Canada Told to Prepare for Possible Pandemic Amidst 7th Case in BC

Introduction

Note: This article is a follow-up to previous reports regarding the presence of COVID-19 in Vancouver and federal recommendations for outbreak preparedness.

On February 24, 2020, Provincial Health Officer Dr. Bonnie Henry identified a seventh case of COVID-19 in BC. This case involves a man in his 40s who was a close contact of the province’s sixth case—a woman who recently returned from Iran [1,2]. The Fraser Health Authority has been working to identify contacts in the region, including issuing warnings to school districts in Burnaby, New Westminster, and the Tri-Cities [4].

Closing the Window of Containment

In a dramatic shift from earlier “low risk” assessments, Chief Medical Officer Dr. Theresa Tam acknowledged that Canada may no longer be able to contain the virus. She stated that “governments, businesses and individuals should prepare for an outbreak or pandemic” [7]. Dr. Tam emphasized that the window for stopping global spread is closing, necessitating community and family-level preparedness [8].

Practical Advice and Social Distancing

Given the thriving international communities in Greater Vancouver, there is concern regarding the rapid growth of outbreaks in Iran and South Korea. Experts suggest it is unlikely that current cases represent the only individuals entering Canada from regions with high transmission rates [8].

Practical steps for individuals include:

  • Avoiding touching the eyes, nose, or mouth after contacting public surfaces.
  • Washing hands with soap and water for at least 20 seconds.
  • Practicing social distancing by avoiding crowded public places like food courts and waiting rooms.

The Role of Distance Consultations

With the virus capable of spreading within approximately 2 meters (6.5 feet), limiting group exposure is prudent. This is where Distance Consultations provide a vital alternative. With over a decade of experience providing virtual nutrition support, I offer a way to continue clinical care without the risks associated with in-person waiting rooms.

More Info?

Learn about me and the Comprehensive Dietary Package that 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. The Globe and Mail. B.C. identifies seventh case of coronavirus. Feb 24, 2020. 
  2. Montreal Gazette. Passenger from Iran on flight from Montreal to Vancouver tests positive. Feb 23, 2020. 
  3. CBC News. B.C.’s 6th presumptive COVID-19 case flew from Montreal to Vancouver. Feb 23, 2020. 
  4. Global News. Passenger on Air Canada flight to Vancouver is not a new case. Feb 23, 2020. 
  5. Ottawa Citizen. Canadians being told to prepare for a possible novel coronavirus pandemic. Feb 24, 2020. [Link]
 
Nutrition is BetterByDesign
 

Privacy Policy | Terms of Use

 

© 2025 BetterByDesign Nutrition Ltd.

LEGAL NOTICE: The contents of this blog, including text, images, and cited statistics, are for informational purposes only. The content is not intended to be a substitute for professional medical advice, diagnosis, or treatment. Always seek the advice of your physician or other qualified health provider with any questions you may have regarding a medical condition. Never disregard professional medical advice or delay in seeking it because of something you have read in this content.

Sixth Case of COVID-19 Coronavirus in Vancouver called a Sentinel Event

Introduction

Note: This article is a follow-up to previous reports regarding COVID-19 in the Vancouver area. This article includes updates posted on February 23rd, 2020.

Provincial Health Officer Bonnie Henry announced on February 20th that a woman in her 30s returning from Iran is British Columbia’s sixth case of the novel COVID-19 coronavirus. This case is particularly unusual as the travel was not to China or Singapore. Dr. Henry described this as a “sentinel event,” a marker that viral activity may be broader than initially expected [1].

Tracking Exposure in the Fraser Health Region

The woman is currently in self-isolation within the Fraser Health region. Health officials are investigating her travel history to determine if other passengers on her flight home require testing. This follows the identification of a fifth case—a woman returning from Shanghai through YVR—where officials worked to contact everyone seated within three rows of the infected passenger [4].

The incubation period for the illness is believed to be up to 14 days. Because individuals can remain asymptomatic while contagious, it is unknown how many people in the Greater Vancouver area may have been exposed through close contact with travelers arriving before quarantines were implemented [5,6].

Relative Risk and Public Concern

While medical officials describe the risk to the public as “low,” concern remains high in local communities. Proximity of less than 2 meters (6.5 feet) in crowded places like food courts, airports, or checkout lines may pose a risk if an individual is contagious. Growing outbreaks in Iran and South Korea are of particular concern due to strong local community ties and unrestricted travel.

The Role of Distance Consultations

For over a decade, I have provided nutrition services via Distance Consultation. As the COVID-19 situation unfolds, many local clients are opting for remote appointments to avoid public waiting rooms and unnecessary travel. This allows for the continuation of clinical care with no risk of exposure.

Update: February 23, 2020

Media reports confirm that the sixth case flew from Montreal to Vancouver on Valentine’s Day (February 14th). The BC Provincial Health Authority is contacting passengers seated within three rows of the individual [8,9]. Additionally, Fraser Health has notified school districts in Burnaby, New Westminster, and the Tri-Cities that contacts of the individual may have attended schools but were asymptomatic and remain well [10].

More Info?

Learn about me and the Comprehensive Dietary Package that 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. The Globe and Mail. B.C. hit with sixth case of coronavirus. Feb 20, 2020.
  2. Global News. B.C. identifies 5th presumptive case of COVID-19. Feb 14, 2020. 
  3. Montreal Gazette. Passenger from Iran on flight from Montreal to Vancouver tests positive. Feb 23, 2020. 
  4. CBC News. B.C.’s 6th presumptive COVID-19 case flew from Montreal to Vancouver on Feb. 14. Feb 23, 2020. 
  5. Global News. Passenger on Air Canada flight to Vancouver is not a new case. Feb 23, 2020.
 
Nutrition is BetterByDesign
 

Privacy Policy | Terms of Use

 

© 2025 BetterByDesign Nutrition Ltd.

LEGAL NOTICE: The contents of this blog, including text, images, and cited statistics, are for informational purposes only. The content is not intended to be a substitute for professional medical advice, diagnosis, or treatment. Always seek the advice of your physician or other qualified health provider with any questions you may have regarding a medical condition. Never disregard professional medical advice or delay in seeking it because of something you have read in this content.

Five Pounds or Fifty Pounds of Fat – in very real terms

Introduction

Whether one loses 5 pounds of fat or 50 pounds of fat, I think it is very helpful to visualize just how much that is. Yes, five pounds of fat is much larger than most people realize! This past week, I purchased a life-sized model of 5 pounds of fat from a nutrition supplier. When I received it, I was quite surprised by how much room it took up and just how heavy it felt.

Fat takes up a fair amount of room around one’s waist, or worse, inside one’s abdomen or organs. If someone has 20 pounds of fat to lose, that is four of those fat models distributed over their body: legs, belly, arms, neck, back, and face—and perhaps some in their liver.

5 pounds of fat being held in my hand – © BBDNutrition

Holding 5 pounds of fat like an infant

5 pounds of fat being carried as one would carry an infant

My Personal Journey with 55 Pounds of Fat

I had 55 pounds of excess fat before beginning my journey. Comparing these two full-length photos, it is easy to see how I had the equivalent of one of those fat models over the length of each leg, one distributed between each arm, one distributed over my neck and face, and two spread out around my waist and hips.

Joy's 11-year difference

Progress comparison: May 2008 vs June 2019.

The fat in my abdomen was wreaking metabolic havoc on my body; I had very high blood pressure and had lived with type 2 diabetes for eight years. I chose to follow a low carbohydrate diet to achieve these results, but there is no one-size-fits-all diet that is right for everyone.

More Info?

Learn about me and the Comprehensive Dietary Package that I offer.

To your good health!

Joy

You can follow me on:

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

 
Nutrition is BetterByDesign
 

Privacy Policy | Terms of Use

 

© 2025 BetterByDesign Nutrition Ltd.

LEGAL NOTICE: The contents of this blog, including text, images, and cited statistics, are for informational purposes only. The content is not intended to be a substitute for professional medical advice, diagnosis, or treatment. Always seek the advice of your physician or other qualified health provider with any questions you may have regarding a medical condition. Never disregard professional medical advice or delay in seeking it because of something you have read in this content.

New ADA Standards of Medical Care Includes Low Carbohydrate Diet

Introduction

The American Diabetes Association (ADA) has released its Standards of Medical Care in Diabetes (2020) [1]. This update reinforces the April 2019 Consensus Report, emphasizing that there is no “one-size-fits-all” eating pattern for diabetes management. Instead, the ADA underscores that Medical Nutrition Therapy (MNT) must be individualized to the patient.

The ADA explicitly recommends that all people diagnosed with diabetes be referred to a Registered Dietitian (RD/RDN). Research indicates that MNT delivered by an RD is associated with a decrease in HbA1C of between 0.3% and 2.0% for those with type 2 diabetes [3].

Macronutrients and Eating Patterns

The 2020 Standards reiterate that there is no ideal percentage of calories from carbohydrates, protein, and fat. Macronutrient distribution should be based on an individualized assessment of metabolic goals and personal preferences. Notably, the ADA continues to recognize a low-carbohydrate eating pattern as a healthful and helpful option for controlling blood glucose [6-8].

“The Mediterranean-style, low-carbohydrate, and vegetarian or plant-based eating patterns are all examples of healthful eating patterns that have shown positive results in research.” [1]

Definitions from the Consensus Report: A low carbohydrate pattern is 26–45% of total calories from carbs. A very low carbohydrate pattern (ketogenic) is defined as 20–50g of non-fiber carbs per day.

Safety and Clinical Guidance

While low-carbohydrate plans show potential to improve glycemia and lipids for up to one year [13-17], the ADA advises regular reassessment of sustainability. Currently, a low-carbohydrate pattern is not recommended for women who are pregnant or lactating, individuals with disordered eating, or those with renal disease. Additionally, caution is advised for patients taking SGLT2 inhibitors due to the potential risk of ketoacidosis [11-12].

Final Thoughts

The 2020 Standards confirm that a well-designed low-carbohydrate diet is considered both healthful and helpful for the second year in a row. As an RD, I am encouraged to see the ADA supporting these evidence-based options, and I hope to see similar updates from Diabetes Canada in the near future.

More Info?

If you would like more information about individualized Meal Plans and MNT, you can learn about me and the Comprehensive Dietary Package that 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. American Diabetes Association. Facilitating Behavior Change and Well-being to Improve Health Outcomes: Standards of Medical Care in Diabetes—2020. Diabetes Care 2020;43(Suppl. 1):S48–S65. https://doi.org/10.2337/dc20-S005
  2. Evert AB, Dennison M, Gardner CD, et al. Nutrition therapy for adults with diabetes or prediabetes: a consensus report. Diabetes Care 2019;42(5):731–754. https://doi.org/10.2337/dci19-0014
  3. Franz MJ, MacLeod J, Evert A, et al. Academy of Nutrition and Dietetics nutrition practice guideline for type 1 and type 2 diabetes in adults. J Acad Nutr Diet 2017;117(10):1659–1679. https://doi.org/10.1016/j.jand.2017.03.022
  4. Esposito K, Maiorino MI, Ciotola M, et al. Effects of a Mediterranean-style diet on the need for antihyperglycemic drug therapy. Ann Intern Med 2009;151(5):306–314. https://doi.org/10.7326/0003-4819-151-5-200909010-00004
  5. Boucher JL. Mediterranean eating pattern. Diabetes Spectr 2017;30(2):72–76. https://doi.org/10.2337/ds16-0063
  6. Sainsbury E, Kizirian NV, Partridge SR, et al. Effect of dietary carbohydrate restriction on glycemic control in adults with diabetes. Diabetes Res Clin Pract 2018;139:239–252. https://doi.org/10.1016/j.diabres.2018.02.026
  7. van Zuuren EJ, Fedorowicz Z, Kuijpers T, Pijl H. Effects of low-carbohydrate- compared with low-fat-diet interventions on metabolic control. Am J Clin Nutr 2018;108(2):300–331. https://doi.org/10.1093/ajcn/nqy096
  8. Snorgaard O, Poulsen GM, Andersen HK, Astrup A. Systematic review and meta-analysis of dietary carbohydrate restriction in patients with type 2 diabetes. BMJ Open Diabetes Res Care 2017;5(1):e000354. https://doi.org/10.1136/bmjdrc-2016-000354
  9. Rinaldi S, Campbell EE, Fournier J, et al. A comprehensive review of the literature supporting CDA recommendations for plant-based diets. Can J Diabetes 2016;40(5):461–467. https://doi.org/10.1016/j.jcjd.2016.02.011
  10. Pawlak R. Vegetarian diets in the prevention and management of diabetes and its complications. Diabetes Spectr 2017;30(2):82–88. https://doi.org/10.2337/ds16-0057
  11. U.S. Food and Drug Administration. FDA Drug Safety Communication: SGLT2 inhibitors warnings. 
  12. Blau JE, Tella SH, Taylor SI, Rother KI. Ketoacidosis associated with SGLT2 inhibitor treatment. Diabetes Metab Res Rev 2017;33(5):e2924. https://doi.org/10.1002/dmrr.2924
  13. Saslow LR, Daubenmier JJ, Moskowitz JT, et al. Twelve-month outcomes of a randomized trial of a moderate-carbohydrate versus very low-carbohydrate diet. Nutr Diabetes 2017;7(12):304. https://doi.org/10.1038/s41387-017-0006-9
  14. Hallberg SJ, McKenzie AL, Williams PT, et al. Effectiveness and safety of a novel care model for the management of type 2 diabetes at 1 year. Diabetes Ther 2018;9(2):583–612. https://doi.org/10.1007/s13300-018-0373-9
  15. van Wyk HJ, Davis RE, Davies JS. A critical review of low-carbohydrate diets in people with type 2 diabetes. Diabet Med 2016;33(2):148–157. https://doi.org/10.1111/dme.12964
  16. Meng Y, Bai H, Wang S, et al. Efficacy of low carbohydrate diet for type 2 diabetes mellitus management. Diabetes Res Clin Pract 2017;131:124–131. https://doi.org/10.1016/j.diabres.2017.07.006
  17. Tay J, Luscombe-Marsh ND, Thompson CH, et al. Comparison of low- and high-carbohydrate diets for type 2 diabetes management. Am J Clin Nutr 2015;102(4):780–790. https://doi.org/10.3945/ajcn.115.112581
  18. Thomas D, Elliott EJ. Low glycaemic index, or low glycaemic load, diets for diabetes mellitus. Cochrane Database Syst Rev 2009;(1):CD006296. https://doi.org/10.1002/14651858.CD006296.pub2
 
Nutrition is BetterByDesign
 

Privacy Policy | Terms of Use

 

© 2025 BetterByDesign Nutrition Ltd.

LEGAL NOTICE: The contents of this blog, including text and cited statistics, are for informational purposes only. The content is not intended to be a substitute for professional medical advice, diagnosis, or treatment. Always consult your physician before implementing changes to your medical regimen.

Is Your New Year’s Resolution to Lose Weight or Improve Your Health?

Introduction

Many people say they plan to lose weight or lower their blood sugar, pressure, or cholesterol in the New Year, but the difference between a “wish” and a “resolution” is having a plan in place to actually do it.

Wish or Resolution?

A “wish” is really just a hope that something will occur, whereas a “resolution” is a firm decision associated with specific qualities. A resolution is a SMART goal; one which is Specific, Measurable, Achievable, Realistic, and Timely.

[Image of SMART goals infographic]

A goal to “lose weight” isn’t specific—it’s just a wish. A resolution to stop eating foods with added sugar or to eat whole, real foods low in refined carbohydrates is specific. A resolution is also measurable; deciding to lose one pound a week for six months is a clear plan for success.

Is the goal achievable and realistic? For example, if you want to incorporate intermittent fasting but still eat dinner with your family, choosing an 18:6 eating window is entirely realistic. Finally, a goal must be timely (or time-bound), meaning it is set to be achieved within a specific timeframe.

The Critical 66 Days

Without a SMART plan, 50% of people give up on their goals by the end of the first week of January [1]. By the end of the month, that number rises to 83% [1]. This happens because it takes approximately 66 days (over two months) for a new habit to become ingrained [2]. Having professional support during this critical window is essential for long-term success.

More Info?

I can help you get off to a good start in achieving your New Year’s resolution. The best time to put a plan in place is now—before the festivities begin. If you would like more information, you can learn about me here.

To your good health!

Joy

You can follow me on:

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

References

  1. Norcross, JC et al. Auld lang syne: success predictors, change processes, and self-reported outcomes of New Year’s resolvers and nonresolvers. J Clin Psychol. 2002 Apr;58(4):397-405. https://doi.org/10.1002/jclp.1151
  2. Lally, P. et al. How are habits formed: Modelling habit formation in the real world. Eur. J. Soc. Psychol. 2010. 40: 998–1009. https://doi.org/10.1002/ejsp.674
 
Nutrition is BetterByDesign
 

Privacy Policy | Terms of Use

 

© 2025 BetterByDesign Nutrition Ltd.

LEGAL NOTICE: The contents of this blog, including text, images, and cited statistics, are for informational purposes only. The content is not intended to be a substitute for professional medical advice, diagnosis, or treatment. Always seek the advice of your physician or other qualified health provider with any questions you may have regarding a medical condition.

When to Eat and Not Eat, How Many Meals and Snacks

Introduction

Historically, “when we eat” was a non-issue; we ate when it was daylight and food was available, and we fasted when it was dark. With modern lighting and refrigeration, our “day” lasts as long as the lights are on, and food is available around the clock. To understand the current science of meal timing, we must look at the history of the three-meal-per-day standard and the rise of snacking.

A Brief History of Meals and Snacks

In the Middle Ages, daylight dictated meal times, with lunch being the main event of the day. Breakfast became popularized in the mid-19th century for laborers and was later marketed heavily by the cereal industry. Snacks were once frowned upon as unhygienic, only becoming a staple in the 1950s due to the rise of processed food manufacturing [1,2]. Between 1977 and 2006, daily caloric intake rose by approximately 570 calories, largely due to snacking [3].

The “Vicious Cycle” of Type 2 Diabetes Treatment

Before insulin, diabetes was managed by strictly restricting carbohydrates. Experts like Dr. William Osler recommended a diet of 65% fat and only 3% carbohydrate [4]. Today, many patients with type 2 diabetes enter a vicious cycle: high carbohydrate intake leads to higher insulin doses, which drives weight gain and increases insulin resistance, further increasing cardiovascular risk [8].

Challenging the “Snacking” Dogma

Since 2009, many have been advised to eat six times a day to “manage” blood sugar. However, a 2019 study in Diabetes Care found that patients who ate three meals per day (without snacks) saw significantly better results than those eating six times, even with the same total calories. The three-meal group lost an average of 12 pounds more and reduced their HbA1C by 1.2% in just 12 weeks [8].

Chronobiology and Circadian Rhythms

Our bodies are governed by circadian rhythms—internal clocks optimized for eating during daylight and fasting at night [16,17]. Blood sugar control fluctuates according to these rhythms; identical foods eaten in the evening cause much higher spikes than when eaten in the morning [18-20]. This suggests that carbohydrate sources are best consumed at breakfast.

When Not to Eat: Intermittent Fasting

While intermittent fasting is popular, timing matters. Fasting until noon has been shown to trigger higher blood sugar spikes after lunch and dinner in those with type 2 diabetes [21]. Aligning your “eating window” with your body’s natural clock is essential for appetite control and glucose regulation.

More Info?

If you would like me to design a Meal Plan for you that aligns your eating times with your natural circadian rhythms, you can learn about me and the Comprehensive Dietary Package that 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. Winterman D. Breakfast, lunch and dinner: Have we always eaten them? BBC News Magazine. Published November 15, 2012. [https://www.bbc.com/news/magazine-20243692]
  2. Carroll A. How Snacking Became Respectable. The Wall Street Journal. Published August 30, 2013. [https://www.wsj.com/articles/how-snacking-became-respectable-1377906874]
  3. Duffey KJ, Popkin BM. Energy Density, Portion Size, and Eating Occasions: Contributions to Increased Energy Intake in the United States, 1977–2006. PLOS Medicine. 2011;8(6):e1001050. [https://doi.org/10.1371/journal.pmed.1001050]
  4. Osler W. The Principles and Practice of Medicine. New York, NY: D. Appleton and Company; 1892. [Archival Source]
  5. Woodyatt RT. Bernhard Naunyn. Diabetes. 1952;1(3):240–241. [https://pubmed.ncbi.nlm.nih.gov/14936838/]
  6. Allen FM. Studies Concerning Diabetes. JAMA. 1914;LXIII(11):939–943. [https://doi.org/10.1001/jama.1914.02570110041011]
  7. Joslin EP. The Treatment of Diabetes Mellitus. 2nd ed. Philadelphia, PA: Lea & Febiger; 1917. [Archival Source]
  8. Jakubowicz D, Landau Z, Tsameret S, et al. Reduction in Glycated Hemoglobin and Daily Insulin Dose Alongside Circadian Clock Upregulation in Patients With Type 2 Diabetes Consuming a Three-Meal Diet: A Randomized Clinical Trial. Diabetes Care. 2019;42(12):2171–2180. [https://doi.org/10.2337/dc19-1142]
  9. Seagle HM, Strain GW, Makris A, Reeves RS. Position of the American Dietetic Association: Weight Management. Journal of the American Dietetic Association. 2009;109(2):330–346. [https://doi.org/10.1016/j.jada.2008.11.033]
  10. Canadian Diabetes Association. Beyond the Basics: Meal Planning for Healthy Eating, Diabetes Prevention and Management. Toronto, ON: Canadian Diabetes Association; 2014. [Clinical Guideline: https://www.rvh.on.ca/wp-content/uploads/2023/07/Beyond-the-Basics-PDF.pdf]
  11. Arnold L, Mann JI, Ball MJ. Metabolic effects of alterations in meal frequency in type 2 diabetes. Diabetes Care. 1997;20(11):1651–1654. [https://doi.org/10.2337/diacare.20.11.1651]
  12. Mekary RA, Giovannucci E, Willett WC, van Dam RM, Hu FB. Eating patterns and type 2 diabetes risk in men: breakfast omission, eating frequency, and snacking. The American Journal of Clinical Nutrition. 2012;95(5):1182–1189. [https://doi.org/10.3945/ajcn.111.028209]
  13. Gouda M, Matsukawa M, Iijima H. Associations between eating habits and glycemic control and obesity in Japanese workers with type 2 diabetes mellitus. Diabetes, Metabolic Syndrome and Obesity: Targets and Therapy. 2018;11:647–658. [https://doi.org/10.2147/DMSO.S173111]
  14. Dyar KA, Ciciliot S, Wright LE, et al. Muscle insulin sensitivity and glucose metabolism are controlled by the intrinsic muscle clock. Molecular Metabolism. 2014;3(1):29–41. [https://doi.org/10.1016/j.molmet.2013.10.005]
  15. Sadacca LA, Lamia KA, deLemos AS, Blum B, Weitz CJ. An intrinsic circadian clock of the pancreas is required for normal insulin release and glucose homeostasis in mice. Diabetologia. 2011;54(1):120–124. [https://doi.org/10.1007/s00125-010-1921-1]
  16. Poggiogalle E, Jamshed H, Peterson CM. Circadian regulation of glucose, lipid, and energy metabolism in humans. Metabolism. 2018;84:11–27. [https://doi.org/10.1016/j.metabol.2017.11.017]
  17. Saad A, Dalla Man C, Nandy DK, et al. Diurnal Pattern to Insulin Secretion and Insulin Action in Healthy Individuals. Diabetes. 2012;61(10):2691–2700. [https://doi.org/10.2337/db11-1478]
  18. Bo S, Fadda M, Castiglione A, et al. Is the timing of caloric intake associated with variation in diet-induced thermogenesis and in the metabolic pattern? A randomized cross-over study. International Journal of Obesity. 2015;39(12):1689–1695. [https://doi.org/10.1038/ijo.2015.138]
  19. Jakubowicz D, Barnea M, Wainstein J, Froy O. High Caloric intake at breakfast vs. dinner differentially influences weight loss of overweight and obese women. Obesity. 2013;21(12):2504–2512. [https://doi.org/10.1002/oby.20460]
  20. Morgan LM, Shi JW, Hampton SM, Frost G. Effect of meal timing and glycaemic index on glucose control and insulin secretion in healthy volunteers. British Journal of Nutrition. 2012;108(7):1286–1291. [https://doi.org/10.1017/S000711451100618X]
  21. Jakubowicz D, Wainstein J, Ahren B, Landau Z, Bar-Dayan Y, Froy O. Fasting Until Noon Triggers Increased Postprandial Hyperglycemia and Impaired Insulin Response After Lunch and Dinner in Individuals With Type 2 Diabetes: A randomized clinical trial. Diabetes Care. 2015;38(10):1820–1826. [https://doi.org/10.2337/dc15-0761]
 
Nutrition is BetterByDesign
 

Privacy Policy | Terms of Use

 

© 2025 BetterByDesign Nutrition Ltd.

LEGAL NOTICE: The contents of this blog, including text and cited statistics, are for informational purposes only. The content is not intended to be a substitute for professional medical advice, diagnosis, or treatment. Always consult your physician before implementing changes to your medical regimen.

Vitamin D Supplementation Can Help Protect Against the Flu

Introduction

There are two large-scale meta-analyses — one from 2013 and the other from 2017 that indicate that Vitamin D supplementation can reduce the risk of getting an upper respiratory infection (URI) including influenza (“the flu”).

Studies Showing that Vitamin D Attenuates the Flu

The first study by Bergman et al [4] analyzed data from 11 placebo controlled trials that involved more than 5,600 subjects and found that those taking a daily dose of Vitamin D had half the risk of developing an upper respiratory infection (URI), including influenza (‘the flu”). This held true even though many of the studies used very low dose of supplementation.

The second of the two large-scale meta-analysis by Martineau et al [5] analyzed the data from 25 randomized controlled trials and involved more than 11,300 subjects. This study found that Vitamin D supplementation reduced the risk of developing an upper respiratory infection (URI), including the flu and those who were the most deficient experienced the most benefit. Even those subjects with very low Vitamin D status had 1/3 the risk when supplementing with Vitamin D, compared to those who did not take any.

Both meta-analysis found that daily dosing with Vitamin D was more effective than taking larger (bolus) doses once a week, or once a month.

There are numerous studies which indicate that people with lower levels of Vitamin D are more likely to get the flu and a 2010 study with healthy adults found that people with lower levels of were twice as likely to get the flu than people with high levels of Vitamin D [6].

Supplementing with Vitamin D

Health Canada’s recommended daily intake (RDAs) for Vitamin D (updated in 2011) are 600 International Units (IUs) for everyone aged one year old to 70 years old and 800 IU for adults over 70 years of age. Health Canada’s safe upper limit (UL) is listed as 4,000 IU per day, however recent scientific publications indicate that there was an error in the calculations used to determine them.

Two researchers from the School of Public Health at the University of Alberta published a paper in October 2014 which indicates that the Institute of Medicine (IOM) that develops the Recommended Dietary Allowances (RDAs) used by both Canadians and Americans made a serious error in their calculations in determining the RDAs for Vitamin D [7] and that rather than 600 IUs being needed to prevent deficiency in 97.5% of individuals, the actual amount is estimated to be 8895 IU of Vitamin D per day — which is above the Health Canada’s tolerable upper intake of 4000 IU per day.

On top of that, researchers from the University of California at San Diego and Creighton University in Omaha, Nebraska published a letter in the same online journal in March 2015 which said that they have confirmed the Institute of Medicine’s miscalculation that was noted by the Canadian investigators [8].

A press release published in Science News on March 17, 2015 indicated that;

“The recommended intake of vitamin D specified by the IOM is 600 IU/day through age 70 years, and 800 IU/day for older ages. Calculations by us and other researchers have shown that these doses are only about one-tenth those needed to cut incidence of diseases related to vitamin D deficiency.

How much Vitamin D should we take?

The Vitamin D Council (a US-based group) recommends adults take 5,000 to 10,000 IU/day, depending on body weight and recommend people have their levels checked to make sure it is > 40 ng/ml (100 nmol/l) and to maintain serum levels at 50 ng/ml (125 nmol/L). Since Vitamin D toxicity manifests as high levels of calcium in the blood and urine, the Vitamin D Council recommends monitoring via blood tests that serum levels don’t exceed 150 ng/ml (374 mmol/L).

Since Health Canada’s current upper limit is 4,000 IUs per day (which may be based on an error in calculation, as noted above), a prudence dosage for supplementation for a healthy adult would not exceed 4,000 IUs per day.

Note: I also recommend people take 100 mcg of Vitamin K2 (menaquinone-4, or menaquinone-7) as Vitamin K2 plays a synergistic role with Vitamin D which regulates blood levels of calcium. Vitamin K prevents calcium from accumulating in soft tissues, such as the blood vessels (contributing to Coronary Artery Calcification)[10].  Put simply, Vitamin K helps ensure that calcium ends up in bone, not arteries.

NOTE: People taking Warfarin (Coumadin) or other anticoagulant medication should not supplement with Vitamin K2 except under the advice of the physician prescribing Warfarin.

Keep in mind that food also provides Vitamin D with natural sources being salmon (447 IU per 3 ounces), tuna (154 IU per 3 ounces), eggs (41 IU per yolk) and cheese (14 IU per 2 ounces of cheddar) and milk and non-dairy beverages made as ‘milk replacements’ are fortified, with 100 IU per cup (250 ml).

If you are a healthy adult under 50 years old with no family risk of cancer* or osteoporosis, 1000 IU Vitamin D3 per day (plus 100 mcg of Vitamin K2) is probably sufficient. Be sure to choose the D3 form (not D2) as it is more efficient at raising serum levels. For adults under 50 with a family history of cancer or who are at risk for osteoporosis, a dosage of 2000 IU Vitamin D3 per day (plus 100 mcg of Vitamin K2) may be more appropriate.

Healthy adults over the age of 50 can safely double the amounts above ⁠— so 2,000 IUs Vitamin D3 per day (plus 100 mcg of Vitamin K2) and for those with a family history of cancer to take 3,000 IUs Vitamin D3 per day (plus 100 mcg of Vitamin K2).

Remember though that Vitamin D is a fat soluble vitamin, so be sure to have your serum levels checked periodically as your body is able to stores for long periods of time. The best indicator of Vitamin D status is a routine blood test called 25-hydroxy vitamin D.

Final thoughts…

There is good evidence that adding Vitamin D3 supplementation to your daily routine may boost your ability to fight of upper respiratory infections, including the flu.

…and if you supplement with Vitamin D, don’t forget to add the Vitamin K2 to help keep the calcium where it ought to be.

More Info

If you would like more information, you can learn about me and the Comprehensive Dietary Package that 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. CTV News, Canadian warns against vaccine apathy after flu sends him to hospital for two months, https://www.ctvnews.ca/health/canadian-warns-against-vaccine-apathy-after-flu-sends-him-to-hospital-for-two-months
  2. Dairy Nutrition, Vitamin D status of Canadians — Results from the Canadian Health Measures Survey, https://www.dairynutrition.ca/nutrients-in-milk-products/vitamin-d/vitamin-d-status-of-canadians-results-from-the-canadian-health-measures-survey
  3. Vitamin D Council, Dr. John Cannell, MD, Influenza, https://www.vitamindcouncil.org/health-conditions/influenza/
  4. Bergman P, Lindh AU, Bjírkhem-Bergman L et al, Vitamin D and Respiratory Tract Infections: A Systematic Review and Meta-Analysis of Randomized Controlled Trials, PLoS One. 2013 Jun 19;8(6):e65835. [https://pubmed.ncbi.nlm.nih.gov/23840373/]
  5. Martineau AR, Jolliffe DA, Hooper RL, Vitamin D supplementation to prevent acute respiratory tract infections: systematic review and meta-analysis of individual participant data, BMJ. 2017 Feb 15;356:i6583 [https://pubmed.ncbi.nlm.nih.gov/28202713/]
  6. Sabetta, J.R., DePetrillo, P., Cipriani, R.J., et al., Serum 25-hydroxyvitamin d and the incidence of acute viral respiratory tract infections in healthy adults. PLoS One, 2010. 5(6): p. e11088. [https://pubmed.ncbi.nlm.nih.gov/20559424/]
  7. Veugelers PJ, Ekwaru JP. A statistical error in the estimation of the recommended dietary allowance for vitamin D. Nutrients. 2014;6(10):4472—4475. Published 2014 Oct 20. doi:10.3390/nu6104472 [https://pubmed.ncbi.nlm.nih.gov/20559424/]
  8. Heaney R, Garland C, Baggerly C, French C, Gorham E. Letter to Veugelers, P.J. and Ekwaru, J.P., A statistical error in the estimation of the recommended dietary allowance for vitamin D. Nutrients 2014, 6, 4472-4475; doi:10.3390/nu6104472. Nutrients. 2015;7(3):1688—1690. Published 2015 Mar 10. doi:10.3390/nu7031688 [https://pubmed.ncbi.nlm.nih.gov/25763527/]
  9. Science News, Recommendation for vitamin D intake was miscalculated, is far too low, experts say, [https://www.sciencedaily.com/releases/2015/03/150317122458.htm]
  10. Theuwissen E, Smit E, Vermeer C, The role of vitamin K in soft-tissue calcification, Adv Nutr. 2012 Mar 1;3(2):166-73.[https://pubmed.ncbi.nlm.nih.gov/22516724/]
 
Nutrition is BetterByDesign
 

Privacy Policy | Terms of Use

 

© 2025 BetterByDesign Nutrition Ltd.

LEGAL NOTICE: The contents of this blog, including text and cited statistics, are for informational purposes only. The content is not intended to be a substitute for professional medical advice, diagnosis, or treatment. Always consult your physician before implementing changes to your me

Why Eating Less and Exercising More DOES Matter As We Age

Introduction

There is much “push back” when it comes to the standard advice to “eat less and exercise more” as a means of losing weight, and for good reason. For one, metabolism will slow as a result of caloric restriction—making it that much more difficult to lose weight when deliberately cutting calories. Another reason is that it is exceedingly difficult for an obese person to exercise. For many, just getting around is a chore. It is for this reason that I focus on helping people be less hungry by eating a different mix of protein, fat and carbohydrate—because a natural byproduct of being less hungry, is eating less. Being active is possible once a person is losing weight and not feeling hungry all the time. Yes, they are still “eating less and moving more”—but as a result, not as the focus.

Addendum (Sept 10 2019)—Weight loss is not only about what we eat. It’s also about when we don’t eat; whether it’s having times between meals where we don’t eat, or not eating from the end of supper until the first meal of the following day (whenever that is). Thanks Dr. Andy Phung for the reminder!

A new study published (September 9, 2019) in the journal Nature Medicine [1] has found that “eating less and exercising more” may actually be good advice as we age—because it turns out that we have decreased fat turnover as we age. If we eat the same amount as we always have and don’t increase the amount we exercise, we will end up gaining approximately 20% over a 10-15 year period [3].

Until recently little was known about fat turnover [2]—which is the storage and removal of fat from adipocytes (fat cells). A 2011 study showed that during the average ten-year lifespan of human fat cells, the fat in them (triglycerides) turns over six times, in both men and women [2], and that when people are obese, the fat removal rate decreases and the amount of fat as triglyceride stored each year increases [2]. What we didn’t know until now is what happened to fat turnover as we age. This follow-up study headed by the same lead researcher as the 2011 study explored this issue, as well as differences in fat turnover after people have bariatric surgery which helps explain why some people regain their weight after weight loss, whereas others don’t.

Eating Less Matters as We Age

Fat turnover is a difference between the rate of fat uptake into fat cells and the fat removal rate. High fat storage but low fat removal is what results in the accumulation of fat and in obesity. The “bad news” of this new study is that fat accumulation due to decreased fat turnover is what happens as we age, leading to accumulation of fat. That is, even if we don’t eat more or exercise less than previously, we will store more fat—which can result in as much as a 20% increase in body weight over 13 years [3].

“Those who didn’t compensate for that (i.e. decrease fat turnover) by eating less calories gained weight by an average of 20 percent” [3].

Researchers from the University of Uppsala in Sweden and the University of Lyon in France studied the fat cells of 54 men and women over an average 13 year period [3] and regardless of whether the subjects gained weight or lost weight, they had a decreased fat turnover. Since fat turnover is decreased as we age, to prevent weight gain we need to take in less calories than we used to, even if we are just as active.

Why We Regain Weight After Weight Loss

The study also looked at fat turnover in 41 women who underwent bariatric surgery. Results showed that only those who had a low lipid turnover rate before the surgery were able to increase their lipid turnover after surgery and maintain their weight loss 4-7 years after surgery [1]. Researchers think that if people had a high lipid turnover rate before surgery, there is less ‘room’ for them to increase their lipid turnover rate after surgery, which is why they regain the weight. This could explain why so many people who lose incredible amounts of weight following any one of a number of “diets” regain it (and then some) afterwards.

Exercise and Lipid Turnover

Previous studies have reported that fat turnover increases as we exercise [2], so based on this new study, the idea of ‘eating less and exercising more’ actually matters as we age. We can either decrease our intake as we age and/or be a little more active and avoid gaining weight—which is easy enough to do for those who are slim, if they know.

But what about those who are already overweight or obese and now find out they are more prone to storing fat now that they’re older, even though they eat the exact same way and haven’t changed their activity level? I believe the solution is the same regardless of a person’s age—focusing on the person eating in such a way as to be less hungry, so that in the end they end up eating less. As they lose weight because they’re not hungry all the time, being more active is easier to implement. The difference between it being “doable” depends on what we focus on.

In light of this new study, what is important is that as people age there is a natural tendency to put on weight, even if they eat the same and don’t change their activity level. This means older people need to modify the amount of calories they take in and/or expend more energy, the question is how.

More Info?

If you would like more information, you can learn about me and the Comprehensive Dietary Package that 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. Arner P, Bernard S, Appelsved K-Y et al. Adipose lipid turnover and long-term changes in body weight. Nature Medicine. 2019 Sep;25(9):1385-1389. [https://pubmed.ncbi.nlm.nih.gov/31501613/]
  2. Arner P, Westermark PO, Spalding KL, et al. Dynamics of human adipose lipid turnover in health and metabolic disease. Nature. 2011 Oct 19;478(7367):110-3. [https://pubmed.ncbi.nlm.nih.gov/21947005/]
  3. Karolinska Institutet. New study shows why people gain weight as they get older. ScienceDaily. Published September 9, 2019. [https://www.sciencedaily.com/releases/2019/09/190909193109.htm]
 
Nutrition is BetterByDesign
 

Privacy Policy | Terms of Use

 

© 2025 BetterByDesign Nutrition Ltd.

LEGAL NOTICE: The contents of this blog, including text and cited statistics, are for informational purposes only. The content is not intended to be a substitute for professional medical advice, diagnosis, or treatment. Always consult your physician before implementing changes to your medical regimen.

Treating Small Intestinal Bacterial Overgrowth (SIBO)

Introduction

In the first two articles of this series on Small Intestinal Bacterial Overgrowth (SIBO), I covered what SIBO is, its prevalence, symptoms, and the various diagnostic tests used to identify it. I also discussed why Irritable Bowel Syndrome (IBS) that does not improve with standard dietary changes may actually be SIBO. In this third installment, I outline the main dietary approaches used in treating SIBO alongside antibiotic and evidence-based herbal antimicrobial therapy, and explore whether dietary changes should occur before or after antimicrobial treatment.

Understanding SIBO Treatment Goals

It is vital to remember that SIBO is the presence of bacteria in the small intestine that are not supposed to be there. While dietary changes improve symptoms, they do not eliminate the bacteria themselves. The foreign bacteria must be eradicated, and the underlying cause—such as low stomach acid, pancreatic insufficiency, or motility disorders—must be addressed to prevent recurrence.

Two factors are critical in treatment: (1) recurrence occurs in nearly half of patients within a year if underlying factors like proton-pump inhibitor use or aging are present, and (2) addressing the root cause is the only way to ensure long-term success.

The Role of Fermentable Carbohydrates

Many clinicians prescribe low-FODMAP or Specific Carbohydrate Diets (SCD) to starve the bacteria. However, this has drawbacks. Long-term restriction can reduce beneficial bifidobacteria. Furthermore, research from Dr. Mark Pimentel suggests that bacteria are easier to eradicate when they are active and replicating. If they are starved, they may become dormant and resistant to antimicrobials.

A 2010 study found that combining the antibiotic Rifaximin with partially hydrolyzed guar gum (PHGG) increased the eradication rate from 62% to 85%, while also protecting beneficial gut flora.

Phase I: Symptom Management and Preparation

The first phase involves 4–6 weeks of a low fermentable carbohydrate diet to improve quality of life. During this time, I include PHGG to allow for the minimal bacterial activity needed to ensure that when antimicrobial treatment begins, it is more likely to be successful. PHGG is also well-known for reducing general IBS symptoms in both constipation and diarrhea subtypes.

Phase II: Antimicrobial Eradication

The second phase coincides with a 4-week antimicrobial protocol. The low fermentable carbohydrate diet is maintained, but small amounts of fermentable foods are gradually reintroduced to “feed” the bacteria, making them vulnerable to treatment.

For methane-positive SIBO, combining Rifaximin with Neomycin or Metronidazole has shown higher success rates. Alternatively, herbal antimicrobials have been shown in some studies to be even more effective than Rifaximin, with the added benefits of lower cost and a strong safety record.

Phase III: Liberalization and Maintenance

The final phase is the gradual reintroduction of foods. Once the gut microbiome is restored, most should tolerate a whole-food diet, though avoiding sugar alcohols and certain gums may prevent future issues. If symptoms return, re-testing for SIBO or investigating other causes like histamine intolerance or A1 beta-casein intolerance is recommended.

Final Thoughts

SIBO remains a debated diagnosis, but for many unsuccessfully treated for IBS, this evidence-based combination of diet and antimicrobials offers significant relief. We are still learning about the gut microbiome, including its link to conditions like fibromyalgia. Until we have more definitive answers, using well-studied tools like PHGG and targeted antimicrobials remains the most effective approach we have.

More Info?

If you would like to know more, you can learn about me and the Small Intestinal Bacterial Overgrowth (SIBO) Package that 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. Lauritano EC, Gabrielli M, Scarpellini E, et al. Small intestinal bacterial overgrowth recurrence after antibiotic therapy. American Journal of Gastroenterology. 2008 Oct;103(8):2031-5. [https://www.ncbi.nlm.nih.gov/pubmed/18802998]
  2. Staudacher HM, Lomer MC, Anderson JL, et al. Fermentable carbohydrate restriction reduces luminal bifidobacteria and gastrointestinal symptoms in patients with irritable bowel syndrome. Journal of Nutrition. 2012 Aug;142(8):1510-8. [https://doi.org/10.3945/jn.112.159285]
  3. Furnari M, Parodi A, Gemignani L, et al. Clinical trial: the combination of rifaximin with partially hydrolysed guar gum is more effective than rifaximin alone in eradicating small intestinal bacterial overgrowth. Alimentary Pharmacology & Therapeutics. 2010 Oct;32(8):1000-6. [https://doi.org/10.1111/j.1365-2036.2010.04436.x]
  4. Quartarone G. Role of PHGG as a dietary fiber: a review article. Minerva Gastroenterologica e Dietologica. 2013 Dec;59(4):329-40. [https://www.ncbi.nlm.nih.gov/pubmed/24212352]
  5. Russo L, Andreozzi P, Zito FP, et al. Partially hydrolyzed guar gum in the treatment of irritable bowel syndrome with constipation: effects of gender, age, and body mass index. Saudi Journal of Gastroenterology. 2015 Mar-Apr;21(2):104-10. [https://doi.org/10.4103/1319-3767.153835]
  6. Peralta S, Cottone C, Doveri T, et al. Small intestine bacterial overgrowth and irritable bowel syndrome-related symptoms: experience with Rifaximin. World Journal of Gastroenterology. 2009 Jun 7;15(21):2628-31. [https://doi.org/10.3748/wjg.15.2628]
  7. Low K, Hwang L, Hua J, et al. A combination of rifaximin and neomycin is most effective in treating irritable bowel syndrome patients with methane on lactulose breath test. Journal of Clinical Gastroenterology. 2010 Sep;44(8):547-50. [https://doi.org/10.1097/MCG.0b013e3181c64c90]
  8. Scarlata K. Small Intestinal Bacterial Overgrowth (SIBO). For a Digestive Peace of Mind blog. [https://blog.katescarlata.com/2014/01/22/small-intestinal-bacterial-overgrowth/]
  9. Chedid V, Dhalla S, Clarke JO, et al. Herbal therapy is equivalent to rifaximin for the treatment of small intestinal bacterial overgrowth. Global Advances in Health and Medicine. 2014 May;3(3):16-24. [https://doi.org/10.7453/gahmj.2014.019]
  10. Minerbi A, Gonzalez E, Brereton NJB, et al. Altered microbiome composition in individuals with fibromyalgia. Pain. 2019 Nov;160(11):2589-2602. [https://doi.org/10.1097/j.pain.0000000000001640]
  11. McGill University Health Centre. Gut bacteria associated with chronic widespread pain for first time. Press Release; June 19, 2019. [https://muhc.ca/news-and-patient-stories/press-releases/gut-bacteria-associated-chronic-widespread-pain-first-time]
 
Nutrition is BetterByDesign
 

Privacy Policy | Terms of Use

 

© 2025 BetterByDesign Nutrition Ltd.

LEGAL NOTICE: The contents of this blog, including text, images, and cited statistics, are for informational purposes only. The content is not intended to be a substitute for professional medical advice, diagnosis, or treatment. Always seek the advice of your physician or other qualified health provider with any questions you may have regarding a medical condition. Never disregard professional medical advice or delay in seeking it because of something you have read in this content.

Diagnosing Small Intestinal Bacterial Overgrowth (SIBO)

Introduction

In the first article of this series about Small Intestinal Bacterial Overgrowth (SIBO), I covered what SIBO is, how common it is, and its primary symptoms. If you haven’t read that introduction yet, it provides essential context for our discussion. In this second article, I cover the different tests used in diagnosing SIBO, exploring the advantages and drawbacks of each method. In the next installment, we will cover various treatment options, including dietary protocols combined with antibiotic or herbal therapies.

The Challenges of Diagnosing SIBO

One of the first challenges in diagnosing SIBO is finding a physician knowledgeable about the condition and its current treatments. Historically, SIBO was diagnosed primarily by gastroenterologists using invasive and expensive surgical tests. Before the widespread use of endoscopy, diagnosis required a surgical procedure to collect liquid from the jejunum of the small intestine for culturing. A positive diagnosis was recorded when bacterial growth exceeded 104 colony-forming units per milliliter.

Endoscopy and the Gold Standard

The invention of the endoscope in the mid-1980s allowed for less invasive fluid collection from the duodenum. While the patient is sedated, a flexible tube is passed through the esophagus and stomach into the small intestine. Despite being the current “gold standard,” this procedure remains expensive and invasive. Furthermore, a significant drawback is that only about 30% of gut bacteria can actually be successfully cultured from these samples, and contamination during withdrawal is common.

The Discovery of Breath Testing

A brilliantly simple solution emerged with the discovery that gases like hydrogen and methane are produced in the small intestine only as a by-product of unabsorbed or incompletely absorbed carbohydrates. Breath tests detect these gases to provide evidence of carbohydrate malabsorption and identify the specific types of bacteria causing the fermentation. The two most common variants are the glucose breath test and the lactulose breath test.

Glucose vs. Lactulose Breath Tests

Clinicians often debate which substrate is more accurate. Glucose is absorbed completely in the upper small intestine, making it very accurate for that region, but it may miss SIBO located in the ileum (the far part of the small intestine). Conversely, lactulose is not absorbed by humans, allowing it to travel the full length of the small intestine and potentially detect overgrowth in the ileum. Preference for these tests varies by practitioner.

How the Breath Test Works

After a patient consumes the substrate, exhaled hydrogen or methane is measured using a gas chromatograph. These gases are produced by bacteria, absorbed into the bloodstream, and then exhaled via the lungs. Notably, 15%-30% of people host Methanobrevibacter smithii, which converts hydrogen into methane. These individuals may not exhale much hydrogen even if they have SIBO, making it vital to measure both gases.

Performing the Test and Interpreting Results

Testing requires an overnight fast and specific oral hygiene to ensure mouth bacteria do not skew results. Breath is analyzed every 15 minutes for 2 to 4 hours. According to the 2017 North American Consensus, a rise in hydrogen of ≥20 ppm within 90 minutes is considered positive for SIBO. Methane levels ≥10 ppm are considered methane-positive. However, some researchers, like Dr. Mark Pimentel, suggest even lower cutoff points for methane (reading >3 ppm) to avoid missing clinical cases.

Distinguishing SIBO from IBS

The symptoms of Irritable Bowel Syndrome (IBS) and SIBO overlap significantly, including bloating, pain, and altered bowel habits. Research has found that nearly 80% of subjects with an abnormal breath test also met the criteria for IBS. This raises the question of how many IBS patients might actually have SIBO. If you have been unsuccessful in resolving IBS symptoms through diet alone, breath testing may be a valuable next step.

Final Thoughts

While some recent studies call into question the validity of breath tests for detecting specific jejunal overgrowth, they remain a vital tool for identifying microbial dysbiosis. Identifying methane-predominant SIBO is particularly important because methane-producing bacteria are often resistant to standard antibiotics and are strongly associated with chronic constipation.

More Info?

If you would like to know more

If you would like to know more, you can learn about me and the Small Intestinal Bacterial Overgrowth (SIBO) Package that 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. Quigley EMM. The Spectrum of Small Intestinal Bacterial Overgrowth (SIBO). Current Gastroenterology Reports. 2019;21(3). [https://doi.org/10.1007/s11894-019-0671-z]
  2. Dukowicz AC, Lacy BE, Levine GM. Small intestinal bacterial overgrowth: a comprehensive review. Gastroenterology & Hepatology. 2007 Feb;3(2):112-122. [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3099351/]
  3. Ghoshal UC. How to interpret hydrogen breath tests. Journal of Neurogastroenterology and Motility. 2011 Jul;17(3):312-317. [https://doi.org/10.5056/jnm.2011.17.3.312]
  4. Levitt MD, Furne JK, Kuskowski M, et al. Stability of human methanogenic flora over 35 years and a review of insights obtained from breath methane measurements. Clinical Gastroenterology and Hepatology. 2006 Feb;4(2):123-129. [https://doi.org/10.1016/j.cgh.2005.11.006]
  5. Pimentel M, Chow EJ, Lin HC. Eradication of small intestinal bacterial overgrowth reduces symptoms of irritable bowel syndrome. American Journal of Gastroenterology. 2000 Dec;95(12):3503-6. [https://doi.org/10.1111/j.1572-0241.2000.03368.x]
  6. Ghoshal UC, Ghoshal U, Ayyagari A, et al. Tropical sprue is associated with contamination of small bowel with aerobic bacteria and reversible prolongation of orocecal transit time. Journal of Gastroenterology and Hepatology. 2003 May;18(5):540-547. [https://doi.org/10.1046/j.1440-1746.2003.03010.x]
  7. Rezaie A, Buresi M, Lembo A, et al. Hydrogen and Methane-Based Breath Testing in Gastrointestinal Disorders: The North American Consensus. American Journal of Gastroenterology. 2017 May;112(5):775-784. [https://doi.org/10.1038/ajg.2017.46]
  8. Scarlata K. Small Intestinal Bacterial Overgrowth (SIBO). For a Digestive Peace of Mind blog. [https://blog.katescarlata.com/2014/01/22/small-intestinal-bacterial-overgrowth/]
  9. Chatterjee S, Park S, Low K, et al. The degree of breath methane production in IBS correlates with the severity of constipation. American Journal of Gastroenterology. 2007 Apr;102(4):837-41. [https://doi.org/10.1111/j.1572-0241.2007.01054.x]
  10. Attaluri A, Jackson M, Valestin J, et al. Methanogenic flora is associated with altered colonic transit but not stool characteristics in constipation without IBS. American Journal of Gastroenterology. 2010 Jun;105(6):1407-11. [https://doi.org/10.1038/ajg.2009.730]
  11. Hwang L, Low K, Khoshini R, et al. Evaluating breath methane as a diagnostic test for constipation-predominant IBS. Digestive Diseases and Sciences. 2010 Feb;55(2):398-403. [https://doi.org/10.1007/s10620-009-0778-4]
  12. Kunkel D, Basseri RJ, Makhani MD, et al. Methane on breath testing is associated with constipation: a systematic review and meta-analysis. Digestive Diseases and Sciences. 2011 Jun;56(6):1612-8. [https://doi.org/10.1007/s10620-011-1590-5]
  13. Schmulson MJ, Drossman DA. What Is New in Rome IV. Journal of Neurogastroenterology and Motility. 2017 Apr;23(2):151-163. [https://doi.org/10.5056/jnm16214]
  14. Sundin OH, Mendoza-Ladd A, Morales E, et al. Does a glucose-based hydrogen and methane breath test detect bacterial overgrowth in the jejunum? Neurogastroenterology & Motility. 2018 Nov;30(11). [https://doi.org/10.1111/nmo.13350]
 
Nutrition is BetterByDesign
 

Privacy Policy | Terms of Use

 

© 2025 BetterByDesign Nutrition Ltd.

LEGAL NOTICE: The contents of this blog, including text, images, and cited statistics, are for informational purposes only. The content is not intended to be a substitute for professional medical advice, diagnosis, or treatment. Always seek the advice of your physician or other qualified health provider with any questions you may have regarding a medical condition. Never disregard professional medical advice or delay in seeking it because of something you have read in this content.

What is Small Intestinal Bacterial Overgrowth (SIBO)?

Introduction

I used to believe that SIBO was a condition that only alternative medicine practitioners, such as naturopaths, identified and treated. I thought it wasn’t a real diagnosis at all, and it seems I was not alone in this belief. This is the first article about SIBO, outlining what it is, its symptoms, and its risk factors. Subsequent articles will explore how SIBO is diagnosed and the various treatment options available.

When I asked on Twitter whether people believed SIBO was a credible diagnosis, only 15% thought it wasn’t legitimate. The majority (62%) felt it was a credible diagnosis that many doctors simply don’t know about yet. My own interest began when a rheumatologist suggested SIBO might be underlying an increase in joint pain I was experiencing. To my surprise, I found that SIBO is not only well-researched but is being studied by academics at prestigious universities.

What is SIBO?

Small Intestinal Bacterial Overgrowth (SIBO) is an increase in the types of bacteria in the small intestine that are normally only found in the large intestine (the colon). The small intestine consists of the duodenum, the jejunum, and the ileum. While it is longer than the large intestine, its diameter is smaller. Normally, the small intestine contains very few bacteria. When the bacteria that normally populate the large intestine “spill over” into the small intestine, it is classified as SIBO.

The body has several mechanisms to prevent this, including high stomach acid which kills most bacteria and the ileocaecal valve, which acts as a barrier between the small and large intestines. Secretions from the pancreas and bile also help keep bacteria from reproducing in the wrong areas.

Risk Factors and Causes

SIBO can occur for several reasons, including low stomach acid (achlorhydria), pancreatic insufficiency, anatomical abnormalities like obstructions or diverticula, and motility disorders common in conditions like diabetes mellitus. Interestingly, while heavy alcohol consumption has long been a known risk factor, recent studies have found an association between moderate alcohol consumption (one drink per day for women) and SIBO, likely due to injury to mucosal cells and slowed intestinal contractions.

How Common is SIBO?

The prevalence of SIBO in young and middle-aged adults appears to be between 6% and 15%. However, this rises to nearly 16% in older adults. This increase may be due to the natural decrease in stomach acid associated with aging, as well as the higher prevalence of type 2 diabetes and diverticulosis in older populations.

Symptoms of SIBO

Many symptoms of SIBO overlap with Irritable Bowel Syndrome (IBS), including abdominal pain, bloating, gas, and alternating bouts of diarrhea or constipation. As I discovered personally, there are also lesser-known symptoms, such as significant joint pain, that can be associated with the condition.

Final Thoughts

If you have been diagnosed with IBS but find that your symptoms do not improve despite appropriate dietary changes, it may be worth investigating SIBO. Understanding the underlying mechanisms—from stomach acid to intestinal motility—is the first step toward effective treatment and recovery.

More Info?

If you would like to know more, you can learn about me and the Small Intestinal Bacterial Overgrowth (SIBO) Package that 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. Bures J, Cyrany J, Kohoutova D, et al. Small intestinal bacterial overgrowth syndrome. World Journal of Gastroenterology. 2010 Jun 28;16(24):2978-90. [https://doi.org/10.3748/wjg.v16.i24.2978]
  2. Medscape. Small Intestine Anatomy. Updated Dec 8, 2017. [https://emedicine.medscape.com/article/1948951-overview]
  3. Hauge T, Persson J, Danielsson D. Mucosal bacterial growth in the upper gastrointestinal tract in alcoholics (heavy drinkers). Digestion. 1997;58(6):591-5. [https://doi.org/10.1159/000201507]
  4. Gabbard SL, Lacy BE, Levine GM, et al. The impact of alcohol consumption and cholecystectomy on small intestinal bacterial overgrowth. Digestive Diseases and Sciences. 2014 Mar;59(3):638-44. [https://doi.org/10.1007/s10620-013-2960-y]
  5. Dukowicz AC, Lacy BE, Levine GM. Small intestinal bacterial overgrowth: a comprehensive review. Gastroenterology & Hepatology. 2007 Feb;3(2):112-22. [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3099351/]
 
Nutrition is BetterByDesign
 

Privacy Policy | Terms of Use

 

© 2025 BetterByDesign Nutrition Ltd.

LEGAL NOTICE: The contents of this blog, including text, images, and cited statistics, are for informational purposes only. The content is not intended to be a substitute for professional medical advice, diagnosis, or treatment. Always seek the advice of your physician or other qualified health provider with any questions you may have regarding a medical condition. Never disregard professional medical advice or delay in seeking it because of something you have read in this content.

When Real Food is Deemed Offensive and Disturbing, not Processed Food

Introduction

Note: This article is not one of my usual Science Made Simple posts, but a commentary regarding an interaction that occurred on social media.

Yesterday, I posted a photo on Instagram, Facebook, and Twitter of some fresh chicken that I had bought and prepared. Real food is a perfectly normal topic for a Dietitian to write about, right? The photo simply showed the chicken before and after I had cut it into legs and breasts. The caption indicated that real food shouldn’t look foreign; real chicken comes with a head, feet, and bones, in contrast to the pre-cut, plastic-wrapped versions found in supermarket Styrofoam trays.

Censorship of Real Food

Presumably, someone found this photo of chicken to be offensive and reported it to Instagram. While I wasn’t notified of the censorship, several followers informed me that the photo was blurred out and deemed to contain “sensitive content.” A physician colleague commented on the absurdity of the situation: “I cannot believe a photo of food is blurred as ‘sensitive content.’ It is absolutely mind-boggling. But it’s totally fine to be constantly inundated with ads for crap that make us feel bad about ourselves, making us buy junk we don’t need.”

What is Truly Offensive?

There is a profound difference between real food and the processed food-like substances we are encouraged to consume. If a photo of whole chicken is considered “disturbing,” we must ask what we should actually be offended by. I find it offensive when individuals face amputations due to uncontrolled diabetes. I find it disturbing when people struggle to lose weight because of insatiable cravings for engineered processed foods. I find it disturbing that many children now view “chicken” only as something boneless, deep-fried, and served with sweetened dipping sauces.

Ultra-Processed vs. Whole Food

I find the use of industrial seed oils, methylcellulose, and pea protein isolates masquerading as “meat” to be offensive. While I support vegetarians and vegans having plant-based options, these products should not be marketed as “better” than meat. An ultra-processed mixture of refined coconut oil, potato starch, maltodextrin, and various gums is not preferable to a whole, real food with a single ingredient: “beef.”

The Right to Choose

Individuals have the right to choose what they eat without judgment. There is no one-size-fits-all diet, and those who choose to eat meat, fish, or poultry should not be vilified or censored. We should focus our concern on the health consequences of ultra-processed diets rather than the sight of actual, whole ingredients.

More Info?

Learn about me and the Comprehensive Dietary Package that I offer.

To your good health!

Joy

You can follow me on:

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

 
Nutrition is BetterByDesign
 

Privacy Policy | Terms of Use

 

© 2025 BetterByDesign Nutrition Ltd.

LEGAL NOTICE: The contents of this blog, including text, images, and personal anecdotes, are for informational purposes only. The content is not intended to be a substitute for professional medical advice, diagnosis, or treatment. Always seek the advice of your physician or other qualified health provider with any questions you may have regarding a medical condition. Never disregard professional medical advice or delay in seeking it because of something you have read in this content.

Tyramine Intolerance – underlying cause of migraine headaches?

Introduction

A migraine is more than just a severe headache; it is a debilitating condition often accompanied by nausea, vomiting, sensitivity to light and sound, and sometimes a preceding aura. For many, these episodes are linked to a reduced ability to clear the amino acid tyramine, a condition known as tyramine intolerance. In individuals with insufficient amounts of the enzyme monoamine oxidase (MAO), tyramine levels can build up, leading to migraines, heart palpitations, and gastrointestinal issues.

What is Tyramine Intolerance?

Just as the amino acid histidine breaks down into histamine, tyrosine breaks down into tyramine. Normally, the enzyme MAO breaks down excess tyramine. However, certain medications—such as MAO inhibitors for depression or Parkinson’s disease—inhibit this enzyme, causing tyramine to accumulate. Some individuals naturally have insufficient MAO levels, which results in the same intolerance. When tyramine builds up, the body responds by releasing neurotransmitters like epinephrine and norepinephrine, triggering a “fight or flight” response that increases blood pressure and heart rate.

Symptoms and Risks

The primary symptoms of tyramine intolerance include migraines, heart palpitations, and nausea. In severe cases, particularly for those on specific medications, a rapid and dangerous increase in blood pressure called a hypertensive emergency can occur. This condition is serious and requires immediate clinical attention, as it can potentially lead to hemorrhagic stroke or organ damage. For most people with intolerance, however, the main struggle is managing the recurring, debilitating migraines triggered by dietary intake.

The Tyramine Intolerance Diet

For those affected, a low-tyramine diet is often recommended to see if symptoms improve. Tyramine occurs naturally in protein-containing foods, but its levels increase as foods age, mature, or ripen. Common triggers include aged cheeses, cured or processed meats, fermented foods, and certain alcoholic beverages. Because tyramine levels fluctuate based on food processing and storage, managing the diet is more complex than simply following a static list.

Personalized Support for Migraines

While some foods are universal triggers, tyramine sensitivity varies between individuals. One person may be triggered by a specific aged cheese, while another is not. Rather than restricting every possible source, it is often more effective to systematically identify and eliminate your specific triggers. This targeted approach provides significant relief without unnecessary dietary restriction, allowing for a more sustainable and enjoyable lifestyle.

More Info?

If you have been diagnosed with tyramine intolerance or suspect you may be sensitive to tyramine, I can help. You can learn about me and the Comprehensive Dietary Package that I offer, to which a Migraine add-on can be added.

To your good health!

Joy

You can follow me on:

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

References

  1. Joneja J. Histamine and tyramine sensitivity — how closely are they linked? Food Matters. October 2017. [https://www.histamine-sensitivity.com/histamine-tyramine-similaraties-10-12.html]
  2. Van Eaton J. Tyramine-Free Diets. Healthline. February 1, 2019. [https://www.healthline.com/health/tyramine-free-diets]
  3. Hall-Flavin D. MAOIs and diet: Is it necessary to restrict tyramine? Mayo Clinic. [https://www.mayoclinic.org/diseases-conditions/depression/expert-answers/maois/faq-20058035]
  4. Costa MR, Glória MBA. Migraine and Diet. Encyclopedia of Food Sciences and Nutrition (Second Edition). 2003. [https://www.sciencedirect.com/science/article/pii/B012227055X007835]
  5. Skypala IJ, Williams M, Reeves L, et al. Sensitivity to food additives, vaso-active amines and salicylates: a review of the evidence. Clinical and Translational Allergy. 2015 Oct 13;5:34. [https://doi.org/10.1186/s13601-015-0078-3]
 
Nutrition is BetterByDesign
 

Privacy Policy | Terms of Use

 

© 2025 BetterByDesign Nutrition Ltd.

LEGAL NOTICE: The contents of this blog, including text, images, and cited statistics, are for informational purposes only. The content is not intended to be a substitute for professional medical advice, diagnosis, or treatment. Always seek the advice of your physician or other qualified health provider with any questions you may have regarding a medical condition. Never disregard professional medical advice or delay in seeking it because of something you have read in this content.

Why So Many Post Menopausal Women and Older Men Have Low Iron

NOTE: This article was written and posted on August 4, 2019, and was completely updated on November 7, 2025.


Introduction

Doctors are often hesitant to order blood tests for post menopausal women who report being more tired or having more hair loss than usual, simply because these women no longer have a period. While menstruation is the most common cause of low iron in younger women, there are multiple reasons why post-menopausal women and men over 50 years of age may be low in iron that warrant investigation. This article explains why iron levels are often low in older adults, what routine blood tests can be done to determine this, and various options available if results come back out of range.

Why Low Iron Matters

Iron is essential for producing red blood cells and supporting energy and brain function. Low iron status can cause fatigue / feeling abnormally tired, weakness, a reduced ability to exercise, and excessive hair loss. These symptoms occur before someone develops full-blown iron-deficient anemia.

Microcytic anemia

Iron deficiency can lead to microcytic anemia, characterized by red blood cells that are smaller than normal. These smaller cells are less effective at carrying oxygen, which leads to feelings of fatigue, weakness, and even shortness of breath [3].

How Common Is Low Iron?

Current data indicate that iron deficiency anemia affects approximately 1 in 7 adults over the age of 50 (U.S. data). Fatigue, brain fog, and decreased physical performance are common early signs [2][11].

Why Low Iron Happens in Adults Over Age 50

Chronic Blood Loss

The most common reason older adults develop iron deficiency is slow, chronic blood loss, which can often be from the gastrointestinal (GI) tract. Sources of GI blood loss include ulcers, diverticulosis, colon or rectal polyps, and GI cancer. As outlined in this earlier article about hemorrhoids, when having bowel movements, internal hemorrhoids can bleed microscopically without detection, resulting in low iron status. Blood loss can be subtle and occur over months or years. For this reason, once iron deficiency is detected, older men and postmenopausal women may be referred to a colorectal surgeon for a colonoscopy to rule out polyps or cancer, or for further assessment if internal hemorrhoids are suspected to be the cause [4][5].

Poor Absorption or Dietary Intake

Another reason for low iron status is dietary, which is not exclusive to older adults. Vegans are often low in dietary iron because they avoid consuming all animal products, the main source of heme, the most bioavailable form. Ovo-lacto vegetarians who consume eggs and dairy but avoid eating red meat and seafood such as oysters and clams also tend to have low iron status because these are rich sources of heme.

It is also not uncommon for older people to eat a narrower range of foods as they age, sometimes due to decreased appetite or a deterioration in their ability to chew, resulting from tooth loss.

A common symptom of celiac disease is low iron status, which is why when I have an adult male client of any age with low iron status (without any obvious reasons for it), I request a routine blood test (IgATTG) to rule that out. Since men don’t metastasize/have “periods”, asking for a requisition for this test in men with low iron makes sense. Since people with celiac disease may be asymptomatic, low iron in men of any age is often the only indication to test for it. One might assume that an older man without any symptoms would have already been tested for celiac disease at some point in his life, but sometimes a diagnosis is made only because someone requested the test. While a biopsy is needed to confirm celiac disease, an IgATTG test to screen for it makes sense in men with low iron lab results.

A Helicobacter pylori (H. pylori) infection can also result in low iron status due to decreased absorption, so requesting a test to rule out H. Pylori is reasonable if no other cause is apparent [5].

Acid-Blocker Medications and H2 Blockers / Antihistamines

Long-term use of Proton Pump Inhibitor (PPIs) medications, which are used to treat acid reflux, heartburn, ulcers, and gastroesophageal reflux disease (GERD), reduces stomach acid, resulting in decreased iron absorption [8]. Some common brand names of PPIs include Prilosec (omeprazole), Nexium (esomeprazole), Prevacid (lansoprazole), and Pantoloc (pantoprazole). In adults who have been taking PPIs long-term, a healthcare provider should monitor iron status (and bone status, which is a separate discussion!).

H2 blockers, also called H2 antihistamines, are another class of medications that reduce stomach acid by blocking histamine receptors in the stomach lining. Some common brand names include Zantac (ranitidine), which has been discontinued in Canada for a while, Pepcid and Pepcid AC (famotidine), and Tagamet (cimetidine). Monitoring iron status in older adults who frequently take these over-the-counter medications is important, but if healthcare providers don’t ask if people take them, they won’t know. I ask.

Note: While H2 blockers are most commonly used for heartburn or mild GERD, they are also used in conjunction with a “regular antihistamine”, also known as an H1 blocker or H1 anti-histamine, for the treatment of Mast Cell Activation Syndrome (MCAS). MCAS is a condition where mast cells release excessive histamine, causing symptoms including hives, flushing, stomach pain, diarrhea, headaches, and very low blood pressure. The use of both an H2 antihistamine (such as ranitidine (Zantac) along with an H1 antihistamine (such as cetirizine hydrochloride, called Reactine in Canada, and Zyrtec in the US) targets different types of histamine receptors, improving overall symptoms in MCAS. It is important to monitor iron status in those using H2 antihistamines long-term for MCAS.

Whether H2 blockers are used to reduce stomach acid or to manage the symptoms of MCAS, the reduction of stomach acid leads to decreased iron absorption, resulting in low iron status over time [8].

How Iron Is Tested

For adults over the age of 50 with symptoms of fatigue, weakness, shortness of breath, or increased hair loss, I will ask their doctor or clinic for a requisition for blood tests to assess iron status, including a Complete Blood Count (CBC), ferritin, transferrin saturation (TSAT) or serum iron, and Total Iron Binding Capacity (TIBC). If the results come back below lab normal values, then determining the underlying cause, or causes, is next.

Treatment Options for Low Iron

Determine the Cause

When blood tests come back out of range, investigations will include ruling out sources of bleeding, such as internal hemorrhoids that can cause undetectable blood loss while having a bowel movement, ulcers, or whether they may have undiagnosed celiac disease or an H. pylori infection [4][5].

Iron Supplementation

Oral iron supplements are effective for treating low iron in most older adults, and there are many different forms of iron — some with better absorption than others. There are a few newer iron formulations that cause no stomach upset or constipation, and alternate-day dosing can increase absorption [7][10]. Oral treatment will usually continue for several months until ferritin levels (ferritin being the storage form of iron) reach adequate levels, not only hemoglobin levels, which are the iron in red blood cells. In severe cases of iron-deficient anemia, intravenous (IV) iron infusions will often be recommended [9].

Practical Tips for Adults Over 50

Tell your healthcare provider — whether it’s your Physician or Dietitian if you feel more tired than usual, easily get out of breath, or have excessive hair loss, as these may indicate that you have low iron status. Routine lab tests can determine if low iron status is underlying the symptoms.

If you have been prescribed PPIs or H2 blockers and have been taking them for several months, someone on your healthcare team should be monitoring your iron status with periodic routine blood tests. If your doctor doesn’t mention it and you think you may have symptoms consistent with low iron, ask to have this tested.

The reason I ask my clients about the medications they take, including over-the-counter medicines and supplements, is to evaluate their existing lab work and identify any areas that may warrant further examination.

Should lab results come back out of range, before heading out to buy an “iron supplement,” it is important to learn about the different formulations that are now available, and the advantages and disadvantages of each (both side effects and costs). I provide my clients with a current comparison chart of the different formulations, including brand-name and generics, and will make recommendations on which type would be the most suitable for them.

Should your iron results come back lower than optimal but not indicating a deficiency, then you may want to consider taking a nutrition education session about how to increase iron absorption from food, and to learn about which foods and beverages interfere with iron absorption, so that you can decide on the best time of day to eat or drink those.

Final Thoughts

Doctors are sometimes hesitant to requisition blood tests to screen post menopausal women for low iron status because they no longer have a period; however, blood loss from menstruation is only one cause. Even in men or in post menopausal women who are not prescribed PPIs or H2 blockers, many regularly take over-the-counter antacid tablets that, over time, can affect iron status.

A colonoscopy is recommended for adults over 50 years every ten years to check for colon polyps or cancer, but unless specifically asked, most people won’t volunteer that they have hemorrhoids, which can bleed microscopically, resulting in low iron status. Since slow GI bleeding is often “silent” in older adults [11], having members of your healthcare team ask the right questions and request blood work when necessary is essential. I ask, and if there is an area that warrants further investigation, I will request routine lab tests to be sure.

More Info

If you are an older adult struggling with ongoing low iron status, I can help. Learn about me and the Healthy Aging and the Comprehensive Dietary packages that 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. British Columbia Women’s Hospital and Health Centre. Iron deficiency in adults. 2019. [https://www2.gov.bc.ca/gov/content/health/practitioner-professional-resources/bc-guidelines/iron-deficiency]
  2. Centers for Disease Control and Prevention. Data brief: Iron deficiency in U.S. adults. 2018. https://www.cdc.gov/nchs/products/databriefs/db519.htm. Accessed November 7, 2025.
  3. Merck Manual Professional Edition. (2024). Overview of microcytic anemia. Merck & Co., Inc. https://www.merckmanuals.com/professional/hematology-and-oncology/anemias-caused-by-deficient-erythropoiesis/overview-of-microcytic-anemia
  4. American Gastroenterological Association. Gastrointestinal evaluation of iron deficiency anemia guidelines. 2023. https://gastro.org/clinical-guidance/gastrointestinal-evaluation-of-iron-deficiency-anemia/. Accessed November 7, 2025.
  5. British Society of Gastroenterology. Iron deficiency in adults: guideline. Gut. 2021;70:203–228. https://pubmed.ncbi.nlm.nih.gov/34497146/. Accessed November 7, 2025.
  6. Medscape. Iron deficiency anemia guidelines. 2023. https://emedicine.medscape.com/article/202333-guidelines. Accessed November 7, 2025.
  7. Weiss G, Goodnough LT. How I treat anemia in older adults. Blood. 2024;143(3):205–215. https://ashpublications.org/blood/article/143/3/205/494702/. Accessed November 7, 2025.
  8. Ganz T, Nemeth E. Inflammation and iron metabolism in older adults. PMC. 2014;5:210–220. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4157323/. Accessed November 7, 2025.
  9. Macdougall IC, et al. IV iron therapy in older adults. PMC. 2006;12:115–124. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10808247/. Accessed November 7, 2025.
  10. Ashcroft DM, et al. Oral iron in older adults. Blood. 2024;143(3):225–234. https://www.cghjournal.org/article/S1542-3565(24)00410-5/fulltext. Accessed November 7, 2025.
  11. Fairweather-Tait SJ, Wawer AA, Gillings R, Jennings A, Myint PK. Iron status in the elderly. Mech Ageing Dev. 2014 Mar-Apr;136-137:22-8. doi: 10.1016/j.mad.2013.11.005. Epub 2013 Nov 22. PMID: 24275120; PMCID: PMC4157323. Accessed November 7, 2025. [https://pmc.ncbi.nlm.nih.gov/articles/PMC4157323/]
 
Nutrition is BetterByDesign
 

Privacy Policy | Terms of Use

 

© 2025 BetterByDesign Nutrition Ltd.

LEGAL NOTICE: The contents of this blog, including text, images, and cited statistics, are for informational purposes only. The content is not intended to be a substitute for professional medical advice, diagnosis, or treatment. Always seek the advice of your physician or other qualified health provider with any questions you may have regarding a medical condition. Never disregard professional medical advice or delay in seeking it because of something you have read in this content.

Histamine Intolerance, MCAS and How Dietary Changes Help

Introduction

Adverse reactions to food can be broadly categorized as either food allergies or food intolerances. A food allergy is an IgE antibody-mediated immune reaction that can range from mild itching to life-threatening anaphylaxis. In contrast, a food intolerance is a non-immune reaction, such as the enzyme deficiency seen in lactose intolerance. Histamine intolerance and Mast Cell Activation Disorder (MCAD)—also known as Mast Cell Activation Syndrome (MCAS)—fall into this category. While rarely life-threatening, these conditions can make daily life quite miserable for those affected.

What is Histamine?

Most people recognize the term “antihistamine” in the context of seasonal allergies, but histamine itself performs many helpful functions, such as stimulating stomach acid production. In the immune system, histamine acts as a defense mechanism. When the body perceives a threat, mast cells release histamine, causing inflammation to signal the immune system to respond. However, in histamine intolerance or MCAD, histamine either isn’t broken down properly or is released inappropriately when no actual allergen is present.

Understanding the Histamine “Bucket”

Histamine intolerance is often compared to an overflowing “bucket.” Normally, histamine is rapidly degraded by two enzymes: diamine oxidase (DAO), which works primarily in the digestive tract, and histamine-N-methyltransferase (HNMT), which deactivates histamine at the receptor level throughout various body tissues. If these enzymes are dysfunctional, histamine accumulates. This differs from Mastocytosis (too many mast cells) or MCAD (mast cells that “spill” their contents inappropriately), though all these disorders result in high histamine levels.

The Four Types of Histamine Receptors

Histamine binds to four specific receptors, each causing different systemic reactions:

  • H1 Receptors: Involved in allergic rhinitis (sneezing), asthma symptoms, and enlarging blood vessels.
  • H2 Receptors: Stimulate stomach acid release and modulate the immune response.
  • H3 Receptors: Affect neurotransmitter release in the central nervous system, including serotonin.
  • H4 Receptors: Found in bone marrow, white blood cells, and the digestive tract.

Common Dietary Triggers

Some foods are naturally high in histidine, which converts to histamine during digestion. High-histamine foods include aged cheeses, yogurt, fermented vegetables like kimchi or sauerkraut, smoked fish, and alcohol. Additionally, some “histamine liberators” like chocolate and tomatoes can trigger mast cells to release their own stored histamine, adding further to the body’s total load.

Symptoms and Diagnosis

Symptoms are incredibly diverse, often leading to misdiagnosis as Irritable Bowel Syndrome (IBS) or simple food poisoning. Gastrointestinal distress can occur within minutes or several hours after eating. Non-GI symptoms include skin hives, facial flushing, heart palpitations, extreme fatigue, and “brain fog.” Because these symptoms appear unrelated, it takes an average of 14 years for a patient to be properly diagnosed with MCAD, usually through an immunologist or allergist.

More Info?

Learn about me and the dietary support I provide for Mast Cell Activation Syndrome (MCAS), Ehlers-Danlos Syndrome – hypermobility subtype (hEDS), Postural Orthostatic Tachycardia Syndrome (POTS), and histamine intolerance. View my Therapeutic Diet Services page.

To your good health!

Joy

You can follow me on:

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

References

  1. Baily N. Histamine Intolerance. Igennus Healthcare Nutrition. [https://www.slideshare.net/igennus/managing-histamine-intolerance-80982438]
  2. Molderings GJ, Brettner S, Homann J, et al. Mast cell activation disease: a concise practical guide for diagnostic workup and therapeutic options. Journal of Hematology & Oncology. 2011 Mar 22;4:10. [https://doi.org/10.1186/1756-8722-4-10]
  3. Hamilton MJ, et al. Mast cell activation syndrome: A newly recognized disorder with systemic clinical manifestations. Journal of Allergy and Clinical Immunology. 2011;128(1):147-152. [https://doi.org/10.1016/j.jaci.2011.04.037]
  4. Jernigan D. Histamine Intolerance Syndrome. Hansa Center for Optimal Health. [https://www.marioninstitute.org/histamine-intolerance-syndrome/]
 
Nutrition is BetterByDesign
 

Privacy Policy | Terms of Use

 

© 2025 BetterByDesign Nutrition Ltd.

LEGAL NOTICE: The contents of this blog, including text, images, and cited statistics, are for informational purposes only. The content is not intended to be a substitute for professional medical advice, diagnosis, or treatment. Always seek the advice of your physician or other qualified health provider with any questions you may have regarding a medical condition. Never disregard professional medical advice or delay in seeking it because of something you have read in this content.

Milk Intolerance May be Caused by A1 Beta-Casein

NOTE: This article was written and posted on July 21, 2019, and was completely updated and expanded on December 29, 2025.


Introduction

Digestive issues resulting from milk consumption are frequently attributed to lactose intolerance. However, emerging clinical research indicates that for many, the culprit is actually an intolerance to a specific protein variant found in most commercial cow’s milk: A1 beta-casein. Understanding the difference between A1 and A2 milk proteins is essential for those who suffer from persistent gastrointestinal distress, as well as those managing complex chronic conditions involving mast cell activation and autonomic dysfunction.

The History of A1 and A2 Beta-Casein

Casein makes up approximately 80% of the protein in milk, and beta-casein accounts for about 30% of that total. Originally, all domesticated cows produced milk containing only the A2 variant of beta-casein. This is the same variant found in human breast milk, as well as milk from goats, sheep, and buffalo. Approximately 8,000 years ago, a genetic mutation occurred in Holsteins, leading to the production of the A1 protein. Today, Holsteins are the primary dairy breed in North America and Northern Europe, meaning most commercially available milk contains a mix of both A1 and A2 proteins.

Why A1 Milk Causes Inflammation

The difference between A1 and A2 beta-casein comes down to a single amino acid at the 67th position of the protein chain. In A2 milk, this position is held by proline. In A1 milk, it is held by histidine. When A1 milk is digested, this histidine bond breaks, creating a peptide called beta-casomorphin-7 (BCM-7). BCM-7 is an opioid peptide that can slow down gastrointestinal transit time and increase inflammatory markers, leading to symptoms that mimic lactose intolerance, such as bloating and abdominal pain.

The “Trifecta” Connection: MCAS, POTS, and EDS

For patients managing the “Trifecta” of Mast Cell Activation Syndrome (MCAS), Postural Orthostatic Tachycardia Syndrome (POTS), and Ehlers-Danlos Syndrome (EDS), the choice of dairy is a critical clinical intervention rather than a minor dietary preference.

MCAS: The Histamine Liberator

BCM-7, the peptide produced during A1 digestion, is a potent “histamine liberator.” In MCAS, mast cells are hyper-reactive; BCM-7 can act as a direct chemical trigger, causing these cells to degranulate and release histamine and other inflammatory mediators systemically [4, 9, 11].

POTS: Autonomic and Motility Interference

Because BCM-7 binds to opioid receptors in the gut, it significantly slows motility [5, 6]. Furthermore, the histamine release triggered by A1 milk causes vasodilation (widening of blood vessels). For POTS patients already struggling with blood pooling, this can exacerbate heart rate spikes and lightheadedness [12].

EDS: Connective Tissue and Permeability

Fragile connective tissue in EDS often results in increased intestinal permeability (“leaky gut”). This may allow larger fragments of the inflammatory BCM-7 peptide to enter systemic circulation more readily, driving the chronic inflammatory state that often accompanies hypermobility disorders [13].

Practical Steps for Relief

If you suspect a sensitivity to A1 proteins, consider switching to A2-only sources. This includes goat’s milk, sheep’s milk, or milk from specific “heritage” cow breeds like Jerseys or Guernseys. It is also worth noting that butter and full-fat whipping cream are almost entirely fat and do not contain significant amounts of casein, meaning they are generally well-tolerated regardless of the source. For many, switching to A2 dairy allows them to enjoy milk products again without inflammation or GI upset.

More Info?

I used to offer a Food Allergy/Food Sensitivity Package; however, most people would be seeking services based on IgG Food Sensitivity tests purchased through a naturpath. rather than IgE-mediated test results obtained through an allergist.  I continue to support those diagnosed with IgE-mediated food allergies and, depending on the severity, will usually do so within the context of add-on services to the Comprehensive Dietary Package. You can learn about me here.

To your good health!

Joy

You can follow me on:

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

References

  1. Ware M. A2 milk: What you need to know. Medical News Today. 2017. [https://www.medicalnewstoday.com/articles/318577.php]
  2. Pasin G. A2 milk facts. California Dairy Research Foundation. 2017. [http://cdrf.org/2017/02/09/a2-milk-facts/]
  3. European Food Safety Authority. Review of the potential health impact of β-casomorphins and related peptides. EFSA Journal. 2009. [https://doi.org/10.2903/j.efsa.2009.231r]
  4. Kurek M, Przybilla B, Hermann K, et al. A naturally occurring opioid peptide from cow’s milk, beta-casomorphine-7, is a direct histamine releaser in man. International Archives of Allergy and Immunology. 1992;97(2):115-20. [https://doi.org/10.1159/000236106]
  5. Pal S, Woodford K, Kukuljan S, et al. Milk intolerance, beta-casein and lactose. Nutrients. 2015;7(9):7285-97. [https://doi.org/10.3390/nu7095339]
  6. Ho S, Woodford K, Kukuljan S, et al. Comparative effects of A1 versus A2 beta-casein on gastrointestinal measures. European Journal of Clinical Nutrition. 2014;68(9):994-1000. [https://doi.org/10.1038/ejcn.2014.127]
  7. Jianqin S, et al. Effects of milk containing only A2 beta casein versus milk containing both A1 and A2 beta casein proteins on gastrointestinal physiology. Nutrition Journal. 2016;15:35. [https://doi.org/10.1186/s12937-016-0147-z]
  8. He M, Sun J, Jiang ZQ, et al. Effects of cow’s milk beta-casein variants on symptoms of milk intolerance in Chinese adults. Nutrition Journal. 2017;16(1):72. [https://doi.org/10.1186/s12937-017-0275-0]
  9. Molderings GJ, et al. Mast cell activation disease: a concise practical guide for diagnostic workup and therapeutic options. Journal of Hematology & Oncology. 2011;4:10. [https://doi.org/10.1186/1756-8722-4-10]
  10. Swiss Interest Group Histamine Intolerance (SIGHI). Histamine Intolerance Food Compatibility List. [https://www.mastzellaktivierung.info]
  11. Stepnik M, & Kurek M. (2002). The influence of bovine casein-derived exorphins on mast cells in rodents. ResearchGate. [https://www.researchgate.net/publication/223521751]
  12. POTS UK. (2025). Mast Cell Activation Syndrome – Associated Conditions. [https://www.potsuk.org/about-pots/associated-conditions/mcas/]
  13. The EDS Clinic. (2025). POTS and MCAS: What is the link? [https://www.eds.clinic/articles/mast-cell-activation-syndrome-postural-orthostatic-tachycardia-syndrome]
 
Nutrition is BetterByDesign
 

Privacy Policy | Terms of Use

 

© 2025 BetterByDesign Nutrition Ltd.

LEGAL NOTICE: The contents of this blog, including text, images, and cited statistics, are for informational purposes only. The content is not intended to be a substitute for professional medical advice, diagnosis, or treatment. Always seek the advice of your physician or other qualified health provider with any questions you may have regarding a medical condition. Never disregard professional medical advice or delay in seeking it because of something you have read in this content.

Arthritis is Not a Normal Part of Aging

Many people mistakenly believe that arthritis is a normal part of the aging process, but many older adults never get it and most of the people that are diagnosed with it are under the age of 65 years old. In fact,  2/3 of those diagnosed are not seniors, and some include children.

US statistics report that almost 1/4 ( 22.7%) adults have doctor-diagnosed arthritis — with significantly higher age-adjusted prevalence in women (23.5%) than in men (18.1%). While arthritis is not a normal part of aging, the likelihood of getting a diagnosis increases with age[1]. Only 7.3% of adults aged 18 to 44 years have been diagnosed arthritis, almost 50% (49.7%) of adults aged 65 years of age have been diagnosed[1].

There are different types of arthritis, including osteoarthritis (OA), rheumatoid arthritis (RA), ankylosing spondylitis, gout, and juvenile arthritis. More on each of these, below.

Osteoarthritis (OA)

Osteoarthritis (OA) is the most common form of arthritis and is a degenerative joint disease that results from a breakdown of the cartilage within a joint. This breakdown results in the bone actually changing, or remodeling in order to try and accommodate the lack of cartilage. The bone does this by producing bone overgrowth called osteophytes, or ‘bone spurs’. An osteophyte is a smooth, bony deposit that grows slowly over time, and often has no symptoms but can be painful if they impinge on nerves or affect the movement of the joint. It most commonly occurs in the hands, hips, and knees and changes usually develop slowly, and get worse over time. OA can cause stiffness, swelling and pain and in some cases it results in some people are no longer able to do daily tasks.

Rheumatoid Arthritis (RA)

Rheumatoid arthritis (RA) an autoimmune and inflammatory disease where the body’s immune system attacks healthy cells in the body, resulting in inflammation and painful swelling. It mainly attacks the joints in the hands, wrists, and knees, and often many joints at once. In a joint with RA, the lining of the joint becomes inflamed, causing damage to joint tissue and this damage is what results in chronic pain, difficulty with mobility and joint deformity.

Ankylosing Spondylitis (AS)

Ankylosing spondylitis (AS) is the most common form of a group of inflammatory arthritis called spondyloarthritis and is an autoimmune disease, which means it is caused by the body’s immune system attacking healthy tissue. AS leads to rigidity of the spine, and the sacroiliac (SI) joints which attach the pelvis (hips) to the base of the spine. Ankylosing’ means “fusing” and spondylitis’ means “inflammation of the spine”. AS 

Gout

Gout is a form of inflammatory arthritis that usually affects one joint at a time, (often the big toe joint. In this form, symptoms wax and wane, with times where there are symptoms being known as ‘flares’. Gout is associated with high levels of uric acid, which can also contribute to kidney stones, so controlling the level of uric acid through diet may be part of treatment.  This includes keeping levels of purine-containing foods constant (not eliminating them). Repeated bouts of gout can lead to ‘gouty arthritis’; a worsening form of arthritis.

Juvenile (childhood) Arthritis

The most common type of childhood arthritis is ‘juvenile idiopathic arthritis’  (JIA), which is also known as juvenile rheumatoid arthritis (J-RA) which can cause permanent physical damage to joints and make it hard for the child to do everyday tasks such as walking, or even getting dressed by themselves.

Arthritis, Other Conditions and Quality of Life

Arthritis in adults is more common in people with other chronic health conditions, including;

– 31% of those with arthritis are obese
– 47% of those with arthritis have diabetes
and
– 49% have heart disease [1].

This isn’t all that surprising given that all of these conditions are linked to different types of systemic inflammation.

Having any of these other chronic conditions ⁠— along with arthritis makes it all the more difficult for people to enjoy life. The pain associated with arthritis may be a barrier to physical activity for those with heart disease[1] and those who are overweight or obese already struggle with having little energy to be active and the pain of arthritis only makes that more difficult [2]. 

That said, physical activity ⁠— whether it is simple aerobic activity like walking or swimming or strength / resistance training can benefit all of those conditions, so reducing the pain in arthritis is an important key to being able to be active, and have a much improved quality of life.

Reducing Inflammation – the role of an Anti-inflammatory Protocol

Many people when they get diagnosed with arthritis want to know if there is an “arthritis diet”.  There is no diet specific to people diagnosed with arthritis, except perhaps a diet that lowers uric acid in those with gout, however eating in such a way as to lower inflammation can help a great deal!

I have offered an Anti-Inflammatory Protocol for close to ten years and recently completely updated the materials that I used to teach it, as well as the 27 pages of handouts I provide, in light of the most current research.

The goal of the Anti-Inflammatory Protocol is simple: to reduce stiffness and pain by lowering inflammation. It is divided into 3 sessions of an hour each and covers everything from the components of foods that contribute to inflammation; from grains and seed oils, to otherwise ‘healthy’ foods and even that may make symptoms worse and why, as well as those that are fine to use. I provide teaching on “nightshades” and the reasons why these should be limited and provide a list of fruits, vegetables and spices are in this family. I teach about the effect of alcohol and sugar alcohols used as sugar-substitutes and their effect on inflammation, as well as different gums and thickeners that are commonly used in many food products and that can contribute to inflammation.

My purpose in offering this package is to help those diagnosed with arthritis (and other inflammatory conditions) to improve their quality of life.

As well, I understand what it’s like to live with osteoarthritis (which I was diagnosed with in my 20’s) and the need to reduce symptoms, through diet whenever possible.

More Info?

If you would like more information, you can learn about me and the Comprehensive Dietary Package that I offer.

To your good health!

Joy

You can follow me on:

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

Copyright ©2019 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.

References

  1. Barbour KE, Helmick CG, Boring MA, Brady TJ. Vital signs: prevalence of doctor-diagnosed arthritis and arthritis-attributable activity limitation — United States, 2013—2015. Morb Mortal Wkly Rep. 2017;66:246—253. DOI: http://dx.doi.org/10.15585/mmwr.mm6609e1External.
  2. Hootman JM, Murphy LB, Helmick CG, Barbour KE. Arthritis as a potential barrier to physical activity among adults with obesity—United States, 2007 and 2009. Morb Mortal Wkly Rep. 2011;60(19):614—618. PubMed PMID: 21597454

 

Three Ways to Put Type 2 Diabetes into Remission

According to the scientific literature to date, there are three ways of putting type 2 diabetes into remission, but an article that was widely circulated on social media earlier this week implied that a ketogenic diet ‘cures’ type 2 diabetes.

The article was titled “What If They Cured Diabetes and No One Noticed?”[1] and said;

“So you’d think that if someone figured out a way to reverse this horrible disease, there would be big bold headlines in 72-point type. You’d think the medical community, politicians and popular press would be shouting it from the rooftops.

Guess what? Someone did. Yet it appears no one noticed.

The cure was simple — so simple, in fact, that it involved no medication, no expensive surgery and no weird alternative supplements or treatments.

What was this miracle intervention? Diet. Specifically, the ketogenic diet.”

The author is entitled to hold the above opinion and to express it, however in my opinion, a ketogenic diet does not “reverse diabetes” — it does not “cure” it. It is one of three scientifically documented ways to put the disease into remission. More on that below.

The distinction between “reversing diabetes” and “reversing the symptoms of diabetes” is very important, and more than a matter of semantics. In an article I posted last year titled The Difference Between Reversal and Remission of Type 2 Diabetes, I wrote that;

“Reversal” of a disease implies that whatever was causing it is now gone and is synonymous with using the term ”cured”.  In the case of someone with Type 2 Diabetes, reversal would mean that the person can now eat a standard diet and still maintain normal blood sugar levels. But does that actually occur? Or are blood sugar levels normal only while eating a diet that is appropriate for someone who is Diabetic, such as a low carbohydrate or ketogenic diet, or while taking medications such as Metformin?

If blood sugar is only normal while eating a therapeutic diet or taking medication then this is not reversal of the disease process, but remission of symptoms.”

I believe that claiming that a keto diet ‘cures diabetes’ or ‘reverses the disease’ does the public a disservice:

  • Firstly, it implies that there is simple, free ‘cure’ that will work for everybody.  As I outline below; some people are able to achieve partial or complete remission of their symptoms following a keto diet, and others are not.
  • Secondly, it implies that there is a simple, free ‘cure’ available, but that it is being ‘withheld’ for some reason — either because doctors don’t know about or are afraid what colleagues might think, or because the agricultural and pharmaceutical industries have ‘big bucks to lose’ by people limiting their intake of bread, pasta and insulin.

There is no question that physicians (and all clinicians) need to be selective about recommending a keto diet for their patients / clients and to be able to document from the literature that it is safe, effective and best clinical practice for the condition for which it is recommended, and appropriate for the individual.

While falling markets for specific types of food products and drugs certainly have an impact on the economics of both the agricultural industry and pharmaceutic industry, it comes across like a ‘conspiracy theory’ to imply there is a ‘cure’ available out there, but that the public is being ‘denied’ access to it by “big food” and “big pharma”.

  • Finally, it implies that if people are unable to ‘reverse their diabetes’ and get ‘cured’ following a keto diet, that it is their fault; they mustn’t have done it properly.  Even if we substitute the terms and say instead “put their diabetes into remission” or “reverse the symptoms of diabetes”, it is unreasonable and unfair to assume that everyone will be successful in doing so, and if they aren’t, the responsibility falls on them.

There is no “one-sized-fits-all-diet” that is good for everybody, nor is there a “better” dietary means to achieve remission of type 2 diabetes. As I will elaborate on below, there are 3 ways to put the symptoms of type 2 diabetes into remission, with two of them being dietary,  and some might prefer one over the other for a variety of reasons. The one that they want to adopt and ‘stick with’ will be the one that will work best for them.

Virta Health Data

The on-going study from the Virta Health has had over 200 adults ranging in age from 46-62 years of age in the intervention group following a ketogenic diet for the last two years, so far. At the one year mark, participants in the ketogenic diet group lowered their glycated hemoglobin (HbA1c) to 6.3% (from 7.7% at the beginning of the study) —  with 60% of them putting their type 2 diabetes into remission based on HbA1C levels >=6.5% (American Diabetes Association and Diabetes Canada guidelines).  HbA1C rose slightly to 6.7% at two years. The keto group did considerably better than the ‘usual care group’ whose average HbA1C actually rose to 7.6% at one-year (from 7.5% at the beginning of the study), and rose again to 7.9% at two years [3]. 

Fasting blood glucose of the intervention group following a keto diet increased slightly from  127 mg/dl (7.0 mmol/L) at one year to 134 mg/dl (7.4 mmol/l) at two years, which was considerably better than the usual care group, whose fasting blood glucose was 160 mg/dl (8.9 mmol/L) at one-year and 172 mg/dl (9.5 mmol/L) at two years [3].

The data so far demonstrates that a well-designed keto diet can be a very effective means of reversing the symptoms of type 2 diabetes, and that it is more effective than what was ‘standard care’ (prior to the new ADA guidelines), but it is by no means a ‘cure’.

Dr. Stephen Phinney and the research team at Virta Health have written on the Virta Health website [3];

“A well-formulated ketogenic diet can not only prevent and slow down progression of type-2 diabetes, it can actually resolve all the signs and symptoms in many patients, in effect reversing the disease as long as the carbohydrate restriction is maintained.” [2]

That is, the Virta researchers state that a well-designed keto diet can resolve the signs and symptoms of the disease in many people, which “in effect” (i.e. ‘is like’) reversing the disease —  as long as the carbohydrate restriction is maintained. They don’t promote the diet as a ‘cure’, but as an effective treatment, which it is.

There is no question that Virta’s results are impressive — so much so that their studies have been included in the reference list of the American Diabetes Association’s (ADA) new Consensus Report of April 18, 2019, where the ADA included adopted the use of both a low carb and very low carb (ketogenic) diet (20-50 g of carbs per day) as one of the management methods for both type 1 and type 2 diabetes in adults. You can read more about that here.

In fact, the ADA said in that report that;

Reducing overall carbohydrate intake for individuals with diabetes has demonstrated the most evidence for improving glycemia*’

* blood sugar

…but a keto diet is not a ‘cure’ for type 2 diabetes.

At this present time, there is no cure for diabetes. There are, however three documented ways to put type 2 diabetes into remission;

  1. a low calorie energy deficit diet [4,5,6]
  2. bariatric surgery (especially use of the roux en Y procedure) [7,8]
  3. a ketogenic diet [3]

Final Thoughts…

I believe that based on what has been published to date, it is fair to say that a well-designed ketogenic diet can;

  • prevent progression to type 2 diabetes, when adopted early in pre-diabetes
  • slow down progression of type 2 diabetes
  • resolve the signs and symptoms of the type 2 diabetes
  • serve in effect like reversing the disease, provided carbohydrate restriction is maintained

…but to claim that a keto diet ‘cures’ type 2 diabetes is simply incorrect.

A ketogenic diet is a safe and effective option for those wanting to put the symptoms of type 2 diabetes into remission. So is a calorie restricted diet. The primary difference is in a calorie restricted diet, calories are drastically reduced in order to lose weight and feeling hungry is simply a side-effect that people come to expect.  In a low carb or ketogenic diet, calories end up being substantially reduced as an inadvertent result of targeting protein and vegetables and adding sufficient healthy fat that comes along with that protein, or that are added to the vegetables to make them more interesting, while limiting carbohydrates.  One isn’t better than the other; it is what is better suited to each individual.

More Info?

If you would like more information, you can learn about me and the Comprehensive Dietary Package that I offer.

To your good health!

Joy

You can follow me on:

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

 

Copyright ©2019 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.

References

  1. Steel, P, “What If They Cured Diabetes and No One Noticed? – if the ketogenic diet can reverse diabetes, why isn’t your doctor recommending it?”, The Startup, July 13 2019, https://medium.com/swlh/what-if-they-cured-diabetes-and-no-one-noticed-keto-diet-ketogenic-virta-study-d49c195bf8f5
  2. Phinney S and the Virta Team, Can a ketogenic diet reverse type 2 diabetes? https://blog.virtahealth.com/ketogenic-diet-reverse-type-2-diabetes/
  3. Athinarayanan SJ, Adams RN, Hallberg SJ et al, Long-Term Effects of a Novel Continuous Remote Care Intervention Including Nutritional Ketosis for the Management of Type 2 Diabetes: A 2-year Non-randomized Clinical Trial.  preprint first posted online Nov. 28, 2018;doi: http://dx.doi.org/10.1101/476275.
  4. Lim EL, Hollingsworth KG, Aribisala BS, Chen MJ, Mathers JC, Taylor R. Reversal of type 2 diabetes: normalisation of beta cell function in association with decreased pancreas and liver triacylglycerol. Diabetologia2011;54:2506-14. doi:10.1007/s00125-011-2204-7 pmid:21656330
  5. Steven S, Hollingsworth KG, Al-Mrabeh A, et al. Very low-calorie diet and 6 months of weight stability in type 2 diabetes: pathophysiological changes in responders and nonresponders. Diabetes Care2016;39:808-15. doi:10.2337/dc15-1942 pmid:27002059
  6. Lean ME, Leslie WS, Barnes AC, et al. Primary care-led weight management for remission of type 2 diabetes (DiRECT): an open-label, cluster-randomised trial. Lancet2018;391:541-51.
  7. Cummings DE, Rubino F (2018) Metabolic surgery for the treatment of type 2 diabetes in obese individuals. Diabetologia 61(2):257—264.
  8. Madsen, L.R., Baggesen, L.M., Richelsen, B. et al. Effect of Roux-en-Y gastric bypass surgery on diabetes remission and complications in individuals with type 2 diabetes: a Danish population-based matched cohort study, Diabetologia (2019) 62: 611. https://doi.org/10.1007/s00125-019-4816-2

Trouble-shooting Ongoing Constipation on a Low Carb Diet

Constipation is one of the most common problems that people face, with between 2 and 28% of the population in Western countries reporting having this [1-3]. In 2007 in the United States, 19.4% of people reported problems with chronic constipation[4] and in Canada between 15% and 27% of people reported having sought health care support for chronic constipation in 2001 [5].

Defining Constipation

The term “constipation” means different things to different people. For some it simply means they don’t pass their stools (feces) often enough, and for others it means that when they do, their stools are hard, difficult to pass, may cause lower abdominal discomfort, or feel like they “still have to go” afterwards (incomplete evacuation).

What is considered a ‘normal range’ in the number of bowel movements per week varies considerably; from anywhere from 3 – 21 times per week, provided the stools are soft and easy to pass, but not loose or unformed.

For some people, having bowel movements 3 times per week may be normal, as long as their stools aren’t hard, dry or compact and there is no abdominal discomfort. For others, 3 times per day (21 times per week) may also be considered fine, provided the stools aren’t unusually loose. There are many factors that can contribute to chronic constipation; including some medications that people take, inadequate fiber or the wrong kind of fiber, insufficient hydration (not drinking enough water, especially when its hotter out, or exercising), high levels of estrogen and progesterone when a woman is pregnant, or disorders such as Irritable Bowel Syndrome (IBS) and diverticulosis.

The Causes of Chronic Constipation

People often think (or are told) that if they are constipated, they just need to eat more fiber, but in some cases increasing fiber from certain sources such as grains may make the problem worse. For example, some people are wheat sensitive, but not gluten-intolerant (i.e. not Celiac). That is, they are sensitive to wheat only, but not rye or barley (which also contain gluten).  Others have something called non-celiac gluten sensitivity which resolves when gluten is eliminated from the diet, yet don’t test positive for Celiac disease. These people feel better when they avoid grain-based carbs, and may opt instead for eating nutritiously-dense starchy vegetables, such as winter squash or yam, for instance. Since a low-carb diet is non-grain-based, people who experience chronic constipation due to wheat intolerance or non-celiac gluten sensitivity will start to feel considerably better eating this way.  The problem may be that for those with non-celiac gluten sensitivity, other sources of gluten, such as those found in malt vinegar or low carb beer may continue to cause them symptoms.

Many people who try a “low-carb” or “keto” diet on their own often complain of being constipated and this may be for a number of other reasons.  They may be taking a medication that causes constipation as a side-effect, they may not don’t drink enough water, or it may be the result of something else.

Inadequate Hydration

I would estimate that ~80% of the people that I assess in my office have observable signs that they are aren’t drinking enough water, so this is something I would recommend most people to consider as a possible contributor to chronic constipation.

The idea that everybody needs to drink “8 glass of water per day” is a fallacy; everyone’s need for water is different. A good rule of thumb to know if you are dehydrated is just to look in the mirror. If your lips are dry and wrinkled, then you probably should aim to increase your water intake. When your lips are plump and without deep lines, you’ve probably had sufficient amount. Water is best, as coffee and tea act as a mild diuretic. They won’t dehydrate you, but you will pass the water contained in them more rapidly.

If you don’t really like plain water, a Sodastream® that enables you to make carbonated water at home may be the answer. My clients know that there is always a bottle of it on my desk, as that is how I make sure to drink enough water. A twist of lime or lemon makes a nice treat too!

What about Getting Enough Fiber?

In Canada, dietary recommendations  for dietary fiber intake varies with age and gender. Men under the age of 50 years are recommended to take in 38 gm / day of dietary fiber, and men over 50 years to take in 30 gm / day. Women under 50 years old are recommended to take in 25 gm of fiber per day and over 50 years, 21 gm per day [6].

In the US, fiber intake recommendations from the Institute of Medicine range from 19 grams to 38 grams per day, depending on gender and age [7].

While people generally think of “healthy whole grains” as good sources of fiber, many are not. For example, medium grain brown rice only has 3.4 g of fiber per 100 g, whereas wild rice (which is actually a grass and not a grain) has 6.2 g of fiber per 100 g [8]. Many vegetables and fruit such as avocado and berries are excellent sources. More on that below.

Two Kinds of Fiber — soluble and insoluble

There are two kinds of fiber; insoluble and soluble.

Insoluble fiber is what most people think about when they think of ”roughage” needed to form stool and prevent constipation. It helps form the bulk of the stool. Insoluble fiber is naturally present in the outside of grains, such as whole grain wheat and the outside of oats and is also found in fruit, legumes (or pulses) such as dried beans, lentils, or peas, some vegetables, and in nuts and seeds. Many of these are eaten on a low carb diet and can provide the recommended amount of fiber (more on that below).

Soluble fiber forms a gel’ in the intestine and binds with fatty acids. It slows stomach emptying and helps to make people feel fuller for longer, as well as slow the rate that blood sugar rises, after eating. Soluble fiber absorbs water in the gut, and helps to form a pliable stool. Soluble fiber is found on the inside of certain grainssuch as oats, chia seeds or psyillium, as well as the inside of certain kinds of fruit such as apple and pear.

For those eating a low carb diet, getting enough fiber is not that difficult. Here are a few examples of the fiber content of foods that can be eaten;

  • Avocado — Surprisingly, avocado which is an excellent source of vegetable fat, is also high in fiber, having more than 10 gm fiber per cup (250 ml). Avocado grown in Florida which are the bright green, smooth-skinned variety have more insoluble fiber than California avocado, which are the smaller, darker green, dimpled variety.
  • Berries — Berries such as blackberries and raspberries are an excellent source of antioxidants, but also have 8 gm fiber per cup (250 ml).
  • Coconut — Fresh coconut meat has 6 gm of net carbs per 100 grams of coconut, but also packs a whopping 9 gms of fiber and is a very rich source of fat (33 gms per 100 gm coconut). It can be purchased peeled, grated and sold frozen in many ethnic stores or in the ethnic section of regular grocery stores.
  • Artichoke — Artichoke is a low-carbohydrate vegetable that is delicious boiled and it’s leaves dipped in seasoned butter. Surprisingly, one medium artichoke has over 10 gm of fiber.
  • Okra — Okra, or lady fingers’ is a staple vegetable in the South Asian diet and is commonly eaten in the Southern US. Just one cup of okra contains more than 8 gm of fiber.
  • Brussels Sprouts — These low-carb cruciferous vegetables are not just for Thanksgiving and Christmas dinner.  Split and grilled on the BBQ with garlic, they are a sweet, nutty addition to any meal, packing almost 8 gm of fiber per cup.
  • Turnip — Turnip, the small white vegetable with a hint of purple is not to be confused with the pale beige, larger rutabaga. Turnip contains almost 10 gm of fiber per cup. It is delicious pickled with salt and one beet and is commonly eaten with Middle Eastern food.

Irritable Bowel Syndrome (IBS) and Diverticulosis

Unfortunately, in addition to the fact that 20-30% of people in the US and Canada experience chronic constipation, approximately 10-15% of the population have Irritable Bowel Syndrome (IBS) [9].

IBS is a functional disorder of the gastrointestinal (GI) tract which means there is no structural or biological abnormality that can be measured on routine diagnostic tests. These people often experience chronic constipation, sometimes alternating with bouts of diarrhea, as often experience abdominal pain and bloating, as well. You can read more about IBS hereAs mentioned in the linked article, many people with IBS feel considerably better when they adopt a low-carb diet because they are no longer eating many of the foods that underlie their symptoms such as grains, milk and fruit, other than berries. Unfortunately, even after adopting a low carb diet about 15- 20% of those diagnosed with IBS still have residual symptoms. I have years of experiencing working with those with IBS and offer an IBS package as well as a low FODMAP package that can help.

Another common problem is diverticulosis, which an estimated 50% of those over 50 years of age have. Diverticulosis is where your colon (large intestine) has small ”pockets” in it called diverticula, which can cause a number of symptoms including chronic constipation. Like those with IBS, many people with diverticulosis feel much better when they adopt a low-carb diet because they are no longer eating foods such as wheat, dairy products with lactose or high fructose fruit that used to contribute to their symptoms. The problem is that many of the low carb vegetables that are low in carbs and may be rich in fiber also may be contributing to their symptoms. So many of my clients have recently been diagnosed with diverticulosis, that I have recently added a one-hour teaching session that can be added to the end of a package, or taken as a stand-alone session to help.

Final Thoughts

In trouble-shooting constipation, I recommend that people ensure they are adequately hydrated, and that they remember to drink extra water when it’s hot out or when they’ve been ill.

Eating wide variety of low-carb veggies, including those listed above that are known to be high in fiber is also good. For those on a moderate low-carb diet (not a ketogenic diet), small amounts of yam or winter squash are other ways to get added nutrients and fiber.

Berries are a wonderful source of nutrients and anti-oxidants, can be enjoyed by those on a low-carb diet and are a wonderful source of fiber! Strawberries have 3g of fiber per cup and blackberries and raspberries have a whopping 8 g of fiber per cup, with blueberries paling in comparison with a mere 2.4 g of fiber (and are higher in carbs, too).

Of course, exercise as simple as a daily walk can often help people move their bowels and many people swear by their morning cup of coffee!

For those doing all of the things above and still experiencing chronic constipation, it may be time to rule out other possible causes such as Celiac disease, or non-celiac gluten sensitivity, IBS, or diverticulosis.

I can help.

More Info?

If you would like more information, you can learn about me and the Comprehensive Dietary Package that I offer.

To your good health!

Joy

You can follow me on:

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

 

Copyright ©2019 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.

References

  1. Higgins PDR, Johanson JF, Epidemiology of constipation in North America: a systematic review, The American Journal of Gastroenterology 99(4); 750—759, 2004.
  2. Corazziari E, Definition and epidemiology of functional gastrointestinal disorders, Best Practice and Research: Clinical Gastroenterology, 18 (4); 613—631, 2004. 
  3. Harris LA, Prevalence and ramifications of chronic constipation, Managed Care Interface, 18 (8); 23—30, 2005.
  4. Johanson JF,  Kralstein J, Chronic constipation: a survey of the patient perspective, Alimentary Pharmacology and Therapeutics, 25(5); 599—608, 2007. 
  5. Pare P, Ferrazzi S, Thompson WG et al, An epidemiological survey of constipation in Canada: definitions, rates, demographics, and predictors of health care seeking, The American Journal of Gastroenterology, 96(11); 3130—3137, 2001.
  6. Health Canada, Fiber, https://www.canada.ca/en/health-canada/ services/ nutrients/fibre.html
  7. Institute of Medicine, Food and Nutrition Board. Dietary Reference Intakes: Energy, Carbohydrates, Fiber, Fat, Fatty Acids, Cholesterol, Protein and Amino Acids. Washington, DC: National Academies Press; 2005
  8. Source: US Department of Agriculture, Agricultural Research Service. 2014. USDA National Nutrient Database for Standard Reference, Release 27. Nutrient Data Laboratory Home Page, http://www.ars.usda.gov/ba/bhnrc/ndl.
  9. Foundation for Gastrointestinal Disorders (IFFGD),  https://www.aboutibs.org/facts-about-ibs/statistics.html

 

What is IBS and Why Do Symptoms Improve on a Low Carb Diet?

Quite a few physicians that I know that recommend a low-carb diet to their patients have mentioned to me that those who had previously been diagnosed with Irritable Bowel Syndrome (IBS) and who suffered for years reported significant improvements within a short time of adopting the dietary changes and have asked me why. That is the topic of this article.

Prior to expanding my Dietetic practice to include this low carb division a little over 4 years ago, my main focus was on helping people who were dealing with food allergies and food sensitivities; including Celiac disease, Mast Cell activation disorder (MCAD) / histamine intolerance, fructose intolerance and Irritable Bowel Syndrome  For many of my clients, it was the gastrointestinal (GI) symptoms that caused them to seek out my help in the first place.

What is IBS?

I have often thought of Irritable Bowel Syndrome (IBS) as the diagnosis that people receive when all the other possible options have been ruled out. For the most part, by the time people are told that they have IBS, they already know for sure that they don’t have Celiac disease or inflammatory Bowel Disease (IBD) such as Ulcerative Colitis or Crohn’s, and they don’t have diverticulosis ⁠—as each of those diagnoses are confirmed after a colonoscopy and/or a biopsy, and are often supported with underlying blood test results.

What makes IBS different is that it is a functional GI disorder ⁠— which means there is no structural or biological abnormality that can be measured on routine diagnostic tests.

Of course, a person experiencing a bout of diarrhea or constipation, or abdominal pain does not mean that person has a GI disorder or disease. Those symptoms could be the result of a virus, bacteria, food-borne illness (“food poisoning”) or food sensitivities. Once these have been ruled out, if the symptoms recur over and over again over time, then an investigation as to what else it could be is often begun.

How is IBS Diagnosed?

While many of the symptoms of IBS and Celiac disease can be quite similar, including diarrhea and abdominal pain and bloating, there are very specific indicators that a person may have Celiac disease that clinicians such as myself notice as evidence to request further testing. The first stage in ruling out Celiac disease is an ordinary blood test looking for an antibody to gluten. If that comes back positive, then the person is referred to a Gastroenterologist for an endoscopy. If the blood test is negative, the next step may be for the person to be scheduled for a colonoscopy.

A colonoscopy which is where the inside of the large intestine (colon) is examined using a flexible probe about 1/2″ in diameter that’s fitted with a light and telescopic camera at one end and endoscopy is where a fine, flexible probe fitted with a light and telescopic camera is inserted via the mouth to view the esophagus, stomach and the upper part of the small intestine.

Celiac disease will be ruled out or confirmed using endoscopy, as the upper small intestine is where the damage to the villi (little hair-like projections on the wall that increase the surface area in order to help absorb nutrients from food) will be visible, or not.

A colonoscopy enables the Gastroenterologist to see what the lining of walls of the colon look like and to look for physiological signs of diverticulosis (little bulges or “pouches” in the colon) or signs of inflammation and damage consistent with Inflammatory Bowel Disease (IBD), such as Ulcerative Colitis or Crohn’s and to rule out colon cancer.

If the endoscopy and colonscopy come back normal, the person is often told that their symptoms of diarrhea or constipation (or both alternating), flatulence (“gas”), bloating, abdominal pain or cramping, mucous in the stool is Irritable Bowel Syndrome (IBS).

Prevalence of IBS

According to the International Foundation for Gastrointestinal Disorders (IFFGD), approximately 10-15% of the population have IBS; with 40% having a mild form, 35% having a moderate form, and 25% having severe IBS. While many people think of IBS as being a woman’s health issue, 35% to 40%  of people with IBS are men and 60-65% are women [1].

IBS is so common, that it is estimated that 12% of all visits to primary care providers (family doctors) is related to symptoms of IBS [1].

Physicians will sometimes suggest their patients try following a “low-FODMAP diet” but since IBS is so common, there are many different diets called by this name that differ significantly. Even if the doctor provides guidance as to which low-FODMAP diet they should follow, people often eliminate a whole host of foods and wind up eating a very limited diet, with no way of knowing which food they stopped eating actually helped.

Why Eating a Low-Carbohydrate Diet often Improves IBS Symptoms?

A low-FODMAP diet eliminates sources of very specific carbohydrates that are fermented by the gut bacteria and that result in the increased gas production that underlies the classic IBS symptoms of abdominal pain and bloating, and the water flooding into the intestine in response to these fermented carbohydrate is what causes the very common symptom of diarrhea. The constipation results when the contractions of the colon are impaired, resulting in the stool sitting longer in the colon resulting in more and more of the water being re-absorbed.

When people eat a low-carb diet, they either eliminate or greatly reduce sources of fructose (the sugar found in fruit and many processed foods, especially processed condiments like ketchup) and significantly reduce one of the key sources of fructans (inulin) found in wheat; which is a highly fermentable carbohydrate. Galactans, another fermentable carbohydrate found in beans, lentils and legumes such as soy is also eliminated or greatly reduced which is why people with IBS feel so much better after beginning eating a low-carb diet!

Before I taught a low-carbohydrate approach, I used to have people take the IBS Package before the Complete Assessment Package, so we could find out what foods underlie their unpleasant symptoms and eliminate them before I designed their Meal Plan. Now, if they are planning to adopt a lower carb lifestyle anyway, then I recommend they don’t take the IBS Package, as it may not be necessary.  I recommend focus on them adopting a diet that greatly reduces the sources of the fermentable carbohydrates mentioned above, plus a few more that I tell them about and see how they feel. If their symptoms are gone, then there is no reason for them to take the IBS Package!  If however, they are feeling quite a bit better, but still have residual symptoms, then I suggest they take the IBS Package so that we can systematically determine what other non-FODMAP foods are contributing to them feeling unwell.

More Info?

If you would like more information, you can learn about me and the Comprehensive Dietary Package that I offer.

To your good health!

Joy

You can follow me on:

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

 

Copyright ©2019 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.

References

Foundation for Gastrointestinal Disorders (IFFGD),  https://www.aboutibs.org/facts-about-ibs/statistics.html

Have You Been Diagnosed with Diverticulosis?

Have you recently been told by your General Practitioner (CP) or gastroenterologist that you have “diverticulosis” and wonder how you should be eating differently to keep it from getting worse?

What is “diverticulosis”?

Diverticulosis is where your colon (large intestine) has small “pockets” in it called diverticula which can cause a number of symptoms or in some people, no symptoms at all.

Diverticula can vary in number from one to literally hundreds. Generally, diverticula increase in number and size over time and range in size from 0.5-1 cm (0.2-0.4 inch) in diameter to 2 cm (0.8 inch)[1]. Diverticulosis occurs in about 5% of adults younger than forty years old, but rise to at least 50% of those older than sixty, with 65% of those who older than 85 having diverticulosis[1].

These little pouches were once thought to be cause by a diet that was too low in fiber[1] which caused the stools to move too slowly though the colon, resulting in constipation. Based on this “fiber hypothesis”, the remedy was thought to be to eat a diet high in fiber; including whole grain bread, unprocessed wheat bran, porridge and fruit. For the last 50 years or so, increased fiber intake has been the recommendation for treatment of diverticulosis, including by the GI Society of Canada and the American Gastrolenterology Association recommends at least 25 g of fiber per day[2,3]. It was thought that increased fiber would increase the volume of the stool and thus require less straining to move the bowels and prevent weakening of the bowel wall, reducing the occurrence of these “pouches”.  Unfortunately, several recent studies have shed doubt on the “fiber hypothesis” [4-8].

Not only did a 2012 study find no association between a low fiber diet and diverticulosis [9], the study found that increasing total fiber intake in the form of grains, insoluble fiber and soluble fiber actually increased the prevalence of diverticulosis!

“People with the lowest fiber intake were 30% less likely to develop diverticula than people whose diets included the most fiber.” [9]

Subsequent studies have either found no association between the amount of fiber intake and diverticulosis [10] or that there was no association between diverticulosis and constipation symptoms [11].

These findings left researchers and clinicians with little evidence for continuing to recommend a high fiber diet in diverticulosis, but no alternative options.

ADDENDUM (July 17 2019): There are a number of hypotheses as to what causes diverticulosis with many thinking it could be related to colonic aging weakening of the smooth muscle bands, motor dysfunction, increased luminal pressure, as well of lack of dietary fiber.

Eating foods with soluble and insoluble fiber and drinking sufficient fluid is good, however the source of that fiber is now thought to be important, as I will outline below.

Logical Hypothesis for Diverticulosis

A recent hypothesis is that the increased pressure in the colon that resulted from the intake of so much fiber; particularly the types of fiber that are easily fermented by gut bacteria is what weakens the colon wall, resulting in these ‘pockets’ or diverticula.

What seemed to add credibility to this hypothesis is that historically (prior to WWII) diverticula were seen in a specific region of the colon (proximal colon) in people in Asian countries, with the condition only affecting the right side. This has been explained by the high prevalence of lactose intolerance (inability to digest the sugar in milk and dairy) which exists in Asians.  As well, the incidence of this right-sided diverticulosis has been lowest in European populations, where lactose intolerance is very low [12]. Similarly, in Western countries, most of the diverticula are on the left side of the colon, which is thought to be associated with the higher ingestion of wheat, compared historically to Asian countries [12]. 

Both lactose and the fructans in wheat are carbohydrates that are easily fermented by gut microbes and which results in high amounts of water being drawn into the colon, resulting in increasing pressure on the colon wall from the gas produced by the microbes, possibly leading to the creation of these diverticula. 

Of interest, consumption of wheat in Japan and in South Korea has increased considerably since WWII and there is now a considerably higher incidence of left colon diverticula now being observed there, as well [12].

Use of a low-FODMAP Diet in diverticulosis

FODMAPS is an acronym for fermentable oligosaccharides, disaccharides, monosaccharides and polyols (sugar alcohols) which are the specific types of carbohydrate that are fermented by the gut bacteria, resulting in increased gas production, abdominal pain, bloating and either diarrhea and constipation or a combination of both. These are very similar symptoms as are observed in Irritable Bowel (IBS) Syndrome and a low-FODMAP diet has long been used to minimize the symptoms in IBS, and is now being used to reduce the same symptoms in diverticulosis.

It is thought that use of a low-FODMAP diet in those with diverticulosis may reduce the occurrence of diverticulitis; which is painful inflammation of these diverticula that often requires medical treatment ranging from antibiotics and pain medication, to bowel resection as is common in Inflammatory Bowel Disease (IBD), such as Ulcerative Colitis and Crohn’s disease.

I offer a Diverticulosis Option for those who want to have specific nutrition education to help them reduce their symptoms and lower the likelihood of their disease progressing to diverticulitis.

Even if you are already following a low-carbohydrate diet and not eating wheat, foods with lactose or fruit, it’s important to know that there are a number of low carbohydrate vegetables that also contain some of these fermentable carbohydrates, as do many of the sugar alcohols many people following a low carb diets use. Reducing the intake of these specific vegetables and sticking to sweeteners that are low FODMAP can greatly help!

More Info

If you would like more information, you can learn about me and the Comprehensive Dietary Package that I offer.

To your good health!

Joy

You can follow me on:

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

 

Copyright ©2019 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.

References

  1. GI Society, Canadian Society of Intestinal research, https://badgut.org/information-centre/a-z-digestive-topics/diverticular-disease/
  2. Painter NS, Diverticulosis of the Colon and Diet. Br Med J. 1969 Jun 21;2(5659):764-5.
  3. American Gastroenterological Association. A Patient Guide: Managing Diverticulitis. Gastroenterology. 2015;149:1977—1978
  4. Tan KY, Seow-Choen F. Fiber and colorectal diseases: separating fact from fiction. World J Gastroenterol. 2007;13:4161—4167. 
  5. Unlu C, Daniels L, Vrouenraets BC, Boermeester MA. A systematic review of high-fibre dietary therapy in diverticular disease. Int J Colorectal Dis. 2012;27:419—427. 
  6. Peery AF, Sandler RS. Diverticular disease: reconsidering conventional wisdom. Clin Gastroenterol Hepatol. 2013;11:1532—1537. 
  7. Tursi A, Papa A, Danese S. Review article: the pathophysiology and medical management of diverticulosis and diverticular disease of the colon. Aliment Pharmacol Ther. 2015;42:664—684. 
  8. Elisei W, Tursi A. Recent advances in the treatment of colonic diverticular disease and prevention of acute diverticulitis. Ann Gastroenterol. 2016;29:24—32.
  9. Peery AF, Barrett PR, Park D, Rogers AJ, Galanko JA, Martin CF, Sandler RS. A high-fiber diet does not protect against asymptomatic diverticulosis. Gastroenterology. 2012;142:266—272
  10. Peery AF, Sandler RS, Ahnen DJ, Galanko JA, Holm AN, Shaukat A, Mott LA, Barry EL, Fried DA, Baron JA. Constipation and a low-fiber diet are not associated with diverticulosis. Clin Gastroenterol Hepatol. 2013;11:1622—1627
  11. Braunschmid T, Stift A, Mittlbí¶ck M, Lord A, Weiser FA, Riss S. Constipation is not associated with diverticular disease – Analysis of 976 patients. Int J Surg. 2015;19:42—45.
  12. Uno Y, van Velkinburgh JC. Logical hypothesis: Low FODMAP diet to prevent diverticulitis. World J Gastrointest Pharmacol Ther. 2016;7(4):503—512. doi:10.4292/wjgpt.v7.i4.503

 

 

Experts: WHO Draft Guidelines Excludes Key Facts and Studies

An analysis was published last week in the British Medical Journal which raised several important concerns about the World Health Organization (WHO)’s draft guidelines on fatty acids; including saturated fat.

The international group of 16 nutrition experts who wrote the paper are concerned as “many governments consider the WHO dietary guidelines to be state of the art evidence, translating them into regional and national dietary guidelines” [1].

In fact, this is exactly the case in Canada. The new Canada Food Guide that was just released on January 22, 2019 relied extensively on the WHO’s 2017 Guidelines for it’s policy regarding decreasing dietary saturated fatty acids (SFA), as indicated by the table below from pg. 5 of Health Canada’s Interim Evidence Update 2018 [2]. 

Pg 5 Health Canada’s Interim Evidence Update 2018 [2]

Regarding the significance of the WHO Guidelines, the authors wrote:

“These guidelines have potential health implications for billions of people, so the consistency of the science behind such recommendations and the validity of the conclusions are crucial”.

The authors state that the WHO, in their draft guidelines released in May 2018 “excluded some important aspects and studies” concerning evidence linking saturated fat intake and cardiovascular (CVD) risk.

“They [WHO] recommend reducing intake of total saturated fatty acids to less than 10% of total energy consumption and replacing with polyunsaturated fat and monounsaturated fat to reduce incidence of cardiovascular disease and related mortality. But this fails to take into account considerable evidence that the health effects vary for different saturated fatty acids and that the composition of the food in which they are found is crucially important.”[1]

The authors point out that the composition of the food in which the fatty acid is found has a substantial effect on lipid digestion and absorption, as well as the amount of emulsified fat that is found in the blood after a meal (postprandial lipemia), which “is an independent risk factor for cardiovascular disease.”[1]

The authors point out that recently there have been several meta-analyses of observational studies and randomized controlled trials (RCTs) that found that total saturated fat is NOT associated with coronary heart disease, cardiovascular disease, and all-cause mortality (i.e. deaths). In addition they report that a Cochrane analysis found no significant association between reducing saturated fatty acids and total mortality, cardiovascular disease deaths, fatal and non-fatal myocardial infarction (MIs), stroke, coronary heart disease events, and coronary heart disease deaths.

Continued Reliance on Surrogate Endpoints

The authors note that the WHO draft guidelines continue, as they have in the past to (1) rely heavily on “surrogate endpoints” of the effect of dietary saturated fat intake on the level of lipid and lipoproteins in the blood — and (2) ignores the food source of the saturated fat.

They raise three key points;

1. Not all saturated fatty acids are equal; the amount and even the direction of the effects (raises or lowers) both surrogate and long term endpoints vary, depending on which fatty acid is involved.

2. Influence of the food source that the fatty acid is found in; the authors note that it has still not been determined whether any changes in blood lipoproteins translates into a lowering of cardiovascular risk and death, regardless of food source.

“Most trials included in the meta-analysis did not investigate whole food sources of saturated fat.”[1]

That is, the studies that WHO considered compared the effect of diets supplemented with fats rich in saturated fatty acids — not the effect of saturated fats in a specific food matrix.

One example of saturated fat in a whole food matrix cited in the paper is one of eggs; where there is “no association with coronary heart disease, and there is a reduced risk of stroke, and that randomized control trial data show that two eggs a day has beneficial effects on cardiovascular disease biomarkers“. (table 1, [1]).

3. Using LDL cholesterol concentration as a marker for cardiovascular disease risk. As I’ve written about in several previous articles, the authors note that the degree to which LDL particles are atherosclerotic is determined by, among other things, their size.

“Small and medium LDL particles show the strongest association with risk of cardiovascular disease, whereas large particles show no association.” [1]

in fact, the authors point out as I did in a recent article about red meat and white meat “raising cholesterol”, that a rise in serum LDL cholesterol concentration from total saturated fat consumption has been linked to a parallel increase in particle size “so it might not translate into an
increased risk of cardiovascular disease.”[1]

Excluding Observational Studies and Prospective Cohort Studies

The authors point out that the WHO draft guidelines exclude two types of studies from consideration; observational studies and prospective cohort studies because they argue that the quality of the evidence is lower than from
analyses of RCTs, and that it was not possible to assess the potential differential effects of replacing saturated fatty acids with different nutrients.

The problem with this is that (1) observational studies enable assessing the association between saturated fat and cardiovascular disease  rather than simply looking at the association between surrogate endpoints” (i.e. saturated fat and LDL-c) and (2) observational studies enable examining of the actual foods that people eat, rather than just individual nutrients, as

“Longstanding evidence indicates that the food matrix is more important than its fatty acid content for predicting the effect of a food on risk of coronary heart disease.”

The authors concluded;

“A recommendation to reduce intake of total saturated fat
without considering specific fatty acids and food sources is not
evidence based
; will distract from other more effective food-
based recommendations; and might cause a reduction in the
intake of nutrient dense foods that decrease the risk of
cardiovascular disease, type 2 diabetes, other serious
non-communicable diseases, malnutrition, and deficiency
diseases and could further increase vulnerability to nutrient
deficiencies in groups already at risk.

Final thoughts

This analysis adds a critical academic “voice” to the concern of limited saturated fat intake which may translate a reduction in the intake of nutrient-dense whole foods.

In fact, this was precisely the concern that I raised in my recent article about the Canada Food Guide “Snapshot” which came out at the end of June and which linked an image of ultra-processed foods with the message “limit foods high in sodium, sugars or saturated fat”. After all, meat is high in saturated fat and cheese is high in saturated fat and sodium, but are these really the types of whole, real foods that Canadians should be advised to limit?

More Info?

If you would like more information, you can learn about me and the Comprehensive Dietary Package that I offer.

To your good health!

Joy

You can follow me on:

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

 

Copyright ©2019 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.

References

  1. Astrup A, Bertram HCS, Bonjour J-P et al, WHO draft guidelines on dietary saturated and trans fatty acids: time for a new approach? BMJ 2019; 366: l4137 doi: 10.1136/bmj.l4137
  2. Health Canada. Food, Nutrients and Health: Interim Evidence Update 2018. Ottawa: Health Canada; 2019.

Focus on Limiting Ultra Processed Food Not Saturated Fat & Sodium

Note: This article is a combination of a Science Made Simple article, with the references below and an editorial which provides my opinion.

Dietary advice ⁠— especially National Dietary Guidelines ought to give clear, consistent messages. It would seem that the new Canada Food Guide ‘snapshot’ outlined in the previous article may inadvertently cause considerable confusion as to which foods are healthy and which are not.

The new Canada Food Guide ‘snapshot’ released last week shows a photo of ultra-processed products as foods to avoid, yet the label beneath the photo reads “limit foods high in sodium, sugars or saturated fat” (see circled part of photo, below).

Canada Food Guide 'Snapshot'
Canada Food Guide ‘Snapshot’

In fact, when the image of these processed foods is clicked on the Health Canada website, it brings the reader to a page listing the “Benefits of Limiting Highly Processed foods” and has paragraphs below for Sodium, Sugars, and Saturated Fat. 

In my opinion, this conflates two issues. 

Advising people to limit ultra-processed food is not the same as advising them to limit saturated fat, sodium and sugar

There are many whole unprocessed foods and minimally processed foods such as meat, eggs, cheese, yogourt, olives and berries that have sustained humans through thousands of years of history that contain these elements and are unlikely to be responsible for our current epidemics of obesity, diabetes, hypertension and cardiovascular disease that we now face.

As mentioned in an earlier article about distinguishing between food and food-like products there is a big difference between the three categories of food as defined by the NOVA food classification system [2,3,4]. Unprocessed Foods such as meat, chicken, fish and eggs are whole, real food in their original state and Minimally Processed Foods such as cheese, yogourt or pickled and cured fish or meat or olives are foods that have been preserved in some fashion by curing, smoking or soaking in brine. Foods such as meat, eggs, cheese and olives may be high in saturated fat or sodium but have been part of the human diet for thousands of years without compelling evidence that these pose a risk to human health.

It may be helpful to recommend that people consume pickled, cured meat and fish in smaller quantities, not because these foods are high in saturated fat or sodium, but because many are now made in less traditional ways that involve the use of chemical additives.

The primary health concern that I see it is that Ultra Processed Foods is making up more than 50% of the Canadian (and American) diet and really isn’t food at all. These are manufactured products made from a combination of refined carbohydrates (including sugar) and seed oils and are convenient, hyper-palatable and cheap — and displace real food from the diet. In fact, some of the most addictive foods available to us are ultra processed foods; including breakfast cerealmuffins, pizza, cheeseburgers, French fries and fried chicken — and desserts such as chocolate, ice cream, cookies and cake, as well as the soda we wash them down with [5]. These ultra processed foods are full of “empty calories” / have little nutritional value, and full of refined fats and refined carbs. It is for this reason ultra processed should be limited — not because it is high in saturated fat and sodium. 

Even though fruit as we now know it has been bred over the last 50-100 years to be hyper-sweet, for metabolically healthy people there is still no comparison between natural whole fruit such as berries or an apple, and sugary pop. One is real, whole unprocessed food and the other is ultra processed.

In my opinion, it makes good sense for Health Canada to show a photo of ultra-processed foods as they had (above)with advice to limit them — but because they are ultra processed, not because they are high in saturated fat or sodium.

 

Shifting the Focus off Saturated Fat Based on the Evidence

As covered in several previous article on this site, while research does indicate that dietary saturated fat raises low density lipoprotein cholesterol (LDL-cholesterol) in the blood, distinction in these studies isn’t made between the small, dense LDL sub-fraction which is atherosclerotic, and the large, fluffy LDL which is not. This recent study makes this distinction; demonstrating that saturated fat from red meat and poultry raises the large, fluffy LDL and cardio-protective HDL, but not the small dense (atherosclerotic) LDL.

Epidemiological studies that do exist provide a very mixed picture of any possible association between saturated fatty acids and cardiovascular disease (heart disease and stroke); with recent studies finding no association [6,7]. Even more compelling, the data from the Prospective Urban and Rural Epidemiological (PURE) Study which was the largest prospective epidemiological study to date involving many different countries found that dietary saturated fat was actually beneficial; with those who ate the largest amounts of saturated fat having significantly reduced death rates and that those that ate the lowest amounts of saturated fat (6-7% of calories) had increased risk of stroke [8].

In addition, according to the Canadian Heart and Stroke Foundation position statement titled ”Saturated Fat, Heart Disease and Stroke” released in September 2015 [9], different saturated fatty acids (e.g. lauric, stearic, myristic and palmitic acids) have different effects on blood cholesterol, so we can’t simply lump all saturated fats together.

Focus on Where Change is Needed

I believe that national guidelines such as Canada’s Food Guide should focus on eliminating ultra-processed foods from the diet because these form almost half of caloric intake with little nutrients and displace real, whole nourishing food from the diet.

This makes good sense.

In my opinion, the linking of ultra processed foods to saturated fat and sodium as has been done in this most recent Canada Food Guide ‘snapshot’ will end up confusing the public that things like fried chicken and cheese are both equally unhealthy because they are high in saturated fat and salt.

It would be far more helpful to highlight the benefits of whole, unprocessed foods and minimally processed foods while encouraging the public to limit ultra-processed foods.

More Info?

If you would like more information, you can learn about me and the Comprehensive Dietary Package that I offer.

To your good health!

Joy

You can follow me on:

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

 

 

Copyright ©2019  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.

References

  1. Health Canada Snapshot: https://food-guide.canada.ca/en/?utm_source=canada-ca-foodguide-en&utm_medium=vurl&utm_campaign=foodguide
  2. Moubarac JC, Batal M, Martins AP, Claro R, Levy RB, Cannon G, et al. Processed and ultraprocessed food products: Consumption trends in Canada from 1938 to 2011. Can J Diet Pract Res. 2014 Spring;75(1):15-21.
  3. Monteiro CA, Moubarac J-C, Cannon G., Ng SW, Popkin B. Ultra-processed products are becoming dominant in the global food system. Obes Rev. 2013
  4. Moubarac JC. Ultra-processed foods in Canada: consumption, impact on diet quality and policy implications. Montréal: TRANSNUT, University of Montreal; December 2017Nov;14 Suppl 2:21-8. doi: 10.1111/obr.12107.
  5. Schulte EM, Avena NM, Gearhardt AN (2015) Which Foods May be Addictive? The Roles of Processing, Fat Content and Glycemic Load. PLoS ONE 10(2); e0117959. https://doi.org/10.1371/journal.pone.0117959
  6. Chowdhury R, Warnakula S, Kunutsor S, Crowe F, Ward HA, Johnson L, et al. Association of dietary, circulating and supplement fatty acids with coronary risk: A systematic review and meta-analysis. Ann Internal Medicine 2014;160:398-406.
  7. Sri-Tarino PW, Sun Q, Hu FB, Krauss RM. Meta-analysis of prospective cohort studies evaluating the association of saturated fat with cardiovascular disease. Am J Clin Nut 2010;91(3):535-546.
  8. Dehghan M, Mente A, Zhang X et al, The PURE Study — Associations of fats and carbohydrate intake with cardiovascular disease and mortality in 18 countries from five continents (PURE): a prospective cohort study. Lancet. 2017 Nov 4;390(10107):2050-2062
  9. Heart and Stroke Foundation of Canada, Position Statement ”Saturated Fat, Heart Disease and Stroke, September 24, 2015, https://www.heartandstroke.ca/-/media/pdf-files/canada/position-statement/saturatedfat-eng-final.ashx

 

CFG Snapshot – conflating Ultra-Processed Food and Whole, Real Foods?

Note: This article is a combination of a Science Made Simple article with references below and an editorial which provides my opinion.

This past Monday, Health Canada released the Canada’s Food Guide “snapshot”[1] in 28 languages which is not intended to be a stand-alone resource, but to be used as a tool to guide people to the Canada’s Food Guide website.

Canada’s Food Guide includes Canada’s Dietary Guidelines[2], the healthy eating recommendations[3], and all of the other resources and information on the Canada’s Food Guide website. Links to the guidelines and healthy eating recommendations are available in the References, below.

The “Snapshot”

The main message of the “snapshot” is that “healthy eating is more than the foods you eat” ⁠— which I think is an excellent way of summarizing the guidelines and recommendations and encouraging the public to want to learn more. From that point of view, the snapshot is successful in that it is likely to guide people to the website.

The main points on the Snapshot are;

  1. Be mindful of your eating habits
  2. Cook more often
  3. Enjoy your food
  4. Eat meals with others
  5. Use food labels
  6. Limit foods high in sodium, sugars or saturated fat*
  7. Be aware of food marketing

Each of these points link to the sections of Canada’s Food Guide which address those points and in my opinion are all very helpful, except for one elaborated on below.

For example, under “Be mindful of your eating habits” is and encouragement for Canadians to be aware of;

  • how you eat
  • why you eat
  • what you eat
  • when you eat
  • where you eat
  • how much you eat

Being mindful can help you:

  • make healthier choices more often
  • make positive changes to routine eating behaviours
  • be more conscious of the food you eat and your eating habits
  • create a sense of awareness around your every day eating decisions
  • reconnect to the eating experience by creating an awareness of your:
    • feelings
    • thoughts
    • emotions
    • behaviours

Cheese, eggs and meat are high in saturated fat, and cured meats are high in sodium and saturated fat, and dates are certainly very high in sugar, but are not ultra-processed foods. Are these really foods that all Canadians should limit?

Is there irrefutable scientific evidence that healthy people should limit eggs, real cheese and whole fresh meats and poultry? Is it “unhealthy” for metabolically well folks to eat dates, which are very high in sugar? Or are we conflating whole, real food with ultra-processed food?

Using the NOVA food classification that foods such as cheeses, cured meats and olives or anchovies are minimally processed foods that have been processed to make them ore durable and palatable, but they are not “ultra-processed foods” akin to hot dogs, pizza and pop!

I don’t believe that it is helpful to lump “ultra-processed food” and whole, real food that are high in saturated fat, sodium and sugar, together.

 

It makes good sense to advise Canadians to limit ultra-processed food because they are high in refined carbohydrates and refined fats, and low in nutrient density — but when ultra-processed food is labelled with the advice “limit foods high in sodium, sugar or saturated fat”, whole, real foods are conflated with food-like products which displace real, whole food from the diet.

More Info?

If you would like more information, you can learn about me and the Comprehensive Dietary Package that I offer.

To your good health!

Joy

You can follow me on:

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

 

Copyright ©2019 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.

References

  1. Health Canada Snapshot: https://food-guide.canada.ca/en/?utm_source=canada-ca-foodguide-en&utm_medium=vurl&utm_campaign=foodguide
  2. Health Canada, Canada’s Dietary Guidelines, https://food-guide.canada.ca/en/guidelines/
  3. Health Canada, Healthy Eating Recommendations, https://food-guide.canada.ca/en/healthy-eating-recommendations/
  4. Schulte EM, Avena NM, Gearhardt AN (2015) Which Foods May be Addictive? The Roles of Processing, Fat Content and Glycemic Load. PLoS ONE 10(2); e0117959. https://doi.org/10.1371/journal.pone.0117959

Only Half of People Have Newer Gene that Controls High Blood Sugar

The maintenance of blood sugar is very tightly regulated; with a healthy person’s blood glucose being kept in the range from 3.3-5.5 mmol/L (60-100 mg/dl) between meals, however a new study indicates that it may be newer variant of a gene that determines how well (or not) we are able to maintain these levels.

After eating, the higher levels of blood glucose that comes from the broken-down carbohydrate-based food triggers the release of insulin by the pancreas, which in turn causes the release of a special transporter called GLUT4.  The GLUT4 transporter acts like a taxi to remove excess glucose from the blood, taking it into muscle and fat tissue.

Newer Variant of an Older Gene

Between meals and with the help of a special protein (CHC22) produced by the CLTCL1 gene, the GLUT4 glucose transporter remains inside muscle and fat, so that some blood sugar will continue to circulate.

A newly published study [1] by research specialists in population genetics, evolutionary biology, ancient DNA and cell biology analyzed the human genomes to understand how the gene producing CHC22 has changed over human history [2].

By examining the genomes of 2,504 people from the global 1000 Genomes Project compared to the genomes of ancient humans, researchers found that almost half of the people in various ethnic groups have a variant of CHC22 protein that is produced by a new variant of the CLTCL1 gene that became more common as humans moved away from being hunter-gathers and began farming and raising crops. Researchers postulate that the increased consumption of carbohydrates may have been the selective force driving this genetic adaptation.

Researchers found that the newer CHC22 variant of the gene is less effective at keeping the GLUT4 glucose transporter inside muscle and fat tissue between meals, which means that the transporter can more readily clear glucose out of the blood*.

As a result, people with the newer variant of the gene will have lower blood sugar than those with the older variant of the gene.

“The older version of this genetic variant likely would have been helpful to our ancestors as it would have helped maintain higher levels of blood sugar during periods of fasting, in times when we didn’t have such easy access to carbohydrates, and this would have helped us evolve our large brains”[2] — lead author Dr Matteo Fumagalli

*Note: It’s important to keep in mind that only GLUT4 transporters are insulin-dependent. There are other glucose transporters that allow glucose into the cell that don’t involve insulin, such as the GLUT1 transporter that works on a concentration gradient. That is, the effect of this gene is not on all glucose regulation, but only glucose regulation in adipose and muscle cells that use GLUT4 transporters.

The higher carbohydrate diets that came as a result of the advent of agricultural meant that this newer variant of the gene could be advantageous, as it moves the excess blood sugar from the blood into the muscle and fat tissue and having the older variant of the gene may make people more likely to develop Diabetes and may also make worse the insulin resistance that underlies the process of developing Diabetes.

“People with the older variant (of the gene) may need to be more careful of their carb intake, but more research is needed to understand how the genetic variant we found can impact our physiology”[2] — co-author Dr. Frances Brodsky 

Along with the 2015 study from Israel[3] that demonstrated substantial differences in blood glucose response between both healthy individuals and those with Diabetes predictable by their gut microbiome, this new research adds to the knowledge that multiple factors are involved with determining whether people can tolerate specific dietary carbohydrate loads.

Nutritional guidelines for maintaining healthy blood glucose levels are portrayed as universally applicable, however this new study and the 2015 Israeli study demonstrates that blood glucose varies significantly between individuals based on genetics as well as on gut microbiota composition, which necessitates the need for personalized nutrition in managing blood glucose levels.

More Info

If you are interested in a personalized approach aimed at helping you gain control of your blood sugar levels, I can help.

I offer both in-person services in my Coquitlam, British Columbia office as well as remote services via Distance Consultation. You can find more information about my packages under the Services tab or in the Shop and if you would like to learn more about how Distance Consultation services work, you can click here.

Have Questions?

If you would like more information, you can learn about me and the Comprehensive Dietary Package that I offer.

To your good health!

Joy

You can follow me on:

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

 

Copyright ©2019 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.

References

  1. Matteo Fumagalli, Stephane M Camus, Yoan Diekmann, Alice Burke, Marine D Camus, Paul J Norman, Agnel Joseph, Laurent Abi-Rached, Andrea Benazzo, Rita Rasteiro, Iain Mathieson, Maya Topf, Peter Parham, Mark G Thomas, Frances M Brodsky. Genetic diversity of CHC22 clathrin impacts its function in glucose metabolism. eLife, 2019; 8 DOI: 10.7554/eLife.41517
  2. University College London. “Gene mutation evolved to cope with modern high-sugar diets.” ScienceDaily. ScienceDaily, 4 June 2019, https://www.sciencedaily.com/releases/2019/06/190604084857.htm
  3.  Zeevi D, et al. Personalized nutrition by prediction of glycemic responses. Cell. 2015;163:1079—1094.
  4. Noecker C, Borenstein E. Getting Personal About Nutrition. Trends Mol Med. 2016;22(2):83—85. doi:10.1016/j.molmed.2015.12.010