Month: July 2019

INTRODUCTION: In the previous article about milk intolerance related to a novel beta casein protein found in commercial cow’s milk, I mentioned both histamine intolerance and Mast Cell Activation Disorder (MCAD) — which is also called MCAS (Mast Cell Activation Syndrome).  Several people with these disorders reached out to me on social media looking for articles about them, so I decided to write this one.

Adverse reactions to food or components of food can be divided into food allergy and food intolerance.

A food allergy is an IgE antibody-mediated immune reaction and can range from mild skin itching or hives, to full-blown anaphylactic attack where a person is unable to breathe. Specific IgE-mediated antibodies can be assessed and quantified by a blood test for an allergen, or assessed via skin scratch test with a small amount of the allergen.

A food intolerance is a non-immune reaction to a food or food component that can result in a disturbance of enzymes of the gastrointestinal (GI) tract. Lactose intolerance is probably the best known food intolerance, where people have a disturbance of the enzyme lactase in the GI tract, which makes them unable to properly digest the sugar in milk.

Histamine intolerance, like tyramine intolerance is a food intolerance and while rarely life-threatening, it can makes people’s lives quite miserable.

What are Histamines

Most people know that term ‘antihistamine’ as medications that people take when they have seasonal allergies, such as trees and grasses or ragweed (“hay fever”), but what are histamines?

Histamine is a chemical that performs many helpful functions in the body such as stimulating the production of stomach acid (via the H2 receptors), but in this context, the interest is in histamine’s role in the immune system.

As it is intended to, histamine is released in response to exposure to an allergen, in the body’s attempt to protect you against something that it perceives as a threat. If you have breathed in some pollen that you you are allergic to for example, a signal is sent to your mast cells to release histamine in the body.  These histamines result in inflammation; a condition which signals the immune system to respond. That response could make you sneeze or make your nose run in order to help get rid of the offending allergen — or in cases with people with IgE mediated allergies it can be a very serious reaction that causes your blood pressure to suddenly drop very low, and you find it very difficult to breathe (anaphylaxis).

In histamine intolerance or mast cell activation disorder, histamine is either not broken down properly so it builds up in the body or is released by the mast cells inappropriately, such as when there is no allergen present. In these people, histamine becomes like gluten to a celiac, or regular milk to someone with lactase deficiency — only worse.

Some foods are high in an amino acid called histidine; which converts to histamine during digestion (via a carboxylation reaction mediated L-histidine decarboxylase).

Foods high in histamine include aged and fermented foods such as cheese, yogurt, pickled foods such as kimchi or saurkraut, and smoked fish. Other foods include dried fruit, specific vegetables, some nuts, well as alcohol.

There are also foods that are histamine-liberators, such as chocolate, milk and tomatoes (just to name a few) that need to be considered to minimize the symptoms of histamine intolerance, as well as certain food additives [1].

Finally, foods high in histidine, which is converted to histamine upon digestion, aslo need to be factored in to the diet of someone with histamine intolerance or mast cell activation disorder.

People with mastocytosis, mast cell activation disorder (MCAD) or histamine intolerance react to foods high in histadine / histamine as well as to foods that liberate histamine from mast cells. While these are separate disorders, they all involve problems with histamine.

Mastocytosis is condition where there are too many mast cells. This can be limited to just the skin or can be systemic (all over the body) and occurs due to a mutation in a specific gene.

Mast Cell Activation Disorder (MCAD) – sometimes called Mast Cell Activation Syndrome (MCAS) is where the mast cells ‘degranulate’ (spill their contents, including histamine) at an inappropriate time.  That is, they release histamine when there is no allergen present.

Histamine Intolerance is where the rate of histamine accumulation in the body is greater than the rate at which histamine degrades. The analogy of histamine intolerance is that of an overflowing “bucket”.

Histamine Intolerance

Normally, histamine is stored in the mast cells, or is rapidly degraded by one of two enzymes; either by diamine oxidase (DAO) or histamine-N-methyltransferase (HNMT) upon release, so it doesn’t accumulate.  Disfunction in these enzymes can

DAO primarily functions in the small intestine, ascending colon (a section of the large intestine), as well as kidney [1]. The primary function of DAO is the elimination of excess histamine, as well as controlling the amount of histamine in the body, coming from the digestive tract [1].

HNMT is primarily functions at the level of the histamine receptors themselves, where it deactivates histamine. This enzyme is active in a wide range of body tissues; but greatest in the kidney and liver, followed by the spleen, colon (large intestine), reproductive organs (prostate, ovary), spinal cord cells and parts of the lungs (bronchi, trachea).

Histamine Receptors

There are 4 types of histamine receptors that bind histamine and cause mast cells to release histamine. The binding of histamine with these receptors result in different types of allergic reactions.

H1 Receptors

H1 receptors are primarily involved in allergic rhinitis symptoms (sneezing, blowing ones nose), broncho-constriction such as what occurs in allergy-induced asthma, as well as systemic vasodilation (enlarging of the blood vessels)[2].

H2 Receptors

H2 receptors stimulate the stomach to release HCL acid, and inhibit the body from making antibodies, as well as activate the immune system response, including T-cell proliferation and the production of cytokines[2].

H3 Receptors

H3 receptors change neurotransmitter release in the central nervous system, including serotonin and norepinephrine (noradrenaline)[2].

H4 Receptors

H4 receptors are found mostly in bone marrow and white blood cells and are also expressed in the colon (large intestine), small intestine, spleen, tonsils and trachea (wind-pipe)[2].

Symptoms of Histamine Intolerance

People with histamine intolerance display a wide variety of symptoms, affecting different parts of the body.  Some people have many symptoms in different parts of the body, whereas others have a few symptoms clustered in specific parts.  Those with histamine intolerance may have chronic reactions and others may have them seemingly ‘randomly’.

That said, the most frequently observed symptoms are acute (sudden) or chronic (long term) gasto-intestinal GI symptoms [2] and can easily  be mistaken for ‘food poisoning’ (acute symptoms) or irritable bowel syndrome (chronic symptoms). That said, there are individuals with MCAD that have anaphylactic-type reactions. 

Gastro-intestinal symptoms often take place several hours after ingestion of the offending food or food component, because the food itself has to be digested (which takes time) for its histamine to be liberated and bind with the histamine receptors.

In other cases, the reaction is faster; especially when eating aged or leftover food or other foods with high histamine content. These foods may trigger abdominal cramps or diarrhea within 15-30 minutes [2].

Other non-GI related symptoms common with histamine intolerance and mast cell activation disorder (MCAD) are skin rashes, hives (with or without itchiness), facial and chest flushing (getting red and ‘hot’ feeling), faster or slower heartbeat (arrhythmia) or low blood pressure or extreme fatigue. Some people also experience mood changes, including inattentiveness or something described as a ‘brain fog’, as well as sleep disturbances [3,4].

Getting Diagnosed

Histamine intolerance and mast cell activation disorder are difficult to diagnose, firstly because people themselves don’t think wide range of symptoms are related, so they often don’t seek medical help. Another challenge is that the very fact that the symptoms are diverse may result in them be discounted by some physicians as being related to stress/anxiety or depression.

Mast cell activation disorder (MCAD) takes on average 14 years to be diagnosed [4] and often only occurs once the person finally gets a referral to an immunologist or allergist knowledgeable in the condition. I can assist in helping people get that referral, as well as provide support once they know they have either MCAD or histamine intolerance.

[Note: You may be interested in this article about similar condition called tyramine intolerance, especially if you suffer from migraine headaches.

More Info?

If you have been diagnosed with histamine-intolerance or Mast Cell Activation Disorder (MCAD), I can help by providing you with nutrition education to make the needed dietary changes to help minimize symptoms.

Learn more by visiting the landing page, or clicking on the Services tab and scroll down to the section on Therapeutic Dietary Services.

To your good health!

Joy

You can follow me on:

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

Reference

1. Baily N, Histamine Intolerance, Igennus Healthcare Nutrition, https://www.slideshare.net/igennus/managing-histamine-intolerance-80982438
2. Jernigan D, Histamine Intolerance Syndrome, Hansa Center for Optimal Health, Bimed Network, https://www.marioninstitute.org/histamine-intolerance-syndrome/
3. Molderings GJ, Brettner S, Homann J et al, 2011, Mast cell activation disease: a concise practical guide for diagnostic workup and therapeutic options, J of Hemat and Onc 4 (10)
4. Hamilton MJ et al, 2011, Mast cell activation syndrome: A newly recognized disorder with systemic clinical manifestations. J of Allergy and Clin Immunology Vol 28 (1), p. 147-153

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.

Digestive issues that result from milk consumption are often attributed to lactose intolerance, but research indicates that it may be the result of an intolerance to a specific type of protein found in some types of cow’s milk; specifically A1 beta-casein.

Casein and whey are the two primary proteins found in milk, with casein accounting for ~ 80 % of the protein in milk. Approximately 30% of the protein in milk is beta-casein.

There are two variants of beta-casein; A1 and A2, however before cows were domesticated, they only produced milk that only contained the A2 form of beta-casein[1,2]. Older breeds of cows such as most Jerseys, Guernseys, Brown Swiss, Normandes, as well as most of the cows in Asia, Africa and southern Europe[2] produce milk with the A2 variant of beta-casein, as do goats, sheep, donkeys, yaks, camel and buffalo [2]. In addition, human milk contains A2 beta-casein.

It is thought that ~8,000 years ago, a single-gene mutation occurred in Holsteins which resulted in the production of the A1 beta-casein protein in this breed. This novel gene variant was passed on to other northern European breeds of cows, including Friesian, Ayrshire and British Shorthorn since Holsteins were bred with them to improve milk production[2]. 

Today’s Holstein breed is the most common dairy cow in the US, Canada, Australia and northern Europe and carries both A1 and A2 forms of beta casein in approximately equal amounts[2].

Milk intolerance may not always be due to lactose intolerance, but due to intolerance to milk containing A1 beta-casein.

Note: Primary lactose intolerance is a result of a lack of the enzyme lactase, which is genetic in origin. This is a permanent condition. Secondary lactose intolerance is temporary and the result of being sick with something that causes diarrhea which sloughs off the lactase from the wall of the intestine. Genuine lactose intolerance can be tested with a hydrogen breath test.

Research suggests that A1 beta-casein protein may be at the root of stomach pain and other gastrointestinal (GI) symptoms associated with consumption of milk from A1 cows and which closely resemble lactose intolerance. These symptoms are not present when consuming milk from cows that only produce A2 beta-casein. Food-derived peptides such as β-casomorphins and others are known to have different effects on the intestines, including the secretions of the stomach and pancreas, as well as gut motility [3]. Studies have found that a peptide called β-(beta) casomorphin (BCM-7) may be behind stomach pain and other symptoms associated with milk containing A1 beta-casein.

The Difference Between A1 and A2 Beta-Casein

If one thinks of proteins as chains of amino acids strung together like train-cars in a train, each one of the ‘cars’ represents a different amino acid.  In the older A2 beta-casein variant, the ‘car’ which occupies the 67th position is an amino acid called proline, but in the newer A1 beta-casein variant, the amino acid in the 67th position is histidine. When milk with A1 beta-casein is digested, the histidine bond breaks, resulting is a peptide made up of 7 amino acids, called β-(beta) casomorphin-7 (BCM-7).

β-(beta) casomorphin-7 (BCM-7) is a naturally occurring opioid peptide, with a structure similar to morphine and is known to bind to opioid receptors [3]. What effect does BCM-7 have on the body as a result of binding with these opioid receptors?

A 2015 review paper cites research demonstrating that milk containing A1 beta-casein increases GI transit time (the amount of time that it takes for food to go through the GI tract) which means in slows it down, and in animal studies, increases inflammatory markers significantly more than A2 beta-casein containing milk[5]. In a small, double-blinded, randomized crossover study from 2014 with 41 subjects, it was found that participants consuming A1 beta-casein cow’s milk had significantly softer stools, more bloating and more abdominal pain than those drinking A2 beta-casein milk [6]. In another unrelated double-blind, randomized, crossover trial from 2016 with 45 Chinese participants with self-reported intolerance to cow’s milk drank  250 mL of either A1/A2 or A2 milk following each of two meals over a 14-day period. When drinking the A1 beta-casein milk, there was an increase in transit time and in GI inflammation, and a worsening of digestive discomfort [7] as well as an increase in inflammatory markers such as IgG, IgE, and IgG1. These were significantly lower in those that drank A2 milk [7].

Addendum (July 22, 2019): *there has been some anecdotal evidence that people with arthritis do considerably better when they do not consume casein (see Arthritis Foundation website).

In a large scale 2017 randomized cross-over design follow-up study, 600 adult who reported lactose intolerance and digestive discomfort following milk consumption were assigned over a 7-day period to consume either 300 mL of conventional milk containing both A1 and A2 beta casein, or only A2 milk. Results indicated digestive symptoms were markedly reduced after consuming A2 milk versus conventional milk [8].

Healthcare professionals have often assumed (without giving people hydrogen breath tests to confirm it) that people with GI symptoms related to consuming dairy products have lactose intolerance, when it is possible that the symptoms could be related to intolerance of A1 beta-casein.

Concerning to those with histamine-intolerance, including those with Mast Cell Activation Disorder (MCAD) who need to lower their intake of histadine-containing foods and histamine-liberators [9] may unknowingly be adversely affected by milk commonly available in the US, Canada, Australia and northern Europe that contains A1 beta-casein, as when it is digested it produces betacasomorphin-7 (BCM-7), a potent histamine liberator. The most well-known Histamine Intolerance Food Compatibility List from the Swiss Histamine Intolerance Group (SIGHI) lists milk as producing a low reaction — perhaps because the milk available in Central Europe, as in southern Europe, contains A2 beta casein, and not A1 beta-casein as in North America, Australia and northern Europe [10]. Those with histamine-intolerance in the US and Canada, for example and other countries with A1 beta-casein in dairy need to be aware that the milk and the hard cheeses listed as being “well-tolerated, no symptoms expected at usual intake” does not apply to the milk and cheese available to them.

Final Thoughts…

While much research has yet to be done to determine the extent that A1 beta-casein proteins impact human health, those with suspected lactose intolerance who continue to have symptoms while consuming lactose-free milk and low-lactose products such as yogurt and hard cheese, should try eliminating milk produced at ordinary large-scale dairies that have milk containing both A1 and A2 beta-casein to see if their symptoms improve.  As a substitute, they could use goat milk or buffalo milk, or find small, local dairies that use “heritage herd” cows, such as specific species of Jerseys, Guernseys, Brown Swiss, and Normandes that only produce milk with A2 beta-casein.

Note: My tried and true recipe for making homemade goat or A2 yogurt in an oven or crock-pot using a temperature controller, as well as turning it into thick Greek yogurt is posted here.

Those with histamine-intolerance in the US, Canada and Australia might feel better avoiding milk, cheese, and yogurt from conventional dairies, as these contain A1 beta-casein, which are high histamine liberators. After a period of dairy avoidance to enable mast cells to calm, dairy products from “heritage herd” cows can then be trialed.

NOTE: Butter and full-fat (whipping) cream are entirely fat, and as such do not contain either A1 or A2 beta-casein proteins. These would be fine to consume regardless of which dairy they were from.

More Info?

If you have food allergies or food intolerances, including what you thought was lactose intolerance, or have been diagnosed with histamine-intolerance or Mast-Cell Activation Disorder (MCAD), I can help.

You can find out more about the packages and hourly consultations I offer under the Services tab or by clicking here. If you would like further information, please send me a note using the Contact Me form above and I will reply as soon as I can.

To your good health!

Joy

You can follow me on:

Twitter: https://twitter.com/lchfRD
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. Ware M, Metropulos M, Medical News Today, A2 milk: What you need to know, July 25, 2017, https://www.medicalnewstoday.com/articles/318577.php
2. Pasin G. A2 milk facts. California Dairy Research Foundation website. http://cdrf.org/2017/02/09/a2-milk-facts/. Published February 9, 2017.
3.  European Food Safety Authority. Review of the potential health impact of β-casomorphins and related peptides. EFSA J. 2009;7(2):1-107.
4. Kurek M, Przybilla B, Hermann K, A naturally occurring opioid peptide from cow’s milk, beta-casomorphine-7, is a direct histamine releaser in man, Int Arch Allergy Immunol. 1992;97(2):115-20.
5. Pal S, Woodford K, Kukuljan S, Ho S. Milk intolerance, beta-casein and lactose. Nutrients. 2015;7(9):7285-7297.
6.  Ho S, Woodford K, Kukuljan S, Pal S. Comparative effects of A1 versus A2 beta-casein on gastrointestinal measures: a blinded randomised cross-over pilot study. Eur J Clin Nutr. 2014;68(9):994-1000.
7. Jianqin S, Leiming X, Lu X, Yelland GW, Ni J, Clarke AJ. Effects of milk containing only A2 beta casein versus milk containing both A1 and A2 beta casein proteins on gastrointestinal physiology, symptoms of discomfort, and cognitive behavior of people with self-reported intolerance to traditional cows’ milk. Nutr J. 2016;15:35
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: a multicentre, randomised controlled study. Nutr J. 2017 Oct 25;16(1):72.
9. Molderings GJ, Brettner S, Homann J, Afrin LB. Mast cell activation disease: a concise practical guide for diagnostic workup and therapeutic options. J Hematol Oncol. 2011;4:10. Published 2011 Mar 22. doi:10.1186/1756-8722-4-10
10. Lamprecht H, Swiss Interest Group Histamine Intolerance (SIGHI), Histamine Intolerance Food Compatibility List, wwww.mastzellaktivierung.info & www.histaminintoleranz.ch

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This article is based in part on material by Judith C. Thalheimer, RD, LDN, Is A2 Milk the Game-Changer for Dairy Intolerance?Today’s Dietitian, Vol. 19, No. 10, P. 26

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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 Package 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?

You can find out more about the Anti-Inflammatory Protocol Package that I offer by clicking here and if you have questions, please feel free to send me a note using the Contact Me form above and I will reply as soon as I can.

To your good health!

Joy

You can follow me on:

Twitter: https://twitter.com/lchfRD
Facebook: https://www.facebook.com/BetterByDesignNutrition/
Instagram: https://www.instagram.com/lchf_rd
Fipboard: http://flip.it/ynX-aq

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

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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 on using diet to seek to put the symptoms of type 2 diabetes into remission or for weight loss, I’d be glad to help.

You can learn more about my services under the Services tab or in the Shop.

If you have questions, please feel free to send me a note using the Contact Me form above and I will reply as soon as I can.

To your good health!

Joy

You can follow me on:

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

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

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 grains, such 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 here. As 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 about how I can help in this regard, you can find the various services I offer related to Food Sensitivities / Food Allergies, Celiac Disease, IBS and Diverticulosis under the Services tab, and in the Shop.

If you have questions please feel free to send me a note using the Contact Me form above, and I will reply as soon as I can.

To your good health!

Joy

You can follow me on:

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

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

 

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 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 about the IBS Package, you can find that under Services tab of my affiliate website, BetterByDesign Nutrition Ltd. and if you’re interested in the low-FODMAP teaching, you can find that in the Shop on that site.

Of course, if you have questions please feel free to send me a note using the Contact Me form above, and I will reply as soon as I can.

To your good health!

Joy

You can follow me on:

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

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 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 a Meal Plan designed just for you in light of your diagnosis, as well as specific nutrition education services on how to minimize the symptoms of diverticulosis and lower the likelihood of it progressing to diverticulitis, please click on the Diverticulosis Option, under the Services tab to learn more.

If you have questions, please feel free to send me a note using the Contact Me form above and I will reply as soon as I can.

To your good health!

Joy

You can follow me on:

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

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

 

 

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]. 

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, 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 about choosing whole, real food and limiting ultra-processed foods, I can help.

You can learn more about my services under the Services tab or in the Shop. If you have questions, please feel free to send me a note using the Contact Me form above and I will reply as soon as I can.

To your good health!

Joy

You can follow me on:

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

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.

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).

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 cereal, muffins, 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 about limiting ultra-processed foods, while including whole, real foods (plant-based and animal-based), I can help.

You can learn more about my services under the Services tab or in the Shop. If you have questions, please feel free to send me a note using the Contact Me form above and I will reply as soon as I can.

To your good health!

Joy

You can follow me on:

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

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