Some Carbs Are Better Than Others – Part 4 – the Insulin Index

In previous articles in this series on Some Carbs are Better than Others, I’ve covered both Glycemic Index  (GI) and Glycemic Load (GL) which are useful measures of how easily carbohydrate-based foods raise the blood sugar of healthy people. For those that are insulin resistant or have Type 2 Diabetes, Insulin Index is much more useful because it indicates how much insulin is required for a specific food. Insulin is the hormone that tells our body to store excess energy as glycogen or fat, and that is also responsible for lowering blood sugar.

Unlike GI and GL, the Insulin Index is not limited to carbohydrate-based foods because protein-based foods (have no carbohydrate in them) still cause an insulin response. Some foods that have a low GI or GL result in a lot of insulin being released — and knowing this is important to those who are insulin resistant or have already been diagnosed with Type 2 Diabetes and are working at lowering their fasting insulin levels.

As presented in Part 3 of this series Some Carbs are Better than Other (for Diabetics), I demonstrated how 25 g of carbs made from highly processed flour and sugar produced a very different glucose response a Type 2 Diabetic (me!) than 25 g of carbs of an unrefined (intact) food — even though at the time I did this ‘experiment’,  I had been eating very low carb for over a year.

Why the difference when both had 25 g of carbs?

The 25 g of carbs as a cracker with chocolate was a combination of highly refined white flour and fat (chocolate) which raises blood glucose to a much higher degree than a food that contains carbohydrates alone (see The Perils of Food Processing, Part 2) . The 25g of carbs as intact chickpeas that were cooked from soaked, dry ones were fully intact — as they were prepared with the minimum necessary cooking.  As covered in Part 1 of the series on The Perils of Food Processing, highly refined and carb-based processed foods cause a much higher and more immediate glucose response due to the incretin hormone GIP, than foods with the same number of carbs that has its plant structure intact (i.e. the chickpeas). This explains WHY I had three times the glucose response with the cracker, as I did with the chickpeas — even though both foods had the same amount (25 g) of carbohydrate in them.

What about Insulin Response in response to these two foods?

The 25 g of carbs as a cracker with chocolate would have resulted in a huge stimulation of the gut (incretin) hormone GIP in the upper intestine and resulted in a pronounced release of insulin. The 25 g of carbs as cooked chickpeas would not have resulted in a huge stimulation of GIP because they were intact and as a result, the starch in them was not readily available to the enzyme that digests it (α-amylase). In fact, some of the carbohydrate in the chickpeas would have passed through the gut undigested.

The insulin response of these two foods (each with 25 g of carbohydrate) would have been very different.

What is the Insulin Index?

Shortly after I was diagnosed as having Type 2 Diabetes in 2007, I came across a research paper from 1997 called “An insulin index of foods: the insulin demand generated by 1000-kJ portions of common foods”. In this paper, the Insulin Score of a food was determined by feeding individual foods that contained exactly 239 calories (kcals) / 1000 kilojoules each to non-diabetic subjects and then measuring their insulin response over three hours. The results from each food were then compared to the insulin response of pure glucose, which was assigned an arbitrary value of 100%. The Insulin Index ranks each individual food compared to the insulin response of pure glucose.

Below is a graph from that paper:

Holt S, Brand-Miller J & Petocz P (1997). An insulin index of foods

At the time, the graph was quite puzzling to me as eggs, cheese, fish and beef —which have no carbohydrate in them at all, still caused insulin to be released. It would take close to 10 years for me to better understand this.

As far as I could see, there were two major limitations to the Insulin Index; the first was that there were only 38 foods evaluated. One really can’t make any inferences based on only 38 foods!  The second limitation was that it measured the insulin response in healthy, non-diabetic people.

Last year, I had heard that a PhD researcher from the University of Sydney , under the oversight of Prof. Jennie Brand Miller (who had worked on the original study in 1997) had conducted a research project on the clinical application of the Insulin Index to Diabetes (Type 1). In addition to her thesis, she had also created a database of the Insulin Index of a large number of foods.

This was huge!

As it turned out, some foods that were high in protein and low in fat (such as lean steak or fish) resulted in a large insulin release and foods such as navy beans or All Bran® cereal resulted in a relatively low insulin response. As it turns out, it’s not only the amount of carbohydrate in a food that influences insulin release, but also protein and fiber.

What is especially helpful about the Insulin Index and the database of Insulin Scores is that it enables those with Type 1 or insulin-dependent Type 2 Diabetes to more accurately estimate their injected insulin needs.

However, for those with insulin-dependent Type 2 Diabetes, there is another option.

Results from recent research studies such as the one-year data from the Virta study have been published and demonstrate that reversal of Type 2 Diabetes symptoms is possible — even for those injecting themselves with insulin!

At the beginning of the study, 87% of participants were taking at least one medication for Diabetes but after only 10 weeks of following a well-formulated ketogenic diet, almost 57% had one or more Diabetes medications reduced or eliminated. At the end of a year, sulfonylurea medication was entirely eliminatedInsulin therapy was reduced or eliminated in 94% of of those following the well-formulated ketogenic diet at a year.

For those taking any of the types of medication listed below, following a well-designed ketogenic diet requires one’s doctor’s oversight. As I wrote about in a previous article, medical supervision is absolutely required  before a person changes the amount of their carbohydrate intake if they have been prescribed any of the following medications;

(1) insulin

(2) medication to lower blood glucose such as sodium glucose co-transporter 2 (SGLT2) medication including Invokana, Forxiga, Xigduo, Jardiance, etc. and other types of glucose lowering medication such as Victoza, etc.

(3) medication for blood pressure such as Ramipril, Lasix (furosemide), Lisinopril / ACE inhibitors, Atenolol / β₁ receptor antagonists

(4) mental health medication such as antidepressants, medication for anxiety disorder, and mood stabilizers for bipolar disorder and schizophrenia.

I don’t provide low carbohydrate / ketogenic dietary services those taking insulin (either Type 1 Diabetes or Type 2 Diabetes), I encourage those that are taking it to consult with their endocrinologist and work with a knowledgeable healthcare professional with CDE certification.

As I said previously, people taking any of these medications should not adjust the dosage of their medication without first consulting with their doctor and being instructed by them to do so. The consequences can be very serious, even life-threatening. For example, people taking SGLT2 inhibitors such as Invokana or Jardiance and who decrease insulin dosage suddenly are at increased risk for a life-threatening condition called “Diabetic ketoacidosis (DKA)”.  Medication dosages and timing must be adjusted by a doctor.

If you are not taking insulin — or have been stable for a period of time after having had insulin withdrawn by your doctor, I’d be happy to work with you to coordinate dietary and lifestyle changes with you and your doctor, as they monitor your health and adjust the levels of prescribed medications. In complex cases, I will ask for written consent to coordinate care with your doctor depending on medications you are prescribed, as your doctor will need to know in advance what level of carbohydrates you have been advised to eat, so that they can monitor your health and make adjustments in your medication dosage.

If you have questions as to how I can help you or how I’d work with you and your doctor as they oversee you adopting a low carb lifestyle, please feel free to drop me a note using the Contact Me form on the tab above.

To your good health!

Joy

References

Holt S, Brand-Miller J & Petocz P (1997). An insulin index of foods: the insulin demand generated by 1000-kJ portions of common foods. Am J Clin Nutr 66, 1264-1276. The American journal of clinical nutrition. 66. 1264-76.

Bell K, University of Sydney, School of Molecular and Microbial Bioscience, Clinical Application of the Food Insulin Index to Diabetes Mellitus, May 14, 2014. https://ses.library.usyd.edu.au/handle/2123/11945


Copyright ©2018  BetterByDesign Nutrition Ltd.

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The Perils of Food Processing (Part 2) – what food components and other factors affect the absorption of carbs

This article on the Perils of Food Processing is based on a lecture given by Gabor Erdosi, MSc, MBA– Food News Conference, May 19, 2018 – Prague, Czech Republic.

Part 1 can be read here.


INTRODUCTION: In the first part of this article on the Perils of Food Processing, we considered the effect of different types of simple food processing such as grinding and cooking on the hormonal response of the incretin hormones to carbohydrate intake. While interesting, we rarely eat meals that are only made up carbohydrate, without any fat or protein. Even if we eat a slice of bread or toast and put peanut butter on top, it is now mixture of carbohydrate, fat and protein. How does a ‘mixed meal” with fat and protein affect the body’s hormonal response to carbohydrate?  Does it matter how often we eat, or how fast? This and more are covered in this article.

Response of Incretin Hormones to Meal with Fat and Carbohydrate

In the first study we’re going to look at, the researchers designed a sandwich that produced a very stable glucose response in healthy individuals.  The sandwich was made of 120 g of white bread, 20 g of butter and 10 g of dried meat. As can be seen from curve A, blood sugar rose to ~150 mg/dl (~8.3 mmol/L) and stayed relatively stable for the next 3 hours (180 minutes).

But what happened to the insulin response when these foods were eaten separately and together in a sandwich?

Effect of fat and protein on incretin effect of a mixed meal – – Gabor Erdosi – Food News 2018

Looking at curve B (bottom), it can be seen when subjects ate only the dried meat, blood insulin levels didn’t rise much at first, but then rose a little bit at ~ 90 minutes and stayed relatively constant. When subjects ate only the butter, insulin levels rose a little bit more and then only increased slightly over the next several hours. But when they ate the sandwich with the white bread, butter and dried meat, you can see that blood insulin levels rose quite steeply, beginning before 30 minutes, reaching a maximum level at 60 minutes, and then decreased very slowly over the next several hours. This makes sense, because of the presence of the carbohydrate in the bread.

What is interesting is what happens to the two gut hormones, GIP (from the K-cells) and GLP-1 (from the L-cells) in response to eating these foods.

Contribution of fat and protein to the incretin effect of a mixed meal – – Gabor Erdosi – Food News 2018

Looking at the second curve (graph on the right) it can be seen that in response to the ‘mixed meal’ of the sandwich, GIP from the K-cells (high up in the intestine) is released rapidly and in large amounts. That is, a mixed meal results in a large stimulation of both insulin and glucagon release. Insulin moves the glucose into the cell for storage at the level of the fat cells increases lipoprotein lipase, which increases triglyceride storage. This is an anabolic process of storing nutrients for use later.

As can be seen from the first curve, when a ‘mixed meal’ is eaten, GLP-1 is released from the L-cells lower down in the intestine responded but is much less pronounced. That is, in response to GLP-1 secretion, insulin is released to a small extent, but there is little of the signalling to decrease glucagon, which means little effect on the hunger signal and little satiety (feeling full).

Incretin Response to a Standard Western Diet Meal versus a Paleo-style Meal

In this next study, we can see the same effect in a plant-based meal, using a reference meal and a paleolithic style meal (called PAL2) that both had the same number of calories (~1600 kcals) and very similar macronutrient distributions (carbohydrate, fat, protein). The only difference between the reference diet and the Paleolithic type diet is the amount of processing.

Plant-rich Paleo-type Meal versus Standard Western-type Meal – – Gabor Erdosi – Food News 2018

The reference meal was made up of cooked, long grain rice, mango and boiled carrots, some fish cooked over dry heat and some olive oil.

The paleo type meal was made up of raw strawberries, raw apple, as well as the same significantly more fish cooked over dry heat, raw mushrooms, seedless raisins, zucchini (courgettes), flax seed, cinnamon and capers. While both of these meals had the same number of calories, as can be seen, there was a significant difference in the weight between these two meals – with the reference meal weighing only 248 g, uncooked and the paleo type meal weighing 718 g.

In each of these two types of meals, the response of the two gut incretin hormones, GIP from the upper intestine K-cells and GLP-1 from the lower intestinal L-cells were very different!

Looking at the bottom of the 3 graphs, it can be seen that GIP from the K-cells (high up in the intestine) was released rapidly and in large amounts in the reference meal – a meal that is quite similar to the Standard Western Diet. Recall that the GIP from the K-cells acts on the pancreas to trigger both insulin release from the beta-cells and to trigger glucagon release from the alpha cells. The insulin results in the body storing glucose from the meal and the glucagon release signals the body to release stored glucose, if the blood sugar falls too low. The rise of GIP in response to the paleo-type meal was very slow and gradual and didn’t rise very high, which means that much less insulin was triggered to be released from the pancreas’ beta-cells and much less glucogon was triggered to be released from the alpha-cells.

What happened to GLP-1 release from the L-cells in the lower intestine in response to these two different types of meals?

The Western-type meal (the reference meal) caused a very short rise in GLP-1 from the lower L-cells, which decreased back to baseline quickly.  That means that very little additional insulin was released to move additional glucose into the cells and significantly, there was very little decrease of glucagon which means that appetite was not decreased and there was little to no stimulus to increase satiety (feeling full) and little to no signal to decrease food intake.

The paleo-type meal resulted in significant release of GLP-1, which caused the pancreas to release insulin from the beta-cells and also decreases glucagon release from the alpha-cells of the pancreas – which at the level of the brain, acts to decrease appetite and increase satiety.

This is key; based on this study, a meal based on a Standard Western Diet did not trigger the signal that the body had taken in sufficient food and that appetite could now decrease.

The Effect of Food Texture even Greater than the Effect of Macronutrient Distribution

This next study is very interesting – showing that food texture has an even greater effect on obesity induced from diet than macronutrient content of the diet.

Disrupted food texture versus a high-fat and high sugar diet – – Gabor Erdosi – Food News 2018

The top graph demonstrates that mice fed a “high fat diet” – which was really high in both sugar and fat (not just high in fat) gained significantly more weight than mice fed standard mice chow.

The bottom graph shows that if you take the standard mice chow and grind it fine into a powder and feed it to the mice, they gain weight to the same degree as when fed a diet high in fat and sugar.  That is, the degree of food processing in the diet has at least as great an effect on obesity as the amount of fat and sugar in the diet itself.

There is something about grinding the food that changes the satiety/hunger signal.

Meal Size and Meal Frequency

Common advice given by nutritionists and Dietitians is that it is better to eat small, frequent meals than large meals less often, but there are some studies that support that it as far as hunger and satiety signalling are concerned, it is better to eat fewer, larger meals due to the effect of the incretin hormones.

The Effect of Meal Size and Meal Frequency on Incretin Hormones – – Gabor Erdosi – Food News 2018

[study on right hand side of slide]

After a low-calorie smaller meal, insulin response is proportionately higher compared to a larger meal. That is, a small meal triggers a proportionately greater insulin response that a larger meal, so if one eats small meals frequently, there is an overall greater amount of insulin released than if one eats larger meals less often.

Interestingly, it is the same for those with Type 2 Diabetes.  It is possible to modulate the beta-cell sensitivity to glucose by giving obese people and those with Type 2 Diabetes fewer large meals compared to more frequent smaller meals.

Eating Speed

If one eats more slowly the incretin hormones that trigger satiety (feeling full) are released in a more pronounced manner.  This holds true even when obese subjects eat calorically dense foods such as ice-cream. More of the satiety hormones are released when people eat slowly.

Glycemic Load as a Proxy for the Amount of Carbohydrate Processing

Glycemic Load indicates how a healthy person’s body will respond to amount of carbohydrate in one serving of a food. One usual serving of a food would be considered to have a very high Glycemic Load if it is ≥ 20, a high Glycemic Load if it is between 11-19 and a low Glycemic Load if it is ≤10.

Glycemic Load as a proxy for amount of carbohydrate processing – – Gabor Erdosi – Food News 2018

When one compares the Glycemic Load estimated from ancient diets at the time of the Agricultural Revolution (A on the graph) compared with the Industrial Revolution (B on the graph), the Glycemic Load at the Industrial Revolution is approaching 20, and after that point, continues to go up in an almost vertical manner.  That is, Glycemic Load is a fairly accurate proxy for the degree of food processing of the diet; the more processed the diet, the higher the Glycemic Load.

Amount of Fiber as a Proxy for the Amount of Carbohydrate Processing

This next graph shows the consumption of total carbohydrate over the last century – from 1909-2000 and the amount of carbohydrate from fiber as a percentage.

Consumption of total carbohydrate from 1909-2000 and the amount of carbohydrate from fiber as a percentage – – Gabor Erdosi – Food News 2018

As can be seen, at the beginning of the century, the total amount of carbohydrate started off high and gradually decreased until about 1954, leveled off, then began to increase again. The decrease in the fiber content in carbohydrate-based foods is also evident on this graph from ~ 1960 onward.

What happened?

Perhaps it was the introduction of supposedly “healthy” polyunsaturated vegetable oils (industrial seed oils) in the 1960s that contributed to the dramatic increase in the consumption of ultra-refined carbohydrates.

At the very same time that ultra-refined carbohydrate appeared on the scene, so were novel industrial seed oils – ultra-refined fats.  Perhaps it is the combination of the two in many processed food products which contributed to carbohydrate content of the diet climbing exponentially – and along with it, obesity and metabolic diseases.

Structure and Speed of Absorption

Recall from Part 1 of this article that there are several nutrient-sensing hormones in the small intestine, but with respect to the effect of food processing, SGLT1 is a glucose sensor and both K-cells and L-cells contain this nutrient-sensing receptor.

Intact versus disrupted structure affects the speed of absorption in morbidly obese – Gabor Erdosi – Food News 2018

In the morbidly obese, intestinal glucose absorption high up in the intestine is accelerated due to SGLT-1 from the K-cells.  SGLT-1, along with GIP from the K-cells results in high insulin and high glucagon release, which results in both hyperinsulinemia and hyperglycemia.

Intact structures in grain are not accessible to the digestive enzyme amylase (which breaks down starch to glucose), so when grain is consumed intact, this delays gastric emptying and creates a barrier to starch digestion.  The degree to which grain is intact was found to be more effective in improving glucose metabolism than dietary fiber, irrespective of the type of cereal

Evidence for Why We Get Hungry 3-4 Hours After Eating Refined Carbohydrate

Recall from Part 1, the hormone ghrelin is the only hormone that can increase hunger.

Effect of Eating Refined Carbs on Ghrelin and Blood Glucose – Gabor Erdosi – Food News 2018

Looking at the graph in the top left, we can see that when one eats carbohydrate, ghrelin decreases at first below baseline for the first two hours (120 minutes), but then begins to rise. It continues to rise, exceeding baseline at three hours (180 minutes) and continues rising until four hours; resulting in significantly increased hunger.

At the same time as ghrelin (the hunger hormone) is increasing between 3 and 4 hours after eating refined carbs, serum glucose has dipped below baseline in response to eating refined carbs (as demonstrated in Part 1 of this article) and from 3 hours to 4 hours (180 minutes – 240 minutes), so that serum glucose remains low.

That is, in response to eating refined carbohydrates alone (without combining them with protein) you end up having low blood sugar and feel hungry 3-4 hours later. Blood glucose only gradually begins to increase until it is returns to baseline again at 6 hours (360 minutes).

This next study is a comparison between normal weight and obese people.

Satiety and Hunger Signaling in Normal-Weight and Obese Subjects – Gabor Erdosi – Food News 2018

On the right-hand side, at the top one can see that normal weight people have normal signalling. Satiety (feeling full) goes up and one can see that PYY correspondingly goes up, hunger goes down and correspondingly, ghrelin goes down.

Below that, one can see that in the morbidly obese, their signalling for hunger and satiety is dysregulated. Satiety is going down even after they’ve eaten and correspondingly, PYY shows this dysregulation in that it also goes down. While hunger goes down and the hormone ghrelin also goes down, it is to a much lesser degree that in normal subjects.

So, the obese individuals may feel slightly less hungry, but they don’t feel satiated. This holds true whether obese individuals eat carbohydrate, protein or fat but it is especially pronounced when carbohydrate is eaten. That is, signalling is largely preserved in the morbidly obese when it comes to protein and fat, but it is lost when it comes to carbohydrate.

Obese people should avoid eating diets high in refined carbohydrate because their hunger and satiety signals are dysfunctional and they don’t receive signals that they have eaten.

Here is another study showing that in obese Chinese men, a high protein meal or a high fat meal produces more satiety and better appetite hormonal response after eating than a high carbohydrate meal.

High protein or high fat meal produces more satiety than high carbohydrate meal – Gabor Erdosi – Food News 2018

In another study, different conditions were looked at such as whether it made a difference in the hunger hormone, ghrelin, if the carbohydrate food was eaten first or last.  It turned out that it is best to eat carbs last, as ghrelin continues to decrease for 2 ½ hours (150 minutes) after eating carbohydrate.

This next illustration shows that there is positive feedback mechanism between insulin and GIP.

Insulin drives GIP expression but requires glucose – Gabor Erdosi – Food News 2018

Insulin drives GIP expression but requires glucose to do it. When you eat food with carbohydrate, GIP in the upper intestines is released, resulting in insulin being released. If you keep eating carb-based foods, there is lots of glucose present, which continues to drive the release of more and more GIP, triggering more and more insulin to be released.

This next slide shows a study with two kinds of sugar, sucrose which is ordinary table sugar and isomaltulose, which is made up of the exact same molecules of fructose and glucose, just attached together in a different configuration.

Sucrose’s effect on Plasma Glucose and GIP, GLP-1 – Gabor Erdosi – Food News 2018

As can be seen, sucrose causes a huge spike in plasma GIP secreted from the K-cells high up in the intestine compared to isomaltulose which triggers high insulin and high glucagon release and which results in both hyperinsulinemia and hyperglycemia. Sucrose also results in much lower release of GLP-1 from the L-cells, lower down in the intestine which results in some release of insulin, but a much smaller decreases glucagon so that at the level of the brain, there is less of a decrease in appetite and less of an increase satiety (feeling full).  As a result, eating foods sweetened with sucrose results in higher glucose, higher insulin, very little decrease in appetite, less feeling full and less decreased food intake, compared with isomaltulose.

As a result, sustained feeding with sucrose in mice results in insulin resistance and fatty liver.

Differential Effect of eating Sucrose with a Meal or Alone – Gabor Erdosi – Food News 2018

If these sugars are eaten with a meal, instead of alone, the effect on blood glucose and insulin is removed, but GIP release is still triggered to be released to a large extent compared with isomaltulose, and fatty liver persists in the mice in the sucrose group.

The Effect of Combining Refined Carbohydrates with Fat

As can be seen from the graph on the left hand side at the bottom, when refined carbs are combined with fat, there is a huge response of GIP.

Effect of having Fat with Carbohydrate-based Food – Gabor Erdosi – Food News 2018

Eating boiled potato and low-fat veal didn’t result in this effect but the addition of butter to the potato dramatically changed this.

From an evolutionary perspective it makes sense, because there are no naturally occurring cases where a food has both high carbohydrates and high fat at the same time.  Our body’s have not evolved to see these two macronutrients together.

The following is from a recent overview from May 2018 which provides a summary of GIP actions in response to a high Glycemic Index meal.

Summary of actions of GIP in response to a high Glycemic Index meal – Gabor Erdosi – Food News 2018

When high GI carbohydrate food is eaten and passes through digestion in the stomach and then as it enters the upper small intestine, the K-cells release GIP which has several actions, including decreasing lipolysis, increasing insulin secretion in the pancreas, decreasing fat oxidation, increasing the AKT-mTOR pathway in the brain, and increasing fat storage in the liver.

How Does Bariatric Surgery / Gastric Bypass Work

Many people assume that the reason gastric bypass works is because the stomach is made smaller, so that the person cannot overeat, but this is not primarily what makes it effective.

Bariatric Surgery / Gastric Bypass – Gabor Erdosi – Food News 2018

But what occurs within a week of the Roux-en-Y gastric bypass surgery is that there is a dramatic change in the balance of the incretin hormones.

Effect of Roux-en-Y Bypass Surgery on Incretin Hormones; first two weeks – Gabor Erdosi – Food News 2018

After only a week, GIP release is ½ what it was before the surgery and GLP-1 is almost doubled.

These changes in only a week are not a result of weight loss, but of the surgery’s impact on correcting the imbalance in the incretin hormones – essentially causing an ‘opposite imbalance’ which corrects the defect cause by the Type 2 Diabetes and overeating of ultra-refined carbs.

There are other types of surgical interventions, such as the Duodenal-Jejunal bypass liner tube that impact incretin hormones, as well as numerous medications. There are selective sodium-dependent glucose transporter 1 inhibitors that block glucose absorption and impair GIP release in the same way that a roux-en-Y gastric bypass does.

“Gastric Bypass in a Pill” – Gabor Erdosi – Food News 2018

There are also numerous other medications such as sodium-glucose co-transporter 2 inhibitors, Glucagon-like Peptide 1 Agonists, and Dipeptidyl Peptidase 4 Inhibitors that impact the incretin hormones to varying degrees (and even some that claim to and do nothing!).

Numerous Other Medications Used to Impact Incretin Hormones – Gabor Erdosi – Food News 2018

…and there are low carbohydrate diets that significantly reduce the release of GIP from the K-cells, because there are low levels of carbohydrate consumed at any one time to trigger it’s release.  As a result, significantly less insulin is release, which is how LCHF diets followed over time lower insulin resistance.

Effect of a Low Carbohydrate Diet on GIP – Gabor Erdosi – Food News 2018

Summary of Part 1 and Part 2 of the Perils of Food Processing

  • Speed and location of intestinal nutrient absorption is crucial in determining metabolic response to a food
  • The greatest effect in incretin hormone response is seen with carbohydrate rich plant processing, therefore retaining the plant or grain structure as much as possible is crucial
  • Diets high in ultra-refined, quick absorbing food plausibly results in altered intestinal hormonal profile, altered hunger / satiety signalling and as a result higher food intake and increased meal frequency
  • The above effect is exaggerated when ultra-processed carbohydrates are consumed in combination with significant amounts of fat (the “doughnut effect”).
  • GIP may be part of a “thrifty mechanism” in mammals; easily digestible, high energy density foods overstimulate it (think “honey” to hunter-gatherers).

Practical “Takeaways”

  • Processing of food that are high in fat and protein has little effect on intestinal hormone levels, so prioritize food items in terms of desired amount of macronutrients
  • Plant or grain foods (carbohydrate containing) should be carefully selected based on their most dense, undisturbed structure. Processing, whether grinding, pureeing or cooking disrupts the plant / grain structure and accelerates absorption of the carbohydrate, which triggers an intestinal hormonal response which results in reduced satiety. Excluding most carbohydrate-based foods also solves this problem
  • Consume carbohydrate foods at the end of the meal (after protein and fat foods)
  • Have fewer, larger meals vs small, frequent ones. Avoid “snacking” between meals
  • Eat meals slowly to maximize the satiety effect and increase the release of the lower intestinal hormones.

Perhaps you wonder what all this information means for you. How should this information change the way you eat and what you eat?  What does this mean in practical terms when planning dinner, or eating dinner – especially if you have Type 2 Diabetes or insulin resistance and also if you are well now, but have a family history with many common metabolic disorders.  How can you change how you eat to stay well?

I can help.

Please send me a note using the “Contact Me” form located on the tab above to find out information about the services I offer (in-person or via Distance Consultation using telephone or Skype) and I will reply shortly.

To your good health!

Joy

 


The full lecture can be watched here:

References

(continued from Part 1)

16. Carrel, G., L. Egli, C. Tran, P. Schneiter, V. Giusti, D. D’Alessio, and L. Tappy. “Contributions of Fat and Protein to the Incretin Effect of a Mixed Meal.” American Journal of Clinical Nutrition 94, no. 4 (2011):
997–1003.

17. Bligh, H. Frances J., Ian F. Godsland, Gary Frost, Karl J. Hunter, Peter Murray, Katrina MacAulay, Della Hyliands, et al. “Plant-Rich Mixed Meals Based on Paleolithic Diet Principles Have a Dramatic Impact on
Incretin, Peptide YY and Satiety Response, but Show Little Effect on Glucose and Insulin Homeostasis: An Acute-Effects Randomized Study.” British Journal of Nutrition 113, no. 04 (2015): 574–84.

18. Desmarchelier, Charles, Tobias Ludwig, Ronny Scheundel, Nadine Rink, Bernhard L. Bader, Martin Klingenspor, and Hannelore Daniel. “Diet-Induced Obesity in Ad Libitum-Fed Mice: Food Texture Overrides the Effect of Macronutrient Composition.” British Journal of Nutrition 109, no. 08 (2013): 1518–27.

19. Vilsbøll, T., T. Krarup, J. Sonne, S. Madsbad, A. Vølund, A. G. Juul, and J. J. Holst. “Incretin Secretion in Relation to Meal Size and Body Weight in Healthy Subjects and People with Type 1 and Type 2 Diabetes
Mellitus.” The Journal of Clinical Endocrinology & Metabolism 88, no. 6 (2003): 2706–13.

20. Alsalim, Wathik, Bilal Omar, Giovanni Pacini, Roberto Bizzotto, Andrea Mari, and Bo Ahrén. “Incretin and Islet Hormone Responses to Meals of Increasing Size in Healthy Subjects.” The Journal of Clinical
Endocrinology & Metabolism 100, no. 2 (2015): 561–68.

21. Koopman, Karin E., Matthan W.A. Caan, Aart J. Nederveen, Anouk Pels, Mariette T. Ackermans, Eric Fliers, Susanne E. la Fleur, and Mireille J. Serlie. “Hypercaloric Diets with Increased Meal Frequency, but Not Meal Size, Increase Intrahepatic Triglycerides: A Randomized Controlled Trial.” Hepatology 60, no. 2 (2014): 545–53.

22. Stote, Kim S., David J. Baer, Karen Spears, David R. Paul, G. Keith Harris, William V. Rumpler, Pilar Strycula, et al. “A Controlled Trial of Reduced Meal Frequency without Caloric Restriction in Healthy, Normal-Weight, Middle-Aged Adults.” The American Journal of Clinical Nutrition 85, no. 4 (April 1, 2007): 981–88.

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25. Rigamonti, A. E., F. Agosti, E. Compri, M. Giunta, N. Marazzi, E. E. Muller, S. G. Cella, and A. Sartorio. “Anorexigenic Postprandial Responses of PYY and GLP1 to Slow Ice Cream Consumption: Preservation in
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37. Pfeiffer, Andreas F.H., and Farnaz Keyhani-Nejad. “High Glycemic Index Metabolic Damage – a Pivotal
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38. Collier, G., and K. O’Dea. “The Effect of Coingestion of Fat on the Glucose, Insulin, and Gastric Inhibitory Polypeptide Responses to Carbohydrate and Protein.” The American Journal of Clinical Nutrition 37, no. 6 (June 1, 1983): 941–44.

39. McClean, P. L., N. Irwin, R. S. Cassidy, J. J. Holst, V. A. Gault, and P. R. Flatt. “GIP Receptor Antagonism Reverses Obesity, Insulin Resistance, and Associated Metabolic Disturbances Induced in Mice by Prolonged
Consumption of High-Fat Diet.” AJP: Endocrinology and Metabolism 293, no. 6 (October 23, 2007):E1746–55.

40. Ceperuelo-Mallafré, Victòria, Xavier Duran, Gisela Pachón, Kelly Roche, Lourdes Garrido-Sánchez, Nuria Vilarrasa, Francisco J. Tinahones, et al. “Disruption of GIP/GIPR Axis in Human Adipose Tissue Is Linked
to Obesity and Insulin Resistance.” The Journal of Clinical Endocrinology & Metabolism 99, no. 5 (May 2014): E908–19.

41. Gögebakan, Özlem, Martin A. Osterhoff, Rita Schüler, Olga Pivovarova, Michael Kruse, Anne-Cathrin Seltmann, Alexander S. Mosig, Natalia Rudovich, Michael Nauck, and Andreas F. H. Pfeiffer. “GIP Increases Adipose Tissue Expression and Blood Levels of MCP-1 in Humans and Links High Energy Diets to Inflammation: A Randomised Trial.” Diabetologia 58, no. 8 (August 2015): 1759–68.

42. Mohammad, S., R. T. Patel, J. Bruno, M. S. Panhwar, J. Wen, and T. E. McGraw. “A Naturally Occurring GIP Receptor Variant Undergoes Enhanced Agonist-Induced Desensitization, Which Impairs GIP Control of
Adipose Insulin Sensitivity.” Molecular and Cellular Biology 34, no. 19 (2014): 3618–29.

43. Nie, Y., R. C. Ma, J. C. N. Chan, H. Xu, and G. Xu. “Glucose-Dependent Insulinotropic Peptide Impairs Insulin Signaling via Inducing Adipocyte Inflammation in Glucose-Dependent Insulinotropic Peptide
Receptor-Overexpressing Adipocytes.” The FASEB Journal 26, no. 6 (2012): 2383–93.

44. Timper, K., J. Grisouard, N. S. Sauter, T. Herzog-Radimerski, K. Dembinski, R. Peterli, D. M. Frey, et al. “Glucose-Dependent Insulinotropic Polypeptide Induces Cytokine Expression, Lipolysis, and Insulin
Resistance in Human Adipocytes.” AJP: Endocrinology and Metabolism 304, no. 1 (2012): E1–13.

45. Miyawaki, Kazumasa, Yuichiro Yamada, Nobuhiro Ban, Yu Ihara, Katsushi Tsukiyama, Heying Zhou, Shimpei Fujimoto, et al. “Inhibition of Gastric Inhibitory Polypeptide Signaling Prevents Obesity.” Nature
Medicine 8, no. 7 (2002): 738–42.

46. Boylan, Michael O., Patricia A. Glazebrook, Milos Tatalovic, and M. Michael Wolfe. “Gastric Inhibitory Polypeptide Immunoneutralization Attenuates Development of Obesity in Mice.” American Journal of
Physiology – Endocrinology And Metabolism 309, no. 12 (2015): E1008–18.

47. Nasteska, D., N. Harada, K. Suzuki, S. Yamane, A. Hamasaki, E. Joo, K. Iwasaki, K. Shibue, T. Harada, and N. Inagaki. “Chronic Reduction of GIP Secretion Alleviates Obesity and Insulin Resistance Under High-Fat
Diet Conditions.” Diabetes 63, no. 7 (2014): 2332–43.

48. Althage, M. C., E. L. Ford, S. Wang, P. Tso, K. S. Polonsky, and B. M. Wice. “Targeted Ablation of Glucose-Dependent Insulinotropic Polypeptide-Producing Cells in Transgenic Mice Reduces Obesity and
Insulin Resistance Induced by a High Fat Diet.” Journal of Biological Chemistry 283, no. 26 (2008): 18365–76.

49. Calanna, S., F. Urbano, S. Piro, R. M. Zagami, A. Di Pino, L. Spadaro, F. Purrello, and A. M. Rabuazzo. “Elevated Plasma Glucose-Dependent Insulinotropic Polypeptide Associates with Hyperinsulinemia in
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50. Chia, Chee W., Juliana O. Odetunde, Wook Kim, Olga D. Carlson, Luigi Ferrucci, and Josephine M. Egan. “GIP Contributes to Islet Trihormonal Abnormalities in Type 2 Diabetes.” The Journal of Clinical Endocrinology & Metabolism 99, no. 7 (July 2014): 2477–85.

51. Chen, Shu, Fumiaki Okahara, Noriko Osaki, and Akira Shimotoyodome. “Increased GIP Signaling Induces Adipose Inflammation via a HIF-1α-Dependent Pathway and Impairs Insulin Sensitivity in Mice.” American
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Copyright ©2018 BetterByDesign Nutrition Ltd.

LEGAL NOTICE: The contents of this blog, including text, images and cited statistics as well as all other material contained here (the “content”) are for information purposes only.  The content is not intended to be a substitute for professional advice, medical diagnosis and/or treatment and is not suitable for self-administration without the knowledge of your physician and regular monitoring by your physician. Do not disregard medical advice and always consult your physician with any questions you may have regarding a medical condition or before implementing anything  you have read or heard in our content.

A New Study Explains Why Carbs and Fat Together are Irresistible

A study that is due to be published on July 3, 2018 in the scientific journal Cell Metabolism is the first to demonstrate that compared to foods high in carbs or fat, foods with both carbs and fats together result in much more dopamine being released from the striatum, which is the reward-center of our brain [1]. Dopamine is the same neurotransmitter that is released during sex and that is involved in the addictive “runner’s high” familiar to athletes. This is one powerful neurotransmitter!

It is thought that there are separate areas of the brain that evaluate carb-based foods and fat-based foods and both are involved in the release of dopamine, but when carbs and fat appear in the same food together, this results in what the researchers called a “supra-additive effect“. That is, both areas of the brain get activated at the same time, resulting in much more dopamine being released and a much bigger feeling of “reward” being produced.

This combination of carbs and fat in the same food is why we find foods such as French fries, donuts and potato chips irresistible.

In fact, the study found that people were willing to pay more for foods that combine both carbs and fat than for foods that were only high in carbs but not fat such as candy, or only high in fat but not carbs, such as cheese.

This powerful reward-system involving dopamine is why we will choose the fries over the baked potato and why we have no difficulty wolfing back a few donuts, even when we’ve just eaten a meal.

This “supra-additive effect” on the pleasure center of our brain, along with the fact that more insulin is released when both carbs and fat are eaten together[2] may help explain the roots of the current obesity epidemic and the metabolic diseases such as Type 2 Diabetes that go along with it.

Carbohydrate intake was high in the early 1900s and gradually decreased until about 1954, leveled off, then began to increase again[3]. What caused that to occur? At that time, ultra-refined carbohydrates began appearing in the market and these by their very nature were devoid of the whole, unprocessed grain that slows the release of insulin [3]. Excess release of insulin triggered by the constant eating of ultra-refined carbohydrate foods underlies the process of how insulin resistance develops and in time, how Type 2 Diabetes develops [3].

The early 1950’s was also when the “diet-heart hypothesis” proposed by Ancel Keys took root, along with the recommendation that Americans (and later, Canadians) reduce their consumption of saturated fat (more in this article).  With the recommendation to decrease saturated fat was the necessity to create fats to replace them, which is when and why both soybean oil and later, canola oil were created (see this article for more information). These industrial seed oils began to replace natural fats such as butter, lard and tallow in home and restaurant cooking, frying and baking.

With the creation of "polyunsaturated vegetable oils", French fries were now a healthy food - after all, they were vegetables fried in "healthy polyunsaturated fat". 

What could possibly go wrong?

This new study provides the missing link as to the mechanism by which the “perfect storm” was created. That “perfect storm” was the simultaneous appearance in the late 1950s and early 1960s of ultra-refined carbohydrates and industrial seed oils (promoted as “heart healthy” by the American and Canadian Dietary Guidelines) that literally hijacked the reward system of our brain!

Is there little wonder why rates of overweight and obesity began rising at in the early 1960s and have continued to rise dramatically ever since?

As far as our brains are concerned, French fries are much more desirable than a baked potato and donuts and pastry much more desirable than toast because they literally make us feel good!  Eating French fries and pastry results in considerably more dopamine being released than eating baked potato or plain toast. Eating these foods produce something comparable to a “runner’s high” in people that have never run a block or have even gotten off the couch!

While discovery of the dopamine-centered mechanism is new to this study, the food industry has known for some time that processed foods containing both carbohydrate and fat will result in people coming back and buying more and more of their product. Carbs and fat is why Pringles® chips could boast “betcha can’t eat just one!“, but it’s not just Pringles®. This combination of carbs and fat is in all processed foods; from so-called “junk food” such as chips and Cheezies® to foods that are perceived as “healthy foods”, such as granola bars and commercial peanut butter.

Carbs and fats together are the essence of “fast food” – from Big Macs® dripping with cheese and mayo sandwiched between several buns, to French fries of all types, super-sized or not.  People may joke about “junk food being addictive”, however understanding the “supra-additive” effect of carbohydrate combined with fat makes these foods as addictive to our brains as a “runner’s high” is to an athlete, or what makes people seek out sex. Addictive? Maybe not in the truest sense of the word except in cases of food addiction, but certainly in the rest of us there is a powerful draw to want to eat them.

Knowing and understanding this mechanism is of no small consequence! It should inform our food choices.

We need to be aware of foods that we eat that “hijack” our appetites. They could be “healthy foods” like cashews that are both high in fat and high in carbohydrate.  Given what we know about the triggering of the reward system in the brain, should those of us with current or past weight problems have them around?

Another way this knowledge should inform our food choices is around the concept of “cheat days”.  People who see me seeking weight loss often ask me about whether they can have one day a week, or one day a month where they eat “cheat foods”.  Knowing the very potent chemically-mediated reward system involved with eating foods such as pizza or French fries or ice cream, do you think these are foods that are helpful to eat once a week, or once a month? How much will eating those foods cause you to crave them later, after your “cheat day”? Is it worth it?

From a purely academic perspective, knowing the mechanism also helps explains why metabolically healthy people can lose weight either following a low-fat diet or a low-carb diet, because it is the combination of both carbs and fats that stimulate the reward centers.

Note: a low-carb approach is preferable for people who have have already become insulin resistant or diagnosed with Type 2 Diabetes because they are no longer able to handle more than small amounts of carbohydrate at a time without it significantly impacting their blood sugar (and insulin) levels.

So, knowing that eating carbs and fat together result in a huge release of dopamine and light up the reward-centers of our brain, how should we choose foods differently?

This is where I can help.

Do you have questions about how I can help you eat healthier and reduce food cravings? Would you like information about having me design a Meal Plan for you to help you reach your health and nutrition goals?

Please send me a note using the “Contact Me” tab above and I will reply as shortly.

To our good health,

Joy

References

  1. Di Feliceantonio et al., 2018, Supra-Additive Effects of Combining
    Fat and Carbohydrate on Food Reward, Cell Metabolism 28, 1–12
  2. Carrel, G., L. Egli, C. Tran, P. Schneiter, V. Giusti, D. D’Alessio, and L. Tappy. “Contributions of Fat and Protein to the Incretin Effect of a Mixed Meal.” American Journal of Clinical Nutrition 94, no. 4 (2011):997–1003.
  3. Gross, Lee S., Li Li, Earl S. Ford, and Simin Liu. “Increased Consumption of Refined Carbohydrates and the Epidemic of Type 2 Diabetes in the United States: An Ecologic Assessment.” The American Journal of Clinical Nutrition 79, no. 5 (2004): 774–779.
  4. O’Dea, K., Nestel, P.J., and Antonoff, L. “Physical Factors Influencing Postprandial Glucose and Insulin Responses to Starch” 33, no. 4 (April 1, 1980): 760–65. https://doi.org/10.1093/ajcn/33.4.760.

Copyright ©2018 BetterByDesign Nutrition Ltd.

LEGAL NOTICE: The contents of this blog, including text, images and cited statistics as well as all other material contained here (the “content”) are for information purposes only.  The content is not intended to be a substitute for professional advice, medical diagnosis and/or treatment and is not suitable for self-administration without the knowledge of your physician and regular monitoring by your physician. Do not disregard medical advice and always consult your physician with any questions you may have regarding a medical condition or before implementing anything  you have read or heard in our content.

10 Common Myths about a Low Carb Diet

I keep coming across the same misconceptions about a “low carb diet” in online articles and on social media, so I decided to write an article dispelling the 10 most common myths.

Myth 1: “A low carb diet will cause clogged arteries and heart attacks because it is too high in saturated fat.”

A recent study[1] published at the end of March 2018 in Nutrients looked at health and nutrition data from 158 countries worldwide and found that total fat and animal fat consumption were least associated with the risk of cardiovascular disease, so even if someone following a low carb diet chose to eat foods high in saturated fat, it does not mean they are necessarily at higher risk of heart attacks or strokes.

Secondly, a low carb diet does not necessarily have to be high in saturated fat. In fact,  it may have very little added fat at all such as when people are aiming to lose weight, so that they burn more of their own body fat.

While there is no increased risk with eating the saturated fat that is naturally found in meat (chicken, beef, pork, etc.), except for specific clinical requirements (for example, a ketogenic diet for epilepsy) there is no reason anyone has to add additional saturated fat. There are other sources of fat that are delicious and have beneficial properties, such as monounsaturated fats found naturally in olive oil and avocados and their oils.

Myth 2: “A low carb diet has way too much protein in it!”

There are different types of low carb diets and a low carb diet may not necessarily have a lot of protein – whether as eggs, cheese, meat, or fish.

In a very low carb (ketogenic) diet used for epilepsy, the diet is mostly fat, however in a low carb diet used for weight loss and improving metabolic conditions such as Type 2 Diabetes or high blood pressure, the amount of protein will be moderate.

How much protein is “too much”?

The RDA for Protein is set at 56 gm per day (based on 0.8 g protein per kg of body weight) is the minimum amount to prevent deficiency.  This is not the optimal amount, but the absolute minimum amount. So, whether a given person is eating 1200 calories a day or 2500 calories per day they have an absolute requirement for 56 gm of protein per day[2].

The maximum amount of protein per day is set at ~200 g / day and is calculated based on >2.5 g protein per kg of body weight, and the range from 56 g to 200 g of protein per day is referred to as the range of safe intake[2].

According to Dr. Donald Layman, Professor Emeritus of Human Nutrition from the University of Illinois, a high protein diet doesn’t start “until well above 170 g / day”[2].

Everybody’s needs for protein is different and many people, especially adults and older adults are either not getting enough protein or it is mostly at dinner, with little at breakfast and lunch, which is a concern in older adults, as it puts them at risk for sarcopenia, the muscle wasting often seen in older adults eating a Westernized diet.

In any case, most low carb diets aren’t anywhere near the level of what is considered a “high protein diet”, let alone “too high in protein”.

Myth 3: “Low Carb Diets involve eating lots of meat”.

While there are some, especially those involved in the body-building or body-sculpting world that choose to follow a variation of a low-carb diet which involves eating lots of meat (and protein, in general), there are some variations of a low-carb diet that don’t involve eating meat at all.  As mentioned above, ketogenic diets used for those with epilepsy or seizure disorder are mostly fat and ketogenic diets used as an adjunct therapy in treatment of specific types of cancer are often mostly fat, as well depending on the specific type of cancer.

Therapeutic low carb or ketogenic diets used for weight loss or improving metabolic conditions such as Type 2 Diabetes, high blood pressure and abnormal cholesterol may be based on a moderate amount of protein, with some of that as meat if the individual eats it and enjoys it. To eat low-carb,  there is no requirement to eat meat at all.

A low carb diet can be designed to accommodate pescatarians (those that only eat fish), as well as vegetarians. There are even some vegans that choose to follow a low carb diet for a variety of reasons, although getting enough of all nutrients is a major challenge, just as it is for those following a Standard American/Canadian Diet.

Myth 4: “Low carb diets are dangerous because the brain needs a certain amount of carbohydrate”.

Except for erythrocytes (red blood cells) every cell in the body has mitochondria (the so-called “powerhouse of the cell”). The mitochondria can use a variety of fuel sources and turn it into Acetyl-CoA, which then enters the Kreb’s Cycle and generates Adenosine Triphosphate (ATP) which is what every cell in the body requires for life. The brain is no different than any other cell in the body that has mitochondria, as it can efficiently and safely use Acetyl-CoA can be made from carbohydrate (e.g. glucose), ketone bodies (a byproduct of fatty acid breakdown) and amino acids from protein to generate Acetyl-Coa. Most parts of the brain have no requirement for dietary carbohydrate, as it can use ketones generated from fat breakdown.

Certain parts of the brain and red blood cells do need glucose (approximately 30 g a day) and that need is fulfilled by a process called gluconeogenesis where glucose is made by the liver and kidneys from substrates other than carbohydrate, including amino acids (from proteins) or glycerol  (from fat breakdown).

In fact, the human body doesn’t require any dietary carbohydrate provided the amount of protein and fat in the diet is sufficient (to be used as substrates, as mentioned above); from page 275 of Dietary Reference Intakes for Energy, Carbohydrate, Fiber, Fat, Fatty Acids, Cholesterol, Protein and Amino Acids (2005)[3];

The lower limit of dietary carbohydrate compatible with life apparently is zero, provided that adequate amounts of protein and fat are consumed. 

This does not mean that low carb diets contain no carbohydrate!

As mentioned above, some liberal low carb diets have enough carbohydrate such that the person does not go into ketosis, while therapeutic ketogenic diets (done under medical supervision) such as those used for the management of epilepsy or as an adjunct to cancer treatment may have < 30 g of carbohydrate.

Myth 5: “A Low carb diet is imbalanced and causes nutrient deficiencies”.

With the exception of a therapeutic ketogenic diet for epilepsy or as an adjunct to cancer treatment, eating a well-formulated low-carb diet provides adequate nutrients, even those such as thiamine (vitamin B1) and folate which are normally associated with grain products. There are many low-carb sources of thiamine, including pork, chicken liver, macadamia nuts and peanuts, flax-seed and asparagus and just 1 serving of each of these can meet an adult’s daily requirement.

Likewise, there are many low-carb sources of folate (vitamin B9), including the low carb leafy vegetables that are abundant in a well-formulated low carb diet, as well as other green vegetables such as asparagus, spinach, Brussels Sprouts and avocado.

Vitamin C is plentiful in foods outside of citrus fruit, including red and green bell pepper, broccoli, cauliflower and strawberries, as well as in lemon and lime that can be used as a seasoning for salad dressing, fish or to flavour water.

Calcium is easily obtained from well-designed meal plans that include cheese and yogurt, fish (such as sardines and canned salmon), almonds and leafy vegetables such as spinach, collards and kale.

A well-designed low carb diet provides a wide range of foods; from cheese and other dairy products, nuts, seeds, fruit, low carb vegetables and meat, fish and poultry and can provide the essential nutrients that a healthy body requires, including vitamins and minerals.

The only two nutrients that will likely be sub-optimal are vitamin D and magnesium– but are certainly not provided in lesser amounts than in the average Canadian or American diet. I advocate for supplementation of both of these nutrients, whether someone is following a Standard American or Canadian diet or a low-carb diet.

Myth 6: “Low carb diets are so restrictive”.

This is one of the two myths that I often joke about around the dinner table, because the food we eat is anything but restrictive.

People can eat a huge variety of vegetables and meat, fish and poultry which require the minimum of cooking and food preparation so even for someone with little or no cooking skill or time to prepare food, a well-designed low carb diet is entirely possible.  I design them for clients all the time, because many people fall into this category or live alone and don’t want to cook elaborate meals for themselves.

For those that enjoy cooking and have the time to do it there are very few, if any traditional foods that can not be made low carb – and made very tasty! 

There is almost no recipe that can’t be easily adapted for those that choose to eat low carb because food should not only be healthy, but enjoyable.

Myth 7: “Low carb diets are not sustainable”.

This is the second myth that makes me chuckle, because I know of people that have been eating this way for 15 or 20 years which in and by itself demonstrates it is quite sustainable. There are one-year and two-years studies on this web page the also indicate that a well designed low carb diet is quite sustainable.

What is “not sustainable“ about eating fresh, healthy, whole foods that can be prepared with a minimum of cooking or as elaborate as one’s imagination allows?

Myth 8: “Low carb diets require you to constantly count carbs and check your ketone levels”.

First of all, a well-designed low carb Meal Plan does all the “carb counting” for you – all you need to do is decide what you want to eat. This is no different whether someone eats a moderate amount of carbs or a low amount of carbs. In fact, how foods are grouped on your Meal Plan, you’ll know how many carbs are in one serving any food in that group, should you want to add something to your Meal Plan.

As far as checking ketones, unless one is on a low level of carbohydrates (ketogenic diet) and either has certain health conditions or taking specific medications, there is no need.

Myth 9: “It doesn’t matter if you eat low carb or low fat, the only thing that matters is Calories In Calories Out”.

This answer may stir up some controversy, because there is a wide range of opinion on this.

Some advocates of a low-carb diet insist that Calories In Calories Out (CICO) is irrelevant because metabolism is different when one eats low carb. Some advocates of a low-fat diet will say that low-carb only works because in the end, people eat less calories.

I think it is “both / and not “either / or”.

Most low-fat diets are calorie-restricted diets and when calories are restricted, people’s metabolism slows down.  That is why people following a  carbohydrate-based low-calorie diet feel cold, tired and lethargic; because their body is conserving the calories it is getting for important metabolic functions. Because the body is primarily using carbohydrate as fuel, fat stores are only accessed when carbohydrate is restricted – which also slows down metabolism.

When people are eating a diet that is low in carbohydrate and which has sufficient protein, and is higher in a variety of fats, people’s bodies are mainly using fat as fuel. If their Meal Plan is designed for weight loss, then some of the fat they are using for fuel is their own fat stores – so ‘fuel’ is never restricted.  If the body needs more energy, it will take the “extra” it needs from fat stores. In this way, the body doesn’t have to slow metabolism to conserve energy, because there is always more fat in the person’s fat stores. Eating a diet based predominantly based on healthy fats and protein with much lower level of carbohydrates makes people feel full after eating much less, so the end result is that they generally eat less calories, which is why they are able to lose weight.

That is, a calorie is still a calorie but all fuels are not considered equal.

Myth 10: “Ketones are dangerous and you can die from them!”

Unfortunately, this is way too common a myth – even one in which some healthcare professionals are confused.

Ketones are naturally produced in our bodies during periods of low carb intake, in periods of fasting for religious or medical tests, and during periods of prolonged intense exercise. This state is called ketosis. It is normal and natural and something everyone’s body does when using glucose as its main fuel source.

Once our glycogen levels are used up, fat is broken down for energy and ketone bodies are a byproduct of that. These ketones enter into the mitochondria of the cell and are used to generate energy (as ATP) to fuel our cells.

Ketosis is a normal, physiological state and we may produce ketones after sleeping all night, if we haven’t gotten up and eating something in the middle of the night.

Ketoacidosis on the other hand is a serious medical state that can occur inuntreated or inadequately treated Type 1 Diabetics, where the beta cells of the pancreas don’t produce insulin. It may also occur in those with Type 2 Diabetes who decrease their insulin too quickly or who are taking other kinds of medication to control their blood sugars.

In inadequate management of Type 1 Diabetes or in insulin-dependent Type 2 Diabetes, ketones production will be the first stage in ketoacidosis. This is not the case when the above medical issues are not present.

Final Thoughts…

There is a wide range of low-carb diets with various levels of carbohydrate, protein and fat. Some are high in meat, others low in meat, while others have no meat at all. Some are very high in protein and others are very high in fat. Some promote weight loss, others make it very difficult. There are different types of low carb diets because they are used for different purposes.

Each person’s requirement for protein is different, so following a generic “low carb diet” downloaded from the internet will be based on an ‘average’ amount of protein for adults and not your needs . The amount of fat you will be encourage to eat will be based around the protein needs that are set by the web page. If you are wanting to lose weight, very often you may find that you lose a bit at first and then weight plateaus for extended periods of time.  Many of my clients come to me after trying this approach, feeling that a “low carb diet doesn’t work for me”.  The issue very often is that the plan wasn’t designed for “them” at all.

Most general types of “low carb diets or plans” allow people to select the level of carbohydrate they want to limit. Often, people will choose a ketogenic level because they want to lose weight quickly, with little regard for making sure they are getting sufficient nutrients.

For otherwise healthy young adults with no major risk factors and who are not taking any medications, this might work out fine however for adults with medical or metabolic conditions – and especially for those taking medications for Diabetes or high blood pressure, this can put them at significant risk. As outlined in more detail in a previous article, medical supervision is absolutely required before a person changes the level of  their carbohydrate intake if they are taking;

(1) insulin

(2) medication to lower blood glucose such as sodium glucose co-transporter 2 (SGLT2) medication including Invokana, Forxiga, Xigduo, Jardiance, etc.

(3) medication for blood pressure such as Ramipril, Lasix (furosemide), Lisinopril / ACE inhibitors, Atenolol / β₁ receptor antagonists

or

(4) mental health medication such as antidepressants, medication for anxiety disorder, and mood stabilizers for bipolar disorder and schizophrenia.

For everyone who does not fall into the above category, it’s important to realize that there is a very big difference between a generic meal plan downloaded from a “low-carb” website and one designed just for you, based on your physiological needs and ensuring that you get adequate nutrients based on your own medical history and family risk factors. For a low-carb style diet to provide the nutrients that you need for your age, gender and activity level, it needs to be designed for you; factoring in your need for specific nutrients.  It’s not simply a matter of choosing a level of “macronutrients”  (“macros”) such as carbohydrate, fat and protein, but ensuring adequate “micronutrients”, too. That is the difference between having an Individual Meal Plan designed specifically for you by a knowledgable Registered Dietitian and one that is based on general cutoff points.

For this to be a way of eating that is balanced in terms of overall nutrients and will meet specific health goals and which is healthy and interesting enough to be sustainable over the long term, it needs to be carefully designed for each individual.

Do you have questions about how I can help design a Meal Plan for you? Or for you and your partner?

Please send me a note using the Contact Me form located on the tab above and I will reply shortly.

To your good health!

Joy

References

  1. Skeaff CM, PhD, Professor, Dept. of Human Nutrition, the University of Otago, Miller J. Dietary Fat and Coronary Heart Disease: Summary of Evidence From Prospective Cohort and Randomised Controlled Trials, Annals of Nutrition and Metabolism, 2009;55(1-3):173-201
  2.  Layman, Donald, The Evolving Role of Dietary Protein in Adult Health, Nutrition Forum, British Columbia, Canada, June 23, 2013 https://youtu.be/4KlLmxPDTuQ
  3. Dietary Reference Intakes for Energy, Carbohydrate, Fiber, Fat, Fatty Acids, Cholesterol, Protein and Amino Acids (2005), pg 275

Copyright ©2018  BetterByDesign Nutrition Ltd.

LEGAL NOTICE: The contents of this blog, including text, images and cited statistics as well as all other material contained here (the “content”) are for information purposes only.  The content is not intended to be a substitute for professional advice, medical diagnosis and/or treatment and is not suitable for self-administration without the knowledge of your physician and regular monitoring by your physician. Do not disregard medical advice and always consult your physician with any questions you may have regarding a medical condition or before implementing anything  you have read or heard in our content.

 

 

CBC Interview with a Low Carb Physician – five minutes and all the basics

Dr. Miriam Berchuk is a Calgary-area physician and active member of the Canadian Clinicians for Therapeutic Nutrition who was interviewed today (June 11, 2018) on CBC Radio (Calgary Eyeopener) about her personal use and promotion of a Low Carb diet for weight loss and specific metabolic conditions related to insulin resistance.

While the interview lasts just a touch over 5 minutes, everything that one needs to know to understand what a low carb diet is (and isn’t!) is clear, as well as when medical supervision should be sought.

If you want to know the basics or are having a difficult time explaining it to others, Dr. Berchuk’s interview should be very helpful.

The Perils of Food Processing – how the preparation of food affects how quickly it is absorbed

This article is based on a lecture given by Gabor Erdosi, MSc, MBA– Food News Conference, May 19, 2018 – Prague, Czech Republic

Introduction – Gabor Erdosi, MSc, MBA is a Molecular Biologist from Debrecen, Hungary who is employed in the Food Industry but whose hobby is reading scientific publications and analyzing the available information. The talk that this article is based on was given at the Food News Conference, May 19, 2018 – Prague, Czech Republic  and is the condensation of approximately 4 years worth of Gabor’s studying of the literature.

Gabor founded and heads up the Lower Insulin group on Facebook which is dedicated to discussing the scientific basis of the relationship between metabolic diseases and food and lifestyle factors. At present, the group has ~5300 members.

This new series titled The Perils of Food Processing reflects Gabor’s conviction that what’s of primary importance in the interaction between food and our physiology (GI tract) is the speed and location of food absorption in the digestive system. This article is arranged according to the same principle.

The reason I am writing this series of articles is because I believe what Gabor Erdosi has come to understand about the effects of food processing on the speed and location of food absorption — especially carbohydrate, and which affects the very nature of hunger and satiety is absolutely crucial to understanding the current epidemic of metabolic diseases we now face.

This first article provides an overview of the gastrointestinal system and the so-called “incretin hormones” and how the amount a food is cooked or ground impacts how quickly it is absorbed and the energy stored.


When talking about Food Processing, the issue arises as to how to properly define the concept of ‘processing’.

How do we define ‘food processing’? Humans have been processing their food in one way or another for hundreds of thousands of years – be it cutting, cooking or grinding their food in some way.  These are all forms of food processing.

In terms of the effect of Food Processing on human physiology, a few main questions that this series of articles will address, arise;

(i) are all forms of food processing created equal?

(ii) does the food processing of different macronutrients and foods have different results?

(iii) could these changes in food processing over the last few hundred years or so have anything to do with the epidemic of metabolic diseases that we now face?

1. Overview of Gastrointestinal Physiology

Before getting into the topic of the effect of different types of food processing on the speed and place of absorption, it’s necessary to provide an overview of the gastrointestinal physiology and how the digestive system works and what hormones are released in response to different nutrients.

1. Overview of Gastrointestinal Physiology – Gabor Erdosi – Food News 2018

The important concept here is that we have “sensor cells” (K-cells, L-cells) within our gastrointestinal tract and these cells release different hormones in response to different nutrients.

K-cells release an incretin hormone called GIP and the L-cells release an incretin hormone called GLP-1, as well as GLP-2, PYY and Oxyntomodulin (OXM).

What is important to note is that the distribution of these cells is not uniform.

The K-cells are more abundant in the upper part of the small intestine and other cells, the L-cells are more abundant in the lower part of the small intestine. This uneven distribution of these incretin-hormone-releasing sensor-cells has profound implications, as will be seen later.

Uneven distribution of the K-cells and L-cells in the small intestine – Gabor Erdosi – Food News 2018

2. Nutrient Sensing, the Incretin Effect and Hunger-Satiety Signalling in the Gut

Nutrient-Sensing

So, what happens when we eat foods that we have evolved to see for millennia? As the food goes through the small intestine, it triggers hormonal release from these incretin-hormone-releasing sensor-cells.

If you eat meat and berries, for example, which are foods we have evolved to see for hundreds of thousands of years, they have a fairly balanced stimulatory effect on these sensor cells. These incretin hormones will be released in a more or less balanced manner.

However, as will be shown later on, when we eat food products that we have not evolved to see – relatively new food products on an evolutionary scale, these patterns are completely disrupted.

There are several nutrient-sensing hormones in the small intestine, but the one to focus on with respect to the effect of food processing is SGLT1 –  which is a glucose sensor. Both the K-cells and the L-cells contain this nutrient-sensing receptor, and most others, as well.

Keep in mind for the next articles that the distribution of these cells is uneven; with more in the K-cells higher up in the small intestine and increasing numbers further down in the L-cells.

The Incretin Effect

When we eat glucose, such as in an oral glucose tolerance test or when someone gets intravenous glucose in a hospital, the difference in the insulin response is called the “incretin effect”.

As you can see from the diagram below, the response to an oral or intravenous glucose load is very large and can be 50-70% of the insulin response.

The “Incretin Effect” to oral or intravenous glucose – Gabor Erdosi – Food News 2018

The majority of the insulin response is stimulated by these incretin hormones (GIP, GLP-1, etc.) secreted by the K-cells and L-cells and not directly via glucose.

The Physiological Effects of the Incretin Hormones

In addition to the insulin-stimulating effect, these incretin hormones have very different effects.

The K-cells, which are more abundant in the upper small intestine, secretes Glucose-dependent Insulinotropic Polypeptide (GIP) which acts on the pancreas – not only to result in insulin release, but also increase glucagon. At the level of the fat cells, the adipose tissue, it increases increases triglyceride storage, resulting in weight gain. In this way, GIP supports insulin’s effect on storing lipids. This is an anabolic-type of hormone and if it is very high, it can cause inflammation in adipose tissue.

The L-cells, which are more abundant in the lower small intestine, secrete Glucagon-like Peptide-1 (GLP-1) which also acts on the pancreas to increase insulin, but decreases glucagon. This GLP-1 at the level of the brain, acts to decrease appetiteincrease satiety (feeling full) and decrease food intake.

  1. Hunger-Satiety Signalling in the Gut
Effects of Intestinal hormones on hunger-satiety signaling – Garbor Erdosi – Food Net 2018

It is important to note that there is only one hormone that can increase hunger and that is ghrelin which is synthesized in the stomach.

All the other hormones, including CCK, PP, PYY, GLP-1 and OXM (Oxyntomodulin) decrease hunger. That is, all of these hormones promote satiety; the feeling of being ‘full’. It is very important to note that four of these hormones, CCK, PYY, GLP-1 and OXM are all synthesized in the small intestine L-cells.

The above is the all the basic physiology that is needed to understand the effects of food processing on the speed and location of nutrient absorption, the nature of hunger and satiety and how the current epidemic in metabolic diseases we now face is a result of disregulation of this system.

3 a. The Effect of Cooking Foods on Body Weight

One of the most ancient forms of food processing is cooking, and there are studies which indicate that there is an association between how many raw foods people eat and their body weight.  There is a generally tendency that the more raw foods a person eats, the lower their body weight. That does not mean that eating a vegetarian diet is more desirable, it is only to point out that with more and more processing – in this case, cooking, the higher body mass tends to be.

The Effect of Cooking Foods on Body Weight – Gabor Erdosi Food News 2018

3b. The Effect of Cooking Foods on Nutrient Availability

Carbohydrate-rich Foods

The relationship between cooking foods and body weight is particularly important with respect to carbohydrate-rich foods. For example, when grains are cooked they become much more digestible – meaning that more of the nutrients in the grain is available to be absorbed. In the case of potatoes, there is double or triple the amount of energy (calories) available to the body when they are cooked versus when they are raw. When a potato is cooked, the digestible starch increases 2-3 times, which means that these calories are now available to the body where they weren’t when they were raw.

The Effect of Cooking Carbohydrate on Nutrient Availability – Gabor Erdosi – Food News 2018
Lipid and Protein-rich Foods
The Effect of Cooking Lipid (fat) and Protein-rich Foods on Nutrient Availability – Gabor Erdosi Food News 2018

When foods that are high in lipids (fats) such as peanuts are cooked, the amount of energy the body is able to derive from the food, increases. As well, significantly more amino acids in protein-rich foods such as egg make it to the large intestine (where their nutrients are absorbed) when the protein-rich food is cooked.

3c. The Effect of Non-Thermal Food Processing on Nutrient Availability

Mechanical processing, such pounding food is also an ancient form of food processing which has an effect on how many nutrients are available to be digested. The nutrients available to the body when food is eaten raw and whole versus raw and pounded is significant, and this holds true whether the food is animal protein such as meat or a starchy vegetable such as sweet potato.

In a study with mice, one group of mice was fed meat either raw and whole or raw and pounded and then the group was crossed over to cooked and whole or cooked and pounded. The other group of mice was fed sweet potato eaten raw and whole or raw and pounded and then crossed over to cooked and whole or cooked and pounded.

When the meat or starchy vegetable (sweet potato) was eaten raw and whole, it was associated with lower body mass than the same foods eaten raw and pounded because the mice lost weight. As expected from what is known about the effect of cooking on nutrient availability (see above), when the mice ate the cooked meat or cooked sweet potatoes, they either didn’t lose as much weight (in the case of the meat) or actually gained weight (in the case of the sweet potato).

The conclusion of this study was worth noting;

“Our results indicate that human dieters who count calories and eat similar mixed diets but cook them to different extents would experience different weight gain outcomes at comparable levels of physical activity. This prediction is consistent with recent long-term data indicating that preparation-specific factors affect the relationship between caloric consumption and weight gain in humans.”

3 d. The Effect of Hydrolyzing Protein on Hormonal Response in the Small Intestine

Hydrolyzed protein, is essentially pre-digested protein and this process has an impact on which hormones are released in the small intestine when it is eaten.

In a 2010 study, comparing soy protein with soy protein hydrolysates and whey protein with whey protein hydrolysates, it was found that significantly more insulin compared to glucagon is released with the hydrolysates versus the intact protein. This means that the insulin to glucagon ratio is higher and insulin is the hormone which signals the body to store energy.  A higher insulin to glucagon ratio means that the body is storing energy rather than responding to glucagon which signals the body to use glucose and fat for energy.

4 a. The Effect of Mechanical Processing on the Blood Glucose Response of a Carbohydrate Food

Grinding / Juicing Fruit

Mechanical processing of a food doesn’t change the amount of carbohydrate that is in it. That is, when we compare 60g of whole apple with 60 g of pureed apple or 60g of juiced apple, there is the same amount of carbohydrate each. When we compare the Glycemic Index of these three, the results are very similar so this isn’t very helpful to tell us about the blood glucose response to actually eating these different foods.

When these foods are eaten, the blood glucose response 90 minutes later, is significantly  different.

Note: It’s not relevant to the outcome, but on this graph, slow and quick puree and juice as just differences in the amount of time it took for the liquid to be drunk.
The Effect of Mechanical Processing of Fruit on Blood Glucose Response – Gabor Erdosi – Food News 2018

As can be seen by the graph on the right, in healthy individuals blood insulin level goes very high with the juiced apple and in response, blood glucose then goes very low, below baseline.

The response that we see with the juiced apple is typical of what is seen with ultra-processed carbohydrates.

Grinding Grains

Grinding grains is another type of ancient food processing which changes the hormonal response in the small intestine.

The Effect of Mechanical Processing of Wheat on Blood Glucose Response – Gabor Erdosi – Food News 2018

When healthy individuals eat grain-based meals, the plasma insulin response increases the smaller the particle size of the grain.  That is, a specific amount of whole grain releases less insulin than the same amount of cracked grains, which is less than the same amount of course flour. The highest amount of insulin is released in response to eating the same amount of fine flour.

What was true for wheat in this study was true for rice as well and what was of interest, is there wasn’t a big difference between the insulin response with brown rice versus white rice.

The Effect of Mechanical Processing of Rice on Blood Glucose Response – Gabor Erdosi – Food News 2018

There is no difference in the Glycemic Index or Glycemic Load of whole wheat versus ground wheat or whole rice versus ground rice, but there is a huge difference in the insulin response with difference types of mechanical processing.

It’s also important to note that the amount of  fiber that was in the grain did not make a difference in the amount of insulin released, only the amount of mechanical processing of the grain. So, eating brown rice versus white rice won’t change the amount of insulin that is released – and insulin is a hormone that signals the body to store energy (calories).

In this next study, the same response that we saw with the pureed and juiced apples (above) is also seen with finely ground wheat bread. We see plasma glucose rise rapidly and then it drops below baseline at 120 minutes (circled).

Plasma glucose rises rapidly with bread made with wheat flour, then drops below baseline at 120 minutes

We know that the difference wasn’t due to the amount of fiber, because in this study they added back the fiber and it didn’t make a difference.

The difference had to do with the amount of disruption to the structure of the grain. So, eating whole wheat bread versus eating white bread — which is just adding the fiber that was taken out back won’t help much in terms of the insulin response.

The disruption of the structure of the grain had very adverse effects on the hormonal response; both the insulin response and GIP response, which can be seen in the next graph;

Disruption to structure of grain has adverse effect on insulin response and GIP response – Gabor Erdosi – Food News 2018

The bread made with flour resulted in a much larger insulin response and plasma GIP response than those made with whole kernel grains

Recall from the first article in this series, that GIP is released from the K-cells, which are dominant in the upper part of the small intestine. Bread made from ground flour results in a much greater and earlier hormonal response than bread made from whole grains.

The same researchers did another study a year later, this time with wheat bread, rye bread with the endosperm, traditional rye bread and high-fiber rye bread. As can be seen from these graphs (whether wheat or rye bread), it is the structural difference of the bread that explains the insulin response after a meal, not the total amount of fiber.

Note: Gabor Erdosi made a table comparing the Area Under the Curve (AUC) of the hormonal response of GIP (from the K-cells in the upper part of the small intestine) and GIP-1 (from the L-cells in the lower part of the small intestines) for the different breads which was very telling.
Area Under the Curve (AUC) of the hormonal response of GIP and GIP-1 for the different breads – Gabor Erdosi – Food News 2018

As can be seen from this table, there was almost double the GIP/GLP-1 ratio in the refined wheat bread (5.02) than the traditional rye bread (2.75) and this difference was largely due to significantly more GIP being released from the K-cells high up in the small intestine with the refined wheat bread than with the traditional rye bread.

It wasn’t due to fiber, because there was less GIP released with the traditional rye bread than even with the high fiber rye bread.

4 b. In-Vitro Hydrolysis of Starch Highly Correlates to Starch Digestion in the Small Intestine

This study shows a striking ability to predict how starch is hydrolyzed (broken down) in the small intestine with how it is broken down in a petri-dish in a lab using alpha-amylase. A perfect correlation would be = 1 and in this case it is 0.95.

Glycemic Response and Insulin Response to Starch Hydrolysis in-vitro and In-vivo – Gabor Erdosi – Food News 2018

As can be seen from these graphs, the glycemic response (blood sugar response) and the insulin response in the body can be accurately predicted using this method.

In this article we considered the effect of various kinds of ‘food processing’ on the speed and location of food absorption of individual macronutrients (such as protein, fat and carbohydrate), but we rarely eat meals that are only carbohydrate, or only protein or only fat.

How does the presence of protein and fat-rich foods influence the hormonal response in the small intestine and how do these affect the hormonal response to carbohydrate? How does fiber content or addition of fiber affect the hormonal response, or does it? These will be the topic of the next article where we’ll look at the hormonal response of the body to mixed meals (meals with different combinations of fat, protein and carbohydrate.

Perhaps you wonder what all this information means for you.

Maybe, like many you’ve become metabolically unwell with Type 2 Diabetes or high blood pressure or high cholesterol despite eating a diet rich in whole wheat bread, whole grain rice and lots of cooked vegetables and are beginning to realize that how your food is processed is as important a factor as the nutrients it contains in it’s unprocessed form.

I can help.

Feel free to send me a note using the “Contact Me” form located on the tab above to find out information about the services I offer, both in-person in my office or via Distance Consultation (using telephone or Skype).

To your good health!

Joy

The conclusion of this lecture is available here.


References

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    021115-105439.
  2. Reimann, Frank, and Fiona M Gribble. “Mechanisms Underlying Glucose-Dependent Insulinotropic Polypeptide and Glucagon-like Peptide-1 Secretion.” Journal of Diabetes Investigation 7 (2016): 13–19. https://doi.org/10.1111/jdi.12478.
  3. Nauck, Michael A., and Juris J. Meier. “Incretin Hormones: Their Role in Health and Disease.” Diabetes, Obesity and Metabolism 20 (2018): 5–21. https://doi.org/10.1111/dom.13129.
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  6. Evenepoel, Pieter, Dirk Claus, Benny Geypens, Martin Hiele, Karen Geboes, Paul Rutgeerts, and Yvo Ghoos. “Amount and Fate of Egg Protein Escaping Assimilation in the Small Intestine of Humans.”
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  9. Morifuji, Masashi, Mihoko Ishizaka, Seigo Baba, Kumiko Fukuda, Hitoshi Matsumoto, Jinichiro Koga, Minoru Kanegae, and Mitsuru Higuchi. “Comparison of Different Sources and Degrees of Hydrolysis of
    Dietary Protein: Effect on Plasma Amino Acids, Dipeptides, and Insulin Responses in Human Subjects.” Journal of Agricultural and Food Chemistry 58, no. 15 (August 11, 2010): 8788–97.
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  11. Heaton, K.W., S.N. Marcus, P.M. Emmett, and C.H. Bolton. “Particle Size of Wheat, Maize, and Oat Test Meals: Effects on Plasma Glucose and Insulin Responses and on the Rate of Starch Digestion in Vitro” 47,no. 4 (1988): 675–82. https://doi.org/10.1093/ajcn/47.4.675.
  12. O’Dea, K., Nestel, P.J., and Antonoff, L. “Physical Factors Influencing Postprandial Glucose and Insulin Responses to Starch” 33, no. 4 (April 1, 1980): 760–65. https://doi.org/10.1093/ajcn/33.4.760.
  13. Juntunen, Katri S., Leo K. Niskanen, Kirsi H. Liukkonen, Kaisa S. Poutanen, Jens J. Holst, and Hannu M. Mykkänen. “Postprandial Glucose, Insulin, and Incretin Responses to Grain Products in Healthy Subjects.”The American Journal of Clinical Nutrition 75, no. 2 (2002): 254–262. https://doi.org/10.1093/ajcn/75.2.254.
  14. Juntunen, K.S., D.E. Laaksonen, Leo K Niskanen Karin Autio Jens J Holst, Kari E Savolainen, Kirsi-Helena Liukkonen, Kaisa S Poutanen, and Mykkänen, H.M. “Structural Differences between Rye and Wheat Breadsbut Not Total Fiber Content May Explain the Lower Postprandial Insulin Response to Rye Bread” 78, no. 5(2003): 957–64. https://doi.org/10.1093/ajcn/78.5.957.
  15. Bornet, F R, A M Fontvieille, S Rizkalla, P Colonna, A Blayo, C Mercier, and G Slama. “Insulin and Glycemic Responses in Healthy Humans to Native Starches Processed in Different Ways: Correlation with in Vitro Alpha-Amylase Hydrolysis.” The American Journal of Clinical Nutrition 50, no. 2 (1989): 315–23. https://doi.org/10.1093/ajcn/50.2.315.

Copyright ©2018 BetterByDesign Nutrition Ltd.

LEGAL NOTICE: The contents of this blog, including text, images and cited statistics as well as all other material contained here (the “content”) are for information purposes only.  The content is not intended to be a substitute for professional advice, medical diagnosis and/or treatment and is not suitable for self-administration without the knowledge of your physician and regular monitoring by your physician. Do not disregard medical advice and always consult your physician with any questions you may have regarding a medical condition or before implementing anything  you have read or heard in our content.

Here is the link to the full lecture;

Evolving Theory of Obesity – the perfect storm of refined carbs and industrial seed oils

Three years ago, my theory about the roots of the current obesity and Diabetes epidemic was simple. I believed that it was largely a matter of us eating too many carbs while having reduced the amount of healthy fat we ate. I now think it is a little more subtle than that, and that it is specifically the combination of a diet too high in refined carbs while high in industrial seed oils (such as soybean and canola oil) that underlies the issue.

When I first started reading and writing about the current obesity and Diabetes epidemic, my thoughts were summarized in two articles written in May and June of 2015. In the first article, I documented how in 1970-72 only 6% of men and 11.7% of women were considered obese (Body Mass Index > 30) in Canada, but by 2013 obesity in men had tripled to 20.1% in men and to  17.4% in women. In the second article, I explained how the changes in the obesity rates coincided with the changes in the Dietary Recommendations that began in 1977 and continued in 1982, 1992 and 2005 and which encouraged people to eat considerably more carbs and a lot less fat coincided with the increased obesity rates, and that the increasing rates of Type 2 Diabetes (9.4% in 2014 in Canada) was just a natural outworking of the higher obesity rates.

The problem was, I really didn’t know of any specific mechanisms that related one to the other.

Now I know of several.

This article summarizes my current theory of obesity, as it relates to previous articles and a brand new study published last week.

Correlation is not Causation

There’s an expression in science is that “correlation is not causation“.

That is, the fact that a dramatic increase in obesity rates correlates (or coincides) with the changes in the Dietary Recommendations doesn’t mean that the Dietary Recommendations ’caused’ the obesity epidemic or the Diabetes epidemic.

One can hypothesize that there is a relationship between these two things, but without some understanding of the mechanism and more data, we don’t know what this relationship might be.

From the reading I have been doing the last number of years, I have some ideas of some of what may be involved.

Evolution of the Theory

A presentation at a conference at the beginning of March got me thinking that the picture was bigger than just “too many carbs” and a “decrease in the satiety effect of saturated fat” from full fat milk, cheese and butter. I was challenged by the fact that in the late 1960s and early 1970s, people in the US and Canada were generally slim, despite eating carbohydrates at just about every meal;

“They ate cereal or toast for breakfast and just about every household had a toaster. Lunch was often sandwiches, as there were no microwaves to heat food up in. Potatoes were a mainstay at dinner, sometimes pasta – yet the majority of young adults and adults were slim. Of course there were always some people that were overweight. Most elementary school classes had one ‘chubby’ kid, but when one looks around the classes of today or on public transit or in stores and supermarkets, most people are considerably heavier than people in the 1950’s and 1960’s”

(from A New Hypothesis for Obesity Part 1)

The question was raised ‘what resulted in overweight and obesity all of a sudden exploding in the 1970’s and just keep rising?’

What changed?

We knew that (based on US data) people began eating ~240 calories a day more as carbohydrate but what was causing them to do this? Was it just because the Dietary Recommendations were encouraging us to eat more carbohydrate or was there something else going on?

Not More Fat but the Type of Fat

While people were eating more carbohydrate, neither people in Canada nor the US were eating more fat, but the type of fat we’ve been eating since the 1970s has changed substantially. This tweaked my interest.

We’d reduced our intake of saturated fat (because the “Diet-Heart Hypothesis” had told us they were the “cause of cardiovascular disease”) and we dutifully ate more and more of ‘polyunsaturated fats’ / vegetable oils – which as I wrote about previously are more appropriately called “industrial seed oils“.  These oils, including soybean, corn oil and canola oil contain high amounts of linoleic acid which is at the very top of the omega 6 (n-6) pathway and these fats which elongate to arachidonic acid are pro-inflammatory products in nature.

There is nothing inherently ‘bad’ about linoleic acid which is found naturally in nuts and seed oils, including walnut, macadamia and sesame oil, but it is the sheer amount of these industrial seed oils which suddenly became excessive in our diet, which I think may be a significant factor.  These fats are in our bread, pastries, salad dressing, margarine and even our peanut butter.  Canned fish is packed in it, our mayonnaise is made from it and everything we eat that is fried from a restaurant is bathed in these industrial seed oils. On top of that, many of us use it our own homes to cook with.

So many of the foods we now eat are prepared with soybean or canola oil and as a result, we consume a much greater amount of linoleic acid than our body ever evolved to handle.

As outline in previous articles, these oils are much more unstable than the saturated fats they were created to replace. What I mean by ‘unstable’ is that they are more easily oxidized – that is, when industrial seed oils are heated in the making of commercial foods using them or in cooking, they react with oxygen in the air to form toxic substances including  aldehydes  and lipid peroxides.  When these oils are heated, they produce oxidized metabolites which have been also been implicated in the development of a variety of conditions, including non-alcoholic fatty liver disease (NAFLD), cardiovascular disease and cancer and it has been proposed that inflammation is involved in the development of Type 2 Diabetes and metabolic syndrome, as well.

Also as written about previously, cardiolipin  is an important component of the inner membrane of the mitochondria (the so-called “powerhouse of the cell”) and the fats that make up cardiolepin change, depending on the types of fats in the diet. That is, the fatty acid composition of cardiolepin is altered by us eating a diet high in linoleic acid, such as soybean and canola oil. This past week a study about cardiolepin was published that added a very interesting piece to my evolving theory of the obesity and Type 2 Diabetes epidemic.

In this new study, researchers at the University of Copenhagen found that when large amounts of cardiolipin are produced in ‘brown fat’ cell mitochondria, there is much stronger calorie-burning. Conversely, when there are low amounts of cardiolepin in brown fat, there is much less calorie-burning. Low amounts of cardiolepin and less calorie-burning in brown fat was reported to be associated with obesity and Type 2 Diabetes [1].

Note: "Brown fat" is a specialized type of fat that burns fat, rather than stores it and cardiolepin acts like a kind of on-off switch for the activity in our brown fat.

This study got me thinking that since it is known that the fatty acid composition of cardiolepin changes according to the fatty acid composition of the diet (covered in previous blogs), what effect has the massive increase in linoleic acid intake in the diet in both Canada and the US had on the function of the cardiolipin? 

Could it be that a shift in the types of fats that make up cardiolepin in brown fat stemming from a very high linoleic acid intake from industrial seed oils has had a similar effect as an absolute decrease in cardiolepin – and that this is somehow related to the increase in obesity and Type 2 Diabetes?

Type of Fats and Refined Carbohydrates

My theory of obesity has evolved and will likely continue to evolve.  I don’t think that increased carbohydrate consumption based on changes in the Dietary Recommendations in the late 1970s / early 1980s in and by itself resulted in the obesity epidemic and huge increase in Type 2 Diabetes we see now.

I currently believe that the introduction of these manufactured industrial seed oils (soybean, canola, corn) that were created in the 1970s and meant to replace saturated fat in the diet (presumably to protect people from heart disease!) may be part of the initiation of the disease process.

As documented in earlier articles, we know that these fats are easily oxidized, have a direct impact on increasing inflammation and triggering the disease generation process in several health conditions and on acting on the endo-cannibinoid receptors in the body, in much the same way as cannabis (marijuana).  Could it be that these created oils that are very high in the average Western diet actually lead people to consuming more and more carbohydrate-based foods; foods that often comes liberally bathed in more industrial seed oils?

The mechanism of how the above might work was presented in an another earlier article and had to do with how energy is generated in the electron transport chain of the mitochondria being different for saturated fats and unsaturated fats.

There are several possible mechanisms that may link consumption of these novel fats to obesity and development of Type 2 Diabetes (oxidation, inflammation, food cravings) and now based on this new study, the possibility of an increase in linoleic acid content in cardiolepin and it’s effect on fat burning.

It will take years more research before we have a fuller picture, so what do we do in the meantime?

Sensible Recommendations based on the Current Knowledge

For someone who is metabolically healthy (i.e. does not have Type 2 Diabetes or Insulin Resistance, hypertension or high cholesterol), it would seem that a whole-foods approach combined with avoiding omega – 6 industrial seed oils such as soybean, canola and corn oil combined with being mindful of the amount and type of carbohydrate in the diet may be sufficient to avoid developing these chronic diseases. Such a scenario would not be unlike the diet of the average American or Canadian in the 1950s and 60s. Not that that diet was that healthy, when compared with a classic Mediterranean diet, Japanese or Okinawan-style diet, or a whole food low-carbohydrate diet. These, it would seem offer a much healthier alternative.

For those who are already are insulin resistant or been diagnosed with Type 2 Diabetes, avoiding industrial seed oils would prudent and eating naturally-obtained vegetable fats such as olive oil or avocado oil instead. Since it does not seem that studies clearly support that saturated fat causes heart disease and not simply increase in surrogate markers of heart disease such as higher LDL (which LDL subfraction?), it would seem that using modest quantities of real butter is preferable to eating margarine made from industrial seed oils. It would also seem that at least initially, eating a diet where the amount and type of carbohydrate is kept to a quantity that does not trigger large amounts of insulin release or spike blood glucose makes good sense. As I wrote about recently, with the availability of Continuous Glucose Monitoring (CGM), this approach can be tailored to each individual person’s response to specific foods. We are no longer reliant on Glycemic Index or Glycemic Load, which are derived from healthy people’s response to foods, not those with Type 2 Diabetes. A suitable diet could be expressed as a variety of different lifestyles (just as for the healthy individual) including a Mediterranean diet, Okinawan-style diet, or whole food low-carbohydrate diet – with carbohydrate levels tailored on an individual basis, based on glycemic response and insulin levels.

Whether a person is healthy or metabolically unwell, based on the studies I have read and some of the mechanisms that have come to light, I can see no benefit in people eating either industrial seed oils or refined, processed carbohydrates. There is every reason to believe that both of these may have been part of the underlying cause of the current obesity and Type 2 Diabetes epidemic.

Unrefined Carbohydrates and Healthy Fats

If someone is metabolically healthy, I recommend eating minimally processed carbohydrates as they reduce the ‘incretin effect‘ of hormones such as GIP, GLP-1 and GLP-2 that are released in the intestine and trigger the release of insulin from the pancreas beta-cells. Eating minimally processed carbs would result in less triggering of the release of insulin, thus reducing the likelihood of developing either insulin resistance or Type 2 Diabetes.

If someone is already insulin resistant or has Type 2 Diabetes, it seems from recent studies that minimizing carbohydrate initially, along with weight loss and some forms of activity may be at least as good if not more beneficial than a low-fat calorie-restricted diet. Certainly, many people find they are a lot less hungry eating a low carbohydrate whole foods diet and are easily able to stick with it long term (a year or two in studies), allowing for a period of improving insulin sensitivity and lower overall blood sugar levels. It certainly has been demonstrated to be safe and effective in periods up to two years.

For both those that are metabolically healthy or insulin resistant or have Type 2 Diabetes, avoiding industrial seed oils makes good sense, for all the reasons outlined above.

What about your specific situation?

Do you have questions about the type and amount of carbohydrates that are most suitable for you based on your blood work and family history? What about which fats are are the best choices given your lifestyle?

I can help.

Please feel free to send me a note using the “Contact Me” form located on the tab above to find out how I can support your needs and I will reply as soon as possible.

To your good health!

Joy


Reference

Sustarsic EG, Ma T, Lynes MD et al, Cardiolipin Synthesis in Brown and Beige Fat Mitochondria Is Essential for Systemic Energy Homeostasis,
Cell Metabolism (2018), https://doi.org/10.1016/j.cmet.2018.05.003

Copyright ©2018 BetterByDesign Nutrition Ltd.

LEGAL NOTICE: The contents of this blog, including text, images and cited statistics as well as all other material contained here (the “content”) are for information purposes only.  The content is not intended to be a substitute for professional advice, medical diagnosis and/or treatment and is not suitable for self-administration without the knowledge of your physician and regular monitoring by your physician. Do not disregard medical advice and always consult your physician with any questions you may have regarding a medical condition or before implementing anything  you have read or heard in our content.

 

The Per Person Yearly Cost of Having Type 2 Diabetes

The most recent data available from 2011 indicates that the cost per person per year of having Type 2 Diabetes in Canada ranges from $1611 (Quebec) to $3427 (New Brunswick) based on an average income of $43,000 per year. Necessary medications, devices and supplies are expensive – costing more than 3% of income. While those with extended health benefits now may not consider this cost now, a change in employment circumstances can affect this overnight.

As Type 2 Diabetes progresses, more medications are often added and the number of times blood sugar needs to be taken each day often increases, as well.  Job loss or retirement suddenly results in Canadians being faced with bearing the burden of their disease, along with the chronic, progressive nature of poorly managed blood sugars.

A per-province breakdown using the 2011 figures from the Canadian Diabetes Association appears below;

Cost of Type 2 Diabetes per person per year by province (2011 figures) – from Canadian Diabetes Association

It doesn’t have to be so.

Long term studies that have been published in the last couple of years (reviewed in previous articles on this site) which demonstrate that a well-designed low carbohydrate or ketogenic diet can and does enable a significant improvement in Type 2 Diabetes symptoms.

After as little as 10 weeks, glycosylated Hemoglobin (HbA1C) has been reported to drop a full percentage point; from 7.6% to 6.6%. After a year, the average HbA1C was 6.3%, which is below the diagnostic criteria for Type 2 Diabetes.  That is, in just a year of following a well-designed low carbohydrate diet, it has been demonstrated that people can get their average blood glucose in the non-Diabetic range.

Medication use drops substantially when people are able to control their blood sugar by limiting the amount and types of carbohydrates they eat.  At the start of the study mentioned above published in Feb of 2018, 87% of people were taking at least one medication for Diabetes and at just 10 weeks, almost 57% had one or more Diabetes medications reduced or eliminated. After one year, Type 2 Diabetes medication prescriptions other than Metformin declined from 57% to below 30%. Insulin injections were reduced or eliminated in 94% of users and sulfonylurea medication was entirely eliminated.

For each one of these individuals, a simple change to a low carbohydrate diet resulted not only in significantly improved health and a reduction in Diabetes symptoms, but in significantly reduced cost, as well.

According to Virta Health who conducted the study referred to above, cost savings are as indicated in this diagram below.

The cost of "Diabetes Reversal" below reflects the estimated cost of an individual being cared for by the Virta Health multi-disciplinary team program, which appears to be an excellent program given the methods used in the studies they have published. 

It should be noted that the cost of working one-on-one with me over the course of a year (and as overseen by your GP) is substantially less. In fact, getting started by being assessed and having me design an individual Meal Plan just for you is significantly less than the yearly cost of achieving better blood sugar control in the graphic below.
Average Per Person Per Year Saving Potential (US dollars, 2018) – from Virta Health

Sometimes people are hesitant to invest in the cost of seeing a Registered Dietitian who can help them adopt a low carbohydrate lifestyle that can enable them to achieve significantly improved blood sugar control – even though the yearly costs of Diabetes supplies is far greater than the cost of being assessed and getting a Individualized Meal Plan. Such an estimate is at the level of health they are today, but waiting a few years, with longer Type 2 Diabetes, more medications, possibly including insulin injections, and the cost is closer to $3500 in 2011 Canadian dollars / $4000 in 2018 (US) dollars.

Does this make any sense?

The sooner someone changes their diet and lifestyle upon being diagnosed with Type 2 Diabetes, the more likely it seems they may be able to achieve full remission of symptoms. If you’ve followed my own story on “A Dietitian’s Journey” then you know how much harder it is for me, after being diagnosed 10 years ago.

If you have extended benefit coverage, then now is the time to invest some time in learning how to make lifestyle changes that will benefit your health and your finances for the years to come.  Even for those without such coverage, the cost of an assessment package which will provide you with a  Meal Plan designed specifically for you is substantially less than you are already paying for your medications, devices and supplies. I provide both in-person services in my Coquitlam, British Columbia office and via Skype Distance Consultations.

If you have questions about this package entails or about the flexible payment options that are available, why not send me a note using the “Contact Me” form located above? I’ll be happy to reply.

To your good health,

Joy

References

Canadian Diabetes Association, The Burden of Out of Pocket Costs for Canadians with Diabetes, 2011,  http://www.diabetes.ca/CDA/media/documents/publications-and-newsletters/advocacy-reports/burden-of-out-of-pocket-costs-for-canadians-with-diabetes.pdf


Copyright ©2018 BetterByDesign Nutrition Ltd.

LEGAL NOTICE: The contents of this blog, including text, images and cited statistics as well as all other material contained here (the “content”) are for information purposes only.  The content is not intended to be a substitute for professional advice, medical diagnosis and/or treatment and is not suitable for self-administration without the knowledge of your physician and regular monitoring by your physician. Do not disregard medical advice and always consult your physician with any questions you may have regarding a medical condition or before implementing anything  you have read or heard in our content.

Therapeutic Ketogenic Diet in Type 2 Diabetes Lowers CVD Risk at 1 year

As demonstrated in a previous article, a low carbohydrate or therapeutic ketogenic diet is a viable option for people to reduce their symptoms of Type 2 Diabetes, but does it increase the risk of cardiovascular disease such as heart attack and stroke?

Results of a peer-reviewed study of cardiovascular outcomes of people with Type 2 Diabetes (T2D) that was published at the beginning of May in the Journal of Cardiovascular Diabetology [1] found that those that followed a ketogenic diet (≤ 30 g carbohydrate per day) significantly improved in 22 of 26 cardiovascular disease risk factors, including biomarkers of cholesterol / lipoproteins, blood pressure, inflammation, and carotid intima media thickness (cIMT).

Previous published results from the same researchers and published in February of 2018 demonstrated that significant improvement of T2D symptoms was able to be achieved and sustained long term using a ketogenic diet [2,3]. A post reviewing that study can be read here.

Simply by decreasing the amount of carbohydrate in the diet over the course of a year there was not only a significant decrease in blood sugar and weight, but a dramatic improvement in lipid and lipoprotein markers associated with markers of cardiovascular risk.

The results of this most recent study do much to dispel the myth that a therapeutic ketogenic diet puts individuals at increased risk for heart attack and stroke. In fact, it reduces their risk.

Methods

Continuous Care Intervention (CCI) Group Participants

At the beginning of the study, there were 238 participants enrolled in the continuous care intervention (CCI) group and all had a diagnosis of Type 2 Diabetes (T2D) with an average HbA1c of  7.6%  ±1.5%.  They ranged in age from 46 – 62 years of age, 67% were women and 33% were men. Weight of the subjects ranged from 200 pounds to 314 pounds (117±26 kg) with an average weight of 257 pounds (117 kg) and Average Body Mass Index (BMI) was 41 kg·m-2 (class III obesity) ±9 kg·m-2, with 82% categorized as obese.  The majority of participants (87%) were taking at least 1 medication for glycemic control medication.

At the end of a year, 218 participants (83%) remained enrolled in the  continuous care intervention (CCI) group.

Intervention and Monitoring of CCI Group

Each participant in the CCI group received an Individualized Meal Plan which enabled them to attain and maintain nutritional ketosis. They also received behavioral and social support, biomarker tracking tools, and ongoing care from a health coach with medication management by a physician.

Subjects typically required <30 g·day−1 total dietary carbohydrates.

Daily protein intake was targeted to a level of 1.5 g·kg−1 based on ideal body weight and participants were coached to incorporate dietary fats until they were no longer hungry.

Other aspects of the diet were individually tailored to ensure safety, effectiveness and satisfaction, including consumption of 3-5 servings of non-starchy vegetables and sufficient mineral and fluid intake.

Participants ability to achieve and maintain nutritional ketosis was determined by subjects monitoring their blood ketone level of β-hydroxybutyrate (BHB) using a portable, handheld device. Blood glucose and β-hydroxybutyrate (BHB) levels were initially tracked daily using a combination blood glucose and ketone meter and frequency of tracking was modified by the care team based based on each individual’s needs and preferences.

Participants with high blood pressure (hypertension) were provided with an automatic home blood pressure machine (sphygmomanometer) and they were instructed to record their readings daily to weekly in the supplied app, depending on recent blood pressure control. Antihypertensive medication prescriptions were adjusted based on home blood pressure readings and reported symptoms.

Downward Adjustment and/or Discontinuation of Medications

As blood pressure came down, diuretic medication was the first antihypertensive medication to be discontinued. This was followed by beta blockers (unless the participant had a history of coronary artery disease).

Angiotensin-converting-enzyme inhibitors (ACE inhibitors) and angiotensin II receptor blockers (ARBs) were generally continued due to their known protective effect on the kidneys in those with Type 2 Diabetes.

Statin medications were adjusted to maintain a goal of LDL-P under 1000 nmol L−1 (or based on participant preference after full risk/benefit discussion with the physician).

The Usual Care (UC) Group

For comparison purposes, an independent group of patients with Type 2 Diabetes were also recruited for the study and were referred to Registered Dietitians that provided dietary advice according to the American Diabetes Association Guidelines [4].

Laboratory Assessors

Since an abnormal lipid / cholesterol profile (“atherogenic dyslipidemia”) is a known risk factor for CVD [5] and is very common in people with Type 2 Diabetes, a number of laboratory tests were conducted at the beginning of the study and the end to determine if they improved, stayed the same or got worse.

Most common in people with Type 2 Diabetes is where there are increased triglycerides (TG), decreased high-density lipoprotein cholesterol concentration (HDL-C) and increased small low-density lipoprotein particle number (small LDL-P).

The authors of this study state that evidence suggests that increased very low-density lipoprotein particle number (VLDL-P) and a large VLDL-P in particular may be one of the key underlying abnormalities in this abnormal lipid / cholesterol profile (“atherogenic dyslipidemia”) associated with T2D.

The authors also outline how higher concentrations of small LDL are often associated with increased total LDL particle number (LDL-P) and increased ApoB which is the main protein constituent of  very low-density lipoprotein (VLDL) and low-density lipoprotein (LDL). The authors provide previous study evidence that demonstrates that in people with insulin resistance and T2D, increased total LDL particle number (LDL-P) and increased ApoB may exist even with normal to low LDL-C concentrations values. For this reason, LDL-C alone was not relied on as a measure of abnormal lipid / cholesterol profile (“atherogenic dyslipidemia”) in this study as it could miss the impact of increased total LDL particle number (LDL-P) and/or ApoB.

The authors mentioned that in previous studies with carbohydrate restriction of up to 1 year, while triglycerides (TG) usually decrease and HDL-C often increase, LDL-C sometimes increased and other times decreases. The authors note that although higher LDL-C is a known risk factor for CVD, low LDL-C may also reflect higher small, dense LDL, total LDL particle number (LDL-P) or ApoB and thus be a risk factor, as well.

Since inflammation is involved at all stages of the atherosclerotic process, higher high-sensitivity C-reactive protein (CRP) and/or higher white blood cell count (WBC) were assessed as risk factors for CVD.

Finally, since high blood pressure (hypertension) is also an added risk factor for CVD in people with T2D, tighter blood pressure control was deemed to reduce the risk of DVD, stroke and other microvascular events.

Continuous Care Intervention (CCI) Group

Standard laboratory fasting blood draws of the CCI group were obtained at the start of the study (baseline), at 70 days (3 months) and at ~ 1 year follow-up.

Lipid/cholesterol-related tests included ApoB, ApoA1, total cholesterol, triglycerides, direct HDL-C concentrations and LDL was calculated using the Friedewald equation.

The LipoProfile3 algorithm was used to determine relationship of lipid subfractions to cardiovascular (CVD) risk – specifically the number of HDL particles (HDL-P) previously reported  to be associated with death, Myocardial Infarction (MI), stroke and hospitalization, HDL-C (HDL cholesterol) which is the amount of cholesterol those particles are carying, which is not associated with these negative outcomes and HDL-P subclasses [6].

Risk was also determined using the lipoprotein insulin resistance score (LP-IR) which was proposed to be associated with the homeostasis model assessment of insulin resistance (HOMA-IR) and glucose disposal rate (GDR) [7].

Finally, risk was also determined using the 10-year atherosclerotic  cardiovascular disease (ACSVD) risk score of the American College of Cardiology [8].

Carotid ultrasonography (cIMT) measure was performed at baseline and 1 year to characterize atherosclerotic risk.

The Usual Care (UC) Group

Body measurements, vital signs and fasting blood draws for the Usual Care (UC) group were obtained at the start of the study (baseline) and at 1 year using the same clinical facilities and laboratory and data collection methods. Carotid ultrasonography (cIMT) measure was also performed at baseline and 1 year to characterize atherosclerotic risk.

Results

There were no significant difference in the baseline characteristics of the two sub groups of CCI participants (web-based on onsite-based) and no significant difference at 1 year, so for the purpose of analysis, data from both groups were combined.

As well, there were no significant difference in the baseline characteristics of the Usual Care (UC) group (which served as an observational comparison group) and the Continuous Care Intervention Group (CCI) except mean body weight and BMI were higher in the CCI versus the UC group.

The within-Continuous Care Intervention group changes in the following lipids and lipoproteins were all statistically significant and were as follows;

ApoA1  [a component of high-density lipoprotein (HDL)] increase by + 9.8%)

ApoB / ApoA1 ratio decreased by − 9.5%

Triglycerides (TG) decreased by − 24.4%

LDL-C increased by + 9.9% but LDL-particle size also increased by + 1.1% (that is, large fluffy LDL increased compared with small, dense LDL)

HDL-C increased by + 18.1%

total HDL-P increased by + 4.9%

large HDL-P increased by 23.5%

Triglyceride/ HDL-C ratio decreased by − 29.1%

large VLDL-P decreased by − 38.9%

small LDL-P decreased by − 20.8%

There were no significant changes in total LDL-P or ApoB.

These results are impressive!

Simply by decreasing the amount of carbohydrate in the diet over the course of a year there was a dramatic improvement in lipid and lipoprotein markers associated with markers of cardiovascular risk.

In addition, the Continuous Care Intervention group had a significant reduction in;

systolic blood pressure decreased − 4.8%

diastolic blood pressure decreased − 4.3%

C-Reactive Protein (CRP) decreased almost 40% (i.e. − 39.3%) 

white blood cell (WBC) count decreased − 9.1%

Below are graphs of the changes in biomarkers for the Continuous Care Intervention (CCI) group (figure 1) and the Usual Care (UC) Group;

FIGURE 1: changes in biomarkers for the Continuous Care Intervention (CCI) group

 

FIGURE 2: changes in biomarkers for the Usual Care (UC) group

Below is a comparative graph of the two groups, the Continuous Care Intervention (CCI) Group and the Usual Care (UG) Group

FIGURE 3: changes in biomarkers for the Continuous Care Intervention (CCI) group compared to the Usual Care (UC) group

Some Final Thoughts…

This study demonstrates that a therapeutic ketogenic diet followed over the course of 1 year significantly improved 22 of 26 cardiovascular disease risk markers in those with Type 2 Diabetes. This is huge!

The size of the study group was large and had an 83% retention rate over the course of the year – which in and by itself demonstrates that the intervention diet was one that people had no difficulty staying with in their day-to-day lives, without the use of meal replacements (shakes or bars).

While not a randomized control trial between CCI and UG groups, this study supports that a ketogenic diet is both safe and effective for periods of up to a year (and in other studies has been documented to be safe and effective for up to two-years). Not only can a well-designed ketogenic diet reverse many of the symptoms of Diabetes it can also significantly improve risk markers for cardiovascular disease.

Do you have questions about how a carefully-designed low carbohydrate or ketogenic diet can help you improve symptoms of Type 2 Diabetes and lower markers of risk factors for cardiovascular disease? Please send me a note using the “Contact Me” form above to find out more.

References

  1. Nasir H. Bhanpuri, Sarah J. Hallberg, Paul T. Williams et al, Cardiovascular disease risk factor responses to a type 2 diabetes care model including nutritional ketosis induced by sustained carbohydrate restriction at 1 year: an open label, non-randomized, controlled study, Cardiovascular Diabetology, 2018, 17(56)
  2. McKenzie AL, Hallberg SJ, Creighton BC, Volk BM, Link TM, Abner MK, Glon RM, McCarter JP, Volek JS, Phinney SD, A Novel Intervention Including Individualized Nutritional Recommendations Reduces Hemoglobin A1c Level, Medication Use, and Weight in Type 2 Diabetes, JMIR Diabetes 2017;2(1):e5, URL: http://diabetes.jmir.org/2017/1/e5, DOI: 10.2196/diabetes.6981
  3. Hallberg SJ, McKenzie AL, Williams, PT et al. Diabetes Ther (2018). Effectiveness and Safety of a Novel Care Model for the Management of Type 2 Diabetes at 1 Year: An Open-Label, Non-Randomized, Controlled Study.
  4. America Diabetes Association, Lifestyle management. Diabetes Care. 2017;40 (Suppl 1):S33–S43
  5. Fruchart J-C, Sacks F, Hermans MP, Assmann G, Brown WV, Ceska R, et al. The Residual Risk Reduction Initiative: a call to action to reduce residual vascular risk in patients with dyslipidemia. Am J Cardiol. 2008;102:1K–34K.
  6. May HT,  Anderson JL, Winegar DA, Utility of high density lipoprotein particle concentration in predicting future major adverse cardiovascular events among patients undergoing angiography, Clinical Biochemistry, 2016;49(15): 1122-1126
  7. Shalaurova I, Connelly MA, Garvey WT, Otvos JD. Lipoprotein insulin resistance index: a lipoprotein particle-derived measure of insulin resistance. Metabol Syndr Relat Disord. 2014;12:422–9.
  8. Goff DC, Lloyd-Jones DM, Bennett G, Coady S, D’Agostino RB, Gibbons R, et al. ACC/AHA guideline on the assessment of cardiovascular risk: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. Circulation. 2013;2014:S49–73 (tool: http://tools.acc.org/ASCVD-Risk-Estimator-Plus/#!/calculate/estimate/)

Copyright ©2018 BetterByDesign Nutrition Ltd.

LEGAL NOTICE: The contents of this blog, including text, images and cited statistics as well as all other material contained here (the “content”) are for information purposes only.  The content is not intended to be a substitute for professional advice, medical diagnosis and/or treatment and is not suitable for self-administration without the knowledge of your physician and regular monitoring by your physician. Do not disregard medical advice and always consult your physician with any questions you may have regarding a medical condition or before implementing anything  you have read or heard in our content.

Two More Good Indicators of Cardiovascular Risk

In a recent article about why Waist Circumference and Waist-to-Height Ratio is so important, I explained that a meta-analysis from 2012 which pooled data from 300,000 adults of different races and ages found that the lowest risk of cardiovascular disease and shorter lifespan was associated with a Waist to Height Ratio (WHtR) of 0.5. That is, we are at lowest risk when our waist circumference is less than half our height (even if our BMI is in the normal range). I also explained exactly how to take waist circumference, so that the results are accurate.

There are other measures of cardiovascular risk that I think are worth considering.

  1. A 2015 study of 3200 adults found that Waist-to-Hip Ratio (WHR) is more accurate in predicting 10-year cardiovascular risk than Waist to Height Ratio (WHtR), however whether this relationship would hold up in a sample as large as the meta-analysis above is unknown. I feel it is worth mentioning Waist-to-Hip Ratio (WHR) as an indicator of cardiovascular risk, as it is easy to do.
  2. Another index this 2015 study found to accurately predict 10-year  cardiovascular risk was something called Conicity Index which I will touch on even though it is not as easily determined as Waist-to-Hip Ratio (WHR) or Waist to Height Ratio (WHtR).

Determining Waist to Hip Ratio

As mentioned in the previous article, to use these indices requires waist measurements and hip measurements to be done accurately and at a specific place on the body.  To make it easier, I will repeat how to measure waist circumference here and below, how to measure hip circumference.

Measuring Waist Circumference

For the purposes of calculating risk associated with increase abdominal girth, waist circumference needs to be measured at the location that is at the midpoint (i.e. half way) between the lowest rib and the top of the hip bone (called the “iliac crest”). Below is a picture that should help.

Where to measure waist circumference

This measurement should be taken with a flexible seamstress-type tape measure, being sure that the tape measure is at the same height in the front and the back, when looking in front of a mirror. That is, the tape measure should be perpendicular to the floor (not higher in the back or the front).

It’s also important that the person’s abdomen (belly) is completely relaxed when taking the measurement, not sucked in.  One way to do that is to taking a deep breath and let it out fully just as the measurement is taken.

If your Waist to Height ratio is greater than 0.5, then you are at increased risk for cardiovascular events and a shortened lifespan. Looking at the graph above, one can see that for every little bit over 0.5, the risk rises steeply.

Measuring Hip Circumference

Hip circumference needs to be measured at the widest portion of the buttocks (butt) and as with waist circumference, the tape measure needs to be parallel to the flood (same height in the front and the back, when looking in front of a mirror).

For both the waist and hip measurement, the tape measure should be snug around the body, but not pulled so tight that it is constricting and it is best if a stretch‐resistant but flexible seamstress-type tape measure is used.

Assessing Waist-to-Hip Ratio

If the waist circumference is measured in inches, then the hip circumference needs to be as well – same if the measurement is in centimeters; both need to be in the same units.

To calculate the Waist-to-Hip Ratio take the waist circumference and divide it by the hip circumference.

Waist-to-Hip Ratio and Risk of Cardiovascular Disease

The following ratios are associated with low, moderate and high risk of cardiovascular risk;

Low Risk: For men, if the ratio is 0.95 or less, for women if the ratio is 0.80 or less

Moderate Risk: For men, if the ratio is 0.96 – 1.0, for women if the ratio is 0.81 – 0.85

High Risk: For men, if the ratio is 1.0 or more, for women if the ratio is 0.85 or more.


The Waist-to-Hip Ratio can also be thought of as people being shaped like “apples” or “pears“.

“Apples” versus “Pears”

People who carry most of their excess weight around their middle (“apples”) have more visceral fat and this type of fat is much more dangerous than the fat under our skin (called “sub-cutaneous fat”) because it is found around the heart, liverpancreas and other organs and increases the risk not only of cardiovascular disease, but also Type 2 Diabetes and hypertension.

People who’s hips are much wider than their waist (so-called “pears”) have less visceral fat and therefore lower risk of these weight-related health problems.

Conicity Index

Conicity Index(CI) is a little more cumbersome a calculation than either Waist-to-Hip (WHR) Ratio or Waist-to-Height (WHtR), but was found in the 2015 study mentioned above with 3200 subjects to be a strong predictor of cardiovascular risk.

Conicity literally means “cone-shaped” and determines how much our  body fat distribution like two end-to-end cones.

In the first figure below, body weight is distributed evenly, however when someone has a conical distribution, their weight is more heavily distributed around the abdomen. As a result, it has increased conicity and is more highly correlated to increased cardiovascular disease (as well as Type 2 Diabetes and hypertension).

For those who are interested in calculating Conicity Index (CI), the formula is below along with the formula for Waist-to-Hip (WHR) Ratio, Waist-to-Height (WHtR).

Indices of central adiposity

Final Thoughts…

Given the sample size of the data on which Waist-to-Height (WHtR) is based (300,000 adults) and that it is an easy to determine and robust measure of cardiovascular risk, this is the one I tend to favour.  That said, Waist-to-Hip (WHR) Ratio was previously used for years and found to be a simple and accurate predictor of risk. From that point of view, either could be used, but why not both?

In my clinical experience, I have encountered many people with much wider hips than waist (so-called “pears”) but whose Waist-to-Height (WHtR) is considerably greater than 0.5, and for this reason I tend to put more credence on Waist-to-Height (WHtR) than Waist-to-Hip (WHR) Ratio as a measure of visceral fat and increased cardiovascular risk.

Since both Waist-to-Height (WHtR) and Waist-to-Hip (WHR) Ratio are very easy to determine, for those with a family risk of cardiovascular disease, Type 2 Diabetes or hypertension, I think it makes sense to aim for a waist measurement that is within both of these easily obtained measures.

Do you have questions about how I can help you lower your risk of cardiovascular disease, Type 2 Diabetes or hypertension? I provide both in-person and Distance Consultation services via Skype or telephone (and remember, many extended benefits plans will reimburse for visits with a Registered Dietitian).

Please feel free to send me a note using the “Contact Me” form on the tab above to find out more.

To our good health,

Joy

References

  1. Rabiee B,  Motamed N, & Perumal D, et al. Conicity index and waist-hip ratio are superior obesity indices in predicting 10-year cardiovascular risk among men and women. Clin. Cardiol. 38, 9, 527–534 (2015)

Copyright ©2018  BetterByDesign Nutrition Ltd. 

LEGAL NOTICE: The contents of this blog, including text, images and cited statistics as well as all other material contained here (the “content”) are for information purposes only.  The content is not intended to be a substitute for professional advice, medical diagnosis and/or treatment and is not suitable for self-administration without the knowledge of your physician and regular monitoring by your physician. Do not disregard medical advice and always consult your physician with any questions you may have regarding a medical condition or before implementing anything  you have read or heard in our content.

Why Waist Circumference and Waist to Height Ratio is so Important

Most of us know that obesity is where a person has high levels of body fat, but at what point does overweight become obese? There are different ways of determining this and one way that many people are familiar with is the Body Mass Index.

Body Mass Index (BMI) classifies whether a person is overweight or obese by looking at their weight to height ratio. It is calculated by taking a person’s weight (in kilograms) and dividing it by their height (in meters squared).

BMI= weight (kg) / height (m) x height (m).

People are considered overweight if their BMI is between 25 and 29.9 and obese if it is above 30.

There are different levels of obesity, too.

Class I obesity is a BMI between 30 and 34.9.

Class II obesity is a BMI between 35 and 39.9.

Class III obesity (also called morbid obesity) is a BMI is greater than 40.

In recent years, research has determined that waist-to-height ratio is a much better predictor of cardiovascular health risk and a shorter lifespan due to illness than BMI, which is weight to height ratio.

A meta-analysis from 2012 pooled data from multiple studies, and examined Waist to Height Ratio (WHTR) in more than 300, 000 adults from several different ethnic groups and found that was a far better predictor of cardiovasular of metabolic risk factors in both men and women, than BMI [1].

A 2014 study found a correlation between Year of Life Lost (YLL) for different values of Waist to Height Ratio (WHtR) and found that YLL increased dramatically in both males and females when above 0.52 – a waist circumference of just over half one’s height [2].

Waist-to-Height Ratio Is More Predictive of Years of Life Lost than Body Mass Index [2]
These two studies found that the least amount of years of life lost is associated with a Waist to Height Ratio of 0.5That is, our waist circumference should be less than half our height, even if our BMI is in the “normal range”*.

*Both males and female non-smokers have a slightly increased Years of Life Lost at waist circumference > 0.50, even when their BMI was in the normal range (18.5 to to 22) - which means that waist circumference is a more important predictor of shortened lifespan due to cardiovascular disease, than BMI. 

Determining Waist to Height Ratio

If you’re a male and 5’10” tall (70″ tall), then to be in the lower risk category, your waist circumference should be 35 inches or less.

If you’re a female and 5’6″ tall (66″ tall), then your waist circumference should be 33 inches or less.

Waist to Height Ratio

But where should we measure waist circumference?

Is it where we wear our pants? Is it at the smallest part of our belly, where it dips in? Is it where our navel (belly button) is? Each one of these will produce very different results.

Measuring Waist Circumference

For the purposes of calculating risk associated with increase abdominal girth, waist circumference needs to be measured at the location that is at the midpoint (i.e. half way) between the lowest rib and the top of the hip bone (called the “iliac crest”). Below is a picture that should help.

Where to measure waist circumference

This measurement should be taken with a flexible seamstress-type tape measure, being sure that the tape measure is at the same height in the front and the back, when standing in front of a mirror. That is, the tape measure should be perpendicular to the floor (not higher in the back or the front).

It’s also important that the person’s abdomen (belly) is completely relaxed when taking the measurement, not sucked in.  One way to do that is to taking a deep breath and let it out fully just as the measurement is taken.

If your Waist to Height ratio is greater than 0.5, then you are at increased risk for cardiovascular events and a shortened lifespan. Looking at the graph above, one can see that for every little bit over 0.5, the risk rises steeply.

How Much Should I Weigh?

People often ask me “how much should I weigh” – wanting me to provide them with a specific weight in pounds or kilos.

While I can give people a ball-park figure based on their height and weight, how much we should weigh is when our waist circumference is half our height. At this weight, we have the lowest risk of heart attack and stroke (cardiovascular disease) and the lowest amount of Years of Life Lost.

Health is not a number on the scale.  Its the measurement of the amount of fat in our abdomen, around our liver, kidneys, pancreas and heart.

If your waist circumference is greater than 0.5 you are at risk.

If you have been diagnosed with Type 2 Diabetes or pre-Diabetes, high blood pressure or high cholesterol, then this risk is compounded.  Add to that a family history of these, and your risks are even higher.

While we can’t change our family history, we can change our diet and lifestyle and lower our risk.

Attaining a waist to height ratio of 0.5 is often associated with lower blood sugars, lower blood pressure and better cholesterol – even more so when the diet to achieve the weight loss is intentionally designed for these outcomes.

If you would like help getting on your own road to better health, please send me a note using the Contact Me form on this web page, and let me know how I can help. Remember, I provide both in-person and Distance Consultation services via Skype and many extended benefits plans will reimburse for visits with a Registered Dietitian.

Please send me a note if you have questions.

To our good health,

Joy

References

  1. Ashwell M, Gunn P, Gibson S (2012) Waist-to-height ratio is a better screening tool than waist circumference and BMI for adult cardiometabolic risk factors: systematic review and meta-analysis. Obes Rev 13: 275–286
  2. Ashwell M, Mayhew L, Richardson J, Rickayzen B (2014) Waist-to-Height Ratio Is More Predictive of Years of Life Lost than Body Mass Index. PLoS ONE 9(9)

Copyright ©2018  BetterByDesign Nutrition Ltd. 

LEGAL NOTICE: The contents of this blog, including text, images and cited statistics as well as all other material contained here (the “content”) are for information purposes only.  The content is not intended to be a substitute for professional advice, medical diagnosis and/or treatment and is not suitable for self-administration without the knowledge of your physician and regular monitoring by your physician. Do not disregard medical advice and always consult your physician with any questions you may have regarding a medical condition or before implementing anything  you have read or heard in our content.

Don’t Try This at Home – when medical supervision is needed

There are some things that people should not do on their own and one of them is to begin a low carb diet without first consulting with their doctor, especially if they take certain types of medication.  Medical supervision is absolutely required before a person changes the level of  their carbohydrate intake if they are taking;

(1) insulin

(2) medication to lower blood glucose such as sodium glucose co-transporter 2 (SGLT2) medication including Invokana, Forxiga, Xigduo, Jardiance, etc.

(3) medication for blood pressure such as Ramipril, Lasix (furosemide), Lisinopril / ACE inhibitors, Atenolol / β₁ receptor antagonists

(4) mental health medication such as antidepressants, medication for anxiety disorder, bipolar disorder (especially Lithium) and schizophrenia.

I don’t provide low carbohydrate dietary services those taking insulin (either Type 1 Diabetes or Type 2 Diabetes), but encourage those considering adopting this type of lifestyle to first consult with a healthcare professional with CDE certification, and their family doctor. This is very important because clinical studies indicate that injected insulin levels need to be adjusted downward very soon after beginning a low carb diet and this must be medically supervised.

I also recommend to those taking medication for mental health conditions that they consult with their psychiatrist and/or family practice physician before changing their diet. A low carb diet may have an effect on the dosage of medication required, especially with mood stabilizing medications such as Lithium. (A recent article written by Psychiatrist Georgia Ede, MD related to a ketogenic diet appeared in Psychology Today and appears here.)

Why do I advise people coming to me to implement a low carbohydrate or ketogenic lifestyle and taking medication to control their blood sugar or blood pressure first consult with their doctor before changing how they eat? It’s because eating less carbohydrate can result in blood sugar levels and blood pressure coming down fairly soon afterward and this can have serious consequences if dosages of these medications are not monitored and adjusted downward (and often being discontinued entirely).  For example, a sudden drop in blood pressure could result in people becoming dizzy or confused and could even result in injury to themselves or others if they ‘blacked out’ while walking or driving a car.

Some medications which lower blood sugar such as sodium glucose co-transporter 2 (SGLT2) medication including Invokana, Forxiga, Xigduo, Jardiance, etc. can result in life-threatening and even fatal cases of a very serious condition called “Diabetic ketoacidosis (DKA)” even with no change in diet, but these risks can be increased for patients on a very low carbohydrate diet as the combination of the medication and the low carb diet may increase the amount of ketone production (see Health Canada’s Safety Review here).

Those with significant alcohol consumption who are taking these medications are at risk for DKA, so it is very important that if you drink alcohol on a regular basis and take these medications to tell your doctor. If you are taking any of these medications and come to me, I will ask you about your alcohol consumption because alcohol and these medications together could potentially result in this serious and potentially life-threatening condition.

People taking any of the above medications (or any medications for other conditions) should not adopt a low carb or ketogenic lifestyle on their own without first checking with their doctor.

Another thing that people should never do on their own is adjust the dosage of any of their prescribed medication without first discussing it with their doctor. The consequences of doing so can be very serious, even life-threatening. For example, people taking SGLT2 inhibitors such as Invokana or Jardiance who decrease their insulin dosage suddenly are at increased risk for DKA. This is very serious. Medication dosages and timing must be adjusted by a doctor.

Another condition which is less common than DKA but is very serious is Hyperosmolar Hyperglycemia State (HHS).  It is life-threatening and has a much greater death rate than DKA, reaching up to 5-10%. It is most commonly seen in people with Type 2 Diabetes (T2D) that have some illness which results in reduced fluid intake, and them becoming seriously dehydrated. Being sick with an infection is one such situation where it is very important for you to see your doctor if you have T2D, so they can monitor you for HHS. You can read more about HHS here.

If you come to see me to adopt a low carb diet, I will work with you to coordinate dietary and lifestyle changes with your doctor, as they monitor your health and adjust the levels of prescribed medications. In more complex cases, I may ask for written consent to coordinate care with your doctor because depending on those medications, your doctor may need to know in advance what level of carbohydrates you have been advised to eat so that they can monitor your health and make adjustments in your medication dosage.

Your health is important and your diet and the medications need to be coordinated and overseen by your doctor. The potential risks are too great to attempt to do this on your own.

Do you have questions as to how I could work with you and your doctor as they oversee you adopting a low carb lifestyle?  Feel free to drop me a note using the Contact Me form on the tab above.

 


Copyright ©2018  BetterByDesign Nutrition Ltd.

LEGAL NOTICE: The contents of this blog, including text, images and cited statistics as well as all other material contained here (the “content”) are for information purposes only.  The content is not intended to be a substitute for professional advice, medical diagnosis and/or treatment and is not suitable for self-administration without the knowledge of your physician and regular monitoring by your physician. Do not disregard medical advice and always consult your physician with any questions you may have regarding a medical condition or before implementing anything  you have read or heard in our content.

 

Some Carbs are Better than Others (for Diabetics) – Part 3

INTRODUCTION: In the first article in this series on carbohydrates, I explained that Glycemic Index (GI) is a way to rate carbohydrates based how easily they raise the blood sugar of healthy people and that some carbohydrates are better than others when they cause much less of a rise in blood sugar. I wanted to know how would I react to carbohydrate-based foods now that I have been eating low carb for over a years and have seen a partial reversal of Type 2 Diabetes that I had for more than 10 years.

I decided to conduct some impromptu ‘experiments’ and the results led to some reading in the scientific literature. The information I discovered is VERY exciting for me and for others with Type 2 Diabetes or Insulin Resistance.

Once people have achieved significant reversal of symptoms following a therapeutic low carb or ketogenic diet, there is a way to logically begin to re-introduce carb-based foods in a way that doesn’t cause their blood sugar to spike.


As you may recall from the first article in this series on Carbohydrates, the Glycemic Index of a food is determine by having healthy people eat 50 grams of digestible carbohydrate of a given food, and then measure their blood glucose response over a 2 hour period (30 minutes, 60 minutes, 90 minutes, 120 minutes), plotting the curve then measuring the area under the curve (AUC) and comparing it to the AUC of pure glucose, the reference food.

The problem with the Glycemic Index or even the Glycemic Load (based on individual serving sizes) is that this data does not apply to those with Diabetes or Insulin Resistance.

Since I have been Diabetic for a long time, I decided to go about conducting my own sample-set-of-one (n=1) ‘experiment’, and one thing led to another…

The ‘Test Food’

I ate 1/2 cup of chickpeas (cooked from dried) which has 25 g of carbohydrate and measured my blood sugar response with the same meter at 30 minutes, 60 minutes, 90 minutes, 120 minutes, 180 minutes and 210 minutes.

blood glucose response to 25 g of chickpeas, cooked from dried

At the time I did this, I hadn’t eaten in 8 hours (considered a fasted state) and my starting blood sugar was 4.8 mmol/L (86 mg.dl). The chickpeas were part of a mixed meal with some chicken (high biological value protein) and a cucumber salad with olive oil.

At the highest point, my blood sugar went up to 5.8 mmol/L (105 mg/dl),  stayed there, then started to drop at 2 hours.

I was amazed.

When I first began changing my lifestyle a year ago, even eating low GI foods such as chickpeas caused my blood sugar to jump dramatically. I recall the first few months when I would eat 1 cup of hummus, which is chickpeas with tahini (ground sesame seeds) and has even more fiber than chickpeas alone and also has only 25 g of carbs, my blood sugar would always go up to ~ 8.6 – 8.9 mmol/L (155- 160 mg/dl). What I’ve since found out (and will explain this more in detail in an upcoming article) is that intact legumes have a very different impact on blood glucose as to ground ones.  The more intact a legume or bean is, the lower the blood glucose response.  As I said, more on that in a future article.

The ‘Reference Food’

Two weeks ago, I was at a social occasion where a milk-chocolate covered cracker was served and I decided (in the interest of science, of course!) to read the nutritional label, measure out exactly 25 g of carbohydrate of this food and eat it, measuring my blood sugar at 0 minutes, 60 minutes, 90 minutes120 minutes, and 180 minutes.

This ‘reference food’ (high GI) was eaten after a dinner that had a fair amount of high biological value protein (steak) as well as some healthy fats (olive oil on vegetables) and fiber in the vegetables, and my starting blood sugar was 6.7 mmol/L (121 mg/dl).

Just look at the blood sugar spike!

When I ate 25 gm of carbohydrate as the cracker and chocolate, my blood glucose went from 6.7 mmol/L to 9.8 mmol/L (121 mg/dl -177 mg/dl)! That is, I had eaten the SAME amount of carbohydrate (25 g of carbs) as when I ate the cooked chickpeas and had THREE TIMES the blood sugar response!!

Both the meals I ate just before the ‘reference food’ (high GI, cracker with chocolate) and the ‘test food’ (low GI, chickpeas) had a high biological value protein (chicken, steak) which slows the blood sugar response of the body, and both had the same amount of fiber (the exact same salad).

Below is a graph of the two responses (chickpeas in blue, chocolate covered cracker, orange) over 3+ hours.

It is quite evident that 25 g of carbs as high GI white flour with milk chocolate is processed VERY differently by my body than 25 g of carbs as low GI chickpeas!!
Comparison of blood glucose response of 25 g of carbohydrate as chickpeas and white flour cracker with chocolate (special thanks to Phil Thompson of the “Lower Insulin” Facebook group for the graph and calculations of area under the curve)

The area under the curve (AUG) was determined by lowering the cracker and chocolate curve down to sit just above the chickpea curve (grey curve) and then assessing where the respective points were and running the AUG formula relative to baseline.

The AUG of 25 g of carbs as chickpeas was 129.

The AUG of 25 g of carbs as white flour cracker with chocolate was 381.

The difference was 2.95.

The blood sugar response of the cracker with chocolate was THREE TIMES GREATER than the blood sugar response of the chickpeas – and both contained 25 g of carbs!

Some carbs are quite clearly better than others for this Type 2 Diabetic.*

* As I will elaborate on below, people's blood sugar response to different carbohydrate-based food is quite individual.

Objective Data

Facsimile for Glycemic Index of Cracker with Chocolate

I was able to find for purposes of estimation, that 25 g of carbohydrate as white bread with 5 g of margarine (a pretty good facsimile for 25 g of carbohydrate as white flour cracker covered with milk chocolate made with palm oil) has a GI of 70.1 when compared to the reference which was 25 g glucose in 125 ml water [1].

Studies of Effect of Eating Legumes (Pulses) Alone

A meta-analysis of 10 studies on the effect of pulses (legumes) eaten alone on blood sugar control in people with and without Diabetes [2] provided some helpful information. The pulses in the meta-analysis included chickpeas, black-eyed peas and various other beans (including red and white kidney, black, pinto, fava and white navy).

Seven of the 10 trials that looked at the effect of eating pulses alone had a crossover design (five had a washout period), studied a total of 253 participants, of which only 21 had Type 2 Diabetes, and 232 that had normal blood sugar.

Background diets were largely high-carbohydrate, low-fat diets (carbohydrate 52% of energy, protein 18% of energy, fat 29% of energy).

Due to the length of time I have had Type 2 Diabetes and the very high degree of persistent insulin resistance over the first 6 months of eating low carb but not ketogenic, the last 6 months my diet has been very low in carbohydrate (5-10% of energy), moderate in protein ~23% and 67-77% healthy fats.

It was found that fasting blood glucose following the eating of pulses alone was decreased by 0.82% (95% CI ), but there was no long term effect on HbA1C (3 month average blood sugar) or on HOMA-IR (fasting blood glucose: fasting insulin).

[Of interest, in low GI diets, eating of pulses lowered HbA1C (3 month average blood sugar) by 0.28% but had no change on fasting blood sugar or HOMA-IR. The average GI of the pulse-containing low-GI diets was 67 and as compared to the GI value of bread alone.]

The conclusions of the meta-analysis found that the strongest modifiers of benefit were in Type 2 Diabetes and that the legumes that modified blood sugar the most were black beans, white/navy beans, pinto beans, red and white kidney beans, chickpeas and fava beans.

“Specific to the pulses alone analysis, pulse species including Phaseolus vulgaris (black, white, pinto, red and white kidney beans), Cicer arietinum (chickpeas) and Vicia faba (fava beans) were also identified as significant modifiers.” [2]

Individual Glycemic Response  – role for personalized nutrition

A 2015 study from Israel[3] with 800 people who were monitored with continuous glucose monitors indicates that there isn’t a ‘universal’ blood sugar response to low GI foods or high GI carbs – that glycemic (blood sugar) response is very individual. 

“We continuously monitored week-long glucose levels in an 800-person cohort, measured responses to 46,898 meals, and found high variability in the response to identical meals, suggesting that universal dietary recommendations may have limited utility.

The study also found that an individual’s blood sugar response to different foods was able to be predicted by type and amounts of bacteria in their intestines (the ‘gut biome’ / ‘microbiome’ / ‘microbiota’) . 

Based on the data they collected, the team has since created and validated a machine-learning algorithm that combines blood parameters, dietary habits, anthropometrics (height, weight data), physical activity and gut microbiota  data that they say accurately predicts a person’s individual post meal blood sugar response to actual meals.

Applications in Dietetic Practice for Personalized Nutrition

There is a tremendous opportunity for Dietitians such as myself to help individuals with Type 2 Diabetes or pre-diabetes determine which carbohydrate-based foods cause the lowest, most gradual rise in blood sugar.

This is huge!

This means that after individuals have had significant reversal of Type 2 Diabetes / Insulin Resistance following a therapeutic low carb diet for a period of time, I can help them re-introduce carb-based foods back into their diet by selecting ones that have the least impact on their blood sugar!

There are two ways this can be done;

  1. USING EXISTING BLOOD GLUCOSE METER – I can help those with Type 2 Diabetes eat a specific amount of a ‘test food’ that contains 50 g of carbohydrate (I will calculate this for them) and have them test their blood sugar every 30 minutes for 2 or 3 hours with the blood glucose meters they already have.  Then, I can take that data, enter it into an Excel sheet just as was done with my data above, and determine their blood sugar response.

  2. USING A CONTINUOUS GLUCOSE MONITOR – continuous glucose monitors (CGMs) such as the FreeStyle Libre have become relatively inexpensive and would be ideal for this kind of testing. Test strips for most standard home blood glucose monitors are $1 a piece, so testing every 30 minutes for 3 hours costs $6. The FreeStyle Libre costs $50 for the unit, and while test patches are $90 and last only two weeks, huge varieties of carbohydrate-based foods can be tried and measured in a short time, with no effort.

As a Dietitian I can not only help individuals carry out this kind of individual testing of carbohydrate-based foods, I can help them interpret the results as we begin to re-introduced some foods back into the diet once significant reversal of insulin resistance has been accomplished.

Do you have Type 2 Diabetes or pre-diabetes and want help to determine which carb-based foods don’t spike your blood sugar? Or do you have questions about how I can help you reverse the symptoms of Type 2 Diabetes or insulin resistance ?

Please send me a note using the “Contact Me” form on this web page and I will respond to you shortly.

To your good health!

Joy

 

References

  1. Aston LM, Gambell JM, Lee DM, Bryant SP, Jebb SA. Determination of the glycaemic index of various staple carbohydrate-rich foods in the UK diet. European journal of clinical nutrition. 2008;62(2):279-285.
  2. Sievenpiper, J.L., Kendall, C.W.C., Esfahani, A. et al. Effect of non-oil-seed pulses on glycaemic control: a systematic review and meta-analysis of randomised controlled experimental trials in people with and without diabetes. Diabetologia (2009) 52: 1479.
  3. Zeevi D, Korem T, Zmora N, et al. Personalized Nutrition by Prediction of Glycemic Responses. Cell. 2015 Nov 19;163(5):1079-1094.

Copyright ©2018  BetterByDesign Nutrition Ltd. 

LEGAL NOTICE: The contents of this blog, including text, images and cited statistics as well as all other material contained here (the “content”) are for information purposes only.  The content is not intended to be a substitute for professional advice, medical diagnosis and/or treatment and is not suitable for self-administration without the knowledge of your physician and regular monitoring by your physician. Do not disregard medical advice and always consult your physician with any questions you may have regarding a medical condition or before implementing anything  you have read or heard in our content.


 

Are Some Carbs Better Than Others – Part 2

In Part 1 of the new series on “Are Some Carbs Better Than Others” I explained what Glycemic Index (GI) is; how it is a way to rate carbohydrates based how easily they raise blood sugar. If you recall, low GI foods (those with a value of 55 or less) are more slowly digested, absorbed and metabolized and cause a lower and slower rise in blood glucose levels and very high GI foods (>70) are digested very rapidly, casing a large spoke in blood sugar. High GI foods (>55) are result in a fairly rapid rise in blood sugar.

The GI value of a food is determined comparing how healthy people’s blood sugar responds over a two hour period to a food containing 50 grams of digestible carbohydrate from that food compared to 50 grams of glucose (pure sugar). The drawback to this rating scale is that the values are only known for a serving that has 50 grams of carbs in it.  That is, they compare the ability for different foods containing the SAME amount of carbohydrate it (50 g) to raise blood sugar. That is, the problem with the Glycemic Index is that its hard to compare foods because a serving size may have considerably less than 50 g of carbs in it.  For example, the Glycemic Index of watermelon is 76, which is as high as the Glycemic Index of a doughnut, but one serving of watermelon (1/2 a cup) has 11 g of carbohydrate in it, while a medium doughnut (one serving) has 23 g of carbs.

This is where the concept of Glycemic Load (GL) is much more helpful, because it tells us how a healthy person’s body will respond to the carbs in one serving of a foodOne usual serving of a food would be considered to have a very high Glycemic Load if it is ≥20, a high Glycemic Load if it is between 11-19 and a low Glycemic Load if it is ≤10.

How to Determine Glycemic Load

To determine Glycemic Load  (GL) of a serving of a food, what needs to be known is:

The Glycemic Index (GI) of that food (found by referring to a table of Glycemic Indexes)

The number of grams of carbohydrate in the quantity of food considered to be one serving.

  • GL  = GI x (amount of carbohydrate per serving) / 100

For purposes of comparison,  let’s look at the Glycemic Load of the same foods we looked at the Glycemic Index for in the first article.

One slice of white bread has a Glycemic Load of 10 and so does one slice of whole wheat bread, which is considered low. Both have 15 g of carbs per slice.

 

One 1 cup of cooked white spaghetti has a Glycemic Load of 25 which is considered very high and while 1 cup of whole grain spaghetti only has a Glycemic Load of 14, this is still not low, just lower than white spaghetti.

A cup of boiled white rice has 53 g of carbs in it and has a very high Glycemic Load = 35. A cup of white spaghetti has 44 g of carbs in it and also has a very high Glycemic Load at 25. These foods are high in carbohydrate and will cause a rapid rise in blood sugar in healthy people. To those who are already Diabetic or pre-Diabetic this is a big problem.

One cup of cooked whole grain spaghetti has a Glycemic Load of 14 which is still not low and has 37 g of carbs in it.

 

A cup of boiled brown rice has a Glycemic Load of 20 which is still considered very high and has 42 g of carbs.  These foods are high in carbohydrate and will cause a fairly rapid rise in blood sugar in healthy people, let alone those who are already having problems.

So what’s the problem?

Eating a high Glycemic Load diet over a period of years and years will result in blood sugar after meals (called “post prandial blood glucose”) to be high. This puts a huge demand on the body to keep releasing insulin to try to move all that glucose into the body’s cells and get it out of the blood. Over time, a high Glycemic Load diet causes the body’s pancreas β-cells (beta cells) to decrease in function or in many cases, to die – resulting in a diagnosis of Type 2 Diabetes. As can be seen above, even eating the “whole grain” version of favourite foods does not necessarily reduce the insulin demand on our pancreas. Our  β-cells are under continual pressure to release insulin every time we eat – from our breakfast toast or cereal, to our mid-morning muffin, to our pasta lunch. Eating a low carb diet is one very effective way to lower the demand on our pancreas to keep producing and releasing insulin to deal with the constant spikes in our blood sugar from carbohydrate containing foods. But does that mean we need to remain eating a low carb diet forever? More on that in future articles in this series.

Glycemic Load will tell us how much a serving of food will increase our blood sugar but it doesn’t tell us how much insulin our body releases as a result of eating a food – that is, the demand we are putting on our pancreatic βcells.

For those that have been eating a high carbohydrate diet for years and years or have a family history of Type 2 Diabetes, knowing how much insulin is needed to process the carb -based foods we eat is hugely important, because we need to eating foods that do not put a large demand on our pancreatic β-cells.  For those that already have Type 2 Diabetes, it is especially important to eat in such a way as to preserve whatever β-cell function we have leftInsulin Index, which will be covered in a future article, will enable us to choose between carb-based foods based on the demand they put on our β-cells and this is the topic of the next article in this series.

If you have questions as to how I can help you choose foods that result in much less glucose being released and also put much less demand on your  β-cells to keep producing and releasing insulin, please send me a note using the “Contact Me” form located on the tab above.

 


Reference

Oregon State University, Linus Pauling Institute, Micronutrient Information Centre, Glycemic Index and Glycemic Load http://lpi.oregonstate.edu/mic/food-beverages/glycemic-index-glycemic-load#glycemic-index


Copyright ©2018  BetterByDesign Nutrition Ltd. 

LEGAL NOTICE: The contents of this blog, including text, images and cited statistics as well as all other material contained here (the “content”) are for information purposes only.  The content is not intended to be a substitute for professional advice, medical diagnosis and/or treatment and is not suitable for self-administration without the knowledge of your physician and regular monitoring by your physician. Do not disregard medical advice and always consult your physician with any questions you may have regarding a medical condition or before implementing anything  you have read or heard in our content.

Are Some Carbs Better Than Others – Part 1

INTRODUCTION: Not all carbohydrate foods (“carbs”) are created equal; some are broken down very quickly into simple sugars and others are broken down very slowly. In the past the terms “simple sugar” and “complex carbohydrate” were used to imply this concept there are newer terms that enable us to know how much eating these foods will raise blood glucose in healthy people. The “in healthy people” is important, as the ability to tolerate carbohydrate in those with insulin resistance (“pre-diabetes”) or Type 2 Diabetes is significantly affected.

This is the first article in a new series on carbohydrate.

Glycemic Index

The Glycemic Index (GI) is a way of rating carbohydrates based on their ability to raise blood sugar. Low GI foods (those with a value of 55 or less) are more slowly digested, absorbed and metabolized and cause a lower and slower rise in blood glucose levels and very high GI foods (>70) are digested very rapidly, casing a large spoke in blood sugar. High GI foods (>55) are result in a fairly rapid rise in blood sugar.

Many of the foods people eat lots of in our society, such as bread, rice, pasta and cereal, even vegetables, are high GI foods. As once healthy people continue to eat these foods on a regular basis, they put a high demand on their body to produce and release insulin, which brings all that glucose into their cells. This insulin is released from the beta cells in the pancreas and people eating these high GI foods means that their beta cells have to release insulin over and over all day long and this constant demand on the beta cells, over time, results in the cells throughout their body becoming insulin resistant (no longer responding to insulin’s signal) or burning out their beta cells, resulting in Type 2 Diabetes.

Many people don’t realize that by the time they are diagnosed with Type 2 Diabetes, they already have beta cell dysfunctionbeta cell death and/or a decrease in beta cell mass. Once beta cells die, they’re gone. Our once healthy body is no longer healthy.  When we eat foods with significant carbohydrate – especially high GI carbohydrates, our ability to release insulin is significantly impacted and as a result, we can no longer tolerate carbs like we used to.  While the mechanism is different, it’s similar to someone that becomes intolerant to gluten; once they’re celiac, they can no longer tolerate foods that contain gluten without causing damage to their body.  Depending how long someone had Type 2 Diabetes when they were finally diagnosed, or how long they had it before they changed their eating habits will all factor in to how much carbohydrate they can process. For this reason, each person is different.

It’s not that carbs are inherently “bad”. It’s that our bodies are no longer able to process some of them they way we could when we were still healthy – so in those cases, the sugar stays in our blood, damaging tissues throughout our body.

Knowing which carbs are high GI is important, because these are the foods that tax our already overtaxed beta cells if we are not Diabetic and limiting these foods significantly, or avoiding may be the best way for healthy people to remain healthy.

The good news is that there are some types of carbohydrates that some people can not only tolerate, but may actually improve their blood sugar control, and that’s the topic of an upcoming article.

How the GI of a Food is Determined

GI Graph

The GI value of a food is determined by feeding a group of healthy people the amount of a food that contains 50 grams of digestible (available) carbohydrate and then measuring the effect on their blood glucose levels over the next two hours. The area under their two-hour blood glucose response (glucose AUC) for this food is then measured.

At another time, the same group of healthy people eat 50 grams of glucose, (which is the reference food) and their two-hour blood glucose response is also measured.

The GI value for the test food is calculated for each person in the group by dividing their glucose AUC for the test food by their glucose AUC.

The final GI value for the test food is the average GI value all the people in the group.

Too Much of a ‘Good’ Thing

Many of the foods that people in the West enjoy and eat a lot such as bread, rice and noodles are High GI foods – these are ones that are rated at  ≥ 55 (compared to pure glucose, which is rated at 100).

White bread has a GI of 75 ± 2 and whole wheat bread isn’t much better, at 74 ± 2.

 

Boiled white rice is high GI at 73 ± 4, and while somewhat better boiled brown rice is still high GI at 68 ± 4.

White spaghetti has a GI of 49 ± 2 and whole grain spaghetti has a GI of 48 ± 5.

 

Rice noodles, such as those in Pho (Vietnamese Beef Noodle soup) are even higher, at 53 ± 7.

 

Breakfast cereals, whether boxed or cooked are also high GI.  Here is a table that summarizes some of these [1];

REAKFAST CEREALS  Glycemic index (glucose = 100)
Cornflakes 81 ± 6
Wheat flake biscuits 69 ± 2
Porridge, rolled oats 55 ± 2
Instant oat porridge 79 ± 3
Muesli 57 ± 2

Many people include vegetables such as potato, sweet potato and squash such as pumpkin in their “vegetable quota” for the day, but let’s look at the Glycemic Index for these;

VEGETABLES  Glycemic index (glucose = 100)
Potato, boiled 78 ± 4
Potato, instant mash 87 ± 3
Potato, french fries 63 ± 5
Carrots, boiled 39 ± 4
Sweet potato, boiled 63 ± 6
Pumpkin, boiled 64 ± 7

People in our culture eat a lot of bread, rice, pasta, starchy vegetables and cereal but one of the things we know is that eating them with good source of protein slows down how quickly they affect blood sugar. Oftentimes bread and cereal form the basis of breakfast, perhaps with a high GI glass of juice and frequently, people eat pasta with a tomato sauce for supper (or leftovers for lunch), and this kind of meal will spike their blood sugar. We also know that the fiber content of a mixed meal will also slow down the rate at which blood sugar rises from these carbs, so there are ways to ‘tone down’ the response.

Some Final Thoughts…

If you have a family history of Type 2 Diabetes, are overweight or have high blood sugar, it’s important to understand that what you eat matters and to eat in a way that does not put high demand on your beta cells to keep releasing insulin to process all that glucose.

The time to consider the effect on your body is now – before you get sick by having overtaxed your pancreas’ beta cells and experience beta cell death or mass loss and are diagnosed with Type 2 Diabetes.

Once we’ve crossed that threshold; once our once healthy body is no longer healthy, we need to learn to eat in a way that does not put high demand on our beta cells, that does not require our body to process large amounts of glucose at a time, in order to preserve whatever beta cell mass and function we have left.

Determining which carb-containing foods we can tolerate and in what quantities will enable us to eat in a way that keeps us from getting worse and keeps us from developing the very serious consequences of not doing so, which can include blindness, toe and food amputations and more.

In coming articles, I’ll explain Glycemic Load and the Insulin Index and I’ll also touch on a role for legumes (pulses) such as chickpeas and sources of “resistant starch” in a moderate carb ‘Mediterranean-style’ diet.  Stay tuned.


If you just found out you are pre-diabetic, now is the time to do something about it. Waiting will not make it better. If you’ve been recently be diagnosed with Type 2 Diabetes, it’s not too late. Studies have shown that changing eating habits and lifestyle soon after diagnosis makes it possible for some people to reverse their symptoms and to have their Diabetes go into remission. One thing is known, that doing nothing will bring needless firsthand understanding to the phrase that “Diabetes is a chronic, progressive disease”.  It doesn’t have to be.

If you want to know how I can help you, please send me a note using the “Contact Me” form located on the tab above.

 


References

  1. https://www.health.harvard.edu/diseases-and-conditions/glycemic-index-and-glycemic-load-for-100-foods

Also see: Atkinson FS, Foster-Powell K, Brand-Miller JC, “International tables of glycemic index and glycemic load values”, Diabetes Care 31(12); 2281-2283


Copyright ©2018  BetterByDesign Nutrition Ltd. 

LEGAL NOTICE: The contents of this blog, including text, images and cited statistics as well as all other material contained here (the “content”) are for information purposes only.  The content is not intended to be a substitute for professional advice, medical diagnosis and/or treatment and is not suitable for self-administration without the knowledge of your physician and regular monitoring by your physician. Do not disregard medical advice and always consult your physician with any questions you may have regarding a medical condition or before implementing anything  you have read or heard in our content.

Concerns with Polyunsaturated Vegetable Oils – Part 2

This article is Part 2 in a two-part series on concerns with Polyunsaturated Vegetable Oils.Part 1 can be read here.

There are a few key things about polyunsaturates vegetable oils that need to be understood to understand this article, so I’ll keep the science simple.

There are two class of polyunsaturated fats; (PUFAs); omega 3 (ω-3 also written n-3) and omega 6 (ω-6 / n-6) which compete with each other for enzymes, and which becomes significant at one branch point (marked with the red and green box).

At that junction point (where the red box is at Arachidonic acid and green box is at Eicosapentanoic acid) if there is more n-6 fats than n-3 fats, then the pathway will favour the n-6 pathway. If there are more n-3 fats than n-6 fats, then the pathway will favour the n-3 pathway. The issue, as I will elaborate on below, is that in the Western diet, the n-6 pathway is always favoured.

Of significance, the n-6 polyunsaturated fats are pro-inflammatory and the n-3 polyunsaturated fats are anti-inflammatory. This is important to understand why eating lots of foods high in n-6 fats can lead to health consequences.

When people take low-dose Aspirin® for example, to lower the risk of heart attack or stroke, it acts on Arachidonic acid in the n-6 polyunsaturated fat pathway, to keep it from making certain inflammatory products that can lead to heart attack or stroke. 

In our evolutionary history it was thought that n-6 fats (from nuts and seeds that were gathered in the wild) and n-3 fats (from the fish and meat we hunted) were eaten in close to a 1:1 ratio – providing the two essential fatty acids from both classes. When man began domesticating grain and growing beans and lentils and nuts and seeds for food (all high in n-6 fats), the shift towards a diet higher in n-6 fats occurred. The modern Western diet is estimated to have an omega-6 to omega-3 fatty acids of 15–20:1 in favour of n-6 fats [6].

Many people take omega-3 fish oil capsules in an effort to protect their body from inflammation, but because the amount of n-6 fats in the diet is so much higher than the amount of n-3 fats, the n-6 pathway is still favoured.

Unless we significantly lower the amount of n-6 fats in the diet, taking fish oil doesn't really help as the n-6 pathway will always be favoured.

Changing the Makeup of Cell Components

Industrial seed oils have very high levels of linoleic acid which is at the top of the n-6 pathway.  These industrial seed oils are pro-inflammatory and will elongate to Arachidonic acid, resulting in many pro-inflammatory products being produced.

When we eat a lot of food made with soybean oil or fried in soybean oil we eat way more linoleic acid then our body has evolved to handle.

A major problem with polyunsaturated fatty acids such as linoleic acid are that they are very unstable fats that are easily oxidized (similar to a fat becoming ‘rancid’ or a metal ‘rusting’). Even if we never buy these industrial seed oils to cook with at home, when we buy French fries at restaurants they are fried in either soybean or canola oil. When we pick up a donuts, same thing.  Bottle salad dressing and mayonnaise (even the one that is called ‘olive oil mayonnaise’) are made with one of these industrial seed oils. These oils are found in products one would never expect to find them, including peanut butter! Start reading labels and you will be shocked how many products they are in – or rather, how few products they are NOT in.

Industrial seed oils are in most of the prepared food we buy and almost all of the food we eat out in fast-food restaurants.

According to a 2011 journal article published in the American Journal of Clinical Nutrition;

“The most striking modification of the US food supply during the 20th century was the >1000-fold increase in the estimated per capita consumption of soybean oil from 0.006% to 7.38% of energy.” [7]

When the linoleic acid content of the diet is high because we are eating foods made with industrial seed oils, important components of our cells membranes incorporate higher amount of linoleic acid into them.

For example, cardioleptin is a phospholipid component found in the inner mitochondrial membrane, which is where all energy metabolism in our body occurs. Cardioleptin plays an important role in the function of several enzymes involved in mitochondrial energy metabolism. 

When we eat a lot of pre-made and processed foods and food made in fast-food restaurants, cardioleptin’s fatty acid content becomes 90% linoleic acid, making it easily oxidized, affecting its function. If the diet is high in coconut oil and olive oil, cardioleptin will be higher in stearic and oleic acids and these fats are more stable fats than linoleic acid.

Literally, we are what we eat!

Cooking with Industrial Seed Oils

When industrial seed oils are heated such as they are in the making of commercial foods using them, they undergo rapid oxidation which means that they react with oxygen in the air to form toxic substances, including aldehydes and lipid peroxides.  Aldehydes are known neurotoxins and carcinogens, and are documented to contribute to DNA mutations, inflammation and hypersensitivity [8].

Heating polyunsaturated vegetable oils for just 20 minutes produces 20 times the permitted levels of ldehydes recommended as a maximum limit by the World Health Organization [8].

Keep in mind that at fast-food restaurants and in the preparation of commercial donuts and other fried food products, these industrial seed oils are used for frying everything from French fries to donuts and are heated over and over for extended periods of time, creating alarming levels of aldehydes and lipid peroxidation products.
Concentrations of aldehyde per litre of oil when heated to 180 C (from Groosvelt et al, 2015)

When heated, industrial seed oils produce oxidized metabolites known as oxidized linoleic acid metabolites (OXLAMs) which have been also been implicated in the development of non-alcoholic fatty liver disease (NAFLD)[9].

In the body cell components such as cardioleptin with high amounts of linoleic acid are easily oxidized producing an oxidation product known as 4-hydroxynonenal (4-HNE) which has been implicated in the development of cancer [10].

Increasing Appetite

The high linoleic acid content of industrial seed oils also act on two endo-cannibinoids in the body (2-AG and Anandamide) which results in us feeling hungry, even when we have recently eaten –  in much the same way as cannabis (marijuana) does [11-12].  As a result, these industrial seed oils are believed to contribute to obesity and the associated health risks such as Type 2 Diabetes and high blood pressure.

Final Thoughts…

For fifty years, the public ate industrially-created trans fats in place of natural saturated fats and we only found out later that they were a major contributor to heart disease.

For the last forty years we have been eating industrial seed oils in greater and greater quantities place of natural saturated fat, but (a) given how these industrial seed oils are produced (solvents, high heats for extended period of time, bleach, etc.) and (b) given what is known about the very toxic products they produce when heated in production and how they are oxidized in the body and oxidized through heating when cooking, it is warranted to be very cautious about eating prepared foods made with them.

To avoid these industrial seed oils will take a concerted effort as they are in virtually everything we buy ready-made and many of the foods we eat out, but one solution is to cook real food using healthy sources of fat and to avoid these industrial seed oils that were created and marketed to us as supposedly healthy substitutes for natural fats.

The butter, lard and tallow of years gone by were made from animals that were pasture raised, not fed soybeans and corn as commercial animals are now, but in light of the mounting number of studies that indicate that saturated fat is not associated with increased risk of cardiovascular disease, perhaps it might be preferable to buy grass fed butter or render tallow or lard from the fat of pasture-raised animals for some cooking applications – rather than use these industrial seed oils that were created as substitutes.  Butter, lard and coconut oil (a vegetarian saturated fat) are all very low in linoleic acid and thus are very stable.  They are not easily oxidized in the body or by heating and produce very low levels of aldehyde and lipid peroxidation products when heated, compared with many of the industrial seed oils.

These are all factors we need to consider when deciding which fats our food should be made with.

The chart below shows the linoleic content of some common fats in blue.  Keep in mind that fats with the smallest amount of linoleic acid are the most stable and the least prone to oxidation (either in the body or when heated).

Comparison of Dietary Fats – linoleic acid content
A personal note:

For non-heating uses, I use natural sources of monounsaturated fat such as cold pressed macadamia nut oil, hazelnut oil, avocado oil, and extra virgin olive oil and for cooking and heating uses I use a mixture of olive oil and coconut oil (to raise the smoke point), clarified butter (ghee) at higher temperatures and butter at lower temperatures and for baking.

I read labels of all products I buy and deliberately avoid purchasing any food products that contain soybean oil, canola oil or sunflower oil and when I eat out, I ask that my food be prepared with coconut oil, butter or ghee.

While the jury is still “out” when in comes to saturated fat, it is my opinion that with the mounting evidence that eating saturated fat does not contribute to heart disease, using moderate use of butter, ghee (clarified butter) and coconut oil seems to me to be a more acceptable risk than eating foods made with, or fried in industrial seed oils.

I trust having the information contained in this article will help you make an informed choice for yourself and for those you cook for.

If you have questions about how I might be able to help you follow a low carb lifestyle -including selecting appropriate fats for use in your own cooking, please feel free to send me a note using the “Contact Me” form located on the tab above.

References

(continued from Part 1)

6. A.P. Simopoulos, Evolutionary aspects of the dietary omega-6:omega-3 fatty acid ratio: medical implications,World Rev Nutr Diet, 100 (2009), pp. 1-21

7. Tanya L Blasbalg, Joseph R Hibbeln, Christopher E Ramsden, Sharon F Majchrzak, Robert R Rawlings; Changes in consumption of omega-3 and omega-6 fatty acids in the United States during the 20th century, The American Journal of Clinical Nutrition, Volume 93, Issue 5, 1 May 2011, Pages 950–962.

8. Grootvelt M, Rodada VR, Silwood CJL, Detection, monitoring, and
deleterious health effects of lipid oxidation products generated in culinary oils during thermal stressing episodes, Lipid Oxidation, November/December 2014, Vol. 25 (10)

9. Maciejewska, Dominika & Ossowski, Piotr & Drozd, Arleta & Karina, Ryterska & Dominika, Jamioł & Banaszczak, Marcin & Małgorzata, Kaczorowska & Sabinicz, Anna & Wyszomirska, Joanna & Stachowska, Ewa. (2015). Metabolites of arachidonic acid and linoleic acid in early stages of non-alcoholic fatty liver disease-A pilot study. Prostaglandins & other lipid mediators.

10. Zhong H, Yin H. Role of lipid peroxidation derived 4-hydroxynonenal (4-HNE) in cancer: Focusing on mitochondria. Redox Biology. 2015;4:193-199. doi:10.1016/j.redox.2014.12.011.

11. Alvheim AR, Malde MK, Hyiaman DO et al; Dietary Linoleic Acid Elevates Endogenous 2-AG and Anandamide and Induces Obesity, Obesity (2012) 20;1984-1994

12. Alveim AR, Torstensen BE, Lin YH et al, Dietary Linoleic Acid Elevates the Endocannabinoids 2-AG and Anandamide and Promotes Weight Gain in Mice Fed a Low Fat Diet, Lipids (2014) 49:59–69


Copyright ©2018 BetterByDesign Nutrition Ltd.

LEGAL NOTICE: The contents of this blog, including text, images and cited statistics as well as all other material contained here (the “content”) are for information purposes only.  The content is not intended to be a substitute for professional advice, medical diagnosis and/or treatment and is not suitable for self-administration without the knowledge of your physician and regular monitoring by your physician. Do not disregard medical advice and always consult your physician with any questions you may have regarding a medical condition or before implementing anything  you have read or heard in our content.

Concerns with Polyunsaturated Vegetable Oils – Part 1

INTRODUCTION: Both the US and Canadian Dietary Guidelines encourage us to limit saturated fat in order to reduce the risk of heart disease and to eat unsaturated fat, including polyunsaturated vegetable oils instead but what are these fats, where do they come from and what role might these play in development of obesity, Type 2 Diabetes, non-alcoholic fatty liver disease and even cancer?  This article is part 3 in the series titled Bad Fats and Enduring Beliefs.


Polyunsaturated vegetable oils” is really a misnomer, as neither soybeans nor rapeseed / Canola are “vegetables”.  More accurately these should be called “industrial seed oils“, as they are seed crops that have been deliberately engineered for food use.  These are created oil products which are quite unlike natural oils that can be easily expressed from nuts, seeds and fruit using a millstone, as has been done since the Bronze Age [1].

Image result for ancient olive press
Ancient olive oil press

If you simply press olives, almonds, sesame or poppy seeds between your fingers you will be able to express a little bit of their oil on your fingers.

Not so with soybeans!

You can squeeze a soybean as hard as you like and for as long as you like and you are not going to get any oil out of it!

The first attempt at trying to express oil from soybeans occurred in the United States, a few years after the creation of Crisco® shortening in 1911.  For 3 long years (1922 – 1925) scientists tried over and over again to extract oil from soybeans  imported from Manchuria using hydraulic presses,  and time and time again they failed. Finally, in 1925 scientists turned to the use of chemical solvents  to get oil from soybeans and solvent extraction of soybean oil has been used ever since.

Trans Fats and Industrially Produced Shortening

In days gone by, deep-fat frying in restaurants (e.g. for French fries) was done in beef tallow, sometimes in lard. Pastry crusts were made with lard or butter, and baked goods such as cakes and brioches were usually made with butter – that is until 1911 when Crisco® shortening was invented. When it was noticed that hardened cottonseed oil used in the soap-making industry had an appearance like lard, scientists decided to further process it to remove the strong odor inherent with cottonseed oil, and market it to housewives as the ‘modern’ way to bake.

Beginning in the 1950s, trans fats (which occurs naturally in very small quantities) were industrially produced from other industrial seed oils such as soybean oil for use in other natural fat substitutes, including  margarine, fat for commercial baked goods and fat for deep-fat frying in the fast food industry [2]. Unfortunately, it was only in the late 1990s and early 2000s that it became widely-accepted by the scientific community that eating foods made with trans fats or fried in trans fats raised LDL-cholesterol while lowering protective HDL cholesterol, and also raised triglycerides; promoting systemic inflammation and contributing to the development of heart disease. 

How ironic that the fats that were created to replace naturally-occurring saturated fats ended up being so detrimental to health!

After trans fats were discontinued due to their adverse health effects, industrial seed oils such as soybean oil and canola oil became the number one and number two oils of the food industry. These unsaturated (liquid) industrial seed oils have replaced saturated (solid) trans fat industrial oils in our food supply, however there is considerable evidence emerging which should cause us to question whether these fats are any safer (more on that below).

The Created Market for Industrial Seed Oils

The market for industrial trans fats and liquid industrial seed oils was itself created based a belief that ‘dietary saturated fat led to heart disease’.  Much  of what we have come to believe about this originated with a pathologist named Ancel Keys who proposed his ‘diet-heart hypothesis‘ in the 1950s.

Physiologist Dr. Ancel Keys.

In 1967, Keys published his “Seven Country  Study” that reported that populations that consumed large amounts of saturated fats in meat and dairy had high levels of heart disease but when data from 22 countries that was available since 1957 was plotted, it was a great deal more scattered, indicating a much weaker association than Keys’ Seven Country  Study data indicated.

In August of 1967, just as Ancel Keys published his study, Stare, Hegsted and McGandy, 3 Harvard researchers paid by the sugar industry published their reviews in the New England Journal of Medicine which vindicated sugar as a contributor of heart disease and laid the blame on dietary fat and in particular, saturated fat and dietary cholesterol (previous article on that topic here). Sponsorship of this research by the sugar industry certainly casts a dark shadow over their findings.

These 3 researchers insisted in their conclusion that there was a link between dietary cholesterol and heart disease and that there was “major evidence” which suggested that there was “only one avenue for diet to contribute to hardening of the arteries and the development of heart disease”,  but as covered in the previous article, it is known that a year after their publications (1968), the report of the Diet-Heart Review Panel of the National Heart Institute made the recommendation that a major study be conducted to determine whether changes in dietary fat intake prevented heart disease because such a study had not yet been done.

Just 10 years after the sugar industry paid Stare, Hegsted and McGandy to write their reviewsHegsted was directly involved with developing and editing the 1977 US Dietary Guidelines which recommended that Americans decrease intake of saturated fat and cholesterol and increase dietary carbohydrate – entrenching the belief that saturated fat caused heart disease into American public health policy. That same year (1977), based on the same body of literature, Canada adopted very similar dietary guidelines around saturated fat…and the rest is history.


Public Health Policy Based Rooted in a Belief

For the last forty years Americans and Canadians have shunned natural fats such as butter, cream and lard in place of man-made margarine, non-dairy creamer and Crisco® – all in the enduring belief that ‘saturated fat is “bad” and leads to heart disease’.  Given that published reports vilifying saturated fat were funded by the sugar industry and that Ancel Keys study left out 2/3 of the nutrition and health data available at the time, it has become evident that public health policy was founded on what is now questionable data.

In addition, more and more current peer-reviewed published studies are concluding that saturated fat is not associated with an increased risk of developing cardiovascular disease.

If saturated fat is not associated with increased risk of heart disease then should we be eating industrial seed oils that were created and marketed as a replacement for them?

Creation of Industrial Seed Oils

Inexpensive soybean oil has been the leading oil used in food production in the United States since 1945 [3]. It was previously made into a hard fat through hydrogenation and sold to consumers as trans-fat based shortening and margarine and came into wide-spread use as both synthetic hard fat and as a food-based oil product in the late-1960s.

In Canada, soybean oil is just behind canola oil in terms of the most used, and canola is another industrial seed oil that was created by science. In 1978 rapeseed, a prairie weed was specially bred in Canada to produce a novel plant that was lower in erucic acid (a toxin found in rapeseed) and this new plant was named “canola” (‘Canadian Oil‘).

A 2015 study on Canadian vegetable oil purchased and eaten in Canada found that in 2013, 42% was canola oil (a Canadian bio-engineered industrial seed oil) and 20% was soybean oil, an industrially-engineered seed oil developed in the US [4]. Keep in mind this figure excludes food products available in Canada that are manufactured in the US, which uses predominantly soybean oil.

Soybean Oil is a Modern, Industrial Product

According to an article titled “Soybeans Are Ancient; Oil Is Not” published in the Wall Street Journal in 2011 [5], soybeans as the basis for tofu and soy sauce is an ancient food in China, but soybean oil was virtually unknown until global food oil shortages during World War I created an interest to extract the fatty part of the soybean for oil. Soybean oil is a modern creation.

How is oil made from seeds such as soybean and canola?

“Soybeans are first crushed into crude oil and then refined to remove impurities like free fatty acids. Over days, the crude is “neutralized” of acidity with phosphoric acid, “winterized” through filters that remove wax, bleached at high heat to lighten the color and finally vacuum “deodorized” to eliminate impurities.” [5]

Related image
soybean extraction plant

The extraction of soybean oil involves the industrial processing of soybeans with solvents at very high heats over an extended length of time in order to have the soybean give up its small amount of oil.

Solvent extraction of canola oil occurs in a similar method, beginning with an hour or more ‘wash’ of the rapeseed with a hexane solvent, then a sodium hydroxide wash. Bleach is then used to lighten the cloudy color of the processed oil and then it is steamed injected at high temperatures to
remove the bitter smell.

Yummy! Now this oil is ready to sell to the public to cook with and eat!

Should we even be eating these industrial seed oils?

Are they any safer than trans fats that were approved for consumption for 50 years and later found to contribute to heart disease?

Part 2 of this article will continue in Concerns with Polyunsaturated Vegetable Oils – Part 2.


References

  1. Alfred Thomas (2002). “Fats and Fatty Oils”. Ullmann’s Encyclopedia of Industrial Chemistry. Weinheim: Wiley-VCH.
  2. “Tentative Determination Regarding Partially Hydrogenated Oils”. Federal Register. 8 November 2013. 2013-26854, Vol. 78, No. 217.
  3. Dutton, HJ. Journal of the American Oil Chemists Society, Vol. 58, No.3 Pages: 234-236 (1981),  https://pubag.nal.usda.gov/pubag/downloadPDF.xhtml?id=26520&content=PDF
  4. Schaer, L., Grainews, Canola gets competition from soybeans, Feb 01, 2016, https://www.grainews.ca/2016/02/01/canola-gets-competition-from-soy/
  5. Wall Street Journal, “Soybeans Are Ancient; Oil Is Not“, 2011, https://blogs.wsj.com/chinarealtime/2011/01/03/soybeans-are-ancient-oil-is-not/

Copyright ©2018 BetterByDesign Nutrition Ltd.

LEGAL NOTICE: The contents of this blog, including text, images and cited statistics as well as all other material contained here (the “content”) are for information purposes only.  The content is not intended to be a substitute for professional advice, medical diagnosis and/or treatment and is not suitable for self-administration without the knowledge of your physician and regular monitoring by your physician. Do not disregard medical advice and always consult your physician with any questions you may have regarding a medical condition or before implementing anything  you have read or heard in our content.

Do Saturated Fats Cause Heart Disease?

The Diet-Heart Hypothesis

The diet-heart hypothesis is the belief that eating foods high in saturated fat contributed to heart disease was first proposed in the 1950s by a scientist named Ancel Keys who believed that by replacing saturated fat from meat, butter and eggs with newly-created industrial polyunsaturated vegetable oil (such as soybean oil) that heart disease and the deaths allegedly associated with it would be reduced by lowering blood cholesterol levels.

In 1952, Keys suggested that Americans should reduce their fat consumption by 1/3 – while at the same time acknowledged that he had no idea whether he was right;

“Direct evidence on the effect of the diet on human arteriosclerosis is very little and likely to remain so for some time” [1].

In 1953, Ancel Keys published the results of his “Six Countries Study“ [1], where he said that he had demonstrated that there was an association between dietary fat as a percentage of daily calories and death from degenerative heart disease.

Four years later, in 1957, Yerushalamy published a paper with data from 22 countries [2], which showed a much weaker relationship between dietary fat and death by coronary heart disease than was suggested by Keys’s Six Countries Study data.

 

Keys et al – Epidemiological studies related to coronary heart disease: characteristics of men aged 40–59 in seven countries [1]

Yerushalmy J, Hilleboe HE. Fat in the diet and mortality from heart disease. A methodologic note [2]
Nevertheless, in 1970, Keys went on to publish his Seven Countries Study in which maintained there was an associative relationship between increased dietary saturated fat and Coronary Heart Disease -basically ignoring the data presented in Yerushalamy’s 1957 study and failing to study countries where Yerushalamy found no relationship, such as France. In a paper published in 1989 based on food consumption patterns in the 1960s in the seven countries [3], Keys said that the average consumption of animal foods (with the exception of fish) was positively associated with 25 year CHD mortality (death) rates and the average intake of saturated fat was strongly related to 10 and 25 year CHD mortality rates. Keys knew of Yerushalamy’s data from 1957 and ignored it.

Keys methodology has been widely criticized for selecting data only from the 7 countries that best fit his hypothesis.

The Sugar Industry Funding of Research Vilifying Fat

In August of 1967, just as Ancel Keys had published his Seven Country Study, Stare, Hegsted and McGandy – the 3 Harvard researchers paid by the sugar industry published their review in the New England Journal of Medicine, titled “Dietary fats, carbohydrates and atherosclerotic vascular disease”[3] which vindicated sugar as a contributor of heart disease and laid the blame on dietary fat and in particular, saturated fat and dietary cholesterol (see previous article on that topic).

Stare, Hegsted and McGandy concluded that there was “only one avenue” by which diet contributed to the development and progression of “hardening of the arteries” (atherosclerosis) and resulting heart disease and that was due to how much dietary cholesterol people ate and its effect on blood lipids;

“Since diets low in fat and high in sugar are rarely taken, we conclude that the practical significance of differences in dietary carbohydrate is minimal in comparison to those related to dietary fat and cholesterol…the major evidence today suggests only one avenue by which diet may affect the development and progression of atherosclerosis. This is by influencing the levels of serum lipids [fats], especially serum cholesterol.” [4]

These researchers concluded that there was major evidence available at the time which suggested that there was only ONE avenue for diet to contribute to hardening of the arteries and the development of heart disease – yet a year later in 1968 the report of the Diet-Heart Review Panel of the National Heart Institute made the recommendation that a major study be conducted to determine whether changes in dietary fat intake prevented heart disease because such a study had not yet been done [5];

“the committee strongly recommended to the National Heart Institute that a major definitive study of the effect of diet on the primary prevention of myocardial infarction be planned and put into operation as soon as possible. ”

This is an important point; prior to a major study having ever been conducted to determine whether changes in dietary cholesterol impacts heart disease, 3 Harvard researchers paid by the sugar industry concluded that there was "only one avenue" by which diet contributed to the development and progression of atherosclerosis (i.e. "hardening of the arteries") and heart disease and that was due to how much dietary cholesterol people ate and its effect on blood lipids.

Researcher Paid by the Sugar Industry Helps Develop the 1977 US Dietary Guidelines

Only ten years after the sugar industry paid Stare, Hegsted and McGandy to write their reviews, the same Dr. Hegsted was directly involved with  developing and editing the 1977 US Dietary Guidelines [6] which recommended an increase in dietary  carbohydrate and a decrease in saturated fat and cholesterol in the diet.

Historic changes in the Dietary Recommendation in Canada have largely been based on changes to the Dietary Recommendations in the US, and as a result both stemmed from a belief that eating saturated fat increases total cholesterol and therefore increases the risk of heart disease.

The problem is this belief is just that, a belief.

There have been many studies that have disproved this including a  randomized, controlled dietary intervention trial from 2008 which compared a low calorie, low in fat with a low carbohydrate, high fat diet of the same number of calories. This study found that overall heart health is significantly improved when carbohydrate is restricted, rather than fat [7,8].

Not all LDL cholesterol is “bad” cholesterol.

Small, dense LDL (“Pattern B”)  causes more “hardening of the arteries” than the large, fluffy LDL particles (“Pattern A”)[9].

It has been reported that when dietary fat is replaced by carbohydrate, the percentage of the small, dense LDL particles  (the ones that cause hardening of the arteries) is increased, increasing risk for heart disease.  Furthermore,  the low carb diet increased HDL (so-called “good” cholesterol), which are protective against heart disease and HDL and small, dense LDL were made worse on the low fat diet. Quite opposite to the “Diet-Heart Hypothesis, this study demonstrated improvements in the risk of heart disease for those eating a low carbohydrate, high fat diet compared to those eating a low fat, low calorie diet – which is not all that surprising given that it had been reported previously that a diet high in saturated fat actually lowers small, dense LDL (the type of LDL that causes hardening of the arteries) and raises the large fluffy LDL; actually improving risk factors for heart disease [15].

There are also other randomized controlled trials from 2004-2008 which demonstrate that a low carb diet improves blood cholesterol test results more than a low fat diet [10,11,12,13,14] – yet despite this, the belief that eating saturated fat increases blood cholesterol, persists.

Both the American and Canadian governments are in the process of revising their Dietary Guidelines and what is clear is that what is needed is an external, independent scientific review of the current evidence-base for the enduring false belief that dietary fat, especially saturated fat contributes to heart disease.

What are the findings of current scientific literature?

Eight recent meta-analysis and systemic reviews which reviewed evidence from randomized control trials (RCT) that had been conducted between 2009-2017 did not find an association between saturated fat intake and the risk of heart disease [16-21].

Furthermore, recently published results of the largest and most global epidemiological study published in December 2017 in The Lancet [23] found that those who ate the largest amount of saturated fats had significantly reduced rates of mortality and that low consumption (6-7% of calories) of saturated fat was associated with increased risk of stroke.

Here is a synopsis of the findings of the eight meta-analysis and systemic reviews;

“Intake of saturated fatty acids was not significantly associated with coronary heart disease mortality” and “saturated fatty acid intake was not significantly associated coronary heart disease events”

Skeaff CM, PhD, Professor, Dept. of Human Nutrition, the University of Otago, Miller J. Dietary Fat and Coronary Heart Disease: Summary of Evidence From Prospective Cohort and Randomised Controlled

“There were no clear effects of dietary fat changes on total mortality or cardiovascular mortality”.

Hooper L, Summerbell CD, Thompson R, Reduced or modified dietary fat for preventing cardiovascular disease, 2012 Cochrane Database Syst Rev. 2012 May 16;(5)

“Current evidence does not clearly support cardiovascular guidelines that encourage high consumption of polyunsaturated fatty acids and low consumption of total saturated fats.”

Chowdhury R, Warnakula S, Kunutsor S et al, Association of Dietary, Circulating, and Supplement Fatty Acids with Coronary Risk: A Systematic Review and Meta-analysis, Ann Intern Med. 2014 Mar 18;160(6):398-406

“The present systematic review provides no moderate quality evidence for the beneficial effects of reduced/modified fat diets in the secondary prevention of coronary heart disease. Recommending higher intakes of polyunsaturated fatty acids in replacement of saturated fatty acids was not associated with risk reduction.”

Schwingshackl L, Hoffmann G Dietary fatty acids in the secondary prevention of coronary heart disease: a systematic review, meta-analysis and meta-regression BMJ Open 2014;4

“The study found no statistically significant effects of reducing saturated fat on the following outcomes: all-cause mortality, cardiovascular mortality, fatal MIs (myocardial infarctions), non-fatal MIs, stroke, coronary heart disease mortality, coronary heart disease events.”

Note: The one significant finding was an effect for saturated fats on cardiovascular events however this finding lost significance when subjected to a sensitivity analysis (Table 8, page 137).

Hooper L, Martin N, Abdelhamid A et al, Reduction in saturated fat intake for cardiovascular disease, Cochrane Database Syst Rev. 2015 Jun 10;(6)

“Epidemiological evidence to date found no significant difference in CHD mortality and total fat or saturated fat intake and thus does not support the present dietary fat guidelines. The evidence per se lacks generalizability for population-wide guidelines.”

Harcombe Z, Baker JS, Davies B, Evidence from prospective cohort studies does not support current dietary fat guidelines: a systematic review and meta-analysis, Br J Sports Med. 2017 Dec;51(24):1743-1749

“Available evidence from randomized controlled trials (1968-1973) provides no indication of benefit on coronary heart disease or all-cause mortality from replacing saturated fat with linoleic acid rich vegetable oils (such as corn oil, sunflower oil, safflower oil, cottonseed oil, or soybean oil).”

Ramsden CE, Zamora D, Majchrzak-Hong S, et al, Re-evaluation of the traditional diet-heart hypothesis: analysis of recovered data from Minnesota Coronary Experiment (1968-73), BMJ 2016; 353

“Available evidence from adequately controlled randomised controlled trials suggest replacing saturated fatty acids with mostly n-6 PUFA is unlikely to reduce coronary heart disease events, coronary heart disease  mortality or total mortality. These findings have implications for current dietary recommendations.”

Hamley S, The effect of replacing saturated fat with mostly n-6 polyunsaturated fat on coronary heart disease: a meta-analysis of randomised controlled trials, Nutrition Journal 2017 16:30

Only one recent meta analysis conducted by the American Heart Association (by the authors of the Diet-Heart Policy for Americans, mentioned above) found a relationship between saturated fat intake and coronary heart disease, yet failed to examine cardiovascular mortality (death) or total mortality [24].

NOTE: In 1961, the American Heart Association was the author of the original policy paper recommending to limit saturated fats to protect against heart disease and therefore has a significant interest in defending its longtime institutional position.

With the exception of the American Heart Association review, the conclusion of 9 different meta-analysis and review papers of randomized control trials conducted by independent teams of scientists worldwide do not support the belief that dietary intake of saturated fat causes heart disease.


The PURE (Prospective Urban Rural Epidemiology) was the largest-ever epidemiological study and was published in The Lancet in December 2017 [25]. It recorded dietary intake in 135,000 people in 18 countries over an average of 7 1/2 years, including high-, medium- and low-income nations.  It found;

“High carbohydrate intake was associated with higher risk of total mortality, whereas total fat and individual types of fat were related to lower total mortality. Total fat and types of fat were not associated with cardiovascular disease, myocardial infarction, or cardiovascular disease mortality, whereas saturated fat had an inverse association with stroke. Global dietary guidelines should be reconsidered in light of these findings.”

Dehghan M, Mente A, Zhang X et al, The PURE Study – Associations of fats and carbohydrate intake with cardiovascular disease and mortality in 18 countries from five continents (PURE): a prospective cohort study. Lancet. 2017 Nov 4;390(10107):2050-2062

Those critical of the study say that it has methodological problems, including problems related to the authors dividing consumption of macronutrients (protein, fat and carbohydrate) into 4 groups (quintiles).  Some say that this is reason the data showed an inverse relationship between saturated fat and cardiovascular disease [26]. Criticisms also include that one cannot compare data between countries of substantially different level of income because “low fat consumption is very uncommon in high income countries” and that ‘the ability to afford certain foods may change the dietary pattern (e.g. high-carbohydrate and low-fat diets may be associated with poverty) [26].

Final thoughts…

Both the American and Canadian governments are currently in the process of revising their Dietary Guidelines and I feel that what is needed now is an external, independent scientific review of the current evidence-base for the belief that saturated fat contributes to heart disease.

 

Have questions about which types of fats are best to include in your diet and which are best to limit? Please send me a note using the “Contact Me” tab above and I will reply shortly.

References

  1. Keys, A. Atherosclerosis: a problem in newer public health. J. Mt. Sinai Hosp. N. Y.20, 118–139 (1953).
  2. Yerushalmy J, Hilleboe HE. Fat in the diet and mortality from heart disease. A methodologic note. NY State J Med 1957;57:2343–54
  3. Kromhout D, Keys A, Aravanis C, Buzina R et al, Food consumption patterns in the 1960s in seven countries. Am J Clin Nutr. 1989 May; 49(5):889-94.
  4. McGandy, RB, Hegsted DM, Stare,FJ. Dietary fats, carbohydrates and atherosclerotic vascular disease. New England Journal of Medicine. 1967 Aug 03;  277(5):242–47
  5. The National Diet-Heart Study Final Report.” Circulation, 1968; 37(3 suppl): I1-I26. Report of the Diet-Heart Review Panel of the National Heart Institute. Mass Field Trials and the Diet-Heart Question: Their Significance, Timeliness, Feasibility and Applicability. Dallas, Tex: American Heart Association; 1969, AHA Monograph no. 28.
  6. Introduction to the Dietary Goals for the United States – by Dr D.M. Hegsted. Professor of Nutrition, Harvard School of Public Health, Boston, MASS., page 17 of 130, https://naldc.nal.usda.gov/naldc/download.xhtml?id=1759572&content=PDF
  7. Volek JS, Fernandez ML, Feinman RD, et al. Dietary carbohydrate restriction induces a unique metabolic state positively affecting atherogenic dyslipidemia, fatty acid partitioning, and metabolic syndrome. Prog Lipid Res 2008;47:307–18
  8. Forsythe CE, Phinney SD, Fernandez ML, et al. Comparison of low fat and low carbohydrate diets on circulating fatty acid composition and markers of inflammation. Lipids 2008;43:65–77
  9. Tribble DL, Holl LG, Wood PD, et al. Variations in oxidative susceptibility among six low density lipoprotein subfractions of differing density and particle size. Atherosclerosis 1992;93:189–99
  10. Foster GD, Wyatt HR, Hill JO, et al. A randomized trial of a low-carbohydrate diet for obesity. N Engl J Med 2003;348:2082–90.
  11. Stern L, Iqbal N, Seshadri P, et al. The effects of low-carbohydrate versus conventional weight loss diets in severely obese adults: one-year follow-up of a randomized trial. Ann Intern Med 2004;140:778–85
  12. Gardner C, Kiazand A, Alhassan S, et al. Comparison of the Atkins, Zone, Ornish, and LEARN diets for change in weight and related risk factors among overweight premenopausal women. JAMA 2007;297:969–77
  13. Yancy WS Jr., Olsen MK, Guyton JR, et al. A low-carbohydrate, ketogenic diet versus a low-fat diet to treat obesity and hyperlipidemia: a randomized, controlled trial. Ann Intern Med 2004;140:769–77
  14. Shai I, Schwarzfuchs D, Henkin Y, et al. Dietary Intervention Randomized Controlled Trial (DIRECT) Group. Weight loss with a low-carbohydrate, Mediterranean, or low-fat diet. N Engl J Med 2008;359:229–41
  15. Dreon DM, Fernstrom HA, Campos H, et al. Change in dietary saturated fat intake is correlated with change in mass of large low-density-lipoprotein particles in men. Am J Clin Nutr 1998;67:828–36
  16. Skeaff CM, PhD, Professor, Dept. of Human Nutrition, the University of Otago, Miller J. Dietary Fat and Coronary Heart Disease: Summary of Evidence From Prospective Cohort and Randomised Controlled Trials, Annals of Nutrition and Metabolism, 2009;55(1-3):173-201
  17. Hooper L, Summerbell CD, Thompson R, Reduced or modified dietary fat for preventing cardiovascular disease, 2012 Cochrane Database Syst Rev. 2012 May 16;(5)
  18. Chowdhury R, Warnakula S, Kunutsor S et al, Association of Dietary, Circulating, and Supplement Fatty Acids with Coronary Risk: A Systematic Review and Meta-analysis, Ann Intern Med. 2014 Mar 18;160(6):398-406
  19. Schwingshackl L, Hoffmann G Dietary fatty acids in the secondary prevention of coronary heart disease: a systematic review, meta-analysis and meta-regression BMJ Open 2014;4
  20. Hooper L, Martin N, Abdelhamid A et al, Reduction in saturated fat intake for cardiovascular disease, Cochrane Database Syst Rev. 2015 Jun 10;(6)
  21. Harcombe Z, Baker JS, Davies B, Evidence from prospective cohort studies does not support current dietary fat guidelines: a systematic review and meta-analysis, Br J Sports Med. 2017 Dec;51(24):1743-1749
  22. Ramsden CE, Zamora D, Majchrzak-Hong S, et al, Re-evaluation of the traditional diet-heart hypothesis: analysis of recovered data from Minnesota Coronary Experiment (1968-73), BMJ 2016; 353
  23. Hamley S, The effect of replacing saturated fat with mostly n-6 polyunsaturated fat on coronary heart disease: a meta-analysis of randomised controlled trials, Nutrition Journal 2017 16:30
  24. Sachs FM, Lichtenstein AH, Wu JHW et al, Dietary Fats and Cardiovascular Disease: A Presidential Advisory From the American Heart Association,  Circulation. 2017 Jul 18;136(3)
  25. Dehghan M, Mente A, Zhang X et al, The PURE Study – Associations of fats and carbohydrate intake with cardiovascular disease and mortality in 18 countries from five continents (PURE): a prospective cohort study. Lancet. 2017 Nov 4;390(10107):2050-2062
  26. Sigurdsson, AF, The Fate of the PURE Study – Fat and Carbohydrate Intake Revisited, Doc’s Opinion, October 16 2017,  www.docsopinion.com/2017/10/16/pure-study-fats-carbohydrates/

Copyright ©2018 BetterByDesign Nutrition Ltd. 

LEGAL NOTICE: The contents of this blog, including text, images and cited statistics as well as all other material contained here (the “content”) are for information purposes only.  The content is not intended to be a substitute for professional advice, medical diagnosis and/or treatment and is not suitable for self-administration without the knowledge of your physician and regular monitoring by your physician. Do not disregard medical advice and always consult your physician with any questions you may have regarding a medical condition or before implementing anything  you have read or heard in our content.

 

The Marketing of Polyunsaturated Vegetable Oils

Yesterday, in preparing to begin a new series of articles on the relationship between polyunsaturated vegetable fats to obesity, I came across an old, yellowed sheet titled “Comparison of Dietary Fats” that I was given as an undergrad Dietetic student at McGill, in 1989.

(reverse side) Comparison of Dietary Fats – “Provided as a Professional Service by Proctor & Gamble”, 1989 – full size photo, below

It was designed to help us teach consumers how to choose the “healthiest” dietary fats.

As indicated at the bottom of both sides of the handout (see full size photos, below), it was “provided as a Professional Service by Proctor and Gamble“.

Why would Proctor and Gamble, a soap company provide future Dietitians with a teaching handout on choosing healthy oils for cooking? A bit of understanding about how soap is made, will help.

At the time, the making of soap required a mixture of animal fats and lye, however William Procter and James Gamble (brothers-in-law living in Cincinnati in the late 1800s and who formed Proctor and Gamble) needed to find an inexpensive replacement for animal fat for the creation of individually wrapped bars of soap.

The source of soap fat they turned to was a waste-product of the cotton industry – cottonseed oil. It was literally the garbage leftover when cotton was produced and is cloudy, red and bitter to the taste, and toxic to most animals.

They needed to make cottonseed oil solid in order to make bar soap and utilized a newly patented technology to produce a creamy, pearly white substance out of cottonseed oil. This fat resembled lard (the most popular natural animal fat baking and frying fat at the time), so with a little more tweaking, this hydrogenated cottonseed oil was then sold in 1911 by Procter & Gamble to home cooks as Crisco® shortening.

All that was needed now was for Proctor and Gamble to market this industrially-produced seed oil fat, and market it they did. They hired America’s first full-service advertising agency, the J. Walter Thompson Agency that employed graphic artists and professional writers.

“Samples of Crisco were mailed to grocers, restaurants, nutritionists, and home economists. Eight alternative marketing strategies were tested in different cities and their impacts calculated and compared.

Doughnuts were fried in Crisco and handed out in the streets.

Women who purchased the new industrial fat got a free cookbook of Crisco recipes. It opened with the line, “The culinary world is revising its entire cookbook on account of the advent of Crisco, a new and altogether different cooking fat.” [1]

From the very beginning, Proctor and Gamble marketed their industrially-created solid fat (Crisco®) to “nutritionists” and “home economists” – the forerunners to Dietitians.

When Procter & Gamble introduced Puritan Oil® in 1976, a liquid cooking oil made of sunflower oil which became 100% canola oil by 1988, it was natural for them to market their newly created oil to Dietitians.  

Proctor & Gamble now had a lucrative business manufacturing industrial seed oils as dietary fats and they wanted to make sure that we, as Dietitians encouraged people to use their “healthy” fats.

I’ve scanned in both sides of the handout (it’s old and yellowed, having been kept in the back of my “new” 1988 Canada’s Food Guide book for almost 30 years). As can be seen, in first place on the front side of the handout is canola oil identified by the trade name “Puritan Oil®“, a registered trademark of Proctor and Gamble.

(front side) Comparison of Dietary Fats – “Provided as a Professional Service by Proctor & Gamble”, 1989

On the reverse side, is what consumers should know about these oils, including that canola oil is “better than all other types of vegetable oil“.

(reverse side) Comparison of Dietary Fats – “Provided as a Professional Service by Proctor & Gamble”, 1989

I’ve highlighted some of the wording that makes Proctor & Gamble’s bias apparent;

(reverse side) Comparison of Dietary Fats – “Provided as a Professional Service by Proctor & Gamble”, 1989 – red text mine

Some Final Thoughts…

From the very beginning, industrially-produced seed  fats and oils have been marketed to nutritionists, home economists and Dietitians by the companies that created them, in some cases as a “Professional Service”.

As will become clear in the next article we, as Dietitians were tasked by the Dietary Guidelines in both Canada and the US with promoting “polyunsaturated vegetable oils” to the public as ‘healthful alternatives’ to presumably unhealthy saturated animal fats. The manufacturers were there to ‘assist’ as a ‘Professional Service’.

Looking back on the role of fat manufacturers and the sugar industry (outlined in the preceding article) on which foods were recommended and promoted, it makes me question what I was taught and who affected what I was taught. Given that it was known at the time the sugar industry funded the researchers that implicated saturated fat as the alleged cause of heart disease, I wonder what we don’t know about which industry funded which research.  After all, the knowledge about the sugar industry having funded the researchers that implicated saturated fat only ‘came out’ in November 2016 when it had occurred decades earlier.


NOTE: It is increasingly my conviction that the simultaneous (1) marketing of polyunsaturated vegetable oil (soybean oil, canola oil) along with (2) changes in the Dietary Recommendations for people to (a) eat no more than 20- 30% of calories from fat and to (b) limit saturated fat to no more than 10% of calories, combined with the recommendations for people to (c) eat 45-65% of calories as carbohydrate was the “perfect storm” that may well explain the current obesity crisis and associated  increase in metabolic health problems that we now see 40 years later.

In subsequent articles I’ll elaborate on why I believe this is the case.

 

References

  1. Ramsey, D*., Graham T., The Atlantic. How Vegetable Oils Replaced Animal Fats in the American Diet, April 26 2012 (www.theatlantic.com/health/archive/2012/04/how-vegetable-oils-replaced-animal-fats-in-the-american-diet/256155/)

*Dr. Drew Ramsey, MD is an assistant clinical professor of psychiatry at Columbia University.


Copyright ©2018 BetterByDesign Nutrition Ltd. 

LEGAL NOTICE: The contents of this blog, including text, images and cited statistics as well as all other material contained here (the “content”) are for information purposes only.  The content is not intended to be a substitute for professional advice, medical diagnosis and/or treatment and is not suitable for self-administration without the knowledge of your physician and regular monitoring by your physician. Do not disregard medical advice and always consult your physician with any questions you may have regarding a medical condition or before implementing anything  you have read or heard in our content.

 

 

Researchers that Blamed Saturated Fat as Cause of Heart Disease – paid by sugar industry

A year ago, I found out from a fellow Dietitian that a recently published article in the Journal of the American Medical Association revealed that the sugar industry had secretly funded a group of renowned Harvard researchers to write an influential series of articles which downplayed, discredited or outright ignored research known at the time, and which demonstrated that sugar was a contributor to heart disease.

I read the article and was stunned at its significance.

As I am in the midst of a new series of articles on the role of saturated fat and polyunsaturated fat in health and disease, I felt it’s important that people understand the sugar’s industry involvement in potentially skewing of the scientific evidence at the very time that the original 1977 low-fat high carb Dietary Guidelines were being formulated and so I researched further and wrote this article.

Two of the prominent Harvard researchers that were paid by the sugar industry and who wrote articles dismissing that sugar was a significant contributor to heart disease and implicating saturated fat as the cause were the late Dr. Fredrick Stare, chair of Harvard’s School of Public Health Nutrition Department and the late Dr. D. Mark Hegsted, a professor in the same department [2].

POST PUBLICATION NOTE (March 12 2018): Dr. Hegsted, one of the 3 Harvard researchers paid by the sugar industry to write these review articles was directly involved in developing and editing the 1977 US Dietary Guidelines [6].

A commentary in the Journal of Accountability in Research [4] summarized the significance of those articles as follows;

“Researchers were paid handsomely to critique studies that found sucrose [sugar] makes an inordinate contribution to fat metabolism and heart disease leaving only the theory that  dietary fat and cholesterol was the primary contributor.”

In the mid-1960’s, the Sugar Research Foundation (which is the predecessor to the Sugar Association) wanted to counter research that had been published at the time which suggested that sugar was a more important cause of atherosclerosis than dietary fat. The Sugar Research Foundation invited Dr. Stare of Harvard’s School of Public Health Nutrition Department to join its scientific advisory board and then approved $6,500 in funds ($50,000 in 2016 dollars) to support a review article that would respond to the research showing the danger of sucrose[2].  Letters exchanged between the parties were brought to light in the November 2016 article published by Kearns et al [1] maintained that the Sugar Research Foundation tasked the researchers with preparing “a review article of the several papers which find some special metabolic peril in sucrose [sugar] and, in particular, fructose [3].”

This would seem akin to the tobacco industry having secretly funded articles demonstrating that something other than smoking was responsible for lung cancer.

In August 1967 the New England Journal of Medicine published the first review article written by Drs. Stare, Hegsted and McGandy titled “Dietary fats, carbohydrates and atherosclerotic vascular disease”[3] which stated;

“Since diets low in fat and high in sugar are rarely taken, we conclude that the practical significance of differences in dietary carbohydrate is minimal in comparison to those related to dietary fat and cholesterol

The report concluded;

“the major evidence today suggests only one avenue by which diet may affect the development and progression of atherosclerosis. This is by influencing the levels of serum lipids [fats], especially serum cholesterol.”

The Harvard researchers went on to say;

“there can be no doubt that levels of serum cholesterol can be substantially modified by manipulation of the fat and cholesterol of the diet.”

The Harvard researchers concluded;

“on the basis of epidemiological, experimental and clinical evidence, that a lowering of the proportion of dietary saturated fatty acids, increasing the proportion of polyunsaturated acids and reducing the level of dietary cholesterol are the dietary changes most likely to be of benefit.”

Stare, Hegsted and McGandy did not disclose that they were paid by the Sugar Research Foundation for the two-part review [4].

In response to Kearns et al article in the Journal of the American Medical Association in November 2016 [1], the Sugar Association responded [5] by stating that it;

should have exercised greater transparency in all of its research activities, however, when the studies in question were published funding disclosures and transparency standards were not the norm they are today.” [5]

Some final thoughts…

The reviews written by these influential Harvard School of Public Health Nutrition Department researchers and paid for by the sugar industry have the appearance of being deliberate manipulation of the perception of the scientific evidence known at the time. 

Whether deliberate or inadvertent, the fact that such sponsorship occurred at the very period in time when the Dietary Guidelines were under revision to emphasize that saturated fat intake must be reduced and carbohydrate consumption must be increased cannot be understated a move which certainly benefited the sugar industry.

POST PUBLICATION NOTE (March 12 2018): Discovered after publication of this article, one of the three Harvard researchers funded by the sugar industry, Dr. D.M Hegsted was one of the scientists that worked on the 1977 US Dietary Guidelines[6].

How has this turned out for us?

For the last 40 years, Americans and Canadians have diligently eaten more carbohydrate (including foods containing sucrose and fructose) and more polyunsaturated fats (especially soybean and canola oil) just as the Harvard researchers paid for by the sugar industry recommended and to what end

Obesity rates have gone from ~10% in the 1950’s and 60’s in both countries to 26.7% in Canada (2015) and ~34% in the US (2017) and Diabetes and high blood pressure (hypertension) rates have risen exponentially.

What’s going on?

Could it be that the shift to a diet abundant in omega-6 polyunsaturated fat (such as soyabean oil) and which supplies 45-65% of daily calories as carbohydrate created the ‘perfect storm‘ which inadvertently fueled the obesity and health epidemic we now see?

This will be the subject of future articles.

Have questions?

Please send me a note using the “Contact Me” tab above and I will reply shortly.


Copyright ©2018 BetterByDesign Nutrition Ltd.

LEGAL NOTICE: The contents of this blog, including text, images and cited statistics as well as all other material contained here (the “content”) are for information purposes only.  The content is not intended to be a substitute for professional advice, medical diagnosis and/or treatment and is not suitable for self-administration without the knowledge of your physician and regular monitoring by your physician. Do not disregard medical advice and always consult your physician with any questions you may have regarding a medical condition or before implementing anything  you have read or heard in our content.

The Role of Protein in the Diet of Older Adults

This article is based largely on a lecture given by Dr. Donald Layman, PhD - Professor Emeritus from the University of Illinois (Nutrition Forum, June 23, 2013, Vancouver, British Columbia, Canada).

People understand it’s important for children to eat enough protein because they’re growing but adults and older adults need to eat enough protein each day, as well.

After youth have finished growing, they are at their maximum physical capacity between age 20 and 30 years old and after the age of 30 years old, adults begin to lose muscle mass at the rate of 1% per year [1].

We’ve come to expect that as people age, they will gain more fat, loose bone mass and that they’ll have decreased muscle strength and that in time, these will lead to difficulty getting around, a greater risk of falls and eventually to physical disability. We commonly see older people with spindly legs and bony arms and we think of this as ‘normal’, but as discussed in a recent “A Dietitian’s Journey” article, we’ve mixed up what is “common” with what is “normal”.  When we look at seniors in Okinawa, Japan for example, we don’t see this. They continue to do manual jobs and practice martial arts well into their 80’s and 90’s. Aborigine elders in Australia also remain lean, fit and active as seniors. This is normal.

The physical deterioration that we associate with aging including weak bones (osteoporosis) and the loss of skeleton muscle mass (sarcopenia) don’t develop suddenly, but take place over an extended period of time – brought on by less than optimal practices in early middle age.

How Much Protein?

The Recommended Dietary Allowance (RDA) for protein is set at 0.8 g protein/kg per day and describes the minimum quantity of protein that needs to be eaten each day to prevent deficiency. Protein researchers propose that while sufficient to prevent deficiency, this amount is insufficient to promote optimal health as people age[2].

There have been several recent “position statements” issued by those that work with an aging population indicating that protein intake between 1.0 and 1.5 g protein / kg per day may provide optimal health benefits during aging [3, 4]. This seems at odds with the 2010 Dietary Guidelines Advisory Committee report [5] which states that ‘protein intake in the US is more than adequate’ and that ‘inadequate protein intake is rare’ [5]. These seemingly contradictory positions are largely due to a difference in terms of how protein adequacy is determined.

The RDA – more specifically the Estimated Average Requirement (EAR) is the minimum amount of protein intake required to prevent deficiency and is based on nitrogen balance studies (since nitrogen is the main component of the amino acids which make up proteins). The EAR is set at the amount of protein that allows the body to achieve nitrogen balance (protein making and protein breakdown is equal) and evaluates overall protein intake.  Evaluation of optimal protein intake not only considers total amount of protein eaten, but also evaluates the metabolic roles of individual amino acidsWhile the EAR may be enough protein for healthy younger adults, higher intakes of specific Essential Amino Acids (ones the body can’t make, e.g.  Leucine and Isoleucine and Valine) have been reported to improve body composition (muscle mass and increased strength) in older adults.

Another factor is that nitrogen balance studies look at the total amount of protein eaten in a day but don’t look at the amount of protein eaten at each meal [6,7] nor the role of the Essential Amino Acid Leucine which is  required to be present for protein synthesis to begin (including synthesis of new protein for muscle and bone)[6].  Leucine is an indispensable amino acid in the making of all types of protein, but has a unique role in signaling the beginning of muscle protein synthesisMuch research has been done with large doses of free leucine, however a 2012 animal study[6] found that in small meals with limited protein intake (often the case for older adults), that there was a specific minimum amount of Leucine required to be be present, before protein synthesis took placeThis “Leucine threshold” had to be met or exceeded before the body would even begin the energy-expensive process of making new proteins!

Typically, the average American eats only 10 g protein for breakfast, 15 g protein for lunch and has most of their daily protein at supper (65 g protein at supper) and since the minimum amount of Leucine that needs to be present in a meal (i.e. “Leucine Threshold“) is not enough at breakfast and lunch with this pattern of protein intake, protein synthesis is only triggered after the evening meal. As elaborated on below, it is recommended that this change.

A 2013 study of muscle protein synthesis in adults in their late 30’s found that when the amount of protein is distributed evenly throughout the day (30 g protein at breakfast, lunch and supper) that significantly more muscle protein was madeOf importance, the (a) making of new protein and (b) the threshold at which protein will be triggered to be made differ with agewith older people needing a higher intake of protein and specifically the amino acid Leucine, than younger adults [8]. This reduced muscle protein synthesis has been called “anabolic resistance” (anabolic means to ‘build’) and studies have shown that this “anabolic resistance” can be overcome with meals containing higher amounts of Essential Amino Acids and appears to be related to the Leucine content of the meal [8]. These findings led to Dietary Recommendations for older adults that emphasize a minimum of 20 g of protein per meal containing more than 2.3 g Leucine to optimize the building of new muscle protein [4].

Final Thoughts…

It is not only growing children and youth that need to eat adequate protein daily, but older adults as well. In many Indigenous cultures, the Elders eat first and eat the best of the animal proteins – which may factor in to the preservation of bone and muscle mass we see in many of these cultures.

The average protein intake for men >20 years old in the US is ~98 g per day and for women it is 68 g per day which may be adequate in total for healthy young adults, but is considered imbalanced in terms of distribution, as a minimum amount of Leucine is required for protein synthesis (specific amount in humans has not yet be determined). Dr. Layton recommends that until further research is conducted and the optimal amount of Leucine is determined that young adults and middle aged adults distribute their protein evening throughout the day with ~25 g (women) -30 g (men) of animal-based protein at each meal. The reason high biological value proteins from animal sources (meal, poultry, fish, egg, dairy) are recommended is because these are high in Leucine (rather than having only 10 g protein for breakfast, 15 g protein for lunch and 65 g protein at supper).

The recommendations above for older adults to eat 1.0 – 1.5 g protein / kg per day distributed evening over three meals which would be on average ~30-40g of animal-based protein at each meal to provide for optimal muscle protein synthesis, preventing sarcopenia – the muscle loss we’ve come to see as ‘normal’ in aging.

How much is too much protein?

According to Dr. Layton, the Upper Limit of Protein according to the Recommended Daily Allowance for Protein is set at ~ 2.5 g protein / kg per day which would put the maximum amount for most adult men at ~200 g protein per day.

Recommended Daily Allowance (RDA) for Protein [slide from Dr. Donald Layman, PhD – The Evolving Role of Dietary Protein in Adult Health]
Have questions?

Need help determining how much protein you should optimally be eating at each meal and from what sources? Please send me a note using the “Contact Me” form and I will reply as soon as possible.

 


References

  1. Keller K, Engelhardt M. Strength and muscle mass loss with aging process. Age and strength loss. Muscles, Ligaments and Tendons Journal. 2013;3(4):346-350.
  2. Volpi E, Campbell WW, Dwyer JT, et al. Is the optimal level of protein intake for older adults greater than the recommended dietary allowance? J Gerontol A Biol Sci Med Sci. 2013 Jun;68(6):677-81
  3. Fielding RA, Vellas B, Evans WJ, Bhasin S, et al, Sarcopenia: an undiagnosed condition in older adults. Current consensus definition: prevalence, etiology, and consequences. International working group on sarcopenia. J Am Med Dir Assoc. 2011 May;12(4):249-56
  4. Bauer J1, Biolo G, Cederholm T, Cesari M, et al. Evidence-based recommendations for optimal dietary protein intake in older people: a position paper from the PROT-AGE Study Group. J Am Med Dir Assoc. 2013 Aug;14(8):542-59
  5. U.S. Department of Agriculture and U.S. Department of Health and Human Services, Dietary Guidelines for Americans, 2010. 7th Edition, Washington, DC.
  6. Norton LE, Wilson GJ, Layman DK, et al. Leucine content of dietary proteins is a determinant of postprandial skeletal muscle protein synthesis in adult rats. Nutr Metab (Lond). 2012 Jul 20;9(1):67
  7. Mamerow MM, Mettler JA, English KL, et al. Dietary Protein Distribution Positively Influences 24-h Muscle Protein Synthesis in Healthy Adults. The Journal of Nutrition. 2014;144(6):876-880.
  8. Layman DK, Anthony TG, Rasmussen BB, et al. Defining meal requirements for protein to optimize metabolic roles of amino acids, The American Journal of Clinical Nutrition, Volume 101, Issue 6, 1 June 2015, Pages 1330S–1338S

Copyright ©2018 BetterByDesign Nutrition Ltd. 

LEGAL NOTICE: The contents of this blog, including text, images and cited statistics as well as all other material contained here (the “content”) are for information purposes only.  The content is not intended to be a substitute for professional advice, medical diagnosis and/or treatment and is not suitable for self-administration without the knowledge of your physician and regular monitoring by your physician. Do not disregard medical advice and always consult your physician with any questions you may have regarding a medical condition or before implementing anything  you have read or heard in our content.

Unreliability of Many Blood Glucose Monitors

Previous to today, I never gave the reliability of blood glucose monitors a second thought. I assumed that if they were sold in Canada, they were reliable. Not all are as good as others, it seems!

Yesterday morning, as I always do, I tested my morning fasting blood glucose with my glucometer. As someone with Type 2 Diabetes, this helps me understand the effect that the food I had for supper may have had and also helps guide me as to whether I may begin the day with time-delayed eating. For Type 1 Diabetics or insulin-dependent Type 2 Diabetics however, the accuracy of this information is critical! They base the dosage of insulin they take on this data and count on it being reliable and accurate.

Accuracy is how close the reading on the meter is to the actual blood glucose value and reliability is the likelihood of repeating the measure with the same meter at the same time and getting the same result.

Yesterday, I swabbed by thumb with an alcohol wipe, let it dry and took my blood glucose reading at 5:27 am and got a reading of 4.8 mmol/L (86 mg/dl) and thought “that can’t be!“, as I know that is a blood sugar reading that I only obtain after more than 18 hours of fasting.

 

I got another test strip from the same vial (recently opened and not expired) and tested the same thumb in a location immediately beside where I had just tested and got a reading of 5.8 mmol/L (105 mg/dl) and thought “that seems more reasonable, but what’s with the meter?”.

Ironically, only several hours prior a physician-friend sent me the link a report from August 14, 2017 that indicated that only 6 out 18 blood glucose meters tested passed the standard for meter accuracy which is for them to be within 15% or 15 mg/dl (0.8 mmol/L) of the laboratory value in 95% of 100 trials. That means there was only a 1/3 pass rate

Naturally, the first thing I did was look up to see how my meter – actually both my meters (which are identical) ranked.  It failed! 

Even though I had brought my glucometer to the lab with me in July when I last had my fasting blood glucose measured and it matched the lab results exactly, my meter failed the test because when tested 100 times, it was NOT accurate 95% of the time.  

To pass a meter had to match or be within 15% or 15 mg/dl (0.8 mmol/L) of the laboratory value on 95/100 trials.

I only tested my meter against the lab value ONCE and assumed it to be accurate. It was accurate on that one occasion, but it was not reliable, because when repeating the measure 100 times with the same meter it did not produce results within the 15% acceptable variation.

At 5:27 AM my blood glucose reading was 4.8 mmol/L and 2 minutes later with a new strip it was 5.8 mmol/L – on the same meter. That is a huge amount of variation, although depending on what the lab value actually would have been at that time, the results may or may not have fallen with range (see box below).

NOTE: The average of the two readings, 4.8 & 5.8 is 5.3 mmol/L and a ±15% tolerance would be ± 0.795 or ~ ± 0.8, for a range of 4.5 mmol/L to 6.1 mmol/L, so the readings would be within that range, ASSUMING the AVERAGE is the CORRECT result.

While 0.8 is +16.7% more than the lower result and -13.8% less than the higher result, the actual ± 0.5 deviation from the mean is +10.4% and -8.6% of the lower & upper results.

If either one result was correct, then 4.8 x 1.15 = 5.52 mmol/L, while 5.8 x 0.85 = 4.93 mmol/L, so the other would be erroneous. 

But,
4.8 ÷ 0.85 = 5.65 mmol/L, and 
5.8 ÷ 1.15 = 5.04 mmol/L, so if the laboratory serum reading fell between 5.04 and 5.65 mmol/L then the meter's two readings would be accurate to within ±15%.

Now ± 15% is 30% of the value which means that 

(a) A serum glucose of 3.5 mmol/L (low end of normal) could mean a glucometer reading range of 1.05, or 3.04 mmol/L to 4.12 mmol/L

A serum glucose of 11 mmol/L (way too high!) would be a 3x larger range of 3.3, or 9.56 mmol/L to 12.94 mmol/L.

[thanks to Dr. L De Foa for the calculations]

Unfortunately, I know that my device(s) are not reliable based on this study data and for people who are insulin-dependent Type 1 or Type 2 Diabetics, they rely on the readings from their blood glucose monitors in order to dose their insulin. When their meters have been proven unreliable, it is cause for major concern.

I am reproducing the main data from this study because it is imperative that people know whether the monitor they are relying on is indeed, reliable.

Overall Results of Blood Glucose Monitoring Systems – Diabetes Technology Society 2018

The full testing protocol and results can be found here.

The rated accuracy from Bayer of the number one rated meter above, the Contour Next USB is 100% within ±0.56 mmol/L for glucose < 5.55 mmol/L and 98.1% within ±10% and 100% within ±15% for blood glucose > 5.55 mmol/L and it was accurate 100% of the time in the tests.

As for me, I have gone back to using a glucometer that I had on hand (which also tests blood ketones), as it is one of the models that passed.

While I am left with almost 1/2 a package of new test strips from the unreliable meter, how much worse could it be for someone who is dosing insulin based on unreliable blood glucose meter reading.

Type 2 Diabetes?

If you have Type 2 Diabetes and have struggled to lower your HbA1C or achieve your weight loss goals please send me a note using the “Contact Me” form above about how I can help and I’ll be happy to reply.


Copyright ©2018 BetterByDesign Nutrition Ltd. 

LEGAL NOTICE: The contents of this blog, including text, images and cited statistics as well as all other material contained here (the “content”) are for information purposes only.  The content is not intended to be a substitute for professional advice, medical diagnosis and/or treatment and is not suitable for self-administration without the knowledge of your physician and regular monitoring by your physician. Do not disregard medical advice and always consult your physician with any questions you may have regarding a medical condition or before implementing anything  you have read or heard in our content.

Significant Improvement in Type 2 Diabetes Symptoms Possible Long Term

In June of 2017 results of a 10-week outpatient study using a  ketogenic diet intervention  were published and demonstrated significant improvements in subject’s body weight, glycated hemoglobin (HbA1C) and medication usage. One year follow-up data has just been published demonstrating that reversal of Type 2 Diabetes symptoms is sustainable over the long term, as participants continue to eat a ketogenic diet.

Participants

There were 238 participants  enrolled in the continuous care intervention at the beginning of the study and all had a diagnosis of Type 2 Diabetes (T2D) when the study began, with an average HbA1c of 7.6% ±1.5%.

Participants ranged in age from 46 – 62 years of age (mean age = 54 years). Sixty-seven (67%) of participants were women and 33% were men.

Weight ranged from 200 pounds to 314 pounds (117±26 kg), with an average weight of 257 pounds (117 kg).  Average Body Mass Index (BMI) was 41 kg·m-2 (class III obesity) ±9 kg·m-2, with 82% categorized as obese.

The majority of participants (87%) were taking at least 1 glycemic control medication at the beginning of the study.

At the end of a year, 218 participants (83%) remained enrolled in the  continuous care intervention group.

Intervention

Each participant received an Individualized Meal Plan for nutritional ketosis, behavioral and social support, biomarker tracking tools, and ongoing care from a health coach with medication management by a physician.

Subjects typically required <30 g·day−1 total dietary carbohydrates. Daily protein intake was targeted to a level of 1.5 g·kg−1 based on ideal body weight and participants were coached to incorporate dietary fats until they were no longer hungry. Other aspects of the diet were individually tailored to ensure safety, effectiveness and satisfaction, including consumption of 3-5 servings of non-starchy vegetables and enough mineral and fluid intake. The blood ketone level of β-hydroxybutyrate was monitored using a portable, handheld device.

Ten Week and One Year Outcomes

Medication Use

At baseline, 87% of participants were taking at least one medication for Diabetes and at 10 weeks, almost 57% had one or more Diabetes medications reduced or eliminated.

After one year, Type 2 Diabetes medication prescriptions other than metformin declined from 57% to just below 30%.

Insulin therapy was reduced or eliminated in 94% of users and sulfonylurea medication was entirely eliminated in the  continuous care intervention group.

Glycosylated Hemoglobin (HbA1C)

At baseline, the average HbA1c level was 7.6% ±1.5%, with less than 20%  of participants having a HbA1c level of <6.5% (with medication usage).

After 10 weeks, HbA1c level was reduced by 1.0% and the percentage of individuals with an HbA1c level of <6.5% was 56%.

Average HbA1C Reduction after One Year [from Effectiveness and Safety of a Novel Care Model for the Management of Type 2 Diabetes at 1 Year: An Open-Label, Non-Randomized, Controlled Study.]
On average after 1 year, participants in the intervention group lowered HbA1c from 7.6% to 6.3% – which is in the sub-Diabetes range.

Weight Loss

At 10 weeks, mean body mass reduction was 7.2% from a baseline average of 117 kg (257.4 pounds) ±26 kg / 57 lbs.

Average Weight Loss at One Year [from Effectiveness and Safety of a Novel Care Model for the Management of Type 2 Diabetes at 1 Year: An Open-Label, Non-Randomized, Controlled Study.]
At one year, mean body mass reduction of participants was  12% of their initial body weight.

Other Metabolic Markers

At 10 months, participants experienced a 20% reduction in triglycerides and after one year, reduction in triglycerides was at 24%.  After one year, LDL increased on average by 10% however HDL increased on average by 18%. Serum  creatinine and liver enzymes (ALT, AST, and ALP) also declined.

Conclusion

This intervention study demonstrated that individualized nutrition care plans that encourage nutritional ketosis can significantly result in reduced weight, HbA1c and medication use within 10 weeks, and that these outcomes can be sustained, or even improved on  over the long term, as participants continue to eat a ketogenic diet.  

Do you have questions about how a carefully-designed low carbohydrate or ketogenic diet can help you improve symptoms of Type 2 Diabetes?

Please send me a note using the “Contact Me” form above to find out more about how I can provide you with in-person or Distance Consultation services (via Skype or long distance telephone).

To our good health,

Joy

Copyright ©2018 BetterByDesign Nutrition Ltd.

LEGAL NOTICE: The contents of this blog, including text, images and cited statistics as well as all other material contained here (the “content”) are for information purposes only.  The content is not intended to be a substitute for professional advice, medical diagnosis and/or treatment and is not suitable for self-administration without the knowledge of your physician and regular monitoring by your physician. Do not disregard medical advice and always consult your physician with any questions you may have regarding a medical condition or before implementing anything  you have read or heard in our content.


References

McKenzie AL, Hallberg SJ, Creighton BC, Volk BM, Link TM, Abner MK, Glon RM, McCarter JP, Volek JS, Phinney SD, A Novel Intervention Including Individualized Nutritional Recommendations Reduces Hemoglobin A1c Level, Medication Use, and Weight in Type 2 Diabetes, JMIR Diabetes 2017;2(1):e5, URL: http://diabetes.jmir.org/2017/1/e5, DOI: 10.2196/diabetes.6981

Hallberg, S.J., McKenzie, A.L., Williams, P.T. et al. Diabetes Ther (2018). Effectiveness and Safety of a Novel Care Model for the Management of Type 2 Diabetes at 1 Year: An Open-Label, Non-Randomized, Controlled Study.  https://doi.org/10.1007/s13300-018-0373-9

Bubby’s Chicken Soup

Many people (including me) are sick with the flu and many are sipping soup, because it is warm and comforting and provides them with some protein, vitamins and minerals. I’m drinking chicken soup, made from my grandmother’s recipe and this isn’t any chicken soup, as you will soon find out.

Whenever someone in my family is sick, it’s me they turn to for chicken soup — but not just any chicken soup, but the one I learned how to make at my grandmother’s knee.

This soup is purported to have curative effects and it must have had something because my Bubby (‘grandmother’) lived until 104 years old and was in very good health until a few months before she passed away (2013).

My grandmother used to joke that she “didn’t lose her marbles” and to be honest, she had more “marbles” at 104 than many do at half that age.

Her chicken soup was amazing — nothing like any similarly named broths by Lipton®’s or Campbell®’s. Bubby’s Chicken Soup was made with love, care and the best of ingredients and was the epitome of what has become known as, “Jewish penicillin“. I still have vivid memories from when I was a little girl of going to the market with my grandmother to pick out a live chicken.

She always served her chicken soup in a “soup plate”, like this and the spoon was deep and round, like a miniature bowl with a handle.

Bubby’s Chicken Soup – served in a ‘soup plate’
same soup – different way to serve

I wonder if she’d be horrified that I drink mine out of a coffee mug!

The first question many people ask me when I talk about my Bubby’s Chicken Soup is “what makes Jewish chicken soup different“?

No, the chickens aren’t “Jewish” (!) — although a kosher soup chicken does make the most amazing broth.

Bubby’s Chicken Soup was made with a special type of chicken and has a texture and a taste unlike any other. To illustrate my point, here is a photo of what Bubby’s Chicken Soup looks like when its chilled;

natural gelatin from the ‘soup chicken” results in this texture, when chilled

It is the special type of chicken that this soup is made from (and a few other special ingredients that I’ll tell you about shortly) that contribute collagen and natural gelatin and result in the chilled broth being like very firm Jello®.

A “soup chicken” (also known as a “stewing hen“) is essential for making this soup. A “roaster” or “broiler” simply won’t do!  They are too young and have too much fat, too much ‘meat’ and too little flavor.

A soup chicken is an old bird that has outlived its usefulness for laying eggs and it’s the age of the chicken that makes it perfect for making soup, because although  the meat is tough it makes the best soup. Old laying hen hav lots of connective tissue and collagen, and it’s this which makes the resulting broth very different. This, and the addition of chicken feet.  Yes, chicken feet.  As my grandmother did, I chop the nails off of them before making soup, but many butchers that sell them, will do this for you, if you ask. One can often find ‘soup chickens’ or ‘stewing chickens’ at independent ethnic butchers or at small supermarkets with a large ethnic clientele and these same markets often sell chicken feet, too.

As you can see from the photo above, soup chickens are small and don’t have hormone-enlarged breasts- in fact, they have very little meat at all, and have almost no fat under the skin. It’s these factors (plus the addition of the feet) that result in the the chilled broth being so gelatinous, with the minimum of fat on it. Jewish Chicken Soup is the original “bone broth“.

Bubby’s Chicken Soup (aka “Jewish Penicillin)

Most people would never give out their grandmother’s family recipe, but since not everyone had a Jewish grandmother,  I thought I’d share mine with you, along with her wonderful recipe for soup!

Bubby’s Chicken Soup 
3 soup chickens / stewing fowl
8 chicken feet (nails removed), cleaned
1 lg onion,  just the outermost skin removed, whole
2 very large carrots,  peeled and cut in chunks
1 parsley root, peeled (I can’t find this in Vancouver, so I use the stems from a bunch of Italian parley plus a very tiny parsnip)
1 stalk of celery, with leaves
Salt to taste
cracked black pepper
Sprig of fresh dill (for garnish)
1 – Put two of the stewing chickens at the bottom of a very large stock pot.
2- Toss the vegetables on top, then the chicken feet.  Cover with very cold water and add salt. Be careful not to put in too much water, otherwise the broth won’t have the correct taste, body or colour. Gently slip in the 3rd soup chicken.
3 – Bring to a boil over medium high heat, skimming off foam with a small mesh designed for this purpose, until it stops producing foam.
4 – Lower heat to medium low and simmer soup for at least 8-10 hours, overnight if possible.
5- Strain the broth through a large colander into another pot (so you only have the rich golden liquid). Pick out the carrot chunks from the colander, and serve with the clear broth. Garnish with fresh dill.

 

Note: for those that are not following a low carbohydrate / ketogenic lifestyle, this soup can also form the basis for “matzoh ball soup”.

Matzoh Ball Soup (from an archived photo)
Enjoy!

What Regulates Body Weight?

Body weight is not under our control as much as we’d like to believe, but is a tightly regulated process that involves a variety hormones with some of the major ones being leptin (a hormone that regulates fat stores by  inhibiting hunger), ghrelin (a hormone that increase hunger when your stomach is empty) and insulin, which plays a very significant role in hunger, eating behavior and fat managementInsulin is one of the major controllers of the body’s “set point”.

What is “set point“?

Think of set point like the thermostat in your house; when the air gets too cold, the thermostat is engaged, and the furnace comes on and when the air gets a little too hot, the thermostat shuts the furnace off. Your body’s set point is maintained by a complex set of hormonal mechanisms that works to maintain your body at its current weight.  If you eat a lot more one day because it’s a special occasion, the next day you won’t feel as hungry as usual, and will eat less. When someone who normally eats a carbohydrate-based diet restricts calories, their body slows its metabolism and lowers the amount of energy (calories) it uses for vital bodily functions in order to ‘save’ the limited calories for use by their brain. In fact, the amount of energy used by your body at rest (called Basal Energy Expenditure) can decrease by as much as 30-50% in order to save those calories!

This saving of calories for essential functions is why when people who are used to eating carbs ‘fast’ or limit the number of calories they eat, they feel cold, tired and find it hard to focus.  This is the body ‘saving’ the few calories for essential body functions, such as for their brain and organs. This doesn’t happen to someone who is fat-adapted, because they use their own fat stores to maintain blood and brain glucose, and for other energy needs.

Equally part of maintaining the body’s set point, when an overweight person takes in too many calories, their body will try to get rid of them by increasing its Basal Energy Expenditure and speeding up breathing rate (respiration), increasing heart rate and generating more body heat.

So, whether we are overweight or underweight, the body will adjust its processes to maintain its ‘set point’.

This is why the so-called calorie in, calorie out model, doesn’t work – because it is not simply a matter of “eating less and moving more“. When people who are carb-dependent restrict their calories, their metabolism slows and so they burn way less calories!

Calories in and calories out are not independent of each other but inter-dependent on each other; when one is lowered (calories in), so is the other (calories out, metabolism).  When one is increased (calories in), so is the other (calories out, respiration, heat generation).

It’s really not as simple as “eating less and moving more” to lose weight, because when we both restrict calories and increase our exercise, our body responds by increasing hungerincreasing craving (especially for foods such as simple carbs that can be broken down quickly for glucose for your blood) and by decreasing the amount of energy it uses. Using the thermostat analogy, our body turns the thermostat down.

Wouldn’t you think that if it were really as simple as “eating less and moving more” that more people would be slim!

Restricting calories doesn’t work for long term weight loss because the body compensates by lowering its energy expenditure. It’s not about how many calories we take in, but about what changes ‘set point’.

It’s mainly about insulin. We have to reduce insulin.

Low-carbohydrate diets and increasing the amount of time between meals (called “intermittent fasting”) are two ways to lower insulin.

Lowering insulin, will in turn will lower blood sugar and when this lifestyle is maintained, over time, it has even shown by researchers to be able to reverse the symptoms of Diabetes. That doesn’t mean people aren’t Diabetic anymore – they are but the symptoms of Diabetes, namely high blood sugar (reflected in high fasting blood glucose and HbA1C) are in remission. Other added benefits include a lowering of blood pressure  (which is closely tied to insulin), gradual, sustainable weight loss and a normalizing of triglycerides as well as some cholesterol  markers.

When people are ‘fat-adapted‘, they have a ready supply of fuel for their bodies (their own fat stores!), and so their metabolism doesn’t slow down when they eat this way. Their bodies continue to burn calories at the usual rate!

Furthermore, they aren’t cold, tired and hungry because they have excess fat stores to serve as a constant supply of fuel for their brain, blood and muscles. Fat is broken down for ketone bodies which can be used for most body processes, and the essential glucose needed by our blood and brain is easily synthesized by the breaking down of fats. 

Thinking about adopting a low-carb or lower-carb lifestyle, but want to read more about it first? Low carb / ketogenic specific articles are located here.

Have questions? Please send me a note using the Contact Us form above.


Copyright © BetterByDesign Nutrition Ltd.

LEGAL NOTICE: The contents of this blog, including text, images and cited statistics as well as all other material contained here (the “content”) are for information purposes only.  The content is not intended to be a substitute for professional advice, medical diagnosis and/or treatment and is not suitable for self-administration without the knowledge of your physician and regular monitoring by your physician. Do not disregard medical advice and always consult your physician with any questions you may have regarding a medical condition or before implementing anything  you have read or heard in our content.

What is the Anti-Inflammatory Protocol and what is it used for?

Changing how and what we eat, as well as managing stress and getting enough restful sleep has been shown in research studies to reduce pain and symptoms in people with chronic inflammatory diseases such as Rheumatoid Arthritis, Fibromyalgia, Hashimoto’s Hypothyroidism, Celiac disease, etc.. As well, there is increasing evidence that cardiovascular disease, including heart attack and stroke are inflammatory in nature and that lowering risk is best managed through dietary and lifestyle changes. For those with a strong family history of heart disease, the Anti-Inflammatory Protocol dove-tails perfectly with a low-carb high healthy fat diet.


Knowing which foods promote inflammation and why and which foods are evidence-based to have anti-inflammatory properties  and why is essential for those seeking to reduce pain and symptoms associated with a chronic inflammatory condition. Choosing foods that are nutrient densepromote gut healthaddress diet-related disruptions in hormone-regulation and that target immune system regulation are key in the Anti-Inflammatory Protocol.

Nutrient density – Every system in the body, including the immune system requires an array of vitamins, minerals, antioxidants, essential fatty acids, and amino acids to function normally. Micronutrient deficiencies and imbalances are considered key players in the development and progression of autoimmune disease, therefor attention is put on consuming the most nutrient-dense foods available. A nutrient-dense diet provides the ‘building blocks’ that the body needs to heal damaged tissues. The goal is to supply the body with a surplus of micronutrients to correct both deficiencies and imbalances, supporting regulation of the immune system, hormone and neurotransmitter production.

Gut health – It is thought that ‘gut dysbiosis’ (gut microbial imbalance) and ‘leaky gut’ may be key facilitators in the development of autoimmune disease. The foods recommended on the Anti-inflammatory Protocol support the growth of healthy levels and a healthy variety of gut microorganisms. Foods that irritate or damage the lining of the gut are avoided, while foods that help restore gut barrier function and promote healing are encouraged.

Diet-related Disruptions in hormone regulation – What we eat, when we eat, and how much we eat affects a variety of hormones that interact with the immune system. Eating foods with too much sugar or ‘grazing’ throughout the day, rather than eating food at set meals spaced apart deregulate these hormones. As a result, the immune system is typically stimulated. Promoting regulation of these hormones through diet, in turn has a modulating effect on the immune system. As well, dietary hormones that impact the immune system are also profoundly affected by how much sleep we get, how much and what kinds of activity we do, and how well we reduce and manage stress, so looking at diet and lifestyle together, is key.

Immune system regulation – Our intestines are home to millions of bacteria which live in symbiotic relationship with us.  We provide food for them and when in balance, they maintain the integrity of the gut wall, which serves as a protective barrier. When our gut ‘flora’ gets out of balance, having an excess of pathogenic bacteria, this protective barrier becomes compromised, resulting in small ‘holes’ that permit exchange between the inside of our gut and the blood stream.  This is what is called “leaky gut“. Endotoxins produced by the proliferation of “bad” bacteria can get into the blood stream, stimulating the immune system, and resulting in systemic inflammation. What becomes critical is to limit the factors that contribute to excess of the “bad bacteria” and restore a healthy amount and diversity of “good” gut microorganisms, so that the gut once again functions as a protective barrier, and immune system regulation is achieved.

What is the Anti-Inflammatory Protocol?

The Anti-Inflammatory Protocol identifies foods that promote inflammation from those that research indicates have anti-inflammatory properties. It isn’t simply a list of “eat this” and “don’t eat that”, but explains what about a particular food promotes inflammation or inhibits it. It explains the role of key inflammatory -producing compounds such as lectinssaponins and protease inhibitors, and which foods they are found in, and how eating those foods contribute to “leaky gut“. Which grains can one eat?  Which should be avoided? What about beans and lentils? Are there some better than others?

The Anti-Inflammatory Protocol explains which healthy cooking and eating fats won’t contribute to the production of Advanced Glycation End-Products (AGEs) – and how this compound causes oxidative damage to the cells in the body. Knowing this enables people to know whether oils such as grapeseed for example, are a good choice and if not, why – as well as which other oils would be preferable.

I want people to understand in simple terms how omega 6 (ω-6) fats compete for binding sites and elongation enzymes with omega 3 (ω-3) fats, as this enables them to determine whether foods such as nuts and seeds should be included in an anti-inflammatory diet. If they understand the role of hormones such as insulin and what causes it’s release, they can determine for themselves whether products like agave syrup or coconut sugar are preferable to table sugar when following an anti-inflammatory protocol. I find that once people understand the theory as to why they should eat less of certain foods (explained in ways that don’t require an educational background in science!) and they also understand which types of foods they should aim to eat more of, they are empowered to make dietary choices that contribute to reducing inflammation, as well as symptoms, along with risk factors for other inflammation-related conditions.

I consider my primary role is as an educator. I don’t want to tell someone they need to eat this food on this day and this other food on the next day.  It is far more rewarding and helpful to them, if I help them know how to make these decisions themselves.

Want to know more?

Why not send me a note using the “Contact Us” form above.

To our good health,

Joy


 https://twitter.com/joykiddieRD

  https://www.facebook.com/BetterByDesignNutrition/


Copyright ©2017 BetterByDesign Nutrition Ltd.  LEGAL NOTICE: The contents of this blog, including text, images and cited statistics as well as all other material contained here (the “content”) are for information purposes only.  The content is not intended to be a substitute for professional advice, medical diagnosis and/or treatment and is not suitable for self-administration without regular monitoring by a Registered Dietitian and with the knowledge of your physician. Do not disregard medical advice and always consult your physician with any questions you may have regarding a medical condition or before implementing something you have read or heard in our content. 

Part 2: How is Insulin Resistance Measured?

The introduction to this article (Part 1: What is Insulin Resistance)  explains what insulin resistance is, the conventional treatment for it and the drawbacks to that treatment: http://www.bbdnutrition.com/2017/07/26/what-is-insulin-resistance/

INTRO: There are a number of tools available for measuring insulin resistance, most of which are more suited to a research setting, including the Quantitative Insulin Sensitivity Check Index (QUICKI) and the Matsuda Index.  Others, such as the McAuley -, Belfiore -, Cederholm -, Avignon – and Stumvoll Index are better suited for epidemiological (population) research studies and are often compared to the “gold standard” for the measurement of insulin sensitivity, the Hyperinsulinemic Euglycemic Clamp (HEC).

The homeostasis model assessment (HOMA-IR) method is suitable for individuals to use with their doctors or Dietitians to assess insulin resistance, and is useful for using over time to measure the impact of dietary and lifestyle changes in lowering insulin resistance.


Visualizing Insulin Resistance

Insulin resistance can be determined by measuring insulin response to a standard glucose load over a 5 hour period and plotting the Insulin Response curves – which is precisely what Dr. Joseph R. Kraft MD, who was Chairman of the Department of Clinical Pathology and Nuclear Medicine, St. Joseph Hospital, Chicago, until his retirement.

Dr. Kraft spent more than a quarter century devoted to the study of glucose metabolism and blood insulin levels – collecting data in almost 15,000 people, aged 3 to 90 years old. Between 1972 and 1998, Dr. Kraft measured the Insulin Response and data from 10,829 of these subjects indicated that 75% of subjects were insulin resistant.

Compiling this data, five distinct Insulin Response Patterns emerged.

Pattern I

The light green curve below, is what a normal insulin response should look like. Insulin levels should rise steadily in the first 45 minutes (in response to the standard glucose load) to no higher than ~60 mIU/L (430.5 pmol/L) and then decrease steadily until baseline by 3 hours.

PATTERN II

People who are in the early stages of insulin resistance (Pattern II, represented by the yellow curve) release considerably more insulin in response to the exact same glucose load. Insulin levels rise to ~ 115 mIU/L (825 pmol/L) in the first hour and then take considerably longer (5 hrs) to drop back down to baseline, than the normal response.

PATTERN III

People who have progressed in insulin resistance to Pattern III have insulin levels that keep rising for the first 2 hours and then drop off more sharply, back down to baseline.

PATTERN IV

Those with Type 2 Diabetes / very high insulin resistance (Pattern IV) release huge amounts of insulin almost immediately, reaching levels of ~ 150 mIU/L (1076 pmol/L) at 1 hour.  Then for the next 2 hours, insulin continues to climb, before it begins to decline to baseline.  Even at 5 hours, insulin levels never decrease to normal values.

PATTERN V

Is what is seen in Type I Diabetes (T1D), when there is insufficient insulin production.

Please see Significance of Insulin Resistance for more details on Dr. Kraft's findings: http://www.bbdnutrition.com/2017/03/22/featured-significance-of-insulin-resistance/

While a 5 hour glucose tolerance test is not available at most labs, a 2 hour glucose tolerance test (2hrGTT) will indicate whether or not a person is insulin resistant or Type 2 Diabetic. 

However, once a person is already diagnosed as Type 2 Diabetic, most medical plans will not cover the cost of having the test re-performed in order to determine if insulin response has changed in response to diet and lifestyle changes.

This is where the the homeostasis model assessment of insulin resistance (HOMA-IR) comes in – a tool easily used by clinicians and relying on standard blood tests.

Homeostasis model assessment of insulin resistance (HOMA1-IR) – Matthew’s Equations (1985)

The homeostasis model assessment was first developed in 1985 by David Matthews et al and is method used which quantifies insulin resistance and β-cell function of the pancreas from fasting blood glucose and either fasting insulin or C-peptide concentrations.

Pancreatic β-cells are responsible for insulin secretion in response to increasing glucose concentrations, so when there is decreased function of the pancreas’ β-cells, there will be a reduced response of β-cell to glucose-stimulated insulin secretion.

In addition, glucose concentrations are regulated by insulin-mediated glucose production in the liver, so insulin resistance is reflected by reduced suppression of hepatic glucose production, stemming from the effect of insulin.

The HOMA-IR model describes this glucose-insulin homeostasis using a simple equation, based on fasting blood glucose and fasting insulin. The equation uses the product of fasting plasma insulin (FPI) x fasting plasma glucose (FPI), divided by a constant of 22.5, providing an index of hepatic insulin resistance:

HOMA1-IR = FPI (mu/I) x FBG (mmol/L) / 22.5

The “Blood Code” book is based on these 1985 equations. The problem with the Matthew’s Equations is that they underestimate Insulin Sensitivity (%S) and overestimate % β-cell function.

Homeostasis model assessment of insulin resistance (HOMA2-IR)

Oxford University, Centre for Diabetes, Endocrinology and Metabolism in the UK, has designed a HOMA2-IR model (2013) that estimates β-cell function (%B) and insulin sensitivity (%S) for an individual from simultaneously measured fasting plasma glucose (FPG) and fasting plasma insulin (FPI) values. It also can be used with fasting specific insulin or C-peptide values, instead of fasting RIA insulin.

The HOMA2-IR calculator provides % β-cell function (% B ) and % Insulin Sensitivity (%S): https://www.dtu.ox.ac.uk/homacalculator/download.php.

Use of Tools

While these tools are primarily used by clinicians, knowing about them is useful in being proactive in managing one’s own health.  For example, if you have already started making the dietary and lifestyle changes to lower insulin resistance, having your fasting insulin measured along with your fasting blood glucose, will enable your doctor or myself to calculate your progress, as well as recommend adjustments in your plan.

Have questions?

Why not send me a note using the “Contact Us” form at the top of this webpage.

To our good health!

Joy


References

Gutch, M, Kumar, S, Razi, SM, et al,  Assessment of Insulin Sensitivity / Resistance, Indian J Endocrinol Metab. 2015 Jan-Feb; 19(1): 160–164.

HOMA Calculator©, University of Oxford, Diabetes Trials Unit, Oxford Centre for Diabetes, Endocrinology and Metabolism: https://www.dtu.ox.ac.uk/homacalculator/download.php


 https://twitter.com/joykiddieRD

  https://www.facebook.com/BetterByDesignNutrition/


Copyright ©2017 BetterByDesign Nutrition Ltd.  LEGAL NOTICE: The contents of this blog, including text, images and cited statistics as well as all other material contained here (the “content”) are for information purposes only.  The content is not intended to be a substitute for professional advice, medical diagnosis and/or treatment and is not suitable for self-administration without regular monitoring by a Registered Dietitian and with the knowledge of your physician. Do not disregard medical advice and always consult your physician with any questions you may have regarding a medical condition or before implementing something you have read or heard in our content. 

Part 1: What is Insulin Resistance?

The hormone insulin plays a number of roles, one of which is to help move the glucose that is produced from the digestion of food – from the blood and into the cells for energy. Insulin resistance is where the body isn’t responding to insulin’s signals to take up glucose, so blood glucose remains high, despite normal or high levels of insulin.

Type 2 Diabetes (T2D) is essentially a state of very high insulin resistance.

Insulin normally goes up when we eat foods that contain carbohydrate (breads, pasta, rice, fruit, milk products, etc.) and acts on the liver to help store the incoming food energy – first as glycogen and when liver and muscle glycogen stores are “full”, it acts to store the excess energy as fat (de novo lipogenesis).

When we haven’t eaten for a while or are sleeping, the hormone glucagon acts to break down the glycogen in our muscles and liver (glycogenolysis) in order to supply our brain and cells with glucoseInsulin acts to inhibit glucagon‘s action, which signals the body to stop making new glucose from its glycogen stores. When our glycogen stores run out (such as when we are fasting), the body turns to non-carbohydrate sources such as fat to make the glucose it needs for essential functions (gluconeogenesis).

When we are insulin resistant, insulin continues to act on the liver to signal it to store energy. When glycogen stores are “full”, it stores the excess energy as fat. When fat stores are “full”, the body starts storing the excess fat that the liver keeps making, inside the liver itself.  There shouldn’t be fat in the liver, but when we are insulin resistant, such as in Type 2 Diabetes excess fat gets stored in the liver in a condition known as “fatty liver disease“.

In insulin resistance, the liver becomes more sensitive to insulin’s signal to make fat (and as a result keeps making more and more fat) yet at the same time, the liver becomes less sensitive to insulin’s inhibition of glucagon – resulting in more and more glucose being produced and released in the blood.

High levels of glucose remain in the blood despite adequate insulin, and it is this high level of blood glucose that is the hallmark symptom of Type 2 Diabetes. For the same quantity of insulin released, the body moves less and less glucose into the cell. 

What does the body do to compensate? It makes more insulin!

KEY POINT: Insulin resistance results in the increased production of insulin. Increasing blood sugar CAN a symptom, caused by the insulin resistance, but blood glucose can be normal and one can still be insulin resistant (see Featured Article on Insulin Resistance).

When we are insulin resistant and keep eating a carb-based diet, the body requires more and more insulin in order to move the same amount of glucose into the cell.

The main issue then becomes too much insulin (hyperinsulinemia).

Defining the Problem Defines the Treatment

In Type 2 Diabetes (which is in essence, very high insulin resistance), the symptom is high levels of glucose in the blood. That is not the cause. It is the symptom.

High levels of glucose in the blood resulting from uncontrolled Type 2 Diabetes, results in proteins in the body becoming “glycosylated“. Glucose, is a highly reactive molecule and easily accepts (or “shares”) electrons from other molecules – especially from the amino acid Lysine, which is found in virtually every protein in the body. When Lysine and glucose share an electron, it creates an irreversible chemical bond between the glucose molecule and the protein – and that protein is said to have become glycosylated. It is this glycosylation that lies behind the complications found in Diabetes.

To reduce the glucose in the blood and the glycosylation of the body’s proteins, current treatment for Type 2 Diabetes involves medications that move glucose from the blood into the cells. This doesn’t really remove the excess glucose from the body, it simply moves it to a different location in the body. While these medications can be very helpful in the short term (until people begin to address the underlying dietary causes), over time these medications become less and less effective at removing glucose from the blood. In a sense, we become “medication resistant”, so additional medications are added.  Once the various combinations of medications loose their effectiveness, people with Type 2 Diabetes are prescribed insulin as a treatment – because insulin moves excess glucose into the cells. But the cells are already overflowing with too much glucose!

Insulin is added as a treatment when the body is already producing too much insulin.  The problem is the cells aren’t responding to the signal from insulin. The body doesn’t need more insulin – it needs the cells that are sensitive to respond to insulin’s signal.

Diabetes as a “chronic, progressive disease”

Type 2 Diabetes is described as a “chronic, progressive disease” because with current medication treatment, people eventually get worse. When they no longer respond to the initial medications  prescribed that help move excess glucose from the blood into the cells, they are prescribed insulin which they take by injection – in order to force more glucose into already over-full cells.  While people’s blood glucose gets better (i.e. the symptom improves), they gain weight as a result of the insulin injections and develop complications such as heart disease, stroke, kidney disease, blindness etc..

In the end, they don’t get better, but worse, fulfilling the belief that T2D is a chronic, progressive disease.

Redefining the Problem, Redefines the Solution

Rather than looking at the symptom (high blood glucose) as something that needs to be “fixed” with medications and later with insulin (when the medications are no longer effective), when we define insulin resistance and Type 2 Diabetes as a problem of excess insulin, we approach addressing the problem differently.

By changing what we eat, we can lower the amount of glucose in the body, which in turn causes the body to produce less insulin.  With less insulin being produced, the cells begin to respond to normal amounts of insulin  – reversing insulin resistance and yes, reversing the symptoms of Type 2 Diabetes.

Eating a low carb high fat diet and extending the amount of time between meals (intermittent fasting) lowers the production of insulin, resulting in the cells become more sensitive to its signal. Rather than addressing the symptom (which is high blood glucose) we are addressing the problem of too much insulin.

Have questions? Would like to know how I could help you?

Why not send me a note using the “Contact Us” form on the tab above.

To our good health!

Joy

In Part 2, I will explain how insulin resistance is measured and how we can track insulin sensitivity returning, as we continue to eat a low carb diet and increase the time between meals.

 https://twitter.com/joykiddieRD

  https://www.facebook.com/BetterByDesignNutrition/


Copyright ©2017 BetterByDesign Nutrition Ltd.  LEGAL NOTICE: The contents of this blog, including text, images and cited statistics as well as all other material contained here (the “content”) are for information purposes only.  The content is not intended to be a substitute for professional advice, medical diagnosis and/or treatment and is not suitable for self-administration without regular monitoring by a Registered Dietitian and with the knowledge of your physician. Do not disregard medical advice and always consult your physician with any questions you may have regarding a medical condition or before implementing something you have read or heard in our content. 

 

 

 

Insulin and Leptin – very different effects in lean versus overweight people

The hormone insulin (involved in storing fat) and leptin (involved in burning fat) work very differently in lean people than in overweight people. This is why excess fat such as is found in “bullet proof coffee” or “fat bombs” results in overweight (or obese) people that follow a Low Carb High Fat diet gaining weight—whereas lean people will simply burn it off. This article explains the role of these hormones and how they impact lean people and overweight people very differently.

When we eat, the hormone insulin is released which signals our body to do two things; (1) it tells our cells to uptake energy (in the form of glucose) and (2) to store excess energy as fat. Insulin is the major driver of weight gain. If we are lean, when we eat more than usual and increase our body fat stores, the body responds by increasing secretion of a hormone called leptin.  Leptin acts as a negative feedback loop on the hypothalamus area of our brain, reducing our hunger, causing us to eat less and preventing us from gaining too much fat.

The problem occurs when we become insulin resistant.

Insulin Resistance

When we eat a diet that is high in carbs and we eat every few hours (3 meals plus snacks), insulin is released each time we eat (in order to cause our cells to take in energy and store the excess as fat). If we continue to eat this way, over time our body is inundated with insulin, so it sends signals to down-regulate the insulin receptors, making our cells less sensitive to insulin signals. This is called insulin resistance. When we are insulin resistant, our body releases more and more insulin to deal with the same amount of glucose in the blood.

Leptin Resistance

Consistently having high levels of insulin, will also keep stimulating the release of leptin, which normally results in us becoming less hungry and eating less. However, when we are insulin resistantwe keep producing more and more insulin, which results in us producing more and more leptin. Over time, this consistently high leptin level will result in the same type of down-regulation of hormonal receptors that occurred with insulin, resulting in leptin resistance.

Leptin resistance interferes with the negative feed back loop on our hypothalamus which normally reduces our hunger, causing us to eat less. When we are leptin resistance, even when we’ve eaten a great deal of food, we don’t feel satiated — even when our abdomens are straining from feeling full. As a result, we just keep eating, as if there is no “off” switch.

It is this leptin resistance that results in obesity. 

Obese people aren’t obese because they lack will-power, but because their body is responding to signals from very powerful hormones produced in response to the types of foods they eat.

Difference between a High Carb Diet and a High Fat Diet

When people consume diets high in carbs it stimulates insulin to be released. In response to all the insulin, energy that is not immediately needed for activity is stored as glycogen in the liver and muscle cells, and the remainder is shipped off to our adipose cells (fat cells), to be stored as fat. When eating a high carb diet, getting excess calories into fat cells is easy, getting the fat out of fat cells, not so much.

When people eat a diet high in fat and low in carbs, the fat is absorbed in the intestines as chylomicrons and is shuttled through the lymphatic system to the thoracic duct, going directly into the blood circulation. From there, the fat is either burned for energy or goes into our fat cells, to be stored. It is important to note that the fat does NOT go to the portal circulation of the liver and as a result, fat needs no help from insulin to be absorbed

That’s good, but if excess fat gets stored in fat cells, doesn’t eating fat make one fat?

Not for lean people, because lean people are leptin sensitive and obese people are leptin resistant. When overweight or obese people eat excess fat, it is a different matter.

Lean People versus Obese People

If a lean person eats a diet high in fat and low in carbs, the excess fat will be stored in fat cells, but insulin does not go up. So a lean person does not become insulin resistant, as described above.  As their fat mass goes up, leptin also goes up. Since the lean person is sensitive to leptin, the negative feedback loop acts on the brain causing them to stop eating, allowing their body weight to go back down. Even if a lean person deliberately eats more and more fat when they aren’t hungry, what happens is their body’s metabolism goes up, and they burn off the extra calories.

If an overweight or obese person eats a diet high in fat and low in carbs with moderate amounts of protein, insulin levels don’t go up — which is good of course, however from years of eating high carb low fat diets and from eating a carb rich foods every few hours, overweight and obese people are insulin resistant. This means that their blood glucose levels remain high for long periods after they’ve eaten and as importantly, it also means that they are also leptin resistant. In this case, if they eat too much fat – such as drinking “bullet-proof coffee” or having “fat bombs”, they will respond (as the lean person does) by making more leptin, but the problem is, they are not sensitive to leptin! Their brain doesn’t respond to the signals from leptin, so when an obese or overweight person eats excess fat, beyond that which is naturally found in a low carb high fat foods, their appetite doesn’t drop – nor does their metabolism go up to burn off the excess fat being stored in fat cells. They simply get fatter.

Weight Loss

For those that are overweight or obese and insulin resistant, it is important to keep in mind that with insulin resistance comes leptin resistance. Leptin resistance by definition means that the signals to stop eating don’t work.  The “off switch” is defective.  As well, the body doesn’t respond to signals from leptin to up-regulate metabolism, so when an overweight or obese person on a low carb diet eats too much fat, they gain weight.

Since increasing carbs is not an option and increasing protein results in glucose being synthesized from the excess (gluconeogenesis), the way to lower insulin resistance (and thus leptin resistance) is by extending the amount of time between meals.  This is known as intermittent fasting – a topic that will be covered in a future article.

Have questions?  

Want to know how I can help you get started on a low carb high healthy fat diet?  Please drop me a note using the “Contact Us” form, located on the tab above.

To our good health!

Joy

Copyright ©2017 BetterByDesign Nutrition Ltd.  LEGAL NOTICE: The contents of this blog, including text, images and cited statistics as well as all other material contained here (the “content”) are for information purposes only.  The content is not intended to be a substitute for professional advice, medical diagnosis and/or treatment and is not suitable for self-administration without regular monitoring by a Registered Dietitian and with the knowledge of your physician. Do not disregard medical advice and always consult your physician with any questions you may have regarding a medical condition or before implementing something you have read in our content. 


You can follow me at:

 https://twitter.com/joykiddieRD

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References

Ebbeling CB, Swain JF, Feldman HA, et al. Effects of Dietary Composition During Weight Loss Maintenance: A Controlled Feeding Study. JAMA : The journal of the American Medical Association. 2012;307(24):2627-2634. doi:10.1001/jama.2012.6607.

Feinman RD, Fine EJ (2003) Thermodynamics and metabolic advantage of weight loss diets. Metabolic Syndrome and Related Disorders, 1:209-219.

Tracking Carbs Instead of Counting Calories

I have found that people wanting to lose weight simply don’t want to weigh or measure food or count calories – and who can blame them! I design Meal Plans for my clients so they don’t need to. As I will explain in this article, with a Standard Meal Plan (based on a traditional macronutrient distribution), carbohydrate, protein and fat are all laid out, based on the food exchanges. With a Low Carb High Healthy Fat Meal Plan or a Hybrid Meal Plan, carbohydrate percent, protein- and fat percent are also laid out, but for those seeking to lower insulin resistance or lose weight or both, tracking carb intake is important.  In this article, I’ll explain tracking carbs.

Firstly, what is a Meal Plan?

What is a Meal Plan?

A Meal Plan isn’t a “menu” that tells you what foods you have to eat, but indicates how many servings of each category of food you should aim to eat at each meal. I explain more about what a food category is, below.

The first step in designing a person’s Meal Plan after I’ve done their assessment, is to determine their overall caloric needs based on age, gender, activity level, desired weight loss (or gain), as well as any special considerations such as growth, weight loss, pregnancy or lactation, etc.

More about calories in the next article, but suffice to say here, calories are generally not the focus in Low Carb High Healthy Fat eating, carbs are.

The next step is to set the macronutrient distribution (% of calories from carbohydrate, protein and fat) of the Meal Plan according to what would best suit the person’s clinical needs, goals and lifestyle. This is something I discuss with people during the assessment, and which is ultimately up to them.  The Standard macronutrient distribution is ~45-65% carbohydrate, ~15-20% protein and ~30% fat. Generally speaking, unless there is a compelling clinical reason for using a Standard Meal Plan, I encourage people to consider the benefits of a low carb high healthy fat eating.

The Low Carb High Healthy Fat macronutrient distribution is ~5-10% carbohydrate, ~20% protein and ~65-70% healthy fat, with the Hybrid macronutrient distribution falling somewhere in between.

In the final step, I design a person’s Meal Plan based on the foods that they’ve told me they like, avoiding those they don’t, and factoring in the time of day they either need to (for scheduling reasons) or prefer to eat. Then we meet for me to go over their Meal Plan with them, and for me to teach them how to easily and accurately estimate their portion sizes, using visual measures. More on visual measures, below.

The only thing left for them to decide is what they want to eat!

Food Categories – Standard Meal Plan

In a Standard Meal Plan or Hybrid, categories include Starchy Vegetables and Grains, Fruit, Non-Starchy vegetables, Meat, Poultry, Meat and Egg or Cheese, and Legumes (pulses). These categories are based on how many grams of carbs are contained in the foods in make up that category.

Take, for example, the Starchy Vegetable and Grain Category.  This group includes all the standard “carbs” such as bread, pasta, rice and cereals as well as “starchy vegetables” such as peas, corn, potatoes, sweet potatoes / yams and winter squash (such as acorn or butternut squash). All foods in this category have 15 gm of carbs per serving (where a serving is 1/2 cup or the equivalent of 1 slice of bread).

So, 1 slice of bread has 15 gms of carb, 1/2 cup of peas has 15 gms of carb, 1/2 cup of rice has 15 gms of carb, 1/2 cup of oatmeal has 15 gms of carb, and 1/2 a hamburger bun has 15 gms of carb.

If a person’s Meal Plan indicates that they can have 2 servings from the Starchy Vegetable and Grain category, that could be 2 pieces of toast, or 1 cup of oatmeal, or 1 cup rice, etc. Their Meal Plan doesn’t tell them what food they have to eat, just how much from each category.

Here is an example of what a Standard Meal Plan looks like;

 

 

As you can see, all the calculations have been done.

In this example, this Meal Plan was for an 85 year old man who wanted to gain weight and was based on 45% of his calories coming from carbs, 21% from fat and 34% from fat.

Estimating Portion Sizes

When I’ve taught someone to accurately estimate their serving sizes using visual measures, the amount of macronutrients (carbs, protein, fat and calories) they will take in following their Meal Plan will be what was planned.

What are Visual Measures?

Visual measures are easy and accurate means to estimate serving sizes. For in-person clients, this might be based on the size of their hand or fingers, such as (depending on the size of a person’s hand) a 1/2 a cup (dry measure) may be the amount of something round (like frozen peas) that could be contained in their scooped hand, without rolling out. An ounce (by weight) might be the size of two specific fingers on their hand, or a Tbsp may be the amount of the last digit on their thumb. For Distance Consultation clients, the standard used in teaching visual measures are standard size items, such as the size of a golf ball or four dice stacked up.

Tracking Carbohydrates

Where tracking carbohydrates comes into play is with Low Carb High Healthy Fat Meal Plan or a Hybrid Meal Plan – especially when lowering insulin levels or losing weight is desired. Keeping track of carbohydrates on these kind of Meal Plans is nothing like needing to count calories! It is very easy.

On a Low Carb High Healthy Fat Meal Plans, the macronutrient distribution for carbs is set quite tightly. For men, total carbs would be somewhere between 80-100 grams and for women, it may be set as low as 35 gms carb or as high as 50 gms. It depends on their needs. Naturally, Hybrid Meal Plans will have higher total daily carbs.

Since there are no Starchy Vegetables and Grains and Milk on these Meal Plans (cheese is used, just not milk due to the carb content), the Food Categories on a Low Carb Meal Plan or Hybrid are different than on a Standard (or traditional) Meal Plan).

Food Categories in a Low Carb Meal Plan include Non-Starchy Vegetables, which exclude “Starchy Vegetables” such as peas, corn, potatoes, sweet potatoes / yams and winter squash – with some intake guidelines around root vegetables such as carrots, beets and parsnips. The Fruit category here is specified more narrowly than in a Standard Meal Plan – generally focused on berries and low sugar citrus such as lime and lemon, as well as tomatoes and cucumbers (yes, both are technically ‘fruit’).

Meat, Poultry, Meat and Egg or Cheese is pretty much the same as with a Standard Meal Plan, with an ounce of any of these protein foods being 1 serving and individuals being able to have several servings at each meal (based on their caloric needs, factoring in any weight loss). The fat contained in the Meat, Poultry, Meat and Egg or Cheese is already calculated when the Meal Plan is made, so “Fat” here means added fat. The Fat category includes everything from olive oil, avocado (both the fruit and the oil), coconut oil, butter, olives and nuts and seeds.

Foods in the Meat, Poultry, Meat and Egg or Cheese category have little or no carbs in them and Non-Starchy Vegetables are generally around 5 gm of carb per cup and berries, which are in the Fruit category are roughly 15 gm of carb for 1/2 a cup. A few berries on a salad isn’t usually a problem, but more than that can easily put us over our maximum amount of carbs for the day, which I call the “carb ceiling“.

Where it becomes particularly important to track carbohydrates when one is seeking weight loss is with foods such as nuts and seeds.  It is very easy to eat a handful of nuts and end up exceeding one’s daily maximum number of carbs.

[an article written a month earlier will provide detailed information regarding the carbohydrate content of nuts: http://www.bbdnutrition.com/2017/05/23/oh-nuts/]

Carb Creep

“Carb-creep” is when we eat more carbs than we think we are, which results in weight loss slowing, or even stopping. When one reaches a plateau  where they haven’t lost any weight for longer than a week or two, then tracking carbs to see if there is carb creep is advised.

A man’s carb limit may be set to 80-100 gms per day and a woman’s may be as low as 35 gms or as high as 50 gms.  That is not a lot and it is easy to inadvertently exceed this amount of carbs in the course of a day. A few splashes of milk in several cups of coffee, a handful of peanuts walking by the bowl near the photocopier and an ounce or two of 72% dark chocolate (for heart health, of course!) can quickly put us over our carb ceiling. This is where it’s important to evaluate food choices that may be putting your over your carb ceiling.

Want to know more about having a Meal Plan designed for you?

Please send me a note using the “Contact Us” form above and I will reply to you, usually by the next business day.

To our good health!

Joy

Copyright ©2017 BetterByDesign Nutrition Ltd.  LEGAL NOTICE: The contents of this blog, including text, images and cited statistics as well as all other material contained here (the “content”) are for information purposes only.  The content is not intended to be a substitute for professional advice, medical diagnosis and/or treatment and is not suitable for self-administration without regular monitoring by a Registered Dietitian and with the knowledge of your physician. Do not disregard medical advice and always consult your physician with any questions you may have regarding a medical condition or before implementing something you have read in our content. 


 https://twitter.com/joykiddieRD

  https://www.facebook.com/BetterByDesignNutrition/


 

 

One in Two People Will Get Cancer – new report finds

A new report released by the Canadian Cancer Society predicts that almost one in two Canadians will be diagnosed with cancer in their lifetime.

One half” is a very sobering number!

Currently, cancer is the leading cause of death in Canada, accounting for almost 1/3 of all  of all deaths (30%).

Heart disease is the second leading cause of death, accounting for 1/5 of all deaths (20%).

In an interview with Peter Goffin of the Toronto Star, Dr. Robert Nuttall, Assistant Director of Health Policy at the Canadian Cancer Society attributed this alarming new statistic that 1/2 will get cancer in their lifetime to the “aging population” – notlifestyle factors“. 

Nutall said;

“The important thing to remember here is that the biggest driver behind this is the aging population. “Canadians continue to live longer, and cancer is primarily a disease that affects older Canadians.”

Japan has the oldest population in the world, with ~1/3 of people aged over 60.

What do their statistics show?

According to the Institute for Health Metrics and Evaluation, Japan’s leading causes of death (2015) were:

  1. cerebrovascular disease (stroke)
  2. cardiovascular disease (heart disease)
  3. lower respiratory infection
  4. Alzheimer’s disease

Lung cancer was 5th, followed by stomach cancer (6th) and colorectal cancer (7th). In Japan, a country with the oldest population in the world, cancer of any kind wasn’t even in the top four!

Are half of us really going to get cancer because of the “aging population” or is it because of “lifestyle factors“?

Looking at the top 4 Causes of Cancer in Canada:

Ten Most Common Cancers in Canada – projected for 2017
  1. Lung cancer is the number one form of cancer and the Canadian Cancer Society indicates that more than 85% of lung cancer cases in Canada are related to smoking tobacco.

  2. Colorectal cancer is the second leading cause of cancer and the Canadian Cancer Society indicates that risk factors for colorectal cancer include (a) diet , (b) being overweight, (c) physical inactivity and (d) smoking.

  3. Breast cancer (in both men and women) is the third leading cause of cancer. Apart for personal and family history of breast cancer and other genetic factors, the Canadian Cancer Society list the following known risk factors: (a) exposure to ionizing radiation, (b) use of oral contraceptives (c) alcohol and (d) being obese.

  4. Prostrate cancer which only affects men, is the fourth leading cause of cancer and the only known risk according to the Canadian Cancer Society is family history.

Major Risk Factors for the top 4 Causes of Cancer

Here are the major risk factors for the top four leading causes of cancer in Canada;

  1. smoking
  2. diet
  3. being overweight
  4. physical inactivity 
  5. exposure to ionizing radiation (x-rays)
  6. use of oral contraceptives
  7. alcohol

Except for use of x-rays, all of these are lifestyle factors!

Diet, being overweight and being inactive are three things that can be changed easily and sustainably!

A low carb approach can be particularly helpful, as it can not only address being overweight, but new studies have found that a number of cancer cells feed exclusively on glucose.  It is thought that a ketogenic lifestyle may play a role in reducing the glucose available for some types of cancer.

We being told that the biggest driver behind the projection that half of us will get cancer in our lifetime is the aging population– when it would seem that the underlying risk factors of these cancers are lifestyle factors.

In fact, the Canadian Cancer Society says themselves that half of the cases are preventable;

“We already know a lot about how to prevent cancer. If we, as a society, put everything we know into practice through healthy lifestyle choices and policies that protect the public, we could prevent about half of all cancers.”

We will all age and this is not preventable, but by addressing lifestyle factors including smoking, diet, overweight and physical inactivity and others, we should be able to prevent almost 1/2 of all cancers.

Have questions on how I can teach you how to eat healthier and work with you to help you tackle being overweight and inactive, then please send me a note using the “Contact Us” form on this web page.

To your good health!

Joy


 https://twitter.com/joykiddieRD

  https://www.facebook.com/BetterByDesignNutrition/

Copyright ©2017 BetterByDesign Nutrition Ltd.  LEGAL NOTICE: The contents of this blog, including text, images and cited statistics as well as all other material contained here (the “content”) are for information purposes only.  The content is not intended to be a substitute for professional advice, medical diagnosis and/or treatment and is not suitable for self-administration without regular monitoring by a Registered Dietitian and with the knowledge of your physician. Do not disregard medical advice and always consult your physician with any questions you may have regarding a medical condition or before implementing something you have read in our content. 


References

Canadian Cancer Society, http://www.cancer.ca/en/cancer-information/cancer-type/lung/risks/?region=on#ixzz4kZ5AnNz6

Canadian Cancer Society, http://www.cancer.ca/en/about-us/for-media/media-releases/ontario/2011/not-enough-canadians-being-screened-for-colorectal-cancer-leading-to-many-unnecessary-deaths/?region=on#ixzz4kZ5vSGSS

Canadian Cancer Society, http://www.cancer.ca/en/cancer-information/cancer-type/breast/risks/?region=on#ixzz4kZ8RvXbm

Canadian Cancer Society, http://www.cancer.ca/en/cancer-information/cancer-type/prostate/risks/?region=on#ixzz4kZ9J6o64

Canadian Cancer Society, http://www.cancer.ca/en/cancer-information/cancer-101/cancer-research/prevention/?region=on#ixzz4kZ9jQJwt

Institute for Health Metrics and Evaluation, http://www.healthdata.org/japan

The Toronto Star, Peter Goffin (Staff Reporter), Tue June 20 2017, https://www.thestar.com/news/gta/2017/06/20/half-of-all-canadians-will-get-cancer-in-their-lifetime.html

New Obesity Study Sheds Light on Dietary Recommendations

As mentioned in the previous article, a new study published Monday, June 12, 2017 in the New England Journal of Medicine analyzed data from 68.5 million adults and children in 195 countries and found that 1/3 of people worldwide are overweight or obese and are at increased risk of chronic disease and death, as a result.

Data from one country, China, stood out among all of them due to record high rates of childhood and adult obesity;

  • In 2015, China had the highest incidence of obese children in the world (~10%) along with India. 
  • In 2015, China along with the US had the highest incidence of obese adults (>35%). 

I wanted to have a look at the Dietary Guidelines for Chinese Residents (Chinese: 中国居民膳食指南) in the years prior to 2015, to determine how they may have contributed to these high rates of overweight and obesity.

The Food Guide Pagoda

The Chinese Dietary Guidelines, known as the ‘Food Guide Pagoda’ was first published in 1989 and revised in 1997. The 2007 revision was developed in conjunction with a committee from the  Chinese Nutrition Society, in association with the Ministry of Health.  A new revision came out in 2016.

The 2007 ‘Food Guide Pagoda’ (the one that was in effect at the time the 2015 overweight and obesity statistics came out) was divided into five levels of recommended consumption corresponding to the five Chinese food groups.

  1. Cereals – in the form of rice, corn, bread, noodles, crackers and tubers make up the base of the Pagoda
  2. Vegetables and Fruits – form the second level of the Pagoda

    According to the Chinese Dietary Recommendations, the majority of foods in each meal should be made up of cereals, including rice, corn, bread, noodles, crackers and tubers (such as potatoes), followed by Vegetables and Fruit.


  3. Meat, Poultry, Fish & Seafood and Eggs form the third level, and it is recommended that should be ‘eaten regularly’, but ‘in small quantities’.

  4. Milk & Dairy and Bean & Bean Products – form the fourth level.
  5. Fat, Oil and Salt – form the roof of the Pagoda and are recommended to be eaten in moderation.

Specific Dietary Recommendations (2007-2015)

The main recommendations of the 2007 Chinese Dietary Guidelines were as follows:

  • Eat a variety of foods, mainly cereals, including appropriate amounts of whole grains.
  • Consume plenty of vegetables, fruits and tubers (e.g. potato, taro, yam etc.)
  • Consume milk, beans, or dairy or soybean products every day
  • Consume appropriate amounts of fish, poultry, eggs and lean meat.
  • Reduce the amount of cooking oil
  • Divide the daily food intake among the three meals and choose suitable snacks.

The Results (2005-2015)

1. Leading cause of death

In 2015, heart disease overtook Chronic Obstructive Pulmonary Disease (COPD) as the second leading cause of death, followed by stroke.

In 1990, the leading cause of death in China was Chronic Obstructive Pulmonary Disease (COPD) largely contributed to by smoking, followed by heart disease and diarrhea.


2. Leading cause of premature death

In 2015 as in 2005, stroke was the leading cause of death, followed by heart disease.

 


3. What caused the most death and disability combined?

In 2015, stroke was leading cause of death in China, followed by heart disease.

 


Magnitude of the Problem – China compared to the US and Canada

In 2015, for every 100,000 people in China, 2,237 people died from heart disease and 1,672 people died from stroke.

In the US, for every 100,000 people, 457 people died from heart disease and 1,617 died from stroke.

In Canada, for every 100,000 people, 327 people died from heart disease and 1,106 died from stroke.

Rates of stroke in the China and US were quite similar. Both China and the US had the highest number of obese adults (>35%) in the world. 

China’s “solution”?

China concluded that “dietary risks drive the most death and disability” – especially stroke and heart disease which were the two leading causes of all forms of death, of premature death and of disability in 2015.

In response to these high rates of stroke and heart disease among Chinese, the Chinese government, with the assistance of the Chinese Nutrition Society produced a revised version of the Chinese Food Pagoda in 2016.

New Dietary Recommendations (2016)

The Chinese have stated that “there have been no significant changes in dietary recommendations” (Wang et al, 2016) when compared with the previous version of the 2007 Food Pagoda and are emphasizing the following recommendations:

Eat a variety of foods, with cereals as the staple – The daily amount of cereals and potatoes consumed for body energy production should be 250–400 g, including 50–150 g of whole grains and mixed beans, and 50–100 g of potatoes. The major characteristic of a balance diet pattern is to eat a variety of foods with cereals as the staple.

Balance eating and exercise to maintain a healthy body weight – this is based on the same “calorie in / calorie out” model that the US and Canadian recommendations have been based on. “Avoiding ingesting excessive food and physical inactivity is the best way to maintain energy balance”.

Consume plenty of vegetables, milk, and soybeans – The daily vegetable intake should be in the range of 300–500 g. Dark vegetables, including spinach, tomato, purple cabbage, pak choy, broccoli, and eggplant, should account for half this amount and should appear in every meal. Fruits should be consumed every day. The daily intake of fresh fruits, excluding fruit juice, should be between 200 and 350 g. A variety of dairy products, equivalent to 300 g of liquid milk, should be consumed per day. Bean products and nuts should be frequently eaten in an appropriate amount for energy and essential oils.

Consume an appropriate amount of fish, poultry, eggs, and lean meat – The consumption of fish, poultry, eggs, and meat should be in moderation. The appropriate weekly intake is set at 280–525 g of fish, 280–525 g of poultry, and 280–350 g of eggs with an accumulated daily intake of 120–200 g on average. Fish and poultry should be chosen preferentially. The yolk should not be discarded when consuming eggs, and less fat and fewer smoked and cured meat products should be eaten.

Final Thoughts…

China now has some of the highest rates of childhood obesity in the world (~10%) and is tied with the US for the highest rate of adult obesity (>35%) yet to address the issue of incredibly high rates of stroke and high rates of heart disease, the 2016 Chinese Dietary Recommendations define a balance diet pattern as a daily adult intake of;

1/2 lb – 1 lb (250-400 gm ) of cereals, grains and potatoes

1/3- 3/4 lb (200 – 350 gm) of fresh fruit

1 1/2 cups of milk

and

1/4 lb – 1/3 lb of fish, poultry or eggs (with meat “in moderation”)

These “new” recommendations seem to be based on the same “calorie in / calorie out” model familiar to us in the West and that fail to take into account how the body compensates on a carbohydrate-based calorie restricted diet diet (see previous blogs).

The Chinese are being told that “the best way to maintain energy balance” (Wang et al, 2016) is to;

  1. exercise more (150 minutes/week plus 6000 steps/day)
  2. eat less fat and animal protein
    and
  3. consume most of their calories as rice, corn, bread, noodles, crackers and potatoes 

Over the last four decades,  Americans and Canadians have reduced their fat consumption from ~40% in the 1970’s to ~30%, increased the amount of carbohydrate as whole grains, fruits and vegetables, are consuming low fat milk, eating more fish and drinking less pop and presently, 2/3 of adults considered overweight or obese.

Should we expect different results in China?

How I can help you

If you are looking to achieve a healthy body weight, lower blood sugar, blood pressure and triglycerides, I can help.

I take a low carb high health fat approach and can teach you how to eat well, without weighing or measuring food, or counting “points”.

Want to know more?

Send me a note using the “Contact Us” form, on the tab above.

To our health!

Joy

Copyright ©2017 BetterByDesign Nutrition Ltd.  LEGAL NOTICE: The contents of this blog, including text, images and cited statistics as well as all other material contained here (the “content”) are for information purposes only.  The content is not intended to be a substitute for professional advice, medical diagnosis and/or treatment and is not suitable for self-administration without regular monitoring by a Registered Dietitian and with the knowledge of your physician. Do not disregard medical advice and always consult your physician with any questions you may have regarding a medical condition or before implementing something you have read in our content. 


You can follow me at:

 https://twitter.com/joykiddieRD

  https://www.facebook.com/BetterByDesignNutrition/


References

Global Burden of Disease (GBD) 2015 Obesity Collaborators, Health Effects of Overweight and Obesity in 195 Countries over 25 Years, N Engl J Med, DOI: 10.1056/NEJMoa1614362

Global Health Data Exchange (GHDx), http://ghdx.healthdata.org/geography/china

Wang S, Lay S, Yu H, Shen S. Dietary Guidelines for Chinese Residents (2016): comments and comparisons. Journal of Zhejiang University Science B. 2016;17(9):649-656. doi:10.1631/jzus.B1600341.

 

Obesity Pandemic – new study

In the last few years, we’ve heard the term “obesity epidemic“, but a new study published this past Monday, June 12, 2017 in the New England Journal of Medicine seems to indicate that it is now an “obesity pandemic“.

Researchers analyzed data from 68.5 million adults and children in 195 countries to assess (1) the prevalence of overweight and obesity in 2015 and (2) the trends in the prevalence of overweight and obesity between 1980 and 2015.

The “short story” is that a 1/3 of people worldwide are now overweight or obeseput another way, two billion people globally are overweight or obese and are at increased risk of morbidity (chronic diseases) and morbidity (death), as a result.

The Significance

Epidemiological studies (studies of different populations from around the world) have identified high BMI as a risk factor for cardiovascular disease, type 2 Diabetes, hypertension, chronic kidney disease and many types of cancer.

Furthermore, overweight children are at higher risk for the early onset of diseases such as type 2 Diabetes, hypertension and chronic kidney disease.

Body Mass Index (BMI) is the weight in kilograms divided by the square of the height in meters

Obesity is defined as having a Body Mass Index (BMI) > 30 kg/(m)2

Overweight is defined as having a BMI between 25 and 29.9 kg/(m)2

Obesity Findings

Data showed that in 2015, there were 603.7 million obese adults worldwide and 107.7 million obese children.

The prevalence of obesity has more than doubled in 70 countries since 1980, and there has been a tripling of obesity in youth and young adults in developing, middle class countries such as China, Brazil, and Indonesia.

Worldwide, the prevalence of obesity is now 5% in children and 12% in adults — findings that mirror global trends in type 2 Diabetes.

Most alarming was that in 2015;

  • high BMI accounted for four million deaths globally
  • almost 40% of deaths resulting from high BMI occurred in people who were overweight, but not obese
  • more than 2/3 of deaths related to high BMI were due to cardiovascular disease

Varying Risk

It is important to note that risk of outcomes related to obesity has not been found to be uniform across populations. For example, it has been reported that at any given level of BMI, Asians have been shown to have a higher absolute risk of Diabetes and hypertension, whereas African Americans have a lower risk of cardiovascular disease than other groups.

Addressing the Problem

To address the problem of overweight and obesity both here and around the world, requires correctly identifying its cause and for the last 40 years, excess dietary fat — especially saturated fat has been blamed as the villain and ostensibly responsible for the “obesity epidemic” and resulting “diabetes epidemic”.

But is it?

When one compares the Dietary Recommendations in both Canada and the United States since 1977 to rates of overweight and obesity in both of these countries, it seems apparent that it has been the promotion of diets high in carbohydrate that lies at the root.

In the next article, I’ll take a look at the Dietary Recommendations of the country with the highest rate of childhood obesity and adult obesity in 2015, as well as some of the highest rates of stroke and heart disease per capita, in the world.

How I can help

If you have eaten a ‘low fat diet’ and counted calories (or points) until you are blue in the face and are tired of doing the same thing over and over again, expecting a different outcome, why not drop me a note using the “Contact Us” form, above. I’d be glad to explain how I can help you achieve a healthy body weight, while normalizing your blood sugar, blood pressure and cholesterol levels.

To your health!

Joy

Copyright ©2017 BetterByDesign Nutrition Ltd.  LEGAL NOTICE: The contents of this blog, including text, images and cited statistics as well as all other material contained here (the “content”) are for information purposes only.  The content is not intended to be a substitute for professional advice, medical diagnosis and/or treatment and is not suitable for self-administration without regular monitoring by a Registered Dietitian and with the knowledge of your physician. Do not disregard medical advice and always consult your physician with any questions you may have regarding a medical condition or before implementing something you have read in our content. 


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References

Global Burden of Disease (GBD) 2015 Obesity Collaborators, Health Effects of Overweight and Obesity in 195 Countries over 25 Years, N Engl J Med, DOI: 10.1056/NEJMoa1614362

Gregg EW, Shaw JE, Global Health Effects of Overweight and Obesity, N Engl J Med, doi: 10.1056/NEJMe1706095

Karter AJ, Schillinger D, Adams AS, et al. Elevated rates of diabetes in Pacific Islanders and Asian subgroups: the Diabetes Study of Northern California (DISTANCE). Diabetes Care 2013; 36:574-9

1977 Dietary Recommendations — forty years on

Since 1977, the dietary recommendations in Canada and the US has been for people to consume a diet with limited fat and where “complex carbohydrates” (starches) comprise the main source of calories.

From 1949 until 1977, the dietary recommendations of Canada’s Food Guide were for people to consume

~20-30% of their daily calories as carbohydrate

~40-50% of daily calories as fat

~20-30% of daily calories as protein

From 1977 onward, Canada’s Food Guide recommended that people consume:

55-60% of daily calories as carbohydrate

<30% of daily calories as fat, with no more than 1/3 from saturated fat

15-20% of daily calories as protein

The US recommendations since 1977 have been similar to those in Canada, with the Dietary Goals for the United States recommending that carbohydrates are 55-60% of daily calories and that calories from fat be no more than 30% of daily calories (of which no more than 1/3 comes from saturated fat).

Eating Well with Canada’s Food Guide which came out in 2015, recommends that people eat even more of their daily calories as carbohydrate;

45-65% of daily calories as carbohydrate

20-35% of daily calories as fat, with no more than 1/3 from saturated fat

10-35% of daily calories as protein

[Reference: http://www.hc-sc.gc.ca/fn-an/nutrition/reference/table/ref_macronutr_tbl-eng.php]

Health Canada recommends limiting fat to only 20-35% of calories  while eating 45-65% of daily calories as carbohydrates and currently advise adults to eat only 30-45 mL (2 – 3 Tbsp) of unsaturated fat per day  (including that used in cooking, salad dressing and spreads such as margarine and mayonnaise).

This is what people have come to call a “balanced diet“.

But is it?

For the past 40 years, the public has come to believe that ‘eating fat made you fat’ and that eating saturated fat caused heart disease. This however is not what evidence-based research shows. More on that in future articles.

Our society has become “fat phobic”. People guzzle skim or 1% milk with little regard to the fact that just 1 cup (250 ml) has almost the same amount of carbs as a slice of bread.  And who drinks only one cup of milk at a time?  Most people’s “juice glasses” are 8 oz and the glasses they drink milk from are 16 oz, which is 2 cups. Who ever stops to think of their glass of milk as having the same amount of carbs as almost 2 slices of bread? 

In addition, carbs are hidden in the 7-10 servings of Vegetables and Fruit they are recommended to eat  – with no distinction made between starchy- and non-starchy vegetables.  Many people eat most of their vegetable servings as carbohydrate-laden starchy vegetables such as peas, corn, potatoes and sweet potatoes and then have a token serving of non-starchy vegetables (like salad greens, asparagus or broccoli) on the “side” at dinner. Who stops to think that just a 1/2 cup serving of peas or corn has as many carbs as a slice of bread – and often those vegetables are eaten with a cup of potatoes, adding the equivalent number of carbs as another 2 slices of bread? 

People drink fruit juice and “smoothies” with no regard for all of the extra carbs they are consuming (not to mention the effect that all of that fructose has).  A “small juice glass” is 8 oz, so just a glass of orange juice has the equivalent number of carbs as another 2 slices of bread! Many grab a smoothie at lunch or for coffee break without even thinking that the average smoothie has the same number of carbs as 5 slices of bread!

Then there is the toast, bagels and cereal or bars that people eat for breakfast, the sandwiches or wraps they eat for lunch and the pasta or rice they have for supper.  These are carbs people know as carbs — which are added to all the carbs they consumed as vegetables, fruit and milk.

What has been the outcome of people following these dietary recommendations to eat a high carb diet since 1977 ?

Obesity Rates

In 1977, obesity rates* were 7.6% for men and 11.7% for women, with the combined rate of < 10 % for both genders.

* Obesity is defined as a Body Mass Index (BMI) ≥30 kg/(m)2

In 1970-72 the obesity rate in Canadian adults was 10% and by 2009-2011, it increased two and a half times, to 26%.

In 1970-72, only 7.6% of men were obese but by 2013, 20.1% of men were categorized as obese. In 1970-72, only 11.7% of women were obese but by 2013, 17.4% of women were obese.

In 1978 in Canada, only 15% of children and adolescents were overweight or obese, yet by 2007 that prevalence almost DOUBLED to 29% of children and adolescents being overweight or obese. By 2011obesity prevalence alone (excluding overweight prevalence) for boys aged 5- to 17 years was 15.1% and for girls was 8.0%.

The emphasis since 1977 on consuming diets high in carbohydrates and low in fat has taken its toll.

Effect on Health

Non-alcoholic liver disease is rampant and not surprisingly, considering 37% of adults and 13% of youth are abdominally (or truncally) obese – that is, they are carrying their excess body fat around and in the internal organs, including the liver.

Since the 1970’s, Diabetes rates have almost doubled.

  • In the 1970s, the rate of Type 2 Diabetes in women was 2.6% and in men was 3.4 %. In the 1980s that number rose in women to 3.8% and in men to 4.5%. In the 1990s the rate was almost double what it was in 1970in women it was 4.7% and  in men, 7.5%.

If people eating a high carb, low fat diet has corresponded to an increase in obesity, overweight and Diabetes, then what’s the alternative?

That is where a ketogenic diet comes in , which is a low carbohydrate, high fat diet which supplies adequate, but not excess protein. Eating this way enables us to use our own fat stores for energy, and to make our own glocose and ketones to fuel our cells and organs. Since humans are designed to run on carbs (in times of plenty) and in our fat stores (when food is less plentiful), ketosis is a normal physiological state. By eating a low carb high fat diet when we’re hungry and delaying eating for short periods, we can mimic the conditions that were common to our ancestors. By eating this way over an extended period of time, we can bring down insulin levels and as a result, decrease the insulin resistance of our cells. We can improve our blood sugar, lower our blood pressure and see our LDL cholesterol and triglycerides come down to normal, healthy levels.

Want to know more?

Why not send me a note using the Contact Us form located above?

To your health!

Joy

Copyright ©2017 BetterByDesign Nutrition Ltd.  LEGAL NOTICE: The contents of this blog, including text, images and cited statistics as well as all other material contained here (the “content”) are for information purposes only.  The content is not intended to be a substitute for professional advice, medical diagnosis and/or treatment and is not suitable for self-administration without regular monitoring by a Registered Dietitian and with the knowledge of your physician. Do not disregard medical advice and always consult your physician with any questions you may have regarding a medical condition or before implementing something you have read in our content. 


follow me at:

 https://twitter.com/joykiddieRD

  https://www.facebook.com/BetterByDesignNutrition/