Year: 2021

Several recent studies have found a relationship between the species of bacteria and fungi that live in our large intestine, carbohydrate intake and Irritable Bowel Disease (IBD), including Ulcerative Colitis and Crohn’s disease. This article elaborates on how this knowledge may help improve symptoms for those with IBD.

The Gut Microbiome & Mycobiome

The trillions of gut bacteria that live in our intestines are collectively referred to as the ‘gut microbiome, ‘gut microbiota’ or ‘gut flora’, along with fungi (called the ‘mycobiome’) and other single cell organisms called archaea.

We are in a symbiotic relationship with these gut bacteria — which means when things are going well, they benefit us and we benefit them. What we eat feeds them, and in turn they produce by-products that are helpful for us. One example of a helpful end-product of fermentation by the so-called “good bugs” of our gut microbiome is the formation of short chain fatty acids (SCFA) [3], which plays an important role in maintaining glucose (blood sugar) levels, fat metabolism and even appetite regulation [2] in humans. As I will elaborate further on in this article, these SCFA also play a role in keeping the “bad bugs” from taking over.

The gut mycobiome, which are the species of fungi that live in our large intestine can have an impact on our gut microbiome, and both are affected by the carbohydrates we take in through the diet — which has important implications for those with Inflammatory Bowel Disease.

Dietary Carbohydrate

What types of foods are carbohydrate-based may seem obvious to some, but many people don’t realize that simple sugars such as glucose (the sugar in our blood) and fructose (the sugar in fruit) are not that much different than ‘starches’, such as bread, pasta and rice. As outlined in a previous article, sugars can come alone come alone, in pairs or strung like pearls on a chain. Knowing the different types of sugars is important to those with Inflammatory Bowel Disease as these sugars and starches can be used as food for our gut microbiome, and which bacteria and fungi we ‘feed’ has important implications on health.

Simple Sugars – monosaccharides & disaccharides

Simple sugars can come alone (monosaccharides, which means ‘one sugar’) or in pairs (disaccharides, which means ‘two sugars’).

Monosaccharides include glucose, fructose and galactose and disaccharides are combinations of these monosaccharides linked together, in pairs. Some common disaccharides include sucrose, lactose and maltose;

Sucrose is ordinary table sugar and made up of glucose-fructose.

Lactose is the sugar in milk and milk products and is made from a glucose-galactose pair.

Maltose which rarely occurs naturally in foods, is glucose-glucose. Maltose is used in food processing such as the shiny glaze on Chinese roast duck.

Complex Carbohydrates – strings of sugar molecules

Complex carbohydrates are made up of more than two monosaccharides (sugar molecules). Oligosaccharides (‘oligo’ means ”scant” or ”few”) are made up of 3-10 sugar molecules, whereas polysaccharides (including starch) are made up of hundred or even thousands of monosaccharides (sugar molecules).

Oligosaccharides

Oligosaccharides are made up of 3-10 sugar molecules and the two most common are some of the complex carbohydrates found in dried beans, peas and lentils[1].  For example, raffinose is an oligosaccharide made from 3 sugar molecules: galactose-glucose-fructose and stachyose is an oligosaccharide made from 4 sugar molecules: galactose-galactose-glucose-fructose. What is important to know is that the body can’t break down either raffinose or stachyose, but these are fermented by certain species of bacteria in our gut microbiome.

Polysaccharides

Polysaccharides are made up of hundreds or thousands of sugar molecules linked together. When those sugar molecules are only glucose, the polysaccharide is called ”starch”.

Some polysaccharides form long straight chains while others are branched like a tree. These structural difference affect how these carbohydrates behave when they’re heated or put in water. The way the monosaccharides are linked together makes the polysaccharides either digestible as in starch, or indigestible as in fiber.

We can’t digest polysaccharides found in plant foods such as fiber, cellulose, hemicellulose, gums and mucilages (such as psyllium) but they can both slow down the absorption of digestible carbohydrate and be fermented by the gut microbiome.

Starch

Starches are long chains of glucose molecules strung together like beads on a string. Starches are found in grains such as wheat, corn, rice, oats, millet and barley, as well as in legumes such as peas, beans and lentils* and tubers such as potatoes, yams and cassava.

*As mentioned above, peas, beans and lentils also have the complex carbohydrates called oligosaccharides which are not broken down by the body, but are broken down by bacteria in our gut microbiome.

There are two types of starches; the long unbranched chains called amylose and the long branched chain ones call amylopectin. The body digests most starches very easily, although those with a high percentage of amylopectin (such as cornstarch) are digested much more easily than those with a high amount of amylose, such as wheat starch [1].

Since starches are just glucose molecules linked together and they are easily broken down to individual glucose molecules, so starches quickly affect the blood sugar and as I will elaborate on in this article are fermented easily by our gut microbiome and may play a role in colitis in genetically susceptible individuals.  Limiting these and other fermentable carbohydrates also can play a role in reducing symptoms of those with IBD.

How Simple Sugars can Induce Colitis by Affecting the Microbiome

A study was published in late 2020 documenting how simple sugars in the diet can induce colitis, an inflammatory bowel disease [2]. The study found that when researchers fed mice simple sugars such as glucose, fructose and sucrose, the high-sugar diet damaged the protective mucus layer of the colon (large intestine) and increased the number of harmful bacteria — especially Akkermansia muciniphila and Bacteroides fragilis which break down the mucus that lines and protects the colon. 

The study found that when the mice were fed a 10% glucose solution for seven days (chosen because soft drinks contain ~15% sugar) and were then given a 2.5% dextran sulfate sodium (DSS) which is known to induce colitis, the mice that had been fed the glucose had extreme sensitivity to DSS treatment and suffered from aggressive colitis, bloody diarrhea and rapid loss of nearly 20% of their body weight. When the researchers looked at the glucose-treated mice three days after giving them the DSS, they found that their colons were shorter than the colons of the control mice that were not fed the glucose, and that the glucose-fed mice had many of the symptoms of colitis, including loss of epithelial crypts, inflammation, and ulceration.

When the researchers saw that the high-sugar intake made the colitis
caused by DSS chemical injury of the colon worse, it led them to then test
whether high sugar intake alone had a similar effect in mice that were genetically susceptible. They treated mice with genetic susceptibility to colitis with a 5% glucose solution from 14 weeks of age, while measuring weekly body weight changes and clinical scorings for 5 weeks. At 19 weeks, 90% of glucose-treated genetically-susceptible mice developed colitis, compared to 40% in the controls that did not have the genetic susceptibility. The glucose-fed susceptible mice had much greater loss of body weight and higher diarrhea and rectal bleeding compared to control the control mice, and when they looked at the colon tissue of the mice, the ones that were glucose-fed had increased inflammation. There was also a much higher expression of inflammatory molecules in the colons of sugar-treated mice.

Of Mice and Men

Even though the results of animal studies can’t be applied directly to humans, this study can give us an indication of what may be going on in people. 

The National Human Genome Research Institute explains it this way;

“Mice and humans share virtually the same set of genes. Almost every gene found in one species so far has been found in a closely related form in the other. Of the approximately 4,000 genes that have been studied, less than 10 are found in one species but not in the other” [3].

Low-FODMAP Diet in Inflammatory Bowel Disease – effect on microbiome

For people with Inflammatory Bowel Disease, including Crohn’s disease and Ulcerative Colitis, a low-FODMAP diet is successfully used to reduce symptoms of the disease once their symptoms have been stabilized using a low residue diet after a flare. A low-FODMAP diet enables people with IBD to gradually normalize their diet, while avoiding foods that can be fermented by the ‘gut microbiome’ and this often leads to those with IBD finding significant relief of symptoms.

FODMAP is an acronym for fermentable, oligo-, di-, monosaccharides and polyols. A low-FODMAP diet reduces foods which contain various sugars such as fructose (the sugar found in fruit), lactose (the sugar in milk), sugar alcohols called ‘polyols’ such as sorbitol and mannitol, fructans which are found in garlic, leeks, artichokes, and wheat, and galacto-oligosaccharides which are found in legumes such as lentils, chickpeas, and black beans. As outlined above, these FODMAPS are fermentable by the gut bacteria and the by-products of that fermentation have long been thought to underlie symptoms experienced in those with Inflammatory Bowel Disease (IBD), as well as Irritable Bowel Syndrome (IBS). 

Over the last 5 years since I began using a therapeutic low carbohydrate diet to reduce the symptoms of type 2 diabetes and for weight loss, I began to wonder if what made a low-FODMAP diet effective in reducing symptoms in IBD was due to its overall low-carbohydrate content — not just the lower amount of fermentable, oligo-, di-, monosaccharides and polyols. Two studies published towards the end of 2020 confirmed a relationship between other types of carbohydrate in the diet and the gut microbiome (bacteria) and mycobiome (fungi). The first study was about the relationship between simple sugars intake and colitis which is outlined above, and the second study was about the effect of a very low carbohydrate diet on species of gut fungi (mycobiome), and is outline below.

Very Low Carbohydrate Diet Reduces Some Fungi in Gut Microbiome

Shortly before the above study showing a relationship between simple sugar intake and colitis is genetically-susceptible mice was published, there was another study that looked at the effect of a Mediterranean ketogenic diet^* to decrease the population of certain species of gut fungi (mycobiome) that populate the gut, along with the bacteria (microbiome).

^*A ketogenic diet is one that is very low in dietary carbohydrates — usually less than 20 grams of carbohydrate per day.

While it was a small pilot study, it was a randomized, double-blind crossover study which is the strongest study design. This type of study has two groups of people that don’t know which of the two groups they are in and who received one diet for half the study period, and then the diets and groups are switched so they receive the other diet for the second half of the study.

This study looked at the effect of Mediterranean Ketogenic Diet (MMKD) compared to the American Heart Association Diet (AHAD) in people with mild cognitive impairment (MCI) and found that symptoms of MCI were improved with the Mediterranean Ketogenic Diet in relationship with changes in the gut mycobiome. 

What researches found was that (1) whether a person had Mild Cognitive Impairment or not, the Mediterranean Ketogenic Diet more positively affected the gut mycobiome than the AHAD diet and (2) in those with MCI, there was a significant reduction in the proportion of Candida species during the Mediterranean Ketogenic Diet phase.

It was this part of the discussion that got my attention in relationship to Irritable Bowel Disease, such as Crohn’s disease and Ulcerative Colitis.

“The genus Candida comprises many opportunistic species implicated in various gut-related diseases including inflammatory bowel diseases, Crohn’s disease, ulcerative colitis, and gut inflammation [78]…In this context, reduced Candida carriage in patients with MCI might reflect another positive outcome of the MMKD intervention.”

What this means is, the researchers wondered whether a Mediterranean Ketogenic Diet (MMKD) might be effective in lowering Candida which has already been implicated in Inflammatory Bowel Disease, including Crohn’s disease and ulcerative colitis.

This part of the discussion section also stood out;

“Notably, we find a significantly negative correlation of Candida with short-chain fatty acid butyrate, a beneficial gut bacterial metabolite which was found to be increased by MMKD in these patients with MCI [24]. One of the ways gut bacteriome keep mycobiome in check is through the production of wide range of small molecules such as SCFAs (e.g., butyrate), which have inhibitory effects against the growth of pathobionts including Candida albicans [79, 80]. Together, these data suggest that the MMKD positively modulates the gut microbiome as well as the bacterial metabolites arrays, which in turn may check the overgrowth of opportunistic pathogens such as Candida.”

Simply said, what this means is that it is well-known that a ketogenic diet increases the amount of the short chain fatty acid (SCFA) butyrate which inhibits the growth of strains of Candida. This relationship implies a therapeutic role for a  Mediterranean ketogenic diet in the management of Irritable Bowel Syndrome.

Final Thoughts

In light of the above two studies, it seems to make good sense for those at genetic risk of developing Irritable Bowel Disease — as well as for those already diagnosed with IBD to

(a) reduce intake of simple sugars, including glucose, fructose and sucrose 

and

(b) consider adoption of a Mediterranean Ketogenic Diet which has been found to reduce the amount of Candida species — which has already been implicated in the development of Irritable Bowel Disease.

More Info?

If you would like more information about my services then please have a look under the tab of that name or send me a note through the Contact Me form.

To your good health!

Joy

You can follow me on:

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

 

Copyright ©2021 BetterByDesign Nutrition Ltd.

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

 

References

1. Morrison DJ, Preston T. Formation of short chain fatty acids by the gut microbiota and their impact on human metabolism. Gut Microbes. 2016;7(3):189-200. doi:10.1080/19490976.2015.1134082
2. Khan S, Waliullah S, Godfrey V et al, Dietary simple sugars alter microbial ecology in the gut and promote colitis in mice, Science Translational Medicine 28 Oct 2020: Vol. 12, Issue 567,  DOI: 10.1126/scitranslmed.aay6218
3. National Human Genome Research Project, Why Mouse Matters, https://www.genome.gov/10001345/importance-of-mouse-genome
4. Nagpal R, Neth B, Wang S et al,  Gut mycobiome and its interaction with diet, gut bacteria and alzheimer’s disease markers in subjects with mild cognitive impairment: A pilot study. EBioMedicine, 2020; 59: 102950 DOI: 10.1016/j.ebiom.2020.102950

The myth persists that a “keto” diet followed for weight loss or improved metabolic health is all about the fat…bacon, heavy whipping cream, and fat bombs. It’s about adding butter and MCT oil to coffee, about eating fatty cuts of meat and lots of avocado.

It isn’t.

What makes a diet “low carb” or “keto” is only how little carbohydrate it contains NOT how much fat it contains.

[Please note that therapeutic ketogenic diets are different from keto diets followed for weight loss and improved metabolic health.]

Defining “Low Carb” and “Keto” Diets

Different individuals and groups define ”low carb” and ”keto” (very low carb) in various ways. Feinman et al [1] defined three categories of reduced-carbohydrate diets;

(a) very low carbohydrate / ketogenic diet: carbohydrate limited to 20—50 g per day or < 10% of total energy intake

(b) low carbohydrate diet: carbohydrate limited to < 130 g per day or < 26% of total energy intake

(c) moderate carbohydrate diet: carbohydrate limited to 130—225 g per day or 26—45% of total energy intake.

In its Consensus Report of April 18, 2019, the American Diabetes Association and the European Association for the Study of Diabetes (EASD) defined a low carbohydrate diet as having 26-45% of total daily calories as carbohydrate (a combination of a low carbohydrate diet and a moderate carbohydrate diet defined by Feinman et al), and defined a very low carbohydrate (ketogenic) diet as 20-50 g carbs per day. In its 2020 Standards of Medical Care in Diabetes, the American Diabetes Association continued to define low carb and very low carb the same way.

Diabetes Canada also defines a low carbohydrate diet as less than <130 g of carbohydrate per day or <45% energy as carbohydrate, and very low carbohydrate (ketogenic) diet as <50 g of carbohydrate per day in its April 2020 Position Statement [3].

What defines a low carbohydrate or very low carbohydrate (“keto”) diet is ONLY the amount of carbohydrate it contains. There isn’t even any mention of how much fat it contains!

How Much Carbohydrate is Essential in the Diet?

The Dietary Reference Intakes for Energy, Carbohydrate, Fiber, Fat, Fatty Acids, Cholesterol, Protein and Amino Acids (2005) which forms the basis for dietary recommendations in both the US and Canada reads;

”The lower limit of dietary carbohydrate compatible with life apparently is zero, provided that adequate amounts of protein and fat are consumed[4].

There are essential amino acids and essential fatty acids that we need to take in through the diet because the body can’t make these, but there is no essential carbohydrate because the body can make any carbohydrate it needs from amino acids (from protein) or fat.

How Much Fat in a Keto Diet?

There is nothing magical or mystical about how much fat or protein is required in a “low carb” or “keto” diet.

Whether one starts a low carb diet at 130 g of carbohydrate per day or a “keto” diet of 20-50 g carbohydrate per day, the the remainder of daily calories is provided as protein and fat.

As outlined below, the popularized “keto” diet sets the amount of fat at approximately 75% of daily calories as fat, but this is only one type of “keto” diet.

It is a misconception is that to be a “keto” diet, most of daily calories needs to be as fat. 

It is also a misconception that added fat that is part of a low carb or “keto” diet must be animal fat.  Added fat as food or to cook with, or to put on salad can be provided by high fat fruit such as avocado or olives (fruit or oil), coconut (meat or oil), and nuts and seeds. If people choose, they can be low carb or “keto” and eat a predominantly whole-food plant-based (vegetarian) meal pattern.

Popularized “Keto” Diet

The popularized “keto” diet promoted widely on the internet is described as 75% fat, 15% protein and 10% carbohydrate, but is only ONE “keto diet” and not “THE keto diet”.

There are other “keto” diets, including the low carb, high protein, moderate fat ketogenic diet called Protein Power published in 1997 by Dr. Michael Eades and his wife Dr. Mary Dan Eades [5], the 2010 New Atkins For a New You [6] — which is a redesign of the original “Atkins Diet” from the 1970s written by Dr. Eric Westman, Dr. Stephen Phinney MD PhD, and Dr. Jeff Volek RD PhD which is only a very high fat ketogenic diet (20-50 g carbs per day) for phase one which lasts only the first two weeks, and there is also Real Meal Revolution [7] by Tim Noakes, Sally-Ann Creed, Jonno Proudfoot. Phinney and Volek’s approach in their 2011 book, the Art and Science of Low Carbohydrate Living has been to establish carbohydrate intake at 7.5-10% of calories for men, 2.5-6.5% of calories for women, protein intake at up to 30% of calories during weight loss, 21% during weight maintenance and fat intake to 60% of calories during weight loss and 65-72% during weight maintenance. Fat intake at 60% of calories during weight loss is NOT the same as the 75% calories as fat of the popularized “keto” diet.

The popularized “keto” diet is based largely on the two 2016 books by Dr. Jason Fung titled the Obesity Code [8] and The Complete Guide to Fasting [9], and the 2017 book titled by Dr. Andreas Eenfeldt, the founder of the popular “Diet Doctor website”, titled A Low Carb, High Fat Food Revolution [10] — both of whom write extensively on the Diet Doctor website.

Defining “High Fat”

In the US, the recommendation has been to limit calories from fat to no more than 30% of daily calories, of which no more than 1/3 comes from saturated fat and in Canada, to limit fat to 20-35% of daily calories as fat, with no more than 1/3 from saturated fat.  By definition, diets higher than 30% fat (US) or 35% fat (Canada) are considered “high fat”.

A “keto” diet which is only 40% fat would be considered “high fat” by the USDA and Health Canada, as would a “keto” diet that is 75% fat.  

But is a diet that is 40% fat really “high fat”?

From 1949 until 1977, dietary intake in Canada was at ~40-50% of daily calories as fat,  ~20-30% of daily calories as protein, and only 20-30% as carbohydrate. Was this the original “low carb high fat” diet?

Clarifying Definitions

In anything, it is important to define terms.

A “low carb” or “keto” diet is ONLY about how little carbohydrate it has (<130 g carbohydrate per day, 20-50 g of carbohydrate per day) and has absolutely nothing to do with how much fat it has.

Or how much protein in has, for that matter.

Contrary to what some on social media want to know, there is no “protein starting point” for a low carb or “keto” diet.  Each individual’s macro needs (energy, protein, fat and carbohydrate) are different, and vary depending on a person’s age, gender, stage of life,  health conditions, and activity for example.

There is no one-sized-fits-all low carb or “keto” diet with a set amount of fat, and set amount of protein. It depends what one is seeking to accomplish. Based on the definition, a low carb or “keto” diet for weight loss could range from 40% fat to 75% fat — and up to 90% for those following a therapeutic ketogenic diet for seizure disorder or glioblastoma.

People are always looking for the “formula for success” when it comes to weight loss but there isn’t one, except the one that works best for them.

More Info?

If you would like more information about my services then please have a look under the tab of that name or send me a note through the Contact Me form.

To your good health!

Joy

You can follow me on:

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

 

Copyright ©2021 BetterByDesign Nutrition Ltd.

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

References

1. Feinman RD, Pogozelski WK, Astrup A, Bernstein RK, Fine EJ,Westman EC, et al. Dietary Carbohydrate Restriction as the First Approach in Diabetes Management: critical review and evidence base. Nutrition. 2015;31(1):1—13
2. Evert, AB, Dennison M, Gardner CD, et al, Nutrition Therapy for Adults With Diabetes or Prediabetes: A Consensus Report, Diabetes Care, Ahead of Print, published online April 18, 2019, https://doi.org/10.2337/dci19-0014
3. Diabetes Canada, Diabetes Canada Position Statement on Low Carbohydrate
   Diets for Adults with Diabetes: A Rapid Review Canadian Journal of Diabetes (2020), doi: https://doi.org/10.1016/j.jcjd.2020.04.001.
4. National Academies of Sciences, Engineering and Medicine, Dietary Reference Intakes for Energy, Carbohydrate, Fiber, Fat, Fatty Acids, Cholesterol, Protein and Amino Acids, 2005, https://www.nap.edu/catalog/10490/dietary-reference-intakes-for-energy-carbohydrate-fiber-fat-fatty-acids-cholesterol-protein-and-amino-acids
5. Eades M, Dan Eades M (1997), Protein Power: The High-Protein/Low-Carbohydrate Way to Lose Weight, Feel Fit, and Boost Your Health—in Just Weeks! Bantam; New edition edition (1 December 1997)
6. Westman E, Phinney SD, Volek J, (2010) The New Atkins for a New You — the Ultimate Diet for Shedding Weight and Feeling Great, Atria Books February 17, 2010)
7. Volek JS, Phinney SD, The Art and Science of Low Carbohydrate Living: An Expert Guide, Beyond Obesity, 2011
8. Noakes T, Creed S-A, Proudfoot J, et al, (2013)The Meal Real Revolution, Quivertree Publications
9. Fung J (2016) Obesity Code, Greystone Books, Vancouver
10. Fung J, Moore J (2016), The complete guide to fasting : heal your body through intermittent, alternate-day, and extended fasting, Victory Belt Publishing
11. Eenfeldt A, Low Carb, High Fat Food Revolution: Advice and Recipes to Improve Your Health and Reduce Your Weight (2017), Skyhorse Publishers