INTRODUCTION:  Not everyone who eats a “low carb” diet can afford to keep buying meat at the today’s current crazy prices. This article looks at options on the basis of protein to energy, in calories (kcals). Yes, it contains some ‘unconventional’ protein sources, but ones that can still fit within a low carb diet. It provides people with options who may not have a choice.

Meat prices have gone crazy and many people are wondering how to eat well on a budget. Steaks and chops are familiar, but they aren’t the only source of protein — or even the best sources.

A rib steak is only 60% protein but skipjack tuna is 92% protein — which is substantially more, and costs a great deal less. Skinless turkey breast is 86% protein and skinless chicken breast is 75% protein— both higher than a rib steak and both considerably less expensive. While medium-lean ground beef (80% lean) is inexpensive it only has 41% protein, and canned pink salmon, beef- or chicken liver, canned mackerel and sardines all have more protein in them than that!

Note: In this article, protein to energy ratio (P:E in kcals) is protein in calories (kcals) compared to the total amount of calories in one ounce (28g) of the food. This is different than the Ted Naiman’s “P:E ratio“, where energy is “non-fiber carbohydrate + fat”. In this calculation the energy provided by protein is not counted, however not all protein is used for muscle accretion, but in a high protein diet, excess protein is burnt for energy, or stored as fat.

Below are some examples of relatively low-cost animal source foods, sorted from the highest amount of protein to the lowest and as animal products, these are all complete proteins — having all 9 essential amino acids.

But what to make out of canned pink salmon? “Salmon patties” were a staple in my home growing up. They are made from drained canned pink salmon, mixed with a little chopped celery, minced green onion and egg to bind them (my mom would add breadcrumbs but I omit them and they come out fine!). They are formed into patties and either fried in a bit of fat or cooked in a non-stick skillet. They are an excellent source of highly bioavailable protein, a good source of omega 3 fatty acids, and are inexpensive and delicious! They can be served with homemade cabbage salad (Cole slaw), or a side of cooked vegetables…and yes, frozen vegetables are just as nutritious as fresh, and much less expensive.

Canned tuna is delicious mixed up with a bit of mayonnaise, with or without some minced celery and of course is terrific added to casseroles that for those not following a low carb diet, are made with pasta. I find that chunks of lightly cooked cauliflower stands in well for noodles and these casseroles can be a complete meal with the addition of a few handfuls of fresh or frozen vegetables.  They are also wonderful with a sprinkle of grated cheese on top.  Tuna is a great source of protein as well as omega 3 fat, and is often on sale. Buying a few cans to have on hand makes it easy to reach for at the end of a long day.

Some people don’t like liver because their only experience with it is something akin to shoe leather, but when it is bought fresh and cooked on a barbeque (or broiled in the oven) until “just cooked”, it is delicious. Chicken liver can be cooked that way too, but is also delicious pan fried with onion, mushroom and peppers, or made into a pí¢té.

Eggs can provide the protein in a spinach soufflé which is delicious with or without some grated parmesan or swiss cheese. Adding extra egg white makes it even higher in protein, and makes for an even better soufflé!

Eggs can stand on their own served as shakshuka as the main dish for dinner. A cucumber and tomato salad makes a delicious side dish and all together, this is a very affordable and tasty meal!

What about some non-animal sources ?

Non-Animal Source of Protein

Tofu is very versatile and to many people’s surprise, contains all 9 essential amino acids.  It comes in so many forms — from firm blocks, to silky and custard-like, and can be cooked into so many wonderful dishes. If you haven’t tried Chinese Ma-Po tofu, you are missing something! It has a delicious sauce made from garlic, green onions and brown bean sauce (and for non-vegetarians includes a small amount of ground meat), and is simply just delicious! Serve it with stir fried broccoli or bok choi and garlic.

Firm tofu, cut in small rectangles, dipped in egg and pan fried with some ginger and green onion and finished by steaming with a bit of broth is just delicious!  The Chinese fondly refer to tofu as “meat without bones” and I call the egg dipped fried with green onion and ginger, as “fish without bones” (because this is often the way the Cantonese prepare fish).

While many people who eat low carb think that legumes such as lentils and chickpeas are “off limits”, 1/2 cup of legumes contain approximately the same amount of carbs as 1/2 cup of yam or squash, but comes with an added bonus of 7g of protein. For those that are concerned about anti-nutrients in pulses, these are reduced with soaking and cooking, and not using the soaking water for cooking them reduces most of the gas that people think of when they think of pulses.

[Note: November 7, 2021 – Best to not purée cooked legumes, as they will raise blood sugar more than if left intact.]

Animal proteins are complete proteins which means they contain all 9 essential amino acids. While lentils and other pulses have a good protein to energy (kcals) ratio, it is important to note that they are missing amino acids. That is why they are considered “incomplete proteins”.  For example, lentils are missing the sulfur-containing amino acids methionine and cysteine, and pinto beans are missing methionine and tryptophan. Since pulses are missing amino acids, it is important for those who are vegetarian to be sure to eat other foods during the day that contain the missing amino acids. It used to be believed they had to be eaten at the same meals, but that is not necessary.

Protein in Some Nuts, Seeds and Grains

Nuts and seeds also provide some protein, but are easy to over-eat. Nuts are high in fat and like hard cheese can stall weight loss, if over eaten. Same with nut butters like peanut butter or tahini which is made from ground sesame seeds. It is helpful to think of these as fat sources that have some protein, rather than protein sources. It is best to use them as a decoration to make other foods like salad taste good, rather than as a protein source.

Cottage Cheese – a surprising low carb high protein staple

Have a look at the protein to energy (kcal) ratio of pressed cottage cheese (see photo) in the table, below.  Ounce for ounce, pressed cottage cheese provides way more protein than steak, or ground beef, and even more than turkey or chicken breast!  Who would have thought? Once the bane of calorie counter’s existence, cottage cheese is an excellent protein source for those following a low carb diet, even high than eggs!

Low carb diets — especially the high fat ones always seem to highlight eggs, but eggs are only 33% protein (see table, above) whereas pressed cottage cheese is 84% protein, Greek yogurt is 74% protein, and creamed cottage cheese is 51% protein!

Different Types of Cottage Cheese Compared [Added November 8, 2021)

I decided to add this  clarification to explain the different types of cottage cheese. 

“Dry cottage cheese” is just the curd that is used for making “creamed cottage cheese”, but without the liquid.  In years gone cream was added to the dry curd to make “creamed cottage cheese” hence the name — but now it is a mixture of milk with various gums, such as carrageenan, guar gum and xanthan gum.

Difference between dry cottage cheese, pressed cottage cheese and regular (creamed) cottage cheese

But how does one eat pressed cottage cheese? It can be mixed with egg, herbs such as parsley and green onion, formed into patties and fried like the salmon patties mentioned above, or mixed with egg and/or spinach and used as a filling for lasagne or manicotti.

Seriously, low carb lasagne is a “thing”! Thin slices of deli chicken make a terrific low-carb substitute for the noodles in lasagne (just choose brands that don’t have added sugar) and the cottage cheese and egg filling can be rolled up in strips of zucchini, like manicotti.

Creamed cottage cheese is an excellent protein source for breakfast or lunch and Greek yogurt is a good source, and delicious with 1/2 cup of berries thrown. Even though Greek yogurt pales in comparison to cottage cheese in terms of its protein to kcal ratio, it still scores higher than steak — and higher than eggs!

There are so many good sources of inexpensive protein that can stand on their own, or mixed together to make so many delicious combinations!  Looking to other cultures that use these ingredients is a great way to find out what to do with them. Chinese, Korean and Japanese have wonderful easy recipes for tofu.  Hispanic cultures including Mexican have so many ways to cook pinto beans, kidney beans, and black beans — both with and without meat and for lentils and chickpeas you need not look far. Middle Eastern recipes abound using these, as do South Asian recipes from India, Pakistan and Sri Lanka. And don’t forget the lowly “offal” meats, like liver and heart! These are inexpensive and good sources of complete protein. Finding out how to cook them properly can make all the difference.

Protein is a very important macronutrient needed as a building block for the body. Carbohydrate and fat are the body’s energy sources, but the body can make its own glucose from protein or fat, provided they are supplied in sufficient quantities. Protein is so important that according to the “protein leverage hypothesis“, people will keep eating and eating until their body gets the protein it needs. Targeting protein first is important to keep from overeating foods that are “protein dilute”. And it is not only children and adolescents that need protein, but older people need more protein as they age, to lower the risk of sarcopenia (muscle wasting).

A “low carb” diet need not fit a philosophy, but a definition. What makes a diet low carb is how few carbs it has, not what the source of those carbs are.

Final Thoughts…

Yes, meat prices are crazy these days, but steaks and chops are not the only source of protein and not even the best source!  Salmon, tuna, chicken and turkey breast are all excellent sources and one doesn’t need to eat the expensive variety to benefit.  Frozen pink salmon or canned tuna are fine! And don’t forget cottage cheese!

More Info?

If you would like more information about how I can help you 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

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.

The idea that there is a specific food that acts as the “off switch” for appetite is very compelling.  Who hasn’t eaten more food than they planned or wanted? Whether it was too much of the same food or too much of a variety of foods, we often eat until we are stuffed. Wouldn’t it be amazing if we could eat something that could satisfy that drive to eat? According to Dr. Stephen Simpson and Dr. David Raubenheimer, that “something” is protein.

In their 2005 paper published in Obesity Reviews, Simpson and Raubenheimer proposed that obesity isn’t primarily caused by eating too much fat, or eating too many ‘carbs’, but by eating food that has too little protein [1]. They called this the “Protein Leverage Hypothesis”.  This states is that humans have a built-in appetite for protein that drives food consumption. When we eat food that contains low amount of protein, we will over-eat until the amount we need is met.  

In paleolithic times, the human diet was ~35% animal protein, 33% fat and the remainder plant protein (which was limited in the diet due to antinutrients such as phytates, oxalates, tannins, trypsin-, amylase-,  and protease inhibitors, and glycosides) [2].  Humans evolved and thrived eating this way. 

In contrast, currently the percentage of protein in diets around the world remains at ~16% of daily calories [3] and Simpson and Raubenheimer believe that it is this ‘protein dilution‘ of the diet that results in us overeating food, to try and obtain sufficient amounts.

In their 2005 paper, they wrote;

”The obesity epidemic is among the greatest public health challenges facing the modern world. Regarding dietary causes most emphasis has been on changing patterns of fat and carbohydrate consumption. In contrast the role of protein has largely been ignored because (i) it typically comprises only approximately 15% of dietary energy and (ii) protein intake has remained near constant within and across populations throughout the development of the obesity epidemic. We show that paradoxically these are precisely the two conditions that potentially provide protein with the leverage both to drive the obesity epidemic through its effects on food intake and perhaps to assuage it. [1]“

What this implies is, if we don’t intentionally prioritize protein in the diet, we will overeat fat and carbohydrate to reach the amount we require (or have evolved to eat).

To complicate matters, the food environment is made up of ultra processed foods that are mostly carbohydrate and fat.  Snack and convenience foods were only introduced the early 1970s — which, coincidently was when the obesity epidemic began.

We have known since 2018 that foods high in both carbohydrate and fat result in more dopamine being released from the reward-center in striatum of our brain, than foods with carbohydrate alone, or fat alone [4]. This is why will often overeat French fries, but rarely a baked potato. Perhaps, the fact that snack and convenience foods are so low in protein is a contributing factor to us overeating them.

Current statistics indicate that 55% of calories eaten by adults [5] and 67% of calories eaten by children and teenagers [6] come from ultra-processed foods — high in both carbohydrate and fat, and low in protein.

A 2018 follow-up paper by Simpson and Raubenheimer based on the 2009-2010 National Health and Nutrition Examination Survey (NHANES) found higher consumption of ultra-processed foods was associated with lower protein density [7].

“Consistent with the Protein Leverage Hypothesis, increase in the dietary contribution of ultra processed foods was also associated with a rise in total energy intake, while absolute protein intake remained relatively constant [7].

“The protein-diluting effect of ultra processed foods might be one mechanism accounting for their association with excess energy intake [7].”

Rather than going in circles arguing whether eating too much fat or eating too many carbs resulted in obesity, perhaps it is more productive to focus on ensuring sufficient intake of high quality protein.

But how much is best? It depends for whom.

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. The RDA is not the optimal requirement, but the absolute minimum to prevent deficiency.

The RDA – enough protein to prevent deficiency

The RDA for protein for healthy adults is calculated at 0.8 g protein / kg of body weight [8]. A sedentary 70 kg / 154 pound man needs a minimum of 56 g and a sedentary 60 kg / 132 pound woman needs a minimum of 48 g protein per day.

Protein Needs for Active Healthy Adults

For physically active adults, the Academy of Nutrition and Dietetics, Dietitians of Canada, and the American College of Sports Medicine [9] recommend an intake of 1.2—2.0 g protein / kg of lean body mass (LBM) per day to optimize recovery from training, and to promote the growth and maintenance of lean body mass.

Protein Needs for Older Adults

Several position statements by groups working with an aging population indicate that intake between 1.0 and 1.5 g protein / kg of lean body mass (LBM) per day may best meet the needs of adults during aging [10, 11].

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 written 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 of LBM 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.

Final Thoughts…

We know that the presence of both carbs and fat together in a food has a supra-additive effect on the pleasure center of our brain [4]. This leads to us eating way more of these foods, than foods with just carbs or just fat.  Given this, it would make sense to avoid foods that have high amounts of both carbs and fat which include almost all of our favourite snack and convenience foods.

With the exception of nuts, seeds and milk most real, whole food is high in either carbs or fat, not both.  Aim to eat these foods the most, but not together at the same meal.

Based on the Protein Leverage Hypothesis, aim to eat sufficient high protein foods based on your individual needs.  Reach for foods such as salmon, tuna, skinless chicken and shrimp the most often. These contain 8 grams of protein per ounce (28 g) and 1.5 grams of fat.  Enjoy a good ribeye, some pork or chicken legs that have on average 6.2 grams of protein per ounce (28g), and 6g of fat.

Vegetarian? No problem!

Cottage cheese has 28 g of highly bioavailable protein per cup, and Greek yogurt has 16 grams of protein per cup. Tofu only has ~4.7 grams of protein per ounce (28g), and is a complete protein containing all the essential amino acids.

Think of protein as a control button for appetite and reach for the types of protein that suit your lifestyle best!

More Info?

If you would like more information about how I can help you 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

References

1. Simpson SJ, Raubenheimer D. Obesity: the protein leverage hypothesis. Obes Rev. 2005 May;6(2):133-42. doi: 10.1111/j.1467-789X.2005.00178.x. PMID: 15836464.
2. Ben-Dor M, Gopher A, Hershkovitz I, Barkai R (2011) Man the Fat Hunter: The Demise of Homo erectus and the Emergence of a New Hominin Lineage in the Middle Pleistocene (ca. 400 kyr) Levant. PLoS ONE 6(12): e28689. https://doi.org/10.1371/journal.pone.0028689
3. Lieberman HR, F.V., Agarwal S, et al. , Protein intake is more stable than carbohydrate or fat intake across various US demographic groups and international populations. The American Journal of Clinical Nutrition, 2020. 112(1): p. 180-186.
4. DiFeliceantonio AG, Coppin G, Rigoux L, et al., Supra-Additive Effects of Combining Fat and Carbohydrate on Food Reward. Cell Metab. 2018 Jul 3;28(1):33-44.e3. doi: 10.1016/j.cmet.2018.05.018. Epub 2018 Jun 14. PMID: 29909968.
5. Zefeng Zhang, Sandra L Jackson, Euridice Martinez, Cathleen Gillespie, Quanhe Yang, Association between ultraprocessed food intake and cardiovascular health in US adults: a cross-sectional analysis of the NHANES 2011—2016, The American Journal of Clinical Nutrition, Volume 113, Issue 2, February 2021, Pages 428—436, https://doi.org/10.1093/ajcn/nqaa276
6. Lu Wang, Euridice Martí­nez Steele, Mengxi Du, Jennifer L. Pomeranz, Lauren E. O’Connor, Kirsten A. Herrick, Hanqi Luo, Xuehong Zhang, Dariush Mozaffarian, Fang Fang Zhang. Trends in Consumption of Ultraprocessed Foods Among US Youths Aged 2-19 Years, 1999-2018. JAMA, 2021; 326 (6): 519 DOI: 10.1001/jama.2021.10238
7. Martí­nez Steele E, Raubenheimer D, Simpson SJ, Baraldi LG, Monteiro CA. Ultra-processed foods, protein leverage and energy intake in the USA. Public Health Nutr. 2018 Jan;21(1):114-124. doi: 10.1017/S1368980017001574. Epub 2017 Oct 16. PMID: 29032787.
8. National Academies Press, Dietary Reference Intakes for Energy, Carbohydrate, Fiber, Fat, Fatty Acids, Cholesterol, Protein and Amino Acids (2005)
9. 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
10. 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
11. 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

    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.

    

As a Dietitian who supports people with food addiction, I was recently asked to speak at a food addiction summit.  The evening prior to speaking, I was given a list of the questions I would be asked. The first one was “How has food addiction impacted your life? How old were you”? The opening question at the summit was “do you identify as a food addict”?

I had to really think about how to answer this. I knew there were two specific foods over which I had no “off button”.  If you’ve listened to some of the podcasts I’ve spoken at, you will know that those two foods are hot Montreal-style bagels that are baked in a wood burning oven, and pizza — but only ones baked in a wood-burning oven (or at a very high heat in a pizza oven).  I have NO idea why these are like “kryptonite” to me, and can think of no memory that offers a clue. When I was a kid, there were “Cheezies ®” (a brand of cheese puff snack food from Canada — essentially they are extruded cornmeal covered in powdered cheddar cheese), and as a teenager, there was Nutella®.  I would eat Cheezies or Nutella over a period of a few hours, until the container was empty.

To answer the question, ‘how has food addiction impacted my life‘, I first had to define ‘food addiction‘. Since my post-graduate research was in the area of mental health nutrition, I turned to the Diagnostic and Statistical Manual (DSM-5) which is used to classify mental health disorders for diagnoses, treatment, and research. The DSM-5 was published in 1994 and recognizes substance use disorders [1] resulting from the use of 10 separate classes of drugs:

1. 1. alcohol;
   2. caffeine;
   3. cannabis;
   4. hallucinogens (such as LSD);
   5. inhalants;
   6. opioids;
   7. sedatives, hypnotics or anxiolytics (anti-anxiety medication);
   8. stimulants (including amphetamine-type substances, cocaine, etc.);
   9. tobacco;
   10. and other or unknown substances

Is food addiction a substance use disorder? I guess it depends who one asks.

On one hand, one’s “kryptonite” foods could fall under “and other or unknown substances,” but as I mentioned in the summit, I don’t think it is the foods themselves that people become addicted to.

I believe that it is the release of dopamine from the pleasure center of the brain that is associated from the release of dopamine from the brain (explained in this article), and supported by endo-cannabinoids and endo-opioids that are also released.

The first question I was asked at the summit was whether I identified as a food addict. 

I referred to the list from the DSM-5 which lists the 11 criteria related to substance use disorder.

In preparation for the talk, I had marked a red “x” beside the ones that applied to foods that I consider my “kryptonite”.

1. 1. Taking the substance in larger amounts or for longer than you’re meant to.
   2. Wanting to cut down or stop using the substance but not managing to.
   3. Spending a lot of time getting, using, or recovering from use of the substance.
   4. Cravings and urges to use the substance.
   5. Not managing to do what you should at work, home, or school because of
      substance use.
   6. Continuing to use, even when it causes problems in relationships.
   7. Giving up important social, occupational, or recreational activities because of substance use.
   8. Using substances again and again, even when it puts you in danger.
   9. Continuing to use, even when you know you have a physical or psychological problem that could have been caused or made worse by the substance.
   10. Needing more of the substance to get the effect you want (tolerance).
   11. Development of withdrawal symptoms, which can be relieved by taking more of the substance.

I could certainly remember eating more hot bagels or pizza than I wanted to, and for longer than I intended, so “yes” to criteria #1.

I certainly wanted to cut down or stop eating hot bagels or pizza, but not managing to, so “yes” to criteria #2.

Criteria #3, was a “no”.  I never spent a lot of time getting, using, or recovering from eating those (or any) foods.

There was no question, criteria #4 was a “yes”. I certainly had cravings and urges to eat these foods that only abated when I went low carb and stopped eating them.

Criteria #5, #6, and #7 and #11 were all “no”. Eating these (or any foods) did not interfere with me doing what I needed to at work, home or school, they didn’t cause problems in relationships and I didn’t give up any important social, occupational, or recreational activities because of them. I didn’t experience withdrawal symptoms when I ate those foods.

The reality of answering criteria #8 and #9 was undeniable.

I ate foods such as bagels and pizza (and foods high in both carbs and fat) again and again — even when it put me in danger.  I continued to eat these foods,  even though I knew (but was in denial!) that I had several physical problems that could have been caused by or made worse by eating these foods.

I was obese, had type 2 diabetes and dangerously high blood pressure — and was a Registered Dietitian with a master’s degree who was in denial as to just how much danger I had put myself in!  If you haven’t heard my story, it is under the Food for Thought tab, and titled A Dietitian’s Journey.

Reading Dr. Vera Tarman’s book, Food Junkies made me come face-to-face with criteria #10. I had given up milk chocolate when I adopted a low carb lifestyle, but reading the book made me realize that I needed more dark chocolate to enjoy it.  This was classic tolerance. 

As I talk about it the food addiction summit, coming to that realization resulted in me giving up all chocolate for a full year.  At present, I am finding that I can eat small amounts of >78% cocoa without it being problematic, but am doing so cautiously. I will abstain* completely if I am unable to do that.

I met the criteria for ‘substance use disorder’ when I applied the definition of “substance’ to specific foods.

In colloquial terms, I am a food addict, however I don’t say “I am a type 2 diabetic,” because I am in remission. I don’t say “I have hypertension or  obesity”, because I am in remission. So, more accurately, I am a person with food addiction, in remission. 

…and like type 2 obesity, hypertension and obesity, I will remain in remission provided I don’t go back and eat how I used to eat before.

If food addiction would be classified as a ‘substance use disorder’, then meeting 6 of 11 criteria indicates it would be “severe”. 

But it’s only hot bagels and pizza! Does that make me a “food addict”?

Here is a rhetorical question that may help answer this.

Does it matter if an alcoholic is powerless over only one type of rum and one type of whiskey?

I don’t think so.

One of the other questions I was asked during the summit was to define  “abstinence” and and what an “abstinence food plan” is.

This is how I defined them; 

“For me, abstinence is “the practice of restraining oneself from indulging in something”. There is alcohol-addiction, drug-addiction, gambling-addiction, sex-addiction, and food-addiction — but it is not possible to completely abstain from food, as it is necessary for survival. I define abstinence as “restraining from indulging in foods over which one has no control”.

Alcoholics Anonymous uses the term “powerless” to describe addiction, so I define abstinence as “restraining from foods over which one is powerless to stop eating.”

An “abstinent food plan” is one that does not include foods over which a person is powerless to control the amount they eat.”

Final Thoughts…

The DSM-5 does NOT define “food addiction”.  It defines “substance use disorder”. That said, I think that looking at whether specific foods or categories of food result in these types of symptoms can be helpful to consider.  It can help one decide whether getting support for food addiction may provide a context and structure that they find helpful.

More Info

I design abstinent meal plans for people with food addiction and support the dietary side as people work with either a food addiction- or sugar addiction counsellor, or in a food addiction 12-step program.

If you would like more information please send me a note through the Contact Me form, on the tab above.

To your good health!

Joy

You can follow me on:

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

References

Hasin DS, O’Brien CP, Auriacombe M, et al. DSM-5 criteria for substance use disorders: recommendations and rationale. Am J Psychiatry. 2013;170(8):834-851. doi:10.1176/appi.ajp.2013.12060782

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.

For as long as I can remember, type 2 diabetes has been called a chronic, progressive disease and people diagnosed with type 2 diabetes have been  taught that (1) the disease will persist (i.e. is chronic), (2) will only get worse (i.e. is progressive), (3) that medication to manage the disease is inevitable, and (4) that as the disease progresses multiple medications may be required, including insulin.

A newly published consensus report (August 31, 2021) from an expert panel made up of representatives from the American Diabetes Association (ADA), European Association for the Study of Diabetes (EASD) and Diabetes UK states that “diabetes may not always be active and progressive” [1,2,3], and the report highlights that remission is possible, and a person may need ongoing support and regular monitoring to prevent relapse. You can read a summary of the report here.

The website of the American Diabetes Association states [4];

“You might start managing your diabetes with diet and exercise alone, but, over time, will have to progress to medication, and further down the line you might need to take a combination of medications, including insulin.”

While this will be the case if diet and lifestyle are not adequately changed, but it is by no means inevitable!

Diabetes Canada in its patient resources on “the basics” of type 2 diabetes states; ”type 2 diabetes is a progressive, life-long disease” [5].

…and in its March 2020 handout on access to diabetes medication states, Diabetes Canada states that; [6];

Diabetes is a chronic, progressive disease that affects the body’s ability to regulate the amount of glucose (sugar) in the blood. It has no cure, but can be managed through education, support, healthy behaviour interventions, and medications.

…and in its advocacy report on bariatric surgery as a type 2 diabetes intervention strategy [7] states;

Diabetes is a chronic, progressive disease affecting more than 3.6 million Canadians; approximately 90 per cent of whom live with type 2 diabetes. Type 2 diabetes is caused by a combination of genetic, lifestyle and environmental factors. It occurs when the body cannot properly regulate the amount of glucose (sugar) in the blood. Insufficient insulin production, insulin resistance, or both, cause hyperglycemia (high blood sugar) which, over time, can damage blood vessels, nerves and organs, and lead to many debilitating and irreversible complications. Type 2 diabetes can be managed with education and support, behaviour interventions (including healthy eating, regular physical activity and stress reduction) and medication.

Why do diabetes associations not explain that there are three documented ways to put type 2 diabetes into remission, two of which are dietary;

1. 1. a ketogenic diet [8,9]
   2. a low calorie energy deficit diet [10,11,12]
   3. bariatric surgery (especially use of the roux en Y procedure) [13,14]

Why are people diagnosed with type 2 diabetes still told that type 2 diabetes is a chronic, progressive disease — rather than told about the two evidence-based dietary options to achieve remission?

Final Thoughts…

In light of this new consensus report stating that “diabetes may not always be active and progressive” [1,2,3],  it is time to stop referring to diabetes as “a chronic, progressive disease”.

People  need to know that remission is possible, as well as information about the evidence-based dietary options that remission can be achieved.

More Info?

If you would like more information about how I can support you in seeking remission of type 2 diabetes, 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

References

1. 1. Riddle MC, Cefalu WT, Evans PH. et al. Consensus Report: Definition and Interpretation of Remission in Type 2 Diabetes, The Journal of Clinical Endocrinology & Metabolism, 2021, dgab585,  https://doi.org/10.1210/clinem/dgab585
   2. Riddle MC, Cefalu WT, Evans PH. et al. Consensus report: definition and interpretation of remission in type 2 diabetes. Diabetes Care (2021) https://doi.org/10.2337/dci21-0034
   3. Riddle MC, Cefalu WT, Evans PH. et al.  Consensus report: definition and interpretation of remission in type 2 diabetes. Diabetologia (2021). https://doi.org/10.1007/s00125-021-05542-z
   4. American Diabetes Association, How Type 2 Diabetes Progresses, https://www.diabetes.org/diabetes/how-type-2-diabetes-progresses
   5. Diabetes Canada, Type 2 diabetes – the basics, https://guidelines.diabetes.ca/docs/patient-resources/type-2-diabetes-the-basics.pdf
   6. Diabetes Canada, Access to Diabetes Medication, March 2020 https://www.diabetes.ca/DiabetesCanadaWebsite/media/Advocacy-and-Policy/Advocacy%20Reports/Access-to-Diabetes-Meds_Time-to-Listing_EN.pdf
   7. Diabetes Canada, Bariatric surgery as a type 2 diabetes intervention strategy, https://www.diabetes.ca/advocacy—policies/advocacy-reports/bariatric-surgery-as-a-type-2-diabetes-intervention-strategy
   8. Hallberg, S.J., McKenzie, A.L., Williams, P.T. et al. Effectiveness and Safety of a Novel Care Model for the Management of Type 2 Diabetes at 1 Year: An Open-Label, Non-Randomized, Controlled Study. Diabetes Ther 9, 583—612 (2018). https://doi.org/10.1007/s13300-018-0373-9
   9. Athinarayanan SJ, Adams RN, Hallberg SJ, McKenzie AL, Bhanpuri NH, Campbell WW, Volek JS, Phinney SD, McCarter JP. Long-Term Effects of a Novel Continuous Remote Care Intervention Including Nutritional Ketosis for the Management of Type 2 Diabetes: A 2-Year Non-randomized Clinical Trial. Front Endocrinol (Lausanne). 2019 Jun 5;10:348. doi: 10.3389/fendo.2019.00348. PMID: 31231311; PMCID: PMC6561315.
   10. Lim EL, Hollingsworth KG, Aribisala BS, Chen MJ, Mathers JC, Taylor R. Reversal of type 2 diabetes: normalisation of beta cell function in association with decreased pancreas and liver triacylglycerol. Diabetologia2011;54:2506-14. doi:10.1007/s00125-011-2204-7 pmid:21656330
   11. Steven S, Hollingsworth KG, Al-Mrabeh A, et al. Very low-calorie diet and 6 months of weight stability in type 2 diabetes: pathophysiological changes in responders and nonresponders. Diabetes Care2016;39:808-15. doi:10.2337/dc15-1942 pmid:27002059
   12. Lean ME, Leslie WS, Barnes AC, et al. Primary care-led weight management for remission of type 2 diabetes (DiRECT): an open-label, cluster-randomised trial. Lancet2018;391:541-51.
   13. Cummings DE, Rubino F (2018) Metabolic surgery for the treatment of type 2 diabetes in obese individuals. Diabetologia 61(2):257—264.
   14. Madsen, L.R., Baggesen, L.M., Richelsen, B. et al. Effect of Roux-en-Y gastric bypass surgery on diabetes remission and complications in individuals with type 2 diabetes: a Danish population-based matched cohort study, Diabetologia (2019) 62: 611. https://doi.org/10.1007/s00125-019-4816-2

Copyright ©2021 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 new consensus report from an expert panel made up of representatives from the American Diabetes Association (ADA), European Association for the Study of Diabetes (EASD) and Diabetes UK [1,2,3] have proposes a standard definition for remission of type 2 diabetes. This new article outlines the different factors involved in that definition, as well as the proposed cut-offs.

As outlined in a previous article, in 2009 the American Diabetes Association defined  partial remission, complete remission and prolonged remission of type 2 diabetes as follows [4];

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

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

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

In 2019, the Association of British Clinical Diabetologists and the Primary Care Diabetes Society [5] defined remission of type 2 diabetes as follows;

“Remission of type 2 diabetes can be diagnosed when a person with confirmed type 2 diabetes has achieved all three of the following criteria: (1) weight loss; (2) fasting plasma glucose or HbA1c below the WHO diagnostic threshold (<7 mmol/L or <48 mmol/mol, respectively) on two occasions separated by at least 6 months; (3) the attainment of these glycaemic parameters following the complete cessation of all glucose-lowering therapies.”

I am by no means an expert in diabetes, but in clinical practice I’ve defined remission of type 2 diabetes as blood sugar levels “at or below the cut-offs for diagnosis” (HbA1C & FBG) without the use of medication. 

Choice of the Term “Remission”

The consensus report’s expert panel outlined that while several terms have been proposed to describe those who have become free of a previously diagnosed disease state, including ‘resolution‘, ‘reversal‘, ‘remission‘, and ‘cure‘,  that with respect to type 2 diabetes ‘remission‘ is the most appropriate term [1,2,3]. They chose the term remission as it is used widely used in the field of cancer treatment (oncology) as defined as a decrease in or disappearance of signs and symptoms of cancer [6].

The expert panel believes that the term remission captures that (1) “diabetes may not always be active and progressive“, while also implying that (2) “notable improvement may not be permanent“, and (3) is consistent with the view that a person may need ongoing support and regular monitoring to prevent relapse [1,2,3].

“Remission” Not Equivalent to No Evidence of Disease

The panel highlighted that the tendency to equate remission with “no evidence of disease” is not appropriate with respect to type 2 diabetes because diabetes is defined by hyperglycemia, which exists on a continuum [1,2,3], and noted that any criterion chosen to define remission is somewhat arbitrary, as it represents a point on a continuum of glycemic levels. They also highlighted that remission is not equivalent to “no evidence of disease” because the underlying cause of type 2 diabetes is rarely resolved by dietary or lifestyle changes, or by bariatric surgery — including insufficient release of insulin from βeta-cells and insulin resistance.

Different Levels of Remission

The panel decided against dividing diabetes remission into partial remission and complete remission using different blood glucose thresholds as this could result in challenges with respect to policy decisions related to insurance premiums, and coding for medical visits and that the 5-year threshold previously used by the ADA for defining prolonged remission “did not have an
objective basis”.

Use of Glucose-Lowering Medication in Defining Remission

The issue of whether remission could be diagnosed while a person was receiving ongoing medication support, was also addressed. This is an important consideration, as some studies such as those from Virta Health [7,8] define remission of type 2 diabetes as a HbA1C < 6.5% and fasting blood glucose ≤ 5.5 (100 mg/dl) while taking no other medication except metformin / glucophage.

The panel concluded that since it is not possible to tell if a person has achieved remission due to dietary and lifestyle changes or due to medication that lowers glucose, “a diagnosis of remission can only be made after all glucose-lowering agents have been withheld for an interval that is sufficient both to allow waning of the drug’s effects and to assess the effect of the absence of drugs on HbA1c values“.

The panel concluded the absence of medication includes the use of metformin for weight maintenance, to improve markers of risk for cardiovascular disease or cancer, or prescribed for polycystic ovarian syndrome (PCOS), GLP-1 receptor agonists (such as Ozempic, Victoza / Saxenda and others) which may be used for weight management or to reduce the risk of cardiovascular events, and sodium glucose cotransporter inhibitors (such as Invokana, Jardiance, Synjardy and others) which may be prescribed for heart failure or renal protection.

The panel concludes that if it is not possible to discontinue these drugs for 3 months or longer, then remission cannot be diagnosed even though
normal or near normal blood sugar values are maintained — and that without doing so “whether true remission has been attained remains unknown”.

Timeline for Determining Remission

Whether the changes made are dietary, lifestyle or surgical (such as gastric bypass), varying amounts of time are required to determine whether remission has been achieved.

Medication Intervention (Pharmacotherapy)

The expert panel determined that when the  intervention has been through medication (pharmacotherapy), there needs to be  a period of at least 3 months after the medication has been completely stopped before tests of HbA1C can reliably evaluate whether remission has been achieved.

Surgical Intervention

In the event of surgical intervention, the panel determined that there needs to be a period of at least 3 months after the surgical procedure and 3 months after the medication has been completely stopped before tests of HbA1C can reliably evaluate whether remission has been achieved.

Lifestyle Changes

When lifestyle changes, including diet and exercise are made, the panel determined that there needs to be a period of at least 6 months after beginning this intervention and 3 months after the medication has been completely stopped before tests of HbA1C can reliably evaluate whether remission has been achieved.

Need for Ongoing Monitoring

As outlined above, since the improvements in blood glucose may not be permanent, a person who has achieved remission from type 2 diabetes as defined above will likely need ongoing support and regular monitoring to prevent relapse as weight gain, stress resulting from other illnesses, and the continued decline of βeta-cell function can all result in recurrence of type 2 diabetes. The panel recommends regular laboratory testing of HbA1c or another measure of blood sugar control should be performed at least once a year.

The panel cautions that since there can still be the “legacy effect” of prior poor blood sugar control in various body tissues that continues after remission of symptoms, there is a need not only for ongoing monitoring of HbA1C, but also regular retinal screening for retinopathy, tests of renal function to rule out nephropathy, foot evaluation to rule out neuropathy, as well as measurement of blood pressure and weight to reduce the risk of cardiovascular disease.

HbA1c as the Defining Measurement of Remission

The expert panel set the cut-off point for defining remission as HbA_1c to < 6.5% (<48 mmol/mol) while stating that “the relative effectiveness of using HbA1C of 6.0% (42 mmol/mol), HbA1c of 5.7% (39 mmol/mol), or some other
level in predicting risk of relapse or microvascular or cardiovascular complications should be evaluated“. As noted above, the panel believes that any criterion chosen to define remission is somewhat arbitrary, as it represents a point on a continuum of glycemic levels. 

Conclusions of the Expert Panel

The expert panel concluded that the term “remission” should be used to describe a sustained metabolic improvement in type 2 diabetes to nearly normal levels defined as a return of HbA_1c to < 6.5% (<48 mmol/mol) that occurs spontaneously, or following an intervention and that persists for at least 3 months in the absence of usual glucose-lowering medication (pharmacotherapy).

When HbA1c is determined to be an unreliable marker of chronic glycemic control, the panel concluded that a fasting blood glucose (FBG) / fasting plasma glucose (FPG) <126 mg/dL (<7.0 mmol/L) or eA1C <6.5% calculated from continuous glucose monitoring (CGM) values can be used as an alternative.

Final Thoughts…

In addition to the new proposed cut-offs, there are three very important points made in this new consensus report:

NOTE: Be sure to read the following post about why it is time to stop calling type 2 diabetes ”a chronic, progressive disease”.

More Info?

If you would like more information about how I can support you in seeking remission of type 2 diabetes as defined above, 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: A consensus report is not an American Diabetes Association (ADA) position statement but represents expert opinion of this international expert panel’s collective analysis, evaluation, and opinion.

References

1. Riddle MC, Cefalu WT, Evans PH. et al. Consensus Report: Definition and Interpretation of Remission in Type 2 Diabetes, The Journal of Clinical Endocrinology & Metabolism, 2021, dgab585,  https://doi.org/10.1210/clinem/dgab585
2. Riddle MC, Cefalu WT, Evans PH. et al. Consensus report: definition and interpretation of remission in type 2 diabetes. Diabetes Care (2021) https://doi.org/10.2337/dci21-0034
3. Riddle MC, Cefalu WT, Evans PH. et al.  Consensus report: definition and interpretation of remission in type 2 diabetes. Diabetologia (2021). https://doi.org/10.1007/s00125-021-05542-z
4. Buse JB, Caprio S, Cefalu WT, et al. How do we define cure of diabetes? Diabetes Care 2009 Nov; 32(11): 2133-2135.https://doi.org/10.2337/dc09-9036
5. Nagi D, Hambling C, Taylor R. Remission of type 2 diabetes: a position statement from the Association of British Clinical Diabetologists (ABCD) and the Primary Care Diabetes Society (PCDS). Br J Diabetes 2019, June 2019; 19 (1):73—76. https://doi.org/10.15277/bjd.2019.221
6. Barnes E. Between remission and cure: patients, practitioners and the transformation of leukaemia in the late twentieth century. Chronic Illness 2008, Jan 2008;3(4):253—264.https://doi.org/10.1177/1742395307085333
7. McKenzie AL, Hallberg SJ, Creighton BC, Volk BM, Link TM, Abner MK, Glon RM, McCarter JP, Volek JS, Phinney SD, A Novel Intervention Including Individualized Nutritional Recommendations Reduces Hemoglobin A1c Level, Medication Use, and Weight in Type 2 Diabetes, JMIR Diabetes 2017;2(1):e5, URL: http://diabetes.jmir.org/2017/1/e5, DOI: 10.2196/diabetes.6981
8. Hallberg, S.J., McKenzie, A.L., Williams, P.T. et al. Diabetes Ther (2018). Effectiveness and Safety of a Novel Care Model for the Management of Type 2 Diabetes at 1 Year: An Open-Label, Non-Randomized, Controlled Study.  https://doi.org/10.1007/s13300-018-0373-9

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’ve recently been asked to explain the difference between a Low Carb High Protein (LCHP) diet and the new P:E Diet, and that is the purpose of this article.  While both these diets prioritize protein, the recommended macros are very different.  This article outlines these two approaches and highlights the similarities and difference between the macro recommendations of these two diets.

Defining Terms

In order to describe how these two diets are similar and different, it is necessary to define some terms — specifically

(1) “low carb“, “keto” and “moderate carb”

(2)  “low fat”

(3) “high protein”

Defining Carbohydrate Intake

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

Since these same cut offs for carbohydrate are used by diabetes associations around the world — including the American Diabetes Association, European Association for the Study of Diabetes (EASD), Diabetes Australia, and Diabetes Canada, I use these established definitions, as well.

Defining “Low Fat”

A low fat diet is defined by the USDA as ”not more than 30% of calories from fat” [2].

Defining “High Protein”

Lower and Higher protein diets were defined in a very recent systematic review and meta-analysis[3] with some overlap;

• • Lower Protein Diets provide 10-23% of calories from protein
  • Higher Protein Diets provide 20-45% of calories from protein

The P:E Diet

P:E Diet -the book

I’ve read the P:E Diet book and find that it provides excellent guidance for healthy individuals who are seeking to build muscle, and lose excess fat. For those seeking to accomplish those goals, the P:E diet is excellent as it encourages people to eat the best quality protein for the least amount of energy (as fat + net carbs).

That said, as I have covered in previous articles and will elaborate on below, I am concerned that the total amount of protein generated in the P:E Macro Generator associated with the P:E Diet (located at the bottom of www.p2eq.com) can get close to the maximum rate at which the kidney can get rid of nitrogen waste from protein in the urine. 

I also have concerns that the P:E Macro Generator associated with the diet provides a carbohydrate intake of >100 g of carbohydrate per day to up to >160 g carbohydrate per day which is fine for healthy individuals, but may be inappropriate for someone who is metabolically unhealthy, especially having difficulty with higher than normal blood sugar levels. There is a clear disclaimer at the beginning of the book that it is not intended for those with health conditions, but none on the P:E Macro Generator.

Recommended Macros for the P:E Diet

The P:E Diet Macro Calculator associated with the P:E Diet is located at the bottom of www.p2eq.com recommends 40% protein and 30% fat and 30% carbohydrate for males or females of different heights. Recommended weight generated by the Macro Calculator is set to Ideal Body Weight (i.e. a BMI of 22) which is halfway through the normal weight category.

Below are some examples of macros from the P:E Macro Generator for different heights for both genders;

Carbohydrate recommendation for a man who is 5’7″ tall are at the low end of the moderate carbohydrate range — providing 131 g of carbs / 30% of total energy intake — where moderate carbohydrate is defined as 130—225g carbohydrate / day, 26—45% of total energy intake.

Fat recommendation of 30% calories as fat is low fat, i.e. ”not more than 30% of calories from fat”.

Protein recommendation of 40% calories as protein is a High Protein Diet i.e. provides 20-45% of calories from protein.

Macros for a man who is 5’10” tall are in the moderate carbohydrate range — providing 144 g of carbs / 30% of total energy intake — where moderate carbohydrate is defined as 130—225g carbohydrate / day, 26—45% of total energy intake.

Fat recommendation of 30% calories as fat is low fat, i.e. ”not more than 30% of calories from fat”.

Protein recommendation of 40% calories as protein is a High Protein Diet i.e. provides 20-45% of calories from protein.

Macros for a woman who is 5’6″ tall are in the low carbohydrate range — providing 117 g of carbs / 30% of total energy intake — where low carbohydrate is defined as < 130 g carbohydrate / day, < 26% of total energy intake.

Fat recommendation of 30% calories as fat is low fat, i.e. ”not more than 30% of calories from fat”.

Protein recommendation of 40% calories as protein is a High Protein Diet i.e. provides 20-45% of calories from protein.

Macros for a man who is 6’2″ tall are in the middle of the moderate carbohydrate range — providing 162 g of carbs / 30% of total energy intake — where moderate carbohydrate is defined as 130—225g carbohydrate / day, 26—45% of total energy intake.

Fat recommendation of 30% calories as fat is low fat, i.e. ”not more than 30% of calories from fat”.

Protein recommendation of 40% calories as protein is a High Protein Diet i.e. provides 20-45% of calories from protein.

Summary of P:E Macros

For the most part, carbohydrates in the P:E Diet are in the moderate carbohydrate range, although are on occasion they are in the high end of the low carbohydrate range, or at the low end of the moderate carbohydrate range [1].

The P:E Diet is a Low Fat Diet as it provides ”not more than 30% of calories from fat” [2].

The P:E Diet is a High Protein Diet providing 40% of calories from protein which is in the 20-45% of calories from protein range [3].

Recommended Macros for Low Carb High Protein Diet

As outlined in the previous article, the way I have taught a Low Carb High Protein (LCHP) diet the past 3 years is that protein is set at 25-30% protein (to a maximum of 2.5-3.0 g protein per kg ideal body weight), fat at 65-70% fat and carbohydrate at 10% carbs. This is at the high end of the protein range recommended by Phinney and Volek [7] of 20% to up to 30% of daily calories as protein — and fat is the same as they recommend, at 65-70% fat and 10% carbs.

A Low Carb High Protein diet is always low carb or very low carb;  low carb when it contains <130g carbohydrate per day,  < 26% of total energy intake, and very low carb (‘keto‘) when it contains 20—50g carbohydrate /day,  < 10% total energy intake.

A Low Carb High Protein diet is a High Fat Diet as it provides 65-70% fat, which is ”more than 30% of calories from fat” [2]. Unlike the popularized Low Carb High Fat diet, most of the fat in a Low Carb High Protein Diet comes from the fat inherent in the protein eaten — such as the fat in high fat fish like salmon and tuna, fat in Greek yogurt or the fat that comes in ground beef.  There is very little added fat, since a Low Carb High Protein Diet is often used for weight loss.

A Low Carb High Protein diet is a High Protein Diet providing 25-30% of calories from protein [3] to a maximum of 2.5-3.0 g protein per kg ideal body weight, and which is in the 20-45% of calories from protein range of a High Protein Diet [3].

Important Differences Between Low Carb High Protein and P:E Diet

From my perspective, there are two significant differences between a Low Carb High Protein diet and the P:E Diet.

The first significant difference is that the P:E Diet may be low carb — but for the most part is a moderate carbohydrate diet.  For those who are metabolically healthy, a diet which provides a carbohydrate intake of >100 g of carbohydrate per day to up to >160 g  carbohydrate per day as real, whole (cellular) food is fine. My concern is that for those who already have pre-diabetes or type 2 diabetes, a carbohydrate intake of >100 g carbohydrate per day up to >160 g per day is not the best way to improve blood sugar levels.

As outlined in the American Diabetes Association’s April 2019 Consensus Report a low carb diet has ”demonstrated the most evidence for improving glycemia (blood sugar) for individuals with diabetes”[4].

A Low Carb High Protein diet is, by definition, a low carb diet — so it has demonstrated the most evidence for improving blood sugar.

The second significant difference between a Low Carb High Protein Diet and the P:E Diet is that protein in the P:E Diet is set at 40% of daily calories — and as described in this earlier article, for some heights and weights, the P:E Macro Calculator generates protein at the high end of the maximum protein intake of 3.2 g protein per kg ideal body weight.

When protein is eaten, the body must get rid of the nitrogen by-product and the main way the body gets rid of this nitrogen is by turning it into ammonia, and then excreting it as urea in the urine. Since 84% of the nitrogen waste produced from protein intake is excreted as urea in the urine [5], the safe upper limit of protein intake is based on the maximum rate of urea production which is 3.2 g protein per kg body weight [6], described in more detail in this article. 

Protein needs should always be calculated as grams of protein per kilogram of body weight of the person and not as a percentage of daily calories e.g. 40 % of daily energy as protein. This is to ensure adequacy and avoid the excess. 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).

By the P:E Diet Macro Generator setting protein intake at 40% of daily calories without limiting a maximum to below the safe upper limit of 3.2 g protein per kg body weight, the protein recommendations generated may sometimes be at the very upper limit.

The Low Carb High Protein Diet, the way I teach it sets protein at 25-30% of daily calories — with a maximum of 2.5 g protein per kg ideal body weight, which is below the safe maximum intake level.

Different Diets for Different Purposes

The P:E Diet is geared towards healthy people seeking to build muscle and lose fat, and as indicated on page 85;

“all bodybuilders are really combining low carb AND low fat AND high protein to the very highest level of success.“

That is what the P:E Diet Macro Calculator located at the bottom of www.p2eq.com is set to do!

It generates macros that are 40% protein, 30% fat and 30% carbohydrate.

A diet that is 30% carbohydrate IS “low carb” when compared with the 45-65% carbohydrate range of the US or Canadian dietary guidelines AND low fat (“”not more than 30% of calories from fat” AND high protein (40% of daily calories as protein) and this is by design.

A Low Carb High Protein Diet, the way I teach it (and as conceptualized by Phinney and Volek in their book) is primarily a therapeutic diet aimed at improving metabolic health including high blood sugar, insulin resistance and for weight loss. 

The P:E Diet book is not directed at those who have medical conditions such as pre-diabetes or type 2 diabetes, or for those who have higher than normal blood sugar.  

These are very different diets, for very different purposes.

Final Thoughts…

I think the P:E Diet as outlined in the book provides excellent guidance for healthy individuals seeking to build muscle and lose excess fat and P:E ratio as a concept is excellent — encouraging people to eat the best quality protein for the least amount of energy (as fat + net carbs).

I also find that the tool for looking up the P:E ratio of individual foods (at the same link as the Macro Generator, except at the top of the page) is very helpful and saves people from having to do the math to determine Protein / (Fat + Net Carbs).

That said, I am concerned that total amount of protein in the P:E Macro Generator is not limited to a maximum of 3.0 g protein / kg ideal body weight — to ensure it does not exceed the 3.2 g protein / kg ideal body weight (the rate at which the kidney can get rid of nitrogen in the urine). This could easily be done, given that the weight it generates is already set at Ideal Body Weight.

For those who are metabolically healthy, the P:E Macro Generator which provides a carbohydrate intake of >100 g of carbohydrate per day to up to >160 g  carbohydrate per day as real, whole (cellular) food is fine, but my concern is that this level of carbohydrate intake may be inappropriate for someone who is already metabolically unhealthy — especially for someone with prediabetes or type 2 diabetes or challenges with higher than normal blood sugar.  This could easily be solved by providing a clear disclaimer such as the one that appears in the book.

More Info?

I design low carb Meal Plans from a variety of perspectives, including a Low Carb High Protein and can help individuals decide between different approaches based on their health, goals and nutritional needs.

For those who are metabolically healthy, I also design Meal Plans from a P:E perspective, however I do limit maximum protein intake to a maximum of 2.5 g protein per kg of ideal body weight.

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

To your good health!

Joy

You can follow me on:

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

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. 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/
3. Vogtschmidt YD, Raben A, Faber I et al, Is Protein the Forgotten Ingredient: Effects of higher compared to lower protein diets on cardiometabolic risk factors: a systematic review and meta-analysis of randomised controlled trials, Atherosclerosis, May 25, 2021, DOI:https://doi.org/10.1016/j.atherosclerosis.2021.05.011
4. A Consensus Report, Diabetes Care, Ahead of Print, published online April 18, 2019, https://doi.org/10.2337/dci19-0014
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. Volek JS, Phinney SD, The Art and Science of Low Carbohydrate Living: An Expert Guide, Beyond Obesity, 2011
8. Naiman T, Shewfelt W, The P:E Diet – Leverage Your Biology to Achieve Optimal Health, June 10, 2020, 330 pages

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 still think that a “keto diet” is all about eating loads of fat, and while a Low Carb High Fat (LCHF) diet is certainly one way to do ‘keto’, it is by no means the only way — or is it even a single diet. There are therapeutic ketogenic diets for epilepsy and adjunct treatment (along with chemotherapy and radiation) for certain types of cancer, as well as for seeking to improve quality of life outcomes in certain neurological disorders, such as MS. There are also different types of “low carb” and “keto” diets that are used for weight loss and for improving metabolic heath — that range from ones that prioritize fat, to those that prioritize protein. This article outlines some of the key advantages and disadvantages of different types of low carb* and keto** diets that are used for weight loss and normalizing blood sugar.

As outlined here, *low carb is defined as < 130g carbohydrate / day, < 26% of total energy intake and very low carb / **keto diets are defined as 20—50g carbohydrate /day,  < 10% total energy intake.

Humans can use protein, fat and carbohydrate for fuel, but our two main energy sources are fat and carbohydrate.  While amino acids from the protein we eat can be used to make glucose to maintain blood sugar and to supply red blood cells when there is inadequate food intake, protein’s main role in the diet is NOT as a fuel source, but to provide amino acids (the building blocks of protein) for the body to make its own proteins. Protein is primarily there to provide structure and function, not energy.

Fat and carbohydrate are human’s two primary energy sources — and carbohydrate is entirely optional from a biological perspective.

Even the Dietary Reference Intakes support that carbohydrate in the diet is optional, provided we eat adequate amounts of protein and fat.

Protein and fat are not optional, carbohydrate is.

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

Our body has an absolute requirement for specific essential nutrients — and these are called “essential nutrients” because we must take them in through our diet because we can’t synthesize them.

As I wrote about back in 2017, there are 9 essential amino acids that must be supplied in the different kinds of protein that we eat, and include histidine, isoleucine, leucine, lysine, methionine, phenylalanine, threonine, tryptophan, valine and there are 2 essential fatty acids — linoleic (an omega 6 fat) and alpha-linolenic (an omega 3 fat) that also must be provided in the diet because that can’t be synthesized by the body.

There are also 13 essential vitamins (vitamin A, vitamin B1 (thiamine), B2 (riboflavin), B3 (niacin), B5 (pantothenic acid), B6 (pyrodoxine), B12 (cyanocobalamine), biotin, vitamin C (ascorbic acid), choline, vitamin D (cholecalciferol), vitamin E (tocopherol) and  folate), and several essential minerals, including major minerals (calcium, phosphorus, potassium, sodium, chloride and magnesium) and minor minerals (chromium, cobalt, copper, fluorine, iodine, iron, manganese, molybdenum, selenium, silicon, sulfur and zinc).

Of the 3 macronutrients (protein, carbs and fat), protein and fat are not optional because they provide the essential amino acids and essential fats — and with them, many (but not all) of the essential vitamins and essential minerals. The remainder of the essential vitamins and minerals are provided by eating a wide range of vegetables and fruit.

Prioritizing Protein

Whether we eat a Low Carb High Fat (LCHF) diet, or Low Carb High Protein (LCHF) diet, we first need to make sure we are eating adequate amounts of high quality protein for our needs, and with high quality proteins come the essential fats. 

Think of protein as the foundation of a balance scale — providing the body with building blocks for structure and function — and the two arms of a balance scale as the two sources of fuel for energy: carbohydrate and fat.

We need to have enough protein for our needs, but not so much as to exceed the body’s ability to get rid of the excess nitrogen in our urine (more about that here).

Basic protein requirements are set in the Recommended Daily Allowance (RDA) for protein, which is the level that is sufficient to meet the needs of 97-98 % of healthy people and to prevent deficiency. The RDA for protein for healthy adults is calculated at 0.8 g protein / kg of reference body weight (i.e. IBM) [1]. Remember, this is the bare minimum to prevent deficiency in most people.

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 IBW per day to optimize recovery from training, and to promote the growth and maintenance of lean body mass.

Older people also need more protein in order to maintain muscle mass, and prevent sarcopenia (muscle loss associate with aging). 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 IBW per day may best meet the needs of adults during aging [3,4].

The Need to “Trade Off” Protein for Ketones

If we need to supply our body with lots of ketones for therapeutic reasons — such as the management of seizure disorder, or as an adjunct treatment for certain types of cancer or neurological disorders, then there is the need to “trade off” supplying the body anything more than the bare minimum of protein, in order to provide it with the very high levels of fat needed to make high levels of ketones.

The classic Ketogenic Diet (KD) has a 4:1 ratio i.e. 4 parts of fat for every 1 part protein and carbs and the Modified Ketogenic Diet (MKD) has a 3:1 ratio i.e. 3 parts fat for every 1-part protein, but unless a person has a therapeutic need for high levels of ketones, then why eat super high levels of fat? 

Higher Fat than Carbs – two very different approaches

As outlined in the American Diabetes Association’s April 2019 Consensus Report, a low carb diet has “demonstrated the most evidence for improving glycemia (blood sugar) for individuals with diabetes“[6], so either a Low Carb High Fat diet or a Low Carb High Protein diet are excellent approaches for those with prediabetes or type 2 diabetes seeking to significantly improve their blood sugar, or to put type 2 diabetes into remission.

Popularized “Keto” Diet

When most people think of a Low Carb High Fat (LCHF) diet, they think of the standard “keto diet” of 75% fat, 15% protein and 10% carbs, which is the popularized high fat approach of Dr. Jason Fung and the Diet Doctor website recommend. As will be outlined below, there are other Low Carb High Fat approaches.

If the goal is to lose weight however, it really doesn’t make a lot of sense to eat tons of fat which provides almost twice as much energy, as either protein or carbs — unless also doing regular periods of intermittent and extended fasting. While people do have success with this type of low carb high fat diet when used this way, this approach has drawbacks for some people.

Intermittent fasting for less than 24 hours has many benefits, but the problem with extended fasting for periods longer than 24 hours is there is a loss of lean body mass (muscle) that goes along with it — which is more of a concern for older adults who are already losing lean body mass, than for younger people.

According to a 1979 research article published in the American Journal of Clinical Nutrition [7], 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 [9,10].

This graph from Virta Health [10] based on the same research [7] 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 [9] 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 [9].

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 [10]”.

This time frame is consistent with the research above [9,10] showing that the slowing of muscle loss only occurs after 10 days of fasting, when ketones become the preferred fuel.

It is for this reason that I do not recommend fasting longer than 24 hours for older adults — especially post-menopausal women who are already at risk of sarcopenia (muscle loss), but daily periods of intermittent fasting (from the end of dinner until the first meal of the day, the following day) is recommended to help normalize blood sugar and circulating levels of insulin.

Another shortcoming with the popularized “keto” macros is that 15% protein may be insufficient for an older adult or for someone to sustain regular physical activity (more here).

For younger adults and those who are not trying to build muscle, this approach can be very helpful for losing weight and controlling blood sugar levels.

A “Well-Formulated” Ketogenic Diet

Another approach which falls in the Low Carb High Fat (LCHF) category are the recommendations of Dr. Stephen Phinney and Dr. Jeff Volek from their book The Art and Science of Low Carbohydrate Living — which recommends ~60-70% fat, 20%-up to 30% protein, and 10% carbohydrate [11].

This style of low carb high fat diet provides up to 30% protein, which is almost twice as much protein as the popularized keto’ diet, which is only 15% protein — and as outlined in an earlier article is insufficient for older adults, as well as people sustaining regular physical activity.

Low Carb High Protein

In a sense, a Low Carb High Protein (LCHP) diet which provides ~25-30% protein really falls at the higher end of the range of Dr. Stephen Phinney and Dr. Jeff Volek’s approach of 20% — up to 30% protein and provides a similar fat range of 65-70% fat, and 10% carbs.

As a “low carb diet” it offers all the benefits for lowering blood sugar, and as such is ideal for those seeking to put pre-diabetes or type 2 diabetes into remission.

It is also ideal for those seeking weight loss without periods of extended fating, as it does not have excessive fat, and provides sufficient protein for older adults and those who participate in regular physical activity.

Final Thoughts…

Both a Low Carb High Fat diet and Low Carb High Protein diet are low carb — so both are great for controlling blood sugar.

A Low Carb High Protein diet has almost twice the protein as a Low Carb High Fat diet — so, great for older adults and those who exercise regularly.

Protein provides satiety (feeling full) for almost half the calories as fat –so, great for weight loss.

If there is no need for a person to have very high levels of ketones, than a person should select which low carb or keto diet they follow on the basis of first meeting their protein needs. Then they can select the amount of carbohydrate that best meets their blood glucose goals. Finally, they can add a little fat to make things taste good as their essential fats come with their protein.

More Info?

If you are interested in learning more about my services, please have a look at the Services tab.  At the top are services provided as a Registered Dietitian to those in Canada, and at the bottom are Nutrition Education services provided to those outside of Canada.

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. 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
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. Kossoff EH, Doward JL. The Modified Atkins Diet. Epilepsia 2008; 49 (Suppl8): 37-41
6. Evert, AB, Dennison M, Gardner CD, et al, Nutrition Therapy for Adults With
   Diabetes or Prediabetes: A Consensus Report, Diabetes Care, Ahead of Print, published online April 18, 2019, https://doi.org/10.2337/dci19-0014
7. G B Forbes, E J Drenick, Loss of body nitrogen on fasting, The American Journal of Clinical Nutrition, Volume 32, Issue 8, August 1979, Pages 1570—1574, https://doi.org/10.1093/ajcn/32.8.1570
8. Owen OE, Felig P, Morgan AP, Wahren J, Cahill GF Jr. Liver and kidney metabolism during prolonged starvation. J Clin Invest. 1969 Mar;48(3):574-83. doi: 10.1172/JCI106016. PMID: 5773093; PMCID: PMC535723.
9. Phinney SD, Volek JS, To Fast of Not to Fast: what are the Risks of Fasting?, December 5, 2017, Virta Health, https://www.virtahealth.com/blog/science-of-intermittent-fasting
10. Cahill GF Jr. President’s address. Starvation. Trans Am Clin Climatol Assoc. 1983;94:1-21.
11. Volek JS, Phinney SD, The Art and Science of Low Carbohydrate Living: An Expert Guide, Beyond Obesity, 2011

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.

The human body is able to use carbohydrate, fat or protein to generate energy, however only carbohydrate and fat are major fuel sources.  Protein’s role in the diet is mainly to provide amino acids needed by the body to make its own proteins, for structure and function.

During digestion, carbohydrate, fat and protein from food are broken down into their basic components — carbohydrates are broken into simple sugar and turned into glucose, proteins are broken down into amino acids, and fat is broken down into fatty acids and glycerol.

During moderate-intensity exercise, our body will use half fatty acids as fuel and half glucose. During high-intensity exercise our body will rely on glucose as fuel — both from the carbohydrates we ate, as well as generated by breaking down fat stores. It is only if we are not getting enough calories in our food or from our fat stores that protein will be used for energy[2] and burned as fuel. If more protein is eaten than is needed by the body, the excess will be broken down and stored as fat [2].

Determining Individual Macros

In determining the amount of protein, fat and carbohydrate that each individual needs (i.e. “macros”), choosing the amount of protein we require comes first. The amount of carbohydrate and fat is chosen after that — based on the needs of the individual for blood sugar control and their metabolic health.

Since it is not a primary fuel source for the body, think of protein as the base of a balance scale — providing the body with building blocks for structure and function. The two arms of the balance are the two sources of fuel for energy: carbohydrate and fat. 

How do we choose the amount of protein we need?

We need to have enough protein for our needs, but not so much as to either store the excess as fat — or worse, to exceed the ability of our body to get rid of the excess nitrogen-by-product in the urine. Since 84% of the nitrogen waste produced from protein intake is excreted as urea in the urine[3], the safe upper limit of protein intake is based on the maximum rate of urea production which is 3.2 g protein per kg of ideal body weight [4] i.e. lean body mass.

NOTE: this calculation is based on lean body mass (also known as Ideal Body Weight or Ideal Body Mass (IBW), 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.

Basic protein requirements are set in the Recommended Daily Allowance (RDA) for protein, which is the level that is sufficient to meet the needs of 97-98 % of healthy people and to prevent deficiency. The RDA for protein for healthy adults is calculated at 0.8 g protein / kg of reference body weight (i.e. IBM) [5]. Remember, this is the bare minimum to prevent deficiency in most people.

For those who are physically active, the Academy of Nutrition and Dietetics, Dietitians of Canada, and the American College of Sports Medicine[6] recommend a protein intake of 1.2—2.0 g protein / kg IBW per day to optimize recovery from training, and to promote the growth and maintenance of lean body mass.

Older people also need more protein in order to maintain muscle mass, and prevent sarcopenia (muscle loss associate with aging). 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 IBW per day may best meet the needs of adults during aging [7,8].

Balancing Carbohydrate and Fat as Fuel

There are 3 ways that carbohydrate and fat as fuel can be balanced — and which one is best for a specific individual depends on their protein needs (outlined above), as well as their metabolic health.

Higher Carbohydrate than Fat

The standard American (and Canadian) diet recommended by national dietary guidelines aims for the majority of fuel (energy intake) to come from carbohydrate.

These diets are High Carb, Low Fat (HCLF) diets.

They are “high carb” because they provide >225g – 300 g carbohydrate / day, 45-65% of total energy intake.

They are “low fat” as they provide “not more than 30% of calories from fat [9].

For those who are metabolically healthy, a high carbohydrate diet where carbohydrate sources are unrefined whole grains (include the husk and the bran), as well as unprocessed starchy vegetables such as yam, peas and winter squash is certainly one option. The problem is that 88% of Americans are already metabolically unwell [10], with presumably a large percentage of Canadians as well (more about that here).

People who are already showing indications that they are not tolerating carbohydrate well; manifest either as high HOMA-IR, pre-diabetes or type 2 diabetes might do better to select another option for their main fuel source  — especially given that the American Diabetes Association (ADA) consensus report on Diabetes and pre-diabetes published on April 2019 indicated that;

”Reducing overall carbohydrate intake for individuals with diabetes has demonstrated the most evidence for improving glycemia and may be applied in a variety of eating patterns that meet individual needs and preferences[11].”

Higher Fat than Carbohydrate

Low Carb, High Fat (LCHF) diets are one type of diet that provides more fuel (energy) from fat, than from carbohydrate. There is another type, outlined below.

These range from the popularized “keto diet” of Dr. Jason Fung and the Diet Doctor website which typically provide ~75% fat, 15% protein, ~10% carbohydrate — to the recommendations of Dr. Stephen Phinney and Dr. Jeff Volek from their book The Art and Science of Low Carbohydrate Living which recommends ~60-70% fat, 20%-up to 30% protein, and 10% carbohydrate [12].

These are considered “low carb” diets when they provide < 130g carbohydrate / day, < 26% of total energy intake and “very low carb” (ketogenic) diets when they provide 20—50g carbohydrate / day, < 10% total energy intake — based on the definition from Feinman et al [13] which defines very low carbohydrate, low carbohydrate, and moderate carbohydrate diets as follows:

1. very low carbohydrate 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 same definitions of “low carbohydrate” and “very low carbohydrate” are also used in the clinical guidelines of the American Diabetes Association [11], as well as Diabetes Canada [15] where these are meal pattern options for those with diabetes and pre-diabetes to control blood sugar.

Balanced Fat and Carbs

This type of diet is a High Protein, Low Fat (HPLF) diet and the best-known is the P:E Diet of Dr. Ted Naiman.

The P:E Diet is “high protein” diet – recommending 40% protein with equal amounts of fat (30%) and carbohydrate (30%) — as generated by the P:E ratio Macro Calculator  (located at the bottom of www.p2eq.com);

The P:E diet is “low fat” as it provides “not more than 30% of calories from fat [9].

For the most part, the P:E diet is “moderate carb” — providing ~130—225g carbohydrate per day — although for some weights and heights, the carbohydrate content is slightly below the 130 g carbs / day cut-off for “low carb” (see examples from the P to E Macro Calculator, above).

While a high protein intake makes sense for those seeking to build and sculpt muscle, as outlined in this previous article setting the recommendation for protein at 40% of dietary intake (instead of as “g protein per kg body weight“) results in protein sometimes coming close to exceeding the excretion rate for urea of 3.2 g protein per kg reference body weight. 

This could be avoided if the P:E Macro Calculator was set a maximum limit of protein of 3.0 g protein / per kg body weight.

Low Carbohydrate High Protein

A Low Carb High Protein (LCHP) diet provides ~25-30% protein, which is significantly higher than the 10-20% protein of the standard American (or Canadian diet), yet without the possibility of exceeding the urea excretion capacity of the kidney as protein intake is set to up to 2.5 grams protein per kg body weight (which is well below the maximum of 3.2 g protein / kg ideal body weight).

Having high protein, it offers more satiety at less than half the calories of fat [16] — which makes much more sense for someone seeking weight loss.

Like the Low Carb, High Fat diets of Dr. Jason Fung and Diet Doctor (~75% fat, 15% protein, ~10% carbohydrate) this diet is “high fat“, and provides 65-70% fat. In a sense, a Low Carb High Protein meal pattern reflects the higher end of the range of Dr. Stephen Phinney and Dr. Jeff Volek’s approach of ~60-70% fat, 20%-up to 30% protein, and 10% carbohydrate.

This meal patterns provides a wide range of fats from olive oil and avocado oil to (depending on the lipid profile of the person) butter and coconut oil. Most of the fat provided in the diet is not from added fat, but from fat that comes along with protein — such as the fat in meat, cheese, nuts or yogurt.

Most significantly, this meal pattern is “low carb” (< 130g carbohydrate / day) or “very low carb” / ketogenic — providing ~20—50g carbohydrate / day and as a low carb diet “has demonstrated the most evidence for improving glycemia” [11].

For those seeking fat loss but already having difficulty handling carbohydrate, a Low Carb High Protein (LCHP) meal pattern offers the “best of both worlds”.

It offers the benefits of being able to build new muscle, as well as lower the risk of muscle loss.

It also offers the higher satiety of high protein — without the possibility of exceeding the body’s ability to excrete ammonia in the urine.

…and it is “low carb” — providing the improved blood sugar control that “low carb” is known for.

Final Thoughts…

Humans only have two primary fuel sources, so meal patterns such as Low Carb High Fat, Low Carb High Protein and P:E (High Protein Low Fat) always come down to a choice between “low carb” or “low fat“.*

*theoretically, one could set all 3 macros at 33% each — making the meal pattern neither low fat or low carb — but to what end?

Whether low carb or low fat is the most suitable for someone depends on their protein needs and metabolic health.

I started out 5 years ago teaching low carb from a Low Carb High Fat (LCHF) perspective, and for the last 3 years have also provided a Low Carb High Protein (LCHP) meal pattern.

For those seeking to improve blood sugar or put type 2 diabetes into remission, either one of the low carb options work, however it has been my experience that peri- and post-menopausal women often do much better on the higher protein version of a low carb diet when it comes to weight loss. 

Over the last few months, I have also been asked to provide metabolically healthy people with a P:E / HPLF Meal Plan — which I do, although I set an upper limit on protein intake to a maximum of 2.0 g protein per kg ideal body weight.

Different people have different goals and health needs, which is why I offer more than one type of meal pattern. While a P:E diet is just on the edge of “low carb” — it is very much “low carb” when compared with the Standard American (and Canadian) diet.

There is no one-sized-fits-all low carb or ketogenic 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:

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

References

1. Fuel Sources. (2020, August 13). Retrieved May 24, 2021, from https://med.libretexts.org/@go/page/7071
2. Youdim A, Merck Manual, Carbohydrates, Proteins and Fats, https://www.merckmanuals.com/en-ca/home/disorders-of-nutrition/overview-of-nutrition/carbohydrates-proteins-and-fats
3. 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
4. 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
5. National Academies Press, Dietary Reference Intakes for Energy, Carbohydrate, Fiber, Fat, Fatty Acids, Cholesterol, Protein and Amino Acids (2005)
6. 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
7. 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
8. 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
9. 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/
10. Araíºjo J, Cai J, Stevens J. Prevalence of Optimal Metabolic Health in American Adults: National Health and Nutrition Examination Survey 2009—2016. Metabolic Syndrome and Related Disorders Vol 20, No. 20, pg 1-7, DOI: 10.1089/met.2018.0105
11. 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
12. Volek JS, Phinney SD, The Art and Science of Low Carbohydrate Living: An Expert Guide, Beyond Obesity, 2011
13. 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
14. 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
15. 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

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 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

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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.