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Low Dose Naltrexone also known as LDN

 

Allot of people in our group have started using LDN.  Keeping this in mind, I thought it was about time we had some information on this medication as well as personal experiences so that others who are interested would be able to make a more educated decision as to whether it is for them or not.  To date I have to honestly say that I have not yet heard anyone on LDN complain of any side effects from its use. 

With permission, I am posting the personal experiences of some chatters who use the LDN.  If you or someone you know is using LDN, please email me your story and permission to post it here.  We are looking for personal experiences both good and bad. 

Personal experiences with LDN

About LDN

Some side effects of LDN

New Private forum!  No more pop up adds.

 

Joan also known as MSBunny's story:

Joan started LDN after hearing stories of other chatters who had great success with it.  Joan reported to me that after the first 2 weeks she noticed she no longer had a soft hard to understand voice...she described it as a retarded sounding voice.  She said her voice became both louder and stronger.  She no longer has to strain to speak.   After another 2 weeks she reports that she felt stronger over all.   Joan has not been on LDN very long.  In fact, she has only been on it a little over a month now maybe 2.   As she sees more improvements in her symptoms and over all healthy with this medication she will let me know and I'll keep updating her story.  So far she has high hopes and is continuing her use of LDN.   Here are her own words on LDN.

IT IS NOT A CURE BUT IT IS THE BEST AND CLOSEST THING WE HAVE TO ONE. A PERSON CAN TAKE LDN BY ITSELF OR WITH ANOTHER TREATMENT BUT ONE CAN’T TAKE LDN WITH ANOTHER CONTROL SUBSTANCE. LDN IS A PRESCRIBED MEDICATION. IF YOU CANNOT FIND A DOCTOR WHO WILL GIVE YOU THE PRESCRIPTION, YOU CAN HAVE A TELEPHONE CONSULTATION WITH ONE OF THE DOCTORS LISTED AT THE YAHOOGROUP SITE. TO LEARN MORE GO TO WWW.YAHOOGROUP.COM. LDN DOES NOT COST A LOT; APPROXIMATELY $30.00 PER MONTH. THE PRESCRIPTION HAS TO BE FILLED AT A COMPOUNDING PHARMACY. IN ONLY 6 WEEKS LDN WILL IMPROVE YOU AND IT HAS BEEN 2 WEEKS I SEE A DIFFERENCE.   LDN IS NOT PERFECT BUT IT DOES HELP.   I DON’T KNOW WHY THE NATIONAL MS SOCIETY HAS NOT SAID ANYTHING MORE ABOUT IT. I DON’T KNOW EVERYTHING ABOUT IT, BUT I KNOW SOME. I WILL CONTINUE TO UPDATE MY PROGRESS. IF YOU WISH TO CONTACT ME ABOUT THIS YOU MAY AND MY E-MAIL ADDRESS IS: JMARCHILDON@PEOPLEPC.COM.

 

Another personal experience from the husbands view of his wife who has been dealing with MS:

 I WOULD SAY IT TOOK MY WIFE ABOUT SIX WEEKS WHERE SHE STARTED TO FEEL BETTER AND STRONGER.   AFTER THE FIRST MONTH OF TAKING IT SHE WAS TOLD TO STOP THE BETAS RON WHICH SHE DID AND THEN IN A FEW WEEKS SHE SEEMED TO GET STRONGER AND STARTED TO WALK WITH HER WALKER WITHOUT ME HELPING HER AT ALL.

SHE ALSO STOPPED WEARING THE POISE PADS AND SHE WOULD WEAR THEM 24/7 BUT HER INCONTINENCE IMPROVED THAT MUCH THAT THE URGENCY JUST STOPPED.  SHE STILL MIGHT HAVE TO GO TO THE BATHROOM MORE THEN THE AVERAGE PERSON BUT SHE DOESN'T HAVE TO HURRY ANYMORE.

EVERYONE THAT SEES HER TELLS HER THAT SHE LOOKS SO MUCH BETTER AND JOAN HER ATTITUDE HAS IMPROVED ALLOT SINCE TAKING THE LDN. SHE IS TAKING 4.5 MG CAPSULE ONCE A DAY BETWEEN 9PM AND 10PM. SHE NEVER HAD ANY SIDE EFFECTS FROM IT EITHER.

HER DOCTOR TOLD HER THAT THINGS SHOULD GET BETTER YET AS TIME GOES BY, AND WE SURE HOPE SO.

SHE WILL NEVER GO BACK TO THE ABC-R MEDS AGAIN SINCE THE LDN HAS IMPROVED HER THIS MUCH. WE DIDN'T HAVE ANY GREAT MIRACLES BUT WE DID HAVE A FEW SMALL ONES SO FAR.

IT'S SURE WORTH A TRY AND SO MUCH LESS EXPENSIVE THE THE ABC MEDS.

BEST OF LUCK TEE

 

LDN and Multiple Sclerosis (MS)


 

In Brief

Over the past few years, growing experience with the clinical use of LDN demonstrates its consistency in preventing further attacks in people with MS. In addition, a majority of such patients note reductions in spasticity and fatigue.

[Ed. note: Patients who are exposed to undue fatigue, heat, or a febrile illness may demonstrate a recurrence of prior symptoms, stemming from an area of old neurologic involvement. These areas tend to have increased irritability of nervous tissue surrounding old healed MS scars ("plaques"). Such an episode may be very transient and may not represent a true relapse.]

 

Recent Developments

As of March 2002:

Clinically the results are strongly suggestive of efficacy. Ninety-eight to 99% of people treated with LDN experience no more disease progression, whether the disease category is relapsing-remitting or chronic progressive. Dr. Bihari has more than 70 people with MS in his practice and all are stable over an average of three years. 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 that led to an attack.

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 e-mail link on the LDN website to ask 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 two-thirds of MS patients starting LDN have some symptomatic improvement generally apparent within the first few days. There are two types of such improvement:

· One is 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, e.g., 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 a direct effect on the MS disease process, but rather an indirect one caused by restoration of normal endorphin levels improving energy.

Patients who are in the midst of an acute exacerbation when they start LDN have generally shown rapid resolution of the attack. In two patients, chronic visual impairment due to old episodes of optic neuritis has shown fluctuating improvement.

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 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.

 

Noteworthy Cases

In May 2000, Bernard Bihari, MD reported four occurrences of surprisingly rapid clinical improvement in people with multiple sclerosis, presumably related to LDN use. Three were female patients for whom Dr. Bihari had prescribed nightly LDN.

As of March 2002, all four have sustained the improvement originally seen. Since those four cases were first reported, there have been several dozen more patients who have had similar relief of spasticity allowing better ambulation and relief of MS-related fatigue.

The occurrences Dr. Bihari originally reported in May 2000 were as follows:

A 31-year-old patient has a history of relapsing-remitting MS, and recently had developed not only slurred speech and trouble finding the right word (dysphasia) but also had noted weakness in one hand and one leg. She started LDN and reported that within one week her problems with speech had substantially cleared,and there was a marked improvement in her gait and in the use of her hand.

The patient who is 44 years old has chronic progressive MS (as do the other two women to be discussed below). She had reached the point some time ago where she needed to use a walker in the home in order to get around. On the third night after starting LDN, she got up and went to the bathroom without using the walker — for the first time in two years. She reports having experienced a prompt 20%-30% improvement in her balance, apparently due to decreased spasticity.

The third patient, a woman in her early 50's, reported prompt improvement in walking within four days after starting LDN, apparently due to decreased spasticity.

The fourth case came to Dr. Bihari's attention in late April 2000 when a woman telephoned his office to leave a message of thanks for him. She has the diagnosis of MS and for the past ten years has had variable visual impairment in one eye, to the extent that she has had to wear eyeglasses to mask that eye. She said her neurologist had begun to prescribe LDN three months earlier. Within two days after starting LDN she regained unimpaired binocular vision. She said that she had recently forgotten to take her LDN at bedtime for two nights in a row, and the eye problem returned — only to subside within a day or two after restarting the medication.

 

Background

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. 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 cleared 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 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

"http://www.lowdosenaltrexone.org/index.htm"

Please Note:

Fundamental questions and answers concerning LDN can be found on the LDN Homepage and on other pages of this website focused on specific diseases such as cancer, HIV/AIDS, and MS.

This page contains other questions frequently asked, along with corresponding answers.

Can LDN be taken with other medications such as tranquilizers or chemotherapy? How about interactions with alcohol or tobacco?

LDN can be taken along with any other medication or substance, so long as it is not narcotic-containing. Naltrexone is a pure opioid antagonist and it will block the action of narcotics. Some examples of narcotic-containing drugs are Ultram, morphine, Percocet, Duragesic patch and any codeine-containing medication.

Can LDN be taken along with any of the standard medications for multiple sclerosis?

It can, and many people with MS do this. However, all of the standard MS drugs, with the probable exception of Copaxone, are immunosuppressant and thus tend to oppose the beneficial immune system upregulation induced by LDN. Therefore, many people with MS try to wean themselves away from these other medications when they find that they are doing well on LDN.

What is the best dosage of LDN to begin treatment with?

For an adult who is not significantly below the normal weight range, the optimal dose of LDN is 4.5mg, taken each night at bedtime; i.e., between 9pm and 3am. One can begin at this dose level. If one were to develop persistent sleep disturbance (i.e., a sleep disturbance lasting longer than 10 to 14 days) after starting LDN, which occurs in less than 2% of users, then the dose may be decreased to 3mg or 2mg.

If I have to work on a night shift, for example from midnight to 8a.m., at what time should I take my LDN?

Continue to take LDN as recommended above; i.e., between 9pm and 3am. This relates to the fact that the endorphins for each day are always produced in the pre-dawn hours, regardless of the hours when one is awake or sleeping.

If LDN is so wonderful, why isn't it FDA-approved or reported in one of the respected medical journals?

Although the Food and Drug Administration approved naltrexone at the 50mg dosage in 1984, "low dose naltrexone" ( LDN ) in the 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 tens of millions of dollars. In the absence of such a current scientific clinical trial, medical journals tend not to be interested in "anecdotal" reports of therapeutic successes.

Can you supply me with the names of physicians in my town who prescribe LDN?

Sorry, we have no such lists of physicians. But any physician may ethically and legally prescribe LDN as an off-label prescription. If you are very interested in starting LDN, and you are absolutely unable to find any local doctor who will prescribe it for you—even though you have shown them information from the website and made it clear to them that LDN is compatible with any other medicine (except narcotics) and that it has no toxicity and no significant side effects—then you may want to set up a consultation with LDN's discoverer, Bernard Bihari, MD. Such consultations are done either by a visit to his office or through a very prolonged telephone interview. His office telephone number in New York City is 212-929-4196.

Can I have my LDN prescription filled at any pharmacy?

Low dose naltrexone prescriptions are generally filled at a compounding pharmacy. The druggist uses either generic naltrexone 50mg tablets or bulk naltrexone powder to prepare the LDN capsules. Because there have been occasional reports from patients of a poor quality product coming from scattered pharmacies, we feature the names of several pharmacies on the website that have shown themselves reliable and experienced in correct LDN preparation. (Please note: Under no circumstances should you accept a preparation of "long-acting" or "slow release" naltrexone.)



About LDN: FDA-approved naltrexone, in a low dose, can up-regulate the immune system -- helping those with HIV/AIDS, cancer, MS, and autoimmune diseases such as systemic lupus, rheumatoid arthritis, Behcet's syndrome, Wegener's granulomatosis, bullous pemphigoid, psoriasis, and Crohn's disease.

 

NALTREXONE -- A SHORT OVERVIEW
Naltrexone (17-(cyclopropylmethyl)-4,5 alpha-epoxy-3, 14 dihydroxymorphinan-6-one) is an analogue of Naloxone and is a relatively pure narcotic antagonist. It is available as an oral semisynthetic compound, which is similar to Naloxone in structure. Its relative antagonistic potency in human studies as reported by Martin et al, and Crabtree B.L 1984, is approximately 17 times that of Nalorphine and about twice that of Naloxone. On administration of 50mg, following a three doses per week schedule, peak plasma concentration was achieved after one hour with almost complete absorption. It is mainly excreted in the urine with 60% of an orally administered dose recovered over a 48-hour period and only 23% excreted in the faeces. It has a half-life of about 10 hours and is approximately 20% bound to protein.

Naltrexone is primarily employed as an adjunct in the therapy of social and psychosocial rehabilitation during the recovery of narcotic addicts, and also partly in the treatment of alcohol dependence. Verebey et al, 1976, showed that 50mg of Naltrexone produced effective blockade of 25mg IV heroin challenge for 24 hours, while 100mg and 150mg blocked narcotic effects for 48 hours and 72 hours respectively. They observed that after the oral administration of 100mg doses, the effects of heroin were blocked for three (3) days as follows: day 1, 96%: day 2, 87%: and on day 3, 46%. Wall et al, 1981, and Bullingham et al 1983, observed that Naltrexone is metabolized in the liver to Beta-Naltrexol which is a weaker antagonist but may contribute to the long duration of action. Bullingham, while working on animals showed that although Beta-Naltrexol is very much weaker than Naltrexone as a narcotic antagonist, its effects last between 4 to 9 times longer. Gritz et al, 1976, reported that no significant cardiovascular toxicity was observed during treatment, however, Martin et al, 1973 and Thomas et al 1976, reported small increases in blood pressure, although these changes may not be clinically significant. About the CNS, Crowley et al 1985, said Naltrexone may induce mild dysphoria in former opiate addicts long after they have stopped using opiates . They suggested that this phenomenon might contribute to the high rate of non-compliance among addicts who receive Naltrexone. Mendelson et al, 1979, and Hollister et al 1981, reported mental confusion, depression, and fatigue in healthy subjects, while other studies reported anxiety, nervousness and sleeping difficulty in 10% of patients receiving Naltrexone. In 1974, Tornabene showed that in patients with narcotic addiction, Naltrexone reversed the effects of the narcotic analgesia producing withdrawal symptoms within five minutes of its ingestion and said that such patients with narcotic addiction should be detoxified before Naltrexone administration. It has been recommended that patients must be opioid-free for 7 to 10 days before initiating Naltrexone treatment. Naltrexone will help patients who have alcohol problems by keeping the body from wanting alcohol. Also, it helps former drug users stay off drugs, but it is not a substitute for active involvement in a recovery program.

Some of the major side effects produced by Naltrexone are:

Severe stomach pains,
Yellowing of the eyes or skin,
Dark colored urine.

Some minor side effects are;-

Diarrhea or constipation,
Headache,
Joint or muscle pain,
Mild stomach pain,
Nausea or vomiting,
Nervousness and sleeping trouble.

Naltrexone produces its effects by competitively displacing opiate molecules at opiate receptor sites as well as by blocking the narcotic access to the opiate receptor sites. Schecter 1980, and Willette, 1982, reported that when Naltrexone is administered to normal individuals or drug-free addicts, no significant effects were observed, but that the drug can block the euphoriant effect of the opiates, suggesting that this type of antagonism would create the proper conditions for eliminating the drug taking response by eliminating re-enforcement of opiate-taking behaviour, especially in the addicts old copping area.

Although Naltrexone is considered a pure narcotic antagonist, serum studies have described agonist-like effects in healthy subjects. Malley et al, 1992, and Volpicelli et al, 1992, said that the endogenous opioid system may modulate the intake of alcohol. They reported, using animal data, that high alcohol consumption is associated with endogenous opioid activity and proposed alterati on in opioid receptor activity through the use of an opiate antagonist such as Naltrexone, to decrease alcohol craving and so decrease drinking of alcoholic beverages; and in 1995, Volpicelli et al, reviewed the role of Naltrexone in the pharmacological a nd psychosocial treatments for alcohol dependence. In 1996, they carried out double-blind placebo controlled trials and further confirmed that patients receiving Naltrexone reported significantly less craving for alcohol. Naltrexone had its most import ant effect in decreasing subsequent drinking once intake of alcohol occurred, thus helping prevent the desire for the next drink. They conducted a six-month follow-up study after discontinuation of Naltrexone therapy for alcohol dependence, which indicate d benefit that tended to diminish with time. They suggested that continued treatment beyond 12 weeks might be useful in some individuals.

Because of its effects on endogenous alpha-interferon, Naltrexone has been studied in AIDS patients by Abb et al, 1984, and Skurkovich et al, 1987, as a possible immuno-modulator in response to foreign antigen but the data has been inconclusive. In an uncontrolled study, using 200mg Naltrexone daily on 5 bulimic women for 6 weeks, Jonas and Gold 1984,noticed that the number of days per week with binges was reduced by the second week of treatment; the number of days with purging was reduced by the fourth week and that there was also a reduction in the duration of the bingeing episodes, which occurred by the sixth week. At the same time, no mood changes were observed. They concluded that more studies were required to truly evaluate the efficacy of Naltrexone in Bulima including comparisons with tricyclic antidepressants. In a controlled study by Mitchell et al, 1989, using 50mg orally nightly, in the treatment of bulimia, reported that this low dosage was no more effective than placebo in normal-weight outpatient women, but they suggest that there is some benefit it at higher doses of 200mg to 300mg daily. Huseman 1990, made similar observations to that of Mitchell et al, using 10 normal-weight women with 50mg Naltrexone daily, but also found significantly elevated levels of beta-endorphins in 6 out of 8 patient s correlated with frequency of binge behavior. In one uncontrolled trial by Sonne et al ,1996, 5 patients, age 26 to 36 years, were followed-up for three weeks. No medication was given during week one and week three. During week 2, 50mg Naltrexone daily was given to 4 patients and 100mg daily given to 1 patient due to concomitant Carbamazepine therapy which is thought to induce Naltrexone metabolism. They observed that self injurious thoughts and behaviors decreased significantly during therapy from an average 15.2 to 5.1 daily.(p= <0.05); but also indicated further studies necessary.

Leboyer et al, 1988, observed decreasing self injurious behaviour (SIB) in 2 autistic girls age 10 and 12 years during Naltrexone therapy using 1-2mg/kg daily. Kars 1990, also noticed decreasing frequency of SIB, during a double blind placebo controlled cross over study with 50mg Naltrexone daily for 3 weeks. Campbell 1990, reported a reduction in hyperactivity and fidgetiness with Naltrexone and said that the most consistent symptom changes observed in each of a group of 18 autistic children, 14 male s and 4 females, were decreases of withdrawal, increase of verbal production and communicative speech, but in 1993, with 41 autistic children, only a small beneficial effect on decreasing SIB was observed. It was also shown by Bystritsky and Strauser, 1996,in a 46year old male, who had a history of obsessive compulsive disorder that 50mg per day of Naltrexone was effective in the termination of cutting behavior but the cutting behavior recurred when Naltrexone was discontinued.






 

 
 
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