New research found that depression may begin in your gut when a common bacterium interacts with a chemical found in most personal care products - Tech paper

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New research found that depression may begin in your gut when a common bacterium interacts with a chemical found in most personal care products

Medical Research & Innovations

8 min read<br>Journal of the American Chemical Society

Depression has been explained to most people as a brain problem. A chemical imbalance. Too little serotonin, too much cortisol, a prefrontal cortex that cannot quiet an overactive amygdala. The treatments that followed from this explanation target the brain directly: antidepressants that adjust neurotransmitter levels, therapy that rewires thought patterns, medications that dampen the stress response.

Harvard Medical School researchers have now traced a pathway to depression that starts somewhere most people would never think to look. Not in the brain. In the gut. And not just in the gut in the general sense that the microbiome affects mood. In a specific bacterium, interacting with a specific chemical found in products sitting in your bathroom right now, producing a specific inflammatory molecule that travels up to the brain and helps create the conditions for major depressive disorder.

The mechanism is precise enough to be disturbing. And it suggests that for a significant number of people, the depression they are experiencing may not be primarily a brain disorder at all.

The Bacterium Nobody Was Watching

Morganella morganii is not a pathogen in the conventional sense. It lives quietly in the digestive tract of most people without causing obvious harm. It does not produce the dramatic symptoms associated with dangerous gut bacteria. For most of its history in medical literature, it was considered an opportunistic organism, occasionally problematic in immunocompromised patients, largely unremarkable otherwise.

Several years ago, large-scale population studies began noticing something unusual. People with major depressive disorder had consistently higher levels of Morganella morganii in their gut microbiomes compared to people without depression. The association appeared across multiple datasets. But an association is not an explanation. The question that nobody could answer was whether the bacterium was somehow contributing to depression, whether depression was altering the gut environment in ways that allowed it to flourish, or whether something else entirely was driving both.

The Harvard team, led by researchers from Harvard Medical School and the Broad Institute of MIT and Harvard, set out to find the mechanism. What they found was more specific than anyone had anticipated.

The Chemical Hitchhiker

The key to the discovery was a molecule called diethanolamine, or DEA. This is not an obscure industrial compound. DEA is found in nearly 20% of all personal care products, present in shampoos, body washes, facial cleansers, lotions, and household cleaning products used by millions of people every day. It is also found in metalworking fluids, pesticides, antifreeze, and pharmaceuticals. The European Commission has already prohibited DEA in cosmetics due to its links to carcinogenic nitrosamines. In the United States, the EPA lists it as a hazardous air pollutant. It enters the body primarily through skin absorption during daily personal care routines and through ingestion of trace amounts in food and water.

Once inside the body, DEA reaches the gut. And in the gut, it encounters Morganella morganii.

Under normal circumstances, Morganella morganii produces a class of fatty molecules called phospholipids as part of its ordinary biological functioning. These molecules sit on the bacterium’s surface and are generally harmless. But when DEA is present in the gut environment, something unexpected happens. The bacterium incorporates DEA into its phospholipid structure, substituting it into a position where a different molecule would normally sit. The result is a chemically altered phospholipid that the body has never encountered in its natural form. And the immune system, encountering this unfamiliar molecule, responds to it as a threat.

The Inflammatory Trigger

The Harvard team used a bioassay-guided approach to identify exactly what these altered phospholipids were doing at the molecular level. What they found was that the DEA-modified molecule produced by Morganella morganii activates two specific receptors on immune cells called TLR1 and TLR2, toll-like receptors that function as the immune system’s pattern recognition sensors for detecting foreign and potentially dangerous molecules.

When TLR1 and TLR2 are activated, they trigger a pro-inflammatory immune response, releasing cytokines and initiating the cascade of systemic inflammation...