There are more factors that contribute to the development of obesity and related conditions than simply what we eat and how much energy we expend. The very notion of calories in, calories out is not what it seems; at least, not at face value. As researchers are discovering, your gut microbes have more to do with your metabolism than you might ever have imagined. A recent study published in the journal Nature gives us a closer look at how our gut inhabitants affect our propensity to develop obesity and related conditions.1
Researchers looked at the gut microbial composition, including the number of microbial genes, of 292 obese and non-obese Danish individuals. They were able to separate the individuals in to two groups based on the number of microbial genes—what they called bacterial richness. Those with the highest gene count had the highest bacterial richness and vice versa. They found that those with the lowest bacterial richness (23 percent of the individuals) also had more abdominal fat, insulin resistance, high insulin, increased triglycerides, decreased HDL-cholesterol (“good” cholesterol), and increased C-reactive protein (hsCRP—a marker of inflammation) when compared to the group with high bacterial richness.
In the people with low bacterial richness, they found 46 different bacteria groups (genera) to be more abundant; these include such potential pathogens as Campylobacter, Porphyromonas, Ruminococcus and Staphylococcus (plus commensals like Bacteroides). In the people with high bacterial richness, they found an abundance of Faecalibacterium, Bifidobacterium, Lactobacillus, Methanobrevibacter, and more. You may notice two stars in that last group—Lactobacillus and Bifidobacterium. These probiotic bacteria are known to have a wide range of human health benefits, so it is no surprise that they were found to be abundant in these healthy people who had higher bacterial richness.
The researchers also found that those who had low bacterial richness exhibited the potential to produce metabolites with possible deleterious health effects, including the ability to produce carcinogens—yes, your gut bacteria can produce carcinogens. On the other hand, those who had high bacterial richness exhibited the potential to produce organic acids known to be beneficial to health, including the short-chain fatty acids lactate, propionate, and butyrate.
Those with low bacterial richness (shall we call them bacterially poor?) showed the following characteristics:
- Reduction in the butyrate-producing bacteria (butyrate nourishes the cells of the intestinal lining)
- Increased potential for mucous degradation (the mucous lining protects the intestinal lining from damage)
- Reduced hydrogen and methane production potential combined with increased hydrogen sulfide formation potential
- Increase abundance of Campylobacter/Shigella (both potential pathogens)
- Increased potential for oxidative stress (production of peroxidase)
About these characteristics the researchers stated, “Overall, this suggests that [those individuals with low bacterial richness] harbor an inflammation-associated microbiota. Together, these analyses suggest that the [low bacterial richness] individuals are featured by metabolic disturbances known to bring them at increased risk of pre-diabetes, type 2 diabetes and ischaemic cardiovascular disorders. We propose that an imbalance of potentially pro- and anti-inflammatory bacterial species triggers low-grade inflammation and insulin resistance.”
Low bacterial richness has also been found in patients with inflammatory bowel disorder,2,3 elderly patients with inflammation,4 and obese individuals.5 In animal studies, this reduced bacterial richness has been induced by repeated antibiotic use.6 In humans, antibiotic use during childhood has been found to lead to increased risk of later being overweight, possibly due to a reduction in bacterial richness.7 In the Danish study, the obese individuals with low bacterial richness gained more weight than did the individuals with high bacterial richness.
As the authors state, “Obesity is not just obesity.” There is more to the story. Even lean people can harbor the wrong microbes, or have a low diversity of microbes, and be more at risk for chronic health conditions normally associated with obesity. This study will certainly lead to more investigation into the diversity of our gut microbes, and more specifically, how those microbes interact to produce health or disease. I eagerly await more insight into this fascinating universe.
- Le Chatelier E, Nielsen T, Qin J, et al., “Richness of human gut microbiome correlates with metabolic markers.” Nature. 2013 Aug 29;500:541–546.
- Manichanh C, Rigottier-Gois L, Bonnaud E, et al., “Reduced diversity of faecal microbiota in Crohn’s disease revealed by a metagenomic approach.” Gut. 2006 Feb;55(2):205-11.
- Lepage P, Hasler R, Spehlmann ME, et al., “Twin study indicates loss of interaction between microbiota and mucosa of patients with ulcerative colitis.” Gastroenterology. 2011 Jul;141(1):227-36.
- Claesson MJ, Jeffrey IB, Conde S, et al., “Gut microbiota composition correlates with diet and health in the elderly.” Nature. 2012 Aug 9;488(7410):178-84.
- Turnbaugh PJ, Hamady M, Yatsuneko T, et al., “A core gut microbiome in obese and lean twins.” Nature. 2009 Jan 22;457(7228):480-4.
- Cho I, Yamanishi S, Cox L, et al., “Antibiotics in early life alter the murine colonic microbiome and adiposity.” Nature. 2012 Aug 30;488(7413):621-6.
- Ajslev TA, Andersen CS, Gamborg M, et al., “Childhood overweight after establishment of the gut microbiota: the role of delivery mode, pre-pregnancy weight and early administration of antibiotics.” Int J Obes (Lond). 2011 Apr;35(4):522-9.