Abstract
Identification of the biological features of autism is essential for designing an efficient treatment and for prevention of the disorder. Though the subject of extensive research, the neurophysiological features of autism remain unclear. One of the proposed biological causes of autism is malfunction of the pineal gland and deficiency of its principal hormone, melatonin. The main function of melatonin is to link and synchronize the body's homeostasis processes to the circadian and seasonal rhythms, and to regulate the sleep-wake cycle. Therefore, pineal dysfunction has been implicated based on the common observation of low melatonin levels and sleep disorders associated with autism. In this perspective, we highlight several recent findings that support the hypothesis of pineal gland/melatonin involvement in autism. Another common symptom of autism is abnormal neuroplasticity, such as cortical overgrowth and dendritic spine dysgenesis. Here, we synthesize recent information and speculate on the possibility that this abnormal neuroplasticity is caused by hyperactivity of endogenous N,N-dimethyltryptamine (DMT). The pineal gland was proposed as the source of DMT in the brain and therefore, our assumption is that besides melatonin deficiency, pineal dysfunction might also play a part in the development of autism through abnormal metabolism of DMT. We hope that this manuscript will encourage future research of the DMT hypothesis and reexamination of several observations that were previously attributed to other factors, to see if they could be related to pineal gland/melatonin malfunction. Such research could contribute to the development of autism treatment by exogenous melatonin and monitored light exposure.
Highlights
Decades of intensive research have revealed a wide-range of physiological features [1, 2], genetic [3], and environmental effectors [4], which have been suggested to be the cause, trigger, or to enhance the risk of autism spectrum disorder (ASD)
Melatonin synthesis and secretion are mainly controlled by photosensory information that arrives from the suprachiasmatic nuclei (SCN)
In addition to the link between melatonin and ASD, we propose new insights in light of the recent work by Calvin Ly et al [27], speculating on the possibility that abnormal metabolism of endogenous N,Ndimethyltryptamine (DMT), possibly from the pineal gland [28], might cause the aberrant neuroplasticity and neural connectivity abnormalities observed in autistic patients [29, 30]
Summary
Pineal dysfunction has been implicated based on the common observation of low melatonin levels and sleep disorders associated with autism. In this perspective, we highlight several recent findings that support the hypothesis of pineal gland/melatonin involvement in autism. The pineal gland was proposed as the source of DMT in the brain and our assumption is that besides melatonin deficiency, pineal dysfunction might play a part in the development of autism through abnormal metabolism of DMT We hope that this manuscript will encourage future research of the DMT hypothesis and reexamination of several observations that were previously attributed to other factors, to see if they could be related to pineal gland/melatonin malfunction.
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