Hi, Sasha and the group.
I would like to give my views on supplementation of essential fatty acids in ME/CFS.
First, some of the main roles of omega 3 and 6 fatty acids in the body are to be part of cell membranes (including mitochondrial membranes) to raise their fluidity and thus to assist the cell receptors and channels in the membranes to operate properly, to help to build the myelin (white matter) in the brain, and to serve as substrates for making eicosanoids (signalling molecules, such as prostaglandins).
In ME/CFS, it is well established that there is a state of oxidative stress, and this is particularly important in the mitochondria.
It is known that the unsaturated (essential) fatty acids are the most vulnerable molecules in the cells to oxidative damage.
It is also known from the microscopic examinations done by Dr. John McLaren Howard at Acumen Lab in the UK that the mitochondria membranes are damaged in ME/CFS. The positive tests using Dr. Hokama's ciguatoxin test (which cross-reacts with cardiolipin, which is found almost exclusively in mito membranes in humans) is also evidence of damage to the mito membranes in ME/CFS, as is the work of Dr. Garth Nicolson using fluorescent indicators.
There is also increasing evidence of white matter deficits in ME/CFS from magnetic resonance brain scanning.
In view of all this evidence, it seems reasonable to believe that supplementing the essential fatty acids should be helpful in ME/CFS. However, there are some things to be aware of:
One is that so long as the state of oxidative stress is present, there will continue to be damage to the unsaturated fatty acids. Furthermore, the formation of lipid peroxides from these fatty acids is a chain reaction process, which feeds on itself. Therefore, while it should be beneficial to supplement these fatty acids, there needs to be a parallel effort to stop the oxidative stress. Otherwise, the situation might actually become worse from the supplementation.
In my view, treating to lift the methylation cycle block is the way to raise glutathione automatically and lower the oxidative stress. The simplified protocol for doing so includes a phospholipids supplement that contains the essential fatty acids.
Another thing to note is that people differ in their fatty acids status, in terms of the ratio of omega 3 to omega 6, depending on their diets and past supplementation. It's true that the average population (at least in the U.S., and I don't know about the UK) gets most of their unsaturated fatty acids from vegetable oils, which are high in omega-6. However, those who consume a lot of fish may be higher in omega-3. The status can be determined from a fatty acids panel, and it's important to run it on the red blood cell membranes, not the serum, in order to reflect to body content.
DHA is particularly important for the myelin in the brain. I don't agree that it should be avoided in ME/CFS.
There are different ways to supplement the essential fatty acids. As I noted, the simplified treatment uses phospholipids, as does Patricia Kane's approach. This has the advantage of also supplying choline, which is in short supply in ME/CFS because of the partial methylation cycle block. NT Factor also uses phospholipid (phosphatidylcholine) but in a liposomal form for better transport. It is also possible to use oils containing omega-3 and omega-6 fatty acids, and rely on the cells to convert them to the phospholipid forms, but this may be limited by the choline shortage.
I realize that my views differ from those of Prof. Puri, but in my opinion, he has misinterpreted the results of his and others' magnetic resonance spectroscopy measurements, in that he has assumed that creatine levels are normal in ME/CFS, so that the high ratio of choline to creatinine observed in brain scanning has been interpreted to mean that choline is high in ME/CFS.
However, both creatine and choline require methylation for their synthesis in the body, and thus, both are low. Creatine drops more than choline in ME/CFS, since its synthesis is normally the main user of methylation in the body, and this is what produces the elevation in the ratio of choline to creatine, but this is deceiving, because both are decreased. Additional evidence comes from 24-hour urine measurements of creatinine excretion, which are often found to be low in ME/CFS. Creatinine is the breakdown product of creatine. The low creatinine excretion may be mistakenly attributed to low lean body mass, but it is actually due to low creatine production because of the methylation deficit, in my view. We need absolute measurements of both creatine and choline in the brain in ME/CFS, and I hope this will be done soon. It is much easier to measure ratios with magnetic resonance spectroscopy, so that is what has commonly been done, but absolute measurements can be made with more effort, and this needs to be done.
Best regards,
Rich
