Author: Joy Kiddie, MSc, RD

I was surprised to read a discussion on social media today which said that the Diet Doctor website recommended that low carbohydrate meal plans be up to 100g of carbohydrate per day, rather than using the generally accepted definition from Feinman et al [1] which defines low carbohydrate < 130g carbohydrate / day.

Feinman et al [1] define very low carbohydrate (“keto”) diet, low carbohydrate diet and moderate carbohydrate diet as follows:

1. very low carbohydrate (keto) diet: 20—50g carbohydrate /day,  < 10% total energy intake

2. low carbohydrate diet: < 130g carbohydrate / day, < 26% of total energy intake

3. moderate carbohydrate diet: 130—225g carbohydrate / day, 26—45% of total energy intake

The above definitions have been used by Diabetes Associations around the world, including the American Diabetes Association, the European Association for the Study of Diabetes (EASD), Diabetes Australia, and Diabetes Canada.

The American Diabetes Association in conjunction with the European Association for the Study of Diabetes (EASD) used the above definition of a low carbohydrate diet and very low carbohydrate diet in their joint 2019 Consensus Report [2] and the American Diabetes Association used the same definition in their 2020 Standards of Medical Care in Diabetes [3].

The same definition for a low carbohydrate diet and moderate carbohydrate diet were also used by Diabetes Australia in their 2018 Position Statement on Low Carbohydrate Eating for People with Diabetes [4].

Diabetes Canada in their 2020 Position Statement on Low Carbohydrate Diets for Adults with Diabetes also defined a very low carbohydrate diets as < 50 g of carbohydrate per day and a low carbohydrate diet as 51 – 130 g of carbohydrate per day [5].

Given that the definitions for low carbohydrate and very low carbohydrate (“keto”) are widely accepted, why define a low carbohydrate meal plan as “up to 100 grams of carbs per day”?

Why does it matter?

Why a Standard Definition of a “Low Carbohydrate” Diet Matters

It matters whether there is a standard definition because otherwise there is no standard in the marketplace or in research for what “low carbohydrate” is.

Product Labelling

There are hundreds, if not thousands of “low carb” products available on the market and none of these are held to any standard as to what makes them suitable for individuals following a low carbohydrate or very low carbohydrate (“keto”) diets. The terms “low carb” or “keto” on product labels are meaningless! Without a standard definition, it is up to each consumer to read the label and try to determine if these products are suitable. 

A Nutrient Content Claim characterizes the level of a nutrient in a food, so terms like “low-fat” have specific nutritional thresholds and nutrition content claims made on labels are regulated by law. At present, there are no nutrient thresholds for carbohydrate content — and these are needed.

Adopting Feinman et al’s widely used definitions makes sense and will make it possible to for the consume to be provided with meaningful labels, enabling the average consumer to know if a product is suitable for their needs, or not.

Scientific Research Requires a Standard Definition for “Low Carbohydrate”

Without a standard definition for “low carbohydrate < 130g carbohydrate / day”, research studies can define “low carbohydrate” anyway they want — which also means that conclusions of studies can state that “a low carbohydrate diet is associated with increased mortality (death)” when the diet used in the study was well over 130 g of carbohydrate per day”.

In fact, this is exactly what has been occurring.

Dr. Sarah Hallberg, Medical Director at Virta Health said it best on Twitter April 20, 2021;

“Honest representation of evidence is important. How many people have heard someone say that a low carb diet is associated with increased mortality? There is no evidence for this. Here are all the studies that make that claim. None were actually low carb. Much closer to SAD [Standard American Diet].

Let’s have a closer look at the studies Dr. Hallberg cited.

The above 10 studies were said to associate “low carbohydrate diets” with increased mortality, however none of the studies were actually “low carbohydrate”, as defined by Feinman et al [1].

The average carbohydrate intake in these studies were 41.34% —not a low carbohydrate diet which is < 26% of total energy intake [1]. These studies were moderate carbohydrate diet, using Feinman et al’s definition.

The range of carbohydrate intake in these studies was 36.2 % – 51.5 % /day — which means even the study with the lowest carbohydrate intake exceeded the cut-off of a low carbohydrate diet of < 26% of total energy intake, defined by Feinman et al [1].

Final Thoughts…

When the media circulates reports that “a low carb diet is associated with increased mortality” it is imperative that “low carb” is defined as <130 g carbohydrate per day. Otherwise what the message that the public receives is that these diets are dangerous, when the diet used in the study wasn’t a low carbohydrate diet at all!

We need to get our terms straight.

We need to be consistent.

Feinman et al’s definition of “low carbohydrate” and “very low carbohydrate” / “keto” have already been adopted by Diabetes Associations around the world, including the American Diabetes Association, the European Association for the Study of Diabetes (EASD), Diabetes Australia, and Diabetes Canada.

Let’s use them.

Let’s lobby our governments to require them to be used on product labels to provide honesty and accuracy in labelling.

Let’s push for academic institutions and scientific publications to adopt these definitions as standard, so that research has meaning — and conclusions to not mislead people to believing something is dangerous, when the thing that was studies was something different.

More Info?

If you would like to know more about the low carbohydrate (<130g carbs / day) and very low carbohydrate (“keto”) services I provide (< 50 g carbs / day), please have a look under the Services tab, above.

To your good health!

Joy

You can follow me on:

Twitter: https://twitter.com/lchfRD
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NOTE: This article was inspired by important discussion on Twitter between Antonio Martinez II and Nina Teicholz, which included the post above from Dr. Sarah Hallberg.

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. A Consensus Report, Diabetes Care, Ahead of Print, published online April 18, 2019, https://doi.org/10.2337/dci19-0014
3. American Diabetes Association, Facilitating Behavior Change and Well-being to Improve Health Outcomes: Standards of Medical Care in Diabetes—2020
   American, Diabetes Care Jan 2020, 43 (Supplement 1) S48-S65; DOI: 10.2337/dc20-S005
4. Diabetes Australia, Position Statement – Low Carbohydrate Eating for People with Diabetes, August 2018, https://www.diabetesaustralia.com.au/wp-content/uploads/Diabetes-Australia-Position-Statement-Low-Carb-Eating.pdf
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.

Copyright ©2021 The LCHF Dietitian (a division of BetterByDesign Nutrition Ltd.)

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

Therapeutic ketogenic diets such as the classic Ketogenic Diet (KD) or the Modified Ketogenic Diet (MKD) are used in the management of epilepsy or seizure disorder or as adjunct therapy in the treatment of glioblastoma and these diets have a purpose; to produce very high levels of ketones that are used by the body to minimize seizures, or to lower glucose availability to cancer cells.  If one does not have a therapeutic need for very high levels of ketones, why eat a very high fat diet that produces lots of them? Why add lots of added fat to diet that is already high in fat?  Likewise, if one is eating a high protein low fat diet like P:E in order to build muscle and lose body fat, what is the benefit to eating even more protein? Are there any risks or possible downsides to eating more protein in a high protein low fat diet, or more fat in a low carb high fat diet? How can a low carb high protein diet avoid the problem of excess fat or excess protein?

Eat Fat to Lose Fat?

Some people have come to believe that they need to eat more dietary fat in order to burn body fat, so they add copious amounts of fat to food in the form of heavy whipping cream, butter, fatty meats and to make sure, they supplement with “fat bombs”. If one is trying to lose body fat, then it makes no sense to add tons of dietary fat that will be used by the body for energy before using their own body fat stores. A very high fat version of a LCHF diet may have a role at the very beginning in order to help people make the transition from being predominantly glucose-burning to being fat-burning (referred to as becoming “fat adapted“), but there is no need to keep eating a very high fat diet (75% of energy as fat) once that has occurred. In fact, for many people, continuing to eat 75% fat “keto” diet after the initial adoption often (but not always) results in a stall in weight loss, and in some cases in weight gain — especially when not also doing extended periods of fasting.  Fat is two and a half times as energy-dense as protein and carbohydrate, so unless one needs very high levels of ketones for therapeutic purposes and is not concerned about losing muscle mass from extended periods of fasting (more about that here), it makes no sense to keep eating lots of fat.

High Fat Diet Needed for Satiety?

Some people believe that eating high dietary fat on a low carbohydrate diet is needed to keep them from feeling hungry— and that it is this which results in them eating less. While fat does keep people from feeling hungry (i.e. produces increased ‘satiety’), it is not the best source of satiety. Protein is far better at producing satiety, and at less than half the calories of fat. According to a 2010 study titled Energy Density of Foods: Effect on Energy Intake [1];

”when the satiating effects of macronutrients on appetite and energy intake (EI) are compared as nutrients come in the diet (and fat contributes disproportionately to energy density (ED), Joule-for-Joule, protein is consistently (at doses above 1.2 to 1.4 MJ) more satiating than carbohydrate (CHO), which is more satiating than fat.

When energy density (ED) is controlled, protein is still far more satiating than fat or carbohydrate.”

Since protein produces more satiety than fat and has less than half the calories, it makes much more sense for someone seeking weight loss to eat more protein in the diet, and not add excess dietary fat.

Impact of High Fat on Blood Glucose Control

For blood glucose improvements, dietary fat has no impact on the body’s (endogenous) insulin levels, so adding dietary fat does not help lower circulating levels of insulin or blood glucose (blood sugar). It is only the “low carbohydrate” part of a low carb high fat (LCHF) diet that helps improve insulin levels, and in turn glucose levels and it is for this reason that a low carbohydrate diet (defined as <130 g of carbs per day) has been approved by the American Diabetes Association for both improved blood sugar control and weight loss [2] and is why the American Diabetes Association’s Consensus report of April 2019 also includes use of a very low carb (keto) diet of 20-50 g carbs per day [3]. for blood sugar management. Since it is only the low carbohydrate part of a low carb high fat (LCHF) diet that is important for glucose control, keeping carbohydrate low is the goal (not keeping fats high). 

For people with pre-diabetes, type 2 diabetes or for those at increased risk due to past medical history or family risk factors, selecting the level of carbohydrate intake that is most appropriate for blood glucose control around prioritizing protein intake based on physiological need, is the first step and the remainder of the diet will be made up of various types of dietary fat. Since the level of fat intake will be above the “not more than 30% of calories from fat” that the USDA defines as a “low fat diet” [4], this diet pattern will still be considered a “high fat diet“.

Depending on whether fat or protein is higher, this type of meal pattern will be either a low carb high fat (LCHF) diet or a low carb high protein (LCHP) diet. More on this second one, below.

Determining Protein Needs without Exceeding the Safe Upper Limit

Protein needs are always calculated as grams of protein per kilogram of body weight of the person and not as a percentage of daily calories e.g. X % of daily energy as protein. This is to ensure adequacy and avoid the d excess.

When protein is eaten, the body must get rid of the nitrogen by-product which is toxic to the body. As can be seen from the table below, the main way the body gets rid of this toxic nitrogen by-product is by turning it into ammonia, and then excreting it as urea in the urine.

Protein intake in high protein diets should not be set as a percentage of daily calories, but as a maximum of 3.2 g protein per kg body weight. This is because an intake of 40% of daily calories as protein for one person may be below the safe upper limit of 3.2 g protein per kg body weight, but for another 40% of calories as protein put them right at the upper limit (more in this article). 

How Much Protein is Best?

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 wanting to prevent protein 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.

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 [7]. 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[8] 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 [9,10].

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.

At present, there is very little data for defining the upper limit of protein beyond the urea cycle, which has been established to be safe at 3.0 g protein / kg body weight (tied to the maximum rate of urea production which is 3.2 g protein per kg body weight [6]), so the range of safe intake is defined as  >0.8 g protein body/ kg body weight to >2.5 g protein/ kg body weight.

*in clinical practice, I have set a maximum of 2.5 g protein / kg IBW but in practice, Meal Plans have routinely been below 2.0 g protein / kg IBW.

Is “More” Better

There is a tendency for people to think that because a high fat diet is “good” — or a high protein diet is “good”, that “more is better”. This is a bit like thinking that since a certain amount of laundry detergent is “good”, that “more detergent is better”, but before adding “more”, a few questions need to be asked. For example, will the clothes come out any cleaner, or is there a possibility that “more” may cause the suds to overflow the machine? There is a benefit / risk to “more” that first needs to be considered.

Considering the benefit / risk of more also needs to be considered when contemplating adding “more fat” in a low carb high fat (LCHF) diet (e.g. 75% fat, 15% protein, 10% carbs).

If one needs high ketones for therapeutic reasons, then “more fat” has a benefit — but if weight loss is the goal, then “more fat” may result in a weight stall, or possibly a weight gain. That isn’t a “risk” as one normally thinks of it, but it certainly isn’t a benefit.

“More” may be better, but not always.

One also needs to consider the benefit / risk of adding “more protein” to a high protein, low fat (HPLF) diet, such as P:E (e.g. 40% protein, 30% carbs, 30% fat).

If one is eating a diet that provides 2.5 g protein / kg body weight is “good” in order to build up muscle or be a swimsuit model, one has to consider if it is really “better” to eat 3.3 g – 4.4 g protein per kg body weight (1.5 or 2 grams protein per pound). 

Just because some “do” does not make it “better”. It has to also be safe.

One has to ask if there are clinical studies that indicate that eating this high amount of protein intake long term is safe, but at present there are not.  All we have at present is the safe upper limit based on the rate of urea excretion of 3.2 g protein per kg body weight, so until it is known that “more” is better AND “safe”, staying within this safe upper limit is what is recommended.

Some will argue that since our ancient ancestors ate a largely meat diet that there is no limit on the amount of protein we can eat, however not all “meat” is protein, some is fat. In addition, it is known that our ancient ancestors also had carbohydrate in the diet as berries, above ground vegetables and tubers and recently it was discovered that~ 6,000 years ago, our ancient ancestors from present-day Kenya and Sudan were also eating milk products, which contains carbohydrate.

Dr. Loren Cordain, Professor from the Department of Health and Exercise Science at Colorado State University who is renowned for his work over the last two decades on the evolutionary and anthropological basis for diet estimates the protein intake of our ancient ancestors at 35% of total caloric intake [11].

A Low Carb High Protein (LCHP) Diet

A low carb high protein (LCHP) diet can be either low carbohydrate (<130g of carbs) or very low carbohydrate / ketogenic (20-50 g of carbs) and a low carbohydrate diet, is suitable for people with pre-diabetes or type 2 diabetes for improved glucose control and weight loss. A low carb high protein diet avoids the problem of excess fat or excess protein by prioritizing protein around individual need (outlined above), then limiting carbs to the level most suited to the individual for glycemic (blood sugar) control. The remainder of dietary intake is just enough fat to make everything taste good, and to provide essential fatty acids. The situation of either excess fat or excess protein is avoided. 

A high protein low fat (HPLF) diet such as the P:E Diet (40% protein, 30% carbs, 30% fat) is very different. It is a moderate carbohydrate diet of ~130—177 g carbohydrate per day, and is not the most suitable for those already not tolerating higher amounts of carbohydrate intake, such as those with pre-diabetes or type 2 diabetes. It’s good for healthy individuals seeking to build muscle mass; provided dietary intake of protein does not exceed the maximum level of urea excretion.

Final Thoughts…

For those seeking to lose weight or normalize blood glucose levels, a low carbohydrate diet is accepted by both the American Diabetes Association and Diabetes Canada and considered both safe and effective, so either a low carb high fat or low carb high protein diet would be suitable. In either, the percentage of fat is considered “high”, because a “low fat diet” is anything at or below 30% of calories[4]. By definition, since either diet provides more than 30% of energy as fat , they are both considered “high fat” diets.

I think it is more reasonable to consider diets with fat intakes of 30-45% of daily calories as fat as moderate fat diets, and those above that level as “high fat” diets, but this is only my opinion.

Whether one sets fat intake at 50% or 75% of calories depends on an individual’s goals. If a person needs low levels of ketones for therapeutic reasons, or are engaging in regular periods of extended fasting and can handle the extra energy intake of a high fat diet, then for weight loss or blood sugar control, a low carb high fat diet might be a good choice.

For those who don’t have any specific need for ketones, or who  practice only daily periods of intermittent fasting (12-16 hours), then for blood sugar control and weight loss, a low carb high protein diet may be a better option.

I have been providing a low carb high fat (LCHF) Meal Plans for the last 5 years and low carb high protein (LCHP) Meal Plans for the last 3 years and design Meal Plans for either.

“There is no one-sized-fits-all low carb or keto diet”.

More Info?

If you are interested in having me design a Meal Plan for you, then please have a look at the Complete Assessment Package under the Services tab (for those in Canada).

If you are outside of Canada and would like me to provide you with Nutrition Education for either low carb high fat or low carb high protein, then please have a look the Meal Plan Package under the Services tab.

To your good health!

Joy

You can follow me on:

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References

1. Stubbs J, Ferres S, Horgan G, Energy Density of Foods: Effects on Energy Intake, Critical Reviews in Food Science and Nutrition, 40:6, 481-515, 2010
2. American Diabetes Association, Lifestyle Management Standards of Medical Care in Diabetes — 2019. Available at: http://care.diabetesjournals.org/content/42/Supplement_1. Accessed: Dec. 17, 2018.
3. 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
4. Institute of Medicine (US) Committee on Examination of Front-of-Package Nutrition Rating Systems and Symbols; Wartella EA, Lichtenstein AH, Boon CS, editors. Front-of-Package Nutrition Rating Systems and Symbols: Phase I Report. Washington (DC): National Academies Press (US); 2010. Appendix B, FDA Regulatory Requirements for Nutrient Content Claims. Available from: https://www.ncbi.nlm.nih.gov/books/NBK209851/
5. Tomé D, Bos C, Dietary Protein and Nitrogen Utilization, The Journal of Nutrition, Volume 130, Issue 7, July 2000, Pages 1868S—1873S, https://doi.org/10.1093/jn/130.7.1868S
6. 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
7. National Academies Press, Dietary Reference Intakes for Energy, Carbohydrate, Fiber, Fat, Fatty Acids, Cholesterol, Protein and Amino Acids (2005)
8. 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
9. 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
10. 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
11. Cordain L, Miller JB, Eaton SB, Mann N, Holt SH, et al. (2000) Plant-animal subsistence ratios and macronutrient energy estimations in worldwide hunter-
    gatherer diets. The American Journal of Clinical Nutrition 71(3): 682—692
12. Bleasdale, M., Richter, K.K., Janzen, A. et al. Ancient proteins provide evidence of dairy consumption in eastern Africa. Nat Commun 12, 632 (2021). https://doi.org/10.1038/s41467-020-20682-3

Copyright ©2021 The LCHF Dietitian (a division of 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.

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  TG:HDL ratio can be used in some cases to see if an apoB is warranted 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 as a rough screening, 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].

Some believe that when apoA is measured along with apoB (found in Very Low Density Lipoprotein (VLDL) and Low Density Lipoprotein (LDL)), it is an even stronger predictor of CVD risk than apoB alone [2]. More on this below. There are those who believe that any ratios (either apoA/apo B or TG:HDL) is problematic and that apoB alone should evaluate risk.

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 Apolipopoprotein B (apoB), the lipoprotein in VLDL.

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 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.

Some believe that an apoB/apoA ratio is an even better predictor of CVD risk, than ApoB alone [2], and that an apo B / apo A ratio of > 0.9 a risk for CVD. Others only consider apoB alone to be a strong assessor of cardiovascular risk.

Triglyceride (TG):HDL Ratio

Measuring apoB requires special blood tests, but studies have found that an estimate of the size of the LDL can be calculated by dividing triglycerides (TG) by HDL-cholesterol (HDL-C) from a standard lipid panel. 

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

While TG:HDL ratio can provide some indication of the size of LDL cholesterol / particle number, when LDL is very high I recommend that a person have an apoB test. When that is not possible, I feel it is prudent to change the types and amounts of fat being eaten, to lower overall LDL cholesterol.

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 two 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.

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 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/lchfRD
Facebook: https://www.facebook.com/lchfRD/
Instagram: https://www.instagram.com/lchf_rd

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 The LCHF Dietitian (a division of BetterByDesign Nutrition Ltd.)

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

Two years ago, I wrote an article about why symptoms of IBS often improve on a low carb diet, but what if they don’t? What if they feel quite a bit better but still have some IBS symptoms? Learning which low-carb foods may be problematic can help — from low-FODMAP and beyond.

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. I teach this through my long-standing private practice which focuses on GI issues and food allergies.

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

In my GI and food allergy focused practice, I teach how to implement a low-FODMAP diet in 3 progressive stages, so that with 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 you would like to learn a low-FODMAP diet please reach out to me and let know.

To your good health!

Joy

You can follow me on:

Twitter: https://twitter.com/lchfRD
Facebook: https://www.facebook.com/lchfRD/
Instagram: https://www.instagram.com/lchf_rd

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 The LCHF Dietitian (a division of 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.

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.

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/lchfRD
Facebook: https://www.facebook.com/lchfRD/
Instagram: https://www.instagram.com/lchf_rd

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 The LCHF Dietitian (a division of 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 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 body 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 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. 4í·5=80%) of calories come from fat and 20% (i.e. 1í·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 can 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/lchfRD
Facebook: https://www.facebook.com/lchfRD/
Instagram: https://www.instagram.com/lchf_rd

References

1. U.S. Department of Health and Human Services: Final MNT regulations. CMS-1169-FC. Federal Register, 1 November 2001. 42 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 The LCHF Dietitian (a division of 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.

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

Macros

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

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

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

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

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

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

The first therapeutic ketogenic diet was used prior to 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. 4í·5=80%) of calories come from fat and 20% (i.e. 1í·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

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) 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 elaborates on the how the protein intake in the P:E diet differs from a regular “low carb” diet and the popularized “keto diet”, and this article compares the popularized “keto diet” (best known through Diet Doctor and Dr. Jason Fung), the ‘higher protein, lower fat’ dietary approach of Drs. Phinney and Volek (described in their book The Art and Science of Low Carbohydrate Living) and the Protein to Energy (P:E) ratio diet of Dr. Ted Naiman in terms of;

• Is protein adequate based on the RDA?
• Is protein enough to sustain someone who is physically active?
• Is protein enough for an older adult?
• Is protein within the safe upper limit?
• Does protein exceed the maximum level of amount of
  protein based on the disposal of ammonia in urea in the urine?

Final Thoughts…

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/lchfRD
Facebook: https://www.facebook.com/lchfRD/
Instagram: https://www.instagram.com/lchf_rd

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 The LCHF Dietitian (a division of 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.

Three years ago (March 12, 2018) I wrote about an article that appeared in the Journal of the American Medical Association in September 2016 [1] that revealed that the sugar industry had funded three renowned Harvard researchers to write a series of articles that downplayed, discredited or ignored known research that demonstrated sugar was a contributor to heart disease — and instead put the blame on fat, especially saturated fat.

When I read it, I was stunned at its significance — and it made me wonder how much of what I learned in my training needed to be revisited in a current light.

As written about in my initial post, two of the three Harvard researchers paid by the sugar industry were the late Dr. Fredrick Stare, chair of Harvard’s School of Public Health Nutrition Department and the late Dr. D. Mark Hegsted, a professor in the same department [2]. I only found out after I had posted the article in March 2018 that one of the 3 Harvard researchers, Dr. D. Mark Hegsted was directly involved in the development of the 1977 US Dietary Goals [4] —which was by Hegsted and his staff at the newly-created Office of Nutrition of the Department of Agriculture as the basis for the 1980 Dietary Guidelines for Americans. These were the first Guidelines that called for Americans to decrease consumption of meat and saturated fat with the belief that it would lower the risk of heart disease. 

I planned to go back at some point and write an updated post that included the historic paper trail, but never did. Today when I was posting on social media about the ~300 articles I have written the last 5 years (under the Food For Thought tab), I realized I inadvertently omitted three articles — with one of them being the one about the sugar industry’s sponsorship of the Harvard researchers. That article was too important to leave off — and it still needed to be updated.

Today, instead of taking the stat holiday off, I rewrote the earlier article with inclusion of documentation of Hegsted’s role — both in writing the sugar industry sponsored papers in 1967, and his role in advising the Select Committee on Nutrition and Human Needs on the 1977 Dietary Goals.

This is the resulting article.

In the mid-1960’s, the Sugar Research Foundation (SRF), the predecessor to the Sugar Association wanted to counter research that had been published at the time which suggested that sugar was a more significant contributor of atherosclerosis, than dietary fat. The Sugar Research Foundation invited Dr. Stare of Harvard’s School of Public Health Nutrition Department to join its scientific advisory board, and then approved $6,500 in funds ($50,000 in 2016 dollars) “to support a review article that would respond to the research showing the danger of sucrose[1]”.

From the 2016 Kearn’s et al article [1],

“On July 13, 1965, the Sugar Research Foundation (SRF)’s executive committee approved Project 226, a literature review on Carbohydrates and Cholesterol Metabolism by Hegsted and Robert McGandy, overseen by Stare.”

According to the article, letters were exchanged between the Sugar Research Foundation and the three Harvard researchers that tasked them preparing ”a review article of the several papers which find some special metabolic peril in sucrose [sugar] and, in particular, fructose [1]”.

In a letter written to Dr. DM Hegsted, the Sugar Research Foundation made its agenda clear [1];

”Our particular interest had to do with that part of nutrition in which there are claims that carbohydrates in the form of sucrose make an inordinate contribution to the metabolic condition, hitherto ascribed to aberrations called fat metabolism. I will be disappointed if this aspect is drowned out in a cascade of review and general interpretation.[2]”

Hegsted replied to the Sugar Research Federation on behalf of the three Harvard researchers, saying;

”We are well aware of your particular interest in carbohydrate and will cover this as well as we can [1].”

Project 226, sponsored by the Sugar Research Foundation resulted in a 2-part literature review by McGandy, Hegsted and Stare that was published in the New England Journal of Medicine in 1967 titled “Dietary Fats, Carbohydrates and Atherosclerotic Disease”. There was no mention of the Sugar Research Federation sponsorship of the research [1].

The first part of the two-part review article written by Drs. Stare, Hegsted and McGandy stated;

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

The report concluded;

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

The Harvard researchers continued;

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

…and concluded;

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

Stare, Hegsted and McGandy did not disclose that they were paid by the Sugar Research Foundation for the two-part review that vindicated sugar and blamed fat — most notably dietary saturated fat. 

Dr. Marion Nestle, Professor of Nutrition, Food Studies and Public Health at New York University wrote an editorial which appeared in the same issue of the Journal of the American Medical Association as the Kearn’s article [1] where she said that the documents provided ”compelling evidence” that the sugar industry initiated Project 226 research ”expressly to exonerate sugar as a major risk factor for coronary heart disease“[4].

Nestle notes;

“The investigators knew what the funder expected, and produced it. Whether they did this deliberately, unconsciously, or because they genuinely believed saturated fat to be the greater threat is unknown [4].”

The story doesn’t end there.

Dr. DM Hegsted went on to play a significant role in advising the Select Committee on Nutrition and Human Needs that oversaw the development of the 1977 Dietary Goals for the United States — and ultimately oversaw the writing of the first Dietary Guidelines for Americans that called for a reduction in saturated fat consumption in order to lower the risk of coronary heart disease. 

Below is front page of the Dietary Goals for the United States from the Select Committee on Nutrition and Human Needs from December 1977 [5], and directly below that is a page from this book that refers to Dr. D.M. Hegsted’s role in advising the Select Committee on Nutrition and Human Needs on the US Dietary Guidelines [5].

Here is the quote about Dr. Hegsted’s role in the Committee that oversaw the 1977 Dietary Goals for the United States;

“Dr. Hegsted has worked very closely and patiently with the committee staff on this report, devoting many hours to review and counselling. He feels very strongly about the need for public education in nutrition and the need to alert the public to the consequences of our dietary trends. He will discuss these trends and their connection with our most killing diseases. [5]”

There were 8 hearings of the Committee titled “Diet Related to Killer Diseases” that were held from July 1976 until October 1977 [7] and which provided an opportunity for US senators to hear from leading scientists, government officials, and business representatives about the risks of diet on heart disease, cancer, and other chronic diseases. 

“Of those who gave testimony at the first hearings, perhaps the two most important were assistant secretary for health and former director of the National Heart and Lung Institute, Theodore Cooper, and Professor Hegsted” [7].

Hegsted admitted to the Committee that the primary evidence for an association between diet and ‘killer diseases’ was ”epidemiologic” [the weakest form of scientific data] [8], and not rooted in clinical studies*. He felt that there was ”a clear linkage between plasma serum lipids, atherosclerosis and coronary disease” and that it was ”clear that diet controls cholesterol levels“[8].

*[Note: April 04, 2021] – There were only 8 randomized clinical trials available at the time with only 2,467 male subjects, and no female subjects [9] and there was no supporting evidence from those studies that reduced total dietary fat or dietary saturated fat decreased death from all causes or death from cardiovascular disease [9]. This is why the “primary evidence was epidemiologic”.

Several researchers pleaded with the Committee to wait for more research. The director of the National Heart, Lung and Blood Institute, Dr. Robert Levy said “no one knew if eating less fat would prevent heart attacks“. Dr. Robert Olson of St. Louis University said, “I plead in my report and will please again orally here for more research on the problem before we make announcements to the American public” and Dr. Peter Ahrens said “advising Americans to eat less fat on the strength of such marginal evidence was equivalent to conducting a nutritional experiment with the American public as subjects“.

Committee Chairman Sen. McGovern responded

”Senators don’t have the luxury that the research scientist does of waiting until every last shred of evidence is in.“

Hegsted believed there could be “no risks” to recommending that the American public eat less meat, less fat — particularly saturated fat, and less cholesterol.

“What are the risks to eating less meat … fat, particularly saturated fat … cholesterol …(and) more unsaturated fat … fruits, vegetables, and cereal products, particularly those made of whole grain cereal. There are none that can be identified and important benefits can be expected.  “[8]

[Note April 4, 2021] The epidemiological data that Hegsted relied on was from Ancel Keys’ yet-unpublished Seven Country Study [9] where he collected data from men aged 40-59 from the USA, Finland, the Netherlands, Yugoslavia, Greece and Japan from 1958 – 1964. The Seven Country Study data has been criticized for several reasons, including the fact that Keys did not choose countries such as Switzerland or France who were known to have very high saturated fat consumption, yet low rates of heart disease.  Data from Greece, Italy and Yugoslavia were thought to have not been representative of what they normally ate, since these countries were still facing poverty post WWII.

Keys had been alleging since 1952 that there was a direct association between saturated fat and heart disease based on a graph that he drawn in a 1952 presentation at Mt. Sinai Hospital in New York, and later published in 1953, in which he plotted CVD deaths per 1000 people (y-axis) against Percent Calories from Fat (x-axis), for six countries; Japan, Italy, England and Wales, Australia, Canada, the USA. The 6 points were a subset of data from a 21 country study published by Yerushalamy and Hilleboe more than a decade earlier [11] — and while the 6 points that Keys’ selected showed a nice linear relationship between fat intake and heart disease, the full data from Yerushalamy and Hilleboe was not linear at all.  Undeterred, Keys set out in his Seven Country Study to demonstrate a relationship between saturated fat intake and heart disease.

“Hegsted was urging action on the basis not of evidence of a demonstrated relationship between exposure and outcome, but a combination of limited studies, prevailing scientific opinion, and risk-benefit probabilities[7].” ~Dr. Marion Nestle

Final Thoughts…

The significance of the sugar industry’s sponsorship of the three Harvard researchers to write review papers vindicating sugar and blaming fat —especially saturated fat for heart disease is important in and by itself. The fact that one of those researchers, Dr. DM Hegsted was a major influencer of the 1977 US Dietary Goals — and then oversaw the writing of the Dietary Guidelines for Americans that called for reducing saturated fat consumption and increasing consumption of cereal products cannot be understated.  Basing national dietary guidelines on epidemiologic studies made the general public the equivalent of subjects in a huge, unplanned experiment.

For 40+ years, we’ve had low fat dietary guidelines in the US and Canada that were based largely on the hypotheses of a link between dietary saturated fat and heart disease. They were not based on clincal research, but weak epidemiological studies such as Ancel Keys’ Seven Country Study that was conducted many years before it was published in 1980. Furthermore, the dietary recommendations arrogantly assumed that decreasing meat and saturated fat consumption and increasing grains and cereals came without risk. 

How have these low fat dietary guidelines turned out?

Heart disease is still the number one killer in the US, and second in Canada, obesity is through the roof, and rates of type 2 diabetes continue to rise.

There were consequences to recommending Americans reduce meat, fat and saturated fat consumption and increase consumption of grain and cereal products — and that is that the subsequent rise in carbohydrate consumption directly contributed to the current obesity epidemic and the metabolic diseases that accompany it. 

A report published in June 2020 in the Journal of the American College of Cardiology based on meta-analysis of randomized control trials (the strongest data available), as well as observational studies found no beneficial effect on either cardiovascular disease (CVD) or death of lowering saturated fatty acid intake and that saturated fat intake is actually protective against stroke [5].

Without industry influence, it is time that the role of sugar and refined carbohydrate consumption on obesity and metabolic disease informs reevaluation of dietary guidelines. 

More Info?

If you would like information about what I do, 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 at:

Twitter: https://twitter.com/lchfRD
Facebook: https://www.facebook.com/lchfRD/
Instagram: https://www.instagram.com/lchf_rd

References

1. Kearns C, Schmidt LA, Glantz SA, et al. Sugar Industry and Coronary Heart Disease Research: A Historical Analysis of Internal Industry Documents. JAMA Intern Med. 2016 Nov 01; 176(11):1680-1685.
2. Husten, L, How Sweet: Sugar Industry Made Fat the Villain, Cardio|Brief, 2016 Sept 13.
3. McGandy, RB, Hegsted DM, Stare,FJ. Dietary fats, carbohydrates and atherosclerotic vascular disease. New England Journal of Medicine. 1967 Aug 03;  277(5):242—47
4. Nestle M. Food Industry Funding of Nutrition Research: The Relevance of History for Current Debates. JAMA Intern Med. 2016;176(11):1685—1686. doi:10.1001/jamainternmed.2016.5400
5. Dietary Goals for the United States, Select Committee on Nutrition and Human Needs, United States Senate. Washington : U.S. Govt. Print. Off., 1977. http://hdl.handle.net/2027/uiug.30112023368936
6. 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
7. Oppenheimer GM, Benrubi ID. McGovern’s Senate Select Committee on Nutrition and Human Needs versus the meat industry on the diet-heart question (1976-1977). Am J Public Health. 2014 Jan;104(1):59-69. doi: 10.2105/AJPH.2013.301464. Epub 2013 Nov 14. PMID: 24228658; PMCID: PMC3910043.
8. United States. Congress. Senate. Select Committee on Nutrition and Human Needs. (1977). Diet related to killer diseases: hearings before the Select Committee on Nutrition and Human Needs of the United States Senate, Ninety-fifth Congress, first session. Washington: U.S. Govt. Print. Off..
9. Keys A. Coronary heart disease in seven countries. 1970. Nutrition. 1997 Mar;13(3):250-2; discussion 249, 253. doi: 10.1016/s0899-9007(96)00410-8. PMID: 9131696.
10. Harcombe, Z., An examination of the randomised controlled trial and epidemiological evidence for the introduction of dietary fat recommendations in 1977 and 1983:   A systematic review and meta-analysis. 2015, University of the West of Scotland.
11. Yerushalmy J, Hilleboe HE, Fat in the diet and mortality from heart disease; a methodologic note. N Y State J Med, 1957. 57(14): p. 2343-54.

Copyright ©2021 The LCHF Dietitian (a division of 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.

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]. 

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/lchfRD
Facebook: https://www.facebook.com/lchfRD/
Instagram: https://www.instagram.com/lchf_rd

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.

People also have the option to self-pay for these tests.

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. Bermíºdez 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 The LCHF Dietitian (a division of 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 – Protein Intake in the High Fat “Keto Diet”

The well-known high fat “keto” diet that is 75% fat,  10% carbs and 15% protein is only one of many keto diets. The amount of protein is not based on body weight, but is a percentage of energy. A diet which is 75% fat means there is lots of added fat in the form of whipping cream, avocado, bacon and fatty meat in order to make up for the very low carbohydrate intake (10%) and only 15% of calories allotted to protein. 

A 100 kg man (220 pounds) with an energy consumption of 2500 kcal/day would be eating 1875 calories / 208g as fat, 250 calories / 62g as carbs and 375 calories / 94g as protein.

A 60 kg woman (132 pounds) with an energy consumption of 2000 kcals/day would be eating 1500 calories / 166 g as fat, 150 calories / 37.5 g as carbs and 225 calories / 56g as protein.

Does this amount meet people’s needs? 

For the 100 kg man;

√ Is protein adequate based on the RDA? His protein intake based on the RDA of 0.8 g protein / kg body weight [1] so his basic needs are only 80g, so this diet is adequate at 94 g. Remember, this is the minimum amount of protein needed to meet the needs of 97-98% of healthy individuals, not an optimal amount.

X Is protein enough to sustain someone who is physically active? Based on the Academy of Nutrition and Dietetics, Dietitians of Canada, and the American College of Sports Medicine[2] which recommends and intake of 1.2—2.0 g protein / kg per day, his protein intake needs to be 120 g – 200 g per day to sustain physical activity, so is inadequate at 94g.

X Is protein enough for an older adult? Based on recent position papers [3,4] his protein intake needs to be between 1.0 and 1.5 g protein / kg per day, which is 100 – 150 g per day, and is inadequate at 94g.

√ Is protein within the safe upper limit? The highest end of the range of safe intake of protein is 2.5 g protein/ kg per day and at 94 g of protein, his intake is below 250 g protein per day based on his weight, so it is safe.

√ Does protein exceed the maximum level of amount of protein based on the disposal of ammonia in urea in the urine? A 100 kg man (220 pounds) with 20% body fat would have 80 kg lean mass and 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). His intake is only 94 g or protein, so it is safe.

For the 60 kg woman;

√ Is protein adequate based on the RDA? Her protein intake based on the RDA of 0.8 g protein / kg body weight [1] needs to be only be 48g, so is adequate at 56 g to prevent deficiency.

X Is protein enough to sustain someone who is physically active? Based on the Academy of Nutrition and Dietetics, Dietitians of Canada, and the American College of Sports Medicine[2] which recommends and intake of 1.2—2.0 g protein / kg per day, her protein intake would need to be 72 g – 120 g per day to sustain physical activity, so is inadequate at 56g.

X Is protein enough for an older adult? Based on recent position papers [3,4] her protein intake would need to be between 1.0 and 1.5 g protein / kg per day, which is 60 – 90 g protein per day, so is inadequate at 56 g.

√ Is protein within the safe upper limit? The highest end of the range of safe intake of protein is 2.5 g protein/ kg per day and at 56 g of protein, her intake is below 150g protein per day based on her weight, so it is safe.

√  Does protein exceed the maximum level of amount of protein based on the disposal of ammonia in urea in the urine? A 60 kg (132 pound) woman with 25% body fat, would have 45 kg of lean mass, and based on energy consumption of 2000 kcals/ day would have a maximum protein ceiling of 144 g/day. Her intake of 56 g of protein in safe.

B – The Higher Protein, Lower Fat Ketogenic Dietary approach

This approach used for weight loss by Drs. Phinney and Volek in their book The Art and Science of Low Carbohydrate Living works out to approximately 60-70% fat, 20% up to 30% protein and 10% carbohydrate (Nutritional Ketogenic), but the macros are determined based on ideal body weight, which is estimated by lean body mass.

From page 210 of their book [6];

”…our studies of muscle retention and function during carbohydrate restriction, we recommend daily protein intakes between 1.5 and 2.5 grams per day per kg of reference body weight [6].”

What would this amount of protein look like in terms of intake?

A man who is 5’9″³ (1.75 m) tall and weighs 100 kg ( 220 pounds) has an IBW (lean body mass) of 155 pounds (70 kg), so protein intake should be 105 g – 175.0 g protein.

A woman who is 5″² 4 “³(1.63 m) tall and weighs 60 kg (132 pounds) has an IBW (lean body mass) of 127 pounds (55 kg), so protein intake according to Phinney and Volek should be between 82.5 g – 137.5 g protein.

For the 100 kg man;

√ Is protein adequate based on the RDA? His protein intake based on the RDA of 0.8 g protein / kg body weight [1] would need only be 80g, so is adequate between 105 g – 175 g protein. 

√ Is protein enough to sustain someone who is physically active? Based on  the Academy of Nutrition and Dietetics, Dietitians of Canada, and the American College of Sports Medicine[2] which recommends and intake of 1.2—2.0 g protein / kg per day, his protein intake would need to be 120 g – 200 g per day to sustain physical activity, so is adequate between 105 g – 175 g protein. 

√  Is protein enough for an older adult? Based on recent position papers [3,4] his protein intake would need to be between 1.0 and 1.5 g protein / kg per day, which is 100 – 150 g per day, and is adequate between 105 g – 175 g protein. 

√ Is protein within the safe upper limit? The highest end of the range of safe intake of protein is 2.5 g protein/ kg of total weight per day, so is safe at 2.5 g protein IBW (i.e. 70 kg / 155 pounds) which is total intake of 105 g – 175 g protein. 

√ Does protein exceed the maximum level of amount of protein based on the disposal of ammonia in urea in the urine? 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). His intake between 105 g – 175 g protein is safe.

For the 60 kg woman;

√ Is protein adequate based on the RDA? Her protein intake based on the RDA of 0.8 g protein / kg body weight [1] would need only be 48g, so is adequate at 82.5 g – 137.5 g protein. Remember, this is the minimum amount of protein needed to meet the needs of 97-98% of healthy individuals.

√ Is protein enough to sustain someone who is physically active? Based on the Academy of Nutrition and Dietetics, Dietitians of Canada, and the American College of Sports Medicine[2] which recommends and intake of 1.2—2.0 g protein / kg per day, her protein intake would need to be 72 g – 120 g per day to sustain physical activity, so is adequate at 82.5 g – 137.5 g protein.

√ Is protein enough for an older adult? Based on recent position papers [3,4] her protein intake would need to be between 1.0 and 1.5 g protein / kg per day, which is 60 – 90 g per day, and is adequate at 82.5 g – 137.5 g protein.

√ Is protein within the safe upper limit? The highest end of the range of safe intake of protein is 2.5 g protein/ kg per day and at 82.5 g – 137.5 g protein her intake is below 150g protein per day based on her weight, so it is safe.

√  Does protein exceed the maximum level of amount of protein based on the disposal of ammonia in urea in the urine? A 60 kg (132 pound) woman with 25% body fat, would have 45 kg of lean mass, and based on energy consumption of 2000 kcals/ day would have a maximum protein ceiling of 144 g/day. Her intake of 82.5 g – 137.5 g protein is safe.

C – Very High Protein, Low Fat Protein to Energy (P:E) Ratio Diet

By definition, the P:E ratio diet (40% protein, 30% carbs, 30% fat) is a High Protein Low Fat diet, as fat is at or below the USDA low fat cutoff of 30% — based on the P:E ratio calculator located at www.p2eq.com.

It is largely a moderate carbohydrate approach (130-225g carbs per day), but for some weights and heights generates carbs of just under 130g / day, the cutoff for low carb.

Based on that calculator:

A man who is 5’9″³ (1.75 m) tall should weigh 155 pounds (70 kg). According to this calculator and assuming this man is metabolically healthy, he should should eat 1,860 kcals as 186 g protein (2.66 g pro/kg IBW), 62 g of fat and 140 g of total carbs.

A woman who is 5″² 4″³ (1.63 m) should weigh 120 pounds (55 kg). According to this calculator and assuming she is metabolically healthy, this hypothetical woman should eat 1,440 kcals per day as 144 g protein (2.67 g protein /kg IBW), 48 g of fat and 108 g of total carbs.

For the 100 kg man;

√ Is protein adequate based on the RDA? His protein intake based on the RDA of 0.8 g protein / kg body weight [1] would need only be 80g, so is more than adequate at 186g. 

√ Is protein enough to sustain someone who is physically active? Based on the Academy of Nutrition and Dietetics, Dietitians of Canada, and the American College of Sports Medicine[2] which recommends and intake of 1.2—2.0 g protein / kg per day, his protein intake would need to be 120 g – 200 g per day to sustain physical activity, so is more than adequate at 186g.

√ Is protein enough for an older adult? Based on recent position papers [3,4] his protein intake would need to be between 1.0 and 1.5 g protein / kg per day, which is 100 – 150 g per day, and is more than adequate at 186g.

√ Is protein within the safe upper limit? The highest end of the range of safe intake of protein is 2.5 g protein/ kg per day and at 186 g of protein, his intake is below 250g protein per day based on his weight, so it is safe.

√ Does protein exceed the maximum level of amount of protein based on the disposal of ammonia in urea in the urine? According to the online calculator, a man who is 5’9″³ (1.75 m) tall should weigh 155 pounds (70 kg), and eat 1,860 kcals as 186 g protein but in this case, he weighs 100 kg (220 pounds) and has 30% body fat. Safe intake is based on his LBM so the fact that he is overweight makes no difference.  Based on the maximum amount of ammonia disposal of 3.21 g of protein / kg of lean body mass his maximum amount of protein would be 225 g / day, so 186 g protein is safe.

For the 60 kg woman;

√ Is protein adequate based on the RDA? Her protein intake based on the RDA of 0.8 g protein / kg body weight [1] would need only be 48g, so is more than adequate at 144 g. 

√ Is protein enough to sustain someone who is physically active? Based on the Academy of Nutrition and Dietetics, Dietitians of Canada, and the American College of Sports Medicine[2] which recommends and intake of 1.2—2.0 g protein / kg per day, her protein intake would need to be 72 g – 120 g per day to sustain physical activity, so is more than adequate at 144 g. 

√ Is protein enough for an older adult? Based on recent position papers [3,4] her protein intake would need to be between 1.0 and 1.5 g protein / kg per day, which is 60 – 90 g per day, and is more than adequate at 144 g. 

√ Is protein within the safe upper limit? The highest end of the range of safe intake of protein is 2.5 g protein/ kg per day and at 144 g of protein, her intake is below 150g protein per day based on her weight, so it is safe.

√ / X? Does protein exceed the maximum level of amount of protein based on the disposal of ammonia in urea in the urine? According to the online calculator, a woman who is 5″² 4″³ (1.63 m) should weigh 120 pounds (55 kg). should eat 1,440 kcals per day as 144 g protein (576 kcal / 1440 kcals = 40% protein). Based on the maximum amount of ammonia disposal of 3.21 g of protein / kg of lean body mass [5], her maximum amount of protein is 144 g / day, so she is at the very high end of the safe range. 

Note: When a high protein diets include supplementation with whey protein (such as the P:E ratio encourages by listing it as one of the best protein to energy sources) it is much easier to exceed the upper limit of protein and exceed the capacity of the body to excrete the ammonia as urea. It should be noted that this is much more difficult to do eating only real, whole food.

Final Thoughts…

Which low carbohydrate dietary approach is best for you will depend on your protein needs. If you want to make sure to have enough protein to be very active or to preserve muscle as an older adult, then the popularized high fat “keto” diet would not necessarily be the best approach.

If you don’t want to exceed the safe range of protein intake and the capacity of your body to get rid of ammonia, yet want to eat a very high protein, low fat diet, then be sure to do the calculations.

I think that the safest approach is the one Drs. Phinney and Volek recommend and which meet the needs of a wide range of people from the very active to older adults and with protein intakes that are well within the safe range of protein intake and a outlined in a recent article, Drs. Phinney and Volek along with Dr. Brittanie Volk updated their recommendations for protein in 2018 to be between 1.5 and 1.75 grams of protein per kg of reference body weight [7] from the earlier 1.5 and 2.5 grams per day per kg of reference body weight [6] — which puts protein recommendations well within the safe range, while meeting or exceeding the needs of a wide range of people.

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/lchfRD
Facebook: https://www.facebook.com/lchfRD/
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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
6. Volek JS, Phinney SD, The Art and Science of Low Carbohydrate Living: An Expert Guide, Beyond Obesity, 2011
7. Phinney SD, Volek JS, Volk B, How Much Protein Do You Need In Nutritional Ketosis? February 21, 2018, Virta Health, https://www.virtahealth.com/blog/how-much-protein-on-keto

Copyright ©2021 The LCHF Dietitian (a division of 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.

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 be calculated as grams of protein per kilogram of body weight.

Note: this article is Part 1 of 2.  Be sure to read the following article titled Protein Intake in Popular Low Carbohydrate / Keto Diets for Weight Loss.

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;

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.

Be sure to read the following article titled Protein Intake in Popular Low Carbohydrate / Keto Diets for Weight Loss which is Part 2 of this one.

To your good health!

Joy

You can follow me on:

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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 The LCHF Dietitian (a division of BetterByDesign Nutrition Ltd.)

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

Some believe that a ketogenic diet was first used to treat epilepsy and that the diet was later adapted for use in treating those with diabetes, but as the previous article titled A Hundred Years of Treating Diabetes with a Low Carb and Ketogenic Diet points out, Dr. Russell Wilder who coined the term “ketogenic diet” and who is famous for his application of the diet in epilepsy, remains virtually unknown for his earlier use of a ketogenic diet for the treatment of diabetes. This short article provides the historic evidence that a ketogenic diet was used first in diabetes treatment, and later applied to the treatment of epilepsy.

Wilder’s First Musings About Use of a Ketogenic Diet in Epilepsy

On July 27, 1921, Dr. Russell Wilder wrote a short article in The Clinic Bulletin of the Mayo Clinic where he explained his thinking regarding Geyelin’s use of fasting in epilepsy, and why he thought that a ketogenic diet could work just as well. Note the highlighted ”as has long been known” which alludes to his and other’s previous use of a ketogenic diet in the treatment of diabetes.

Wilder’s First Use of a Ketogenic Diet in Diabetes

In 1958, Wilder’s published ”Recollections and Reflections on Education, Diabetes, Other Metabolic Diseases, and Nutrition in the Mayo Clinic and Associated Hospitals, 1919-1950” in which he said;

”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. 

While the first printing of the book A Primer for Diabetic Patients was in 1921, it is clear from what Wilder wrote in “Recollections and Reflections” (1958) that a ketogenic diet was already being used by Dr. Frederick M. Allen to treat those with diabetes (prior to 1920):

“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.

A book titled “The Starvation Treatment of Diabetes Mellitus” written by Dr. Walter R. Steiner was published in 1916 and outlines the treatment protocol of Dr. Frederick M. Allen on which Dr. Russell Wilder based his method at the Mayo Clinic.

[Note: Special thanks to Doug Gilliland, Engineer of Connellsville, Pennsylvania for bringing this book to my attention.]

Note: The following protocol should not be attempted on one’s own.  This was used in a supervised hospital setting.

As outlined on page 177-179 of Steiner’s book, Dr. Allen’s treatment consisted of first fasting the patient for 2-4 days (up to 8-10 days) while the patient could drink as much water, coffee, tea and meat broth as they wished.

Once the patient’s urine was free of sugar for a period of 24-hours, they were given 150g of low carbohydrate vegetables (5 g carbohydrate) that were boiled three times and the water discarded to further reduce the amount of carbohydrate in them. Then 5 grams of carbohydrate was added every other day from the list of low carb vegetables (5 grams carbohydrate), then medium carbohydrate vegetables (10 gram carbohydrate) and finally high carbohydrate vegetables (15 grams carbohydrate). Finally, the carbohydrate content of the diet was gradually titrated up by adding fruit, potato, oatmeal and bread — provided that no sugar appears in the urine.  Once the urine has been sugar free for 2 days, protein was added in the form of 3 eggs and then 15 grams of protein were added per day until the patient is receiving 1 gram of protein per kilogram body weight. Once protein tolerance (1 gram protein per kilogram body weight) was reached) 25 grams of fat were added daily until the patient stopped losing weight — or until 40 calories per kilogram body weight was reached.

Dr. Frederick Allen’s ketogenic diet was in use prior to 1916 when Dr. Walter Steiner published his book, and Dr. Russell Wilder later based his treatment protocol on Allen’s “generally accepted treatment”.

“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 which 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.“

A ketogenic diet was used in treating diabetes prior to 1916 — several years before Dr. Wilder proposed using it in epilepsy in July 1921.

Wilder’s Outline of the Timeline of Use of a Ketogenic Diet – from treatment of diabetes to use in epilepsy

Page 243 of ”Recollections and Reflections on Education, Diabetes, Other Metabolic Diseases, and Nutrition in the Mayo Clinic and Associated Hospitals, 1919-1950” Dr. Russell Wilder clearly spells out the timeline that use of a ketogenic diet in diabetes came first, then his idea that a ketogenic diet might also have application in epilepsy. 

“At an Atlantic City meeting, I had heard Gehelin’s report of the benefit in epilepsy of periods of absolute fasting and was led thereby to look into the effect of prescribing a diet so designed that it would provoke ketosis— that is, a diet very high in fat and rigidly restricted in its content of carbohydrate.”

This is what Wilder wrote about in July 27, 1921 in The Clinic Bulletin– at least a year after he was already using a ketogenic diet in the treatment of diabetes (see above) .

Final Thoughts…

People think of a ”keto diet” to treat diabetes as something new — as a “fad” even, but it has been used for over 100 years to do just that. Its therapeutic application in the treatment of epilepsy is rarely disputed yet its therapeutic use in the treatment of diabetes remains a hotly debated topic. This ought not to be.

While not everyone with type 2 diabetes wants to seek remission, those with diabetes who want choose a diet-first approach to treating the disease should be made aware that (1) such a choice exists, and as outlined in previous articles posted on this website (2) is considered safe and effective by Diabetes Australia, the American Diabetes Association (ADA), the European  Association for the Study of Diabetes (EASD), as well as Diabetes Canada. In addition, those with diabetes (3) should have the support of their healthcare team to implement such a diet with medical oversight and where needed to have their physician adjust their dosage of insulin / insulin analogues and to adjust / gradually deprescribe their oral diabetes medications, as carbohydrates are decreased.

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/lchfRD
Facebook: https://www.facebook.com/lchfRD/
Instagram: https://www.instagram.com/lchf_rd

Copyright ©2021 The LCHF Dietitian (a division of 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. Wilder RM, The Clinic Bulletin Vol 2. No. 307, The Effect of Ketonemia on the Course of Epilepsy, July 27, 1921, https://www.neslazeno.cz/wilder-1921-the-effect-of-ketonemia-on-the-course-of-epilepsy/
2. 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 MUSE, doi:10.1353/pbm.1958.0019.
3. Steiner WR, The Starvation Treatment of Diabetes Mellitus, Transactions of the Connecticut State Medical Society, 1916
4. 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

Note (February 12, 2021): This article is provided for nutrition information only and is not an endorsement of any specific type of low carbohydrate diet. Everyone’s nutritional needs are different.

Except for specific conditions such as epilepsy, seizure disorder and glioblastoma — or for those seeking the specific benefits of high ketones,  I tend to recommend a higher protein, lower fat version of a ketogenic diet when helping people with weight loss. The main reason is that for weight loss, the high fat version is normally paired with frequent- or extended-periods of fasting which, as I will outline below has some key drawbacks. 

The popularized keto diet which is 75% fat has, by definition lots of added fat in the form of whipping cream, avocado, bacon and fatty meat to make up for the lower protein of 15%, as well as very low carbs (10%). While it is enticing to eat this way, ~1/3 of my clients come to me for dietary support after either failing to lose more than a little initial weight, or gaining weight. I think that is because they may have ‘missed’ that a high fat keto diet for weight loss necessarily goes along with frequent periods of fasting, but not everyone “gets” that message or even wants to ‘fast’. 

Often times people will implement the ‘high fat keto diet part’ without implementing the ‘regular or extended fasting part’ —  adding tons of dietary fat to food. This approach will not enable someone to reduce their own body fat stores, which is why in such cases I will recommend a slightly lower fat, higher protein approach.

Something I have observed over the last several years is that the very high fat approach often does not work well for peri- and post-menopausal women.  I hypothesize that it is the change in  hormones — especially estrogen at menopause that may lower metabolic rate and thus contribute to a slowing of weight loss. Combined with lots of added fat, this becomes a recipe for failure with many peri- and post-menopausal women. I’ve also noticed that in some older women, a very high fat approach triggers cravings for ‘fat bombs’ and high-fat “keto treats” and I think this may be related to the dopamine release associated with either high fat or high carb intake — and which becomes substantially higher when with foods with both fat and carbs are eaten together.  Many of these women became obese eating high-fat high-carb foods, which leads me to believe that the reward-centre of the brain may be triggering that same desire via eating lots of high fat foods. 

I have discovered from those who come to me after eating a high fat keto diet that they came to believe from what they’ve read online that (1) dietary fat is “the” source of satiety (no longer feeling hungry) and that (2) that when “eating “keto”, calories don’t count”. 

In this article I will address these two beliefs, starting with the second.

Calories Don’t Count When Eating “Keto” 

Proponents of the popularized keto diet are often heard to say that the “calories in calories out (CICO) model” is irrelevant, and that counting calories doesn’t apply “when eating keto”.

The problem is that calories are thought of as a “thing”, rather than a process. A calorie isn’t counted, but is calculated from heat and work. 

A calorie was originally defined as “the amount of heat required to raise the temperature of 1 gram of water by 1° Celsius at a standard atmospheric pressure”.  Since the amount of heat required to raise the temperature of 1 gram of water by 1° Celsius is known to vary by as much as 1% at different temperatures, a calorie (small “c”) is defined as “the amount of heat that will raise the temperature of 1 gram of water from 14.5° to 15.5° Celsius. This is based on the first  law of thermodynamics (Law of Conservation of Energy) — that energy cannot be created or destroyed. 

The number of calories in a given food is determined by burning that food in a bomb calorimeter, which is a box with two chambers, one inside the other. A sample of the food is weighed, put on a dish in the inner chamber of the calorimeter., and burned. When the food burns, if the temperature of the water goes up 1 degree Celsius per kilogram, the food is said to have 1 calorie.

As Professor Dr. Richard Feinman said recently on social media, it’s impossible to keep track of ‘grams-in of food’ and ‘grams-out of energy’ (CO2 and exhaled water) in daily life, so in that sense the “calories in calories out model” isn’t meaningful.

The law of thermodynamics doesn’t stop applying because one is eating a keto diet. In fact, when using therapeutic ketogenic diets for conditions such as epilepsy, seizure disorder and glioblastoma, diets such as the classic Ketogenic Diet (KD) with a 4:1 ratio of fat to protein, a Modified Ketogenic Diet (MKD) with a 3:1 ratio of fat to protein, and a Modified Atkins Diet (MAD) with a 2:1 ratio of fat to protein are all calculated based on the caloric needs of the individual. These high fat diets are intended to produce large amounts of ketones for therapeutic purposes and calories definitely count when following a ketogenic (keto) diet. 

The popularized keto diet which is usually thought of as being ~75% fat, 15% protein and 10% carbohydrate is basically a hybrid between the Modified Ketogenic Diet (MKD) and the Modified Atkins Diet (MAD) — neither of which are weight loss diets. In fact, these diets were specifically designed to not result in weight loss. Unless the popularized high fat ‘keto’ diet is combined with frequent periods of fasting <24 hours and/or extended periods of fasting >24 hour, weight loss is unlikely to occur. This is why the two main proponents of the high fat ‘keto’ diet, Dr. Jason Fung and Diet Doctor both promote the high fat ‘keto’ diet together with periods of fasting. While many people are successful losing weight this way, the question is does weight loss occur because of the fasting?

Many who follow this type of diet will say that it is the high fat that makes the fasting possible, and point to fat providing “satiety” (feeling of not being hungry) but as I will elaborate on below, high fat is not the only — or even the best way to increase satiety.  Not only is protein far better at providing satiety, the amount of protein recommended by Dr. Stephen Phinney, MD, PhD and Dr. Jeff Volek, PhD, RD in their 2011 book the Art and Science of Low Carbohydrate Living is up to double the amount of the popularized keto diet.

Fat (9 calories per gram) is more than twice the calories of carbohydrate and protein (4 calories per gram each), so unless one is fasting frequently and/or for extended periods of time, it makes absolutely no sense to eat a high added fat diet if one is seeking weight loss and fasting has its drawbacks.

Frequent and/or Extended Fasting

The problem with fasting for periods longer than 24 hours is there is a loss of lean body mass (muscle) that goes along with it.

According to a 1979 research article published in the American Journal of Clinical Nutrition[1], protein is lost during extended fasting beginning on day 1 and continues until it reaches at maximum on day 3, then slowly declines. These results are validated in other studies, including one from Owen and Cahill in 1969 [2,3]. 

This graph from Virta Health [3] based on the same research [1] shows the losses in grams of nitrogen per day, where each gram represents the loss of about 1 ounce of lean tissue.

This graph also from Virta Health [3] and based on the same research shows the long-term loss of body nitrogen (protein) as % of pre-fasting value. While loss of protein slows somewhat after day 10, it continues right up to 60 days.

Based on this data, healthy overweight adults who fast for 10 days will lose 5 pounds of lean muscle [3].

According to a 1983 study by by Cahill, normal protein breakdown is ~75 g per day and while protein breakdown will eventually slow by ~25% when people are fasting long term in order to spare muscle, this is only as the “final stage of adaptation” and only “once ketoacid levels (ketones) reach a plateau and the brain is preferentially using ketoacids as fuel [4]“.  

This time frame is consistent with the research above [1,2] showing that the slowing of muscle loss only occurs after 10 days of fasting, when ketones become the preferred fuel.

For older adults — especially post-menopausal women who are already at risk of sarcopenia (muscle loss), I do not recommend fasting longer than 24 hours.

Dietary Fat or Dietary Protein as the Source of Satiety

Proponents of the high fat ‘keto’ diet say that it is the high dietary fat that makes them so much less hungry, which makes them able to fast frequently and for extended period of time, and which results in them eating less over all.  I don’t doubt this, but fat is not the only — or even the best source of satiety.  Protein is far better at producing satiety and at less than half the calories of fat!

According to a 2010 study titled Energy Density of Foods: Effect on Energy Intake [3];

“when the satiating effects of macronutrients on appetite and energy intake (EI) are compared as nutrients come in the diet (and fat contributes disproportionately to energy density (ED), Joule-for-Joule, protein is consistently (at doses above 1.2 to 1.4 MJ) more satiating than carbohydrate (CHO), which is more satiating than fat.

When energy density (ED) is controlled, protein is still far more satiating than fat or carbohydrate.”

Given that protein produces more satiety than fat and has less than half the calories as fat, it makes much more sense if someone is seeking weight loss, to provide substantially more protein in the diet and significantly less dietary fat.

But how much protein?

Protein Intake in a Ketogenic Diet

In their classic 2011 book the Art and Science of Low Carbohydrate Living, Dr. Stephen Phinney, a physician with a PhD and Dr. Jeff Volek, a Dietitian with a PhD recommend that during weight loss, fat intake be 60% of calories and protein intake be to up to 30% of calories, with carbohydrate intake be 7.5-10% of calories for men, 2.5-6.5% of calories for women [4].  This mix of 60% fat, up to 30% protein and ~10% carbohydrate has up to twice the protein intake of the popularized ‘keto’ diet (75% fat, 15% protein, 10% carbohydrate).

NOTE (February 8, 2021): A ketogenic diet that is 30% protein might have most of its fat in the meat, eggs, and cheese that comprise it — and need not have any “added fat”. It is definitely not “low fat” (<30% fat) but is approximately ~60% fat. A ketogenic diet that has only 15% protein has to have lots of added fat (75%) to make up the rest of calories, because carbs are limited to 10%.

In relation to protein intake, Phinney and Volek write on page 210;

”…our studies of muscle retention and function during carbohydrate restriction [27,78,87], we recommend daily protein intakes between 1.5 and 2.5 grams per day per kg of reference body weight [6].”

What would this amount of protein look like in terms of intake?

A woman who is 5′ 4.25″(1.63 m) tall has an IBW (lean body mass) of 127 pounds (55 kg), so protein intake according to Phinney and Volek should be between 82.5 g protein (at 1.5 g/kg) to 137.5 g protein (at 2.5 g/kg).

A man who is 5’9″ (1.75 m) tall has an IBW (lean body mass) of 155 pounds (70 kg), which means that based on of reference body weight which is the half according to Phinney and Volek, protein intake should be 105 g protein (at 1.5 per kg) to 175.0 g protein (at 2.5 g/kg).

In a more recent 2018 article published online by Drs. Phinney and Volek along with Dr. Brittanie Volk, who is also a Dietitian with a PhD write;

”While a precise analysis of dose-response to varying protein intakes during nutritional ketosis has not been done in humans, we have performed a number of studies indicating that most healthy humans maintain lean body mass and function during a ketogenic diet providing between 1.5 and 1.75 grams of protein per kg of reference body weight’ (Phinney 1983, Davis 1990). Furthermore, there are no convincing human studies showing any benefit from dietary protein above 2.0 g/kg reference weight for adults following a ketogenic diet.” [7]

Reference body weight is considered to be “roughly normal lean body mass, rather than total body weight.“ [7].

So what does this updated recommendation look like in terms of intake?

A woman who is 5′ 4.25″(1.63 m) tall has an IBW (lean body mass) of 121 pounds (55 kg), so protein intake during nutritional ketosis according to Phinney, Volek and Volk should be between 82.5 g protein (at 1.5 g/kg) to 96.25 g protein (at 1.75 g/kg).

A man who is 5’9″ (1.75 m) tall has an IBW (lean body mass) of 155 pounds (70 kg), which means that according to Phinney, Volek and Volk should be 105 g protein (at 1.5 per kg) to 122.5 g protein (at 1.75 g/kg).

Protein to Energy (P:E) Ratio

In 2019, I was following with interest the evolving thoughts of Dr. Ted Naiman with regards to the amount of protein he was thinking that we should be eating.

As I wrote about in a 2019 article, his ”P:E” ratio determines the Protein to Energy ratio of a food — with a focus on eating the most amount of protein for the least amount of energy (calories).

The P:E Diet was published as a book in 2020 and can best be described as a high protein, low fat and low-ish carb diet.  I say “low-ish” carb because some calculations recommend carbs >130 g per day, which is the cut-off for low carb in most of the literature.  On his web site the macros are clearly represented as being for healthy people without metabolic conditions, but I question whether they could even be considered for use in those with type 2 diabetes because of the higher carb intake.  After all, type 2 diabetes is the end-state of an inability to appropriately handle carbohydrates in the diet.

After listening to a recent talk of Dr. Naiman’s last week on YouTube, I have begun following his posts on social media to try to understand his implementation of these recommended macros. It is important to keep in mind that Dr. Naiman’s focus is on healthy individuals seeking optimal muscle / lean body mass and not for those seeking remission of metabolic conditions, such as type 2 diabetes.

I was curious what the P:E calculator (available at p2eq.com) would assess the macros for the sample woman and sample man, above.

Note: Since it was not possible to select 5.4.25 in the tool for the height of the sample woman, I chose 5’4.5″ — the closest match.

According to the P:E ratio, a woman who is 5′ 4.5″ (1.64 m) should weigh 121 pounds (55 kg). According to this calculator and assuming she is metabolically healthy, this hypothetical woman should eat 1,470 kcals per day as 147 g protein (2.67 g protein /kg IBW), 49 g of fat and 110 g of total carbs.

According to Dr. Naiman’s P:E ratio, a man who is 5’9″ (1.75 m) tall should weigh 155 pounds (70 kg). According to this calculator and assuming this man is metabolically healthy, he should should eat 1,860 kcals as 186 g protein (2.66 g pro/kg IBW), 62 g of fat and 140 g of total carbs.

In this calculation, the amount of protein recommended for both the woman and the man in the P:E ratio at ~2.66 g protein/kg IDW is higher than the range that Phinney and Volek determined in their 2011 book, The Art and Science of of Low Carbohydrate Living, which is based on 2.0 g protein/kg of ideal body weight.

As I wrote about in an earlier article, according to Dr. Donald Layman, PhD, Professor Emeritus, University of Illinois, the highest end of the range of safe intake of protein is 2.5 g protein/ kg per day (maximum of 200 g / day).

The high end of Phinney and Volek’s recommendations from their 2011 book of 2.5 g protein/kg IDW are at what Dr. Layman indicates is the high end of the safe range. While Dr. Naiman’s recommendations at 2.66 g protein/kg IDW is slightly higher than the 2.5 g protein/kg IDW, it is not in terms of the absolute number of grams of protein (>200 g/day).

NOTE (February 23, 2021): 

The “best macros” are the one’s based on your individual needs and health- and weight-loss goals.

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

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