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The use of Low Dose Naltrexone in the treatment of Multiple Sclerosis. (A personal view)
After the licensing of Naltrexone for treatment of heroin addiction in 1984, Dr Bihari, a neurologist working with New York drug addicts, went on to develop a treatment for Aids using low doses of Naltrexone, which he subjected to a small but successful clinical trial. He then offered LDN as an experimental treatment for MS, seemingly with great success, and patented this application in 1987. LDN is now in widespread use around the world and is believed by many to be the most effective treatment for MS currently available.
LDN as a treatment for MS has been recognised in a written answer to parliament (2.3.05 Dr Ladyman). There have been two conferences in the USA where doctors have given their clinical experience of using LDN to treat MS. The results of surveys of patient experiences have been published on the web. An independent medical article by YP Agrawal states that anecdotal evidence is absolutely overwhelming. It is clear that LDN does not work for absolutely everyone. However anecdotal evidence suggests that halting the progress of MS is a reasonable expectation for very many sufferers.
But what is the scientific evidence?
First, I guess, it is reasonable to ask what scientific evidence is anyway. The normally
accepted benchmark in the medical community is that of clinical double blind trials
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The Cochrane Collaboration makes this point with their analysis of Copaxone trials for MS.
Another obvious drawback is the cost. Any treatment that cannot make a reasonable return for the sponsoring company will not be tested however impressive it appears.
Once a drug has been licensed for any purpose it may well be used off label for
other conditions -
The safety of Naltrexone in large doses is proven -
Clearly long term safety cannot be guaranteed, but then products with known safety issues are now licensed for the treatment of MS.
In any case, accuracy of reported drug safety data has come in for serious criticism recently from respectable sources such as Panorama and a House of Commons Health Committee report.
So is the evidence for using LDN to treat MS sufficient to take the seemingly low risk of using it? A personal choice I would suggest, but it would certainly be first on my list to try.
I think my additional comment on this would be that my perception is that LDN is very effective in percentage terms at stopping disease progression and not very effective at symptom improvement.
LDN is in my wife's case very dose critical and did do harm at 4.5Mg which may have been permanent if we had stuck with that dose. The problem is no one will do a truly random survey, this could only be done by the medical authorities who clearly are not interested in doing so.
Linda's survey suggests a success rate in the region of 90% but of course her results as presumable are yours are based on those who volunteer to give evidence and therefore not random.
The other problem is that the random survey would need to be done on people who have chosen LDN as the only therapy, which would now exclude us.
I think part of the way LDN is being rubbished by vested interests is to get people to regard it as a therapy with symptomatic benefits and thus when people find they receive no symptom improvements they drop it.
It is interesting to note that both the clinical trials on LDN have only concentrated on symptom relief and not adjusted the dose to the individual. Whilst they have both been successful to an extent still no one is testing on disease progression with a dose adjusted to suit individual participants.
Dave Taylor
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