This Is MS Multiple Sclerosis Community: Knowledge & Support

Hi Search,
I have most of those statistics and have them over a 10 year period. They move around over time and have been tending to normalise more recently. Absolutely numbers are useful but I like trend data as a better indicator.
The OO is superoxide, the ON is nitric oxide. They need to come into close proximity to create peroxynitrite. The OO is provided by EBV infected B cells. The ON is naturally occurring in the brain and CNS. The two combine as 10 x 10 not 10 + 10 so it quickly results in an overload in the body. If the B cell issue isn't addressed then the process never stops. Low uric acid arises because of insufficient production of ATP in the citric acid cycle. Boosting Uric acid via supplements helps control peroxynitrite as Uric acid is a scavenger.
The issue with peroxynitrite is it disables the proper functioning of the citric acid cycle. Once that occurs a lot of readings you are looking at start to go pop up as other cycles are impacted.
I don't agree with your view that MS has different varieties according to gender. It may have different rates of incidence but that is a second round outcome. I'm not saying you are wrong dealing with measured deficiences but I think you need to go one round deeper to what causes the imbalance. Thats where I think you will implicate OO via EBV.

Regards

O2- is a product of mitochondrial metabolism, immunity, etc, which is why CuZnSOD is so important. Unfortunately, it is damaged by among all the things I mentioned, H2O2 which is also constantly produced by the cell and normally eliminated by catalase (an Fe enzyme), pseudocatalase (an Mn enzyme) and selenium-glutathione peroxidase.
NO is produced by the cell and has myriad functions, including vasodilation, immunity, etc, Zn inhibits NO synthase, so when Zn is low or displaced by Cd, there can be excess NO (which is not much of a problem if there is no O2- and if the cell has plenty of Mg and can expell NO to perform its vasodilation function, etc, in other cells. Unfortunately, when the neuron is low in Mg, NO cannot be expelled, and when there is O2- it reacts with it.
Sorry but I dont see how 2 substances can combine as 10x10, that vioates the conservation of matter. Simply O2- + NO = ONOO-.

The citric acid cycle has many functions. One function described a decade ago in a paper in Medical Hypethesis titled Do mitochondira regulate iron homeostasis? is that when the mitochondrion is low in Fe (which it uses to make heme for hemoglobin and other enzymes), the cycle is interrupted and citrate is released by the mitochondrion. The citrate chelates an Fe atom from IBP-1, and causes it to detach from the gene codes for transferrin receptor production, so that transferrin receptors are produced and displayed on the cell membrane, allowing iron to access the cell. Once the cell has plenty of iron the cycle is restored and the IBP-1 floating around in the cell binds to an Fe atom and becomes aconitase, an enzyme that destroys the remaining citric acid in cytosol and then binds again to the gene for tranferrin receptor, blocking it. IBP-1 does the opposite with ferritin gene, blocking it when Fe is low and inducing it when there is excess Fe in the cell, so that the Fe is safely sequestered in ferritin and cannot cause oxidative damage.

A very important process in MS is lipid peroxidation, which produces acrolein, which in turn blocks Cu enzymes, damages mitochondrial, lysosome and cell membranes, etc, and interferes with lysosomal proteolysis of many harmful substances.

http://physrev.physiology.org/content/8 ... l.pdf+html

Download the file. The whole thing is worthwhile. There is a lot in it.

Page 316 talks about the 10x 10 thing. Orginally, I thought as you do.

Peroxynitrite is a superfast molecule. It has a very short life but constantly keeps reforming.

Regards

Thanks for the article (or rather book) Scott1. It is typical of an expert's report, loaded with useless information and devoid of useful information.
I could not find even the mention of a single ONOO- scavenger. It mentions the effect of NO on Ca proteins, but does not mention the cruacial role of Mg in this interaction. Strangely, it states that NO is hydrophobic, but that it moves freely through cytosol, which is basically water.
Regarding MS it mentions that urate inhibits tyrosine nitration but is not an ONOO- savenger. It does not mention explain that being a sulfur-iron protein, xanthine oxidase (the enzyme that produces uric acid and which appears in the long list of proteins damaged by ONOO-) it is damaged by ONOO- and hence the low urate levels in people with MS.

Instead of using a million words I like to address the crux of the matter.
There are several vicious cycles or rather descending spirals: A person MS propensity and with low levels of uric acid, PQQ, Zn, Mg, vit D, CuZnSOD, folate, etc, starts to produce some ONOO-, which damages the MnSOD and C-cytochrome in mitochondria and the remaining CuZnSOD, Zn-thionein, xathine oxidase and many other heme enzymes in cytosol and induces lipid peroxidation, causing high levels of very harmful aldehydes, cush as acrolein, malon dealdehyde, etc, Acrolein damages some Cu proteins, which blocks homocysteine elimination, causing homocysteine elevation, which in turn damages more Cu proteins, etc,

Hi Search,

Do you have MS?

Regards

Hi Scott1,
No I don't. I have the gout gene and started doing research at age 40 because all my male relatives over 40 had it and I wanted to avoid it. All the books, articles, wiki, etc, stated that uric acid was the problem but that only 10% of people with hyperuricemia ever developed gout and even though many of the people with hyperuricemia had uric acid in excess of 12 and no gout and people with gout often developed attacks with levels below 9. It didn't make any sense to me. It didn't make sense to me either that if I was born with the gene the disease didn't appear until after 40. I figured out that high Fe, Mo, etc and low Cu, Mg, etc, was the problem. I donate blood to keep my ferritin between 30 and 55 and take copper, drink no more than one glass of wine or beer a day and eat well and never deloped gout (I´m 55 now). I cured all my relatives and acquaintances by suggesting that they do the same.
I research many other diseases, always trying to get to the bottom.
take care

Maybe you should stay with Gout.

I've had both which makes me fairly rare.

I'm a C282Y heterozygote, so is my sister (and brother too), so we don't have classic HH.
My ferritin has always been >120, (even when heavily pregnant over 15 years ago).
It was 175, at my sickest point about 3 years ago now, iron was around 28, transferrin saturation at 62%.

My sisters ferritin sits steadily at 150, iron high 20's, TS around 36%, but we have only recently started to collect these results. Other tests don't show she has inflammation. Her iron results are
not particularly like mine, as she has high transferrin which would suggest she is anaemic(?), and this skews her transferrin saturation result.
She definitely isn't anaemic, the only correlation I can find for that is that pre-type 2 diabetes can raise transferrin. She can't donate because she has MS. She would love to try this, as it fixed me up a treat. She gets the stiff sore joints as well.

It has also been suggested that I have porphyria by one of my specialists (a rheumotologist).
That of course opens up a whole new nest of worms I can't drink alcohol, or tolerate hormones (birth control), I can get a rash also, especially when I've taken hormones in the past. I also react to some drugs, over the past few years it's been to local anaesthetics (dental) twice. I avoid these types of things where at all possible.

Anyway, the iron reduction works really well, quite magical really

Hi Bethr,
Thanks for the info. Just remember that everytime you donate you not only dump excess Fe, but also many other elements, some of which were probably low even before your first donation.
I would like to know uric acid, urea creatinine, Na, Cl, Ca, P, ALP, AST, ALT, GGT, albumin, globulins, insulin, MCV, hgb, etc, for both of you.

If she has excess iron and hgb>15, etc, and benefits from eliminating blood she can go to a doctor to extract the blood in the same way a donation is performed (which is costly), but the doctor will discard the blood or if she does not have money and her MS is not advanced, she can simply learn to do bloodletting. One way is to stand up for a half hour and to sever an obvious vein on the foot with a sterile scalpel or exacto and remove a pint. To stop the bleeding, lie down, raise the foot above the heart and apply ice. However, we need the lab values above and after seeing them maybe others, in order to know her deficiencies and to correct them, otherwise, they will be exacerbated by phlebotomy.

Another downward spiral in MS:
As mentioned above lipid peroxidation results in high acrolein in MS. In turn acrolein inhibits the synthesis of beta-alanine, which is blocks acrolein, so that as MS progresses acrolein increases and carnosine decreases. The same thing occurs in diabetic neuropathy, but affectng mostly the eyes and kidneys, instead of the CNS. Fortunately, beta alanine supplementation can help to restore carnosine production and reduce acrolein levels and the damage that acrolein causes (which includes damage to the Cu enzymes among others, which in turn elevates homocysteine, which causes more damage to Cu proteins, resulting in weak blood vessles, low dopamine, more lipid peroxidation, etc,).
Acrolein is not only produced in the body by lipid peroxdation, it is also acquired by eating fried food, smoking, etc, As mentioned, acrolein has a short life in alkaline media, but persists and is more active in acidic media, hence the importance of maintaining blood pH between 7.4 and 7.44 with a good diet, Mg supplements, etc,

I want to mention a quick and inexpensive way to get an idea of blood pH and hydration level:
Ideally 138<Na<142 and 102<Cl<106, if both are higher than these values the person is probably dehydrated, if both are low the person is probably retaining fluid (is hyperhydrated). Moreover, if both are in the low range i.e. Na=138 and Cl=102 or both are in the high range i.e. Na=142, Cl=106 pH is probably between 7.36 and 7.4, if Na=138 (low range), but Cl=106 (high range) then pH is 7.35 or lower. In contrast if Na=142 (high range) and Cl=102 (low range) the blood pH is probably between 7.4 and 7.44 (alkaline, healthy pH).

I believe that a chart or diagram that shows the most important processes involved in MS is more helpful than a million words. I'am still working on it, but it already diplays a lot of information in a small area and would like to post it, but dont know how to do it (I'm more of a 19th century man than a 21st century one). I have it in a word file. Can anybody please tell me what to do to post it here?
thanks

When blood is donated or plasmapheresis (plasma exchange) is performed, insulin in the blood is also removed temporarily, until the pancreas secretes more.

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NHE

Thanks NHE,
I went to photobucket and after typing 6 recapchas I gave up. So never mind the flow chart.

There is a big controversy about methanol causing MS. Methanol is said to be found in cigarrete smoke (along with Cd, As, acrolein, CO, etc,) and in canned foods, especially fruits, vegetables and their juices. Methanol toxicity causes optic neuritis and other symptoms of MS.

Although most people can eat lots of cans without any problem (my 89 year old father spent WW II in the Pacific with the navy as a pilot and still consumes several cans a week, so he probably has eaten several thousand cans in his life, yet he is healthier than some 50 year organic vegetarians I know), people with low molybdenum, iron or sulfur or high ONOO- (which damages the enzymes containing these elements) have impaired function of the Mo-Fe-S enzymes that metabolize ethanol, methanol, aldehydes (acrolein, malon dialdehyde, etc,) and sulphites (dired fruits, wine, etc,) and purines (to make uric acid). Therefore, ethanol, methanol, sulphites (dried fruits, wine, etc,), etc, would affect these people more, increasing their already high risk of developing MS.