hi cure, i am afraid that i am not being very scientific with my attempts. i am pretty much firing all guns at this thing. but, i don't think i started anything else new at the same time as i went on the candida offensive. it's just that there was a background of longer term supplementation in the picture.
when i say it did a great job, hmm... well, i never put any of my miscellaneous little things together into the candida framework until i started reading about it in the context of MS. then, i suddenly had links for diverse things about me, that i either thought was something else, or didn't realize wasn't normal, etc. then i also remembered having to go on a yeast-free diet when i was maybe in my early teens or something. there were many other personal factors that fit the scenario perfectly.
so, i started starving the candida and throwing in a bunch of acidophilus, and all my diverse things cleared up. i wouldn't say that i specifically noticed an improvement in ms symptoms. (certainly not like the time i megadosed some b vitamins and could type again in hours.) i think the impact would be more like halting disease progression by taking away toxicity, not promoting healing. but, i was satisfied to have evidence that i was keeping the little neurotoxic buggers under control. i include some interesting articles on the subject below. one thing i find very interesting is the immunosuppression thing. it seems to go against the autoimmune theory.
J Neurol Sci. 1998 Feb 5;154(2):209-21.
A gliotoxic factor and multiple sclerosis.
Menard A, Amouri R, Dobransky T, Charriaut-Marlangue C, Pierig R, Cifuentes-Diaz C, Ghandour S, Belliveau J, Gascan H, Hentati F, Lyon-Caen O, Perron H, Rieger F.
INSERM, Laboratoire de Neuromodulations Interactives et Neuropathologies, Paris, France.
The pathogenesis of multiple sclerosis (MS) is unknown. Searching for possible toxic factors, it was found that 3-day exposure to heat-treated cerebrospinal fluid (CSF) from MS patients caused apoptotic death of astrocytes and oligodendrocytes, but not fibroblasts, myoblasts, Schwann cells, endothelial cells and neurons, in vitro. CSFs from other inflammatory or non-inflammatory neurological diseases showed no toxicity. Exposure of these glial cells to partially purified MS CSF produced DNA fragmentation, apoptotic bodies, chromatin condensation, cell shrinkage, and changes in the levels of known cytokines. A cytotoxic factor, called gliotoxin, was characterized chromatographically as a stable 17-kDa glycoprotein. Since this protein is highly cytotoxic for astrocytes and oligodendrocytes, it may represent an initial pathogenic factor, leading to the neuropathological features of MS, such as blood-brain barrier involvement and demyelination.
Arh Hig Rada Toksikol. 2004 Nov;55(4):313-20.
[Chemistry and biological effects of gliotoxin]
[Article in Croatian]
Kosalec I, Pepeljnjak S.
Zavod za mikrobiologiju Farmaceutsko-biokemijskog fakulteta Sveucilista u Zagrebu, Zagreb. email@example.com
Gliotoxin is a mycotoxin from the epipolythiodioxypipeazine family with biological active internal disulfide bridge. Gliotoxin has an antibacterial and antiviral activity, but it was discarded from clinical practice due to its toxicity. The most studied effect of gliotoxin is its influence on the cell of the immune system. Today, researches are focused on treating transplantation organs ex situ and making them immunologically silent. Its toxicity has been proven on several cells (macrophages, thymocites, splenocytes, and fibroblasts) causing apoptosis and necrosis and it has acted as inhibitor of several enzymes (farnesyl-transefases, NF-kappaB, and alcohol-dehydrogenases). Its mechanism of toxicity is connected with the production of mixed disulfide and covalent bonds, and oxidative effects. An important medical mould Aspergillus fumigatus and yeast Candida albicans can secrete gliotoxin in infected tissues and, because of the proven toxic effects of gliotoxin, it is suggested that gliotoxin can exacerbate mycoses (invasive aspergillosis or candidiasis). Gliotoxin can also affect the invasiveness of fungi and their dissemination from the primary site throughout the organism.
Clin Immunol. 2006 Jan;118(1):108-16. Epub 2005 Oct 6.
Fungal metabolite gliotoxin blocks mast cell activation by a calcium- and superoxide-dependent mechanism: implications for immunosuppressive activities.
Niide O, Suzuki Y, Yoshimaru T, Inoue T, Takayama T, Ra C.
Division of Molecular Cell Immunology and Allergology, Advanced Medical Research Center, Nihon University Graduate School of Medical Sciences, 30-1 Oyaguchikami-cho Itabashi-ku, Tokyo 173-8610, Japan.
Fungal secondary metabolites such as gliotoxin, an epipolythiodioxopiperazine toxin produced by pathogenic fungi like Candida and Aspergillus, possess immunosuppressive activities and have been thought to contribute to pathology of fungal infections in animals and humans. Since recent studies show that mast cell plays a crucial role in the front of host defense, we examined whether fungal secondary metabolites affected mast cell activation. We found that gliotoxin had suppressive effects on FcepsilonRI-dependent or -independent mast cell activation, including degranulation, leukotriene C4 secretion, and TNF-alpha and IL-13 production. Gliotoxin also suppressed intracellular Ca2+ rise through store-operated Ca2+ channels with a minimal effect on depletion of internal Ca2+ stores. Finally, gliotoxin induced intracellular production of superoxide possibly through a thiol redox cycling, which appeared to mediate suppressive effects on mast cell activation. These findings suggest that suppression of mast cell activation might contribute to the establishment of infections with gliotoxin-producing fungi.