In the early 1960’s a compound was developed to treat addicts by blocking opioid receptors on the surface of our cells (mostly brain cells). Naltrexone would block the opioid receptor sites for 24 hours stopping the high from heroin, and the addictive behavior.  In 1984 the FDA approved Naltrexone for use in opioid abuse at doses of 50-150 mg per day.  In 1994 the FDA approved it for alcohol abuse at a dose of 50 mg, and in 2014 the FDA approved it for use in weight loss when prescribed along with Wellbutrin (an anti-anxiety medication).  These applications for Naltrexone would go on to help many suffering from addictive behaviors and this alone would qualify Naltrexone as a monumental drug in the annals of medicine.  However, there is more to this story.

Dr. Bernard Bihari, a Harvard educated M.D., was working with Naltrexone and addicts in the mid 1980’s in NYC when he was suddenly inundated with AIDS patients. In an interview filmed 11 years ago, he said that “he knew the immune system was in large part controlled by the opioid system, and having sufficient endorphin levels was essential to stimulate the immune system to help these AIDS patients”. When testing AIDS patients, he found that their endorphins levels were only 30% of what they should be. Knowing that Naltrexone blocked endorphins, Bihari did a study that included fifty patients to find the lowest dose of Naltrexone hoping that it might function as an immune system modulator and increase endorphins. He discovered at a dose as low as 3 mg, he would get the same endorphin release as he would with 50 mg. Even though Low Dose Naltrexone leaves the body within 4-5 hours instead of 24 hours at the higher dose, there is an endorphin rise that lasts for 24 hours. The low dose and short-term blocking of the opioid receptors paradoxically triggers a rebound phenomenon with an overproduction of more endorphins (and enkephalins) than would have been done normally.