Anti-LDN article debunked
We have saved both the NMSS' original article, plus the abstract for the research they incorrectly cited, for posterity on this page on 5-19-2004.
The Infamous NMSS LDN "Article"
Low Dose Naltrexone Update
May 2004—We have received a number of inquiries about the use of low dose naltrexone as a treatment for multiple sclerosis. There are no published clinical data to support the use of naltrexone in MS.
Naltrexone is an opioid antagonist that has been approved by the U.S. Food and Drug Administration (FDA) since the early 1990s for the treatment of addictions to opioids and alcohol. At significantly lower doses, it has been marketed on the Internet as a treatment for a variety of diseases, including various types of cancers, HIV/AIDS, Parkinson's disease, Alzheimer's disease, amyotrophic lateral sclerosis (ALS), emphysema, as well as MS and other autoimmune diseases. There are, however, no published reports of placebo-controlled clinical trials demonstrating the safety and efficacy of naltrexone in any of these diseases. The marketing efforts rely entirely on anecdotal reports.
Naltrexone is said to work in MS and other diseases by adjusting the level of endorphins in the body to enhance immune function. Enhancement of the immune system, however, is not recommended for anyone with MS. Because MS is thought to be an autoimmune disease, in which the immune system mistakenly attacks the myelin in the central nervous system, the goal of currently approved treatments is to inhibit the overactive immune response rather than boost it. In fact, the one study of low dose naltrexone in experimental allergic encephalomyelitis (EAE)-the animal model of MS-demonstrated a disease worsening (Panerai et al. 1994. J Neuroimmunol 51(2):169-176).
People with MS are advised to avoid any medication, dietary supplement, or other treatment that is touted as strengthening the immune response.
Clinical Programs Department
in collaboration with
Allen Bowling, MD, PhD
Rocky Mountain MS Center
Last updated May 11, 2004
Originally posted to: http://www.nationalmssociety.org/Clinup-Naltrexone.asp
Cited research article which actually indirectly SUPPORTS the use of LDN
Beta-endorphin concentrations in brain areas and peritoneal macrophages in rats susceptible and resistant to experimental allergic encephalomyelitis: a possible relationship between tumor necrosis factor alpha and opioids in the disease.
Panerai AE, Radulovic J, Monastra G, Manfredi B, Locatelli L, Sacerdote P.
Department of Pharmacology, University of Milan, Italy.
Since the central nervous system and neuropeptides modulate immune functions, we investigated whether the different susceptibility of Lewis and Brown Norway rats to experimental allergic encephalomyelitis could also reflect differences in beta-endorphin and substance P concentrations in brain areas and macrophages during the development of the disease. We show that beta-endorphin concentrations increase much more in the hypothalamus and macrophages of Lewis rats during the development of the disease, while the increase is much lower or absent in Brown Norway rats. Tumor necrosis factor-alpha seems to play an important role in this difference. The administration of the opiate receptor antagonist naltrexone worsens the development of the disease, suggesting that the increase of the opioid beta-endorphin might represent a mechanism to downregulate the immune response. In both strains, the concentrations of substance P do not change.
PMID: 7514185 [PubMed - indexed for MEDLINE]
J Neuroimmunol. 1994 May;51(2):169-76.
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