A new concept and treatment options for MS

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Re: A new concept and treatment options for MS

Postby Anonymoose » Thu Apr 24, 2014 10:05 am

Hi Leonard,
The acyclovir will only stop lytic viral replication. It won't do anything for latent ebv infected/immortalized B cells or their clonal expansion and it doesn't kill lytic infected cells either. It just stops the spread of lytic infection so your immune system can have a better chance of getting things under control. So, with only two weeks under your belt, you may have done little to address your ebv load and may have inspired a reactivation of the virus (my issues with valtrex prior to rituxan started to clear as soon as I stopped taking it so we've had different difficulties).

Have you read scott1's threads about his whole anti-ebv program? Ten years on valtrex plus avonex and some nutrient/supplement work as well. No quick solutions here.

Off topic...these days, whenever I hear of significant progression after trying a new med, I always think of changes in nutrient levels. Might be something to look into if you're at a loss.

Hope the worsening is only temporary.
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Re: A new concept and treatment options for MS

Postby Kronk » Thu Apr 24, 2014 8:54 pm

So then would you recommend these meds during a relapse?

That would make the most sense to me, as EBV levels spike in tune with MS relapses, that point has been proven with many studies.
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Re: A new concept and treatment options for MS

Postby Leonard » Fri Apr 25, 2014 12:31 am

@Anonymoose: thank you for these very useful comments. I would agree, the experience of one patient after 2 weeks of anti-viral medication is nothing, is very subjective in the first place where such things as nutritional change or even an assumed increase in energy level and activity may be the cause for a backlash... and as you say, hopefully things are only temporary. nothwithstanding, the overall picture that emerges here not in the least through your great comments and insights is fascinating. I think - and hope - that we come ever closer to the root cause of MS. As said, I would agree that the primary angle of attack is to strengthen the immune function where I am sure that mitochondrial energy is a key component...

@Kronk: thank you for sharing your views on the fat metabolism, the March 2013 UK paper on errors in our dietary advice and what constitutes saturated fat, and papers on the possible implications of fat for EBV replication. as regards your last posting, I don't want to recommend anything. I am just reporting as a patient somewhere on the fringes of this global play what I see happen or how I see things connect.

while we may not be able to find the solution, the idea that the medical industry in the wide sense may not necessarily be interested either in finding the solution keeps crossing my mind. what would happen if it were all clear what is MS, what causes the disability progression? lots of investment and prospects in this global bonanza of medicin development for MS would be lost, and a lot more in current worldwide sales. therefore, what I see happening on these fora is just great, if it were not only to counter the perverse drivers in the medical system and help drive the system towards finding a real solution for our problem. I say this without necessarily making any accusations or allusions as inadvertently current practice has grown it did and has brought us some great benefits as well.
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Re: A new concept and treatment options for MS

Postby Scott1 » Fri Apr 25, 2014 4:08 am

Hi Leonard,

I'm afraid the acyclovir is a long term treatment. I took 500g twice a day, every day, for a decade. The reason is the active life of single tablet is around 15 hours and you need to work on total cover. All it does is put a stop in the codan of the RNA of the EBV so when your B cells divide you can make an uninfected B cell instead of an EBV immortalized cell. The reason you want to limit the EBV proliferation is an EBV infected B cell gives off two molecules of oxygen (superoxide). Whilst we need superoxide to control pathogens we don't need an overproduction of it. I think the reason why some people don't develop MS and we do tell us that EBV is not the whole story. The other part is the so called predisposition. My thinking is this condition is due to our kidney/renal system producing asymmetric dimethylarginine (ADMA) whereas healthy people produce the symmetrical form. ADMA is an endogenous inhibitor of all forms of Nitric Oxide synthase. The capacity to vasodilate is dependent on how much endothelial Nitric Oxide synthase we have to make Nitric Oxide. In people with MS there is a very high level of inducible Nitric Oxide synthase (iNOS) rather than endothelial (eNOS). iNOS is made by the body in response to injury. The ADMA depletes eNOS and iNOS arises as a natural response. Why is this important? When superoxide and Nitric Oxide come into close proximity they spontaneously make Peroxynitrite which is, by far, the worst free radical. Peroxynitrite mucks up many functions as well as nitrating the lipids. The most important factor is the disabling of Glyceraldehyde-3-phosphate. If this doesn't function, ADP can't become ATP. We need ATP to drive the sodium-potassium pump in each cell. If that doesn't function we can't make energy. EBV contributes superoxide toward the production of peroxynitrite ,but if you have a renal malfunction that is producing ADMA leading to too much iNOS ,you are likely become compromised as an MS person when the peroxynitrite runs rampant.
The lack of energy is due to the collapse of the function of the pump as is the loss of mitochondrial vitality. The inability to vasodilate is due to the lack of Arginine. The lack of Arginine is due to a renal malfunction.
The renal problem may be as simple as late maturity of function or we may have a mutant form of Megalin. I often read posts about Vitamins D, B12 and A. They are all transported through the renal proximal tube by Megalin where some metabolizing occurs. Vitamin A is sorely lacking in the general conversation but it is very involved in gut health.
I prefer to break the problem into two separate issues 1) a renal problem and 2) a viral infection that promotes the proliferation of Peroxynitrite that poisons the system. I posted a unfortunately long winded explanation called "Beyond Avonex and Valtrex" which goes into more detail with links to research.

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Re: A new concept and treatment options for MS

Postby Anonymoose » Fri Apr 25, 2014 5:12 am

Scott1,
Do you have a link to a paper that says acyclovir affects B cell replication or is that explanation based on your more in depth understanding of what is published about lytic infected cells being applied to B cells?

I think Leonard, unlike me, will be able to grasp the nitty gritty of your explanations. :P
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Re: A new concept and treatment options for MS

Postby Leonard » Fri Apr 25, 2014 6:42 am

Anonymoose, I think you are too modest. I am at best a semi-literate trying to connect things not limited or hindered by old knowledge or concepts. Where I don't necessarily need to understand it all, the world is full of professionals who could be asked...

Scott, wow... the high load of EBV is something that I see in the family: grandfather with nasal carcinoma, uncle and other further relative with coronary artery aneurism, father had Meniere's attacks (and diabetes 2 from his mother's side).

but my brother has a mitochondrial energy failure. this is highly genetic so probably I have the same or it may be that he has MS. with this knowledge, our diagnoses were re-examined and both were confirmed! I have MS, he does not have MS. interestingly, apart from the disability, I migrate more and more towards an energy failure...

your posting above and the detailed elaboration on regimens-f22/topic24019.html relate it all together. a million thanks for that!! and thank you Anonymoose for making the connection. leave it with me for while, I have to ponder on this now...
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Re: A new concept and treatment options for MS

Postby Scott1 » Fri Apr 25, 2014 10:35 pm

Hi Leonard,

It may not be genetic. There can also be clusters of infection in populations. It would be interesting to compare your brothers readings with your own. In particular, compare your fasting amino acid studies and look closely at the nonessential amino acids. If he lacks energy but you have MS, you may both have problems with Peroxynitrite but you may also have lower Arginine. You are in a unique position to compare and contrast.
Also compare your uric acid levels plus magnesium and zinc. If possible test for chlamydias, rickettsia, mycoplasmas and lyme. I have always felt it was important to know as much as you can about yourself and not guess.

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Re: A new concept and treatment options for MS

Postby Scott1 » Fri Apr 25, 2014 11:16 pm

Hi Anonymoose,

It's probably not right to say Acyclovir affects B cell replication. EBV is a herpes family virus which means it borrows the machinery of a host cell and when the host divides the EBV replicates along with it. The Acyclovir interrupts the RNA of the EBV although I usually see people say DNA!
There are many articles under google talking about this. There are also many articles that say it is least effective against EBV and best against genital herpes. The problem with all the studies is they are nowhere near long enough. There is a divided opinion whether it can swing between a latent and lytic cycle. In a perfect world you would induce the lytic cycle so you could hit it. Cells divide. When they do, there is a very brief window where Acyclovir might work in a latent cycle. All I know is you need to keep attacking EBV constantly for a very long time.
Leonards interest in cell machinery is well placed. You need properly respiring cells which Coenzyeme Q10 can help with and you need to overcome ADMA which L-Arginine can assist. Taking L-Arginine can be tricky because Arginine uses the same pathway as Lysine which suppresses viruses but it will always outcompete it so if you have herpes viruses they can get worse if Lysine is compromised. If you take L-Arginine you need to take Valacyclovir as well. After many years you can really taper back on Acyclovir as I have now done.
So I don't think Acyclovir affects the B cell as such but it does attack EBV in the Lytic phase and, I think, sometimes in the latent phase. (and only if the use is constant)

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Re: A new concept and treatment options for MS

Postby Anonymoose » Sat Apr 26, 2014 5:27 am

Thanks scott1. That makes sense.

I think they can reactivate ebv with a combination of rituxan and dexamethasone...and then hit it with gancyclovir. http://www.ncbi.nlm.nih.gov/pmc/article ... rt=classic

It seems they can do it with methotrexate as well. http://www.ncbi.nlm.nih.gov/m/pubmed/15547182/
Interesting to think of that in the context of ms mtx experiences.
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Re: A new concept and treatment options for MS

Postby Leonard » Thu May 08, 2014 6:51 am

I would like to recap based on our learnings.

MS has many aetiologies. The picture is not black and white. MS is multifacetted with considerable variation among patients (the NO / OHNOO cycle interacts with distinct tissues to produce varying patterns of symptoms and signs) http://www.allergyresearchgroup.com/Exp ... sp-35.html . Variation may also be seen in pattern/degree of ccsvi, immune system handling of EBV and gradations of ADMA generation by the kidney/renal system.

The pattern of thinking by most medical experts is too linear and singular rather than lateral and heterogeneous. http://en.wikipedia.org/wiki/Paul_Feyerabend Everybody wants a magic bullet but for MS that does not work. Doctors should have a veterinarian look at things. As regards the therapy, it is the sum of all the things you do that makes a difference and it will take time to be effective.

Ccsvi links the drainage of the dural nerve system, the dural sinuses, and meningeal inflammation. It provides a possible explanation for meningeal inflammation and subpial cortical lesions exclusively observed in MS patients. Environmental factors such as exposure to heavy metals (even of previous generations) and related genetic factors of veins may play their role here (Boston document, Texas study). Still apart from the whole discussion on amalgam, on average PwMS seem to have a worse than average dental health which may find an explanation here as well.

Quite a bit of research implicates EBV is central in the development of MS. One ingenious study looked at blood samples collected from 3 million US military personnel at their time of enlistment, and their subsequent development of MS. Those who had high anti-bodies to EBV at the time of enlistment, that is those who had a chronic viral infection, even up to 5 years before the onset of MS, had a 20-30 times higher risk of getting the disease than those with low antibody levels.

Researchers in Houston, Texas have speculated that some of the effects of interferons in MS might be due to their anti-viral properties (in fact as much as their effects on the immune system).

In susceptible people, or it is probably better to say people that have a certain predisposition, that is those with the 'right' genetic make-up, and the right sort of environmental triggers e.g. lack of sunshine, fish oil, infection with EBV may trigger the onset of the disease later in life. The kidney/renal system producing ADMA is a highly suspect factor predisposing people.

The mechanisms causing disability progression and the lesions are only loosely coupled: the EBV envelop protein vs EBV infected B cells inducing peroxynitrite nitrating the lipids. Studies also confirm that disability progression and lesions are not 1:1 correlated.

Autoimmunity is explained by chronic high concentration EBV immune complexes cross-coupling with epitodes of EBV remnants in transgenetic cells. About 8% of cells in our body is transgenetic, after about 120 million years of evolution.

In MS disability progression, because the effects of poor health of dendrocytes and a lack of energy come together, they appear one and the same process. But I think underlying are in fact two different processes: the EBV envelop protein causing the replenishment of new dendrocytes to stall vs peroxynitrite disabling glyceraldehyde-3-phosphate and ADP/ATP conversion causing mitochondrial energy / the pump to fail. In casu, I see my own disability progress but at the same time to migrate more and more towards an energy failure. And although there is a common causal factor, they are different processes. An explanation for the big temperature effects seen in PwMS, who are inevitably running more on the borderline, should probably be sought in this corner as well.

The count of mitochondria in our cells is important too. If you have more mitochondria and active membranes, you are less susceptible for developing MS, I think because it just takes longer for the system to get jammed. The number is proprotionate to the vitamin D level in the circulation of the mother from say the 2nd to the 6th month of pregnancy and of the adolecent during the main phase of cellular growth. Where the vitamin D level is influenced by cholesterol and sunlight. That is why I think that our modern low fat diet that may be good for mid-aged and elderly people and helps protect against heart disease etc is not necessarily good for young mothers and children.

Women are reported to produce more nitric oxide than men, possibly explaining the gender bias seen in MS. A similar gender bias is seen in autoimmune diseases characterized by excessive peroxynitrite (i.e. CFS, lupus, rheumatoid arthritis).

Nitric oxide is known to stimulate the nociceptors that initiate the perception of pain. I am sure nitric oxide is sky high in MS patients explaining the pain in limbs.

The cycle seems self-reinforcing: EBV infection gives ever weaker immune protection which aggravates EBV infection. Strengthening the immune function would seem central to any therapy.

I find the theory Beyond Avonex and Valtrex by Scott on regimens-f22/topic24019.html beautiful thinking and highly plausible as it connects all the things that I see in my own family. It is fully complementary to and reinforces the overall concept below. I cannot be naïve anymore and simply accept that this is all coincidence. It is just too good to be dismissed. I encourage you all to read Scott's theory.

Perverse drivers in the medical system and fear of stepping outside accepted practice hamper the exploration of new ideas. Fortunately, the collective cognition on the Internet leads to new concepts beyond old thinking in traditional quarters. Together with prof. Peter Finke http://www.perlentaucher.de/buch/peter- ... ience.html , we can only hope that this citizen science that now thrives on social fora may find "ways out of the impasse of reality".




A new concept and treatment options for MS II

update 29 April 2014

1. Causes

MS has multiple aetiologies

CCSVI (probably in part a birth defect) positively correlates with MS (1)
and is a factor that contributes to an early compromise of the BBB

Venous reflux/hypoperfusion combined with weakening immune system (see also point 3. below):
- promotes local inflammatory processes (2)
- reactivates HERV-W (Herpes, VZV, EBV) in cerebral meninges (as in cartilage of joint as in RA)

With broken BBB:
- Phase 1: Herpes simplex/VZV or Cpn blocks receptors --> inflammation --> RR (time constant days to weeks)
The virus may be latent for many years and reactivate only sporadically after so many years. In the beginning, for me reactiviation repeated only every 8 or 9 years, always in the Spring when the immune system is low.

- Phase 2: EBV envelop protein inhibits OPC differentiation; EBV --> injury of cell types i.e. dendrocytes --> progressive (time constant months to years)
EBV promotes the proliferation of Peroxynitrite that is by far the worst free radical, poisoning the system in several ways e.g. causing mitochondrial failure, nitrating fat tissue giving rise to inflammation (lesions in combination with fats?) etc... see also Part III below and regimens-f22/topic24019.html
The problem of inhibition of OPC differentiation -which is the real problem in MS, studies have clearly shown this- may well be a bit more than the envelop protein e.g. be intermingled in some way with fats, immune complexes, peroxinitrite and ADP/ATP. But for now and for the overall concept that does not seem so important.

Graph of age of onset of MS has double peak --> different mechanisms underlie Ph1 and Ph2;
Ph2 is age dependent, not on RR severity

(1) CCSVI = Venous insufficiency of Internal Jugular Veins in the neck, draining the Cerebro Spinal
(2) Local inflammatory processes combined with inflammation induced high levels of nitric oxide cause narrowing of cerebral veins and autonomous nervous system dysfunction


2. Auto-immunity

Uncontrolled EBV infection reactivates in ectopic B-cell follicles in cerebral meninges --> chronically active EBV

Infection of autoreactive B-cells

Elevated EBV anti-bodies (already years before the first MS symptoms begin)

Cross-coupling of immune complexes with epitodes of remnant virus parts (in transgenic cells) explains the action against the "self"
- is secondary process (The MSRV-Env protein has also pro-inflammatory properties which translate into the production of different cytokines)
- EBV is chronic; immune complexes not effective against EBV; fat metabolism involved in EBV replication

Note: Chronically active EBV presents
- coronary artery aneurysm (uncle, farther's cousin)
- nasopharyngeal carcinoma (grand farther)
- Meniere (farther)
- mitochondrial energy failure? (brother)
- MS (me, with very high readings of Herpes simplex and EBV immune)


3. Weakening immune system

Immune system gets ever weaker <-- mitochondria get weaker
(poor quality of food e.g. high carb, lack of phytonutrients, stress, lack of sunshine/vit D/fat, environment, vaccinations, HERV/EBV)

Immune system is producing useless /non-working antibodies against EBV

B-lymphocytes unbridled multiplication

Hypo gamma globulin (shortage IgG3)

Immune system forgets about the rest

Chronic infection, for example:
- leaky gut --> Ɛ toxin
- mycoplasma
- Cpn infection (in RR)
- even toenails fungus which has crossed here several times

Diagnosis:
- CFS
- Rheuma Arthritis
- Lupus
- MS

- Autonomic dysfunction smooth muscle layer
(my own titre was very high, eating own muscles, is this the regulatory system attempting to relax smooth muscle of cerebral veins?)


4. Treatment options

Main options:

Lots and lots of antioxidants and flavonoids (incl. supplements such as CoQ10)

Neuro Muscular Electric Stimulation (NMES) see pg 14-17 of http://www.ms-uk.org/files/npwm_2009_0053.pdf

Hormonal and amino acid support as L-Arginine

Anti-viral as Valacyclovir

Gamma globulin IgG3

------

Other issues for consideration:

Vitamin D gut/immune system support
Vit A to help restore gut function

Nutritional support / diet
Detoxification for strong mitochondria; strenghten B-cells, epithelium, meninges
Food rich in anti oxidants incl. polyphenols, acathpocyanids (bue black), lutein (red) and caretnoids (yellow orange)
CoQ10 (e.g. MitoQ effective form)
High quality food phyto nutritients
Oxygen in bed room (when at rest in supine position)
Low fat / Swank / FAS = EBV inhibit (Fatty Acid Synthase inhibitor, no palmitoylated proteins, no palmitic acid)
Magnesium Zinc

Promote brain perfusion
stimulate Chinese 'axis'; electrically stimulate vagus nerve (as in RA)
Prozac derivative
Bosenthal

Hormonal support
Arginine
DHEA
Testosterone
HPA axis
Adrenal – cortisol - gut

Anti viral (e.g. Zovirax/acyclovir or Valacyclovar or anti-HIV/HAART)?

Anti biotics – Cpn RR

Gamma globulin IgG3 to help normalise the immune system



A new concept and treatment options for MS III

Scott1 wrote:
I'm afraid the acyclovir is a long term treatment. I took 500g twice a day, every day, for a decade. The reason is the active life of single tablet is around 15 hours and you need to work on total cover. All it does is put a stop in the codan of the RNA of the EBV so when your B cells divide you can make an uninfected B cell instead of an EBV immortalized cell. The reason you want to limit the EBV proliferation is an EBV infected B cell gives off two molecules of oxygen (superoxide). Whilst we need superoxide to control pathogens we don't need an overproduction of it.

I think the reason why some people don't develop MS and we do tell us that EBV is not the whole story. The other part is the so called predisposition. My thinking is this condition is due to our kidney/renal system producing asymmetric dimethylarginine (ADMA) whereas healthy people produce the symmetrical form. ADMA is an endogenous inhibitor of all forms of Nitric Oxide synthase. The capacity to vasodilate is dependent on how much endothelial Nitric Oxide synthase we have to make Nitric Oxide. In people with MS there is a very high level of inducible Nitric Oxide synthase (iNOS) rather than endothelial (eNOS).

iNOS is made by the body in response to injury. The ADMA depletes eNOS and iNOS arises as a natural response. Why is this important? When superoxide and Nitric Oxide come into close proximity they spontaneously make Peroxynitrite which is, by far, the worst free radical. Peroxynitrite mucks up many functions as well as nitrating the lipids. The most important factor is the disabling of Glyceraldehyde-3-phosphate. If this doesn't function, ADP can't become ATP. We need ATP to drive the sodium-potassium pump in each cell. If that doesn't function we can't make energy.

EBV contributes superoxide toward the production of peroxynitrite, but if you have a renal malfunction that is producing ADMA leading to too much iNOS ,you are likely become compromised as an MS person when the peroxynitrite runs rampant.
The lack of energy is due to the collapse of the function of the pump as is the loss of mitochondrial vitality. The inability to vasodilate is due to the lack of Arginine. The lack of Arginine is due to a renal malfunction.

The renal problem may be as simple as late maturity of function or we may have a mutant form of Megalin. I often read posts about Vitamins D, B12 and A. They are all transported through the renal proximal tube by Megalin where some metabolizing occurs. Vitamin A is sorely lacking in the general conversation but it is very involved in gut health.

I prefer to break the problem into two separate issues 1) a renal problem and 2) a viral infection that promotes the proliferation of Peroxynitrite that poisons the system. I posted a unfortunately long winded explanation called "Beyond Avonex and Valtrex" which goes into more detail with links to research.



see also regimens-f22/topic24019.html
Last edited by Leonard on Sat Jun 21, 2014 2:20 am, edited 35 times in total.
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Re: A new concept and treatment options for MS

Postby Kronk » Fri May 09, 2014 8:48 am

Huge kudos to you trying this out Scott.

Scott1 wrote:I'm afraid the acyclovir is a long term treatment. I took 500g twice a day, every day, for a decade.


http://jvi.asm.org/content/83/22/11857.full

"...we estimate that it would take 6 years of 500 mg of valacyclovir once each day to eradicate 99% of EBV from the B-cell compartment and 11.3 years to eliminate the virus completely from the body if persons were not reinfected during this time. Reinfection with the virus is likely, however, since multiple strains of EBV are detected in many individuals, suggesting that multiple episodes of infection occur..."

Long term treatment indeed... The risk of reinfection is so high I would question the benefits of going this route though. Wouldn't be able to kiss your partner or drink from the same cup.
Another interesting study giving some food for thought was on the benefits of Acyclovir vs. Valacyclovir.

http://www.ncbi.nlm.nih.gov/pubmed/7492102

"... The limited oral bioavailability of acyclovir necessitates frequent dosing. Valaciclovir, the l-valyl ester of acyclovir, is rapidly and almost completely converted to acyclovir in vivo and gives three- to fivefold increases in acyclovir bioavailability..."
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Re: A new concept and treatment options for MS

Postby Scott1 » Fri May 09, 2014 3:12 pm

I should clarify, the Avonex (and later generics) I took were Valacyclovir. That's how I got the Acyclovir.
That's an interesting quote about clearing EBV. I'm not sure we should treat it as anything more than a guess. It's not the only thing either, just a key part of a protocol to lower superoxide overproduction. There's lots of other things to address as well.

Also, I wouldn't worry about the issue of avoiding kissing or sharing utensils. EBV is so common throughout the whole population that it renders that sort of behavior redundant. It is how we manage the EBV that counts not the infection itself. Eliminating the infection is aspirational but the focus should be on our health to help us keep the adverse effects at bay. You should say to those you love "kiss me as much as you like, I won't give you MS" and go for it! It is the broader picture of health that matters most. EBV is a part not the whole thing.

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Re: A new concept and treatment options for MS

Postby Leonard » Tue May 27, 2014 8:12 am

This page completes the circle: http://en.wikipedia.org/wiki/Flavonoid
It connects iNOS (see above posting from Scott1) with flavonoids/antioxidants in our food.
quote:
Preliminary studies indicate that flavonoids may affect anti-inflammatory mechanisms via their ability to inhibit reactive oxygen or nitrogen compounds. Flavonoids have also been proposed to inhibit the pro-inflammatory activity of enzymes involved in free radical production, such as cyclooxygenase, lipoxygenase or inducible nitric oxide synthase (iNOS), and to modify intracellular signaling pathways in immune cells.

Among the most intensively studied of general human disorders possibly affected by dietary flavonoids, preliminary cardiovascular disease research has revealed the following mechanisms under investigation in patients or normal subjects:

inhibit coagulation, thrombus formation or platelet aggregation
reduce risk of atherosclerosis
reduce arterial blood pressure and risk of hypertension
reduce oxidative stress and related signaling pathways in blood vessel cells
modify vascular inflammatory mechanisms
improve endothelial and capillary function
modify blood lipid levels
regulate carbohydrate and glucose metabolism
modify mechanisms of aging.


The Wahls diet is very rich in flavonoids. And we know how well Terry Wahls has done.
But on the same wikipedia page, we find that the FDA and the European Food Safety Authority say that nothing has been proven about the role of flavonoids. Is not it time to turn around the burden of proof, apply the precautionary safety principle and recommend an abundance of vegetables, as men has eaten for millions of years? And from that starting point to advice, if and only if it is blatantly clear that flavonoids do not contribute to the health of our vessel walls, make these bold statements about the negligable systemic activity of flavonoids on our vessels walls? I think time will show they were wrong and will have to revise their advice.
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Re: A new concept and treatment options for MS

Postby Leonard » Wed Jun 04, 2014 6:17 am

with reference to the other thread on "No easy answers for managing secondary progressive MS" on general-discussion-f1/topic24869.html

yes, yes, old therapies .... were badly flawed....
you can smell there is change in the air.
neurologists become more critical to DMTs.

it will be interesting to see what this ACTRIMS/ECTRIMS conference will deliver: http://www.msboston2014.org/index.php/s ... ic-program
re: the last points
12.Society and MS: roles of the expert patient, social media, and health policy
8.Critically examine how the expert patient, news media, social media, and health policy affect the relationships between patients with MS, health care providers, and researchers.

I do not know how the agenda came together.
but I do see a much stronger reference to expert patients than ever before, the role of social media etc.
I think the professional world starts to take more serious this 'Citizen Science'.

it gets particularly interesting when health policy gets mentioned.
I did not know there was any explicit or serious health policy with regard to the role of expert patients or social media, on either side of the ocean.
at least I have never felt it like that.
so what is this about? is this ACTRIMS/ECTRIMS being advocate and judge at the same time, to make new policies long overdue? :sad:
new policies to make the medical establishment - to speak with the words of Nigel Crisp - more "the servant and not the master of humanity"...

in any event, I am quite happy with this joint US/Europe event.
in the US, when things show to be wrong, you are much better than we are in Europe in making a fast turn-around.
I hope this meeting will become a landmark event and indeed profoundly change the paradigm.
and that the US will take Europe along in its slipstream.
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Re: A new concept and treatment options for MS

Postby Leonard » Mon Jun 09, 2014 9:24 am

oh my God, it is all the same.... this theory from prof. Martin Pall on CFS fully overlaps with the above theory on MS.

http://chronicfatigue.about.com/od/trea ... otocol.htm

I think they reinforce each other and make the line of thought even more credible, and plausible.
this line of thought must become the main issue at the next ACTRIMS/ECTRIMS conference (see above posting).
some program changes will be necessary.
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