Can we blame our gut bacteria for being overweight ?
What science tells us
Over the last 10 years scientists have investigated the connection between body fat and gut bacteria. A lot of attention has been given to the connection between the disruption of the normal gut bacteria population, referred to as dysbiosis, and obesity.
In a study from 2004, it was shown that transferring gut bacteria from normal healthy mice to germ free mice (mice that are kept in a sterile environment and have no gut bacteria) resulted in a large increase in their body fat.) Later, Rob Knight and his colleagues showed that obese mice had significantly different gut bacteria compared to lean mice. They also showed that the most significant difference, namely the relative proportion of two groups of bacteria, the Firmicutes and the Bacteroidetes, was also seen in humans. Even more notably, they showed that transplanting bacteria from obese mice or obese humans into germ-free mice increased the animals body weights when compared to animals given bacteria from lean donors. The easiest way to explain this is that some bacteria are better at digesting certain food groups and also stimulating the body to convert the energy generated into fat. Recently it has also been shown that in Zebrafish the gut bacteria can influence the animal’s ability to adsorb fat.
On a more positive note, some bacteria are known to be very good at making the short-chain fatty acid (SCFA) butyrate which is known to be beneficial for the intestinal wall and help prevent potentially harmful chemicals getting into the blood stream. However, other short-chain fatty acids often produced by gut bacteria when exposed to a high fat diet are though to be harmful, weakening the gut lining. This effect, that is often associated with obesity, is thought to be due to the combined effect of a high fat diet and the specific bacteria that this diet stimulates, resulting in continual low-level inflammation of the intestines. Of course the open question which remains is whether the gut bacteria associated with obesity also causes the obesity phenotype or if the obese phenotype stimulates those specific bacterial species.
"Bacteria are known to be very good at making the short-chain fatty acid (SCFA) butyrate which is known to be beneficial for the intestinal wall and help prevent potentially harmful chemicals getting into the blood stream."
Antibiotics & Probiotics
A number of treatments and food types have been identified which can change the make-up of the gut bacteria population, these include antibiotic, probiotic and prebiotic use. In this light there has been some evidence in recent studies that antibiotic use can not only change the make-up of the gut bacteria but also lead to increased risk of obesity. These studies, however, are far from conclusive and have been mostly performed on animal. Additionally, recent work by Wand and colleagues has shown that mice fed with probiotics (live bacteria) show reduced weight gain and a healthier condition when concurrently fed on high fat diets. However, to date, evidence of the anti-obesity effects of probiotics have only been generated from animal models.
A further treatment possibility which is current attracting a lot of attention is FMT or fecal microbiota transplant. This is a treatment where the gut content of an often unhealthy or obese recipient is replaced by a sample of fecal microbiota (poop!) from a healthy (lean) donor. Some studies on animal models have shown that this can reduce obesity. A similar test was also performed in humans by Vrieze and collegues at the Amsterdam Medical Centre (AMC), who showed that poop transplant from lean healthy people to obese patients resulted in a reduction of insulin resistance, a sign of early diabetes. These results were published in 2012 in Gastroenterology. These experiments showed again that the gut bacteria may play a critical role in determining if you are over weight or not.
Your genes play an important role
Of course your genes also play a significant role in determining whether you have increased risk of becoming over weight. Many studies looking at the body mass index (BMI) within families and more specifically between twins have clearly shown that having a high BMI is between 40 and 70% the result of our genes. Human genome sequencing has also helped identify a number of specific genetic variations (SNPs) which have been linked to a higher BMI. A number of these variations have been found in the so-called fat mass and obesity gene (FTO) which has been consistently linked with increased risk of obesity. Recent work by Tim Spector and colleagues on the UK Twin cohort have additionally shown that a persons gut bacterial composition may be influenced by their genes, linking the presence of specific bacterial species to genetic variations on the human genome. This strongly suggests the co-evolution of specific host genotypes and microbiota composition.
Are diet and exercise not important?
Not surprisingly, a poor diet, or more specifically the increased intake of high energy and high fat foods are generally considered to increase your risk of becoming over weight. Additionally, too little exercise or a sedentary lifestyle are also seen as clearly increasing the risk of becoming overweight and developing related diseases. Therefore, a common advice is not to eat too much high energy food (carbohydrate and fat), eat a varied high fibre diet and to take regular exercise. Of course, the food you consume also impacts your microbiota and influences the interplay between your body, diet and gut bacteria.
Overall then, while the scientific evidence is now clear that your gut bacteria do play a role in determining whether or not you will become overweight, they are clearly not the only factor involved. Therefore, the role played by the gut bacteria should be seen in the context of multiple contributing factors including your genes, diet and lifestyle, all of which have an impact on your weight and BMI. Therefore, whether you are thin, lean, overweight or obese depends on an interplay and balance between your environment, lifestyle, diet, your genes and of course your gut bacteria.
In conclusion, if you want to blame the bacteria in your gut, please do not consider them to be the only villains!
Cani PD. (2014) Metabolism in 2013: The gut microbiota manages host metabolism. Nat Rev Endocrinol.; 10(2):74-6.
Cox AJ, West NP, Cripps AW. (2015) Obesity, inflammation, and the gut microbiota. Lancet Diabetes Endocrinol.;3(3):207-15.
Fredrik Bäckhed, Jill K. Manchester, Clay F. Semenkovich‡, and Jeffrey I. Gordon. (2006) Mechanisms underlying the resistance to diet-induced obesity in germ-free mice; vol. 104 no. 3, 979–984.
Goodrich JK, Davenport ER, Waters JL, Clark AG, Ley RE. (2016) Cross-species comparisons of host genetic associations with the microbiome. Science; 29;352(6285):532-5.
Hung CF, Breen G, Czamara D, Corre T, Wolf C, Kloiber S, Bergmann S, Craddock N, Gill M, Holsboer F, Jones L, Jones I, Korszun A, Kutalik Z, Lucae S, Maier W, Mors O, Owen MJ, Rice J, Rietschel M, Uher R, Vollenweider P, Waeber G, Craig IW, Farmer AE, Lewis CM, Müller-Myhsok B, Preisig M, McGuffin P, Rivera M. (2015) A genetic risk score combining 32 SNPs is associated with body mass index and improves obesity prediction in people with major depressive disorder.BMC Med.; 13:86.
Kallus SJ, Brandt LJ.; (2012) The intestinal microbiota and obesity. J Clin Gastroenterol. 46(1):16-24.
Ley RE, Bäckhed F, Turnbaugh P, Lozupone CA, Knight RD, Gordon JI. (2005) Obesity alters gut microbial ecology. Proc Natl Acad Sci U S A. Aug 2;102(31):11070-5. Epub Jul 20.
Nova E, Pérez de Heredia F, Gómez-Martínez S, Marcos A. (2016) The Role of Probiotics on the Microbiota: Effect on Obesity.Nutr Clin Pract. 31(3):387-400.
Parekh PJ, Balart LA, Johnson DA., (2015)The Influence of the Gut Microbiome on Obesity, Metabolic Syndrome and Gastrointestinal Disease.;Clin Transl Gastroenterol.; 18;6.
Semova I, Carten JD, Stombaugh J, Mackey LC, Knight R, Farber SA, Rawls JF. (2012) Microbiota regulate intestinal absorption and metabolism of fatty acids in the zebrafish.Cell Host Microbe.; 13;12(3):277-88.
Swinburn B, Gill T, Kumanyika S. (2005) Obesity prevention: a proposed framework for translating evidence into action. Obes Rev.; 6(1):23-33. Review.
Vrieze A, de Groot PF, Kootte RS, Knaapen M, van Nood E, Nieuwdorp M. (2013) Fecal transplant: a safe and sustainable clinical therapy for restoring intestinal microbial balance in human disease? Best Pract Res Clin Gastroenterol.; 27(1):127-37.