http://www.eurekalert.org/pub_releases/2011-12/uocp-rcm122211.php?utm_source=twitterfeed&utm_medium=twitter

Jan Wexler found this gem

It makes sense! Logic!! I love it! It explains why diet has helped Terry L. Wahls and her friends, and probably explains why digestive enzymes have dramatically helped a nasty symptom of mine. And it gives us all back a bit of control if we take it and make some sensible changes. No instant cure but something I think we all can use to our advantage while we wait for one.

An article to be published Friday (Dec. 23) in the December 2011 issue of The Quarterly Review of Biology argues that multiple sclerosis, long viewed as primarily an autoimmune disease, is not actually a disease of the immune system. Dr. Angelique Corthals, a forensic anthropologist and professor at the John Jay College of Criminal Justice in New York, suggests instead that MS is caused by faulty lipid metabolism, in many ways more similar to coronary atherosclerosis (hardening of the arteries) than to other autoimmune diseases.

Framing MS as a metabolic disorder helps to explain many puzzling aspects of the disease, particularly why it strikes women more than men and why cases are on the rise worldwide, Corthals says. She believes this new framework could help guide researchers toward new treatments and ultimately a cure for the disease.

Multiple sclerosis affects at least 1.3 million people worldwide. Its main characteristic is inflammation followed by scarring of tissue called myelin, which insulates nerve tissue in the brain and spinal cord. Over time, this scarring can lead to profound neurological damage. Medical researchers have theorized that a runaway immune system is at fault, but no one has been able to fully explain what triggers the onset of the disease. Genes, diet, pathogens, and vitamin D deficiency have all been linked to MS, but evidence for these risk factors is inconsistent and even contradictory, frustrating researchers in their search for effective treatment.

"Each time a genetic risk factor has shown a significant increase in MS risk in one population, it has been found to be unimportant in another," Corthals said. "Pathogens like Epstein-Barr virus have been implicated, but there's no explanation for why genetically similar populations with similar pathogen loads have drastically different rates of disease. The search for MS triggers in the context of autoimmunity simply hasn't led to any unifying conclusions about the etiology of the disease."

However, understanding MS as metabolic rather than an autoimmune begins to bring the disease and its causes into focus.

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http://www.eurekalert.org/pub_releases/2011-12/uocp-rcm122211.php?utm_source=twitterfeed&utm_medium=twitter