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As outlined in a previous article, the standard screening test for abnormal thyroid function is thyroid-stimulating hormone (TSH), but if those results come back within normal range and a person has no known risk factors or obvious symptoms of thyroid disease, no testing of thyroid hormones occurs,  and thyroid function is presumed to be normal.

In British Columbia, unless a person is of advanced age, has a family history or personal medical history of thyroid disease or an autoimmune disorder, takes medications such as lithium or amiodarone, or is from a a developing country with iodine deficiency, they do not qualify for TSH testing unless they display the specific symptoms listed in Table 1, below.

This approved checklist does not include some of the well-documented symptoms of hypothyroidism, such as non-pitting edema of the lower legs and ankles, a puffy, swollen face, enlarged tongue with or without scalloped edges, loss of the outer third of eyebrows, or having pale or bluish lips. The downloadable checklist below contains a list of these and other common symptoms.

Signs and Symptoms of Hypothyroidism – downloadable checklist

This downloadable checklist of common hypothyroid symptoms is not intended for self-diagnosis. It is provided to help people who feel unwell to have an informed discussion with their doctor as to whether thyroid hormone testing should be considered.

   Signs and Symptoms of Hypothyroidism – downloadable and fillable checklist

More Info?

As a Dietitian who is knowledgeable about hypothyroidism, I support adults who have been diagnosed as well as those who suspect they may be hypothyroid based on family history and symptoms. 

I understand the weight gain that accompanies hypothyroidism from both sides of the clinical desk and provide services to help people address this. I also provide nutrition education about key nutrients that are often low in hypothyroidism and that are needed by the body to convert inactive thyroid hormone (fT4) into its active form (fT3).  

Please reach out if you would like my help.

To your good health!

Joy

You can follow me on:

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

References

1. BC Guidelines & Protocols Advisory Committee, Thyroid Function Testing in the Diagnosis and Monitoring of Thyroid Function Disorder, October 24, 2018

Copyright ©2022 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.

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/

Note: This article was originally posted on July 14, 2022, and was completely updated and reposted on November 3, 2025.

Introduction

When people have blood tests to “check their thyroid,” the test that is performed is a TSH test. TSH is a pituitary hormone, not a thyroid hormone. Provincial guidelines have established that even if TSH comes back in the high-normal range, no testing of thyroid hormones is performed (i.e., no testing of free T4 or free T3) — unless the person meets the criteria that warrant a closer look. 

This article covers everything you need to know about hypothyroidism, including common causes of an underactive thyroid, typical signs and symptoms associated with hypothyroidism, and outlines the various options available for having thyroid hormone blood tests done.

The Thyroid Gland

The thyroid is a butterfly-shaped gland located in the middle of the lower front part of the neck. While small, it plays a critical role in regulating metabolism—the process by which the body converts food into energy (2).

When the thyroid is underactive (hypothyroid), metabolism slows. This can affect heart rate, heat production, muscle function, thinking, and information processing (1).

The Two Main Thyroid Hormones – T4 and T3

The thyroid produces two main hormones: thyroxine (T4) and triiodothyronine (T3). About 80–90% of thyroid hormone is T4, and 10–20% is T3, most of which is converted from T4 in body tissues (6). On average, the thyroid produces roughly 85 mcg of T4 and 6.5 mcg of T3 per day—a T4:T3 ratio of about 13:1 (1).

T4 is inactive until converted to T3, the active form. In its free form, thyroxine is called free T4 (fT4), and triiodothyronine is called free T3 (fT3) (1).

T4 and T3 production is regulated by the pituitary gland, which responds to the hypothalamus. The hypothalamus releases Thyrotropin-Releasing Hormone (TRH), prompting the pituitary to release TSH (Thyroid Stimulating Hormone), signaling the thyroid to produce hormones (6).

Hypothyroidism – how it is diagnosed

In Canada and many parts of the U.S., TSH is the standard screening test for thyroid function. If symptoms are present or TSH is high-normal, doctors may also check free T4 (7).

Central hypothyroidism occurs when the hypothalamus or pituitary gland fails to signal the thyroid gland properly. Lab tests reveal low TSH and low free T4 levels, and patients are often treated with thyroid medication, including T3 (1).

Primary hypothyroidism occurs when the thyroid itself is underactive. Diagnosis is based on high TSH with normal or low free T4 (1).

Hypothyroidism – main causes

Hashimoto’s disease is the most common cause of primary hypothyroidism in developed countries. It is an autoimmune disorder producing antibodies against the thyroid, including TPO-ab and TG-ab (3). Diagnosis is based on symptoms and antibody testing (3). Iodine deficiency can also underlie hypothyroidism and is more common in developing countries. In the last 20-30 years, it has been largely reduced through global iodization programs (8). Other causes include thyroid surgery or radioactive iodine treatment for hyperthyroidism (1, 2).

Hypothyroidism – getting tested and diagnosed

Many early symptoms of hypothyroidism are non-specific and may have multiple causes.

In British Columbia, unless a person is of advanced age, has a personal or family history of thyroid or autoimmune disorders, takes medications such as lithium or amiodarone, or grew up in a region where salt was not iodized, TSH testing is only covered by MSP if the person has symptoms listed in Table 1 below (4).

One limitation of the checklist is that it does not include well-documented symptoms such as non-pitting edema in the lower legs, a puffy face, an enlarged tongue (with or without scalloped edges), loss of the outer third of the eyebrows, or pale/blue lips (see downloadable checklist, below).

Even if TSH is tested and comes back in the high-normal range, further testing is not done (4). Some clinicians may manually request free T4, but without checking free T3, the assessment is incomplete (7). In order to have TSH, free T4, and free T3 tests done, the doctor needs to write them on the requisition manually. When I request that a doctor write a requisition for thyroid testing for one of my clients, I provide them with a sample requisition of how these tests need to be written based on the current MSP guidelines.

Without a doctor knowing that their patient has risk factors for hypothyroidism based on family history, or that they grew up in a place where salt was not iodized, or that they have several of the known symptoms for hypothyroidism, diagnostic tests may not be requisitioned unless the person becomes sicker.

Downloadable Checklist of Common Hypothyroid Symptoms

To support a more informed discussion with a healthcare provider, below is the link to a downloadable, fillable checklist of common hypothyroid symptoms, which includes a simple explanation for each. For example, “periorbital edema” is described as “swelling under the eyes.”

Keep in mind that these symptoms are not exclusive to hypothyroidism and may exist with other conditions.  Only a doctor can determine if there are enough symptoms to warrant further investigation.

This checklist is not exhaustive and is not intended for self-diagnosis. It is provided to help people who suspect they may have hypothyroid symptoms discuss their concerns with their doctor. Only a licensed medical professional can diagnose and treat hypothyroidism.

As a Dietitian, I liaise with my client’s doctors to request that they be tested based onfamilial risk factors and/or symptoms of hypothyroidism and I also support the dietary side of those diagnosed with hypothyroidism, including ensuring that nutrients of importance in the conversion of inactive thyroid hormone (free T4) to the active form (free T3) are sufficient in the diet or supplemented.

Signs and Symptoms of Hypothyroidism – downloadable and fillable checklist

Thyroid Panel Lab Tests – 3 options to test for hypothyroidism

Final Thoughts

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References

1. Jonklaas J, Bianco AC, Bauer AJ, et al. Guidelines for the treatment of hypothyroidism: prepared by the American Thyroid Association task force on thyroid hormone replacement. Thyroid. 2014 Dec 1;24(12):1670–1751. [https://pubmed.ncbi.nlm.nih.gov/25266247/]

2. Berkow R, Beers MH, Fletcher AJ. The Merck Manual of Medical Information. Whitehouse Station, N.J.: Merck Research Laboratories; 1997. [https://cmc.marmot.org/Record/.b10805436]

3. Puszkarz I, Guty E, Stefaniak I, Bonarek A. Role of food and nutrition in pathogenesis and prevention of Hashimoto’s thyroiditis. 2018. https://doi.org/10.5281/zenodo.1320419

4. BC Guidelines & Protocols Advisory Committee. Thyroid Function Testing in the Diagnosis and Monitoring of Thyroid Function Disorder. October 24, 2018. [https://www2.gov.bc.ca/assets/gov/health/practitioner-pro/bc-guidelines/thyroid-function-testing.pdf]

5. Laboratory Services Act. Laboratory Service Regulation. October 1, 2015 (last amended September 20, 2020 by B.C. Reg. 263/2020). [https://www.bclaws.gov.bc.ca/civix/document/id/crbc/crbc/52_2015_pit_2020_09_20]

6. NCBI Bookshelf. Physiology of thyroid hormones. 2023. Available at: https://www.ncbi.nlm.nih.gov/books/NBK499850/

7. Canadian Thyroid Association. Thyroid Testing Guidelines. 2023. Available at: https://www.thyroid.ca/thyroid-testing-guidelines/

8. World Health Organization. Iodine Deficiency Disorders. 2024. Available at: https://www.who.int/news-room/fact-sheets/detail/iodine-deficiency-disorders

Copyright ©2022 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 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.

Introduction

A therapeutic diet is used to treat a medical condition, and when prescribed by a Physician and implemented by a Dietitian, it is referred to as Medical Nutrition Therapy (MNT) [1]. 

Therapeutic ketogenic diets are a form of medical nutrition therapy using a specific ratio of fat to protein plus carbohydrate. These diets are also referred to as ketogenic diet therapy or ketogenic metabolic therapy, and may be used as an adjunct treatment for specific physical health conditions. 

Therapeutic ketogenic diets are very high in fat and help the body enter and stay in a state called ketosis. In ketosis, the body burns fat for energy instead of carbohydrates. Nutritional ketosis occurs when the ketone called beta-hydroxybutyrate (BHB) reaches levels between 0.5 and 3.0 mmol/L[2].

In therapeutic ketogenic diets, like those used to treat epilepsy and seizure disorders, BHB levels can go up to 4.0 mmol/L [3], and for conditions such as glioblastoma, where a therapeutic ketogenic diet is used as an adjunct treatment alongside chemotherapy and radiation, BHB levels can reach up to 3.0 mmol/L [4,5,6].

Note: Just because a therapeutic diet may help in glioblastoma does not mean it is suitable for all types of cancer. Most cancers use glucose to grow, while a few use ketone bodies.

Types of Therapeutic Ketogenic Diets

Ketogenic diets are a type of low-carbohydrate diet.

Low-carbohydrate diets are defined as diets in which less than 130 grams of carbohydrates per day, or less than 26% of total energy intake, are consumed [7]. This level of carbohydrate intake is considered too high for therapeutic purposes, such as the treatment of epilepsy or seizure disorders, or when used as an adjunct therapy for glioblastoma. However, they are often used to manage type 2 diabetes.

Moderate-carbohydrate diets are defined as diets in which 130–225 grams of carbohydrates per day, or 26–45% of total energy intake, are consumed [7]. While these diets can be used to help manage type 2 diabetes or obesity, the carbohydrate intake is still too high for the treatment of epilepsy, seizure disorders, or as an adjunct therapy in glioblastoma.

A very low-carbohydrate diet is also referred to as a “ketogenic diet.” In this diet, carbohydrate intake is limited to 20–50 grams per day, or about 10% of total energy intake [7]. It is considered safe and effective for the treatment of type 2 diabetes and obesity [2], and it is also used in the treatment of epilepsy, seizure disorders [3], and as an adjunct therapy in glioblastoma [4,5,6]. Because carbohydrate intake is kept very low, protein and fat intake are increased.

In therapeutic ketogenic diets used for obesity management or to help manage type 2 diabetes, protein intake is set between 15% and 35–40% of total calories. Nutritional ketosis is induced because the diet is very high in fat and very low in carbohydrates, allowing β-hydroxybutyrate (BHB) levels to reach 0.5–3.0 mmol/L [2].

For the treatment of epilepsy, seizure disorders, or as an adjunct therapy in glioblastoma, protein intake is kept as low as 15% of calories to allow BHB levels to rise to between 3.0 and 4.0 mmol/L.

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

A therapeutic ketogenic diet has been used since the 1920s by Dr. Russell Wilder for the treatment of diabetes and later for the treatment of epilepsy.

In fact, the term “ketogenic diet” is credited to Wilder himself. The precise percentages of carbohydrate, fat, and protein in what is now called the “classic” Ketogenic Diet (KD) were calculated by Dr. M.G. Peterman in 1925 [8], and these same ratios are still used today.

Therapeutic ketogenic diets that are used for epilepsy, seizure disorders, and as adjunct therapy in glioblastoma are very high in fat, low in protein, and low in carbohydrates. Ratios range from 4:1 (4 parts fat for every 1 part protein plus carbohydrate) to 3:1 (3 parts fat for every 1 part protein plus carbohydrate), and for maintenance, ratios as low as 2:1 (2 parts fat for every 1 part protein plus carbohydrate) may be used.

The Diet Prescription

As a Dietitian who designs therapeutic ketogenic diets, the first step is to determine the amount of energy (calories, in kcal) the individual needs. This is calculated based on the person’s weight, height, activity level, nutritional requirements, and whether weight loss is to be avoided, such as in the treatment of glioblastoma.

The second step is to determine the percentage of calories that needs to come from fat, protein, and carbohydrate is calculated based on the specific dietary prescription, whether 4:1 or 3:1. Because of the very high fat and very low carbohydrate content of a 4:1 or 3:1 ketogenic diet, and the small amount of protein, the design of these diets is time-consuming. It is very challenging to create palatable food combinations at each meal to meet the precise macronutrient ratios (protein, fat, and carbohydrate).

To keep ketone production constant over the day, each meal must contain the exact amounts of fat, protein, and carbohydrate specified in the diet prescription. Just as medication has a “dosage,” the specific types and exact amounts of food in the diet prescription are treated as a “food dosage.”

When adults are trialing a 4:1 or 3:1 ketogenic diet for seizure disorders, or during chemotherapy and radiation for glioblastoma, the diet calculations are performed, and a simple breakfast, lunch, and dinner meal plan is designed for use during the first six weeks. Occasionally, an extra dinner meal is included to allow for alternation.

If the diet is found to improve symptoms, those with seizure disorders may choose to remain on the therapeutic diet for an extended period. In such cases, additional lunch and dinner options may be designed, while most people are content to continue eating the same breakfast.

For those with glioblastoma, a 2:1 Modified Atkins Diet is usually requested to be designed for use between rounds of chemotherapy and radiation, and this is done. This diet allows for more protein while keeping carbohydrate intake low and provides a more pleasant “break” for those who have found the restrictive meals of a 4:1 or 3:1 ketogenic diet difficult. Another advantage is that, because it is unknown whether the type of glioblastoma may feed on ketones, alternating between a high-ketone and low-ketone diet in this way reduces the risk of providing high ketone levels when chemotherapy or radiation is not being administered.

For those who are first starting a therapeutic ketogenic diet for epilepsy or as an adjunct treatment in glioblastoma, a challenge is presented by the requirement that the amounts of food on the final meal plan must be weighed precisely and accurately. Even the smallest amount of vegetables, which contain some protein and carbohydrates, can affect the macronutrient ratios and reduce the therapeutic benefit of the diet. Therefore, all foods must be weighed to the gram.

In addition, daily monitoring of blood ketone levels is required at the beginning to determine when the desired therapeutic range has been achieved. For epilepsy and seizure disorders, this range is often defined as β-hydroxybutyrate (BHB) levels between 3.0 and 4.0 mmol/L. Once the desired levels can be maintained by following the diet, less frequent testing can be performed.

Classic Ketogenic Diet (KD) – 4:1

In the classic Ketogenic Diet (KD), the total number of calories is matched to the amount of calories needed by the person. Protein is usually set at 1 gram per kilogram of body weight, carbohydrate is limited to 10–15 grams per day in total, and the remaining calories are provided as fat. For very young children, the diet may be prescribed based on body weight, for example, 75–100 calories for each kilogram (2.2 pounds) of body weight.

Since the 1920s, several other therapeutic ketogenic diets have been developed for the treatment of epilepsy and seizure disorders, including the Modified Ketogenic Diet (MKD) and the Modified Atkins Diet (MAD). All of these diets are very low in carbohydrates and high in fat, which by definition makes them ketogenic, and they differ in the amount of protein that is provided.

In addition to their use in epilepsy and seizure disorders, any of these therapeutic ketogenic diets may be prescribed as adjunct treatment for glioblastoma or as adjunct treatment for Alzheimer’s disease.

The classic Ketogenic Diet (KD) is based on a 4:1 ratio, meaning 4 parts fat for every 1 part protein plus carbohydrates. In other words, for every 5 grams of food, 4 grams are fat and 1 gram is protein and/or carbohydrate.

In the classic Ketogenic Diet, 80% of calories (4 out of 5) are provided from fat, and 20% of calories (1 out of 5) are provided from a combination of protein and carbohydrates. 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%, with carbohydrate as high as 10%.

Modified Ketogenic Diet (MKD) – 3:1 ratio

The Modified Ketogenic Diet (MKD) has a 3:1 ratio, which means 3 parts fat for every 1 part protein and carbohydrate. This diet is 75% of calories 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

In the Modified Atkins Diet (MAD), a 2:1 ratio is used, meaning 2 parts fat for every 1 part protein and carbohydrate. In this diet, carbohydrate intake is restricted to less than 15 grams per day for children and less than 20 grams per day for adults. For adults following a Modified Atkins Diet, 60% of calories are provided from fat, 30% of calories from protein, and 10% of calories from carbohydrate [5].

“Chasing Ketones” – betahydroxybutyrate, the therapeutic goal

While people following the popular “keto diet” for weight loss or type 2 diabetes management are often teased for “chasing ketones” (because their goal is fat loss or improved blood sugar, rather than high ketone production), those following a therapeutic ketogenic diet for epilepsy or seizure disorders, are seeking to maintain ketones between 3.0 mmol/L and 4.0 mmol/L.

The therapeutic goal of a 4:1 or 3:1 therapeutic ketogenic diet is to have the person’s blood ketone level reach 3.0 mmol/L of β-hydroxybutyrate (BHB) as quickly as possible and to maintain it at that level (or, in some cases, increase to up to 4.0 mmol/L). Since the therapeutic benefit is provided by the ketones, nothing that is not part of the diet prescription should be eaten.

It is recommended that for those starting a therapeutic ketogenic diet, a medical-grade Abbott Precision Freestyle Neo meter be obtained from a pharmacy. This meter measures both blood glucose and ketones and is very accurate and reliable, unlike some meters purchased online and used by people following the popular “keto diet” for weight loss. The meter is provided at no cost when 100 glucose strips are purchased (about $1 per strip). It is also recommended that 30 ketone strips be purchased for the same monitor ($3 each), which will last approximately one month when blood glucose is checked three times per day and ketones once per day.

Blood glucose should not fall below 4.0 mmol/L when measured with the meter, and blood ketone levels should ideally measure 3.0 mmol/L, and up to 4.0 mmol/L for epilepsy and seizure disorders—but not higher. If ketone levels exceed 4.0 mmol/L, one’s doctor should be contacted, and if levels rise higher, medical help should be sought immediately.

For people diagnosed with glioblastoma, a 4:1 (or 3:1) therapeutic ketogenic diet is ideally started upon discharge from the hospital so that chemotherapy and radiation treatments are begun while ketone levels are already at 3.0 mmol/L BHB.

For seizure disorders, neurologists who refer patients for dietary management generally seek ketone levels as close to 4.0 mmol/L as possible, because this is where the most benefit is seen. Once seizures have stopped, a gradual transition to a 3:1 or 2:1 diet may be attempted, as long as seizures remain in remission.

To achieve the precise level of ketones required, a certain amount of trial and error in adjusting the diet is involved, but for those seeking to extend life (as in glioblastoma) or improve quality of life (as in epilepsy or seizure disorders), the process may be worthwhile.

NOTE: (April 13, 2021): While some research papers indicate that advanced gliomas do not use ketones as a fuel source, a research paper published in September 2020 has called this into question. According to this paper, different types of glioblastoma cells exist, and some are able to oxidize fatty acids and use ketones for energy. It is suggested that when glucose levels are reduced, some glioblastoma cells may adapt by partially shifting their metabolism to use oxidized fatty acids and ketones. Therefore, seeking lower levels 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 are extended to Cliff Harvey, PhD, for helping to complete this understanding.

More Info?

Under the Services tab, you can learn about the 3:1 and 2:1 therapeutic ketogenic diets that I design for 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).

For those who have received a new diagnosis of glioblastoma and need the earliest available appointment, please reach out through the Contact Form. 

To your good health!

Joy

You can follow me on:

Twitter: https://twitter.com/jyerdile
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: a 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.