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

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

What are Hemorrhoids?

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

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

Most people are unaware that internal hemorrhoids are there until one becomes irritated and swollen, or worse, prolapses and protrudes from the anus. 

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

Grade 1: Not at all prolapsed.

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

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

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

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

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

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

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

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

Treatment for Hemorrhoids

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

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

Causes of Hemorrhoids

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

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

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

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

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

Squatting versus Sitting Toilet   

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

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

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

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

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

The Length of Time Sitting on a Pedestal Toilet 

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

Think of a single-hole paper punch. 

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

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

Washrooms as Phonebooths

In the early 1950s, most houses only had one washroom or bathroom, so multiple members of the same household had to do what they needed to in a limited time and get out. It was rare to have the luxury of being able to sit on the toilet for an extended period of time, reading the newspaper. Now, 97% of new home construction has more than one washroom or bathroom [4] — most often having two full washrooms, plus an additional 1/2 bathroom containing a toilet and a sink. 

With three toilets per house for an average family size of three in Canada [5] means that each member of the average household has access to a toilet on demand, and can — and does spend inordinate amounts of time sitting on it.

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

Final Thoughts

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

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

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

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

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

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

To your good health. 

Joy 

You can follow me on:

Twitter: https://twitter.com/jyerdile

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

References 

1. UT Southwestern Medical Centre, Treating hemorrhoidal disease: Conservative vs. surgical approaches, April 14, https://utswmed.org/medblog/best-ways-to-treat-hemorrhoids/ 
2. McKeown DG, Goldstein S. Hemorrhoid Banding. [Updated 2024 Feb 14]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2024 Jan-. Available from:https://www.ncbi.nlm.nih.gov/books/NBK558967/
3. Hawkins AT, Davis BR, Bhama AR, Fang SH, Dawes AJ, Feingold DL, et al. The American Society of Colon and Rectal Surgeons Clinical Practice Guidelines for the Management of Hemorrhoids. Dis Colon Rectum. 2024 May 1. 67 (5):614-623. 
4. Eye on Housing, Number of Bathrooms in New Homes in 2021, November 3, 2022, https://eyeonhousing.org/2022/11/number-of-bathrooms-in-new-homes-in-2021/
5. Statistics Canada, Average Family Size in Canada, 2021 https://www.statista.com/statistics/478948/average-family-size-in-canada/
6. Toronto Sun, Two-thirds of Canadians take smart phones into the bathroom: Survey, May 16, 2022, https://torontosun.com/news/national/survey-65-of-canadians-take-their-smart-phones-into-the-bathroom

Copyright ©2025 BetterByDesign Nutrition Ltd.

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

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

What is “Old People Smell”?

“Old people smell” is the characteristic ‘greasy, grassy odor’ most noticeable in nursing homes and long term care homes,  beyond that of urine, feces, and spilled food. In fact, many independent-living older adults also have “old people smell” — although they have become desensitized to it themselves as it had increased gradually since middle age. Many times, their children and grandchildren are very aware of it. 

While body odour can be caused by foods containing a lot of onion, garlic, ginger and certain spices, or may be a side-effect of some medications, “old people smell” originates from 2-noneal, a volatile chemical compound caused by the oxidative degradation of palmitoleic acid and vaccenic acid, two omega-7 unsaturated fatty acids that increase on the skin from age 40 years, onwards [1].

Compared to adults under 40 years of age, 2-noneal increases by up to 6 times beginning at 40 years of age [1], although the reason for this increase is not yet known.

Research has also shown that the more omega-7 unsaturated fatty acids or lipid peroxides that are on the skin’s surface, the more 2-nonenal there is in body odour [1].  

As with all unsaturated fats, omega-7 unsaturated fats are more prone to getting oxidized — literally going rancid, just as unsaturated kitchen fats, such as seed oils.

Keeping omega-7 fats from going rancid, as well as cleaning the skin, bedding, and clothing from these unstable unsaturated fats, will significantly reduce, if not eliminate, “old people smell”. Since 2-noneal is fat-soluble, it is not removed from skin or clothing using ordinary water-soluble soaps and detergents. As a result, targeted products are required.

Targeting “Old People Smell” — lifestyle and dietary changes 

Lifestyle Changes

Lifestyle changes that have been recommended to reduce kareishu (“old people smell”) include wearing clothes made of natural fibers, such as cotton, linen, or silk, so that the fatty acid compounds on skin can more easily transfer to clothing, and then be washed.

Regular washing of bedding and clothing in an enzyme-activated detergent can break up the fatty acids that cause the smell. Washing with body soap that contains polyphenols extracted from Japanese persimmon tannins* has been shown to remove 2-noneal from the skin [2].

*It is important to note that widely available soaps containing persimmon juice, or persimmon leaf, are not the same as those containing the concentrated tannins from Japanese persimmon extract used in the study. 

Dietary Changes

Since it is known that the more palmitoleic acid and vaccenic acid (omega-7 unsaturated fatty acids) on the skin’s surface, the more 2-nonenal there will be in body odour, two dietary approaches are to reduce the intake of foods high in these fatty acids, and to increase the intake of dietary antioxidants that can neutralize 2-nonenal.  

Reducing Intake of Palmitoleic acid and Vaccenic acid

Reducing the intake of foods high in palmitoleic acid and vaccenic acid is one dietary approach to decreasing 2-nonenal body odour.

Palmitoleic acid is found primarily in macadamia nuts and macadamia nut oil, avocado and avocado oil, olive oil, sea buckthorn oil, and anchovies..

Vaccenic acid is a naturally occurring trans fat found in the fat of ruminant animals, including the fat of cows and sheep, and dairy or butter from the milk of these animals [3].

While decreasing the amount of foods high in palmitoleic acid and vaccenic acid may decrease the amount of 2-noneal, it is important to note that since omega-7 fats are non-essential, they don’t need to be available in the diet. The body can make them by converting carbohydrates, other types of fat, and proteins we eat, in a process known as de novo lipogenesis [3].

While seed oils such as soybean and canola are not high in omega-7s, they are easily oxidized, especially when heated, and quite inflammatory. As a result, they are best not used at home, and avoided at restaurants by not ordering food fried in them. Another way to avoid these fats is not to eat highly processed foods, which are made with them.

At the same time, storing real, whole food that is high in palmitoleic acid and vaccenic acid, such as macadamia nuts and oil, avocado and avocado oil, anchovies, and olive oil in the fridge, will significantly slow the process of them going rancid. Many of these oils are sold in dark glass bottles, which slow oxidation, but keeping them in the refrigerator, especially during the summer, is prudent.

Increasing Intake of Dietary Antioxidants 

Eating real foods naturally high in vitamin C, vitamin E, selenium, and polyphenols, which are all natural antioxidants, can neutralize free radicals and lipid peroxidation products, preventing oxidative damage and rancidity.

Catechins are a type of antioxidant flavonoid polyphenol found in plants, including green tea and berries. A study from 2006 found that green tea, which contains the catechins epigallocatechin gallate, epigallocatechin, epicatechin gallate, and gallic acid, showed a strong deodorizing effect against 2-noneal [4]. 

A double-blind placebo-controlled parallel-group study conducted in Japan in 2015 with 80 men and women subjects aged 50–79 years found that daily ingestion of 50 mg/day, 500 mg/day, and 1000 mg/day of mushroom extract made from champignons (white button mushrooms) had increasing benefit in the reduction of both pillow and pyjama odor that was caused by 2-noneal. The study concluded that white button mushroom extract can be a safe and effective target for a dietary supplement to reduce the incidence of kareishu (“old person smell”) [5]. Increasing dietary consumption of different types of mushrooms known to be high in polyphenols is a delicious way to increase intake of these odor-fighting polyphenols. Mushrooms that are very good sources include shitake and oyster mushrooms, and to a lesser degree, porcini and portobello mushrooms. 

A recent study from 2025 determined that the polyphenol N–trans-feruloylputrescine in eggplant can significantly reduce the body’s production of 2-nonenal [6]. While some people avoid eggplant because it is part of the nightshade family, eating a wide variety of eggplant may be another way to limit the production of 2-nonenal.

A 2019 study found that the presence of 2-nonenal on the skin of middle-aged and older adults was reduced by 28% when they consumed a powder made from New Zealand blackcurrants for 7 days [7]. This effect was thought to be the result of the high anthocyanin content of blackcurrants. Other berries, such as elderberry, blackberries, blueberries, and raspberries, also have very high amounts of anthocyanins, as do acai berries and pomegranate [8].

Final Thoughts…

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

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

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

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

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

More Info?

If you would like to learn about how I can help support you in your goal of being the best you can be as you age, please visit the landing page to learn about the different services that I provide, including the Healthy Aging Package.

To your good health!

Joy

You can follow me on:

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

References

1. Haze S, Gozu Y, Nakamura S, Kohno Y, Sawano K, Ohta H, Yamazaki K. 2-Nonenal newly found in human body odor tends to increase with aging. J Invest Dermatol. 2001 Apr;116(4):520-4. doi: 10.1046/j.0022-202x.2001.01287.x. PMID: 11286617.
2. Tatsuguchi, I., Matsuoka, T. et al, Preventive effect against the aged men’s body odor by the soap containing polyphenol, Journal of Japan Association on Odor Environment, 2012, Volume 43, Issue 5, Pages 362-366.
3. Venn-Watson, E., Fatty 15, Omega 7: What To Know About This Fatty Acid, https://fatty15.com/blogs/news/what-is-omega-7
4. Cabrera C, Artacho R, Giménez R. Beneficial effects of green tea–a review. J Am Coll Nutr. 2006 Apr;25(2):79-99. doi: 10.1080/07315724.2006.10719518. PMID: 16582024.
5. Nishihira J, Nishimura M, Tanaka A, Yamaguchi A, Taira T. Effects of 4-week continuous ingestion of champignon extract on halitosis and body and fecal odor. J Tradit Complement Med. 2015 Dec 11;7(1):110-116. doi: 10.1016/j.jtcme.2015.11.002. PMID: 28053896; PMCID: PMC5198824.
6. Kim HM, Kim JH, Jeon JS, Kim CY. Eggplant Phenolamides: 2-Nonenal Scavenging and Skin Protection Against Aging Odor. Molecules. 2025 May 12;30(10):2129. doi: 10.3390/molecules30102129. PMID: 40430302; PMCID: PMC12114487.
7. Willems, M, Todaka M, et al, Effect of New Zealand Blackcurrant Powder on Skin Emission of Volatile Organic Compounds in Middle-Aged and Older Adults, 2019, Current Developments in Nutrition,, Volume 3, Supplement 1,
   2019, https://doi.org/10.1093/cdn/nzz031.P06-092-19
8. Lakshmikanthan M, Muthu S et al, A comprehensive review on anthocyanin-rich foods: Insights into extraction, medicinal potential, and sustainable applications, Journal of Agriculture and Food Research, Volume 17, 2024.
   101245, https://doi.org/10.1016/j.jafr.2024.101245.

Copyright ©2025 BetterByDesign Nutrition Ltd.

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

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

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

Two Main Types of Intermittent Fasting

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

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

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

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

Periods of Fasting of 24 hours or more

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

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

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

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

Time Restricted Eating 

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

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

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

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

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

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

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

Erratic Eating Patterns in Adults

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

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

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

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

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

Supporting Time-Restricted Eating 

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

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

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

Implementing a 16:8 Time Restricted Eating Schedule

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

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

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

Chrononutrition 

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

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

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

When We Eat Matters

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

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

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

Early or Late Time-Restricted Eating – some considerations

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

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

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

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

Final Thoughts…

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

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

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

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

More Info?

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

To your good health!

Joy

You can follow me on:

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

References

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

Copyright ©2025 BetterByDesign Nutrition Ltd.

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

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

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

Functional Dyspepsia and IBS Surge After the Pandemic

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

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

The Role of the Gut-Brain Axis

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

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

Symptoms Vary Between Individuals 

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

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

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

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

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

Role of Behaviour Interventions in Functional Dyspepsia 

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

Some Final Thoughts

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

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

More Info?

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

To your good health!

Joy

You can follow me on:

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

Reference

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

Copyright ©2025 BetterByDesign Nutrition Ltd.

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

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

What is Vitamin B12?

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

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

Vitamin B12 Deficiency Symptoms

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

Findings of the Study

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

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

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

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

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

Findings of the Study

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

Final Thoughts…

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

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

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

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

More Info?

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

To your good health!

Joy

You can follow me on:

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

References

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

Copyright ©2025 BetterByDesign Nutrition Ltd.

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

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

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

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

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

Gastrointestinal (GI) Concerns in EDS

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

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

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

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

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

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

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

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

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

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

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

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

Dietary support may include

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

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

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

How to Encourage Normal Gut Biosis

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

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

Vitamin and Mineral Deficiency Common in Ehlers-Danlos Syndrome

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

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

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

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

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

Specific Dietary Recommendations

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

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

More Info?

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

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

To your good health!

Joy

You can follow me on:

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

References

1. 1. Hakim A. Hypermobile Ehlers-Danlos Syndrome. 2004 Oct 22 [Updated 2024 Feb 22]. In: Adam MP, Feldman J, Mirzaa GM, et al., editors. GeneReviews® [Internet]. Seattle (WA): University of Washington, Seattle; 1993-2025.
   2. Hakim AJ, Tinkle BT, Francomano CA. Ehlers-Danlos syndromes, hypermobility spectrum disorders, and associated co-morbidities: Reports from EDS ECHO. Am J Med Genet C Semin Med Genet. 2021;187:413-5.

   3. Dr. Heidi Collins MD, Nutritional Approaches to Treating GI Concerns in Persons with Ehlers-Danlos Syndrome, The Ehlers-Danlos Syndrome Society, 2020 Virtual Summer Conference

Copyright ©2025 BetterByDesign Nutrition Ltd.

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

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

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

Yearly Limits

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

Reasonable and Customary Fees

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

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

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

Multi-Province Dietetic Registration

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

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

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

British Columbia – reasonable and customary limits

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

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

Alberta – reasonable and customary limits

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

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

Ontario – reasonable and customary limits

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

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

Pricing Based on Inter-Provincial Reasonable and Customary Fee Limits

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

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

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

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

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

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

Final Thoughts…

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

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

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

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

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

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

To your good health,

Joy

You can follow me on:

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

References

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

Copyright ©2024 BetterByDesign Nutrition Ltd.

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

Therapeutic Ketogenic Diets

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

These are very high-fat diets that range from 65-72% fat (2:1), to as high as 90% fat (4:1) [1], and since the amount of protein, fat, and carbohydrate is tightly controlled, ingredients are weighed. Monitoring and tracking blood glucose and blood ketone levels are also required to ensure that the desired Glucose to Ketone Index (GKI) is achieved and maintained.

Three Types of Therapeutic Ketogenic Diets 

A Popularized Keto Diet

There is no one “keto diet”, but rather a range of keto diets. What these diets have in common is that they limit carbohydrate intake to 10% or less of daily calories to promote the body’s production of ketones.

A Well-Formulated Ketogenic Diet

Final Thoughts…

References

Copyright ©2024 BetterByDesign Nutrition Ltd.

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

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

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

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

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

Prediction of Risk of Type 2 Diabetes

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

Diagnosis of Type 2 Diabetes

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

Benefits of the 1-hour Post-Load Glucose Test

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

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

Conclusion

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

Final Thoughts

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

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

To your good health,

Joy

You can follow me on:

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

Reference

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

Copyright ©2024 BetterByDesign Nutrition Ltd.

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

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

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

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

Accredited Facilities for DEXA Bone Density Scans

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

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

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

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

Summary of the Accreditation Standards for Diagnostic Imaging for Bone Densitometry

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

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

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

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

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

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

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

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

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

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

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

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

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

Imaging Center Providing DEXA bone density scans

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

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

Image Quality

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

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

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

Measurement Accuracy – hips

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

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

Measurement Accuracy – spine

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

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

Finding an Accredited Facility

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

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

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

Final Thoughts…

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

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

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

How I Can Help

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

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

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

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

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

DEXA Body Composition Scan

The DEXA Body Composition Scan measures

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

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

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

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

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

DEXA Body Composition Scan Data of Fat and Lean 

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

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

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

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

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

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

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

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

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

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

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

Final Thoughts…

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

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

Take Away Message

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

Getting accurate information using the right diagnostic tool is essential.

How I Can Help

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

To your good health,

Joy

You can follow me on:

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

Reference

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

Copyright ©2024 BetterByDesign Nutrition Ltd.

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

Some people are considering going “plant-based” for perceived health reasons, or for ethical considerations and while these are important, evaluating plant protein quality is a necessary consideration. Evaluating protein quality using the Digestible Indispensable Amino Acid Score [DIAAS] can help.

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

Amino Acids and Bioavailability

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

Bioavailability means the degree to which the essential amino acids in a food can be used by the body to make its own proteins [2] such as muscle.

Essential amino acids, including leucine, which is required for muscle growth and repair, must be eating in protein foods in the diet. This is why they are called “essential” amino acids. The leucine content of a protein is vital because leucine is what triggers mTOR signaling in muscle, which stimulates muscle growth[3]. Dietary Recommendations for older adults emphasize obtaining 2.3 g leucine at each of 3 meals to ensure the building of new muscle protein [4], and 3g leucine per meals [5] to rebuild muscle. Protein recommendations for older adults range from between 20g per meal [3] to 25-30g protein per meal [5] for those recovering muscle mass. For physically active adults, the Academy of Nutrition and Dietetics, Dietitians of Canada, and the American College of Sports Medicine recommend a protein intake of 1.2—2.0 g protein / kg per day to optimize recovery from training, and to promote the growth and maintenance of lean body mass [6].

Plant Protein vs Animal Protein for Building Muscle 

Plant protein generally contains lower levels of the essential amino acid leucine than animal proteins[7] but those seeking to eat a more plant-based diet often turn to legumes (“beans”) for protein. Most legumes are incomplete proteins – meaning they are missing essential amino acids. For example, lentils have only 0.7g of leucine per half cup and chickpeas contain only 0.42g of leucine per half cup.  This means that so for an older adult to get the minimum amount of leucine at a meal (2.3 g leucine) they would have to eat more than 3 cups of lentils, or 5 ½ cups of chickpeas at a meal.

But what about the protein content of foods? Are plant-based proteins equivalent to animal-based proteins?

Is Plant Protein Equivalent to Animal Protein?

A newly randomized, investigator-blinded, crossover study was first performed with a group of young adults, and then in a group of older adults [1]. Researchers compared ounce-equivalents (oz-eq) of animal-based protein (lean pork or whole eggs) with plant-based protein (black beans or sliced almonds) in a mixed whole foods meal. The goal was to see how well the body can use essential amino acids from each type of protein to make body protein. To determine essential amino acid bioavailability, as well as blood sugar and insulin levels, blood samples were taken before they ate the meal, and at 30, 60, 120, 180, 240, and 300 minutes after eating.

Researchers chose the measure of ounce-equivalent (oz-eq) because the Dietary Guidelines for Americans (DGA) uses ounce-equivalent to “identify the amount of (protein group) foods with similar nutritional content” [1, 8]. For example, the DGA indicates that one ounce-equivalent equals one ounce of meat, or one whole egg, or 0.25 cups of beans, or 0.5 ounces of nuts but the authors of the study note that the ‘basis for stating these protein foods are “equivalent” and have “similar nutritional content” is unclear’ [1].

As pointed out by the authors, protein foods differ in energy content and macronutrient contents, including both protein quantity, and protein quality. With regards to protein quantity, one ounce-equivalent of pork loin contains ~7 g of total protein, and one ounce-equivalent of almonds contains only ~3 g of total protein [1]. 

With regards to protein quality, the authors define this ‘as the ability of a dietary protein source to provide adequate amounts and proportions of essential amino acids (EAA) that are digestible and as a result are bioavailable for use in the body for stimulating protein synthesis, and maintaining or growing body tissues’. 

The Bioavailability of Plant Protein – Digestible Indispensable Amino Acid Score

The bioavailability of amino acids in different types of proteins have been determined and is available in the The Digestible Indispensable Amino Acid Score [DIAAS]. In 2013, the DIAAS was recommended by the Food and Drug Administration to replace their previous method called the Protein Digestibility Corrected Amino Acid Score (PDCAAS) [9]. In the DIAAS system, each essential amino acid is recognized as an individual nutrient, rather than lumping all amino acids together and this is very important because the bioavailability of a protein source must to be taken into account when determining if a diet is adequate in protein, and in specific essential amino acids such as leucine.

High quality proteins are those with a DIAAS score ≥100, and are considered excellent quality proteins. DIAAS scores of 75–99 are considered high-quality proteins, and those with scores of <75 are considered to be able to make no quality protein claim [8]. Based on this recent research, plant protein from most grains and legumes (“beans”) are <75 on the DIAAS score, with pea and soy falling between 75 and 100.  Animal protein such as pork consistently score over 100 on the DIAAS [10].

If regulatory guidelines such as the Dietary Guidelines for Americans and Canada’s Food Guide for Health Eating used the protein values generated by the Digestible Indispensable Amino Acid Score, rather than the PDCAAS, consumers would easily be able to see that a 4oz plant-based patty is not equivalent in protein quantity of quality as a 4oz beef patty, and 20g of vegan protein powder is not equivalent to 20g of whey protein powder. Use of the DIAAS in both countries would more accurately reflect protein quality [11] and enable consumers to make better choices.  

Plant Protein versus Animal Proteins – conclusions of the study

The study found that consuming meals with equivalent amounts of animal-based proteins versus plant-based proteins resulted in more essential amino acids in the blood compared with meals containing animal-based proteins in both young and older adults, separately and combined.

Also found was that there was greater essential amino acid bioavailability in lean pork, than in eggs in both young adults and older adults, separately or combined, and there as no difference in essential amino acid bioavailability between black beans and almonds.

The researchers concluded that it is inappropriate to say that different protein sources on an ounce-equivalent basis are “equivalent” .

Final Thoughts…

If you are an active adult seeking to build and repair muscle, then knowing which is better (plant protein vs animal protein for building muscle) is important. If you are an older adult wanting to retain muscle mass, eating high quality protein that contains all the essential amino acids including leucine is essential. While the US Dietary Guidelines states that one ounce of meat or one whole egg or 0.25 cups of beans or 0.5 ounce of nuts are equivalent, this recent study finds that the protein in beans and nuts is not equivalent to that in meat and eggs. 

If you are toying with the idea of becoming more plant-based, be sure that you understand the science of protein bioavailability so you can make a sound decision. 

For those who already eat a vegetarian diet for religious or ethical reasons, ensuring that your meals contain the most bioavailable plant-based proteins at each meal requires knowledge and effort.

More Info

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

To your good health, 

Joy

You can follow me on:

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

References

1. Connolly G, Hudson JL, Bergia RE, Davis EM, Hartman AS, Zhu W, Carroll CC, Campbell WW. Effects of Consuming Ounce-Equivalent Portions of Animal- vs. Plant-Based Protein Foods, as Defined by the Dietary Guidelines for Americans on Essential Amino Acids Bioavailability in Young and Older Adults: Two Cross-Over Randomized Controlled Trials. Nutrients. 2023; 15(13):2870. https://doi.org/10.3390/nu15132870
2. Gaudichon C, Calvez J. Determinants of amino acid bioavailability from ingested protein in relation to gut health. Curr Opin Clin Nutr Metab Care. 2021 Jan;24(1):55-61. doi: 10.1097/MCO.0000000000000708. PMID: 33093304; PMCID: PMC7752214.
3. Layne E Norton, Donald K Layman, Leucine Regulates Translation Initiation of Protein Synthesis in Skeletal Muscle after Exercise12, The Journal of Nutrition,
   Volume 136, Issue 2, 2006, Pg 533S-537S, doi.org/10.1093
   (https://www.sciencedirect.com/science/article/pii/S0022316622080956)
4. Bauer JI, Biolo G, Cederholm T, Cesari M, et al. Evidence-based recommendations for optimal dietary protein intake in older people: a position paper from the PROT-AGE Study Group. J Am Med Dir Assoc. 2013 Aug;14(8):542-59
5. Nutrition Heart Beat, Leucine: perform better and maximize your muscle through diet, https://nutritionheartbeat.com/sports-nutrition/leucine-diet-muscle
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 Jan;49(1):222]. Med Sci Sports Exerc. 2016;48(3):543-568. doi:10.1249/MSS.0000000000000852
7. Berrazaga I, Micard V, Gueugneau M, Walrand S. The Role of the Anabolic Properties of Plant- versus Animal-Based Protein Sources in Supporting Muscle Mass Maintenance: A Critical Review. Nutrients. 2019 Aug 7;11(8):1825. doi: 10.3390/nu11081825. PMID: 31394788; PMCID: PMC6723444.
8. U.S. Department of Agriculture and U.S. Department of Health and Human Services. Dietary Guidelines for Americans, 2020–2025, 9th ed.; U.S. Department of Agriculture and U.S. Department of Health and Human Services: Washington, DC, USA, 2020. Available online: DietaryGuidelines.gov
9. Herreman, L, Nommensen, P, Pennings, B, Laus, MC. Comprehensive overview of the quality of plant- And animal-sourced proteins based on the digestible indispensable amino acid score. Food Sci Nutr. 2020; 8: 5379–5391. https://doi.org/10.1002/fsn3.1809
10. Food and Agriculture Organization of the United Nations. Dietary Protein Quality Evaluation in Human Nutrition: Paper 92. Rome, Italy: Food and Agriculture Organization of the United Nations; 2013.
11. Marinangeli CPF, House JD. Potential impact of the digestible indispensable amino acid score as a measure of protein quality on dietary regulations and health. Nutr Rev. 2017 Aug 1;75(8):658-667. doi: 10.1093/nutrit/nux025. Erratum in: Nutr Rev. 2017 Aug 1;75(8):671. PMID: 28969364; PMCID: PMC5914309.

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.

In the interest of time, many people will throw a cup or more of fruit, some green veggies and maybe some protein powder into a blender to make a smoothie for breakfast without realizing the effect that blending has on their blood sugar, gut microbiome, and even the overall amount of food they eat.

Making a Smoothie 

Cellular versus Acellular Carbohydrate

Cellular carbohydrates come from whole, intact food that remains in the cell wall. These take longer to be digested and absorbed into our bloodstream than carbohydrates that have been ground or pureed. As well, cellular carbohydrates have a lower “carbohydrate density” than processed carbohydrate, where the carbohydrate density are the grams of carbohydrate in a food, minus  the grams of fiber, based on the total gram weight of the food [1].

Acellular carbohydrates are no longer are contained within their cell wall, because they have been pureed (like fruit in a smoothie), or ground, such as flour, from grain. As a result, these foods have a much higher “carbohydrate density” because the fiber is no longer contained in the cell wall, along with the carbohydrate.

A Smoothie as “Pre-Chewed” Food

Most people think digestion begins in the stomach, but it doesn’t. It starts in the mouth when we chew food. As unpalatable as it sounds, smoothies are really “pre-chewed” food, and consuming carbs this way can disrupt our blood sugar, gut microbiota, and even affect the amount of food we consume.

1. A 1977 study published in the journal Lancet demonstrated 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 [2]. This is because the blender or juicer has made the carbohydrate acellular, by doing some of the work that chewing does. In this way, carbohydrate-containing smoothies are essentially “pre-chewed”. For those with pre-diabetes or diabetes, having a morning smoothie instead of eating the same foods intact has a very different effect on blood glucose. Keep in mind, that while 60g of a whole fruit, 60g of pureed fruit, and 60g of fruit that has been juiced have the same amount of carbohydrate and similar Glycemic Index (GI), the GI only indicates how quickly a food or drink will increase blood sugar, not how much higher blood sugar will go.  The two-part article, titled The Perils of Food Processing explains in scientific terms the effect of food processing on blood sugar.
2. Carbohydrates that remain with their cell structure such as whole berries or fruit (i.e. cellular carbohydrates) have their carbohydrate density preserved until the digestive juices in the stomach begin to break down the cell wall of the fruit. Once free from the cell wall, the carbohydrate is absorbed in the large intestine, or colon. Acellular carbohydrates, on the other hand such as fruit-containing smoothies begin to be digested in the small intestine, instead of the colon (where cellular carbohydrates are digested). It is thought that this early fermentation may raise the risk of gut dysbiosis and leaky gut syndrome [1].
3. Finally, the processing of acellular carbohydrates in a blender so we can drink our food, as opposed to eating it makes it too easy to have more than one would if eating the same amount of the intact food. Since acellular carbohydrates are higher in carbohydrate density than the diets made of intact, whole food, it is thought that this may raise the risk for obesity, and leptin resistance [1]. Leptin is the hormone that tells us when we are hungry, and it is thought that this negative feedback loop becomes dysregulated when we consume large amounts of acellular carbohydrates, including pureed fruit, flour-based baked goods, and refined grains.
4.  

Final Thoughts…

It is important to keep in mind that digestion begins in the mouth when we chew food and how we absorb the carbohydrate contained in those foods is very different when we eat whole, intact food, as opposed to pureeing them into a smoothie. Smoothies are really “pre-chewed” food that can disrupt our blood sugar, gut microbiota, and affect the overall amount of food we consume.

Instead of throwing some fruit, veggies and protein powder into a blender, why not eat a half cup of berries, with a cup of cottage cheese or plain Greek yogourt, and grab a handful of snap peas for the low carb veggies, instead? This is a quick, light meal that has all the protein and leucine required for adults to preserve their muscle mass — and there is no blender to clean, afterwards!

How I Can Help

I understand that not everyone who wants to eat healthy loves to cook. I often design Meal Plans for people based on easy-to-obtain foods that require minimum preparation and little to no cooking. Whether you love to cook or can’t be bothered, I can help.

For more information, please look under the Service tab or contact me through the Contact Me form above.

To your good health, 

Joy

You can follow me on:

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

References

1. Spreadbury, I., Comparison with ancestral diets suggests dense acellular carbohydrates promote an inflammatory microbiota and may be the primary dietary cause of leptin resistance and obesity. Diabetes, Metabolic Syndrome and Obesity: Targets and Therapy. 2012:5 175-189.
2. 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

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 inability to retain muscle and strength associated with aging is called sarcopenia, and it is not only a concern for older adults. Loss of muscle mass begins to occur after the age of thirty at the rate of 1% per year [1], and the gradual inability to retain muscle mass and strength generally begins occurring by age fifty [2]. Muscle loss affects 5-13% of adults between the ages of sixty to seventy, and up to half of adults older than eighty years of age have sarcopenia [3].

Not being able to retain muscle mass results in older adults no longer being able to remain active, a reduced quality of life, osteoporosis, increased risk of falls, and a worsening of metabolic health [4].

Most people have never paid attention to the amount and quality of the protein they eat – choosing instead to select protein foods based on taste preference, economics, or ethical or religious reasons. These are all important considerations; however, they are not the only ones. As outlined in a previous article about the role of protein in the diet of older adults, high biological value protein that contain sufficient amounts of the amino acid leucine are necessary for the health of muscle [5], but in this regard not all protein foods are equal.

Amino acids are the building blocks of protein, including muscle, and there are twenty amino acids categorized into two groups: essential and non-essential amino acids. Essential amino acids, including leucine which is required for muscle growth and repair are not produced by the body in sufficient amounts. Leucine must be obtained through diet, which is what makes it an “essential” amino acid.

The leucine content of proteins is critical because leucine is what triggers mTOR signaling in muscle that stimulates muscle growth. For this reason, the proteins people need to contain sufficient leucine – especially older adults who want to retain muscle mass, and mobility.

Plant proteins generally contain lower levels of leucine compared to animal proteins [6]. Grains such as wheat contain less than 7% leucine [7] and even quinoa which is considered a “complete protein” because it has all essential amino acids only contain only 4.5% leucine [8]. People who want to eat a more plant-based diet to retain muscle may turn to legumes (“beans”) for protein, but they are usually incomplete proteins – meaning they are missing essential amino acids, and are generally poor sources of leucine. Even soybeans, which are complete proteins, contain only 8% leucine [9].

Dietary Recommendations for older adults emphasize a minimum of 20g of protein per meal, with more than 2.3 g leucine at each of 3 meals to ensure the building of new muscle protein [10].

Furthermore, to retain muscle and to recover the loss of muscle mass in older adults, the recommended intake of leucine is 3g per at each of 3 meals, along with 25-30g of protein [11].

Protein Sources to Help Retain Muscle 

Animal proteins are highly bioavailable complete proteins and the richest sources of leucine.  Only 1 cup of 1% fat cottage cheese contains 2.9g of leucine per cup – the amount needed for an entire meal! A cup of plain yogurt contains 1.3g of leucine, and a cup of Greek yogurt contains 1.2 g of leucine. Only 3 oz. of ground beef or pork contains 1.8g of leucine and the same amount of chicken breast contains 2.25g – all the leucine that is needed in a meal [11]. These are excellent protein and leucine containing food to help retain muscle. 

Soybeans which are a complete plant-based protein contain only 0.28g leucine per half cup, and firm tofu which is a concentrated form of soy protein has between 0.73g of leucine for three ounces, so to get sufficient leucine from firm tofu would require an older adult to eat ¾ of a pound – well beyond the appetite of many older adults. Incomplete proteins such as lentils have only 0.7g of leucine per half cup, and black beans only 0.61g leucine per half cup – so for an older adult to get the minimum amount of leucine at a meal (2.3 g leucine) from either of these, they would have to eat more than 3 cups at a meal, or 5 ½ cups of chickpeas (0.42g of leucine per half cup). 

For older adults who want to eat a more plant-based diet, ensuring adequate highly bioavailable protein that are also rich sources of leucine is essential to retain muscle – so I recommend “prioritizing protein” along with eating plenty of non-starchy vegetables, like broccoli, green beans, and leafy greens.

[NOTE: This recent article explains the difference in bioavailability between plant-based protein and animal based protein.]

Prioritize Protein to Retain Muscle 

“Prioritizing protein” means to first decide what protein you are going to eat at a meal, and then build the rest of the meal around that.  For older adults, the protein should have between 25-30g of highly bioavailable protein, and 2.3-3g of leucine.

For breakfast, choosing high leucine proteins such as a cup of cottage cheese, or a cup of plain Greek yogurt will provide the needed minimum amount of highly bioavailable protein, as well as sufficient leucine. On the other hand, 2 eggs only contain 12 g of highly bioavailable protein, and 1.2g leucine less than half the recommended amount for older adults.

Choosing 4 oz (113g) of canned tuna for lunch will provide 4g of leucine and 21g of protein, and 3 oz of chicken breast (113g) will provide 2.4g of leucine and 26.5g of protein. To top up the leucine contents, you can serve that with some salad greens sprinkled with an ounce (28g) of pumpkin seeds that contains 0.7g of leucine or an ounce (28g) of sunflower seeds that contains 0.46g of leucine.

In terms of dinner options, while steak is one of the richest sources of leucine – having 3.4 g leucine per 4 oz (113g), cost is a factor. More cost-effective options for those that eat it are 4 oz. (113g) of pork chops which contains 27g of protein, and 2.5 g of leucine. Four ounces of ground beef contains only 16 g of protein but has 2.5 g of leucine, so boosting the protein content of the meal can be as simple as adding some Greek yogurt for dessert.

UPDATE (August 20, 2023) – Be sure to read the new article “Is Plant Protein and Animal Protein Equivalent” based on a recently published study.

Final Thoughts…

The quality of life of older adults and their health depends on remaining active, which requires adequate muscle mass, and preventing sarcopenia requires sufficient protein with all the essential amino acids, as well as enough of the amino acid leucine.

Given that we lose muscle mass at the rate of 1% per year after the age of thirty, which proteins we choose to eat at each of our meals is essential.

If you would like support ensuring you or a loved one eats sufficient high quality protein and leucine as well as other nutrients of concern, please reach out to me through the Contact Me form, above.

To your good health, 

Joy

You can follow me on:

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

References

1. Keller K, Engelhardt M. Strength and muscle mass loss with aging process. Age and strength loss. Muscles, Ligaments and Tendons Journal. 2013;3(4):346-350.
2. Lexell J. Human aging, muscle mass, and fiber type composition. Journals of Gerontology Series A: Biological and Medical Sciences. 1995;50:11–16
3. Cruz-Jentoft AJ, Bahat G, Bauer J, Boirie Y, Bruyère O, Cederholm T, et al. Sarcopenia: revised European consensus on definition and diagnosis. Age Ageing. (2019) 48:16–31. 10.1093/ageing/afy169
4. Hunter GR, Singh H, Carter SJ, Bryan DR, Fisher G. Sarcopenia and Its Implications for Metabolic Health. J Obes. 2019 Mar 6;2019:8031705. doi: 10.1155/2019/8031705. PMID: 30956817; PMCID: PMC6431367.
5. Tessier AJ, Chevalier S. An update on protein, leucine, omega-3 fatty acids, and vitamin d in the prevention and treatment of sarcopenia and functional decline. Nutrients. (2018) 10:1099. 10.3390/nu10081099
6. Berrazaga I, Micard V, Gueugneau M, Walrand S. The Role of the Anabolic Properties of Plant- versus Animal-Based Protein Sources in Supporting Muscle Mass Maintenance: A Critical Review. Nutrients. 2019 Aug 7;11(8):1825. doi: 10.3390/nu11081825. PMID: 31394788; PMCID: PMC6723444.
7. Norton, L.E., Wilson, G.J., Layman, D.K. et al. Leucine content of dietary proteins is a determinant of postprandial skeletal muscle protein synthesis in adult rats. Nutr Metab (Lond) 9, 67 (2012). https://doi.org/10.1186/1743-7075-9-67
8. El-Sohaimy, Sobhy & Mehany, Taha. (2015). Physicochemical and functional properties of quinoa protein isolate. Annals of Agricultural Sciences. 60. 10.1016/j.aoas.2015.10.007.
9. Amino Acid Analysis of Soybean, https://www.drugfuture.com/chemdata/Soybean.html
10. Bauer JI, Biolo G, Cederholm T, Cesari M, et al. Evidence-based recommendations for optimal dietary protein intake in older people: a position paper from the PROT-AGE Study Group. J Am Med Dir Assoc. 2013 Aug;14(8):542-59
11. Nutrition Heart Beat, Leucine: perform better and maximize your muscle through diet, https://nutritionheartbeat.com/sports-nutrition/leucine-diet-muscle
12. Rondanelli M, Nichetti M, Peroni G, Faliva MA, Naso M, Gasparri C, Perna S, Oberto L, Di Paolo E, Riva A, Petrangolini G, Guerreschi G, Tartara A. Where to Find Leucine in Food and How to Feed Elderly With Sarcopenia in Order to Counteract Loss of Muscle Mass: Practical Advice. Front Nutr. 2021 Jan 26;7:622391. doi: 10.3389/fnut.2020.622391. PMID: 33585538; PMCID: PMC7874106.

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.

People’s interest in following a ketogenic diet for improved mental health has significantly increased over the past year. Emerging evidence suggests that this diet may be helpful as an adjunct treatment, along with medication, for improving mental health symptoms of anxiety, depression, and some types of bipolar disorder. However, not everyone is prepared for the demands of adopting a diet that contains twice (2:1) or three times (3:1) the amount of fat compared to protein and carbohydrates combined.

A therapeutic ketogenic diet is used for ketogenic diet therapy (also known as ketogenic metabolic therapy), and it may be prescribed on its own by a Physician or implemented by a Dietitian under a doctor’s oversight as an adjunct treatment for some mental health disorders. 

Some people assume that a 2:1 therapeutic ketogenic diet is the same as the popularized “keto” diet used for weight loss and improved metabolic health. While there are similarities, the 2:1 diet is therapeutic in its design, and the popularized “keto diet” is used therapeutically to improve weight and metabolic health. You can read more here.

In a 2:1 therapeutic ketogenic diet, the amount of protein, carbs, and fat is regulated at each meal so that ketone levels are consistent through the day. In the popularized “keto diet,” the goal is to be in ketosis with little to no regard to the level of ketosis or the relationship between glucose levels and ketone levels.

Different Types of Ketogenic Diets

As outlined in a previous article titled “Use of a Therapeutic Ketogenic Diet in Mental Health,” there are three basic types of therapeutic ketogenic diets: a Classic Ketogenic Diet that uses a 4:1 ratio of fat to protein plus carbs, a Modified Ketogenic Diet that uses a 3:1 ratio, and a Modified Atkins Diet that uses a 3:1 ratio.

There are anecdotal reports of individuals doing very well following a Modified Atkins Diet (2:1) under the supervision of their doctors, and very recently (June 3, 2023), a pre-print pilot study came out where this approach was successfully trialed in people with bipolar disorder [2].

This alternative approach is less time-consuming in terms of the amount of calculations and work needed to design it. It enables people to get into ketosis under medical oversight, then, in consultation with their doctors, decide if the improvements are sufficient to maintain their diet as is, or whether it may be worth seeing if a gradual increase in fat and decrease in protein may work better.

Working with Your Doctor to Support Mental Health

As mentioned in the previous article, Dr. Palmer recommends that Psychiatrists first determine if trialing a ketogenic diet is appropriate for a specific patient. For people considering using a ketogenic diet as an adjunct treatment for mental health, the first place to start is by having this discussion with your doctor, especially if taking any medications for depression, anxiety disorder, or bipolar disorder, or for metabolic conditions such as high blood pressure or to control blood sugar.

Dr. Palmer also recommends that doctors have their patients remain on their medication while trialing the diet for a period of three months, during which they are evaluated to see if there has been any significant change in symptoms [1]. If the doctor finds that the diet is helping, they may begin to gradually deprescribe some medications. As I’ve said in many other articles, changing dosages of medication is not something people should ever do on their own. 

There is an important point that Dr. Palmer makes that should not be overlooked. With the gradual decrease in medications, people must realize that they are more reliant on the ketogenic diet to keep symptoms under control. Since the diet is therapeutic, taking “cheat days” may result in it taking several days to get back into ketosis — during which symptoms can dramatically reappear [1]. I do not recommend “cheat days” when following a ketogenic diet for therapeutic purposes.  While a 2:1 diet is much easier to maintain long term than a 3:1, consistently maintaining the correct ratio of fat to protein and carbohydrate is essential.

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

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

2. Read the book “Ketogenic Therapies” by Dr. Eric Kossoff [3]

Dr. Eric Kossoff’s book, Ketogenic Diet Therapies for Epilepsy and Other Conditions is one that have referred to often over the last 5 years of designing therapeutic ketogenic diets for other conditions.

Steps to Getting Started

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

If you have already discussed this and your doctor is willing to oversee your health and medications while you adopt the diet, I can provide you with a Request for Medical Supervision Form. 

More Info

If you would like more information about having a therapeutic ketogenic diet designed for you, please visit the Services tab and scroll down to Therapeutic Diets. 

To your good health!

Joy

You can follow me on:

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

References

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

Copyright ©2023 BetterByDesign Nutrition Ltd.

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

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

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

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

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

One Difference Between the US and Canadian Ketchup 

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

High Intakes of Fructose and Non-Alcoholic Fatty Liver Disease

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

What is fructose?

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

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

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

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

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

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

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

Final Thoughts…

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

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

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

To your good health!

Joy

You can follow me on:

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

References

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

Copyright ©2023 BetterByDesign Nutrition Ltd.

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

Most people have heard of the high-fat, low-carb “keto” diet that is often followed for weight loss and for improving blood sugar, but a therapeutic ketogenic diet is very different. A therapeutic ketogenic diet is used for ketogenic diet therapy (also known as ketogenic metabolic therapy). It may be prescribed on its own by a Physician or implemented by a Dietitian under a doctor’s oversight as an adjunct treatment for some mental health disorders.

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

Therapeutic Ketogenic Diet for Mental Health 

A research article published on July 6, 2022, in Frontiers of Psychiatry was my first exposure to the use of a therapeutic ketogenic diet in the treatment of mental health disorders. This was of great interest to me because my graduate research was in the area of mental health nutrition, and for the last 5 year,s I have supported people following therapeutic ketogenic diets for seizure disorder, and as adjunct treatment in specific forms of cancer. The use of a therapeutic ketogenic diet in mental health brings these two formerly separate areas of my experience together. 

In this pilot study, thirty-one adults in a psychiatric hospital in Toulouse, France, who had treatment-resistant depression, bipolar disorder, and schizoaffective disorder were placed on a therapeutic ketogenic diet that restricted their carbohydrate intake to 20g per day. Of the 28 patients who followed the diet for longer than two weeks, symptoms of depression and psychosis improved in all 28 patients, with improvements becoming noticeable within three weeks or less. Most impressive was that 43% of patients achieved clinical remission of symptoms, and 64% were discharged from the hospital on less psychiatric medication [1].  There have also been other pilot studies [2,3] using a therapeutic ketogenic diet in both bipolar disease and schizophrenia.

“Brain Energy” Book – role for therapeutic ketogenic diet 

The release of the best-selling book Brain Energy in mid-November 2022, written by Harvard psychiatrist Dr. Chris Palmer, one of the pioneers in the use of a therapeutic ketogenic diet in treating psychiatric disorders [4], brought the use of this type of diet in mental health to public awareness. As a result of the book, I have had many more individuals contact me about designing such a diet to see if it would improve their mental health.  

But what is a therapeutic ketogenic diet?

Types of Therapeutic Ketogenic Diets

There are several types of therapeutic ketogenic diets, each designed according to a specific “ketogenic ratio” which specifies the amount of fat in the diet compared to the total amount of protein plus carbohydrate.

Classic Ketogenic Diet (KD)

The Classic Ketogenic Diet uses a 4:1 ratio, which means it is made up of 4 grams of fat for every 1 gram of protein plus carbohydrate. That is, for every 5 grams of food eaten, there are 4 grams of fat and 1 gram of protein and/or carbohydrate. A 4:1 ketogenic diet contains 80% fat (4÷5=80%) and 20% protein plus carbohydrate (1÷5=20%), and protein may be set at 15% of calories with a maximum of 5% of calories coming from carbohydrate, or protein may be set lower at 10%, and carbohydrate as high as 10%. This type of diet may be used when the need to achieve and maintain high levels of ketones is necessary.

It is important to note that the ketogenic ratio compares the amount of fat, protein, and carbohydrates in grams, which is a measure of weight. The diet is calculated in grams, since food is measured by weight, in grams.

As you will see below, the amount of fat, protein, and carbohydrate in the diet can also be calculated as a percentage of calories.

Modified Ketogenic Diet (MKD)

The Modified Ketogenic Diet uses a 3:1 ratio, which means it is made up of 3 grams of fat for every 1 gram of protein plus carbohydrate. For every 4 grams of food eaten, there are 3 grams of fat and 1 gram of protein and carbohydrate. A 3:1 ketogenic diet contains 75% fat (3÷4=75%) and 25% protein plus carbohydrate (1÷4=25%). Some psychiatrists will start their patients on a 3:1 therapeutic ketogenic diet and once their patient is producing significant levels of ketones and is stable with respect to symptoms, may gradually have them transition over to a Modified Atkins Diet (see below) while monitoring their symptoms.

Modified Atkins Diet (MAD)

The Modified Atkins Diet uses a 2:1 ratio and is often used when people are taking a break from a 4:1 or 3:1 therapeutic ketogenic diet, and is also used as a therapeutic diet in mental health, as it is the easiest for people to sustain long-term. As mentioned above, some psychiatrists will start their patients on a 3:1 ketogenic diet to generate higher levels of ketones and then gradually have their clients transition over to a Modified Atkins Diet as it is more sustainable long term. This diet is also very helpful for those who do not tolerate the very high fat content of a 4:1 or 3:1 diet. In a Modified Atkins Diet, for every 3 grams of food eaten, there are 2 grams of fat and 1 gram of protein and carbohydrate. A 2:1 ketogenic diet contains 67% fat (2÷3=67%) and 33% protein plus carbohydrate (1÷3=25%).

Calculating Ratios Based on a Percentage of Calories

The first step for me, as a Dietitian in designing a therapeutic ketogenic diet is to determine the amount of calories (kcals) a person requires. This is routine work in designing any Meal Plan.

The next step is unique to the design of therapeutic ketogenic diets, and that is calculating the specific percentage of calories that needs to come from fat, protein, and carbohydrate.

It is important to note that calculating the ratio provided from fat, protein, and carbohydrate based on calories arrives at a different percentage than when calculating the ratio based on grams of food. This is because fat provides more calories per gram (9 kcal/g) than protein and carbohydrates (4 kcal/g).

To get 500 calories as protein, one would need to eat 125g of protein (500÷4=125), but to get the same 500 calories as fat, one would only need to eat 55.5 g of fat (500÷=55.5), because fat is much more calorically dense. Therapeutic ketogenic diets have much smaller meals because fat provides the same number of calories, for much less mass (weight, in grams).

Classic Ketogenic Diet – 90% fat as a percentage of calories

On a 4:1 ketogenic diet, 90% of the calories in the diet come from fat when measuring by calories (80% fat if you are measuring by weight, in grams). This can be confusing, but remember that a 4:1 ketogenic ratio represents 4 grams of fat for every 1 gram of carbohydrate plus protein.

• • Four grams of fat (which provides 9 calories per gram) provides a total of 36 calories (4 x 9 = 36).
  • One gram of protein or carbohydrate (which provides 4 calories per gram) provides a total of 4 calories (1 x 4 = 4). 

That is, the ratio of calories from fat to calories from protein plus carbohydrate is 36:4. This means that for every 40 calories consumed, 36 calories come from fat and 4 calories come from protein and/or carbohydrate. Thus, 90% of the calories come from fat (36÷40=90%), and 10% comes from protein and carbohydrate (4÷40=10%) [5]. 

Modified Ketogenic Diet (MKD) – 87% fat as a percentage of calories

On a 3:1 ketogenic diet, about 87% of the calories come from fat, and 13% comes from protein plus carbohydrate. 

• Three grams of fat (which provides 9 calories per gram) provides a total of 36 calories (3 x 9 = 27).
  • One gram of protein or carbohydrate (which provides 4 calories per gram) provides a total of 4 calories (1 x 4 = 4) [5]. 

On a Modified Ketogenic diet, the ratio of calories from fat to calories from protein plus carbohydrate is 27:4. This means that for every 31 calories consumed, 27 calories come from fat and 4 calories come from protein and/or carbohydrate. Thus, 90% of the calories come from fat (27÷31=87%), and 13% comes from protein and carbohydrate (4÷31=13%) [8]. 

A Dietitian’s Role in Therapeutic Ketogenic Diets

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

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

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

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

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

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

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

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

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

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

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

Dr. Eric Kossoff’s book, Ketogenic Diet Therapies for Epilepsy and Other Conditions is one that have referred to often over the last 5 years of designing therapeutic ketogenic diets in different applications. 

Steps to Getting Started 

If you are thinking of adopting a ketogenic diet for improved mental health, then the first step is to reach out to your doctor.  To assist you in having this type of discussion, please feel free to download this letter. 

If you have already discussed this and your doctor is willing to oversee your health and medications while you adopt the diet, I can provide you with a Request for Medical Supervision Form. 

[UPDATE (June 21, 2023): There is emerging evidence from a June 3, 2023, pre-publication paper that the easier-to-follow 2:1 ketogenic diet may work well as an adjunct treatment in mental health disorders, such as bipolar disorder. You can read more about that in this more recent article.

More Info

If you would like more information about having a therapeutic ketogenic diet designed for you, please send me a note using the Contact Me form at the top of this page.

To your good health!

Joy

You can follow me on:

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

References

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

Copyright ©2023 BetterByDesign Nutrition Ltd.

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

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. 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.

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

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

Androgenic Alopecia

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

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

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

Three Main Types of Hair Loss

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

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

Androgenic 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 nutritional supplements can be helpful in helping restore hair loss.

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

Dihydrotestosterone (DHT) as a Main Cause of Hair Loss

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

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

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

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

Pumpkin Seed Oil as a nutritional supplement in hair loss

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 nutritional supplement showed significantly superior hair growth, with a mean hair count increase of 40% in the pumpkin seed oil-treated men compared to 10% in the placebo-treated men. There were no differences in adverse effects between the two groups.

Nutritional Supplements in Hair Loss – Saw Palmetto

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 nutritional supplement extract (Serenoa repens) daily for 24 months, or 1 mg Finasteride daily for the same time period.  While Finasteride was significantly more effective at slowing hair loss, at 24-months the Saw Palmetto extract did stabilize hair loss. [12].

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

The Role of Specific Micronutrients in Restoring Hair Loss

Nutritional Supplements for Hair Loss – Vitamin D

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

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

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.

Nutritional Supplements for Hair Loss – Zinc

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

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

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.

Nutritional Supplements for Hair Loss – Vitamin B12

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

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

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. 

Nutritional Supplements – the role of antioxidants in restoring hair loss

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

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

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

Nutritional Supplements – more is not always better

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

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

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.

Other Nutritional Supplements – 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/

References

1. 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 Loss: A Systematic Review. JAMA 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.

Hypothyroid 101 provides an overview of what the thyroid does, the main thyroid hormones, the main causes of hypothyroidism, how hypothyroidism is diagnosed, as well as options for having thyroid 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 (hypothyroid) this 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.

Hypothyroid – how it is diagnosed

In Canada and many places in the US, the standard screening test for abnormal thyroid function, including hypothyroid, 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.

Hypothyroid – main causes 

In the developed world, the most common form of primary hypothyroid in is Hashimoto’s disease. In developing countries, it is mostly caused from a lack of iodine in the diet. Other causes of hypothyroid 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 hypothyroid 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 as hypothyroid 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 pain, fatigue, 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. 

Hypothyroid – 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].

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

• • • 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 

• • TSH
  • Free Thyroxine (FT4)
  • Free Triiodothyronine (FT3)
  • Reverse T3
  • Thyroperoxidase Antibody (TPO-ab)
  • Anti-Thyroglobulin (TG-ab)

3. Patient-Pay 

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.