I think it was a British uni doing the study... I think that it's one of the most intriguing trials out there at the moment, and I have high hopes for it!
Also, is anyone currently using hook/whip worm and is seeing substantial benefits?
I have been using hookworm since Spring 2011, increasing the dose gradually, and now host over 100 helminths. This is a safe dose level, I have no ill effects from the worms, and I have not had a relapse since starting. Of course its "only" been 18 months, so I'm not jumping to any conclusions, but so far so good.
The science behind this is very strong, though I dont claim to understand it all. Here is the Argentinian study http://www.ncbi.nlm.nih.gov/pubmed/17230481 convinced me that this was worth a try.
The problem with the trials is that it will take a long time for anything to come of them. In order for anyone to invest in full phase 3 trials they need something patentable. So they'll want to find, isolate, and patent the particluar active molecule(s) from the worms and turn it into a patented drug - this is where the money is. But this will take years.
So why wait for this when the natural product (that has evolved over thousands of years in symbiosis with humans) is available now. There is at least one company currently providing safe doses of hookworms and whipworms.
Are you going to go up to 300, which I have heard is the target for Ms?
Meanwhile 18 months is a good start. It does apparently take the worms a while to reach full efficacy - probably up to a year. So I am hoping to see the full benefit now they are fully up and running. I actually have close to 200, and no plans to go higher at the moment. In a year or so I'll probably top up, as its likely that some will gradually dying off.
Yes I do do still have residual symtpoms from previous attacks, especially when my temperature is raised - but no new symptoms. I would say that the helminths work to control inflammation to prevent or drastically reduce further relapses. This will hopefully allow the body to heal itself as much as possible.
Yes, I'm using AIT. They've been great, and they - Jasper and Marc - really believe in what they're doing.
Also, out of interest, what are your particular symptoms when it gets hot? Is it the usual fatigue or something else?
The data is only limited by the relatively low number of subjects. In the Argentinian study they compared 12 people with helminth infection against 12 without infection, and followed them for 4.6 years....... only 3 relapses from 12 infected people in 4.6 years, compare to 48 relapses in the 12 non-infected people. No change in EDSS in infected people. WOW
These results are simply incredible, and the study is of really high quality. It was published in Annals of Neurology in 2007 and I only wish I'd seen it, and acted on it, sooner. I cant believe the study is not more widely known, but then I guess there is no big money behind it
Theres a follow-up study where they 'treated' some of the people to remove their helmiths... this population reverted to a higher number of relapses over the next few years. Further convincing evidence that the helminths excert a protective influence on MS.
See my thread in Regimens section
Wellcome Centre for Molecular Parasitology, Institute of Infection, Immunity and Inflammation, University of Glasgow, Glasgow, United Kingdom
The Helminth Parasite Heligmosomoides polygyrus Attenuates EAE in an IL-4Rα-Dependent Manner
Helminth parasites are effective in biasing Th2 immunity and inducing regulatory pathways that minimize excessive inflammation within their hosts, thus allowing chronic infection to occur whilst also suppressing bystander atopic or autoimmune diseases. Multiple sclerosis (MS) is a severe autoimmune disease characterized by inflammatory lesions within the central nervous system; there are very limited therapeutic options for the progressive forms of the disease and none are curative. Here, we used the experimental autoimmune encephalomyelitis (EAE) model to examine if the intestinal helminth Heligmosomoides polygyrus and its excretory/secretory products (HES) are able to suppress inflammatory disease. Mice infected with H. polygyrus at the time of immunization with the peptide used to induce EAE (myelin-oligodendrocyte glycoprotein, pMOG), showed a delay in the onset and peak severity of EAE disease, however, treatment with HES only showed a marginal delay in disease onset. Mice that received H. polygyrus 4 weeks prior to EAE induction were also not significantly protected. H. polygyrus secretes a known TGF-β mimic (Hp-TGM) and simultaneous H. polygyrus infection with pMOG immunization led to a significant expansion of Tregs; however, administering the recombinant Hp-TGM to EAE mice failed to replicate the EAE protection seen during infection, indicating that this may not be central to the disease protecting mechanism. Mice infected with H. polygyrus also showed a systemic Th2 biasing, and restimulating splenocytes with pMOG showed release of pMOG-specific IL-4 as well as suppression of inflammatory IL-17A. Notably, a Th2-skewed response was found only in mice infected with H. polygyrus at the time of EAE induction and not those with a chronic infection. Furthermore, H. polygyrus failed to protect against disease in IL-4Rα-/- mice. Together these results indicate that the EAE disease protective mechanism of H. polygyrus is likely to be predominantly Th2 deviation, and further highlights Th2-biasing as a future therapeutic strategy for MS.