Melatonin supplementation, hyperprolactinemia, and incident heart failure: A proposed prolactin-mediated pathway for cardiovascular risk.

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Europe PMCPublished 2026Medicine & Clinical ResearchClinical Trials & Treatments
Journal
World journal of experimental medicine
Record source
Europe PMC Research Library

Abstract / Description

The problem of heart failure (HF) is complicated and is continuously growing, making the need for novel solutions critical. The role of melatonin, widely used as an over-the-counter medication for sleep disorders, has been historically researched for its cardioprotective actions based on its established antioxidant properties. Recent preliminary evidence, however, points to a possibly alarming association: A statistically significant increased risk of new onset HF, HF requiring hospitalization, and all-cause mortality was observed in association with long-term melatonin therapy (one year or longer in duration), in adult patients suffering from insomnia. However, these were reported in a single, as-yet unpublished conference abstract that has not undergone peer review or independent validation. This hypothesis-generating observation warrants careful investigation of possible mechanisms. In this article we speculatively propose a plausible - but as yet unconfirmed - mechanistic pathway mediated through prolactin (PRL). Melatonin may increase the release of PRL through its modulation of hypothalamic dopaminergic neurons, though whether this effect is sustained with long-term use remains an unresolved critical knowledge gap. This is particularly relevant given that peripartum cardiomyopathy, a dangerous, pregnancy-related variant of HF, has as its central mechanism the cardiotoxic effect of a cytotoxic 16-kDa fragment of PRL. We hypothesize that chronic exogenous melatonin use might - if it were shown to sustain hyperprolactinemia - provide excess PRL that could theoretically be cleaved to the cardiotoxic 16-kDa fragment in patients with pre-existing oxidative stress and cardiovascular risk factors, in a manner analogous to peripartum cardiomyopathy. This speculative mechanism should be tested in prospective mechanistic and clinical studies, with appropriate adjustment for confounders including insomnia severity.
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