Low Dose Naltrexone & Second-Hand Smoke

There is ongoing research regarding the benefits of low dose naltrexone (LDN) in MS patients.  Naltrexone was originally approved by the FDA (in 1984) for the purpose of helping heroin or opium addicts.  It did this by blocking the effect of the drugs. "By blocking opioid receptors, naltrexone also blocks the reception of the opioid hormones that our brain and adrenal glands produce: beta-endorphin and metenkephalin. Many body tissues have receptors for these endorphins and enkephalins, including virtually every cell of the body's immune system."  Subsequently, in 1985, a physician discovered the effects of a much smaller dose of naltrexone on the body's immune system. "He found that this low dose, taken at bedtime, was able to enhance a patient's response to infection by HIV, the virus that causes AIDS."  The phycisian learned in the 1990s that cancer patients and patients with autoimmune diseases could also benefit from LDN. 

Information from http://www.lowdosenaltrexone.org/:

Up to the present time, the question of "What controls the immune system?" has not been present in the curricula of medical colleges and the issue has not formed a part of the received wisdom of practicing physicians. Nonetheless, a body of research over the past two decades has pointed repeatedly to one's own endorphin secretions (our internal opioids) as playing the central role in the beneficial orchestration of the immune system, and recognition of the facts is growing.
The brief blockade of opioid receptors between 2 a.m. and 4 a.m. that is caused by taking LDN at bedtime each night is believed to produce a prolonged up-regulation of vital elements of the immune system by causing an increase in endorphin and enkephalin production. Normal volunteers who have taken LDN in this fashion have been found to have much higher levels of beta-endorphins circulating in their blood in the following days.
In general, in people with diseases that are partially or largely triggered by a deficiency of endorphins (including cancer and autoimmune diseases), or are accelerated by a deficiency of endorphins (such as HIV/AIDS), restoration of the body's normal production of endorphins is the major therapeutic action of LDN.

Regarding its efficacy in patients with autoimmune diseases, including MS, the website states, "Within the group of patients who presented with an autoimmune disease, none have failed to respond to LDN; all have experienced a halt in progression of their illness. In many patients there was a marked remission in signs and symptoms of the disease. The greatest number of patients within the autoimmune group are people with multiple sclerosis, of whom there were some 400 [patients]. Less than 1% of these patients has ever experienced a fresh attack of MS while they maintained their regular LDN nightly therapy."

Regarding the question of when LDN will be FDA Approved, the website says:

The FDA approved naltrexone at the 50mg dosage in 1984. LDN (in the 3mg or 4.5mg dosage) has not yet been submitted for approval because the prospective clinical trials that are required for FDA approval need to be funded at the cost of many millions of dollars.
The successful results of the first US medical center research on LDN, an open-label trial that tested the use of LDN in Crohn’s disease, was presented in May 2006 by Professor Jill Smith of the Pennsylvania State University College of Medicine. The National Institutes of Health has granted $500,000 for Dr. Smith's group to continue the study as a larger placebo-controlled scientific trial of LDN in Crohn's disease.
All physicians understand that appropriate off-label use of an already FDA-approved medication such as naltrexone is perfectly ethical and legal. Because naltrexone itself has already passed animal toxicity studies, one could expect that once testing is able to begin, LDN could complete its clinical trials in humans and receive FDA approval for one or more uses within two to four years.

Note: It appears as though this website is up to date (at least as of December 2010).

I received an email regarding LDN in a mailer sent out by the Multiple Sclerosis International Federation.  The email, discussing research published last month, said:

The use of low dose naltrexone (LDN) in patients with MS in clinical practice is controversial. This study examined the long term effects of the opioid growth factor (OGF, [Met5]-enkephalin) and LDN on expression of myelin oligodendrocyte glycoprotein (MOG)-induced [experimental autoimmune encephalomyelitis] (EAE). The results indicate that treatment with LDN and OGF had no deleterious long-term repercussions and did not exacerbate EAE, but i) halted progression of disease, ii) reversed neurological deficits, and iii) prevented the onset of neurological dysfunction across a considerable span of time.

That may not make a whole lot of sense, but I think the important take-away is that no harmful, long-term, side-effects of LDN were noted, but results showed that LDN halted the progression of the MS disease, reversed neurological deficits, and prevented the onset of additional neurological dysfunction.

I think we should really be looking into this more!  It sounds like it is a promising option for treating MS, but has not gained enough notoriety and funding to get FDA approval.


Another area of research that was discussed in the mailer from the Multiple Sclerosis International Federation was regarding second-hand smoke and its association with an increased risk of developing MS.  The mailer stated:
Exposure to environmental tobacco smoke is associated with increased risk for MS:

This interesting population-based case-control study reports the incidence of passive smoking in patients with MS and controls who had never smoked. Through comparison of rates of the incidence of multiple sclerosis among never-smokers who had been exposed to passive smoking and comparison with that of never-smokers who had never been exposed, an odds ratio was calculated of 1.3 (95% CI 1.1-1.6). The authors also found that the risk increased with increasing duration of exposure to passive smoke.
The authors conclude that passive smoking is associated with an increased risk of developing MS, and that the underlying mechanism may relate to irritation within the lung, as oral tobacco in the form of moist snuff is not associated with increased risk.

The increased risk of developing MS by smoking was discussed in the 2/14/11 Teleconference.  I didn't pay too munch attention to it, however, because I have never smoked so it clearly didn't apply to me.  However, this study seems to show that ANY exposure to cigarette smoke is associated with an increased risk of developing MS.  This is disturbing, considering most public places, including restaurants had "smoking sections" (where you, in the non-smoking section, could still smell the smoke) until very recently.  I am sure there are still places that allow smoking in public places, but luckily many towns/cities across the country have banned smoking in bars and restaurants.  I was rarely exposed to smoke as a child, but I do recall being at restaurants, in the "non-smoking section" and being bothered by the smoke wafting in from the "smoking section."  As I grew older, I was exposed to smoke a little more although I tended to avoid it at all costs.  I cannot say that I believe that second-hand smoke was a major contributing factor to me developing MS, but, according to this study, it could have played a small role.  So the lesson to be learned is that smoking is bad, whether you are the smoker or just around smokers.  I know this is not new, earth-shattering news, but it is one more way we know that smoking is bad.