|The alien inside - billions of bacteria in your gut interact with your central nervous system and take command over your metabolism and - probably - even about what you want to put into your mouth.|
Well, in today's SuppVersity Article we're going to take a look at a bunch of studies and hypothesis that may actually allow you to find a new excuse for your inability to lose weight. But beware! While I wouldn't say that researchers who favor the "evolutionary conflict between host and microbes" theory as an alternative explanation for the ever-increasing obesity rates are totally off. What I will say, however, is that this is at best a contributing, maybe even just a corollary factor in the etiology of the obesity epidemic.
We know for quite some time that individual members of the microbiota, and consortia of those microbes are highly dependent on the nutrient composition of the diet.
- Prevotella grows best on carbohydrates; dietary fiber provides a competitive advantage to Bifidobacteria (González‐Rodríguez. 2013)
- Bacteroidetes has a substrate preference for certain fats (Wu. 2011)
We have tons of associations, but little experimental evidence: All this does yet not mean that the specialized gut microbiome will also affect the dietary intake of the host. You could after all argue that you could get rid of Prevotella by simply cutting out all carbs from your diet, but scientists believe that the specialization works both ways.There is circumstantial evidence for a connection between cravings and the composition of gut microbiota. Individuals who are “chocolate desiring” have different microbial metabolites in their urine than “chocolate indifferent” individuals, despite eating identical diets (Rezzi. 2007).
|Figure 1: A study by Rezzi et al. showed that chocolate cravers have a different microbiome than their peers (Rezzi. 2007)|
It's not as if there was no evidence, it's just not really compelling (yet?)
An area where the mechanisms appear to be more evident is the effect of certain bacteria on the expression of certain molecular receptors in the gut. Germ-free mice for example have altered taste receptors for fat on their tongues and in their intestine compared to mice with a normal microbiome (Duca. 2012). Since an increase in fat receptors is associated with an increased preference and intake for fatty foods and energy, an over-expression of these receptors could certainly be involved in the etiology of obesity.
In conjunction with other scientific evidences, such as the increased intestinal expression of cannabinoid and opioid receptors in mouse and rat intestines in response to the oral supplementation of L. acidophilus NCFM in rats and similar effects in human epithelial cell culture (Rousseaux. 2006), the Duca study suggests that the composition of microbes in our guts could in fact actively alter our food preferences by modulating the receptor expression or transduction (Collins. 2012).
Is a "gut dysbiosis" the reason we are fat?
The idea that not having the "right" bacterial make-up could be at the heart of the obesity epidemic has recently received significant scientific attention. Backhed and colleagues showed that mice genetically predisposed to obesity remained lean when they were raised without microbiota (Bäckhed. 2004).
Let's put everything together, now!
As you can see in the graphical illustration in Figure 3, the taste receptor interactions are not the only scientifically proven changes. There are also well-known endotoxin induced effects on mood and anxiety (Amaral. 2008; Chiu. 2013) of which Hill et al. have shown (albeit in a different context) that it will affect food cravings (Hill. 1991).
Beware! If the scientists are right, the same probiotics that are good for people on a mixed diet may be bad for those who consume a low carb or ketogenic diet. I would thus be very reluctant to make any form of one-size-fits it all supplement recommendation! If there is one take home message from what we already know, it's that, in the long run, unbalanced diets (low-to-no whatever) will obviously put you at greater risk of developing a highly specialized obesity-promoting gut microbiome.
If microbial control is mediated through the vagus nerve, then microbial signals should interfere to some extent with the physiological regulation coordinated by the vagus nerve. [...] We predict that people experiencing cravings should have lower vagal tone. Furthermore, it is possible to block or sever the vagus, which we predict would subdue microbial signaling via the vagus nerve, and thereby alter food preferences. This would be consistent with studies showing that blocking the vagus nerve can lead to weight loss." (Alcock. 2014)In conjunction with the aforementioned effects and the influence of population size and composition on cravings and high fat, high carbohydrate preferences foods Alcock et al. believe to have enough evidence for the existence of what they call an "evolutionary conflict between the host and microbiota" which may lead to cravings and cognitive conflict with regard to food choice.
- Alcock, Joe, Carlo C. Maley, and C. Aktipis. "Is eating behavior manipulated by the gastrointestinal microbiota? Evolutionary pressures and potential mechanisms." BioEssays (2014).
- Amaral, F. A., et al. "Commensal microbiota is fundamental for the development of inflammatory pain." Proceedings of the National Academy of Sciences 105.6 (2008): 2193-2197.
- Bäckhed, Fredrik, et al. "The gut microbiota as an environmental factor that regulates fat storage." Proceedings of the National Academy of Sciences of the United States of America 101.44 (2004): 15718-15723.
- Chiu, Isaac M., et al. "Bacteria activate sensory neurons that modulate pain and inflammation." Nature (2013).
- Collins, Stephen M., Michael Surette, and Premysl Bercik. "The interplay between the intestinal microbiota and the brain." Nature Reviews Microbiology 10.11 (2012): 735-742.
- Cox et al. "Altering the Intestinal Microbiota during a Critical Developmental Window Has Lasting Metabolic Consequences." Cell 158 (2014):705–721.
- De Filippo, Carlotta, et al. "Impact of diet in shaping gut microbiota revealed by a comparative study in children from Europe and rural Africa." Proceedings of the National Academy of Sciences 107.33 (2010): 14691-14696.
- Duca, Frank A., et al. "Increased oral detection, but decreased intestinal signaling for fats in mice lacking gut microbiota." PloS one 7.6 (2012): e39748.
- Fava,Francesca, et al. "The type and quantity of dietary fat and carbohydrate alter faecal microbiome and short-chain fatty acid excretion in a metabolic syndrome ‘at-risk’population." International Journal of Obesity 37.2 (2012): 216-223.
- González‐Rodríguez, Irene, et al. "Factors involved in the colonization and survival of bifidobacteria in the gastrointestinal tract." FEMS microbiology letters 340.1 (2013): 1-10.
- Gotthardt, J. D., et al. "Exercise Promotes Enhanced Gut Microbial Diversity Compared to Sedentary Counterparts." International Journal of Exercise Science: Conference Proceedings. Vol. 9. No. 2. 2014.
- Hehemann, Jan-Hendrik, et al. "Transfer of carbohydrate-active enzymes from marine bacteria to Japanese gut microbiota." Nature 464.7290 (2010): 908-912.
- Hill, Andrew J., Claire FL Weaver, and John E. Blundell. "Food craving, dietary restraint and mood." Appetite 17.3 (1991): 187-197.
- Hold, Georgina L. "The gut microbiota, dietary extremes and exercise." Gut (2014): gutjnl-2014.
- Kadooka, Y., et al. "Regulation of abdominal adiposity by probiotics (Lactobacillus gasseri SBT2055) in adults with obese tendencies in a randomized controlled trial." European Journal of Clinical Nutrition 64.6 (2010): 636-643.
- Miras, Alexander D., and Carel W. le Roux. "Mechanisms underlying weight loss after bariatric surgery." Nature Reviews Gastroenterology and Hepatology 10.10 (2013): 575-584.
- Mozaffarian, Dariush, et al. "Changes in diet and lifestyle and long-term weight gain in women and men." New England Journal of Medicine 364.25 (2011): 2392-2404.
- Rezzi, Serge, et al. "Human metabolic phenotypes link directly to specific dietary preferences in healthy individuals." Journal of proteome research 6.11 (2007): 4469-4477.
- Ridaura, Vanessa K., et al. "Gut microbiota from twins discordant for obesity modulate metabolism in mice." Science 341.6150 (2013): 1241214.
- Rousseaux, Christel, et al. "Lactobacillus acidophilus modulates intestinal pain and induces opioid and cannabinoid receptors." Nature medicine 13.1 (2006): 35-37.
- Wu, Gary D., et al. "Linking long-term dietary patterns with gut microbial enterotypes." Science 334.6052 (2011): 105-108.