Yet another study that exposes the “happiness hormone” 5-HT as anything but. In addition, the study also raises serious questions in regards to how much of the current CVD epidemic is iatrogenic in origin, considering the widespread use of the serotonergic SSRI drugs in virtually all age groups of the general population. In corroboration of the findings of the study below that 5-HT may be a causative factor in CVD, studies done decades ago with the serotonin antagonist ketanserin (a drug developed to treat hypertension, which by itself is pretty telling about the role of 5-HT in CVD) demonstrated robust decrease in CVD rates and progression in animal models, as well as reduction in ischemic events (heart attacks and strokes) in the animals receiving ketanserin.
https://doi.org/10.1186/s12929-025-01172-4
“…In recent years, the role of smooth muscle cells (SMCs) in arterial health and disease has garnered significant attention. Understanding the molecular mechanisms by which these cells contribute to vascular conditions, particularly intimal hyperplasia following arterial injury, is critical in developing effective therapeutic strategies. A compelling study published in the Journal of Biomedical Science explores this phenomenon, shedding light on the impact of hydroxyindole O-methyltransferase (HIOMT) expression specifically within smooth muscle cells. The study highlights a transformative discovery: the expression of HIOMT in smooth muscle can markedly reduce arterial injury-induced intimal hyperplasia. This pathophysiological condition arises when there is injury to the arterial wall, leading to an excessive proliferation of smooth muscle cells, contributing to the thickening of the vessel wall and narrowing of the lumen. Such events can predispose individuals to severe cardiovascular complications, including ischemia and thrombosis.”
“…HIOMT is an enzyme critical for the metabolism of serotonin and other indoleamine substances. By influencing serotonin levels, the expression of HIOMT in vascular smooth muscle cells appears to have a cascading effect on SMC behavior. Serotonin is known for its role not only in neurotransmission but also in various vascular processes, including vasoconstriction and modulation of vascular smooth muscle proliferation. Consequently, increasing HIOMT activity may lead to reduced levels of bioactive serotonin in the vicinity of the arterial wall, blunting the pathological cellular responses associated with arterial injury.”
