Looks pretty fishy to me. Any substance that is supposed to cure that
many diseases is not likely to actually cure anything. I might be wrong,
but I doubt it.

Here's the list:
Autoimmune diseases
multiple sclerosis, systemic lupus erythematosus (SLE/LED), rheumatoid
arthritis, ankylosing spondylitis, pemfigoidi, sarcoidosis, scleroderma,
Crohn's disease, ulcerative colitis aka colitis ulcerosa, Celiac
disease, psoriasis, Wegener's granulomatosis, transverse myelitis

Cancers
bladder cancer, breast cancer, carcinoid tumor, colorectal cancer,
glioblastoma, liver cancer, non-small cell lung cancer (NSLC), chronic
lymphocytic leukemia, lymphoma (both Hodgkin's and non-Hodgkin's),
melanoma, multiple myeloma, neuroblastoma, ovarian cancer, pancreatic
cancer, prostate cancer, renal cell carcinoma, throat cancer, uterine
cancer

Other illnesses
HIV/AIDS, hepatitis C, amyotrophic lateral sclerosis (ALS)/primary
lateral sclerosis (PLS), autism, Alzheimer's disease, Parkinson's
disease, Behcet's disease, chronic obstructive pulmonary disease (COPD,
emphysema), endometriosis, fibromyalgia, chronic fatigue
syndrome/myalgic encephalomyelitis (CFS/ME), irritated bowel syndrome
(IBS)

Possible indications
myasthenia gravis, eczema, asthma, allergies, narcolepsy, chronic Lyme
disease/post Lyme syndrome, acne, rosacea, insomnia and some other sleep
disorders, migraine, depression, chronic urticaria (hives), interstitial
cystitis, obsessive compulsive disorder (OCD), type II diabetes,
dementia, post-traumatic stress disorder (PTSD), schizophrenia

Impressive... but hard to believe.
Thomas

quack quack quack, it is a duck?  so how does it walk?  like a duck? well,
LDN is an agent for releasing the addictive clutch that opiates have on the
body, over a long term rather than the on-scene rescue agent used by
paramedics on overdose victims. But it is a close cousin.  It has been found
to not only relieve addiction withdrawls, but also have beneficial effects
on the autoimmune system.  It was first cross-prescribed for control of
Crohn's Disease, and it appears to work (study 2007, see abstract NIH.GOV)

I copied the files below from:
http://neurotalk.psychcentral.com/thread46492.html  There appear to be a lot
more articles and discussions on LDN and potential benefits.  Therefore I
suspect a duck is indeed a duck.  And this is not quackery, as it appears to
be cross-precribed for Parkinson's Disease patients, the only limitation of
beneficial effects appear to be receptor issues in individual patients (?).

Google this: Low Dose Naltrexone Hepatitis C?

This stuff has some kind of promise for people that are infected with Hep C
and other killer bugs, but as yet sits parked because specialized medicine
is so scattered all over the map and does not seem to understand teamwork on
testing and symptoms issues.  This may stay on the shelf, right next to the
gizmo that can reduce viral load in the bloodstream.  The only reason we see
small molecule research for Hep C treatment now at this late stage is
because of the high incidence of co-infection with HIV, where small molecule
medicine was first investigated, and where they have a lot more grant money
to experiment and prove treatments.

Hey chuck, thanks for bringing this up here.  Where did you hear about LDN?

-cactus jammies-

Clinical Studies demonstrating Naltrexone's Beneficial Effects to the Liver:
The following are nine Clinical Studies which demonstrate the safety and
very beneficial effects of Naltrexone to the liver for dosages below 300 mg
a day. While the below are not specific to Low Dose Naltrexone (which is
taken in much smaller dosages of approximately 1 to 4.5 mg a day), the below
studies demonstrate the beneficial affect that opioid antagonists can have
in liver disease in the following ways:
1.Reducing Liver Enzymes Levels, including Hepatitis (Studies 1 & 2)
2.Reducing Liver Damage in Hepatitis (Study 3)
3.Reducing Liver Injury in Cholestasis (Study 4)
4.Reducing Liver Enzymes in Cholestasis (Study 5)
5.Reducing Liver Fibrosis (Study 6)
6.Anti-inflammatory effects & improving hepatic dysfunction (Study 7)
7.Benefits in Cholestatic Pruritus (Studies 8 & 9)
All of the below Clinical Studies / Articles are quoted from the National
Institutes of Health / National Library of Medicine/Pub Med Website:
(http://www.ncbi.nlm.nih.gov/sites/entrez?db=pubmed)
****************************************
Study 1 - Benefit of reducing liver enzyme (ALT/AST) levels:
Study of hepatotoxicity of naltrexone in the treatment of alcoholism.
Alcohol. 2006 Feb;38(2):117-20. Links
Yen MH, Ko HC, Tang FI, Lu RB, Hong JS.
Department of Pharmacology, National Defense Medical Center, Taipei, Taiwan.
Since a black box warning was issued by the Food and Drug Administration
regarding the use of the opiate antagonist naltrexone (NTX), many clinicians
have been concerned about current labeling of the potential hepatotoxicity
risk of NTX in the treatment of opiate dependence and alcoholism. Despite
many reports that demonstrated that the use of NTX did not cause elevation
of liver enzymes, controversy concerning whether NTX is hepatotoxic
continues. The current study monitored 74 alcoholic patients who received
25mg of NTX daily in the first week and then 50mg of NTX daily for the rest
of the 12-week period. After the 12-week treatment, levels of the hepatic
enzymes alanine aminotransferase (ALT) and aspartate aminotransferase (AST)
did not show any elevation, except in one subject, and the results strongly
support that NTX did not induce abnormalities in liver function tests or
elevate the liver enzymes. Instead, a statistical significance of decreasing
levels of ALT and AST in the liver was shown throughout the study. These
findings provide further support that NTX is not hepatotoxic at the
recommended daily dose and may be beneficial for patients with elevated
liver enzymes.
PMID: 16839858 [PubMed - indexed for MEDLINE]

*******************************************
Study 2 - Benefit of reducing liver enzyme levels in Hepatitis C patients:
Effect of methadone or naltrexone on the course of transaminases in
parenteral drug users with hepatitis C virus infection

[Article in Spanish]
Lozano Polo JL, Gutiérrez Mora E, Martínez Pérez V, Santamaría Gutiérrez J,
Vada Sánchez J, Vallejo Correas JA.
Hospital Santa Cruz de Liencres,Servico de Medicina Interna, Cantabria.

A prospective study was conducted on the evolution of serum transaminases in
116 patients infected with hepatitis C virus (HCV), parenteral drug abusers,
included for 6 months in treatment programs with methadone, naltrexone or
"drug free" regimen. Treatment with methadone or naltrexone did not result
in a transaminase increase in these patients. In contrast, patients included
in the drug-free program appear to have a higher increase in serum
transaminase levels than those treated with methadone or naltrexone (146.1
+/- 122.29 vs 91.88 +/- 81.96 and 86.99 +/- 64.26 Ul/ml, respectively). Such
an increase originated mainly from patients who anytime during follow-up had
a liver necrosis outbreak in the acute hepatitis range, and is offset if,
instead of a given transaminase value, we consider a simplified liver
necrosis index (1.28 +/- 0.74 vs 0.95 +/- 0.72 and 1.01 +/- 0.65,
respectively; p > 0.05). HIV infected patients have serum transaminase
values similar to those in HIV-negative patients (80.61 +/- 58.81 vs 113.63
+/- 99.59, respectively; p > 0.05).
PMID: 9411543 [PubMed - indexed for MEDLINE]
Note: Basically, the above study showed that ALT/AST levels of those with
Hepatitis C who used Naltrexone, had liver enzymes significantly lower
(86.99 +/- 64.26) than those patients who did not use Naltrexone (i.e. were
`drug free' - 146.1 +/- 122.29)
*************************
Study 3 - Benefit by reducing liver damage of hepatitis:
Opioid receptor blockade reduces Fas-induced hepatitis in mice.

Hepatology. 2004 Nov;40(5):1136-43.
Jaume M, Jacquet S, Cavaillès P, Macé G, Stephan L, Blanpied C, Demur C,
Brousset P, Dietrich G.
INSERM U563, Institut Claude de Préval, IFR 30, Hôpital Purpan, Université
Paul Sabatier Toulouse III, Toulouse, France.
Fas (CD95)-induced hepatocyte apoptosis and cytotoxic activity of
neutrophils infiltrating the injured liver are two major events leading to
hepatitis. Because it has been reported that opioids, via a direct
interaction, sensitize splenocytes to Fas-mediated apoptosis by upregulating
Fas messenger RNA (mRNA) and modulated neutrophil activity, we assumed that
opioids may participate in the pathophysiology of hepatitis. Using the
hepatitis model induced by agonistic anti-Fas antibody in mice, we showed
that opioid receptor blockade reduced liver damage and consequently
increased the survival rate of animals when the antagonist naltrexone was
injected simultaneously or prior to antibody administration. Treatment of
mice with morphine enhanced mortality. Naloxone methiodide-a selective
peripheral opioid antagonist-had a protective effect, but the absence of
opioid receptors in the liver, together with lack of morphine effect in
Fas-induced apoptosis of primary cultured hepatocytes, ruled out a direct
effect of opioids on hepatocytes. In addition, the neutralization of opioid
activity by naltrexone did not modify Fas mRNA expression in the liver as
assessed with real-time quantitative polymerase chain reaction. Injured
livers were infiltrated by neutrophils, but granulocyte-depleted mice were
not protected against the enhancing apoptotic effect of morphine. In
conclusion, opioid receptor blockade improves the resistance of mice to
Fas-induced hepatitis via a peripheral mechanism that does not involve a
down-modulation of Fas mRNA in hepatocytes nor a decrease in proinflammatory
activity of neutrophils.
PMID: 15389866 [PubMed - indexed for MEDLINE]

*******************************

Study 4 - Benefit of reducing liver injury:
Opioid system blockade decreases collagenase activity and improves liver
injury in a rat model of cholestasis.

J Gastroenterol Hepatol. 2007 Mar;22(3):406-13.
Kiani S, Ebrahimkhani MR, Shariftabrizi A, Doratotaj B, Payabvash S, Riazi
K, Dehghani M, Honar H, Karoon A, Amanlou M, Tavangar SM, Dehpour AR.
Department of Pharmacology, School of Medicine, Tehran University of Medical
Sciences, Tehran, Iran.
BACKGROUND: Following bile duct ligation (BDL) endogenous opioids accumulate
in plasma and play a role in the pathophysiology and manifestation of
cholestasis. Evidence of centrally mediated induction of liver injury by
exogenous opioid agonist administration, prompts the question of whether
opioid receptor blockade by naltrexone can affect cholestasis-induced liver
injury.
METHODS: Cholestasis was induced by BDL and cholestatic and sham-operated
rats received either naltrexone or saline for 7 consecutive days. On the 7th
day, liver samples were collected for determining matrix metalloproteinase-2
(MMP-2) activity, S-adenosylmethionine (SAM) and S-adenosylhomocysteine
(SAH) content and blood samples were obtained for measuring plasma
nitrite/nitrate and liver enzyme activities.
RESULTS: Naltrexone-treated BDL animals had a significant reduction in
plasma enzyme activity and nitrite/nitrate level. Liver SAM : SAH ratio and
SAM level improved by naltrexone treatment in cholestatic animals compared
to saline-treated BDL ones. Naltrexone treatment in BDL rats led to a
decrease in the level of liver MMP-2 activity, which had already increased
during cholestasis.
CONCLUSION: Opioid receptor blockade improved the degree of liver injury in
cholestasis, as assessed by plasma enzyme and liver MMP-2 activities. The
beneficial effect of naltrexone may be due to its ability to increase liver
SAM level and restore the SAM : SAH ratio.
PMID: 17295775 [PubMed - indexed for MEDLINE]

******************************

Study 5- Reducing Liver Enzymes in Cholestatis
Do endogenous opioids contribute to the bradycardia of rats with obstructive
cholestasis?
Fundam Clin Pharmacol. 2002 Aug;16(4):273-9.
Gaskari SA, Mani AR, Ejtemaei-Mehr S, Namiranian K, Homayoun H, Ahmadi H,
Dehpour AR.
Department of Pharmacology, School of Medicine, Tehran University of Medical
Sciences, Tehran, Iran.

Endogenous opioids have nitric oxide (NO)-dependent cardiovascular actions.
In the light of biological evidence of accumulation of endogenous opioids in
cholestasis and also existence of NO-dependent bradycardia in cholestatic
subjects, this study was carried out to evaluate the role of endogenous
opioids in the generation of bradycardia in a rat model of cholestasis. Male
Sprague-Dawley rats were used to induce cholestasis by surgical ligation of
the bile duct, with sham-operated animals serving as a control. The animals
were divided into six groups which received naltrexone [20 mg/kg/day,
subcutaneously (s.c.)], N(G)-L-nitro-arginine methyl ester (L-NAME, 3
mg/kg/day, s.c.), aminoguanidine (200 mg/kg/day, s.c.), L-arginine (200
mg/kg/day, s.c.), naltrexone + L-NAME (20 and 3 mg/kg/day, s.c) or saline.
One week after the operation, a lead II electrocardiogram (ECG) was recorded
and the spontaneously beating atria of the animals were then isolated and
the chronotropic responses to epinephrine evaluated. The plasma
L-nitro-tyrosine level and alanine amino transferase and alkaline
phosphatase activities were also measured. The heart rate of cholestatic
animals was significantly lower than that of control rats in vivo and this
bradycardia was corrected with daily adminstration of naltrexone or L-NAME.
The basal spontaneous beating rate of atria in cholestatic animals was not
significantly different from that of sham-operated animals in vitro.
Cholestasis induced a significant decrease in the chronotropic effect of
epinephrine. This effect was corrected by daily injection of naltrexone or
L-NAME, or concurrent administration of naltrexone + L-NAME, and was not
corrected by aminoguanidine. L-arginine had an equivalent effect to L-NAME
and increased the chronotropic effect of epinephrine in cholestatic rats but
not in control animals. Bile duct ligation increased the plasma activity of
liver enzymes as well as the level of L-nitro-tyrosine. L-arginine and
naltrexone treatment significantly decreased the elevation of liver enzymes
in bile duct-ligated rats. Pretreatment of cholestatic animals with
naltrexone or L-NAME decreased the plasma L-nitro-tyrosine level. The
results suggest that either prevention of NO overproduction or protection
against liver damage is responsible for recovery of bradycardia after
naltrexone administration.
PMID: 12570015 [PubMed - indexed for MEDLINE]

*********************************

Study 6- Benefit of reducing liver fibrosis:

Naltrexone, an opioid receptor antagonist, attenuates liver fibrosis in bile
duct ligated rats.
Gut. 2006 Nov;55(11):1606-16. Epub 2006 Mar 16.
Ebrahimkhani MR, Kiani S, Oakley F, Kendall T, Shariftabrizi A, Tavangar SM,
Moezi L, Payabvash S, Karoon A, Hoseininik H, Mann DA, Moore KP, Mani AR,
Dehpour AR.
The UCL Institute of Hepatology, Department of Medicine, Royal Free and
University College Medical School, University College London, Rowland Hill
St, London NW3 2PF, UK.
AIM: The aim of this study was to investigate the hypothesis that the opioid
system is involved in the development of hepatic fibrosis.
METHODS: The effect of naltrexone (an opioid receptor antagonist) on hepatic
fibrosis in bile duct ligated (BDL) or sham rats was assessed by histology
and hepatic hydroxyproline levels. Liver matrix metalloproteinase 2 (MMP-2)
was measured by zymography, and alpha smooth muscle actin (alpha-SMA) and
CD45 (leucocyte common antigen) by immunohistochemistry. The redox state of
the liver was assessed by hepatic glutathione (GSH)/oxidised glutathione
(GSSG) and S-nitrosothiol levels. Subtypes of opioid receptors in cultured
hepatic stellate cells (HSCs) were characterised by reverse
transcriptase-polymerase chain reaction, and the effects of selective delta
opioid receptor agonists on cellular proliferation, tissue inhibitor of
metalloproteinase 1 (TIMP-1), and procollagen I expression in HSCs
determined.
RESULTS: Naltrexone markedly attenuated the development of hepatic fibrosis
as well as MMP-2 activity (p<0.01), and decreased the number of activated
HSCs in BDL rats (p<0.05). The development of biliary cirrhosis altered the
redox state with a decreased hepatic GSH/GSSG ratio and increased
concentrations of hepatic S-nitrosothiols, which were partially or
completely normalised by treatment with naltrexone, respectively. Activated
rat HSCs exhibited expression of delta1 receptors, with increased
procollagen I expression, and increased TIMP-1 expression in response to
delta(1) and delta(2) agonists, respectively.
CONCLUSIONS: This is the first study to demonstrate that administration of
an opioid antagonist prevents the development of hepatic fibrosis in
cirrhosis. Opioids can influence liver fibrogenesis directly via the effect
on HSCs and regulation of the redox sensitive mechanisms in the liver.
PMID: 16543289 [PubMed - indexed for MEDLINE]

********************************
Study 7- Benefit of anti-inflammatory effects & improving hepatic
dysfunction:
Effects of naltrexone on lipopolysaccharide-induced sepsis in rats.
J Biomed Sci. 2005;12(2):431-40. Links
Lin SL, Lee YM, Chang HY, Cheng YW, Yen MH.
Department of Anesthesiology, Tri-Service General Hospital, Taipei, Taiwan.

Naltrexone, an opioid antagonist, has been reported to possess an
anti-inflammatory effect via blockade of opioid receptor. The aim of this
study is to evaluate the protective effect of naltrexone on LPS-induced
septic shock in rats. Sepsis was induced by administration of LPS (10 mg/kg,
i.v.) in anesthetized rats. Results demonstrated that pretreatment with
naltrexone (10 mg/kg, i.v.) significantly ameliorated hypotension and
bradycardia of rats 6 h after LPS administration. In isolated blood vessel,
study showed that pretreatment with naltrexone significantly improved
norepinephrine-induced vasoconstriction and ACh-induced vasorelaxation in
aorta of endotoxemic animals. Naltrexone significantly reduced the elevation
of serum glutamate-oxalacetate transaminase and glutamate-pyruvate
transaminase (as index of hepatic function) induced by LPS. The infiltration
of polymorphonuclear neutrophils into liver 48 h after LPS treatment in mice
was also reduced by naltrexone. On the other hand, naltrexone significantly
decreased the levels of plasma TNF-alpha and inhibited overproduction of
superoxide anions in aortic rings. However, naltrexone did not suppress the
overproduction of NO (measured by its metabolites nitrite/nitrate in plasma)
and iNOS expression in lungs induced by LPS. In in vitro study, naltrexone
did not attenuate non-enzymatic iron-induced lipid peroxidation in rat brain
homogenates. In conclusion, pretreatment with naltrexone significantly
improved circulatory failure and hepatic dysfunction in sepsis. These
effects were associated with reduction of TNF-alpha levels and superoxide
anion formation, which may be attributed to antagonism of opioid receptors.
PMID: 15917999 [PubMed - indexed for MEDLINE]
*********************************