from Medscape
_http://www.medscape.com/viewarticle/547019?src=mp_
(http://www.medscape.com/viewarticle/547019?src=mp)
"We don't know exactly what causes these abnormalities," Dr. Paterson said.
"We believe that it's a developmental process that begins in utero, involving
probably environmental as well as genetic factors. Finding out exactly what
the pathogenesis is is a big step toward trying to intervene and stop this."
Other known facts about SIDS that are compatible with these findings are
that infants younger than 6 months of age, when control systems for homeostatic
functions are still immature, {emphasis mine if it comes through} are most
vulnerable to SIDS. The triple risk model suggests that sudden death results
from a combination of an underlying vulnerability, an exogenous stressor such
as prone sleep position or bed sharing, and the critical developmental period
during the first 6 months of postnatal life, when the infant is at greatest
risk for SIDS.
Some environmental factors, such as maternal smoking and alcohol use, may
adversely affect prenatal development of the brainstem serotoninergic system.
Researchers in this field are currently trying to develop some animal models
to test different interventions, according to Dr. Paterson.
Until screening tests and potential interventions become available, Dr.
Paterson recommends following the mandates of the national "Back to Sleep"
campaign, which urges caregivers to put babies to bed on their backs. In fact, 65%
of the SIDS cases in this study were sleeping prone or on their side at the
time of death, indicating the need for continued public health messages on
safe sleeping practices. Other recommended sleeping practices for infants are
use of firm sleeping surfaces and avoidance of soft bedding, overheating, and
exposure to prenatal and postnatal cigarette smoke.
Comments:
Does it seem odd to anyone that neurophysiological immaturity and poor
homeostasis control are linked with "bed sharing" while solitary sleep is a
neurophysiological stressor and a challenge to decent homeostasis and here is not ev
en recognized as such? Will researchers ever get beyond their bias against
normal sharing of sleep ( within the limits we think we know, like no soft
bedding, no drugs or alcohol or smoking)? And that many of those solitary
sleeper's brains are not developing normally because they are being ' fed '
artificially for most or all of infancy? Does SIDS happen at the same rate among
animals who are not fed artificially or are artificially separated from the
family? This is probably not even researchable since test animals are in
totally abnormal social and nutritional environments. The researcher's own study
limitations might cause a problem rather than study one...Other comments?
Peace,
Judy
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