Sids Research Paper

Sids Research Paper-72
I do not suggest that solitary nocturnal sleep “causes” SIDS, that all parents should sleep with their infants, or that traditional SIDS research strategies should be abandoned.However, using evolutionary data, I do suggest that an adaptive fit exists between parent-infant sleep contact and the natural physiological vulnerabilities of the neurologically immature human infant, whose breathing system is more complex than that of other mammals owing to its speech-breathing abilities.During this less stable period of breathing control, infants are most susceptible either to colic or may be the result of these integrating neural tracks developing at different rates, leading to a sleeping infant experiencing sleep apnea, or an involuntary pause in breathing, that is not stopped by either sub-system.

I do not suggest that solitary nocturnal sleep “causes” SIDS, that all parents should sleep with their infants, or that traditional SIDS research strategies should be abandoned.However, using evolutionary data, I do suggest that an adaptive fit exists between parent-infant sleep contact and the natural physiological vulnerabilities of the neurologically immature human infant, whose breathing system is more complex than that of other mammals owing to its speech-breathing abilities.During this less stable period of breathing control, infants are most susceptible either to colic or may be the result of these integrating neural tracks developing at different rates, leading to a sleeping infant experiencing sleep apnea, or an involuntary pause in breathing, that is not stopped by either sub-system.

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And while serotonin, a neurotransmitter, helps regulate breathing, the chemical’s connection to SIDS isn’t completely clear.

To explore this connection, Harvard Medical School geneticist Susan Dymecki and her colleagues genetically altered mice so that their-neurons, which produce serotonin, stopped working after the animals received an injection of a chemical called clozapine-N-oxide.

In a paper published recently in the journal Family Relations, lead researcher James Mc Kenna, director of the Mother-Baby Behavioral Sleep Lab and Rev. For the first month or so of life, Mc Kenna explains, the breathing process is controlled exclusively by the brain stem, with the infant having no control over vocalizing.

But through about seven months of age, the brain stem becomes increasingly more functionally integrated with the cortex, essentially sharing the control of breathing between two sub-systems.

It’s still unclear whether SIDS stems from the acute inhibition of serotonin neurons.

Kevin Cummings, a biomedical scientist at the University of Missouri who wasn’t involved in the study, is skeptical that that’s the case.

More than 2,000 infants die each year in the US from sudden infant death syndrome (SIDS).

Studies have linked the condition, in which babies stop breathing while sleeping, with drops in the activity of serotonin-producing neurons in the brain.

They suggest that important clinical data on the relationship between infantile constitutional deficits and microenvironmental factors relevant to SIDS can be acquired by examining the physiological regulatory effects (well documented among nonhuman primates) that parents assert on their infants when they sleep together.

I attempt to show why access to parental sensory cues (movement, touch, smell, sound) that induce arousals in infants while they sleep could possibly help one of many different subclasses of infants either to override certain kinds of sleep-induced breathing control errors suspected to be involved in SIDS or to avoid them altogether.

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