Oxidative Stress and SIDS

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Could too much oxidative stress from toxins, vaccines and other environmental exposures

be 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 SIDS

may be the result of mitochondrial dysfunction in key organs such as the lungs, heart, or brain

caused by excessive oxidative stress on infants’ tiny bodies.

Simplified, oxidative stress is when peroxides and free radicals damage our DNA, cells and

tissues. More specifically, oxidative stress can damage mitochondria in our cells. The

mitochondria are our cells’ “power plants” helping us to make energy that is used for everything

from breathing to thinking. When mitochondria are damaged by oxidative stress, this can result

in mitochondrial dysfunction, a condition where we lose the ability to effectively produce energy

in 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 mitochondrial

dysfunction 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 upon

inoculation)

• 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 scientific

finding over a decade ago. However, scientists are now looking into the possibility that

environmentally-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 monkeys

show 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 have

confirmed 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 created

in mouse pups by altering or damaging serotonin pathways. Interestingly, mitochondrial

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dysfunction is one of the factors that can affect how serotonin is utilized in the brain, particularly

because it seems to affect neurons that have high firing rates.

A 2010 study out of University Hospital in Norway found that babies who died of SIDS had signs

of inflammation and ischemia in their lungs. Researchers must now whether oxidative stress

caused by environmental exposures causes inflammation and ischemia in the lungs of the babies

who died of SIDS.

While more research is needed to confirm the suspected connection between oxidative stress,

mitochondrial dysfunction and SIDS, it seems clear that reducing exposures to factors that cause

oxidative stress is a safe and responsible step to take for all infants.

http://www.ncbi.nlm.nih.gov/pubmed/19773461





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Oxidative Stress and SIDS

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