Year: 2025

 

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

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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

 

 

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