Amyotrophic lateral sclerosis and EGCG from green tea
ALS or Lou Gehrig’s disease is currently irreversible and fatal.
Beginning in the extremities (usually the hands or feet), the motor nerves of all the muscles begin to die. Muscles become weaker until paralysis sets in. The nerve degeneration usually moves from the outside to the center of the body, eventually affecting the diaphragm muscle.
Once this muscle is paralyzed, people with amyotrophic lateral sclerosis cannot breathe and they die.
About half of the diagnosed people die within three years and most die within 5 years of diagnosis.
Almost 20 years of green tea research has shown that EGCG green tea extract can protect nerve cells from oxidative stress damage and iron dysregulation that lead to their death.
While many studies have shown the neuroprotective effects of EGCG with Parkinson’s disease and Alzheimer’s disease, now a new study examines amyotrophic lateral sclerosis and EGCG.
In an animal model of Lou Gehrig’s disease, mice were given EGCG in their drinking water daily beginning at age 2 months.
At higher amounts (above 2.9 micrograms of EGCG per gram of body weight), animals given the green tea antioxidant EGCG had a significantly longer lifespan and significantly longer time before the onset of symptoms (Koh SH, The effect of epigallocatechin gallate on suppressing disease progression of ALS model mice, Neuroscience Letters, March 2006).
This research is considered preliminary.
Also of note is the history of Dr. Roy Walford. While most people die from ALS within 5 years, he survived ALS for approximately 12 years, dying at age 79. He believed he acquired the disease in Biosphere II.
Dr. Walford was the primary lead scientist to develop the massive information about the benefits of calorie restriction with optimal nutrition and practiced calorie restriction with his personal diet.
Additional studies from Northwestern University on amyotrophic lateral sclerosis and DNA have identified two faulty genes that are failing to recycle damaged proteins in the body. Those damaged proteins then become malformed and accumulate in the motor neurons of the spinal cord as well in neurons in the brain, causing progressive degeneration (F. Fecto et al, SQSTM1 Mutations in Familial and Sporadic Amyotrophic Lateral Sclerosis, Archives of Neurology, November 2011, p 1440).
This research can lead to new targets for therapeutic drug development for ALS patients as well as for other neurological diseases like the dementias, Parkinson's, and Alzheimer's disease.
About 5000 new cases of ALS are diagnosed in the United States each year and there are an estimated 350,000 people diagnosed worldwide. It affects all ethnic groups, but only 10% is considered familial.
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