This Is MS Multiple Sclerosis Community: Knowledge & Support

cheer i need to go take another look at jeff's regimen but i imagine zinc must be factored into it? - i think i remember your saying he took some daily? what was that amount again? i'll go see if i can find.

Sarah,
Do you or David think this would bed contrary to ABX thinking?

C pneumoniae is known to patchily parasitize the cells which line small blood-vessels, causing episodes of vasculitis. This is a local inflammatory process characterised by tiny punctures in the vessel walls and leakage of blood-components into the surrounding tissue space. It can be visualized directly in the retinal veins, where the vessels appear to be coated with a thin greyish sheath. This sheath is comprised of T lymphocytes. A very similar pathology takes place in the brain in early MS. The association between sheathing of retinal veins and MS was first made in 1944. The anatomical distribution of lesions within the brain in MS is often centred on small veins; elongated plaques may follow the sinuous curves of the vessels they surround. [Esiri MM, ed. Oppenheimer's Diagnostic Neuropathology, 2nd edition, 1996 Blackwell: 256-9.] Vasculitic phemomena were recognised surprisingly early: in 1873 Rindfleisch commented: "If one looks carefully at freshly altered parts of the white matter in the brain, one sees with the naked eye a red point or line in the middle of each individual focus, the transversely or obliquely cut lumen of a small vessel engorged with blood. . . All vessels running inside the foci, but also that traverse the immediately surrounding but still intact parenchyma are in a state of chronic inflammation." Rindfleisch had recognized, over 130 years ago, that inflammation of small vessels — vasculitis — precedes neural damage.

Examination of the eye reveals retinal vasculitis in about a third of persons with early MS, but it is probably present in far more. It is especially common following optic neuritis (a common precursor of MS), and is characterised by leakage of dye in a fluorescein dye test, blood cells, and cuffing of the vessel walls by inflammatory cells. Where it is seen, there is a raised likelihood that MS will follow. I have noted that episcleritis (an inflammatory condition of the connective tissue between the conjunctiva and sclera involving vasculitic features) is also a frequent finding in those with MS. (Unpublished data.)

MS is currently considered an autoimmune demyelinating disease. Myelin is an insulating lipoprotein; its sudden local loss causes the acute MS relapse. But this myelin loss may well be a secondary phenomenon. The very fact that retinal vasculitis is commonly associated with MS casts considerable doubt on myelinopathy being the root cause of MS; myelin, and the oligodendrocyte cells which produce it, are not found in the retina, and the earliest pathological manifestations of MS are in blood-vessels, not nerves and glial cells. Demyelination has recently been shown to be a secondary phenomenon in the acute, typical lesion of MS: the first visible event in a newly-forming fatal MS lesion is the sudden, orderly, non-inflammatory local mass death of oligodendrocytes, the cells which make and support myelin. [Barnett MH, Prineas JW. Relapsing and remitting multiple sclerosis: pathology of the newly forming lesion. Ann Neurol. 2004; 55(4): 458-68.] This casts further doubt on the notion of MS as a primary autoimmune disease. The removal of unsupported myelin by inflammatory cells may well be a secondary 'housekeeping' activity. We may be witnessing the beginning of a sea-change in thought. [Chaudhuri A, Behan PO. Multiple sclerosis: looking beyond autoimmunity. J Roy Soc Med 2005; 98: 303-306.] These authors cite ten important considerations about MS which cannot be explained by the concept of a myelin-specific autoimmune process.

...A significant increase in the activity of AMP deaminase—an enzyme involved in the purine catabolic pathway—in the muscle of the zinc-deficient rats was also observed; this alteration may also contribute to hyperammonemia in zinc-deficient animals and humans (2, 3). Zinc supplementation in patients with SCD resulted in a significant improvement in secondary sexual characteristics, in the normalization of plasma ammonia concentrations, and in the reversal of abnormalities in dark adaptation (3).
...It is well known that patients with SCD are susceptible to infection ... Mycoplasma and Chlamydia pneumoniae are the most common infections associated with the acute chest syndrome in patients with SCD. It is believed that a large percentage of patients with pulmonary infiltrates probably have associated viral infections (6).
...A placebo-controlled trial of the effect of 50–75 mg elemental Zn/d orally for <=3 y resulted in significant increases in lymphocyte and granulocyte zinc concentrations and interleukin 2 production and fewer documented bacteriologically positive infections, numbers of hospitalizations, and numbers of vaso-occlusive pain crises (6). These effects were seen when zinc was administered in therapeutic doses.