LDL Cholesterol is Not the Best Assessor of Cardiovascular Risk

There continues to be a reliance on LDL cholesterol (LDL-C) as the main means to assess cardiovascular (CVD) risk, despite the fact that apolipoproteinB (apoB) has been found to be a much better predictor. This new article looks at why total LDL cholesterol is inadequate to assess cardiovascular risk, what apoB is and why it is considered a better assessor, and how apoB, apoB/apoA ratio and its proxy TG:HDL ratio could be used to assess CVD risk.

An article published in Current Opinion in Lipidology (April 16, 2021) [1] states;

There is now a robust body of evidence demonstrating the superiority of apoB over LDL-C and non-HDL-C as a clinical marker of cardiovascular risk. LDL-C is not the appropriate marker to assess the benefits of statin / ezetimibe / PCSK9 therapy”

The paper outlines that in 2019 the European Society of Cardiology and the European Atherosclerosis Society Guidelines both concluded that apolipoprotein B (apoB) was a more accurate measure of cardiovascular risk and a better guide to using lipid lowering medication, than low-density lipoprotein cholesterol (LDL-C) or non-high-density lipoprotein cholesterol (HDL-C) — yet the American College of Cardiology and the American Heart Association continue to use both LDL-C as the primary means to assess CVD risk and to guide statin therapy.

To understand why apoB is a more accurate measure of cardiovascular risk than LDL, as well as how apoB/apoA ratio and its proxy triglyceride to HDL ratio (TG:HDL) can be used, a simple overview of the different types of cholesterol is needed — and it holds some surprises when it comes to both what we’ve believed about HDL being “good cholesterol”, and LDL being “bad cholesterol”.

Different Types of Cholesterol

What we call “cholesterol” are really lipoproteins which are particles made up of lipids (fat) and protein and that vary in size, density, and lipid and apolipoprotein composition. They can be separated into different classes based on physical and chemical parameters and include;

    • high density lipoprotein (HDL)
    • low density lipoprotein (LDL)
    • very low density lipoprotein (VLDL)

High Density Lipoprotein (HDL) – so-called “good cholesterol”

Most people think of high density lipoprotein (HDL) as “good cholesterol” and while it is known as a strong inverse indicator of CVD risk, HDL cholesterol is not one entity, but there are different sub-classes of HDL.

We have known since the 1990s that there are several sub-particles of LDL and we now know that HDL is made up of 5 different sub-fractions based on their size and density (very large, large, medium, small, and very small)  and that these five subclasses seem to be associated with different levels of CVD risk [2]. HDL Cholesterol measured on blood tests measures the total cholesterol content in all the different sub-fractions of HDL (HDL-C)[2].

Each High Density Lipoprotein (HDL) carries one apolipoprotein-A (apoA) which makes up ~65% of its mass and has been found in most studies to not to be associated with CVD risk [2].

When apoA is measured along with apoB (found in Very Low Density Lipoprotein (VLDL) and Low Density Lipoprotein (LDL)), it is considered to be an even better predictor of CVD risk than apoB alone [2]. More on this below.

Low Density Lipoprotein (LDL) – so-called “bad cholesterol”

Most people think of low density lipoprotein (LDL) as “bad cholesterol” — but low density lipoprotein (LDL) is not a single entity either — but is made up of four subclasses of LDL particles[2] where decreased size and increased density of LDL are associated with increased cardiovascular risk [3,4].

It is the small, dense LDL sub-fraction (sdLDL) that is associated with atherosclerotic plaque, whereas the large, fluffy (or buoyant) LDL sub-fraction is not [3].

Here’s an analogy that may help think of the different sub-fractions of LDL.

If I have a basket filled with balls — is how many I can get inside a basket affected by whether they are basketballs, or golf balls?

Of course it is!

I can put many more golf balls in a basket, than I can basketballs.

Think of golf balls as small, dense LDL (sdLDL) and basketballs as large, buoyant LDL.

LDL Cholesterol on Lab Test Results

LDL cholesterol measured on lab tests indicates total LDL-cholesterol (LDL-C) — that is, the total concentration of cholesterol within all four sub-fractions of LDL sub-particles. What is very important to note is that total LDL cholesterol (LDL-C) is what is usually used in studies that report an association between higher levels of LDL and cardiovascular disease, but these studies fail to distinguish between small dense LDL which are atherosclerotic, and the large, buoyant LDL which are not.  All the different subtypes of LDL are lumped together as if they were a one thing — and they are very different!

Usually, when someone is told their “cholesterol is high” it usually means that their LDL cholesterol is high — but many doctors are unaware of the different sub-fractions of LDL and that it is only the small, dense LDL (sdLDL) ones that pose a risk.  This is why I encourage my clients when told their LDL is high to ask “which LDL“? 

Very Low Density Lipoprotein (VLDL)

Very low density lipoprotein (VLDL) is produced in the liver and the best way to understand its role is to think of it as a “taxi” which the liver makes and then releases into the bloodstream to shuttle triglycerides (TG) around the body, to the various tissues.  VLDL cholesterol on blood test results isn’t actually measured, but is estimated as a percentage of the triglyceride value.

It is important to note that very low density lipoproteins (VLDL) and the Low Density Lipoproteins (LDL) that results after it off-loads it triglycerides each carry one apolipoprotein-B (apoB) molecule, and while a high VLDL value is said to be a risk for cardiovascular disease, a more accurate measure is the ratio of Apolipopoprotein B (apoB), the lipoprotein in VLDL compared to Apolipoprotein A (apoA), lipoprotein in HDL. More on that below.

Where does LDL come from?

Once a large amount of triglyceride (TG) has been off-loaded in the tissues by the VLDL “taxi”, it then becomes a new, smaller lipoprotein called low density lipoprotein, or LDL which contains mostly cholesterol, and some protein.  Some LDLs are removed from the circulation by cells around the body that need the cholesterol contained in them and the rest is taken out of the circulation by the liver.

LDL is what is left once the VLDL which is made by the body has offloaded its triglyceride ‘passenger’ to the tissues.

Assessing Cardiovascular Risk – particle number, apoB : apo A and TG:HDL ratio

LDL particle number (LDL-P)

Since the amount of cholesterol in each LDL particle varies, measuring total LDL cholesterol (LDL-C) tells us nothing about the actual number of particles they are or their size but an increased number of LDL particles indicates that a person has more small, dense particles.

To best understand this, think of the ball analogy, above. There will be increased number of balls with golf balls as compared to basketballs in the same size container.

LDL-particle number (LDL-P) has a strong and independent association with the development of atherosclerosis, as well as with CVD events [2] and is considered a more accurate predictor of cardiovascular events, than total LDL cholesterol (LDL-C) [2].

A nuclear magnetic resonance spectroscopy (NMR) lipid profile test directly measures the number of LDL particles (as well as HDL particles). For LDL particles, a value of less  than 1.000 in nmol/L is considered ideal, a value of 1000-1299 is considered moderate,  a value of 1300-1599 is considered borderline high, and a value >1600 is considered high.

Apolipoprotein B:Apolipoprotein A

Apolipoprotein B (apo B), which is the main lipoprotein in VLDL (and in LDL after the VLDL has offloaded its triglycerides to the tissues) and is correlated with LDL particle number, which makes it a very good assessor of cardiovascular disease risk.

Remember, the golf ball / basketball analogy; the higher number of LDL particles means the more small, dense LDL particles there are.

When an apoB test is used in conjunction with an apoA test (which measures the main lipoprotein in HDL), the apoB/apoA ratio is considered to be an even better predictor of CVD risk, than ApoB alone [2].

An apo B / apo A ratio of > 0.9 considered a risk for CVD.

Triglyceride (TG):HDL Ratio

Measuring apoB to apoA requires special blood tests, but reliable proxy can be calculated by dividing triglycerides (TG) by HDL-cholesterol (HDL-C) from a standard lipid panel and studies have found this to be a very good assessor of cardiovascular risk.

TG:HDL ratio reflects LDL particle size, which means it is an excellent proxy for particle number.

Remember, the golf ball / basketball analogy; the more small, dense LDL particles there are, the higher the LDL particle number. 

One study from 2004 reported that almost 80% of people with a TG:HDL-C ratio of greater than 3.8 (when values are expressed in mg/dl) had mostly small, dense LDL particles, indicating cardiovascular risk. This same study found that more than 80% with a TG:HDL-C ratio of less than 3.8 (when values are expressed in mg/dl) had mostly large, fluffy LDL particles, indicating lower cardiovascular risk[5].

A 2005 study [6] reported that a TG:HDL-C ratio of 3.5 or greater was highly correlated with atherosclerosis in men, as well as insulin resistance and metabolic syndrome.

A recent 2014 [7] study found that a high TG:HDL-C ratio was a strong independent predictor of cardiovascular disease, coronary heart disease and all-cause mortality both before- and after adjustment for age, smoking, BMI and blood pressure.

In Canada (as well as Europe), values are expressed as mmol/L and the ratios are interpreted as follows [8];

TG:HDL-C < 0.87 is ideal

TG:HDL-C > 1.74 is too high

TG:HDL-C > 2.62 is much too high

In the US, values are expressed in mg/dl and the ratios are interpreted as follows [8];

TG:HDL-C < 2 is ideal

TG:HDL-C > 4 is too high

TG:HDL-C > 6 is much too high

Final Thoughts…

If someone’s lab test results show they have high LDL cholesterol, all we know for certain is that the total concentration of cholesterol counting all four sub-fractions of LDL sub-particles together is high. 

This would be like telling someone that the total number of balls they have is 25 and then asking them if this will fit in their container — but not telling them if they were golf balls or basketballs. We need to know how big they are to know what “25” means.

Someone having “high LDL cholesterol” i.e. high total LDL (LDL-C) tells us nothing in and by itself. We need to know about either particle size or particle number.

This leaves several options;

An LDL-particle (LDL-P) test will indicate the LDL particle number and the higher the number, the more small dense LDL the person would have. While not routinely done, I have had had clients come to me with results from this specialized test.  They had it done when their total LDL cholesterol was found to be high, and their doctor wanted to know if this was problematic. If the number was low, then most of the LDL would be the large, buoyant type and not a problem — it would only be if the number was high, indicating lots of small, dense LDL that high total LDL is indicative of CVD risk.

An apoB test which measures the lipoprotein in VLDL and LDL is a good indicator of LDL particle number, so is a very good assessor of cardiovascular disease risk.

An apoB / apoA ratio is considered to be an even better predictor of CVD risk, than ApoB alone so if someone’s total LDL cholesterol (LDL-C) came back high, an apoB / apoA test would provide information with regards to the LDL particle number compared to the HDL particle number. ..but before requesting any special tests, one can simply look at TG:HDL ratio to see if LDL-C being high may be a concern.

Being told we have high LDL cholesterol doesn’t mean much if we don’t know which LDL is high. Small, dense LDL are a risk, but large, buoyant LDL are not. To assess the need for dietary, lifestyle or medication changes we need to know “how many” or “how big”. We can estimate this using a TG:HDL ratio from routine blood work — all we need is a calculator, and knowing the cut-off points. Then, if warranted, we can run an apoB test or both apoB and apoA tests to assess apoB/apoA and know for sure if there are too many small dense LDL.

Prescribing statins on the basis of high (total) LDL cholesterol alone — without knowing anything about size of the LDL particles or total number of LDL particles is, according to this most recent article, inappropriate.

NOTE (April 26, 2021): It should be noted that while it is the opinion of the writers of the article in Current Opinion in Lipidology, and that of the European Society of Cardiology and the European Atherosclerosis Society that LDL-C is not the best clinical marker of cardiovascular risk or the appropriate marker to assess the benefits of statin medication, an individual should always discuss whether or not to take a medication with their doctor.  Lab tests may not be the only reason for medications to be prescribed — and such a recommendation may also include past medical history, lifestyle factors and/or family risk factors. Always discuss these matters with your doctor.

More Info?

If you’ve been told you have high cholesterol and would like to know if dietary changes might be helpful, please reach out.  I’ll look at your your diet, blood work and family history and let you know what may be the most prudent approach to minimize risk.

To your good health!

Joy

You can follow me on:

Twitter: https://twitter.com/JoyKiddie
Facebook: https://www.facebook.com/BetterByDesignNutrition/

References

  1. Sniderman A; Langlois M, Cobbaert C, Update on apolipoprotein B, Current Opinion in Lipidology: April 16, 2021 – Volume Publish Ahead of Print – Issue – doi: 10.1097/MOL.0000000000000754
  2. Harada PHN, Akintunde A, Mora S, Advanced Lipoprotein Testing: Strengths and Limitations. 2014 Jun 20, Am Col of Cardiology, Expert Analysis, https://www.acc.org/latest-in-cardiology/articles/2014/08/25/15/07/advanced-lipoprotein-testing-strengths-and-limitations
  3. Diffenderfer MR, Schaefer EJ. The composition and metabolism of large and small LDL. Curr Opin Lipidol. 2014 Jun;25(3):221-6. doi: 10.1097/MOL.0000000000000067. PMID: 24811298.
  4. Ivanova EA, Myasoedova VA, Melnichenko AA, Grechko AV, Orekhov AN. Small Dense Low-Density Lipoprotein as Biomarker for Atherosclerotic Diseases. Oxid Med Cell Longev. 2017;2017:1273042. doi:10.1155/2017/1273042
  5. Hanak V, Munoz J, Teague J, Stanley A Jr, Bittner V. Accuracy of the triglyceride to high-density lipoprotein cholesterol ratio for prediction of the low-density lipoprotein phenotype B. Am J Cardiol. 2004 Jul 15;94(2):219-22. doi: 10.1016/j.amjcard.2004.03.069. PMID: 15246907.
  6. McLaughlin T, Reaven G, Abbasi F, et al. Is there a simple way to
    identify insulin-resistant individuals at increased risk of cardiovascular
    disease? Am J Cardiol. 2005;96(3):399Y404.
  7. Vega GL, Barlow CE, Grundy SM et al, Triglyceride to High Density Lipoprotein Cholesterol Ratio is an Index of Heart Disease Mortality and of Incidence of Type 2 Diabetes Melletus in Men, Journal of Investigative Medicine & Volume 62, Number 2, February 2014
  8. Sigurdsson AF, The Triglyceride/HDL Cholesterol Ratio, updated January 12, 2019, https://www.docsopinion.com/2014/07/17/triglyceride-hdl-ratio/

 

Copyright ©2021 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 a Low-FODMAP Diet and How Can it Improve Symptoms of IBS?

FODMAP is an acronym for fermentable oligosaccharides, disaccharides, monosaccharides and polyols which are the types of carbohydrate that are fermented by the microorganisms that live in our intestines know as the “microbiome”, resulting in increased gas production (methane), abdominal pain, bloating, diarrhea or constipation, or sometimes a combination of both.

The carbohydrate fermented by our gut organisms include simple sugars such as monosaccharides and disaccharides, as well as slightly longer molecules known as oligosaccaharides and a group of sugar alcohols known as polyols.

Monosaccharides are simple sugars such as glucose, fructose, galactose. Fructose is the sugar that makes fruit such as apples, pears and peaches sweet. Honey, prunes and dates, mango and papaya are also very high in fructose.

Disaccharides are two monosaccharide sugars joined together. Common table sugar is a disaccharide made up of a molecule of glucose and fructose.

An oligosaccharide is a short carbohydrate chain whose molecules are composed of a relatively small number of monosaccharide (such as glucose, fructose, galactose) units. Chains of fructose with one glucose molecule on the end are oligosaccharides known as fructans. Wheat is a major source of fructans in the diet, which means most breads, pasta, and pastry contain large amounts of fructans. Chains of galactose with one fructose molecule on the end are known as galactans. Foods rich in galactans are legumes (including soybeans, chickpeas, lentils), cabbage, and brussels sprouts.

Polyols are sugar alcohols that are found in sugar substitutes such as mannitol, xylitol, and sorbitol but they are also found naturally in fruit and vegetables such as cherries, avocado, plums, and mushrooms.

What is a low-FODMAP Diet?

A low FODMAP diet was first created in the early 2000s by Dr. Peter Gibson and Dr. Sue Shepherd to improve symptoms in Functional Gastrointestinal Disorders (FGIDs). Functional GI disorders are ones where there is no structural abnormality that can be seen when the person has tests including endoscopy, but they have frequent symptoms. These symptoms are thought to be related to gut–brain interaction, such as motility disturbance, visceral hypersensitivity, altered gut microbiota, and include a wide range of disorders or which Irritable Bowel Syndrome (IBS) is only one.

A low-FODMAP diet is frequently used to help reduce symptoms of Irritable Bowel Syndrome (IBS) and can be helpful for those who have been diagnosed with Inflammatory Bowel Disease (IBD) such as Crohn’s disease and Ulcerative Colitis when re-introducing foods after they have reduced symptoms following a Low Residue Diet.

Why do FODMAPs trigger symptoms?

FODMAPs are carbohydrates that are used by the gut microbiome as food. These bacteria, yeast and single-cell organisms live in the intestines help digest the food we eat and release by-products, as a result. Some of these by-products such as short-chain fatty acids can be helpful to the body, whereas other by-products may underlie unpleasant gastrointestinal (GI) symptoms.

When certain types of microbes ferment FODMAPs, one of the by-products they produce is methane gas which can contribute to feelings of bloating, abdominal pain, or cramping in individuals with IBS. Some types of FODMAPS also result in water being pulled into the intestines rather quickly, and which results in the diarrhea. Depending on the microbes and the FODMAPS they rely on, constipation can also be a symptom – whereas some people experience alternating periods of diarrhea and constipation.

What is the low FODMAP diet?

When used for those with functional GI disorders such as IBS, a low FODMAP diet is an elimination diet that involves removing high FODMAP foods from the diet for a period of 4 weeks or so and assessing whether the person feels better. If they do, it is assumed that some of the FODMAP foods are the ones underlying their symptoms problematic and we go about determining which ones they are not tolerating. After several weeks of the person not eating any foods with FODMAPS, we gradually reintroduce small amounts of foods that have lower amounts of FODMAPs and see how they feel. Foods that do not cause any symptoms are left in the diet, but those that result in symptoms are eliminated.

One Diet – in three stages

The Initial Stage of the Low-FODMAP Diet is where there is total elimination of FODMAP foods, and this stage lasts approximately 4 weeks. At the end of this stage, we evaluate to what degree symptoms have decreased. If symptoms have not decreased, I may recommend that we change approaches to evaluate other non-FODMAP factors that may be contributing to symptoms. If symptoms have decreased, then we carry on to the next stage of the Low-FODMAP Diet.

During the Intermediate Stage, specific foods with low levels of FODMAPs are gradually re-introduced over the following several weeks. How long a person remains at this stage varies with the person, the severity of their symptoms, and they level of comfort they have with reintroducing foods.

Finally, there is the Liberalization Stage of the Low-FODMAP Diet where the person gradually increases the amount of slightly higher FODMAP foods and begin to re-introduce new foods.

The Low-FODMAP Specialty Hour Service

I offer a one-hour specialty hourly service for those who want to take a low-FODMAP approach to reducing their unpleasant gastrointestinal symptoms.  I teach how to implement a low-FODMAP diet in 3 progressive stages, so that with my guidance people can find the level of FODMAP restriction that suits them best, without unnecessarily restricting foods that don’t cause them distress.

The first stage begins with a period of one-on-on instruction where I go over the detailed handout that I give them for following the elimination diet over the next 4 weeks. During that time, they can consult with me via email if they have questions, or if they want additional direction. At the end of the 4 weeks, we meet again and review their progress and make adjustments in what they are eating, if necessary. Then I go over the handouts for the next two stages and answer any questions they may have about implementing them sequentially.

Beyond FODMAP

People sometimes have ongoing problems with IBS – despite having learned a low-FODMAP diet elsewhere. They remain at a loss as to why they are still having symptoms. Sometimes it is because they did not implement the diet in distinct sequential stages – beginning with a period of complete elimination then gradually re-introducing foods from lower to higher FODMAP, and as a result never learned which foods are problematic, and which are not.

Oftentimes it is because they have not had any teaching about a specific category of food outside the standard low-FODMAP diet that even people without IBS do not tolerate well. These are foods which contain two specific oligosaccharides that should be cautiously re-introduced or avoided in people who know that they do not do well with some of those foods and which are beyond the scope of a standard low-FODMAP diet.

I teach these as part of the low-FODMAP service that I provide.

Gut Microbiome – environment and genetics

It was once thought that people are born with their unique types of gut bacteria, but recent twin studies have found that identical twins have very different types and amounts of gut bacteria — leading researchers to conclude that what we eat determines which gut bacteria multiply and which don’t. The extent to which different people produce methane gas in response to food seems to depend on the types of bacteria in one’s gut microbiome.

By avoiding the specific FODMAP foods that underlie symptoms we can greatly reduce the severity and frequency of symptoms that these gut bacteria produce as by-products.

More Info?

If your doctor has suggested that you could benefit from following a low-FODMAP diet, or you have previously learned a low-FODMAP somewhere but feel you missed some important aspects, please reach out to me and let know how I can help.

To your good health!

Joy

You can follow me on:

Twitter: https://twitter.com/JoyKiddie
Facebook: https://www.facebook.com/BetterByDesignNutrition/

References

1. Gibson, PR, Shepherd SJ. Evidence-based dietary management of functional gastrointestinal symptoms: The FODMAP approach. Journal of Gastroenterology & Hepatology 2010;25(2):252-8.
2. Drossman DA, et al. Rome IV, the functional gastrointestinal disorders. Gastroenterology 2016;150:1262–1279.
3. V. Jain, K. Gupta, in Encyclopedia of Analytical Science (Second Edition), 2005
4. Cahana, I, Iraqi, FA. Impact of host genetics on gut microbiome: Take‐home lessons from human and mouse studies. Anim Models Exp Med. 2020; 3: 229– 236. https://doi.org/10.1002/ame2.12134
5. Rothschild, D., Weissbrod, O., Barkan, E. et al. Environment dominates over host genetics in shaping human gut microbiota. Nature 555, 210–215 (2018). https://doi.org/10.1038/nature25973

Copyright ©2021 BetterByDesign Nutrition Ltd.

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

Why Drinking a Smoothie isn’t the Same as Eating the Food Contained in it

People are busy. I “get” that, and morning routines are often the most challenging. Taking time to have breakfast is often seen as “one more thing to do”, so the idea of making a smoothie and “taking it with” may seem like a good idea. But is it? Is drinking a smoothie the same as eating the foods it is made out of? It isn’t.

In an earlier article, I covered the effect of various types of food processing (including mechanical processing such as pureeing fruit in a smoothie) on blood glucose. While 60g of whole apple, 60 g of apple that has been pureed, and 60g of apple that has been juiced have the same amount of amount of carbohydrate and a very similar Glycemic Index (GI) [1], neither the carbohydrate content nor GI tell us anything about how high blood sugar is going to go when eating or drinking them. Glycemic Index only indicates how slowly or quickly foods will increase blood sugar, not how much higher blood sugar will go [2].

A raw apple has a GI of 36  ± 2, and apple juice has a GI of 41  ± 2, so factoring in the error range, raw apple can have a GI of 38, and apple juice a GI of 39. A medium apple (3″ across) has ~25 g of carbs, and even when we make it into unsweetened apple sauce, it still has the same amount of carbs. If we press it into juice, the amount of carbohydrate in it doesn’t change. But we know from a 1977 study published in the Lancet that when fruit is pureed fruit or juiced and then eaten, the glucose response 90 minutes later is significantly higher, than if the fruit were eaten whole [3]. This is because the blender or juicer has done some of the work of digesting the food for us!

Most people think that digestion begins in the stomach, but it doesn’t. It begins in the mouth when we chew food.

When we eat a bowl of berries for example, chewing makes the glucose (sugar) in the berries that we chewed more available to the body — but when we put the same amount of berries in a blender and whir them up, the contents of all the berries are now completely available for the body to act on. We never chew food as fine as a blender makes it, so blending food results in a faster spike in blood sugar than the whole food, eaten intact. This is one reason why drinking a smoothie is not the same as eating the same food it is made from.

The order we eat foods in during a meal also makes a big difference on blood sugar and on the insulin response to eating (or drinking) carbohydrate-containing food. We know from a 2015 study about the effect of food order on the response of glucose and insulin that if the carbohydrate-containing food is eaten last, the glucose curve will be ~74% smaller than if it were eaten first! Likewise, if we eat the carbohydrate-containing food last, the insulin spike will be 49% smaller, than if we eat it first [4]!

Having a smoothie for breakfast instead of a meal made out of the same foods means there is no way of having the carbs last!

Final Thoughts…

It really doesn’t take very long to eat the some veggies (like snap peas or baby carrots) and a dish of yogurt and berries for breakfast and the response on blood sugar and demand on our pancreas for insulin is significant!  This is why I tell people who come to me seeking to loose weight and improve their metabolic health to eat their food, not drink it — because it does matter!

This is also one of the reasons that I felt Diabetes Canada’s “7-day Low Carb Meal Plan” which had a 30g of carbs (and only 9 g of protein) was not the best recommendation for people with diabetes to have for breakfast 3 days per week.

More Info?

If you would like more information about how I can support your nutritional needs, please click on the Services tab above to learn more.

To your good health!

Joy

You can follow me on:

Twitter: https://twitter.com/JoyKiddie
Facebook: https://www.facebook.com/BetterByDesignNutrition/

References

  1. Atkinson FS, Foster-Powell K, Brand-Miller JC, “International tables of glycemic index and glycemic load values”, Diabetes Care 31(12); 2281-2283
  2. Harvard Health Publishing, Glycemic index for 60+ foods (from American Diabetes Association, 2008), https://www.health.harvard.edu/diseases-and-conditions/glycemic-index-and-glycemic-load-for-100-foods
  3. Haber GB, Heaton KW, Murphy D, Burroughs LF. Depletion and disruption of dietary fibre. Effects on satiety, plasma-glucose, and serum-insulin. Lancet. 1977 Oct 1;2(8040):679-82. doi: 10.1016/s0140-6736(77)90494-9. PMID: 71495
  4. Shukla AP, Iliescu RG, Thomas CE, Aronne LJ. Food Order Has a Significant Impact on Postprandial Glucose and Insulin Levels. Diabetes Care. 2015;38(7):e98-e99. doi:10.2337/dc15-0429

 

Copyright ©2021 BetterByDesign Nutrition Ltd.

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

A Therapeutic Ketogenic Diet – treatment and adjunct treatment

therapeutic diet is one that is used in the treatment of a medical condition and can be prescribed by a physician and implemented by them, or prescribed by a physician and implemented by a dietitian. When implemented by a dietitian, a therapeutic diet is referred to as Medical Nutrition Therapy (MNT) [1]. 

A ketogenic diet is a very high fat diet that induces and sustains a state of ketosis, which is a natural metabolic state where the body burns fat as its primary fuel, rather than carbohydrate. Ketosis is where the ketone betahydroxybutyrate (BHB) reaches levels between 0.5 – 3.0 mmol/L known as nutritional ketosis [2] — right up to levels of 4.0 mmol/L for specific therapeutic ketogenic diets used in the treatment of epilepsy[3] and seizure disorder, or levels of up to 3.0 mmol/L when used as adjunct treatment along with chemo and radiation, in glioblastoma [4,5,6]*.

*Just because a therapeutic diet may be useful in glioblastoma, one can not and should not assume it is an appropriate adjunct treatment for all types of cancer, or in all types of glioblastoma. Some types of cancer feed on glucose, whereas other feed on ketone bodies. 

Types of Therapeutic Ketogenic Diets

Ketogenic diets are a subtype of a low carbohydrate  diets.

Low carbohydrate diets are ones where carbohydrate intake is limited to <130 g per day or < 26% of total energy intake[7] but that level of carbohydrate intake is much too high for therapeutic purposes in the treatment of epilepsy or seizure disorder, or as adjunct treatment of glioblastoma but are used in the treatment of type 2 diabetes. 

Moderate carbohydrate diets are where carbohydrate intake is limited to 130–225 g per day or 26–45% of total energy intake [7] and while this level of carbohydrate intake can be helpful in the treatment of type 2 diabetes and obesity, a much lower level of carbohydrate intake is required for the treatment of epilepsy, seizure disorder or as adjunct treatment in glioblastoma.

A very low carbohydrate diet is also called a “ketogenic diet” and is one where carbohydrate intake is limited to 20-50 g per day or 10% of total energy intake[7]. It can be used safely and effectively in the treatment of type 2 diabetes and obesity [2], and is also used the treatment of epilepsy, seizure disorder [3], and as adjunct treatment in glioblastoma [4,5,6]. The carbohydrate content of the diet is kept very low, so as a result protein and/or fat need to be increased significantly.

In therapeutic ketogenic diets used for obesity management and for seeking remission from the symptoms of type 2 diabetes, protein intake can range from 15% of calories as protein right up to 35-40% of calories. Since it is a very high fat, low carbohydrate diet it induces a state of nutritional ketosis where the primary ketone of interest, betahydroxybutyrate (BHB) can range from 0.5 -3.0 mmol/L[2].

For the treatment of epilepsy and seizure disorder or as adjunct treatment in glioblastoma, a much lower level of protein is required so that for therapeutic purposes, levels of betahydroxybutyrate (BHB) can reach between 3.0 and 4.0 mmol/L (depending on the specific condition and length of time the person has been following a therapeutic ketogenic diet).

Therapeutic Ketogenic Diets for Epilepsy, Seizure Disorder and Adjunct Treatment in Glioblastoma

A therapeutic ketogenic diet has been used prior to the 1920s by Dr. Russell Wilder for the treatment of diabetes and later for the treatment of epilepsy, in fact it was Wilder himself who is credited with coining the term “ketogenic diet”. The precise percentage of carbohydrate, fat and protein in what is now called the “classic” Ketogenic Diet (KD) was worked out by Dr. M.G. Peterman in 1925 [8], and are the same ratios used today. 

Therapeutic ketogenic diets used in epilepsy and seizure disorder and as adjunct treatment in glioblastoma are very high fat, low protein and low carbohydrate diets — ranging from 4 : 1 ratio (4 parts fat for every 1 part protein plus carbohydrate) to a 3 : 1 ratio (3 parts fat for every 1 part protein plus carbohydrate) — and for maintenance may be as low as a 2 : 1 ratio (2 parts of fat for every 1 part protein plus carbohydrate).

The Diet Prescription

Based on the diet prescription written by the doctor, the amount of energy (calories) that the person needs will be calculated based on the person’s weight and height, activity level, and nutritional requirements and whether there is a goal to avoid weight loss, such in glioblastoma treatment.

Given the very high fat, low carbohydrate content of a 4 : 1 and 3 : 1 ketogenic diet, and the very small amount of protein, Meal Plan design is time consuming and challenging. It’s not that easy to come up with palatable food combinations that meet the precise macros (amount of protein, fat and carbohydrate) of the diet. Each meal has to have the exact amount — as it is a diet prescription.  In a therapeutic diet, the amount and types of food are an integral part of treatment. Just as medication has a “dosage”, the specific and exact amount of food on the diet prescription is like the “food dosage”.

Vitamin, mineral and trace element supplementation (such as potassium citrate) are also necessary to avoid nutritional deficiencies and recommendations are provided along with the Meal Plan.

In working with adults who are trialing a 4 : 1 or 3 : 1 ketogenic diet for seizure disorder, or during chemo and radiation for glioblastoma,  I do the diet calculations, and then design a simple breakfast-lunch-and-dinner Meal Plan for them to use during the initial 6 weeks. Sometimes people with  will want an extra dinner meal to alternate with. 

If things go well and the diet is improving their symptoms, those with seizure disorder may decide to stay on the therapeutic diet over an extended period of time, and in such a case, I may be asked to design a few lunch and dinner options — with most people content to eat the same breakfast.

Those with glioblastoma will usually ask me to design a 2 : 1 Modified Atkins Diet for them to follow between rounds of chemo and radiation, which I will do for them.  This allows for more protein in their diet (while still keeping the carbohydrate content low) and provides a pleasant ‘break’ for those who have been finding the restrictive meals of a 4 : 1 or 3 : 1 ketogenic diet difficult. The other advantage is that since it is unknown whether the type of glioblastoma involved may feed on ketones, alternating between a high ketone and low ketone diet in this manner minimizes providing high ketone levels when not taking the chemo- or radiation treatment.  

What is challenging for those first starting out in eating a therapeutic ketogenic diet for epilepsy or as an adjunct treatment in glioblastoma, is that the amount of food on the final Meal Plan must be precisely and accurately weighed — as even the smallest amount of vegetable (which has some protein and some carbohydrate in it) can affect the macros, and thus reduce the therapeutic benefit of the diet. Everything needs to be weighed to the gram.

In addition, at the beginning there is the need for daily monitoring of blood ketone levels to determine when the person has achieved the desired therapeutic range, which for epilepsy and seizure disorder is often where betahydroxybutyrate (BHB) is between 3.0 and 4.0 mmol/L. Once they are able to keep it there by maintaining the diet, testing less frequently is possible. 

Classic Ketogenic Diet (KD) – 4 : 1

In the classic Ketogenic Diet (KD), the total amount of calories are matched to the number of calories the person needs. Protein is usually determined as being 1 g of protein per kg body weight, 10-15 g of carbohydrate per day total, and the remainder of calories provided as fat. For very young children, the diet may be prescribed based on body weight (e.g. 75-100 calories for each kg (2.2 pounds) of body weight.

Since the 1920s, several other therapeutic ketogenic for the treatment of epilepsy and seizure disorder have been developed, including the Modified Ketogenic Diet (MKD) and the Modified Atkins Diet (MAD). They are all very low carbohydrate diets high fat diets which is by definition what makes them ketogenic, differ in the amount of protein they contain.

As well as their use in epilepsy and seizure disorder, any of the above therapeutic ketogenic diets may be prescribed for patients as adjunct treatment in glioblastoma, or as adjunct treatment in Alzheimer’s disease.

The classic Ketogenic Diet (KD) has a 4:1 ratio i.e. 4 parts of fat for every 1 part protein and carbs. That is, for every 5 grams of food there are 4 grams of fat and 1 gram of protein and/or carbohydrate.

In the classic Ketogenic Diet, 80% (i.e. 4÷5=80%) of calories come from fat and 20% (i.e. 1÷5=20%) from a combination of protein and carbohydrate.

Protein may be set at 15% of calories with a maximum of 5% of calories coming from carbohydrate, or protein may be set lower at 10%, and carbohydrate as high as 10%.

Modified Ketogenic Diet (MKD) – 3 : 1 ratio

The Modified Ketogenic Diet (MKD) has a 3:1 ratio i.e. 3 parts fat for every 1-part protein and carbohydrate. In a Modified Ketogenic Diet, 75% of calories come from fat and 25% from a combination of protein and carbohydrate. Protein may be set at 15% of calories with a maximum of 10% of calories coming from carbohydrate[5].

Modified Atkins Diet (MAD) – 2 : 1 ratio

The Modified Atkins Diet (MAD) has a 2 : 1 ratio, with 2 parts fat for every 1-part protein and carbohydrate. In a Modified Atkins Diet, carbohydrates are restricted to <15 g / day for children, <20 g / day for adults. In a Modified Atkins Diet for adults, 60% of calories come from fat, 30% of calories come from protein, and 10% of calories come from carbohydrate[5].

“Chasing Ketones” – betahydroxybutyrate, the therapeutic goal

The therapeutic goal of a 4 : 1 or 3 : 1 therapeutic ketogenic diet is to get the person’s blood ketone level (as measured with an accurate meter!) to measure 3.0 mmol/L betahydroxybutyrate (BHB) as soon as possible — and to have them sustain it at that level (or in some cases, up to 4.0 mmol/L). Since it is the ketones that provide the therapeutic benefit, not adding anything to the diet that isn’t part of the diet prescription is important.

I usually recommend for a person starting out on a therapeutic ketogenic diet get a Abbott Precision Freestyle Neo meter from their pharmacy, as it measures both blood glucose and ketones, is very accurate and reliable (unlike some purchased online and used by people following the popularize “keto diet” or weight loss) and is provided at no cost when purchasing 100 glucose strips (~$1 each).  I then recommend they purchase 30 ketone strips for the same monitor ($3 each) — so the strips will last a month with checking blood glucose 3x / day and checking ketones 1 x / day. 

Blood glucose should not go below 4.0 mmol/ L when measured using the glucose strip in the meter, and blood ketone levels should ideally measure 3.0 mmol/L (and as high as 4.0 mmol/Lin epilepsy and seizure disorder – but not over). If ketones exceed 4.0 mmol/L, the person should contact their doctor — and if they go much higher, should seek medical help immediately.

People diagnosed with glioblastoma ideally begin a 4 : 1 (or 3 : 1) therapeutic ketogenic diet upon discharge from hospital so that they begin chemo and radiation treatment already at a ketone level of 3.0 mmol/L betahydroxybutyrate. For seizure disorder, the neurologists that refer their patients to me are seeking levels as close to 4.0 mmol/L as possible — because that is where the most benefit is seen.  Once seizures have ceased, people may want to begin to try gradually eating a 3 : 1, then a 2 : 1 diet — so long as their seizures remain in remission.  There is a lot of trial and error involved, but for those seeking to extend their life (as in glioblastoma) or improve their quality of life (as in epilepsy or seizure disorder), it may be worth it.

While people following the popularized “keto diet” for weight loss or remission of type 2 diabetes are often teased about “chasing ketones” — when their goal is fat loss or improved blood sugar (and not producing high levels of ketones!), for those following a therapeutic ketogenic diet for the treatment of epilepsy or seizure disorder, “chasing ketones” between 3.0 mmol/L and 4.0 mmol/L may be desirable.

NOTE: (April 13, 2021): While some research papers indicate that advanced gliomas do not use ketones as a fuel source, a research paper from September 2020 was brought to my attention which calls this into question.  According to this paper, there are different types of glioblastoma cells and some oxidize fatty acids and use ketones for energy. Since it appears that when glucose levels are decreased, some types of glioblastoma cells may adapt by partially shifting their metabolism to use oxidized fatty acids and ketones, seeking lower level of ketone production may be advantageous.
[Sperry J, Condro MC, Guo L, et al, Glioblastoma Utilizes Fatty Acids and Ketone Bodies for Growth Allowing Progression during Ketogenic Diet Therapy, iScience  Volume 23, Issue 9, 25 September 2020, 101453].

Many thanks to Cliff Harvey, PhD. for rounding out this understanding.

More Info?

If you would like more information about how I support adults with epilepsy or seizure disorder, or those diagnosed with glioblastoma who are seeking to use a therapeutic ketogenic diet as adjunct treatment (along with chemo and radiation), please send me a note through the Contact Me form.

If you are newly diagnosed with glioblastoma, I will fit you in even when I have no openings for the next several weeks. Your clinical needs are a priority.

To your good health!

Joy

You can follow me on:

Twitter: https://twitter.com/JoyKiddie
Facebook: https://www.facebook.com/BetterByDesignNutrition/

References

  1. U.S. Department of Health and Human ServicesFinal MNT regulationsCMS-1169-FCFederal Register1 November 200142 CFR Parts 405, 410, 411, 414, and 415
  2. Nasir H. Bhanpuri, Sarah J. Hallberg, Paul T. Williams et al, Cardiovascular disease risk factor responses to a type 2 diabetes care model including nutritional ketosis induced by sustained carbohydrate restriction at 1 year: an open label, non-randomized, controlled study, Cardiovascular Diabetology, 2018, 17(56)
  3. Meira ID, Romao TT, Pires do Prado HJ, Ketogenic Diet and Epilepsy: What We Know So Far, Front. Neurosci., 29 January 2019, https://doi.org/10.3389/fnins.2019.00005
  4. van der Louw EJTM, Olieman JF, van den Bemt PMLA, et al. Ketogenic diet treatment as adjuvant to standard treatment of glioblastoma multiforme: a feasibility and safety study. Ther Adv Med Oncol. 2019;11, 2019 Jun 21. doi:10.1177/1758835919853958
  5. Schwartz KA, Noel M, Nikolai M, Investigating the Ketogenic Diet As Treatment for Primary Aggressive Brain Cancer: Challenges and Lessons Learned, Front. Nutr., 23 February 2018 | https://doi.org/10.3389/fnut.2018.00011
  6. Klein P, Tyrlikova I, Zuccoli G, Tyrlik A, Maroon JC. Treatment of glioblastoma multiforme with “classic” 4:1 ketogenic diet total meal replacement. Cancer Metab. 2020;8(1):24. Published 2020 Nov 9. doi:10.1186/s40170-020-00230-9
  7. Feinman RD, Pogozelski WK, Astrup A, Bernstein RK, Fine EJ,Westman EC, et al. Dietary Carbohydrate Restriction as the First Approach in Diabetes Management: critical review and evidence base. Nutrition. 2015;31(1):1–13
  8. Peterman MG, The Ketogenic Diet, JAMA. 1928;90(18):1427–1429. doi:10.1001/jama.1928.02690450007003

Copyright ©2021 BetterByDesign Nutrition Ltd.

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

A Simple Guide to Different Types of Diet and Macros

People on social media argue about which is the “best diet” for humans — vegan or carnivore? Low carb or keto? Vegetarian or vegan? I avoid these “diet wars” largely because I don’t believe there is a “best” diet for everybody. Some diets are preferable over others for a variety of reasons, including religious constraints, ethical reasons and specific health conditions — so the “best diet” is one that meets an individual’s personal health goals and objectives, and that is consistent with their belief system. 

One of my clients recently mentioned that the more they read about different types of diets online, the more confused they became. They wanted to know if I could write an article to explain them simply. That is the purpose of this post.

Macros

Macros defined

Foods are made up of protein, fat and carbohydrate in different ratios, and these together are commonly referred to as “macros“. This term is shortened from “macronutrients“, where macro means “big” in Greek. Micronutrients is the term used for all the vitamins and minerals, where micro means “small” in Greek.

Macros refer to the three categories of nutrients (protein, carbohydrates and fat) that make up the food that people eat, and which together provide them with their source of energy, as calories.

When people are “counting macros” or “calculating their macros”, they are counting the grams of proteins, carbohydrate (carbs) and fat they are eating.

Different Diet Types

This is not an exhaustive list of all the different diet types, but a summary of popular categories.

Standard American Diet

Standard American Diet

The average American (or Canadian diet) is often referred to as the “SAD Diet” — which is a shortened form of the “Standard American Diet“.

The Standard American Diet is one where the majority of calories come from carbohydrate and fat — mostly vegetable fat, as recommended by both the American and Canadian dietary guidelines. Vegetable fats are also called “seed oils” and include soybean, canola, and corn oil.

Carbohydrate (“carbs”) are most commonly thought of in terms of various types of bread, rolls, pizza, pasta, rice, and potatoes (French fries, mashed, baked potato, boiled potato), but also include fruit (other than berries which are eaten on a low carb diet), as well as fruit juice, and milk (but not cheese or yogurt that are low in carbs). Milk is included as “carbs” because of its high carbohydrate content.

Vegetarians and Vegans

Vegetarians

Vegetarian

Vegetarians are those that don’t eat meat, fish or poultry, but do eat eggs and milk.  These are also known as ovo-lacto vegetarians, as they eat eggs (“ovo” meaning eggs) and milk (“lacto” meaning milk).

Pescatarians are vegetarians that eat fish.

People who eat a vegetarian or pescatarian diet can also eat low carb or very low carb (keto). They are not mutually exclusive.

Vegans

Vegan

Vegans don’t eat any food of animal origin, including eggs, milk, butter or cream (and products made from them) may do so for religious or ethical reasons. Vegans are sometimes considered a subclass of vegetarian, or an entirely different category. 

They often refer to themselves eating an entirely “plant-based” diet.

A vegan diet can be done low carb, but to obtain adequate nutrients takes a great deal of time and knowledge, but it can be done.

“Low Carb” – LCHF

Low Carb – LCHF

In a research context [1] and in the clinical guidelines of the American Diabetes Association [2] and Diabetes Canada [3], low carbohydrate diets (“low carb”) are those where carbohydrate intake is limited to <130 g per day or < 26% of total energy intake[1].

These are also referred to as low carb high fat diets (LCHF) or low carb healthy fat diets (also LCHF).

Moderate carbohydrate diets are where carbohydrate intake is limited to 130–225 g per day or 26–45% of total energy intake [1].

A “Paleo diet” is modelled after what is understood to have been the diet of our ancient hunter-gatherer ancestors. It varies considerably between individuals, but is essentially a low carbohydrate diet that uses protein and fat sources that have been known to mankind for millennia.

A Keto Diet

“Keto” Diet

A keto diet is a subtype of low carb diet and in a research context [1], and in the clinical guidelines of the American Diabetes Association [2] and Diabetes Canada [3] are referred to as “very low carbohydrate diets“. A “very low carbohydrate diet”, or “keto diet” is one where carbohydrate intake is limited to 20-50 g per day or 10% of total energy intake [1,2,3].

They are called “keto” diets because at this very low level of carbohydrate intake, blood ketones (by-products of the body burning fat for energy) increase at or above 0.5 mmol/L, resulting in a state known as “ketosis”.

Keto diets used predominantly for weight loss or improving symptoms of type 2 diabetes are where ketone levels are usually set with betahydroxybutyrate (BHB) levels between 1.5-3.0 mmol/L [4].

There is no one “keto diet” but some versions of the popularized high fat keto diet are associated with Dr. Jason Fung and Diet Doctor.

Therapeutic Ketogenic Diet

Therapeutic Ketogenic Diets

The first therapeutic ketogenic diet was used in the 1920s by Dr. Russell Wilder, for the treatment of diabetes and later, for epilepsy.

The percentage of carbohydrate, fat and protein in what has since become called the “classic” Ketogenic Diet (KD) was worked out by Dr. M.G. Peterman in 1925 [4], and are the same as used today. 

In the classic KD, the total amount of calories are matched to the number of calories the person needs. Protein is usually determined as being 1 g of protein per kg body weight, 10-15 g of carbohydrate per day total, and the remainder of calories provided as fat.  For very young children, the diet may be prescribed based on body weight (e.g. 75-100 calories for each kg (2.2 pounds) of body weight.

Since the 1920s, several other therapeutic ketogenic for the treatment of epilepsy and seizure disorder have been developed, including the Modified Ketogenic Diet (MKD) and the Modified Atkins Diet (MAD). They are all very low carbohydrate diets high fat diets which is by definition what makes them ketogenic, differ in the amount of protein they contain. 

As well as their use in epilepsy and seizure disorder, any of the above therapeutic ketogenic diets may be prescribed for patients as adjunct treatment in glioblastoma, or as adjunct treatment in Alzheimer’s disease.

The classic Ketogenic Diet (KD) has a 4:1 ratio i.e. 4 parts of fat for every 1 part protein and carbs. That is, for every 5 grams of food there are 4 grams of fat and 1 gram of protein and/or carbohydrate. 

In the classic Ketogenic Diet, 80%  (i.e. 4÷5=80%) of calories come from fat and 20% (i.e. 1÷5=20%) from a combination of protein and carbohydrate.

Protein may be set at 15% of calories with a maximum of 5%  of calories coming from carbohydrate, or protein may be set lower at 10%, and carbohydrate as high as 10%.

The Modified Ketogenic Diet (MKD) has a 3:1 ratio i.e. 3 parts fat for every 1-part protein and carbohydrate. In a Modified Ketogenic Diet, 75% of calories come from fat and 25% from a combination of protein and carbohydrate. Protein may be set at 15% of calories with a maximum of 10% of calories coming from carbohydrate[5].

The Modified Atkins Diet (MAD) has a 2:1 ratio, with 2 parts fat for every 1-part protein and carbohydrate.  In a Modified Atkins Diet, carbohydrates are restricted to <15 g / day for children, <20 g / day for adults. In a Modified Atkins Diet for adults, 60% of calories come from fat, 30% of calories come from protein, and 10% of calories come from carbohydrate[5].

These high fat diets are not weight loss diets. These are therapeutic ketogenic diets used with the goal of producing high amounts of ketones (> 4.0 mmol/L / 40 mg/dl) for therapeutic reasons.

Carnivore

Carnivore

Carnivores are people who eat only protein and fat of animal origin, including any edible part of mammals (including organ meats), birds of many types including poultry such as chicken and turkey as well as their eggs, and fish and seafood. Fats include butter, rendered chicken or duck fat, beef fat (tallow), and lard (rendered pig fat).

Carnivores and vegans are polar opposites — one eating ONLY animal products and the other not eating any animal products.

Protein to Energy (P:E)

Protein to Energy (P:E)

Protein to Energy (P:E) is an entirely new class of diet created by Dr. Ted Naiman. It focusses on eating the most amount of protein for the least amount of energy (calories).

It is not a low carbohydrate diet as the P:E calculator recommend carbohydrate intake  >130 g per day, which is the cut-off for low carb in most of the literature.

This article explains how everyone’s protein needs are different, and how protein should be calculated to prevent deficiency, to sustain exercise and to preserve muscle mass in older adults. Each of these calculations are different but at the same time, total protein should not exceed the ability of the kidney to excrete urea. 

There is no “best diet” for everyone. The “best diet” is an individual is one that meets their personal health goals and objectives and that is consistent with their beliefs.

More Info?

If you would like more information about my services, please have a look around my web page and if you have questions, please send me a note through the Contact Me form.

To your good health!

Joy

You can follow me on:

Twitter: https://twitter.com/JoyKiddie
Facebook: https://www.facebook.com/BetterByDesignNutrition/

Please read the terms and conditions (link below) regarding use of images on this web page.

References

  1. Feinman RD, Pogozelski WK, Astrup A, Bernstein RK, Fine EJ,Westman EC, et al. Dietary Carbohydrate Restriction as the First Approach in Diabetes Management: critical review and evidence base. Nutrition. 2015;31(1):1–13
  2. Evert, AB, Dennison M, Gardner CD, et al, Nutrition Therapy for Adults With Diabetes or Prediabetes: A Consensus Report, Diabetes Care, Ahead of Print, published online April 18, 2019, https://doi.org/10.2337/dci19-0014
  3. Diabetes Canada, Diabetes Canada Position Statement on Low Carbohydrate
    Diets for Adults with Diabetes: A Rapid Review Canadian Journal of Diabetes (2020), doi: https://doi.org/10.1016/j.jcjd.2020.04.001.
  4. Nasir H. Bhanpuri, Sarah J. Hallberg, Paul T. Williams et al, Cardiovascular disease risk factor responses to a type 2 diabetes care model including nutritional ketosis induced by sustained carbohydrate restriction at 1 year: an open label, non-randomized, controlled study, Cardiovascular Diabetology, 2018, 17(56)

Copyright ©2021 BetterByDesign Nutrition Ltd.

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

Why Is Type 2 Diabetes Still Called “a Progressive, Lifelong Disease”?

[NOTE: This is a combination Science Made Simple article and editorial, expressing my opinion.]

This past Wednesday March 24, 2021, Dr. James Muecke, a South Australia ophthalmologist who was the 2020 Australian of the Year, posted on Facebook that Diabetes Australia reworded their webpage from “Type 2 diabetes is a progressive condition” to “Type 2 diabetes is often a progressive condition” — wording that Dr. Muecke calls;

a small, but significant change that will give some degree of hope to the 280 Australians diagnosed [with type 2 diabetes] every day“. 

Diabetes Australia’s change in phraseology occurred shortly after Diabetes Victoria  removed the words “Type 2 diabetes is a progressive condition” entirely from its Type 2 Diabetes webpage — replacing it with nothing. This, Dr. Muecke said;

“gives tremendous hope to patients that their newly diagnosed condition can potentially be put into remission.”

I was curious what Diabetes Canada’s web site said and was saddened to discover that it stated that Type 2 diabetes is a progressive, life-long disease“.

Diabetes Canada: “Type 2 diabetes is a progressive, lifelong disease” (https://guidelines.diabetes.ca/docs/patient-resources/type-2-diabetes-the-basics.pdf)

We don’t tell people diagnosed with cancer they have “a progressive, lifelong disease” — but speak to them instead about treatment options and the possibility of remission. While some types of cancer are incurable and untreatable, in general people diagnosed with cancer are not told they have a “progressive, lifelong disease”. Why are people with type 2 diabetes told this? 

I think calling type 2 diabetes a progressive, lifelong disease is a vestige from before there was evidence that it could be put into remission. I think we need to change our terminology to reflect that it is now possible.

In February 2018, one year data from Virta Health’s outpatient study using a ketogenic diet intervention demonstrated that reversal of type 2 diabetes symptoms is sustainable over the long term — with HbA1c level at baseline being 7.6% ± 1.5% being reduced by 1.0% and the percentage of individuals with a HvA1C of <6.5% was 56% [1].

Virta Health’s 2-year data indicated that there were improvements in body weight and that improved blood sugar control was also largely sustained, and that significant metabolic markers and health improvements occurred while using a ketogenic approach in an outpatient setting, over the usual care model approach [2]. On average after one year, participants in the intervention (ketogenic) group lowered HbA1c from 7.7% to 6.3% and at two years, HbA1C of participants in the intervention group increased slightly to 6.7%. By comparison, HbA1C of the usual care control group was 7.5% at baseline, 7.6% at one-year, and 7.9% at two years.

Even a 2019 study using an calorie-restricted diet found that remission of type 2 diabetes within 1-year can be achieved at a cost below the annual cost of diabetes, including complications [3] .

There is no cure for diabetes — at least not yet, but there are three documented ways to put type 2 diabetes into remission;

  1. a ketogenic diet [1,2]
  2. a low calorie energy deficit diet [4,5,6]
  3. bariatric surgery (especially use of the roux en Y procedure) [7,8]

Since there is evidence that both a well-designed ketogenic diet and a well-designed calorie-restricted diet put type 2 diabetes into remission (i.e. maintaining blood glucose  below the diabetes cut-offs), we need to stop referring to type 2 diabetes as “a progressive, lifelong disease” — as if it is always the case. 

It can be a progressive, lifelong disease for those who would rather not make the significant dietary and lifestyle changes that are required to put it into remission (and as I outline in this article, this is a valid choice, too!)

People can choose to live WITH diabetes or to seek remission FROM it  — but they deserve to know that remission is possible.

More Info?

If you would like more information about how I can support you in aiming to put type 2 diabetes into remission, please let me know.

To your good health!

Joy

You can follow me on:

Twitter: https://twitter.com/JoyKiddie
Facebook: https://www.facebook.com/BetterByDesignNutrition/

 

References

  1. Hallberg, S.J., McKenzie, A.L., Williams, P.T. et al. Effectiveness and Safety of a Novel Care Model for the Management of Type 2 Diabetes at 1 Year: An Open-Label, Non-Randomized, Controlled Study. Diabetes Ther 9, 583–612 (2018). https://doi.org/10.1007/s13300-018-0373-9
  2. Athinarayanan SJ, Adams RN, Hallberg SJ, McKenzie AL, Bhanpuri NH, Campbell WW, Volek JS, Phinney SD, McCarter JP. Long-Term Effects of a Novel Continuous Remote Care Intervention Including Nutritional Ketosis for the Management of Type 2 Diabetes: A 2-Year Non-randomized Clinical Trial. Front Endocrinol (Lausanne). 2019 Jun 5;10:348. doi: 10.3389/fendo.2019.00348. PMID: 31231311; PMCID: PMC6561315.
  3. Xin Y, Davies A, McCombie L, Briggs A, Messow CM, Grieve E, Leslie WS, Taylor R, Lean MEJ. Type 2 diabetes remission: economic evaluation of the DiRECT/Counterweight-Plus weight management programme within a primary care randomized controlled trial. Diabet Med. 2019 Aug;36(8):1003-1012. doi: 10.1111/dme.13981. PMID: 31026353.
  4. Lim EL, Hollingsworth KG, Aribisala BS, Chen MJ, Mathers JC, Taylor R. Reversal of type 2 diabetes: normalisation of beta cell function in association with decreased pancreas and liver triacylglycerol. Diabetologia2011;54:2506-14. doi:10.1007/s00125-011-2204-7 pmid:21656330
  5. Steven S, Hollingsworth KG, Al-Mrabeh A, et al. Very low-calorie diet and 6 months of weight stability in type 2 diabetes: pathophysiological changes in responders and nonresponders. Diabetes Care2016;39:808-15. doi:10.2337/dc15-1942 pmid:27002059
  6. Lean ME, Leslie WS, Barnes AC, et al. Primary care-led weight management for remission of type 2 diabetes (DiRECT): an open-label, cluster-randomised trial. Lancet2018;391:541-51.
  7. Cummings DE, Rubino F (2018) Metabolic surgery for the treatment of type 2 diabetes in obese individuals. Diabetologia 61(2):257–264.
  8. Madsen, L.R., Baggesen, L.M., Richelsen, B. et al. Effect of Roux-en-Y gastric bypass surgery on diabetes remission and complications in individuals with type 2 diabetes: a Danish population-based matched cohort study, Diabetologia (2019) 62: 611. https://doi.org/10.1007/s00125-019-4816-2

Copyright ©2021 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.

Assessing Insulin Resistance – Homeostasis Model Assessment (HOMA)

In November 2018, the American Association of Clinical Endocrinologists (AACE) released a Position Statement [1] which identified four separate disease stages associated with an abnormal glucose response, including Type 2 Diabetes;

Stage 1: Insulin Resistance
Stage 2: Prediabetes
Stage 3: Type 2 Diabetes
Stage 4: Vascular Complications — including retinopathy, nephropathy and neuropathy

Long before blood sugar becomes abnormal in the stage known as prediabetes, the progression to type 2 diabetes has already begun in the form of insulin resistance — and identifying insulin resistance at this stage (while blood glucose is still normal) enables people to implement dietary changes to avoid the progression to pre-diabetes, and type 2 diabetes.

Discovering insulin resistance in those who lack the more obvious outward signs can be especially helpful — including those who appear slim, but who may have visceral or ectopic fat  (so-called TOFIs, “thin on the outside, fat on the inside”), or those who may have undetected hyperinsulinemia due to their abnormal response to dietary carbohydrate. Some people that fall in this category may include those with a significant family history of type 2 diabetes, or previous gestational diabetes, even though they currently appear healthy.

The Homeostatic Model Assessment (HOMA-IR) is a test that uses a simultaneous fasting blood glucose test and fasting insulin test to accurately estimate the degree of insulin resistance (IR) and β-cell function (the cells of the pancreas that produce insulin). Alternatively, HOMA-IR can also be determined from a simulteous fasting blood glucose test and a fasting C-peptide test [2]. C-peptide is released in proportion to insulin, so it can be used to estimate insulin.

The Homeostatic Model Assessment (HOMA) equations have been widely used in research to estimate insulin resistance and the two equations which use fasting blood levels of insulin and glucose are as follows, with HOMA-IR used to assess insulin resistance and HOMA-B used to assess pancreatic β–cell  (beta-cell) function [3,9]. 

HOMA-IR= (glucose in mmol/L x insulin in mIU/mL)/22.5
HOMA-B= (20 x insulin in mIU/mL)/(glucose in mmol/L – 3.5)

Individual results are best compared to local population cut off values for HOMA1-IR [3] (1985) or the updated HOMA2-IR* [4] (1998).

HOMA2-IR* is easily and accurately calculated using the online HOMA2 calculator released by the Diabetes Trials Unit, University of Oxford available at http://www.dtu.ox.ac.uk/homacalculator/index.php.

The original HOMA1-IR equation proposed by Matthews in 1985 [3] was widely used due to its simplicity, however it was not always reliable because it did not consider the variations in the glucose resistance of peripheral tissue and liver, or increases in the insulin secretion curve for blood glucose concentrations above 10 mmol/L (180 mg/dL), or the effect of circulating levels of pro-insulin. [5]. The updated HOMA2-IR computer model [6] mentioned above and available from Oxford University has been used since 1998 and corrects for these — and estimates both insulin resistance and β-cell function.

Cut-off for insulin resistance using the original Matthews values (1985) [3] for HOMA-IR ≥ 2.7

  • Insulin sensitive is considered less than 1.0
  • Healthy is considered 0.5-1.4
  • Above 1.8 is early insulin resistance
  • Above 2.7 is considered significant insulin resistance

Cuff-off values for insulin resistance using the HOMA2-IR calculator (1998) [6] is HOMA2-IR ≥ 1.8. Three population based studies found the same or very close cut-offs applied, including a 2009 Brazilian study [6] which found HOMA2-IR ≥ 1.8, a 2014 Venezuelan study [7] which found HOMA2-IR ≥ 2.0 and a 2014 Iranian study [8] which found HOMA2-IR ≥ 1.8.

Use of HOMA-IR to Assess Insulin Resistance and β-cell Function in the Individual

HOMA-IR has been used to assess Insulin Resistance (IR) and β-cell function as a one-off measures in individuals in >150 epidemiological studies of subjects of various ethnic origins, with varying degrees of glucose tolerance [9].

In the Mexico City Study which used single glucose-insulin pairs (not the mean of three samples at 5-min intervals) [10], β-cell function and insulin resistance were assessed using HOMA-IR in ~1500 Mexicans with normal or impaired glucose tolerance (IGT). Subjects were followed up for 3.5 years for the incidence of diabetes and to examine any possible relationship with baseline β-cell function and IR. At 3.5 years, ~4.5% of subjects with normal glucose tolerance at baseline and ~23.5% with impaired glucose tolerance at baseline had progressed to type 2 diabetes. That is, the development of diabetes was associated with higher HOMA-IR at baseline.

The use of HOMA-IR on an individual basis enables clinicians to quantify both the degree of insulin sensitivity and β-cell function on assessment — before the person makes any dietary changes. Once the individual understands the significance of their HOMA-IR results, it can provide significant motivation for them to make dietary changes in order to prevent the progression toward abnormal glucose tolerance, or type 2 diabetes. When HOMA-IR is repeated 6 months into dietary changes, it provides significant feedback to the individual regarding the effectiveness of dietary changes, and the motivation to continue.

“HOMA-IR can be used to track changes in insulin sensitivity and β-cell function longitudinally in individuals. The model can also be used in individuals to indicate whether reduced insulin sensitivity or β-cell failure predominates[10].

Assessing HOMA2-IR is the reason I may request a simultaneous fasting blood glucose and fasting insulin from those that come to me and who have insulin resistance and/or hyperinsulinemia. My goal is to find out even when blood sugar results are still normal in order find out if their pancreas is working too hard in order to keep them that way.

More Info?

If you would like more information about how I can support you in meeting your health and nutrition goals, please have a look around my web page, or send me a note through the Contact Me form.

To your good health!

Joy

You can follow me on:

Twitter: https://twitter.com/JoyKiddie
Facebook: https://www.facebook.com/BetterByDesignNutrition/

 

Note: In British Columbia, family MDs may decline to order the fasting insulin test for the investigation of insulin resistance as the BC government does not authorize payment for that use, but many physicians will if they feel it is clinically warranted. Alternatively, a fasting C-peptide test can be ordered without restriction and can be used to determine HOMA2-IR using the Oxford calculator.

References

  1. American Association of Clinical Endocrinologists Announces Framework for Dysglycemia-Based Chronic Disease Care Model, November 28, 2018, AACE Online Newsroom, url: https://media.aace.com/press-release/american-association-clinical-endocrinologists-announces-frameworkdysglycemia-based-c
  2. Crofts, C., Understanding and Diagnosing Hyperinsulinemia. 2015, AUT University: Auckland, New Zealand. p. 205.
  3. Matthews, D. R; Hosker, J. P; Rudenski, A. S; Naylor, B. A; Treacher, D. F; Turner, R. C; ―Homeostasis model assessment: insulin resistance and β-cell function from fasting plasma glucose and insulin concentrations in man‖; Diabetologia; July, 1985; Volume 28, Number 7: Pp 412-419
  4. Levy JC, Matthews DR, Hermans MP. Correct homeostasis model assessment (HOMA) evaluation uses the computer program. Diabetes Care. 1998;21:2191–2192
  5. Song YS, Hwang Y-C, Ahn H-Y, Comparison of the Usefulness of the Updated Homeostasis Model Assessment (HOMA2) with the Original HOMA1 in the Prediction of Type 2 Diabetes Mellitus in Koreans, Diabetes Metab J. 2016 Aug; 40(4): 318–325
  6. Geloneze B, Vasques AC, Stabe CF et al, HOMA1-IR and HOMA2-IR indexes in identifying insulin resistance and metabolic syndrome: Brazilian Metabolic Syndrome Study (BRAMS), Arq Bras Endocrinol Metabol. 2009 Mar;53(2):281-7
  7. Bermúdez V, Rojas J, Martínez MS et al, Epidemiologic Behavior and Estimation of an Optimal Cut-Off Point for Homeostasis Model Assessment-2 Insulin Resistance: A Report from a Venezuelan Population, Int Sch Res Notices. 2014 Oct 29;2014:616271
  8. Tohidi M, Ghasemi A, Hadaegh F, Age- and sex-specific reference values for fasting serum insulin levels and insulin resistance/sensitivity indices in healthy Iranian adults: Tehran Lipid and Glucose Study, Clin Biochem. 2014 Apr;47(6):432-8
  9. Wallace TM, Levy JC, Matthews DR, Use and Abuse of HOMA Modeling, Diabetes Care 2004 Jun; 27(6): 1487-1495. https://doi.org/10.2337/diacare.27.6.1487
  10. Haffner SM, Kennedy E, Gonzalez C, Stern MP, Miettinen H: A prospective analysis of the HOMA model: the Mexico City Diabetes Study. Diabetes Care 19:1138–1141, 1996

Copyright ©2021 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 a Hiatal Hernia and How Can Dietary Changes Help?

More than half of middle aged people have a hiatal hernia (sometimes referred to as a “hiatus hernia“), but most people are only diagnosed when their symptoms become a problem or when having medical tests for something else.

A hiatal hernia is where part of the stomach bulges up through the space (called a “hiatus”, meaning a “gap”) in the diaphragm/ abdominal wall where the esophagus normally passes. 

Illustration of a hiatal hernia (“hiatus hernia”)

There are two types of hiatal hernias; the sliding type and the fixed type.

The sliding type of hiatal hernia is the more common type and occurs intermittently (i.e. from time to time), when the pressure in the abdomen increases.  This increased pressure pushes part of the stomach up through the gap in the diaphragm where only the esophagus is supposed to pass, and the little bulge is caused the hiatal hernia.

The fixed type of hiatal hernia is also called a paraesophageal hiatal hernia and occurs when the opening for the esophagus in the abdominal wall is bigger than usual. The stomach, and sometimes other organs including the small intestine or colon (large intestine) may also bulge into the chest cavity through this paraesophageal hernia. Paraesophageal hernias often get worse over time, in which case surgery is required to treat the problem. 

A strangulated hernia is not a type of hernia, but rather a complication in any one of a number of different types of hernias that can occur in different parts of the body — such as an inguinal hernia which can occur near the pubic bone, an umbilical hernia which occurs near the umbilicus (or “belly button”), or in a hiatal hernia in the upper part of the abdominal wall. A strangulated hernia is a serious condition where the blood supply to the stomach, intestines or other organ is being cut off because of that part of the body being forced into the small hole of the hernia, and requires immediate medical attention.

What Causes Hiatal Hernia?

A common contributing factor to development of a hiatal hernia is obesityespecially when people are carrying their weight around their middles.  The presence of increased fat around their internal organs (called visceral fat), as well as the excess fat under their skin (called sub-cutaneous fat — meaning “under the skin”) contributes to increased abdominal pressure especially when they are sitting, frequently bending, or lifting heavy objects.

Other contributing factors are frequent coughing (sometimes secondary to smoking), straining due to constipation, or it may simply be hereditary.

Symptoms of a Hiatal Hernia

Hiatal hernias are usually diagnosed when people go to their doctors complaining of symptoms such as frequent heartburn, or are having a test such as a barium swallow or endoscopy, for some other reason.

Many people with hiatal hernias have no symptoms — and because of that, they don’t even know they have one! People without symptoms usually don’t require treatment — although they may be advised to lose weight — especially if they are carrying excess weight around their abdomen. If their waist-to- height ratio is greater than 0.50, this means they are carrying more weight around their middle then optimal, so reducing this is a great place to start to prevent symptoms from occurring. Reducing fat around the abdomen may reduce abdominal pressure caused by the excess fat in the belly pushing the stomach up through the hernia.

Symptoms may include heartburn, chest pain or pressure, coughing, or frequent burping and since these symptoms may be caused by other conditions, it is important that people first see their doctor to find out the cause.  In addition, many people with hiatal hernia have also been diagnosed with  GERD (gastroesophageal reflux disease) and by teaching people how to make simple dietary and lifestyle changes often greatly reduces and even eliminates the symptoms of both.

Final Thoughts…

Losing weight, especially around the belly, and simple dietary and lifestyle changes can significantly improve the symptoms that result from hiatal hernia, as well as GERD which often accompany it.

More Info?

I provide nutrition education for reducing the symptoms of hiatal hernia which can be taken as a one-hour stand alone session, or at reduced cost as an add-on option for those taking the Complete Assessment Package. You can read more about that here.

To your good health!

Joy

You can follow me on:

Twitter: https://twitter.com/JoyKiddie
Facebook: https://www.facebook.com/BetterByDesignNutrition/

References

Ashwell M, Mayhew L, Richardson J, Rickayzen B (2014) Waist-to-Height Ratio Is More Predictive of Years of Life Lost than Body Mass Index. PLoS ONE 9(9)

HealthlinkBC, Hiatal Hernia, https://www.healthlinkbc.ca/health-topics/hw239946

Simic, P. John, Hiatal Hernia, emedicinehealth, March 3, 2020, https://www.emedicinehealth.com/hiatal_hernia/article_em.htm

 

Copyright ©2021 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.

Allergies to Trees or Grasses can Result in Reactions to Food

When  people come to me because they think they may be allergic to certain foods, the first thing I ask is if they have an allergy to any trees or grasses. This may seem like a strange question but some people who are allergic to tree or grass pollen may have symptoms when eating certain foods because the pollen of the tree or grass is similar to the pollen that forms the fruit or vegetable and the body recognizes the similarity. This is known as cross-reactivity.

A person who is allergic to a tree or grass pollen reacts to the food — not because they are allergic to the food itself, but because they are allergic to a pollen from a tree or grass that has similar protein sequences. If a person has never been tested for environmental allergies (pollens, for example) or for food allergies, the first place I get started is to recommend that their doctor have them tested by an allergist. 

What is a Food Allergy?

An allergy is an immune-system mediated reaction which results in the body producing specific allergen IgE antibodies to the substance they are allergic to (the allergen). When people are exposed to the substance they are allergic to, the specific IgE antibody binds with their mast cells (a type of white blood cell that is part of the immune system) which result in the release histamine which causes the symptoms of an allergic reaction, which most often are sneezing, itching, difficulty breathing, or other symptoms. A true allergy is always involve IgE antibodies therefore food sensitivity tests based on IgG antibodies commonly performed by naturopaths do not diagnose food allergy.

Each IgE antibody is specific to one type of allergen, but some types of environmental substances (such as pollen or grass) or foods have several components that have protein sequences that can produce allergy. Using a food as an example, a person with a “milk allergy” may produce IgE antibodies to β-Lactoglobulin or α-Lactalbumin — two completely different proteins found in the whey fraction of milk, or they may be allergic to casein, a protein that makes up another fraction of milk.  A person with a milk allergy may produce specific IgE antibodies to αLactalbumin but not to β-Lactoglobulin, or to casein but not the others. Or, they may allergic to all three.

Similarly, a person allergic to a tree pollen may produce IgE antibodies to only one protein in that pollen, or to several.

Oral Allergy Syndrome (OAS) – pollen allergy

Most food allergies in adults who never had food allergies as children are the result of cross-reactions between food and inhaled allergens such as pollen[1] that they are allergic to. This is this known as Oral Allergy Syndrome (OAS)

If a person has seasonal allergies in the early spring, it is most likely caused by allergies to tree pollen [2], and as many as 50%–70% of people who are allergic to birch pollen will have Oral Allergy Syndrome [3,4].

Alder is another common pollen allergen that results in OAS, as is latex found in rubber trees.

OAS reactions are most often thought of involving people’s lips, tongue or the roof of their mouth — where the cross-reacting food comes into contact with their body, but some people can also experience gastro-intestinal symptoms as a result of OAS — particularly related to birch pollen allergy[5].

It can get complicated, too.

An allergy to either birch or alder pollen can cause a Oral Allergy Syndrome to apples — but so can an allergy to apples, themselves.

How do we know if the person is reacting to apple because they are allergic to either birch or alder pollen (or both!), or because they are allergic to apples?

Only an allergist can determine that.

Since an allergist is specialized physician (MD), the costs of allergy tests done by an allergists are covered by provincial health plans

Once I’ve assessed someone, if I think they may be experiencing either food allergy of oral allergy syndrome, I will recommend that they speak to their doctor about being referred to an allergist for testing.

Once a person has been tested, the allergist’s office faxes me their report (with their permission, of course) and then person returns to me for teaching.  If they have tested positive to foods or to pollens, I teach them how to avoid coming into contact with foods they are allergic to, as well as which foods may result in cross-reactions because they are allergic to specific pollens.

If they have tested negative to food or pollen allergies and the person’s symptoms are gastro-intestinal (involving their stomach or intestines), then if they haven’t already been tested, the next thing I usually rule out is celiac disease (gluten intolerance). This is determined with a simple blood test that their family doctor can requisition.

If the person has no food or pollen allergies, doesn’t have celiac disease, and their doctor has ruled out inflammatory conditions such as Crohn’s or colitis, then very often they are diagnosed with Irritable Bowel Syndrome (IBS). Since symptoms of IBS can be significantly minimized with changes in diet, I provide them with this type of teaching.

Final Thoughts…

Spring is almost here, and if you have seasonal allergies and find yourself having more reactions to food, it may be an indication that you have Oral Allergy Syndrome.

More Info?

Under the Services tab, you can find out more information about the Food Sensitivity / Food Allergy Package and the Irritable Bowel Syndrome (IBS) Package and if you have questions, you can send me a note using the Contact Me form on this web page.

To your good health!

Joy

You can follow me on:

Twitter: https://twitter.com/JoyKiddie
Facebook: https://www.facebook.com/BetterByDesignNutrition/

References

  1. Pong AH. Oral allergy syndrome. Vaughan (ON): Allergy/Asthma Information
    Association (AAIA); 2000. Available: www.calgaryallergy.ca /Articles/English
    /Oral_Food_Allergy.htm (accessed 2009 Dec. 3).
  2. Sussman G, Sussman A, Sussman D, Oral Allergy Syndrome, CMAJ 2010. DOI:10.1503/cmaj.090314
  3. Mogensen JE, Wimmer R, Larsen JN, et al. The major birch allergen, Bet v 1
    shows affinity for a broad spectrum of physiological ligands. J Biol Chem 2002;
    277: 23684-92.
  4. 8. Hoffmann-Sommergruber K, O’Riordain G, Ahorn H, et al. Molecular characterization of Dau c 1, the Bet v 1 homologous protein from carrot and its cross-reactivity with Bet and Api g 1. Clin Exp Allergy 1999; 29:840-7.
  5. Rentzos G, Lundberg V, Stotzer PO, Pullerits T, Telemo E. Intestinal allergic inflammation in birch pollen allergic patients in relation to pollen season, IgE sensitization profile and gastrointestinal symptoms. Clin Transl Allergy. 2014;4:19. Published 2014 May 30. doi:10.1186/2045-7022-4-19

Copyright ©2021 BetterByDesign Nutrition Ltd.

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

Why Grazing Can Look Like a Scene From Hoarders

Most people know that prediabetes and diabetes is having “high blood sugar” but just how much sugar is actually in the human body? And how does grazing on food, rather than eating set meals affect this?

An adult has 5 liters of blood circulating in their body at any one time.  A healthy person’s body keeps the range of sugar in the blood (called ‘blood glucose’) tightly-controlled between 3.3-5.5 mmol/L (60-100 mg/dl) — that is, when they eat food with carbohydrate the body breaks it down to sugar,  and insulin takes the extra sugar out of the blood and moves it into cells.

Where does it put it?

First, the body makes sure that glycogen stores are sufficient, which is the body’s “emergency supply of energy”. There’s about a day’s worth of energy (2000 calories) in our muscle and liver glycogen. Once the liver and muscle glycogen is full, the rest of the blood sugar is moved to the liver where it is converted into LDL cholesterol and triglycerides and then the rest stored in fat cells. Fat is where the sugar that we make from the food we’ve eaten goes if it is not needed right away. Fat is storage for later.

So how much sugar is there in the blood of a healthy adult?

Doing the math (see illustration below), there are only 5 grams of sugar in the entire adult human body — which is just over one teaspoon of sugar.

That’s it!

One heaping teaspoon of sugar in the entire adult body!

understand sugar in body
The amount of sugar in the blood of a healthy adult

How Do We Understand Diabetes in Terms of Blood Sugar?

How much sugar does someone with diabetes have in their blood compared to a healthy person?

Someone with a fasting plasma glucose level of 7 mmol/L (126 mg/dL) meets the diagnostic criteria for Diabetes — which is just 6.25 grams of sugar or 1 -1/4 teaspoons. That is, the difference between the amount of sugar in the blood of a healthy person and the amount of sugar in the blood of someone with  Diabetes is just a quarter of a teaspoon of sugar.

That’s it!

A quarter teaspoon of sugar is such a small amount but it makes the difference between someone who is healthy and someone who has Diabetes.

The difference between the amount of sugar in the blood of a healthy person and the amount of sugar in the blood of someone with Diabetes is just a quarter of a teaspoon of sugar.

In a person with type 2 diabetes, the once tightly-controlled system that is supposed to keep the range of sugar in the blood between 3.3-5.5 mmol/L  (60-100 mg/dl) is “broken” — and it may get this way by them “grazing” all day long, or eating more carbohydrate than their body can handle. When someone with diabetes eats food with carbohydrate in it, their insulin is unable to take the sugar out of their blood fast enough, so the sugar stays in their blood longer than it should. Just as with a healthy person, the body of someone with type 2 diabetes takes the sugar that results from the food they’ve eaten and ‘tops up’ their liver and muscle glycogen stores, then the rest is sent to the liver where it is converted into LDL cholesterol and triglycerides, and then the rest is stored in fat cells. But what if the person is grazing all day long? The sugar just keeps on coming!

Some people have the ability to store the excess sugar in the form of fat under the skin (called sub-cutaneous fat). In this way, obesity is a way of protecting the body from this sugar overflow.  Eventually though, if the constant flow of carbohydrate continues, the ability of the body to store the excess as sub-cutaneous fat is limited and then fat around the organs (called visceral fat) increases and this is what ends up contributing to type 2 diabetes and fatty liver disease. It is easy to pack away excess carbohydrate when one is grazing instead of eating, because they don’t eat enough at anyone time to feel satiated (full).

subcutaneous vs visceral fat
Sub-cutaneous fat (LEFT) versus visceral fat (RIGHT) – from Klöting N, Fasshauer M, Dietrich A et al, Insulin-sensitive obesity, Am J Physiol Endocrinol Metab 299: E506–E515, 2010, pg. 5

The problem often is that we never get to access our fat stores because we are grazing on food with carbohydrate in it every few hours, storing the excess sugar in our fat stores. According to recent statistics, three-quarters of us lead sedentary (inactive) lives and barely get to make a dent in the energy we take in each day.  We just keep getting fatter and fatter.

We eat breakfast — maybe a bowl of cereal (30 gms of carbs) or two toast (30 gms of carbs) or if we’re in a rush we grab a croissant breakfast sandwich at our favourite drive-through (30 gms of carb). Each of these contains the equivalent of a bit more than 6 teaspoons of sugar. Mid-morning, maybe we eat a fruit – say, an apple (30 gm of carbs) to hold us together until lunch — and take in another 6+ teaspoons of sugar in the process. If we didn’t bring a fruit, maybe we go out for coffee and pick up an oat bar at Starbucks® (43 gms of carbs) — the equivalent of almost 10 teaspoons of sugar. The grazing continues…

At lunchtime, maybe we’ll have a sandwich (30 gm of carbs) or some leftover pasta from the night before (30 gm of carbs) or we’ll go to the food court and have a small stir-fry over rice (30 gm of carbs) — the equivalent of another 6+ teaspoons of sugar. Then, believing grazing is better than eating 3 big meals, maybe we eat another piece of fruit mid-afternoon, this time an orange (30 gms of carb) — and we’ve provided our body with the equivalent of another  6+ teaspoons of sugar.

In the scenario above, by mid afternoon (assuming we didn’t eat any fast-food or convenience foods, but only eating the food from home) we’ve eaten the equivalence of 24 teaspoons of sugar! But isn’t grazing, and eating food we bring from home supposed to be healthier?

What if we go to MacDonald®’s and eat a Big Mac® (20 g of carbs), large fries (66 g of carbs) and a large soft drink (86 g of carbs) – we’ve eaten a total of 172 g of carbs – which is equivalent to 43 teaspoons of sugar in just one meal!

In short, a healthy person will keeps moving the excess carbohydrate they eat off to their liver and will keep making triglyceride and LDL cholesterol out of it and storing the rest as fat and a person who is not insulin resistant or does not have type 2 diabetes will have normal blood sugar level, but their high carbohydrate intake can be reflected in their “cholesterol tests” (called a lipid panel) – where we may see high triglyceride results or high LDL cholesterol results or both.

The body takes the triglycerides into very-low-density lipoprotein (VLDL) cholesterol. Think of these as “taxis” that  move cholesterol, triglycerides and other lipids (fats) around the body. When the VLDL reach fat cells (called “adipose tissue”), the triglyceride is stripped out and absorbed into fat cells. The VLDLs shrink and becomes a new, smaller, lipoprotein, which is called Low Density Lipoprotein, or LDL — the so-called ‘bad cholesterol’. This is a misnomer, because not all LDL is harmful.  LDL which is normally large and fluffy in texture is  a good cholesterol (pattern A) that can become bad cholesterol (pattern B) when it becomes small and dense.

In a healthy person, LDL is not a problem because they find their way back to the liver after having done their job of delivering the TG to cells needing energy. In a person with insulin resistance however, the LDL linger a little longer than normal, and get smaller and denser, becoming what is known as “small, dense LDL” and these are the ones that put us at a risk for cardiovascular disease.

There are two important points here: (1) the only source of LDL is VLDL not the fat we take in though our diet and (2) only the “small dense LDL are “bad” cholesterol and these occur as a result of insulin resistance.

People often believe that because their blood sugar is ‘normal’ on a lab test, that there isn’t any problem, but as Dr. Joseph Kraft discovered in his 25+ years of research measuring blood glucose and insulin response in some 10,000 people, 75% of people with normal glucose levels are actually insulin resistant and are at different stages of pre-diabetes or “silent Diabetes” (what Dr. Kraft called “Diabetes in situ”).

These people (and maybe their doctors) think they are “fine” because their blood sugar seems normal. Perhaps however, their triglycerides and LDL blood tests come back high. The origin of the problem is not because they are eating too much fat, but grazing on too much carbohydrate.

The body is trying to store the excess sugar somewhere.  First it stores it in glycogen, then the rest is made into triglyceride and LDL and shipped all over the body, with the rest stored as fat.  The fat cells in the body keep filling up — in the muscle, in and around our organs, and some get “fatty liver disease” and some even get fat cells in their bones if their body needs a place to put it.  Bone is not supposed to have fat cells it in, but the body has to store it somewhere, because the carbohydrates just keep arriving every few hours!

Think of grazing it this way;

Imagine you are at home and you hear the doorbell ring. You go to the door and there’s a package and it’s for you.  You take the package, close the door and head to the kitchen table to open it.  Just as you’re about to open it, the door bell rings again.  You go to the door, and there’s another package — and it’s for you, again.  You take the package and head back to the kitchen and set it down beside the first, when (you guessed it) the doorbell rings again. You take that package and the ones that keep arriving, finding places to put them.  When the kitchen table is full, you put the packages on the floor underneath the table, but then you get a delivery of several packages.  You set those down wherever there’s a spot, just in time to answer the door yet again.  Package after package arrives and before you know it, you look like something out of the TV series Hoarders.  You can barely move for all the boxes, and all of them are unopened.

This is what grazing on meals and snacks with carbohydrates in them every few hours is like.

We overwhelm our body’s tightly-regulated system that is supposed to maintain our blood sugar level between 3.3 and 5.5 mmol/L (60-100 mg/dl) by continually requiring it to process the equivalent of anywhere from 6 teaspoons of sugar in a bowl of cereal or two toasts to the equivalent of 43 teaspoons of sugar in a fast-food meal.

This is how the system gets “broken”.

In time, we may get Type 2 Diabetes or fatty liver disease or high triglycerides or high cholesterol or group of symptoms called Metabolic Syndrome. This is the result of the constant strain we put our bodies under by eating a steady diet of foods containing a large percentage of  carbohydrate.

It is easy to see where the high rates of obesity and Diabetes have come from. We have become a nation of “hoarders”.

What’s the solution?

We stop the constant delivery of packages of carbohydrate every few hours.

We feed our body the protein and the nutrients it needs with enough fat to use as fuel (in place of carbs) and allow it to take the extra energy it needs from our “stored fat”.  We finally take the fat out of storage and we do this by following a low carb high fat diet.

Science made simple.

To your good health!

Joy

You can follow me on:

Twitter: https://twitter.com/JoyKiddie
Facebook: https://www.facebook.com/BetterByDesignNutrition/

References

Michigan State University, How to convert grams of sugars into teaspoons,  http://msue.anr.msu.edu/news/how_to_convert_grams_of_sugars_into_teaspoons

Klöting N, Fasshauer M, Dietrich A et al, Insulin-sensitive obesity, Am J Physiol Endocrinol Metab 299: E506–E515, 2010, http://www.physiology.org/doi/10.1152/ajpendo.00586.2009

 

Copyright ©2021 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.

How Much Protein is Best Depends on Different People’s Needs

I often hear the question, “how much protein is best?” but that depends for whom. Different people have a different protein needs. A healthy man or woman seeking to build muscle has a different protein need than an older adult wanting to reduce the risk of sarcopenia (muscle loss) or someone simply wanting to prevent deficiency. The amount of protein someone needs depends on many factors, including whether a person is growing, pregnant or lactating (breastfeeding), or has been sick or just had surgery. Even for those who aren’t in these special circumstances, protein needs may be calculated to prevent deficiency, to sustain exercise or to preserve muscle mass in older adults, and each of these calculations are different.

Protein needs are calculated as grams of protein per kilogram of body weight of the person, and not as a percentage of daily calories (energy). As explained below, 40% of calories as protein may be safe for one person and be in excess for someone else. For this reason, protein must to be calculated as grams of protein per kilogram of body weight.

Basic Needs – the Recommended Daily Allowance (RDA) for Protein

The Recommended Daily Allowance (RDA) for any nutrient is the average  daily dietary intake level that is sufficient to meet the needs of 97-98 % of healthy people. It is important to keep in mind that the RDA is not the optimal requirement, but the absolute minimum to prevent deficiency.

The RDA for protein for healthy adults is calculated at 0.8 g protein / kg of body weight [1]. A sedentary 70 kg / 154 pound man needs a minimum of 56 g of protein and a sedentary 60 kg / 132 pound woman needs a minimum of 48 g protein per day.

Protein Needs for Active Healthy Adults

For those who are physically active, the Academy of Nutrition and Dietetics, Dietitians of Canada, and the American College of Sports Medicine[2] recommend a protein intake of 1.2–2.0 g protein / kg per day to optimize recovery from training, and to promote the growth and maintenance of lean body mass.

Protein Needs for Older Adults

There have been several 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 best meet the needs of adults during aging [3,4].

For the average, healthy 70 kg / 154 pound sedentary man this would be daily protein intake of 70 -105 g per day and for the average, healthy 60 kg / 132 pound sedentary woman this would be a protein intake of 60-90 g protein per day.

Range of Safe Intake

As I wrote about in an earlier article, according to Dr. Donald Layman, PhD, Professor Emeritus, of Nutrition from the University of Illinois, the highest end of the range of safe intake of protein is 2.5 g protein/ kg per day.

For the average 70 kg / 154 pound sedentary man this would be a maximum daily protein intake of 175 g per day and for the average 60 kg / 132 pound sedentary woman, this would be a maximum protein intake of 150 g/ day.

Someone eating on occasion above their safe range is a different scenario than someone eating above or at the very high end of that range on a regular basis. The body has a flexible capacity to tolerate higher protein intake on occasion, but regularly eating too much protein can result in protein toxicity.

Maximum Amount of Protein the Body can Safely Process

[Special thanks to Richard Morris, research biochemist from Canberra, Australian for the information contained in this section.]

When protein is eaten, the body needs to get rid of the ammonia that results and this is done by turning the ammonia into urea and excreting it in the urine.

The disposal rate of ammonia isn’t able to be calculated because ammonia is literally given off by the lungs and skin, and tracer studies suggest that the disposal rate is higher than the rate that urea appears in urine. This means that there are probably several reservoirs for ammonia (such as urea building up in circulation before filtration in the kidneys) and this ‘elastic’ or flexible capacity for ammonia enables us to survive high protein days interspersed with low protein days.

The rate limit for maximal disposal of urea through urine is 0.53 g of N per kilo of 3/4 body weight[4], as a proxy for lean body mass. The ratio of molecular weights between a nitrogen atom and the average molecular weight of amino acids is a factor of 6.05x, so the effective rate limit for maximal disposal of urea through urine is .53 x 6.05 = 3.21 g of protein/kg lean body mass. If someone were to eat above that amount of protein for too long, they will have filled their ‘elastic’ (flexible) reservoirs with urea, and would then be at risk of ammonia intoxication.

This calculation for determining the maximum amount of protein based on urea clearance requires know a person’s energy consumption (in kcals / calories), as well as lean body mass (LBM).  Note that this is lean body mass, not total body weight. Lean body mass is essentially one’s total body weight minus the amount of fat they have.

Lean body mass can be assessed using a DEXA scan, or estimated by using relative fat mass (RFM). The amount of fat someone has can be estimated from total body weight (taken on a scale), minus their estimated RFM as described in this article

Once we know a person’s lean body mass, we can use the equation (3.21 g of protein / kg lean body mass) to determine the maximum amount of protein they can eat on an ongoing basis while being able to safely dispose of the ammonia via urea through urine.

Here are some examples of calculations;

Example 1:

A 100 kg man (220 pounds) with 20% body fat would have 80 kg lean mass, so would have a maximum protein ceiling of ~256g/day (based on the maximum amount of ammonia disposal of 3.21 g of protein / kg of lean body mass). Assuming his energy consumption is 2500 kcal/day, 256 g of protein is ~41% of total energy.

A 60 kg woman with 25% body fat, would have 45 kg of lean mass, so would have a maximum protein ceiling of 144 g/day. Assuming her energy consumption is 2000 kcal/day, 144 g of protein would be 29% of total energy as protein. The maximum amount of protein that this woman could regularly eat based on the disposal rate of ammonia in urea is only 29% of energy as protein.  

Since the amount of protein one can eat is tied to the amount of lean body mass, what if this woman were leaner, say at the very lowest end of the body fat range? Could she eat 40% protein on an ongoing basis and excrete all the resulting ammonia as urea in her urine?

The same 60 kg woman at only 10% body fat would have 54 kg lean mass, with a maximum protein ceiling of 173 g protein / day. Assuming her energy consumption is the same 2000 kcal/day, 173 g pro/ day would be 35% of total energy as protein.

While this woman can safely have a higher percentage of energy as protein because she has more lean body mass, the maximum amount of protein based on disposal of ammonia is still only 35% of energy as protein.

It is important to note that 10% body fat for a woman is at the very low end of essential fat range and could result in amenorrhea (loss of menstrual cycles).

Final thoughts…

To know if a diet has adequate protein, one needs to ask ‘adequate for whom’. If you are an older adult trying to preserve muscle mass to avoid the increased risk of falls that comes with sarcopenia (loss of muscle mass) then your protein needs will be very different than if you just want to make sure your protein intake is adequate, or if you are about to train for a half-marathon.

When evaluating diets and whether they have adequate protein, they should at least meet the bare minimum requirements of the RDA. Then, ask yourself if the diet has enough protein to sustain someone who is physically active or enough for an older adult? Finally, make sure that the amount of protein is within the safe upper limit and does it exceed the maximum level of amount of protein based on the disposal of ammonia in urea in the urine.

If you are unsure how much protein you need, and how much and what type of fats and carbohydrate are most suitable for you, then please reach out for assistance.

More Info?

If you would like more information about my services then please have a look under the tab of that name or send me a note through the Contact Me form.

To your good health!

Joy

You can follow me on:

Twitter: https://twitter.com/JoyKiddie
Facebook: https://www.facebook.com/BetterByDesignNutrition/

References

  1. National Academies Press, Dietary Reference Intakes for Energy, Carbohydrate, Fiber, Fat, Fatty Acids, Cholesterol, Protein and Amino Acids (2005)
  2. Thomas DT, Erdman KA, Burke LM. American College of Sports Medicine Joint Position Statement. Nutrition and Athletic Performance [published correction appears in Med Sci Sports Exerc. 2017 Jan;49(1):222]. Med Sci Sports Exerc. 2016;48(3):543-568. doi:10.1249/MSS.0000000000000852
  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. Rudman D, DiFulco TJ, Galambos JT, Smith RB 3rd, Salam AA, Warren WD. Maximal rates of excretion and synthesis of urea in normal and cirrhotic subjects. J Clin Invest. 1973;52(9):2241-2249. doi:10.1172/JCI107410

Copyright ©2021 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.

Standard Treatment for Diabetes Prior to the Discovery of Insulin

A hundred years ago, Dr. Russell M. Wilder and two Dietitians from the Mayo Clinic wrote a 69-page book titled “A Primer for Diabetic Patients – A Brief Outline of The Principles of Diabetic Treatment, Sample Menus and Food Tables[1]” which outlined the dietary treatment for diabetes that was used and which had different levels of a low carbohydrate, as well as short periods of fasting. I read through this book over the weekend and was quite surprised with how similar this approach was to current low carbohydrate diets that are being by those seeking remission from symptoms of the disease using a diet-first approach.

“The effect of ketonemia on the course of epilepsy” (1921), Russell M. Wilder

The name Dr. Russell Wilder was familiar to me, but I knew him as the physician who in 1921 proposed use of a very high fat, low carbohydrate diet for the treatment of epilepsy to produce the same benefits as fasting[2]? It was Wilder himself who is credited with coining the term “ketogenic diet” — and his version of the classic 4:1 ketogenic diet (KD) is still used today in the management of epilepsy, as well as in adjunct treatment for glioblastoma (a very aggressive type of brain cancer) — along with chemo and radiation, as well as in some neurological disorders.  But his first work using the diet was in diabetes.

How could it be that Wilder is so famous for being a very early implementer of a ketogenic diet for epilepsy, yet virtually unknown for his earlier use of low carbohydrate and ketogenic diet for the treatment of diabetes? I wondered if it could it be that the discovery of insulin a short time later by Dr. Fredrick Banting and medical student Charles Best[3] and its manufacture by Eli Lilly [3] relegated the use of a low carbohydrate diet in diabetes to the pages of history? I found out, that is exactly what happened!

While it makes total sense to me that use of insulin as treatment of those with type 1 diabetes (where a person’s pancreas produces little or no insulin) took a front and center role to keep them from literally wasting away without it, it is unfathomable to me that Wilder’s dietary recommendations did not continue to be widely used in the management of type 2 diabetes —  an impairment in the way the body uses glucose and which results in too much sugar circulating in the blood. Again I wondered if perhaps it was because type 2 diabetes wasn’t identified as being different than type 1 diabetes until Harold Percival Himsworth differentiated between the two in 1936 — and by then, use of insulin was standard treatment.

Oral diabetes medications such as Metformin and other biguanide derivatives, as well as sulfonylurea such as Carbutamide and Tolbutamide were not developed until 1955-1956,  so prior to 1955 insulin was the only treatment for type 2 diabetes[4].

As it turned out, a paper published in 1958 by Dr. Russell Wilder provides some much needed understanding as how the discovery of insulin and its free provision to those with diabetes by the drug company Eli Lilly ended up shaping the use — and eventual disuse of low carb diets in diabetes treatment.

“Insulin at that time cost five cents a unit in the market. However, the patients in our early cases received theirs gratis (i.e. free) for a period of several years, thanks to the Eli Lilly Company.” (p.247-8 [4])

In Wilder’s 1958 paper, he outlines how the A Primer for Diabetic Patients [1] (the book on which this article is based) went from being a diet-first approach to the treatment of diabetes prior to the discovery of insulin to a diet that was indistinguishable from the carbohydrate and protein rich diet of non-diabetics, as the result of the use of insulin.

“The nine editions of the little book A Primer for Diabetic Patients, the first written in 1921, the last in 1950, provide a panorama of diabetic therapy in that interval. The first printing was based on mimeographed instruction sheets prepared in 1920 for the diabetic patients. We were then following the generally accepted treatment of that time, which was based on the research of Dr. Frederick M. Allen at the Rockefeller Institute in New York. It involved an initial period of starvation and the effort afterward to maintain control of glycosuria by a very rigidly restricted diet and periodic fast days. The second edition (1923 ) introduced insulin and diets made more liberal in fat. The pre-insulin diets were continued because of the cost of insulin—5 cents a unit then—and because of a disinclination to give more of this new drug than was absolutely necessary, since it was not yet known whether ill effects would result from the continued use of insulin. As the years went by, greater and greater liberality was permitted, until, in the later editions of the book, the diets recommended, although still controlled as to composition, provided almost as much protein and carbohydrate as would be contained in the well-selected diets of normal persons [4].

Perhaps the reason diabetes has been considered a “chronic and progressive disease” is because dietary treatment had been all but forgotten after the discovery of insulin.

In 1921, Wilder understood that;

“Diabetes is a disease which in manifested by excretion of sugar in the urine. This sugar comes from the foods which the patient eats, but which is body, owing to the disease, is unable to utilize.”

and his treatment recommendations (pg.12) were;

suiting the diet to the condition of the patient and feeding no more sugar-forming foods than the patient’s body is able to use.”

The concept of “eat what you want and cover it with insulin” simply wasn’t an option for those with diabetes, as insulin hadn’t been discovered yet. Diet was the only choice for managing symptoms of the disease — which begs the question, for those with type 2 diabetes who want to get off of diabetes medications now, why isn’t carbohydrate restriction offered as a choice?

No one denies the safety and efficacy of a ketogenic diet for the treatment of epilepsy, yet many deny that a low carb or ketogenic diet appropriate for those with diabetes — when both have been used safely for 100 years! While there is an absolute need to manage the dosage of oral hypoglycemic medications before and during reduction in the amount of carbohydrate in the diet there is no reason that we cannot support a diet-first, not drug-first approach to diabetes treatment and management when people want.

Determining Carbohydrate Tolerance in Diet

Diabetes is at its very essence “carbohydrate intolerance” and Wilder describes ‘tolerance‘ as ‘the amount of sugar-forming foods which a person can eat in twenty-four hours without causing sugar in the urine’.

“The tolerance of a given patient is ascertained by feeding foods of known composition in weighed and gradually increasing amounts.”

“The actual procedure will vary with different patients, but, in general, foods of known composition in weighted amounts are fed, the total intake of carbohydrate, protein and fat being increased very gradually as high as possible without the return of sugar in the urine.”

“Some patients will be found to have low tolerance, others may stand 100 gm. of carbohydrate. Every patient should be treated as an individual case, but for convenience in prescribing diets, the following arbitrary grouping is made:

Group A — tolerance below 40 gm. carbohydrate

Group B — tolerance between 40 and 60 gm. carbohydrate

Group C — tolerance between 60 and 100 gm. carbohydrate

Group D — tolerance above 100 gm. of carbohydrate

Use of Fasting and Protein Sparing Modified Fasts in Diet

Wilder’s approach incorporates short fasts of 12 – 24 hours as part of the management of blood sugar and up to 2-days if spilling sugar in the urine (i.e. exceeding their carbohydrate tolerance).

Those in Group A who have carbohydrate tolerance of less than 40 grams of carbohydrate (ketogenic level for women and men) are instructed to “interrupt their diet by a “fast day” once a week” — but its not a complete fast.  They are told to “take liberally of liquids”, including beef broth and coffee or tea.

Those in Group B who have carbohydrate tolerance between 40 and 60 grams of carbohydrate are instructed to “institute weekly days of half-fasts” on which they restrict their diet to 20 grams of carbohydrate, as well as 12 grams of protein and 12 grams of fat.

On the appearance of sugar in the urine at any time, the patient, irrespective of his group, must institute a fast day. If the sugar persists, a second fast day should follow the first.

Of interest,  if sugar persists in the urine Wilder’s recommendations are to institute what would be known today as a “protein sparing modified fast“;

If sugar persists, the patient should return to one-half of his diet, continue on this for a week, and then again try the effect of a fast day. After the urine is again sugar-free, he can return gradually to his previous diet.”

Wilder cautions that “longer fasts should never be attempted outside of an institution”, but it’s important to keep in mind that there was no distinction at this point between type 1 and type 2 diabetes.

There is no fasting protocol for those whose carbohydrate tolerance is between 60 and 100 grams.

Daily Macros

Those in Group A who have a carbohydrate tolerance of less than 40 grams of carbohydrate (ketogenic level for women and men) are instructed to eat breakfast, lunch and dinner such that the value of three such meals has 20 grams of carbohydrate, 70 grams of protein and 100 grams of fat (pg. 30 [1]).

Those in Group B who have carbohydrate tolerance between 40 and 60 grams of carbohydrate are instructed to eat breakfast, lunch and dinner such that the value of three such meals has 40 grams of carbohydrate, 70 grams of protein and 100 grams of fat (pg. 33 [1]).

Those in Group C who have carbohydrate tolerance between 60 and 100 grams of carbohydrate are instructed to eat breakfast, lunch and dinner such that the value of three such meals has 60 grams of carbohydrate, 70 grams of protein and 100 grams of fat (pg. 37 [1]).

Those in Group D who have carbohydrate tolerance above 100 grams of carbohydrate are instructed to eat breakfast, lunch and dinner such that the value of three such meals 100 grams of carbohydrate, 70 grams of protein and 140 grams of fat (pg. 41 [1]).

At 70 grams of protein per day irrespective of a person’s weight or gender, these low carb / ketogenic diets provided plenty of satiety and this amount is above the current DRIs of 46 g protein for the average sedentary woman, and 56g protein per day for the average sedentary man.

Fat sources in the sample menus were butter, cream, cheese and eggs and the fat found in the protein.

Carbohydrate sources in the diets were mainly from recipes for something called “Hepco Cakes” made from eggs, cream, Hepco flour, butter and water or from “Cullu-flour Griddle Cakes” made from eggs, salt, water and cellu-flour. Very low carb meals included low carb vegetables and a little bit of fruit, and the higher carbohydrate meals included low carb vegetables, root vegetables such as onion and beet, as well as a bit of fruit.

Final Thoughts…

Wilder understood that diabetes is a disease of carbohydrate intolerance and that each person with diabetes should be treated as an individual.

He was aware that some people with diabetes will have very low carbohydrate tolerance of less than 40 grams per day requiring a very low level of carbohydrate intake, while others can tolerate up to 100 grams of carbohydrate per day.

Over the last 5 years that I have been helping people with type 2 diabetes to follow a low carbohydrate diet to improve their symptoms, and to seek to put the disease into remission, my understanding turns out to be remarkably similar Wilder’s.  I have found that each person with type 2 diabetes (and even pre-diabetes) has different levels of carbohydrate tolerance and I don’t believe that everyone needs to be on “a keto diet”.

When I first started teaching low carbohydrate diets 5 years ago, unless someone was already on a ketogenic diet, I would start those with type 2 diabetes (who were not on any of the medications previously mentioned) at 130 grams of carbohydrate per day and gradually lower carbohydrates until clinical outcomes were reached. In the past two or three years I came to the realization that none of my clients with type 2 diabetes were tolerating carbohydrate intakes above 100 grams per day — which interestingly is consistent with Wilder’s categories.

People think of a low carb or “keto diet” to treat diabetes as something new — a “fad” even, but this diet has been around for over 100 years and was standard treatment at the Mayo Clinic for those with the disease until the discovery of insulin.  I have heard anecdotal stories of those who were diagnosed before the widespread use of insulin and who used a low carb diet their entire lives, avoiding the unnecessary complications that are thought to be part and parcel of having type 2 diabetes.

For those seeking to take a diet-first approach in managing their symptoms, this diet has stood the test of time in terms of safety and efficacy and very similar approaches have solid studies supporting their use. Is it any wonder that Diabetes Australia, American Diabetes Association and the European  Association for the Study of Diabetes (EASD) and Diabetes Canada accept a low carb and very low carb (keto) diet as medical nutrition therapy for the treatment and and management of diabetes?

More Info?

If you would like more information about how I might be able to support your needs, please have a look under the Services tab or send me a note through the Contact Me form.

To your good health!

Joy

You can follow me on:

Twitter: https://twitter.com/JoyKiddie
Facebook: https://www.facebook.com/BetterByDesignNutrition/

NOTE: Special recognition to Jan Vyjidak of London, England, Founder and CEO at Neslazeno.cz for finding this book!

References

  1. Wilder RM, Foley MA, Ellithorpe D, A Primer for Diabetic Patients – a brief outline of the principles of diabetic treatment, sample menus and food tables,  The Mayo Clinic, W.B. Saunders Company Publishing, 1922
  2. Wheless JW. History of the ketogenic diet. Epilepsia. 2008 Nov;49 Suppl 8:3-5. doi: 10.1111/j.1528-1167.2008.01821.x. PMID: 19049574.
  3. The History of Insulin, diabetes.co.uk, diabetes.co.uk/insulin/history-of-insulin.html
  4. Krochmal M, 10 Facts About the History of Diabetes, https://type2diabetes.com/living/10-facts-history-diabetes/
  5. Wilder, Russell M. “Recollections and Reflections on Education, Diabetes, Other Metabolic Diseases, and Nutrition in the Mayo Clinic and Associated Hospitals, 1919-50.” Perspectives in Biology and Medicine, vol. 1 no. 3, 1958, p. 237-277. Project MUSEdoi:10.1353/pbm.1958.0019.

Copyright ©2021 BetterByDesign Nutrition Ltd.

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

 

A Choice: Living With Diabetes, Seeking Remission From Diabetes

People come to me as a Dietitian with different goals with respect to type 2 diabetes. Most people who have been diagnosed with type 2 diabetes come to see me in my low carb division seeking to put their diabetes into remission — that is, to no longer meet the criteria for diagnosis. 

As stated throughout this web site and on my forms, I do not counsel people with type 1 diabetes, or with insulin-dependent type 2 diabetes because I am not a Certified Diabetes Educator (CDE). 

As explained in this earlier article, the American Diabetes Association has defined partial remission, complete remission and prolonged remission from type 2 diabetes, as follows;

    • Partial remission is having blood sugar that does not meet the classification for Type 2 Diabetes; i.e. either HbA1C < 6.5% and/or fasting blood glucose 5.5 – 6.9 mmol/l (100–125 mg/dl) for at least 1 year while not taking any medications to lower blood glucose.*

* some studies such s those from Virta Health define partial remission as a HbA1C < 6.5% and fasting blood glucose ≤ 5.5 (100 mg/dl) while taking  no medication, or only generic Metformin.

    • Complete remission is a return to normal glucose values i.e. HbA1C <6.0%, and/or fasting blood glucose < 5.6 mmol/L (100 mg/dl) for at least 1 year while not taking any medications to lower blood glucose.
    • Prolonged remission is a return to normal glucose values (i.e.
      HbA1C <6.0%, and/or fasting blood glucose < 5.6 mmol/L (100 mg/dl) for at least 5 years while not taking any medications to lower blood glucose.

Complete and prolonged remission can be achieved after bariatric surgery such as the roux-en-y procedure, and partial remission and complete remission have been documented with dietary and lifestyle changes, including a very low calorie diet and a very low-carbohydrate (ketogenic diet). To date, there is limited long-term data of 5 years or more documenting prolonged remission with dietary and lifestyle changes alone, although there are case studies.

I support people with a wide-range of goals when it comes to diabetes through my long-standing general dietetic practice, BetterByDesign Nutrition, and for those seeking remission through either that division or my low carbohydrate focussed practice, The Low Carb Healthy Fat Dietitian.  

    • Some people come to me with a diagnosis of pre-diabetes wanting to implement dietary changes to avoid getting type 2 diabetes.
    • Others come to me once they are diagnosed with type 2 diabetes, wanting to better control their blood sugar level through dietary changes and avoid complications.
    • Those who found me searching for a Dietitian with experience with low carbohydrate- and very low carbohydrate (ketogenic) diets most often are coming to avoid developing diabetes after a pre-diabetes diagnosis, or to have me help them put the disease into remission.

These are each valid goals.

Those who know that remission of type 2 diabetes is entirely possible find it difficult to understand that not everyone with type 2 diabetes wants to put the disease into remission.

Some people simply don’t known that this is even a possibility — believing that the disease is automatically both chronic (long-term) and progressive (getting worse with time). This type of a situation gives me the opportunity to explain to them that type 2 diabetes can be put into remission, and the different ways that I can support them in aiming to achieve that.

Other people may simply want to ‘manage’ their blood sugar levels to keep them from getting higher in order to avoid complications. They don’t want to have normal blood sugar, but want to avoid losing toes or going blind. These people have every right to choose these goals and to be supported by their healthcare team including me, in meeting them. I will make sure that they know that it is possible to achieve remission (because many don’t know), but if they don’t want to make the significant lifestyle changes required, then I will help them manage their diet to keep their blood sugar from getting higher. That said, they before they even begin services with me, they know that the Meal Plan I will design for them will not be “high carb” by any stretch of the imagination. Since type 2 diabetes is, in essence end-stage carbohydrate intolerance, the amount and type of carbohydrate on a Meal Plan that I will design for them will be limited, and specific. 

Note: Those coming to me on SGLT2 medication, such as Jardiance and Victosa or ACE inhibitors for high blood pressure will be asked to first consult with their doctor to have them monitor their dosages, as the carbohydrate content of their diet is gradually reduced.

For those coming to me to avoid having their pre-diabetes progress to type 2 diabetes or seeking to put their type 2 diabetes into remission, I will present to them the various dietary options available and explain how I am best able to support them in each. In my long-standing general dietetic practice I support three main approaches, including a very low calorie diet (including time-restricted eating), a whole-food predominately plant-based (vegetarian) diet, a modified DASH diet, a Mediterranean diet, and a very low carbohydrate / ketogenic diet. Through my low carb division, I offer a low carb and very low carbohydrate / ketogenic diet which can be tailored to someone being a vegetarian, if that is their preference. To those coming to me for support in following a carnivore diet (all meat / animal product consumption) or a vegan diet (one devoid of any animal products), I recommend they seek the support of another Dietitian with expertise in those areas.  I simply don’t feel equipped to ensure a nutritionally-adequate diet following either of those approaches.

The byline of my low carb division (The Low Carb Healthy Fat Dietitian) is “there is no one-sized-fits-all low carb or ketogenic diet” — because there isn’t.  A high-fat moderate protein ketogenic diet may be appropriate in some circumstances, whereas a higher lean protein, moderate fat approach may be better suited in others. Everyone’s medical conditions, risk factors and personal preferences are different, so I go over the different options and make my recommendations while explaining my reasons for them and let the person decide for themselves. Nothing is carved in stone.  Meal Plans can be changed or “tweaked” to best meet the individual’s needs.

The byline of my long-standing general dietetic practice is “Nutrition is BetterByDesign“. This emphasises the same conviction that Meal Plans need to be designed for the individual.  A person who doesn’t eat meat for religious, cultural or ethical considerations, for example needs to have an individual Meal Plan that helps them achieve their health goals — in the same way that someone who eats meat does. Those who choose to live with diabetes have just as much right to dietary support to meet those goals, as someone who desires to seek remission from diabetes. It doesn’t matter that remission is possible if they don’t want to achieve that, or they don’t want to make the lifestyle changes necessary to make that a possibility. They are free to make that decision. As a Dietitian, my responsibility is to support them in meeting their goals, and not to try and convince that other goals are “better”.  As long as they know that the possibility for remission exists and how that can be accomplished, I will whole-heartedly support them in their desire to live better with diabetes.

One of the reasons why I continue to maintain both my long-standing dietetic practice, BetterByDesign Nutrition (BBDNutrition), as well as my low carb division, The Low Carb Healthy Fat Dietitian is to providing people with different dietary approaches to type 2 diabetes. The other reason is that some people come to me seeking support for GI disorders or food allergies / sensitivities, or for nutritional support in pregnancy or for their children, which I do only through BBDNutrition. My two divisions give people options. People who want only low carb and ketogenic dietary support in a practice that does nothing else have that at the Low Carb Healthy Fat Dietitian.

Individuals have different goals and various needs. People are also at different stages of change when it comes to them having type 2 diabetes. Some may start with wanting to manage their symptoms — and only later arrive at a point where they want to seek remission.  If and when they do, I support them in doing that.

This is why I do, what I do, the way I do.

Please let me know if I can help.

To your good health!

Joy

You can follow me on:

Twitter: https://twitter.com/JoyKiddie
Facebook: https://www.facebook.com/BetterByDesignNutrition/

 

Copyright ©2021 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.

 

Diabetes Canada’s 7-day Low Carb Meal Plan – includes bread, pasta, rice

I was excited when I saw a thread on social media over the weekend about Diabetes Canada’s new 7-day Low Carb Meal Plan. After all, last May they released a Position Statement summarizing the evidence for the role of low carbohydrate diets (<51-130g carbohydrate/day) and very low- carbohydrate diets (<50g carbohydrate/day) in the management of type 1 and type 2 diabetes and I thought “great!” — they are going to be providing support for people with diabetes to be able to choose a low carb or very low carb (keto) diet as one of the available healthy eating patterns.  Not quite.

This was the ad I saw on Facebook;

Diabetes Canada – healthy low carb meal plan (low glycemic and plant-based), January 23, 2021

Clicking on the link associated with the ad, the text reads;

“Current evidence suggests that a low-carbohydrate diet can be safe and effective for people with diabetes. This dietary pattern can help with weight loss and blood sugar management. Keep in mind that a low-carbohydrate diet can also reduce the need for certain diabetes medications. People living with diabetes who want to follow a low-carbohydrate diet should seek professional advice from their healthcare provider to avoid any adverse effects, such as hypoglycemia (low blood sugar) or an increased risk for diabetic ketoacidosis (DKA).

This meal plan features healthy plant-based foods, low glycemic index carbohydrates, and less than 130 grams carbohydrates per day. [1]”

At the bottom of the meal plan it indicates;

sponsors of Diabetes Canada’s 7-day low carbohydrate meal plan [1]
While the promotion on Facebook indicated that it features ‘plant-based foods’, it is not a plant-based menu. It includes eggs and yogurt, fish (tuna, fish fillet, salmon),  a (bun-less) cheeseburger, beef or pork meatballs, and chicken breast — along with tofu, legumes such as chick peas and black beans. Not surprisingly given one of the sponsors of the menu, each day includes one or more servings of plant-based beverages and recipes use canola oil.

The Diabetes Canada “low carb” meal plan is like no other I have ever come across, as it includes servings of starches such as bread, potato, rice, pasta and legumes.

Breakfast on day 1, 3 & 5 of the menu features a smoothie made with 200 ml of a sugar-sweetened soy beverage manufactured by one of the menu’s sponsors, along with 65 g of blueberries, 85 g of pomegranate and 2 g of ginger. This is hardly the best way for someone with diabetes (an inability to adequately handle carbohydrate) to begin the day — and that’s all there is for breakfast! One little glass of smoothie totalling almost 30g of carbs and only 9 g of protein.

1 cup of soy protein smoothie – 28.4 g carbs, 8.9 g pro, 5.2 g fat

Lunches and Dinners included either a slice of whole-grain bread, 1 small baked potato, 1/2 cup cooked brown rice, 3/4 cup (150 ml) cooked pasta, 1/2 cup (125 ml) mashed sweet potato or chick peas or black beans. Sure, small amounts of sweet potato can be appropriate as part of a real, whole food low carbohydrate meal plan, and a small amount of chick peas or black beans can be included from time to time, but there is no established “low carb” diet that includes bread, rice and pasta!

Low Carb — and low protein and fat too

I was curious how much food there was at each meal on this plan, as well as  the total amount of carbs and protein per day, so I decided to analyze Day 1, Day 3 and Day 5 to get a rough idea.

Where a recipe was not provided as part of the menu, I looked up the food item in Cronometer and used the nutritional information for the specified quantity.

These meals were <130 g of carbohydrate per day — so technically these are considered “low carb“, but they are also low fat, and low or inadequate in protein.

Day 1

Breakfast on Day 1 had a small glass of the “smoothie” (28.4 g carbs, 8.9 g pro, 5.2 g fat) and that was it until lunch! Given the high amount of ground-up fruit in it as well as the low amount of fat and protein, the first thing I thought of was how soon an adult with diabetes would be ravenous after drinking this. Then I wondered how high would their blood sugar go?

[Note: February 5, 2021]: In an earlier article, I covered the effect of various types of food processing on blood glucose, including mechanical processing such as the pureeing of the fruit in this smoothie. While 60g of whole apple, 60 g of pureed apple, and 60g of juiced apple have the same amount of carbohydrate and similar Glycemic Index neither of these indicate how blood glucose responds to eating pureed fruit, versus intact fruit.  We know from a 1977 study published in the Lancet (reference below) that when pureed fruit or juiced fruit is consumed, the glucose response 90 minutes later is significantly higher than if the fruit were eaten whole. 

[Haber GB, Heaton KW, Murphy D, Burroughs LF. Depletion and disruption of dietary fibre. Effects on satiety, plasma-glucose, and serum-insulin. Lancet. 1977 Oct 1;2(8040):679-82. doi: 10.1016/s0140-6736(77)90494-9. PMID: 71495]

This is typical of what is seen with any ultra-processed carbohydrate. So, the first problem with someone with diabetes having a fruit smoothie such as this as a meal is that the fruit is ground up, and not whole.  A smoothie will spike blood glucose much more than if the same food was eaten not pureed. 

We also know from a 2015 study on the effect of food order on the response of glucose and insulin, that if carbs are eaten last, the glucose curve will be approximately 74% smaller, with a 49% smaller insulin spike.

[Shukla AP, Iliescu RG, Thomas CE, Aronne LJ. Food Order Has a Significant Impact on Postprandial Glucose and Insulin Levels. Diabetes Care. 2015;38(7):e98-e99. doi:10.2337/dc15-0429]

The second problem with someone with diabetes drinking a fruit smoothie like this for breakfast with no other food is that there is no way of having the carbs last!

Lunch on Day 1 was a small serving of vegetable frittata (3 g carbs, 13.6 g pro, 14.9 g fat), 1 slice whole-grain bread (13.2 g carbs, 4.5 g pro, 1.3 g fat) and 1 cup unsweetened plant based beverage such as Silk plain Oat milk (7.6 g carbs, 0.4 g pro, 0.3 g fat). A slice of frittata, a slice of plain bread and a glass of oat milk and that’s it for lunch. Maybe a nice lunch for child home from school?

Dinner was 1 cup of Indonesian tofu stew with vegetables (8 g carbs, 5 g pro, 8 g fat) and ½ cup (125 mL) cooked brown rice (24.2 g carbs, 2.8 g pro, 1.0 g fat). That’s it. This might be an adequate serving for an older adult with a small appetite.

So what did this day provide in terms of carbohydrate and total protein?

Well, it was low carb (84.4 g) but it was also inadequate in protein — having only 35.2 g PRO. Based on “average” body weight and a minimum 0.36 g of protein per pound of body weight (0.8 g protein per kg), this is less than the 46g protein required for the average sedentary woman, and much less than the 56g of protein required for the average sedentary man.

Day 3

Breakfast was small glass of the same smoothie (28.4 g carbs, 8.9 g pro, 5.2 g fat) and that was it until lunch!

Lunch was a “cup” of low fat cream of cauliflower soup that was actually only 3/4 cup / 175ml in size ( 10 g carbs, 7g PRO,  2g fat), 3.5 oz / 100 g grilled chicken breast (0 carbs, 41.7 g pro, 6.1 g fat) and a cup of unsweetened plant based beverage (7.6 g carbs, 0.4 g pro, 0.3 g fat). No salad, no side of veggies, that was it.

Dinner was 1 serving (3 oz) of grilled fish fillet (pink salmon – 0 g carbs, 17.4 g pro, 3.7 g fat), ½ cup (125 mL) cooked quinoa (17.1 g carbs, 4.1 g pro, 1.8 g fat) and 1.5 cups green salad with dressing (2.8 g carbs, 0.8 g pro, 2.5 g fat). What adult would find a small piece of fish, a small serving of quinoa and a small salad enough for supper — unless they had a big lunch?

What did this day provide, in terms of carbohydrate and total protein? Well, it was low carb (65.9 g) and adequate (71.4 g) protein, but had very few vegetables, little healthy fat, and very small portions.

Day 5

Breakfast was small glass of the same smoothie (28.4 g carbs, 8.9 g pro, 5.2 g fat) and that was it.

Lunch was 1 egg on 3/4 cup of Mexican baked black beans (19 g carbs, 12 g pro, 9 g fat) and 1 cup unsweetened plant based beverage (7.6 g carbs, 0.4 g pro, 0.3 g fat). Nothing else. No veggies, no salad, not even a dollop of guacamole!

Dinner was 1 serving (3.5 oz) of beef or pork meatballs without sauce (10.5 g carbs, 19.3 g pro, 16.6 g fat) and ¾ cup (150 mL) of plain cooked pasta (30.5 g carbs, 6.1 g pro, 1.0 g fat). How is this an appropriate “low carb” dinner for someone with diabetes? How is this a complete meal?

It was low carb (96.0 g) and adequate (46.7 g) protein for a sedentary woman but inadequate protein for even a sedentary man. It had few vegetables, very little healthy fat, and very small portions.

Final Thoughts…

There are parts of this menu that are certainly usable, and it can be modified to make it into a lovely low-carb meal plan.

The frittata, for example could be a great start to a low-carb lunch when paired with a nice big salad, with a bit of crumbled cheese, a few pumpkin seeds and a bit of avocado — and skip the bread!

Double the amount of tofu stew and vegetables, and make a nice Asian style cucumber salad on the side and skip the rice!

The cauliflower soup with a splash of cream and the grilled chicken breast would go every well with a nice helping of steamed veggies or mixed greens on the side — and why not? They are low carb, and high in micronutrients. The cooked ones would taste great with a dab of butter and the raw ones, with a squeeze of lemon and some extra virgin olive oil. Now there’s lunch!

And why on earth would a person with diabetes be encouraged to drink that smoothie 3 times per week if not to promote the product of one of the menu’s sponsors?  Why not suggest an omelette made with some leftover cooked veggies from the night before — and they could even add an ounce of sharp cheddar to it, which would easily get them through to lunch. Or, how about a bowl of Greek yogurt with 1/2 cup of blueberries and a tablespoon of hemp heart? That is a high protein breakfast with far fewer carbs than the smoothie and will keep a person going with stable blood sugars until lunch.

Ditch the carbs.  Who needs the bread and pasta and rice — especially on a “low carb” meal plan?

People can get all the B-vitamins they need, including B1 (thiamine), B2 (riboflavin), B3 (niacin) and folate from real, whole food such as chicken liver, sardines, eggs and sunflower seeds. They can plenty of the most bioavailable iron from seafood and meat and get ample magnesium from nut, seeds, dark chocolate and avocados, and selenium from Brazil nuts and eggs.

The American Diabetes Association understands that a low carbohydrate diet “limits sugar, cereals, pasta, bread, fruit & starchy vegetables” and “consist mostly of protein foods like meat and dairy, fatty foods like oil, nuts, seeds, avocado, and butter, and non-starchy vegetables” [2].

 

 

 

Canadian with diabetes deserve to have a low carb menu based on these same principals, and which provides them with adequate protein, a good source of healthy fats and adequate size servings of food.

We can do better.

Canadians with diabetes deserve better.

More Info?

If you would like more information about how I can help support your nutrition needs, please click on the Services tab to learn more.

To your good health!

Joy

You can follow me on:

Twitter: https://twitter.com/JoyKiddie
Facebook: https://www.facebook.com/BetterByDesignNutrition/

 

Copyright ©2021 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.

Reference

  1. Diabetes Canada, 7-day low carbohydrate meal plan, https://diabetes.ca/nutrition—fitness/meal-planning/7-day-low-carbohydrate-meal-plan
  2. American Diabetes Association, Diabetes Food Hub, Meal Prep: meals for any eating pattern, Low Carb, https://www.diabetesfoodhub.org/articles/meal-prep-meals-for-any-eating-pattern.html

Negative Effect of Dietary Carbohydrate on the Gut Microbiome in IBD

Several recent studies have found a relationship between the species of bacteria and fungi that live in our large intestine, carbohydrate intake and Irritable Bowel Disease (IBD), including Ulcerative Colitis and Crohn’s disease. This article elaborates on how this knowledge may help improve symptoms for those with IBD.

The Gut Microbiome & Mycobiome

The trillions of gut bacteria that live in our intestines are collectively referred to as the ‘gut microbiome, ‘gut microbiota’ or ‘gut flora’, along with fungi (called the ‘mycobiome’) and other single cell organisms called archaea.

We are in a symbiotic relationship with these gut bacteria — which means when things are going well, they benefit us and we benefit them. What we eat feeds them, and in turn they produce by-products that are helpful for us. One example of a helpful end-product of fermentation by the so-called “good bugs” of our gut microbiome is the formation of short chain fatty acids (SCFA) [3], which plays an important role in maintaining glucose (blood sugar) levels, fat metabolism and even appetite regulation [2] in humans. As I will elaborate further on in this article, these SCFA also play a role in keeping the “bad bugs” from taking over.

The gut mycobiome, which are the species of fungi that live in our large intestine can have an impact on our gut microbiome, and both are affected by the carbohydrates we take in through the diet — which has important implications for those with Inflammatory Bowel Disease.

Dietary Carbohydrate

What types of foods are carbohydrate-based may seem obvious to some, but many people don’t realize that simple sugars such as glucose (the sugar in our blood) and fructose (the sugar in fruit) are not that much different than ‘starches’, such as bread, pasta and rice. As outlined in a previous article, sugars can come alone come alone, in pairs or strung like pearls on a chain. Knowing the different types of sugars is important to those with Inflammatory Bowel Disease as these sugars and starches can be used as food for our gut microbiome, and which bacteria and fungi we ‘feed’ has important implications on health.

Simple Sugars – monosaccharides & disaccharides

Simple sugars can come alone (monosaccharides, which means ‘one sugar’) or in pairs (disaccharides, which means ‘two sugars’).

Monosaccharides include glucose, fructose and galactose and disaccharides are combinations of these monosaccharides linked together, in pairs. Some common disaccharides include sucrose, lactose and maltose;

Sucrose is ordinary table sugar and made up of glucose-fructose.

Lactose is the sugar in milk and milk products and is made from a glucose-galactose pair.

Maltose which rarely occurs naturally in foods, is glucose-glucose. Maltose is used in food processing such as the shiny glaze on Chinese roast duck.

Complex Carbohydrates – strings of sugar molecules

Complex carbohydrates are made up of more than two monosaccharides (sugar molecules). Oligosaccharides (‘oligo’ means “scant” or “few”) are made up of 3-10 sugar molecules, whereas polysaccharides (including starch) are made up of hundred or even thousands of monosaccharides (sugar molecules).

Oligosaccharides

Oligosaccharides are made up of 3-10 sugar molecules and the two most common are some of the complex carbohydrates found in dried beans, peas and lentils[1].  For example, raffinose is an oligosaccharide made from 3 sugar molecules: galactose-glucose-fructose and stachyose is an oligosaccharide made from 4 sugar molecules: galactose-galactose-glucose-fructose. What is important to know is that the body can’t break down either raffinose or stachyose, but these are fermented by certain species of bacteria in our gut microbiome.

Polysaccharides

Polysaccharides are made up of hundreds or thousands of sugar molecules linked together. When those sugar molecules are only glucose, the polysaccharide is called “starch”.

Some polysaccharides form long straight chains while others are branched like a tree. These structural difference affect how these carbohydrates behave when they’re heated or put in water. The way the monosaccharides are linked together makes the polysaccharides either digestible as in starch, or indigestible as in fiber.

We can’t digest polysaccharides found in plant foods such as fiber, cellulose, hemicellulose, gums and mucilages (such as psyllium) but they can both slow down the absorption of digestible carbohydrate and be fermented by the gut microbiome.

Starch

Starches are long chains of glucose molecules strung together like beads on a string. Starches are found in grains such as wheat, corn, rice, oats, millet and barley, as well as in legumes such as peas, beans and lentils* and tubers such as potatoes, yams and cassava.

*As mentioned above, peas, beans and lentils also have the complex carbohydrates called oligosaccharides which are not broken down by the body, but are broken down by bacteria in our gut microbiome.

There are two types of starches; the long unbranched chains called amylose and the long branched chain ones call amylopectin. The body digests most starches very easily, although those with a high percentage of amylopectin (such as cornstarch) are digested much more easily than those with a high amount of amylose, such as wheat starch [1].

Since starches are just glucose molecules linked together and they are easily broken down to individual glucose molecules, so starches quickly affect the blood sugar and as I will elaborate on in this article are fermented easily by our gut microbiome and may play a role in colitis in genetically susceptible individuals.  Limiting these and other fermentable carbohydrates also can play a role in reducing symptoms of those with IBD.

How Simple Sugars can Induce Colitis by Affecting the Microbiome

A study was published in late 2020 documenting how simple sugars in the diet can induce colitis, an inflammatory bowel disease [2]. The study found that when researchers fed mice simple sugars such as glucose, fructose and sucrose, the high-sugar diet damaged the protective mucus layer of the colon (large intestine) and increased the number of harmful bacteria — especially Akkermansia muciniphila and Bacteroides fragilis which break down the mucus that lines and protects the colon. 

The study found that when the mice were fed a 10% glucose solution for seven days (chosen because soft drinks contain ~15% sugar) and were then given a 2.5% dextran sulfate sodium (DSS) which is known to induce colitis, the mice that had been fed the glucose had extreme sensitivity to DSS treatment and suffered from aggressive colitis, bloody diarrhea and rapid loss of nearly 20% of their body weightWhen the researchers looked at the glucose-treated mice three days after giving them the DSS, they found that their colons were shorter than the colons of the control mice that were not fed the glucose, and that the glucose-fed mice had many of the symptoms of colitis, including loss of epithelial crypts, inflammation, and ulceration.

When the researchers saw that the high-sugar intake made the colitis
caused by DSS chemical injury of the colon worse, it led them to then test
whether high sugar intake alone had a similar effect in mice that were genetically susceptible. They treated mice with genetic susceptibility to colitis with a 5% glucose solution from 14 weeks of age, while measuring weekly body weight changes and clinical scorings for 5 weeks. At 19 weeks, 90% of glucose-treated genetically-susceptible mice developed colitis, compared to 40% in the controls that did not have the genetic susceptibility. The glucose-fed susceptible mice had much greater loss of body weight and higher diarrhea and rectal bleeding compared to control the control mice, and when they looked at the colon tissue of the mice, the ones that were glucose-fed had increased inflammation. There was also a much higher expression of inflammatory molecules in the colons of sugar-treated mice.

Of Mice and Men

Even though the results of animal studies can’t be applied directly to humans, this study can give us an indication of what may be going on in people. 

The National Human Genome Research Institute explains it this way;

“Mice and humans share virtually the same set of genes. Almost every gene found in one species so far has been found in a closely related form in the other. Of the approximately 4,000 genes that have been studied, less than 10 are found in one species but not in the other” [3].

Low-FODMAP Diet in Inflammatory Bowel Disease – effect on microbiome

For people with Inflammatory Bowel Disease, including Crohn’s disease and Ulcerative Colitis, a low-FODMAP diet is successfully used to reduce symptoms of the disease once their symptoms have been stabilized using a low residue diet after a flare. A low-FODMAP diet enables people with IBD to gradually normalize their diet, while avoiding foods that can be fermented by the ‘gut microbiome’ and this often leads to those with IBD finding significant relief of symptoms.

FODMAP is an acronym for fermentable, oligo-, di-, monosaccharides and polyols. A low-FODMAP diet reduces foods which contain various sugars such as fructose (the sugar found in fruit), lactose (the sugar in milk), sugar alcohols called ‘polyols’ such as sorbitol and mannitol, fructans which are found in garlic, leeks, artichokes, and wheat, and galacto-oligosaccharides which are found in legumes such as lentils, chickpeas, and black beans. As outlined above, these FODMAPS are fermentable by the gut bacteria and the by-products of that fermentation have long been thought to underlie symptoms experienced in those with Inflammatory Bowel Disease (IBD), as well as Irritable Bowel Syndrome (IBS)

Over the last 5 years since I began using a therapeutic low carbohydrate diet to reduce the symptoms of type 2 diabetes and for weight loss, I began to wonder if what made a low-FODMAP diet effective in reducing symptoms in IBD was due to its overall low-carbohydrate content not just the lower amount of fermentable, oligo-, di-, monosaccharides and polyols. Two studies published towards the end of 2020 confirmed a relationship between other types of carbohydrate in the diet and the gut microbiome (bacteria) and mycobiome (fungi). The first study was about the relationship between simple sugars intake and colitis which is outlined above, and the second study was about the effect of a very low carbohydrate diet on species of gut fungi (mycobiome), and is outline below.

Very Low Carbohydrate Diet Reduces Some Fungi in Gut Microbiome

Shortly before the above study showing a relationship between simple sugar intake and colitis is genetically-susceptible mice was published, there was another study that looked at the effect of a Mediterranean ketogenic diet* to decrease the population of certain species of gut fungi (mycobiome) that populate the gut, along with the bacteria (microbiome).

*A ketogenic diet is one that is very low in dietary carbohydrates — usually less than 20 grams of carbohydrate per day.

While it was a small pilot study, it was a randomized, double-blind crossover study which is the strongest study design. This type of study has two groups of people that don’t know which of the two groups they are in and who received one diet for half the study period, and then the diets and groups are switched so they receive the other diet for the second half of the study.

This study looked at the effect of Mediterranean Ketogenic Diet (MMKD) compared to the American Heart Association Diet (AHAD) in people with mild cognitive impairment (MCI) and found that symptoms of MCI were improved with the Mediterranean Ketogenic Diet in relationship with changes in the gut mycobiome. 

What researches found was that (1) whether a person had Mild Cognitive Impairment or not, the Mediterranean Ketogenic Diet more positively affected the gut mycobiome than the AHAD diet and (2) in those with MCI, there was a significant reduction in the proportion of Candida species during the Mediterranean Ketogenic Diet phase.

It was this part of the discussion that got my attention in relationship to Irritable Bowel Disease, such as Crohn’s disease and Ulcerative Colitis.

“The genus Candida comprises many opportunistic species implicated in various gut-related diseases including inflammatory bowel diseases, Crohn’s disease, ulcerative colitis, and gut inflammation [78]…In this context, reduced Candida carriage in patients with MCI might reflect another positive outcome of the MMKD intervention.”

What this means is, the researchers wondered whether a Mediterranean Ketogenic Diet (MMKD) might be effective in lowering Candida which has already been implicated in Inflammatory Bowel Disease, including Crohn’s disease and ulcerative colitis.

This part of the discussion section also stood out;

“Notably, we find a significantly negative correlation of Candida with short-chain fatty acid butyrate, a beneficial gut bacterial metabolite which was found to be increased by MMKD in these patients with MCI [24]. One of the ways gut bacteriome keep mycobiome in check is through the production of wide range of small molecules such as SCFAs (e.g., butyrate), which have inhibitory effects against the growth of pathobionts including Candida albicans [79, 80]. Together, these data suggest that the MMKD positively modulates the gut microbiome as well as the bacterial metabolites arrays, which in turn may check the overgrowth of opportunistic pathogens such as Candida.”

Simply said, what this means is that it is well-known that a ketogenic diet increases the amount of the short chain fatty acid (SCFA) butyrate which inhibits the growth of strains of Candida. This relationship implies a therapeutic role for a  Mediterranean ketogenic diet in the management of Irritable Bowel Syndrome.

Final Thoughts

In light of the above two studies, it seems to make good sense for those at genetic risk of developing Irritable Bowel Disease — as well as for those already diagnosed with IBD to

(a) reduce intake of simple sugars, including glucose, fructose and sucrose 

and

(b) consider adoption of a Mediterranean Ketogenic Diet which has been found to reduce the amount of Candida species — which has already been implicated in the development of Irritable Bowel Disease.

More Info?

If you would like more information about my services then please have a look under the tab of that name or send me a note through the Contact Me form.

To your good health!

Joy

You can follow me on:

Twitter: https://twitter.com/JoyKiddie
Facebook: https://www.facebook.com/BetterByDesignNutrition/

 

Copyright ©2021 BetterByDesign Nutrition Ltd.

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

 

References

  1. Morrison DJ, Preston T. Formation of short chain fatty acids by the gut microbiota and their impact on human metabolism. Gut Microbes. 2016;7(3):189-200. doi:10.1080/19490976.2015.1134082
  2. Khan S, Waliullah S, Godfrey V et al, Dietary simple sugars alter microbial ecology in the gut and promote colitis in mice, Science Translational Medicine 28 Oct 2020: Vol. 12, Issue 567,  DOI: 10.1126/scitranslmed.aay6218
  3. National Human Genome Research Project, Why Mouse Matters, https://www.genome.gov/10001345/importance-of-mouse-genome
  4. Nagpal R, Neth B, Wang S et al,  Gut mycobiome and its interaction with diet, gut bacteria and alzheimer’s disease markers in subjects with mild cognitive impairment: A pilot study. EBioMedicine, 2020; 59: 102950 DOI: 10.1016/j.ebiom.2020.102950

A Keto Diet is Only About How Much Carbohydrate it Contains

The myth persists that a “keto” diet is all about the fat…bacon, heavy whipping cream, and fat bombs. It’s about adding butter and MCT oil to coffee, about eating fatty cuts of meat and lots of avocado.

It isn’t.

What makes a diet “low carb” or “keto” is only how little carbohydrate it contains NOT how much fat it contains.

Defining “Low Carb” and “Keto” Diets

Different individuals and groups define “low carb” and “keto” (very low carb) in various ways. Feinman et al [1] defined three categories of reduced-carbohydrate diets;

(a) very low carbohydrate / ketogenic diet: carbohydrate limited to 20–50 g per day or < 10% of total energy intake

(b) low carbohydrate diet: carbohydrate limited to < 130 g per day or < 26% of total energy intake

(c) moderate carbohydrate diet: carbohydrate limited to 130–225 g per day or 26–45% of total energy intake.

In its Consensus Report of April 18, 2019, the American Diabetes Association and the European Association for the Study of Diabetes (EASD) defined a low carbohydrate diet as having 26-45% of total daily calories as carbohydrate (a combination of a low carbohydrate diet and a moderate carbohydrate diet defined by Feinman et al), and defined a very low carbohydrate (ketogenic) diet as 20-50 g carbs per day. In its 2020 Standards of Medical Care in Diabetes, the American Diabetes Association continued to define low carb and very low carb the same way.

Diabetes Canada also defines a low carbohydrate diet as less than <130 g of carbohydrate per day or <45% energy as carbohydrate, and very low carbohydrate (ketogenic) diet as <50 g of carbohydrate per day in its April 2020 Position Statement [3].

What defines a low carbohydrate or very low carbohydrate (“keto”) diet is ONLY the amount of carbohydrate it contains. There isn’t even any mention of how much fat it contains!

How Much Carbohydrate is Essential in the Diet?

The Dietary Reference Intakes for Energy, Carbohydrate, Fiber, Fat, Fatty Acids, Cholesterol, Protein and Amino Acids (2005) which forms the basis for dietary recommendations in both the US and Canada reads;

“The lower limit of dietary carbohydrate compatible with life apparently is zero, provided that adequate amounts of protein and fat are consumed[4].

There are essential amino acids and essential fatty acids that we need to take in through the diet because the body can’t make these, but there is no essential carbohydrate because the body can make any carbohydrate it needs from amino acids (from protein) or fat.

How Much Fat in a Keto Diet?

There is nothing magical or mystical about how much fat or protein is required in a “low carb” or “keto” diet.

Whether one starts a low carb diet at 130 g of carbohydrate per day or a “keto” diet of 20-50 g carbohydrate per day, the the remainder of daily calories is provided as protein and fat.

As outlined below, the popularized “keto” diet sets the amount of fat at approximately 75% of daily calories as fat, but this is only one type of “keto” diet.

It is a misconception is that to be a “keto” diet, most of daily calories needs to be as fat. 

It is also a misconception that added fat that is part of a low carb or “keto” diet must be animal fat.  Added fat as food or to cook with, or to put on salad can be provided by high fat fruit such as avocado or olives (fruit or oil), coconut (meat or oil), and nuts and seeds. If people choose, they can be low carb or “keto” and eat a predominantly whole-food plant-based (vegetarian) meal pattern.

Popularized “Keto” Diet

The popularized “keto” diet promoted widely on the internet is described as 75% fat, 15% protein and 10% carbohydrate, but is only ONE “keto diet” and not “THE keto diet”.

There are other “keto” diets, including the low carb, high protein, moderate fat ketogenic diet called Protein Power published in 1997 by Dr. Michael Eades and his wife Dr. Mary Dan Eades [5], the 2010 New Atkins For a New You [6] — which is a redesign of the original “Atkins Diet” from the 1970s written by Dr. Eric Westman, Dr. Stephen Phinney MD PhD, and Dr. Jeff Volek RD PhD which is only a very high fat ketogenic diet (20-50 g carbs per day) for phase one which lasts only the first two weeks, and there is also Real Meal Revolution [7] by Tim Noakes, Sally-Ann Creed, Jonno Proudfoot. Phinney and Volek’s approach in their 2011 book, the Art and Science of Low Carbohydrate Living has been to establish carbohydrate intake at 7.5-10% of calories for men, 2.5-6.5% of calories for women, protein intake at up to 30% of calories during weight loss, 21% during weight maintenance and fat intake to 60% of calories during weight loss and 65-72% during weight maintenance. Fat intake at 60% of calories during weight loss is NOT the same as the 75% calories as fat of the popularized “keto” diet.

The popularized “keto” diet is based largely on the two 2016 books by Dr. Jason Fung titled the Obesity Code [8] and The Complete Guide to Fasting [9], and the 2017 book titled by Dr. Andreas Eenfeldt, the founder of the popular “Diet Doctor website”, titled A Low Carb, High Fat Food Revolution [10] — both of whom write extensively on the Diet Doctor website.

Defining “High Fat”

In the US, the recommendation has been to limit calories from fat to no more than 30% of daily calories, of which no more than 1/3 comes from saturated fat and in Canada, to limit fat to 20-35% of daily calories as fat, with no more than 1/3 from saturated fat.  By definition, diets higher than 30% fat (US) or 35% fat (Canada) are considered “high fat”.

A “keto” diet which is only 40% fat would be considered “high fat” by the USDA and Health Canada, as would a “keto” diet that is 75% fat.  

But is a diet that is 40% fat really “high fat”?

From 1949 until 1977, dietary intake in Canada was at ~40-50% of daily calories as fat,  ~20-30% of daily calories as protein, and only 20-30% as carbohydrate. Was this the original “low carb high fat” diet?

Clarifying Definitions

In anything, it is important to define terms.

A “low carb” or “keto” diet is ONLY about how little carbohydrate it has (<130 g carbohydrate per day, 20-50 g of carbohydrate per day) and has absolutely nothing to do with how much fat it has.

Or how much protein in has, for that matter.

Contrary to what some on social media want to know, there is no “protein starting point” for a low carb or “keto” diet.  Each individual’s macro needs (energy, protein, fat and carbohydrate) are different, and vary depending on a person’s age, gender, stage of life,  health conditions, and activity for example.

There is no one-sized-fits-all low carb or “keto” diet with a set amount of fat, and set amount of protein. It depends what one is seeking to accomplish. Based on the definition, a low carb or “keto” diet for weight loss could range from 40% fat to 75% fat — and up to 90% for those following a therapeutic ketogenic diet for seizure disorder or glioblastoma.

People are always looking for the “formula for success” when it comes to weight loss but there isn’t one, except the one that works best for them.

More Info?

If you would like more information about my services then please have a look under the tab of that name or send me a note through the Contact Me form.

To your good health!

Joy

You can follow me on:

Twitter: https://twitter.com/JoyKiddie
Facebook: https://www.facebook.com/BetterByDesignNutrition/

 

Copyright ©2021 BetterByDesign Nutrition Ltd.

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

References

  1. Feinman RD, Pogozelski WK, Astrup A, Bernstein RK, Fine EJ,Westman EC, et al. Dietary Carbohydrate Restriction as the First Approach in Diabetes Management: critical review and evidence base. Nutrition. 2015;31(1):1–13
  2. Evert, AB, Dennison M, Gardner CD, et al, Nutrition Therapy for Adults With Diabetes or Prediabetes: A Consensus Report, Diabetes Care, Ahead of Print, published online April 18, 2019, https://doi.org/10.2337/dci19-0014
  3. Diabetes Canada, Diabetes Canada Position Statement on Low Carbohydrate
    Diets for Adults with Diabetes: A Rapid Review Canadian Journal of Diabetes (2020), doi: https://doi.org/10.1016/j.jcjd.2020.04.001.
  4. National Academies of Sciences, Engineering and Medicine, Dietary Reference Intakes for Energy, Carbohydrate, Fiber, Fat, Fatty Acids, Cholesterol, Protein and Amino Acids, 2005, https://www.nap.edu/catalog/10490/dietary-reference-intakes-for-energy-carbohydrate-fiber-fat-fatty-acids-cholesterol-protein-and-amino-acids
  5. Eades M, Dan Eades M (1997), Protein Power: The High-Protein/Low-Carbohydrate Way to Lose Weight, Feel Fit, and Boost Your Health–in Just Weeks! Bantam; New edition edition (1 December 1997)
  6. Westman E, Phinney SD, Volek J, (2010) The New Atkins for a New You – the Ultimate Diet for Shedding Weight and Feeling Great, Atria Books February 17, 2010)
  7. Volek JS, Phinney SD, The Art and Science of Low Carbohydrate Living: An Expert Guide, Beyond Obesity, 2011
  8. Noakes T, Creed S-A, Proudfoot J, et al, (2013)The Meal Real Revolution, Quivertree Publications
  9. Fung J (2016) Obesity Code, Greystone Books, Vancouver
  10. Fung J, Moore J (2016), The complete guide to fasting : heal your body through intermittent, alternate-day, and extended fasting, Victory Belt Publishing
  11. Eenfeldt A, Low Carb, High Fat Food Revolution: Advice and Recipes to Improve Your Health and Reduce Your Weight (2017), Skyhorse Publishers

No Underlying Health Conditions – likely assumed not assessed

News outlets highlight when someone has died of complications of COVID-19, stressing that the person “had no underlying health conditions“,  but the problem is that this is often assumed,  not assessed.  Just because a person wasn’t diagnosed with diabetes, heart disease or high blood pressure (or some other disease) does not mean that they have no underlying health conditions. 

Not Assessed – assumed “fine”

We have known since 2018 that 88% of Americans are metabolically unhealthy[1], which means that only 12% of adults are metabolically healthy. An adult dying with “no underlying health conditions” may simply mean they hadn’t been assessed. Many people have never had their waist circumference measured by a health care professional, nor had their blood sugar, blood pressure or cholesterol checked, and the results compared to healthy standards. If these things haven’t been measured, can we assume that a person is metabolically healthy?

Measures of metabolic health include [1]:

  • Waist Circumference: < 102 cm (40 inches) for men and 88 cm (34.5 inches) in women
  • Systolic Blood Pressure: < 120 mmHG
  • Diastolic Blood Pressure: < 80 mmHG
  • Glucose: < 5.5 mmol/L (100 mg/dL)
  • HbA1c: < 5.7%
  • Triglycerides: < 1.7 mmol/l (< 150 mg/dL)
  • HDL cholesterol: ≥ 1.00 mmol/L (≥40 mg/dL) in men and ≥ 1.30 mmol/L (50 mg/dl) in women.

If a person hasn’t had their waist circumference, blood sugar or pressure, or cholesterol assessed, then they are assumed to have no underlying health conditions. Not measuring it doesn’t mean it doesn’t exist.

Given that only 12% of US adults are metabolically healthy,  it is more likely that an adult who dies of complications of COVID-19 and are said to have “no underlying health conditions” simply had not been  previously assessed for markers of metabolic health. If one is not assessed, they can’t be diagnosed.

Tested and everything is “fine”

Adults may be screened for risk of becoming diabetic using a fasting blood glucose test and when the results come back ‘normal’ they are told (or assume) that everything’s fine. But is it?

In a fasting blood glucose test, we only know what happens to blood sugar when the person is fasting — but if we don’t know what happens to their blood sugar between 30 minutes and 60 minutes after consuming a carbohydrate load, then we simply don’t know if they are at risk.

A glycated hemoglobin test (HbA1C) provides an estimate of average blood sugar over a 3-month period at all times (both fasted and after eating), and provides more information than only having a fasting blood glucose test. It will spot those that have overall higher-than-normal blood sugar, even if it is normal in the morning when they’ve been fasting.  However, even these two tests together will still miss a significant percentage of people who have normal blood sugar at fasting, and 2 hours after a carbohydrate load.

A 2-hour Oral Glucose Tolerance Test (OGTT) is usually only given to pregnant women and to those who already show abnormal fasting blood sugar and/or HbA1C and is considered the best way to determine if someone is at risk of becoming diabetic. It measures blood sugar at fasting and again 2-hours after a glucose load, but it will completely miss those who have significant blood sugar spikes between 30 minutes and 60 minutes, because it doesn’t measure it.

We know from research that a higher blood glucose peak >7.0 mmol/L (126 mg/dl), a delayed glucose peak >30 minutes), or blood sugar levels >7.0 mmol/L (126 mg/dl) at 30 minutes and >6.5 mmol/L (117 mg/dl) at one hour are all signs of insulin resistance and hyperinsulinemia, and correlate with higher insulin levels[2] — abnormal conditions outline in this previous article). If blood sugar 30 minutes and/or 60 minutes after a glucose load isn’t assessed, it can’t be assumed to be “fine”?

We also know from the research that if a person has a blood sugar spike >8.6 mmol/l (155 mg/dl) one-hour after a carbohydrate load that this is a better predictor of future diabetes, cardiovascular disease and death than a blood sugar reading of 7.8 mmol/l at 2 hours [3]. The problem is, a standard Oral Glucose Tolerance Tests doesn’t measure blood glucose except at baseline (fasting) and at two hours. It doesn’t look at blood sugar at 30 minutes and/or 1 hour. If it isn’t assessed then we simply don’t know.

Not tested – not fine

A large-scale 2016 study looked at the blood sugar responses and circulating insulin responses in almost 4000 men aged 20 years and older, and 3800 women aged 45 years or older found that while more than half (53%) had normal blood sugar at 2 hours after a standard glucose load, of these people 75% had abnormal blood sugar results between 30 minutes and 60 minutes[4]. This means that someone can have totally normal blood sugar levels 2-hours after a glucose load in a 2-hour Oral Glucose Tolerance Test and be presumed to be “fine”. The test doesn’t measure what happens to the person’s blood sugar at 30 minutes and/or one-hour, so we simply don’t know.
We can’t assume people have no underlying health conditions if we don’t assess it.

Three quarters of adults overweight or obese

New NHANES data released this week indicates that more than 73% of US adults are either overweight or obese[5].  Rates of overweight are so prevalent, that many people considered overweight ‘normal’, and only obesity and severe obesity as a problem. Just because something is common, does not make it normal.

Rates of overweight in men are going down, but this is not a good thing because rates of obesity are skyrocketing (see solid lines in the graph below)[5].

Rates of overweight in women are about the same as it was 20 years ago, but rates of obesity (see dashed lines in the graph above) are skyrocketing, and severe obesity is climbing too[5].
from Fryar C, et al “Prevalence of overweight, obesity, and severe obesity among adults aged 20 and over: United States, 1960–1962 through 2017–2018” NCHS Health E-Stats; 2020

People who are overweight have a BMI > 24.9, and those who are obese have a BMI > 29.9. Based on the latest data, almost three-quarters of US adults are overweight or obese, but BMI does not assess metabolic health, only weight to height ratio. BMI doesn’t tell us the whole story, as athletes who are very muscular may have a high BMI and those with normal BMI may be metabolically unhealthy.

People who are overweight or obese will have waist circumferences that are >40 inches (102 cm) for men, and >34.5 inches (88 cm) for women — and based on the definition above, this increased weight carried around their abdomen is what causes them to be considered metabolically unhealthy[1].   In addition, they often have high blood pressure, high fasting blood glucose and/or HbA1C, and may also have high triglyceride levels and/or low HDL cholesterol levels…and we haven’t even assessed what happens to their blood sugar 30 minutes or 60 minutes after a carbohydrate load!


Final thoughts…

America is a nation with underlying health conditions; only 12% of adults are metabolically healthy and only slightly more than a 1/4 have a normal body weight.

While Canada’s obesity rates were slightly better when last measured, how many Canadians have normal waist circumference — let alone normal blood pressure, normal fasting blood sugar, HbA1C or triglycerides or HDL cholesterol? In fact, how many people in either country even know what a healthy waist circumference is?

Until we realize that we are “sick”,  getting “well” is simply not possible.

More Info?

If you would like more information about restoring your weight and metabolic health, please send me a note using the Contact Me form on the tab above.

To your good health!

Joy

 

You can follow me on:

Twitter: https://twitter.com/JoyKiddie
Facebook: https://www.facebook.com/BetterByDesignNutrition/


References
  1. Araújo J, et al Prevalence of Optimal Metabolic Health in American Adults: National Health and Nutrition Examination Survey 2009–2016. Metabolic Syndrome and Related Disorders Vol 20, No. 20, pg 1-7, DOI: 10.1089/met.2018.0105
  2. Hulman A, Simmons RK, Vistisen D. et al. Heterogeneity in glucose response curves during an oral glucose tolerance test and associated cardiometabolic risk. Endocrine 55, 427–434 (2017). https://doi.org/10.1007/s12020-016-1126-z
  3. Pareek M, Bhatt DL, Nielsen ML, et al, Enhanced Predictive Capability of a 1-Hour Oral Glucose Tolerance Test: A Prospective Population-Based Cohort Study,
  4. Crofts, C., et al., Identifying hyperinsulinaemia in the absence of impaired glucose tolerance: An examination of the Kraft database. Diabetes Res Clin Pract, 2016. 118: p. 50-7.
  5. Fryar C, et al “Prevalence of overweight, obesity, and severe obesity among adults aged 20 and over: United States, 1960–1962 through 2017–2018” NCHS Health E-Stats; 2020.

Copyright ©2020 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 Difference Between Food Sensitivity Tests and Food Allergy Tests

One of the more frustrating things that I experience as a Dietitian who works with people with food allergy is when people come to me with a lab report listing foods they are ‘allergic’ to — only for me to get a multi-page report that they paid $650-750 out of pocket for, and which measures IgG antibodies, not the IgE antibodies which are associated with food allergy. These people paid good money to find out what foods underlie them not feeling well and received an impressive looking multi-page document that doesn’t measure what they think — or are led to believe it measures.

Our body makes different types of antibodies, including IgA antibodies, IgG antibodies, IgM antibodies, and IgE antibodies. IgA antibodies are found in high concentrations in the respiratory passages, as well as the GI tract and one of the best known IgA antibody tests is the IgA TTG test which tests for whether someone has celiac disease. IgM antibodies are found in the blood and lymphatic system and are found when our body is fighting a new infection. IgE and IgG antibodies are covered below.

Immunoglobin E (IgE)

IgE antibodies are produced by the immune system and are normally found in very small amounts in the blood. When someone has an allergy — whether to an environmental substance such as pollen from trees or grasses, or to food, the body overreacts and produces high amounts of specific allergen IgE antibodies.  What is important to know is that each type of IgE is specific to one type of allergen. When the IgE antibody binds with our mast cells, a type of white blood cell that is part of our immune system, they release histamine which causes us to have an allergic reaction, which may be sneezing, itching, difficulty breathing, or other symptoms [1].

When people have some types of environmental allergies such as to pollen from grass or trees, they might be prescribed antihistamines to calm that allergic reaction down. 

When people are diagnosed with food allergies, they are advised to avoid that food completely, which is often sufficient to avoid symptoms. Sometimes completely different foods that have proteins with similar amino acid sequences as the food they are allergic to cause them to have a “cross-reaction”. This is where the body recognizes the similar amino acid sequence as being the same as part of the amino acid sequence in food that they are allergic to (and to which they have IgE antibodies).  In some cases the body will react to this other food as if it is allergic, but it is usually it a lower level of a reaction that the food to which they have a full-blown reaction.  

When people have very serious food allergies, they are advised to carry an Epipen in the event they have a very serious reaction called anaphylaxis.  Anaphylaxis is a serious, life-threatening allergic reaction where a person’s immune system over-reacts to a specific allergen (such as insect sting, peanut or latex) and which results in difficulty breathing and a sudden drop in blood pressure. This requires immediate medical treatment, including a person (or someone else) administers an Epipen injection which contains epinephrine (adrenaline) to get them breathing, and then a visit to the emergency department of a local hospital.

Tests for food allergy always involve assessing the amount of IgE antibody response to a specific allergen or allergens — either by skin-scratch testing, or by a specific antigen IgE blood test.

Immunoglobin G (IgG)

IgG antibodies are found in our blood and other body fluids and recognize foreign proteins — including those from bacterial and viral infections.  These are the type of antibodies we are looking for when we’ve had an vaccine or immunization to diseases like chicken pox, or measles.

Our body also produces IgG antibodies in response to foods — and this is a normal response in a person with a healthy immune system.

Our body knows the difference between the proteins it makes, and the proteins contained in our food, so if we eat beef or a banana, our body will make IgG antibodies to the proteins in those foods. These IgG antibodies serve as a form of “memory” of our exposure to that food. Positive IgG antibodies to a food do NOT indicate a food allergy [2]. A positive IgG antibody response to a food means that our body as been exposed to that food recently and recognizes the protein in it.

Food Sensitivity / Food Allergy Testing

Sometimes, people have symptoms that make them feel unwell and they want to determine which foods, or food-components underlie their symptoms.

If the person goes to their doctor, they may be referred to an Allergist who will determine if they have IgE mediated antibodies to specific proteins in various food.  If they do, the person may be advised to avoid eating these foods, or if a potentially serious food allergy, to carry an Epipen. They may be advised to see a Dietitian that specializes in food allergies to help them know which foods are similar to the ones they are allergic to (i.e. cross reactants), so they can minimize their symptoms.

Sometimes the person will go to a Dietitian that is experienced with food allergy first — in an attempt to determine if they are allergic or sensitive to specific foods.  After taking a thorough history — including whether the person is allergic to certain trees which are known to cross-react with specific vegetables, fruit or nuts, the Dietitian may be recommended the person ask their doctor to requisition specific antigen IgE blood tests to determine of they are allergic to a food or tree pollen that is known to underlie Oral Allergy Syndrome. Oral Allergy Syndrome is where the body recognizes amino acid sequences in certain foods that are similar to the tree pollen(s) they have IgE antibodies to.

Note: Specific antigen IgE antibody testing is completely covered by provincial health insurance. In British Columbia, general practitioner MDs / family physicians can requisition up to 5 specific antigen IgE blood tests per year per patient.

If the specific antigen IgE blood test results come back positive, then the doctor may refer the person to an Allergist for further testing, and the Dietitian will teach them about avoiding foods they are allergic to, as well as their cross-reactants.

Alternative Food Sensitivity Testing – immunoglobin G (IgG)

Sometimes, instead of going to their doctor or to a Dietitian experienced with food allergies, people will sometimes seek out the help of a Naturopath. Typically, they will recommend “food sensitivity testing”, for which they charge between $650-$750. In this type of testing, the person will have their blood drawn and sent off to one of several labs that do this type of testing. The blood is exposed to different types of foods, and food components in a petri dish and the degree to which immunoglobin G (IgG) binds to each food is measured. The results are then printed off in a multi-page report that is given to the person by their Naturopath who explains that the positive results indicate the degree to which the person has an “allergy” or “sensitivity” to those foods [2]. The problem is, IgG antibodies only indicate that the person’s body recognizes that foodNOT that they are allergic or sensitized to the food.

Note: Only IgE antibodies assess true allergy — either by skin scratch testing, or specific allergen IgE blood tests.

These multi-page reports come in different formats, and here are a couple of examples (with names removed);

Based on these results, people will be advised by their Naturopaths which food(s) they should avoid.

Sometimes the person is provided with accompanying information which lists specific conditions that are supposedly associated with positive IgG antibodies, including weight gain, bloating, hyperactivity, depression, asthma, high blood pressure and others [1].

Alternative Food Sensitivity Testing – MSAS Food Sensitivity Testing, Kinesiology Muscle Testing

There are other types of alternate testing that are supposed to indicate whether a person is “sensitive” to a food. The procedure called MSAS Food Sensitivity testing uses a device which conducts an electrical current on acupuncture points (called meridian points) on the fingers and arm.

Here is an example of MSAS report:

MSAS Food Sensitivity Testing Results

One client of mine was told by their Naturopath that they were allergic to food if their arm went down when they were rubbed gently with the food, while holding their arms out by their sides. This technique is known as Kinesiology Muscle Testing (unaffiliated with the health science of Kinesiology).

Food intolerance

Food Intolerance is non-IgE mediated food sensitivity which usually involves a difficulty in digesting certain foods, and often involves a lack of a specific enzyme.

Lactose Intolerance is a well-known food intolerance in which a person can’t digest the sugar in milk because they have a shortage of the enzyme, lactase. Primary lactose intolerance is where a person doesn’t make enough lactase, and secondary lactose intolerance is where the person lacks lactase because they’ve had diarrhea which sloughed off the lactase enzyme which resides in the intestinal wall.

Tyramine Intolerance is also caused by a lack of an enzyme — in this case monoamine oxidase (MAO). As a result, levels of tyramine can build up, causing migraine, heart palpitations or GI issues, including nausea and vomiting.

As mentioned above in the section about IgE mediated allergy, histamine is released from mast cells and mediates allergic reactions. Histamine is produced by the body, along with an enzyme known as diamine oxidase (DAO). DAO is responsible for breaking down histamine that is made from foods you eat that contain histadine. Some people have a deficiency of DAO, which is called histamine intolerance. It may be secondary to a person having Mast Cell Activation Disorder (MCAD), or due to some other cause, such as certain medications that cause them not to be able to break down histamine properly. In such cases, limiting foods that are high in histadine — which gets converted to histamine can be helpful, or by limiting foods that trigger histamine release from mast cells.

If You Think You May Be Allergic 

If you think you may be allergic to certain foods, or that some of the food you are eating may underlie specific symptoms you are experiencing, then go see your doctor and seek the help of  a Dietitian that specializes in food allergy and sensitivity.

The first step would be to rule out genuine food allergy, which is IgE antibody mediated. This can be done by scratch tests from an Allergist or by specific allergen IgE tests (both types of tests are covered by provincial health insurance). If you have food allergies, then the Dietitian will teach you how to avoid those foods, and how to watch out for cross-reacting foods.

If you don’t have food allergies, then the Dietitian can assist you in identifying which foods are making you feel unwell, then by recommending an appropriate approach once the specific foods, or food components are identified. For some, this may mean avoiding the food, but often times it is a matter of eating less of the food at a time, or eating it less often. Each person is different.

More Info?

If you think you may have food allergies or sensitivities, I offer a package called the Food Sensitivity Food Allergy Package which walks people through the process mentioned above.

If you have questions please send me a note through the Contact Me form on the tab above.

To your good health!

Joy

You can follow me on:

Twitter: https://twitter.com/JoyKiddie
Facebook: https://www.facebook.com/BetterByDesignNutrition/

References

  1. American Academy of Allergy, Asthma and Immunology, Immunoglobin E (IgE)  definition, https://www.aaaai.org/conditions-and-treatments/conditions-dictionary/immunoglobulin-e-(ige)
  2. American College of Allergy, Asthma and Immunology (ACAAI), Can IgG blood testing check for delayed food allergies?https://acaai.org/resources/connect/ask-allergist/can-igg-blood-testing-check-delayed-food-allergies
  3. Lavine E. Blood testing for sensitivity, allergy or intolerance to food. CMAJ. 2012;184(6):666-668. doi:10.1503/cmaj.110026

Copyright ©2020 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.

Stages of Change and Why Most People Regain Weight Loss

Studies have found that more than half of weight loss is regained within two years and by five years, more than 80% of weight loss is regained [1]. In fact, people who have had previous failed attempts at maintaining their weight-loss often believe that weight loss is a futile endeavor[2], so why bother even trying to change?

There are lots of different reasons why people seek weight loss and in my experience it is much less about how people feel about how they look, than their health.  People already know that they need to lose weight to lower high blood sugar and high blood pressure (hypertension), but the last few months there is a greater sense of urgency due to recent studies which indicate that people requiring hospitalization for Covid-19 had one or more of these underlying conditions. But where to start?

Some people think that all they need to do is “make up their mind” to change and they will, yet in most cases these same people have “made up their minds” multiple times — lost weight, and then put it all back and then some.

Change is not a state of mind, but a process.

The Stages of Change model was developed in 1979 by James Prochaska [3] and expanded on by Prochaska, Norcross and DiClemente in a 1994 book titled Changing for Good: a Revolutionary Six-Stage Program for Overcoming Bad Habits and Moving Your Life Positively Forward.

The Stages of Change are Precontemplation, Contemplation, Preparation, Action, Maintenance and Relapse.

They were originally seen as five stages (with Preparation and Action forming one stage) but are now seen as six distinct stages.

The Six Stages of Change

  1. Precontemplation – in this stage, people are just beginning to see that there is a problem, but not necessarily what it is. Oftentimes, people see the problem as being something outside of their control, or the result of someone- or something else. They may be experiencing negative consequences related to their behaviour, but don’t see the problem as being serious enough to motivate them to changing it.
  2. Contemplation – in this stage, the person realizes that the behaviour is problematic for them, but they have mixed feelings. They have a desire for the situation to change, but are not ready to commit to making changes.
  3. Preparation – in this stage, the person still has some mixed feelings about the problem, but begins to make plans to take action within a specific amount of time (usually a few weeks). At this point, most people have weighed the positive versus negative consequences of not changing their behavior and have concluded that the negative aspects outweigh any benefits they perceive their current behavior brings them, and are coming up with a plan to support their success.
  4. Action – at this stage, the person is actively involved in changing their behaviour and carrying out their plan to support their success.
  5. Maintenance – at this stage, people are consolidating what they’ve accomplished during the action stage. TA person can remain in this stage for an extended periods of time — with an adequate support system in place.
  6. Relapse – the person falls back (lapses) into their former pattern of behaviour. Some people start the process of change over again after a brief “slip”, while others continue in their lapsed behaviour patterns.

Is Relapse Inevitable?

The standard model sees relapse as part of the stages of change, and to a certain extent, it is.  No one perfectly maintains their goal weight, or their goal blood sugars or blood pressure. For some, a lapse may be eating a meal or a dessert that isn’t part of their plan, but then the next day they are “back on track”. For others, eating a meal or a dessert results in them feeling like a failure. They feel like since they’ve “already blown it”, so they might as well “go for it” and eat all the things they want.

I believe that what makes the difference between those that “slip” and then relapse and those that “slip” and get back on track is having a long-term plan for maintenance.

A Long-Term Plan for Maintenance

Just as one contemplates their plan for weight loss, then prepares to execute that plan, and takes action to carry out that plan — to be successful long term requires not only having a plan in place to support successful weight loss, but also having a plan for maintenance in place for afterwards.

Understanding what contributed to gaining weight in the first place often helps people come up with a successful plan both to lose weight, as well as a long-term plan for weight maintenance. Each person needs to find what is an appropriate plan for them.

For some, that might be an accountability partner, for others it may be support and follow-up with a Dietitian, and for others it may be getting support for a larger issue such as food addiction at a 12-step support group or addictions counsellor.

It doesn’t have to be a “vicious cycle”!

If a person was driven to eat due to high cortisol and insulin levels, then having a plan in place to keep those in check after they’ve reached their goal weight will enable them to maintain their weight loss long term.

If they came to realize that they meet many of the 11 DSM (Diagnostic and Statistical Manual) criteria for substance abuse disorder related to specific foods or food in general, then seeking support of a food addictions counsellor would be worth exploring.

If they realize that they mainly eat when they are angry, lonely, tired or stressed then coming up with healthier alternative behaviours to do instead, might be part of what would enable them to achieve and maintain long-term weight loss, or by working through some of those underlying issues with a counsellor.

A 2018 paper by Hall and Kahan titled Maintenance of Lost Weight and Long-Term Management of Obesity put it well:

“Treatment of obesity requires ongoing attention and support, and weight maintenance-specific counseling, to improve long-term weight management.” [4]

I support my clients with services through all stages of change — from the SMART goal setting session, to the Complete Assessment Package, and the Dietary Management Package and refer to others with expertise in counselling or food addiction, as appropriate.

I want you to be part of the 20% that are able to maintain your weight loss to five years and beyond, and I believe that it is entirely “doable” with good planning and appropriate support.

More Info?

If you would like more information about the different types of low carb or ketogenic diets I teach, please send me a note using the Contact Me form on the tab above.

To your good health!

Joy

You can follow me on:

Twitter: https://twitter.com/JoyKiddie
Facebook: https://www.facebook.com/BetterByDesignNutrition/

Reference

  1. Anderson JW, Konz EC, Frederich RC, Wood CL. Long-term weight-loss maintenance: a meta-analysis of US studies. Am J Clin Nutr. 2001;74(5):579–584.
  2. Mann T, Tomiyama AJ, Westling E, Lew AM, Samuels B, Chatman J. Medicare’s search for effective obesity treatments: diets are not the answer. The American psychologist. 2007;62(3):220–233.
  3. Prochaska, J. O., & DiClemente, C. C. (1982). Transtheoretical therapy: Toward a more integrative model of change. Psychotherapy: Theory, Research & Practice, 19(3), 276–288. https://doi.org/10.1037/h0088437
  4. Hall KD, Kahan S. Maintenance of Lost Weight and Long-Term Management of Obesity. Med Clin North Am. 2018;102(1):183-197. doi:10.1016/j.mcna.2017.08.012

 

Copyright ©2020 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.

Is a Diet High in Carbohydrate Appropriate for Humans?

This post comes out of some recent lively discussion on social media where I was challenged to re-consider my position that a low carbohydrate or very low carbohydrate (keto) diet can put people into remission of type 2 diabetes (T2D), but does not reverse it, and is not a cure. The discussion centred around whether some metabolic diseases such as T2D may come about as the result of us eating a diet that humans have not evolved to see, and whether eating a species-appropriate diet could be viewed as “curative”.


Back in 2018, I wrote my first article on the topic of whether a low carbohydrate diet actually “cures” type 2 diabetes, or puts it into remission.  In that article, titled The Difference Between Reversal and Remission of Type 2 Diabetes I wrote;

“Reversal” of a disease implies that whatever was causing it is now gone and is synonymous with using the term “cured”. In the case of someone with Type 2 Diabetes, reversal would mean that the person can now eat a standard diet and still maintain normal blood sugar levels. But does that actually occur? Or are blood sugar levels normal only while eating a diet that is appropriate for someone who is Diabetic, such as a low carbohydrate or ketogenic diet, or while taking medications such as Metformin? If blood sugar is only normal while eating a therapeutic diet or taking medication then this is not reversal of the disease process, but remission of symptoms.”

I argued that since type 2 diabetes is the result of beta cell failure, for someone to indeed be “cured”, there would need to be evidence of a restoration of beta cell function. 

In that article, I explained how in 2009 the American Diabetes Association defined the terms partial remission, complete remission and prolonged remission as follows;

  • Partial remission is having blood sugar that does not meet the classification for Type 2 Diabetes; i.e. either HbA1C < 6.5% and/or fasting blood glucose 5.5 – 6.9 mmol/l (100–125 mg/dl) for at least 1 year while not taking any medications to lower blood glucose.
  • Complete remission is a return to normal glucose values i.e. HbA1C <6.0%, and/or fasting blood glucose < 5.6 mmol/L (100 mg/dl) for at least 1 year while not taking any medications to lower blood glucose.
  • Prolonged remission is a return to normal glucose values (i.e. HbA1C  <6.0%, and/or fasting blood glucose < 5.6 mmol/L (100 mg/dl) for at least 5 years while not taking any medications to lower blood glucose.

Different studies, including those from the DiRECT diabetes remission trial and Virta Health define remission differently. The DiRECT diabetes remission trial defines remission as having a HbA1C below 6.5%, which is the cut-off for a type 2 diabetes diagnosis, as well as discontinuation of all diabetes medications for at least two months [1].  Virta Health, on the other hand defines remission in their studies as a HbA1C < 6.5% and fasting blood glucose ≤ 5.5 (100 mg/dl) while taking no medication, il with the exception of Metformin (or generic equivalent) [2].

There are 3 ways that are known for people to achieve remission of type 2 diabetes symptoms and these are;

  1. a low calorie energy deficit diet [1,3,4]
  2. bariatric surgery (especially use of the roux en Y procedure) [5,6]
  3. a ketogenic diet [2]

…but in each of these cases, we are defining remission in terms of the disease state and based on lab standards for defining normal cut-off values. That is, remission is defined as having normal fasting blood sugar and/or HbA1C, that are below the cut-off points for the disease, based on current diet.

This past weekend, I was appropriately challenged by someone on Twitter who said that this logic is flawed, because it assumes that the diet causing the disease is somehow natural. That is, if the diet causing the disease is unnatural, then couldn’t the natural diet indeed be viewed as curative?

I agreed to ponder this — and in fact, gave a great deal of thought to it. Several things came to mind that reinforced the idea that a high carbohydrate diet is not a “natural” human diet, and may not be appropriate for humans.

Human’s Evolutionary Diet

Over the course of man’s existence, there have been a number of major shifts in the human diet and with that change came the necessity of the body to adapt by producing enzymes capable of digesting and absorbing nutrients from these novel foods. This required the human genome (our genes) to adapt, evolve and change, and this type of adaptation takes a great deal of time [8].

There is good evidence for use of human-controlled fires which would have given us the ability to cook our meat, but is only about 800,000 years old [9] with less certain sites dating back 1,500,000 years [10,11].

The origin of domestication of animals is considered to be ~10,000 – 12,000 years and represents a relatively recent shift in the human diet — moving humans from being a hunter-gatherer species, to being an agricultural species [8]. The innovation of human agriculture not only greatly reduced diversity in the human diet, it resulted in an estimated 50%–70% of calories coming from starch (carbohydrates) [12].

According to Dr. Donald Layman, Professor Emeritus from the University of Illinois, looking at it from the perspective of man’s evolutionary history, the appearance of a diet centered around carbohydrates is very recent [9]. According to Dr. Layman, cereal grains as food were non-existent in the human evolutionary diet, and the same with legumes, such as chickpeas and lentils [13]. As well, refined sugar made up of sucrose was also non-existent in the evolutionary diet. While humans would eat wild fruit, these contained a fraction of the digestible carbohydrate content of domesticated fruitOn the rare occasion when humans came across a beehive and would eat honey (which is half glucose, half fructose), the idea of a diet high in sucrose and fructose was simply non-existent. According to Dr. Layman, consumption of dairy products and alcohol are also very recent in terms of human history [13]. We didn’t milk wild animals, we ate them and fermentation of fruit for wine is also very recent in terms of the evolutionary diet [13]. According to Dr. Layman if we look at contemporary agriculture, what has fundamentally changed is that these foods were totally non-existent in the history of man’s diet previous to the agricultural revolutionHumans did not evolve to see cereal grains, legumes, refined sugar, dairy foods and alcohol as human food and all of these are very rich in carbohydrate.  Interestingly, Dr. Layman stressed that the human body responds to dietary carbohydrate as if it were highly toxic, and that it must be rapidly cleared after eating in order for our body to maintain blood sugar within the very narrow range between 3.3-5.5 mmol/L (60-100 mg/dl).

Why would our body react this way?

According to Dr. Layman, over the span of human history we have developed very extensive and elaborate patterns for handling protein; for digesting and metabolizing it and have also developed a very high ‘satiety’ (feeling full) in response to eating protein, and that it is the only macronutrient that provides sufficiently strong feedback such that we can’t over eat it. He said that fat is a very passive nutrient and has very little direct effect on our body. We store it effectively and this ability to store excess intake as fat is what enabled us to survive as hunter-gatherers, but according to Dr. Layman, the macronutrient that is at odds in this picture is carbohydrate, simply because humans did not evolved to eat large amounts of carbohydrate.

Could it be that the diet that underlies metabolic disease like type 2 diabetes be one that is unnatural for humans? We certainly did not evolve to eat 300 grams of carbohydrate per day!

As I was contemplating this idea, I suddenly remembered seeing a video clip about a year or so ago that was mind-blowing to me at the time. It was of Dr. Walter Willett, Professor of Epidemiology and Nutrition at Harvard School of Public Health and a well-known advocate for diets very low in animal protein and high in carbohydrate (including the recent EAT-Lancet diet [14,15]) saying something along the lines that it is not the eating of dietary fat that makes people fat, but eating lots of carbohydrate.

Here is verbatim what Dr. Willett said;

 “There had been part of a belief that fat in the diet is what makes you fat and I even had colleagues who said that you can’t get fat eating carbohydrates because the body can’t convert carbohydrates to fat. I grew up in Michigan in a rural community and I can tell you that farmers have known for thousands of years if you want to fatten an animal a lot, what you feed them is grains, high carbohydrate diets, and you put them in a pen so they don’t run around and they get fat very predictably… most recent literature showed very clearly, you can really do randomized trials looking at weight change because you need just a hundred or few hundred people and you don’t need decades; you need a year or two and it’s very clear from those randomized trials that low-fat diets…ummm… fat is really not determinant of body weight. The percentage of calories from fat in the diet is not a determinant. In fact, lot of evidence suggesting it is easier for many people to get fat on a low-fat high carbohydrate diets. If anything, that’s what the literature is suggesting. So, it is interesting that fat in the diet just has almost nothing to do with fat in the body. We can get very fat on just lots and lots of carbohydrates.”

Lest anyone think I am taking the video clip out of context, here is the link to the full video from Willett’s keynote lecture from the 2012 Annual Advances in Cancer Prevention Lecture of July 25, 2012. The question and answer period which contains the clip above, begins 49 minutes into the full-length video.

So, it is well-known that eating lots and lots of carbohydrate can make pigs fat, and pigs are used in many research settings because of their similarities to humans. Is it not reasonable to deduce that humans eating lots and lots of carbohydrate can also make us fat?

But it’s not only are cereal grains and legumes that are relatively new in the human diet as food, but so are the oils extracted from cereal grains and seed, such as soybean oil and canola and that are in almost every manufactured food we eat.   

(I’ve previously written about concerns with these seed oils known as “polyunsaturated vegetable oils” in a two-part article from mid-2018 that can be read here and here.)

We, as humans have not evolved to eat these as food — and not only to eat them as food, but to eat them in HUGE quantities!

A study published in November 2018 in Metabolic Syndrome and Related Disorders reported that 88% of Americans are already metabolically unhealthy. That is, only 12% have metabolic health defined as have levels of metabolic markers “consistent with a high level of health and low risk of impending cardiometabolic disease“[16].

Metabolic Health is defined as ;

Waist Circumference: < 102 cm (40 inches) for men and 88 cm (34.5 inches) in women
Systolic Blood Pressure: < 120 mmHG
Diastolic Blood Pressure: < 80 mmHG
Glucose: < 5.5 mmol/L (100 mg/dL)
HbA1c: < 5.7%
Triglycerides: < 1.7 mmol/l (< 150 mg/dL)
HDL cholesterol: ≥ 1.00 mmol/L (≥40 mg/dL) in men and ≥ 1.30 mmol/L (50 mg/dl) in women

When looking at only 3 of the above 7 factors (waist circumference, blood glucose levels and blood pressure) more than 50% of Americans were considered metabolically unhealthy [16].

Given the slightly lower rates of obesity in Canada [17] as in the United States [18], presumably there is a slightly lower percentage of Canadians who are metabolically unhealthy, but the similarity of our diets may make that difference insignificant — which begs the question: what is it about our diet that results in 3/4 of us being metabolically unhealthy?

I believe the answer has something to do with the amount of refined carbs and refined fat that we eat together — something that was not part of our evolutionary history, and something that is now known to be irresistible.

Maybe the logic behind thinking about “remission” from diseases such as type 2 diabetes IS flawed because it DOES assume that our current human diet is “natural”. Genetic adaptation to dietary changes takes time, and in the context of human evolution, the foods that we eat so much of are relatively new.

Given this, is it not possible that some of the metabolic disease we as humans are facing in ever-increasing numbers might be related to us eating a diet that is not a natural human diet?

Could it be that consuming a diet that humans evolved to eat — and which reverses the symptoms associated with some metabolic diseases be indeed viewed as “curative”?

Definitely food for thought!

More Info?

If you would like more information about the different types of low carb or ketogenic diets I teach, please send me a note using the Contact Me form on the tab above.

To your good health!

Joy

You can follow me on:

Twitter: https://twitter.com/JoyKiddie
Facebook: https://www.facebook.com/BetterByDesignNutrition/

Reference

  1. Lean ME, Leslie WS, Barnes AC, et al. Primary care-led weight management for remission of type 2 diabetes (DiRECT): an open-label, cluster-randomised trial.  Lancet. 2018 Feb 10;391(10120):541-551. doi: 10.1016/S0140-6736(17)33102-1.
  2. Athinarayanan SJ, Adams RN, Hallberg SJ et al, Long-Term Effects of a Novel Continuous Remote Care Intervention Including Nutritional Ketosis for the Management of Type 2 Diabetes: A 2-year Non-randomized Clinical Trial.  preprint first posted online Nov. 28, 2018;doi: http://dx.doi.org/10.1101/476275.
  3. Lim EL, Hollingsworth KG, Aribisala BS, Chen MJ, Mathers JC, Taylor R. Reversal of type 2 diabetes: normalisation of beta cell function in association with decreased pancreas and liver triacylglycerol. Diabetologia2011;54:2506-14. doi:10.1007/s00125-011-2204-7 pmid:21656330
  4. Steven S, Hollingsworth KG, Al-Mrabeh A, et al. Very low-calorie diet and 6 months of weight stability in type 2 diabetes: pathophysiological changes in responders and nonresponders. Diabetes Care2016;39:808-15. doi:10.2337/dc15-1942 pmid:2700205
  5. Cummings DE, Rubino F (2018) Metabolic surgery for the treatment of type 2 diabetes in obese individuals. Diabetologia 61(2):257–264.
  6. Madsen, L.R., Baggesen, L.M., Richelsen, B. et al. Effect of Roux-en-Y gastric bypass surgery on diabetes remission and complications in individuals with type 2 diabetes: a Danish population-based matched cohort study, Diabetologia (2019) 62: 611. https://doi.org/10.1007/s00125-019-4816-2
  7. Evert, AB, Dennison M, Gardner CD, et al, Nutrition Therapy for Adults With Diabetes or Prediabetes: A Consensus Report, Diabetes Care, Ahead of Print, published online April 18, 2019, https://doi.org/10.2337/dci19-0014
  8. Luca F, Perry GH, Di Rienzo A. Evolutionary Adaptations to Dietary Changes. Annual review of nutrition. 2010;30:291-314. doi:10.1146/annurev-nutr-080508-141048.
  9. Goren-Inbar N, Alperson N, Kislev ME, Simchoni O, Melamed Y, et al. Evidence of hominin control of fire at Gesher Benot Ya’aqov, Israel.  Science.  2004;304:725–727
  10. Brain CK, Sillent A. Evidence from the Swartkrans cave for the earliest use of fire. Nature. 1988;336:464–466.
  11. Evidence for the use of fire at Zhoukoudian, China Weiner S, Xu Q, Goldberg P, Liu J, Bar-Yosef O Science. 1998 Jul 10; 281(5374):251-3.
  12. Copeland L, Blazek J, Salman H, Chiming Tang M. Form and functionality of starch. Food Hydrocolloids. 2009;23:1527–1534
  13. Layman, Donald, The Evolving Role of Dietary Protein in Adult Health, Nutrition Forum, British Columbia, Canada, June 23, 2013 https://youtu.be/4KlLmxPDTuQ
  14. The EAT-Lancet Commission on Food, Planet and Health,  https://eatforum.org/eat-lancet-commission/
  15. The EAT-Lancet Commission on Food, Planet and Health – EAT-Lancet Commission Brief for Healthcare Professionals,  https://eatforum.org/lancet-commission/healthcare-professionals/
  16. Araújo J, Cai J, Stevens J. Prevalence of Optimal Metabolic Health in American Adults: National Health and Nutrition Examination Survey 2009–2016. Metabolic Syndrome and Related Disorders Vol 20, No. 20, pg 1-7, DOI: 10.1089/met.2018.0105
  17. Statistics Canada, Health at a Glance, Adjusting the scales: Obesity in the Canadian population after correcting for respondent bias,  https://www150.statcan.gc.ca/n1/pub/82-624-x/2014001/article/11922-eng.htm
  18. State of Obesity, Adult Obesity in the United States, https://stateofobesity.org/adult-obesity/

 

Copyright ©2020 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.

Another Therapeutic Ketogenic Diet and How it Differs from “the Keto Diet”

In addition to the several types of therapeutic ketogenic diets mentioned in the previous post, such as the Classic Ketogenic Diet (KD), the Modified  Ketogenic Diet (MKD) and the Modified Atkins Diet (MAD) used in the treatment of epilepsy and seizure disorder and as adjunct treatment in glioblastoma, there is another type of therapeutic ketogenic diet used in the treatment of type 2 diabetes and for weight loss which is referred to in the literature as a Very Low Carbohydrate Diet (VLCD). This post outlines two examples of this type of therapeutic ketogenic diet, and how it differs considerably from the popularized “keto diet”.

When compared with a Very Low Carbohydrate Diet (VLCD), the popularized “keto diet” which focuses on high intake of eggs and fatty cuts along with copious amounts of added fat in the form of ‘fat bombs’ and ‘bulletproof coffee’ is like a caricature compared with a portrait.  A portrait seeks to accurately represent physical attributes, and a caricature uses hyperbole to exaggerate some, and over-simplify others. 

This new article picks up from the previous one in outlining another type of therapeutic ketogenic diet used for putting type 2 diabetes into remission as well as for weight loss, and how it is very different from the popularized “keto diet”.


A Therapeutic Ketogenic Diet

A ketogenic diet is one that induces and sustains a state of ketosis which is a natural metabolic state where the body burns fat as its primary fuel, rather than carbohydrate. What makes any diet ketogenic is not how much fat it contains, but the amount of carbohydrate it contains.

In reference to the treatment of type 2 diabetes and obesity, ketogenic diets are often referred to in the literature as a “Very Low Carbohydrate Dies (VLCD)”, which is where carbohydrate intake is limited to 20-50 g per day or 10% of total energy intake[1]. It is this low carbohydrate intake that results in the body using fat as its primary fuel, rather than carbohydrate and at this very low level of carbohydrate intake, blood ketone levels increase at or above 0.5 mmol/L, resulting in ketosis.

Ketosis is where the ketone betahydroxybutyrate (BHB) reaches levels between 0.5 – 3.0 mmol/L (and up to 4.0 mmol/L for therapeutic ketogenic diets  used in the treatment of epilepsy, seizure disorder and glioblastoma). In a Very Low Carbohydrate Diet (VLCD) used in the treatment of type 2 diabetes, BHB levels are usually set between 1.5-3.0 mmol/L, a level described as nutritional ketosis [2].

A drug or diet is said to be therapeutic when it is used in the treatment of a disease or medical condition(s). When implemented by a Dietitian, a therapeutic diet is referred to as Medical Nutrition Therapy (MNT) [3].

Use of a Very Low Carbohydrate Diet (VLCD) as Medical Nutrition Therapy in the treatment of type 2 diabetes is recognized by numerous organizations around the world, including the European Association for the Study of Diabetes (EASD).

The American Diabetes Association has stated that reducing carb intake has the most evidence for improving blood sugar and has included both a low carbohydrate (LC) and very low carbohydrate (VLC) eating pattern for treating type 2 diabetes as listed in their 2019 Consensus Report, and has included both in their 2019 Standards of Medical Care in Diabetes (2019) and Standards of Medical Care in Diabetes (2020).  This year,  Diabetes Canada released a Position Statement outlining that a low carbohydrate (LC) and very low carbohydrate diet (VLCD) are both safe and effective treatment for non-pregnant or lactating adults with type 2 diabetes.

The American Diabetes Association’s  Consensus Report defines low carbohydrate and very low carbohydrate as follows;

“In this review, a low carbohydrate (LC) eating patterns is defined as reducing carbohydrates to 26-45% of total calories [4].”

and

“In this review a very low carbohydrate (VLC) eating pattern is defined as reducing carbohydrate to <26% of total calories [4].”

Diabetes Canada also defines low carbohydrate and very low carbohydrate diets in terms of the amount of carbohydrate the diet contains. Low carbohydrate diets are defined as less than <130 g of carbohydrate per day or <45% energy as carbohydrate,  and very low carbohydrate diets as <50 g of carbohydrate per day [5].

Very Low Carbohydrate Diet (VLCD) for Treatment of Type 2 Diabetes

Back in 2018, the American Diabetes Association cited Virta Health’s one-year study data [6] as evidence for the safety and efficacy of a Very Low Carbohydrate Diet (VLCHD) in lowering blood sugar and diabetes medication usage and the new Diabetes Canada’s recommendations refers to the same study. As a result, Virta Health’s study is a good place for defining what a Very Low Carbohydrate Diet (VLCD) for the treatment of type 2 diabetes looks like.

Note: It should be noted that at the time the ADA’s 2019 Standards of Medical Care in Diabetes was published, Virta Health’s 2-year data had not yet been published, so the ADA and in turn, Diabetes Canada recommendations which were based on it, as well as other international organizations support for low and very low carbohydrate diets were only able to say conclusively that low carbohydrate diets and very low carbohydrate diets were safe and effective both in managing weight, as well as lowering glycated hemoglobin (HbA1C) in people with type 2 diabetes over the short term (<3 months). 

Virta Health’s Approach

As covered in this article on my affiliate site about Virta Health’s 2-year update and in this article with their 1-year update , subjects in their studies typically ate;

  1. <30 g per day of total dietary carbohydrate
  2. daily protein intake was targeted to a level of 1.5 g / kg based on ideal body weight
  3. Participants were coached to incorporate dietary fats until they were no longer hungry (i.e. to satiety)

Note (August 31, 2020): To put the protein requirements in perspective, a male whose ideal body weight is 150 pounds (68 kg) would be eating over 100 g of protein per day and a female whose ideal body weight is 135 pounds (61 kg) would be eating 92 g of protein per day.  That is, protein is targeted for its nutrient-density and satiety, and fat is incorporated only until satiety is reached.

Phinney and Volek’s Approach

Dr. Stephen Phinney MD, PhD, a medical doctor and Dr. Jeff Volek, RD, PhD a Registered Dietitian with a PhD have decades of combined scientific and clinic research experience in the area of low carbohydrate diets. In 2011 they published their expert guide titled The Art and Science of Low Carbohydrate Living [7] documenting the clinical benefits of carbohydrate restriction and how it can be used for weight loss.

In Phinney and Volek’s book [7], the Very Low Carbohydrate Diet (VLCD) outlined is one that is higher protein during the weight loss phase than during the weight maintenance stage, with ~30% of caloric intake coming from protein during weight loss, but which decreases to ~21% of caloric intake during weight maintenance. Fat is 60% of calories during the weight loss phase, and is increased to 65-72% during weight maintenance. Carbohydrate intake is kept very low (7.5-10% of calories for men, 2.5-6.5% of calories for women) in order to induce nutritional ketosis.

The reason dietary fat intake is lower during the weight loss phase in Phinney and Volek’s approach is to allow for the using of body fat stores for energy.

In Phinney and Volek’s approach;

  1. Carbohydrate intake is 7.5-10% of calories for men, 2.5-6.5% of calories for women
  2. Protein intake is up to 30% of calories during weight loss, 21% during weight maintenance
  3. Fat is 60% of calories during weight loss, 65-72% of calories during weight maintenance

Note (August 31, 2020): Protein intake for someone eating 2000 kcals per day is 150 g and for someone eating 1700 kcals per day is 141 g per day. Again, protein is targeted for its nutrient-density and satiety, and fat is only 60% of calories during weight loss.  This is very different than the popularized “keto diet”.

Popularized “Keto Diet”

The popularized “keto diet” is described as 70 – 80% fat, 15-20% protein* and 5% carbohydrate, with websites and articles promoting it frequently show plates laden with bacon and eggs, large fatty steaks with added butter melting on top, and loads of whipping cream over berries, and lots of avocado.

*while many “keto” proponents still stick with the lower protein intake [8], others have more recently increased the protein macro to 20% of calories, with fat at 70%.

This popularized “keto diet” is not the Very Low Carbohydrate Diet (VLCD) used by either Virta Health for putting type 2 diabetes into remission, or the VLCD approach used by Phinney and Volek for weight loss.

The popularized “keto diet” has ~50% less protein than a Very Low Carbohydrate Diet (VLCD) and ~20% more fat which has twice the energy density as protein.

Furthermore, the popularized “keto diet” is a very high fat, very low carbohydrate diet and is often promoted along with periods of intermittent fasting (IF), as frequent periods of less than 24 hours, or longer fasting periods which may include 5:2 (5 days of normal diet, 2 days restricting total calories to 500 per day), alternate day fasting, 36 hour fasts, or 42 hour fasts. This approach may suit some, but one has to ask if only eating ~1/3 of the time, is any weight loss really due to eating super high fat all the time, or due to the periods of fasting?

Like a caricature, the “keto diet” exaggerates some aspects of a Very Low Carbohydrate Diet (VLCD) and over-simplifies others. It exaggerates the fallacy that one needs to add extra fat into everything in order to lose weight, and overlooks the satiety of protein.

[Personal note: Approximately 1/3 of clients come to me for support after having followed this popularized “keto diet” without the fasting, and having failed to lose more than a bit of weight initially, or having gained weight.] 

Final Thoughts

There is no one-sized-fits-all low carb or ketogenic diet for weight loss, because each person’s nutrition needs are different. As covered in the preceding article, for those seeking safe and effective weight loss, there are a range of low carbohydrate diets available to choose from, with some that includes periods of ketosis, and others that don’t.

For those seeking to put type 2 diabetes into remission, a well-designed ketogenic diet using the Virta Health approach, or for weight-loss using Phinney and Volek’s approach are both safe and effective, if individualized for each person and done with adequate oversight. 

Remember, if you are taking any medication for type 2 diabetes, please read this article for why it can be dangerous to begin a very low carbohydrate diet (VLCD) / ketogenic diet without the involvement of your diabetes team.

More Info?

If you would like more information about type of low carb or ketogenic diet that might be best suited to you, please send me a note using the Contact Me form on the tab above.

To your good health!

Joy

You can follow me on:

Twitter: https://twitter.com/JoyKiddie
Facebook: https://www.facebook.com/BetterByDesignNutrition/

References

  1. Feinman RD, Pogozelski WK, Astrup A, Bernstein RK, Fine EJ,Westman EC, et al. Dietary Carbohydrate Restriction as the First Approach in Diabetes Management: critical review and evidence base. Nutrition. 2015;31(1):1–13
  2. Nasir H. Bhanpuri, Sarah J. Hallberg, Paul T. Williams et al, Cardiovascular disease risk factor responses to a type 2 diabetes care model including nutritional ketosis induced by sustained carbohydrate restriction at 1 year: an open label, non-randomized, controlled study, Cardiovascular Diabetology, 2018, 17(56)
  3. U.S. Department of Health and Human ServicesFinal MNT regulationsCMS-1169-FCFederal Register1 November 200142 CFR Parts 405, 410, 411, 414, and 415
  4. Evert, AB, Dennison M, Gardner CD, et al, Nutrition Therapy for Adults With Diabetes or Prediabetes: A Consensus Report, Diabetes Care, Ahead of Print, published online April 18, 2019, https://doi.org/10.2337/dci19-0014
  5. Diabetes Canada, Diabetes Canada Position Statement on Low Carbohydrate
    Diets for Adults with Diabetes: A Rapid Review Canadian Journal of Diabetes (2020), doi: https://doi.org/10.1016/j.jcjd.2020.04.001.
  6. Hallberg SJ, McKenzie AL, Williams PT, et al. Effectiveness and safety of a novel care model for the management of type 2 diabetes at 1 year: an  open-label, non-randomized, controlled study. Diabetes Ther 2018;9:583–612
  7. Volek JS, Phinney SD, The Art and Science of Low Carbohydrate Living: An Expert Guide, Beyond Obesity, 2011
  8. Zoe Harcombe, LCHF and Butter, January 29, 2018, https://www.zoeharcombe.com/2018/01/lchf-and-butter/

Copyright ©2020 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 Stereotypical High Fat Keto Diet is Only ONE Type

There is a common, but mistaken belief that there is such as thing as “THE keto diet” (singular) — which is high in fat of all types, including cream, butter, bacon, avocado and fatty cuts of meat. In fact, there are a wide range of “keto diets” (plural) — including several different therapeutic ones, as well as those that have been popularized the last several years for weight loss.  This article will explains the range of ketogenic diets that are available, and what they are used for as well as the unintended consequence of believing that a “keto diet” has to be high in fat.

What is a Ketogenic Diet?

A ketogenic diet is one that induces and sustains a state of ketosis, which is a natural metabolic state where the body burns fat as its primary fuel, rather than carbohydrate.

There are a number of different therapeutic ketogenic diets, as well as a number of weight-loss ketogenic diets

What makes any diet ketogenic is not how much fat it contains, but the amount of carbohydrate it contains.

This bears repeating.

A ketogenic diet is determined solely on the basis of how much carbohydrate it contains, and not on how much fat in contains.

Ketogenic diets, which are also referred to in the literature as “very low carbohydrate diets” are where carbohydrate intake is limited to 20-50 g per day or 10% of total energy intake [1].  It is this low carbohydrate intake that results in the body using fat as its primary fuel, rather than carbohydrate and at this very low level of carbohydrate intake, blood ketone levels increase at or above 0.5 mmol/L, resulting in ketosis. 

Ketosis is where the ketone betahydroxybutyrate (BHB) reaches levels between 0.5 – 3.0 mmol/L — and up to 4.0 mmol/L for therapeutic ketogenic diets used in the treatment of epilepsy, seizure disorder and glioblastoma.

Nutritional ketosis used predominantly for weight loss is usually set with BHB levels between 1.5-3.0 mmol/L [2].

Low carbohydrate diets are those where carbohydrate intake is limited to < 130 g per day or < 26% of total energy intake [1] and moderate carbohydrate diets are where carbohydrate intake is limited to 130–225 g per day or 26–45% of total energy intake [1].

Again, the amount of fat in the diet has nothing to do with a diet being ketogenic only the amount of carbohydrate it contains.

Therapeutic Ketogenic Diets

First of all, what does “therapeutic” mean?

Something is therapeutic when it is used in the treatment of a disease. This may be a pharmaceutical drug or a diet.  What makes a diet therapeutic is that it is used to treat a medical condition, or conditions.

A therapeutic diet may be prescribed by a Physician, and implemented by a Dietitian or the Physician themselves.  When implemented by a Dietitian, a therapeutic diet is referred to as Medical Nutrition Therapy (MNT) [3].

The first therapeutic ketogenic diet was used in the 1920s for the treatment of epilepsy. Physicians at Harvard Medical School had begun experimenting with periods of extended fasting as a treatment, and discovered that seizures improved after 2-3 days. In 1921 , Dr. R.M. Wilder[3] used a very high fat, low carbohydrate, and restricted protein diet in a series of patients with epilepsy, and found that it was as effective as fasting and had the advantage that it could be maintained for much longer a period of time than fasting.

The percentage of carbohydrate, fat and protein in what has since become called the “classicKetogenic Diet (KD) was worked out by Dr. M.G. Peterman in 1925 [4] and are the same as used today.  In the classic KD, the total amount of calories are matched to the number of calories the person needs. Protein is usually determined as being 1 g of protein per kg body weight, 10-15 g of carbohydrate per day total, and the remainder of calories provided as fat.  For very young children, the diet may be prescribed based on body weight (e.g. 75-100 calories for each kg (2.2 pounds) of body weight. 

Since the 1920s, several other therapeutic ketogenic for the treatment of epilepsy and seizure disorder have been developed, including the Modified Ketogenic Diet (MKD) and the Modified Atkins Diet (MAD). These are all high fat diets, but differ in the amount of protein they contain. They are all very low carbohydrate diets, which is by definition what makes them ketogenic.

The classic Ketogenic Diet (KD) has a 4:1 ratio i.e. 4 parts of fat for every 1 part protein and carbs. In the classic Ketogenic Diet, 90% of calories come from fat, 6% from protein, and only 4% of calories come from carbohydrate.

The Modified Ketogenic Diet (MKD) has a 3:1 ratio i.e. 3 parts fat for every 1-part protein and carbohydrate. In a Modified Ketogenic Diet, 80-90% of calories come from fat, 12-15% of calories come from protein, and 5-6 % calories come from carbohydrate[5].

The Modified Atkins Diet (MAD) has a 2:1 ratio, with 2 parts fat for every 1-part protein and carbohydrate.  In a Modified Atkins Diet, carbohydrates are restricted to <15 g / day for children, <20 g / day for adults. In a Modified Atkins Diet, 60% of calories come from fat, 30% of calories come from protein, and 10% of calories come from carbohydrate[5].

As well as their use in epilepsy and seizure disorder, any of the above therapeutic ketogenic diets may be prescribed for patients as adjunct treatment in glioblastoma, or as adjunct treatment in Alzheimer’s disease.

These high fat diets are not weight loss diets. These are therapeutic ketogenic diets used with the goal of producing high amounts of ketones (> 4.0 mmol/L / 40 mg/dl) for therapeutic reasons.

Other Types of Therapeutic Ketogenic Diets – for treatment of type 2 diabetes and obesity

In addition to the three types of therapeutic ketogenic diets above, ketogenic diets where carbohydrate is restricted to 50g of carbohydrates per day or less are considered Medical Nutrition Therapy (MNT) in the treatment of type 2 diabetes.

The American Diabetes Association has stated that reducing carb intake has the most evidence for improving blood sugar and has included the use of a very low carbohydrate (ketogenic) eating pattern for treating type 2 diabetes as listed in their 2019 Consensus Report and both the 2019 Standards of Medical Care in Diabetes (2019) and Standards of Medical Care in Diabetes (2020).  In addition, Diabetes Canada released a Position Statement in April of this year outlining that a low carb and very low carb / keto (<50 g of carbohydrates per day) are both safe and effective treatment for adults with diabetes. 

According to the American Diabetes Association, what makes a diet low carbohydrate (LC) or very low carbohydrate (VLC) / ketogenic is defined by the amount of carbohydrate contained in the diet, not the amount of fat. The American Diabetes Association’s  Consensus Report defines low carb and very low carb as follows;

“In this review, a low carbohydrate (LC) eating patterns is defined as reducing carbohydrates to 26-45% of total calories [6].”

and

“In this review a very low carbohydrate (VLC) eating pattern is defined as reducing carbohydrate to <26% of total calories [6].”

Diabetes Canada also defines low carbohydrate and very low carbohydrate diets in terms of the amount of carbohydrate the diet contains. Low carbohydrate diets are defined as less than <130 g of carbohydrate per day or <45% energy as carbohydrate,  and very low carbohydrate diets as <50 g of carbohydrate per day [7].

Weight-Loss “Keto” Diets

There are a wide range of weight-loss approaches that have a ketogenic (keto) component to them.

The 1997 Protein Power[8] published by Dr. Micheal Eades and his wife Dr. Mary Dan Eades is a low carb, high protein, moderate fat ketogenic diet. In fact, the authors warn in the book that eating a large number of calories as fat would make it impossible to lose weight, so this is not a high fat diet at all.

The New Atkins For a New You [9], was redesigned in 2010 by Dr. Eric Westman, Dr. Stephen Phinney MD PhD, and Dr. Jeff Volek RD PhD, and while considered a low carbohydrate high fat, moderate protein weight loss diet, it has 4 phases, with only the first phase being ketogenic (20-50 g carbs per day), but only for two weeks. This first stage is where the Modified Ketogenic Diet (MKD) used in epilepsy and seizure disorder came from — but as a weight-loss diet, the high fat stage in The New Atkins for a New You is very short lived. In phase two, more carbohydrate is added (nuts & seeds, berries, cherries and melon, cheese,  dairy products, legumes (pulses), tomato juice and vegetable cocktail) and this level is maintained until close to goal weight when higher carbohydrate amounts are added in phase 3, then phase 4. It is only higher fat for the first two weeks. 

Then there is the 2013 Real Meal Revolution [10] by Tim Noakes, Sally-Ann Creed, Jonno Proudfoot which is a handbook on the Banting lifestyle (which originated in the late 1800s), with foods broken down into green list, orange list and red list, with varying levels of carbohydrate intake.

Note: there is also the 2014 Bulletproof Diet by former Silicon-Valley biohacker, Dave Asprey but since he doesn’t have a clinical background, I have not included it.  That said, the diet is very high fat and is where “bulletproof coffee” (with added butter and coconut oil) comes from.

In 2016, Dr. Jason Fung, a Toronto nephrologist (kidney specialist) wrote the Obesity Code [11] which promotes a high fat version of a very low carb / keto diet, which is used in conjunction with his 2016 book written with Jimmy Moore titled The Complete Guide to Fasting [12]. In 2020, Fung published Life in the Fasting Lane [13], written with Eve Meyer and Megan Remos which builds on his approach of using a low carb high fat diet along with intermittent fasting.

In 2014, the web site “Diet Doctor” was launched by Dr. Andreas Eenfeld. This was initially mostly with articles translated from his Swedish site and later added content from a variety of other people, including Dr. Jason Fung, Dr. Eric Westman and Dr. Ted Naiman.  In 2017, Eenfeld wrote his own diet book titled Low Carb High Fat Food Revolution [14], which promoted a high fat version of a very low carb / ketogenic weight loss diet.  Later, Dr. Eric Westman went on to found his own Adapt weight loss program which is a very low carb / keto, moderate protein, moderate fat approach and Dr. Ted Naiman went on to write his P:E Diet [15] which promotes a low carb, high protein, low fat approach.

Of ketogenic weight-loss diets outlined above, the two that promote a very high fat intake are Dr. Jason Fung’s approach, and the “Diet Doctor” approach. While both fat and protein result in satiety (not feeling hungry), fat has almost two and a half the caloric density as protein. In addition, fat can trigger the reward system of the brain in the same way carbs do, resulting in many over-eating fat, especially added fat. What many people fail to take into consideration is that both of these approaches also promote periods of intermittent fasting (IF) which as Diet Doctor teaches may be frequent periods of less than 24 hours, to longer fasting periods which may include 5:2 (5 days of normal diet, 2 days restricting total calories to 500 per day) or alternate day fasting, as well as two types of fasts that Dr. Fung promotes, including 36 hour fasts, and 42 hour fasts. If one is only eating ~1/3 of the time, is any weight loss really due to the high fat diet, or the fasting?

“In our clinic, we will often recommend 36-hours fasts 2-3 times per week for type 2 diabetes.” ~Dr. Jason Fung

[ADDED NOTE, August 24, 2020: a well-formulated ketogenic diet such as used by Virta Health (covered here and here) which is high in fat and moderate in protein but that consists of a diet of real, whole food is not the same as popularized “keto diets” high in fat and moderate protein, but that consist of lots of added fat in both food and beverages. There is more to a well-designed ketogenic diet for remission of type 2 diabetes and obesity than macros, alone.

August 27, 2020: There is a fundamental difference between a well-designed ketogenic diet that is high in fat and that is comprised of real, whole food — and the popularized “keto diet”, which is all about added fat. It’s not about macros, but nutrients.]

The Stereotypical High Fat Keto Diet is Only ONE Type

Over the last several years, about 1/3 of people that come to me do so after following “the keto diets” without realizing that there is not just one.  Most lost some weight initially on this high fat diet, and then stalled and quite a few actually ended up gaining weight.

Whether following Dr. Fung’s approach or the Diet Doctor approach, people reported eating 75% fat, 15% protein and 10% carbohydrate — which is essentially a hybrid between the Modified Ketogenic Diet (MKD) and the Modified Atkins Diet (MAD) which as mentioned above are NOT weight loss diets — in fact, they were designed to not result in weight loss. These high fat, moderate protein diets are diets are solely intended to produce large amounts of ketones for therapeutic purposes. 

It is no wonder high fat “keto” diets don’t deliver weight loss results. That’s not what they were designed to do! 

Unless these high fat “keto” diets are combined with the frequent periods of <24 hours of fasting, >24 hour periods of fasting several times per week, weight loss is unlikely to occur unless as byproduct of the higher satiety of the fat, and over all eating less food.

Losing Body Fat is Not About Eating Less Carbs and More Fat!

If we want to lose body fat, then eating food that is very high in dietary fat won’t accomplish that UNLESS one is only eating every second or third day, which is what the stereotypical high fat “keto” diets promote. If we are eating a high fat diet and regularly fasting for extended periods of time, it is the fasting itself that underlies body fat loss and lower insulin, not all the added dietary fat.

Eating tons of bacon, butter, cream and avocado makes perfect sense in a therapeutic diet for epilepsy, seizure disorder or as an adjunct treatment in glioblastoma or Alzheimer’s disease, because the goal is to produce lots of ketones but if one wants to lose weight without using frequent periods of fasting, then adding tons of fat to food makes no sense. We want to utilize our fat stores for energy, not burn dietary fat.

One can use any one of a number of low carbohydrate approaches to accomplish weight loss, as well as improve blood sugar — by focusing on eating nutrient dense foods with a high protein-to-energy ratio, and that are rich in micronutrients.  Protein also increases satiety, helps build muscle and is much less calorically dense than fat [16].

Whether starting at a brief ketogenic level and working up (such as the method used by Protein Power, New Meal Revolution or Westman, Phinney and Volek’s approach in the New Atkins, or using an approach I often do which is to start people off at 130 g of carbohydrate per day, and lower carbohydrate as required to achieve clinical outcomes. In either approach, weight loss and lower insulin and glucose can be achieved without extended or frequent periods of fasting.

That doesn’t mean there aren’t benefits to doing short daily periods of fasting, such as from after dinner on one day until the first meal the following day — there are.  It simply isn’t required for weight loss.

Final Thoughts…

There are several therapeutic ketogenic diets that can be used in epilepsy and seizure disorder as well as other conditions, and other types of therapeutic ketogenic diets that are considered Medical Nutrition Therapy (MNT) for the treatment of type 2 diabetes and obesity.

The idea that there is “THE keto diet” which is high in fat is a fallacy — one that has the unintended consequence of many people failing to lose weight (and often gaining weight) because they don’t realize that it needs to be combined with periods of intermittent fasting.  A weight-loss “keto diet” that is 75% fat, 15% protein and 10% carbs is only ONE type of ketogenic diet. It is by no means “THE keto diet!”A diet that is low in carbohydrate and rich in nutrient-dense lean protein, as well as a wide range of vegetables and fruit is just as much a “keto diet” because it is low in carbohydrate — and one that can be used successfully to achieve weight loss, with no fasting required.

In short, there is no one-size-fits-all-low-carb or keto diet, but rather a range of low carb and keto diets that can be chosen from, based on each person’s personal preference, as well as their specific medical needs.

More Info?

If you would like more information about type of low carb or ketogenic diet that might be best suited to you, please send me a note using the Contact Me form on the tab above.

To your good health!

Joy

You can follow me on:

Twitter: https://twitter.com/JoyKiddie
Facebook: https://www.facebook.com/BetterByDesignNutrition/

References

  1. Feinman RD, Pogozelski WK, Astrup A, Bernstein RK, Fine EJ,Westman EC, et al. Dietary Carbohydrate Restriction as the First Approach in Diabetes Management: critical review and evidence base. Nutrition. 2015;31(1):1–13
  2. Nasir H. Bhanpuri, Sarah J. Hallberg, Paul T. Williams et al, Cardiovascular disease risk factor responses to a type 2 diabetes care model including nutritional ketosis induced by sustained carbohydrate restriction at 1 year: an open label, non-randomized, controlled study, Cardiovascular Diabetology, 2018, 17(56)
  3. U.S. Department of Health and Human ServicesFinal MNT regulationsCMS-1169-FCFederal Register1 November 200142 CFR Parts 405, 410, 411, 414, and 415
  4. Peterman MG, The Ketogenic Diet, JAMA. 1928;90(18):1427–1429. doi:10.1001/jama.1928.02690450007003
  5. Kossoff EH, Doward JL. The Modified Atkins Diet. Epilepsia 2008; 49 (Suppl8): 37-41
  6. Evert, AB, Dennison M, Gardner CD, et al, Nutrition Therapy for Adults With Diabetes or Prediabetes: A Consensus Report, Diabetes Care, Ahead of Print, published online April 18, 2019, https://doi.org/10.2337/dci19-0014
  7. Diabetes Canada, Diabetes Canada Position Statement on Low Carbohydrate
    Diets for Adults with Diabetes: A Rapid Review Canadian Journal of Diabetes (2020), doi: https://doi.org/10.1016/j.jcjd.2020.04.001.
  8. Eades M, Dan Eades M (1997), Protein Power: The High-Protein/Low-Carbohydrate Way to Lose Weight, Feel Fit, and Boost Your Health–in Just Weeks! Bantam; New edition edition (1 December 1997)
  9. Westman E, Phinney SD, Volek J, (2010) Diet for Shedding Weight and Feeling Great, Atria Books February 17, 2010)
  10. Noakes T, Creed S-A, Proudfoot J, et al, (2013)The Meal Real Revolution, Quivertree Publications
  11. Fung J (2016) Obesity Code, Greystone Books, Vancouver
  12. Fung J, Moore J (2016), The complete guide to fasting : heal your body through intermittent, alternate-day, and extended fasting, Victory Belt Publishing
  13. Fung J, Meyer E and Ramos M (2020), Life in the Fasting Lane: The Essential Guide to Making Intermittent Fasting Simple, Sustainable, and Enjoyable, Harper Wave
  14. Eenfeld A, Low Carb, High Fat Food Revolution: Advice and Recipes to Improve Your Health and Reduce Your Weight (2017), Skyhorse Publishers
  15. Naiman T, Shewfelt W,  The PE Diet: Leverage your biology to achieve optimal health (2020)
  16. Paddon-Jones D, Westman E, Mattes RD et al, Protein, weight management, and satiety, The American Journal of Clinical Nutrition, Volume 87, Issue 5, May 2008, Pages 1558S–1561S, https://doi.org/10.1093/ajcn/87.5.1558S

Copyright ©2020 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 Keto Diet — a potentially dangerous and an unhealthy diet

INTRODUCTION: I’ve heard other Dietitians say that the keto diet is a potentially dangerous and an overall unhealthy diet because it focuses on ‘high intakes of processed meat, butter and cream’. Some have said that harmful effects were seen as much as three years post keto —  with one case involving symptoms of uncontrollable food cravings and “a head rush” after ingesting any carbs, and another three cases of people having developed severe adverse health effects, including one with newly diagnosed diabetes that wasn’t present before the diet, and two others with non-alcoholic fatty liver disease. All of these individuals were said to have gained all the weight back plus more, and the concern was raised as to whether the keto diet can really be called “a key to diabetes reversal or diabetes remission” because we haven’t actually fixed a broken pancreas. This article will address some of these beliefs.


The belief that there is such as thing as “the keto diet” (singular) which is high in processed meat, butter and cream is common, but incorrect. More on that below.

As a Dietitian, I am expected to be well-informed about a wide range of dietary options and to speak and write from an evidenced-based perspective, but the reality is that as Dietitians we can’t be knowledgeable in all available diets. While I am by no means an expert on low carb or ketogenic diets, I have written over 200 articles on the topic (published on my dedicated low-carb practice website), and have been using low carb and ketogenic diets as two of several dietary options in clinical practice for the past 5 years.

Firstly, with regards to the severe adverse health effects that the 3 individuals reportedly developed as a result of following the keto diet, it has been documented that abnormal glucose responses are present as long as 20 years before a diagnosis of Type 2 Diabetes[1] and the American Association of Clinical Endocrinologists (AACE) concluded that both insulin resistance and prediabetes precede a diagnosis of type 2 diabetes[2] — which means that people presenting with type 2 diabetes after following “the keto diet” had been developing the disease for many years prior.

Furthermore, non-alcoholic fatty liver disease (NAFLD) is strongly associated with insulin resistance, which is characterized by excessive hepatic glucose production (high production of glucose by the liver) and compensatory hyperinsulinemia [3-9], which is the response of the liver to produce high amounts of insulin in order to remove the excess glucose. The association of NAFLD with insulin resistance indicates that the fatty liver was developing for years prior to these individuals following “the keto diet”.  Furthermore, it has been documented that a classic ketogenic diet (KD) is an effective treatment for nonalcoholic fatty liver disease [10] and “rapidly reverses NAFLD and insulin resistance despite increasing circulating non-esterified fatty acids, the main substrate for synthesis of intrahepatic triglycerides” [10].

As for “the keto diet” being a key to diabetes reversal or diabetes remission, I’ve addressed this in detail in a previous article.

So, let me address the misconception that there is such a thing as “the keto diet” (singular), which is high in processed meat, butter and cream.

Many Types of Keto Diets

There are a variety of therapeutic ketogenic diets, including the Ketogenic Diet (KD), the Modified Ketogenic Diet and the Modified Atkins Diet, as well as a variety of ketogenic diets that are used both for therapeutic reasons (such as the management of type 2 diabetes), as well as those that are followed for personal choice.

What makes a diet therapeutic is that it is used to treat a medical condition or conditions and is recommended by a Physician, and implemented by a Dietitian, or by the MD themselves. When a doctor sends me a referral to implement a Modified Atkins Diet for one of their patients with seizure disorder, it is a therapeutic diet. So is a referral to implement a very low carbohydrate / ketogenic diet for the treatment of type 2 diabetes or fatty liver disease.

Use of a very low carb / keto diet by Physicians or Dietitians in the management of type 2 diabetes should come as no surprise to anyone given that these dietary patterns are considered Medical Nutrition Therapy (MNT) in the treatment of type 2 diabetes.

The American Diabetes Association has stated that reducing carb intake has the most evidence for improving blood sugar and has included the use of a very low carbohydrate (ketogenic) eating pattern for treating type 2 diabetes as listed in their 2019 Consensus Report and both the 2019 Standards of Medical Care in Diabetes (2019) and Standards of Medical Care in Diabetes (2020).  In addition, Diabetes Canada released a Position Statement in April of this year outlining that a low carb and very low carb / keto (<50 g of carbohydrates per day) are both safe and effective treatment for adults with diabetes. 

Therapeutic ketogenic diets such as the classic Ketogenic Diet (KD), the Modified Ketogenic Diet and the Modified Atkins Diet are by necessity high fat diets — because the goal is to produce very high levels of ketones in order to improve clinical outcomes in epilepsy and seizure disorder, and as adjunct treatment in glioablastoma ( a type of brain cancer) and in Alzheimer’s disease.  The Ketogenic Diet (KD) has a 4:1 ratio i.e. 4 parts of fat for every 1 part protein and carbs, the Modified Ketogenic Diet (MKD) has a 3:1 ratio; 3 parts fat for every 1-part protein and carbs, and the Modified Atkins Diet (MAD) has a 2:1 ratio, with 2 parts fat for every 1-part protein and carbs.

What makes a weight loss diet ketogenic is not how much fat it contains, but the amount of carbohydrate it contains. Very low carbohydrate / ketogenic diets are diets where carbohydrate is limited to 20-50 g per day or 10% of total energy intake [11]. It is this low carbohydrate intake that results in the body using fat as its primary fuel, rather than carbohydrate.  At this level of carbohydrate intake, blood ketone levels increase at or above 0.5 mmol/L, resulting in ketosis. 

Ketosis is where betahydroxybutyrate (BHB) reaches levels between 0.5 – 3.0 mmol/L (and up to 4.0 mmol/L for therapeutic ketogenic diets such as those used in the treatment of epilepsy, seizure disorder and glialblastoma), whereas nutritional ketosis for optimal weight loss is commonly set with BHB levels between 1.5-3.0 mmol/L [12].

There is no one “keto diet” for weight loss but a range of choices, only some of which I will mention here.

I will start by looking at one of the earlier known diets that used a ketogenic level of carbohydrate intake; the 1972 Dr. Atkins’ Diet Revolution[13], by Dr. Robert Atkins. The so-called “Atkins’ Diet” had an introductory phase which limited carbohydrate intake to 20-25 grams of net carbs from nuts, seeds, and low carb vegetables, and this phase resulted in people going into ketosis.  In fact, this first phase of the Atkin’s Diet is what forms the basis for the Modified Atkins Diet, a therapeutic diet used in the treatment of epilepsy and seizure disorder.

The 1997 Protein Power[14] published by Dr. Micheal Eades, and his wife Dr. Mary Dan Eades is a low carb,  high protein, moderate fat ketogenic diet. In fact, the authors warn in the book that eating a large number of calories as fat would make it impossible to lose weight, so this is not a high fat diet at all.

The New Atkins For a New You [15], was redesigned in 2010 by Dr. Eric Westman, Dr. Stephen Phinney MD PhD, and Dr. Jeff Volek RD PhD, and is a low carb high fat, moderate protein weight loss diet that has 4 phases, with the first phase being ketogenic to start with (20-50 g carbs per day), but is only ketogenic for two weeks.  In phase two, more carbohydrate is added as nuts & seeds, berries, cherries and melon, cheese,  dairy products, legumes (pulses), tomato juice and vegetable cocktail and this level is maintained until close to goal weight when phase 3, then phase 4 (both higher carb) are implemented.

The 2011 book by Dr. Stephen Phinney MD PhD, and Dr. Jeff Volek RD PhD, The Art and Science of Low Carbohydrate Living [16] is not a diet book, but elaborates on type 2 diabetes as ‘carbohydrate intolerance’ and on the importance of electrolyte and mineral management to avoid side effects of a ketogenic diet. In this approach, added dietary fat is incorporated after weight loss, for long term weight maintenance, to prevent further weight loss.

Then there is the 2013 Real Meal Revolution [17] by Tim Noakes, Sally-Ann Creed, Jonno Proudfoot which is a handbook on the Banting lifestyle (which originated in the late 1800s), with foods broken down into green list, orange list and red list, with varying levels of carbohydrate intake.

In 2016, Dr. Jason Fung, a Toronto nephrologist (kidney specialist) wrote the Obesity Code [18] which promotes a high fat version of a very low carb / keto diet, which is used in conjunction with his 2016 book written with Jimmy Moore titled The Complete Guide to Fasting [19]. In 2020, Fung published Life in the Fasting Lane [20], written with Eve Meyer and Megan Remos which builds on his approach of using a low carb high fat diet along with intermittent fasting.

In 2014, the web site “Diet Doctor” was launched by Dr. Andreas Eenfeld. This was initially mostly with articles translated from his Swedish site and later added content from a variety of other people, including Dr. Jason Fung, Dr. Eric Westman and Dr. Ted Naiman.  In 2017, Eenfeld wrote his own diet book titled Low Carb High Fat Food Revolution [21], which promoted a high fat version of a very low carb / ketogenic weight loss diet.  Later, Dr. Eric Westman went on to found his own Adapt weight loss program which is a very low carb / keto, moderate protein, moderate fat approach and Dr. Ted Naiman went on to write his P:E Diet [22] which promotes a low carb, high protein, low fat approach.

Of ketogenic weight-loss diets above, the only ones that promote a high fat intake with processed meat (bacon), butter and cream are Dr. Jason Fung’s approach and the “Diet Doctor” approach. These are not THE “keto diet” — but one type of ketogenic approach, amongst many.

Self Administered Diets

If an individual hears about a diet from friends, or reads about it online and implements it, and is unsuccessful at losing weight or at keeping it off, or has adverse side effects, is this a reflection of the diet itself or is it a problem inherent in self-administered diets?

Does it matter if the failed “diet” is a calorie-restricted diet, a ketogenic diet, a grapefruit diet or any other diet?

Self administered diets of any type may or may not be appropriate for an individual, because the person’s individual nutritional needs, risk factors, metabolic conditions, and medications are not factored in. Weight-loss failure is one issue, as are potential adverse side-effects.  For example, if a person decides to follow a very low-calorie diet, experiences hypoglycemia and falls and injures themselves, is this the fault of the diet itself, or their self-administration of a diet?  Likewise, if a person decides to follow a very low carbohydrate / ketogenic diet and has an adverse reaction because of some medications they are taking, is this the fault of the particular version of a ketogenic diet they are following?

All diets have potential benefits and risks and self-administered diets pose additional risks that simply haven’t been factored in — regardless what type of diet is chosen.

Failed Weight Loss

Studies show that the failure rate with weight-loss diets is high — often as much as 80 – 90%, and regain of weight is thought to possibly be higher because follow-up rates are very low, and weights are often self-reported either by phone or mail [23].

The fact that most people will gain most of the weight they lost while dieting back, and sometimes end up weighing more than before dieting is not disputed, and is irrespective of the type of diet followed.

Regardless of the dietary approach chosen, “dieting” is not the answer for sustained weight loss. If someone goes “on” a diet that means that at some point they will go “off” of it.  In my opinion, a lifestyle change is a preferred approach and what will work for one person long-term, may not work for another. That is why I say that there is no one-sized-fits-all diet.

Final Thoughts…

Low carb and very low carb / ketogenic diets are two approaches that can suit some, but not all people.  A Mediterranean Diet or a whole food plant based (vegetarian) diet may be better suited to others. 

The misconception that there is one “keto diet” that is high in fat, especially processed meat, butter and cream is simply incorrect. There are a range of ketogenic (keto) diets and even in a high fat ketogenic diet, the fat can come from avocado, nuts and seeds and olives.

A high fat versions of a keto diet may be appropriate and work well in some individuals when used with periods of intermittent fasting, such as OMAD (one meal a day). In my clinical experience, I have observed that high fat versions of a keto diet often result in weight stalls and even weight gain in peri- or post-menopausal women. Since I don’t recommend extended fasting > 24 hours in older adults due to the muscle-loss which can result from the fasting, combined with the muscle loss that is already associated with aging, I generally recommend a higher protein, lower added fat version in such cases. In any case, there are lots of ways to do a ketogenic weight-loss diet — which is ultimately about the total amount of carbohydrate in the diet, not the amount of fat.

More Info?

If you would like more information about the services I offer, please send me a note using the Contact Me form on the tab above.

To your good health!

Joy

You can follow me on:

Twitter: https://twitter.com/JoyKiddie
Facebook: https://www.facebook.com/BetterByDesignNutrition/

References

  1. Sagesaka H, S.Y., Someya Y, et al, Type 2 Diabetes: When Does It Start? Journal of the Endocrine Society, 2018. 2(5): p. 476-484.
  2. American Association of Clinical Endocrinologists Announces Framework for Dysglycemia-Based Chronic Disease Care Model, November 28, 2018, AACE Online Newsroom, url: https://media.aace.com/press-release/american-association-clinical-endocrinologists-announces-frameworkdysglycemia-based-c
  3.  Fabbrini E., et al. , Alterations in adipose tissue and hepatic lipid kinetics in obese men and women with nonalcoholic fatty liver diseaseGastroenterology 134, 424–431 (2008). 
  4. Gastaldelli A., et al. , Relationship between hepatic/visceral fat and hepatic insulin resistance in nondiabetic and type 2 diabetic subjectsGastroenterology 133, 496–506 (2007). 
  5. Korenblat K. M., Fabbrini E., Mohammed B. S., Klein S., Liver, muscle, and adipose tissue insulin action is directly related to intrahepatic triglyceride content in obese subjectsGastroenterology 134, 1369–1375 (2008). 
  6. Kotronen A., Juurinen L., Tiikkainen M., Vehkavaara S., Yki-Järvinen H., Increased liver fat, impaired insulin clearance, and hepatic and adipose tissue insulin resistance in type 2 diabetesGastroenterology 135, 122–130 (2008).
  7. Bugianesi E., et al. , Insulin resistance in non-diabetic patients with non-alcoholic fatty liver disease: Sites and mechanismsDiabetologia 48, 634–642 (2005).
  8. Seppälä-Lindroos A., et al. , Fat accumulation in the liver is associated with defects in insulin suppression of glucose production and serum free fatty acids independent of obesity in normal menJ. Clin. Endocrinol. Metab. 87, 3023–3028 (2002).
  9. Ryysy L., et al. , Hepatic fat content and insulin action on free fatty acids and glucose metabolism rather than insulin absorption are associated with insulin requirements during insulin therapy in type 2 diabetic patientsDiabetes 49, 749–758 (2000). 
  10. Luukkonen PK, Dufour S, Lyu K, et al. Effect of a ketogenic diet on hepatic steatosis and hepatic mitochondrial metabolism in nonalcoholic fatty liver disease. Proc Natl Acad Sci U S A. 2020;117(13):7347-7354.
  11. Feinman RD, Pogozelski WK, Astrup A, Bernstein RK, Fine EJ,Westman EC, et al. Dietary Carbohydrate Restriction as the First Approach in Diabetes Management: critical review and evidence base. Nutrition. 2015;31(1):1–13.
  12. Nasir H. Bhanpuri, Sarah J. Hallberg, Paul T. Williams et al, Cardiovascular disease risk factor responses to a type 2 diabetes care model including nutritional ketosis induced by sustained carbohydrate restriction at 1 year: an open label, non-randomized, controlled study, Cardiovascular Diabetology, 2018, 17(56)
  13. Atkins, R. C. (1972). Dr. Atkins’ diet revolution; the high calorie way to stay thin forever. New York: D. McKay Co.
  14. Eades M, Dan Eades M (1997), Protein Power: The High-Protein/Low-Carbohydrate Way to Lose Weight, Feel Fit, and Boost Your Health–in Just Weeks! Bantam; New edition edition (1 December 1997)
  15. Westman E, Phinney SD, Volek J, (2010) Diet for Shedding Weight and Feeling Great, Atria Books February 17, 2010)
  16. Phinney SD, Volek J, (2011), The Art and Science of Low Carbohydrate Living, Beyond Obesity LLC
  17. Noakes T, Creed S-A, Proudfoot J, et al, (2013)The Meal Real Revolution, Quivertree Publications
  18. Fung J (2016) Obesity Code, Greystone Books, Vancouver
  19. Fung J, Moore J (2016), The complete guide to fasting : heal your body through intermittent, alternate-day, and extended fasting, Victory Belt Publishing
  20. Fung J, Meyer E and Ramos M (2020), Life in the Fasting Lane: The Essential Guide to Making Intermittent Fasting Simple, Sustainable, and Enjoyable, Harper Wave
  21. Eenfeld A, Low Carb, High Fat Food Revolution: Advice and Recipes to Improve Your Health and Reduce Your Weight (2017), Skyhorse Publishers
  22. Naiman T, Shewfelt W,  The PE Diet: Leverage your biology to achieve optimal health (2020),
  23. Mann T, Tomiyama AJ, Westling E, Lew AM, Samuels B, Chatman J. Medicare’s search for effective obesity treatments: diets are not the answer. Am Psychol. 2007;62(3):220-233. doi:10.1037/0003-066X.62.3.220

 

Copyright ©2020 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.

 

American College of Cardiology: No Benefit to Lower Saturated Fat Intake

The recommendation to lower the consumption of saturated fat in the diet to reduce the risk of cardiovascular disease (CVD) has been the central theme in both the US and Canadian since 1977, and has been carved into our respective Dietary Guidelines since the 1980s.

A newly published study published by the American College of Cardiology has found no beneficial effect on either cardiovascular disease (CVD) or death of lowering saturated fatty acid (SFA) intake and that saturated fat intake is actually protective against stroke [1]. This reassessment of dietary saturated fat intake was based on a meta-analysis of randomized control trials (the strongest data available), as well as observational studies.

The newly published report stated;

Whole-fat dairy, unprocessed meat, eggs and dark chocolate are SFA-rich foods with a complex matrix that are not associated with increased risk of CVD. The totality of available evidence does not support further limiting the intake of such foods.”[1]

The Significance of These Findings

From 1977 onward, based on a belief that saturated fat caused heart disease, both Canada and the US changed their respective dietary recommendations to move the diet away from consuming fat — especially saturated fat, to a diet where more than half the calories (55-60% in Canada, 45-65% in the US) were from carbohydrate. The goal was to lower the risk of cardiovascular disease based on the fact that eating saturated fat raised total LDL (LDL-C), and it was assumed that higher total LDL was tied to increased risk of heart disease. The problem was that it wasn’t known until many years later that there are different types of LDL particles (you can read more about that here) and that it is the small, dense LDL particles that are associated with heart disease, not all LDL particles [2].  

Coinciding with the recommendation for people to eat less saturated fat and more carbohydrate as the main source of calories, we have seen obesity rates go from ~10% of the population in both countries, to 1 in 3 people in the US, and 1 in 4 people in Canada — with another 1/3 of people falling in the overweight category.

What this newly published reassessment of the data indicates is that the American and Canadian diet, which has shunned whole-fat dairy, unprocessed animal meats and eggs for the last 40+ years did so without benefit to cardiovascular disease rates, or rates of death.

Telling people to eat “low fat” everything and to avoid butter, red meat and eggs not only did not do what it was intended to do, it has likely been a significant contributor to the obesity epidemic we now face, along with astronomical rates of type 2 diabetes, hypertension and yes, cardiovascular disease. How ironic.

The report summarized;

“The dietary recommendation to reduce intake of SFAs without considering specific fatty acids and food sources is not aligned with the current evidence base. As such, it may distract from other more effective food-based recommendations, and may also cause a reduction in the intake of nutrient-dense foods (such as eggs, dairy, and unprocessed meat) that may help decrease the risk of CVD, type 2 diabetes, and other non-communicable diseases, but also malnutrition, deficiency diseases and frailty, particularly among “at-risk” groups. Furthermore, based on several decades of experience, a focus on total SFA has had the unintended effect of misleadingly guiding governments, consumers, and industry toward foods low in SFA but rich in refined starch and sugar.“[1]

The Study’s Conclusion

The report concluded;

The long-standing bias against foods rich in saturated fats should be replaced with a view towards recommending diets consisting of healthy foods. What steps could shift the bias? We suggest the following measures:

1) Enhance the public’s understanding that many foods (e.g., whole-fat dairy) that play an important role in meeting dietary and nutritional recommendations may also be rich in saturated fats.

2) Make the public aware that low-carbohydrate diets high in saturated fat, which are popular for managing body weight, may also improve metabolic disease.”

“There is no robust evidence that current population-wide arbitrary upper limits on saturated fat consumption in the US will prevent CVD or reduce mortality.”

Final Thoughts…

I  remember when the 1977 guidelines first came out, and when the 1988 Canada’s Food Guide was new.  I also remember when the majority of people were normal body weight and it was the exception for someone to be overweight or obese. Here it is, more than 40 years later and we now have strong evidence that saturated fat from unprocessed meat, full fat dairy and eggs does NOT contribute to heart disease or death, and is protective against stroke.

Given this evidence, will Health Canada revisit its most recent Canada Food Guide of January 2019 and adjust it’s recommendation to “limit the amount of foods containing saturated fat, such as cream, higher fat meats…cheeses and foods containing a lot of cheese“?

More Info?

If you would like more information about restoring your weight and healthy by eating a diet lower in carbohydrate and which includes real, whole food such as unprocessed meat, full-fat dairy and eggs, please send me a note using the Contact Me form on the tab above.

To your good health!

Joy

You can follow me on:

Twitter: https://twitter.com/JoyKiddie
Facebook: https://www.facebook.com/BetterByDesignNutrition/

References

  1. Astrup A, Magkos F, Bier, DM, et al, Saturated Fats and Health: A Reassessment and Proposal for Food-based Recommendations: JACC State-of -the-Art Review, J Am Coll Cardiol. 2020 Jun 17. Epublished DOI:10.1016/j.jacc.2020.05.077
  2. Lamarche, B., I. Lemieux, and J.P. Després, The small, dense LDL phenotype and the risk of coronary heart disease: epidemiology, patho-physiology and therapeutic aspects. Diabetes Metab, 1999. 25(3): p. 199-211.

 

Copyright ©2020 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.

New Protocols for In-Person Clinical Operation for Health Professionals

WorkSafeBC has just released what will be required of regulated health professionals such as myself, as a Dietitian to safely run an in-person clinical practice in British Columbia during the ongoing Covid-19 outbreak, and it is much more involved than I imagined when I wrote a recent article. As well, these protocols are in addition to the obligations required prescribed by our professional college, as well as to abide by any relevant orders, notices, or guidance issued by the provincial health officer, and the relevant health authority, in my case Fraser Health.

The WorkSafeBC protocols include sections on Understanding the Risk, Selecting Protocols for the Workplace, as well as detailed Protocols for Health Professionals.

Understanding the Risk

The WorkSafeBC website outlines that the virus that causes COVID-19 is spread in several ways, including through droplets when a person coughs or sneezes, and from touching a contaminated surface before touching the face. It is outlined that risk or person-to-person transmission is increased the closer a healthcare professional comes to other people, the amount of time a healthcare professional spends near them, and the number of people seen by a healthcare professional.  The site emphasizes that “physical distancing measures help mitigate this risk”. The WorkSafeBC website also emphasizes that the risk of surface transmission is increased when many people contact same surface, and when those contacts happen in short intervals of time, therefore “effective cleaning and hygiene practices help mitigate this risk”[1].

Selecting Protocols for the Workplace

The WorkSafeBC website notes that there are different protocols which offer different levels of protection and emphasize that “Wherever possible, use the protocols that offer the highest level of protection and add additional protocols as required”[1].

WorkSafeBC Covid-19 Hierarchy of Controls [1]
Elimination first level protection –  Limit the number of people in the workplace  by implementing work-from-home arrangements where possible, limiting occupancy, rescheduling work tasks, or by other means. Rearrange work spaces to ensure that health professionals are at least 2 m (6 ft) from co-workers, customers, and other members of the public.

Engineering controls second level protection : if it is not always possible to maintain physical distancing, then install barriers such as plexiglass to separate people.

Administrative controlsthird level protection – WorkSafeBC encourges the establishing of clinic rules and guidelines, such as cleaning protocols, making sure there is no sharing of equipment, and implementing one-way doors, or walkways, in order to minimize risk.

Personal Protective Equipment (PPEs) – fourth level protection – If the first three levels of protection aren’t enough to control the risk, WorkSafeBC recommends considering the appropriate use of non-medical masks, and to be aware of limitation of non-medical masks to protect the wearer from respiratory droplets.

Protocols for Health Professions

The list of protocols for healthcare professionals is extensive and includes several categories, including those for;

(a) hygiene, cleaning and disinfection – Ensure adequate hand washing facilities are available, and provide approved alcohol-based hand sanitizers,
Encourage staff and clients to practice hand hygiene upon entering and exiting the clinic. Identify all common areas such as clinical space, washrooms, etc. and high contact surfaces such as door handles, stair rails and develop and implement a cleaning and disinfection schedule and associated procedures. Increase cleaning and sanitizing of shared equipment and facilities (e.g. scales, washrooms). Develop and implement protocols for sanitizing treatment areas and equipment to prevent surface transmission between clients. Ensure safe handling and effective application of cleaning products.

(b) modifying staff areas and workflow – Work remotely whenever possible, develop and enforce policy that staff stay home when sick, hold meetings virtually through use of teleconference or online meeting technology and where in-person meetings are required ensure people are positioned at least two metres apart. Consider staggering start times / appointment times to reduce the number of people in the workplace at a given time. Minimize the number of co-workers that staff are interacting with, prioritize the work that needs to occur at the workplace in order to offer services. Minimize the shared use of equipment where possible, consider the requirement for staff to have dedicated work clothes and shoes, provide a place for staff to safety store their street clothes while working and change in/out of clothes to prevent cross-contamination upon entry and exit. Consider adjusting the ventilation such as increasing the amount of outdoor air while maintaining the indoor air temperature and humidity at comfortable levels for building occupants. 

(c) scheduling appointments and communicating with clients – Determine how many clients can be within the clinic at a given time while maintaining at least two metres of physical distance and do not book appoints above this number. In order to accommodate physical distancing, appointment times may need to be staggered. When speaking with clients during scheduling and appointment reminders, ask clients to consider rescheduling if they become sick, are placed on self-isolation, or have travelled out of the country within the last 14 days and attending appointments alone where possible, and not bring friends or children. Consider emailing the client forms that need to be filled out so clients can complete them prior to arriving, and clinics with a website should consider posting information on modifications made to the location and appointment visit procedures.

(d) reception – Post signage at the entrance and within the clinic to assist with communicating expectations, such as hand hygiene, physical distancing, respiratory etiquette, reporting illness or travel history, occupancy limits and no entry if unwell or in self-isolation. Consider placing lines on the floor to mark a two metres distance from the reception desk. Consider use of a transparent barrier such as a plexiglass shield around reception desk, when there is insufficient space to maintain two metre distance between staff and clients. Screen all clients when they check-in for their appointment by asking if they have symptoms associated with COVID-19, have been advised to self-isolate, or have travelled outside of Canada within the last 14 days. Clients that respond in the positive should be asked to leave and reschedule the appointment when deemed clinically appropriate. During transactions, limit the exchange of papers such as receipts if possible and where possible, payments should be accepted through contactless methods.

(e) waiting area – Arrange the waiting area in a way that allows at least two metres of physical distance between each client and consider removing extra chairs and coffee tables from the area to support this. Remove unnecessary items and offerings such as magazines etc. and use disposable cups or single- use items where necessary for beverages. Instruct clients to arrive no more than five minutes before their expected appointment. Where room size or layout presents challenges to physical distancing, consider alternative approaches, such as asking clients not to enter the clinic until they receive a text message or phone call to advise that their appointment can start.

(f) provision of health servicesConduct appointments virtually where clinically appropriate, conduct a point of care assessment for risk of COVID-19 for every client interaction and health services should not be performed on ill or symptomatic clients. Where the client requires timely treatment, ensure PPE is used in accordance with BC-CDC guidance. When possible, the clinical staff should position themselves at least 2 metres from the client and where physical distancing cannot be maintained consider the use of barriers and masks to reduce the risk of transmission. Clients should be required to wear masks for services in order to protect workers and workers should also wear masks to protect clients. Consider treating only one client at a time to minimize risks associated with moving between two or more clients, ensure clients are positioned at least 2 metres apart and shared equipment is cleaned and disinfected between uses by clients. If products / equipment is shared, they must be cleaned and disinfected between uses. Practice effective hand hygiene after each client by washing hands with soap and water or using an alcohol-based hand sanitizer approved by Health Canada. Where feasible, workers should avoid sharing equipment or treatment rooms and treatment rooms should be allocated to a single worker per shift.

(g) preparing for the next appointment and the end of the day – Ensure waiting and treatment areas and equipment are sanitized to prevent surface transmission between clients. Commonly touched surfaces and shared equipment must be cleaned and disinfected after contact between individuals even when not visibly soiled. Towels or any other items contacting a client are to be discarded or laundered between each use. Change into a separate set of street clothes and footwear before leaving work and work clothing should be placed in a bag and laundered after every shift. Shower immediately upon returning home after every shift.

As well, the WorkSafeBC website has protocols for documentation and training of staff, as well as links to the various professional colleges for health professionals to check additional requirements for their profession.

The Effect of these Necessary Protocols

These enhance protocols take time away from healthcare professionals being able to schedule actual clinical appointments. They require PPEs to be available and provided when necessary, as well as require extra time and labour for cleaning and disinfecting waiting areas, office equipment and washrooms, and to dispose of the waste. As much as we would all like things to “return to normal”, there is the need to accept that for now, this is the “new normal”.

For clinical practices that require a clinician to touch a client in the provision of services, such as in dentistry or registered massage therapy or physiotherapy there is no choice, but this is not the case in my practice. Thankfully, we are living in an era where there is secure video conferencing available which is ideal for the services that I provide as a Registered Dietitian, and is recommended by WorkSafeBC as the first approach when possible in the provision of health services.

Use of professional HIPAA and PIPEDA compliant telemedicine software

I have been providing Distance Consultations for over a decade; which are virtual ‘face-to-face’ visits that are functionally indistinguishable from the in-person services I provided prior to Covid-19. They are a very efficient use of my client’s time, as well as my own, and no PPEs are required, no disinfecting or extra hand-washing, or sanitizing of waiting areas, office space and washrooms between each client, and appointments are not spread out through the day due to the need to carry out decontamination tasks between clients.

I use secure HIPAA & PIPEDA compliant telemedicine software – with no download required.

During virtual appointments my clients and I see each other’s faces when we meet, and can comfortably talk, laugh and even sneeze without concern, and weight obtained from people’s own scales is more than adequate for the types of clients I see — and I provide my clients with written instructions for measuring their waist circumference the same way I would do it if they were in my office.

More Info?

If you would like more information about the different type of Dietetic services I provide, please have a look under the Services tab or in the Shop. If you have any service-related questions please feel free to send me a note using the Contact Me form above and I will reply as soon as I can.

To your good health!

Joy

You can follow me on:

Twitter: https://twitter.com/JoyKiddie
Facebook: https://www.facebook.com/BetterByDesignNutrition/

References

WorkSafeBC – Health professions: Protocols for returning to operation,  https://www.worksafebc.com/en/about-us/covid-19-updates/covid-19-returning-safe-operation/health-professionals

Copyright ©2020 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.