Sudden infant death syndrome: a genetically determined impaired maturation of the photoneuroendocrine system. A unifying hypothesis.

Sudden Infant Death Syndrome (SIDS) is the unexpected, and after autopsy, unexplained death of an apparently healthy infant. SIDS exhibits circannual, circadian, and ontogenetic features which may reflect an impaired maturation of the photoneuroendocrine system caused by a genetic absence or mutation of the enzyme N-acetyltransferase which is the rate-limiting enzyme for the biosynthesis of the hormone melatonin in the pineal gland. The failure of normal pineal gland development and subsequent impaired production of its main secretory product, melatonin, may cause a lethal imbalance in the chemical interactions among serotonin, progesterone, and catecholamines.

The photo-biochemical basis of infant colic: pineal intracellular calcium concentrations controlled by light, melatonin, and serotonin.

Infant crying during the first 3 months of life exhibits a circadian rhythm with peak crying in the evening hours. Intracellular calcium ion within the pineal gland may be influenced by alternating light and dark, melatonin concentrations, and serotonin concentrations which both exhibit circadian rhythmicity. Differences in light by latitude and differences in the ontogenic development of melatonin and serotonin rhythmicity could combine to effect the pineal intracellular concentrations of calcium and result in high levels of infant crying called colic.

Infant colic: the effect of serotonin and melatonin circadian rhythms on the intestinal smooth muscle.

It is hypothesized that in the evening, peak serotonin concentration causes intestinal cramps associated with colic because serotonin increases intestinal smooth muscle contractions. Melatonin has the opposite effect of relaxing intestinal smooth muscles. Both serotonin and melatonin exhibit a circadian rhythm with peak concentrations in the evening.

Colic, sleep inertia, melatonin and circannual rhythms.

Colic is periodic behavior occurring at the end of the day during the first 3 months of life characterized by crying. It is hypothesized that the crying at the end of the day is due to sleep inertia or a state dissociation during which the infant is simultaneously partially awake and partially asleep because of the absence of a melatonin diurnal rhythm. The melatonin timing mechanisms, which codes for day length, is initiated prenatally by the maternal pineal gland, and after 3 months postnatally, the melatonin nocturnal secretion rhythm is maintained by the infant's pineal gland.