Anthony Komaroff: The Microbiome and Risk for Obesity and Diabetes

*Link to the 1st page of the article above. The rest is gated.*

Research has begun to demonstrate that the quality of bacteria in one's gut is important for human health. Let me call the quality of bacteria in one's gut "microbiome capital." Anthony Komaroff makes the argument that microbiome capital could plausibly be important early in his Journal of the American Medical Association summary article "The Microbiome and Risk for Obesity and Diabetes":

Beginning at the moment of birth, each human increasingly coexists with microbes. By the time individuals reach adulthood, they are colonized by many more microbial cells than the roughly 13 trillion human cells. More important still, these microbial cells (the microbiota), collectively, have exponentially more genes (the microbiome) than do human cells, around 250 to 800 times more.

Moreover, many genes in the human microbiome generate proteins, including hormones, neurotransmitters, and molecules of inflammation, that can enter the circulation and affect health. In light of this, it is reasonable to question whether the genes of the microbiome might play a greater role in health than do human genes. Recent evidence suggests that the microbiome may affect the probability of many major diseases, including obesity and diabetes.

Current knowledge hints that it might be possible to create a proxy for the quality of bacteria in one's gut—and thus for microbiome capital—from the ratio of bacteria from the phylum Bacteroidetes to bacteria from the phylum Firmicutes. Anthony writes:

About 90% of gut bacteria are in 1 of 2 phyla: Bacteroidetes and Firmicutes. Firmicutes generate more harvestable energy than Bacteroidetes. Obese humans have relatively more Firmicutes ...

Many experiments in mice, detailed as follows by Anthony, indicate that microbiome capital matters:

Gut microbiota from obese mice and from lean mice were transplanted into germ-free, lean mice, all of whom had the same daily caloric intake. Over the next 2 weeks, the mice receiving microbiota from obese mice became obese, whereas those receiving microbiota from lean mice remained lean.1
Gut microbiota from conventionally raised animals were placed in the guts of lean germ-free mice. Without any increase in daily caloric intake, the body fat content of the animals increased by 60% within 14 days, and they developed insulin resistance.2
Obese mice underwent Roux-en-Y gastric bypass (RYGB) surgery or sham surgery. Mice that underwent RYGB surgery had the expected weight loss and a characteristic change in the gut microbiome, whereas mice that underwent the sham surgery did not. Transfer of bacteria from mice that underwent RYGB surgery to mice that underwent the sham surgery resulted in weight loss, although not as great as seen following RYGB surgery. ...

The last experiment is important because in many ways it has been somewhat mysterious exactly why gastric bypass surgery helps so much in weight loss, given that greater hunger could easily counteract any purely mechanical reduction in food intake at a given sitting.

The comparison to capital accumulation is tightened by the influence of obesity on microbiome capital. Here is Anthony's description of that:

These experiments suggest that the composition of gut microbiota can influence obesity. However, other experiments suggest that obesity can influence the composition of gut microbiota. For example, when obese people diet and lose weight, the proportion of Bacteroidetes increases relative to Firmicutes. Conversely, when obese people resume their previous diets and gain weight, the proportion of Firmicutes increases.

All of this is only tantalizing if a therapeutic result for humans cannot be confirmed. The closest thing so far is this result that Anthony reports:

... only experimental evidence can suggest a causal connection. At least 1 study does. Treatment-naive men with the metabolic syndrome had their gut flora eliminated by polyethylene glycol lavage. Then they were randomized to receive small intestinal infusions (through a gastroduodenal tube) either from lean male donors or from their own feces. In men who received infusions from lean individuals, insulin sensitivity increased. This effect declined over time, and there was considerable individual variability.

That is, getting gut bacteria from someone thin tended to move the recipient away from the insulin-resistance that is so closely related to diabetes, though it only did so for a while.

This is an important area of research. I hope it proceeds expeditiously. For economists theorizing about obesity and diabetes, it points to changes in microbiome capital as a possible mechanism for phenomena. One big missing piece in the research is that it does not address whether or not high-quality probiotics taken by mouth can help with weight loss and with restoring insulin sensitivity.

Don't miss these other posts on diet and health and on fighting obesity:

Also see the last section of "Five Books That Have Changed My Life" and the podcast "Miles Kimball Explains to Tracy Alloway and Joe Weisenthal Why Losing Weight Is Like Defeating Inflation." If you want to know how I got interested in diet and health and fighting obesity and a little more about my own experience with weight gain and weight loss, see my post "A Barycentric Autobiography."