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Scientists find the key to cot deaths (Sudden Infant Death Syndrome - SIDS)
Times Online (U.K.) ^ | November 1, 2006 | Nigel Hawkes

Posted on 10/31/2006 6:32:51 PM PST by Stoat

Scientists find the key to cot deaths


 
It is hoped that babies with the brain abnormality that leads to cot death may be identified by a scan in the womb
 

SCIENTISTS believe that they have found the underlying cause of cot death, a condition that claims the lives of hundreds of babies every year.

 

Research into dozens of infant fatalities identified as the result of sudden infant death syndrome showed that the victims had a brain abnormality that prevents the detection of insufficient oxygen levels in the body. As a result, babies with the condition can be smothered in their bedclothes, especially if they are sleeping on their fronts.

The researchers said yesterday that this was the strongest evidence yet of a common cause for cot death, and that it opened up the possibility of detecting those at risk and treating them.

Three hundred babies died of cot death in Britain last year, a 16 per cent fall on 2004. The year-on-year decrease is credited to greater alertness among parents and better ways of determining causes of death, resulting in fewer cases classified as cot death.

The US team, led by David Paterson, of Boston Children’s Hospital, examined post-mortem samples from the brainstems of thirty-one babies who had suffered a cot death, comparing them with ten babies who had died of other causes. They were following up research suggesting that cot-death babies had an innate difference in the brainstem, the part of the brain responsible for controlling breathing, heart rate, blood pressure, temperature and arousal.

Three studies had found that cot-death babies had a reduced ability to use and recycle serotonin, a chemical best known for regulating mood but which has other roles. Scientists said the new study, which was published in the Journal of the American Medical Association, offered the most convincing confirmation yet of the link.

The babies examined had twice as many brain cells that either manufacture or use serotonin as did those of the babies who died of other causes. But the cells that use serotonin also had significantly fewer binding sites — places on the outside of the cells where serotonin “docks” and acts as a signalling chemical.

The study suggests that the slight abnormalities in the brainstem may impair a baby’s ability to sense high carbon dioxide and low oxygen levels in its body. This would increase the risk that a baby will inhale its own exhaled breath and become deprived of oxygen. Hannah Kinney, the paper’s senior author, said: “These findings provide evidence that sudden infant death syndrome is not a mystery but a disorder that we can investigate and some day may be able to identify and treat.

“A normal baby will wake up, turn over, and start breathing faster when carbon dioxide levels rise.” But in babies who die from sudden infant death syndrome, defects in the serotonin system may impair these reflexes.

 

Such circumstances are far more likely to arise if a baby is placed face down in the cot. Campaigns to put babies on their backs have had great success, halving the numbers of cot deaths in the past decade.

Strikingly, boys who had died of cot death had significantly fewer serotonin binding sites than girls, a finding that would be consistent with the fact that cot deaths are more common among boys.

The Scottish Cot Death Trust, which part-funded the new research, said: “It looks like a really interesting piece of work and we welcome it as a way of starting to sift out the many possible factors in cot death.”

Marian Willinger, of the US National Institute of Child Health and Human Development, which funded the study, said that the research improved the understanding of the developmental disease process that underlies cot death, and the chances of providing at-risk infants with appropriate interventions.

However, George Haycock, scientific adviser to the Foundation for the Study of Infant Deaths, added that a brain abnormality was unlikely to be the sole cause.

“Much more research is needed in order to understand and, ultimately, to prevent these tragedies,” he said.



TOPICS: Miscellaneous; News/Current Events
KEYWORDS: cotdeath; physiology; science; sids

1 posted on 10/31/2006 6:32:53 PM PST by Stoat
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To: Stoat

SIDS is a general description of many causes.


2 posted on 10/31/2006 6:39:26 PM PST by kinoxi
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To: Stoat

not to mention vaccines...


3 posted on 10/31/2006 6:39:34 PM PST by Zechariah_8_13 (Courage is not simply one of the virtues, but the form of every virtue at the testing point.)
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To: neverdem

ping


4 posted on 10/31/2006 6:47:26 PM PST by raybbr (You think it's bad now - wait till the anchor babies start to vote.)
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self-ping.


5 posted on 10/31/2006 8:55:30 PM PST by SunkenCiv (Dhimmicrati delenda est! https://secure.freerepublic.com/donate/)
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To: Stoat
Three studies had found that cot-death babies had a reduced ability to use and recycle serotonin

I bet Ritalin fixes this...................
6 posted on 10/31/2006 9:40:08 PM PST by festus (The constitution may be flawed but its a whole lot better than what we have now.)
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To: Stoat; raybbr
Multiple Serotonergic Brainstem Abnormalities in Sudden Infant Death Syndrome

David S. Paterson, PhD; Felicia L. Trachtenberg, PhD; Eric G. Thompson, MS; Richard A. Belliveau, BA; Alan H. Beggs, PhD; Ryan Darnall, BA; Amy E. Chadwick, BA; Henry F. Krous, MD; Hannah C. Kinney, MD

JAMA. 2006;296:2124-2132.

Context The serotonergic (5-hydroxytryptamine [5-HT]) neurons in the medulla oblongata project extensively to autonomic and respiratory nuclei in the brainstem and spinal cord and help regulate homeostatic function. Previously, abnormalities in 5-HT receptor binding in the medullae of infants dying from sudden infant death syndrome (SIDS) were identified, suggesting that medullary 5-HT dysfunction may be responsible for a subset of SIDS cases.

Objective To investigate cellular defects associated with altered 5-HT receptor binding in the 5-HT pathways of the medulla in SIDS cases.

Design, Setting, and Participants Frozen medullae from infants dying from SIDS (cases) or from causes other than SIDS (controls) were obtained from the San Diego Medical Examiner's office between 1997 and 2005. Markers of 5-HT function were compared between SIDS cases and controls, adjusted for postconceptional age and postmortem interval. The number of samples available for each analysis ranged from 16 to 31 for SIDS cases and 6 to 10 for controls. An exploratory analysis of the correlation between markers and 6 recognized risk factors for SIDS was performed.

Main Outcome Measures 5-HT neuron count and density, 5-HT1A receptor binding density, and 5-HT transporter (5-HTT) binding density in the medullary 5-HT system; correlation between these markers and 6 recognized risk factors for SIDS.

Results Compared with controls, SIDS cases had a significantly higher 5-HT neuron count (mean [SD], 148.04 [51.96] vs 72.56 [52.36] cells, respectively; P<.001) and 5-HT neuron density (P<.001), as well as a significantly lower density of 5-HT1A receptor binding sites (P.01 for all 9 nuclei) in regions of the medulla involved in homeostatic function. The ratio of 5-HTT binding density to 5-HT neuron count in the medulla was significantly lower in SIDS cases compared with controls (mean [SD], 0.70 [0.33] vs 1.93 [1.25] fmol/mg, respectively; P = .001). Male SIDS cases had significantly lower 5-HT1A binding density in the raphé obscurus compared with female cases (mean [SD], 16.2 [2.0] vs 29.6 [16.5] fmol/mg, respectively; P = .04) or with male and female controls combined (mean [SD], 53.9 [19.8] fmol/mg; P = .005). No association was found between 5-HT neuron count or density, 5-HT1A receptor binding density, or 5-HTT receptor binding density and other risk factors.

Conclusions Medullary 5-HT pathology in SIDS is more extensive than previously delineated, potentially including abnormal 5-HT neuron firing, synthesis, release, and clearance. This study also provides preliminary neurochemical evidence that may help explain the increased vulnerability of boys to SIDS.

7 posted on 10/31/2006 9:41:47 PM PST by neverdem (May you be in heaven a half hour before the devil knows that you're dead.)
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To: festus
Three studies had found that cot-death babies had a reduced ability to use and recycle serotonin

I bet Ritalin fixes this...................

Well, considering that Ritalin has apparently been judged as being a universal cure for all childhood behavioral ailments, I suppose it's only a matter of time before they give it a shot with at-risk infants   :-)

Unfortunately, it seems that your pal Doc Adams passed away in 1980, and so the town may be in need of a new Practitioner....perhaps you might like to fill that void when you aren't protecting the townsfolk from Leftists as they sashay into town?  If you can prove the efficacy of Ritalin in a SIDS study, you would most likely get enough of a reward from that to buy a brand new buckboard, a new six-shooter and maybe even a new dress for Miss Kitty.   :-)

8 posted on 11/01/2006 12:17:06 AM PST by Stoat (Rice / Coulter 2008: Smart Ladies for a Strong America)
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To: Stoat

I was lead to this, and I am just astounded...

http://www.mercola.com/2000/nov/5/victory_over_sids.htm


9 posted on 08/27/2008 1:21:26 PM PDT by diamond6 (Everyone who is for abortion has been born. Ronald Reagan)
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To: diamond6

Unfortunately, the link that you provided goes to a screen that demands a valid email address and a site signup to progress to the article.


10 posted on 08/27/2008 9:16:39 PM PDT by Stoat (Rice / Coulter 2012: Smart Ladies for a Strong America)
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To: Stoat

I’m sorry, why don’t you try: http://www.cotlife2000.com


11 posted on 08/28/2008 8:32:37 AM PDT by diamond6 (Is SIDS preventable? www.cotlife2000.com)
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