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. 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 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 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 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 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.

Lotions Potions and Pills – a new three part series on hair growth supplements for various types of hair loss

Lotions, Potions and Pills is new three-part series about evidence-based oral and topical nutritional supplements that are documented to improve hair number and/or hair density in different types of hair loss.

This first article in this series summarized oral nutritional supplements with the highest-quality evidence to support restored hair growth.

The second article in the series is also based on the findings of this recently published systematic review and will summarize the studies commercial oral hair growth mixtures with the best quality evidence to support hair growth.

The third article in this series will be about the evidence-based topical hair supplements including essential oils, botanicals, and herbals 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.


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 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 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 dietary 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. ]

The Role of 5-α reductase (5-AR) Inhibitors in Restoring Hair Loss

Pumpkin Seed Oil

Pumpkin 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 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.

Saw Palmetto 

In 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 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

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.

Before 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.

Foods that are naturally good sources of vitamin D include fatty fish such as salmon, mackerel and tuna.

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.

If 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.

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.

The 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. 

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. 

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].

The 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.

Probiotics and Growth Hormone Modulators

Probiotics 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, 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/


Personal Note (updated January 10, 2023):

September 3, 2022 (3 months after being diagnosed and beginning treatment for hypothyroidism)

My interest in nutritional supplements with evidence to restore hair loss was more than academic. Just like 50% of people over 40 years old with thyroid disorders, I not only developed telogen effluvium three months after showing symptoms of profound hypothyroidism, but also androgenic alopecia. My search for evidence-based solutions began in the scientific literature, and this article comes out of that research.

To find what worked for me, I first needed to understand the type of hair loss that I had, as well as my dietary intake and nutrient status of specific nutrients. Once I knew this, developing an effective regime of oral and topical supplements wasn’t difficult. Each person’s needs will be different.

People pay so much money for “hair regrowth formulas” that promise results “in just a month,” but if it sounds too good to be true, it probably is.

First, hair loss has to stop. Unfortunately, even with using nutritional supplements with solid evidence of effectiveness, it can take ~1 to 1.5 years for hair to be fully restored, and complete restoration may not be possible, depending on the reason for the hair loss.

Below is a photo of my progress after 4 months of treatment. Again, everyone’s progress will be different, depending on the cause of their hair loss, the medication treatment they receive, and the type of nutritional support they have. This is what it has been like for me, and it will still take another year for my hair to be fully restored.

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 articletelogen 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. The one on the left was taken at one of my son’s wedding in June 2022, just prior to being diagnosed with 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.

 

 

 

Hypothyroidism 101

This article provides an easy-to-understand overview of hypothyroidism, including what the thyroid gland does, the main thyroid hormones, how hypothyroidism is diagnosed, the main causes of hypothyroidism, getting evaluated and diagnosed, as well as the 3 options for having thyroid panel blood tests done.

The Thyroid Gland

The thyroid is butterfly-shaped gland situated in the middle of the lower front part of the neck. While it isn’t very big, it plays a very important role in the regulation of metabolism which is the process by which the food we eat is converted to energy.

When the thyroid doesn’t function properly, it affects metabolism. In the case that the thyroid is underactive, it results in a slowing of everything from heart rate, our ability to generate heat to stay warm, for muscles to do work, and for us to think properly and process information.

The Two Main Thyroid Hormones – T4 and T3

The thyroid produces two main hormones, T4 (thyroxine) and T3 (triiodothyronine). When it’s working properly, 93% of the thyroid hormone produced by the body each day is T4, and only 7% is T3 [1]. The thyroid manufactures ~85mcg of T4 and 6.5mcg of T3 per day [1], which is a T4 to T3 ratio of 13:1.  

T4 is the inactive form of thyroid hormone and has four molecules of iodide bound to it. When it becomes activated, it loses one of the iodides and becomes T3, which is the active form.

In its free, unbound form, thyroxine is known as free T4 (abbreviated fT4) and in its free, unbound form triiodothyronine is known as free T3 (abbreviated fT3). 

The production of T4 and T3 in the thyroid is regulated by the pituitary gland, but the signal for the pituitary gland to tell the thyroid gland to make thyroid hormones comes from the hypothalamus region of the brain.  The hypothalamus releases a hormone called TRH (Thyrotropin-Releasing Factor) that acts on the pituitary gland, causing it to release a hormone called TSH (Thyroid Stimulating Hormone). It is TSH released from the pituitary gland that acts on the thyroid gland, causing it to release thyroxine.

 

from [2] The Merck Manual of Medical Information (1997)

How Hypothyroidism is Diagnosed

In Canada and many places in the US, the standard screening test for abnormal thyroid function is a blood test measuring thyroid stimulating hormone (TSH), which is a pituitary hormone

If TSH results falls within normal range, no testing of thyroid hormones occurs. The thyroid response to TSH is presumed to be normal. 

Central Hypothyroidism occurs when there is a problem with either the hypothalamus or the pituitary gland.

On lab tests, a low TSH and low free T4 indicates central hypothyroidism and this is often treated by prescribing medication, including T3 containing medications. 

Primary hypothyroidism is where there is no abnormality in the hypothalamus or the pituitary gland. It is diagnosed when there is high TSH, and normal or low free T4.

Main Causes of Hypothyroidism

In the developed world, the most common form of primary hypothyroidism in is Hashimoto’s disease. In developing countries, it is mostly caused from a lack of iodine in the diet. Other causes of hypothyroidism includes the trauma from surgery to remove a benign or cancerous tumour, or the result of radioactive iodine treatment for overactive thyroid.

Hashimoto’s disease is the most common cause of hypothyroidism in the West. It is an autoimmune disorder where the body’s immune system, specifically the lymphocytes attack the thyroid. In response to this attack,  the thyroid produces antibodies, specifically thyroperoxidase antibodies (TPO-ab) and thyroglobulin antibodies (TG-ab) [3]. A diagnosis of Hashimoto’s is made based on both the presence of symptoms of hypothyroidism, as well as the presence of TPO-ab or TG-ab.


One of the main challenges with getting diagnosed with hypothyroidism is that many of the early symptoms of hypothyroidism are non-specific  — meaning they can have several different causes.

In a post-pandemic world of telephone doctor appointments, such vague symptoms may seem too inconsequential to bring up.

Below is a downloadable checklist that can help you have a conversation with your doctor.



Symptoms such as body aches, joint painfatigue, feel chilled, weight gain, frequently being constipation, having dry skin don’t seem ‘serious’ enough to make an appointment with one’s doctor and could be due to a number of different causes from  not eating well, to having a virus, and are very often discounted as being due to “age”. Even forgetfulness and depression which are known symptoms in more advanced hypothyroidism are often attributed to aging. 

Getting Evaluated and Diagnosed 

As outlined in an earlier article, in British Columbia unless a person is of advanced age, has a family history or personal medical history of thyroid disease or another autoimmune disorder, takes medications such as lithium or amiodarone, or is from a developing country with iodine deficiency, they do not even qualify for TSH testing unless they display the specific symptoms listed in Table 1, below [4].

Table 1: Signs and Symptoms of Hypothyroidism (from [4])


One drawback to the above approved checklist is that it does not include some of the well-documented symptoms of hypothyroidism, such as non-pitting edema of the lower legs and ankles, a puffy swollen face, an enlarged tongue (with or without scalloped edges), loss of the outer third of eyebrows, or having pale or bluish lips.

Even if one has a blood test for TSH, if it comes back at the high end of the normal range, no further testing is done [4]. 

Without a person having known risk factors, or having symptoms that appear in the official  list in the Guidelines and Protocols [4] (Table 1, above), diagnostic tests may not be requisitioned unless or until a person becomes sicker and the reason for this is explained below, in the section about ordering lab tests.

To help people have an informed discussion with their doctor, below is a 2-page downloadable, fillable checklist that contains a list of common hypothyroid symptoms, along with a simple explanation of what that symptom is. For example, in this checklist “periorbital edema” is explained as ‘swelling under eyes.’

Please note that this checklist list is not exhaustive and is NOT intended to be used for self-diagnosis purposes. It is only provided so that people who think they may have symptoms of hypothyroidism can consult with their doctor, and discuss the matter with them. Remember, only a medical doctor can diagnose and treat

Signs and Symptoms of Hypothyroidism – 2-page downloadable and fillable checklist

 

Thyroid Panel Lab Tests –  3 options 

[updated: November 3, 2022]

In Canada, there is no such thing as a standard “thyroid panel,” although naturopaths offer thyroid assessment panels on a client-pay basis. Medical doctors can order thyroid function tests based on the guidelines of their specific province, and naturopaths can order different thyroid assessment panels, depending on the province they are located in.

1. Medical Doctor (MD)

Thyroid function blood tests can be ordered by medical doctors (MDs) including family practice physicians, general practitioners (GPs), and specialists such as Endocrinologists and the cost of testing will be covered by the provincial health plan if it meets their guidelines. 

In most provinces in Canada, a requisition needs to be written by a licensed medical doctor for the cost of the test to be covered by the provincial health plan. In New Brunswick and Nova Scotia Health authorities and lab regulators have placed restrictions on how lab tests can be ordered, and patents are charged fees to order them privately.

In Ontario, Saskatchewan and British Columbia, the following guidelines apply;

Furthermore, in British Columbia, physician-ordered lab tests must be requisitioned in accordance with the Laboratory Services Act to be covered by MSP (Medical Service Plan). Doctors are in a very challenging position in BC as MSP can seek recovery for lab-test cost from a doctor if they feel that the test(s) ordered were not clinical  justified

Most physician-initiated lab test investigation into thyroid function begins with a TSH test. One reason for this is to rule out Central Hypothyroidism which is where there is a problem with either the hypothalamus, or the pituitary gland. As explained above, a low TSH will likely result in a free T4 test being requisitioned. If free T4 is also low, then T3 medication or some other type of medication might be prescribed, or the person referred to an endocrinologist.

If the TSH test comes back high (above the upper limit of normal) this will likely result in a free T4 test being requisitioned. Depending on whether the free T4 is normal or low, and how far above the upper limit the TSH is, the doctor may recommend one of a variety of treatment options, and/or refer their patient to an endocrinologist.
 
The provincial health plan in British Columbia (MSP) pays the laboratory that performs the analysis the following amount for thyroid function tests, and thyroid antibody tests:
 
      • TSH: $9.90
      • free T4: $12.12
      • free T3: $9.35
      • thyroperoxidase antibody (TPO-ab): $20.22 (payable only for possible autoimmune thyroid disease)
      • thyroglobin antibody (TG-ab): $27.90 (only performed as an adjunct to thyroglobulin measurement for the conditions such as thyroid tumors, cancer, etc.)
      • reverse T3: uninsured test 
 
from http://www.bccss.org/bcaplm-site/Documents/Programs/laboratory_services_schedule_of_fees.pdf
Where it becomes challenging is when TSH is in the high-normal range and/or the person has symptoms consistent with hypothyroidism but not symptoms listed on Table 1 of the Guidelines & Protocols for Thyroid Function Testing [4]. In BC, it used to be up to a physician’s discretion to requisition blood tests based on their best clinical judgement, but since the Laboratory Services Act (LSA) came into effect on October 1, 2015 [5], the Medical Service Plan (MSP) can seek recovery for lab-test cost from the doctor if they feel that the test(s) ordered were not clinical  justified. Needless to say, this puts doctors in a very challenging position.
 
As a clinician, when I provide one of my clients with a Lab Test Request Form to bring to their doctor, with their permission I will mark the clinical reason that I am requesting specific tests on the form, so that their doctor can consider whether they feel the test(s) are warranted.
 

2. Naturopathic doctor (ND)

[updated: November 3, 2022] 
 
In British Columbia, Ontario and Saskatchewan, thyroid assessment panels require a visit to a naturopath, and would take at least two sequential visits; one to get the lab test requisition to go to the lab, and the second to have the naturopath provide their interpretations of the results, and their recommendations. The costs of naturopath’s services are not covered by provincial health care, so clients need to pay out of pocket.  Fees for naturopathic visits and blood test vary between provinces and within the same province between practitioners.
 
In Ontario, fees for visits to a naturopath are regulated by the College of Naturopaths of Ontario and are set per block of time . Typically the cost of first visit, second visit and subsequent visits vary, with the first visit of 75 minutes costing ~$200, and the second visit of 45 minutes) costing ~$115. 
 
In the first visit the naturopath would ask questions as part of their assessment and complete and sign a Naturopathic Requisition Form which enables their client to go to the lab and have the tests done. The client pays the naturopath for the visit as well as the cost of the lab tests. In Ontario, the College of Naturopaths of Ontario allows naturopaths to add a markup to goods and services they offer, such as supplements, and blood test panels. With respect to blood tests, the naturopath pays a special negotiated lab fee for the thyroid panel to the lab, then bills their clients, often with a mark-up.   In the second visit, the naturopath will interpret the results.
 
In BC, fees are set by the BC Naturopathic Association Fee Guidelines. Naturopaths are also able to add a mark-up to the cost of supplements and blood tests. From experience, some naturopaths in BC keep their mark-up for lab tests minimal (e.g. $7 per test).  
 
The Enhanced Thyroid Assessment available in Ontario has the following 6 tests ;
    • TSH
    • Free Thyroxine (FT4)
    • Free Triiodothyronine (FT3)
    • Reverse T3
    • Thyroperoxidase Antibody (TPO-ab)
    • Anti-Thyroglobulin (TG-ab)
Prices for thyroid panels charged to naturopaths are available online for Ontario (see above) but in BC the prices aren’t marked.
 
Compared to the (MSP) government pricing, the above tests (minus the Reverse T3 which isn’t paid for by MSP) costs $80, so presumably naturopaths are charged prices similar to what MSP pays and then can add a mark-up to them. From the client’s perspective, they need to pay for the two naturopath visits, as well as the cost of the lab tests. 
  • TSH: $9.90
  • free T4: $12.12
  • free T3: $9.35
  • thyroperoxidase antibody (TPO-ab): $20.22 (payable only for possible autoimmune thyroid disease)
  • thyroglobin antibody (TG-ab): $27.90 (only performed as an adjunct to thyroglobulin measurement for the conditions such as thyroid tumors, cancer, etc.)
Total: $79.49
 
In British Columbia, naturopaths can only order the Basic Thyroid Assessment which includes the following 4 tests;
  • TSH
  • Free Thyroxine (FT4)
  • Free Triiodothyronine (FT3)
  • Thyroperoxidase Antibody (TPO-ab)

Reverse T3 and Anti-Thyroglobulin (TG-ab) are not available.

3. Patient-Pay 

If a doctor does not want to take the risk of requisitioning specific lab tests that the provincial plan may seek to recover costs from them, there is the option of the doctor writing on the requisition that specific test(s) will be “patient-pay” and the individual can pay for that specific lab test themselves. 
It should be made clear that a person does need a requisition from a doctor that indicates “patient pay” for the specific test(s) and cannot go to the lab directly and request the test themselves.
 
***It should also be noted that the cost of thyroid lab tests paid for by the individual are NOT the same as the cost paid for by MSP, and naturopaths, but are significantly higher. 
 
Last week, as a private individual with a physician lab requisition, I was charged 3 times the MSP cost for a free T3 test. As I found out at that lab visit, there is no patient-pay price list available at the lab, online, or by writing the lab office. The staff at the lab will disclose the cost of the test once the person is at the lab with the requisition, but this first requires the individual making an appointment, and going there at their appointment time.  
 
A fellow clinician told me several days later that there is a patient-pay price list available to Physicians, Registered Dietitians, Nurse-Practitioners, and other healthcare professionals, and I now have a copy of this list. It is titled the British Columbia Private Price List for Commonly Ordered Lab Tests, and is dated April 2021. It is labelled as “a confidential document,” and it is indicated at the top that clinicians are not to disclose their prices publicly, however we are able to share that information in conversations with our patients / clients. 
 
 
 
While I am unable to disclose the patient-pay lab test prices publicly (such as in this article), I am able to share the patient-pay prices of lab tests with any of my clients who are considering asking their doctor to requisition patient-pay test(s).  
 
 

Final Thoughts

Determining whether the symptoms one has may be related to their thyroid, and going about getting tested can be challenging. It is my hope that by providing the information in this article, you can have an informed discussion with your doctor.

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

To your good health!

Joy

 

You can follow me on:

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

 

References

  1. Jonklaas J, Bianco AC, Bauer AJ, et al, Guidelines for the treatment of hypothyroidism: prepared by the American thyroid association task force on thyroid hormone replacement. thyroid. 2014 Dec 1;24(12):1670-751.
  2. Berkow, R., Beers, M. H., & Fletcher, A. J. (1997). The Merck Manual of Medical Information. Whitehouse Station, N.J.: Merck Research Laboratories.
  3. Puszkarz, Irena, Guty, Edyta, Stefaniak, Iwona, & Bonarek, Aleksandra. (2018). Role of food and nutrition in pathogenesis and prevention of Hashimoto’s thyroiditis. https://doi.org/10.5281/zenodo.1320419
  4. BC Guidelines & Protocols Advisory Committee, Thyroid Function Testing in the Diagnosis and Monitoring of Thyroid Function Disorder, October 24, 2018
  5. Laboratory Services Act, Laboratory Service Regulation, October 1, 2015 (last amended September 20, 2020 by B.C. Reg. 263/2020)

 

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.

Hypothyroidism Signs and Symptoms Checklist

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


As outlined in a previous article, the standard screening test for abnormal thyroid function is thyroid stimulating hormone (TSH), but if those results come back within normal range and a person has not known risk factors or obvious symptoms of thyroid disease, no testing of thyroid hormones occurs,  and thyroid function is presumed to be normal.

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

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

Signs and Symptoms of Hypothyroidism – downloadable checklist

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

 

Signs and Symptoms of Hypothyroidism – larger type, 4-page downloadable checklist

 

   NEW Signs and Symptoms of Hypothyroidism – 2-page downloadable and fillable checklist


All Articles as of December 30, 2022 on Hypothyroidism

July 14, 2022 – Thyroid Function Assumed to be Normal When Only TSH is Tested –

August 7, 2022 –  Symptoms of Hypothyroidism Mistakenly Blamed on Aging 

August 12, 2022 – Beyond Diet – the role of hormones in metabolic health 

August 26, 2022 – More Than Skin Deep – skin symptoms associated with hypothyroidism 

September 4 , 2022 – Hair Loss – root causes (Part 1) 

October 14, 2022 Hypothyroidism Signs and Symptoms – a downloadable checklist

November 1, 2022 Hypothyroidism 101- about the thyroid, its hormones and diagnosis

November 17, 2022 – Hair Loss in Hypothyroidism (Part 2) – Nutrients of Importance


More Info?

If you would like to know how I can help support your nutritional needs, 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. BC Guidelines & Protocols Advisory Committee, Thyroid Function Testing in the Diagnosis and Monitoring of Thyroid Function Disorder, October 24, 2018

 

Copyright ©2022 BetterByDesign Nutrition Ltd.

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

Hair Loss – root causes (Part 1)

Hair loss can be a very distressing symptom, especially when it is noticeable to ourselves and others. However, before outlining strategies for addressing it, we first need to understand what’s causing it. That is the purpose of this article.  The next article will address strategies for helping to restore hair loss through diet and nutrient supplementation.

There are different types of hair loss with various causes, including genetic, autoimmune, severe stress, as well as nutrient deficiency and nutrient excess. Below are a three of the most common types of loss. 

Male pattern baldness

Androgenic Alopecia is the most common type and affects up to 50% of men and women [1]. In men, it is called ‘male pattern baldness,’ and is mainly seen on the crown of the head and on the temples.  In women, it  is called ‘female pattern baldness,’ and is mainly seen at the crown of the head, with a wider center part [2].  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 [1]. Since it is genetic, there is no ‘cure,’ but growth may be improved by using products such as minoxidil (Rogaine®) or rosemary extract which has been found to be as effective as minoxidil in studies [2]. One drawback is that treatment needs to continue indefinitely or loss will reoccur when treatment is discontinued [6].

Alopecia areata is an autoimmune disorder where the body’s immune system attacks the follicles. Hair often comes out in clumps, usually the size and shape of a quarter but it can affect wider areas of the scalp [3]. It can occur in those who already have some form of autoimmune conditions, including thyroid disease. Treatment may involve use of oral or topical corticosteroid medication [3] which are very powerful anti-inflammatory medications, or other medications used in autoimmune conditions. Individual bald spots may be treated using Minoxidil (Rogaine®) [3]. 

Telogen effluvium – is the most common form of diffuse hair loss [7]. It usually occurs after a profound stress, shock or traumatic event including after childbirth, as the result of a thyroid disorder, as well as rapid weight loss. It has been reported after a sudden and significant calorie restriction diet (“crash dieting”) [8],  and has also been reported associated with the popularized ‘keto’ diet [9,10], but I am in agreement with Dr. Stephen Phinney of Virta Health that it should not occur in a well-designed keto diet [11].  

In telogen effluvium, hair often comes out in clumps in the shower, or in a brush [6]. Loss is usually from all over the scalp, but may occur more on the temples, the part and the crown of the head [7].  Once the cause telogen effluvium is removed, regrowth will usually begin within two to six months [6].

There are three phases of growth; the growth (anagen) phase, the transition (catagen) phase, and the resting (telogen) phase [5]. During the growth phase, follicles produce a shaft beginning from tip to root [5]. During the catagen and telogen phase, the follicles reset and prepare to start making a new hair. 

hair growth phases – based on Reference [7]

Normal Hair Loss vs Hair Loss in Telogen Effluvium

Normally,  90-95% of 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 [7] 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 [7].

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., loss becomes 5-10 greater than normal, with people losing up to 50% of their hair.  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.

Identifying the cause of hair loss is essential, as once identified, and corrected, regrowth will occur [7], but it can take 3-6 months for hair shedding to stop. While many people are anxious that they will go bald, hair loss does not usually exceed 50% of their hair [7].  Once the cause is identified and corrected, regrowth can begin to be seen 3-6 months later [7], but significant regrowth can take 12-18 months [7].

Medications that can interfere with hair regrowth include beta-blockers such as metoprolol and propranolol used in the treatment of abnormal heart rhythms, after a heart attack, or high blood pressure, anti-thyroid medication used in the treatment of hyperthyroidism and anticoagulants [7].

As outlined in this previous article, hair loss is one of the identifying markers of hypothyroidism that results from a lack of thyroid hormones. Hair growth will begin to occur once optimal thyroid hormone replacement is reached, however as mentioned above, it may take 3-6 months for hair shedding to stop, and another 3-6 months for regrowth to be able to be seen [7].  For someone dealing with hair loss, six months to a year to begin to see hair growth can seem like an eternity.  

[I understand this firsthand, as the two photos below are of me.  The one on the left was taken June 3, 2022 at my youngest son’s wedding — a few weeks before being diagnosed of hypothyroidism, and the one on the right was taken yesterday, September 3, 2022, exactly three months later. I share these photos so that people can better understand what the hair loss associated with hypothyroidism may look like.]

Hair loss 3 months after diagnosis

Dr. Izabella Wentz, a clinical pharmacist who focuses on thyroid disorders believes that hair loss is best improved on a medication that contains both T4 and T3, such as desiccated thyroid extract like WP Thyroid®, Nature-Thyroid® or Armour Thyroid®, or a mixture of T4 medication (such as Synthroid®) and a T3 medication such as Cytomel®.  Dr. Wentz also provides a general “rule of thumb” that TSH after treatment should be between 0.5 and 2 μIU/mL [12].

Hair Loss in Nutrient Deficiencies and Nutrient Excess

There are specific nutrient deficiencies that are also linked to different types of hair loss, with the most well-known being iron deficiency. Vitamin C deficiency is also a factor as it is needed  for intestinal absorption of iron.  Zinc deficiency, as well as some B-vitamin deficiency (e.g. niacin, biotin, riboflavin) as well as vitamin D deficiency can also be associated with hair loss [13].  As importantly, excess in vitamins such as vitamin E, vitamin A and folic acid are also associated with hair loss [13]. Ensuring  adequate but not excess nutrient intake is essential and this will be covered in the next part of this article.

Final Thoughts…

Hair loss can be a very distressing symptom, especially when it is noticeable to ourselves and others. Once the cause has been identified and treated, can all we do is be patient and wait for the hair to grow?

Hair regrowth can be supported by ensuring a nutrient-adequate diet, as well as with nutrient supplementation, when there is nutrient deficiency. This will be the topic in Hair Loss – Part 2.

More Info

If you would like more information about how I might be able to support your nutritional needs, please send me a note through the Contact Me form, above.

To your good health!

Joy

You can follow me on:

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

 

References

  1. 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_
  2. Panahi Y, Taghizadeh M, Marzony ET, Sahebkar A. Rosemary oil vs minoxidil 2% for the treatment of androgenetic alopecia: a randomized comparative trial. Skinmed. 2015;13(1):15-21.
  3. Medical News Today, Alopecia areata: Causes, diagnosis and treatments, April 7, 2022, https://www.medicalnewstoday.com/articles/70956
  4. Medical News Today, Is Telogen Effluvium reversible? April 23, 2018, https://www.medicalnewstoday.com/articles/321590
  5. Alonso L, Fuchs E; The Hair Cycle. J Cell Sci 1 February 2006; 119 (3): 391–393. doi: https://doi.org/10.1242/jcs.02793
  6. Phillips TG, Slomiany WP, Allison R. Hair Loss: Common Causes and Treatment. Am Fam Physician. 2017;96(6):371-378.
  7. Malkud S. Telogen Effluvium: A Review. J Clin Diagn Res. 2015;9(9):WE01-WE3. doi:10.7860/JCDR/2015/15219.6492
  8. Goette DK, Odom RB. Alopecia in crash dieters. JAMA. 1976;235(24):2622-2623.
  9. Hallberg, S., Do Ketogenic diets cause hair loss? https://www.youtube.com/watch?v=PxkfM84lxMU
  10. Westman E., Hair Loss and Keto, https://www.youtube.com/watch?v=Cgv92mfTj4k
  11. Phinney S., Virta Health, Does Keto Cause Hair Loss, https://www.virtahealth.com/faq/keto-hair-loss
  12. Wentz I., Hair Loss and Your Thyroid, https://thyroidpharmacist.com/articles/hair-loss-and-thyroid/
  13. Guo EL, Katta R. Diet and hair loss: effects of nutrient deficiency and supplement use. Dermatol Pract Concept. 2017;7(1):1-10. Published 2017 Jan 31. doi:10.5826/dpc.0701a01

 

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.

 

More Than Skin Deep – skin symptoms associated with hypothyroidism

According to the American Thyroid Association, 6% of the population have some type of thyroid disease and 60% of them (~12 million people) are unaware of it. Assuming the same rate applies in Canada, 2.3 million people in Canada have thyroid disease and almost 1.4 million people are unaware of it. Since changes in the skin may be one of the first clinical signs of hypothyroidism [2] and are often important indications of its progression [4], this article outlines how some of those skin changes may appear.

DISCLAIMER (August 26, 2022): The information in this post should in no way be taken as a recommendation to self-diagnose, self-interpret skin symptoms or diagnostic tests, or self-treat any suspected disorder. It is essential that people who suspect they may have symptoms of any condition consult with their doctor, as only a medical doctor can diagnose and treat.

NOTE: This article also contains aspects of my personal story which are clearly marked. My personal experience is not objective data. The pictures are provided only so that people can better understand what some skin symptoms of hypothyroidism may look like. Many more pictures are available in clinical online. 


INTRODUCTION: My interest in hypothyroidism is more than academic, as I was recently diagnosed with it. I realize in retrospect that I missed almost all the early signs because I didn’t know what the range of possible symptoms could be. Just as my interest in hyperinsulinemia and type 2 diabetes was birthed in my own diagnosis and eventual partial remission, my interest in this hypothyroidism is no different. Since hypothyroidism can be dangerous if left untreated, my goal in writing this series of articles is to help people know the wide range of symptoms that may be associated with it, and to seek medical attention for themselves or their loved one, when necessary.

As outlined in the article Symptoms of Hypothyroidism Mistakenly Blamed on Aging, people think it is normal for ‘older adults’ to have body aches, joint pain, fatigue, to feel chilled when others do not, experience constipation, hair loss, be forgetful, or to experience depression. However, these are NOT typical signs of aging but ARE common symptoms of hypothyroidism. 

In retrospect, in my case, these types of symptoms came long after the skin symptoms, but cutaneous symptoms were so non-specific that I had no idea they might indicate that something clinical was going on.  

Of course, as a Dietitian, I knew that people often gained weight before they were diagnosed with hypothyroidism, and that they needed to take one of several medications prescribed as treatment. I knew they had to take their medication a half an hour before eating but until recently, my support was limited to teaching them what hypothyroidism is, the nutrients of importance in thyroid function, and foods and beverages that may impact thyroid function.

Until recently, I didn’t know that undiagnosed hypothyroidism can be dangerous and can progress to a myxedema crisis that can be fatal, with a death rate between 20-60%even with treatment [3]. 

Until today, I had no idea that the majority of people with thyroid disease (60%) are undiagnosed [1].

Putting these two sets of statistics together was concerning to me.  Since many of the symptoms of hypothyroidism such as joint and muscle pain, difficulty getting up from a seated position, or feeling cold are often discounted as normal signs of aging, I wanted people to also know what some of the skin symptoms of hypothyroidism are in the hope that is might help them put the clues together, and seek medical attention.

Skin Symptoms Associated with Hypothyroidism

As mentioned in a previous article about the role of hormones in metabolic disease, thyroid hormones act on every organ system of the body, and their affect on the skin is no exception. Some skin symptoms such as myxedema don’t appear until much later in the progression of hypothyroidism, while other appear early on.

In this article, I will describe the later symptoms first because they are hallmarks of the progression of disease and indicate that getting medical attention is important. In my own case, it was the symptoms associated with myxedema that made me begin to realize that the tiredness and achy muscles and sore joints that I had been experiencing for over a year was more than post-Covid symptoms.

As explained in Symptoms of Hypothyroidism Mistakenly Blamed on Aging, myxedema describes advanced hypothyroidism that occurs when the condition is left untreated or inadequately treated and is also applied to hypothyroidism’s effects on the skin, where it looks puffy and swollen and takes on a waxy consistency [4]. 

[Personal note: It was me looking for clinical answers this morning that resulted in me stumbling across the some of the other skin symptoms associated with hypothyroidism. I wanted to know how long it would take since beginning treatment with thyroid hormone medication for the myxedema to resolve in my legs.]


NOTE: these photos are for illustrative purposes only. Photos of myxedema in the clinical literature are available but are copyrighted. It is for this reason that I am posting my photos only as example, or illustrations.

Below is a photo showing the change in appearance in my left leg from November 3, 2021 (left), to July 16, 2022 (middle), to August 26, 2022 (right).

The photo on the left was taken by me last November while I was doing some stretches. It was still on my phone in mid-July when I took a picture of the swelling in my lower legs and ankles caused by mucin accumulating in the skin. The photo on the right was taken this morning, and while much of the swelling has been reduced, I am still unable to pinch any skin on my legs due to the remaining mucin. I have read that it can take 6 – 8 months for this to resolve.

It has been only 2 months since I began treatment for hypothyroidism, beginning with a very low dose. The above photo shows what I looked like 2 ¾ months ago at my son’s wedding, and how quickly the myxedema in my face resolved with treatment. 


What Causes the Skin Change Known as Myxedema

Myxedema is one several skin significant changes associated with the progression of hypothyroidism. A recently updated dermatology textbook describes myxedema as ‘skin that is cold and pale with abnormally widespread dryness (xerosis) and where a diffuse loss of hair (alopecia) may be present [5].’

When I first saw my doctor after my son’s wedding at the beginning of June, he pointed this out on my legs and said that the cold, waxy skin, along with the swelling is “benchmark symptom” of hypothyroidism.  He showed me how it was impossible to pinch and lift any skin on my legs and that pressing on it left no ‘dent’ mark.  This lack of a dent means the type of edema (swelling) is “non-pitting edema.” Pitting edema occurs in many other conditions, but this non-pitting edema, along with the cold, waxy skin is characteristic of progressing hypothyroidism. The coldness of the skin is the result in the drop in body temperature due to decreased metabolism [2] and is another hallmark symptom of hypothyroidism, discussed in a previous article. The swelling is caused by the accumulation of mucin in the skin.

Mucin is a type of glycoprotein (a protein with a side chain of hyaluronic acid, a sugar molecule) [5] which is naturally produced in the skin. Hyaluronic acid normally binds water to collagen, trapping it in the skin and is injected into the skin by dermatologists to cause aging skin to appear plump, moist and younger looking. The problem is, in hypothyroidism mucin accumulates under the skin, giving it that “tight, waxy” texture. (I would describe it as feeling like an over-inflated balloon). The accumulation of mucin around hair follicles contributes to the resulting hair loss on the arms and legs (and other areas where it occurs). 

[Personal Note: if you look at the composite picture of my left foot (above), you can see in the right hand photo taken this morning (more than 2 months after beginning thyroid hormone medication) that I still cannot pinch any skin on my legs.  While my face has improved, there is still significant improvement yet to occur in my legs, and other parts of my body. ]

Other Skin Symptoms of Hypothyroidism

In addition to myxedema, other skin changes that are associated with hypothyroidism include;

    • dry skin (xerosis)
    • thin scaly skin
    • carotinemia
    • purpura
    • telogen effluvium (hair loss)
    • decrease sweating
    • poor wound healing

As explained in an earlier article, since the presentation of symptoms in hypothyroidism varies so much between individuals, symptoms that were “early” for me, may not be for others, and may not appear at all. 

Purpura is caused when small blood vessels burst, resulting in blood pooling just under the skin. It looks a bit like a bruise, but without pain or swelling and it does not change colour in time.  Purpura is a non-serious skin hemorrhage that is almost always a symptom of something else and looks like small, reddish-purple spots just beneath the skin’s surface.

[Personal account: This morning, when I saw the term “purpura” it jumped out at me. Since May of 2021, I have had a large purple area on my left ankle that I had first attributed to a particularly grueling hike I did in Maple Ridge, BC with one of my young adult sons.  I noticed it when I got home, as did my son, and I assumed it would clear up on its own, but it never did. When I saw my doctor right after my son’s wedding, I showed it to him and he nodded as if to take note, but didn’t say anything. I now know that in my case, it was one of the very early skin signs of hypothyroidism.  I thought I had taken photos of what my purple ankle looked like at its worse, but I may have deleted them because I thought it was simply leftover damage to blood vessels from a hike. The good news is, that two months after beginning thyroid hormone treatment, the purpura is ~75% resolved.] 

August 20, 2022: purpura 75% resolved, thin dry skin, telogen effluvium (hair loss) yet to be resolved

Another early symptom of hypothyroidism for me, was telogen effluvium, a loss of hair on my arms and legs and to a lesser extent, on my scalp. 

[Personal account: Last summer I was joking with a family member that one of the advantages of getting older was no longer needing to shave my legs.  I didn’t realize until recently that the loss of hair on my legs and arms as long as two years ago was NOT a perk of aging (like no longer having a “period”), but was an early symptom of hypothyroidism! I also didn’t realize that decreased sweating wasn’t a benefit of aging, either. I feel stupid in retrospect, but I wasn’t taught it and when I looked it up it said that hair on the body “thins” as one ages, so I thought it was normal.  I hadn’t realized that I had NO hair on my arms and legs. Two months after beginning thyroid medication, that is beginning to change. I feel like a pubescent boy excited by his first facial hair.

I mentioned the dry skin in previous posts, so won’t do so again here, but that was a very early sign for me.  Again, I thought it was a normal part of aging.]

Another term that jumped out at me this morning, was the term carotinemia. This is where beta-carotene accumulates in the blood and gives skin a yellowish pigmentation. In my case, it was not due to eating too much beta-carotene rich foods like carrots, squash or sweet potato, but was a skin symptom of hypothyroidism.  

Two days ago, I posted the photo below on social media. I now understand the significance of what I wrote;

“Update from A Dietitian’s Journey – Part II: It’s been exactly 2 ½ months since my son’s wedding and 2 months since I began thyroid treatment. I think what is most noticeable is that the yellowish skin colour is gone.”

I now know this was carotinemia which has recently resolved —  between the photo of last week (August 17, 2022) and this week (August 24, 2022).
 

 

How my Clinical Practice is Impacted

Just as my clinical practice changed 5 years ago when I came to understand what hyperinsulinemia was, and how early clinical signs of developing type 2 diabetes are evident as long as 20 years before diagnosis, it is changing again as a result of what I am learning about hypothyroidism.

Understanding the wide range of clinical and subclinical symptoms that people may have leads me to ask additional questions, to look at lab test results differently, and to ask for additional ones if it seems clinical warranted. While it is beyond the scope of practice of a Dietitian to diagnose any disease or to treat hypothyroidism, I am more aware of what to look and this helps me to refer people back to their doctor if I feel there may be a clinical concern.

Final Thoughts…

The list of skin symptoms in hypothyroidism in this article is by no means exhaustive.  There are others discussed in the literature that present, particularly as the disease progresses.  Since the goal of this article was to present symptoms that may present early or with advancing hypothyroidism, additional symptoms are beyond the scope of this article.

If you think that you, or someone you know may have symptoms of hypothyroidism, please consult with a medical doctor. 

More Info

If you would like more information about the services I provide people who are newly diagnosed with hypothyroidism, please send me a note through the Contact Me form, above.

To your good health!

Joy

 

You can follow me on:

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

 

Previous articles in the Hypothyroidism Series

07/14 – Thyroid Function Assumed to be Normal When Only TSH is Tested 

08/07 Symptoms of Hypothyroidism Mistakenly Blamed on Aging 

08/12 – Beyond Diet – the role of hormones in metabolic health

08/14 – Don’t Try This at Home (Part 2) – when a doctor’s diagnosis is required

References

    1. American Thyroid Association, Prevalence and Impact of Thyroid Disease, https://www.thyroid.org/media-main/press-room/, accessed August 26, 2022
    2. Kasumagic-Halilovic E. Thyroid Disease and the Skin. Annals Thyroid Res. 2014;1(2): 27-31.
    3. Elshimy G, Chippa V, Correa R. Myxedema. [Updated 2022 May 22]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing. https://www.ncbi.nlm.nih.gov/books/NBK545193/#_NBK545193_pubdet_
    4. Medical News Today, What is Myxedema and How is it Treated, April, 22, 2022, https://www.medicalnewstoday.com/articles/321886
    5. Patterson, JW, Weedon’s Skin Pathology, Cutaneous Mucinoses, Elsevier Canada; 5th edition (April 20, 2020)

 

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.

Beyond Diet – the role of hormones in metabolic health

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

The role of diet in metabolic health is well-known, but many people do not realize that hormones, including those from the thyroid impact that.

The Role of Thyroid Hormones

from The Merck Manual of Medical Information (1997)

The thyroid and the hormones it produces play an important role in metabolic health but it is a hormone from the pituitary gland called Thyroid Stimulating Hormone (TSH) that causes the thyroid gland to release the hormone thyroxine, also called free T4. Free T4 is the inactive form of thyroid hormone. Free T4 is activated (reduced) to free T3 (triiodothyronine), the active form of thyroid hormone.

Overt hypothyroidism is where TSH >10 mU/L, with normal or low free T4). 

Subclinical hypothyroidism (SCH), which is where TSH is higher than the normal cutoffs (TSH >4 mU/L) but less than the criteria for overt hypothyroidism (TSH >10 mU/L), but with normal free T4. 

Metabolic Changes due to Hypothyroidism

It has been well established for decades that people with overt (established) hypothyroidism experience several clinical changes that one might assume to be diet-related at first glance. For example, people with hypothyroidism have a decrease in red blood cells and experience different types of anemia, including the anemia of chronic disease. In addition, ten percent of people with hypothyroidism develop pernicious anemia, which is associated with vitamin B12 and folate (folic acid).  

The slowing of metabolism associated with hypothyroidism also results in a decrease in cardiac (heart) output, which results in both slower heart rate and less ability for the heart to pump blood. 

High Blood Pressure

The decreased ability of the heart to pump leads to increased resistance in the blood vessels, which results in increased blood pressure (hypertension).

In those who had normal blood pressure previous to developing hypothyroidism, blood pressure can rise as high as 150/100 mmHg. Hypothyroidism may increase it further for those previously diagnosed with high blood pressure.

It is not only diet that can contribute to high blood pressure but thyroid hormones (as well as other factors).

Weight Gain

Thyroid hormones act on every organ system in the body, but the thyroid is well-known for its role in energy metabolism. When someone has overt hypothyroidism, there is a slowing of metabolic processes, which results in symptoms such as fatigue, cold intolerance, constipation, and weight gain. 

Weight gain is not only about diet or how much someone eats versus how much they burn off. It is also about the person’s metabolic rate, which can be impacted by several things, including decreased thyroid hormones.

High Cholesterol

It has long been known that those with overt hypothyroidism have high total cholesterol, high low-density lipoproteins (LDL) [14], and high triglycerides (TG) [15], which results from a decrease in the rate of cholesterol metabolism. While many assume that “high cholesterol” results from diet, such as the assumption it is related to eating too many eggs, thyroid hormones may also play a role.

Subclinical Hypothyroidism

It has been found that some people with subclinical hypothyroidism have high low-density lipoproteins (LDL) and triglycerides (TG) and low high-density lipoproteins (HDL) [16]. 

But it is not only high cholesterol that is also found in subclinical hypothyroidism. For example, a 2016 paper referred to above reported that previous studies found no significant difference in symptoms between people with subclinical hypothyroidism and those with overt hypothyroidism [9]. That is, all the symptoms associated with overt hypothyroidism are also seen in subclinical hypothyroidism. Therefore, to assume that high blood pressure, serum cholesterol, or blood sugar is solely the result of diet is to possibly overlook the role of the pancreas and/or the thyroid.

As I wrote about in the previous post, all too often common symptoms of hypothyroidism are assumed to be normal signs of aging. Given the potentially serious consequences leaving hypothyroidism undiagnosed and untreated, it is important that people are able to recognize these symptoms in themselves, and loved ones.

Thyroid Hormones Affect Insulin Secretion of the Pancreas

Just as we cannot look at diet without considering the role of hormones such as insulin, we cannot look at pancreas function in isolation from thyroid function. 

As mentioned above, thyroid hormones influence every organ in the body, including the pancreas. It is now known that there are functional thyroid receptors in the pancreas that affect insulin secretion, and it is thought that thyroid hormones may play a role in the development of diabetes. 

Diagnosis and Treatment

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

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

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

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

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

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

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

Final Thoughts…

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

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

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

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

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

If you suspect you may have hypothyroidism (or any other clinical condition), consult with your doctor, and “don’t try this at home.”

More Info

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

To your good health!

Joy

 

You can follow me on:

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

 

References

    1. Crofts, C., et al., Identifying hyperinsulinaemia in the absence of impaired glucose tolerance: An examination of the Kraft database. Diabetes Res Clin Pract, 2016. 118: p. 50-7.
    2. Pareek, M., Bhatt, D.L., Nielsen, M.L., et al,  Enhanced Predictive Capability of a 1-Hour Oral Glucose Tolerance Test: A Prospective Population-Based Cohort Study. Diabetes Care 1 January 2018; 41 (1): 171–177. https://doi.org/10.2337/dc17-1351
    3. Sagesaka H, S.Y., Someya Y, et al, Type 2 Diabetes: When Does It Start? Journal of the Endocrine Society, 2018. 2(5): p. 476-484.
    4. Government of British Columbia, Ministry of Health, Schedule of Fees for Laboratory Services – Outpatient, Payment Schedule, revised April 1, 2022, http://www.bccss.org/bcaplm-site/Documents/Programs/laboratory_services_schedule_of_fees.pdf
    5. BC Guidelines, Hormone Testing – indications and appropriate use, Insulin, https://www2.gov.bc.ca/gov/content/health/practitioner-professional-resources/bc-guidelines/special-endocrine-testing#Insulin
    6. BC Guidelines, Hormone Testing – indications and appropriate use, C-peptide, https://www2.gov.bc.ca/gov/content/health/practitioner-professional-resources/bc-guidelines/special-endocrine-testing#C-peptide
    7. Canadian Diabetes Association, The Burden of Out of Pocket Costs for Canadians with Diabetes, 2011,  http://www.diabetes.ca/CDA/media/documents/publications-and-newsletters/advocacy-reports/burden-of-out-of-pocket-costs-for-canadians-with-diabetes.pdf
    8. Statistics Canada. Table 11-10-0239-01 Income of individuals by age group, sex and income source, Canada, provinces and selected census metropolitan areas, DOI: https://doi.org/10.25318/1110023901-eng
    9. Javed Z, Sathyapalan T. Levothyroxine treatment of mild subclinical hypothyroidism: a review of potential risks and benefits. Ther Adv Endocrinol Metab. 2016;7(1):12-23. doi:10.1177/2042018815616543
    10. Danese MD, Ladenson PW, Meinert CL, Powe NR. Clinical review 115: effect of thyroxine therapy on serum lipoproteins in patients with mild thyroid failure: a quantitative review of the literature. J Clin Endocrinol Metab 2000; 85:2993.
    11. Caraccio N, Ferrannini E, Monzani F. Lipoprotein profile in subclinical hypothyroidism: response to levothyroxine replacement, a randomized placebo-controlled study. J Clin Endocrinol Metab 2002; 87:1533.
    12. Nakajima Y, Yamada M, Akuzawa M, et al. Subclinical hypothyroidism and indices for metabolic syndrome in Japanese women: one-year follow-up study. J Clin Endocrinol Metab 2013; 98:3280.
    13. Janovsky CCPS, Bittencourt MS, Goulart AC, et al. Unfavorable Triglyceride-rich Particle Profile in Subclinical Thyroid Disease: A Cross-sectional Analysis of ELSA-Brasil. Endocrinology 2021; 162.
    14. Lithell, H., Boberg, J., Hellsing, K., Ljunghall, S., Lundqvist, G., Vessby, B., & Wide, L. (1981). Serum lipoprotein and apolipoprotein concentrations and tissue lipoprotein-lipase activity in overt and subclinical hypothyroidism: the effect of substitution therapy. European journal of clinical investigation11(1), 3–10. https://doi.org/10.1111/j.1365-2362.1981.tb01758.x
    15. Nikkila E, Kekki M, Plasma triglyceride metabolism in thyroid disease, J Clin Invest. 1973;51:203. 
    16. Kung, A. W., Pang, R. W., & Janus, E. D. (1995). Elevated serum lipoprotein(a) in subclinical hypothyroidism. Clinical endocrinology43(4), 445–449. https://doi.org/10.1111/j.1365-2265.1995.tb02616.x
    17. Canaris, G. J., Manowitz, N. R., Mayor, G., & Ridgway, E. C. (2000). The Colorado thyroid disease prevalence study.  Archives of internal medicine160(4), 526–534. https://doi.org/10.1001/archinte.160.4.526
    18. BC Guidelines & Protocols Advisory Committee, Thyroid Function Testing in the Diagnosis and Monitoring of Thyroid Function Disorder, October 24, 2018, pg. 6
    19. Biondi B., The Normal TSH Reference Range: What Has Changed in the Last Decade?, The Journal of Clinical Endocrinology & Metabolism, Volume 98, Issue 9, 1 September 2013, Pages 3584–3587, https://doi.org/10.1210/jc.2013-2760
    20. Surks MI, Hollowell JG.2007Age-specific distribution of serum thyrotropin and antithyroid antibodies in the US population: implications for the prevalence of subclinical hypothyroidismJ Clin Endocrinol Metab 92:4575–4582
    21. Kabadi U. M. (1993). ‘Subclinical hypothyroidism’. Natural course of the syndrome during a prolonged follow-up study. Archives of internal medicine153(8), 957–961. https://doi.org/10.1001/archinte.153.8.957Huber, G., Staub, J. J., Meier, C.,
    22. Vanderpump, M. P., Tunbridge, W. M., French, J. M., Appleton, D., Bates, D., Clark, F., Grimley Evans, J., Hasan, D. M., Rodgers, H., & Tunbridge, F. (1995). The incidence of thyroid disorders in the community: a twenty-year follow-up of the Whickham Survey. Clinical endocrinology43(1), 55–68. https://doi.org/10.1111/j.1365-2265.1995.tb01894.x
    23. Mitrache, C., Guglielmetti, M., Huber, P., & Braverman, L. E. (2002). Prospective study of the spontaneous course of subclinical hypothyroidism: prognostic value of thyrotropin, thyroid reserve, and thyroid antibodies. The Journal of clinical endocrinology and metabolism87(7), 3221–3226. https://doi.org/10.1210/jcem.87.7.8678
    24. Rodondi, N., den Elzen, W. P., Bauer, D. C., Cappola, A. R., Razvi, S., Walsh, J. P., Asvold, B. O., Iervasi, G., Imaizumi, M., Collet, T. H., Bremner, A., Maisonneuve, P., Sgarbi, J. A., Khaw, K. T., Vanderpump, M. P., Newman, A. B., Cornuz, J., Franklyn, J. A., Westendorp, R. G., Vittinghoff, E., … Thyroid Studies Collaboration (2010). Subclinical hypothyroidism and the risk of coronary heart disease and mortality. JAMA304(12), 1365–1374. https://doi.org/10.1001/jama.2010.1361
  1.  

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.

 

Symptoms of Hypothyroidism Mistakenly Blamed on Aging

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

NOTE: This article contains aspects of my personal story which are clearly marked. My personal experience is not objective data. The pictures are provided only so that people can better understand what the “weight gain” of hypothyroidism can look like, and how different it is from ordinary weight gain. 


In-person visits to the doctor have been minimal over the past two years, and it has been easy for people to discount symptoms such as body achesheadaches, fatigue, and ‘brain fog‘ to having had Covid, or to having ‘long Covid’ [1]. It was only when I began having symptoms that were not consistent with Covid that I began to think that it might be hypothyroidism. You can read my personal account here.

I am not that old, but at the beginning of June (two months ago), 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, up the path to the hotel, or get up from 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 last summer. I knew that it was abnormal for me to feel so exhausted and for my muscles to feel so weak, and one look in the mirror told me something was very wrong.

In a matter of just a few weeks, I went from looking as I have the last two years to looking as I did when I was 55 pounds overweight. For the sake of this special occasion, I said nothing to my family, but was very concerned for my health.  It was also exceedingly hard for me to be in family photographs that I knew would be viewed for years to come.

I planned to contact my doctor when I returned home and have him assess me to determine whether I had what I suspected was hypothyroidism. 

Last Friday, my doctor confirmed that my symptoms were consistent with that diagnosis. I was surprised when he said that it was not unexpected in light of my lab work over the previous nine years, my past thyroid surgery many years ago, and my having experienced periodic hypothyroid symptoms since that time. Unfortunately, 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. 

Common Hypothyroid Symptoms May Often be Assumed to be Aging

from https://www.thyroid.org/thyroid-disease-older-patient/

People assume that it is normal for ‘older adults’ to have body aches, joint painfatigue, feel chilled when others do not, experience constipation, have dry skin or hair loss, be forgetful, or to even experience depression. However, these are NOT typical signs of aging but ARE common symptoms of hypothyroidism. 

The above-mentioned symptoms are so non-specific that many would not give them a second thought. An older person who is already limited to a one-issue-ten-minute remote doctor’s appointment would likely be hesitant to book a phone call to discuss these symptoms with their doctor. After all, they would conclude, these could be the result of so many different things, or “just the normal effect of aging”. 

Consider constipation as an example. Chronic constipation affects 15% of adults and is the sixth most commonly reported GI symptom [3]. Within the context of a lack of mobility that we have all faced due to lockdown restrictions, how many people would give increased constipation a second thought?

Consider mood changes as another example. It is well-documented that the social isolation associated with the pandemic lockdowns has taken a toll on the mental health of people of all ages. It is easy to attribute symptoms of  decreased cognitive function, forgetfulness, or even depression in older adults to increased social isolation rather than considering a diagnosis of hypothyroidism.

Symptoms such as loss of hair on the legs or arms may be attributed to the natural process of aging, and while it is normal to have less hair on the arms or legs as people age, it is not normal to lose all the hair. Although no longer needing to shave or wax one’s legs may be perceived as a benefit of aging (like no longer having a ‘period’ after menopause), a complete loss of hair on the legs or arms is something that is not a normal part of aging. Symptoms like these should be brought to the attention of one’s doctor. Likewise, while it may be nice for someone not to feel as sweaty in the heat of the summer as one did when they were younger, sweating is how humans stay cool, and decreased sweating can be dangerous! 

Symptoms of constipationhair loss on legs and armsdecreased sweating, forgetfulness, and mood changes such as depression are not part of “aging” but are symptoms that one’s doctor should assess.  

Untreated Hypothyroidism can be Dangerous

Myxedema describes advanced hypothyroidism that occurs when the condition is left untreated or inadequately treated [4]. This term is also applied to hypothyroidism’s effects on the skin, where it looks puffy and swollen and takes on a waxy consistency [4]. 

Below is a photo of what I looked like hiking 3 months before my son’s wedding, what I looked like with myxedema at his wedding, and what I look like today. I don’t share these photos easily because my son’s wedding was a special occasion, and not only did I look and feel terrible, in retrospect, I was very unwell. I am sharing them so that people can understand what the edema / myxedema of hypothyroidism looks like and how quickly it can progress, and how serious hypothyroidism can be if left untreated or undertreated.

Myxedema of hypothyroidism is very different from ordinary weight gain. I hope that by sharing these photos people will be better equipped to recognize this symptom in themselves or in others, and ensure that medical attention is sought. 

Getting Diagnosed

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

In British Columbia, thyroid testing covered by the provincial health plan is determined by a 2018 document titled Thyroid Function Testing in the Diagnosis and Monitoring of Thyroid Function Disorder [2]. These guidelines outline testing for thyroid stimulating hormone (TSH), free thyroxine (fT4), free triiodothyronine (fT3), and anti-thyroid peroxidase (TPO).  

Unless someone has specific risk factors for thyroid disease (older age, strong personal or family history of thyroid disease, taking drugs such as lithium (used in bipolar disorder) or amiodarone (used in cardiac dysrhythmia), or grew up in a developing country known to have either iodine excess or deficiency),  individuals are required to exhibit several of the specific symptoms listed below to even qualify for thyroid hormone testing

The problem is that typical symptoms such as cold intoleranceedemadecreased sweating, and skin changes often don’t appear until much later in the progression of the disease.  Moreover, in some individuals, these symptoms do not appear at all.

Furthermore, as outlined in the previous article, even if a person meets the criteria for a TSH test, the results would need to come back significantly higher than the cutoffs to qualify for a free T4 (fT4) or free T3 (fT3) test. 

People here and in other places with similar policies have no choice but to live with many symptoms documented to be associated with hypothyroidism but outside narrowly defined diagnostic criteria until they become sick enough to warrant testing


NOTE: these photos are for illustrative purposes only. 

[LEFT: me hiking March 5, 2022.  MIDDLE: me at my youngest’s son’s wedding on June 3, 2022, only 2 months ago. RIGHT: Me today (August 8, 2022), only two months after my son’s wedding with 75% of the edema resolved.

UPDATE [August 25, 2022] The photo on the left was taken 2 ¾ months ago. The photo on the right was taken today, 2 months after beginning treatment for hypothyroidism. They are provided only as an illustration of what symptoms can look like and how quickly they can resolve with medical treatment. (I deliberately left the lines marking the hairline and chin to make comparison easier.) 

LEFT: before diagnosis and treatment RIGHT: 2 months after diagnosis and starting treatment [for illustrative purposes only]

The photos below are of my left leg without edema and with it. While my legs are still ‘waxy’ looking from the myxedema, the extreme swelling resolved within a few days of beginning thyroid hormone replacement. This photo is for illustrative purposes only and does NOT provide any clinical information.

While each person may exhibit different symptoms, this is fairly typical of the length of time over which the “weight gain” of hypothyroidism can occur, and also the time-frame over which it can resolve with treatment.


It is important to understand that untreated hypothyroidism can progress and the results of a myxedema crisis which can be fatal. The death rate for a myxedema crisis is between 20-60%, even with treatment [5]. 

A myxedema crisis is often incorrectly called a ‘myxedema coma,’ but this term is misleading since the person rarely experiences a coma.

The most noticeable feature of a myxedema crisis is the person’s significant deterioration in mental function [5]. The slowness of thoughtdecrease in attention, and apathy can easily be confused with symptoms of depression[6], but in severe untreated hypothyroidism, people can exhibit significant agitation and even psychosis and paranoia, referred to as “myxedema madness” [6]. In addition, there have been cases reported in the literature of people hospitalized with suspected affective (mood) disorders such as bipolar disorder— even psychosis that turned out to be a myxedema crisis and that resolved with thyroid hormone treatment [7].

A myxedema crisis may occur because someone had untreated hypothyroidism. It can also happen because someone stopped taking their medication or was taking an incorrect dosage. Therefore, being correctly diagnosed, treated and followed by a physician is essential.

I found the following explanation from a recent article on hypothyroidism [8] very helpful as it explains how different people with the condition may have various symptoms.

“It is important to maintain a high index of suspicion for hypothyroidism since the signs and symptoms can be mild and nonspecific and  different symptoms may be present in different patients. Typical features such as cold intolerancepuffinessdecreased sweating and skin changes may not be present always. Inquire about dry skinvoice changes, hair loss, constipationfatiguemuscle crampscold intolerancesleep disturbancesmenstrual cycle abnormalitiesweight gain, and galactorrhea  (nipple discharge not associated with lactation / breastfeeding). Also obtain a complete medical, surgical, medication, and family history” [8].

Note (August 15, 2022): Over-treatment with thyroid hormones also poses a risk of thyrotoxicosis, orthyroid storm,” outlined in this newer article.

Final Thoughts…

By virtual of their age, older adults in British Columbia qualify for thyroid testing. If older people exhibit even a few of the common symptoms of hypothyroidism, such as long standing body aches or joint pain, unexplained fatigue, feeling usually chilled, constipation, dry skin or hair loss, forgetfulness or depression, this should be brought to their doctor’s attention. These are not typical signs of aging but are common symptoms associated with hypothyroidism. 

For younger individuals without preexisting risk factors and that do not have the specific symptoms listed on the diagnostic criteria, the reality is that they do not qualify for testing. Unfortunately, they will need to get quite unwell before they are able to be diagnosed and treated, and their doctor’s hands are tied by a system that will not enable them to test T3 or T4 — even in the presence of high-normal TSH, or symptoms known to be associated with hypothyroidism, but not on the diagnostic criteria list.

Surely, there has to be a way that people can be tested, but that does not put additional financial strain on an already overtaxed public healthcare system?

Currently people have two alternative options;

(1) pay significant out of pocket costs to see a Functional Medicine MD or Integrative Health MD where they can be properly diagnosed and treated.

(2) pay a naturopath added costs for them to requisition thyroid tests, but one concern is since they are not medical doctors, they do not have the training to rule out liver, kidney or heart disease that can mimic many of the same symptoms as hypothyroidism, and that requires medical attention.

In the previous post, I mentioned the option of enabling patients to self-pay at the same cost as the government pays for TSH, T3 and T4 tests. This way if the lab tests results come back abnormal, their doctor can oversee both diagnosis and treatment (or refer them to an endocrinologist).

In British Columbia, someone can pay (at government rates) $9.90 for a TSH test, $12.12 for a free T4 test, or T4 or total thyroxine test, and pay $9.35 for a free T3 test [9]. Under the current system, the government only applies a lab volume discount (based on 2011-2012 volumes) for some fee-for-service (FFS) tests [10] so under this model, only 38% of tests are reimbursed at 100% of the published fee, whereas 62% are only reimbursed at 50% of the published fee [3].  It is not clear from the government publication which rate applies to thyroid testing, but even if people are required to pay 100% of the costs, the total cost of a TSH test, and a free T4 test, and a free T3 test is just over $30.  

I was disheartened to learn recently that even if patients are willing to pay the full cost of thyroid testing, their doctor is under no obligation to write the lab requisition. This is because licensing requirements require doctors who write a lab test requisition to also take responsibility to oversee care based on those results. Unfortunately, not all doctors are willing to treat those with subclinical hypothyroidism. 

How I May be Able to Assist

I currently assist my clients in requesting that their doctor refer them to an allergist if I believe there is clinical reason to suspect IgE mediated food allergies. I also will request that a doctor requisition a fasting insulin (or c-peptide test) along with a fasting glucose if based on assessment I have reason to suspect a person’s pancreas may be working too hard to keep fasting blood glucose and HbA1C in the normal range. In the same way, if I have clinical reason to be concerned about a person’s thyroid function, I will request that a doctor requisition thyroid testing. These requests are by no means a guarantee that a person’s doctor will agree to requisition blood tests, but it has been my experience that when clinical concerns are documented, most doctors are willing investigate further. 

More Info

If you would like more information about the services I provide people who are newly diagnosed with hypothyroidism, please send me a note through the Contact Me form, above.

To your good health!

Joy

 

You can follow me on:

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

 

References

    1. John Hopkins Medicine, Long COVID: Long-Term Effects of COVID-19, June 14, 2022, https://www.hopkinsmedicine.org/health/conditions-and-diseases/coronavirus/covid-long-haulers-long-term-effects-of-covid19
    2. BC Guidelines & Protocols Advisory Committee, Thyroid Function Testing in the Diagnosis and Monitoring of Thyroid Function Disorder, October 24, 2018
    3. Bharucha AE, Lacy BE. Mechanisms, Evaluation, and Management of Chronic Constipation. Gastroenterology. 2020;158(5):1232-1249.e3. doi:10.1053/j.gastro.2019.12.034
    4. Medical News Today, What is Myxedema and How is it Treated, April, 22, 2022, https://www.medicalnewstoday.com/articles/321886
    5. Elshimy G, Chippa V, Correa R. Myxedema. [Updated 2022 May 22]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing. https://www.ncbi.nlm.nih.gov/books/NBK545193/#_NBK545193_pubdet_
    6. Samuels MH. Psychiatric and cognitive manifestations of hypothyroidism. Curr Opin Endocrinol Diabetes Obes. 2014;21(5):377-383. doi:10.1097/MED.0000000000000089
    7. Heinrich TW, Grahm G. Hypothyroidism Presenting as Psychosis: Myxedema Madness Revisited. Prim Care Companion J Clin Psychiatry. 2003;5(6):260-266. doi:10.4088/pcc.v05n0603
    8. Patil N, Rehman A, Jialal I. Hypothyroidism. [Updated 2022 Jun 19]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing;
    9. Government of British Columbia, Ministry of Health, Schedule of Fees for Laboratory Services – Outpatient, Payment Schedule, revised April 1, 2022, http://www.bccss.org/bcaplm-site/Documents/Programs/laboratory_services_schedule_of_fees.pdf
    10. BC Agency for Pathology and Laboratory Medicine (BCAPLM), Outpatient Payment Schedule, Laboratory Volume Discounting (LVD), http://www.bccss.org/clinical-services/bcaplm/health-professionals/outpatient-payment-schedule

 

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.

 

Thyroid Function Assumed to be Normal When Only TSH is Tested

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


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

Overview of Thyroid Hormones and Lab Tests

from [5] The Merck Manual of Medical Information (1997)

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

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

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

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

Different Causes of Primary Hypothyroidism

Hashimoto’s Disease

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

Prior Thyroid Surgery or Radiation of the Neck

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

Dietary Deficiency

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

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

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

Testing for Hypothyroidism

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

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

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

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

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

Indications for Testing

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

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

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

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

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

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

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

Table 1: Signs and Symptoms of Hypothyroidism [9]

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

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

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

Hypothyroid signs and symptoms 1 of 3 (the ones in italics do NOT warrant TSH testing in British Columbia)
Hypothyroid signs and symptoms 2 of 3 (the ones in italics do NOT warrant TSH testing in British Columbia)
Hypothyroid signs and symptoms 3 of 3 (the ones in italics do NOT warrant TSH testing in British Columbia)

The Guidelines Summarized

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

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

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

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

Summary

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

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

Thyroid Function

TSH                    4.0  (0.27-4.2) mU/L

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

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

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

Final Thoughts…

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

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

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

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

More Info?

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

To your good health!

Joy

You can follow me on:

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

 

References

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

 

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.

Chronic Constipation — do we really just need more fiber and water?

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

posted with written permission from Glenn McCoy

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

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

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

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

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

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

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

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

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

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

Constipation and Fiber

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

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

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

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

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

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

Soluble Fiber and the Gut Microbiome/Mycobiome

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

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

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

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

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

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

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

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

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

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

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

Putting it Into Practice

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

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

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

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

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

More Info?

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

To your good health!

Joy

You can follow me on:

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

Special Thanks

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

References

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

Copyright ©2021 BetterByDesign Nutrition Ltd.

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

When Meat Prices Go Crazy – the best protein sources on a budget

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

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

Below are some examples of relatively low-cost animal source foods, sorted from the highest amount of protein per ounce (28g), to the lowest and as animal products, these are all complete proteins — having all 9 essential amino acids.

Highest protein animal source foods, from highest to lowest

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

Canned tuna is delicious mixed up with a bit of mayonnaise, with or without some minced celery and is terrific added to casseroles with pasta, or for those eating low carb — with chunks of lightly cooked cauliflower, instead of noodles. These casseroles can be a complete meal with the addition of frozen vegetables, and are lovely with a sprinkle of grated cheese on top.  Tuna is such a great source of protein as well as omega 3 fat, and is often on sale making it even less expensive.

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

Spinach soufflé

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

Shakshuka

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

What about some non-animal sources ?

Non-Animal Source of Protein

Ma-Po tofu

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

fish without bones

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

Highest protein non-animal source foods, from highest to lowest

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

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

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

Protein in Some Nuts, Seeds and Grains

Highest protein per kcal foods, from highest to lowest (nuts, seeds and grains)

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

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

Dairy Sources

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

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

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

 

 

Pressed cottage cheese” is sometimes called baker’s cottage cheese, or “Farmer’s cheese”.

“Dry cottage cheese” is just the curd that is used for making “creamed cottage cheese”, but without the liquid.  In years gone cream was added to the dry curd to make “creamed cottage cheese” hence the name — but now it is a mixture of milk with various gums, such as carrageenan, guar gum and xanthan gum.
As can be seen from the table below, these have very different amounts of protein per ounce.
Difference between dry cottage cheese, pressed cottage cheese and regular (creamed) cottage cheese

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

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

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

low carb manicotti, in process
Highest protein per kcal foods, from highest to lowest (dairy source, with eggs)

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

There are so many good sources of inexpensive protein that can stand on their own, or mixed together to make so many delicious combinations!  Looking to other cultures that use these ingredients is a great way to find out what to do with them. Chinese, Korean and Japanese have wonderful easy recipes for tofu.  Hispanic cultures including Mexican have so many ways to cook pinto beans, kidney beans, and black beans — both with and without meat and for lentils and chickpeas you need not look far. Middle Eastern recipes abound using these, as do South Asian recipes from India, Pakistan and Sri Lanka.

Remember, protein is a very important macronutrient needed as a building block for the body. Carbohydrate and fat are the body’s energy sources, but the body can make its own glucose from protein or fat, provided they are supplied in sufficient quantities.

Protein is so important that according to the “protein leverage hypothesis“, people  will just keep eating and eating until their body gets the protein it needs. Targeting protein first is important to keep from overeating foods that are “protein dilute”. Remember, it is not only children and adolescents that need protein, but older people actually need more protein as they age, to lower the risk of sarcopenia (muscle wasting).

Final Thoughts…

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

More Info?

If you would like more information about how I can help you please send me a note through the Contact Me form.

To your good health!

Joy

You can follow me on:

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

Copyright ©2021 BetterByDesign Nutrition Ltd.

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

Could Protein be the Appetite’s Control – the Protein Leverage Hypothesis

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

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

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

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

In their 2005 paper, they wrote;

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

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

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

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

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

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

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

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

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

But how much is best? It depends for whom.

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

The RDA – enough protein to prevent deficiency

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

Protein Needs for Active Healthy Adults

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

Protein Needs for Older Adults

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

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

Range of Safe Intake

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

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

Final Thoughts…

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

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

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

Vegetarian? No problem!

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

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

More Info?

If you would like more information about how I can help you please send me a note through the Contact Me form.

To your good health!

Joy

You can follow me on:

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

References

  1. Simpson SJ, Raubenheimer D. Obesity: the protein leverage hypothesis. Obes Rev. 2005 May;6(2):133-42. doi: 10.1111/j.1467-789X.2005.00178.x. PMID: 15836464.
  2. Ben-Dor M, Gopher A, Hershkovitz I, Barkai R (2011) Man the Fat Hunter: The Demise of Homo erectus and the Emergence of a New Hominin Lineage in the Middle Pleistocene (ca. 400 kyr) Levant. PLoS ONE 6(12): e28689. https://doi.org/10.1371/journal.pone.0028689
  3. Lieberman HR, F.V., Agarwal S, et al. , Protein intake is more stable than carbohydrate or fat intake across various US demographic groups and international populations. The American Journal of Clinical Nutrition, 2020. 112(1): p. 180-186.
  4. DiFeliceantonio AG, Coppin G, Rigoux L, et al., Supra-Additive Effects of Combining Fat and Carbohydrate on Food Reward. Cell Metab. 2018 Jul 3;28(1):33-44.e3. doi: 10.1016/j.cmet.2018.05.018. Epub 2018 Jun 14. PMID: 29909968.
  5. Zefeng Zhang, Sandra L Jackson, Euridice Martinez, Cathleen Gillespie, Quanhe Yang, Association between ultraprocessed food intake and cardiovascular health in US adults: a cross-sectional analysis of the NHANES 2011—2016, The American Journal of Clinical Nutrition, Volume 113, Issue 2, February 2021, Pages 428—436, https://doi.org/10.1093/ajcn/nqaa276
  6. Lu Wang, Euridice Martí­nez Steele, Mengxi Du, Jennifer L. Pomeranz, Lauren E. O’Connor, Kirsten A. Herrick, Hanqi Luo, Xuehong Zhang, Dariush Mozaffarian, Fang Fang Zhang. Trends in Consumption of Ultraprocessed Foods Among US Youths Aged 2-19 Years, 1999-2018JAMA, 2021; 326 (6): 519 DOI: 10.1001/jama.2021.10238
  7. Martí­nez Steele E, Raubenheimer D, Simpson SJ, Baraldi LG, Monteiro CA. Ultra-processed foods, protein leverage and energy intake in the USA. Public Health Nutr. 2018 Jan;21(1):114-124. doi: 10.1017/S1368980017001574. Epub 2017 Oct 16. PMID: 29032787.
  8. National Academies Press, Dietary Reference Intakes for Energy, Carbohydrate, Fiber, Fat, Fatty Acids, Cholesterol, Protein and Amino Acids (2005)
  9. Thomas DT, Erdman KA, Burke LM. American College of Sports Medicine Joint Position Statement. Nutrition and Athletic Performance [published correction appears in Med Sci Sports Exerc. 2017 Jan;49(1):222]. Med Sci Sports Exerc. 2016;48(3):543-568. doi:10.1249/MSS.0000000000000852
  10. Fielding RA, Vellas B, Evans WJ, Bhasin S, et al, Sarcopenia: an undiagnosed condition in older adults. Current consensus definition: prevalence, etiology, and consequences. International working group on sarcopenia. J Am Med Dir Assoc. 2011 May;12(4):249-56
  11. Bauer J1, Biolo G, Cederholm T, Cesari M, et al. Evidence-based recommendations for optimal dietary protein intake in older people: a position paper from the PROT-AGE Study Group. J Am Med Dir Assoc. 2013 Aug;14(8):542-59

    Copyright ©2021 BetterByDesign Nutrition Ltd.

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

Do You Identify as a Food Addict?

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

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

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

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

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

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

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

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

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

Food addiction in terms of the definition of “substance use disorder” (DSM-5)

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

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

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

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

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

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

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

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

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

I was obese, had type 2 diabetes and dangerously high blood pressure — and was a Registered Dietitian with a master’s degree who was in denial as to just how much danger I had put myself in!  

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

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

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

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

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

Food addiction in terms of substance use disorder

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

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

Here is a rhetorical question that may help answer this.

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

I don’t think so.

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

This is how I defined them; 

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

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

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

Final Thoughts…

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

More Info

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

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

To your good health!

Joy

You can follow me on:

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

References

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

 

Copyright ©2021 BetterByDesign Nutrition Ltd.

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

Time to Stop Calling Type 2 Diabetes a “chronic, progressive disease”

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

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

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

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

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

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

 

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

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

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

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

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

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

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

Final Thoughts…

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

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

What We’ve Been Taught and What We Need to Know

More Info?

If you would like more information about how I can support you in seeking remission of type 2 diabetes as defined above, please have a look around my web page, or send me a note through the Contact Me form.

To your good health!

Joy

You can follow me on:

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

References

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

Copyright ©2021 BetterByDesign Nutrition Ltd.

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

Type 2 Diabetes Remission – proposed definition from international experts

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


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

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

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

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

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

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

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

Choice of the Term “Remission”

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

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

“Remission” Not Equivalent to No Evidence of Disease

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

Different Levels of Remission

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

Use of Glucose-Lowering Medication in Defining Remission

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

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

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

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

Timeline for Determining Remission

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

Medication Intervention (Pharmacotherapy)

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

Surgical Intervention

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

Lifestyle Changes

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

Need for Ongoing Monitoring

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

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

HbA1c as the Defining Measurement of Remission

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

Conclusions of the Expert Panel

The expert panel concluded that the term “remission” should be used to describe a sustained metabolic improvement in type 2 diabetes to nearly normal levels defined as a return of HbA1c to < 6.5% (<48 mmol/mol) that occurs spontaneously, or following an intervention and that persists for at least 3 months in the absence of usual glucose-lowering medication (pharmacotherapy).

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

Final Thoughts…

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

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

More Info?

If you would like more information about how I can support you in seeking remission of type 2 diabetes as defined above, please have a look around my web page, or send me a note through the Contact Me form.

To your good health!

Joy

You can follow me on:

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

Note: A consensus report is not an American Diabetes Association (ADA) position statement but represents expert opinion of this international expert panel’s collective analysis, evaluation, and opinion.

References

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

 

Copyright ©2021 BetterByDesign Nutrition Ltd.

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

High Protein Matcha Drink — role in abdominal fat loss

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


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

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

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

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

How do Green Tea Catechins in Matcha Work?

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

Timing of Matcha Catechin Consumption

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

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

Effect of Milk Casein on Catechins

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

Final Thoughts…

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

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

WARNING TO PREGNANT WOMEN

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

High Protein to Energy Matcha Drink

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

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

Ingredients

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

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

12 cubes ice cubes

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

Optional: 1.5 tsp monk fruit / erythritol sweetener

Method

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

Macros

from chronometer®

Protein to Energy Ratio = 3.17

from ptoe.com

More Info?

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

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

To your good health!

Joy

You can follow me on:

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

 


References

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

 

Copyright ©2021 BetterByDesign Nutrition Ltd.

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

 

Risk of Dehydration in Older Adults During Heatwaves

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

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

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

forecast from The Weather Network

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

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

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

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

Age 12—18 years Age 19—50 years Age 51 years and older
Male Average: 59%
Range: 52—66%
Average: 59%
Range: 43—73%
Average: 56%
Range: 47—67%
Female Average: 56%
Range: 49—63%
Average: 50%
Range: 41—60%
Average: 47%
Range: 39—57%

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

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

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

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

But what to look for?

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

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

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

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

To your good health!

Joy

You can follow me on:

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

References

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

Copyright ©2021 BetterByDesign Nutrition Ltd.

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

 

Staying Hydrated Without a Caffeine or Carbonated Drink – Limonana

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

This week’s weather forecast – hot and hotter (from the Weather Network)

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

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

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

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

How about Limonana?

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

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

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

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

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

Limonana

  • 3 lemons
  • 1620 fresh mint leaves
  • 4 Tbsps. Monk Fruit / erythritol sweetener (or to taste)
  • 450 ml cold water
  • a whole tray of ice cubes
  • Sprig of mint to garnish (optional)
  1. Dissolve the Monk Fruit / erythritol sweetener in a bit of hot water and set aside.
  2. Using a knife, remove the peel from the lemon and be sure to cut off all the white pith as it is bitter. Separate the sections of lemon flesh from the membranes – like one does for orange suprí¨mes. Discard the membranes and any seeds, and put the flesh of the lemon into a blender.
  3. Add the mint and Monk Fruit / erythritol sweetener and pulse a few times until the mint leaves are well chopped. Add the ice cold water and pulse again to mix. Taste the Limonana and add more sweetener, if necessary.
  4. Allow to chill in the fridge for a bit, to let the flavour mature.
  5. When ready to serve, put plenty of ice cubes into a tall glass and pour the Limonana over them. Drink as is, or garnish with the mint sprig and serve.
Enjoy!

 

To your good health!

Joy

You can follow me on:

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

References

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

Copyright ©2021 BetterByDesign Nutrition Ltd.

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

 

The Three Ways to Balance Carbohydrate and Fat as Fuel

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

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

Figure 16.4.4 : The Effect of Exercise Intensity on Fuel Sources (from [1])
Protein is not usually used for energy, although small amounts of amino acids from broken down protein are used by the body when we’re resting, and even smaller amounts are used when we’re doing moderate-intensity exercise[1].

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

Determining Individual Macros

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

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

How do we choose the amount of protein we need?

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

NOTE: this calculation is based on lean body mass (also known as Ideal Body Weight or Ideal Body Mass (IBW), not total body weight. Lean body mass is essentially one’s total body weight minus the amount of fat they have.

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

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

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

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

Older people also need more protein in order to maintain muscle mass, and prevent sarcopenia (muscle loss associate with aging). There have been several position statements issued by those that work with an aging population indicating that protein intake between 1.0 and 1.5 g protein / kg IBW per day may best meet the needs of adults during aging [7,8].

Balancing Carbohydrate and Fat as Fuel

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

Higher Carbohydrate than Fat

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

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

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

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

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

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

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

Higher Fat than Carbohydrate

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

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

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

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

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

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

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

Balanced Fat and Carbs

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

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

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

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

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

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

Low Carbohydrate High Protein

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

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

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

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

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

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

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

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

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

Final Thoughts…

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

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

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

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

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

Nutrition is BetterByDesign!

More Info?

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

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

To your good health!

Joy

You can follow me on:

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

References

  1. Fuel Sources. (2020, August 13). Retrieved May 24, 2021, from https://med.libretexts.org/@go/page/7071
  2. Youdim A, Merck Manual, Carbohydrates, Proteins and Fats, https://www.merckmanuals.com/en-ca/home/disorders-of-nutrition/overview-of-nutrition/carbohydrates-proteins-and-fats
  3. Tomé D, Bos C, Dietary Protein and Nitrogen Utilization, The Journal of Nutrition, Volume 130, Issue 7, July 2000, Pages 1868S—1873S, https://doi.org/10.1093/jn/130.7.1868S
  4. Rudman D, DiFulco TJ, Galambos JT, Smith RB 3rd, Salam AA, Warren WD. Maximal rates of excretion and synthesis of urea in normal and cirrhotic subjects. J Clin Invest. 1973;52(9):2241-2249. doi:10.1172/JCI107410
  5. National Academies Press, Dietary Reference Intakes for Energy, Carbohydrate, Fiber, Fat, Fatty Acids, Cholesterol, Protein and Amino Acids (2005)
  6. Thomas DT, Erdman KA, Burke LM. American College of Sports Medicine Joint Position Statement. Nutrition and Athletic Performance [published correction appears in Med Sci Sports Exerc. 2017
  7. Fielding RA, Vellas B, Evans WJ, Bhasin S, et al, Sarcopenia: an undiagnosed condition in older adults. Current consensus definition: prevalence, etiology, and consequences. International working group on sarcopenia. J Am Med Dir Assoc. 2011 May;12(4):249-56
  8. Bauer J1, Biolo G, Cederholm T, Cesari M, et al. Evidence-based recommendations for optimal dietary protein intake in older people: a position paper from the PROT-AGE Study Group. J Am Med Dir Assoc. 2013 Aug;14(8):542-59
  9. Institute of Medicine (US) Committee on Examination of Front-of-Package Nutrition Rating Systems and Symbols; Wartella EA, Lichtenstein AH, Boon CS, editors. Front-of-Package Nutrition Rating Systems and Symbols: Phase I Report. Washington (DC): National Academies Press (US); 2010. Appendix B, FDA Regulatory Requirements for Nutrient Content Claims. Available from: https://www.ncbi.nlm.nih.gov/books/NBK209851/
  10. Araíºjo J, Cai J, Stevens J. Prevalence of Optimal Metabolic Health in American Adults: National Health and Nutrition Examination Survey 2009—2016. Metabolic Syndrome and Related Disorders Vol 20, No. 20, pg 1-7, DOI: 10.1089/met.2018.0105
  11. Evert, AB, Dennison M, Gardner CD, et al, Nutrition Therapy for Adults With Diabetes or Prediabetes: A Consensus Report, Diabetes Care, Ahead of Print, published online April 18, 2019, https://doi.org/10.2337/dci19-0014
  12. Volek JS, Phinney SD, The Art and Science of Low Carbohydrate Living: An Expert Guide, Beyond Obesity, 2011
  13. Feinman RD, Pogozelski WK, Astrup A, Bernstein RK, Fine EJ,Westman EC, et al. Dietary Carbohydrate Restriction as the First Approach in Diabetes Management: critical review and evidence base. Nutrition. 2015;31(1):1—13
  14. Diabetes Canada, Diabetes Canada Position Statement on Low Carbohydrate
    Diets for Adults with Diabetes: A Rapid Review Canadian Journal of Diabetes (2020), doi: https://doi.org/10.1016/j.jcjd.2020.04.001
  15. Stubbs J, Ferres S, Horgan G, Energy Density of Foods: Effects on Energy Intake, Critical Reviews in Food Science and Nutrition, 40:6, 481-515, 2010

 

Copyright ©2021 BetterByDesign Nutrition Ltd.

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

LDL Cholesterol is Not the Best Assessor of Cardiovascular Risk

There continues to be a reliance on LDL cholesterol (LDL-C) as the main means to assess cardiovascular (CVD) risk, despite the fact that apolipoproteinB (apoB) has been found to be a much better predictor. This new article looks at why total LDL cholesterol is inadequate to assess cardiovascular risk, what apoB is and why it is considered a better assessor, and how apoB, apoB/apoA ratio and its proxy TG:HDL ratio could be used to assess CVD risk.

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

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

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

To understand why apoB is a more accurate measure of cardiovascular risk than LDL, as well as how apoB/apoA ratio and its proxy triglyceride to HDL ratio (TG:HDL) can be used as a rough screening, a simple overview of the different types of cholesterol is needed — and it holds some surprises when it comes to both what we’ve believed about HDL being “good cholesterol”, and LDL being “bad cholesterol”.

Different Types of Cholesterol

What we call “cholesterol” are really lipoproteins which are particles made up of lipids (fat) and protein and that vary in size, density, and lipid and apolipoprotein composition. They can be separated into different classes based on physical and chemical parameters and include;

    • high density lipoprotein (HDL)
    • low density lipoprotein (LDL)
    • very low density lipoprotein (VLDL)

High Density Lipoprotein (HDL) – so-called “good cholesterol”

Most people think of high density lipoprotein (HDL) as ”good cholesterol” and while it is known as a strong inverse indicator of CVD risk, HDL cholesterol is not one entity, but there are different sub-classes of HDL.

We have known since the 1990s that there are several sub-particles of LDL and we now know that HDL is made up of 5 different sub-fractions based on their size and density (very large, large, medium, small, and very small) and that these five subclasses seem to be associated with different levels of CVD risk [2]. HDL cholesterol measured on blood tests measures the total cholesterol content in all the different sub-fractions of HDL (HDL-C)[2].

Each High Density Lipoprotein (HDL) carries one apolipoprotein-A (apoA) which makes up ~65% of its mass and has been found in most studies to not to be associated with CVD risk [2].

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

Low Density Lipoprotein (LDL) – so-called “bad cholesterol”

Most people think of low density lipoprotein (LDL) as ”bad cholesterol” — but low density lipoprotein (LDL) is not a single entity either — but is made up of four subclasses of LDL particles[2] where decreased size and increased density of LDL are associated with increased cardiovascular risk [3,4].

It is the small, dense LDL sub-fraction (sdLDL) that is associated with atherosclerotic plaque, whereas the large, fluffy (or buoyant) LDL sub-fraction is not [3].

Here’s an analogy that may help think of the different sub-fractions of LDL.

If I have a basket filled with balls — is how many I can get inside a basket affected by whether they are basketballs, or golf balls?

Of course it is!

I can put many more golf balls in a basket, than I can basketballs.

Think of golf balls as small, dense LDL (sdLDL) and basketballs as large, buoyant LDL.

LDL Cholesterol on Lab Test Results

LDL cholesterol measured on lab tests indicates total LDL-cholesterol (LDL-C) — that is, the total concentration of cholesterol within all four sub-fractions of LDL sub-particles. What is very important to note is that total LDL cholesterol (LDL-C) is what is usually used in studies that report an association between higher levels of LDL and cardiovascular disease, but these studies fail to distinguish between small dense LDL which are atherosclerotic, and the large, buoyant LDL which are not.  All the different subtypes of LDL are lumped together as if they were a one thing — and they are very different!

Usually, when someone is told their “cholesterol is high” it usually means that their LDL cholesterol is high — but many doctors are unaware of the different sub-fractions of LDL and that it is only the small, dense LDL (sdLDL) ones that pose a risk.  This is why I encourage my clients when told their LDL is high to ask “which LDL“? 

Very Low Density Lipoprotein (VLDL)

Very low density lipoprotein (VLDL) is produced in the liver and the best way to understand its role is to think of it as a ”taxi” which the liver makes and then releases into the bloodstream to shuttle triglycerides (TG) around the body, to the various tissues.  VLDL cholesterol on blood test results isn’t actually measured, but is estimated as a percentage of the triglyceride value.

It is important to note that very low density lipoproteins (VLDL) and the Low Density Lipoproteins (LDL) that results after it off-loads it triglycerides each carry one apolipoprotein-B (apoB) molecule, and while a high VLDL value is said to be a risk for cardiovascular disease, a more accurate measure is Apolipopoprotein B (apoB), the lipoprotein in VLDL.

Where does LDL come from?

Once a large amount of triglyceride (TG) has been off-loaded in the tissues by the VLDL ”taxi”, it then becomes a new, smaller lipoprotein called low density lipoprotein, or LDL which contains mostly cholesterol, and some protein.  Some LDLs are removed from the circulation by cells around the body that need the cholesterol contained in them and the rest is taken out of the circulation by the liver.

LDL is what is left once the VLDL which is made by the body has offloaded its triglyceride passenger’ to the tissues.

Assessing Cardiovascular Risk – particle number, apoB : apo A and TG:HDL ratio

LDL particle number (LDL-P)

Since the amount of cholesterol in each LDL particle varies, measuring total LDL cholesterol (LDL-C) tells us nothing about the actual number of particles they are or their size but an increased number of LDL particles indicates that a person has more small, dense particles.

To best understand this, think of the ball analogy, above. There will be increased number of balls with golf balls as compared to basketballs in the same size container.

LDL-particle number (LDL-P) has a strong and independent association with the development of atherosclerosis, as well as with CVD events [2] and is considered a more accurate predictor of cardiovascular events, than total LDL cholesterol (LDL-C) [2].

A nuclear magnetic resonance spectroscopy (NMR) lipid profile test directly measures the number of LDL particles (as well as HDL particles). For LDL particles, a value of less  than 1.000 in nmol/L is considered ideal, a value of 1000-1299 is considered moderate,  a value of 1300-1599 is considered borderline high, and a value >1600 is considered high.

Apolipoprotein B

Apolipoprotein B (apo B), which is the main lipoprotein in VLDL (and in LDL after the VLDL has offloaded its triglycerides to the tissues) and is correlated with LDL particle number, which makes it a very good assessor of cardiovascular disease risk.

Remember, the golf ball / basketball analogy; the higher number of LDL particles means the more small, dense LDL particles there are.

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

Triglyceride (TG):HDL Ratio

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

Remember, the golf ball / basketball analogy; the more small, dense LDL particles there are, the higher the LDL particle number. 

One study from 2004 reported that almost 80% of people with a TG:HDL-C ratio of greater than 3.8 (when values are expressed in mg/dl) had mostly small, dense LDL particles, indicating cardiovascular risk. This same study found that more than 80% with a TG:HDL-C ratio of less than 3.8 (when values are expressed in mg/dl) had mostly large, fluffy LDL particles, indicating lower cardiovascular risk[5].

A 2005 study [6] reported that a TG:HDL-C ratio of 3.5 or greater was highly correlated with atherosclerosis in men, as well as insulin resistance and metabolic syndrome.

A recent 2014 [7] study found that a high TG:HDL-C ratio was a strong independent predictor of cardiovascular disease, coronary heart disease and all-cause mortality both before- and after adjustment for age, smoking, BMI and blood pressure.

In Canada (as well as Europe), values are expressed as mmol/L and the ratios are interpreted as follows [8];

TG:HDL-C < 0.87 is ideal

TG:HDL-C > 1.74 is too high

TG:HDL-C > 2.62 is much too high

In the US, values are expressed in mg/dl and the ratios are interpreted as follows [8];

TG:HDL-C < 2 is ideal

TG:HDL-C > 4 is too high

TG:HDL-C > 6 is much too high

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

Final Thoughts…

If someone’s lab test results show they have high LDL cholesterol, all we know for certain is that the total concentration of cholesterol counting all four sub-fractions of LDL sub-particles together is high. 

This would be like telling someone that the total number of balls they have is 25 and then asking them if this will fit in their container — but not telling them if they were golf balls or basketballs. We need to know how big they are to know what “25” means.

Someone having “high LDL cholesterol” i.e. high total LDL (LDL-C) tells us nothing in and by itself. We need to know about either particle size or particle number.

This leaves two options;

An LDL-particle (LDL-P) test will indicate the LDL particle number and the higher the number, the more small dense LDL the person would have. While not routinely done, I have had had clients come to me with results from this specialized test.  They had it done when their total LDL cholesterol was found to be high, and their doctor wanted to know if this was problematic. If the number was low, then most of the LDL would be the large, buoyant type and not a problem — it would only be if the number was high, indicating lots of small, dense LDL that high total LDL is indicative of CVD risk.

An apoB test which measures the lipoprotein in VLDL and LDL is a good indicator of LDL particle number, so is a very good assessor of cardiovascular disease risk.

Being told we have high LDL cholesterol doesn’t mean much if we don’t know which LDL is high. Small, dense LDL are a risk, but large, buoyant LDL are not. To assess the need for dietary, lifestyle or medication changes we need to know ”how many” or ”how big”. We can estimate this using a TG:HDL ratio from routine blood work — all we need is a calculator, and knowing the cut-off points. Then, if warranted, we can run an apoB test and know for sure if there are too many small dense LDL.

Prescribing statins on the basis of high (total) LDL cholesterol alone — without knowing anything about size of the LDL particles or total number of LDL particles is, according to this most recent article, inappropriate.

NOTE (April 26, 2021): It should be noted that while it is the opinion of the writers of the article in Current Opinion in Lipidology, and that of the European Society of Cardiology and the European Atherosclerosis Society that LDL-C is not the best clinical marker of cardiovascular risk or the appropriate marker to assess the benefits of statin medication, an individual should always discuss whether or not to take a medication with their doctor.  Lab tests may not be the only reason for medications to be prescribed — and such a recommendation may also include past medical history, lifestyle factors and/or family risk factors. Always discuss these matters with your doctor.

More Info?

If you’ve been told you have high cholesterol and would like to know if dietary changes might be helpful, please reach out.  I’ll look at your your diet, blood work and family history and let you know what may be the most prudent approach to minimize risk.

To your good health!

Joy

You can follow me on:

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

References

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

 

Copyright ©2021 BetterByDesign Nutrition Ltd.

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

What is a Low-FODMAP Diet and How Can it Improve Symptoms of IBS?

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

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

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

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

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

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

What is a low-FODMAP Diet?

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

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

Why do FODMAPs trigger symptoms?

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

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

What is the low FODMAP diet?

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

One Diet – in three stages

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

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

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

The Low-FODMAP Specialty Hour Service

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

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

Beyond FODMAP

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

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

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

Gut Microbiome — environment and genetics

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

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

More Info?

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

To your good health!

Joy

You can follow me on:

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

References

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

Copyright ©2021 BetterByDesign Nutrition Ltd.

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

Why Drinking a Smoothie isn’t the Same as Eating the Food Contained in it

People are busy. I “get” that, and morning routines are often the most challenging. Taking time to have breakfast is often seen as “one more thing to do”, so the idea of making a smoothie and “taking it with” may seem like a good idea. But is it? Is drinking a smoothie the same as eating the foods it is made out of? It isn’t.

In an earlier article, I covered the effect of various types of food processing (including mechanical processing such as pureeing fruit in a smoothie) on blood glucose. While 60g of whole apple, 60 g of apple that has been pureed, and 60g of apple that has been juiced have the same amount of amount of carbohydrate and a very similar Glycemic Index (GI) [1], neither the carbohydrate content nor GI tell us anything about how high blood sugar is going to go when eating or drinking them. Glycemic Index only indicates how slowly or quickly foods will increase blood sugar, not how much higher blood sugar will go [2].

A raw apple has a GI of 36  ± 2, and apple juice has a GI of 41  ± 2, so factoring in the error range, raw apple can have a GI of 38, and apple juice a GI of 39. A medium apple (3″ across) has ~25 g of carbs, and even when we make it into unsweetened apple sauce, it still has the same amount of carbs. If we press it into juice, the amount of carbohydrate in it doesn’t change. But we know from a 1977 study published in the Lancet that when fruit is pureed fruit or juiced and then eaten, the glucose response 90 minutes later is significantly higher, than if the fruit were eaten whole [3]. This is because the blender or juicer has done some of the work of digesting the food for us!

Most people think that digestion begins in the stomach, but it doesn’t. It begins in the mouth when we chew food.

When we eat a bowl of berries for example, chewing makes the glucose (sugar) in the berries that we chewed more available to the body — but when we put the same amount of berries in a blender and whir them up, the contents of all the berries are now completely available for the body to act on. We never chew food as fine as a blender makes it, so blending food results in a faster spike in blood sugar than the whole food, eaten intact. This is one reason why drinking a smoothie is not the same as eating the same food it is made from.

The order we eat foods in during a meal also makes a big difference on blood sugar and on the insulin response to eating (or drinking) carbohydrate-containing food. We know from a 2015 study about the effect of food order on the response of glucose and insulin that if the carbohydrate-containing food is eaten last, the glucose curve will be ~74% smaller than if it were eaten first! Likewise, if we eat the carbohydrate-containing food last, the insulin spike will be 49% smaller, than if we eat it first [4]!

Having a smoothie for breakfast instead of a meal made out of the same foods means there is no way of having the carbs last!

Final Thoughts…

It really doesn’t take very long to eat the some veggies (like snap peas or baby carrots) and a dish of yogurt and berries for breakfast and the response on blood sugar and demand on our pancreas for insulin is significant!  This is why I tell people who come to me seeking to loose weight and improve their metabolic health to eat their food, not drink it — because it does matter!

This is also one of the reasons that I felt Diabetes Canada’s “7-day Low Carb Meal Plan” which had a 30g of carbs (and only 9 g of protein) was not the best recommendation for people with diabetes to have for breakfast 3 days per week.

More Info?

If you would like more information about how I can support your nutritional needs, please click on the Services tab above to learn more.

To your good health!

Joy

You can follow me on:

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

References

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

 

Copyright ©2021 BetterByDesign Nutrition Ltd.

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

A Therapeutic Ketogenic Diet – treatment and adjunct treatment

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

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

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

Types of Therapeutic Ketogenic Diets

Ketogenic diets are a subtype of a low carbohydrate  diets.

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

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

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

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

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

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

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

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

The Diet Prescription

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

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

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

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

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

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

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

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

Classic Ketogenic Diet (KD) – 4 : 1

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

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

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

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

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

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

Modified Ketogenic Diet (MKD) – 3 : 1 ratio

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

Modified Atkins Diet (MAD) – 2 : 1 ratio

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

“Chasing Ketones” – betahydroxybutyrate, the therapeutic goal

The therapeutic goal of a 4 : 1 or 3 : 1 therapeutic ketogenic diet is to get the person’s blood ketone level (as measured with an accurate meter!) to measure 3.0 mmol/L betahydroxybutyrate (BHB) as soon as possible — and to have them sustain it at that level (or in some cases, up to 4.0 mmol/L). Since it is the ketones that provide the therapeutic benefit, not adding anything to the diet that isn’t part of the diet prescription is important.

I usually recommend for a person starting out on a therapeutic ketogenic diet get a Abbott Precision Freestyle Neo meter from their pharmacy, as it measures both blood glucose and ketones, is very accurate and reliable (unlike some purchased online and used by people following the popularize “keto diet” or weight loss) and is provided at no cost when purchasing 100 glucose strips (~$1 each).  I then recommend they purchase 30 ketone strips for the same monitor ($3 each) — so the strips will last a month with checking blood glucose 3x / day and checking ketones 1 x / day. 

Blood glucose should not go below 4.0 mmol/ L when measured using the glucose strip in the meter, and blood ketone levels should ideally measure 3.0 mmol/L (and as high as 4.0 mmol/Lin epilepsy and seizure disorder — but not over). If ketones exceed 4.0 mmol/L, the person should contact their doctor — and if they go much higher, should seek medical help immediately.

People diagnosed with glioblastoma ideally begin a 4 : 1 (or 3 : 1) therapeutic ketogenic diet upon discharge from hospital so that they begin chemo and radiation treatment already at a ketone level of 3.0 mmol/L betahydroxybutyrate. For seizure disorder, the neurologists that refer their patients to me are seeking levels as close to 4.0 mmol/L as possible — because that is where the most benefit is seen.  Once seizures have ceased, people may want to begin to try gradually eating a 3 : 1, then a 2 : 1 diet — so long as their seizures remain in remission.  There is a lot of trial and error involved, but for those seeking to extend their life (as in glioblastoma) or improve their quality of life (as in epilepsy or seizure disorder), it may be worth it.

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

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

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

More Info?

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

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

To your good health!

Joy

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References

  1. U.S. Department of Health and Human ServicesFinal MNT regulationsCMS-1169-FCFederal Register1 November 200142 CFR Parts 405, 410, 411, 414, and 415
  2. Nasir H. Bhanpuri, Sarah J. Hallberg, Paul T. Williams et al, Cardiovascular disease risk factor responses to a type 2 diabetes care model including nutritional ketosis induced by sustained carbohydrate restriction at 1 year: an open label, non-randomized, controlled study, Cardiovascular Diabetology, 2018, 17(56)
  3. Meira ID, Romao TT, Pires do Prado HJ, Ketogenic Diet and Epilepsy: What We Know So Far, Front. Neurosci., 29 January 2019, https://doi.org/10.3389/fnins.2019.00005
  4. van der Louw EJTM, Olieman JF, van den Bemt PMLA, et al. Ketogenic diet treatment as adjuvant to standard treatment of glioblastoma multiforme: a feasibility and safety study. Ther Adv Med Oncol. 2019;11, 2019 Jun 21. doi:10.1177/1758835919853958
  5. Schwartz KA, Noel M, Nikolai M, Investigating the Ketogenic Diet As Treatment for Primary Aggressive Brain Cancer: Challenges and Lessons Learned, Front. Nutr., 23 February 2018 | https://doi.org/10.3389/fnut.2018.00011
  6. Klein P, Tyrlikova I, Zuccoli G, Tyrlik A, Maroon JC. Treatment of glioblastoma multiforme with “classic” 4:1 ketogenic diet total meal replacement. Cancer Metab. 2020;8(1):24. Published 2020 Nov 9. doi:10.1186/s40170-020-00230-9
  7. Feinman RD, Pogozelski WK, Astrup A, Bernstein RK, Fine EJ,Westman EC, et al. Dietary Carbohydrate Restriction as the First Approach in Diabetes Management: critical review and evidence base. Nutrition. 2015;31(1):1—13
  8. Peterman MG, The Ketogenic Diet, JAMA. 1928;90(18):1427—1429. doi:10.1001/jama.1928.02690450007003

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