Past research has suggested that weight may be influenced by genes. A new study builds on this concept, revealing that our genetic makeup shapes what type of bacteria live in the gut, which may affect how heavy we are.

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The results of a twin study suggest that our genes influence what type of bacteria we have in our gut, and that the abundance of bacteria could affect our weight.

The findings come from a twin study conducted by researchers from Cornell University in Ithaca, NY, and King’s College London in the UK.

The research team, including Prof. Tim Spector, head of the Department of Twin Research and Genetic Epidemiology at King’s College London, says the results may open the door to personalized probiotic treatments that could reduce the risk of obesity and its related diseases.

For their study, published in the journal Cell, the researchers sequenced the genes of microbes present in over 1,000 fecal samples taken from 416 pairs of twins who were part of the Twins UK data registry.

Of these twins, 171 pairs were identical and 245 were non-identical. Identical twins share 100% of their genes, while non-identical twins share around 50% of their genes.

Results of the analysis revealed that identical twins had a similar abundance of specific types of gut bacteria, compared with non-identical twins. The team says this indicates that genes influence the type of bacteria present in the gut.

What is more, the researchers found that the presence of a class of bacteria called Christensenellaceae was most influenced by genes. A certain strain of this bacteria – Christensenellaceae minuta – was found to be more common among individuals of a low body weight.

On introducing this bacteria to the guts of mice, the team found the animals gained less weight than those that did not receive the bacteria. This suggests that increasing the amount of Christensenellaceae minuta bacteria in the gut could help to reduce or prevent obesity, the researchers say.

Commenting on their results, Prof. Spector says:

Our findings show that specific groups of microbes living in our gut could be protective against obesity – and that their abundance is influenced by our genes. The human microbiome represents an exciting new target for dietary changes and treatments aimed at combating obesity.”

Senior author Ruth Ley, an associate professor of microbiology at Cornell University, notes that this study is the first to determine that specific gut microbes are heritable and that the variation of these microbes is not solely influenced by diet, environment, lifestyle and health.

Numerous other studies have reported on the association between obesity and gut bacteria, but all of them have different theories.

In September, Medical News Today reported on a study suggesting that Granny Smith apples could protect against obesity by balancing the proportions of “good” gut bacteria.

The researchers of that study, from Washington State University, explain that the fibers and polyphenols present in Granny Smith apples are unscathed when they reach the colon, even after exposure to stomach acid and digestive enzymes. The bacteria in the colon then ferment these compounds, producing butyric acid that triggers the growth of good gut bacteria.

Another study, reported in July, detailed the creation of a probiotic that researchers say could prevent obesity.

Senior study author Sean Davies, of Vanderbilt University in Nashville, TN, and colleagues genetically modified a strain of bacteria that colonizes the human gut – Escherichia coli Nissle 1917 – to produce a compound called N-acyl-phosphatidylethanolamine (NAPE), which can reduce food intake.

On giving this bacteria to mice fed a high-fat diet for 8 weeks, the team found that it significantly reduced their food intake, body fat and incidence of hepatosteatosis (fatty liver), compared with control mice.

“There are lots of people who are doing their best to change their lifestyle and it still isn’t enough for them to get to and keep a healthy weight. We think this strategy will really help them,” Davies told MNT.