Multiple sclerosis is a complex neurodegenerative disease, thought to arise through autoimmunity against antigens of the central nervous system.
The autoimmunity hypothesis fails to explain why genetic and environmental risk factors linked to the disease in one population tend to be unimportant in other populations.
Despite great advances in documenting the cell and molecular mechanisms underlying MS pathophysiology, the autoimmunity framework has also been unable to develop a comprehensive explanation of the etiology of the disease.
I propose a new framework for understanding MS as a dysfunction of the metabolism of lipids [fatty acids].
Specifically, the homeostasis of lipid metabolism collapses during acute-phase inflammatory response triggered by a pathogen, trauma, or stress, starting a feedback loop of increased oxidative stress, inflammatory response [somewhat like what happens in hardening of the arteries], and proliferation of cytoxic foam cells that cross the blood brain barrier and both catabolize [break down] myelin and prevent remyelination [rebuilding of the nerve’s myelin sheath, damaged in MS].
Understanding MS as a chronic metabolic disorder illuminates four aspects of disease onset and progression:
1. Its pathophysiology;
2. Genetic susceptibility;
3. Environmental and pathogen triggers;
4. The skewed sex ratio of patients. [The sexes metabolize fats differently.]
It also suggests new avenues for treatment.
Source: The Quarterly Review of Biology, Dec 23, 2011;86(4). Corthals AP. Department of Sciences, John Jay College of Criminal Justice, City University of New York, NYC, USA. [Email: firstname.lastname@example.org]