Serotonin is a hormone that plays a major role in maintaining mood. Lack of serotonin has thereby been associated with depression, thus the use of “selective serotonin reuptake inhibitors,” or SSRIs, that slow down degradation of brain serotonin. Widely prescribed drugs for depression such as Prozac, Lexapro, and Zoloft are meant to achieve this effect.

Although serotonin plays a major role in the brain, most of the body’s serotonin does not originate there. You may have heard that 90% of the body’s serotonin originates from the intestinal wall, yet another pathway involving the so-called “gut-brain axis.” And more recent evidence tells us that about half of the serotonin produced by the intestines is under the control of intestinal microbes. While earlier work did not identify which species were responsible for this serotonin effect, an elegant study from a group at UCLA has recently narrowed it down to one primary species: Turicibacter sanguinis, responsible for around half of total serotonin production.

Even though this microbe has been fully genetically mapped, we don’t know a lot about it. Since its discovery in 2002, limited attention has been paid to this microbe. Interestingly, one analysis of an 11th century Andean mummy revealed Turicibacter species in its stool. Turicibacter species can also be recovered from the microbiomes of indigenous populations unexposed to antibiotics, herbicides, etc, such as isolated tribes in Papula, New Guinea, suggesting that is a longstanding inhabitant of the human gastrointestinal tract. But I believe that the UCLA findings are going to cause an explosion of both research and methods to commercialize the availability of this microbe. Think of it: a microbial alternative to antidepressant pharmaceuticals. And microbes don’t come with side-effects such as impaired libido, weight gain, and suicide, as pharmaceuticals SSRIs do. While the microbe has been shown to increase serotonin in a mouse experimental model, the actual mood and biological effects have not yet been explored in humans—that’s coming.

Turicibacter sanguinis is not yet commercially available. I’ve asked my microbial sources if they have access and they do not yet. I also don’t know if this species can be fermented in various foods, such as our yogurts, to boost microbial counts that increase the odds of big benefits, as we do with L reuteri and other yogurts.

Now, combine restoration of Turicibacter with efforts to reduce LPS endotoxemia that also adds to depression, and I think we may be privy to a potentially powerful alternative method to not “treat” depression, but to get at its root causes. (If this argument is new to you, see my extended discussion about LPS endotoxin-driven depression in my Super Gut book.) If disruptions of the intestinal microbiome and its accompanying endotoxemia are major root causes underlying depression, is it any wonder that conventional antidepressants have such a poor track record? And are you getting a better sense of the exceptional power that understanding of the microbiome can yield?