note: High levels of serotonin 1a receptor likely means low levels of free serotonin,
a substance that is important in cell-firing to send chemical messages regulating heart
rate, body temperature and breathing. It seems in the editor's opinion
that maintaining an adequate level of serotonin can be critical in preventing
sudden infant death syndrome or SIDS.
studies have associated increased risk of SIDS with use of infant formulas some
of which contain low levels of tryptophan, an amino acid that serve as a
precursor for serotonin, which would result in low levels of serotonin.
SUNDAY July 5, 2008 (foodconsumer.org) -- Weakened serotonin
signaling in the brain may at least partially be responsible for sudden infant
death syndrome (SIDS), according to a study published in the July 5 issue of
SIDS is a lethal and unpredictable affliction that kills
about 2500 seemingly healthy infant each year in the United States.
Sleeping stomach-down and overheating during
sleep are believed to be risk factors for SIDS.
But biological risk factors remain unknown
except that low serotonin has been long suspected as a risk factor.
Dr. Enrica Audero at the European Molecular Biology
Laboratory in Monterotondo, Italy and colleagues used a mouse model of SIDS to
examine how over-expression of a serotonin receptor triggers serotonin
dysfunction and frequently results in death in the animals, a phenomenon
similar to SIDS.
The researchers focused in their study on the serotonin 1a
receptor, a protein on nerve cells that works with serotonin to signal chemical
When serotonin 1a receptor is
overproduced, the serotonin activity would be shut off. Nerve cells that
produce serotonin are located in the brainstem regulating basic body functions
including heart rate and breathing.
Early studies have demonstrated that activating serotonin 1a
receptors causes less firing of serotonin-containing nerve cells and decreases
heart rate, body temperature and respiration, which are some of physiological
factors for SIDS.
The mice used in the study were genetically modified in a
way that they produced about 10 times more serotonin 1a receptor protein than
their normal littermates.
When brain tissue from the transgenic mice was sprayed with
tryptophan, a precursor for serotonin, less cell-firing was observed compared
to the control mice, according to the study.
When a drug blocked the serotonin 1a receptor, cell-firing
was restored to the level seen in the tissue from the control mice, suggesting
that the high levels of serotonin 1a receptor blocks the serotonin functions.
Cornelius Gross, senior author of the report and researcher
at the European Molecular Biology Laboratory said they also looked at what's
happening in the serotonin 1a over producing animals and found a "dramatic
drop" in heart rate and body temperature.
Among the transgenic mice that over expressed serotonin 1a
receptor, 73 percent experienced at least one drip in heart rate and body
temperature called "sporadic autonomic crisis" and it took hours or
even days for them to recover.
crisis was so severe that 37 percent of the mice died.
"The events that precipitated crises in our animals are
not known, and thus far we have not been able to identify environmental
stressors that induce crises," wrote Audero and colleagues. "However,
we speculate that crises may occur preferentially after rapid changes in
serotonin neuron activity." Such activities could occur during sleep-wake
The researchers cautioned that the results may not directly
explain SIDS because infants who suffer SIDS do not show greater amounts of
serotonin 1a receptors. But they said other "functionally equivalent
deficits in serotonin signaling may play a role in SIDS.
American Association for the Advancement of Science, the publisher
of the journal Science, released an article on its website regarding the study
quoting Marian Willinger, SIDS expert at the Eunice Kennedy Shriver National
Institute of Child Health and Human Development as saying during a AAAS/Science
teleconference on July 3 that "I think it (the study results) says to
parents that their babies had a developmental disorder that they were born
Willinger was cited as saying that having an infant die of
SIDS is a "devastating event" for a family and the study "should
provide them with some sense of comfort that there was nothing they could have
done to prevent it—it is a real disease."
A foodconsumer.org health observer did not completely agree. He said
although those who suffered SIDS may likely have some disorder in the brain or
some deficit in certain physiological functionality involving serotonin,
environmental factors may also play a significant role in SIDS.
He also said the study could have yielded more important
information if the researchers tested tryptophan supplementation to see whether
increased intake of tryptophan could prevent the transgenic mice from dying
Early studies suggested decreased intake of tryptophan, the precursor
of serotonin, resulting for instance from consumption of soy-based infant formulas,
may attribute to increased risk of SIDS.
Low tryptophan means the body may produce low serotonin, an effect
similar to what is caused by high levels of serotonin 1a receptor as demonstrated
in the current study.
A meta-analysis of 19 previous studies conducted by Kristine
L.S.P. McVea, MD, MPH at Nebraska Medical Center in Omaha, Nebraska and
colleagues showed infants who were bottle-fed were 2.11 times more likely to
suffer SIDS than those who were breastfed.
Soy-based infant formulas are one of common types.
The authors said the results showed there is an association
between bottle-feeding and SIDS. But they also said confounding variables may
also contribute to the association.
study was published in Journal of Human Lactation, Vol. 16, No. 1, 13-20
Sarwar G. from Nutrition Research Division, Health
Protection Branch, Health Canada published a study in Plant Foods for Human Nutrition
2001, vol. 56, no3, pp. 275-284 reporting that tryptophan were 40 percent lower
in soy-based formulas than human milk, 10.0-12.3 mg/g protein versus 17 - 19
Sarwar also found that supplementation of tryptophan in an
animal model increased serotonin and 5-HIAA (5-hydroxyindole-3-acetic acid), a
metabolite of serotonin, in the brains of mice fed soy-based formula.
Many studies have suggested that low serotonin may be a
major risk factor for SIDS.
Okado N. from the University of Tsukuba in Japan and
colleagues said in their study report published in 2002 in the March issue of
Med Hypotheses that "alone with the genetic factors, environmental
temporal factors appear additively to lower the excitatory
function of 5-HT (serotonin) to the
respiratory center, and finally SIDS might occur. Now the pathophysiological
mechanisms and symptoms of SIDS are explained by decreased levels of
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