October E-zine
The Georgia SIDS
Project E-Zine is an on-line educational update offered monthly by the Georgia
Sudden Infant Death Information, Referral and Support Project, an affiliate of
First Candle/SIDS Alliance. To comment on this issue, request additional
information, refer families in need of support, make a donation or be added or
removed from the list please contact us at
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publication is made available through the generous donation of friends and
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Through
the State Charitable Campaign Program state employees can select and donate to
the Georgia SIDS Project. Help us support bereaved families, increase risk
reduction education, make safe cribs available to low-income high-risk infants
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Volume 2 - Issue Number 10, October
2006
1. NEW STUDY RESULTS MAY MEAN
DIAGNOSTIC TOOL FOR INFANTS AT RISK FOR SIDS ON THE HORIZON!!!! New
autopsy data provides the strongest evidence yet that sudden infant death
syndrome (SIDS) is not a “mystery” disease, but has a concrete biological
basis. Based on their findings, researchers at Children’s Hospital Boston hope
to develop a diagnostic test to identify newborns at risk, and envision
treatments to protect them during the vulnerable period.” The study by
Dr. Kinney was partially funded by donations from Georgia SIDS Alliance and
First Candle.
2.
Georgia SIDS Project Georgia SIDS continues
to offer risk reduction training on a fee scale basis. CEU’s for nurses and
child care workers available. New information and recommendations are making
updated training a must. For information or to schedule a training contact
Georgia SIDS Project at 678-342-3360.
3. NICU
Nurses' Knowledge and Discharge Teaching Related to Infant Sleep Position and
Risk of SIDS. Georgia SIDS collaborates in continuing this research effort in a
current NICU study.
4. DHR Crib matching donation program initiation delayed until November. See
information about how to participate below.
5. Study
finds that complicated first births of live born infants are associated with an
increased risk of unexplained stillbirth in the next pregnancy.
6. Understanding the impact of preterm birth on US infant mortality rates
reviewed in new study.
7. Weight increases between pregnancies could be source of poor subsequent
pregnancy outcomes.
8.
Sudden infant death syndrome and reported maternal
smoking during pregnancy in
9. Evidence-based
guidelines for the diagnosis and treatment of complicated bereavement outlined
10. Gene Linked To Autism In Families
With More Than One Affected Child found.
1.
Infants who die of sudden infant
death syndrome have abnormalities in the brainstem, a part of the brain that
helps control heart rate, breathing, blood pressure, temperature and arousal,
report researchers. The finding is the strongest evidence to date
suggesting that innate differences in a specific part of the brain may place
some infants at increased risk for SIDS. The abnormalities appeared to affect
the brainstem's ability to use and recycle serotonin, a brain chemical which
also is used in a number of other brain areas and plays a role in
communications between brain cells.
Serotonin is most well known for its role in regulating mood, but it
also plays a role in regulating vital functions like breathing and blood
pressure. The study appears in the
November 1 "Journal of the American Medical Association" and was
conducted by researchers in the laboratory of Hannah Kinney, M.D., at
Children's Hospital Boston and
"This
finding lends credence to the view that SIDS risk may greatly increase when an
underlying predisposition combines with an environmental risk -- such as sleeping
face down -- at a developmentally sensitive time in early life," said
Duane Alexander, M.D., Director of the NIH's National Institute of Child Health
and Human Development. SIDS is the sudden and unexpected death of an infant
under 1 year of age, which cannot be explained after a complete autopsy, an
investigation of the scene and circumstances of the death, and a review of the
medical history of the infant and his or her family. Typically, the infant is found dead after
having been put to sleep and shows no signs of having suffered. In previous
studies, researchers have hypothesized that abnormalities in the brainstem may
make an infant susceptible to situations in which they re-breathe their own
exhaled breath, depriving them of oxygen.
This hypothesis holds that certain infants may not be able to detect
high carbon dioxide or low oxygen levels during sleep, and do not wake up. To
conduct the current study, researchers examined tissue from the brainstems of
31 infants who died of SIDS and 10 infants who died of other causes. The tissue was provided by the office of the
chief medical examiner in
Serotonin
belongs to a class of molecules known as neurotransmitters, which serve to
relay messages between neurons. Neurons
release neurotransmitters, which fit into special sites, or receptors, on
surrounding neurons, somewhat like a key fits into a lock. Once in place, the neurotransmitter either
promotes or hinders electrical activity in the receiving neuron -- next in line
in a particular brain circuit -- causing it to release its neurotransmitters,
which either excite or inhibit still more neurons, and so on. Although the
brainstem tissue from the SIDS infants contained more serotonin-using neurons,
these serotonin-using neurons appeared to contain fewer receptors for serotonin
than did the brainstems of control infants.
Dr. Paterson noted that there are at least 14 different subtypes of
serotonin receptor. In their study, the
researchers tested the infants' brainstem tissue for a serotonin receptor known
as "subtype 1A." Tissue from both the SIDS infants and the control
infants contained roughly equal amounts of a key brain protein, serotonin
transporter protein. This protein
recycles serotonin, collecting the neurotransmitter from the surrounding spaces
outside the neuron and transporting it back into the neuron so it can be used
again. Dr. Paterson explained, however,
that because the SIDS infants had proportionately more serotonin-using neurons
than did the control infants, they would also be expected to have more
serotonin transporter protein. So even
though they had equal amounts of serotonin transporter protein, the levels were
nevertheless reduced -- relative to the increased number of serotonin-using
neurons -- and, for this reason, unlikely to meet the needs of these cells.
Dr.
Paterson added that from the observations in this study it was not possible to
determine how much serotonin the infants' brainstems contained when the infants
were alive. He noted, however, that the
pattern of abnormalities -- more serotonin neurons, an apparent reduction of
serotonin 1A receptors, and insufficient serotonin transporter -- suggested
that the level of serotonin in the brainstems of SIDS infants was abnormal.
"Our hypothesis right now is that we're seeing a compensation
mechanism," Dr. Paterson said.
"If you have more serotonin neurons, it may be because you have
less serotonin and more neurons are recruited to produce and use serotonin to
correct this deficiency." The researchers also found that male SIDS infants
had fewer serotonin receptors than did either female SIDS infants or control
infants. The finding may provide insight
into why SIDS affects roughly twice as many males as females. "These
findings provide evidence that SIDS is not a mystery but a disorder that we can
investigate with scientific methods, and some day, may be able to identify and
treat," said Dr. Hannah Kinney, the senior author of the paper.
A large
body of research has shown that placing an infant to sleep on his or her
stomach greatly increases the risk of SIDS.
The NICHD-sponsored Back to Sleep campaign urges parents and caregivers
to place infants to sleep on their backs, to reduce SIDS risk. The campaign has reduced the number of SIDS
deaths by about half since it began in 1994.
The campaign also cautions against other practices that increase the
risk of SIDS, such as soft bedding, smoking during pregnancy, and smoking
around a baby after birth. Despite the fact that the Back to Sleep Campaign
recommendations had been widely distributed by the time the study began, a
large proportion of the SIDS cases in the study by Drs. Paterson, Kinney and
their coworkers were correlated with known SIDS risk factors: 15 (48 percent)
were found sleeping on their stomachs, 9 (29 percent) were found face down, and
7 (23 percent) were sharing a bed, at the time of death. "The majority (65
percent) of the SIDS cases in this data set, however, were sleeping prone or on
their side at the time of death, indicating the need for continued public
health messages on safe sleeping practices, the study authors wrote."
2. Georgia SIDS Project has
training available on a sliding fee scale. Be
sure your SIDS training includes updated information like results from the
study above – stay current with new findings and recommendations! See our
training options at www.sidsga.org
3. NICU Nurses' Knowledge and Discharge
Teaching Related to Infant Sleep Position and Risk of SIDS. Aris
C, Stevens TP, Lemura
C, Lipke
B, McMullen S, Cote-Arsenault D, Consenstein
L. Adv Neonatal Care. 2006 Oct. Infants requiring neonatal intensive care are often placed prone during
their acute illness. After hospital discharge the
4.
5.
Previous Preeclampsia, Preterm Delivery, and Delivery of a Small for
Gestational Age Infant and the Risk of Unexplained Stillbirth in the Second
Pregnancy: A Retrospective Cohort Study, Scotland, 1992-2001. Smith GC, et al Am J
Epidemiol. 2006 Oct 25;
Women with a previous stillbirth are known to be at
increased risk of stillbirth in subsequent pregnancies. However, few studies
have addressed the association between other complications of pregnancy and the
future risk of stillbirth. Using linkage of national pregnancy and perinatal
death registries, the authors performed a retrospective cohort study of 133,163
women having a second birth in
6.
The
contribution of preterm birth to infant mortality rates in the
Although two thirds of infant deaths in the
7.
Interpregnancy weight change and risk of adverse pregnancy
outcomes: a population-based study. Villamor E,. Lancet.
2006 Sep 30. Maternal obesity has been positively associated with risk of
adverse pregnancy outcomes, but evidence of a causal relation is scarce.
Authors examined the associations between change in pre-pregnancy body-mass
index (BMI) from the first to the second pregnancies, and the risk of adverse
outcomes during the second pregnancy in a nationwide Swedish study of 151 025
women who had their first two consecutive singleton births between 1992 and
2001. Compared with women whose BMI changed between -1.0 and 0.9 units,
the adjusted odds ratios for adverse pregnancy outcomes for those who gained 3
or more units during an average 2 years were: pre-eclampsia, 1.78 (95% CI
1.52-2.08); gestational hypertension 1.76 (1.39-2.23); gestational diabetes
2.09 (1.68-2.61); caesarean delivery 1.32 (1.22-1.44); stillbirth 1.63
(1.20-2.21); and large-for-gestational-age birth 1.87 (1.72-2.04). The
associations were linearly related to the amount of weight change and were also
noted in women who had a healthy prepregnancy BMI for both pregnancies.
Interpretation: These findings lend support to a causal relation between
being overweight or obese and risks of adverse pregnancy outcomes. Additionally
they suggest that modest increases in BMI before pregnancy could result in
perinatal complications, even if a woman does not become overweight. Our
results provide robust epidemiological evidence for advocating weight loss in
overweight and obese women who are planning to become pregnant and, to prevent
weight gain before pregnancy in women with healthy BMIs.
8. Sudden infant death syndrome and
reported maternal smoking during pregnancy. Shah
T, Sullivan K, Carter J. Am J
Public Health. 2006 Oct. We investigated the
effect of maternal smoking during pregnancy on the relative risk of sudden
infant death syndrome (SIDS) by linking data from
9.
Update on bereavement research: evidence-based guidelines
for the diagnosis and treatment of complicated bereavement. Zhang
B, et. al. Palliat Med. 2006 Oct. The past decade has witnessed
considerable growth in the evidence-base from which clinical recommendations
for bereavement care can be made. Research now provides guidance to assist
clinicians in: a) recognizing differences between complicated and uncomplicated
bereavement reactions, b) identifying risk factors that may make certain
individuals more vulnerable to bereavement-related complications, c) appreciating
and monitoring for potential adverse outcomes associated with bereavement and
d) taking actions to prevent or minimize maladjustment to the loss. In this
article we distinguish between the course of normal grief and abnormally
prolonged, or complicated grief; clarify distinctions between Complicated Grief
Disorder and other mental disorders secondary to bereavement; review outcomes
associated with Complicated Grief Disorder; describe research on resilience in
bereavement; present findings on stigmatization and the use of mental health
services among recently bereaved persons; and summarize where the field is with
respect to establishing the efficacy and effectiveness of bereavement
interventions. Promising new psychotherapies for Complicated Grief Disorder
have shown clinical efficacy. Nevertheless, further research is needed to
enhance the detection of vulnerable bereaved persons, to promote resilience
following significant interpersonal loss, and to tailor interventions to
address the attachment issues that lie at the heart of this disorder.
10.
Gene Linked To Autism In
Families With More Than One Affected Child A version of a gene has been linked to
autism in families that have more than one child with the disorder. Inheriting
two copies of this version more than doubled a child's risk of developing an
autism spectrum disorder, scientists supported by the National Institutes of
Health discovered. In a large sample totaling 1,231 cases, they traced the
connection to a tiny variation in the part of the gene that turns it on and
off. People with autism spectrum disorders were more likely than others to have
inherited this version, which cuts gene expression by half, likely impairing
development of parts of the brain implicated in the disorder, report Drs. Daniel
Campbell, and colleagues, online during the week of the October 16, 2006 in the
"Proceedings of the National Academy of Sciences." "This common
gene variant likely predisposes for autism in combination with other genes and
environmental factors," said Levitt. "It exerts the strongest effect
detected thus far among autism candidate genes." Autism is one of the most
heritable mental disorders. If one identical twin has it, so will the other in
nearly 9 out of 10 cases. If one sibling has the disorder, the other siblings
run a 35-fold greater-than-normal risk of having it. Still, scientists have so
far had only mixed success in identifying the genes involved. While most
previous studies had focused on genes expressed in the brain, Levitt's team saw
a clue in the fact that some people with autism also have gastrointestinal,
immunological or neurological symptoms in addition to behavioral impairments.
They focused on a gene that affects such peripheral functions as well as the
development of the cortex and cerebellum, brain areas disturbed in autism.
Moreover, it is located in a suspect area of chromosome 7 that has been
previously linked to autism spectrum disorders. This MET receptor tyrosine
kinase gene codes for a protein that relays signals that turn on a cell's
internal machinery and is known to play a key role in both normal and abnormal
development, such as cancer metastases (hence its name). Levitt's group and
others had earlier found that impairing the receptor's signaling interferes
with neuron migration and disrupts neuronal growth in the cortex and similarly
shrinks the cerebellum -- abnormalities also seen in autism.
To explore this possible connection, the researchers looked for
associations between the brain disorder and nine markers in the MET gene, sites
where letters in the genetic code vary among individuals. They tested two
samples: the first, 204 families, including 26 with more than one child with
autism spectrum disorders, the second, 539 families, including 452 with such
multiple affected children. One marker, the C version, emerged as
over-transmitted at "highly significant" levels in people with autism
spectrum disorders in both samples. Moreover, this association held only for
families with more than one affected child and was strongest in a sub-sample of
those with more narrowly-defined autism. The C version was significantly less
prevalent in a group of 189 unrelated controls than in the individuals with
autism or their parents. In cell culture tests, the researchers determined that
the C version is weak at making the MET receptor protein, resulting in a
two-fold reduction in gene expression compared to the other common G version of
the gene, with presumably adverse consequences on brain development. Inheriting
two copies of the C version boosted risk for autism spectrum disorders
2.26-fold, while inheriting one copy of C and one of G increased risk
1.54-fold. "Since autism likely
involves complex interactions between many different genes and other factors,
common genetic predisposing factors are likely more influential in families
with multiple affected members," explained Levitt. "Some cases in
families with only one affected member more likely stem from rarer genetic
glitches or other sporatic events. Hence, finding the link with the MET gene
variant only in the former 'multiplex' families strengthens its
candidacy." The researchers propose
that in some individuals with autism spectrum disorders who also develop
digestive and immune system or non-specific neurological problems, the MET gene
variant might play a role in impairing both brain and peripheral organ
development. "We know that autism
is the most heritable of neuropsychiatric disorders, but, thus far, we have not
identified genes that consistently are associated with this developmental brain
disease," said NIMH Director Thomas Insel, M.D. "This new finding is an important clue,
which if replicated in an independent sample, will take us closer to
understanding the genetic basis of autism."
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