Diets and Mechanism of action

A board to discuss various diet-centered approaches to treating or controlling Multiple Sclerosis, e.g., the Swank Diet

Diets and Mechanism of action

Postby Kronk » Sat Jan 25, 2014 10:04 pm

I am dairy free with the exception of whey protein shakes, would like to go gluten free and I am currently trying to modify my diet to eliminate as much as possible. I started Swank last May and lost a great deal of weight which caused me to relax on most of the restrictions with the exception of the 15g saturated fat limit. I was a rather lean guy to start with and dropped 40lbs becoming uncomfortably skinny. There are many MS diets like paleo, Jelinek, Wahls, Fuhrman, Swank etc. but very few seem to point to the mechanism of action. I adopted the Swank diet because it made a great deal of sense to me, although Jelinek is almost the same with a few more restrictions...

original swank study ... ultClick=1

PwMS have higher levels of saturated fatty acids in plasma. This fact has been proven by many studies and has many implications. Through 5-lipoxygenase activation (5-LOX, a protein activator of leukocytes) Very Long Chain Fatty Acid accumulation causes a lipotoxic response (demyelination) consistent with cALD brain pathology. cALD is very similar to MS in that it is auto-immune mediated, affects the CNS, and is mediated by the presence of fatty acids. What is interesting is that monoeonics (un-saturated fatty acids) were shown to block the expression of 5-LOX and prevent the demyelination. This again points to the imbalance of saturated to unsaturated fatty acid in auto-immune disorders.

Study showing high lysolecithins in pwMS (derived from saturated fat)

Study showing fatty acid ratio in MS

Lipotoxicity accumulation of lipids (fats) ... _Treatment

In addition to this demyelination process there is another related to Lysophosphatidylcholines (LPC), also called lysolecithins. In the average person they are in (≤ 3%) the cell membrane and in the blood plasma (8-12%). But due to pwMS having additional saturated fat in our plasma it would mean higher levels of LPCs. LPCs are quickly metabolized by lysophospholipase and LPC-acyltransferase enzymes, meaning they last only shortly in vivo. However a product of metabolization is lysophosphatidic acid which promotes pro-inflammatory events that lead to the development of atheroma (disease affecting circulation) as well as encouraging progression of the disease. There is evidence that it is involved in such inflammatory diseases as rheumatoid arthritis and multiple sclerosis. LPCs can be used in the lab to cause demyelination of brain slices, to mimic the effects of demyelinating diseases such as multiple sclerosis.

Description of a lysolecithin

Study with fatty acids and rheumatoid arthritis (an anuto-immune disease) ... 8.full.pdf

Study showing fatty acid profiles the same in all neurologic disorders ... x/abstract

In addition to the demyelinating effects of the excess saturated fat its increased percentage in the cell membrane would reduce permeability. Unsaturated fats have a lower melting temperature, that's why saturated fats like butter and coconut are solid at room temperature. This is the same in the body, with unsaturated fats creating a more fluid membrane allowing allowing peptides and hormones through cell walls to bind with their receptors and modulate the cells. Saturated fats on the other hand are solid, essential to hold the cell together but too much and the cell would be sealed off from interaction. I believe this is a possible reason why LDN is not effective in all people. It increases the number of endorphin's in the body but if they cannot connect with the opiod receptors in the nuclear matrix of the cells they are useless.

I believe there is sufficient evidence to lower saturated fat intake in pwMS.
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