tazzygirl -> RE: pregnant women who lose babies face murder charges (7/3/2011 8:22:07 PM)
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You claim to work with drug damaged infants. I would be completely amazed if the healthcare community you work with smiled upon smoking while pregnant. I was STRONGLY warned 21 years ago against the dangers of smoking while pregnant, and yet you treat it like it is no big deal. The article I quoted said 1/3 of SIDs deaths could be averted by smoking cessation while a woman is pregnant... that article was 5 years old. I found another article from 2008 that said the evidence was strong that SIDs is causally related to smoking. That is very strong wording, because as you know it is hard to say one thing is the cause of another... Actually, what was said was this... quote:
about one-third of SIDS deaths might have been prevented if all fetuses had not been exposed to maternal smoking in uter We changed the positions of infants while sleeping. It dropped the rate of SIDS by 11%. A 2006 study states a brain abnormality is seen in SIDS babies. Oct. 31, 2006 - Researchers have identified a brain defect they think is a major contributor to sudden infant death syndrome (SIDS). The findings provide the strongest evidence yet of a specific neurological cause for SIDS, a little-understood condition that kills roughly 2,500 infants each year in the United States. In the study, autopsy tissue taken from babies who had died of SIDS and other causes showed abnormalities in the lower brain stems of the SIDS babies. Among other things, this region of the brain is thought to help regulate breathing and arousal. Environmental factors, such as stomach sleeping, overheating, and exposure to cigarette smoke are all believed to increase a baby's risk of death from SIDS. But the search for a biological link has turned up little, until now. "This is very good evidence that there definitely is a biological problem that contributes to SIDS," neuroscientist and study co-author David S. Paterson, PhD, tells WebMD. "There very well may be other biological causes which have not been identified. This gives us a good starting point to keep looking," says Paterson, of Boston Children's Hospital. The Serotonin System Boston Children's Hospital neuropathologist Hannah Kinney, MD, has searched for a biological cause for SIDS for the past two decades. She and Paterson had previously identified defects in the serotonin system of the lower brain stem in babies who had died of SIDS. The brain stem serotonin system is believed to help coordinate breathing, blood pressure, sensitivity to carbon dioxide, arousal, and temperature. Serotonin works as a chemical messenger in this system. Kinney and Paterson believe babies who die of SIDS actually suffocate from breathing the carbon dioxide they exhale during sleep. Normal babies wake up when the air they breathe contains too much carbon dioxide and not enough oxygen, but the thinking is that babies susceptible to SIDS lack this arousal reflex. In their latest study, which appears in the Nov. 1 issue of The Journal of the American Medical Association, the researchers confirmed their earlier findings and expanded on them. http://www.data-yard.net/10p2/sids.htm Then, we have this... 2010. Conclusion Compared with controls, SIDS was associated with lower 5-HT and TPH2 levels, consistent with a disorder of medullary 5-HT deficiency. Sudden infant death syndrome (SIDS) is the sudden death of an infant younger than 1 year that remains unexplained after a complete autopsy and death scene investigation.1 Typically, an apparently healthy infant is found dead after a sleep period,2 with death presumably occurring during sleep or one of the many transitions between sleep and waking.3,4 The recognition that prone sleep position increases the risk for SIDS led to national campaigns,5 but despite initial success, the overall SIDS rate has plateaued over the last decade.3,4 SIDS remains the leading cause of postneonatal infant mortality in the United States, with an overall rate of 0.54 per 1000 live births.6,7 One model underlying SIDS research is the triple-risk model, which posits that SIDS results from the simultaneous occurrence in the infant of an underlying vulnerability, a critical developmental period, and an exogenous stressor.8 In 3 independent data sets assessing infants with SIDS, our laboratory has consistently reported serotonin (5-hydroxytryptamine [5-HT]) receptor binding abnormalities in regions of the medulla oblongata critical to state-dependent homeostatic regulation,9,10,11 ie, the medullary 5-HT system.3,12 In the third data set, we also found increased 5-HT neuronal densities as well as decreased 5-HT transporter binding relative to 5-HT neuronal number.11 Thus, we propose that SIDS results from an abnormality of the medullary 5-HT system that causes an inability to restore homeostasis following life-threatening challenges, eg, asphyxia, during a sleep period and leads to sudden death in the critical first year of life, when homeostatic systems are still maturing.12 The question remains as to whether underproduction or overproduction of 5-HT is associated with abnormal 5-HT receptor binding in SIDS. In this study we tested the main hypothesis that SIDS is associated with reductions in tissue levels of 5-HT, its key biosynthetic enzyme (tryptophan hydroxylase [TPH2]), or both, thereby representing a 5-HT deficiency disorder. The 3 other study objectives were (1) to compare infants dying from SIDS with hospitalized infants who had chronic hypoxia-ischemia prior to death to evaluate the putative effects of impaired oxygenation on 5-HT tissue markers, given that some infants with SIDS experience repetitive apnea and agonal impaired gasping prior to death4,12,13,14,15; (2) to analyze 5-HT1A receptor binding to verify that this data set displays the same alterations we observed previously9,10,11; and (3) to examine levels of norepinephrine and dopamine and the metabolite 3,4-dihydroxyphenylacetic acid to address whether medullary abnormalities in SIDS involve the catecholamine system. 5-HT, Catecholamine, and Metabolite Levels Samples were available from 35 SIDS cases, 5 controls, and 5 hospitalized infants. Age-adjusted mean levels of 5-HT in SIDS cases were 26% lower than in controls in both the PGCL (31.4 pmol/mg protein [95% confidence interval {CI}, 23.7 to 39.0] vs 40.0 pmol/mg protein [95% CI, 20.1 to 60.0], P = .04) and the raphé obscurus (55.4 pmol/mg protein [95% CI, 47.2 to 63.6] vs 75.5 pmol/mg protein [95% CI, 54.2 to 96.8], P = .05) (Table 2). However, 5-HIAA levels and 5-HIAA:5-HT ratio did not indicate excessive degradation of 5-HT in SIDS cases. There were no significant differences in catecholamine levels between SIDS cases and controls. Dopamine levels, however, were 640% higher in the raphé obscurus in the hospitalized group compared with the SIDS group (81.7 pmol/mg protein [95% CI, 37.6 to 125.8] vs 11.1 pmol/mg protein [95% CI, −3.6 to 25.8], P = .006). Moreover, 5-HT levels were 55% higher in the raphé obscurus (85.6 pmol/mg protein [95% CI, 61.8 to 109.4] vs 55.4 pmol/mg protein [95% CI, 47.2 to 63.6], P = .02) and 126% higher in the PGCL (71.1 pmol/mg protein [95% CI, 49.0 to 93.2] vs 31.4 pmol/mg protein [95% CI, 23.7 to 39.0], P = .002) in the hospitalized group compared with the SIDS group (Table 2) Risk Factors in the SIDS Cases To determine if known risk factors for SIDS were associated with abnormalities in 1 or more 5-HT parameters in the medulla, an analysis of risk factors relative to the 5-HT parameters was undertaken. Risk factors for SIDS (Table 1, eTable 2, and eTable 3) were subdivided into “extrinsic” and “intrinsic” categories.11 Extrinsic factors, eg, prone sleep position,3,4,6,7 are physical stressors that place a vulnerable infant at risk for homeostatic derangements around the time of death; intrinsic factors, eg, prematurity and male sex,3,4,6,7,21,22 are postulated to affect the underlying vulnerability in the infant. Ninety-five percent (39/41) of SIDS cases had 1 or more risk factor, and 88% (36/41) had 2 or more. Ninety-three percent had at least 1 extrinsic risk factor, ie, prone (49%) and side (14%) sleep position, face down (37%), bed sharing (20%), and trivial illness prior to death (44%) (eTable 2). We found no associations between risk factors and 5-HT tissue levels (eTable 3). Significant differences were found, however, for 5-HT1A receptor binding in the raphé obscurus if the infant with SIDS was found dead in a risky sleep position (47.32 fmol/mg tissue [95% CI, 38.23 to 56.38] for prone or side sleep position vs 26.76 fmol/mg tissue [95% CI, 15.64 to 37.88] for supine position) or in an adult bed (49.06 fmol/mg tissue [95% CI, 34.20 to 63.92] vs 32.76 fmol/mg tissue [95% CI, 21.38 to 44.14] in a crib) (eTable 3). Binding levels were significantly lower if the infant with SIDS did not have the risk factor. In addition, TPH2 levels were lower in the infants with SIDS and with recent illness (165.7% [95% CI, 143.3% to 188.0%]) than those without recent illness (138.0% [95% CI, 126.6% to 149.4%]). In this data set we found no effect for male sex (eTable 3). ........ The finding of at least 1 risk factor in 95% of SIDS cases underscores the importance of risk factors in the pathogenesis of SIDS, even in the era of the recommendation for supine sleep position. The finding of 2 or more risk factors in 88% of SIDS cases further underscores that SIDS results from the simultaneous occurrence of multiple events.3 Infants with SIDS but without known extrinsic risk factors had significantly lower 5-HT1A receptor binding, suggesting that additional risk factors are necessary to precipitate death when the medullary 5-HT system is less compromised. These findings raise the question as to how reduced 5-HT and TPH2 levels are related to the increased 5-HT cell density,11 morphologic 5-HT neuronal immaturity,11 reduced 5-HT transporter binding relative to 5-HT cell number,11 and altered 5-HT receptor binding9,10,11 in the SIDS cases. We hypothesize that TPH2 levels are reduced in the medullary 5-HT system for as-yet unknown developmental, genetic, and/or environmental reasons, with a secondary reduction in 5-HT levels and impaired 5-HT neurotransmission. We further propose that insufficient 5-HT levels early in development, potentially as early as the first or second trimester, result in a compensatory increase in immature 5-HT neurons with immature (decreased) 5-HT1A binding and 5-HT transporter levels.34 That the defect is partial rather than total could explain why medullary 5-HT-mediated pathways function reasonably well at baseline or during waking but are unable to respond to homeostatic stressors during sleep when the partial deficit is potentially unmasked, thereby resulting in sudden death. Our data suggest that future animal models mimicking the 5-HT abnormalities of SIDS should focus on underproduction, rather than overproduction, of 5-HT and TPH2. Funding/Support: This study was supported by the First Candle/SIDS Alliance, CJ Martin Overseas Fellowship (National Health and Medical Research Council of Australia), CJ Murphy Foundation for Solving the Puzzle of SIDS, CJ Foundation for SIDS, National Institute of Child Health and Development (R37-HD20991 and PO1-HD036379), and Developmental Disabilities Research Center, Children's Hospital Boston (P30-HD18655) http://jama.ama-assn.org/content/303/5/430.full?home Dr Kinney has researched this for over 20 years. So, who do we believe?
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