A new concept and treatment options for MS

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Re: A new concept and treatment options for MS

Postby vesta » Tue Mar 20, 2018 2:31 am

David1949 wrote:
But recent new insights supported by an abundance of publications in the medical literature change this. MS is no longer that big unknown, is not in its origin a neurological disease, but is a metabolic disease caused by a virus, the herpes virus.

Leonard where is the proof of that?

David


frodo wrote:
Could be this the explanation of the relationship between CCSVI and MS?

This article points out that endogenous retroviruses that are normally latent reactivate under hypoxia (bad blood flow) conditions.

Investigation of Endogenous Retrovirus Sequences in the Neighborhood of Genes Up-regulated in a Neuroblastoma Model after Treatment with Hypoxia-Mimetic Cobalt Chloride

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5826361/

Human endogenous retroviruses (ERVs) have been found to be associated with different diseases, e.g., multiple sclerosis (MS). Most human ERVs integrated in our genome are not competent to replicate and these sequences are presumably silent.

However, transcription of human ERVs can be reactivated, e.g., by hypoxia. Interestingly, MS has been linked to hypoxia since decades. As some patterns of demyelination are similar to white matter ischemia, hypoxic damage is discussed. Therefore, we are interested in the association between hypoxia and ERVs.

As a model, we used human SH-SY5Y neuroblastoma cells after treatment with the hypoxia-mimetic cobalt chloride and analyzed differences in the gene expression profiles in comparison to untreated cells. The vicinity of up-regulated genes was scanned for endogenous retrovirus-derived sequences.


WAIT A MINUTE !

Before we get too excited about Endogenous Retroviruses (ERVs), allow me to point out that the Epstein Barr Virus (EBV) – cause of Mononucleosis which has struck all MSers -also reactivates in a hypoxia situation. As early as my May 4, 2014 blog post I observed that poor blood flow due to CCSVI reactivates the Epstein Barr Virus and with it MS « attacks». (See Blogs for May 4, 2014 « MS, Body Tension, Oxygen and EBV (Revised), May 23, 2014 « Vit D, Veins and EBV » Oct 12, 2016 « Oxygenate » the Brain, Nov 29, 2017 « MS : Linking Hormones, Diet, Blood Flow, EBV, Myelin Sheath – 2)

So what comes first, the Hypoxia or EBV or ERV ?

There appears to be a pathological need in Western Allopathic medicine to find a drug to "cure" MS. But what if Hypoxia is the main culprit for which there are myriad causes and subsequent « cures » and the « cures » aren’t drug related. So who gets the money ? (Well yes, MS patients often want an easy way out. Take a pill and the problem goes away. Who wants to change their diet and way of life ?)

Below find the 3 principal causes, potential cures, for MS hypoxia in the Central Nervous System/

1.The Chiropractor Dr Michael Flanagan believed that up to 25% of MS cases were caused by skeletal obstructions of blood and cerebro-spinal fluid circulation. Dr. Scott Rosa uses the FONAR upright cine MRI to see the obstructions. Specialty needed ? Usually Chiropractic or Osteopathy.

2. Dr. Zamboni’s CCSVI theory and treatment proposes using angioplasty to enlarge stenosed veins draining the brain/spine in order to free obstructed fluid circulation. Specialty Interventional Radiology

3. Dr. Owiesy observed that when the smooth muscle layers of the CNS veins constrict or go into spasm, they obstruct blood flow. This very critical observation helps correct and enlarge Dr. Zamboni’s CCSVI theory/treatment. It’s not always a problem inside the vein but exterior to it. But it IS a venous blood circulation pathology.

a). Dr. Owiesy proposes administration of a mixture of dexamethasone/lidocaine/thiamine in the area around the Internal Jugular veins to relieve the spasms. (Well, yes these are drugs.)

b). I (and many others) propose a healthy non-inflammatory diet and supplements to prevent toxicity and overcome body tension which basically prevents the spasms and veinous constriction– in my opinion the best, non drug idea.

Currently Neurologists monopolize diagnosis and treatment of MS. They apparently completely ignore the Hypoxia phenomena. They use immune suppressing Disease Modifying Drugs (DMDs). Worse, they believe that early treatment of DMDs assures a better outcome to prevent « attacks ». They don’t consider the three hypoxia issues noted above. MSers get railroaded into treatment which may not be the best solution for them. Physical Therapists in France have told me that the drugs tend to suppress vital energies and that the MSer just gradually declines over time.

So I believe these drugs represent a great misfortune which unnecessarily compounds the MS misfortune. They give the illusion of treatment when in fact the true MS problem is not being addressed. The poor patient gets hooked on drugs before she considers anything else and then the inevitable decline sets in.

See George Ebers research. “Critical Review of outcomes used in MS clinical trials” which was posted on You Tube November 4, 2013 by the European Medicines Agency. http://www.youtube.com/watch?v=OqY-_K1fYJY

Previously published on my site MSCureEnigmas.net https://www.mscureenigmas.net/

Regards, Vesta


Consider that the Viruses are secondary to the CNS fluid circulation problem, i.e. CCSVI

Regards, Vesta
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Re: A new concept and treatment options for MS

Postby Leonard » Thu Mar 22, 2018 6:53 am

David, Vesta,

Thanks for your comments.

CCSVI is a certain factor.
Compromised immunity of the nasopharynx leads to viral spreading into CNS.
The rest follows.

The story of Dr. Zamboni is almost anecdotal. As a young doctor, while he was stationed on the island of Sardinia, he diagnosed many young people with venous insufficiencies in the neck.
Many years later, he was long back on the Italian mainland, his wife developed MS. He went back to Sardinia and found that over 90% of the young people that he had diagnosed with vascular problems in the neck had developed MS.

Nobody can deny this. It is empirical. I got it straight from the horse's mouth.

Lately I hear neurologists say: CCSVI is not a factor. Period.
To these neurologists I would say: You ain't understood what is MS. Period.

But it may be even more serious than that where one could ask the question: do neurologists break their Hippocratic Oath "first, do no harm," or the Latin, primum non nocere?
I quote from Vesta's comment from above:
Currently Neurologists monopolize diagnosis and treatment of MS. They apparently completely ignore the Hypoxia phenomena. They use immune suppressing Disease Modifying Drugs (DMDs). Worse, they believe that early treatment of DMDs assures a better outcome to prevent « attacks ». They don’t consider the three hypoxia issues noted above. MSers get railroaded into treatment which may not be the best solution for them. Physical Therapists in France have told me that the drugs tend to suppress vital energies and that the MSer just gradually declines over time.

So I believe these drugs represent a great misfortune which unnecessarily compounds the MS misfortune. They give the illusion of treatment when in fact the true MS problem is not being addressed. The poor patient gets hooked on drugs before she considers anything else and then the inevitable decline sets in. Unquote

To the neurologists I say: Treating patients without understanding at the very least the basic underlying mechanisms is dangerous...

Reg,
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Re: A new concept and treatment options for MS

Postby Leonard » Mon Mar 26, 2018 2:34 am

From the prose of MS unraveled, let’s go back now to the technicalities:

The above book of Martin Pall on Explaining Unexplained Illnesses is from 2007. In 2010, Pall published a further paper with the title “How can we cure NO/ONOO- cycle diseases?” http://nunm.edu/images/CE/cureabst.pdf

I take the following interesting observations from the paper:
- … such multiagent protocols have not produced any significant number of cures
- Fig 1 shows a central role of the NDMA receptor in the biochemistry with multiple interacting vicious cycles

I am sure the process of learning is not far removed from here. Where invariably people with MS are affected in their cognitive capabilities, from the outset they may be smarter than average because their biochemistry allows them to learn more easily. https://www.everydayhealth.com/columns/ ... are-smart/

Another observation I would like to make is that although Pall has done a magnificent job and mentions the respiratory burst in some place in his book, there is a major source of superoxide missing in his work namely the EBV B cells. This latter source is believed to be central to maintaining the oxidative stress cycle with MS and many other EBV related diseases such as CFS/ME (see for instance the book of Francis Coucke on the role of EBV in CFS/ME). To this end, I think it is the EBV B cells that “fuel” the cycle.

Hence, where diet and supplements are influences, managing EBV B cells (i.e. depleting old ones and growing new ‘clean’ ones) is a necessary prerequisite for any cure. In fact, evidences are accumulating that chemo stops the cycle and allows people to get back on a recovery path. Terry Wahls is our best example.

To emphasize the role of chemo, I have revised step 8 of the above skeleton accordingly. general-discussion-f1/topic15188-825.html#p251748
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Re: A new concept and treatment options for MS

Postby Leonard » Wed Apr 04, 2018 4:39 am

Chronic disease begins in the mitochondria. Mitochondria dysfunction and early death are common pathways in all those illnesses. 24 million people in the US have an autoimmune diagnosis, but another 50 million do not feel well and have autoantibodies but do not yet have enough antibodies to make a diagnosis. So, that means about 75 million have autoimmune problems. That’s extremely significant, and it is a sign that our lifestyles have led us down a very dangerous path. Even more disturbing, more and more children are being diagnosed with an autoimmune problem as children.

Despite the increase in longevity which may be attributed to new medical techniques, drugs and technology, we are as a society progressively less well. Why is this happening to us? What has given rise to the single largest epidemic of chronic disease in human history? Have our genes gone bad or have we adopted a lifestyle that could explain the current scourge of autoimmune diseases? ref: https://www.amazon.com/Minding-Mitochon ... tochondria and articles

Since the weight of genetic changes is insignificant in just such a short period of a few generations, we will need to search the causes at the environmental level. Has our modern Western lifestyle over the last 20 - 50 years broken with the evolutionary path of the last many millions of years?

The answer to that last question is an unequivocal yes. The opinion on MS unraveled explains why, explains what happens if our cells and the microbiome composition become ever weaker. general-discussion-f1/topic15188-825.html#p252698
This recent thread on TIMS on "Gut microbes and the brain" adds to this thinking: general-discussion-f1/topic30043.html

Where the health problem itself is a huge global medical issue, solving the problem is perhaps an even bigger issue because the medical world is highly fragmented and compartmentalized in often monolithic structures where it seems that no one has the power and the democratic legitimacy needed to take control and knit the various interdependent innovations together.

I call on MS societies and patient representations to bring this matter to the forefront and demand change.
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Re: A new concept and treatment options for MS

Postby Leonard » Fri May 11, 2018 8:19 am

In progressive MS, there is short of ATP generation. The lack of energy causes problems for the ion pump to recharge and muscular stiffness/rigidity for muscular bonds are failing to break.

The big question now is: is it the mitochondria themselves that perform insufficiently or is it structural damage to the endoplasmic reticulum that impedes the transfer of crude energy supply into the mitochondria?

In my own case, I have difficulty walking and normally I walk with a cane. But fortunately I can still ride the bicycle. When on a chilly morning, I go out for a tour of 15 - 20 miles and then come back home, I walk almost as a normal person without a cane. This despite the fact that the bicycling tour has taken a lot of energy.

It is known that cooled limbs go better. It has always been like that for me. I understand in MS clinics they sometimes use ice to cool down the legs of patients.

From my own experience, where normally the right leg goes very difficult, if it’s cold the neuro path and muscles work much better. This has often taken me by surprise but it happens, all the time. My explanation is that the production of ATP must in some way be restored to semi normal if cold and that mitochondria do work.

A key question now is: why is that happening? Clearly, where there is more ATP, mitochondria just work better and produce more ATP.

But is it the mitochondria themselves that function better when cold? Or is the transport of crude energy across cellular membranes and/or the endoplasmic reticulum improved when cold?

I tend to think the latter, i.e. that the problem is damage to the cellular structure that impedes energy transport while in fact my mitochondria themselves are quite ok. There are several indications that would seem to hint into that direction:

- Apparently the mitochondria are still capable of working (when cold outside), they are not dead, they may just lack the necessary supply of crude energy
- Supplementing CoQ10, acetyl-L-carnitine, D-ribose etc does not really seem to help me, I would even say to the contrary
- Many years ago, when I was still walking 5 km’s, and the legs got empty, eating some grapes (fast sugars) would rapidly replenish the energy and the walking ability
- If I eat a carbon/sugar rich meal and then start physical exercise, I have to pee four times in an hour in big volumes, almost like water. An endocrinologist once suggested to me “the cells are too slow to open up”. [a fasting serum insulin test showed a perfectly normal reponse, I don’t have diabetes 2]
- Swank has shown that a sustained low saturated fat diet may stop progression of disability.
- The effect of statins on slowing down disability progression
- And of course, and perhaps most importantly, our decline that is the result of high oxidative stress as a result of peroxinitrite which would seem to work more on membranes and the ER than on mitochondria which are located deeper inside the cell.

I wonder whether anyone reading here has any views that he or she would like to share with me. I feel we are coming ever closer to understanding the root causes of MS disability progression. The answer to this question on locating the mechanism of disability progression is important.
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Re: A new concept and treatment options for MS

Postby Scott1 » Fri May 11, 2018 5:44 pm

Hi Leo,
I think you might be confusing two issues here. ATP is fundamental to how the body works. If you can’t make it on demand (as very little is stored) then you will fatigue. If fatigue is an issue the CoQ10 etc will help but you can ride those long distances without fatigue so that’s not your problem.
What you’re describing are issues with muscles. When you ride your torso is in a “C” shape as opposed to when you stand you’re an “I” shape and when you sit you’re in an “L” shape.
When you shift from “L” to “I” you’re using different muscles than when you’re in a “C” shape.
In the “C” your psoas is shortened, your QL muscles (lower back) are lengthened and your iliacus is shortened.
The fact that you can swing your leg over a bike to get on it suggests your external rotators are fine and that’s a fantastic place to start.

When you stand your psoas is stretched, your QL is shortened and your iliacus is lengthened. In the standing position your glute minimus, glute medius and your periformis are required to do more work to stabilise the pelvis. As the psoas is stretched now it needs to do more of the work to lift the leg compared to when you’re cycling.
In a standing position the psoas is the thing that lifts the leg and it needs help from the iliacus which is now also stretched. If they are taut then it will be hard to make them work. When you’re cycling the position of your body means they’re not under tension.
If you don’t release the psoas and iliacus and, possibly, the ITB down the side of your upper leg, then gradually your glute muscles will tighten whenever you stand and squeeze significant nerves like the sciatic nerve. If the glutes tighten they will pull on the head of the hamstrings and make them tighten and that will feed all the way down the leg.
The tightness you have is collateral damage from MS but it doesn’t have to be permanent.
I got out of it by doing Pilates based stretches three times a week, getting aggressively massaged at least once a week and dry needled to break up the fascia about monthly.
As you know, I also take Dantrium to relax my muscles but would be horrified by it if I didn’t exercise as well. The exercise needs to be eccentric not concentric movement. It’s not about weights or endurance.

The other aspect is glycolysis. When you consume sugars (from food) they go through a pathway to make pyruvate which, in the presence of oxygen, becomes a feedstock for the mitochondria to make ATP. However, if there is insufficient oxygen then the pyruvate becomes lactate. So the bike ride is encouraging an intake of oxygen compared to just going for a walk. You make less lactate in your bike ride because your oxygen uptake is improved.

See http://hyperphysics.phy-astr.gsu.edu/hb ... elres.html

I don't quite follow the temperature argument as a ride that long will elevate the heat in your body. Perhaps there is something else that you haven't highlighted.

Regards,
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Re: A new concept and treatment options for MS

Postby Leonard » Sat May 12, 2018 5:05 am

Hi Scott,

I think we are talking different things.

What I was after is why is there this temperature effect that I sense?
My explanation is simple: about 38% of energy is converted to ATP in the cells, the rest is produced as heat.
I presume this is the way we keep our normal temperature of 37 degrees Celcius or 98.6 degrees Fahrenheit.

It will be one of the very basic mechanisms of the cell to produce more heat if it gets cold.
That is, it opens its gates further to allow raw fuel to flow into the cell and energy to be produced.
This energy production gives heat and about 1/3 is stored in ATP.

When I arrive home from a tour in the cold, I go better for about half anhour.
I presume some surplus ATP is in fact stored that can be used.
With the ATP, the muscles work, and that energy is externalised.

Having said that, I am not sure whether my problem is an insufficient working of my mitochondria (I tend to think not)
or whether there is an insufficient supply of crude energy into the cell and the mitochndria.

Reg,
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Re: A new concept and treatment options for MS

Postby Scott1 » Sat May 12, 2018 6:02 am

Hi Leo,

On the single aspect of temperature, I guess it will involve Nitric Oxide. However, I'm struggling to make sense of the reaction you have when your body is cool because the air is cold compared to when your body is warm because you have exercised. In both cases you feel better.

The only conclusion I can draw is that temperature is not the issue. It might be PH. I can make sense of the cycling increasing oxygen respiration but not the benefit of cold itself.

Regards.
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Re: A new concept and treatment options for MS

Postby Leonard » Sun May 13, 2018 5:04 am

Thank you Scott for your comments and views. Very inspiring as always...

For me, the temperature effect is definitely there and not only after bicycling in the cold. In fact, I saw a bit of that same phenomenon when I could still walk for 2 - 3 miles. When it was really cold outside, my legs would definitely carry me farther.

And it is more than just an issue of not feeling well with higher temperatures, I sense the muscle control itself actually gets better when exposed to a cool/cold environment for a while. I won't have that same effect when I have been bicycling in the heat.

Likewise, I am sure that air pressure is an issue too. At least for me it is. With high air pressure I definitely go better. With a low pressure area as we have now over here - it's raining, my physical abilities get more limited. [It is known MS patients do better after they have been in an oxygen pressure tank.]

So it seems we end up with a long list of possible influences on cellular working including, besides temperature and air pressure, issues such as NO, PH, state of oxygen respiration etc.

In any event, this may all be more of an academic discussion on cellular respiration for idiots like me. Where, in the end, what really counts for us as MS patients is the fact that the cells just don't work good enough and that EBV B cells seem an important contributary factor to the oxidative stress cycle and cellular damage.

Regards,
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Re: A new concept and treatment options for MS

Postby Scott1 » Sun May 13, 2018 6:13 am

Hi Leo,

I know a walk around the park is easier for me in cooler weather than mild weather also. I agree with all the influences you have mentioned as possible factors.

Recently, I have been re-reading Martin Palls book and the common issue for both of us is how do we maintain calcium homeostasis? Presumably, that means limiting the possible sources of inflammation which include EBV. That's why I have been taking valacyclovir for nearly 20 years .

In Palls work on page 8 he has a schematic of the Nomenclature of the NO/ONOO cycle. Step 5 has inflammatory cytokines that promote the production of iNOS. Those cytokines are products of the EBV cycle as well so controlling EBV with an antiviral just makes sense to me. The NO/ONOO cycle will destroy calcium homeostasis and we will feel it in our muscles.

Magnesium will help block the NMDA receptor so I take that also.

Have you tried either of those things?

Regards,
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Re: A new concept and treatment options for MS

Postby Leonard » Sun May 13, 2018 6:58 am

Hi Scott,

Well yes I have tried Magnesium. It was in conjunction with CoQ10, acetyl-L-carnitine, d-ribose etc in an effort to pump up the mitochondria. Did not work for me. I should try it stand alone I guess, but lately I have become a bit wary of all these sort of supplements. Pall tried extensively multi-supplement protocols to get the cycle broken and he did not succeed. I am sure we need to work on the B cells to break the cycle in our case.

But what you are saying in your last posting on the calcium homeostasis is much more interesting. I looked up the regulation and find indeed an effect on nerves and muscle cells! https://courses.washington.edu/conj/bes ... lcium.html

So may be we can add a very important factor to our list of possible influences, not so much at the intra cellular level this time but at the extracellular level. Where, when the concentration of calcium ions in the extra-cellular fluid is too high, voltage-gated ion channels don't open as easily anymore, and there is depressed nervous system function.

And then we may find an explanation here for the better functioning of our muscles in cold weather. It may not necessarily be intracellular but rather related to the calcium homeostasis. Where of course, cells under the stress condition produce cytokines that in turn promotes iNOS and reinforces the cycle as per Pall's book. With an effect on the calcium homeostasis.

A key question for us and for all progressive MS patients would then seem to become: apart from managing EBV B cells and breaking the cycle, is there something else we could do to improve the calcium homeostasis under the stress condition?
[post script: perhaps here fits in the Vitamin D supplementation, see the above link]

Thanks a whole lot for this interaction. I think I may have learned something very important on this rainy afternoon. :smile:

Regards,
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Re: A new concept and treatment options for MS

Postby Scott1 » Sun May 13, 2018 3:38 pm

Hi Leonard,

The magnesium will help block NMDA receptors as well as doing other things. The Dantrium I take blocks the Ryanodine receptor which which the gateway to the calcium stored in the sarcoplasmic reticulum.

If you jump on Youtube and type "excitation coupling" there are a heap of videos about this. They will explain why the muscles get hard to move.

The other aspect is fascia. If your muscles stay tight the fascia in and around them will remodel itself to the shape of the muscle. Sometimes you need to make a small cut by dry needling the exact spot where it is tightest. That needs someone else going over you to find the spot. Sometimes where you feel it pulling is actually not the tightest spot. Then you need to move the muscle.
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Re: A new concept and treatment options for MS

Postby hellokc » Mon May 14, 2018 1:31 pm

Scott1 wrote:Hi Leo,
I think you might be confusing two issues here. ATP is fundamental to how the body works. If you can’t make it on demand (as very little is stored) then you will fatigue. If fatigue is an issue the CoQ10 etc will help but you can ride those long distances without fatigue so that’s not your problem.
What you’re describing are issues with muscles. When you ride your torso is in a “C” shape as opposed to when you stand you’re an “I” shape and when you sit you’re in an “L” shape.
When you shift from “L” to “I” you’re using different muscles than when you’re in a “C” shape.
In the “C” your psoas is shortened, your QL muscles (lower back) are lengthened and your iliacus is shortened.
The fact that you can swing your leg over a bike to get on it suggests your external rotators are fine and that’s a fantastic place to start.

When you stand your psoas is stretched, your QL is shortened and your iliacus is lengthened. In the standing position your glute minimus, glute medius and your periformis are required to do more work to stabilise the pelvis. As the psoas is stretched now it needs to do more of the work to lift the leg compared to when you’re cycling.
In a standing position the psoas is the thing that lifts the leg and it needs help from the iliacus which is now also stretched. If they are taut then it will be hard to make them work. When you’re cycling the position of your body means they’re not under tension.
If you don’t release the psoas and iliacus and, possibly, the ITB down the side of your upper leg, then gradually your glute muscles will tighten whenever you stand and squeeze significant nerves like the sciatic nerve. If the glutes tighten they will pull on the head of the hamstrings and make them tighten and that will feed all the way down the leg.
The tightness you have is collateral damage from MS but it doesn’t have to be permanent.
I got out of it by doing Pilates based stretches three times a week, getting aggressively massaged at least once a week and dry needled to break up the fascia about monthly.
As you know, I also take Dantrium to relax my muscles but would be horrified by it if I didn’t exercise as well. The exercise needs to be eccentric not concentric movement. It’s not about weights or endurance.

The other aspect is glycolysis. When you consume sugars (from food) they go through a pathway to make pyruvate which, in the presence of oxygen, becomes a feedstock for the mitochondria to make ATP. However, if there is insufficient oxygen then the pyruvate becomes lactate. So the bike ride is encouraging an intake of oxygen compared to just going for a walk. You make less lactate in your bike ride because your oxygen uptake is improved.

See http://hyperphysics.phy-astr.gsu.edu/hb ... elres.html

I don't quite follow the temperature argument as a ride that long will elevate the heat in your body. Perhaps there is something else that you haven't highlighted.

Regards,


I've seen research on CoQ10 for antfatigue effects using cycling as a test parameter. It looks like there was not much change at 100mg, but those on 300mg reported less fatigue. Regular CoQ10 in tablet form is really hard for us to absorb, so those who want to give it a try need to pick a form that will actually make an impact on blood levels. There is solid research on water-soluble forms of CoQ10 improving bio-availability.

Here is the research article on the anti-fatigue effects: https://www.ncbi.nlm.nih.gov/pubmed/18272335
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Re: A new concept and treatment options for MS

Postby Leonard » Tue May 15, 2018 8:21 am

hellokc, thanks for your comment. very useful..

Hi Scott,

Something very weird happened to me this morning. I was spraying the box trees in the garden with poison against the box moth. This time I did that with a mouth cap, my wife had bought some new mouth caps. After about half an hour I could not go anymore at all, as if the disability / muscle rigidity had progressed by another 2 - 4 years or so.

This makes me think about the foregoing discussion about temperature effects on MS. I think now that oxygen homeostasis could in fact be a major issue; my old theory of cells to open up a bit further when cold is probably too simplistic. In cold weather, after bicycling or walking, the level of oxygen in the blood will rise. I remember when I was still walking 3 – 4 km’s, towards the end inhaling very deeply and consciously would extend the range.

Conversely, breathing half an hour through a mouth cap (inhaling your own exhausted air) or sleeping in a heated bedroom (I can’t handle, I sense numbness on my hands in the morning) will actually drop the oxygen level in your blood and thus deteriorate ATP production and neuro conduction. In particular for those cells/mitochondria that are already running close to the edge.

Hence, I do not think our mitochondria as such are the problem, but the transport of oxygen and crude energy into the mitochondria is impaired in some way. Of course, we know about the devastating effect of the oxidative stress cycle fueled by EBV B cells on cellular membranes and the ER.

Reg,

Leo
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Re: A new concept and treatment options for MS

Postby Scott1 » Tue May 15, 2018 2:58 pm

Hi Leo,

Yes, I think that will be part of it. Pyruvate needs oxygen to enter the mitochondria to be part of the feedstock for ATP. Otherwise it goes to the muscles as lactate.

Prof Joanne Ingwalls book, ATP and the heart, highlights that ATP isn't stored. It's made on demand from ADP to which a phosphate molecule needs to be attached.

We often have people talking about hypoxia but ischemia causes a faster breakdown of ATP into purines and rebuilding ATP from purines is slower than from ADP. As a consequence a lack of oxygen fatigues you because ATP production is slowing but pyruvate is going to lactate at the same time.

You may have seen an elite athlete suddenly experience a cramp when competing. What's happening there is the demand for oxygen is greater than the supply so the lactic acid builds up in the muscle. It's about demand and supply rather than stored ATP.

https://www.labce.com/spg585251_mechani ... ctate.aspx

Just to make it more complicated, peroxynitrite or superoxide can play havoc with the mitochondria so any cause of inflammation will upset this process.

This article is probably the most complete https://www.nature.com/articles/emm2017194

Regards,
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