SSRIs

Serotonin is not the "happy hormone" but a primarily inflammatory and stress-related molecule, and the drugs known as selective serotonin reuptake inhibitors (SSRIs) are a class of antidepressants whose clinical effects are widely misunderstood. 2 Ray Peat argued that the foundational myth of SSRIs was a culturally conditioned promotional construction, born from the government's criminalization of psychedelic substances in the 1960s. 6 Because LSD and psilocybin were known to be anti-serotonin agents that blocked serotonin's constricting actions on smooth muscle and turned off serotonin nerves in the brain, Peat contended that the drug industry inverted this reality to market serotonin-increasing drugs as the path to sanity, implying that if anti-serotonin agents made you "insane," then products to increase serotonin must be the cure. 6 Georgi Dinkov has extended this historical account, stating that the government needed a compliant population and vicious soldiers for the Vietnam War, so they deliberately sought a drug that did the exact opposite of the anti-authoritarian LSD, leading to the birth of SSRIs despite clinical trial evidence of increased suicide risk. 11

Peat maintained that the drugs sold as SSRIs do not reliably produce their named effect, and that any genuine antidepressant action occurs by lowering serotonin in the long run. 2 He cited a study in which aggressive, vicious dogs were found to have high serotonin; after a month of treatment with an SSRI, the dogs became pleasant and their serotonin had gone down significantly. 2 Peat noted that the first generation of antidepressants, monoamine oxidase (MAO) inhibitors, increased adrenaline, dopamine, and serotonin, but when their patents expired, the industry selectively attributed their efficacy to serotonin to sell new products. 3 He pointed to tianeptine, a serotonin uptake promoter that reduces serotonin's activity in the synapse, as a more effective antidepressant with beneficial effects on arthritis, diabetes, and inflammatory conditions. 8 Other anti-serotonin drugs like cyproheptadine, ondansetron, lisuride, and bromocriptine have demonstrated therapeutic value by blocking serotonin's effects. 2

The biological actions of serotonin are overwhelmingly degenerative and catabolic. Peat detailed that serotonin constricts smooth muscle in the intestine, blood vessels, and uterus, and is known to cause blood clotting, coronary artery spasms, and inflammation. 2 It activates every pituitary hormone, including the ACTH-adrenal stress axis, and serotonin slows oxidative metabolism, reducing the brain's use of glucose and oxygen in a pattern characteristic of depression, hypothyroidism, aging, and dementia. 2 Serotonin promotes aerobic glycolysis, the inefficient cancer-like metabolism in which lactic acid is produced despite the presence of oxygen, and it reduces cerebral blood circulation. 5 Peat emphasized that serotonin and estrogen have systematically interrelated functions, with estrogen activating mast cells to release histamine and serotonin, contributing to the higher incidence of depression, Alzheimer's disease, multiple sclerosis, and liver disease in women. 9 In Parkinson's disease, anti-serotonin drugs alleviate symptoms while serotonin precursors worsen them, and in autism, serotonin is elevated in the blood of affected children and their relatives. 9

The chronic use of SSRIs produces a distinct profile of iatrogenic harm. Peat observed that by increasing exposure to serotonin or decreasing adrenaline, these drugs slow the metabolic rate, making it harder to burn calories and leading to weight gain. 2 He identified a well-documented association of SSRIs with osteoporosis, explaining that serotonin produced in an inflamed intestine or potentiated by the drugs reaches the bones and interferes with bone metabolism, causing rapid bone loss. 2 The drugs are also associated with sexual malfunction, hair loss, and a lengthening of the heart's QT interval that can cause cardiac arrest. 5 Peat noted that the public is slowly becoming aware of these effects, but the information is always contextualized within the drugs' supposed therapeutic value, even though electroshock therapy—used when SSRIs fail—works only by increasing neurosteroid synthesis at the cost of brain cell death. 5 Dinkov added that Germany's Commission E initially refused to approve Prozac after their own trials showed people killing themselves, and only relented under political pressure while issuing the first black box warning for suicide risk. 11

Recovery from SSRI use requires a systematic metabolic intervention. Peat stated that high serotonin trains the nervous system to stay in a stress state by activating the pituitary ACTH and adrenal system, creating an inflammatory state in the nerves and body that increases fat production and stress. 7 He advised that breaking this pattern requires restoring a good, intense metabolic rate—increasing cellular energy production, keeping thyroid function up, and keeping estrogen down—and noted that even doing everything right, people seem to take about a year to feel fairly normal again. 7 Eating frequently to avoid running on adrenaline was one of his specific recommendations. 7 The broader context Peat provided is that serotonin, nitric oxide, and ATP spread damage signals through the body in a bystander effect, and that the brain's capillaries treat serotonin as a toxin to eliminate, much like the lungs. 5