The microbial flora that inhabits the gut, skin, lung, and oral cavity of humans and other animals is thought to play a critical role in regulating metabolism and immunity. Any disruption or imbalance in that mix, a growing body of literature suggests, may trigger inflammation that contributes to conditions such as diabetes, heart disease, and cancer.
A new theory expands on this view, suggesting that social connections profoundly influence the composition of a person’s microbiome—at least as much as the growing number of probiotic supplements found on grocery store shelves.
Doctoral student Amar Sarkar and colleagues describe this concept as the social microbiome. Although people often focus on avoiding catching harmful bacteria or viruses from others, one of the intriguing hypotheses they recently advanced in Cell is that the social microbiome may contribute positively to health outcomes, independent of genes and lifestyle factors.
“Some keys to human evolution are encoded outside the human genome,” said Sarkar’s adviser, associate professor of human evolutionary biology Rachel Carmody. Culture plays a critical role, but the trillions of microbes that have taken up residence in and on humans likely play a part as well.
Since 2016, members of Carmody’s lab have explored how diet influences the microbiome, and how the microbiome in turn affects human metabolism [see “You Are What (Your Microbes) Eat,” November-December 2023, page 30]. But their conception of the microbiome has recently expanded from thinking about its role for individuals to considering how individuals in the same social group might come to develop similar microbiomes—and what that might mean for the health of the community.
The social microbiome is the collective sum of the microbiomes within an interacting group of organisms: family, classmates, or friends.
Sarkar, Carmody, and teaching fellow Cameron McInroy define the social microbiome as the collective sum of the microbiomes within an interacting group of organisms: family members, classmates, or a circle of friends. But there could also be transmission from more remote connections, such as an international traveler or another species—to take a recent, ominous instance, from a flock of chickens or a cow to a farmworker.
Sarkar synthesized the existing evidence on the various modes of spread—from mother to infant, direct contact between individuals, or contact with microbes on a doorknob or table—and the effects of that transmission, which often have surprising impacts on metabolism.
“Microbes that actually confer or improve sensitivity to certain forms of cancer therapy are also shown to be socially transmissible,” he said. Certain bacteria commonly found in the gut have also been shown to modulate patients’ responses to vaccines and other drugs used to treat Parkinson’s Disease, heart failure, and depression (see “The Sleuth,” July-August 2021, page 36).
Another example pertains to obesity, which often occurs in families and in social networks, a phenomenon often attributed to genetics and shared habits such as an affinity for sugary sodas or video games. But it too, could be driven by microbial exchange during social association.
Although no one has tested this hypothesis in humans, McInroy pointed to one of his favorite examples, a study in which fecal flora from a pair of human twins, one lean and one obese, was fed to germ-free mice. The mice exposed to microbes from the lean twin stayed thin, while their counterparts put on weight. “So, when obese and lean mice are then co-housed, the obese mice actually lose weight, in part by taking on some of these lean microbes,” explained McInroy. “It’s proof that social interactions and the community of people you surround yourself with can have real implications for host phenotype” (the observable characteristics of an individual that spring from interactions between his genes and the environment).
Conducting such research can be challenging outside the laboratory, where it’s harder to control interactions among study subjects. If a scientist finds that several research subjects living together have similar biomes, is that a result of eating similar foods or direct transmission among close contacts?
Sarkar described the approach to answering this question. Metagenomic sequencing, which involves sequencing the entire genome (not just a single gene) of each of the microbes found in a fecal sample, can help track the spread of gut microbes between two individuals. “Metagenomics lets us describe genetic mutations across the entire genome,” he said. Because these mutations are unique to an individual bacterium, explained Sarkar, “If two people have bacteria belonging to the same species and those bacteria have the same pattern of mutations across the whole genome, then we can be confident that they are clonemates.” That, he said, is “the gold standard for transmission.”
His next project will enable him to explore the influence of social connections on the microbiomes of individuals living in a wild population. As part of a collaboration with assistant professor of human evolutionary biology Martin Surbeck, who studies bonobo social behavior at a field site in the Congo, Sarkar will perform metagenomic sequencing on bonobo fecal samples. He’ll then examine characteristics of these primates’ microbiomes based on their family social ties and detailed behavioral data collected by Surbeck’s research team. The data will be an important step toward developing a better understanding of how social microbial transmissions can ultimately lead to new knowledge and even therapies for diseases such as cancer and diabetes that aren’t typically thought of as communicable.
