It's a big jump to assume the lesions on an MRI from one case can translate to another. We'd probably need to see the results of biopsies that looked at the residues in the lesions. In MS there are a number but I don't know if lesions associated with MS will be comparable with what you are thinking of.
When I went on the antibiotic it was after I felt that taking N-acetyl-glucosamine had triggered something. A bit of reading revealed that NAG was a major component of the bacterial cell wall called a peptidoglycan. There is plenty of research that shows even fragments of peptidoglycan can induce an inflammatory response. My reaction was to assume that I was "feeding" a bacteria so I needed an antibiotic that would work on the bacterial cell wall. If I was right it was all too late as I wasn't controlling the inflammation. I'm amazed I could function now I look back on it.
I'm still a big fan of that research that Leonard found noting that EBV primed cells induce arachidonic acid and inflammation when an agonist is introduced while non infected cells don't. So maybe the second trigger could be anything as long as the EBV has laid the foundation for an inappropriate response. Maybe it covers more than cell walls; it could be hormonal, chemical, physical etc.
The problem with EBV infection is it promotes peroxynitrite and that is very disabling. As Szabo noted some of the changes are more or less permanent so we still need to keep peeling an onion to deal with our spot fires.
The lactoferrin is really interesting. My understanding is it influences the binding of iron but it's a bit beyond me. I suspect it's an important area. After my experiment, which I found really mentally challenging, my bowel has been completely normal. There was no lasting negative effect and I'm not concerned about recommending it. For me, I just felt paranoid. It may be just my response but if you stop taking it then the paranoia goes away so it is dose dependent.
The benefit of my current blood pressure issues is I have a better understanding of how calcium operates in the cell. This helps me understand what keeps our muscles tight and why there is so much research on potassium and calcium channel blockers.
As usual, I don't think there is one magic bullet.
If you want something to explore, I think Stephen Sinatras book on metabolic cardiology has many explanations that are useful for us. The heart is just another muscle made up of cells so the work is valuable if you take a read through. Buhners book on Lyme disease coinfections has some very good work on mycoplasmas in particular. Know your enemy if nothing else.
I'm glad the Rituxan helped you. Good luck peeling your onion.
I'll let you know how I go.
I have been meaning to update what has been happening to me recently but wanted to leave it as long as possible to build the most complete picture. In many ways I would have preferred to take more time but I have seen enough to draw some conclusions which should be helpful.
Since my attack had passed, my ongoing problem revolved around spasticity- numbness in the arms, a pronounced limp, soreness, cold hands and general tightness. More recently, the tightness in my muscles had helped elevate my blood pressure so the systolic reading was 194-197 and diastolic reading sat at 84-97. I did spike on the diastolic to 110-115 for one dreadful day. Blood pressure would be better at 130/80 or lower for my age (57).
At my neurologist’s suggestion, I commenced taking a very old muscle relaxant called Baclofen 16 days ago. His advice was to start at 5mg before bed for the first week and add 5mg in the morning in week two. If I tolerated that, I should increase the evening dose to 10mg.
The morning after my first dose my systolic reading fell to 150. I continued over time to produce series of lower readings and I even had a 127 one morning. The diastolic began to decline about a week later to regularly read 73-78. Additionally, my very spastic left calf began to relax and overall I had an impression that I felt a bit better. Each day I recorded my blood pressure and after the first week I decided not to increase from the 5mg in the evening because the blood pressure had not reached a plateau. There were some ordinary days where I was sorely tempted to increase the dose but resisted. Now, 16 days later, I think I will stay on the original dose.
As my muscles began to relax, it became easier to identify where my real trouble spots were. The shoulders were really tight and a subsequent investigation showed I had two frozen shoulders. (adhesive capsulitis). I think this has been due to the relentless spasms just constantly crushing them. The other real trouble spot was in the thoracic region of my back. The nerves felt tight and tortured and at times my back ached. Interestingly, when my back really hurt my blood pressure would be elevated and I could notice my heart thumping in my chest. Both a physio and an Osteo had both said that I reminded them of someone with Thoracic Outlet Syndrome.
To deal with the shoulder issue I have had some hydrodilation work which may be successful but will take a few weeks to really know.
To deal with the back, I had some intensive pressure point massage done just on the area presented as very ropey and tight.
I am a very big fan of the Baclofen because it has helped. The issue now is to explain how it works and how it fits into the overall protocol.
For this discussion, I won’t bother with any infection or metabolic issue that might drive our muscles to tighten but just look at the mechanism.
We are interested in the skeletal muscles. This type of muscle is a form of striated muscle (as is cardiac muscle). It has basic units called sacomeres which are long fibrous proteins that slide past each other when muscles contract or relax. One of the proteins is called myosin and its filaments are thick and the other major protein is called Actin which is thin.
The Myosin has little hooks or heads that bind to the Actin by using ATP for energy. However, this can’t happen without calcium being present. There are a range of bands in the muscle and some can contract. When the Myosin hooks attach to the Actin they can pull the Actin along and contract the muscle.
The cycle of contraction and relaxation works like this-
The calcium is stored in a place called the Sarcoplasmic Reticulum. When stimulated, a motor neuron releases a neurotransmitter called Acetylcholine. This causes Sodium to enter the cell. In turn, that causes a reaction that triggers some calcium to enter the cell which opens the gates of the sarcoplasmic reticulum and even more calcium enters the muscle cell.
That calcium flow causes the Myosin heads to attach to the Actin fibre and the muscle can contract. When the two are bound it is a state called Rigor. To release the rigor an ATP molecule needs to bind to the Myosin. Then the muscle relaxes. This is not the only path but they are all similar.
So ATP is very important for muscle relaxation. It doesn’t spend phosphate molecules as occurs at the Sodium/Potassium pump but it does play a big role.
The muscle fibres lie in bundles but different bundles lie in different directions to create force and that builds into the architecture of the body.
Prior to the neuron releasing the neurotransmitter it has a negative ion charge inside it. The cell has a positive charge. Calcium has two positive charges and sodium and potassium have one positive charge and chloride has a negative charge. This charge is what stops Sodium and Potassium easily passing through membrane. A balance inside and outside the cell must be maintained. When it is unbalanced something needs to happen to restore a balance. The imbalance is called the Action potential. When balance is restored, it is called the resting potential. After the neuron fires there is a refactory period during which the Potassium channels open and the Sodium channels close to go back to resting potential.
So when the neuron signals the Action potential to commence both Sodium and Calcium flood into the cell. The Sodium triggers Calcium and the Calcium triggers the muscle to contract. As long as the balance of ions (which is determined by the balance of Sodium and Potassium in the cell) is polarised the neuron will fire. If the Potassium stays in the cell then the Sodium channels won’t open and the neuron will be hyperpolarised so calcium will not be triggered to flow into the cell and the muscle will not contract.
The Potassium channels are controlled by receptors called gamma-aminobuytric acid (GABA) receptors. Strictly speaking GABA is an amino acid but it is gamma while the ones we call amino acids are alpha amino acids. GABA is synthesised by neurons so it is autocrine (acting on the same cell) and paracrine (acting on nearby cells).
Baclofen is a homologue for GABA (specifically GABA beta) so it can help us keep the Potassium channels closed and hyperpolarise the neuron so the muscle is not compelled to contract.
I do not know why GABA absorption is awry but a homologue looks a good alternative if it works. It is for me. Others may need a different dose. Mine is (apparently) unusually low but I do take other supplements and I can’t find any literature on combinations except for some covering N-aceytl-cysteine.
If spasticity is a problem Baclofen is probably worth trying but remember the entire process of muscle relaxation is ATP dependent.
For ATP production I continue to favour Q10 and N-Aceytl-Carnitine.
Possibly. I don't know what happens to it when you ingest it. It's still just an amino acid so I don't know if it can survive in the correct conformation. What form is it sold in and what do they use it for? I found very little Baclofen has a big effect on me so I don't know how the amino acid itself would go.
The other thing is the Baclofen works on GABA beta receptor rather than the alpha receptor. So I don't know if a supplement does the same thing.
I also found this "ad"- http://nootriment.com/gaba-supplements/
A bit more knowledge on the manufacturing might be needed.
A quick "google" also highlights Baclofen crosses the blood brain barrier while it looks like the supplement doesn't.
- Volunteer Moderator
- Posts: 5164
- Joined: Sat Nov 20, 2004 3:00 pm
- Has thanked: 1 time
- Been thanked: 17 times
It's a good question. The best I could come up with is 1) GABA is the chief neurotransmitter in the brain so it may interact directly with prescription medication or antidepressants, 2) It is normally self limiting in neural settings but if it is too high it becomes depressive and I'd rather be happy.
All I want to do is influence the GABA receptor not GABA levels themselves. By doing that the potassium channel can be stay closed long enough to keep the potassium in the cell so the sodium does not flow in too rapidly and trigger the calcium to flood in leading to tight muscles. Baclofen is a homologue for GABA-not GABA itself.
It seems to be working for me but I am really juiced with Q10 and L-carnitine so I make a lot of ATP. If you don't make enough ATP, I have doubts it will be as successful unless the dose is much higher and that could come with the price of other side effects such as sleepiness or passivity.
More on Baclofen.-
As my tight muscles lessen I notice new things. It struck me today that my stomach seems a lot less uncomfortable than usual so a bit of a peek showed me that GABA is throughout the GI tract and has an influence on bowel motility as a modulator of activity. The article here -http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3153004/ also postulates that Baclofen may be a useful therapeutic. The interesting thing is it shows what may be faulty with the bowel troubles that some have.
I just finished skimming Buhner's book 1 and I'm dipping into book 2 as 3 warms by my side. Good stuff. I love that he offers natural remedies for symptoms, including herxes! (I tried hawthorn extract which he hails as cardio protective but it's mentioned elsewhere as a herx softener. It worked!) So, I've started Buhnering...maybe I'll hit something crucial by accident.
Wanna Buhner with me? So far it seems pretty tame (though I did have to rearrange furniture and order a new shelving unit for my out of control supplement/herb hoard).
(your NAC breaks up bio films and sends the contents throughout the body to do as they will. Are you taking anything to kill the nasties you free? Maybe that's why people on CAP sometimes herx on NAC...which they're supposed to take for some time before starting abx)
After all that candida harping, I read that diflucan is part of a Lyme protocol too. (Hence my adventures in Lyme land). Maybe Scott1 is right about the Lyme/bartonella thing. I've no idea if I have anything lymey (I certainly don't present as a typical Lyme patient) but I'm trying the Buhner stuff (and some Cowden) anyway to see if it knocks something out by accident. Maybe that's the way to go? Paint with a broad brush?
I hope you're doing better...
Now Buhner is a verb! It's a very flattering offer.
I think he writes very coherently and gives us a lot of things to consider. I've tried some of his things but I'm never sure he'd be happy with what I bought. Hawthorn, Red root and Sida are all up there in the interesting taste category. I tried a full Mycoplasma regime at one point and had a long course of the antibiotic Zinnat right through my last big attack so I may have really smacked the infections that NAC affects. Now I maintain it because it helps scavenge a number of free radicals. NAC also is used synergistically with Baclofen (high doses) to treat addiction in alcoholics and heroin users. My head is very clear so maybe that has an effect.I'm happy to use it and haven't had any problems.
Post my attack I also tried Cordyceps but it was a bit rough on my tummy. I think it sounded great but I am a big sook when it comes to the stomach.
At least what he says is well based and it builds our knowledge. We should have a Buhnering good time!
Have you read book 2 & 3? It seems like he explains his whole philosophy more clearly in 2 (the one that addresses bartonella and mycoplasmas...haven't gotten to 3 yet and I just skimmed 1 as I've already learned a lot of the basics). I've barely started really reading 2, but his plan of attack is to primarily to make our bodies inhospitable by stopping the cytokine cascades and protecting major systems. Killing the invaders directly is just a tiny part of his protocol and most of the killing is done by the remedies he uses to correct the cytokine cascade and protect our systems. So, you have to do the whole thing for it to work according to his philosophy.
So far, nothing tastes as interesting as gse. That stuff is awful! Luckily, it's not part of Buhner...it is a cyst buster though.
Back on Baclofen again.
I had been on the subclinical dose of 5mg before bed and it had improved my flexibility and lowered my blood pressure. A few days back I decided to go to 10mg before bed and see if there was an improvement. The result was stomach cramps, diarrhea and I was tighter in some muscles than I expected. Consequently, I've gone back to 5mg and feel good again and benefit from it. The lesson is more is not always better.
Ever since I came out of hospital I've been gradually sorting out tight muscles and neural problems. By and large I've been successful. My hands and fingers are still not right. My left leg has a spastic ankle and is generally stiff.
A huge amount of exercise (mainly Pilates) has worked wonders but the stiffness is still a problem. Baclofen has generally helped but doesn't resolve some specific muscles.
The next step is a series of botox injections into my foot, ankle, calf, hip flexors and possibly my hamstrings.
The idea is to partially "kill off" the neurons in the target area. As the neuron recovers the new growth is free of the damage to the old neurons so the muscles behave more normally. Apparently, it works but the process seems a bit hit and miss. The basic message is I will need to exercise all through the regrowth period or I have wasted my time.
The injections will be done in mid August. They will do their work over the first week and the new growth will occur over three months.
My plan is to be a fit as I can before the injections. Today I walked my dogs for 10km along goat trails around a river. Up and down, on rough surfaces and on narrow paths. It was all rather tricky with a bung leg. The aim was to work my leg through a range of movement, not just bounce it up and down in one plane. I will do this as many times as I can both before and after the shots. A fit leg will move through a wide range of flexion. That's the plan. I'll let you know how I go.
The Botox injections were pretty straight forward. They made me walk around a bit to observe my movement then did a very fussy version of tests for flexion and spasticity while they shook my leg all over the place. In the end there was a shot into the soleus and two into the hamstring. Now I have to exercise as much as possible and they will review in mid October. It should take a week to have an impact.
- Similar Topics
- Last post