Synopsis

Source of validity: Scientific
Rating (out of 5): 4

Serotonin is a key neurotransmitter involved in the regulation of mood, emotion, and cognition. Scientific evidence strongly supports the "serotonin hypothesis" of depression, which posits that reduced serotonergic neurotransmission in the brain is associated with depressive symptoms. This hypothesis is primarily supported by the efficacy of selective serotonin reuptake inhibitors (SSRIs) and other antidepressants that increase the availability of serotonin in the synaptic cleft. Numerous randomized controlled trials and meta-analyses have demonstrated that medications enhancing serotonin signaling can significantly alleviate depressive symptoms in many patients. However, it is important to note that direct supplementation with serotonin itself is not a standard treatment, as serotonin cannot cross the blood-brain barrier when taken orally, making it ineffective as a direct therapy.

Instead, treatments aim to modulate endogenous serotonin levels or receptor activity. While the serotonin hypothesis does not fully explain all cases of depression, and not all patients respond to serotonergic medications, the overall body of clinical and mechanistic evidence provides robust scientific validation for targeting serotonin in depression management. Thus, serotonin’s role in depression treatment is well established in modern medicine, and its manipulation via pharmacological agents constitutes a cornerstone of current therapeutic approaches.

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