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Oxidative Stress and SIDS

Oxidative Stress and SIDS

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Published by Meryl Dorey
The link between oxidative stress and Sudden Infant Death SIDS
The link between oxidative stress and Sudden Infant Death SIDS

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Categories:Types, Research
Published by: Meryl Dorey on May 10, 2013
Copyright:Attribution Non-commercial

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11/20/2013

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Could too much oxidative stress from toxins, vaccines and other environmental exposuresbe the cause of SIDS?By Beth Lambert, Author,
 A Compromised Generation: The Epidemic of Chronic Illness in America’s Children
(Sentient, 2010)
The cause of Sudden Infant Death Syndrome, or SIDS, has long been a mystery. Recent research,however, may point to pre- and postnatal toxic exposures such as flame-retardants in mattresses,nicotine smoke or chronic immune stimulation as contributors to SIDS. It is believed that SIDSmay be the result of mitochondrial dysfunction in key organs such as the lungs, heart, or braincaused by excessive oxidative stress on infants’ tiny bodies.Simplified, oxidative stress is when peroxides and free radicals damage our DNA, cells andtissues. More specifically, oxidative stress can damage mitochondria in our cells. Themitochondria are our cells’ “power plants” helping us to make energy that is used for everythingfrom breathing to thinking. When mitochondria are damaged by oxidative stress, this can resultin mitochondrial dysfunction, a condition where we lose the ability to effectively produce energyin our cells.Mitochondrial dysfunction can affect all major organs in the body including the brain, heart,lungs, GI tract, in addition to the immune system. New research reveals that mitochondrialdysfunction is at least part of what causes the symptoms of many conditions including autism,asthma, ADHD, Parkinson’s disease, and many others.Oxidative stress and mitochondrial dysfunction can be caused by:
 
Exposure to toxins like pesticides, mercury, flame retardants, aluminum, or PVC
 
Exposure to food or environmental allergens
 
Immunological responses (especially chronic infections with viruses, bacteria, or uponinoculation)
 
Radiation (e.g. from WiFi, cellphones, computers, etc.)
Oxidative Stress, Mitochondrial Dysfunction and SIDS
Research shows that at least some cases of SIDS result from mitochondrial dysfunction, includingmitochondrial DNA defects and fatty acid oxidation disorders (considered inherited disorders).Geneticist, Dr. Richard Boles of Children’s Hospital Los Angeles documented this scientificfinding over a decade ago. However, scientists are now looking into the possibility thatenvironmentally-derived mitochondrial dysfunction could be one of the potential causes of SIDS.In other words, exposures that cause oxidative stress in tiny bodies, like toxins, allergens, or vaccinations, could be causing mitochondrial dysfunction and sudden death in infants.Parental smoking has long been known to be a risk factor for SIDS. Studies in rhesus monkeysshow that monkey fetuses exposed to nicotine smoke (a source of oxidative stress) have a higher risk of SIDS, but prenatal administration of an antioxidant like vitamin C (known to protectagainst oxidative stress) reduced the risk of SIDS in infant monkeys. Other studies haveconfirmed that prenatal administration of antioxidants can reduce oxidative stress on the fetus.Respiratory and gastrointestinal infections are also known to increase the risk of SIDS. The risk may be from the increased level of oxidative stress triggered by the infections. In addition,defects in serotonergic pathways (how serotonin is utilized) are believed to be part of the pathophysiology of SIDS. Mouse models have shown that a SIDS-like condition can be createdin mouse pups by altering or damaging serotonin pathways. Interestingly, mitochondrial

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