‘What portion of our dietary calories do our gut bacteria consume? Our guts support a wide array of microorganisms. These must either survive off of our food, or off of bodily secretions made with energy from food (e.g. bile). How much of a typical daily diet is consumed by microorganisms rather than being absorbed by the body?‘
Is it even possible to consider the caloric consumption by our gut microbes as a separate activity? By implying theis imposed upon the human body, this question’s implicit assumption of an us versus them dynamic is problematic to say the least. We can eliminate swaths of human microbiota through antibiotics and try to add others through probiotics but does an autonomous microbe-free human body exist in nature? The human and microbial parts of our body are bound together inextricably. After all, microbes aren’t limited to our gut but encompass other mucosal surfaces such as the respiratory and reproductive tracts, not to mention the ‘largest organ’ in our body, the skin. Thus to ask what portion of dietary calories is consumed by the ‘human body’ versus its ‘microbiota’ is akin to seeking to slice a bowl of water.
That said, energy from diet depends on diet type. Diet type in turn favors stable colonization by certain microbes over others. As we are now discovering almost by the day, to a great extent, microbial metabolism of diet determines caloric yield. Research suggests gut microbiota interact with diet in as-yet not totally deciphered ways to
a) help more efficiently digest food and generate more calories,
b) generate metabolites capable of causing great harm over the long term, for example in cardiovascular diseases, and
c) generate metabolites important for regulating bile acid synthesis, something that may have great bearing in obesity.
A 2016 review by Sonnenburg and Bäckhed () is a handy source that summarizes how and what gut microbiota could contribute to such varied aspects of human metabolism.
Generated Primarily By Gut Microbes, Calories Derived From Dietary Fiber Depend On Diet Type
Gut microbes are critical fordigestion through the process of fermentation, which converts this otherwise indigestible material into energy (ATP) optimal for use by the cells in the anaerobic environment of the intestine ( , 2, , , , 6, , 8).
- Fermentation generates (SCFA) such as acetate, butyrate and propionate.
- SCFA are important for all manner of normal physiological processes (8,
- SCFA were estimated to provide 5 to 10% of the calories available for absorption from the typical industrialized world diet that’s fiber-poor, and saturated fat- and sucrose-rich (10).
- OTOH, plants are the main source of dietary fiber (11). People such as the hunter-gatherer Hazda community in Tanzania consume 7X more dietary fiber ( ) compared to that in the prototypical industrialized world diet. Such diets would naturally generate much more SCFA, which would thereby embody a much larger portion of their daily calories, courtesy the work of gut microbes needed for such conversion.
Examined in this light, competition between our body’s human and microbial cells could arise through resource conflict arising from diets from which both can efficiently extract energy (see figure below from).
How Microbial Metabolism of Diet Could Influence A Human’s Heart Health
- High levels of (TMA) are generated by microbial metabolism of L- and from diets rich in red meat, and cheese, eggs, meats and seafood, respectively.
- Absorbed into bloodstream from the gut, TMA’s enzymatically oxidized to (TMAO).
- Some recent high profile studies suggest TMAO could promote ( , ; see figure below from ).
- Connection between diet and microbiota is suggested by the fact that microbiota of vegans remained poor producers of TMA, even when they were transiently provided TMA precursors in their diet ( ) though we don’t yet fully understand the precise conditions under which TMAO promotes cardiovascular disease.
- Gut microbiota modify human host-derived bile acids synthesized by hepatocytes from cholesterol. Originally the idea was these secondary bile acids acted as detergents to help absorb dietary fats.
- Since the 1990s, however, research has uncovered additional functions in the form of signaling capacity in metabolic pathways. In fact, microbial modification of bile acids could function as a negative feedback loop to reduce bile acid production (see figure below from 17).
- Altered microbiota are associated with imbalances in this pathway ( , ), as seen in obesity and . This suggests inhibition of bile acid synthesis may not be occurring normally in obese people.
1. Sonnenburg, Justin L., and Fredrik Bäckhed. “Diet-microbiota interactions as moderators of human metabolism.” Nature 535.7610 (2016): 56-64.
2. Grabitske, Hollie A., and Joanne L. Slavin. “Low-digestible carbohydrates in practice.” Journal of the American Dietetic Association 108.10 (2008): 1677-1681.
3. Koropatkin, Nicole M., Elizabeth A. Cameron, and Eric C. Martens. “How glycan metabolism shapes the human gut microbiota.” Nature reviews Microbiology 10.5 (2012): 323-335.
4. Flint, Harry J., et al. “Microbial degradation of complex carbohydrates in the gut.” Gut microbes 3.4 (2012): 289-306.;
5. Boutard, Magali, et al. “Functional diversity of carbohydrate-active enzymes enabling a bacterium to ferment plant biomass.” PLoS Genet 10.11 (2014): e1004773.
6. Terrapon, Nicolas, and Bernard Henrissat. “How do gut microbes break down dietary fiber?.” Trends in biochemical sciences 39.4 (2014): 156-158.
7. Larsbrink, Johan, et al. “A discrete genetic locus confers xyloglucan metabolism in select human gut Bacteroidetes.” Nature 506.7489 (2014): 498-502.;
8. Andoh, Akira. “Physiological Role of Gut Microbiota for Maintaining Human Health.” Digestion 93.3 (2016): 176-181.
9. Hijova, E., and A. Chmelarova. “Short chain fatty acids and colonic health.” Bratislavské lekárske listy 108.8 (2007): 354.
10. McNeil, N. I. “The contribution of the large intestine to energy supplies in man.” The American journal of clinical nutrition 39.2 (1984): 338-342.
11. Bergman, E. N. “Energy contributions of volatile fatty acids from the gastrointestinal tract in various species.” Physiological reviews 70.2 (1990): 567-590.
12. Schnorr, Stephanie L., et al. “Gut microbiome of the Hadza hunter-gatherers.” Nature communications 5 (2014).
13. Wasielewski, Helen, Joe Alcock, and Athena Aktipis. “Resource conflict and cooperation between human host and gut microbiota: implications for nutrition and health.” Annals of the New York Academy of Sciences (2016).
14. Wang, Zeneng, et al. “Gut flora metabolism of phosphatidylcholine promotes cardiovascular disease.” Nature 472.7341 (2011): 57-63.
15. Koeth, Robert A., et al. “Intestinal microbiota metabolism of L-carnitine, a nutrient in red meat, promotes atherosclerosis.” Nature medicine 19.5 (2013): 576-585.
16. Tang, WH Wilson, et al. “Intestinal microbial metabolism of phosphatidylcholine and cardiovascular risk.” New England Journal of Medicine 368.17 (2013): 1575-1584.
17. Joyce, Susan A., and Cormac GM Gahan. “Bile acid modifications at the microbe-host interface: potential for nutraceutical and pharmaceutical interventions in host health.” Annual review of food science and technology 7 (2016): 313-333.
18. Parséus, Ava, et al. “Microbiota-induced obesity requires farnesoid X receptor.” Gut (2016): gutjnl-2015.
19. Ryan, Karen K., et al. “FXR is a molecular target for the effects of vertical sleeve gastrectomy.” Nature 509.7499 (2014): 183-188.
For Further Reading:
1. Krajmalnik-Brown, Rosa, et al. “Effects of gut microbes on nutrient absorption and energy regulation.” Nutrition in Clinical Practice 27.2 (2012): 201-214.
2. Martens, Eric C., et al. “The devil lies in the details: how variations in polysaccharide fine-structure impact the physiology and evolution of gut microbes.” Journal of molecular biology 426.23 (2014): 3851-3865.
3. Blaut, Michael. “Gut microbiota and energy balance: role in obesity.” Proceedings of the Nutrition Society 74.03 (2015): 227-234.