Naltrexone in Low Dose
There is growing recognition in the scientific community that autoimmune diseases result from immunodeficiency, which disturbs the ability of the immune system to distinguish “self” from “non-self”. The normalization of the immune system induced by LDN(Low Dose Naltrexone) makes it an obvious candidate for a treatment plan in such diseases.
The experience of people who have autoimmune diseases and who have begun LDN treatment has been remarkable. Patients with diagnoses such as systemic lupus, rheumatoid arthritis, Behcet’s syndrome, Wegener’s granulomatosis, bullous pemphigoid, psoriasis, and Crohn’s disease have all benefited.
Because LDN(Low Dose Naltrexone) clearly halts progression in multiple sclerosis, its use has been more recently extended to other neurodegenerative diseases, such as Parkinson’s disease and amyotrophic lateral sclerosis (ALS or Lou Gehrig’s disease) whose etiology remains unknown but for which there is suggestive evidence of a possible autoimmune mechanism.
In addition, people with fibromyalgia and chronic fatigue syndrome have had marked improvement using LDN, suggesting that these entities probably have an important autoimmune dynamic as well.
Naltrexone was licensed in 1984 by the FDA in a 50 mg dose as a treatment for heroin addiction. It is a pure opiate antagonist (blocking agent) and its purpose was to block the opioid receptors that heroin acts on in the brain. When it was licensed, Dr. Bihari, then involved in running programs for treating addiction, tried it in more than 50 heroin addicts who had stopped heroin use. None of the patients would stay on the drug because of side effects experienced at 50 mg such as insomnia, depression, irritability and loss of feelings of pleasure, all due to the effect of the drug at this dose in blocking endorphins. These are the hormones in the body that heroin resembles. Physicians treating heroin addicts therefore, for the most part, stopped prescribing naltrexone. In 1985, a large number of heroin addicts began to get sick with AIDS—studies showed that 50% of heroin addicts were HIV Positive.
Dr. Bihari and his colleagues decided to shift their research focus to AIDS, in particular focusing on ways of strengthening the immune system. Since endorphins are the hormones centrally involved in supporting and regulating the immune system, levels of endorphins were measured in the blood of AIDS patients. They were found to average only 25% of normal.
Naltrexone, when given to mice and people at high doses, raises endorphin levels in the body’s effort to overcome the naltrexone blockade. This drug became the focus of Dr. Bihari’s research group. When the group discovered that endorphins are almost all produced in the middle of the night, between 2 AM and 4 AM, the studies focused on small doses (1.5-4.5 mg at bedtime) with the hope that a brief period of endorphin blockade before 2 AM might induce an increase in the body’s endorphin production. In fact, the drug did so in this dosage range. It had no effect below 1.5 mg and too much endorphin blockade at doses over 5 mg. A placebo-controlled trial in AIDS patients showed a markedly better outcome in patients on the drug as compared with those on placebo.
During the trial, a close friend of Dr. Bihari’s daughter had three acute episodes of multiple sclerosis over a nine-month period with complete spontaneous recovery from each.
The apparent mechanism of action of LDN in this disease parallels that in AIDS and other immune-related diseases. A small dose of the drug taken nightly at bedtime doubles or triples the endorphin levels in the body all of the next day restoring levels to normal. Since endorphin levels are low in people with MS, immune function is poorly orchestrated with significant impairment of the normal immune supervisory function of CD4 cells. In the absence of normal orchestration of immune function, some of the immune system cells “forget” their genetically determined ability to distinguish between the body’s 100,000 unique chemical structures (called “self”) and the chemical structures of bacteria, fungi, parasites and cancer cells (called “non-self”). With this loss of immunologic memory, some cells begin to attack some of the body’s unique chemical structures. In the case of people with MS, the tissue attacked by immune cells (particularly macrophages) is primarily the myelin that insulates nerve fibers. These attacks result in scars in the brain and spinal cord called plaques. LDN in such patients works by restoring endorphin levels to normal, thereby allowing the immune system to resume its normal supervision and orchestration.
There exists a common notion that the immune system in a person with an autoimmune disorder is too strong and, in its exuberance, targets a body tissue for attack. Rather, the evidence is more consistent with autoimmunity resulting from immunodeficiency.1 Kukreja et al have demonstrated that multiple immunoregulatory T cell defects lie behind Type 1 diabetes both in humans and in non-obese diabetic mice.2
Multiple scientific papers from various other research centres have demonstrated that an underlying immunodeficiency is characteristic of any tested autoimmune disease. Examples thus far reported include multiple sclerosis, rheumatoid arthritis, Crohn’s disease, and chronic fatigue syndrome.3, 4, 5
Multiple scientific papers from various other research centers have demonstrated that an underlying immunodeficiency is characteristic of any tested autoimmune disease. Examples thus far reported include multiple sclerosis, rheumatoid arthritis, Crohn’s disease, and chronic fatigue syndrome.3, 4, 5
Sacerdote et al measured low beta-endorphin levels in two animal examples of autoimmune disease — a mouse strain with a lupus-like syndrome and a strain of chicken with an autoimmune thyroiditis.6 They had significantly lower hypothalamic concentrations of the opioid than normal controls. In each case, the low levels of beta-endorphin were found well before the expression of autoimmune disease. This adds to considerable evidence of a key role for endorphins in regulating immune responses and suggests a therapeutic pathway.
Bihari et al found that a low oral dose of the opioid antagonist naltrexone, when taken at bedtime, led to a doubling or tripling of low levels of circulating beta-endorphin.7 Bihari has since treated some 100 people with autoimmune disorders. None of them has progressed further while the patient continued taking low dose naltrexone each night at bedtime. Since no side effects are apparently associated with its use, this medication might well be studied as a possible preventive for Type one Diabetes.
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