Saturday, September 3, 2011

Forget the Blood Type Diet, Embrace the Gut Type Diet: Eating According to the Likes or Dislikes of Your Bacterial Subtenants Could Keep You Healthy, Lean & Sane.

Image 1: You better feed them right, or your gut bacteria could will disbehave just like the Alien in Ellen Ripley (Sigourney Weaver) in Alien 3 (20th Century Fox).
Eating right for your type, probably is not what it takes to have dietary success. Scientists from the US and Brazil have now found that eating according to the likes an dislikes of your bacterial subtenants seems to could eventually have a much greater potential (Wu. 2011) in keeping you healthy and, as the results of the joint research efforts of Canadian and Irish scientists shows, psychologically sane (Bravo. 2011).

Scientists estimate that the genome of the sum of our gut microbia is about 100x more complex than our own gene-sequence and the type and ratio of the 300-1000 different species within your intestinal tract have a major impact not only on how you digest your food, but also on how you look, feel and perform. It is therefore particularly interesting that Gary D. Wu and his colleagues established (for the first time) the existence of a stable microbiome composition that appears to be specialize to strive on a specific diet.
Note: Currently, the data is still too scarce and the variety of gut microbia, as well as their interactions too complex, for any reliable conclusions on whether it is "optimal" to eat according to your current gut biome or whether and in which way it would benefit your health, performance or body composition to modify / tweak the composition of the latter by dietary strategies and/or supplements or even medications. Even the idea of "optimizing" the microbial composition of our guts for "optimal" macro-nutrient usage is illusive, as it could well be that the specialization of our gut bacteria, i.e. their efficiency in using only little of the dietary energy for themselves and redirecting the rest to us, could theoretically be among the reasons for the obesity epidemic, as well.
In a preliminary analysis Wu et al. had established that in 98 healthy volunteers, whose stool they had analyzed for its individual microbiome composition there was a high correlation between habitual diets (measured by dietary questionnaires; data cf. figure 1, below) and the predominant type of bacteria.
Bacteroide enterotype was highly associated with animal protein, a variety of amino acids, and saturated fats, suggesting that meat consumption as in a Western diet characterized this enterotype. [...] The Prevotella enterotype, [...] was associated with [...] high values for carbohydrates and simple sugars, indicating association with a carbohydrate-based diet more typical of agrarian societies.
As one would expect, "self-reported vegetarians (n = 11) showed enrichment in the Prevotella
enterotype (27% Prevotella enterotype vs. 10% Bacteriodes enterotype; p = 0.13)" and the one self-reported vegan was in the Prevotella enterotype group, as well.

Image 2: Prevotella histicola is a major driving force of tooth decay (King's College). Its relatives in the gut, on the other hand, have been found to be implicated in insulin resistance and infertility due to endotoxin-related inflammation.
Now, if you are a dentist or did some research in the area of "caries" for whatever reason, the name "Prevotella" will probably sound remotely familiar. After all, the Prevotella species has been found to be associated with severe early childhood caries (e.g. Tanner. 2011). These are also the guys, whose poisonous lipolysaccharide dung increases the synthesis of the inflammatory cytokine TNF-alpha (Kim. 2007), which, in turn, has long been known to induce insulin resistance (Hotamisligil. 1999) - quite smart from the bacteria, isn't it? After all, if your body does not suck up the glucose the Prevotella will have more sugar to feed on. What may be less smart, though ,is that the endotoxin (lipolysaccharides are considered endotoxins) induced inflammation will also compromise testicular function on multiple levels, which in turn would deprive future generations of bacteria of their hosts.

Figure 1: Associations (Spearman correlation; -1: max neg. / +1 max pos.) between habitual dietary intake of sugars, vitamins & minerals, fats, amino acids, proteins and micronutrients and bacterial composition, where enterotype 1 is bacteriode dominant, and enterotype 2 is prevotella dominant (data adapted from Wu. 2011)
The polysaccharide A (PSA) produced by Bacteroides, an even larger class of bacteria which obviously strives on a high fat, high protein diet (or rather what mainstream dietitians call "high protein"), on the other hand, has recently been implicated in beneficial modulations of the immune system (Troy. 2010) and apparently even protects the nerves from he central nervous system from demyelation (Ochoa-Repáraz. 2010), i.e. the destruction of the insulating myelin layer. There is however a broad variety among the Bacteroides and as Wexler in his aptly titled paper "Bacteroides: the good, the bad, and the nitty-gritty." points out (Wexler. 2010):
The bacteria maintain a complex and generally beneficial relationship with the host when retained in the gut, but when they escape this environment they can cause significant pathology, including bacteremia and abscess formation in multiple body sites.
Based on the results of Wu's study, which also showed that a short-term dietary intevention (10 days) could not change the Bacteriode dominance of the 10 subjects who had been randomly assigned to high fat/low or a low fat/high fiber diets, we can thus only say that we probably are "optimized" for a certain macronutrient composition. Whether this is a beneficial or detrimental adaptation has still to be determined. What has however been established (in a rat model) is that chronic treatment with the probiotic bacteria Lactobacillus rhamnosus
[...] induced region-dependent alterations in GABAB1b mRNA in the brain [, ...] reduced GABAAα2 mRNA expression in the prefrontal cortex and amygdala, but increased GABAAα2 in the hippocampus [and] reduced stress-induced corticosterone and anxiety- and depression-related behavior.
Bravo et al. ascribe these beneficial psycho-physiological effects to the "modulatory constitutive communication pathway between the bacteria exposed to the gut and the brain". And highlight the "bidirectional communication of the gut–brain axis" as a possible target to treat stress-related disorders.
Image 3: The antibiotic vancomycin could potentially induce obesity month after treatment.
Did you know that Thuny et al. clearly showed that (Thuny. 2010) combined treatment with vancomycin-plus-gentamycin in patients with infective endocarditis was associated with a significant gain in BMI of +2.3kg/m² in the first year after discharge from hospital. For a man of 180cm this would be ~7.5kg. Vancomycin, by the way happens to be the cousin of Avoparcin an antimicribial growth promoter that has been used in the EU for fattening animals for about a year before it was prohibited in 1997.

In defense of "antibiotics" and as a word of caution against exuberant enthusiasm for all bacteria it should yet be mentioned that alternative antibiotics did not exhibit the same profound effects in the Thuny study. Moreover, observations in germ-free mice suggest that (Bäckhed. 2006)
[germ-free] animals are protected from diet-induced obesity by two complementary but independent mechanisms that result in increased fatty acid metabolism: (i) elevated levels of Fiaf, which induces Pgc-1α; and (ii) increased AMPK activity.
In view of the ever increasing resistance towards antibiotics, it is however unrealistic to assume that we will see similar effects in humans after the administration of individual or even combined high-dose antibiotics.
Moreover, more and more scientists argue that, based on the growth-promoting effects of antibiotics in food animals (Linn. 2011), it is more than likely that the long thought of relation between gut microbiota and the human obesity epidemic is real and that research into the detailed working principles of antimicrobial growth promoters (AGP) in animals may reveal hitherto overlooked underpinnings of obesity an respective treatment strategies.

We will see what future research will bring. Yet, while you are waiting for me to keep you on par with the results, I suggest you better stay away from growth or non-growth promoting antibiotics if you want to stay healthy, sane and slim.