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The following article is published by the Brewer Science Library. Single copies of the article may be printed for the reader's personal research and study. Reproduction in any other manner, format or location is expressly prohibited.

    Can Naltrexone Relieve MS Symptoms?
  (modified from the Winter 1999 issue of New Horizons)

The following case was reported by a former patient of Dr. Bernard Bihari, a New York physician who has pioneered the use of low-doses of the drug naltrexone for over a decade.

   Most of his work has been with HIV patients.  He has a large group of them that have been stable with no disease progression for as long as eight years from taking a once daily evening dose of 3 mg of naltrexone.  He has also tried naltrexone in other patients who suffered with different immune system disorders, whom he felt might benefit from its immune modulating actions. 

   What follows is a truly remarkable story of the positive help naltrexone might provide to some people with multiple sclerosis.
   Over twelve years ago Dr. Bihari’s daughter had a college friend who experienced three severe exacerbations in the first year of her recently diagnosed MS.  She was hospitalized with two of them.  These were episodes of transverse myelitis with the MS activity in her spinal cord mimicking severance of the cord.  Two were at the waist level, affecting movement and sensation in her legs as well as bladder and bowel functions.  She experienced a quick spontaneous recovery of 90-95% from each episode, being left with some residual numbness in her feet.  The third attack was in her spinal cord at a high level in her neck. In this attack the numbness was throughout her whole body, from her feet up to her face, and was terrifying to her.   Although she regained over ninety per cent of her physical functions after these severe attacks, she obviously was worried about the course of this illness.  Dr. Bihari suggested she try low-dose naltrexone, 3 mg at night.

   For the next several years she took naltrexone and experienced no exacerbations or deterioration in her condition, remaining quite physically active.  In fact, she was doing so well she thought she probably didn’t need the naltrexone any longer.  So she stopped taking it.    Several weeks after she had discontinued the naltrexone, she had an exacerbation with severe muscle spasms in her left arm causing her extreme pain.

   She called Dr. Bihari in desperation and was again started back on naltrexone.  She reported to him that the day after she took her first naltrexone pill again the muscle spasms in her arm decreased significantly and with continued use stopped altogether.  She had some residual loss of nerve function in her left arm, but was able to adopt her active lifestyle again.

   She has now been on low-dose naltrexone for over 12 years, and continues to do very well.   She reported to Dr. Bihari that occasionally she forgets to take her one naltrexone pill at night and the next day she might experience some muscle spasms.  That reminds her exactly how helpful naltrexone is to her body.
    Although some people may find it easy to negate this wonderful long-term success by suggesting that her MS just coincidentally remitted, that is certainly not what this young woman thinks.  Without naltrexone her predicted progress in twelve years might have been directly to a wheelchair, considering the severity of her exacerbations in her twenties.  The relief of muscle spasms alone would be considered beneficial by most MS patients.

   Intervention in this young woman’s MS was begun very early in her disease process.  Until a significant number of cases are followed and clinical trials are completed, it is unknown whether naltrexone can provide any help for individuals who have chronic progressive MS or whose disease process is much more advanced. A few other multiple sclerosis patients as well as patients with other autoimmune disorders have also responded positively to low-dose naltrexone.

  A small dose of naltrexone (LDN) taken in the evening before bed indirectly results in the pituitary gland increasing its production of beta-endorphin during the middle of the night.  It also causes a rise in the adrenal gland’s production of metenkephalin, another type of endorphin.   These endorphins have a modulating effect on the body’s immune functions.            

   Some individuals who have experienced either no benefit or side effects from other MS therapies may request their doctor’s cooperation in a personal trial of naltrexone.




By Christina White from Winter 2000 – Spring 2001 New Horizons)


Low-dose naltrexone (LDN) for autoimmune disorders has been suggested by Dr. Bernard Bihari of New York City.  He has used it to keep a large group of AIDS patients from progressing to a more advanced stage.  His experience using it with MS patients and other autoimmune disorders has been limited but very encouraging.   Dr. Bihari said that his experience has been that LDN usage in the first year would reduce exacerbations by 90%. 

One of the great responders to LDN is a female MS patient who has had MS for 16 years.  Betaseron and steroid usage did not stop her progression.  This year she also tried the histamine treatment and found some minor symptom improvement.  The dramatic and significant improvements she obtained in her balance, optic neuritis, brain fog, and leg pain she credits to naltrexone.  She began taking it in the middle of an exacerbation and it stopped the severe spacticity she was experiencing.  Continued use of LDN has changed her life.  She is now able to travel and do things she hasn’t done in years.  She also maintains herself on a low-fat, allergy-free diet, gets enough rest and tries to keep her stress level down.  As she enthusiastically says, “but I was doing those things before I started naltrexone, and they did not make this much improvement in my life.”

Another person with optic neuritis who improved  on Dr. Nieper’s calcium EAP protocol, found even greater improvement when she added LDN to her protocol.  She has had to be off of naltrexone for over six weeks due to surgery that required her to take morphine based pain killers (naltrexone should not be taken at the same time as morphine based pain killers since they use the same receptors and then the morphine will not work to reduce pain). She is looking forward to going back on the LDN protocol.

Another MS patient who has experienced an unusually stressful year in her personal life, feels that without the LDN she would have completely fallen apart and had many exacerbations.  

Another MS patient reported that she wasn’t sure if LDN had made her feel any better, but without it she recognized that she definitely felt worse.

Starting Low-Dose Naltrexone:   
Dr. Bihari has found LDN (naltrexone) to be helpful in autoimmune disorders in a dosage range of 1.5 mg to 4.5 mg.  The majority of people are given a prescription for 3 mg, which is taken just before bed.  The only side effect that many people have experienced has been sleep disturbance in the first few weeks of usage.  In order to avoid the sleep disturbance many MS patients are started on a lower dose of LDN, 1.5 mg to 2 mg for a few weeks to a month.  After a month, most people can take the full 3 mg capsule without it causing any disturbance in their sleep.  The individuals who start at the 3 mg dosage and do experience some sleep disturbance might take a magnesium supplement in the evening to help increase their relaxation, and might take a very small amount of melatonin, 300 to 500 micrograms (less than one gram) before bed.

There are some rare individuals who can’t seem to tolerate naltrexone at the three milligram dosage.  In those cases Dr. Bihari has suggested that they remain at a lower dosage of 2 mg or even 1.5 mg. 

Expected Results:  
Some people expect an immediate and significant response to naltrexone use.  Although this may occur in a small number of cases, Dr. Bihari’s experience has been that naltrexone should be tried for six to nine months before giving up on it. 

It is proposed that LDN works by “tweaking” the pituitary to increase the production and release of endorphins, which “communicate” with and help to regulate the immune system.  It may take some time to correct an imbalanced immune system. 

One person reported that by taking a LDN capsule in the daytime she was able to stop her spasticity. 

The amino acid DL-phenylalanine, has been reported to slow down the breakdown of endorphins and other painkillers.  Daytime use of this amino acid (taken on an empty stomach) may help to sustain the benefit of night time use of naltrexone by maintaining high levels of endorphins.

Fillers:   Check with the pharmacy to make sure either calcium, corn starch or some other fast release filler is used in the naltrexone capsules.  Those with lactose sensitivities need to check for lactose-free capsules.



Low Dose Naltrexone (LDN) and Multiple Sclerosis
By Dr. Bernard Bihari, M.D.
(as reprinted in the Summer 2002 New Horizons)

   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, who was 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 with 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 and studies showed that 50% 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.
   Because of his knowledge of MS as a neurologist and of recent evidence of an autoimmune component in the disease, Dr. Bihari started his daughter’s friend on naltrexone at 3 mg every night at bedtime.  She took it for five years with no further attacks.  At that point, when a particular month’s supply ran out, she stopped it because of some denial that she had MS.  Three and a half weeks later, she developed an episode of weakness, numbness, stiffness and spasms in her left arm and resumed LDN, which she has stayed on since.  This episode and over the 12 years since, she has had no further disease activity.
   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 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 T4 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, funguses, 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.
   Clinically the results are strongly suggestive of efficacy.  Ninety-eight to 99% of people treated with LDN experienced no more disease progression, whether the disease category is relapsing-remitting or chronic progressive.  The original patient on LDN for MS, now on it for 17 years, has not had an attack or disease progression for 12 years since the one missed month which led to an attack.  Dr. Bihari has more than 70 people with MS in his practice and all are stable over an average of three years.  In addition, 2,000 or more people with MS have been prescribed LDN by their family MDs or their neurologists based on what they have read on the LDN website or heard about in internet chat rooms focused on MS.
   Many such patients with MS, not under Dr. Bihari’s care, use the website to review information and e-mail their questions.  Many prescribing physicians do not generally know about LDN.  Only once has a patient reported disease progression while on LDN.  In this case, it showed itself five days after he had started the drug.  The onset of the episode had apparently preceded the start of LDN.
   In addition to the apparent ability of LDN to stop disease progression, approximately 2/3 of MS patients starting LDN have some symptomatic improvement generally apparent within the first few days.  The two types of such improvement are reduction in spasticity when this is present, sometimes allowing easier ambulation when spasticity in the legs has been a prominent element of a patient’s difficulty in walking or standing.  This is unlikely to represent a direct effect of LDN on the disease process, but rather reduction in the irritability in nervous tissue surrounding plaques.  Endorphins have been shown to reduce irritability of nervous tissue, i.e. by reducing seizures in patients with epilepsy.  The other area of symptomatic improvement in some patients is a reduction in MS-related fatigue.  This is, also, not likely due to direct effect on the MS disease process, but rather an indirect one caused by restoration of normal endorphin levels improving energy.
   It should be emphasized that in spite of the plentitude of clinical experience described above, in the absence of a formal clinical trial of LDN in MS, these results cannot be considered to be scientific, but rather anecdotal.
   A clinical trial, preferably by a pharmaceutical company with some experience with MS, is clearly needed to determine whether these results can be replicated.  If they can be, they are likely to lead to widespread use of this extremely non-toxic drug in the treatment of MS. 
Dr. Bihari is retired at this time (2009).

EDITOR’S COMMENT:    Many people taking LDN for the first two weeks at dosages of 3 or 4.5 mg will experience difficulty sleeping for the first two weeks.  Due to this temporary sleep disturbance some people may feel worse.  Within a few weeks the body adjusts to the evening dose of LDN and most people report sleeping much better than before LDN use.  There are also a small number of extremely sensitive individuals whose bodies just cannot tolerate the dosage of 4.5 or even 3 mg a day.  Some of them might find they do well on 1.5 or 2 mg a day.  


2008   UPDATE:

The above three articles were written many years ago.  Since that time LOW DOSE NALTREXONE has been tried by thousands of MS patients, as well as many people with other autoimmune disorders.   Although not all MS patients have experienced benefits, many of them have.  A consumer based interest in LDN has engaged some parts of the medical community, and in the last year or so, several clinical studies have been undertaken to determine the actual potential of this treatment for neurological disorders as well as autoimmune Crohn’s disease.  Here is a summary of the some of the recent studies. 

For a thorough investigation of LOW DOSE NALTREXONE, go to the website dedicated to documenting the history of its use with various patient groups at:




After years of consumer interest in the potential of LDN to help MS patients, several animal and human studies have been undertaken or reported in the last two years. 


Animal Model of MS Treated with 2 Different Dosages of Naltrexone:

Dr. Ian Zagon, PhD, at Pennsylvania State University in Hershey, Pennsylvania, focused on an animal study of experimental autoimmune encephalomyelitis (E.A.E.), which is a model of MS.  The research results gave verification to his hypothesis:  that a high dose of naltrexone would actually exacerbate the course of the disease in the animals, while a low dose would delay the development and reduce the severity of the disease process.  This research study brings new evidence to support the role of opioids (naltrexone raises levels of beta endorphin and met-enkephalin, both opioids produced in the human body), and opioid receptors in the progression or delay of MS.   


8 Week Study of MS Quality of Life Inventorywith 4.5 mg LDN with 70 Patients:

This study was done by neurological researcher Dr. Bruce Cree from the University of California in San Francisco.  Each subject was given LDN or a placebo for the first 8 weeks of the study.  After a week without any product, the patients were then switched (this is a cross-over study) to the opposite product, either LDN or placebo, so that all patients who completed the study were on LDN for 8 weeks.   The patient self-reported results indicated that during treatment with LDN they did experience improvement in their level of pain, their sense of well being and their cognitive function.   These improvements were experienced regardless of the age or disease level of the participants, and whether they were on Copaxone or interferon beta.  The physical symptoms of MS, which usually include fatigue, visual disturbances, and bowel and bladder control problems were not affected during this short study.


40 Patient 6-Month Trial of LDN in PPMS (Primary Progressive MS):

Italian neurological researcher, Dr. Maira Gironi led a six-month study of PPMS patients on LDN.  This study looked not only at the safety and tolerability of patients on LDN, but also at changes in their typical symptoms of fatigue, pain, depression, spasticity and quality of life.   Dr. Gironi’s research determined that blood levels of beta-endorphin did increase in response to LDN use.  The research team also measured  a significant decrease in spasticity in the trial group by the end of the study.   During the six-month study, only one patient, of the 35 that completed the trial, experienced further neurological progression.  Considering the lack of treatment options for PPMS, these results are very encouraging for this group of MS patients.  


Anti-inflammatory Effects in Brain Cells from Naltrexone in Animal Studies:

Inflammation has been implicated in all kinds of disease states, including neurodegenerative disorders such as Parkinson’s disease, Alzheimer’s disease and MS.  Dr. J. S. Hong, Ph.D., under the auspices of the National Institute of Environmental Health Sciences, led some animal studies with several morphine-type drugs, which are drugs that cause effects on morphine receptor sites.  Both naltrexone and naloxone were two of the drugs that were used in these animal studies.  His research team studied and reported on the role for these types of medications to modulate inflammatory reactions in microglia brain cells with the potential for reducing the progression of neurodegeneration by providing a protective role.   The full report from this research appears in the January 2007 issue of Nature Reviews Neuroscience [8(1):57-69]. 

Note:  LDN has also shown positive results in Crohn’s disease patients from 2 studies carried out at Penn State.  Check out the LDN website for more information on that:


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