Wednesday, June 15

Gut flora

One of the key aspects of being healthy is maintaining a proper gut flora. Lately, this has been stressed out by many people, including Chris Kesser, Art Ayers, among others. Gut microbiome is a new area of research which will influence all areas of health, specially chronic diseases caused by inflammation. 

Fiber has been promoted for a long time as necessary and healthy. We are supposed to eat fiber because it feeds our gut bacteria and produces short chain fatty acids (SCFA) which serve as fuel to colonocytes (butyrate) and controls cell metabolism and renewal, as well as expression and synthesis of some important biomolecules (mucin, for instance). Current guidelines dictate that fiber's daily intake should be around 25-30g, the more, the better. This, from my perspective, is completely unnatural and its only purpose serves to "justify" whole grain/cereal consumption. 

Fiber is one of the great exclusions when adopting a ketogenic diet. Fiber rich foods tend to be high in starch (cereals/grains/legumes) or sugar (some fruits). Vegetables are viewed as fine by most standards, and overall tend to be just water plus fiber. So when someone restricts his carbohydrate intake to trace amounts, it is not strange that they experiment constipation. This can be potentiated by possible dehydration (not drinking enough water/electrolyte imbalance). In a nutshell, from the fiber-hypothesis, a ketogenic diet is harmful to gut flora and consequently, to health. 

Duncan et al. (1) found that when obese subjects switched to a low carbohydrate diet (24g/day) butyrate production (estimated from fecal samples) fell linearly with carbohydrate intake. Changes in bacterial species included a reduction in Roseburia intestinalis and Eubacterium rectale, both which produce butyrate from glucose from soluble sugars in vitro. Brinkworth et al (2) found that fecal butyrate excretion was 30-60% lower in subjects eating a high fat-low carbohydrate diet compared to a high carbohydrate diet. The level of Bifidobacteria also decreased. 

The results of these studies show a clear trend: carbohydrate intake and levels of butyrate correlate directly. Ergo, it is assumed that a healthy diet must have a good amount of starch/glucose and non-digestible polysaccharides to produce butyrate and promote colon health. 

In my opinion, the interpretation is backwards. Considering the effects of butyrate on colon health, increasing the number of gut bacteria capable of fermenting carbohydrates and producing butyrate is an evolutionary adaptation to a lack of dietary butyrate.

Eating a high fat diet with more butyrate (specially from butter and full fat dairy) decreases the need for species which produce butyrate. Most butyrate (approximately 85%) is absorbed in the gut, so fecal samples may not be a good indicator of overall butyrate levels in the colon. At least not the butyrate that matters. It must be kept in mind that the content of other SCFA (such as propionate and acetate) is also important. 

Gut flora is extremely succeptible to diet. It also controls almost every physiological process in our bodies. It is not rare that a decrease in the supply of essential nutrients (in this case butyrate) changes bacterial population in the gut, trying to maintain homeostasis and proper functioning. After all, it is a symbiotic phenomenon, we need them and they need us. A clear example is fasting induced adipose factor (FIAF) (3). Gut microbiota is needed to digest dietary polysaccharides. Studies with germ-free mice have shown that gut bacteria promotes absorption of monosaccharides from the gut lumen, increasing de novo hepatic lipogenesis, and promotes adiposity via supression of FIAF (4). Germ-free mice are protected from diet-induced obesity partially because of increased levels of FIAF (5). Backhed et al. made an elegant scheme of the process:

Conventionalization of adult germ-free mice with normal microbiota from conventional raised animals has a dramatic impact on metabolism and nutrient partioning, increasing bodyfat by 60% and causing insulin resistance in only 14 days. This despite reduced food intake. 

This results can be interpreted as a mechanism by which gut microbiota promote food storage during ample food intake, associated with an increase in polysaccharide supply. This depends on the amount of bacteria capable of fermenting glucose, which in turn depends on the composition of the diet*.

In conclusion, a proper ketogenic diet should not compromise gut flora. The increase in the need for non digestible carbohydrates may only be relevant when a diet is nutrient deficient. Avoiding most inflammatory foods can help reducing both the number of pathogenic bacteria and the fat storage properties associated with some glucose fermenting bacteria. 

* The importance of diet in determining the effect of gut flora in nutrient partioning has been shown recently.

ResearchBlogging.orgDuncan SH, Belenguer A, Holtrop G, Johnstone AM, Flint HJ, & Lobley GE (2007). Reduced dietary intake of carbohydrates by obese subjects results in decreased concentrations of butyrate and butyrate-producing bacteria in feces. Applied and environmental microbiology, 73 (4), 1073-8 PMID: 17189447
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