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High hopes for low dose medication

The story of naltrexone is a good example of how scientific discoveries are often made unintentionally.

In this case, it started with research into what hooks addicts to the heroin or alcohol they so desperately crave.

INNER PAINKILLER

If you’re an athlete or a body builder, you’ve probably heard of endorphins. These are the body’s natural painkillers and are secreted whenever parts of your body are injured or placed under stress. Endorphins have a euphoric effect on the brain, described as a “runner’s high”, which is felt during or directly after a heavy bout of exercise. This occurs because the endorphins stimulate specialised cells in the brain, known as opioid receptors.

These cells are also sensitive to “external” painkillers, such as morphine and heroin. Alcohol, on the other hand, affects the opioid receptors indirectly, because it stimulates the production of other types of internal opioids.1 The more external stimulation the opioid receptors receive, the less endorphins the body produces. This deficiency worsens over time as the body becomes more and more dependant on alcohol or heroin.

IMMUNE REGULATOR

Naltrexone, in a large 50mg dose, was licensed by the US Food and Drug Administration in 1984 as a treatment for heroin addiction. This was thanks to its ability to “block out” endorphins at the opioid receptors in the brain, making them immune to the euphoric effects of heroin.2

In 1985, a US doctor by the name of Dr Bernard Bihari tried naltrexone with more than 50 heroin addicts who had stopped using the drug, but the side effects at that dose were unbearable.3  Then, later that year, a large number of heroin addicts became sick with AIDS, which prompted Dr Bihari and his colleagues to shift their focus to this disease and to ways of strengthening the patients’ immunity.

Since endorphins are the hormones centrally involved in supporting and regulating the immune system, Dr Bihari’s team measured levels of endorphins in the blood of AIDS patients and found them to be less than 20% of normal.

He knew that when naltrexone is administered, it first stimulates the body to produce more endorphins. But if the dosage is too high, the effects are blocked. Dr Bihari found that with lower doses – a fraction of those given to addicts

– which are taken at night when the body’s own production of endorphins is highest, the blockage doesn’t occur.4

WEAKENED DEFENCES

Autoimmune conditions are confusing because they’re often assumed to be caused by an overly strong immune system. This isn’t the case. Underlying these conditions, is an immune system that's poorly regulated.5 The immune cells, or lymphocytes, then fail to distinguish between foreign invading organisms and the body’s own cells, and when the immune system begins to attack, it triggers the widespread inflammation and scarring seen in the affected parts.

In autoimmune patients, low-dose naltrexone (LDN) works by restoring endorphin levels to normal, thereby allowing the immune system to resume its usual function.

Many studies have shown that an immunodeficiency is a characteristic of autoimmune diseases, including multiple sclerosis, rheumatoid arthritis, Crohn’s disease and chronic fatigue syndrome.6,7,8 There are even studies suggesting that

LDN’s role of modulating immune function may eventually play a role in disease prevention, rather than treatment.9

One of the most promising and recent results, however, comes from a study that looked at the effects of LDN on people who suffer from Crohn’s disease, an autoimmune inflammatory condition of the bowel.10 After 12 weeks, as many as 78% of those treated with LDN experienced a dramatic decline in the severity of their symptoms, while 33% were in complete remission. With dramatic results such as these to encourage further research, there’s hope on the horizon for those suffering from autoimmune disorders, albeit in the form of a medicine not initially created for that purpose. It is, however, no magical cure-all, and an integrative and comprehensive approach to autoimmune conditions is still the best treatment route.

References

  • 1 Sinclair JD. Evidence about the use of naltrexone and for different ways of using it in the treatment of alcoholism. Alcohol and Alcoholism. 2001;36(1):2-10
  • 2 Shader RI. Antagonists, Inverse Agonists, and Protagonists. Journal of Clinical Psychopharmacology. Aug 2003;23(4):321-22
  • 3 Kokayi KB. Dr Kamau B Kokayi Interviews Dr Bihari. Global Medicine Review. 2003. www.lowdosenaltrexone.org/gazorpa/interview.html
  • 4 Bihari B, Drury FM, et al. Low Dose Naltrexone in the Treatment of Acquired Immune Deficiency Syndrome. Oral Presentation at the IV International AIDS Conference, Stockholm. Jun 1988
  • 5 Buckley RH. Primary Immunodeficiency Diseases Due to Defects in Lymphocytes. N Engl J Med. 2000;343:1313-24
  • 6 Thewissen M, Linsen L, et al. Premature immunosenescence in rheumatoid arthritis and multiple sclerosis patients. Ann N Y Acad Sci. Jun 2005;1051:255-62
  • 7 Marks DJ, Harbord MW, et al. Defective acute inflammation in Crohn’s disease: a clinical investigation. Lancet. Feb 2006;367(9511):668-78
  • 8 Vernon SD, Reeves WC. The challenge of integrating disparate high-content data: epidemiological, clinical and laboratory data collected during an in-hospital study of chronic fatigue syndrome. Pharmacogenomics. Apr 2006;7(3):345-54
  • 9 Brown N, Panksepp J. Low-dose naltrexone for disease prevention and quality of life. Med Hypotheses. Mar 2009;72(3):333-7
  • 10 Smith JP, Bingaman SI, et al. Therapy with the Opioid Antagonist Naltrexone Promotes Mucosal Healing in Active Crohn’s Disease: A Randomized Placebo-Controlled Trial. Dig Dis Sci. 8 Mar 2011. www.ncbi.nlm.nih.gov/pubmed/21380937
 
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