Nocturnal melatonin suppression is the acute, light-induced inhibition of the pineal gland’s production and secretion of the hormone melatonin during the biological night. Melatonin is the body’s primary dark signal, and its suppression by artificial light, even at low intensity, compromises the central circadian rhythm and signals a false “daytime” state to the body. This disruption is a key factor in sleep disorders, metabolic dysfunction, and has been implicated in increased risks for certain hormone-sensitive cancers.
Origin
This concept emerged from classic chronobiology experiments in the 1980s that demonstrated the profound sensitivity of the human pineal gland to light exposure after dark. The phenomenon is a direct evolutionary consequence of the body’s need to synchronize its internal clock with the natural solar cycle. The term nocturnal emphasizes the inappropriate timing of the light exposure.
Mechanism
The mechanism is mediated by the intrinsically photosensitive retinal ganglion cells (ipRGCs) in the eye, which contain the photopigment melanopsin and are maximally sensitive to short-wavelength (blue) light. When light strikes these cells at night, the signal travels via the retinohypothalamic tract to the suprachiasmatic nucleus (SCN). The SCN then sends an inhibitory signal down the sympathetic nervous system pathway, which directly suppresses the activity of the enzymes responsible for converting serotonin into melatonin in the pineal gland.
We use cookies to personalize content and marketing, and to analyze our traffic. This helps us maintain the quality of our free resources. manage your preferences below.
Detailed Cookie Preferences
This helps support our free resources through personalized marketing efforts and promotions.
Analytics cookies help us understand how visitors interact with our website, improving user experience and website performance.
Personalization cookies enable us to customize the content and features of our site based on your interactions, offering a more tailored experience.