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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
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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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