A Very Special Get-Ready-for-Summer-Special

Every year from May 1st until the first day of summer (June 21st) I offer a ‘Get-Ready-for-Summer Special’, but this year I wanted to do something different. Since this past year was the year that I literally reclaimed my life and my health, I wanted to offer a special that enables others to make this the summer they begin to do the same.

This summer, I am doing something I’ve never done before.

For those that let me know that they want to reclaim their health, I will take $100 off a Complete Assessment Package. That means you’ll pay the same price that this package cost in 2008…ten years ago!

Why am I doing this?

Because when I finally made the decision last spring to take care of “me”, I still had my own denial and resistance to change to overcome, but I didn’t have to pay a Dietitian to assess me, determine my risk factors, design a meal plan for me and teach me what I needed to know to be successful.  I just had to do it.

The photograph on the left is what I looked like when I began reclaiming my health (March 5 2017) and on the right is what I looked like exactly a year later.

To make reclaiming your health a reality for you, I am offering the Complete Assessment Package at a cost of $250, instead of $350.  All you need to do to qualify is send me a note using the “Contact Me” form on this web page and write “reclaiming my health” at the top of the note, and write the rest of your note below that.  That’s it! I’ll send you the Intake form and we can get started.

This offer is only available from now until June 21, 2018 (the first day of summer).

Will this be the summer that you reclaim your health? Let me help.

I look forward to hearing from you and encouraging you that you can do it.  I did. You can, too.

To our good health!

Joy

 

 

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.

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. 


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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. 


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

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. 


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Humans – the perfect hybrid machine

Long before the ‘hybrid car” there was the human body – a hybrid ‘machine’ perfectly designed to use either carbohydrates or fat for energy. Like a hybrid car, we can run on one fuel source or the other at any one time.

If we are eating a largely carbohydrate based diet, we will be in ‘carbohydrate mode‘ by default. Carb-based foods will be broken down by our bodies to simple sugars and the glucose used to maintain our blood sugar levels. Our liver and muscle glycogen will be topped up, then the rest will be shuttled off to the liver where it will be converted into LDL cholesterol and triglycerides and stored in fat cells.

Historically, in times of plenty, we’d store up glycogen and fat and in lean times, we’d use up our glycogen and then switch fuel sources to be in “fat-burning mode” — accessing our own fat stores, for energy.

The problem is now that we rarely, if ever access our stored fat because we keep eating a carb-based diet.  So we keep getting fatter and fatter.

GLUCOSE OR FAT AS FUEL

When we are in “carb burning mode”, the carbs we eat are broken down by different enzymes in our digestive system to their simplest sugar form (monosaccharides) such as glucose, fructose and galactose.

Glucose is the sugar in our blood, so starchy foods such as bread and pasta and potatoes are broken down quickly so they are available to maintain our blood sugar levels.

Monosaccharides are the building blocks of more complex sugars such as disaccharides, including sucrose (table sugar) and lactose (the sugar found in milk), as well as polysaccharides (such as cellulose and starch). When we drink milk for example, the galactose found in it is broken down into lactose and glucose.  When we eat something sweetened with ‘sugar’ (sucrose), it is quickly broken down to glucose and fructose.

Any glucose that is needed to maintain our blood sugar level is used immediately for that purpose and the remainder is used to “top up” our glycogen stores in our muscle and liver. There are only ~ 2000 calories of glycogen – enough energy to last most people one day, so when our glycogen stores are full, excess energy from what we eat is converted to fat in the liver and stored in adipocytes (fat cells).

One problem is that our diets are high in fructose – naturally found in fruit but also as high fructose corn syrup in many processed foods. Fructose can’t be used “as is”, so it is brought to the liver.  If our blood sugar is low, it will be used to make glucose for the blood (via gluconeogenesis) otherwise it will be converted into LDL cholesterol and triglycerides and stored as fat.

Feasting and Fasting

When we don’t eat for a while, such as would have occurred when our ancestors were hunter-gatherers, we’d use up our glycogen stores hunting for an animal to eat, or gathering other edible foods and if we weren’t successful at finding food to eat, then our bodies would access our fat stores, for energy.  This is known as lipolysis. This process is regulated mainly by a hormone called glucagon, but other hormone such as epinephrine (the “fright and flight” hormone), cortisol (the “stress hormone”) as well as a few others (ACTH, growth hormone, and thyroxine) also play a role.

In times of plenty, we’d store up glycogen and fat and in lean times, we’d use up our glycogen, switch into “fat-burning mode” and then rely on our stored fat for energy.

The problem for most of us in North America and Europe is that we have access to food in our homes, in stores and at fast food restaurants 24/7. We can’t go for a walk without passing places selling or serving food and if the weather is bad or we are too tired, food is just a phone call or web-click away. So we just keep storing up our fat for ‘lean times’ that never come.

In addition, irrespective of our cultural background, our eating style is carb based; pasta, pizza, sushi, curry and rice or naan, potato, pita – you name it.  Every meal has bread or cereal grains, pasta, rice or potatoes – and even what we consider “healthy foods” such as fruit and milk have the same number of carbs per serving as bread, cereal, pasta, rice and potatoes. That wasn’t always so. Our indigenous cultural foods were very different.

Compounding that, many “low-fat” products have added sugar (sucrose) in order to compensate for changes in taste from reducing naturally occurring fat, which then adds to excess carb intake.  Sucrose (ordinary table sugar) is made up of half fructose, so a diet high in sugar adds even more fructose transport to the liver, for conversion to cholesterol and fat.

The vilification of fat

In 1977, both the Canadian and US food guides changed in response to the promoted belief that eating diets high in saturated fat led to heart disease. Multiple studies and reanalysis of the data of older studies indicates that saturated fat is not the problem, but that diets high in carbohydrate combined with chronic inflammation and stress, is.

In 2016, it came to light that the sugar industry funded the research in the 1960’s that downplayed the risks of sugar in the diet as being related to heart disease and highlighted the hazards of fat instead – with the results having been published in the New England Journal of Medicine in 1967 with no disclosure of the sugar industry funding*. The publication suggested that cutting fat out of the American diet was the best way to address coronary heart disease, and which resulted in the average American and Canadian as inadvertent subjects in an public health experiment gone terribly wrong. Overweight and obesity has risen exponentially and with that Diabetes, hypertension (high blood pressure) and high cholesterol.

*(Kearns CE, Schmidt LA, Glantz SA. Sugar Industry and Coronary Heart Disease Research A Historical Analysis of Internal Industry Documents. JAMA Intern Med. 2016;176(11):1680-1685. doi:10.1001/jamainternmed. 2016. 5394). 

Over the last 40 years the promotion of “low fat eating” by governments and the food industry has resulted in carbohydrate-intake skyrocketing. Every high-carb meal is followed by another high-carb meal, and if we can’t wait, a snack, too. We eat every 2-3 hours, and eating carb-based foods every 2 or 3 hours all day, every day is quite literally killing us.

How do we get fat out of “storage”?

The “key” to unlocking our fat stores, is decreasing overall intake of carbohydrates by decreasing the amount of carbohydrates we eat, both by eating much less of it and on occasion, by delaying the amount of time between meals.

Decreasing carb intake lowers insulin, the fat-storage hormone. At first our bodies access liver and muscle glycogen for energy, but since that is only about a one day’s supply, our bodies then turn to our own fat stores as a supply of energy.

By eating a diet rich in fat and keeping protein at the level needed by the body but not in excess, dietary protein is not used to synthesize glucose, but fat is.

An added bonus is that since insulin also plays a role in appetite, as insulin falls, appetite decreases.

This is the role of a low carb high healthy fat diet, a topic covered in this article: http://www.bbdnutrition.com/2017/03/22/a-low-carb-high-healthy-fat-diet/

Have questions?

Why not send me a note, using the “Contact Us” form above?  I’d be happy to answer your questions.

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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Low Carb Green Tea Matcha Smoothie – role in weight and abdominal fat loss

This delicious low carb high fat Matcha Smoothie can help you lose weight & abdominal fat. The science behind it, the recipe & the nutritional info in this article.


Green tea is the unfermented leaves of the Camellia sinensis plant and contains a number of biologically active compounds called catechins of which epigallocatechin gallate (EGCG) makes up ~ 30% of the solids in green tea [Kim et al]. Studies have found that green tea catechins, especially EGCG play a significant role in both weight loss and lower body fat composition.

Population studies and several randomized controlled studies (where one group is “treated” and the other group is not) have shown that waist circumference is smaller and levels of body fat is less the more green tea consumed   [Phung et al].  The anti-obesity effects of green tea are usually attributed to the presence of catechins [Naigle].

Several large-scale population studies have linked increased green tea consumption with significant reductions in metabolic syndrome – a cluster of clinical symptoms which include insulin resistance or hyperinsulinemia (high levels of circulating insulin), Type 2 Diabetes, hypertension or high blood pressurecardiovascular disease including coronary heart disease and atherosclerosis.

It is thought that epigallocatechin gallate (EGCG), the most abundant catechin in green tea, mimics the actions of insulin.  This has positive health implications for people with insulin resistance or Type 2 Diabetes [Kao et al]. 

EGCG also lowers blood pressure  almost as effectively as the ACE-inhibitor drug, Enalapril, having significant implications for people with hypertension (high blood pressure) and cardiovascular disease [Kim et al].

Research indicates that drinking 8-10 cups of green tea per day is enough to increase blood levels of EGCG into a measurably significant range [Kim et al]. 

The most effective way to reduce the symptoms associated with metabolic syndrome is through a low carb high healthy fat diet, however the addition of green tea as a beverage – especially as matcha green tea powder, may provide a means to preferentially target abdominal weight loss. 

GREEN TEA CATECHINS

Catechins make up ~ 30% of green tea’s dry weight (of which 60–80% are catechins) and oolong and black tea  (which are produced from partially fermented or completely fermented tea leaves) contains approximately half the catechin content of green tea.

Matcha, a powdered green tea used in the Japanese tea ceremony and popular in cold green tea beverages contains 137 times greater concentration of EGCG than China Green Tip tea (Mao Jian) [Weiss et al]. 

GREEN TEA CATECHIN CONTENT OF BREWED GREEN TEA VS MATCHA POWDER

A typical cup (250 ml) of brewed green tea contains 50–100 mg catechins and 30–40 mg caffeine, with the amount of tea leaves, water temperature and brewing time all affecting the green tea catechin content in each cup.

A gram (~1/3 tsp) of matcha powder contains 105 mg of catechins – of which 61 mg are EGCGs and contains 35 mg of caffeine. Most matcha drinks made at local tea and coffee houses are made and served cold and contain ~1 tsp of matcha powder which contains ~315 mg of catechins – of which ~183 mg are EGCs.   

WEIGHT LOSS EFFECT OF GREEN TEA CATECHINS

A 2009 meta-analysis (combining the data from all studies) of 11 green tea catechin studies found that subjects consuming between 270 to 1200 mg green tea catechins / day (1 – 4 tsp of matcha powder per day) lost an average of 1.31 kg (~ 3 lbs) over 12 weeks with no other dietary or activity changes [Hursel].

Body composition EFFECT OF GREEN TEA CATECHINS

The effect of green tea catechins on body composition is significant – even when the weight loss between “treated” and “untreated” groups is small (~5 lbs in 12 weeks).

Even with such small amounts of weight loss;

the total amount of abdominal fat decreased 25 times more with green tea catechin consumption than without it (−7.7 vs. −0.3%)

and

 total amount of subcutaneous abdominal fat (the fat just below the skin of the abdomen) decreases almost 8 times more with green tea catechin consumption than without it (−6.2 vs. 0.8%). 

HOW DO GREEN TEA CATECHINS WORK?

The mechanisms by which green tea catechins reduce body weight  and reduce the amount of total body fat and in particular reduce the amount of abdominal fat are still being investigated.  It is currently thought that green tea catechins;

–          increased thermogenesis; i.e. increased heat production which would result in increased energy expenditure (or calorie burning)

–          increase fat oxidation i.e. using body fat as energy. For those on a low fat high fat diet, this is good!

–          decrease appetite

–          down-regulation of enzymes involved in liver fat metabolism (fat storage)  

WARNING TO PREGNANT WOMEN

While EGCG has also been found to be similar in its effect to etoposide anddoxorubicin, a potent anti-cancer drug used in chemotherapy [Bandele et al], high intake of polyphenolic compounds during pregnancy is suspected to increase risk of neonatal leukemia. Bioflavonoid supplements (including green tea catechins) should not be used by pregnant women [Paolini et al].


Betterbydesign’s low carb Green Tea Matcha Smoothie Recipe

Total carbs: 2.5 gm per serving – contains ~315 mg catechins

Ingredients

1 tsp matcha (green tea) powder * (1 tsp = 2 gm)

12 cubes ice, crushed

1/2 cup (125 ml) coconut milk  

optional: 1/2 tsp Silan (Middle Eastern date syrup) – will add an additional 3.5 g carbs to the recipe

Method

  1. Place 1 tsp matcha powder in a small stainless steel sieve and gently press through the sieve into a small bowl with the back of a small spoon
  2. Put the sieved matcha powder into a ceramic or glass bowl (not metal, as the tannins in the tea will react and give the beverage and “off” metalic taste)
  3. With a bamboo whisk (available at Japanese and Korean grocery stores) or a plain spoon, whisk 3 Tbsp boiled and cooled water into the matcha powder, until all the lumps are gone and the mixture is smooth
  4. Place a whole tray of ice cubes (12) into a blender
  5. Pour matcha and water mixture over ice in the glass
  6. Pour coconut milk on top of ice and matcha
  7. Pulse until desired texture is achieved*

*I blend mine just fine enough to be able to drink it through a straw.

Enjoy!


Nutritional Information

Calories 91.48
Saturated Fat 7.7 gm
Cholesterol 0 mg
Sodium 7.5 mg
Carbohydrates 1 gm
Dietary Fiber 770 mg
Protein 1.1 gm

Calcium 8.8 mg
Vitamin A (Retinol Equivalents) 198.4 mg
B-Carotene 1.2 gm
Magnesium 4.6 mg
Vitamin B1 .12 mg
Potassium 54 mg
Vitamin B2 .027 mg
Phosphorus 7.0 mg
Vitamin B6 .018 mg
Iron .34 mg
Vitamin C .12 mg
Sodium .12 mg
Vitamin E .562 mg
Zinc .126 mg
Vitamin K 58 mcg
Copper .012 mg

Polyphenols 200 mg
Caffeine 50 mg
Theophylline 0.84 mg


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References

Bandele, OJ, Osheroff, N. Epigallocatechin gallate, a major constituent of green tea, poisons human type II topoisomerases”.Chem Res Toxicol 21 (4): 936–43, April 2008.

Hursel R, Viechtbauer W, Westerterp-Plantenga MS. The effects of green tea on weight loss and weight maintenance: a meta-analysis. Int J Obes (Lond) 2009;33:956–61.

Kao YH, Chang MJ, Chen CL, Tea, Obesity, and Diabetes, Molecular Nutrition & Food Research, 50 (2): 188–210, February 2006

Kim JA, Formoso G, Li Y, Potenza MA, Marasciulo FL, Montagnani M, Quon MJ., Epigallocatechin gallate, a green tea polyphenol, mediates NO-dependent vasodilation using signaling pathways in vascular endothelium requiring reactive oxygen species and Fyn, J Biol Chem. 2007 May 4;282(18):13736-45. Epub 2007 Mar 15.

Nagle DG, Ferreira D, Zhou YD. Epigallocatechin-3-gallate (EGCG): chemical and biomedical perspective. Phytochemistry 2006;67:1849–55.

Park JH, Jin JY, Baek WK, Park SH, Sung HY, Kim YK, et al. Ambivalent role of gallated catechins in glucose tolerance in humans: a novel insight into nonabsorbable gallated catechin-derived inhibitors of glucose absorption. J Phyisiol Pharmacol 2009;60:101–9.

Phung OJ, Baker WL, Matthews LJ, Lanosa M, Thorne A, Coleman CI. Effect of green tea catechins with or without caffeine on anthropometric measures: a systematic review and meta-analysis. Am J Clin Nutr 2010;91:73–81.

Paolini, M, Sapone, A, Valgimigli, L, “Avoidance of bioflavonoid supplements during pregnancy: a pathway to infant leukemia?”. Mutat Res 527 (1–2): 99–101. (Jun 2003)

Rains, TM, Agarwal S, Maki KC, “Antiobesity effects of green tea catechins; a mechanistic review” J or Nutr Biochem 22(2011):1-7

Weiss, DJ, Anderton CR, Determination of catechins in matcha green tea by micellar electrokinetic chromatography, Journal of Chromatography A, Vol 1011(1–2):173-180, September 2003

 

The Limitations of Common Ways of Determining Weight Loss

People who are eating differently in an effort to lose weight often hop on the scale daily to see how they’re doing. What they fail to consider is that an average adult’s body weight can fluctuate by as much as 4  1/2 pounds per day — solely as a result of changes in the amount of water they are retaining or excreting.

The Limitations of Using a Scale to Determine Fat Loss

An 80 kg person has, on average 48 liters of water in their body. The problem with using body weight as an assessor of fat loss is that the human body does not precisely regulate body water content.

Above 49 liters of water, the kidneys of an 80 kg person will clear the excess water by causing the person to urinate more and below 47 liters of water, the 80 kg person will feel thirsty and increase their fluid intake. People’s “weight” is affected by this change in body water content of ~2 liters per day — which weighs approximately 2 kg or 4.4 pounds! Put another way, each day our “weight” can fluctuate by this amount solely due to the difference in retained or excreted water.

Since there is no way to measure this daily change in water weight in non-clinical settings, the standard scale is a very imprecise way to measure fat loss over the short-term.

Waist Circumference

Many people know that carrying excess weight around the middle increases one’s risk of cardiovascular disease, including heart attack so they measure their waist circumference frequently. Even if waist circumference is measured halfway between the lower rib and the top of the hip bone, with a fully relaxed abdomen, their are limitations to using this as a short term measure of weight loss.

The Limitations of Using a Tape Measure to Determine Fat Loss

Since the average person’s body weight fluctuates by as much as ~4 1/2 pounds per day due only to changes in body water, a tape measure fails to capture decreases in waist circumference stemming from the kidneys excreting water.

That said, waist circumference is helpful as a long-term indicator of weight loss, just not a short-term one.

Body Fat Percent

Some people have bathroom scales that have body fat analyzers built in and think that what it is measuring is the amount of fat they are carrying, however a number of factors can influence this reading.

The Limitations of Using a Body Fat Analyzer to Determine Fat Loss

Body Fat Analyzers use electrical impedance to determine fat percentage, and this measurement is affected by a number of conditions, including environmental (room) temperature, a person’s hydration status, as well as emotional stress. Since hydration status can fluctuate by ~4 pounds per day, a body fat analyzer is no more accurate as a short-term measure than a standard bathroom scale, without it.

HOW TO Assess short-term weight loss

How one’s own clothes fit and comparative ‘before’ and ‘after’ photos are a much better short-term assessor of fat loss than a scale, a tape measure and a body fat analyzer. Since body water fluctuates considerably on a low carb high fat diet due to changes in sodium levels, I recommend that people eating a low carb high fat diet weigh themselves once every two weeks on the same day of the week, at the same time of day and measure their waist circumference at the same time. If they have a scale that assesses body fat percent once every two weeks is sufficient for taking these measurements.

None of these will provide much information on actual fat loss over the short term…so why rely on them for that, but they will be helpful measurement over the longer term.

Sodium and Body Water Content

As mentioned in a previous article, by eating only when hungry and only until no longer hungry, insulin levels have the opportunity to fall to baseline – something they do naturally after not eating for 12 hours.

On days where the time until eating is extended by a few hours (i.e. “intermittent fasting”), insulin levels stay low for an even longer period of time.  In response, our kidneys excrete sodium in a process called naturesis.

Failing to supplement sodium while eating low-carb high fat can result in intense headaches – and if sodium remains low, potassium will also be excreted to keep the necessary sodium-potassium balance. This drop in potassium often results in irregular heart beats, known as arrhythmia.

Phinney and Volek (The Art and Science of Low Carbohydrate Living) recommend that if one is eating less than 60 gms of carbs per day, that 2-3 grams of sodium should be added to the diet (provided the person is not taking any diuretics or other blood pressure medication).

A half a teaspoon of table salt or sea salt provides 1000 mg or 1 gram of sodium.

Final Thoughts

Since hopping on the scale daily or even several times a week won’t provide any useful information, nor will measuring our waist circumference or using a body fat analyzer too often – why do it? Part of ‘getting healthy’ ought to include having a healthy body self image – something that won’t be nurtured by obsessing about such “numbers”.

Short-term measures of success

Short-term success is best measured visually – with comparative photos taken from the same distance away, from the same relative height and wearing the same clothing.

How one’s clothes are fitting is another way.

A person who is insulin resistant or Type 2 Diabetic should be seeing both their fasting blood glucose and post-prandial (2 hours after a meal) glucose levels gradually coming down. If they aren’t then they should schedule an appointment with their Dietitian to find out why that is.

Medium-term measures of success

Medium-term measures of success in eating low carb high fat can be measured both subjectively and objectively. Subjective measures include weighing oneself and taking one’s own waist circumference once every two weeks. Objective measures include having your Dietitian weigh you on a clinical scale, having her assess your waist circumference and body fat percentage using both a device that measures electrical impedance, as well as using good old-fashioned calipers, that measure subcutaneous (under the skin) fat, in 3 or four specific locations on the body.

A person with high blood pressure should be seeing both systolic (the first number) and diastolic (the second number) blood pressure coming down and Type 2 Diabetics or those with insulin resistance should be continuing to observe lower fasting blood glucose and post-prandial (2 hours after a meal) glucose levels.

Longer-term measures of success

After 6 or 8 months eating low carb high fat, both subjective and objective measures should be continuing to lower in a reasonably linear fashion. Of course there will be times where a ‘plateau’ is reached, but if that lasts more than two or three weeks, then its important to check in with your Dietitian to make sure the amount of carbs you think you are eating is what your Dietitian has been determined as being best for you.

A Type 2 Diabetic should be seeing both their fasting blood glucose and post-prandial (2 hours after a meal) glucose levels approaching more normal levels and both Type 2 Diabetics and those with insulin resistance (“pre-diabetes”) should have their HbA1C assessed at a lab every three months, as this provides insights into one’s 3-month average blood glucose level. Fasting blood glucose provides a ‘snap-shot’ of blood sugar in the morning after not eating, and should be done twice a year by a lab, especially if one is Diabetic. Comparing lab test results to previous lab test results is an objective indicator of the effect that eating low-carb high fat is having on specific markers and provides an opportunity to determine if the amount of carbs being eaten may still be too high.

The most accurate assessor is a 2 hour glucose tolerance test, however few doctors will requisition this after one is diagnosed as Type 2 Diabetic.

Finally, every year or so, it is helpful for those who have been diagnosed as Diabetic to have their fasting insulin, C-Protein and AM Cortisol levels assessed and compared to previous results. For these, your doctor may refer you to an Endocrinologist.

Remember, achieving health is a journey and takes time and like most journeys, it is best not done alone.

Have questions about how I can help or about the services I provide?

Please send me a note using the form on the “Contact Us” tab, above.

To your 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. 


follow me at:
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