Category: article

Diagnosis and Treatment

The most recent population-based study data from the US with almost 26,000 adults aged 18 – 74 years found 9.5% had TSH levels >5.1 mIU/L, with a higher prevalence in women and older adults. Among the 9.5% with elevated TSH, 74% had subclinical hypothyroidism (TSH 5.1 and 10 mIU/L), and 26% had overt hypothyroidism (TSG >10 mIU/L) [17].

Note (August 14, 2022): From a practical point of view, this study shows that almost 10% of adults have some form of hypothyroidism, with 7/10% being subclinical and 2½ % having clear hypothyroidism. Given its prevalence and significant risk of being undiagnosed, identifying symptoms and lab markers before it progresses is essential. 

In British Columbia, a diagnosis of subclinical hypothyroidism is made at a TSH > 4 mIU/L, but treatment is only recommended when TSH is above 10 mIU/L [18]. This leaves those with a TSH >4 mIU/L but <10 mIU/L in the situation where they need to get much sicker before treatment is recommended.

The goal of treatment with thyroid hormone replacement is to reduce the patient’s serum TSH concentration into the normal reference range. Since the mean serum TSH for the general population is around 1.4 mIU/L, with 90% having serum TSH levels <3.0 mIU/L, many experts recommend a therapeutic TSH target ranging from 0.5 to 2.5 mIU/L in young and middle-aged patients [19] to 7.7 mIU/L in elderly people over the age of 80 years [20].

Studies with 10 to 20-year follow-up have reported that 33 to 55% of people with subclinical hypothyroidism progress to overt hypothyroidism [21,22,23]. This means that 1/3 to >1/2 of people with subclinical hypothyroidism will develop overt hypothyroidism within that period.

Most experts do not recommend treating people with a TSH > 10 mIU/L but with no symptoms (asymptomatic). However, since a meta-analysis of data from 1950-2010 found no increased risk of coronary heart disease in asymptomatic people with a TSH of 4.5 to 6.9 mIU/L, treating them is generally not recommended [24]. 

There is, however, an increased risk of coronary heart disease in those with a TSH of 7.0 to 9.9 mIU/L, so some experts recommend treating those with a TSH > 7.0 mIU/L whether or not they have symptoms [24]. Unfortunately, despite this elevated risk, individuals in British Columbia do not currently have access to treatment with a TSH < 10 mIU/L under the guidelines [18].

Final Thoughts…

Making recommendations on how someone should change their diet can’t be made in a vacuum and it is for this reason, I evaluate a person’s lab test results in light of their medical history and enquire about family history of type 2 diabetes, heart disease, high cholesterol, blood pressure, thyroid disorders and other conditions as part of my assessment. Then I look at how people eat in light of their risk factors for those conditions.

If I feel that it would be beneficial to have additional lab work such as fasting insulin, or thyroid stimulating hormone (TSH), then I will request that their doctor requisition these tests. Often, when I provide the doctor with my clinical reasons for asking for them, they write the requisition; however, sometimes, they decline. If I don’t think it would not be a financial burden and that having the results will provide the client with a much better understanding of how their diet relates to their weight or health, I will discuss the option of obtaining the tests on a patient-pay basis.  If self-paying for the tests is not feasible, and the risk factors are significant, then I will tailor my dietary recommendation to lower the risk.

NOTE (August 15, 2022): It is important to keep in mind that too little, or too much thyroid hormone can have serious consequences.

Untreated or under-treated hypothyroidism can be serious and is when the body gets too little thyroid hormone. This can lead to a myxedema crisis (covered in this article).

Thyrotoxicosis can also be serious and is when the body gets too much thyroid hormone. This can occur in untreated hyperthyroidism, or by self-treating hypothyroidism (covered in this article).

More Info

If you would like more information about how I can support you in your goal of improved health, please send me a note through the Contact Me form above.

To your good health!

Joy

You can follow me on:

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

DISCLAIMER (August 14, 2022): The information in this post should in no way be taken as a recommendation to self-diagnose, self-interpret diagnostic tests, or self-treat any suspected disorder, including thyroid function. It is essential that people who suspect they may have symptoms of any condition consult with their doctor, as only a medical doctor can diagnose and treat.

In Canada and many places in the US, the standard screening test for abnormal thyroid function is thyroid stimulating hormone (TSH). As outlined below, TSH is a hormone that is released from the pituitary gland, not the thyroid. If TSH results falls within normal range, no testing of thyroid hormones occurs. Thyroid response to TSH is presumed to be normal.

Thyroid Hormones and Lab Tests Used to Assess Thyroid Function

Thyroid Stimulating Hormone (TSH) is a hormone that is produced by the pituitary gland in response to a hormone called Thyrotropin-Releasing Factor (TRF) that is released by the hypothalamus of the brain.

Thyroid Stimulating Hormone (TSH) released from the pituitary gland acts on the thyroid gland, a butterfly shaped gland in the front of the neck. The action of pituitary TSH on the thyroid results in the release of thyroxine, also called Free T4 (fT4).  Thyroxine (fT4) is reduced to Triiodothyronine also called Free T3 (fT3), which is the active form of thyroid hormone.

Central Hypothyroidism is where a problem exists in either the hypothalamus or the pituitary gland that results in a decreased in TSH release from the pituitary gland. On lab tests, a low TSH and low T4 indicates central hypothyroidism. This is often treated by administration of growth hormone, or using T3 containing medications. 

Primary hypothyroidism is where there is no abnormality in the hypothalamus or the pituitary gland. Primary hypothyroidism is diagnosed when there is high TSH and normal or low free thyroxine (free T4 / fT4). In many places in Canada and the USA, if TSH is normal, no further testing is done. It is assumed that the action of pituitary TSH on the thyroid gland results in sufficient release of T4.

Thyroid Function – different causes of primary hypothyroidism

Hashimoto’s Disease

The most common form of primary hypothyroidism in the western world is Hashimoto’s disease which is an autoimmune disorder where the body attacks the thyroid. Thyroid Peroxidase Antibody (TPO antibody) is the marker for Hashimoto’s hypothyroidism [6]. 

Prior Thyroid Surgery or Radiation of the Neck

According to Endocrinologist, Dr. Theodore C. Friedman MD, PhD,  Professor of Medicine at UCLA, primary hypothyroidism can also result from prior thyroid surgery to remove a tumor or nodule, or due to radiation of the neck [6].

Dietary Deficiency

Iodine is essential for thyroid function and in the developing world, the most common type of primary hypothyroidism is related to iodine deficiency. Iodine deficiency is assumed to be rare in the West since iodine is added to salt (iodized salt), in the same way that vitamin D is routinely added to milk.  I have noticed a significant increase in the use of Himalayan pink salt and sea salt for home use in the last decade or so, and wondered how much of the salt being used currently is iodized. Data from 2015 indicates that only 53% of salt sales in the US were iodized [7], so I have to wonder what effect this decreased intake of iodized salt may be having on the prevalence of hypothyroidism. 

Selenium is another mineral that is essential for thyroid function as it functions in the conversion of (inactive) T4 to (active)T3. Like iodine deficiency, selenium deficiency is a significant problem in the developing world, but thought to be rare in the West. Research from 2012 indicates that the selenium content of the soil in the US was already lowest in the major agricultural areas of the Northwest, Northeast, Southeast, and areas of the Midwest near the Great Lakes[8] and at the time, only the Great Plains and the Southwest were reported to have adequate selenium content in the soil [8].

Given the decreased use of iodized salt and decreased presence of selenium in the soil where much of domestic food is grown, I wonder what effect this may be having on formerly rare incidence of nutrient-related hypothyroidism in the US and Canada.

Assessing Thyroid Function – testing for hypothyroidism

Each province in Canada sets its own policy for which laboratory tests are covered by provincial medical plans, and in the US which testing is covered is determined by whether they are performed by in-network or out-of-network labs. 

In British Columbia, thyroid testing covered by the provincial plan is determined by a 2018 document titled Thyroid Function Testing in the Diagnosis and Monitoring of Thyroid Function Disorder [9]. These guidelines outline testing for thyroid stimulating hormone (TSH), free thyroxine (fT4), free triiodothyronine (fT3) and anti-thyroid peroxidase (TPO).

According to the guidelines, risk factors for thyroid disease include [9]:

• men: age ≥ 60 years
• women: age ≥ 50 years
• personal history or strong family history of thyroid disease
• diagnosis of other autoimmune diseases
• past history of neck irradiation
• previous thyroidectomy or radioactive iodine ablation
• drug therapies such as lithium and amiodarone
• dietary factors (iodine excess and iodine deficiency in patients from developing countries)
• certain chromosomal or genetic disorders

Note: Iodine nutrient deficiency for those who are not from developing countries is not included. 

Indications for Testing

1. 1. Routine thyroid function testing is not recommended in asymptomatic patients Testing may be indicated when non-specific symptoms or signs are present in patients who have specific risk factors for thyroid disease.
   2. Testing is indicated for patients with a clinical presentation consistent with thyroid disease as delineated in Table 1: Symptoms and Signs of Thyroid Disease, below.
   3. Where thyroid testing in an asymptomatic patient has occurred and the patient has been diagnosed with subclinical thyroid disease (subclinical hypothyroidism: TSH is elevated in the presence of normal levels of fT4)
   4. If initial testing (i.e. TSH) is normal, repeat testing is unnecessary unless there is a change in clinical condition*.  

The Guidelines (page 3) states, “A TSH value within the laboratory reference interval excludes the majority of cases of primary thyroid dysfunction.

[The reference provided for this is: Jameson, JL., Weetman, A.P.,  Disorders of the Thyroid Gland, Harrison’s Principles of Internal Medicine. 17th ed. New York: McGraw-Hill; 2008. p. 2224–47]

The guide also indicates that “the TSH reference interval will vary depending on the testing laboratory. ” What that means is the cutoff points for an abnormal level of TSH vary between labs in BC.

*What this means is, if TSH lab test results come back in the normal range, no further testing is performed unless the person begins to show some of the accepted hypothyroid signs and symptoms in Table 1, below.

Note: As outlined above, if TSH is found to be normal we know that TSH release from the pituitary gland is normal. There is no testing for the thyroid gland’s response to TSH released from the pituitary gland, it is assumed to be functioning.

Below are the accepted hypothyroid signs and symptoms that warrant testing (from Table 1 [9]).

Only the above list of clinical presentation symptoms is recognized as consistent with hypothyroidism, warranting lab testing.

Looking at the list in Table 1, how many other conditions, including having Covid-19 result in people feeling depressed, having decreased mental function (“brain fog”), feeling physically tired, feeling cold, having reduced degree of movement and muscle weakness, dry flaking skin, and a hoarse voice?  Unless a person has burning or prickling sensation in their hands or feet, or swelling under their eyes, or are sweating less than usual, it is unlikely they would notice anything unusual outside of common flu or Covid symptoms that would have them mention the above to their doctor.

Below is a fuller list of clinical presentation symptoms associated with hypothyroidism, with the ones NOT recognized for testing in italics.

The Guidelines Summarized

Unless you are either a man ≥ 60 years, or a woman ≥ 50 years with a personal history or strong family history of thyroid disease, a diagnosis of other autoimmune diseases, a past history of neck irradiation or previous removal of your thyroid or destruction of your thyroid for medical reason using radioactive iodine, are not on medications such as lithium or amiodarone, and aren’t from a developing country with either iodine excess or iodine deficiency, or have a specific chromosomal or genetic disorder listed, you do not qualify for TSH testing unless you display the specific symptoms listed in Table 1, above).

What if the other common presentations that are NOT also common in colds, flu or Covid-19 were included in the checklist such as;

• • non-pitting edema (swelling) in the lower legs and ankles
  • a puffy swollen face
  • an enlarged tongue (with or without scalloped edges)
  • enlarged saliva glands including under the tongue
  • hair thinning
  • loss of the outer third of eyebrows
  • pale or bluish lips

…would it be more likely that people experiencing these symptoms would go to their doctors, and be tested?

Summary of Assessing Thyroid Function

1. To be diagnosed with hypothyroidism, requires a high TSH and normal or low free free T4 but in many places in Canada and the USA, if TSH is normal, no further testing is done.

2. How one defines “high TSH” is important. In British Columbia, the cutoff points vary between labs, but lab normal values at the labs near me are the normal range is 0.27-0.42 mU/L, but is a result of 3.9 mU/L or 4.0 mU/L really “normal”?

Thyroid Function

TSH                    4.0  (0.27-4.2) mU/L

It is “normal enough” that no further testing is done.

3. Someone can have common clinical manifestations of hypothyroidism (non-pitting edema in the lower legs and ankles, a puffy swollen face, enlarged tongue (with or without scalloped edges), enlarged saliva glands, hair thinning, loss of the outer third of eyebrows or pale or bluish lips but if their symptoms are not on the list in Table 1, they are not eligible for testing of thyroid hormones, fT4 / fT3.

4. Unless a person is from a family with specific risk factors (older age with other autoimmune conditions, or had neck irradiation, a thyroidectomy or radioactive iodine ablation,  or take lithium or amiodarone, or are from a developing country that had iodine excess and iodine deficiency) they are not eligible for testing of thyroid hormones, fT4 / fT3.

Final Thoughts…

If some one has their TSH tested and the results come back in the normal range for that particular lab, no further testing is done — even if they have symptoms documented in the literature to be associated with hypothyroidism. 

My concern is if the definition of who qualifies for fT4 testing may be too narrow,. People with high-normal TSH and symptoms that are associated with hypothyroidism, but not on the “list” in Table 1, will not be tested. Could it be that some people could have greatly improved quality of life if thyroid hormones were evaluated, found to be low, and treatment initiated? [Please see note added July 17, 2022 about a diagnosis of subclinical hypothyroidism where TSH > 4mIU/ with normal T4.]

NOTE, July 16, 2022: It is not the normal TSH test result in the absence of symptoms that I am addressing in this article, but the absence of T4 testing in someone with presenting symptoms of hypothyroidism beyond the official “list”. It is my hope that if someone has those symptoms and a TSH value that is normal, that physicians would remain curious and ask for additional testing.

NOTE: July 17, 2022: I came across an academic paper from 2016 that indicates that diagnosis of subclinical hypothyroidism (SCH) exists in western countries for TSH >4 mIU/L, with normal T4 [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4740939/], whereas the cutoff here for a diagnosis of SCH is >10 mIU/L. (which is based on 2008 reference, as outlined above). Also of interest, another paper I came across from 2016 reported that several previous studies found no significant difference in symptoms between people with  subclinical hypothyroidism  and those with overt hypothyroidism [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4740939/] . The most common symptoms reported of both SCH and overt hypothyroidism were poor memory, slow thinking, muscle cramps, muscle weakness, tiredness, dry skin, feeling colder, hoarse voice, puffy eyes, more constipation.

More Info?

If you have been diagnosed with hypothyroidism and would like to better understand the condition, or would like make sure that you have adequate intake of nutrients known to be important in thyroid health, please send me a note through the Contact Me form and I will reply when I can.

To your good health!

Joy

You can follow me on:

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

References

1. Crofts, C., et al., Identifying hyperinsulinaemia in the absence of impaired glucose tolerance: An examination of the Kraft database. Diabetes Res Clin Pract, 2016. 118: p. 50-7.
2. Pareek, M., Bhatt, D.L., Nielsen, M.L., et al,  Enhanced Predictive Capability of a 1-Hour Oral Glucose Tolerance Test: A Prospective Population-Based Cohort Study. Diabetes Care 1 January 2018; 41 (1): 171–177. https://doi.org/10.2337/dc17-1351
3. Bergman M, Chetrit A, Roth J, Dankner R (2016) One-hour post-load plasma glucose level during the OGTT predicts mortality: observations from the Israel Study of Glucose Intolerance, Obesity and Hypertension. Diabet Med 33:1060–1066
4. Hulman, A., Vistisen, D., Glümer, C. et al. Glucose patterns during an oral glucose tolerance test and associations with future diabetes, cardiovascular disease and all-cause mortality rate. Diabetologia 61, 101–107 (2018). https://doi.org/10.1007/s00125-017-4468-z
5. Berkow, R., Beers, M. H., & Fletcher, A. J. (1997). The Merck Manual of Medical Information. Whitehouse Station, N.J.: Merck Research Laboratories.
6. Freidman, Theodore C., Nuances of Hypothyroidism, The MAGIC Foundation’s Annual Conference for Adults With Endocrine Disorders (Phoenix, AZ),  March 3, 2019
7. Maalouf J, Barron J, Gunn JP, Yuan K, Perrine CG, Cogswell ME. Iodized salt sales in the United States. Nutrients. 2015 Mar 10;7(3):1691-5. doi: 10.3390/nu7031691. PMID: 25763528; PMCID: PMC4377875.
8. Mistry HD, Broughton Pipkin F, Redman CW, Poston L. Selenium in reproductive health. Am J Obstet Gynecol. 2012 Jan;206(1):21-30
9. BC Guidelines & Protocols Advisory Committee, Thyroid Function Testing in the Diagnosis and Monitoring of Thyroid Function Disorder, October 24, 2018

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I have been wanting to write an article about constipation and the role of fiber for a while, but yesterday I saw a cartoon drawn by Glenn McCoy that was the final motivation. 

The old song “all I want for Christmas is my two front teeth” may apply to children, but many adults can relate to this cartoon! The number of people I see in my practice who complain about constipation is ~1/4 to 1/3 — and I know this because one of the questions I routinely ask during an assessment is ‘how many times per day, or per week do you poop’, and I ask them to describe their poop (soft, hard, like bunny poop, floats, etc.).  Yes, really! I ask about pooping because it is important, and I also ask about sleep, because that is important too.

The percentage of adults that I see who struggle with chronic constipation is ~15- 20%, which fits what is seen in the literature. Based on self-report or using the Rome IV criteria, constipation is a problem for between 2% and 27% of the population, with an average of 15% [1].  

Constipation defined by the Rome IV criteria needs to meet at least two of the following symptoms over the previous three months [2]. Put in common language, those symptoms are;

1. 1. having fewer than 3 bowel movements (BMs) per week without taking something to “go” (i.e. having spontaneous bowel movements)
   2. pushing or straining for at least 1/4 of BM attempts
   3. lumpy or hard stools for at least 1/4 of BM attempts
   4. a feeling of something blocking the anus or rectum for at least 1/4 of BM attempts
   5. feeling of still needing to poop after pooping (i.e. incomplete defecation) for at least 1/4 of BM attempts
   6. physically positioning differently or using manual manipulation for at least 1/4 of BM attempts

It is important to note that the Rome IV criteria also states that to meet the criteria for constipation one must NOT also meet the criteria for Irritable Bowel Syndrome (IBS). These are different disorders. While people with IBS may have constipation, they may also have diarrhea, or may have alternating symptoms of constipation and diarrhea.  IBS’ main symptom is abdominal pain related to bowel movements.

The Rome IV criteria for IBS [3] requires having reoccurring symptoms of abdominal pain at least one day per week during the previous three months and associated with 2 or 3 of the following;   

1. 1. defecation (pooping)
   2. a change in the amount of times one poops (stool frequency)
   3. a change in stool form or appearance 

Chronic constipation and IBS are both referred to as “functional gastrointestinal diseases” (FGIDs). These are common disorders that are ongoing and reoccurring and whose symptoms but are not caused by some underlying disease, or structural abnormality of the GI tract [4].  These are different than something like diverticulosis which is a pouch that forms in the large intestine and which requires monitoring the amount of fiber one takes in to avoid constipation. 

[NOTE: December 24, 2021:  I think a better term for these conditions is “functional gastrointestinal disorders” because these do not have a structural cause. A physician I know described it this way; “a rule of thumb is that a disease is something a pathologist can see.”]

There are no tests for constipation or IBS. They are diagnosed based on symptoms, or function.

Constipation and Fiber

Most people who are diagnosed with “constipation*” are told by their doctors to “eat more fiber and drink more water”. 

A diagnosis of “idiopathic constipation” means that the constipation occurred spontaneously on its own, and has no known cause.  “Chronic idiopathic constipation” is chronic constipation which has no known cause.

Most people that come to me think of fiber as “roughage” that include things such as whole, unrefined grains, wheat bran, oat husks, and the like. Horse food! The term “insoluble fiber” is used to describe these because these fibers do not dissolve in water. Insoluble fiber is not digested so it just adds “bulk” to the stools.

Soluble fiber dissolves in water, and as a result creates a gel-like texture in the intestine when mixed with the water contained in food, or in beverages. This is where the “drink more water” advice comes in — it is for the soluble fiber to form that gel. Soluble fiber helps slow down digestion enabling people to feel fuller longer, and helps form a soft, bulky stool. While people don’t usually think of these types of foods as “high in fiber”, foods high in soluble fiber include onions, chicory root, Jerusalem artichoke, oats, apples, strawberries, psyllium husk, and some legumes (or pulses).

The six million dollar question is whether increasing dietary fiber actually improves constipation.  In fact, a ground-breaking study from 2012 found the exact opposite! Symptoms of ‘idiopathic constipation’ were significantly reduced when people in the study lowered, or even stopped their high intake of dietary fiber [5]. This made sense to the researchers who explained that ‘since increasing dietary fiber increases the volume and bulk of the stools, in patients where there is already difficulty in passing large stools, it is illogical to actually expect that bigger or more feces will ameliorate (i.e. improve) this problem.’ Of interest, people in the study who went on to eat the least amount of fiber in their diet had the greatest reduction in symptoms, and those who went back to eating a high fiber diet also began to experience their previous symptoms of constipation — in proportion to the amount of fiber they ate in their diet [5]! ]

So, if increasing fiber intake is not the answer to maintaining ‘regularity’ in our colon, what is?

Soluble Fiber and the Gut Microbiome/Mycobiome

Soluble fiber helps feed the healthy bacteria that live in our bowel (large intestine) called the ‘gut microbiome’ or ‘gut flora’. We are in a mutually beneficial (symbiotic relationship) with them — which means they benefit us, and we benefit them. What we eat feeds them, and in turn they produce by-products that are helpful for us. 

Post Publication Update: (December 24, 2021) The gut microbiome use soluble fiber as “food” and in return produce three short chain fatty acids; acetate,  butyrate and propionate [Rios-Covian, D. et al. Intestinal Short Chain Fatty Acids and their Link with Diet and Human Health. Front Microbiol 7, 185 (2016).]. The butyrate produced by the gut microbiota is the main “food” (energy source) of the cells of our intestine — especially the colonocytes (cells in the lumen of our colon). [Donohoe, D. R. et al. The microbiome and butyrate regulate energy metabolism and autophagy in the mammalian colon. Cell Metab 13(5), 517 (2011).]. Our gut microbiome feed on the fiber in our food and produce short chain fatty acids in return, and in turn, these short chain fatty acids feed the cells of our colon! These short chain fatty acids that are fermented by our gut microbiome are what maintain the homeostasis (balance) of our intestines [Venegas DP, de la Fuente MD, Landskron G, et al, Short Chain Fatty Acids (SCFAs)-Mediated Gut Epithelial and Immune Regulation and Its Relevance for Inflammatory Bowel Diseases, Front. Immun 10, 277 (2019).]

People who eat a very low carbohydrate (ketogenic) diet produce a closely-related short chain fatty acid known as β (beta)-hydroxybutyrate, that can be measured in the blood.  Recent studies have found that β (beta)-hydroxybutyrate acts very similarly to butyrate [Chriett, S., DÄ…bek, A., Wojtala, M. et al. Prominent action of butyrate over β-hydroxybutyrate as histone deacetylase inhibitor, transcriptional modulator and anti-inflammatory molecule. Sci Rep 9,742 (2019). https://doi.org/10.1038/s41598-018-36941-9] and β (beta)-hydroxybutyrate also feeds the cells of the colon, as well as the cells of the small intestine. The main difference is that when the cells of the intestine are fed β-hydroxybutyrate via the capillaries of the blood, this is thought to be less irritating to the cells of the colon than when they feed on butyrate produced by the gut microbiota.

[Many thanks to Dr. Lance de Foa of Wawa, Ontario for bringing the above information to my attention.]

Something else which is very important to note is that the gut microbiome / mycobiome can also be adversely affected by the type of carbohydrate we eat.

A study was published in late 2020 documented how simple sugars in the diet can induce colitis, an inflammatory bowel disease [6] in mice. The study found that when researchers fed the mice simple sugars such as fructose (fruit sugar), sucrose, (table sugar made up of glucose and fructose) and glucose,  the high simple sugar diet damaged the protective mucus layer of the colon (large intestine) and increased the number of specific bacteria — especially Akkermansia muciniphila and Bacteroides fragilis which break down the mucus that lines and protects the colon. When the mice were fed a 10% glucose solution for seven days (chosen because soft drinks contain ~15% sugar) and were then given a 2.5% dextran sulfate sodium (DSS) which is known to induce colitis, the mice that had been fed the glucose had extreme sensitivity to DSS treatment and suffered from aggressive colitis, bloody diarrhea and rapid loss of nearly 20% of their body weight. When the researchers looked at the glucose-treated mice three days after giving them the DSS, they found that their colons were shorter than the colons of the control mice that were not fed the glucose, and that the glucose-fed mice had many of the symptoms of colitis, including loss of epithelial crypts, inflammation, and ulceration [5].

The control mice remained healthy, with stable weight [5]. Both the glucose-treated mice and the mice that were not given glucose ate comparable amounts of food and water during DSS administration — which implied that the colitis susceptibility of glucose-fed mice was not due to any increase in DSS intake.

A second arm of the study (more here) found that a high sugar intake alone had a similar effect as the DSS in mice that were genetically susceptible to colitis. 

A different small randomized, double-blind crossover study pilot study from 2020 [6] looked at the effect of a very low carbohydrate (ketogenic) diet on the population of the gut fungi (mycobiome) and microbiome and found that a very low carbohydrate diet more positively affected the gut mycobiome, than the diet used in the control group, the American Heart Association Diet. What was notable was a significant reduction in the proportion of Candida yeast — which are implicated in various gut-related diseases including inflammatory bowel diseases such as Crohn’s disease and ulcerative colitis, as well as gut inflammation [7].

In my practice I describe the relationship between us (as the host) and our microbiome and mycobiome using the analogy of “feeding turtles”.  If we think of our intestines as a terrarium with two types of turtles — “good turtles” and “bad turtles”, if we only feed the good turtles, and don’t feed the bad turtles, the bad ones will die off, and the good ones will get stronger and proliferate.  If we feed our “good” microbiome and mycobiome and starve out the “bad” ones, we will have a healthier gut.  While the above studies are preliminary, it makes sense that if we reduce simple carbohydrate intake in the diet (sucrose, lactose and glucose) we won’t be feeding the “bad bugs”, which means they will be reduced or even die off. If we eat foods high in soluble fibers that feed the “good bugs”, they will get stronger and proliferate.

In addition to insoluble fiber and soluble fiber, there is another class of fibers which are water-soluble, non-gelling fibers, including one called partially hydrolyzed guar gum (PHGG). This fiber plays an important role in alleviating symptoms of constipation or diarrhea because it is not probiotic, but a prebiotic. It is like “turtle food” for the “good turtles”.  Partially hydrolyzed guar gum (PHGG) has been shown in clinical trials to both decrease symptoms in constipation-predominant IBS and diarrhea-predominant type IBS, as well as decrease the hallmark symptom of abdominal pain [8], and works very well to alleviate symptoms of chronic constipation. 

Putting it Into Practice

For those who want to know which foods are high in non-soluble fiber, these include red cargo rice (4 g fiber per 1/2 cup), or wholegrain brown basmati rice, such as Tilda® brand (4g fiber per 1/2 cup), and wholegrain breads made with whole and cracked wheat berries, or whole and cracked rye berries. Wholegrain breads are not the same as “brown bread” or “whole wheat bread”, but the type of bread one would find in a European bakery, a natural food store, or in a regular supermarket imported from Germany (e.g. Mestemacher® brand). I describe them to clients as heavy enough that if you dropped it on your food, it might leave a bruise. In specific condition, or stages of conditions, it is recommended to limit these foods. 

As for soluble fiber,  legumes are good source and while they contain 15g of carbohydrate per 1/2 cup they also are good sources of protein (~7g per 1/2 cup). Black beans have 8.7 g soluble fiber per 100 g, lentils have 7.3 g soluble fiber / 100g, chickpeas have 7 g soluble fiber / 100g, and kidney beans have 6.8 g soluble fiber / 100g.

Low carb vegetables that are a good source of soluble fiber include carrots (2.8 g/100g), beets (2.8g/100g), broccoli (2.6 g/100g), artichoke (5.4 g/100g), and Brussels sprouts (3.8g/100g) and fruit such as raspberries have 6.5g fiber / 100g, blackberries have 5.3 g fiber / 100g, and apples have 2.4g fiber/100g.

Even excellent sources of fat can come with soluble fiber, including avocado (6.7 g/100g) and Brazil nuts (8g / 100g).

The above foods can be incorporated into a wide range of dietary patterns — from omnivore, to vegetarian and pescatarian, Mediterranean, and low carb, and by also reducing intake of simple carbohydrates such as sucrose, lactose and glucose, you can nourish yourself, as you feed your healthy microbiome.

More Info?

If you would like a Meal Plan to help you reduce chronic constipation, or simply to increase intake of all types of fiber, please send me a note through the Contact Me form and I will reply when I can.

To your good health!

Joy

You can follow me on:

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

Special Thanks

Special thanks to Glenn McCoy for permission to post his cartoon!

References

1. Sanchez MI, Bercik P. Epidemiology and burden of chronic constipation. Can J Gastroenterol. 2011;25 Suppl B(Suppl B):11B-15B. doi:10.1155/2011/974573
2. Drossman DAm Change L, Chey WD, et al, Rome IV Diagnostic Questionnaires and Tables for Investigators and Clinicians, Rome Foundation, http://romeonline.org/?product=rome-iv-diagnostic-questionnaires-and-tables-for-investigators-and-clinicians-first-edition
3. Schmulson MJ, Drossman DA. What Is New in Rome IV. J Neurogastroenterol Motil. 2017;23(2):151-163. doi:10.5056/jnm16214
4. UNC Centre for Functional GI & Motility Disorders, What is a Functional GI Disorder?2017,  https://www.med.unc.edu/ibs/wp-content/uploads/sites/450/2017/10/What-Is-Functional-GI.pdf
5. Ho KS, Tan CY, Mohd Daud MA, Seow-Choen F. Stopping or reducing dietary fiber intake reduces constipation and its associated symptoms. World J Gastroenterol. 2012;18(33):4593-4596. doi:10.3748/wjg.v18.i33.4593
6. Khan S, Waliullah S, Godfrey V et al, Dietary simple sugars alter microbial ecology in the gut and promote colitis in mice, Science Translational Medicine 28 Oct 2020: Vol. 12, Issue 567,  DOI: 10.1126/scitranslmed.aay6218
7. Nagpal R, Neth B, Wang S et al,  Gut mycobiome and its interaction with diet, gut bacteria and alzheimer’s disease markers in subjects with mild cognitive impairment: A pilot study. EBioMedicine, 2020; 59: 102950 DOI: 10.1016/j.ebiom.2020.102950
8. Giannini EG, Mansi C, Dulbecco P, Savarino V. Role of partially hydrolyzed guar gum in the treatment of irritable bowel syndrome. Nutrition. 2006 Mar;22(3):334-42. doi: 10.1016/j.nut.2005.10.003. Epub 2006 Jan 18. PMID: 16413751.

Copyright ©2021 BetterByDesign Nutrition Ltd.

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

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!

Below are some examples of relatively low-cost animal source foods, sorted from the highest amount of protein per ounce (28g), 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, 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 frozen vegetables (which 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 is terrific added to casseroles with pasta, or for those eating low carb — with chunks of lightly cooked cauliflower, instead of noodles. These casseroles can be a complete meal with the addition of frozen vegetables, and are lovely with a sprinkle of grated cheese on top.  Tuna is such a great source of protein as well as omega 3 fat, and is often on sale making it even less expensive.

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 pate.

Eggs can provide most of the protein in a spinach soufflé with or without the addition of some grated cheese…

…or they 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 a bit of ground meat (or omitted for vegetarians), garlic, green onions and brown bean sauce, 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).

Lentils of many types have a good protein to energy (kcals) ratio and are a good source of most essential amino acids, but are missing sulfur-containing methionine and cysteine. Lentils are delicious made Middle Eastern or Indian style and serving them with a 1/2 cup of rice or 1/2 a pita bread will provide the missing amino acids, making it a “complete protein”.

Pinto beans can be made into a delicious vegetarian chili with canned tomatoes and while they lack the amino acids methionine and tryptophan, serving the chili with a few corn tortillas make these complete.

Hummus isn’t the only way to enjoy chickpeas!  They are wonderful cooked into a curry with onions and a bit of tomato or stewed with big chunks of fresh garlic and made into Moroccan Chick Peas (Pois Chiche Moroccan). Hummus with a half of pita, or Pois Chiche Moroccan with couscous complete the missing amino acids.

Protein in Some Nuts, Seeds and Grains

As you can see from the table above, the pita bread or basmati rice provide some protein and so does the tahini in the hummus.

Nuts and seeds, while not inexpensive do provide some protein and can be used with bread or pita to make a complete protein.

Dairy Sources

And don’t forget dairy! While most people think of hard cheese such as cheddar or feta as high in protein, these are high in fat and not that high in protein.  But cottage cheese is amazing! Ounce for ounce, cottage cheese provides way more protein than steak, or ground beef, and even more than turkey or chicken breast!  Who would have thought?

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.

The pressed cottage cheese (see photo, below) can be mixed with egg, herbs such as parsley and green onion and formed into patties and fried (like the salmon patties, above) or mixed with egg and used as a filling for lasagne.

Eating low carb? Slices of deli chicken make a great substitute for the noodles (really!) and the cottage cheese and egg filling can be rolled up in strips of zucchini like manicotti.

Have a look at the protein to energy (kcal) ratio of pressed cottage cheese in the table, below.

Creamed cottage cheese is delicious for breakfast but is also terrific has a protein source for lunch, and Greek yogurt is also amazing with 1/2 cup of berries thrown in and both of these are still higher than steak…and 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.

Remember, 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 just 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”. Remember, it is not only children and adolescents that need protein, but older people actually need more protein as they age, to lower the risk of sarcopenia (muscle wasting).

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!

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

Copyright ©2021 BetterByDesign Nutrition Ltd.

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

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 an amount, 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 material (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 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 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 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 an 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 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/JoyKiddie
Facebook: https://www.facebook.com/BetterByDesignNutrition/

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 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!  

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

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

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 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 HbA1c 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 HbA1c 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:

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

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 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.

INTRODUCTION: Green tea which is high in the catechin EGCG (epigallocatechin gallato) has been associated in two meta-analysis with a reduction in body weight and body fat — especially abdominal fat [1,2] and matcha powder is especially high in EGCG.

Catechins make up ~ 30% of green tea’s dry weight and while ordinary brewed green tea contains ~50—100 mg catechins [3], just 1 gram (~1/3 teaspoon) of matcha powder contains 105 mg of catechins of which 61 mg are EGCs.

A 2009 meta-analysis of 11 green tea catechin studies found that subjects consuming between 270 to 1200 mg green tea catechins / day ( 1 — 4 tsp of matcha powder per day) lost an average of 1.31 kg (~ 3 lbs) over 12 weeks [2], but that the effect of green tea catechins on body composition was significant, even when the weight loss between treated and untreated groups is small (~5 lbs in 12 weeks).

Even with as little as a 3 pound weight loss, the total amount of abdominal fat decreased 25 times more with green tea catechin consumption than without it (−7.7 vs. −0.3%) [2] and the total amount of subcutaneous abdominal fat (fat just below the skin on the abdomen) decreased almost 8 times more with green tea catechin consumption than without it (−6.2 vs. 0.8%) [2].

A 2017 meta-analysis found that consuming as little as 100 and 460 mg/day has shown significant effectiveness on body fat and body weight reduction in intervention periods of 12 weeks or more [1].

How do Green Tea Catechins in Matcha Work?

The mechanisms by which green tea catechins reduce body weight and reduce the amount of total body fat and in particular reduce the amount of abdominal fat are still being investigated but it is thought that green tea catechins increase thermogenesis (increased heat production which would result in increased energy expenditure), increase fat oxidation (using body fat as energy), decrease appetite, result in the down-regulation of enzymes involved in liver fat metabolism, and decrease nutrient absorption [2].

Timing of Matcha Catechin Consumption

Green tea catechins such as EGCG found in matcha are absorbed in the intestine and since the presence of food significantly decreases their absorption, green tea catechins are best consumed 1/2 an hour before meals, or 2 hours after meals.

The timing of green tea catechin intake may also affect the absorption and metabolism of glucose. A study by Park et al [4] found that when green tea catechins were given one hour before to a glucose (sugar) load, glucose uptake was inhibited and was also accompanied by an increase in insulin levels.

Effect of Milk Casein on Catechins

It was previously thought that the protein casein found in milk binds green tea catechins, making them unavailable for absorption in the body, however a recent study found that while the antioxidant activity of polyphenols is lowered from 11-27% by the presence of casein, EGCG which is the catechin in matcha is actually increased by the presence of casein [5].

Final Thoughts…

Consuming between 1 — 4 tsp of matcha powder per day (270 to 1200 mg green tea catechins / day) is sufficient to contribute to weight loss of ~ 3 lbs in 12 weeks (with no other dietary or activity changes) and more significantly decrease body fat composition, especially abdominal fat.

Along with a well-designed meal plan, beverages containing matcha powder may be helpful for those who have already lost significant amounts of weight and who would like to lose remaining fat on their abdomen.

WARNING TO PREGNANT WOMEN

While EGCG has also been found to be similar in its effect to etoposide anddoxorubicin, a potent anti-cancer drug used in chemotherapy [6 al], high intake of polyphenolic compounds during pregnancy is suspected to increase risk of neonatal leukemia. Bioflavonoid supplements (including green tea catechins) should not be used by pregnant women [7].

High Protein to Energy Matcha Drink

This drink is great after a workout, or as a quick high protein, low carb meal replacement when time doesn’t allow for real, whole food. It may be helpful for those who have already lost significant amounts of weight, yet are having difficulty losing residual fat around their abdomen.

Since matcha does contain caffeine, I recommend drinking these before 2 PM in the afternoon so that the caffeine does not interfere with sleep.

Ingredients

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

1 scoop unflavoured whey isolate powder (25 g protein per scoop)

12 cubes ice cubes

1 cup (250 ml) fat free Fairlife® milk (low carb, high protein) 

Optional: 1.5 tsp monk fruit / erythritol sweetener

Method

1. Place 1 tsp matcha powder in a small stainless steel sieve and gently press through the sieve into a small bowl with the back of a small spoon
2. Put the sieved matcha powder into a ceramic or glass bowl (not metal, as the tannins in the tea will react and give the beverage and ”off” metallic taste)
3. Whisk 3 tbsps. boiled and cooled water into the matcha powder using a bamboo matcha whisk (available at Japanese and Korean grocery stores) until the mixture is smooth and frothy
4. Add low carb erythritol sweetener, if desired
5. Add 1 scoop of unflavoured whey isolate powder
6. Stir in 1 cup Fairlife® (low carb, high protein) milk
7. Pour mixture over ice cubes

Macros

More Info?

I design low carb Meal Plans from a variety of perspectives, including a Low Carb High Protein perspective.

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

References

1. Vázquez Cisneros LC, López-Uriarte P, López-Espinoza A, et al. Effects of green tea and its epigallocatechin (EGCG) content on body weight and fat mass in humans: a systematic review. Nutr Hosp. 2017 Jun 5;34(3):731-737. Spanish. doi: 10.20960/nh.753. PMID: 28627214.
2. Hursel R, Viechtbauer W, Westerterp-Plantenga MS. The effects of green tea on weight loss and weight maintenance: a meta-analysis. Int J Obes (Lond). 2009 Sep;33(9):956-61. doi: 10.1038/ijo.2009.135. Epub 2009 Jul 14. PMID: 19597519.
3. Weiss DJ, Anderton CR, Determination of catechins in matcha green tea by micellar electrokinetic chromatography, Journal of Chromatography A, Vol 1011(1—2):173-180, September 2003
4. Park JH, Jin JY, Baek WK, Park SH, Sung HY, Kim YK, et al. Ambivalent role of gallated catechins in glucose tolerance in humans: a novel insight into nonabsorbable gallated catechin-derived inhibitors of glucose absorption. J Phyisiol Pharmacol 2009;60:101—9.
5. Bourassa P, Cote R, Hutchandani S, et al, The effect of milk alpha-casein on the antioxidant activity of tea polyphenols, J Photochem Photobiol 2013;128, 43-49.
6. Bandele, OJ, Osheroff, N. Epigallocatechin gallate, a major constituent of green tea, poisons human type II topoisomerases”.Chem Res Toxicol 21 (4): 936—43, April 2008.
7. Paolini, M, Sapone, A, Valgimigli, L, ”Avoidance of bioflavonoid supplements during pregnancy: a pathway to infant leukemia?”. Mutat Res 527 (1—2): 99—101. (Jun 2003)

Copyright ©2021 BetterByDesign Nutrition Ltd.

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

This morning, I posted on social media about the extreme heat wave that the Vancouver-area will be having over the weekend, with temperatures hitting as high as 40° C or higher, which is almost 105°F. One of the people that follows me on social media mentioned about the risk of leaving clear water bottles in a car on a hot sunny day, and which I had read about this in previous years, but never thought much about it, as I always parked in a garage.

Since my car was currently out on the street and I remembered that I had a partly filled water bottle in it,  I went out to remove it. On my way back inside I thought of writing a social media post about the risk of leaving a partially- or completely-filled water bottle in a vehicle, which results from sunshine passing through the windshield, and then through the water in the bottle — acting like a magnifying glass.

While there is a risk of burn marks to the interior of a vehicle and smoldering as a result of this type of light magnification through water bottles, reports of full-blown vehicle fires resulting from this are unheard of, although theoretically possible. What is well-established, however is that there are over 600 deaths per year in the US as a result of extremely hot weather [1].

Extreme heat are summer temperatures that are much hotter and/or humid than average [1] — such as the 40° C temperatures that are expected for the Vancouver-area this coming weekend. While extreme heat makes people of all ages more prone to getting dehydrated, infants under the age of 4 and adults over the age of 65 are especially at risk [1].

As people age, the amount of available water in their body decreases largely as a result of having decreased lean body mass (muscle), compared to younger people. I’ve mentioned decreased lean body mass as people age in previous articles about sarcopenia — which is the loss of muscle as people age. I’ve highlighted the importance of older adults being eating sufficient protein to reduce the risks of falls, and about how much protein older adults should eat but since muscle holds more water than fat, retaining muscle mass as people age also has the added benefit of helping older people to stay adequately hydrated.

[UPDATE (August 14, 2023) Here is the most recent article about protein intake in older adults and the importance of ensuring adequate intake of the amino acid leucine.]

Women are at higher risk of becoming dehydrated in the heat than men of the same age, because men at any age have a higher amount of muscle and therefore a higher percentage of body water than women. This means that older women (compared to older men) are often at greater risk of dehydration.

The following table lists the average percentage of water in the body, according to age and gender, as well as their ranges [2].

As can be seen from the above table, adult men and older men have, on average almost 10% more body water than women of the same age, so it can take a less time for a woman to get dehydrated in the heat, than for a man.

While we remind children and young adults to be sure to drink when they are thirsty, older adults also are less aware that they are dehydrated because the feeling of thirst decreases as people age [3]. For this reason, it is important that older adults drink more especially when they don’t feel thirsty.

Another reason that older people get dehydrated easier is that kidney function decreases with age, and the hormonal response to dehydration (which is handled in part by the kidney) may be impaired [4]. Other factors that contribute to older people becoming dehydrated easier include conditions such uncontrolled (or undiagnosed) diabetes which can cause more urination, or as the result of the effect of various medications that they may be taking, such as diuretics for high blood pressure. Older adults with osteoarthritis in the knees or hips may find it more difficult to go get water, while others may have some memory impairment that keeps them from remembering when they last drank some water.

A heat wave is an excellent time to check in more frequently on an aging parent, or even on elderly neighbours that you are friendly with.

But what to look for?

Symptoms of dehydration may include dry mouth, or feeling overly tired, but dry mouth is a common side-effect of many medications that older people may be taking, and feeling fatigued may not  be that unexpected. Finding out if they are feeling dizzy, or light-headed may be helpful and if is comfortable to ask, find out if the person is urinating less, or if their urine is darker in colour. The can provide helpful clues that they are already dehydrated.

Serious symptoms may include confusion or disorientation, feeling faint, or having diarrhea or vomiting, so be sure to seek medical treatment if these symptoms are present. Severe dehydration can result in the person going into hypovolemic shock as a result of low blood volume, or having seizures if they have lost too much sodium and potassium in the urine.

If you are checking on older parents or on elderly neighbours, consider bringing along a few bottles of sparkling water, or a non-sweetened flavoured soda such as Bubbly® which can encourage them to drink more when it’s hot outside, and seeing if they have a fan that is safely set up may also help them stay cooler. These are not “big” things to do, but to older adults can make a great deal of difference in extreme heat.

…and when you are out and about, remember not to leave partially- or completely-filled water bottles in your car, as sunlight passing through the windshield and then the water bottle can cause burn marks and even a smoldering fire.

To your good health!

Joy

You can follow me on:

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

References

1. Centres for Disease Control and Prevention (CDC), About Extreme Heat, https://www.cdc.gov/disasters/extremeheat/heat_guide.html
2. National Academies Press, Dietary Reference Intakes for Water, Potassium, Sodium, Chloride and Sulfate, Chapter 6: Water, 2005. https://www.nap.edu/read/10925/chapter/6, pg 73
3. Picetti D, Foster S, Pangle AK, et al. Hydration health literacy in the elderly. Nutr Healthy Aging. 2017;4(3):227-237. Published 2017 Dec 7. doi:10.3233/NHA-170026
4. British Nutrition Foundation, Dehydration in the Elderly, https://www.nutrition.org.uk/nutritionscience/life/dehydrationelderly.html

Copyright ©2021 BetterByDesign Nutrition Ltd.

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

This week, the weather forecast for the Vancouver area is for hot and hotter, so I thought it would good to revisit a wonderful summer drink that I enjoy to help cool off, and replace fluids.

Most people know that when it’s hot out that they need to drink more but are concerned that caffeine-containing drinks such as iced coffee, tea, or matcha or various types of sodas such as cola which contain caffeine can cause dehydration. But is it true?

While caffeine is a mild diuretic (makes you urinate more), a 2014 study which compared the effect of drinking coffee with the effects of drinking the same amount of water (keeping other things constant) found no difference in hydration status between the two groups.  In the study [1], fifty men who usually drank 3-6 cups of coffee per day were asked to drink 4 x 200 ml cups of coffee containing 4 mg/kg caffeine per day for 3 days, while having their total body water calculated.  Then the men switched and drank 4 x 200 ml of water for 3 days, while having total body water calculated — and during both arms of the study, amounts of physical activity, food and other fluids were controlled for. The study found that there were no differences in several markers of hydration status between the groups — so no, caffeine won’t dehydrate you but for many, too much caffeine interferes with sleep, gives them headaches if they drink varying amounts on different days or causes them to feel agitated or nervous. As well, for those with Gastroesophageal Reflux Disease (GERD), caffeine can increase heartburn and other symptoms due to its effect on relaxing the lower esophageal sphincter (LES) — resulting in the contents of the stomach more easily backing up into the lower esophagus, resulting in discomfort.

But what’s the alternative? Plain water? It is a choice, but some find it boring.

Others enjoy bottled club soda or make their own using a Sodastream, or they drink one of the brands of commercial unsweetened bubbly drinks that are available in various flavours — but some people can’t tolerate carbonated drinks, so what’s left?

How about Limonana?

Limonana is a drink that I only learned about a few years ago (and wrote about here) and that I enjoyed so much yesterday that I put up a new pitcher at lunch time, and have it chilling in the fridge for later. Since I wrote about it in 2016, I have lost more than 50 pounds and put my type 2 diabetes and high blood pressure into remission, so no longer make that sugary version that I wrote about previously.  The recipe below is what I am making now.

“Limonana” is named for it’s two main ingredients, lemon and mint. In Arabic or Hebrew, “limon” means lemon, and “nana” means mint and this drink is lemonade with a twist. It is a wonderfully refreshing and cooling drink on the hottest of days, like today or this weekend.

I make Limonana using a sugar-free Monk Fruit and erythritol sweetener, so it is very low in carbohydrate and doesn’t spike insulin or blood glucose, and I use fresh mint that I grow on my counter — but any fresh mint will do. Dried mint is a very last resort.

There are two essentials (in addition to fresh mint) that are needed for Limonana, and the first is it must be made with fresh lemons and the pulp of the lemon (none of that bottled stuff!!). The second thing is it must be served over lots of ice cubes.

Here is the recipe for one liter (~a quart) of Limonana. Enjoy!

Limonana

• 3 lemons
• 16-20 fresh mint leaves
• 4 Tbsps. Monk Fruit / erythritol sweetener (or to taste)
• 450 ml cold water
• a whole tray of ice cubes
• Sprig of mint to garnish (optional)

1. Dissolve the Monk Fruit / erythritol sweetener in a bit of hot water and set aside.
2. Using a knife, remove the peel from the lemon and be sure to cut off all the white pith as it is bitter. Separate the sections of lemon flesh from the membranes – like one does for orange suprí¨mes. Discard the membranes and any seeds, and put the flesh of the lemon into a blender.
3. Add the mint and Monk Fruit / erythritol sweetener and pulse a few times until the mint leaves are well chopped. Add the ice cold water and pulse again to mix. Taste the Limonana and add more sweetener, if necessary.
4. Allow to chill in the fridge for a bit, to let the flavour mature.
5. When ready to serve, put plenty of ice cubes into a tall glass and pour the Limonana over them. Drink as is, or garnish with the mint sprig and serve.

To your good health!

Joy

You can follow me on:

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

References

1. Killer S.C, Blannin A.K., Jeukendrup A.E., No Evidence of Dehydration with Moderate Daily Coffee Intake: A Counterbalanced Cross-Over Study in a Free-Living Population, PLOS One, January 4, 2014, https://doi.org/10.1371/journal.pone.0084154

Copyright ©2021 BetterByDesign Nutrition Ltd.

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

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.

Protein is not usually used for energy, although small amounts of amino acids from broken down protein are used by the body when we’re resting, and even smaller amounts are used when we’re doing moderate-intensity exercise[1].

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.

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, setting the recommendation for protein at 40% of dietary intake (instead of as “g protein per kg body weight”) can result 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”.

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

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 High Protein 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.

Nutrition is BetterByDesign!

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

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 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 apoB, apoB/apoA ratio and its proxy TG:HDL ratio could be used to assess CVD risk.

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

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

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

To understand why apoB is a more accurate measure of cardiovascular risk than LDL, as well as how apoB/apoA ratio and its proxy triglyceride to HDL ratio (TG:HDL) can be used 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/JoyKiddie
Facebook: https://www.facebook.com/BetterByDesignNutrition/

References

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

Copyright ©2021 BetterByDesign Nutrition Ltd.

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

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

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

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

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

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

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

What is a low-FODMAP Diet?

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

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

Why do FODMAPs trigger symptoms?

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

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

What is the low FODMAP diet?

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

One Diet – in three stages

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

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

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

The Low-FODMAP Specialty Hour Service

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

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

Beyond FODMAP

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

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

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

Gut Microbiome — environment and genetics

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

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

More Info?

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

To your good health!

Joy

You can follow me on:

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

References

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

Copyright ©2021 BetterByDesign Nutrition Ltd.

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

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 smoothies and “taking it with” may seem like a good idea. But is it? Are smoothies the same as eating the foods it is made out of? It isn’t.

Smoothies As Processed Food

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! That is what happens with smoothies. 

What’s Different About Smoothies? 

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 into smoothies, 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 smoothies 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 smoothies 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 at smoothies — 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/JoyKiddie
Facebook: https://www.facebook.com/BetterByDesignNutrition/

References

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

Copyright ©2021 BetterByDesign Nutrition Ltd.

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

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

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

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

Types of Therapeutic Ketogenic Diets

Ketogenic diets are a subtype of a low carbohydrate  diets.

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

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

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

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

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

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

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

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

The Diet Prescription

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

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

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

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

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

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

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

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

Classic Ketogenic Diet (KD) – 4 : 1

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

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

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

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

In the classic Ketogenic Diet, 80% (i.e. 4/·5=80%) of calories come from fat and 20% (i.e. 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 may want to begin to try gradually eating a 3 : 1, then a 2 : 1 diet — so long as their seizures remain in remission.  There is a lot of trial and error involved, but for those seeking to extend their life (as in glioblastoma) or improve their quality of life (as in epilepsy or seizure disorder), it may be worth it.

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

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

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

More Info?

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

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

To your good health!

Joy

You can follow me on:

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

References

1. U.S. Department of Health and Human 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 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 recently mentioned that the more they read about different types of diets online, the more confused they became. They wanted to know if I could write an article to explain them simply. That is the purpose of this post.

Macros

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 in the 1920s by Dr. Russell Wilder, for the treatment of diabetes and later, for epilepsy.

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

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

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

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

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

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

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

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

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

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

Carnivore

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

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

More Info?

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

To your good health!

Joy

You can follow me on:

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

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

References

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

Copyright ©2021 BetterByDesign Nutrition Ltd.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

More Info?

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

To your good health!

Joy

You can follow me on:

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

References

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

Copyright ©2021 BetterByDesign Nutrition Ltd.

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

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 simultaneous 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.

To your good health!

Joy

You can follow me on:

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

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

References

1. American Association of Clinical Endocrinologists Announces Framework for Dysglycemia-Based Chronic Disease Care Model, November 28, 2018, AACE Online Newsroom, url: https://media.aace.com/press-release/american-association-clinical-endocrinologists-announces-frameworkdysglycemia-based-c
2. Crofts, C., Understanding and Diagnosing Hyperinsulinemia. 2015, AUT University: Auckland, New Zealand. p. 205.
3. Matthews, D. R; Hosker, J. P; Rudenski, A. S; Naylor, B. A; Treacher, D. F; Turner, R. C; “•Homeostasis model assessment: insulin resistance and β-cell function from fasting plasma glucose and insulin concentrations in man”–; Diabetologia; July, 1985; Volume 28, Number 7: Pp 412-419
4. Levy JC, Matthews DR, Hermans MP. Correct homeostasis model assessment (HOMA) evaluation uses the computer program. Diabetes Care. 1998;21:2191—2192
5. Song YS, Hwang Y-C, Ahn H-Y, Comparison of the Usefulness of the Updated Homeostasis Model Assessment (HOMA2) with the Original HOMA1 in the Prediction of Type 2 Diabetes Mellitus in Koreans, Diabetes Metab J. 2016 Aug; 40(4): 318—325
6. Geloneze B, Vasques AC, Stabe CF et al, HOMA1-IR and HOMA2-IR indexes in identifying insulin resistance and metabolic syndrome: Brazilian Metabolic Syndrome Study (BRAMS), Arq Bras Endocrinol Metabol. 2009 Mar;53(2):281-7
7. 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 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.

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

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

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

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

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

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

What Causes Hiatal Hernia?

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

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

Symptoms of a Hiatal Hernia

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

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

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

Final Thoughts…

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

More Info?

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

To your good health!

Joy

You can follow me on:

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

References

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

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

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

Copyright ©2021 BetterByDesign Nutrition Ltd.

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

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

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

What is a Food Allergy?

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

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

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

Oral Allergy Syndrome (OAS) – pollen allergy

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

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

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

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

It can get complicated, too.

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

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

Only an allergist can determine that.

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

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

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

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

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

Final Thoughts…

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

More Info?

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

To your good health!

Joy

You can follow me on:

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

References

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

Copyright ©2021 BetterByDesign Nutrition Ltd.

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

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

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

Where does it put it?

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

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

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

That’s it!

One heaping teaspoon of sugar in the entire adult body!

How Do We Understand Diabetes in Terms of Blood Sugar?

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

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

That’s it!

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Think of grazing it this way;

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

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

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

This is how the system gets “broken”.

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

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

What’s the solution?

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

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

Science made simple.

To your good health!

Joy

You can follow me on:

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

References

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

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

Copyright ©2021 BetterByDesign Nutrition Ltd.

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

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

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

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

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

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

Protein Needs for Active Healthy Adults

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

Protein Needs for Older Adults

There have been several position statements issued by those that work with an aging population indicating that protein intake between 1.0 and 1.5 g protein / kg per day may best meet the needs of adults during aging [3,4].

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

[UPDATE (August 15, 2023): Protein needs for older adults are now established at above 90g per day, with the optimal amount of 30g highly bioavailable protein over each of 3 meals, along with sufficient amounts of the amino acid leucine, which is needed to trigger muscle protein synthesis.  This updated article explains.

Range of Safe Intake

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

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

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

Maximum Amount of Protein the Body can Safely Process

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

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

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

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

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

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

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

Here are some examples of calculations;

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

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

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

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

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

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

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

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

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

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

In 1921, Wilder understood that;

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

and his treatment recommendations (pg.12) were;

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

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

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

Determining Carbohydrate Tolerance in Diet

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

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

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

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

Group A — tolerance below 40 gm. carbohydrate

Group B — tolerance between 40 and 60 gm. carbohydrate

Group C — tolerance between 60 and 100 gm. carbohydrate

Group D — tolerance above 100 gm. of carbohydrate

Use of Fasting and Protein Sparing Modified Fasts in Diet

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

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

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

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

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

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

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

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

Daily Macros

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

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

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

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

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

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

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

Final Thoughts…

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

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

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

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

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

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

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