Naltrexone
Orignally published in eMS News July 23, 2009
Naltrexone was approved by the FDA in 1984 – in a 50mg dose – to treat opium and heroin addiction. A year later, Dr. Bernard Bihari, a physician in New York City, found that a much lower dose of naltrexone affected the body’s immune system. Initially, LDN was used off-label to treat HIV-positive patients and, in the 1990s, certain types of cancer. However, very limited scientific data has been collected on these treatment uses, and LDN has not been approved by the FDA to treat either disease. More recently, LDN has been promoted as an off-label treatment for MS.
How does LDN work? The proposed effect of the therapy is that LDN causes an artificial blockade in the brain of endorphin/opioid receptors. The larger dose – used to treat addictions – causes a constant blockade, whereas the lower dose only blocks the endorphin receptors for a few hours. The blocking effect means that because endorphins aren’t able to attach to receptors, the body compensates by producing more endorphins, which are reported to boost the immune system and normalize immune function. However, there is very little scientific data to support this.
Proponents of LDN point to recent studies that conclude that immunodeficiency exists in MS – meaning the disease causes low levels of beta-endorphins. This claim remains controversial, and researchers insist that additional studies are necessary in order to more thoroughly understand the role of endorphins in MS.
Although many physicians have publicly encouraged the pursuit of more clinical trials on LDN and MS, few studies have been done. To date, all the studies have been brief, small, and with a focus on subjective outcomes – all facts that concern many MS specialists. Specialists point to the lack of scientific evidence, and insist that the variable nature of MS makes it essential for the therapy to be tested on a larger scale, for longer periods of time, and with more scientifically based criteria.
One Italian pilot study, the results of which were released in 2008, involved 40 patients with primary progressive MS who took LDN for 6 months. The study was set up to primarily evaluate the safety and tolerability of LDN, and to secondarily look at the effect of LDN on spasticity, pain, fatigue, depression, and quality of life. During the course of the study, investigators analyzed protein concentration of beta-endorphins.
Of the 40 study participants, 5 dropped out, two of those due to major adverse events. Of those remaining, investigators were encouraged to see that only one participant experienced neurological disease progression during the course of the study. Despite this seemingly positive result, the fact that the study lasted only 6 months – a very short amount of time in terms of neurological progression – left many MS specialists unconvinced of the efficacy of LDN. Study investigators also noted a possible reduction in spasticity, as well as an increase in the concentration of beta-endorphins.
In another recent clinical trial on LDN and MS, the results of which were also presented in 2008, investigators measured study participants quality of life using the MS Quality of Life Inventory. The Inventory focuses were subjective outcomes such as mental health, pain, and self-reported cognitive function. Among the 80 study participants who were given either LDN or placebo, those on LDN experienced “significantly improved quality of life,” although no physical benefits were seen. During the 8-week trial, the therapy was well-tolerated and the only side-effect that study participants experienced was vivid dreams.
Most MS physicians agree that further studies on LDN and MS are necessary before they will be able to comfortably prescribe the drug off-label, and most remain skeptical that there is a place for LDN in the world of MS treatment. Despite this, patient interest persists and websites on LDN continue to pop up. Supporters of LDN remain hopeful that the therapy will soon become a more available treatment for MS.