Thanks for your excellent research and suggestions. We have read and re-read your posts. We are not in anyway trying to pick holes but as none experts would like to clarify one or two aspects before adding them to the present regime. Carrot juice and co-enzyme Q 10 make perfect sense and we will add these straight away.
NO is required by the body. So in your posts is this aspect of the problem that the bias towards iNOS leads to the overproduction of NO which combines with the over abundance of super-oxide (provided by EBV) to produce the peroxinitrite. i.e. we must have NO but is too much not good.
Later in your posts you suggest taking L-Argenine which facilitates vasodilation through the production of NO but will out compete lysine an essential amino acid.. This raises two questions. First does this not lead to even more NO i.e. too much NO. Secondly how long does the L-arginine out compete the essential lysine?
Finally if Valtrex blocks EBV and attacks other viruses why do you say this might that be a problem wouldn't fighting all visuses be beneficial.
What are your thoughts on Green tea extract as an alternative or complimentary to valtrex.
Thank you for reading my post. When I looked at it again I gave myself a fail mark because it's about as clear as mud.
The NO concept is the hardest to grasp. Remember it's highly unstable and constantly breaking down and reforming and that's what we want it to do. The three different isoforms of nitric oxide synthase is really where our attention should focus, not NO itself. The problem is the reaction rate of the different forms. On this page here - https://sites.google.com/a/udel.edu/nit ... /mechanism there is a chart called figure 9. You can see that iNOS has a lower rate of ferric heme reduction and disassociation than eNOS or nNOS but a significantly higher rate of oxidation. As it reduces more slowly that creates the problem. In simple terms, NO made from iNOS hangs around longer providing more opportunity to combine with superoxide to make peroxynitrite. iNOS is a healthy response to injury. If eNOS is absent then the body's response is to make iNOS. The ADMA problem inhibits all isoforms of NOS and I think that the response to that ultimately leads to more iNOS. Don't even think about NO. Only worry about iNOS.
L-Arginine and Lysine is an interesting question and I don't know the answer. When I have used both I take the L-Arginine in the mid evening and the Lysine in the morning. It will really depend on the viral load of EBV that you are carrying. I had used Valacyclovir for a long time before I understood the importance of L-Arginine so my viral load was down by then. I suspect that if you can manage Valacyclovir then taking that rather than Lysine would be the best option.
On the question of fighting multiple infections at the same time; that may be just too hard. I think Leonard is finding that out right now if you look at his post. Ideally, yes, do fight them all but it could be very difficult and you will give up. The best approach is to be tested for as many things as possible and clear the obvious ones out of the way. Some are susceptible to tetracycline or rulide etc etc... Some treatments are long term and some are quick. I think the reason Avonex is so hard to take is it alerts the body to all the underlying issues and induces a response. Valacyclovir may have a similar response. We are peeling Onions not Apples so go slowly and be as well informed as you can.
On Green Tea; I haven't found anything adverse about it. It just seems to be a good guy but it won't be a cure. It seems to be an inhibitor of bad pathways. If you take Green Tea extract expect to lose a bit of fat.
Thanks for the very thorough reply - very helpful.
I believe you started your regime successfully with just Avonex and Valtrex, before adding the other components, and you thought that it was the combination of these two that was essential. In my case I dont take any of the DMDs, never have done since first symptom in 2003, and am reluctant to start on interferons now.
So the question is: do you still think the combination of both Avonex and Valtrex is critical? or could I feasibly follow your regime with the exclusion of Avonex?
No it isn't a requirement. It is the sum of all the things we do that makes a difference but all things are not always right for all people. Avonex is a signaling agent to activate an immune response. I needed it but it didn't make me better. It will depend how your overall health is. I feel that a lot of DMDs are prescribed on a rote basis with little thought given. If you are on any medications you should check for contraindications (eg blood thinners and Q10, Valtrex and antipurines). If you are on a blockbuster drug and it is tolerable then keep going but augment with the things I suggested.
The objective is twofold;1) lower the EBV by stopping it replicating and 2) heal the effects of renal/kidney malfunction as described in my note.
This will take time. Don't forget I took 1 gram a day of valacyclovir every day for 10 years.
If you give it a go, do let me know how you get on. Please do check for every bug possible before you start the Valtrex. Failing to clear them seems to be the obvious stumbling block.
I did well - now age 71 - retired and I am now a "triple dipper".
My second approach was to block the actual final damage of MS by lowering/blocking the nasty MMP-9s plus I take lots of flavonoids that protect the BBB(Blood Brain Barrier).
See my posting on "How to maximize Interferon beta".
jackD aka Braindead Jack n dalton
Thank you for the thread.
I can see a lot of things in there that made me sit up straight away. A number of them I have been adding recently such as Green Tea extract, Resvesterol, Curcumin etc and I have been having a look at limiting hyaluronidase as a topic of interest. No firm ideas formed yet.
The link to the nature magazine article is very helpful. Thanks again.
As it's 6am here and I have to go to work I will have to read this tonight.
I'll have some fun with this.
Everything I have discussed so far leaves many questions still unanswered; the variation in reactions, the variance in responses to treatment, demyelination, cramping, bowel disorders as well as the graduation of the degree of severity are not explained by the description to date. The arguments presented are not invalidated by what is not adequately explained as the avenue is still open that more than one pathway needs to be explained. The trick will then be to link them as elements in a chain of symptoms.
Experimentation is a way of life for me and inevitably I will make mistakes. As an example some time back I added analine to my regime. For three days I thought I was a genius as my flexibility improved- then the yawning started and it took me some time to realise that analine promotes EBV so I was overproducing superoxide and consequently Peroxynitrite. The analine promoted fatigue for me.
Recently I have made another giant leap in the wrong direction but the positive side of the experiment is I have learned something new. The cost has been a painful and confronting initiation into the world of the MS hug. I could imagine this experience could be terrifying to the uninitiated as it is genuinely painful and the pressure it places on the spine leads to referred sensations in the arms, fingers and soles of the feet of heightened sensitivity, numbness and cramping in addition to extraordinary tightness around the thoracic region and intestines.
Before I look at the pathway I triggered I would like to share my thought on the MS hug and what I did about it. Let us assume it is an immediate problem to be dealt with rather than a concept.
My experience is the hug hits quickly and hard. Fatigue, by comparison, creeps up on you. The hug is typically described as a cramping of the intercostal muscles leading to a sensation of a tight band constricting the ribcage. In my case I felt as if a bolt had been shoved into my back and out through the solar plexus right under the middle of the rib cage. Then nuts are tightened again and again without relief at each end. It is very intimidating. The intestines feel bloated and cramp and the whole torso feels like a big painful slab as any suppleness is replaced with rigidity.
The difference for me compared to most people is I think I know how I caused it so I am able break the reaction down into component parts.
How I physically treated the MS hug.
The first thing is to recognise is the hug has a proper name. It is a spasm. Avoid calling it MS as that term is too generic. The speed of onset in my case suggests my cramp was a pro inflammatory response to a trigger. Others may have a different experience. As it was so rapid and vicious I felt the appropriate response was to dampen the immune response which I did by using Prednisolone and then turned my attention to removing the trigger using a broad spectrum antibiotic against gram positive bacteria. The reason for this will become clearer further on.
What was cramping? Obviously the intercostal muscles were uncontrollably tightening. A more important signal may have been some weakness in my legs which manifested as tight hamstrings and some weakness in the strength of the hip flexors when I lifted my leg. The classic mistake is to blame the legs but they are the innocent party. Go back into the torso and go under the intestine and look at the psoas muscle. If we were butchers we would call this muscle the Tenderloin. A description of the muscle can be found here - http://en.wikipedia.org/wiki/Psoas_major_muscle .
The psoas originates attached to the spine and passes down through the lumbar and on through the hip region in the area you would call your lap. The ability to lift your upper leg to a right angle to your torso is determined by the ability of the psoas to contract to lift the leg. My interpretation is I had a major cramp in this muscle and a lot of pain and altered sensation in my fingers and the soles of my feet was referred from the spine as a result of the cramp. The psoas and the intercostal muscles are independent of each other but may directly or indirectly share fascia which helped the cramp transfer sensations.
The key thing to do is treat the psoas first then the intercostal muscles. You will need a good trainer preferably with a Yoga or Pilates background. A good Osteo would work and some physios may be ok although I would prefer the other groups for the best stretch patterns.
I am a Pilates nut so the studio was the first place I went. My initial stretch was across a high barrel like this - https://www.pilates.com/img/store/arcs- ... ser-01.jpg
This will be too advanced for many but I want to illustrate what I did. This position exaggerates the stretch on the psoas but alone it was not enough. I then had my Pilates instructor vigorously rub a tennis ball over the muscle groups on my stomach and solar plexus whist I lay there. The action was aimed at smoothing out the cramp and was quite successful. Additionally I practiced leg slides whist lying on the floor like this -
I asked my Pilates instructor to apply pressure to my ribcage whilst I lay on a small noodle which was along my spine lengthways. This meant the ribcage was presented as flared up and out and the pressure applied evenly to both sets of ribs flattened the ribcage laterally which expanded the intercostals. This was of great relief but the spasm would return shortly afterward.
On day 6 from the start of the attack I saw a good myotherapist. It was a very painful session of massage focussed on the back. An interesting set of observations flowed from the meeting. Some muscles, in particular, were extremely tight and the feel of my back to him was “a mess” with obvious indications of inflammation in the pattern of the muscles. He identified problems with the iliocoslalsis thoracis (see- http://www.anatomyexpert.com/structure_detail/5229/ ) and the splenus capitus (see - ) Additionally and importantly he described the condition I presented as almost T4 syndrome (see - http://www.physio-pedia.com/T4_Syndrome and http://www.shoulderdoc.co.uk/article.as ... ection=906 ) Both descriptors accurately describe how I felt. By now I was accustomed to the tightness in the torso but the pain in my fingertips was acute. The sensation is like diving your hands into bags of ice then running the sensitive parts under water creating a stinging pain. It just doesn’t go away. My reading suggests it is a referral from the spine.
I still have no relief from the cramp on day 8 but it is no worse. A long way to go. All my other disciplines are working. There is no fatigue although I am weary of the cramp. My mental facilties are fine. If I had fatigue and was confronted by this I would be extremely upset. Such a combination would be very confronting and difficult to convey to anyone else.
The description of the origin of MS earlier in this post looks at the role of ADMA and iNOS flowing from a renal/kidney malfunction. As part of this malfunction the role of megalin is compromised leading to inadequate processing of the precursors of Vitamin A, B12 and D. In particular we should look again at Vitamin A and the retinoids. As described earlier, a failure due to Vitamin A insufficiency will compromise the lining of the gut leaving it susceptible to the introduction of pathogens. In the event bacteria with thick cell walls are introduced to our system by this mechanism there is a pathway to create an inflammatory response that can serve as a trigger for an immune system mediated response.
A big mistake with benefits for learning
In my reading I had been looking at lesions in myelin. There were some indications of an accumulation of Hyaluronic acid in damaged myelin (see - http://www.ohsu.edu/xd/about/news_event ... repair.cfm ) The blame was attributed not the Hyaluronic acid itself but to the enzyme that broke it down, hyaluronidase. Hyaluronic acid can hold many times its weight in water. Given the anistrophic nature of MS myelin it seemed to be a plausable target to assess. I stupidly decided that I would concentrate on adding to the supply of precursors of hyaluronic acid rather than reducing the impact of the enzyme. The most available precursor was n-acetyl-glucosamine, an advanced form of glucosamine. Research on various websites seemed to support it may be useful with no tangible negative events. This was a bad mistake on my part. I did not look closely at other involvements.
The leaky gut lets some bacteria in.
Of specific importance is the type of bacteria. The thickest cell walls belong to the bacteria that can be stained crystal violet and retain the stain. They are known as gram positive bacteria. It has been noted for some time that gram positive bacteria play a role in neurodegeneration (see - http://www.ncbi.nlm.nih.gov/pubmed/17956303 ) “Gram-positive bacterial infections of the central nervous system, such as meningitis, induce an extensive inflammatory response, which in turn may damage neurons. LTA (lipoteichoic acid) is a component of the Gram-positive bacterial cell wall that induces glial inflammatory activation in vitro and in vivo. It does so by binding to Toll-like receptor-2 on microglia and astrocytes, rapidly activating ERK1/2 (extracellular-signal-regulated kinase 1/2) and p38 MAPKs (mitogen-activated protein kinases), causing NF-kappaB (nuclear factor kappaB) activation and leading to the production of pro-inflammatory cytokines and expression of inducible nitric oxide synthase (in synergy with muramyl dipeptide). LTA-activated microglia kill co-cultured neurons apparently via nitric oxide, superoxide and peroxynitrite, which may induce apoptosis of neurons that are then phagocytosed by microglia “
Quite a mouthful. In simple terms, Gram positive bacteria can be proinflammatory when stimulated and add to the overproduction of iNOS simultaneously.
The cell wall as a source of autoimmune stimulation
To quote from Wikipedia- “Peptidoglycan, also known as murein, is a polymer consisting of sugars and amino acids that forms a mesh-like layer outside the plasma membrane of all bacteria (except Mycoplasma), forming the cell wall. ( see - http://en.wikipedia.org/wiki/Peptidoglycan )
Antibodies specific to peptidoglycan are found in the CSF of patients with active MS. ( see - http://brain.oxfordjournals.org/content ... 4.full.pdf )
Peptidoglycan is made of N-acetyl-glucosamine and N-acetylmuramic acid. (see http://en.wikipedia.org/wiki/Peptidoglycan )
Effectively, by loading with n-acetyl-glucosamine I was promoting cell walls that could stimulate proinflammatory responses.
Importantly, even a fragment of peptidoglycan can induce Th1 to promote IFN gamma and CD4 activation. (http://brain.oxfordjournals.org/content ... 4.full.pdf ) .
As a result of my mistake I can see I have fed the cell wall of gram positive bacteria by priming with n-acetyl-glucosamine. This has created a proinflammatory response from Th1 which fits the usual autoimmune model. The important thing is I did it to myself, My body did not initiate this. I did.
I will use the prednisolone to dampen my immune response to avoid damage and an antibiotic to treat the peptidoglycan. (see - http://microbelibrary.org/library/bacte ... -they-work ).
And now I wait…
Perhaps I should add a long term antibiotic to everything else I do. There may be herbal inhibitors but I have a way to go working that out. I expect to completely recover.
Its funny...the more I read about bacteria being involved, the more I think about those who constantly claim that MS is in fact Lyme...
Hope you are feeling better?
It does have a thin peptidoglycan wall.
Still stiff as a board. Will try some dry needling tomorrow otherwise all good, thanks.
The prednisolone stopped after day 7 but I am still taking the antibiotic, Zinnat, and will be for some time to combat gram positive bacteria. The whole thing makes me more convinced that we have differing influences at work. The fatigue can be managed following the anti ADMA, anti iNOS path very successfully. This sort of flare up needs an antibacterial plus time but I am able to treat them as two different things. I still expect to make a total recovery.
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