This Is MS Multiple Sclerosis Knowledge & Support Community

Sent you a PM Scott.

Thank you Kronk for your encouraging words. Thank you Scott for referring me to Czabo.


The world of the herpes virus and the endothelium

Probably tucked deep inside our endothelium lies somewhere the viral cause of MS. The virus of the herpes family settles deep in the endothelium.
The virus itself is no longer detectable in the blood. An eminent immunologist once told me that the virus infection itself is removed from the blood within a day. Thus, there is more to it. We probably have to look for this low-level chronic EBV infection tucked deep inside the endothelium.

The immune system and the virus have evolved alongside, for millions of years, most probably for hundreds of millions of years. Even fish carry the virus. This article (unfortunately in Dutch) shines some light on the virus.
http://www.ntvn.org/artikel/pdf/2011-1_ ... enomen.pdf

What applies to CMV probably applies to all herpes viruses including EBV. Quote from the article:
The virus nests in the vessel wall, and occasional breaks out and causes major changes in the immune system by the formation of highly aggressive effector T-cells (CD4 + and CD8 +). This type of immune cells for their survival depends on the presence of the herpes virus and comes in healthy people only when they are infected with the virus which itself is no longer detectable.

The relationship between the well detectable CD4 + and the CD8 + T cells, and the virus means that the virus itself is somewhere in the body.
The fact that cytomegalovirus-like viruses are found in very many species – including in fish - suggests that it evolved along side with us for a very long time and adjusted itself entirely on the man. In fact, humans and virus keep each other in balance and the virus helped along the long, joint road through attack and defense to build up our present immune system. Unquote


The fat metabolism and the virus

Omega-3 is anti-inflammatory, probably because it suppresses the virus. Texas researchers suggested the effects of interferon may be attributed to virus suppression.

Omega-6 is not anti-inflammatory, it is said to be pro-inflammatory but whether and how the virus is involved is not clear to me.

The Omega-6/Omega-3 ratio in our diet has dramatically changed over the last 150 years, from 1:1 to 16:1. The emergence of inflammatory diseases corresponds/correlates. The articles set out the evolutionary aspects of our diet.
http://www.hindawi.com/journals/jnme/2012/539426/
http://www.sciencedirect.com/science/ar ... 2206002435

The last article explains how many chronic conditions, including cancer, cardiovascular disease, autoimmune diseases, rheumatoid arthritis, are associated with factors that increase by increases in Omega-6 fatty acid intake and decrease by Omega-3 fatty acid intake. The balance is important for homeostasis and normal development.

On the conversion of Omega-6 (LA to arachidonic acid AA an inflammatory precursor) and Omega-3 (ALA to anti-inflammatory precursors EPA and DHA), it is interesting to note that conversions occur along the same rate-limited enzymatic pathways, this means they “compete" for a spot.

Both Omega-3 and Omega-6 influence gene expression. Since many chronic diseases begin in utero or early in infancy, proper dietary intake of PUFA even prior to pregnancy may be important. It would thus seem that an ever weakening society could go across the boundaries of generations. Oh my God, I think this may be very serious and important.

Dietary Omega-6 fatty acids promote whereas marine Omega-3 fatty acids EPA and DHA inhibit leukotriene-mediated inflammation that leads to atherosclerosis.

Leukotrien is a potent fast acting lipid mediator. What is very interesting here is to find a clear relationship with the EBV:
http://www.eurekaselect.com/85606/artic ... nity-vitro

And this one: quote Preincubation of PMN with EBV resulted in an increased release of arachidonic acid .... These data indicate that binding of EBV to human PMN results in the activation of intracellular events involved in the release of pro-inflammatory lipid mediators.
http://www.ncbi.nlm.nih.gov/pubmed/11737068

Or this one: Importantly, the results indicate that endogenous LTB4 can induce T-cell activation that inhibits the EBV-induced proliferation of B lymphocytes.

Wow, this link of the fat metabolism with EBV is incredible. Have we arrived here at the very centre of MS? To the core of the inflammatory fat metabolism with a clear link to EBV?


Peroxynitrite: a natural immune reponse to the virus?

The microcosm at the submicron level of viral activity is poorly understood. Szabo suggested in this paper that peroxydation inhibits viral replication.
http://www.enzim.hu/~lbarna/articles/17667957.pdf

Is this peroxynitrite part of the immune defense mechanism? Or is the peroxynitrite just a consequence of the superoxide (the immune system) trying to kill the virus? That then reacts with the NO where besides the superoxygen also the peroxynitrite works against the virus?

Could it be that in the initial phase of MS there may be some limited suffering of normal cells due to the peroxynitrite while in our case the mechanism has tumbled over too far to the other side?

In conclusion, I think that the cause of MS is somewhere at the intersection of the lipid mechanism, the virus and immune action. There may be a number of other (side-)factors too that play a role such as psychological mechanisms in immune modulator (cortisol and cholesterol mechanism involved?), platelet aggregation (causing further nutritional failure?), the incorporation of EFA in cell membrane phospholipids etc.
http://pni.osumc.edu/KG%20Publications% ... 29/062.pdf

Letermovir would seem a potentially very promising drug that breaks the viral cycle, possibly at the submicron level.

Hi Leo,

There is so much in that Szabo article. The side notes and explanations below the figures are so informative but massively complex. He doesn't draw it out in laymans language but so much of what he is talking about are the different pathways to ATP production. I agree peroxynitrite, of itself, is neither good nor bad but an excess is bad because we end up with too many electrons from it that aren't going on to ATP formation. In the article he talks about PARP. The 'R' is ribose. His diagrams include the membrane around the mitochondria and how ADP converts to ATP. It is very complex. The book I suggested by Sinatra has the beginners version of the process. Szabo talks about imbalance and I think that might be the right way to look at it. Szabo has a side note about Radical-Radical termination. The implication is we do try to heal ourselves by making stuff like Peroxynitrite but its out of balance.
Figure 3 on the Structures of metalloporphyrins is interesting. The point he makes on the side bar of page 666 about how peroxynitrite and several reactive oxygen and nitrogen species can trigger DNA strand breakage which then rapidly activates the nuclear enzyme, PARP, which causes the depletion of the intracellular concentration of its substrate, NAD, thus slowing the rate of glycolysis, electron transport and subsequently ATP formation is probably what it is all about. So Sinatra's focus on Q10, ribose and carnitine for cardiac patients is just as relevant for us. We obviously have to limit peroxynitrite formation but we really need to boost ATP formation. Doing that will help us maintain adequate stores of purines which will be neuroprotective and create energy. Hopefully other processes work better when we do that.
Regards

I always like to focus on the actions we can take more than the theory behind it... therefore the following would be strategies to support the theory above.

- Exercise, particularly heavy lifting leave the treadmills for the hampsters.

- Consume a creatine supplement. Older forms of Creatine the "monohydrates" required a loading phase of 5 g creatine, 4 times a day for one week, and maintenance is 2 to 5 g daily. Newer forms such as the Hydrochlorides do not require loading. Creatine is an amino acid naturally made by the body and can be converted into ATP, particularly during exercise.

- Take daily doses of coenzymeQ10, (CoQ10) or better yet Ubiquinol which is the more stable form of CoQ10. This compound is involved in the body's production of ATP and helps increase energy levels. Since CoQ10 is fat-soluble, it is best absorbed by the body when taken with food. Taking it at night may also yield better results than taking the supplement in the morning.

- Consume Vitamin B-1, or thiamine, which is is especially necessary for the production of ATP. Taking a B-complex ensures that you are getting all eight B vitamins necessary for optimal bodily functioning.

- Take Inosine, which is proven to reduce peroxynitrite. Its thought that Inosine increases uric acid which is a peroxynitrite scavenger but it does much more than that. Inosine is a purine ribonucleoside made within the body within the muscle of the heart and skeletal muscle. It is comprised of the purine base- hypoxanthine and the sugar D-ribose and has been shown to exert potent effects on the immune, neural, and cardiovascular systems. Inosine also has a responsibility in the regeneration of adenosine triphosphate (ATP) during endurance exercise. Be sure to consume adequate amounts of water during supplementation as it can lead to the formation of kidney stones.

Thank you for your reactions. I agree that therapeutic options are very important for us to get control over the disease.
But first I would like to go just a little bit deeper on the viral connection.
Having read dozens of articles, I am sure our microcosm contains many pathways, variables, concepts etc. that we haven't yet seen or fully understood.
The line of thinking below is looking through one particular keyhole at the enormous complexity of this microcosm.
Swank and the low incidence of MS in coastal areas seem to confirm this line of thinking.

The co-evolution theory

Our immune system weakens for a variety of reasons.
The virus emerges, deep in our endothelium.
In reaction, the cells release arachidonic acid (AA). http://www.ncbi.nlm.nih.gov/pubmed/11737068

The immune system recognises that there is something wrong.
It has been with us for tens of millions of years and is trained to react.

Slowly, the ratio Omega-3 to Omega-6 changes because of AA release.
And ApoA1 level (HDL is directly related) is reduced (25% in RR, 50% is SP and 75% in PP). http://ccsviinms.blogspot.be/2013/11/go ... brain.html
ApoA1 is anti-inflammatory but is outcompeted by AA which is inflammatory (because the immune system thinks there is a virus there).
And the endothelioum inflammates. http://www.ncbi.nlm.nih.gov/pubmed/24416810

The other chain follows: immune cells, superoxide, peroxynitite.
These are very localised processes, short lived and restricted diffusion but still go across cell membranes. http://www.enzim.hu/~lbarna/articles/17667957.pdf
Initiation of lipid peroxidation processes, the lesions follow etc etc.

It seems that therapeutic options would need to start with getting control over the fat metabolism (get the balance right / EPA and DHA) and over the virus.
Improving nutritional conditions and antioxidations are important too but seem more of the type of symptom relieve.

Hi Leo,

That full article on arachidonic acid is a cracker. What it points out is EBV infected cells are primed for a further stimulus to lead to arachidonic acid release. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1906243/ .
It's not the EBV itself but that is integral. It is EBV infected polymorphonuclear leucocytes that when stimulated that start a response.
It's the second stimulus that does the damage as the cell is already primed. It's a great article. They don't identify the second stimulus but I guess it could be from a number of sources. The justification for controlling EBV is stronger having read this as, if the cell is not primed, then the second stimulus is neutered.

Regards

Hi Leo,

I found this article which I find very interesting.- http://www.ncbi.nlm.nih.gov/pubmed/10086187

It points out that Adenosine is an endogenous inhibitor of arachidonic acid. If you recall, ATP is made of 3 phosphates, D-Ribose and Adenosine. When we can't make enough ATP the response in the cell is to convert 2 ADP to 1 ATP and 1 AMP . The AMP is then lost from the cell to ensure a constant ratio of ATP:ADP:AMP exists (per Sinatra). Over time the vitality of the cell declines as ATP levels decline and the loss of some AMP leads to a fall in Adenosine and, in time, a loss of purine from Adenosine loss. Ultimately energy levels decline and uric acid levels fall. This article points out that the loss of Adenosine will lower the ability to control inflammation.
It is a system that feeds on itself: the EBV infected B cell is a prolific producer of superoxide and over time we produce excess peroxynitrite, The peroxynitrite disables glyceralderhyde 3 phosphate which impacts the sodium/potassium pump and cell viability. The imbalance of the ratio of ATP to ADP to AMP causes the cell to shed AMP which further lowers ATP, the fall in adenosine lowers purine levels and uric acid falls so we lose a potent scavenger of peroxynitrite. Now we can see the fall in adenosine increase the risk of proinflammatory reactions. And on we go.... EBV infected polymorphonuclear leucoytes will release arachidonic acid when stimulated. So inflammation starts.
It would seem to me that helping ATP to reform becomes critical. In particular, Sinatra points out that Carnitine is the shuttle across the mitochondrial membrane, Q10 is the active element in the electron transport chain inside the inner membrane and D-Ribose would help bind the elements in ATP. He also likes Zinc and Magnesium from memory.

Regards,

Hi Scott,

I think MS is somewhere on the intersection of virus, fat metabolism and immunity. The assessment in your last posting is probably close to it. But the precise concept still needs to be set out.

I therefore think that the main angle of attack of our disease is through the fat metabolism; other supplements work more on the ‘symptomatic side’ of things.

As I understand, the body cannot make the fatty substances itself, so it has to take them from our diet. Our diet thus becomes all important.
This thinking goes into that same direction, taking control of MS through our diet. The reference list at the end of the page contains many very interesting publications.
http://www.overcomingmultiplesclerosis. ... gram/Diet/
http://www.maneyonline.com/doi/pdfplus/ ... 0000000117
and its ref 19: http://www.ncbi.nlm.nih.gov/pubmed/22384749 quote: I propose a new framework for understanding MS as a dysfunction of the metabolism of lipids.

Many of these things are too complicated for me as a semi-literate. I am happy that the most eminent experts in virology and immunology in my country are now looking at this matter.

In the meanwhile, for as long as the ‘solution’ for MS has not been found, I would recommend all patients with MS to strictly adhere to the protocol devised by George Jelinek at http://www.overcomingmultiplesclerosis. ... -Overview/

His book is fabulous. Some time ago, I took a sentence from his book and put it up against the wall of my office. It reads: “It is extremely important for people with MS to tackle this disease early because much of the damage occurs without us aware of it.” And although I put these letters up on the wall, I failed to live up to them, until now.

In 2008, I followed the low fat diet for about 8 or 9 months, and then a sort of gave up, just let it go.. I remember that in that period, my walking distance increased from 2.5 to 4.5 kms. For sure, it did not go down. With hindsight, this is the only period during my 10-year MS career where things improved. Now it is down to a few hundred meters. What have I done?

The initiative to make the book “Overcoming Multiple Sclerosis” available for free for people in Australia and New Zealand is just great. The book should be translated and we should all have access to it, in all countries of the world.

Regards,
Leo

Hi Leo,
I'll be interested to see how you go. I'm going the other way at the moment, consuming a lot more meat, avocado and coconut to get the saturated fat rather than avoiding it. I'm staying well away from gluten and dairy. I agree the fats are really important to look at but I guess it's all about which fat or fatty acids. The word that keeps coming up again and again in articles is "inflammation". How fats and which fats are involved in the inflammatory processes will be a big part of it. You're right, though, it's an intersection that we sit at. Not on a simple point to point highway. Will you be dodging most fats or concentrating a shift in the omega 3:6 ratio?


Regards

I was raised in a catholic family. When I was a child, now more than 50 years ago, we eat fish every Friday. The fish on Friday must have been a good catholic tradition. Where, just like with fasting, there is probably a legacy of many generations in support of this tradition. Traditions that were carried over for thousands of years as they must have contributed to good societal health. We should not forget here that up to a few hundred years ago, the church was still the only governing body in our societies with a similar length of legacy and a key interest in a healthy society, both mentally and physically.

On your question whether I will be dodging most fats or concentrating on a shift in the omega 3:6 ratio, I think it is not an either or. I think the two will go together. If I shift to a higher consumption of fish, fats consumed will change as will the omega 3:6 ratio. In general though, I think these simple concepts on fats are not sufficient. If you take some of the terms in http://www.ncbi.nlm.nih.gov/pubmed/11737068 and cross them in a Google search with terms that you find in other publications such as ApoA1 and ApoA2, you arrive at all sorts of fat related proteins that are mentioned in one breath. I find interesting the figure on the statin pathway on http://en.wikipedia.org/wiki/APOA2 (you can unfold the figure it by clicking on the icon in the right bottom).

You may well be right that not all saturated fats are equally bad. And perhaps the biggest problems are with the transfats. Jelinek´s book gives some insights. But I have some good experience with low saturated fat so I will go this way for now. I don't know where and how this journey will end but it is true that I feel increasingly frustrated with the situation. So perhaps I best take a break.

Increasing saturated fats… can I ask why?

Several studies have concluded that the plasma of people with MS has TOO MUCH saturated fat. Saturated fat is critically important in cell production making up to 50% of the cell membrane and giving it rigidity. The cell membrane is selectively permeable, determined by the ratio of saturated to unsaturated fatty acids. Additional unsaturated fats increase the fluidity and therefore the permeability of the cell. Whereas additional saturated fats increase the rigidity of the cell. Too much saturated fats and the cell would be effectively sealed off, limiting the binding of cells to interact with or produce immune modulating hormones.

There are many studies regarding the distorted fatty acid profile in MS a google search will produce many. I linked an older one below because I like some of the quotes in it.
http://www.pnas.org/content/86/12/4720.full.pdf

“…The abnormal profile of fatty acids in multiple sclerosis has features in common with profiles of other syndromes involving viral infections…”
“…Whatever the cause of MS, accompanying PUFA deficiencies may respond beneficially to nutritional supplementation of PUFA…”
“…Loss of polyunsaturated fatty acids and replacement by nonessential acids lowered mean chain length and raised mean melting point significantly…”
“…Duration and Kurtzke score varied inversely with saturated fatty acids …”
“…Metabolic defects in MS caused a decrease of total PUFA from 47% to 42%, compensated by saturated FA increasing from 36% to 42% in MS. The Double Bond Index of serum phospholidpids (PL) was reduced to 85% of normal as a consequence of PUFA deficiencies in PL…”

I agree with increasing protein significantly to raise the production of growth hormone IGF-1 even agree with raising caloric intake but I believe there is enough evidence to stay away from the saturated fats.

I’m looking at Wahls book first, (excuse my spelling mistakes- I had to type it out)

From page 156

“Essential fatty acids are the fats that our cells need but cannot make themselves. We must consume them or we can become deficient, to the detriment of our own health. These include alpha-linolenic acid (ALA), an omega-3 fatty acid and linolenic acid (LA), an omega-6 fatty acid. In addition, there are two conditionally essential fats: docosahexaenoic acid (DHA), an omega -3 fatty acid and gamma-linolenic acid (GLA) an omega-6 fatty acid. The conditionally essential fatty acids, DHA and GLA are more likely to be required if the person has developed a brain problem, autoimmune problem, or disease involving too much inflammation.”

She goes on to remind us the ratio of omega 3: omega 6 in traditional diets was 1:1 then says

"That ratio has been dramatically skewed in favour of omega-6 fatty acids, and the amount of omega-3 fatty acid has dramatically declined…..The current omega-6 to omega-3 ratio for some Americans is as high as 15:1 or even 45:1…..many of our chemical pathways tilt towards inflammation and the development of chronic disease…. (then page 157) This can easily be reversed, however, by ramping up the amount of grass fed meat and wild caught fish in your diet (while simultaneously eliminating or markedly decreasing the amount of vegetable oil). On a vegetarian diet it is especially difficult to achieve a 1:1 balance."

From page 188

"Eat more fat! I want you to add at least 5 tablespoons of coconut oil or ¾ can or more of full-fat coconut milk."

From page 190

"In a ketogenic diet, fat is high and carbohydrates are low, so that the body begins to burn fat as fuel instead of sugar from carbohydrates…(page 191) when your body is in a state of nutritional ketosis, the liver begins to produce ketone bodies- acetoacetate, acetone, and beta-hydroxybutrate. The brain cannot burn long chain fats because long chain fats can’t cross the blood brain barrier. Instead the brain uses for fuel what can cross the blood brain barrier: ketone bodies….these then proceed to cross the blood brain barrier to be burned as fuel in your brains mitochondria."

From page 202

"I want the majority of your calories to come from fat. You should eat sufficient protein to meet the dietary requirements of your body, but not more…Your goal is to have a source of medium chain fats at each eating occasion. You will get the most ketones from coconut oil as opposed to other types of fats."

From page 277

"Ideally, ask your doctor to do a lipid panel that includes fatty acid analysis to know what your bloodstreams omega-6 to omega -3 fatty acid ratio is. This looks at AA to EPA (arachidonic acid to eicosapentaenoic acid). Your goal is to get that ratio between 1.5 to 3."

She is, of course, highly critical of trans fats.

From The Sinatra solution-Metabolic Cardiology by Stephen Sinatra

Page 204

"L-carnitine facilitates the beta-oxidation of fatty acids as energy fuel. And since fatty acids are the preferred fuel for energy recycling in cells, this action is critical to cell and tissue function….L-carnitine deficiency disrupts the normal metabolism of fatty acids, reducing available energy supplies and leading to the accumulation of toxic byproducts of fatty acid metabolism. L-carnitine supplementation revives fatty acid metabolism and restores normal mitochrondrial function."

Needless to say L-carnitine is part of my routine. I don't disagree that if the processing of fats is disordered then it can be a problem for health. So the question is- are the abnormality of fatty acids profiles in MS because of the type of fat or is it an L-Carnitine deficiency leading to a disorder?

Your note points out the profile is consistent with syndromes involving viral infections. Buhner (Healing Lyme disease coinfections) says

Page 125

" Mycoplasmas scavenge particular fatty acids, in specific oleic (the most), linoleic, palmitic (a.k.a. hexadecanoic), linolenic, and myristic acids"

Page 119
"A number of websites that discuss the treatment of mycoplasmas insist that such things as arginine and fatty acids should not be taken in the diet as these "feed the bacteria". Again this will only result in a worsening of the illness- the mycoplasmas need these substances and they are going to get them from your body one way or another; they are very good at doing so. If you don't replace what they take, the host cells are depleted of these nutrients, a plethora of symptoms will occur, most of them extremely annoying...in terms of diet, if you want to replace the nutrients scavenged by the mycoplasmas, here is what you should eat at least every other day (altering it with other things on the liston the off days) until you are well: eggs, calf or beef liver, oysters, one Brazil nut, sesame seeds(or Tahini) avocados, chlorella/spirulina/seaweed green drink (which is basically chlorella, spirulina, and seaweed powders in water or juice)

So the antibacterial approach of Buhner has a lot of overlaps with Wahls.

Pages 120 to 123 of Buhner look at nutrients to replace due to scavenging: B Vitamins, Choline, Zinc, Copper, Selenium, Amino acids (L-arginine, L-Tryptophan, L-threonine and L-Serine in particular) and Fatty acids (particularly adds Olive oil).

Just looking at fats seems too simple to me. If the fatty acids synthesis is already compromised and we don't adjust for bacterial or metabolic influences then how should we interpret studies that are looking at one thing? We would need to review the context of the ratio of omega-3 to omega-6. We would need to look at the adequacy of L-carnitine and nature of infections that can lead to scavenging.

I'm not sure I would lean too much on that study; 14 MS people measured against 100 30 year old controls could have a lot of variables in 1989 that weren't checked. The MS people were all observed as having metabolic defects and it was only surmised that increasing polyunsaturated fatty acids may help correct an imbalance relative to saturated fats. It didn't test the idea. A follow up test to that may have been done and it would be useful.

I hope you're feeling better today, Leo. Your work is very valuable and obviously followed by many.

Regards

Thanks for the explanation Scott, I hope you do well on the Wahls diet I have heard good things.

I think Wahls and Swank do similar things where Swank has you restrict it Wahls has you consume so much of the "good" fats and vegetables that it pushes the ratio closer to proper balance. I think its important to try different diets, medications, protocols, regimens or what have you to see what works. If it is not, change it up similar to what Leo is doing. I have been on my diet for 2 years and doing well so I am sticking with it.

That linked study was but one of many pointing to the fat imbalance in MS. I posted a some more links below that made me move away from Saturated Fats. I do agree with the almost all of Wahls statements. But I think the exclusion of saturated fat from the diet is important. The argument about any diet could be whether or not the consumption of fats actually affect serum phospholidpids?

To echo Scott's comments I hope you are doing well Leo, I have learned a great deal about MS from this thread...

Best of Luck!

Consumption of saturated fat impairs the anti-inflammatory properties of high-density lipoproteins and endothelial function.
http://www.ncbi.nlm.nih.gov/pubmed/16904539

Consumption of an SAFA-rich meal is harmful for the endothelium, while a MUFA-rich meal does not impair endothelial function
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2584179/

Sat fat effect on the endothelium
http://www.ncbi.nlm.nih.gov/pubmed/3606733

Sat fat damaging endothelial cells particularly palmitic and stearic
http://www.ncbi.nlm.nih.gov/pubmed/1604444

Low fat diets reduce thrombin
http://www.researchgate.net/publication ... w_fat_diet

Thrombin and subendothelium
http://www.ncbi.nlm.nih.gov/pubmed/11307830

Thrombin activity correlates with disease severity
http://www.msdiscovery.org/news/news_br ... on-protein

Clear link between sat fat and thrombin activity
http://books.google.ca/books?id=xY9mnvC ... at&f=false

saturated NEFAs (palmitate and stearate) are proapoptotic, and unsaturated NEFAs (palmitoleate, oleate, and linoleate) are antilipoapoptotic
http://diabetes.diabetesjournals.org/co ... /3121.full

inactivation of thrombin on the subendothelium. Healthy endothelium is able to inactivate thrombin and not produce a clot.
http://www.ncbi.nlm.nih.gov/pubmed/3660348

BBB issue in MS
http://www.ncbi.nlm.nih.gov/pubmed/14664465

BBB functional roles
http://www.ncbi.nlm.nih.gov/pubmed/17453713

Thank you to both of you for all the thought you have put in.

I'm probably not going to obsess about the fats. The thing that really seems to be helping me at the moment is the introduction of Aceytl-L-Carnitine and more recently N-Aceytl-Cysteine. It's on top of everything else I do so I am still taking Q10, Valtrex, L-arginine etc as well. I have absolutely no fatigue issues but I have damage from demyelination that is causing me some grief particularly with my hands and arms. My approach is to think of it like the effect of pinched nerves but it can be quite painful and I have had a couple visits by the ambulance. The main concern is whether I have slipped back into AF which, so far, hasn't been the case. Perhaps the Aceytl-L-Carnitine is normalizing fat metabolism and we just worry too much about the fat rather than the transport agents themselves. Honestly don't know.
The lack of fatigue during my attack and how I am going now gives me cause to hope I am on the right track. More and more I am drawn to focusing on the recycling of ATP as what works for me.

Regards

Thank you for your kind words of appreciation. Don't worry, I'm doing all right. My main frustration probably stems from the fact that things don't go as fast as I would want them to go...

From the link on Kronk's posting (Jan 7, 9:32), by googling a bit I found this trail which brings us back to the herpes virus.

http://www.pnas.org/content/86/12/4720.full.pdf
Involvement of a virus that may release PUFA from PL (25) could be a cause of the PUFA deficiencies observed, and abnormalities of PUFA metabolism may be expected in other viral diseases.
and then on to its ref 25:

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC345862/
Fatty acid patterns of the serum lipids were measured in 17 children with Reye's syndrome (RS). Serial measurements of total serum free fatty acids (FFA) showed that levels were increased during RS and, after recovery, were significantly lower in the patients who survived. Fatty acid patterns of serum FFA, triglycerides, and phospholipids in patients with RS were significantly different from those in controls. In RS the polyunsaturated fatty acid content of phospholipids was less than control values; in the FFA, it was higher. This was consistent with the possible involvement of increased phospholipase activity. The increase in polyunsaturated fatty acids in FFA, the precursors of prostaglandins, suggests that a grossly disturbed prostaglandin pattern may occur in RS. These changes in lipid metabolism may be related to the abnormal hepatic and neurological functions observed in RS.

http://en.wikipedia.org/wiki/Reye_syndrome
Causes for similar symptoms include ... Viral encephalitis...

http://en.wikipedia.org/wiki/Viral_encephalitis
Types of viral encephalitis include:
....
Herpes simplex
Human Herpesvirus-6
Varicella zoster virus
...

Now it occurs to me that -and I repeat myself here- in our current system for medicare, we see a very large number of overlapping autoimmune diseases with different names. Every expression of a neurological set of symptoms got its own name, based on several types of observations. You just have to look at the above weblinks to see the wide variety of observations and symptoms.

But in fact, a bigger common scheme may be underlying. A scheme that encompasses the wide variety of observations, their patterns of case initiation, their chronic nature and many of their shared and unique symptoms and signs of the chronic phase of the disease. A scheme that explains many unexplained observations and the multiple similarities of these illnesses by a simple conceptual framework.

Now you may think this is all far-fetched but this very simple trail confirms to me that the way we currently look at these immune diseases simply starts from the wrong premise altogether where over time things got institutionalised with fences built around them. It confirms to me that we need to develop and accept a new paradigm based on the understanding of a viral cause (herpes) of autoimmunity and indeed MS.