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After a number of days of worsening symptoms the angiogram was deferred and furthertests carried out. These showed a continuing infection with no resolution of thesepticaemia. After trying a second antibiotic, when the infection again appeared topersist it was deduced that the likely fixed source of the infection was the cannula itself.This was duly removed and my temperature, and the infection, resolved within twentyfourhours. I continued the antibiotic for a few more days to ensure completeeradication of the infection, when the angiogram was at last booked and carried out.This showed only moderate narrowing of some of the branch arteries of the coronarycirculation and I was offered two drugs, one a calcium antagonist, and the other a betablocker.I soon became aware of the dramatic side-effects of the beta-blocker when mysleep became grossly disturbed, with bizarre dreams for the maximum of two hourssleep I would attain, plus daytime hallucinations that made me wonder if I was actuallyawake or not!The beta-blocker was thus changed for one that did not cause these strange sideeffectsand I was finally discharged home.After some days I became aware that the drugs, although temporarily effective inreducing the pain, had no prolonged effect in preventing its recurrence. I thereforesurmised that, as I was already taking a moderate dose of vitamin E, a potentvasodilator, and that the nature of the angina could be due to vasospasm of the arteriesof the heart, I might gain a significant benefit by doubling my dose of this simplevitamin. I promptly increased the dose from 400iu to 800iu, when almost instantly,within just a couple of days, the pain had gone entirely.I abandoned both the drugs, that had proved so ineffective, and I have continued withthis high dose of vitamin E with no further recurrence of the pain ever since.My logic, and the results I obtained, were later reaffirmed by a study at AddenbrookeHospital in Cambridge, conducted in 1996, when a double blind, placebo controlled trialof a single daily dose of vitamin E, 400iu, in patients already having suffered a heartattack, showed a 79% reduction in further risk by taking this simple vitamin.I continued my work, now gradually limiting the range of problems I chose to deal with.Eventually, I was dealing almost entirely with just MS, plus a few related conditions,such as colitis or rheumatoid arthritis.Slowly, as my work increased, my reputation grew and, by 1997, as I had begun tomake increasing use of the internet, I had become sufficiently well known to be able tostop advertising entirely and just rely on word-of-mouth recommendations to gathernew inquiries.It was this connection with the internet that was to later reveal the final link in thetreatment regime that was to complete the stability of my MS.This was the discovery, in late 2000, of low-dose naltrexone (LDN), a method initiallyapplied in significant numbers by Dr Bernard Bihari, a New York physician. At that timeDr Bihari was treating about 70 patients with a variety of complaints, by this treatmentmethod.Produced by LDN Research Trust for International LDN Awareness Week 19-25 October 2009© LDN Research Trust 200930