Sugar Industry Paid to Shift Blame for Heart Disease to Fat

 

Introduction

Today I was reminded about a post that I wrote almost eight years ago (March 12, 2018), about an article that had been published in the Journal of the American Medical Association in September 2016 [1]. The article revealed that the sugar industry had funded three renowned Harvard researchers to write a series of articles that downplayed or ignored known research that demonstrated sugar was a contributor to heart disease and instead put the blame solely on fat — especially saturated fat. I was shocked by its significance,  and it made me wonder how much of what I learned in my training needed to be revisited in this light. 

The three Harvard researchers were the late Dr. Fredrick Stare, Chair of Harvard’s School of Public Health Nutrition Department, the late Dr. Robert McGandy, Assistant Professor of Nutrition at the Harvard School of Public Health, and the late Dr. D. Mark Hegsted, a Professor in the same department. 

Dr. Hegsted went on to be directly involved in the development of the 1977 US Dietary Goals, which served as the basis for the 1980 Dietary Guidelines for Americans. These were the first Guidelines that called for Americans to decrease consumption of meat and saturated fat with the belief that it would lower the risk of heart disease.

Following suit, in 1977, Canada’s Food Guide went through a major revision with a shift to increased carbohydrates in the diet and decreased fat. Following a report submitted to Health Canada in 1977 by the Committee on Diet and Cardiovascular Disease, which advised the government to take action to prevent diet-related chronic diseases such as heart disease and high blood pressure, the revised 1982 Canada’s Food Guide shifted towards even lower-fat products.

I wondered today how many people know that decades of “low fat” messaging in both the US and Canada began by the sugar industry paying three prominent Harvard researchers to blame fat as the cause of heart disease, while discounting the role of sugar. I decided it was time to write another article. 


Sugar Industry Funding Helped Shift Blame to Fat — Especially Saturated Fat

In the mid-1960s, the Sugar Research Foundation (SRF), predecessor to the Sugar Association, aimed to counter research which suggested that sugar, not fat, might be a bigger contributor to atherosclerosis. The committee invited Dr. Frederick Stare of Harvard’s School of Public Health Nutrition Department to join its scientific advisory board and approved $6,500 ($65,750–$66,850 in 2025 dollars) “to support a review article that would respond to the research showing the danger of sucrose [1]”.

From the 2016 Kearns et al. article [1]:

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

 

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

In a letter written to Dr. D.M. Hegsted, the Sugar Research Foundation made its agenda clear:

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

Hegsted replied on behalf of the Harvard team, saying:

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

Project 226, sponsored by the Sugar Research Foundation, resulted in a two-part review by McGandy, Hegsted and Stare that was published in the New England Journal of Medicine in 1967 titled “Dietary Fats, Carbohydrates and Atherosclerotic Disease” [3]. There was no mention of the Sugar Research Federation sponsorship of the research [1].  

Article in JAMA - Dietary Fats, Carbohydrates and Atherosclerotic Disease - part 1 and 2
Dietary Fats, Carbohydrates and Atherosclerotic Disease

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

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

 

The report continued: 

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

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

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

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

Hegsted and the 1977 US Dietary Goals

Dietary Goals for the United States, Select Committee on Nutrition and Human Needs, United States Senate. Washington : U.S. Govt. Print. Off., 1977. http://hdl.handle.net/2027/uiug.30112023368936, title page
Dietary Goals for the United States, 1977

Dr. Hegsted went on to play a significant role in advising the Select Committee on Nutrition and Human Needs that oversaw the development of the 1977 Dietary Goals for the United States — and oversaw the writing of the first Dietary Guidelines for Americans that called for a reduction in saturated fat consumption to lower the risk of coronary heart disease [5], [6]. 

Below is a quote about Dr. Hegsted’s role in the Select Committee on Nutrition and Human Needs that oversaw the 1977 Dietary Goals for the United States.

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

There were 8 hearings of the Committee titled “Diet Related to Killer Diseases” that were held from July 1976 until October 1977 [6], which provided an opportunity for US senators to hear from leading scientists, government officials, and business representatives about the risks of diet on heart disease, cancer, and other chronic diseases.

“Of those who gave testimony at the first hearings, perhaps the two most important were assistant secretary for health and former director of the National Heart and Lung Institute, Theodore Cooper, and Professor Hegsted” [6].

Interestingly, Dr. Hegsted admitted that the primary evidence for “killer diseases” was epidemiologic, the weakest form of scientific data, and not clinical data [8]. Despite this admission, Hegsted stated that there was ”a clear linkage between plasma serum lipids, atherosclerosis and coronary diseaseand that it was ”clear that diet controls cholesterol levels“[8].

Hegsted’s statement that there was “a clear linkage” between plasma fat and heart disease was based on only 8 randomized clinical trials that were available at the time, and which had only 2,467 male subjects, and no female subjects [9].

Furthermore, there was no clinical evidence that reducing total fat or saturated fat lowered death from all causes or cardiovascular disease [9].

Several researchers pleaded with the Committee to wait for more research.

The director of the National Heart, Lung and Blood Institute, Dr. Robert Levy, said “no one knew if eating less fat would prevent heart attacks“. 

Dr. Robert Olson of St. Louis University said, “I plead in my report and will plead again orally here for more research on the problem before we make announcements to the American public.” 

Dr. Peter Ahrens said, “advising Americans to eat less fat on the strength of such marginal evidence was equivalent to conducting a nutritional experiment with the American public as subjects“.

Committee Chairman Senator McGovern responded:

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

 

Hegsted believed there could be “no risk” to recommending that the American public eat less meat, less fat, particularly saturated fat, and less cholesterol.[8].

Long-Term Outcomes and Modern Evidence

Hegsted relied heavily on Ancel Keys’ yet-unpublished Seven Countries Study [9], which compared men aged 40–59 in the USA, Finland, the Netherlands, Yugoslavia, Greece, and Japan.

The Seven Country Study data have been criticized for decades for several reasons, including the fact that Keys omitted countries such as Switzerland or France, which were known to have very high saturated fat consumption, yet low rates of heart disease. 

In addition, data from Greece, Italy and Yugoslavia were thought to have not been representative of what they normally ate, since these countries were still facing poverty post WWII.

Despite the limitations, a hypothesis linking saturated fat to heart disease formed the basis for 40+ years of low-fat dietary advice in the US and Canada. These recommendations were largely epidemiology-based and assumed that reducing meat and saturated fat while increasing grains and cereals carried no risk.

The results?

Heart disease remains the leading killer — not only in the US, but according to the CDC, worldwide. Decreasing dietary saturated fat did nothing to change this. In fact, a 2020 meta-analysis in the Journal of the American College of Cardiology found no benefit in lowering saturated fat for cardiovascular disease or mortality, and suggested saturated fat may be protective against stroke [7].

Meanwhile, over the past 40+ years, obesity and type 2 diabetes rates have skyrocketed, along with carbohydrate intake — both if which are known to increase the risk of cardiovascular disease. 

Final Thoughts

It is historically significant that the sugar industry’s funding of three Harvard researchers resulted in the absolving of sugar as having a role in the development of heart disease and placed the blame solely on saturated fat.

Dr. Hegsted’s subsequent influence on the 1977 US Dietary Goals and the 1980 Dietary Guidelines highlights the adverse role that industry-sponsored research can have on people’s health.

National dietary guidelines concerning saturated fat intake based on weak epidemiologic data “was equivalent to conducting a nutritional experiment with the American public as subjects“.

As a Dietitian, making recommendations to individuals to lower dietary saturated fat intake based on lab work and family history is good clinical practice.

Establishing general population based dietary guidelines to reduce the intake of saturated fat based on weak evidence is not. 

National dietary guidance must be based on robust clinical data, as well as epidemiological studies — including the impact of different types of fats in heart disease. It also needs to factor in the role of sugar and refined dietary carbohydrates as drivers of obesity and metabolic disease, which can contribute to heart disease.

To your good health. 

Joy 

 

You can follow me on:

Twitter: https://twitter.com/jyerdile

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

References

  1. Kearns C, Schmidt LA, Glantz SA, et al. Sugar Industry and Coronary Heart Disease Research: A Historical Analysis of Internal Industry Documents. JAMA Intern Med. 2016;176(11):1680-1685. [https://pubmed.ncbi.nlm.nih.gov/27617709/]
  2. Husten L. How Sweet: Sugar Industry Made Fat the Villain. Cardio|Brief, Sept 13, 2016. [https://www.cardiobrief.org/2016/09/13/how-sweet-sugar-industry-made-fat-the-villain/]
  3. McGandy RB, Hegsted DM, Stare FJ. Dietary fats, carbohydrates and atherosclerotic vascular disease. N Engl J Med. 1967;277(5): part 1: pg. 186-192 and part 2: pg. 242–247. 
    [part 1: https://www.nejm.org/doi/10.1056/NEJM196708032770505],
    [part 2: https://www.nejm.org/doi/abs/10.1056/NEJM196707272770405]
  4. Nestle M. Food Industry Funding of Nutrition Research: The Relevance of History for Current Debates. JAMA Intern Med. 2016;176(11):1685–1686. doi:10.1001/jamainternmed.2016.5400. [https://pubmed.ncbi.nlm.nih.gov/27618496/]
  5. Dietary Goals for the United States, Select Committee on Nutrition and Human Needs, United States Senate. Washington: U.S. Govt. Print. Off., 1977. [https://www.govinfo.gov/content/pkg/CPRT-95SPRT98364O/pdf/CPRT-95SPRT98364O.pdf]
  6. Oppenheimer GM, Benrubi ID. McGovern’s Senate Select Committee on Nutrition and Human Needs versus the meat industry on the diet-heart question (1976-1977). Am J Public Health. 2014;104(1):59–69. doi:10.2105/AJPH.2013.301464. [https://pmc.ncbi.nlm.nih.gov/articles/PMC3910043/]
  7. Astrup A, Magkos F, Bier DM, et al. Saturated Fats and Health: A Reassessment and Proposal for Food-based Recommendations. J Am Coll Cardiol. 2020;75(24):3118–3135. doi:10.1016/j.jacc.2020.05.077. [https://pubmed.ncbi.nlm.nih.gov/32562735/]
  8. United States. Congress. Senate. Select Committee on Nutrition and Human Needs. (1977). Diet related to killer diseases: hearings before the Select Committee on Nutrition and Human Needs of the United States Senate, Ninety-fifth Congress, first session. Keys A. Coronary heart disease in seven countries. Nutrition. 1997;13(3):250–252; discussion 249, 253. doi:10.1016/s0899-9007(96)00410-8. [https://babel.hathitrust.org/cgi/pt?id=uc1.a0000416073&seq=3]
  9. Harcombe Z. An examination of the randomized controlled trial and epidemiological evidence for the introduction of dietary fat recommendations in 1977 and 1983: A systematic review and meta-analysis. University of the West of Scotland, 2015. [https://pubmed.ncbi.nlm.nih.gov/25685363/]
  10. Yerushalmy J, Hilleboe HE. Fat in the diet and mortality from heart disease: a methodologic note. N Y State J Med. 1957;57(14):2343–2354. [https://pubmed.ncbi.nlm.nih.gov/13441073/]

 

Copyright ©2025 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.

 

Nutrition is BetterByDesign

The Worst Carb For Blood Sugar You’ve Probably Never Heard Of

[Update, November 17, 2025: This article was updated to include several powerful graphics from a 2025 paper about the health implications of maltodextrin as an additive in processed foods]

Introduction

A recently updated article titled Complex Carbohydrates as Long Chains of Sugar Molecules, explained that “complex carbohydrates” are really just long chains of sugar molecules, like pearls on a string, and that how quickly blood sugar rises depends on the specific types of sugars in those chains. 

Monosaccharides (made up of a single sugar molecule) are sugars such as glucose and fructose that break down very quickly and quickly impact blood glucose. 

Disaccharides (made up of two sugar molecules), such as sucrose (table sugar), are made up of glucose and fructose combined, and break down more slowly than monosaccharides like glucose and fructose. As a result, the rise in blood glucose is slightly slower than glucose. 

What if you found out that the worst carbohydrate for blood sugar is one that you’ve probably never heard of?

What if you found out that this carbohydrate is often found in sugar-free foods, but is not considered a sugar under Canadian food labeling regulations? 

That is what this article is about.

Glycemic Index (GI)

The Glycemic Index (GI) is a ranking system for carbohydrate-containing foods based on how quickly they raise blood sugar (blood glucose) levels after they are eaten.

Foods are ranked on a scale of 0 to 100, with pure glucose assigned a value of 100. 

High GI foods (ranked with a GI of 70 or more) are rapidly digested and absorbed, causing a quick and high spike in blood sugar levels.

Medium GI foods (ranked with a GI of 56-69) have a moderate effect on blood sugar levels.

Low GI foods (ranked with a GI of 55 or less) are digested and absorbed slowly, releasing glucose gradually into the bloodstream and causing a slower, smaller rise in blood sugar. 

As mentioned in the previous article, factors such as the amount of fiber in the food, as well as the amount of food processing of that food, including cooking, can affect a food’s GI value. 

The Glycemic Index of pure glucose (also called dextrose) is 100, the highest score.

The Glycemic Index of table sugar (i.e., sucrose) is rated with a GI of 65-80 (depending on the source) [4]. Sucrose is a disaccharide made of a mixture of glucose (which has a GI of 100) and fructose (which has a GI of 25). While its overall impact on blood glucose is significant, it is less than pure glucose, which is a monosaccharide, because sucrose takes longer to digest, and thus to spike blood sugar. 

The carbohydrate that you’ve probably never heard of has a Glycemic Index between 85 and 105 (depending on the source), which is higher than table sugar (sucrose) and higher than pure glucose

This carbohydrate is maltodextrin. 

Glycemic Index and Glycemic Load of Maltodextrin - from https://glycemic-index.net/maltodextrin/
Glycemic Index and Glycemic Load of Maltodextrin – from https://glycemic-index.net/maltodextrin/

Maltodextrin plays a functional role in food manufacturing, primarily serving as a bulking agent, thickening agent, and stabilizer. Products known to contain some of the highest maltodextrin content include sports and energy drinks.

Maltodextrin is also often found in sugar-free foods, but it is not considered a sugar under Canadian food labeling regulations; rather is classified as a “complex carbohydrate”, a polysaccharide food additive.

Note: The reliability of the Glycemic Index in predicting blood sugar responses in individuals was called into question in research conducted in 2016 and 2019, as outlined in this earlier article. However, it is still used, and for comparative purposes, it is used in this article.

What Is Maltodextrin and What Does It Do to Blood Sugar?

Maltodextrin is a refined carbohydrate made from starch — usually from corn, rice, potato, or wheat. Food manufacturers use it as a thickener, filler,  or stabilizer in a wide range of foods and drinks.

Although maltodextrin doesn’t taste very sweet, the body digests it similarly to pure glucose, so it can raise blood sugar very quickly.

Maltodextrin is created when starch is treated with enzymes to break it down into shorter chains of glucose molecules. Because it’s already partially digested, the body absorbs it quickly, giving it a Glycemic Index (GI) between 85 and 105 (depending on the source), which is significantly higher than regular table sugar (sucrose), which has a GI ≈ of 65 and can even be higher than pure glucose (dextrose). 

While maltodextrin has practical applications in the manufacturing of sports drinks or medical nutrition products where quick energy is needed, it is also found in a wide range of foods, including infant formula, protein supplements, and even sugar-free foods. 

Its presence in sugar-free foods is concerning because it can result in a very significant spike in blood sugar in those who are deliberately trying to avoid sugar.

Splenda® brand sucralose packet
Splenda® brand sucralose packet

Sucralose, used in the sugar-free sweetener Splenda®. It is made from sucrose (table sugar), where three hydroxyl groups (-OH) are replaced by chlorine. It is approximately 600 times as sweet as table sugar, so most of a packet of Splenda® is maltodextrin, used as a filler.  A 2008 research study found Splenda® to be 1.1% sucralose, 1.1 % glucose, 4.23% moisture, and >93.59% maltodextrin.

While Splenda® is “sugar-free”, the maltodextrin in it can cause blood glucose to spike significantly higher than table sugar. 

Below is a graph comparing the glucose spike from maltodextrin, glucose, and sucrose (table sugar). Table sugar (sucrose) spiked blood glucose to ~145 mg/dl (8.0 mmol/L) at 30 minutes, and maltodextrin spiked blood glucose to ~165 mg/dl (9.0 mmol/l) at 40 minutes.

Comparison sample blood glucose response to maltodextrin, glucose and sucrose (table sugar) - from [6]
Comparison sample blood glucose response to maltodextrin, glucose, and sucrose (table sugar) – from [6]

Below is a bar chart illustrating the percentage of products containing maltodextrin.

Some of the highest maltodextrins are found in sports and energy drinks (84%); however, protein supplements have the same percentage of maltodextrin (84%), and infant formula has an even higher percentage (89%).

Product Categories with the Highest Maltodextrin Inclusion - from [6] Yarley EJ, Unveiling Hidden Sugars: A Critical Analysis of Maltodextrin as a Polysaccharide Additive in Processed Foods and Its Health Implications
Product Categories with the Highest Maltodextrin Inclusion – from [6]

Maltodextrin is also present in a wide range of foods that are marketed as “healthy options”, including protein powders and meal replacement bars. As is the case with sugar-free foods containing maltodextrin, consumers rely on labels on these products to make informed dietary choices, unaware of the impact that maltodextrin can have on their blood sugar.

Top 10 Processed Foods with the Highest Maltodextrin Content in mg/serving - from [6] Yarley EJ, Unveiling Hidden Sugars: A Critical Analysis of Maltodextrin as a Polysaccharide Additive in Processed Foods and Its Health Implications
Top 10 Processed Foods with the Highest Maltodextrin Content in mg/serving [6]

Why Blood Sugar Spikes Matter

Since maltodextrin digests and absorbs rapidly, it can cause rapid spikes in blood glucose and insulin levels.

Over time, repeated spikes can lead to:

    • Energy crashes or fatigue after meals

    • Increased hunger and sugar cravings

    • Blood sugar instability in people with diabetes, PCOS, or insulin resistance

    • Possible gut microbiome disruption when consumed in large amounts 

Final Thoughts…

Maltodextrin is a common hidden carbohydrate used in processed foods.

While maltodextrin may serve a useful role in the manufacturing of specialized products for athletes or in medical nutrition products, people relying on a  “healthy” protein shake or a meal replacement bar are usually unaware of the effect it can have on their blood sugar.  How much more do those with prediabetes or diabetes (type 1 or type 2) need to know which products, including sugar-free products, contain maltodextrin?

For those needing to control their blood sugar, it is recommended to read labels closely and limit foods containing maltodextrin. Choosing whole-food carbohydrate sources in amounts that can be monitored (“carb counting”) makes controlling blood sugar possible.

To your good health. 

Joy 

 

You can follow me on:

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

 

 

References

    1. Brand‑Miller JC, Foster‑Powell K, Atkinson F. The International Tables of Glycemic Index and Glycemic Load Values. Am J Clin Nutr. 2002;76(1):5–56. 2008: DOI 10.2337/dc08-1239) [https://pubmed.ncbi.nlm.nih.gov/18835944/]
    2. U.S. Department of Agriculture (USDA). FoodData Central: Maltodextrin – Ingredient Profile and Energy Content. Washington, DC: USDA; Accessed 2024. URL: https://fdc.nal.usda.gov
    3. U.S. Food and Drug Administration (FDA). Code of Federal Regulations Title 21 – Maltodextrin (21 CFR 184.1444). Silver Spring, MD: FDA. URL: https://www.ecfr.gov/current/title-21/chapter-I/subchapter-B/part-184#p-184.1444
    4. Health Canada. List of Permitted Food Additives with Other Accepted Uses. Ottawa, ON: Health Canada; Updated 2023. URL: https://www.canada.ca/en/health-canada/services/food-nutrition/food-additives/permitted-use-additives.html
    5. Hofman, D. L., van Buul, V. J., & Brouns, F. J. P. H. (2015). Nutrition, Health, and Regulatory Aspects of Digestible Maltodextrins. Critical Reviews in Food Science and Nutrition56(12), 2091–2100. https://doi.org/10.1080/10408398.2014.940415
    6. Yarley EJ, Unveiling Hidden Sugars: A Critical Analysis of Maltodextrin as a Polysaccharide Additive in Processed Foods and Its Health Implications, International Journal of Medical Science and Clinical Invention 12(04): 7602-7621, 2025DOI:10.18535/ijmsci/v12i.04.02 https://valleyinternational.net/index.php/ijmsci
    7. Magnuson BA, Roberts A, Nestmann ER, Critical review of the current literature on the safety of sucralose, Food and Chemical Toxicology,
      Volume 106, Part A, 2017, Pages 324-355, https://doi.org/10.1016/j.fct.2017.05.047.
    8. Abou-Donia MB, El-Masry EM, Abdel-Rahman AA, McLendon RE, Schiffman SS. Splenda alters gut microflora and increases intestinal p-glycoprotein and cytochrome p-450 in male rats. J Toxicol Environ Health A. 2008;71(21):1415-29. [http://www.ncbi.nlm.nih.gov/pubmed/18800291]

 

Copyright ©2025 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.

 

Nutrition is BetterByDesign

Hemorrhoids — more than the butt of jokes

[This article was written on November 10, 2024, and was updated on October 10, 2025.]

We are finally breaking the stigma and talking about mental health. Men grow moustaches in November to raise awareness about prostate health, so it is time to move past embarrassment and talk about colorectal health. This is my first article in this area and is about ways to reduce the incidence of painful conditions related to hemorrhoids. An article related to alcohol consumption as a risk factor for colon or rectal cancer is next.

What are Hemorrhoids?

The most well-known type of hemorrhoids, sometimes called “piles,” are swollen, inflamed veins (like varicose veins) in the rectum, or on the anus that can be painful, itchy, and may bleed, and are frequently (pardon the pun) the butt of jokes. These are external hemorrhoids that form under the skin around the anus and may resolve with a few days of over-the-counter ointment, but can become enlarged and painful.

Internal hemorrhoids are located on the lining of the rectum above what is called the dentate line (2-4 cm / 3/4 – 1.5 inches from the opening of the anus). These are normal structures that are aligned in three columns in the rectum and function like bubble wrap — cushioning the rectum against irritation from the stool until a bowel movement [1].

Most people are unaware that internal hemorrhoids are there until one becomes irritated and swollen, or worse, prolapses and protrudes from the anus. Internal hemorrhoids may result in chronic, low-grade internal bleeding can indeed lead to iron deficiency or iron-deficient anemia, even when people have no idea they are losing blood.

There are four grades of internal hemorrhoids based on the degree of prolapse. 

Grade 1: Not at all prolapsed.

Grade 2: Prolapses with a bowel movement, but retracts by itself. 

Grade 3: Prolapses with a bowel movement and has to be manually pushed it back in. 

Grade 4: Prolapsed but can’t be pushed back in, or only with a lot of pain.

Since internal hemorrhoids lie above the dentate line, they don’t have nerve endings, and are painless and remain that way until one becomes irritated — or worse, becomes inflamed and protrudes from the rectum like a large, angry grape.

If an inflamed internal hemorrhoid is located on the left lateral side, it may be too painful to sleep on that side, and if it is located on the right posterior side, it may be too painful to sleep on one’s back. Regardless of where it’s located, a Grade 3 or 4 hemorrhoid may make it too uncomfortable to sleep much at all — and since people are generally too embarrassed to talk about hemorrhoids, this pain is largely endured in silence.

Note: external hemorrhoids that lie at the dentate line are internally located but are considered external hemorrhoids because they are at or below the dentate line. These have many nerve endings and, once inflamed, can also prolapse outside the anus. If they don’t resolve with over-the-counter treatment, surgical procedures to remove them are required. 

A blood clot may form within a hemorrhoid, causing it to become thrombosed, and if this causes the blood supply to get cut off, a strangulated hemorrhoid results, which is excruciatingly painful. 

The pain of hemorrhoids ranges considerably. It’s only once an internal hemorrhoid becomes irritated, swollen, and inflamed that it becomes painful. If an internal hemorrhoid or an external hemorrhoid at the dentate line prolapses, the pain can go from a 1-3 on a Likert pain scale of 1- 10 (with 10 being the worst) to an 8 or 9 on 10, and this can occur suddenly, without warning. A person can literally go from having no awareness of having internal hemorrhoids or external hemorrhoids at the dentate line, to having a prolapsed hemorrhoid, and significant pain.

Treatment for Hemorrhoids

Internal hemorrhoids above the dentate line can be treated with rubber band ligation (RBL), which is the most common first-line treatment [2, 3]. This is where a small rubber band is applied to the base of the hemorrhoid and cuts off the blood supply to it. In essence, this is a planned strangulated hemorrhoid. Over a week or two (depending on the hemorrhoid’s size), the walls will thicken, and the overall size of it will shrink. After approximately 10-14 days, the rubber bands fall off the hemorrhoid, leaving an ulcer. The ulcer may bleed slightly with bowel movements over a few days as it heals [4]. Finally, what will remain is a bit of scar tissue on the rectal wall, and that may continue to bleed lightly during bowel movements until it heals completely over the following few weeks. While the banding procedure itself is painless when done properly, and is usually performed without anesthesia, the pain from the hemorrhoid itself can be significant until it finally falls off after ligation, and heals. If banding doesn’t work or if the hemorrhoid becomes inflamed or prolapsed, surgery will likely be required.

In some cases, after hemorrhoid banding, or after an external hemorrhoid at the dentate line gets better on its own, a rectal polyp may form from the ulcer that remains where the hemorrhoid was. In some cases, the polyp can become larger than the original hemorrhoid and may become inflamed and prolapse out of the anus.  Since rectal polyps can form for reasons other than a previously existing hemorrhoid, surgery will be recommended to remove the polyp, and a biopsy will be performed to determine if the polyp is benign (not cancerous) or pre-cancerous.

Causes of Hemorrhoids

Hemorrhoids, both internal and external, were previously thought to be preventable mainly through dietary changes; yet diet is only part of reducing the likelihood of getting hemorrhoids. More than two-thirds of Canadians and Americans engage in a daily habit that significantly increases the risk of developing hemorrhoids, and simple lifestyle changes can help reduce that risk.

Half of adults will have had hemorrhoids by age fifty, yet it’s rare for people to talk about them. Only 4% of people go to their doctor for help because they’re embarrassed, and the last thing they want is to have someone have a look “down there” and poking around. They just want their hemorrhoids to stop hurting and to go away— and the faster, the better. Most people will self-treat with Epsom salt sitz baths and over-the-counter topical creams or wipes, and only seek medical help if the symptoms persist or get worse.

As a Dietitian, I have routinely asked my clients about their bowel function, including how often they poop and its texture — and most are fine with answering these questions because they know this is within my scope of practice. Even though I was taught that part of what can help people avoid hemorrhoids is dietary, until recently, I never asked anyone whether they’ve been experiencing hemorrhoids. This has changed. While getting enough of the right type of fiber and drinking sufficient water are important, two lifestyle factors are thought to contribute to the development of hemorrhoids, and these are the focus of this article. 

The good news is that by adopting a few simple dietary changes and modifying two lifestyle habits, the risk of developing hemorrhoids can be reduced. 

Most people know that avoiding constipation is important to reduce the risk of getting hemorrhoids, and think that drinking enough water and eating lots of “roughage” is the way to accomplish that. What few realize is that some types of fiber can make constipation worse — especially if there is insufficient water intake. But reducing the risk of hemorrhoids involves more than diet. The length of time that we sit on the toilet, as well as the position that we sit on it, both play a significant role in the risk of developing hemorrhoids. 

Squatting versus Sitting Toilet   

In much of Asia, South East Asia, and Africa, the squatting toilet is the norm. The user positions themselves in a squat position over a floor-level porcelain bowl, which results in the colon and rectum being positioned in a straight line. This enables bowel movement to occur significantly faster and without straining than what occurs when using a western-style pedestal toilet. These are more than “holes in the ground” but are real toilets with a flush mechanism that the user engages to empty the bowl — just like on a Western toilet. 

In Europe and most of the West, the pedestal toilet is the norm, which is used in a sitting position. This type of toilet results in a bend in the alignment between the colon and the rectum, causing it to take longer to have a bowel movement, and frequently requiring more than one “visit” to accomplish it. Of importance, the seat design of a pedestal toilet results in increased pressure on the rectum and anus, which significantly increases the risk of developing hemorrhoids.

Middle Eastern and North African countries have both squatting and pedestal toilets, depending on the region. 

There are various types of squatting platforms available for purchase that can be placed over a standard Western pedestal toilet, converting it into a squatting toilet. These are popular with people who have emigrated from countries where squatting toilets are the norm. 

Also available online are various types of squatting footstools that are placed in front of a standard Western pedestal toilet and enable the user to sit in a semi-squatting position. These squatting stools allow for better alignment of the colon and the rectum, and are frequently recommended to people recovering from hemorrhoids, hemorrhoid ligation (banding), and hemorrhoid surgery. These squatting stools allow for less pressure on the anus and pelvic floor, and as a result, may help reduce the development of hemorrhoids or deterioration of unknown internal hemorrhoids. 

The Length of Time Sitting on a Pedestal Toilet 

Due to the shape of the seat on a Western-style pedestal toilet, the length of time that one sits on it increases the risk of developing hemorrhoids. This is due to the increased pressure on the pelvic floor, lower rectum, and anus resulting from the seat’s shape. 

Think of a single-hole paper punch. 

The pressure exerted over a small hole is what makes a one-hole paper punch so effective. Good for paper,  not good for rectums.

To limit pressure on the rectum and anus, it is recommended to limit “seat time” to 3-5 minutes at a time, 10 minutes maximum in 24 hours [1]. 

Washrooms as Phonebooths

In the early 1950s, most houses only had one washroom or bathroom, so multiple members of the same household had to do what they needed to in a limited time and get out. It was rare to have the luxury of being able to sit on the toilet for an extended period of time, reading the newspaper. Now, 97% of new home construction has more than one washroom or bathroom [5] — most often having two full washrooms, plus an additional 1/2 bathroom containing a toilet and a sink. 

With three toilets per house for an average family size of three in Canada [6] means that each member of the average household has access to a toilet on demand, and can — and does spend inordinate amounts of time sitting on it.

A recent study found that 2/3 of Canadians and even more Americans are on their smartphones while sitting on the toilet [6]. The washroom is the new phone booth. It is one of the only places in the house where some can have time alone, and all this increased sitting on the toilet scrolling on the phone is thought to be related to the increased rates of hemorrhoids seen in younger and younger adults. 

Final Thoughts

There are simple things we can do to lower the risk of developing hemorrhoids.

We can drink more water and eat enough of the right types of fiber.

A squatting stool can help align our colon, making defecation time shorter, while reducing the amount of pressure on our rectum.

It is recommended to limit “seat time” to 3-5 minutes. Not scrolling on the phone while sitting on the toilet will make it possible to do what is needed in the recommended amount of time, significantly reducing the risk of developing hemorrhoids.

Remembering how a one-hole punch works may be a helpful reminder. 

For those who have never experienced the pain of a large, prolapsed hemorrhoid, implementing these changes may help avoid the experience. For those who have, I hope that learning how to minimize the risk of another will be welcomed news. 

To your good health. 

Joy 

 

You can follow me on:

Twitter: https://twitter.com/jyerdile

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

References 

  1. UT Southwestern Medical Centre, Treating hemorrhoidal disease: Conservative vs. surgical approaches, April 14, https://utswmed.org/medblog/best-ways-to-treat-hemorrhoids/ 
  2. Zagriadskiĭ EA, Bogomazov AM, Golovko EB. Conservative Treatment of Hemorrhoids: Results of an Observational Multicenter Study. Adv Ther. 2018 Nov;35(11):1979-1992. doi: 10.1007/s12325-018-0794-x. Epub 2018 Oct 1. Erratum in: Adv Ther. 2018 Nov;35(11):1993. doi: 10.1007/s12325-018-0817-7. PMID: 30276625; PMCID: PMC6223991. [https://pmc.ncbi.nlm.nih.gov/articles/PMC6223991/]
  3. McKeown DG, Goldstein S. Hemorrhoid Banding. [Updated 2024 Feb 14]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2024 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK558967/
  4. Hawkins AT, Davis BR, Bhama AR, Fang SH, Dawes AJ, Feingold DL, et al. The American Society of Colon and Rectal Surgeons Clinical Practice Guidelines for the Management of Hemorrhoids. Dis Colon Rectum. 2024 May 1. 67 (5):614-623. [https://pubmed.ncbi.nlm.nih.gov/38294832/]
  5. Eye on Housing, Number of Bathrooms in New Homes in 2021, November 3, 2022, https://eyeonhousing.org/2022/11/number-of-bathrooms-in-new-homes-in-2021/
  6. Statistics Canada, Average Family Size in Canada, 2021 https://www.statista.com/statistics/478948/average-family-size-in-canada/
  7. Toronto Sun, Two-thirds of Canadians take smart phones into the bathroom: Survey, May 16, 2022, https://torontosun.com/news/national/survey-65-of-canadians-take-their-smart-phones-into-the-bathroom

 

Copyright ©2025 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.

 

Nutrition is BetterByDesign

Dietary and Lifestyle Changes to Avoid “Old People Smell”

 

In Western culture, the main focus as we age is to keep ourselves “looking young,” usually pursued by buying special skin and hair-care products. In Japan, avoiding “kareishu”, or “old people smell,” is a significant focus in aging. There are special soaps and washing products promoted to meet this need, as well as research into foods that can neutralize it.

What is “Old People Smell”?

“Old people smell” is the characteristic ‘greasy, grassy odor’ most noticeable in nursing homes and long-term care facilities, beyond the smells of urine, feces, and spilled food. Many independent-living older adults also have it, though they may have become desensitized to it. Children and grandchildren are often more aware of it.

Body odor can be influenced by eating foods such as onions, garlic, ginger, and certain spices, as well as by medications. However, “old people smell” mainly comes from 2-nonenal, a volatile compound formed by the oxidative breakdown of palmitoleic acid and vaccenic acid, which are two omega-7 unsaturated fatty acids that increase on the skin from about age 40 onwards [1].

Compared to adults under 40, 2-nonenal can increase by up to 6-fold, though the exact reason is unclear [1]. More omega-7 fatty acids or lipid peroxides on the skin correlate with higher 2-nonenal levels [1]. Like other unsaturated fats, omega-7s are prone to oxidation.

Limiting the oxidation of omega-7 fats, as well as keeping skin, bedding, and clothing clean, can significantly reduce “old people smell.” Because 2-nonenal is fat-soluble, ordinary water-based soaps may not be effective in removing it. Polyphenol-containing soaps have been shown to reduce 2-nonenal on the skin [2].

Targeting “Old People Smell” — Lifestyle and Dietary Changes

Lifestyle Changes

Recommended lifestyle measures include wearing natural fibers such as cotton, linen, or silk to allow fatty acid compounds to transfer to the clothing, which can then be easily washed. Washing bedding and clothes in enzyme-activated detergents can break down odor-causing fatty acids. Soaps containing polyphenols, such as concentrated Japanese persimmon extracts, have been demonstrated to reduce 2-nonenal on the skin [2]. Note: Regular persimmon juice or leaves are not equivalent to concentrated tannin extracts used in studies.

Dietary Changes

Since higher levels of palmitoleic acid and vaccenic acid on the skin increase 2-nonenal, dietary strategies include reducing intake of these fats and increasing dietary intake of antioxidants.

Reducing Intake of Palmitoleic Acid and Vaccenic Acid

Foods rich in palmitoleic acid include macadamia nuts, macadamia oil, avocado, avocado oil, olive oil, and sea buckthorn oil [3]. Vaccenic acid is found in ruminant fats, including beef, lamb, and dairy products [3]. Reducing these foods may decrease 2-nonenal formation. Omega-7 fats are non-essential, as the body can synthesize them via de novo lipogenesis [3]. 

Increasing Intake of Dietary Antioxidants

Certain antioxidants and polyphenols may help reduce lipid oxidation and 2-nonenal formation:

green tea to neutralize 2-noneal

Green tea catechins have antioxidant activity that may help reduce oxidative odor precursors [4].

 

eggplant to neutralize 2-noneal

Champignon (white button mushroom) extract was shown in a 4-week trial to reduce body odor in adults, although the study is limited in sample size [5].

Eggplant phenolamides have demonstrated 2-nonenal scavenging activity in vitro and in animal models, suggesting potential reduction in odor [6].

berries to neutralize 2-nonealBlackcurrant powder rich in anthocyanins reduced 2-nonenal skin emission in middle-aged adults [7]. Other anthocyanin-rich foods, such as elderberries, blackberries, blueberries, raspberries, acai, and pomegranate, may have similar effects [8]. 

Final Thoughts

As the saying goes, “beauty is more than skin deep“, and just as young skin and hair aren’t achieved by applying cosmetics and hair dyes, “smelling young” isn’t achieved only by using special soaps.

While cosmetics, special soaps, and detergents can certainly help, the essence of looking young and smelling young is primarily achieved by eating real, whole food rich in natural antioxidants and nourishing oneself from the inside out.

Unfortunately, to limit costs, public long-term care centers rarely provide their residents with the types of antioxidant-rich foods known to minimize the characteristic ‘greasy, grassy odor’ found in these residences. They don’t have to smell like that.

When we become parents, we learn how to feed our infants and children — but who teaches us how to feed ourselves as we age, or our aging parents? Eating well at any age doesn’t just happen by chance. 

Enabling seniors to remain independent into their advanced years begins with dietary and lifestyle changes in middle age (or sooner) — including eating sufficient amounts of the right types of protein to maintain muscle and bone mass, and eating real, whole food rich in antioxidants. 

More Info?

I help adults to be the best they can be at any age, offering services such as the Healthy Aging Package to meet this need. Visit the Services tab to learn more.

To your good health!

Joy

You can follow me on:

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

References

  1. Haze S, Gozu Y, Nakamura S, Kohno Y, Sawano K, Ohta H, Yamazaki K. 2-Nonenal newly found in human body odor tends to increase with aging. J Invest Dermatol. 2001 Apr;116(4):520‑524. doi:10.1046/j.0022-202X.2001.01287.x https://pubmed.ncbi.nlm.nih.gov/11286617/]

  2. Tatsuguchi I, Matsuoka T, Izumi R, Ijichi S, Shibata H. Preventive effect against the aged men’s body odor by the soap containing polyphenol. Jpn Assoc Odor Environ. 2012;43(5):362–366 [https://www.jstage.jst.go.jp/article/jao/43/5/43_362/_article/-char/en]

  3. Venn-Watson E. Fatty 15, Omega 7: What To Know About This Fatty Acid. https://fatty15.com/blogs/news/what-is-omega-7

  4. Cabrera C, Artacho R, Giménez R. Beneficial effects of green tea — a review. J Am Coll Nutr. 2006 Apr;25(2):79‑99. doi:10.1080/07315724.2006.10719518 [https://pubmed.ncbi.nlm.nih.gov/16582024/]

  5. Nishihira J, Nishimura M, Tanaka A, Yamaguchi A, Taira T. Effects of 4‑week continuous ingestion of champignon extract on halitosis and body and fecal odor. J Tradit Complement Med. 2015 Dec 11;7(1):110‑116. doi:10.1016/j.jtcme.2015.11.002 [https://pmc.ncbi.nlm.nih.gov/articles/PMC5198824/]

  6. Kim HM, Kim JH, Jeon JS, Kim CY. Eggplant Phenolamides: 2‑Nonenal Scavenging and Skin Protection Against Aging Odor. Molecules. 2025 May 12;30(10):2129. doi:10.3390/molecules30102129 [https://pmc.ncbi.nlm.nih.gov/articles/PMC12114487/]

  7. Willems M, Todaka M, Banic M, Cook M, Sekine Y. Effect of New Zealand Blackcurrant Powder on Skin Emission of Volatile Organic Compounds in Middle‑Aged and Older Adults. Curr Dev Nutr. 2019;3(Suppl 1):nzz031.P06‑092-19. doi:10.1093/cdn/nzz031.P06‑092-19 [https://pmc.ncbi.nlm.nih.gov/articles/PMC6576077/]

  8. Lakshmikanthan M, Muthu S, et al. A comprehensive review on anthocyanin-rich foods: Insights into extraction, medicinal potential, and sustainable applications. J Agric Food Res. 2024;17:101245. doi:10.1016/j.jafr.2024.101245 [https://www.sciencedirect.com/science/article/pii/S2666154324002825]

 

 

Copyright ©2025 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.

 

Nutrition is BetterByDesign

Intermittent Fasting and Time Restricted Eating — duration and timing

 

People have heard about the benefits of intermittent fasting and time-restricted eating; however, the duration and timing of fasting are important considerations. 

Intermittent fasting refers to specific times for ‘eating’ and ‘not eating’ (fasting) on a set schedule. There are two main types, which are (1) partial fasting or alternate-day fasting, and (2) time-restricted feeding (TRF).

Two Main Types of Intermittent Fasting

Partial Fasting or Alternate Day Fasting is a type of intermittent fasting where fasting days are set to a specific number of days out of the week and may include one day out of seven, or ‘alternate day fasting’ — where the usual amount of food is consumed every other day.

Time-Restricted Eating (TRE), also called time-restricted feeding (TRF), is a type of intermittent fasting where eating occurs during a specific period each day, and ‘not eating’ (fasting) occurs the remainder of the time.

The “5:2 diet” is a type of time-restricted eating that has people eating 25% of their normal caloric intake on two non-consecutive days per week (i.e., ~400-500 calories per day for women and ~500-600 calories for men), and consuming normal intake on the other five days. Since the focus is on restricted caloric intake and not intermittent eating, it has not been elaborated on in this article.

A common TRE schedule is 16:8, and is where all eating occurs during 8 hours, and the remaining 16 hours per day is a period of fasting. This is often done by people skipping breakfast and eating from midday until ~8 PM. 

Periods of Fasting of 24 hours or more

Except as required for specific clinical or religious reasons, I do not recommend that people engage in periods of fasting of 24 hours or more based on the effect of fasting on lean body mass (muscle). For this, I refer to the work of medical doctor Dr. Stephen Phinney, MD, PhD, and Registered Dietitian Dr. Jeff Volek, RD, PhD.

Phinney and Volek have documented that, in periods of prolonged fasting (1-42 days), nitrogen loss, which is a marker of protein loss, begins on day 1 and reaches a maximum on day 3, then gradually declines[1].

“Net protein breakdown begins within the first day of fasting, reaches its maximum rate within 2-3 days – typically a pound of lean tissue lost per day.[1]”

While the human body has fat stores that can easily sustain us during extended periods where we don’t eat, the body does not have reserve protein stores to sustain us over long periods of fasting. All the protein in the body — whether as muscle, red blood cells, antibodies, or neurotransmitters is functional, so “whenever the body loses protein, it loses some of its functional reserve[1].” 

Time Restricted Eating 

Time-restricted eating (TRE), also called time-restricted feeding (TRF), is, for most people, the easiest form of intermittent fasting to do because the period of not eating only occurs for part of the day.

An early pilot study from 2019 in adults with metabolic syndrome which includes high blood pressure, elevated blood sugar, excess fat around the abdomen, and abnormal cholesterol levels found that limiting eating to only 10 hours per day (i.e. a 10 hour “eating window”) promoted weight loss, reduced abdominal fat, and led to more stable blood sugar and insulin levels in those taking standard medication to lower cholesterol and blood pressure [2].  

The researchers from the Salk Institute, including circadian biologist Dr. Satchidananda Panda, concluded that the 10-hour time-restricted eating schedule supported an individual’s circadian rhythms, which results in health benefits evidenced by previous and subsequent mouse studies published by the Salk team[3].

Circadian rhythms are the regular 24-hour cycles of biological processes that affect nearly every cell in the body. 

“Eating and drinking everything (except water) within a consistent 10-hour window allows your body to rest and restore for 14 hours at night. Your body can also anticipate when you will eat, so it can prepare to optimize metabolism.[3]”

A follow-up study from the researchers at Salk Institute that was published in 2024, found that people who ate within a consistent eight-to-ten-hour window each day for three months saw improvements in several markers of blood sugar and metabolic function, compared to those who received standard treatment [4].

Given that more than 1/3 of adults in the US [4], and more than 19% — or 1 in 5 adults in Canada have metabolic syndrome[5] which rises to ~40% in adults over the age of 65, the implication that simply changing the amount of time each day in which eating occurs can significantly improve markers or metabolic syndrome, is significant. 

Erratic Eating Patterns in Adults

A landmark study from 2015 by circadian biologist Dr. Satchidananda Panda of Salk Institute had healthy, normal-weight adults who did not perform shift work track everything they ate each day for 21 days (3 weeks) by taking pictures of it using a smartphone app. The time-stamp on each photo enabled analyses of the time at which eating occurred. Participants were recruited through a newspaper advertisement, paper flyers, and online advertisements, and inclusion and exclusion criteria were determined by an online questionnaire and in-person interview.

In contrast to the popular belief that most people eat three meals per day within a 12-hour interval, this study found that eating patterns are much more erratic and differ between weekdays and weekends.

The amount of time spent eating each day (95% interval) approached 15 hours per day for half the people in the study, and the only time they were not eating was when they were sleeping.

In addition, less than 25% of calories were eaten before noon, and more than 35% of calories were eaten after 6 PM.

While the sample set in this study was small, my clinical experience has found that at least half of adults eat this way. 

Supporting Time-Restricted Eating 

It’s important to keep in mind that for some people, the idea of eating actual meals over a 10-hour period without eating snacks IS intermittent fasting when compared to the way that they usually eat. 

For those accustomed to eating meals and snacks or grazing over 15 hours, the idea of eating meals with nothing between over 10 hours can seem daunting. Many are concerned they will be hungry, and others that their blood sugar will drop, making them feel lightheaded or dizzy. By ensuring that meals are made up of sufficient amounts of highly bioavailable protein and healthy fats, both of these concerns are easily addressed. 

Studies support that eating and sleeping according to one’s natural circadian rhythms will, in and of itself, improve many health markers, and when one’s Meal Plan is designed to factor in desired fat loss and/or muscle gain, the benefits are additive.

Implementing a 16:8 Time Restricted Eating Schedule

As mentioned above, a common time-restricted eating schedule is 16:8, where eating occurs during an 8-hour eating window, and the remaining 16 hours per day are fasting. Most people skip breakfast and begin eating from 11 AM or noon until ~7 or 8 PM. This is called a late time-restricted eating window (TREL). That, however, is not the only way to eat within a 16:8 window,

Some will eat breakfast at ¬7 or 8 AM and finish eating at 3 or 4 PM (with one or no meals in between), and this is called an early time-restricted eating window (TREE).

Does it matter whether someone does an early or a late 16:8 time-restricted eating window? Chrononutrition studies seem to indicate that it can.

Chrononutrition 

Chrononutrition is a field of study that examines the complex relationship between when eating occurs relative to normal human circadian rhythms and metabolic health, and studies indicate that the timing of eating matters — both the timing of the first eating occasion, and how late the last meal occurs. 

Circadian rhythms are regular fluctuations of physiological processes over 24 hours and include the production of hormones such as cortisol, insulin, and melatonin, as well as certain enzymes used in digestion.

Studies have shown that glucose tolerance as well as insulin sensitivity are at their peak in the morning and decrease significantly later in the day. As a result, when meals are eaten late in the evening, when insulin production is at its lowest, there is an increase in blood glucose, insulin release, appetite, and the risk of obesity [8,9].

When We Eat Matters

In the 16-year prospective Health Professionals Follow-up Study, which had almost 27,000 middle-aged male subjects, men who skipped breakfast had a 27% higher risk of coronary heart disease found to be mediated by higher BMI, high blood pressure, diabetes, and high cholesterol [10]. In other studies, breakfast skipping has been linked to greater type 2 diabetes risk, higher total and LDL cholesterol levels, body weight, fat mass, and abdominal adiposity, and lower HDL cholesterol [11,12]. In the same study, there was a 55% higher coronary heart disease risk in men who ate late at night [11]. 

In a 2014 study from Japan, breakfast skipping was associated with 28% and 57% higher odds of developing metabolic syndrome and obesity, but only when it was in combination with eating late-night dinners within 2 hours of bedtime [13]. While it is hard to tease out whether the issue is skipping breakfast or eating late into the evening, an earlier fasting window TREE solves both issues.

In the 2019 national Korean dataset, night eating, which was defined as eating after 9 PM, was associated with 48% higher odds of metabolic syndrome in men but not women, suggesting that there may be sex differences in these associations [14]. In ~900 middle-aged to older adults in the same Korean data set, a higher percentage of daily energy eaten within 2 hours of bedtime was associated with 82% higher odds of being overweight and obese, whereas a higher percent of of daily energy intake consumed during the morning window, within 2 hours of waking up was associated with 47% lower odds of being overweight and obese [15].

Early or Late Time-Restricted Eating – Some Considerations

To a large extent, for most adults, deciding to adopt either an early or late time-restricted eating schedule comes down to a matter of personal preference and convenience.

For older adults, however, the need to prioritize protein and the amino acid leucine first thing in the morning favours an early time-restricted eating window, but that will be a topic of an upcoming post. 

Adults who need to eat their dinner with other family members will often adopt a late time-restricted eating window (TREL). They will feed their family breakfast, but not begin to eat themselves until 11 AM or noon. They will eat their second meal with their family around 5-6 PM, then eat their final meal of the day at ¬8 or 9 PM.  A drawback to this is that eating this late can delay sleep onset because one of the signals required for the body to release melatonin from the brain is a drop in core body temperature. Since digestion of food produces a lot of heat, late consumption of food delays the release of melatonin and, subsequently, delays sleep. As well, eating within 2 – 3 hours of bedtime may be associated with some of the metabolic drawbacks observed in studies — especially for those who already have abnormal blood sugar, blood pressure, cholesterol, or weight.

Those who adopt an early time-restricted eating window (TREE) will usually have their breakfast at ¬7 AM, lunch at around 11:00 AM, and their last meal of the day around 4 PM. By having sufficient highly bioavailable protein at each of the three meals along with sufficient amounts of healthy fats, hunger is a non-issue, and blood glucose is well controlled because eating occurs when the body is the most insulin sensitive.

Final Thoughts…

For those who are used to eating or grazing over 15 hours, having a Meal Plan that distributes meals over a 10-hour eating window may be the best place to start. This will allow for improvements in metabolic markers, fat loss, and muscle gain, while being able to eat their meals with family members.

Those who need to eat dinner with other family members may find adopting a late time-restricted eating window (TREL) the most convenient because it lets them feed their family breakfast while beginning to eat themselves closer to 11 AM, eat their second meal with their family around 5-6 PM, and eat their final meal of the day at ¬8 PM. While it can have an impact on sleep onset and be less than optimal in terms of metabolic improvements, it will likely be a significant improvement to how they were eating before.

Finally, those who can adopt an early time-restricted eating window (TREE) often enjoy having breakfast at ¬7 or 8 AM, lunch, if they eat it at around 11:00 AM, and eat their last meal of the day around 4 PM. Those who are responsible for making meals for their families do very well following this eating window by eating their dinner early, then sitting with their family while they eat dinner.  This way, they don’t miss out on this important time of connecting with the families.

As in other areas, there is no one-size-fits-all approach.

More Info?

If you would like to learn about how I can help support you with a style of time-restricted eating that best suits your lifestyle, please visit the landing page to learn about the services that I provide.

To your good health!

Joy

You can follow me on:

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

References

    1. Virta Health, Phinney S., Volek J., To Fast or Not to Fast: What are the Risks of Fasting, December 5, 2017, https://www.virtahealth.com/blog/science-of-intermittent-fasting
    2. Wilkinson MJ, Manoogian EN, et al Ten-Hour Time-Restricted Eating Reduces Weight, Blood Pressure, and Atherogenic Lipids in Patients with Metabolic Syndrome, Cell Metabolism, Volume 31, Issue 1, 92 – 104.e5, doi: 10.1016/j.cmet.2019.11.004 [https://pubmed.ncbi.nlm.nih.gov/31813824/]
    3. Salk News, December 5, 2019, Clinical Study Finds Eating Within a 10-hour Window May Stave Off Diabetes, Heart Disease, https://www.salk.edu/news-release/clinical-study-finds-eating-within-10-hour-window-may-help-stave-off-diabetes-heart-disease/
    4. Manoogian ENC, Wilkinson MJ, et al. Time-Restricted Eating in Adults With Metabolic Syndrome: A Randomized Controlled Trial. Ann Intern Med.2024;177:1462-1470. doi:10.7326/M24-0859 [https://pubmed.ncbi.nlm.nih.gov/39348690/]
    5. Rao DP, Dai S, et al, (2014) Metabolic syndrome and chronic disease, Chronic Diseases and Injuries in Canada (CDIC), Vol. 34, No. 1, https://doi.org/10.24095/hpcdp.34.1.06
    6. Gill, S., and Panda, S. (2015). A Smartphone App Reveals Erratic Diurnal Eating Patterns in Humans that Can Be Modulated for Health Benefits. Cell Metabolism. 22. 10.1016/j.cmet.2015.09.005. [https://pmc.ncbi.nlm.nih.gov/articles/PMC4635036/]
    7. Raji OE, Kyeremah EB, Sears DD, St-Onge MP, Makarem N. Chrononutrition and Cardiometabolic Health: An Overview of Epidemiological Evidence and Key Future Research Directions. Nutrients. 2024 Jul 19;16(14):2332. doi: 10.3390/nu16142332. PMID: 39064774; PMCID: PMC11280377. [https://pubmed.ncbi.nlm.nih.gov/39064774/]
    8. Poggiogalle E, Jamshed H, Peterson CM. Circadian regulation of glucose, lipid, and energy metabolism in humans. Metabolism. 2018 Jul;84:11-27. doi: 10.1016/j.metabol.2017.11.017. Epub 2018 Jan 9. PMID: 29195759; PMCID: PMC5995632. [https://pubmed.ncbi.nlm.nih.gov/29195759/]
    9. Saad A, Man, CD et al, Diurnal Pattern to Insulin Secretion and Insulin Action in Healthy Individuals. Diabetes 1 November 2012; 61 (11): 2691–2700. https://doi.org/10.2337/db11-1478
    10. Cahill L.E., Chiuve S.E., Mekary R.A., Jensen M.K., Flint A.J., Hu F.B., Rimm E.B. Prospective Study of Breakfast Eating and Incident Coronary Heart Disease in a Cohort of Male US Health Professionals. Circulation. 2013;128:337–343. doi: 10.1161/CIRCULATIONAHA.113.001474. [https://pubmed.ncbi.nlm.nih.gov/23877060/]
    11. Paoli A., Tinsley G., Bianco A., Moro T. The Influence of Meal Frequency and Timing on Health in Humans: The Role of Fasting. Nutrients. 2019;11:719. doi: 10.3390/nu11040719. [https://pubmed.ncbi.nlm.nih.gov/30925707/]
    12. Witbracht M., Keim N.L., Forester S., Widaman A., Laugero K. Female Breakfast Skippers Display a Disrupted Cortisol Rhythm and Elevated Blood Pressure. Physiol. Behav. 2015;140:215–221. doi: 10.1016/j.physbeh.2014.12.044. [https://pubmed.ncbi.nlm.nih.gov/25545767/]
    13. Kutsuma A., Nakajima K., Suwa K. Potential Association between Breakfast Skipping and Concomitant Late-Night-Dinner Eating with Metabolic Syndrome and Proteinuria in the Japanese Population. Scientifica. 2014;2014:253581. doi: 10.1155/2014/253581 [https://pubmed.ncbi.nlm.nih.gov/24982814/]
    14. Ha K., Song Y. Associations of Meal Timing and Frequency with Obesity and Metabolic Syndrome among Korean Adults. Nutrients. 2019;11:2437. doi: 10.3390/nu11102437. [https://pubmed.ncbi.nlm.nih.gov/31614924/]
    15. Xiao Q., Garaulet M., Scheer F.A.J.L. Meal Timing and Obesity: Interactions with Macronutrient Intake and Chronotype. Int. J. Obes. 2019;43:1701–1711. doi: 10.1038/s41366-018-0284-x. [https://pubmed.ncbi.nlm.nih.gov/30705391/]

 

Copyright ©2025 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.

 

Nutrition is BetterByDesign

 

 

Significant Increase in Functional Dyspepsia Since the Pandemic

 

Functional Dyspepsia is a disorder similar to Irritable Bowel Syndrome (IBS) which affects the stomach rather than the bowel and just like IBS, it is diagnosed after ruling out underlying structural, or biochemical causes such as peptic ulcers, gastritis, or Gastro-Esophageal Reflux Disorder (GERD).

Symptoms of Functional Dyspepsia may include pain or burning called epigastric pain syndrome (EPS), getting full quickly when eating and/or feeling excessively full after eating called postprandial distress syndrome (PDS), feeling bloated, or experiencing reflux. Significantly, not all individuals have the same symptoms.

Functional Dyspepsia and IBS Surge After the Pandemic

A recent study[1] of over 4000 adults in both the US and UK that was done in two stages (a) in 2017 before the pandemic then (b) again in 2023, after the pandemic found that Functional Dyspepsia rose almost 44% (from 8% to 12%), and IBS increased 28% (from 5% to 6%) after the pandemic.

It was also found that Functional Dyspepsia and IBS were often associated with people experiencing long-COVID, or diagnosed with anxiety disorder, or depression.

The Role of the Gut-Brain Axis

Functional Dyspepsia is sometimes referred to as having a “nervous stomach” because of the known interaction between the gut and the brain, along what is called the “gut-brain axis”. The gut-brain axis involves the vagus nerve, which is the longest nerve in the human body and which connects the brain to the organs, including the stomach, intestines,  heart and lungs.

Since symptoms of Functional Dyspepsia and some cases of IBS are more pronounced when the individuals are under stress, interventions may not only include dietary modifications, but may also include behavior interventions that can help relax the gut by affecting the vagus nerve.

Symptoms Vary Between Individuals 

Individuals with Functional Dyspepsia may experience some symptoms, but not others, so dietary treatment must be individualized for each person, and some of the interventions used may be similar to those used for other functional disorders, such as IBS, or for digestive disorders such as Gastro-Esophageal Reflux Disorder (GERD), hiatus hernia, or Small Intestinal Bacterial Overgrowth (SIBO), or interventions that are unique to Functional Dyspepsia. 

For example, addressing the symptom of bloating may involve use of a low-FODMAP diet implemented over three stages which is also used in some individuals with Irritable Bowel Syndrome (IBS), depending on which foods are causing the symptoms.

If acid reflux is one of the symptoms that people are experiencing, dietary interventions and lifestyle interventions may be similar to those used in Gastro-Esophageal Reflux Disorder (GERD), or to help decrease stomach pain, dietary recommendations may involve reducing irritants such as spices, alcohol, coffee and caffeine. 

Some dietary inventions are specific to those with Functional Dyspepsia, such as when people are experiencing feeling “overfull” after eating, even when the meals are small.

Dietary interventions for Functional Dyspepsia are definitely not “one-sized-fits-all”, and as it is with Irritable Bowel Syndrome, dietary treatment must be individualized to each person’s symptoms.

Role of Behaviour Interventions in Functional Dyspepsia 

Since Functional Dyspepsia (and sometimes IBS, as well) involve gut-brain interaction, there are some behavioral interventions that often used such as specific types of breathing exercises that affect the vagus nerve, help relax the gut, thus minimizing symptoms. 

Some Final Thoughts

Functional disorders like Functional Dyspepsia or IBS are diagnosed based on symptoms, rather than lab tests because they don’t involve a structural or biological abnormality. As with IBS, a diagnosis of Functional Dyspepsia is made by a doctor after ruling out disease states, or biological causes.

Just as the diagnosis of Functional Dyspepsia is made based on symptoms, so too is which dietary modifications will be most appropriate. Choosing which approaches to use and the order in which to implement those dietary modifications can significantly shorten the length of time it takes until someone begins to feel better, and this is where the help of a Dietitian experienced in both digestive disorders and functional disorders comes in.

More Info?

If you would like to learn about how I can help support you with dietary changes related to Functional Dyspepsia or IBS, please visit the landing page to learn about the services that I provide.

To your good health!

Joy

You can follow me on:

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

Reference

  1. Palsson, Olafur et al. The Prevalence and Burden of Disorders of Gut-Brain Interaction (DGBI) before versus after the COVID-19 Pandemic, Clinical Gastroenterology and Hepatology, Volume 0, Issue 0, DOI: 10.1016/j.cgh.2025.07.012

 

Copyright ©2025 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.

 

Nutrition is BetterByDesign

Vitamin B12 Levels May Be Set Too Low to Prevent Cognitive Decline in Older Adults

 

A recent study published in the Annals of Neurology on February 10, 2025, suggests that levels of vitamin B12 considered within lab-normal values may be too low to prevent cognitive decline in healthy older adults [1].

What is Vitamin B12?

Vitamin B12, also known as cobalamin, is a water-soluble vitamin found in foods of animal origin, including fish, meat, poultry, eggs, and dairy products. It is essential for the proper functioning of the central nervous system, as well as for the formation of healthy red blood cells, and the synthesis of DNA.

Vitamin B12 is absorbed in the gastrointestinal (GI) tract, however, a deficiency may result due to inadequate dietary intake in those following a vegan or vegetarian diet, and from conditions which impair its absorption in the GI tract, including decreased intrinsic factor (IF). IF is a protein secreted in the stomach that enables vitamin B12 to be absorbed from food, and which generally decreases with age due to lower amounts of stomach acid production [2].

Vitamin B12 Deficiency Symptoms

If left untreated, vitamin B12 deficiency can lead to health complications, including megaloblastic anemia (where red blood cells are too large), fatigue, muscle weakness, gastrointestinal problems, nerve damage, and mood disturbances. It can also cause neurological issues, including peripheral neuropathy, cognitive decline, and gait (walking) abnormalities [1].

Findings of the Study

The study was led by researchers at the University of California, San Francisco (UCSF) who investigated whether vitamin B12 levels, despite falling within the lab normal range, might still be associated with neurological damage or impaired function in healthy older adults [1].

The study included 231 healthy individuals, all without dementia or mild cognitive impairment, who were recruited from the Brain Aging Network for Cognitive Health (BrANCH) at UCSF. Participants had an average age of 71, with a median blood vitamin B12 concentration of approximately 414.8 pmol/L.

To assess neurological status, researchers used multifocal visual evoked potential testing, cognitive processing speed evaluations, and magnetic resonance imaging (MRI) and measured serum biomarkers associated with neuroaxonal injury, astrocyte activity, and amyloid pathology. To accurately estimate the body’s capacity to utilize vitamin B12, variables such as age, sex, education level, and cardiovascular risk factors were factored in.

Cognitive testing revealed that individuals with lower levels of active vitamin B12 exhibited slower processing speeds, indicating subtle cognitive decline, an effect more pronounced with advancing age. Older participants also showed significant delays in responding to visual stimuli, suggesting slower visual processing and reduced overall brain conductivity.

MRI results showed that individuals with lower levels of transcobalamin (Holo-TC), the active form of vitamin B12, had greater volumes of white matter hyperintensities—an indicator of brain damage. Additionally, researchers found that elevated levels of the inactive form of B12 were associated with increased concentrations of T-Tau protein in the blood, a biomarker linked to neurodegeneration.

Findings of the Study

The findings of this study suggest that the current recommended levels of vitamin B12 may be insufficient to protect against neurological decline, especially in older adults.

Final Thoughts…

Ensuring sufficient B12 intake can be difficult for older adults who consume less food overall, eat fewer animal-based foods, or have reduced levels of intrinsic factor due to aging. 

While taking a supplement may seem like a relatively straightforward solution to ensure adequate vitamin B12 levels, most B12 supplements available on the market contain types of cobalamin that are not able to be used by people who have the relatively common MTHFR genetic variation which affects their ability to convert folate (vitamin B9) and other B vitamins, including B12 into their active form.  

Another factor that needs to be considered is that long-term use of Metformin to manage blood sugar is, by itself, significantly associated with low vitamin B12  levels [4]. Since many older adults are prescribed this medication, and vitamin B12 levels may already be set too low for healthy older adults not taking any medication, the need for assessing and monitoring vitamin B12 status in older adults is essential.

Further complicating the issue, low iron levels lead to smaller-than-normal red blood cells, while low B12 levels cause them to become larger. When both deficiencies are present, which is not uncommon in individuals with low intake of animal-based foods, they can offset each other, causing red blood cells to appear normal in size and potentially masking the underlying problem. A dietary assessment can help identify these risks, while blood tests can determine the extent to which these nutrients may be sub-optimal, guiding appropriate dietary changes and supplementation.

More Info?

If you’re interested in how I support dietary intake in older adults, please visit the landing page to learn about the services that I provide.

To your good health!

Joy

You can follow me on:

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

References

    1. Beaudry-Richard, A., Abdelhak, A., Saloner, R., et al (2025), Vitamin B12 Levels Association with Functional and Structural Biomarkers of Central Nervous System Injury in Older Adults. Ann Neurol. https://doi.org/10.1002/ana.27200
    2. National Institutes of Health (NIH) Office of Dietary Supplements, B12, https://ods.od.nih.gov/factsheets/VitaminB12-HealthProfessional/
    3. Vitamin B12-Associated Neurological Diseases. Medscape. News release. Updated February 4, 2025. Accessed April 1, 2025. https://emedicine.medscape.com/article/1152670-overview
    4. Atkinson M, Gharti P, Min T. Metformin Use and Vitamin B12 Deficiency in People with Type 2 Diabetes. What Are the Risk Factors? A Mini-systematic Review. touchREV Endocrinol. 2024 Oct;20(2):42-53. doi: 10.17925/EE.2024.20.2.7. Epub 2024 Jul 12. PMID: 39526048; PMCID: PMC11548349.

 

Copyright ©2025 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.

 

Nutrition is BetterByDesign

Dietary Support for Hypermobile Ehlers-Danlos Syndrome (hEDS)

 

Ehlers-Danlos syndrome (EDS) is a group of genetic connective-tissue disorders that often present as symptoms of joint hypermobility (joints that bend in unusual ways), joint instability, stretchy, fragile skin, with accompanying gastrointestinal symptoms.

There are approximately 13 subtypes of Ehlers-Danlos syndrome, with the most common type and the one that I support being Hypermobile Ehlers-Danlos syndrome (hEDS). There is a 50% chance that hEDS will be inherited by children of a parent with the condition [1]. 

It is not uncommon for people with Hypermobile Ehlers-Danlos syndrome to also have symptoms of Mast Cell Activation Disorder (MCAD) (also known as Mast Cell Activation Syndrome /MCAS), which is a reactivity to histamine as well as other bioactive amines [2], previously written about here, which means that it’s nessessary to address the symptoms of both, together. In some cases, Postural Orthostatic Tachycardia Syndrome (POTS) is often involved, too. 

While many of the symptoms of Ehlers-Danlos Syndrome (EDS) are gastrointestinal (GI) and food-reactive in nature, there is no single EDS Diet, but rather general dietary principles on which specific individual recommendations that factor in co-presenting MCAD and POTS can be layered. This includes addressing some associated nutrient deficiencies, as well as dietary interventions to help minimize GI symptoms.

Gastrointestinal (GI) Concerns in EDS

    1. Abnormal connective tissue structure, growth, maintenance, or function in EDS may make the GI tract structurally abnormal, sluggish, painful, inflamed, and/or “leaky”.

(i) Functional Gastrointestinal Disorders (e.g., Irritable Bowel Syndrome, chronic constipation)

Dietary approaches to functional GI symptoms are similar to those utilized in Irritable Bowel Syndrome (IBS), and these can be addressed using the following approaches:

(a) Use of a Time Food Time Symptom Journal to determine which foods or food components trigger adverse symptoms

(b) Trialing a low FODMAP diet introduced in three progressive stages

(ii) Dysmotility (e.g., esophageal dysmotility, gastroparesis, slow colonic transit)

This requires medical diagnosis and treatment first, with dietary support.

2. Autonomic nervous system abnormalities (dysautonomia) common in EDS may cause additional GI symptoms or complications (i.e. fight or flight versus rest and digest).

Functional Dyspepsia affects the upper gastrointestinal tract (stomach), and symptoms include nausea, feeling bloated, and stomach pain. It is sometimes referred to as having a “nervous stomach.”

Some people think that Functional Dyspepsia is caused by food sitting too long in the stomach, or food not moving properly through the upper gastrointestinal tract, both of which may be related to the function of the vagus nerve.

Understanding the role of the Vagus Nerve in Functional Dyspepsia and learning some simple techniques to calm the vagus nerve can be helpful to those with GI symptoms related to dysautonomia.

    1. Dysbiosis and dysregulation of gut-related immune function common in EDS may cause further inflammation, food intolerances, true food allergies (IgE mediated), local or systemic autoimmune conditions, as well as GI or systemic issues.

Dietary support may include

    • IgE-mediated food allergy including avoiding cross-reactants (e.g., latex cross-reactivity manifesting as intolerance to avocado, banana…)
    • other types of antigen-induced immune reactions (e.g. Food Protein-Induced Enterocolitis Syndrome, FPIES) – a delayed, non-IgE mediated food sensitivity to cow’s milk, soy, rice, oats
    • auto-immune targeting of the body’s own tissue (celiac disease, Hashimoto’s)
    • dietary support for cell-mediated reactions (e.g. Mast Cell Activation Disorder, MCAD)
    • determining whether there is food intolerance using a Time Food Time Symptom Journal so that foods that trigger symptoms can be avoided or reduced (e.g. nightshade intolerance)

Eating a less inflammatory diet, avoiding gluten-based foods, artificial sugar substitutes, processed foods, and foods high in simple carbohydrates, and non-cultured dairy can be helpful – while learning to eat a nutritionally adequate diet without these foods. In some people, avoiding corn and eggs can also be helpful.

If Mast Cell Activation Disorder (MCAD) is also diagnosed, then along with over-the-counter H1 and H2 antihistamines, and mast cell stabilizing prescription medication, learning how to reduce the amount of histamine and other bioactive amines in the diet can be very helpful in managing symptoms, with the first step being learning which specific foods trigger a reaction. 

How to Encourage Normal Gut Biosis

A diet rich in prebiotics such as Jerusalem artichoke, dandelion greens, garlic, leeks, onion, and asparagus, as well as probiotics such as fermented dairy and vegetables including kefir, yogurt, kimchi, sauerkraut, and salt-cured pickles, can support encouraging a normal gut microbiome.

Eating a diet rich in leafy greens and other non-starchy vegetables, as well as specific types of fruit can provide ample amounts of antioxidants and soluble fiber to support a healthy microbiome.

Vitamin and Mineral Deficiency Common in Ehlers-Danlos Syndrome

There are several micronutrient deficiencies (i.e. vitamins and minerals) that are often present in people with Ehlers-Danlos Syndrome, including vitamin B6 and B12, magnesium, vitamin D, and vitamin C.

Sometimes, nutrient deficiency is present for some other reason other than Ehlers-Danlos Syndrome, such as due to one of the MTHFR polymorphisms, in which case supplementation with the bioavailable form of folate or vitamin B12, is required.

Since deficiencies in these nutrients can make the symptoms of EDS worse, it is important to have lab tests to assess levels of these nutrients in the body, so that appropriate supplementation can occur – and to understand that in some nutrients such as magnesium, routine lab tests may be inadequate to be able to assess low nutrient status.

Whenever possible, it is best to get these vitamins and minerals from food, rather than supplements but that said, some supplements are used in specific situations, such as quercetin in Mast Cell Activation Disorder, or methylated B-vitamins when someone has one of the MTHFR polymorphisms.

Having a Meal Plan designed to support your specific diagnoses (i.e. Ehlers-Danlos Syndrome (EDS), Mast Cell Activation Disorder (MCAD), and/or Postural Orthostatic Tachycardia Syndrome (POTS) is important.

Specific Dietary Recommendations

While there is no specific diet for Ehlers-Danlos Syndrome, following the general recommendations below can be a helpful place to start, before seeking the support of a knowledgeable Dietitian.

    • Avoid refined carbohydrates
    • Limit daily intake of fructose to less than 25g/day, and limit natural sugar substitutes (e.g., stevia, agave)
    • Eliminate sugar substitutes: sugar alcohols (e.g., xylitol, sorbitol), natural sugar substitutes (e.g., stevia, agave), artificial sweeteners (e.g., aspartame)
    • Eliminate artificial colors/flavors, preservatives, stabilizers, and emulsifiers (gums)
    • Eliminate or minimize casein (especially A-1 beta-casein), gluten, and corn (which contains the storage protein zein)
    • Limit cured meat
    • Limit alcohol consumption

More Info?

If you have been diagnosed with Hypermobile Ehlers-Danlos Syndrome (hEDS), Mast Cell Activation Disorder (MCAD) with or without Postural Orthostatic Tachycardia Syndrome (POTS), I can help you minimize your symptoms.

Please visit the landing page to learn about the therapeutic dietary services I offer.

To your good health!

Joy

You can follow me on:

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

References

    1. Hakim A. Hypermobile Ehlers-Danlos Syndrome. 2004 Oct 22 [Updated 2024 Feb 22]. In: Adam MP, Feldman J, Mirzaa GM, et al., editors. GeneReviews® [Internet]. Seattle (WA): University of Washington, Seattle; 1993-2025.
    2. Hakim AJ, Tinkle BT, Francomano CA. Ehlers-Danlos syndromes, hypermobility spectrum disorders, and associated co-morbidities: Reports from EDS ECHO. Am J Med Genet C Semin Med Genet. 2021;187:413-5.
    3. Dr. Heidi Collins MD, Nutritional Approaches to Treating GI Concerns in Persons with Ehlers-Danlos Syndrome, The Ehlers-Danlos Syndrome Society, 2020 Virtual Summer Conference

 

 

Copyright ©2025 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.

Nutrition is BetterByDesign

Extended Benefits: What are Reasonable and Customary Charges?

Approximately 90% of Canadians (87%) have extended health benefit plans; 64% of people have them through their employer, another 14 % access them  through another type of group plan, and 9% of people buy private health insurance [1] and most major insurers (7 out of 10) cover Registered Dietitian services in their standard plan [2]. 

While all Canadian insurers provide coverage for Registered Dietitian services [3], each individual company chooses to purchase (or not) different amounts of coverage for their employees. As a result, insurance coverage varies significantly company to company, even with the same insurer, so it’s important to check with your insurer, or group benefits representative to determine what your yearly limits are for coverage for a Registered Dietitian, as well as how much they cover per visit.

Yearly Limits

Yearly limits for Registered Dietitian services on extended benefits plans frequently range from $500/year to $1500/year however this is only one aspect of what determines the amount that each insurer will reimburse.

Reasonable and Customary Fees

In addition to yearly limits, each plan sets how much they will cover per visit.

Some benefit plans set out how much they will cover for the initial assessment visit and how much they will cover for each subsequent visit. Other plans reimburse the same amount per visit, regardless if it is the initial assessment visit or not — up to the maximum of the yearly limit.

The insurer uses what is called “reasonable and customary fees” to determine the basis for pricing their benefit plans, as well as the basis for reimbursing claims, and these limits are based on the usual cost for a service in each province.

Multi-Province Dietetic Registration

Since the “reasonable and customary fee” is based on the usual cost for the service in each province, my clients in British Columbia, Alberta and Ontario (the three provinces that I am licensed in) have different reasonable and customary amounts related to my services.

Below are the reasonable and customary limits for Dietitian services from five of the major benefit insurers in Canada. As can be seen, the range that the same provider covers in each province for the same service varies widely. 

In pricing my services, I not only take yearly limits into consideration, I also factor in the reasonable and customary fee amounts in each province that I am licensed. 

Reasonable and Customary Charges by Province – 5 different insurers

British Columbia – reasonable and customary limits

For an initial Assessment visit to a Registered Dietitian, benefit plans in British Columbia reimburse from $200/hour, to $180/hour, to $170/hour, to $150/ hour.

For subsequent visits to a Registered Dietitian, benefit plans in British Columbia will reimburse from $170/hour, to $155/hour, to $150/ hour, to $120/hour.

Alberta – reasonable and customary limits

For an initial assessment visit to a Registered Dietitian, benefit plans in Alberta will reimburse from $210/hour, to $195/hour, to $180/hour.

For subsequent visits to a Registered Dietitian, benefit plans in Alberta will reimburse from $190/hour,  to $180/hour, to $165/hour, to $150/ hour, to $127/hour.

Ontario – reasonable and customary limits

For an initial assessment visit to a Registered Dietitian, benefit plans in Ontario will reimburse from $215/hour, to $195/hour, to $150/ hour, to $145/hour.

For subsequent visits to a Registered Dietitian, benefit plans in Ontario will reimburse for from $155/hour,  to $145/hour, to $140/ hour, to $122/hour.

Pricing Based on Inter-Provincial Reasonable and Customary Fee Limits

When planning to go to any paramedical practitioner, including Registered Dietitians, it is important that people keep in mind that because of these reasonable and customary fee limits, how receipts are issued determines how much reimbursement they will get.  Packages must broken down into the individual services that make up the package, and each service must have the date and time it was provided, and the individual cost for that service. 

I ensure that the receipts provided contain all the information that a client’s benefits plan requires, so that reimbursement is maximized, and occurs quickly. Since many extended benefits plans reimburse per visit, all the packages that I offer are broken down into their respective services, beginning with the Initial Assessment visit, and each subsequent visit. The date and time of each service is listed, and the cost of each service.

Below is an example of a receipt for the Comprehensive Dietary Package, but all packages are broken down similarly to maximize refunds and to make reimbursement easy.

Packages Broken Down into Their Individual Services

I have been in private practice since 2008, and I have always charged $150/hour for an Initial Assessment visit, and $100/hour for all subsequent visits in a package. That’s a long time. 

I recently found out that in 2024, the minimum amount covered for subsequent visits from the above five major insurers in the provinces to which I provide services was $127/hour.  I have been billing $100 since 2008.

Beginning January 1, 2025, the costs of subsequent visits will increase to $120/hour — and even with the increase, the new price will remain lower than the Reasonable and Customary Fees for each province to which I provide services. Prices for the Initial Assessment visit will remain $150/hour — the same price it has been since 2008.

Final Thoughts…

The amount that each extended benefits plan reimburses for visits to a Registered Dietitian is based on the reasonable and customary fees in each province.

Beginning on January 1, 2025, the cost of subsequent visits will change to $120/hour, and this is still lower than the Reasonable and Customary Fee limits in each province that I provide services. The cost of an Initial Assessment visit will remain unchanged at $150/hour — the same price it has been since 2008.

If you would like to learn about the many Routine Services, Digestive Health Services, and Therapeutic Diet Services that I provide please have a look the Services tab and to learn about pricing, payment options, and clinical hours, please visit the Book an Appointment tab.  

If you want to maximize your extended benefits for this year, please keep in mind that October, November and December are my busiest months, so I recommend not waiting too long.

I am currently booking ~2-3 weeks ahead, but I do have a cancellation list.

Please check your with your plan provider or company benefits representative to find out what your specific extended benefit plan covers.  

To your good health,

Joy

 

You can follow me on:

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

 

References

 

  1. Coletto, David, Abacus Data, “Canadians and Health Care: Workplace and Group Insurance Plans”, April 6, 2023, https://abacusdata.ca/healthcare-canadians-clhia-workplace-and-group-insurance-plans/
  2. Dietitians of Canada, “Dietitians are the Best Choice for Employee Benefit Plans”, https://www.dietitians.ca/Advocacy/Priority-Issues-(1)/Dietitian-coverage-on-employee-benefits-plans
  3. Dietitians of Canada, “Providing access to nutrition services in employee health benefits plans”, https://www.dietitians.ca/Advocacy/Priority-Issues-(1)/Dietitian-coverage-on-employee-benefits-plans/Nutrition-Services-(Test)

 

Copyright ©2024 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.

 

Nutrition is BetterByDesign

A Keto Diet and a Therapeutic Ketogenic Diet are Very Different

 
 

Introduction

With the release of several books outlining a role in mental health, therapeutic ketogenic diets have grown in popularity. Some people think they are the same as keto diets for weight loss or blood sugar control in type 2 diabetes. They are similar but very different.
 
A therapeutic ketogenic diet is used for ketogenic diet therapy (also called ketogenic metabolic therapy, a type of medical nutrition therapy). A doctor may prescribe it, or a dietitian may implement it under a doctor’s supervision as part of treatment for mental health and other conditions. [1]
 
There is no single “keto diet.” Most keto diets restrict carbohydrates and offer different levels of protein. They usually do not require weighing food or checking blood sugar or ketones, though some people choose to.
 
Therapeutic ketogenic diets tightly control protein and carbohydrate amounts relative to fat. Diet plans such as 4:1, 3:1, or 2:1 require weighing ingredients and monitoring blood glucose and ketones. [1]
 

Therapeutic Ketogenic Diets

Therapeutic ketogenic diets have been used for more than 100 years in the treatment of epilepsy and diabetes, and more recently as adjunct treatment in some types of cancer and in mental health.

These diets are very high in fat, from 65–72% (2:1) up to 90% (4:1). [1] Protein, fat, and carbohydrate are strictly controlled, so ingredients are weighed. Blood glucose and ketone levels are monitored to reach the desired Glucose to Ketone Index (GKI). [1]

Three Types of Therapeutic Ketogenic Diets 

Since a therapeutic ketogenic diet is like a prescription, each ingredient is weighed to achieve the correct ratio, just as medicine has a dosage.

High-fat, low-protein diets such as 4:1 and 3:1 ketogenic diets make Meal Plan design both time-consuming and challenging. It is not easy to come up with palatable food combinations with the precise amounts of protein, fat, and carbohydrate required. Meals in a 4:1 and 3:1 therapeutic ketogenic diet are precise amounts of ingredients that are assembled to be as palatable as possible.

Classic Ketogenic Diet (KD) – 4 : 1

The 4:1 KD is used for epilepsy and seizure disorders, and is sometimes used along with chemo or radiation for cancers like glioblastoma.

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

Depending on the use, protein may be set at 1 g of protein per kg body weight, carbohydrate at 10-15 g per day total, and the remainder of calories provided as fat. Sometimes, protein is set at 10% or 15% of calories, and carbohydrate ranges from 5% – 10% of calories. [1].

Modified Ketogenic Diet (MKD) – 3 : 1 ratio

The Modified Ketogenic Diet (MKD) has a 3:1 ratio, i.e., 3 parts fat for every 1 part protein and carbohydrate, with 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.

Modified Atkins Diet (MAD) – 2 : 1 ratio

The Modified Atkins Diet (MAD) has a 2:1 ratio, with 2 parts fat for every 1 part protein and carbohydrate. Fat is set at 60% of calories, protein at 30% of calories, and carbohydrate at 10% of calories.

The Popularized “Keto Diet”

There is no one “keto diet”, but rather a range of keto diets.  They all limit carbs to about 10% of daily calories to encourage ketone production.
 
The popular high-fat / moderate protein version of a keto diet with ~75% fat and 15% protein is commonly referred to as “the keto diet,” but as outlined below, this is not the only keto diet, nor the first.  The high-fat, moderate-protein version (~75% fat, 15% protein) became popular in 2016 with the publication of Dr. Jason Fung’s two books, The Obesity Code [2] and The Complete Guide to Fasting [3], as well as Dr. Andreas Eenfeldt’s The Low Carb, High Fat Revolution [4].
 
Unlike therapeutic diets, protein is not tightly regulated in the popularized keto diet. Food does not need to be weighed, and ketones do not need to be monitored. These diets are often used for weight loss or blood sugar control, but are not therapeutic diets.
 
Earlier keto diets include the high-protein/moderate-fat diet in Protein Power (1997) by Drs. Michael and Mary Dan Eades [5], and The New Atkins For a New You (2010) by Drs. Eric Westman, Stephen Phinney, and Jeff Volek [6]. Unlike modern keto, New Atkins was very high fat and very low carbohydrate (20–50 g/day) during phase one, which lasts the first two weeks. [5][6]
 

A Well-Formulated Ketogenic Diet

Shortly after completing the 2010 book, New Atkins for a New You, with Dr. Eric Westman,  Dr. Stephen Phinney (an MD), and Dr. Jeff Volek (a Registered Dietitian) wrote their book, The Art and Science of Low Carbohydrate Living [7].  Since ketosis can occur within a fat intake range between 65-85% of calories [pg. 77], protein intake can range from 21-30% and still result in a “well-formulated ketogenic diet”. 
 
Although this diet specifies the amount of protein, fat, and carbs for weight loss and maintenance, it is not classified as a therapeutic ketogenic diet.  Carbohydrate for men ranges from 7.5–10%, and for women, between 2.5–6.5%, and protein can be as high as 30% for either gender. Fat is restricted to 60% during weight loss, and 65–72% during maintenance.
 
It is my opinion, a well-formulated ketogenic diet containing 21–30% protein [7] is preferable for older adults to the 15% protein provided by popularized keto diets, as the higher amount will help older adults retain muscle mass and avoid sarcopenia.
 

Final Thoughts…

Both therapeutic ketogenic diets and keto diets limit carbohydrates, but therapeutic diets also tightly control protein. Therapeutic ketogenic diets also require precise weighing and tracking of glucose and ketones, as these diets are dietary prescriptions.

Meals high in bacon, eggs, and meat, common in popularized keto diets, are not part of therapeutic ketogenic diets. 
 
While popularized keto diets offer benefits such as weight loss and improved blood sugar, they are not therapeutic diets.
 
There is no one-size-fits-all therapeutic ketogenic diet or keto diet. There are different types of therapeutic ketogenic diets and a range of keto diets that can be utilized, depending on an individual’s needs and goals.
 
I design both therapeutic ketogenic diets and different types of keto diets and support people in implementing and transitioning to other types of ketogenic diets.
 

To your good health,

Joy

 

You can follow me on:

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

 
 

References

 
  1. Kossoff, Eric & Turner, Zahava & Cervenka, Mackenzie & Barron, Bobbie. (2020). Ketogenic Diet Therapies For Epilepsy and Other Conditions. 10.1891/9780826149596.
  2. Fung J (2016) Obesity Code, Greystone Books, Vancouver
  3. Fung J, Moore J (2016), The complete guide to fasting: heal your body through intermittent, alternate-day, and extended fasting, Victory Belt Publishing
  4. Eenfeldt A, Low Carb, High Fat Food Revolution: Advice and Recipes to Improve Your Health and Reduce Your Weight (2017), Skyhorse Publishers
  5. Eades M, Dan Eades M (1997), Protein Power: The High-Protein/Low-Carbohydrate Way to Lose Weight, Feel Fit, and Boost Your Health—in Just Weeks! Bantam; New edition (1 December 1997)
  6. Westman E, Phinney SD, Volek J, (2010) The New Atkins for a New You — the Ultimate Diet for Shedding Weight and Feeling Great, Atria Books February 17, 2010)
  7. Volek JS, Phinney SD, The Art and Science of Low Carbohydrate Living: An Expert Guide, Beyond Obesity, 2011

 

Copyright ©2024 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.

 

 

Nutrition is BetterByDesign

International Diabetes Federation – evidence for 1-hour glucose assessor

International Diabetes Federation has just released a new Position Statement that indicates that an oral glucose tolerance test performed at 1-hour after a glucose load is more effective in screening at-risk individuals for prediabetes and type 2 diabetes than a 2-hour Oral Glucose Tolerance Test (OGTT). 

The International Diabetes Federation is a non-profit umbrella organization of more than 240 national diabetes associations from 161 countries including the United States (represented by the American Diabetes Association), Canada, Australia, as well as many countries in Europe, Asia and Africa. This global reach means that the IDF’s reports and recommendations have significant international implications.

This international Position Statement provides the evidence to support the practice of requisitioning a 1-hour post load glucose test in place of 2 hour Oral Glucose Tolerance Test to diagnose prediabetes and type 2 diabetes in at-risk individuals.

For physicians who prefer to choose to continue to order a 2-hour Oral Glucose Tolerance Test, this new Position Statement provides support for adding an additional extra assessor at 1-hour, something I have asked for over the last several years based on existing evidence

Prediction of Risk of Type 2 Diabetes

The new Position Statement highlights that a 1-hour post-load plasma glucose level of 8.6 mmol/L (155 mg/dL) or higher during in people with normal glucose tolerance strongly predicts the development of type 2 diabetes as well as various complications such as micro- and macrovascular issues, obstructive sleep apnea, metabolic dysfunction-associated fatty liver disease, and death in individuals with risk factors. The recommendations are for  individuals with 1-hour plasma glucose of 8.6 mmol/L (155 mg/dL) or higher to be prescribed lifestyle intervention and referred to a diabetes prevention program.

Diagnosis of Type 2 Diabetes

The Position Statement indicates that a  1-hour post-load plasma glucose level of 11.6 mmol/L (209 mg/dL) or higher confirms a diagnosis of type 2 diabetes and recommends that a repeat test be conducted to confirm the diagnosis of type 2 diabetes and once confirmed, to refer the individual for treatment.

Benefits of the 1-hour Post-Load Glucose Test

The Position Statement indicates that the 1-hour post glucose load test;

    1. shows glucose dysregulation earlier than the 2-hour post glucose load test
    2. provides an opportunity to avoid misclassification of glucose status if fasting blood glucose or HbA1c are used alone.
    3. predicts diabetes and associated complications including death in populations of different ethnicity, sex and age
    4. allows for early detection in high-risk individuals which enables the ability to provide intervention to prevent a progression to type 2 diabetes.

Conclusion

The conclusion of the International Diabetes Federation Position Statement is that there is strong evidence to support redefining current diagnostic criteria for prediabetes and type 2 diabetes to include testing at 1-hour post glucose during an Oral Glucose Tolerance Test.

Final Thoughts

There is strong evidence for the use of a 1-hour post glucose load test to diagnose or rule out prediabetes or type 2 diabetes in at-risk individuals.

Most significantly, use of the 1-hour post glucose load test allows for early detection and provision of dietary and lifestyle intervention support to prevent the progression to type 2 diabetes. 

To your good health,

Joy

 

You can follow me on:

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

Reference

 

  1. Bergman M,  Manco M., Satman I., et al, International Diabetes Federation Position Statement on the 1-hour post-load plasma glucose for the diagnosis of intermediate hyperglycaemia and type 2 diabetes, Diabetes Research and Clinical Practice, Vol. 209, 111589, March 6, 2024 https://doi.org/10.1016/j.diabres.2024.111589

 

Copyright ©2024 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.

 

 

Nutrition is BetterByDesign

DEXA Bone Density Scans – accuracy depends on where it is done

If you are considering having a DEXA bone density scan to assess your risk of osteoporosis, where you have it done will significantly impact the accuracy of the results, and whether they will provide you with the information you want.

While dual-energy X-ray absorptiometry (DEXA) bone density scans are considered the gold standard for assessing bone mineral density (BMD), it is important to note that there is a large difference in the accuracy of DEXA scans obtained from non-accredited imaging centers offering bone density scans as a service, and facilities specializing in bone densitometry (the clinical assessment of bone density). An accurate scan enables doctors to rule out or establish a diagnosis and provides opportunity for timely treatment recommendations, including dietary and lifestyle modifications.

To illustrate the difference, the first part of the article will explain the standards for accredited facilities, and then contrast them to non-accredited imaging centers. This comparison will underscore the differences between the two.

Accredited Facilities for DEXA Bone Density Scans

For bone density scan data to be reliable in ruling out or diagnosing osteopenia or osteoporosis, it’s important that the scans are conducted by a trained bone densitometry technologist, in a facility that adheres to accreditation standards established by the International Society for Clinical Densitometry (ISCD), and in Canada, by the local College of Physicians and Surgeons of the province. Finally, the scans must be reviewed by a Radiologist, a doctor who specializes in medical imaging before a report is generated.

In British Columbia, the accreditation of bone densitometry facilities as well ensuring that bone densitometry technologists have the appropriate training is overseen by the College of Physicians and Surgeons of British Columbia (CPSBC). They operate the Diagnostic Accreditation Program (DAP), which ensures the quality and safety of a range of diagnostic services, including DEXA bone density scans. The DAP not only verifies that a facility meets the necessary quality standards but ensures that they consistently maintain those standards.

Accredited facilities must adhere to the Accreditation Standards for Diagnostic Imaging from the College of Physicians and Surgeons(1). This comprehensive 312 page document contains imaging standards for x-rays, mammograms, ultrasounds, MRIs , with the standards for bone densitometry beginning on page 274. These standards ensure the quality and safety of bone density scanning procedures.

These standards also outline that bone densitometry facilities must have a Medical Director overseeing operations, and that bone densitometry technologists performing scans must either be certified with the International Society for Clinical Densitometry (ISCD), or have obtained 12 Continuing Medical Education (CME) credits in bone densitometry. Additionally, technologists in accredited facilities are mandated to regularly update their knowledge by acquiring 24 CME credits in bone densitometry every three years.

Summary of the Accreditation Standards for Diagnostic Imaging for Bone Densitometry

The bone densitometry section of the Accreditation Standards for Diagnostic Imaging (1) consists of ten pages of standards, including;

    • patient preparation for the exam
    • standard imaging procedure protocols to ensure that the examination is appropriate for its intended use in clinical decision making
    • ensuring that current and accurate medical records are kept for each person
    • that diagnostic reports are in a standardized format and provide comprehensive and necessary information for clinical decision making / interpretation 
    • safe operation and maintenance of equipment
    • acceptance testing for equipment to ensure it is tested prior to use, and quality assurance programs to ensure that the required quality is attained

These standards provide additional mandatory requirements and best practices that supplement the accreditation standards established by the International Society for Clinical Densitometry (ISCD) (2).

Below is the first of the ten pages of standards (this page is on patient preparation).

from page 375 of 312, CPSBC Accreditation Standards for Diagnostic Imaging for Bone Densitometry (1)
from page 375 of 312, CPSBC Accreditation Standards for Diagnostic Imaging for Bone Densitometry (1)

These standards require that the following information be collected before a bone density scan takes place.

(1) taking clinically relevant medical history, including family history, prior fractures, bone trauma, surgery, chronic illness, and any relevant medication that may affect bone density such as corticosteroids, or thyroid medications. 

(2) ensuring that the person has not had any procedures such as a barium x-ray or radionucleotide study that can affect the results,

(3) assessing whether the person has arthritis, deformity or other degenerative changes that can affect measurement,

(4) ensuring the person hasn’t had any implants in the area being assessed, such as a hip replacement,

(5) that a qualified physician is involved in assessing any interference or contraindications,

(6) review of previous bone density scans to determine if a specific site should be excluded from the current scan,

(7) patient height and weight are accurately measured at the time of examination.

None of this, or any of the other 9 pages of standards are required to be followed in an imaging center that provides bone density scans as a service. 

Imaging Center Providing DEXA bone density scans

Imaging centers that provide DEXA bone density scans as a service are businesses, and as such are not clinically regulated.  There are no physicians or radiologists involved. These businesses are not required to meet the international standards of the International Society for Clinical Densitometry (ISCD), or local clinical standards outlined above.

For example, these centres may assess the person’s height using a tape measure or meter stick attached to a wall, rather than a stadiometer. Weight may not even be measured — or even asked, but calculated from the results of a whole body composition scan performed at the same time. Estimating height and weight does not provide the quality data required to interpret the results of the Dexa scan. In addition, questions about personal medical history, family medical history, risk factors, medications or procedures that could affect results are limited, or non-existent.

Image Quality

In accredited facilities, rigorous standards are in place to ensure high image quality, as all scans undergo review by a radiologist prior to report generation.

Images are required to be clear and well defined, such as the top pair of images from HealthLink BC (3). 

Images from imaging centers, such as the pair of images on the bottom often lack the contrast and definition which limits their usefulness.

 

Measurement Accuracy – hips

For hip scans to be useful in diagnosing osteoporosis, it is essential that the neck of the femur (hip bone) is measured at the narrowest part (4), such as the image on the far right (4).

The image on the left from an imaging center does not measure the neck of the femur at the narrowest part, and as illustrated in the middle image, the narrowest part is to the right of where it was measured.

Measurement Accuracy – spine

Spinal images from accredited facilities (left photo from (4)) are clear, and show equal amounts of soft tissue on either side of the spine. In addition, the height of each vertebrae is roughly the same height, with markers in the disk space (4).

   

The image on the right from an imaging center is not clear and has little contrast. It does not show equal amounts of soft tissue on either side of the spine, and the height of each vertebrae varies considerably.

Finding an Accredited Facility

In British Columbia, a full list of accredited diagnostic imaging facilities in the province is available on the College of Physicians and Surgeons web site (5).

The International Society for Clinical Densitometry (ISCD) has a searchable list of accredited facilities by country, as well as US states and Canadian provinces.

The College of Physicians and Surgeons in your province or state may also have a list.

Final Thoughts…

For data from a DEXA bone density scan to be reliable and useful for ruling out or diagnosing osteopenia or osteoporosis, it needs to be performed at an accredited facility.

This can be compared to the difference between home lab test testing and lab tests. While at-home blood testing kits are available to screen for different conditions, diagnoses of a medical condition requires blood tests from an accredited laboratory that are reviewed and assessed by a physician.

If you want to have a DEXA bone density scan to assess your risk of osteoporosis, then speak with your doctor to get a referral to an accredited facility.

How I Can Help

If you have been diagnosed as being at risk for osteoporosis, or have been diagnosed with osteopenia or osteoporosis, implementing appropriate dietary and lifestyle changes can be beneficial.  Please let me know if you would like some support.

To your good health,

Joy

 

You can follow me on:

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

 

References

  1. College of Physicians and Surgeons of British Columbia, Accreditation Standards, Diagnostic Imaging, https://www.cpsbc.ca/accredited-facilities/dap/accreditation-standards-DI
  2. International Society for Clinical Densitometry (ISCD), Official Positions, DEXA Best Practices, https://iscd.org/wp-content/uploads/2021/08/Best-Practices-DXA-Article.pdf
  3. Health Link BC, Bone Density Tests, Treatments, Medications Categories, Media Gallery, https://www.healthlinkbc.ca/tests-treatments-medications/medical-tests/bone-density
  4. Bone Health & Osteoporosis Foundation, DXA Basics- ISO 2021 Interdisciplinary Symposium on Osteoporosis ISO 2024, https://interdisciplinarysymposiumosteoporosis.org/
  5. College of Physicians and Surgeons of British Columbia, Provisional Accreditation Facilities – Diagnostic Imaging, https://www.cpsbc.ca/files/pdf/DAP-Accredited-Facilities-DI.pdf

 

Copyright ©2024 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.

 

Nutrition is BetterByDesign

 

DEXA Body Composition Scans as Assessors of Bone Density

DEXA Bone Density Scans are the gold standard for assessing the quality of the inside of bone, and determining whether a person has osteopenia or osteoporosis. More on those scans, soon.

A DEXA Body Composition Scan is designed for assessing the amount of body fat and the distribution of that fat, yet often come with a report that includes “bone mineral density” information. It is essential to understand that “bone mineral density” on a DEXA Body Composition Scan is estimated, not measured. 

This article is about the DEXA Body Composition Scan and what information it reliably provides.

NOTE: (February 14, 2024) If you are thinking of having a DEXA Body Composition Scan, be sure the facility you choose is accredited by the College of Physicians and Surgeons in your area.  More on this in the next article!

DEXA Body Composition Scan

The DEXA Body Composition Scan measures

(a) total amount of fat mass in grams, and

(2) total amount of Lean Body Mass plus bone, in grams.

It does not measure bone mass, but adds both lean body mass and bone mass together. This is important because reports that often accompanying DEXA Body Composition Scans include information about “bone mineral density”, but this information is estimated, rather than assessed. 

The DEXA Body Composition Scan reliably indicates how much total fat someone has, and the distribution of that fat over the body. It does not differentiate between sub-cutaneous fat (the fat under the skin) and visceral fat (the fat around the organs) which is associated with increased health risk.

Since fat mass is what is being directly evaluated in a DEXA Body Composition Scan, the total amount of body fat determined by this method is accurate.

DEXA Body Composition Scan Data of Fat and Lean 

Below are two pages from a DEXA Body Composition Scan report. 

Body Fat Composition and Total Lean Body Mass (muscle) plus bone
Body Fat Composition and Total Lean Body Mass (muscle) plus bone

This above page from a DEXA Body Composition Scan report is mostly related to what it assesses directly, which is Total Fat Mass in grams, and Lean Body Mass plus bone in grams, and evaluates the distribution of that fat.

While a DEXA Body Composition Scan does not differentiate between subcutaneous fat and visceral fat, the report indicates “Estimated Visceral Adipose Tissue (fat)” in the table of adipose (fat) indices. It is important to note that visceral fat is not assessed, but estimated. 

DEXA scanners (both GE and Hologic brands) have the National Health and Nutrition Examination Survey (NHANES) data integrated into their software, this which enables them to generate Z-scores for total amount of fat in grams, as well as localized Z-scores for fat in arms, legs, and trunk (1).

Z-scores compare the an individual subject’s results to those of an aged-matched population, and since a DEXA Body Composition Scan measures total fat directly, the z-score in this report for adiposity (fat) is valid.

T-scores compare an individual’s results to how many standard deviations it is from the results of a 30-year old young adult, and since a DEXA Body Composition Scan measures total fat directly, the t-score for adiposity (fat) is also valid.

DEXA Body Composition Scan Data on Bone Mineral Density and Bone Mineral Composition

This is where reports that may be provided with a DEXA Body Composition Scan can get really crazy.

A DEXA Body Composition Scan does not differentiate between Lean Body Mass as muscle and bone, so any information about “bone mineral density” and “bone mineral composition” is based on estimations!  

Whole Body Composition Scan - estimation of Bone Mineral Content and Bone Mineral Density
Whole Body Composition Scan – estimation of Bone Mineral Content and Bone Mineral Density

Since there is no measurement of bone mass in grams separate from Lean Body Mass (muscle),  z-scores for “Bone Mass Density” from a Whole Body Composition Scan make no sense.  This is a comparison of estimated bone data to actual data from an aged-matched population! 


Have a look at the table below from a 55 year old woman whose DEXA Body Composition Scan report indicates that she had osteoporosis based on estimated bone density numbers. Without having a DEXA Bone Density Scan, of both hips and lower spine she really doesn’t know if she has osteopenia or osteoporosis or not. A DEXA Body Composition Scan is designed to assess fat mass and the distribution of that fat, not bone.

"Bone Mineral Density" based on a DEXA Whole Body Scan
“Bone Mineral Density” based on a DEXA Whole Body Scan

Final Thoughts…

If you have had a DEXA Body Composition Scan and been told that you have osteopenia or osteoporosis remember that this is based on estimates of total amount of bone, and not actual measurement of bone. In such a case, I would recommend discussing with your doctor having a DEXA Bone Density Scan of both hips and lower spine.

If the DEXA Bone Density Scan indicates that you meet the criteria for osteopenia or osteoporosis, then meet with you doctor to discuss the results and their recommendations. In some cases, a doctor may recommend medication to keep bone from breaking down too quickly, and/or a program designed by a Physical Therapist to enable you to safely exercise and retain as much of bone mass you still have, while minimizing the risk of fractures. 

Take Away Message

Remember, that estimated data of “bone mineral density” from a DEXA Body Composition Scan is not the same as data from a DEXA Bone Mineral Density scan which is based on direct assessments.

Getting accurate information using the right diagnostic tool is essential.

How I Can Help

If you are an older adult who wants to optimize your diet and lifestyle to retain as much bone mass as possible as you age, I can help.

To your good health,

Joy

 

You can follow me on:

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

Reference

  1. Shepherd JA, Ng BK, Sommer MJ, Heymsfield SB. Body composition by DXA. Bone. 2017 Nov;104:101-105. doi: 10.1016/j.bone.2017.06.010. Epub 2017 Jun 16. PMID: 28625918; PMCID: PMC5659281.

 

 

Copyright ©2024 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.

 

Nutrition is BetterByDesign

Is Animal-based and Plant-based Protein Equivalent?

Note: This article was originally posted on August 20, 2023, and was revised and reposted on November 2, 2025. It now includes the latest research on protein quality, amino acid bioavailability, and the Digestible Indispensable Amino Acid Score (DIAAS). References and recommendations for both plant and animal proteins have been updated for accuracy.

Some people are considering going “plant-based” for perceived health reasons or for ethical considerations, and while these are important, evaluating plant protein quality is also necessary. Assessing protein quality using the Digestible Indispensable Amino Acid Score (DIAAS) can help identify the best sources of protein for maintaining and building muscle.

A recent study found that essential amino acids from animal protein are more bioavailable than those from plant protein [1]. These findings are especially important for older adults who need to preserve muscle mass, and for active adults wanting to build or repair muscle.

Amino Acids and Bioavailability

Amino acids are the building blocks of protein, including muscle. There are twenty amino acids, divided into two groups: essential amino acids (EAA) and non-essential amino acids.

Bioavailability refers to the degree to which essential amino acids in food can be used by the body to build its own proteins [2], such as muscle tissue.

Essential amino acids, including leucine, must be consumed in the diet because the body cannot make them. Leucine plays a key role in muscle growth and repair by triggering mTOR signaling in muscle cells, which stimulates protein synthesis [3].

Dietary recommendations for older adults emphasize obtaining about 2.3 g of leucine per meal to support muscle growth [4], and around 3 g per meal to rebuild muscle after exercise [5].

Recent research suggests a practical target range of 2.5–3.0 g of leucine per main meal, roughly equivalent to 25–30 g of high-quality protein. This level best supports muscle protein synthesis in older adults and enhances recovery when paired with light resistance exercise — such as a breakfast of eggs or Greek yogurt.

Plant Protein vs. Animal Protein for Building Muscle

Plant proteins generally contain lower levels of leucine than animal proteins [6]. People choosing a more plant-based diet often rely on legumes like beans or lentils for protein. However, most legumes are incomplete proteins, meaning they lack one or more essential amino acids.

For example:

  • Lentils contain about 0.7 g of leucine per half cup.

  • Chickpeas contain about 0.42 g of leucine per half cup.

An older adult would need to eat more than 3 cups of lentils or 5½ cups of chickpeas at one meal to reach the 2.3 g leucine threshold needed to trigger muscle protein synthesis.

Is Plant Protein Equivalent to Animal Protein?

A randomized, investigator-blinded, crossover study was conducted with both young and older adults [1]. Researchers compared ounce-equivalents (oz-eq) of animal-based protein (lean pork or whole eggs) with plant-based protein (black beans or sliced almonds) in a mixed meal. The goal was to determine how efficiently the body uses amino acids from each source.

The Dietary Guidelines for Americans (DGA) defines ounce-equivalents to identify protein foods with similar nutritional content [7]. However, the researchers noted that the assumption of “equivalence” between these sources is questionable.

For instance, one ounce-equivalent of pork loin provides about 7 g of protein, while one ounce-equivalent of almonds provides only 3 g [1]. Beyond quantity, protein quality — the digestibility and bioavailability of essential amino acids — also differs substantially between these sources.

The Bioavailability of Plant Protein – Digestible Indispensable Amino Acid Score (DIAAS)

In 2013, the Food and Agriculture Organization (FAO) introduced the DIAAS method to replace the older PDCAAS system for assessing protein quality [9].

DIAAS measures how well individual essential amino acids are digested and absorbed at the end of the small intestine, giving a clearer picture of how well the protein supports the body’s needs.

High-quality proteins have a DIAAS ≥100, while scores of 75–99 are considered good, and <75 cannot make a quality protein claim [8].

  • Most grains and legumes score below 75.

  • Pea and soy protein range from 75–100.

  • Animal proteins such as beef typically score well above 100 [10].

Although DIAAS provides a more accurate measure of protein quality, it has not yet been adopted for food labeling in Canada or the U.S. Implementation will require regulatory review and harmonized data across food categories. Until then, dietitians and consumers can use academic data to understand the real quality of different protein sources.

Plant Protein versus Animal Protein – What Studies Show

The recent trial found that meals containing animal-based proteins resulted in higher blood levels of essential amino acids compared with meals made from plant-based proteins — in both young and older adults [1].

Additionally, lean pork produced greater amino acid bioavailability than eggs, and no difference was found between black beans and almonds.

Researchers concluded that it is inaccurate to treat different protein sources as equivalent based on ounce-equivalents alone.

Final Thoughts

If you are an active adult wanting to build and repair muscle, or an older adult aiming to maintain strength, it’s essential to choose high-quality proteins that contain all essential amino acids — especially leucine. While the DGA lists one ounce of meat, one egg, 0.25 cups of beans, or 0.5 ounces of nuts as equivalent, this study shows they are not truly equivalent in quality or bioavailability.

If you are exploring a more plant-based lifestyle, understanding the science of protein bioavailability can help you make informed, health-supporting choices.

For those following a vegetarian or vegan diet for ethical or cultural reasons, combining complementary plant proteins and choosing higher-DIAAS options like soy or pea protein can help you meet your needs.

More Info

If you would like support ensuring that you or someone you love eats sufficient high-quality protein at each meal to trigger muscle synthesis, please reach out through the Contact Me form, available on the tab above.

To your good health,

Joy

Follow Me

Twitter (X): https://x.com/jyerdile
Facebook: https://www.facebook.com/BetterByDesignNutrition/

References

[1] Connolly G, Hudson JL, Bergia RE, Davis EM, Hartman AS, Zhu W, Carroll CC, Campbell WW. Effects of Consuming Ounce-Equivalent Portions of Animal- vs. Plant-Based Protein Foods, as Defined by the Dietary Guidelines for Americans, on Essential Amino Acid Bioavailability in Young and Older Adults: Two Cross-Over Randomized Controlled Trials. Nutrients. 2023; 15(13): 2870. https://doi.org/10.3390/nu15132870

[2] Gaudichon C, Calvez J. Determinants of Amino Acid Bioavailability from Ingested Protein in Relation to Gut Health. Curr Opin Clin Nutr Metab Care. 2021 Jan; 24(1): 55-61. doi: 10.1097/MCO.0000000000000708. PMID: 33093304; PMCID: PMC7752214. [https://pubmed.ncbi.nlm.nih.gov/33093304/]

[3] Norton LE, Layman DK. Leucine Regulates Translation Initiation of Protein Synthesis in Skeletal Muscle after Exercise. J Nutr. 2006 Feb; 136(2 Suppl): 533S–537S. doi: 10.1093/jn/136.2.533S. [https://www.sciencedirect.com/science/article/pii/S0022316622080956]

[4] Bauer J, 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. doi: 10.1016/j.jamda.2013.05.021. [https://pubmed.ncbi.nlm.nih.gov/23867520/]

[5] Thomas DT, Erdman KA, Burke LM. American College of Sports Medicine Joint Position Statement: Nutrition and Athletic Performance. Med Sci Sports Exerc. 2016 Mar; 48(3): 543–568. doi: 10.1249/MSS.0000000000000852. Correction in Med Sci Sports Exerc. 2017 Jan; 49(1): 222. [https://pubmed.ncbi.nlm.nih.gov/26891166/]

[6] Berrazaga I, Micard V, Gueugneau M, Walrand S. The Role of the Anabolic Properties of Plant- versus Animal-Based Protein Sources in Supporting Muscle Mass Maintenance: A Critical Review. Nutrients. 2019 Aug 7; 11(8): 1825. doi: 10.3390/nu11081825. PMCID: PMC6723444. [https://pubmed.ncbi.nlm.nih.gov/31394788/]

[7] U.S. Department of Agriculture and U.S. Department of Health and Human Services. Dietary Guidelines for Americans, 2020–2025, 9th ed. Washington, DC: U.S. Government Publishing Office; 2020. Available from: https://www.dietaryguidelines.gov

[8] Herreman L, Nommensen P, Pennings B, Laus MC. Comprehensive Overview of the Quality of Plant- and Animal-Sourced Proteins Based on the Digestible Indispensable Amino Acid Score. Food Sci Nutr. 2020; 8(9): 5379–5391. https://doi.org/10.1002/fsn3.1809

[9] Food and Agriculture Organization of the United Nations. Dietary Protein Quality Evaluation in Human Nutrition (FAO Food and Nutrition Paper 92). Rome, Italy: FAO; 2013. Available from: https://www.fao.org/3/i3124e/i3124e.pdf

[10] Marinangeli CPF, House JD. Potential Impact of the Digestible Indispensable Amino Acid Score as a Measure of Protein Quality on Dietary Regulations and Health. Nutr Rev. 2017 Aug 1; 75(8): 658–667. doi: 10.1093/nutrit/nux025. PMCID: PMC5914309. [https://pubmed.ncbi.nlm.nih.gov/28969364/]

 

Copyright ©2023 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.

 

 

Nutrition is BetterByDesign

Why A Smoothie is “Pre-Chewed” Food

 

Note: This article was originally posted on August 13, 2023, and was updated and reposted on November 25, 2025

Introduction

In the interest of time, many people throw a cup or more of fruit, some green veggies, and maybe some protein powder into a blender to make a smoothie for breakfast. But most people don’t realize how blending affects their blood sugar, gut microbiome, and how much food they eat.

Making a Smoothie

A smoothie as "pre-chewed food"

For people with challenges keeping blood sugar stable, or having pre-diabetes or diabetes, a smoothie made with fruit is something to reconsider. Pureed fruit affects blood sugar very differently from eating the same type and amount of fruit, whole and intact. 

Cellular versus Acellular Carbohydrate

Cellular carbohydrates come from whole, intact foods where the carbohydrate is still inside the cell wall. These foods take longer to digest and to be absorbed into the bloodstream than ground or pureed foods.

Carbohydrates that have been pureed, like fruit in a smoothie, or ground, like flour made from grain, are now outside their cell wall (acellular carbohydrate). As a result, pureed and ground foods are digested more quickly because the fiber that normally slows absorption is disrupted.

A Smoothie as “Pre-Chewed” Food

Most people think digestion begins in the stomach, but it starts in the mouth, when we chew food. As unappealing as it sounds, smoothies are “pre-chewed” food.

Drinking carbohydrates, rather than eating them, can result in spikes in blood sugar, affect gut bacteria, and can even impact how much food we eat due to hunger that follows a quick rise and then fall in blood sugar from the insulin response to quickly digested carbs.

Research shows that when fruit is pureed or juiced, blood glucose rises more rapidly and remains higher than when the same fruit is eaten whole [1]. This occurs because the blender has already broken down the cell walls, doing some of the work that chewing would normally do. For people with higher than ideal blood sugar, or pre-diabetes or diabetes, drinking a morning smoothie instead of eating the same foods intact can lead to a significantly different blood sugar response.

It is important to note that 60 g of whole fruit, 60 g of pureed fruit, and 60 g of juiced fruit all contain the same amount of carbohydrate and have similar Glycemic Index (GI) values. But the GI only tells us how quickly a food raises blood sugar, not how high blood sugar will go. Recent research also emphasizes that food structure, not just carbohydrate content, plays a critical role in blood glucose control [2].

Whole berries or fruit (cellular carbohydrate) are preserved within their cell walls until the digestive juices in the stomach begin to break them down. Once released, the carbohydrate is then absorbed mainly in the large intestine (colon).

Acellular carbohydrates, such as the fruit in smoothies, begin digestion in the small intestine rather than the colon. Early digestion of acellular carbohydrates can alter gut microbial fermentation and is thought to contribute to an imbalance in gut microbes (gut dysbiosis) or leaky gut (increased intestinal permeability) [3].

Drinking carbohydrate-containing foods, rather than eating them, may promote overconsumption and contribute to leptin resistance. Leptin is the hormone that signals us when we are hungry via a negative feedback loop. This feedback loop is thought to become dysregulated when we consume large amounts of acellular carbohydrates, such as pureed fruit. Leptin resistance occurs when the body fails to respond properly to leptin. Some research suggests that acellular carbohydrates alter leptin signaling, increase inflammation, and disturb the gut microbiota, which over time can blunt the body’s feedback loop that signals the brain that we are full [4].

Final Thoughts

Digestion begins in the mouth when we chew food, and there is a big difference between how whole, intact carbohydrates are absorbed and how blended smoothies are absorbed.

Smoothies are “pre-chewed food” that can disrupt blood sugar, alter our gut microbiome, and increase the total amount of food we consume.

Instead of throwing fruit, veggies, and protein powder into a blender, reach for half a cup of berries to put over top a cup of cottage cheese or plain Greek yogourt with a few spoons of hemp hearts, and grab a handful of snap peas or baby carrots. This quick, light meal that has the protein and leucine adults need to preserve their muscle mass — and there is no blender to clean afterwards!

More Info

I understand that not everyone who wants to eat healthy loves to cook. I am experienced at designing Meal Plans using readily available foods that require minimal preparation and little to no cooking. Whether you love to cook or prefer simplicity, I can help. You can learn more under the Services tab. 

To your good health, 

Joy

You can follow me on:

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

 

References

[1] Haber GB, Heaton KW, Murphy D, Legg NJ. 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. [https://pubmed.ncbi.nlm.nih.gov/71495/]

[2] Forde CG, Frank T, Leong C. Interrelations Between Food Form, Texture, and Matrix. Nutrients. 2022;14(4):731. doi:10.3390/nu14040731 [https://pmc.ncbi.nlm.nih.gov/articles/PMC9174310/]

[3] Stull AJ, Apolzan JW, Thalacker-Mercer AE, Iglay HB, Campbell WW. Liquid and solid meal replacement products differentially affect postprandial appetite and food intake in older adults. J Am Diet Assoc. 2008 Jul;108(7):1226-30. doi: 10.1016/j.jada.2008.04.014. PMID: 18589034; PMCID: PMC2556245. [https://pubmed.ncbi.nlm.nih.gov/18589034/]

[4] Spreadbury I. Comparison with ancestral diets suggests dense acellular carbohydrates promote an inflammatory microbiota, and may be the primary dietary cause of leptin resistance and obesity. Diabetes Metab Syndr Obes. 2012;5:175-89. doi: 10.2147/DMSO.S33473. Epub 2012 Jul 6. PMID: 22826636; PMCID: PMC3402009. [https://pubmed.ncbi.nlm.nih.gov/22826636/]

 

 

Copyright ©2023 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.

Nutrition is BetterByDesign

 

Types of Protein to Help Older Adults Retain Muscle

 

Note: this article was originally posted on August 11, 2023, and has been updated and reposted on November 23, 2025.

Understanding Sarcopenia

The inability to retain muscle and strength associated with aging is called sarcopenia. Since adults lose approximately 1% of muscle mass each year after the age of thirty [1], knowing how to retain muscle as an adult is essential, even though the decline in strength normally only becomes noticeable by age fifty [2].

Muscle loss affects 5–13% of adults between sixty and seventy, and up to 50% of adults over eighty years of age have sarcopenia [2].

Inability to retain muscle affects mobility Not being able to retain muscle mass reduces activity levels, lowers quality of life, increases risk of falls, and worsens metabolic and bone health [3].

Most people have never paid close attention to the amount and quality of protein they eat, often choosing foods based on taste, cost, or ethical or religious reasons. These are important considerations, but they are not the only ones that matter.  As outlined in a previous article on protein for older adults, high-quality protein containing sufficient leucine is necessary for maintaining muscle [4], but not all protein foods are equal.

Amino acids are the building blocks of protein, including muscle. There are twenty amino acids, grouped as essential or non-essential. Essential amino acids, such as leucine, cannot be produced by the body in sufficient amounts and must be obtained through diet [5].

The leucine content of protein is critical because leucine triggers mTOR signaling in muscle, which stimulates muscle protein synthesis. For this reason, proteins consumed by older adults must contain enough leucine to support muscle maintenance and mobility[5].

Plant proteins generally contain lower levels of leucine compared to animal proteins [7]. Grains such as wheat contain less than 7% leucine [6], and even quinoa, considered a “complete protein,” contains only 4.5% leucine [6]. People who want a more plant-based diet may turn to legumes (“beans”), but these are usually incomplete proteins, meaning that they are missing some essential amino acids, and generally low in leucine. Even soybeans, a complete protein, contain only about 8% leucine [6].

Older adult walking

Dietary recommendations for older adults emphasize a minimum of 20–30 g of protein per meal, with at least 2.3–3 g of leucine per meal, to effectively stimulate muscle protein synthesis [7][8].

To recover lost muscle mass, the recommended intake is 3 g of leucine at each of three meals, along with 25–30 g of protein per meal [7][8].

Protein Sources to Help Retain Muscle 

Animal proteins are highly bioavailable, complete proteins, and the richest sources of leucine. One cup of low-fat (1%) cottage cheese contains approximately 2.9 g of leucine, enough for a full meal. A cup of plain yogurt contains roughly 1.3 g, and a cup of Greek yogurt provides about 1.2 g. Only 3 oz (85 g) of ground beef or pork contains ~1.8 g, and the same amount of chicken breast provides about 2.25 g — all close to the per-meal leucine target for older adults [9].

Soybeans, a complete plant-based protein, contain only 0.28 g of leucine per half-cup, and firm tofu, a concentrated form of soy protein, provides approximately 0.73 g per 3 oz (85 g). To reach the minimum leucine threshold from firm tofu, an older adult would need to eat about ¾ pound, which may exceed their typical appetite [9].

Incomplete plant proteins, such as lentils, contain 0.7 g of leucine per half-cup, and black beans contain 0.61 g per half-cup. This means an older adult would need to consume more than 3 cups of lentils or black beans, or 5½ cups of chickpeas (0.42 g leucine per half-cup), to meet the minimum leucine requirement per meal [9]

Older adults who want to eat a more plant-based diet need to ensure they consume adequate, highly bioavailable protein rich in leucine to maintain their muscle mass. A practical approach is to “prioritize protein” at each meal [8].

[NOTE: A recent article explains differences in protein bioavailability between plant-based and animal-based sources.]

Prioritize Protein to Retain Muscle 

“Prioritizing protein” means first deciding which protein you will eat at a meal, and then building the rest of the meal around that. For older adults, the protein chosen should provide 25–30 g of highly bioavailable protein and 2.3–3 g of leucine per meal [7].

For breakfast, choosing high-leucine proteins such as 1 cup of cottage cheese or 1 cup of plain Greek yogurt will provide enough protein and leucine to meet the minimum target. In contrast, 2 eggs contain only 12 g of protein and ~1.2 g leucine, which is less than half of the recommended per-meal leucine for older adults [9].

For lunch, 4 oz (113 g) of canned tuna provides about 4 g of leucine and 21 g of protein, and 3 oz (85 g) of cooked chicken breast provides 2.4 g of leucine and 26.5 g of protein. To increase leucine further, you can add 1 oz (28 g) of pumpkin seeds (~0.7 g leucine) or 1 oz (28 g) of sunflower seeds (~0.46 g leucine) to a salad [9].

For dinner, steak is one of the richest sources of leucine, with 4 oz (113 g) providing ~3.4 g, although cost may be a consideration. More budget-friendly options for those who don’t avoid it for religious reasons would be 4 oz (113 g) of pork chops (~27 g protein, 2.5 g leucine) or 4 oz of ground beef (~16 g protein, 2.5 g leucine). If there is a slight shortfall, the protein content of the meal can be boosted by adding a small serving of Greek yogurt [9].

Final Thoughts…

The quality of life and overall health of older adults depend on staying active, which requires adequate muscle mass. Preventing sarcopenia requires consuming sufficient high-quality protein that contains all essential amino acids, including an adequate amount of leucine to stimulate muscle growth.

Since muscle mass is lost at an estimated rate of 1% per year after age thirty, the choice of protein at each meal is crucial for maintaining strength and mobility. 

For those who would like help, we offer the Healthy Aging Package, which helps ensure that middle-aged and older adults eat sufficient protein and leucine at each meal to maintain their muscle and bone mass as they age.

To your good health, 

Joy

You can follow me on:

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

 

References

  1. Keller K, Engelhardt M. Strength and muscle mass loss with aging process. Age and strength loss. Muscles, Ligaments and Tendons Journal. 2013;3(4):346-350. [https://pmc.ncbi.nlm.nih.gov/articles/PMC3940510/]
  2. von Haehling S, Morley JE, Anker SD. An overview of sarcopenia: facts and numbers on prevalence and clinical impact. J Cachexia Sarcopenia Muscle. 2010 Dec;1(2):129–133. doi:10.1007/s13539-010-0014-2. Epub 2010 Dec 17. PMID: 21475695; PMCID: PMC3060646 [https://pmc.ncbi.nlm.nih.gov/articles/PMC3060646/]
  3. Fielding RA, Vellas B, Evans WJ, et al. Sarcopenia: an emerging public health problem. StatPearls. 2021. [https://www.ncbi.nlm.nih.gov/books/NBK560813/]
  4. Szwiega S, Pencharz PB, Rafii M, et al. Dietary leucine requirement of older men and women is higher than current recommendations. Am J Clin Nutr. 2020;113(2):410–419. doi:10.1093/ajcn/nqaa323 [https://pmc.ncbi.nlm.nih.gov/articles/PMC7851820/]
  5. Cruz-Jentoft AJ, Baeyens JP, Bauer JM, et al. Sarcopenia in older people: European consensus on definition and diagnosis. J Gerontol A Biol Sci Med Sci. 2010;65A(3): 101–116. doi:10.1093/gerona/glp018 [https://pubmed.ncbi.nlm.nih.gov/20392703/]
  6. Guo Y, Fu X, Hu Q, Chen L, Zuo H. The effect of leucine supplementation on sarcopenia-related measures in older adults: a systematic review and meta-analysis of 17 randomized controlled trials. Front Nutr. 2022;9:929891. doi:10.3389/fnut.2022.929891 [https://www.frontiersin.org/journals/nutrition/articles/10.3389/fnut.2022.929891/]
  7. Tanaka T, Simonsick E, Ferrucci L, et al. Leucine intake and risk of impaired physical function and frailty in older adults. J Gerontol A Biol Sci Med Sci. 2022;78(2):241–247. doi:10.1093/gerona/glac219 [https://pubmed.ncbi.nlm.nih.gov/36107140/]
  8. MDPI Nutrients. Beneficial effects of leucine supplementation on sarcopenia: a systematic review. Nutrients. 2019;11(10):2504. doi:10.3390/nu11102504 [https://www.mdpi.com/2072-6643/11/10/2504]
  9. USDA FoodData Central. Leucine content of common foods. U.S. Department of Agriculture, Agricultural Research Service. https://fdc.nal.usda.gov. Accessed [November 23, 2025].

 

 

Copyright ©2023 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.

 

Nutrition is BetterByDesign

 

 

 

A 2:1 Ketogenic Diet for Mental Health

 

Introduction

In the last several years, there has been increased interest in the use of a ketogenic diet to support mental health; however, some types of therapeutic ketogenic diets used in mental health conditions, such as bipolar disorder with psychosis, and schizophrenia, can be challenging to follow because they involve eating two to three times more fat than the combined amount of protein and carbohydrates. For example, a Classic Ketogenic Diet (4:1) is 80% fat, and a Modified Ketogenic Diet (3:1) is 75% fat. 

Different Types of Ketogenic Diets

As explained in a previous article called “Use of a Therapeutic Ketogenic Diet in Mental Health,” there are three main types of therapeutic ketogenic diets. The Classic Ketogenic Diet uses a 4:1 ratio of fat to protein plus carbohydrates, the Modified Ketogenic Diet uses a 3:1 ratio, and the Modified Atkins Diet uses a 2:1 ratio.

There have been anecdotal reports of individuals doing very well following a Modified Atkins Diet (2:1) under the supervision of their doctors, and recently, (June 3, 2023), a pre-print pilot study tested this diet in people with bipolar disorder and found it to be successful [2].

It is hoped that a Modified Atkins Diet, which has a 2:1 ratio and is only 60-65% fat, may be useful, along with medication, for reducing symptoms of anxiety, depression, and bipolar disorder without psychosis, where higher levels of ketones produced by 4:1 and 3:1 ketogenic diets may not be required. 

The advantages are that this approach is less time-consuming in terms of the amount of calculations and work needed to design it. It also enables individuals to get into ketosis under medical oversight, then, in consultation with their doctors, decide if the improvements are sufficient to maintain their diet as is, or if gradually increasing fat and reducing protein might work better.

A 2:1 Therapeutic Diet is Not the Same as a “Keto Diet”

Some people mistakenly believe that a 2:1 therapeutic ketogenic diet is the same as the popular “keto” diet used for weight loss and improved metabolic health. While they have some similarities, a therapeutic ketogenic diet is very different. 

In a therapeutic ketogenic diet, the amount of protein, carbohydrates, and fat is carefully weighed at each meal to keep ketone levels steady throughout the day. No weighing of food is required in the popularized “keto diet”. 

Secondly, in a regular keto diet, the goal is simply to get into and stay in ketosis; however, in a therapeutic ketogenic diet, there is a need to monitor both glucose and ketone levels so that a specific therapeutic level called the Glucose to Ketone Index (GKI) is achieved.

Working with Your Doctor to Support Mental Health

If you are thinking about trying a therapeutic ketogenic diet to help support mental health and you are taking medications for depression, anxiety, or bipolar disorder, the first step is to talk with your doctor.

As outlined in the previous article, Harvard Psychiatrist Dr. Palmer recommends that doctors have their patients remain on their medication while trialling a therapeutic ketogenic diet for a period of three months, and be evaluated by their doctor during the stages of ketosis to see if there has been any significant change in symptoms [1]. If the doctor finds that the diet is helping, they may begin to gradually discontinue some medications.  As stated in previous articles, changing dosages of medication is not something people should ever do on their own. 

There is an important point that Dr. Palmer makes that should not be overlooked. With the gradual decrease in medications, people are more reliant on the ketogenic diet to keep symptoms under control. The ketogenic diet is therapeutic; therefore, taking “cheat days” is not an option. Dr. Palmer notes that it takes several days to get back into ketosis after breaking the diet, and during this time, symptoms can dramatically reappear [ [1]. 

Dr. Palmer recommends the following two steps to doctors who want to use ketogenic diets with their patients [1]; 

  1. Find a licensed Dietitian knowledgeable in therapeutic ketogenic diets and partner with them. 
  2. Read the book “Ketogenic Therapies” by Dr. Eric Kossoff.

Dr. Eric Kossoff’s book, Ketogenic Diet Therapies for Epilepsy and Other Conditions, is one that I have referred to often in designing therapeutic ketogenic diets for different physical conditions. 

Steps to Getting Started

If you are thinking of adopting a therapeutic ketogenic diet for improved mental health, then the first step is to reach out to your doctor and discuss it.  

If your doctor is willing to oversee your health and medications while you adopt the diet, then the next step is to have them complete and return a Request for Medical Supervision Form by fax to our office.

More Info

Under the Services tab, you can learn about the 3:1 and 2:1 therapeutic ketogenic diets that I design, and where you will also find the corresponding Request for Medical Supervision Form.

To your good health!

Joy

 

You can follow me on:

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

 

References

  1. Dr. David Puder, MD, Psychiatry Podcast, Episode 163, Dr. Chris Palmer: Ketogenic Diet for Mental Health, M=November 15, 2022, https://www.psychiatrypodcast.com/psychiatry-psychotherapy-podcast/163-treating-mental-health-disorders-with-a-ketogenic-diet
  2. Needham Nicole, Campbell Ian, Grossi Helen et al, Pilot Study of a Ketogenic Diet in Bipolar Disorder, June 3, 2023, doi.org/10.1101/2023.05.28.23290595, https://www.medrxiv.org/content/10.1101/2023.05.28.23290595v1
  3. Kossoff, Eric & Turner, Zahava & Cervenka, Mackenzie & Barron, Bobbie. (2020). Ketogenic Diet Therapies For Epilepsy and Other Conditions. 10.1891/9780826149596.

 

 

Copyright ©2023 BetterByDesign Nutrition Ltd.

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

 

Is High Fructose Corn Syrup (HFCS) Linked to Fatty Liver Disease?

A recent social media post about a Canadian woman living in the United States who discovered that the ingredients in a major brand of ketchup manufactured in Canada and the United States were different caused quite a stir.  Online discussion centered around whether the inclusion of high fructose corn syrup (HFCS) in the US product posed an increased risk of fatty liver disease.

twitter post that was almost viral about high fructose ketchup

The ingredients listed in the US and Canadian products were as follows;

Heinz Tomato Ketchup (America): Tomato concentrate from red ripe tomatoes, distilled vinegar, high fructose corn syrup, corn syrup, salt, spice, onion powder, natural flavoring.

Heinz Tomato Ketchup (Canada): Tomato paste (from fresh, ripe tomatoes), sugar, vinegar, salt, spices

One Difference Between the US and Canadian Ketchup 

The significant difference between the two ingredient lists was that the US-manufactured ketchup used high fructose corn syrup (HFCS) and corn syrup to sweeten the product, whereas the Canadian ketchup was sweetened using sugar (sucrose). 

High Intakes of Fructose and Non-Alcoholic Fatty Liver Disease

There have been a few research articles over the last several years which seemed to indicate that large intakes of fructose may be linked to non-alcoholic fatty liver disease (NAFLD) but I had not yet written anything about it, largely due to a lack of time. This recent social media post going viral made me want to write a brief post pointing to some recent evidence that large intakes of fructose, including high fructose corn syrup (HFCS) may pose a risk of NAFLD.

What is fructose?

Fructose is a natural occurring sugar that is present in fruit, some vegetables and honey and which is used as a component in the manufacture of high-fructose corn syrup (HFCS) which is used as a sweetener in soda (soft drinks, pop), in candies, and in condiments such as ketchup.

Approximately a quarter (24%) of US adults have non-alcoholic fatty liver disease (NAFLD) which results in the excess build-up of fat in the liver that is unrelated to heavy alcohol use [1]. NAFLD is a serious condition that can progress to chronic liver damage, and lead to death [1].

academic presentation about fructose and NAFLDAn expert talk given this time last year at Endo 2022, the annual meeting of the Endocrine Society which took place from June 11-14, 2022, in Atlanta, Georgia, titled Fructose Consumption and NAFLD in US Adult Population presented evidence that non-alcoholic fatty liver disease (NAFLD) is associated with high intakes of fructose.

The researchers analyzed data from the 3,292 US adults enrolled in the National Health and Nutrition Examination Survey (NHANES) from 2017-2018 and found that those who consumed the greatest amount of fructose were Mexican Americans (48%), non-Hispanic Blacks (44%), with a lower percentage of fructose consumption amongst non-Hispanic whites (33%).

The researchers found the highest prevalence of non-alcoholic fatty liver disease (NAFLD) amongst Mexican Americans who consumed the highest amount of fructose (70%) which was significantly different than the prevalence of NAFLD in Mexican Americans that consumed the lowest amount of fructose (52%) [2]. When researchers adjusted for body composition and laboratory variables, they found that high fructose consumption was related to a higher risk of NAFLD in the total population, not only in Mexican Americans [2].

The researchers concluded that “there is an association between fructose consumption and the odds of developing non-alcoholic fatty liver disease (NAFLD)” and that “interventions should aim to decrease consumption of fructose overall” [1,2].

The researchers recommended that health care providers encourage people to consume less food and beverages with high-fructose corn syrup to prevent the development of NAFLD [1].

Final Thoughts…

Consuming small amounts of ketchup sweetened with high-fructose corn syrup in and by itself does not pose a risk of developing non-alcoholic fatty liver disease.

Where the risk lies is for people who are consuming fruit juice, soda pop, candy and condiments including ketchup that contain high-fructose corn syrup.

The recommendation of the Endocrinologists above is to encourage people to consume less of these foods and beverages to prevent the development of non-alcoholic fatty liver disease.

To your good health!

Joy

 

You can follow me on:

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

References

 

  1. Williams, Colleen, Reports and Proceedings of the Endocrine Society, News Release June 12, 2022, People who consume too much high fructose corn syrup could be at risk for NAFLD, https://www.eurekalert.org/news-releases/955131
  2. Kermah D, Najjar S, Puri V, Schrode K, Shaheen M, Zarrinpar A, Friedman T. OR10-5 Fructose Consumption and NAFLD in US Adult Population of NHANES 17-18. J Endocr Soc. 2022 Nov 1;6(Suppl 1):A17. doi: 10.1210/jendso/bvac150.035. PMCID: PMC9625025.

 

Copyright ©2023 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.

Nutrition is BetterByDesign

Use of a Therapeutic Ketogenic Diet in Mental Health

Most people have heard of the high-fat, low-carb “keto” diet for weight loss and blood sugar control, but a therapeutic ketogenic diet (TKD) is different (read more here). A therapeutic ketogenic diet is a type of medical nutrition therapy used as adjunct treatment for specific physical or mental health conditions that is either prescribed by a Physician (doctor) and implemented by a Dietitian, or implemented by a Dietitian under Physician oversight.

In a therapeutic ketogenic diet, the amount of protein, carbohydrates, and fat is carefully controlled to keep ketone levels steady throughout the day, and both glucose and ketone levels must be monitored so that a specific therapeutic level called the Glucose to Ketone Index (GKI) is achieved. 

Therapeutic ketogenic diets have been used for over 100 years for epilepsy and diabetes, and more recently, in the treatment of various mental health disorders, including depression, bipolar disorder, and schizophrenia.

Therapeutic Ketogenic Diet for Mental Health 

A 2022 study in Frontiers in Psychiatry included 31 adults with treatment-resistant depression, bipolar disorder, or schizoaffective disorder in a psychiatric hospital in Toulouse, France. They followed a therapeutic ketogenic diet that restricted carbohydrates to 20g per day. Of the 28 individuals who stayed on the diet for more than two weeks, all showed symptom improvements within three weeks. Forty-three percent achieved full remission, and 64% were discharged on less psychiatric medication [1].

Other pilot studies show similar results in bipolar disorder and schizophrenia [2][3].

“Brain Energy” Book – role of therapeutic ketogenic diets 

The release of the book Brain Energy by Harvard Psychiatrist Dr. Chris Palmer in 2022 brought public attention to the role of therapeutic ketogenic diets in mental health [4], which has led to an increase in inquiries about using them. 

But what is a therapeutic ketogenic diet?

Types of Therapeutic Ketogenic Diets

Therapeutic ketogenic diets are a form of medical nutrition therapy using a specific ratio of fat to protein plus carbohydrate.

Classic Ketogenic Diet (KD)

The Classic Ketogenic Diet has a 4:1 ratio, which means 4g of fat is provided for every 1g of protein plus carbohydrate. This diet is 80% fat and 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%. This type of diet is used when the need to achieve and maintain high levels of ketones is necessary.

Modified Ketogenic Diet (MKD)

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.

Some Psychiatrists will start their patients on a 3:1 therapeutic ketogenic diet. Once their patient is producing significant levels of ketones and is stable with respect to symptoms, they may gradually have them transition to a Modified Atkins Diet (2:1) while monitoring their symptoms, as this can be easier to maintain long-term and is more suitable for those who cannot tolerate very high-fat diets.

Modified Atkins Diet (MAD)

The Modified Atkins Diet has a 2:1 ratio, and is only 60-65% fat, and is used in specific mental health conditions that do not require the higher levels of ketones that can be produced using a Modified Ketogenic Diet (3:1). 

As mentioned above, some Psychiatrists will start their patients on a 3:1 therapeutic ketogenic diet, and once the desired level of ketones has been achieved and the person is stable with respect to symptoms, they may gradually transition them to a Modified Atkins Diet (2:1).

Calculating Ratios Based on a Percentage of Calories

As a Dietitian who designs therapeutic ketogenic diets, the first step is to determine the amount of energy (calories, in kcal) the individual needs. Then, I calculate the percentage of calories that need to come from fat, protein, and carbohydrate based on the specific dietary prescription.

Meals of therapeutic ketogenic diets are much smaller than conventional meals because they are higher in fat. Fat provides the same number of calories for much less mass (weight, in grams), so to get 500 kcals as protein, one would need to eat 125g of protein, but to get the same amount of calories as fat, one would only need to eat 55.5 g of fat. Fat is much more calorically dense, providing 9 kcal/g, whereas protein and carbohydrate have only 4 kcal/g.

A Dietitian’s Role in Therapeutic Ketogenic Diets

In a recent Psychiatry and Psychotherapy podcast where Dr. Chris Palmer was interviewed, he talks about how Psychiatrists can incorporate the use of a therapeutic ketogenic diet in their practice [8].  The first thing he said was that there was a need for the physician to determine if this approach is appropriate for a specific patient.

As outlined in a 2018 article titled “Don’t Try This at Home – when medical supervision is needed“, following a ketogenic diet needs to be done with the knowledge and oversight of one’s doctor — especially when taking specific types of medication such as;

    1. insulin (or insulin analogues)
    2. medication to lower blood glucose, such as sodium glucose co-transporter 2 (SGLT2) medication, including Invokana, Forxiga, Xigduo, Jardiance, etc..
    3. medication to control blood pressure, such as Ramipril, Lasix (furosemide), Lisinopril / ACE inhibitors, Atenolol / βeta receptor antagonists, etc..
    4. mental health medications such as antidepressants, medication for anxiety disorder, bipolar disorder (such as Lithium), and schizophrenia

Dr. Palmer recommends that doctors have their patients remain on their medication while starting a therapeutic ketogenic diet and be evaluated during the stages of ketosis to see if there has been any significant change in symptoms [6]. 

[People who follow a therapeutic ketogenic diet for medical reasons are often asked to track their Glucose-Ketone Index (GKI) so their doctors can monitor the benefit of the diet. I teach people how to do that.]

Dr. Palmer suggests that individuals should trial a therapeutic ketogenic diet for a period of three months [4], and if the doctor finds that the diet is helping, they may begin to gradually discontinue some medications. As mentioned in the “Don’t Try This at Home” article, changing dosages of medication is not something people should do on their own. 

In the podcast, Dr. Palmer emphasizes that with the gradual decrease in medications, people are more reliant on the ketogenic diet to keep symptoms under control. The ketogenic diet is therapeutic; therefore, taking “cheat days” is not an option. Dr. Palmer notes that it takes several days to get back into ketosis after breaking the diet, and during this time, symptoms can dramatically reappear [8].

Dr. Palmer says that if a Psychiatrist is interested in beginning to use a therapeutic ketogenic diet in their clinical practice, they must be “well-informed on the science behind a therapeutic ketogenic diet, as well as metabolic functioning as a whole”.

Dr. Palmer recommends that doctors begin with the following first two steps [6]:

    1. Find a licensed Dietitian knowledgeable in therapeutic ketogenic diets and partner with them. 

    2. Read the book “Ketogenic Therapies” by Dr. Eric Kossoff

Dr. Eric Kossoff’s book, Ketogenic Diet Therapies for Epilepsy and Other Conditions, is one that I have referred to often in designing therapeutic ketogenic diets for different physical conditions. 

Steps to Getting Started 

If you are thinking of adopting a therapeutic ketogenic diet for improved mental health, then the first step is to reach out to your doctor and discuss it.  

If your doctor is willing to oversee your health and medications while you adopt the diet, then the next step is to have them complete and return a Request for Medical Supervision Form by fax to our office.

More Info

Under the Services tab, you can learn about the 3:1 and 2:1 therapeutic ketogenic diets that I design, and where you will also find the corresponding Request for Medical Supervision Form.

To your good health!

Joy

 

You can follow me on:

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

 

References

  1. Danan A, Westman EC, Saslow LR, Ede G. The Ketogenic Diet for Refractory Mental Illness: A Retrospective Analysis of 31 Inpatients. Frontiers in Psychiatry, 06 July 2022. https://doi.org/10.3389/fpsyt.2022.951376 
  2. Sethi S, Wakeham D, Ketter T, Hooshmand F, Bjornstad J, Richards B, et al. Ketogenic Diet Intervention on Metabolic and Psychiatric Health in Bipolar and Schizophrenia: A Pilot Trial. Psychiatry Research,  2024 May 1,
    https://www.sciencedirect.com/science/article/pii/S0165178124001513
  3. Campbell IH, Needham N, Grossi H, Kamenska I, Luz S, Sheehan S, et al. A Pilot Study of a Ketogenic Diet in Bipolar Disorder: Clinical, Metabolomic and Magnetic Resonance Spectroscopy Outcomes,  Oct 2023,
    https://www.medrxiv.org/content/10.1101/2023.10.23.23297391v1
  4. Palmer, C.M., J. Gilbert-Jaramillo, E.C. Westman. “The Ketogenic Diet and Remission of Psychotic Symptoms in Schizophrenia: Two Case Studies.” Schizophrenia Research. 2019 June; 208: 439-440, ISSN 0920-9964. https://doi.org/10.1016/j.schres.2019.03.019
  5. Sarnyai, Z, Palmer, C.M.,Ketogenic Therapy in Serious Mental Illness: Emerging Evidence, International Journal of Neuropsychopharmacology, Volume 23, Issue 7, July 2020, Pages 434–439, https://doi.org/10.1093/ijnp/pyaa036
  6. Norwitz, N., G.A. Dalai, S. Sethi; C. Palmer. “Ketogenic diet as a metabolic treatment for mental illness.” Current Opinion in Endocrinology & Diabetes and Obesity: 2020 Oct: 27(5): 269-274.
  7. Eastman, M., KetoConnect, The Ketogenic Ratio Explained, September 16, 2014, https://www.myketocal.com/blog/the-ketogenic-ratio-explained/
  8. Dr. David Puder, MD, Psychiatry Podcast, Episode 163, Dr. Chris Palmer: Ketogenic Diet for Mental Health, November 15, 2022, https://www.psychiatrypodcast.com/psychiatry-psychotherapy-podcast/163-treating-mental-health-disorders-with-a-ketogenic-diet

 

Copyright ©2023 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.

 

Nutrition is BetterByDesign - therapeutic ketogenic diets

Thyroid Medication can Worsen Blood Sugar Control in People with Diabetes

Did you know that thyroid medication can worsen blood sugar? The ‘highlights of prescribing information” sheets available to pharmacists and doctors for medications such as Synthroid® (generic: levothyroxine) and Cytomel® (generic liothyronine) warn that both these types of thyroid medication can worsen blood sugar control in diabetics, and increase the need for diabetes medications, including insulin. 

I didn’t know this.

Even though I had been diagnosed with type 2 diabetes more than twelve years ago and with hypothyroidism this past August, when I was prescribed thyroid medication, the pharmacist didn’t mention it when I first filled my prescription, nor was I provided with any printed information when my thyroid medication was delivered. My doctor didn’t mention it either but understandably, he knew I had been in remission of diabetes for three years prior to be diagnosed with hypothyroidism and probably didn’t think of me as being diabetic.  He was well-aware that for three years prior to be diagnosed with hypothyroidism, I did not meet the diagnostic criteria for type 2 diabetes either on the basis of fasting blood glucose or HbA1C because I controlled my blood sugar through diet.

When I began taking thyroid medication after my diagnosis of hypothyroidism, I began to periodically feel unwell as I did when I had high blood sugar.  I began to test my blood glucose more often and discovered that it was routinely spiking as high as the mid- to high 10 mmol/L (~190 mg/dl) for seemingly no reason. 

Effect of thyroid medication on blood sugar

I was totally puzzled as to why.  I didn’t eat simple carbs or starch-based food. I wasn’t sick, or under any new stress. I was sleeping well, was  properly hydrated, and there was no reason that I could think of that my blood sugar would keep spiking. In my search for answers, I stumbled across information that indicated that it should be well known that thyroid medication can worsen blood sugar control in people diagnosed with diabetes. For some reason, this information was not communicated to me, and when I asked others with both disorders, they were also unaware.

While I have already been eating low carb for the past three years, I began eating very low carb in order to get a better handle on the blood glucose spikes, and it is helping. I am also, in conjunction with my doctor, adjusting the timing of my thyroid medication around the timing of my meals to minimize the impact of the thyroid medication on my blood sugar and will continue to monitor my blood sugar several times per day. If need be, I will have my doctor either prescribe a medication such as Metformin to support normal blood sugar and/or trial different doses of thyroid medications. The important factor is I now know and can monitor this and make changes, as necessary. 

How many people have no idea?

Diabetes and Thyroid Medication 

It is essential that people diagnosed with any form of diabetes (type 1, type 2, gestational diabetes) as well as hypothyroidism know that their thyroid medication can impact their blood sugar control, as well as their need for diabetes medications, if they take any. Since those with type 1 diabetes and gestational diabetes have to monitor their blood glucose very closely, they would notice any changes, but many people with type 2 diabetes rarely regularly check. 

Thyroid Medication — highlights of prescribing information (product monographs) 

The “Highlights of Prescribing Information” sheets for both Synthroid® and Cytomel® that are available to doctors and pharmacists warn that therapeutic used of “these medications in patients with diabetes mellitus may worsen glycemic control and result in increased antidiabetic agent [i.e., diabetes medications] or an “increase in insulin requirements.” In addition, there is a warning on prescribing both medications to “carefully monitor glycemic control (i.e., blood sugar) after starting, changing, or discontinuing thyroid hormone therapy.” This means that people with diabetes need to be continuing to monitor their own blood sugar and contact their doctors if there is a need to address worsening blood sugar control related to taking thyroid replacement medication.

The “Highlights of Prescribing Information” for Synthroid® [1] is a 19-page product monograph about this medication which states that it does “not include all the information needed to use this medication safely and effectively.” For that, there is the need to read the full prescribing information. In other words, these 19 pages are only a summary of all that is needed to use the medication safely and effectively! 

Below is page 1 of the 19 of the “Highlights of Prescribing Information” for Synthroid®.

Highlights of Prescribing Information for Synthroid – page 1 of 19 highlighted

If the relevant section wasn’t highlighted in yellow by me, how likely would it be that a pharmacist or physician would have noticed this warning amongst the 19 pages of fine type?

The “Highlights of Prescribing Information” for Cytomel® [2] is an 11-page product monograph about that medication. It also states that it does “not include all the information needed to use this medication safely and effectively.” Those sheets are just a summary, and there is the need to read the full prescribing information.

Below is page 1 of the “Highlights of Prescribing Information” for Cytomel®.

Highlights of Prescribing Information for Cytomel – page 1 of 11 highlighted

Again, if the relevant section wasn’t highlighted in yellow by me, how likely would it be that a pharmacist or physician would have noticed this warning amongst the 11 pages of fine type?

 


[Post publication note (May 1, 2023)] 

Since natural desiccated thyroid (NDT) also called natural desiccated extract (NDE) are not approved by the FDA or Health Canada as medications, there are no Prescribing Information sheets for products such as the US product Armour Thyroid®, or equivalent ERFA desiccated thyroid®,  in Canada, but both products contain the same warning.

Page 3 of 24 of the Product Monograph from Armour®  contains a warning under Contraindications;

“Thyroid hormone therapy in patients with concomitant diabetes mellitus or diabetes insipidus or adrenal cortical insufficiency aggravates the intensity of their symptoms. Appropriate adjustments of the various therapeutic measures directed at these concomitant endocrine diseases are required.”

Page 3 of 24 of the Product Monograph from Armour thyroid®

Page 1 of 9 of the Product Monograph from ERFA desiccated thyroid®  contains the same warning under Precautions;

page 4 of 9 Product Monograph Erfa Thyroid®

Recently published studies report that 11%–23% of people with type 2 diabetes also have hypothyroidism [6] making it essential that people with both diagnoses know about the possible effect of thyroid replacement on blood sugar control.

For those interested in the mechanism, a paper published last month explains how thyroid hormones contribute to a rise in blood glucose.  In the liver, thyroid hormones increases expression of glucose transporter 2 (GLUT2), which increases in both gluconeogenesis and glycogenolysis.  In liver, the thyroid hormone T3 increases gluconeogenesis by increasing activity of phosphoenolpyruvate carboxykinase (PEPCK), and in adipose tissue, thyroid hormones increase lipolysis, resulting in an increase in free fatty acid that stimulates hepatic gluconeogenesis [7].

Additional References

4.  Product monograph for Armour Thyroid: https://dailymed.nlm.nih.gov/dailymed/getFile.cfm?setid=56b41079-60db-4256-9695-202b3a65d13d&type=pdf

5. Product monograph for Erfa: https://pdf.hres.ca/dpd_pm/00034857.PDF

6. Talwalkar P, Deshmukh V, Bhole M. Prevalence of hypothyroidism in patients with type 2 diabetes mellitus and hypertension in India: a cross-sectional observational study. Diabetes Metab Syndr Obes. 2019 Mar 20;12:369-376. doi: 10.2147/DMSO.S181470. PMID: 30936734; PMCID: PMC6431000.

7. Eom YS, Wilson JR, Bernet VJ. Links between Thyroid Disorders and Glucose Homeostasis. Diabetes Metab J. 2022 Mar;46(2):239-256. doi: 10.4093/dmj.2022.0013. Epub 2022 Mar 24. PMID: 35385635; PMCID: PMC8987680.


Final Thoughts…

If you have any type of diabetes and have also been diagnosed with hypothyroidism (including Hashimoto’s disease, the autoimmune form), it is very important that you monitor your blood glucose regularly. 

Contact your doctor if you notice a worsening in your blood sugar control, and to have your doctor evaluate your need for an increased dosage of existing diabetes medications, or the introduction of these medications if you don’t currently take any.

Consider adopting a style of eating that is lower in carbohydrate than you currently eat. According to a 2019 consensus report from the American Diabetes Association, reducing overall carb intake has “the most evidence for improving glycemia [blood sugar]” [3] . But please keep in mind that while a low carb diet is safe and effective for those with diabetes, if you take certain types of medications it is necessary to have medical oversight before adopting a very low carbohydrate (“keto”) diet.

More Info

If you have diabetes or pre-diabetes* and would like information on how I can support you in better managing your blood sugar, please send me a note through the Contact Me form at the top of this page.

To your good health!

Joy

*Please note that I do not design Meal Plans for people currently taking insulin or insulin-analogue medication for diabetes as I do not have CDE certification.

You can follow me on:

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

 

References

  1. Food and Drug Administration, Highlights of Prescribing Information for Synthroid, https://www.accessdata.fda.gov/drugsatfda_docs/label/2020/021402s034lbl.pdf
  2. Food and Drug Administration, Highlights of Prescribing Information for Cytomel, https://www.accessdata.fda.gov/drugsatfda_docs/label/2018/010379s054lbl.pdf
  3. Evert, AB, Dennison M, Gardner CD, et al, Nutrition Therapy for Adults With
    Diabetes or Prediabetes: A Consensus Report, Diabetes Care, Ahead of Print, published online April 18, 2019, https://doi.org/10.2337/dci19-0014

 

Copyright ©2023 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.

 

Hypothyroidism Update – six months of treatment since diagnosis

This update marks just over six months since I was diagnosed with profound hypothyroidism and began medication and nutritional treatment. It is written from a subjective perspective and thus is categorized as part of my personal story.


At the beginning of June 2022, our family was in Tofino (Vancouver Island) for the marriage of my youngest son. The groom’s eldest brother assumed that my inability to walk on the sand for family photos, up the path to the hotel, or to get up out of a chair was a result of me having “aged.” He had no idea that I was hiking in North Vancouver and Golden Ears Provincial Park for several hours at a time just the summer prior.

I knew something was wrong, and for several months, I assumed my feeling exhausted and having joint and muscle pain was a carry-over effect from having had Covid. But a cell phone picture of myself taken just before the wedding told me it had to be something else. Gradually, over several months, I went from looking as I had been the previous two years after losing 55 pounds to looking like I had regained everything. I later found out, it wasn’t fat but an accumulation of mucin in the skin that is one of the hallmark signs of myxedema. You can read more about myxedema and the skin changes associated with hypothyroidism here

Since it was a special occasion, I didn’t say anything to my family about how sick I felt, but I was beginning to think that I had become significantly hypothyroid since I last saw my doctor in person (due to Covid protocols). My plan was to contact him when I returned to the mainland, which I did.

Two weeks later, my doctor confirmed that my symptoms were consistent with a diagnosis of hypothyroidism. In fact, I was surprised when he mentioned that it was not unexpected in light of my lab work over the previous nine years, my past thyroid surgery several decades ago, and my having experienced periodic hypothyroid symptoms since that time. Nevertheless, it took almost a decade for me to get diagnosed because of the limitations placed on doctors regarding which tests they can requisition under what circumstances (more about the challenges of getting diagnosed with hypothyroidism here).

In addition to the clinical challenges of getting diagnosed, there is also the reality that the most common symptoms of hypothyroidism are often assumed to be “just aging.” For example, many people believe it is normal for ‘older adults’ to have body aches, joint pain, fatigue, feel chilled when others do not, experience constipation, have dry skin or hair loss, be forgetful, or to even experience depression. Unfortunately, many don’t realize that these are not typical signs of aging but ARE common symptoms of hypothyroidism. What compounds the challenge of getting diagnosed is that the symptoms of hypothyroidism are so non-specific that many would not give them a second thought. An older person limited to a “one-issue-ten-minute remote doctor’s appointment” would be unlikely even to bring them up.

For those who have been following this story, my diagnosis was not the end but the beginning of my journey. Three months later, I lost half my hair due to telogen effluvium, the most common form of diffuse hair loss that can occur after a profound stress, shock or traumatic event including childbirth, a thyroid disorder, or rapid weight loss. You can read more about that here.

When my hair loss continued due to androgenic alopecia (also common in hypothyroidism), I began to research which nutrients of importance had evidence for helping restore hair loss, and wrote this article. Knowing I had a second son’s wedding mid-February, I incorporated both nutritional supplements (oral and topical) to support me in my recovery from what my doctor called “profound hypothyroidism.”

This weekend was my second son’s wedding, and the difference between how I felt in June and now is incredible! Instead of wearing medical compression stockings and orthopedic shoes so I could walk, I wore regular nylons and dress pumps.

While my doctor said it would still take another six months or longer for the mucin to resolve in my legs and trunk of my body, I was SO pleased that my legs didn’t look like water-logged tree stumps, as they did in June! In addition, my face was no longer swollen beyond recognition. I looked like “me” rather than like I had been “inflated” with an air pump.  I felt human and presentable and unlike I did in June, I wasn’t self-conscious being in the family photos.

Looking at the two wedding pictures side-by-side (see below), it is evident that being on the correct dose and mix of thyroid hormones (thanks to the excellent support of my doctor) has made a significant difference! In addition to thyroid medication, I have also been supplementing with nutrients of importance in hypothyroidism, as well as nutritional supplements with evidence to restore hair loss in androgenic alopecia which I developed secondary to my diagnosis. My hair is gradually growing back in, and where once there was a bald shiny scalp, I have hair an inch or two long. I also have eyelashes again, and the outer thirds of my eyebrows are also coming back in. 

 

It is my hope that when the most recent newlyweds celebrate their first anniversary, that the residual symptoms of hypothyroidism will be behind me.

Final thoughts…

If you have wondered if you have symptoms that may be consistent with hypothyroidism, you can download a checklist of common hypothyroid symptoms here to help you have an informed discussion with your doctor to determine whether thyroid hormone testing is warranted.

More Info?

If you would like more information about how I could support you from a nutritional perspective, please send me a note through the Contact Me form at the top of this page.

To your good health!

Joy

You can follow me on:

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

 

Copyright ©2023 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.

 

 

Alopecia Universalis – a clinician’s personal story of complete hair loss

Three years ago, Tim Rees, a clinician from Germany, lost all his hair a second time to alopecia universalis (AU).  As a registered clinical nutritionist he felt he had lost his credibility to help others with autoimmune conditions, and when he expressed those feelings in a recent blog (link below), it struck a chord with me. 

Tim Rees with his son in 2022

“All my hair fell out, but it was my response to it that destroyed me. You could be forgiven for thinking this is all centered around vanity, but the thing that crushed me was that it made me feel like a fraud.” ~Tim Rees, registered clinical nutritionist

As a clinician, I felt similarly when I lost half my hair in September of 2022. I wondered if others would consider me a “failure” for not having been able to prevent it.

Neither Tim nor I are physicians and thus are not qualified to diagnose conditions (in ourselves or in others). Our role is to provide nutrition education or medical nutrition therapy for conditions diagnosed by physicians. 

I was so struck by Tim’s recent post sharing about his complete hair loss and how he felt about it as a clinician, that I asked his permission to share his story. Below is an excerpt of his recent post. My goal in sharing this is so that people can understand what alopecia universalis is, and how it feels as a clinician to be diagnosed with an auto-immune disorder. It is my hope that sharing Tim’s post will enable people to better understand that clinicians with health conditions (whether autoimmune or not) are no less able to support their clients. What makes a clinician knowledgeable is their training and ongoing study in their area of clinical practice and I do not believe that a clinician diagnosed with an autoimmune disorder or metabolic disease is disqualified from being able to help others. On the contrary, provided they remain objective, I think a clinicians’ ability to understand their clients’ clinical struggles from “both sides of the clinical desk” while offering evidence-based support may be an asset.

I will begin with a very brief explanation of the disorder itself, so Tim’s words make sense.

Alopecia Universalis

Alopecia universalis (AU) is an advanced form of alopecia areata (AA) which is a condition that causes round patches of hair loss. This recent article describes alopecia areata and shows pictures of what it looks like.

In alopecia universalis, there is a complete loss of hair on the scalp and all over the body and it is thought to be an autoimmune condition in which the person’s immune system mistakenly attacks the hair follicles [1].


This Year I Stopped Hiding – a clinician story

(written by registered clinical nutritionist, Tim Rees)

“Three years ago my hair started falling out for the second time. In fact, I’d only had it all back for about 6 months before I got gut-punched standing before the mirror. “It’s not as bad as last time,” I said to myself.

But like an unstoppable rebel force (name the movie) my immune system killed my hair follicles and the hair dropped away like oak leaves in autumn, minus the orange. Alopecia Universalis, not a single hair remained on or in (I’m told) my body.

At the same time, the entire world went into lockdown and the corporate presenting side of my business died along with my self-esteem, my confidence and my monthly hairdressing appointment. There had never been a better time to hide.

You could be forgiven for thinking this is all centered around vanity, but the thing that crushed me was that it made me feel like a fraud. I was so embarrassed the thought of people discovering my secret presented as physical pain. Alopecia, one of the most visible autoimmune diseases one can have, undermined my work and, I thought, my credibility as a nutritionist helping people with autoimmune conditions.

But that’s not true. I’ve done amazing things with nutrition for myself and my clients. Until fairly recently I had lost my hearing to the point that I could no longer use the phone and was conducting sessions using Skype subtitles and talking non-stop in the hope I’d cover their questions before they thought them up. I have a whole list of reasons-why-I’m-not-a-fraud but I won’t bore you with them, after all, most of these insecurities are in my head.

But, here’s the thing. I think I can reverse this condition. Two years ago I stuck to my exclusion diet for four months by which time I had quite a lot of regrowth. Fluffy like a baby owl but still, living follicles. In fact, I remarked to my helpless doctor that I wasn’t worried about the hair, that it was coming back and all was fine. Ever the optimist. But after some bad luck, I began compromising a little here, and a little there, it was Christmas after all, and before I knew it I was doing a passable impression of a bowling ball again.

This year will be different. I’m plastering this all over social media for a number of reasons. Firstly, it’s a part of my acceptance. I fought hard against acceptance mistaking it for defeat. The truth is, you must accept how things are today in order to make a difference tomorrow.

Secondly, after posting a couple of photos on Twitter, I already feel better. And, thirdly it’ll help to keep me motivated and compliant for however long it takes to allow my body to heal.

I’ve been drifting and failing as a husband, as a new father and as a man. Not because I have alopecia but because I’ve let it destroy me. There’s a stoic lesson in there.”

[Shared with permission from Tim Rees’ blog.]


As Tim outlines in the full article, it is his goal this year to reverse his alopecia universalis, and like I did when I set out to recover my own hair loss from telogen effluvium and androgenic alopecia, he will be sharing his progress on social media for all the world to see. 

Tim plans to use an exclusion diet as well as nutritional supplements and to document why he is using them.  He also intends to integrate other approaches which he hopes will support his goal, including the use of sauna, cold thermogenesis, exercise, circadian rhythm / light exposure, etc. and document what he found helpful. While this will be Tim’s personal account of what he is doing to improve his hair loss, I am confident that as a clinician, he will document his choice of approaches and provide references.

I applaud Tim’s boldness and bravery to stop “hiding” and to live his hair loss story and goal of hair loss restoration in a public way. I wish him all the very best in achieving his goal.  

Final Thoughts…

It is important to keep in mind that what may work for Tim may not work for others diagnosed with the alopecia universalis, anymore than the nutrients I took would work for others diagnosed with telogen effluvium and androgenic alopecia. I chose to not write about which nutrients I took and in what dosages because it was not relevant to anyone other than me. I did write two referenced articles related to nutrient supplementation and hair loss and the first one was Hair Loss in Hypothyroidism (Part 2) – Nutrients of Importance  and the second was Nutritional Supplements With Evidence to Restore Hair Loss.

Since taking some nutritional supplements is not without risk, I would encourage anyone considering doing this to first consult with a qualified healthcare professional. Let them assess you to help determine which nutrients may be low or deficient based on dietary intake, and lab work.

A registered clinical nutritionist such as Tim Rees, BSc mBANT rCNHC from Ebersberg, Germany is licensed to support people in that country and I can support people in several provinces in Canada. If you would like more information on how I can help, please send me a note through the Contact Me form at the top of this page and you can reach out to Tim on his blog.

[Please note that I do not know Tim personally and as such this article is not an endorsement.]

To your good health!

Joy

You can follow me on:

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

References

  1. National Institute of Health, Genetic and Rare Diseases Information Centre, Alopecia universalis, https://rarediseases.info.nih.gov/diseases/614/alopecia-universalis

 

Copyright ©2023 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 Androgen Paradox of Hair Growth and Hair Loss

Androgens are male hormones and as explained below, contribute to hair growth in both men and women. But, androgens also contribute to hair loss, such as in androgenetic alopecia. This is known as the “androgen paradox”.

As explained in the previous article, one of the main contributors to both male pattern baldness and female pattern baldness, also known as androgenetic alopecia, is the hormone dihydrotestosterone (DHT). DHT is a male hormone (androgen) that is a metabolite of testosterone made by the enzyme  5 alpha-reductase (5-AR) acting on testosterone. 

But androgens also play an important role in hair growth.

The Androgen Paradox

Before people go through puberty, most parts of the body (except for the scalp) are covered in thin, fine hair known as vellus hair (“peach fuzz”). Vellus hair is generally lighter and shorter than terminal hair that grows on the scalp, which is longer and thicker [1]. As androgens increase during puberty, vellus hair follicles are change into terminal hair follicles which then produce larger, curlier, and darker hair which appears in the public area, and “arm pits” (axillary area) [1].

During puberty, androgens stimulate beard growth in men [1], but even though androgens such as testosterone, androstenedione, dehydroepiandrosterone (DHEA), and DHEA sulfate (DHEAS) are produced by the ovaries and adrenal glands of healthy women, these are not in large enough quantities to stimulate hair growth on the face. In women with Polycystic Ovarian Syndrome (PCOS) however, hair on the upper lip and chin area (hirsutism) is common and is believed to be due to high levels of male androgens and abnormal levels of luteinizing hormone (LH) from the pituitary interfering with the normal function of the ovaries [2,3].

Paradoxically, androgens also contribute to hair loss in androgenetic alopecia (AGA) [4].  A double blind control study from 1994 of people with androgenetic alopecia found that DHT levels were significantly higher in areas of bald scalp, than in areas of the scalp that contained hair [5]. In 1996, it was determined that the parts of the scalp that show balding in androgenetic alopecia have higher levels of the enzyme 5 alpha-reductase (5-AR) in the hair follicles, than the hair follicles in the parts of the scalp that do not bald [6]. These higher levels of 5-AR in the hair follicles converts testosterone to DHT, and when DHT binds to the receptors in the oil glands of hair follicles, it causes the follicles to shrink, or “miniaturize” until they eventually stop producing hair, resulting in baldness. 

As mentioned in the previous article, 5 alpha-reductase (5-AR) can be inhibited by the drug Finasteride® which lowers levels of DHT in the hair follicle, reducing the attack and slowing, or stopping hair loss.  Finasteride® also reduces the amount of DHT in the blood and scalp [7,8] and slowing androgenic alopecia progression.

As outlined in the first article in the three-part series titled, “Lotions, Potions, and Pills”, there are nutritional supplements available that are documented to restore hair growth and that are supported with the highest-quality evidence. A few of them are 5 alpha-reductase (5-AR) Inhibitors, and function similarly to Finasteride®.

The upcoming second article in the series will outline several oral hair growth supplement mixtures with the best quality scientific evidence to support hair growth — some of which also act as 5 alpha-reductase (5-AR) Inhibitors.

In addition, the third upcoming article in the series will outline evidence-based topical hair supplements that either serve as 5-AR reductase inhibitors to reduce the effect dihydrotestosterone (DHT) on hair follicles, support scalp health through their antibacterial or antimicrobial properties, or stimulate hair growth by increasing blood flow to hair follicles.

Final thoughts…

Androgens can paradoxically stimulate hair growth and cycling and this results in men having more hair on their face, and both men and women having hair in their pubic region and arm pits. Androgens can also contribute to balding on the scalp in the same individual, regardless of gender [9].

The balding effect of dihydrotestosterone (DHT) acting on hair follicles of the scalp can be reduced with use of medication treatment such as Finasteride®, as well as by evidence-based oral nutritional supplements and topical applications of essential oils, botanicals, and herbals.

While  Finasteride® is very effective at treating the hair loss associated with androgenic alopecia (as well as benign prostate hyperplasia (BPH)), its use is not without potential side effects. These can include decreased libido, the inability of men to have or maintain an erection, or problems with ejaculation [10]. 

Use oral nutritional supplements supported by robust scientific studies to promote hair growth and/or the use of topical applications of essential oils, botanicals, or herbals that have been demonstrated to be both safe and effective at reducing or stopping hair loss is also an available option.  Click here to read the first of three articles in a series on this topic.

More Info?

If you would like more information about how I could support you from a nutritional perspective, please send me a note through the Contact Me form at the top of this page.

To your good health!

Joy

You can follow me on:

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

References

    1. Inui, S., Itami, S. (2013). Androgen actions on the human hair follicle: perspectives. Exp. Dermatol. 22, 168–171. doi: 10.1111/exd.12024
    2. Barbieri RL, Ehrmann, DA. UpToDate Patient education: Polycystic ovary syndrome (PCOS) (Beyond the Basics), December 20, 2021, https://www.uptodate.com/contents/polycystic-ovary-syndrome-pcos-beyond-the-basics/
    3. Abdelazim IA, Alanwar A, AbuFaza M, et al. Elevated and diagnostic androgens of polycystic ovary syndrome. Prz Menopauzalny. 2020;19(1):1-5. doi:10.5114/pm.2020.95293
    4. Randall, V. A. (2007). Hormonal regulation of hair follicles exhibits a biological paradox. Semin. Cell Dev. Biol. 18, 274. doi: 10.1016/j.semcdb.2007.02.004
    5. Dallob, A. L., Sadick, N. S., Unger, W., Lipert, S., Geissler, L. A., Gregoire, S. L., et al. (1994). The effect of finasteride, a 5 alpha-reductase inhibitor, on scalp skin testosterone and dihydrotestosterone concentrations in patients with male pattern baldness. J. Clin. Endocr. Metab. 79, 703–706. doi: 10.1210/jcem.79.3.8077349
    6. Itami, S., Nakanishi, J., Yoshikawa, K., Takayasu, S. (1996). 21 Expression of androgen receptor, type I and type II 5 α-reductase in human hair follicle cells. J. Dermatol. Sci. 12, 86–86. doi: 10.1016/0923-1811(94)90434-0
    7. Drake, L., Hordinsky, M., Fiedler, V., Swinehart, J., Unger, W. P., Cotterill, P. C., et al. (1999). The effects of finasteride on scalp skin and serum androgen levels in men with androgenetic alopecia. J. Am. Acad. Dermatol. 41, 550–554. doi: 10.1016/s0190-9622(99)80051-6
    8. Price, V. H. (1999). Treatment of hair loss. New Engl. J. Med. 341, 964–973. doi: 10.1056/NEJM199909233411307
    9. Miranda, B. H., Charlesworth, M. R., Tobin, D. J., Sharpe, D. T., Randall, V. A. (2018). Androgens trigger different growth responses in genetically identical human hair follicles in organ culture that reflect their epigenetic diversity in life. FASEB J. 32, 795–806. doi: 10.1096/fj.201700260RR
    10. MedlinePlus [Internet]. Bethesda (MD): National Library of Medicine (US); [updated 2022 Jun 15]. Finasteride, Available from: https://medlineplus.gov/druginfo/meds/a698016.html 

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.

Nutritional Supplements With Evidence to Restore Hair Loss

People’s identity is tied to their appearance, which makes significant hair loss at any age or gender devastating, but can nutritional supplements help?

Those experiencing different types of hair loss are often desperate to find a solution, and there is no shortage of lotions, potions, and pills promising new hair growth. Are these safe and effective, or are they simply “snake oil”? This article is about evidence-based nutritional supplements that may help restore hair loss, depending on its cause. It’s important to keep in mind that nutrient needs between people differ, so supplementation is not one-size-fits-all.

Androgenic Alopecia

Androgenic alopecia is commonly known as “male pattern baldness” or “female pattern baldness,” and the leading cause of it is an androgenic hormone known as dihydrotestosterone (DHT). DHT binds to the hair follicle, causing it to shrink, and eventually, the hair stops growing entirely. Some nutritional supplements positively affect DHT and help support hair growth, but many “hair growth nutritional supplements” contain ingredients for which evidence of benefit is lacking.

A study at an alopecia clinic [1] found that 81% of the patients were female, and 63% of them used nutritional supplements, compared to the US average of 40% [2]. The most common hair loss supplements used include biotin, vitamin B12, and B-complex multivitamin and while taking these nutritional supplements may seem benign, biotin, for example, is well-known to interfere with diagnostic tests for Thyroid Stimulating Hormone (TSH). The implication of this is that people taking biotin-containing supplements to self-treat hair loss without first being evaluated for a thyroid disorder may result in missing the diagnosis and underlying cause of their hair loss. In addition to interfering with diagnostic tests, some ‘hair loss nutritional supplements’ may be toxic in high doses, while still others may interact with medications, or supplements that people are taking to restore a diagnosed nutrient deficiency [3]. 

A systematic review that was recently published in the Journal of the American Medical Association (JAMA) Dermatology (November 30, 2022) evaluated the effectiveness of nutritional supplements for treating hair loss in people without nutritional deficiency [4]. This first article is based on this current systematic review.

Three Main Types of Hair Loss

There are three main types of hair loss, telogen effluvium, androgenic alopecia (AGA), and alopecia areata (AA).

Telogen effluvium (TE) is the most common form of diffuse hair loss [5] and usually occurs after a profound stress, shock or traumatic event including childbirth,  a thyroid disorder, or rapid weight loss. This type of hair loss was covered in this earlier article. But TE is not the only type of hair loss in hypothyroidism. In a study of more than 1200 people with thyroid disorder, half (50%) of people aged 40 years old and older had either alopecia areata, or androgenetic alopecia [6].

Androgenic alopeciaAndrogenic alopecia (AGA) affects up to 50% of men and women. In men is called ‘male pattern baldness’ and is mainly seen on the crown of the head and the temples. In women, it is called ‘female pattern baldness’ and is primarily seen at the crown of the head, with a broader center part. Androgenic alopecia is a genetic disorder that involves both maternal (mother’s) and paternal (father’s) genes, with sons being 5-6 times more likely to have it if their fathers were balding [7]. 

Alopecia areataAlopecia areata (AA) is an autoimmune disorder where the body’s immune system attacks the follicles. As a result, hair often comes out in clumps, usually the size and shape of a quarter, but it can affect more expansive areas of the scalp [8]. It can occur in those with other autoimmune conditions, including thyroid disease. 

There are medication treatments available for the different types of hair loss, and there is increasing evidence that taking specific nutritional supplements can be helpful in helping restore hair loss.

A systematic review published in JAMA Dermatology [4] published November 30, 2022 — just a month ago, evaluated the effectiveness of nutritional supplements for treating hair loss in people without nutritional deficiency. The dietary supplements with the highest-quality evidence of potential benefit were categorized according to their mechanism of action and are outlined in this article.

Dihydrotestosterone (DHT) as a Main Cause of Hair Loss

One of the main contributors to androgenetic alopecia (AA) is the male hormone (androgen) called dihydrotestosterone (DHT). DHT is made by an enzyme called 5 alpha-reductase (5-AR) acting on testosterone. When DHT binds to the receptors in the oil glands of hair follicles, it causes the follicles to shrink, shortening their life span. Eventually, these follicles shrink so much that they stop producing hair. The end result is baldness. DHT can be suppressed by medications such as Finasteride®, which lowers levels of DHT. This reduces the attack on hair follicles, slowing or stopping hair loss.

(Minoxidil® is a hair loss medication that works by an entirely different mechanism. It acts as a vasodilator, increasing blood flow in the scalp by making blood vessels wider. It is thought that this increased blood flow slows hair loss and encourages hair to regrow.)

[Update, December 29, 2022: While androgens such as DHT contribute to baldness by their detrimental effect on hair follicles in the scalp, androgens like DHT are also a key player in hair growth. This contradictory role of androgens is known as the “androgen paradox”. This short supplemental article explains more. ]

Nutritional Supplements – the role of 5-α reductase (5-AR) inhibitors in restoring hair loss

Pumpkin Seed Oil as a nutritional supplement in hair loss

nutritional supplements - Pumpkin seedsPumpkin seed oil is known to be effective in treating benign prostate hyperplasia (BPH) because it acts as a 5AR inhibitor [9,10], so it was an excellent candidate to study for its effect on hair growth. In a 2014 study, 76 male androgenic alopecia (AGA) patients were divided into two groups. For 24 weeks, one group of subjects took a 400 mg capsule of pumpkin seed oil each day, while the other group took a placebo. The group taking the pumpkin seed oil nutritional supplement showed significantly superior hair growth, with a mean hair count increase of 40% in the pumpkin seed oil-treated men compared to 10% in the placebo-treated men. There were no differences in adverse effects between the two groups.

Nutritional Supplements in Hair Loss – Saw Palmetto

nutritional supplements -Saw PalmettoIn a 2004 pilot study, six of ten subjects (60%) that took an extract made from 200 mg Saw Palmetto extract (Serenoa repens), 50 mg betasitosterol, along with 50 mg lecithin, 100 mg inositol, 25 mg phosphatidyl choline, 15 mg niacin, and 100 μg biotin for 5 months were reported to have improved hair growth compared to the placebo controlled group (11%), however the difference was not statistically significant [11]. Studies with larger groups of both treatment and control groups is needed before conclusions can be made. Most importantly, it is hard to know if the benefits were due to the Saw Palmetto, or some of the other ingredients in the supplement.  For this reason, I think this next study is more helpful.

A two year randomized control study of 100 male patients with mild to moderate androgenic alopecia took either 320 mg of dry Saw Palmetto nutritional supplement extract (Serenoa repens) daily for 24 months, or 1 mg Finasteride daily for the same time period.  While Finasteride was significantly more effective at slowing hair loss, at 24-months the Saw Palmetto extract did stabilize hair loss. [12].

The results of this study suggest that Saw Palmetto can stabilize hair loss over two years, but is less effective than the medication Finasteride.

The Role of Specific Micronutrients in Restoring Hair Loss

Nutritional Supplements for Hair Loss – Vitamin D

Three studies from the last 5-10 years have demonstrated that that lower levels of vitamin D, or vitamin D deficiency have been associated with all three forms of hair loss, including androgenic alopecia [13], alopecia areata [14], and telogen effluvium [15].

A small 2021 study supplemented 40 women with telogen effluvium with very high oral vitamin D3 (200,000 IU every two weeks for six weeks). The study reported that more than 80% had improved results on a hair pull test after six months, with no adverse side effects [16]. However, the limitation of this study was that it was unknown if any of these subjects were deficient in vitamin D before taking the supplements, there was no control group, and telogen effluvium tends to resolve by itself over the same six-month period without treatment.

nutritional supplements - vitamin D capsulesBefore beginning supplementation, it would be prudent to assess vitamin D status and to determine how low or deficient it is, then increase dietary intake of vitamin D, and supplement as necessary to attain and maintain sufficient blood levels of vitamin D.

nutritional supplements - salmon as a source of vitamin DFoods that are naturally good sources of vitamin D include fatty fish such as salmon, mackerel and tuna.

Nutritional Supplements for Hair Loss – Zinc

A deficiency of zinc is associated with telogen effluvium, and lower zinc levels have been observed in people with alopecia areata (AA) [17-19]. Two small studies of zinc supplementation in patients with alopecia areata both reported benefits. The first study with 38 subjects was from 1981 [20] and supplemented using 220 mg of zinc sulfate per day. The second study from 2012 [21] had 67 subjects supplemented with 5 mg/kg body weight per day of zinc sulfate. Both studies reported benefits at three months; however, larger studies are needed.

It would be best to assess zinc status for those with hair loss (especially alopecia areata) prior to supplementing with zinc.

sea urchin roe as a source of zincIf zinc status is low, increasing dietary intake of zinc would be a great place to start. Good sources of zinc include red meat, poultry, seafood such as oysters, crab, lobster, and sea urchin (uni, in Japanese), as well as nuts.

If needed to achieve adequate blood levels of zinc, a supplement can be added to attain, and maintain zinc adequacy, but it’s important to ensure there is adequate copper intake as well, as zinc depletes copper. Beef liver is a very good source of dietary copper, but eating 3 or 4 ounces once a week may be enough, as it has 6 times the recommended dietary intake of copper, and high amounts of preformed vitamin A. It is also important not to take zinc supplements within several hours of taking iron supplements, as they complete for binding sites.

Nutritional Supplements for Hair Loss – Vitamin B12

Vitamin B12 is necessary for DNA synthesis and it was proposed in a 2017 report on the role of micronutrients in alopecia areata that vitamin B12 could be helpful in increasing the number of hair follicles [17].

A 2018 study of people with telogen effluvium that included symptoms of itching, pain, soreness, and/or burning were evaluated for symptoms of B12 deficiency. While lab normal values were 200-400 pg/mL, deficiency was evaluated to be <550 pg/ml, a cutoff limit reported to be used in other countries. After four months, 90% of subjects that received either a daily B12 tablet or monthly B12 injection had significant decrease or even an absence of hair shedding [23]. The main shortcoming of this study was the self-resolving nature of telogen effluvium — which means that over the same period of time, doing nothing could have resulted in improvement is hair loss.

nutritional supplements - liver as a source of vitamin B12The best dietary sources of vitamin B12 are organ meats, including liver and kidney, clams, sardines, and beef, however, some disorders and advanced age can result in reduced dietary absorption of vitamin B12. Testing vitamin B12 status is important especially in older adults who have decreased absorption of B12 due to decreased intrinsic factor, as well as testing B12 status in those taking medication to lower stomach acid. 

Nutritional Supplements – the role of antioxidants in restoring hair loss

Oxidative stress has been thought to play a role in all three types of hair loss [24-26] and antioxidants such as selenium, vitamins A, E and C, and carotenoids (yellow, orange or red coloured fat-soluble pigments found in vegetables, fruit, and some fish. 

A 2015 randomized control study compared the effects of giving a supplement containing omega 3 fat from fish, omega 6 fat from blackcurrant seed oil, as well as the antioxidants lycopene (from tomato), vitamin C, and vitamin E versus giving no supplement to 188 women diagnosed with stage 1 androgenic alopecia [27]. The intervention group had significantly increased hair density and hair thickness at six months.

A 2010 randomized control study compared giving a supplement containing mixed tocotrienol from the vitamin E family versus a placebo to patients with unspecified hair loss. The 50 mg mixed capsules given to the intervention group had 30.8% alpha-tocotrienol, 56.4% gamma-tocotrienol, and 12.8% delta-tocotrienol, as well as 23 IUs alpha-tocopherol). Twenty one subjects were randomly assigned receive 2 x 50 mg (100 mg) of mixed tocotrienols daily, while 17 subjects were assigned to receive an oral placebo capsule. At 8-months, the number of hairs of the subjects in the intervention group increased by 34.5% compared to the placebo group which had a 0.1% decrease [28]. The shortcomings of this study were the small sample size and that the study did not define hair loss in the inclusion criteria of subjects. 

Nutritional Supplements – more is not always better

Caution needs to be taken when choosing types and amounts of antioxidant supplements as excessive use of supplements such as selenium, for example has been tied both to toxic effects and hair loss [29]. Even when getting selenium in the diet by eating Brazil nuts, only 2 is already at the maximum daily amount. Eating 4 or 5 Brazil nuts can exceed the safe upper tolerance of selenium for adults, so more is not better. 

Excess vitamin A intake can result in vitamin A intoxication which can result in seizures or blurred vision, and long term (chronic) over supplementation with vitamin A can result in several symptoms, including muscle and bone pain, high blood lipids and ironically alopecia, or hair loss [30].

nutritional supplements - cod livers as a source of vitamin AThe best sources of preformed vitamin A (retinol) are beef liver, fish, and eggs and a delicious and very rich source is Icelandic cod livers.

Cod livers are very high in retinol, and just half a 115g can contains 450% the recommended daily intake for vitamin A. To avoid getting too much preformed vitamin A, it is best not to eat cod livers more than once every week or two, and even further apart if also regularly consuming beef liver which is also high in preformed vitamin A.

Before beginning to take supplements it is important to assess intake form food sources, so as not to take too much as a supplement.

Other Nutritional Supplements – probiotics and growth hormone modulators

kim chee as a probioticProbiotics have been hypothesized to improve blood flow to the scalp and one study from 2020 used a kimchi and fermented soybean paste (cheonggukjang) probiotic product.

Twenty-three men and twenty-three women with androgenic alopecia (AGA) were given the supplement and at four months, 93% showed significant improvement in either hair thickness and/or hair count, with no serious side effects [31]. The limitations of this study were the small sample size and lack of a control group.

capsaicin Capsaicin, is the chemical that give hot chilis their spiciness and is used as a topical pain reliever. When  applied to the scalp has been found to increase Insulin-like Growth Factor I (IGF-1) which is involved in hair growth [32].

A randomized control study of a capsaicin and isoflavone supplement (6 mg capsaicin, 75 mg isoflavone (from soy) in 48 adults with either androgenic alopecia (AGA) or alopecia areata (AA) compared to controls found significantly more hair growth in the capsaicin and isoflavone group at 5 months, and no adverse effects were reported. The limitations of this study were its small sample size as well as the inclusion of various types of alopecia.

Final Thoughts…

In the United States, dietary supplements are normally considered a food and as such, their safety or effectiveness are not evaluated by the Food and Drug Administration (FDA). It is only if a product is labelled to treat a disease that the product meets the definition of a drug and needs to establish its efficacy [33].

In Canada, however, dietary supplements are considered Natural Health Products (NHP) by Health Canada and are treated as non-prescription drugs which are regulated under the Natural Health Product Regulations. According to Health Canada, in the ten years from 2004 (when the Natural Health Product Regulations came into existence) and 2014, nearly 55,000 licenses for NHPs were issued [34].

The ease by which Canadians can order supplements online from the US essentially bypasses any governmental safeguards put into place by Health Canada so it is important that people in both countries are aware that there is no FDA oversight for safety or efficacy for supplements purchased from the US. For this reason, it is best that before people begin using dietary supplements to self-treat hair loss, that they discuss this with a knowledgeable healthcare professional, such as their doctor or Registered Dietitian. In addition, for those already taking dietary supplements, it is important before going for lab tests to mention to your doctor and Dietitian which supplements you are taking so that they can ensure that you discontinue use of specific supplements for an sufficiently long period of time before the test (such biotin before a Thyroid Stimulating Hormone (TSH) test).

More Info?

Hair loss can be devastating, but before parting with substantial sums for money for lotions, potions, or pills that promise new hair growth, first take the time to find out what you need. 

Consider finding out if your diet or lifestyle may put you at risk for nutrient deficiencies, and if so to have those evaluated. Ask yourself if it is possible you may have a thyroid disorder (this article may help) so that you can have diagnostic tests before taking supplements that can interfere with getting accurate results.

Finally, if blood tests come back indicating that you may have low nutrient status or a deficiency, find out which nutrients can be adequately obtained from food, and which may need to be supplemented.

Nutritional supplements can be very helpful if used correctly, but taken in the wrong dosage, or at the wrong timing, supplements can interfere with the absorption of medications you may take, and/or with other nutrients you are already low on.

If you would like more information on how I can help assess your dietary intake or nutrient status of specific nutrients, please send me a note through the Contact Me form at the top of this page.

To your good health!

Joy

You can follow me on:

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

 

References

    1. Burns LJ, Senna MM. Supplement use among women experiencing hair loss. Int J Womens Dermatol. 2020;6(3):211. doi:10.1016/j.ijwd.2020.01.002
    2. E.D. Kantor, C.D. Rehm, M. Du, E. White, E.L. Giovannucci, Trends in dietary supplement use among U.S. adults from 1999–2012, JAMA, 316 (14) (2016), pp. 1464-1474
    3. Ronis MJJ, Pedersen KB, Watt J. Adverse effects of nutraceuticals and dietary supplements. Annu Rev Pharmacol Toxicol. 2018;58:583-601. doi:10.1146/annurev-pharmtox-010617-052844
    4. Drake L, Reyes-Hadsall S, Martinez J, Heinrich C, Huang K, Mostaghimi A. Evaluation of the Safety and Effectiveness of Nutritional Supplements for Treating Hair LossA Systematic ReviewJAMA Dermatol. Published online November 30, 2022. doi:10.1001/jamadermatol.2022.4867
    5. Malkud S. Telogen Effluvium: A Review. J Clin Diagn Res. 2015;9(9):WE01-WE3. doi:10.7860/JCDR/2015/15219.6492
    6. Vincent M, Yogiraj K. A descriptive study of alopecia patterns and their relation to thyroid dysfunction. Int J Trichol 2013;5:57-60
    7. Ho CH, Sood T, Zito PM. Androgenetic Alopecia. Updated Nov 15, 2021. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing, https://www.ncbi.nlm.nih.gov/books/NBK430924/#_NBK430924_pubdet_
    8. Medical News Today, Alopecia areata: Causes, diagnosis and treatments, April 7, 2022, https://www.medicalnewstoday.com/articles/70956
    9. Hong H, Kim CS, Maeng S. Effects of pumpkin seed oil and saw palmetto oil in Korean men with symptomatic benign prostatic hyperplasia. Nutr Res
      Pract. 2009;3(4):323-327. doi:10.4162/nrp.2009.3.
      4.323
    10. Cho YH, Lee SY, Jeong DW, et al. Effect of pumpkin seed oil on hair growth in men with androgenetic alopecia: a randomized, double-blind, placebo-controlled trial. Evid Based Complement Alternat Med. 2014;549721. doi:10.1155/2014/549721
    11. Prager N, Bickett K, French N, Marcovici G. A randomized, double-blind, placebo-controlled trial to determine the effectiveness of botanically
      derived inhibitors of 5-alpha-reductase in the treatment of androgenetic alopecia. J Altern Complement Med. 2002;8(2):143-152. doi:10.1089/
      107555302317371433
    12. Rossi A, Mari E, Scarno M, et al. Comparative effectiveness of finasteride vs Serenoa repens in male androgenetic alopecia: a two-year study. Int J
      Immunopathol Pharmacol. 2012;25(4):1167-1173. doi:10.1177/039463201202500435
    13. Banihashemi M, Nahidi Y, Meibodi NT, Jarahi L, Dolatkhah M. Serum vitamin D3 level in patients with female pattern hair loss. Int J Trichology. 2016;
      8(3):116-120. doi:10.4103/0974-7753.188965
    14. Rasheed H, Mahgoub D, Hegazy R, et al. Serum ferritin and vitamin D in female hair loss: do they play a role? Skin Pharmacol Physiol. 2013;26(2):101-107. doi:10.1159/000346698
    15. Lee S, Kim BJ, Lee CH, Lee WS. Increased prevalence of vitamin D deficiency in patients with alopecia areata: a systematic review and
      meta-analysis. J Eur Acad Dermatol Venereol. 2018;
      32(7):1214-1221. doi:10.1111/jdv.14987
    16. Sattar F, Almas U, Ibrahim NA, et al. Efficacy of oral vitamin D3 therapy in patients suffering from diffuse hair loss (telogen effluvium). J Nutr Sci
      Vitaminol (Tokyo). 2021;67(1):68-71. doi:10.3177/jnsv.67.68
    17. Thompson JM, Mirza MA, Park MK, Qureshi AA, Cho E. The Role of micronutrients in alopecia areata: a review. Am J Clin Dermatol. 2017;18(5):
      663-679. doi:10.1007/s40257-017-0285-x
    18. Abdel Fattah NS, Atef MM, Al-Qaradaghi SM. Evaluation of serum zinc level in patients with newly diagnosed and resistant alopecia areata. Int J
      Dermatol. 2016;55(1):24-29. doi:10.1111/ijd.12769
    19. Mussalo-Rauhamaa H, Lakomaa EL, Kianto U, Lehto J. Element concentrations in serum, erythrocytes, hair and urine of alopecia patients.
    20. Ead RD. Oral zinc sulphate in alopacia areata-a double blind trial. Br J Dermatol. 1981;104(4): 483-484. doi:10.1111/j.1365-2133.1981.tb15323.x
    21. Sharquie KE, Noaimi AA, Shwail ER. Oral zinc sulphate in treatment of alopecia areata (double blind; cross-over study). J Clin Exp Dermatol Res.
      2012;3(150).
    22. Siavash M, Tavakoli F, Mokhtari F. Comparing the effects of zinc sulfate, calcium pantothenate, their combination and minoxidil solution regimens
      on controlling hair loss in women: a randomized controlled trial. J Res Pharm Pract. 2017;6(2):89-93. doi:10.4103/jrpp.JRPP_17_17
    23. Daly T, Daly K. telogen effluvium with dysesthesia (ted) has lower B12 levels and may respond to B12 supplementation. J Drugs Dermatol.
      2018;17(11):1236-1240.
    24. Prie BE, Iosif L, Tivig I, Stoian I, Giurcaneanu C. Oxidative stress in androgenetic alopecia. J Med Life. 2016;9(1):79-83.
    25. Savci U, Senel E, Oztekin A, Sungur M, Erel O, Neselioglu S. Ischemia-modified albumin as a possible marker of oxidative stress in patients with
      telogen effluvium. An Bras Dermatol. 2020;95(4): 447-451. doi:10.1016/j.abd.2020.01.005
    26. Öztürk P, Arıcan Ö, Kurutaş EB, Mülayim K. Oxidative stress biomarkers and Adenosine deaminase over the alopecic area of the patients with alopecia areata. Balkan Med J. 2016;33(2):188-192. doi:10.5152/balkanmedj.2016.16190
    27. Le Floc’h C, Cheniti A, Connétable S, Piccardi N, Vincenzi C, Tosti A. Effect of a nutritional supplement on hair loss in women. J Cosmet
      Dermatol. 2015;14(1):76-82. doi:10.1111/jocd.12127
    28. Beoy LA,WoeiWJ, Hay YK. Effects of tocotrienol supplementation on hair growth in human volunteers. Trop Life Sci Res. 2010;21(2):
      91-99.
    29. Sutter ME, Thomas JD, Brown J, Morgan B. Selenium toxicity: a case of selenosis caused by a nutritional supplement. Ann Intern Med. 2008;148
      (12):970-971. doi:10.7326/0003-4819-148-12-200806170-00015
    30. Olson JM, Ameer MA, Goyal A. Vitamin A Toxicity. [Updated 2022 Aug 8]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2022 Jan-.
    31. Park DW, Lee HS, Shim MS, Yum KJ, Seo JT. Do kimchi and cheonggukjang probiotics as a functional food improve androgenetic alopecia? a clinical pilot study. World J Mens Health. 2020;38 (1):95-102. doi:10.5534/wjmh.180119
    32. Harada N, Okajima K. Effect of topical application of capsaicin and its related compounds on dermal insulin-like growth factor-I levels in mice
      and on facial skin elasticity in humans. Growth Horm IGF Res. 2007;17(2):171-176. doi:10.1016/j.ghir. 2006.12.005
    33. US Food and Drug Administration. Questions
      and Answers on Dietary Supplements. Accessed December 27, 2022. https://www.fda.gov/food/information-consumers-using-dietary-supplements/questions-and-answers-dietary-supplements
    34. Health Canada, Natural Health Products Program Quarterly Snapshot – Quarter 1 (Fiscal year 2014-2015), https://www.canada.ca/en/health-canada/services/drugs-health-products/natural-non-prescription/activities/quarterly-snapshot-quarter-1-2014-2015.html

 

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.

 

Hair Loss in Hypothyroidism – nutrients of importance

In the previous article titled Hair Loss – root causes was about the three most common types of hair loss, including androgenic alopecia, alopecia areata, and the most common form of diffuse hair loss, telogen effluvium which is the type often associated with hypothyroidism.  This article explains the role of specific vitamin and mineral deficiencies in hair loss and how treating them can help restore hair growth.

As explained in the previous article, telogen effluvium (TE) is the most common form of hair loss in hypothyroidism and is where the hair often comes out in clumps in the shower or a brush. Hair loss is usually from all over the scalp but may occur more on the temples, the part, and the crown of the head [1]. But TE is not the only type of hair loss in hypothyroidism. In a study of more than 1200 people with thyroid disorder, half (50%) of people aged 40 years old and older had either alopecia areata, or androgenetic alopecia [2].

What makes the hair loss associated with thyroid dysfunction particularly challenging is that it occurs 2-3 months after the overt symptoms of thyroid disorder began, which is usually once they’ve already begun thyroid hormone treatment for hypothyroidism.

The pictures below are of me and are provided for illustrative purposes only. The one on the left was taken at one of my son’s wedding in June 2022, just prior to being diagnosed with profound hypothyroidism.  I clearly had the symptom of edema (facial swelling, leg and hand swelling) associated with undiagnosed / untreated hypothyroidism, the hair on my head was minimally affected. The photo on the right was taken three months later, after beginning hormone replacement treatment for hypothyroidism, and the hair loss and shiny scalp is very apparent. 

No hair loss at height of untreated hypothyroidism, telogen effluvium hair loss 3 months later

Hair loss in hypothyroidism

Normally,  90-95% of hair follicles are in the growth (anagen) phase, with only 5–10% being in the resting (telogen) phase. Only a few follicles are in the transitional (catagen) phase [1] at any one time.  At the end of the telogen phase, the hair falls out and under normal circumstances that would amount to ~ 100-150 hairs per day.

Hair growth stages

 

In telogen effluvium, the growth (anagen) phase slows down and up to 50% of the follicles move into the telogen phase, where shedding occurs. i.e., hair loss becomes 5-10 greater than normal, with people losing up to 50% of their hair.  As can be seen in the photo above, at 3 months I had lost 50% of my hair. 

It wasn’t only half the hair on my head that I lost, also lost 1/2 my eyelashes and part of the outer third of my eyebrows.

Since the period of the most dramatic loss occurs approximately 2-3 months after the triggering event, many people don’t relate the shedding to the event that caused it. 

Hypothyroidism can result in hair loss, but nutrient deficiencies can sometimes underlie hypothyroidism (such as in iodine or iron deficiency) and can often make the symptoms of hypothyroidism worse.  Each person is different and the degree to which underlying nutrient deficiencies may make hair loss worse, varies.  As a result, the sufficiency of the key nutrients related to hypothyroidism should be evaluated. 

If any of these nutrients are found to be deficient or suboptimal, correct supplementation can support the regrowth of hair, but it should be noted that the timing of supplements with respect to each other and in relation to the timing of thyroid medication is essential. The reason for this is that some nutrients complete for binding sites (e.g., iron, zinc and copper) and need to be taken separated from each other. In addition, thyroid medication needs to be taken at least a half hour before and food or vitamin / mineral supplementation, or two hours afterwards. When there are several nutrient deficiencies and multiple doses per day of thyroid medication, this can take quite a bit of planning to get the timing right.

Iron deficiency is very common and one of the deficiencies that contributes to telogen effluvium [3,4], and iron is often low in hypothyroidism [5]. In some cases, treating iron deficiency may in itself be sufficient to restore thyroid function [5]. The reason is that the body requires sufficient iron to convert the inactive thyroid hormone thyroxine (T4) into the active thyroid hormone triiodothyronine (T3) and insufficient iron stores could interfere with this conversion. 

It has been recommend that to reverse significant hair loss due to telogen effluvium to maintain serum ferritin at levels of >157 pmol/L (70 ng/dL) [4].

Some of the best food sources of heme iron (the most bioavailable form) are oysters, clams and liver.

Adequate vitamin C intake is required for intestinal absorption of iron, so ensuring adequate vitamin C intake is important those with hair loss associated with iron deficiency.

Selenium was identified in the 1990s as a component of the enzyme that activates thyroid hormone through the conversion of (inactive) T4 to (active)T3 [6]. Selenium is also used to by the body for the formation of glutathione, a powerful antioxidant that protects the thyroid from inflammation and oxidative stress.

Food sources of selenium include Brazil nuts, with 2 Brazil nuts meeting the daily requirement of 200 mcg of selenium. Other good sources of selenium are mushrooms, eggs, fish such as cod and halibut, chicken and eggs. 

Selenium deficiency is a significant problem in the developing world, but thought to be rare in the West. Research from 2012 indicates that the selenium content of the soil in the US was already lowest in the major agricultural areas of the Northwest, Northeast, Southeast, and areas of the Midwest near the Great Lakes[7] and at the time, only the Great Plains and the Southwest were reported to have adequate selenium content in the soil [6].

Zinc plays a key role in the metabolism of thyroid hormones, specifically by regulating the enzymes that are involved in the activation of T4 to T3, as well as regulating thyrotropin releasing hormone (TRH), and thyroid stimulating hormone (TSH) synthesis [8]. Zinc also modulates structures of essential transcription factors that are involved in the synthesis of thyroid hormones, as well as influence the levels of TSH, T4,  and T3 in the blood [8]. It is important to be tested first to know if there is a zinc deficiency before taking a supplement, because supplemental zinc can result in a reduction in copper, and if taking zinc, it is important not to take it with iron or calcium supplements as they complete for binding sites.

Eating foods rich is zinc is the safest way to ensure adequate intake and good sources of zinc include red meat, poultry, seafood such as oysters, crab and lobster, as well a nuts. 

Vitamin D – in Canada which is above the 49th parallel, it is  known that between 70% and 97% of the population demonstrates vitamin D insufficiency, with 32% in Canada being Vitamin D deficient [9].  Deficiency of Vitamin D in the US is even higher, at 42% [10]. It has been known that there was a relationship between Hashimoto’s (autoimmune) hypothyroidism and Vitamin D deficiency [11], it is now known that non-autoimmune hypothyroidism is associated with vitamin D deficiency [12]. A randomized, double-blind, placebo-controlled trial from 2018 in over 200 hypothyroid patients aged 20-60 years old found that supplementing with vitamin D improved TSH levels and calcium levels in hypothyroid patients [13]. 

In addition to dairy foods that are fortified with Vitamin D, foods that are naturally good sources of Vitamin D include fatty fish such as salmon, mackerel and tuna.

 

Vitamin B12  – It is known that people with Hashimoto’s disease (autoimmune hypothyroidism) have a higher prevalence of pernicious anemia [14], which is caused by a deficiency of vitamin B12, either due to a lack of B12 the diet or an inability to absorb it. In addition, vitamin B12 deficiency can mimic many of the symptoms of hypothyroidism such as fatigue, weakness, yellowish skin, some of the mental health symptoms. The best sources of vitamin B12 are organ meats, including liver and kidney, clams, sardines, and beef.


[UPDATE: December 11, 2022] The photo on the top, below was taken three months after being diagnosed with hypothyroidism and beginning hormone replacement treatment. The hair loss is obvious, as is my shiny scalp. The photo on the bottom was taken today — three months later. It clearly shows the regrowth of hair which is the result of both hormone replacement treatment, and three months of nutrient supplementation to support regrowth. [Note: Each person’s results will be different of course, depending which nutrient deficiencies they may have, and whether these deficiencies were due to the hypothyroidism itself, the result of inadequate dietary intake, or both].

 

Hair regrowth after 3 months thyroid treatment and nutrient supplementation

…and the hair regrowth wasn’t only on my scalp.  When I first lost so much hair, I also lost most about half of my eyelashes, too.  A month ago (Nov. 18, 2022), I took a picture of them growing back in, and below is that photo and what they look like almost a month later (December 13, 2022), without any mascara or eyeliner.

Eyelashes growing back in

POSTSCRIPT (November 18, 2022):  In writing this post yesterday, I came across several research papers that referred to the role of several of the nutrients of importance to hair loss in hypothyroidism, to premature hair greying. While my grey hair certainly was not “premature,”  look what I found today! 

A recent study mapped hundreds of proteins inside of hair and found that white hairs contained more proteins linked to mitochondria and energy use which suggests that metabolism and mitochondria may play a role in hair greying. Since thyroid hormones are known to be the major controllers of metabolic rate, it makes sense that hair that was previously dark might turn grey as the result of hypothyroidism, and revert back to dark with thyroid hormone correction. 

[Rosenberg AM, Rausser S, Ren J, et al. Quantitative mapping of human hair greying and reversal in relation to life stress. Elife. 2021;10:e67437. Published 2021 Jun 22. doi:10.7554/eLife.67437]


Final Thoughts…

While treating hypothyroidism is a medical prescription of thyroid replacement medication in an optimal dosage, determining if any nutritional deficiencies may be contributing to the condition, or mimicking its symptoms, is essential.

Having dietary intake assessed and, if indicated, having blood tests to determine if nutrient deficiencies exist and correcting them can go a long way to helping people feel better and supporting regrowth from hair loss.

It is important to remember that taking supplements needs to be done wisely. “More is not better” when it comes to taking nutrient supplements.

For example, nutrients such as selenium can be toxic in excess amounts, even when eaten as Brazil nuts.

Some nutrients, such as biotin which is often taken by people for hair growth can interfere with thyroid hormone tests.

Iodine is another nutrient that should not be supplemented when people are taking thyroid hormone replacement medication.

If you aren’t sure if your nutrient intake or nutrient status of specific nutrients sufficient, then having a nutritional assessment and blood tests when needed is a great place to start. 

More Info?

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

To your good health!

Joy

 

You can follow me on:

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

 

References

    1. Malkud S. Telogen Effluvium: A Review. J Clin Diagn Res. 2015;9(9):WE01-WE3. doi:10.7860/JCDR/2015/15219.6492
    2. Vincent M, Yogiraj K. A descriptive study of alopecia patterns and their relation to thyroid dysfunction. Int J Trichol 2013;5:57-60
    3. Almohanna HM, Ahmed AA, Tsatalis JP, Tosti A. The Role of Vitamins and Minerals in Hair Loss: A Review. Dermatol Ther (Heidelb). 2019;9(1):51-70. doi:10.1007/s13555-018-0278-6
    4. Trost LB, Bergfeld WF, Calogeras E. The diagnosis and treatment of iron deficiency and its potential relationship to hair loss. J Am Acad Dermatol. 2006;54(5):824–844.
    5. Ghiya R, Ahmad S. SUN-591 Severe Iron-Deficiency Anemia Leading to Hypothyroidism. J Endocr Soc. 2019 Apr 30;3(Suppl 1):SUN-591. doi: 10.1210/js.2019-SUN-591. PMCID: PMC6552785.
    6. Winther, K.H., Rayman, M.P., Bonnema, S.J. et al. Selenium in thyroid disorders — essential knowledge for clinicians. Nat Rev Endocrinol 16, 165–176 (2020). https://doi.org/10.1038/s41574-019-0311-
    7. Mistry HD, Broughton Pipkin F, Redman CW, Poston L. Selenium in reproductive health. Am J Obstet Gynecol. 2012 Jan;206(1):21-3
    8. Severo JS, Morais JBS, de Freitas TEC, et al. The Role of Zinc in Thyroid Hormones Metabolism. Int J Vitam Nutr Res. 2019;89(1-2):80-88. doi:10.1024/0300-9831/a00026
    9. Schwalfenberg GK, Genuis SJ, Hiltz MN. Addressing vitamin D deficiency in Canada: a public health innovation whose time has come. Public Health. 2010;124(6):350-359. doi:10.1016/j.puhe.2010.03.00
    10. Forrest KY, Stuhldreher WL. Prevalence and correlates of vitamin D deficiency in US adults. Nutr Res. 2011;31(1):48-54. doi:10.1016/j.nutres.2010.12.001
    11. Botelho IMB, Moura Neto A, Silva CA, Tambascia MA, Alegre SM, Zantut-Wittmann DE. Vitamin D in Hashimoto’s thyroiditis and its relationship with thyroid function and inflammatory status. Endocr J. 2018;65(10):1029-1037. doi:10.1507/endocrj.EJ18-0166
    12. Ahi S, Dehdar MR, Hatami N. Vitamin D deficiency in non-autoimmune hypothyroidism: a case-control study. BMC Endocr Disord. 2020;20(1):41. Published 2020 Mar 20. doi:10.1186/s12902-020-0522-9
    13. Talaei A, Ghorbani F, Asemi Z. The Effects of Vitamin D Supplementation on Thyroid Function in Hypothyroid Patients: A Randomized, Double-blind, Placebo-controlled Trial. Indian J Endocrinol Metab. 2018;22(5):584-588. doi:10.4103/ijem.IJEM_603_17
    14. Ness-Abramof R, Nabriski DA, Braverman LE, et al. Prevalence and evaluation of B12 deficiency in patients with autoimmune thyroid disease. Am J Med Sci. 2006;332(3):119-122. doi:10.1097/00000441-200609000-00004

 

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.