Multiple sclerosis, protein, fats, and progesterone
by Ray Peat PhD
We are always subjected to antigenic burdens. The important question has to do with our ability to limit the inflammatory response to these burdens.
In MS [multiple sclerosis], it is clear that the inflammatory process itself is destructive, and that estrogen is a major predisposing factor. Unsaturated fatty acids, and dietary imbalance of amino acids interact closely with hyperestrogenism and hypothyroidism to produce the autoimmune degenerative diseases.
Reduction of the mediators of inflammation is better than augmenting a single antiinflammatory agent such as cortisol. Although immunosuppressive drugs, including the “essential fatty acids,” do alleviate inflammatory symptoms temporarily, they probably contribute to the underlying pathology.
People with MS have chronically increased production of cortisol. This creates a distortion of protein assimilation, resembling a nutritional protein deficiency. Excessive serotonin and estrogen cause a relatively uncontrolled production of cortisol. A vicious circle of inflammatory mediators and amino acid imbalance can result.
Depression, lupus, migraine, menopause, diabetes, and aging have several important metabolic features in common with MS.
Popular therapies are illogical, and are likely to cause disease progression.
High quality protein, thyroid, pregnenolone and progesterone tend to correct the underlying pathology. These are antiinflammatory, but they are not immunosuppressive or catabolic.
High altitude and sunny climate are associated with a low incidence of MS.
