17 oktober 2016: zie ook deze informatie: 

https://kanker-actueel.nl/NL/ldn-low-dose-naltrexone.html

29 april 2010:

LDN - low dose naltrexone krijgt in de complementaire wereld in vooral Engeland en Amerika veel aandacht. Ook de FDA heeft dit middel goedgekeurd en er zijn een aantal studies mee gedaan of lopen nog. Het lijkt erop dat LDN - low dose Naltrexone een aanvullende hulp kan betekenen bij auto-imuunziektes zoals Aids, MS en ook bij  kanker. Hieronder enkele studies daarmee, bv. hoe LDN effectief blijkt bij ziekte van Crohn en een dierstudie en een gerandomiseerde mensenstudie die effectiviteit laat zien bij MS.  Maar lees onderaan een door ons al in 2002 vertaald artikel over LDN - low dose naltrexone of kijk op deze website  voor meer informatie en lopende of al afgesloten studies enz.

Am J Gastroenterol. 2007 Apr;102(4):820-8. Epub 2007 Jan 11.

Low-dose naltrexone therapy improves active Crohn's disease.

Smith JP, Stock H, Bingaman S, Mauger D, Rogosnitzky M, Zagon IS.

Department of Medicine, Pennsylvania State University College of Medicine, Hershey, Pennsylvania 17033, USA.

Abstract

OBJECTIVES: Endogenous opioids and opioid antagonists have been shown to play a role in healing and repair of tissues. In an open-labeled pilot prospective trial, the safety and efficacy of low-dose naltrexone (LDN), an opioid antagonist, were tested in patients with active Crohn's disease. METHODS: Eligible subjects with histologically and endoscopically confirmed active Crohn's disease activity index (CDAI) score of 220-450 were enrolled in a study using 4.5 mg naltrexone/day. Infliximab was not allowed for a minimum of 8 wk prior to study initiation. Other therapy for Crohn's disease that was at a stable dose for 4 wk prior to enrollment was continued at the same doses. Patients completed the inflammatory bowel disease questionnaire (IBDQ) and the short-form (SF-36) quality of life surveys and CDAI scores were assessed pretreatment, every 4 wk on therapy and 4 wk after completion of the study drug. Drug was administered by mouth each evening for a 12-wk period.

RESULTS: Seventeen patients with a mean CDAI score of 356 +/- 27 were enrolled. CDAI scores decreased significantly (P= 0.01) with LDN, and remained lower than baseline 4 wk after completing therapy. Eighty-nine percent of patients exhibited a response to therapy and 67% achieved a remission (P < 0.001). Improvement was recorded in both quality of life surveys with LDN compared with baseline. No laboratory abnormalities were noted. The most common side effect was sleep disturbances, occurring in seven patients.

CONCLUSIONS: LDN therapy appears effective and safe in subjects with active Crohn's disease. Further studies are needed to explore the use of this compound.

PMID: 17222320 [PubMed - indexed for MEDLINE]

Pilot trial of low dose naltrexone and quality of life in MS
Bruce A.C. Cree, Elena Kornyeyeva, Douglas S. Goodin
Multiple Sclerosis Center at UCSF

Abstract

Objective:
To evaluate the efficacy of 4.5 mg nightly naltrexone on the quality of life of multiple sclerosis patients.

Methods:
This single center, double-masked, placebo-controlled, crossover studied evaluated the efficacy of eight weeks of treatment with 4.5 mg nightly naltrexone (Low dose naltrexone or LDN) on self reported quality of life of MS patients.

Results:
80 subjects with clinically definite multiple sclerosis were enrolled and 60 subjects completed the trial. 10 withdrew before completing the first trial period: 8 for personal reasons, 1 for a non-MS related adverse event and 1 for perceived benefit. Database management errors occurred in 4 other subjects and quality of life surveys were incomplete in 6 subjects for unknown reasons. The high rate of subject dropout and data management errors substantially reduced the trial's statistical power. LDN was well tolerated and serious adverse events did not occur. LDN was associated with significant improvement on the following mental health quality of life measures: a 3.3 point improvement on the Mental Component Summary score of the SF-36 (P=.04), a 6 point improvement on the Mental Health Inventory (P<.01), a 1.6 point improvement on the Pain Effects Scale (P=.04) and a 2.4 point improvement on the Perceived Deficits Questionnaire (P=.05).

Interpretation:
LDN significantly improved mental health quality of life indices. Further studies with LDN in MS are warranted.


Figure 2: SF-36, PCS=physical component summary scale score, range 13.6 - 61.9 baseline 34.9. MCS=mental component summary scale score, range 15.6 – 70.0, baseline 44.2.



Figure 3: PES=pain effects scale, range 6 – 30, baseline 16.1. MHI=mental health inventory, range 0 – 100, baseline 63.5

Brain Res. 2010 Jan 15;1310:154-61. Epub 2009 Nov 18.

Opioid growth factor suppresses expression of experimental autoimmune encephalomyelitis.

Zagon IS, Rahn KA, Bonneau RH, Turel AP, McLaughlin PJ.

Department of Neural and Behavioral Sciences, The Pennsylvania State University College of Medicine, Hershey, PA, USA. isz1@psu.edu

Abstract

Naltrexone, an opioid antagonist, has been shown to modulate expression of experimental autoimmune encephalomyelitis (EAE), an animal model of MS, suggesting that endogenous opioids are inhibitory trophic factors in EAE. In the present study, we investigated the effects of one native opioid peptide, opioid growth factor ([Met(5)]-enkephalin), on the onset and progression of EAE. C57Bl/6 mice injected with myelin oligodendrocyte glycoprotein (MOG) received daily injections of 10 mg/kg OGF (MOG+OGF) or saline (MOG+Vehicle). Over 60% of the MOG+OGF animals did not exhibit behavioral signs of disease (EAE) in contrast to 100% of the mice in the MOG+Vehicle group. The severity and disease indices of EAE in the OGF-treated mice were markedly reduced from MOG+Vehicle cohorts. By day 30, 60% of MOG+OGF mice had a remission, relative to 4% in the MOG+Vehicle group. MOG-injected mice receiving OGF had significant reductions in activated astrocytes and damaged neurons compared to MOG+Vehicle animals. Unlike MOG+Vehicle and MOG+OGF mice with behavioral signs of disease, MOG+OGF animals without manifestation of disease had no lumbar spinal cord demyelination. Both OGF and OGF receptor were detected in splenic-derived T lymphocytes by immunohistochemistry. OGF treatment decreased both DNA synthesis and cell proliferation in comparison to vehicle-treated T cell lymphocyte cultures. These results indicate that an endogenous opioid, OGF, inhibits the onset and progression of EAE, and suggest that clinical studies on the use of OGF treatment for MS are merited. Copyright 2009 Elsevier B.V. All rights reserved.

PMID: 19931226 [PubMed - indexed for MEDLINE]

18 februari 2002: Een alternatief middel dat de laatste tijd aandacht krijgt op internet is een lage dosis van naltrexone. Wat ik ervan begrijp is het een soort van kruidenolie, een beetje te vergelijken met Flor Essence. (zie andere alternatieven Flor Essence). Dr. Bihari is de arts die over dit middel enthousiast is en vertelt op zijn site dat Lowdosisnaltrexone in eerste instantie bewees effect te hebben bij aidspatiënten. Een dubbelblinde placebo gecontroleerde studie gaf al in 1986 significante positieve resultaten in de behandeling van HIV/AIDS. Ook werkte naltrexone uitstekend als aanvullend in de behandeling bij heroïne verslaafden. In deze introductie wordt Dr. Bihari opgevoerd. Deze arts deed dat onderzoek naar naltrexone bij HIV/AIDS patiënten. Een vriendin van hem was ze in die tijd behandeld voor non-Hodgkin lymfomen en vroeg zich af nadat de resultaten uit de HIV/AIDDS trial zo positief waren of dit middel haar niet zou kunnen beschermen tegen een terugkomen van haar kanker. Deze vrouw heeft nooit geen kanker teruggehad en stierf aan haar derde hartaanval, die volgens deze informatie niets van doen had met de naltrexone.

Ik heb te weinig kennis van medisch Engels om precies te beschrijven wat voor proces er plaats vindt bij de toediening van lage dosis naltrexone, maar belangrijk lijkt de exacte dosis. In deze introductie wordt gesproken over een exacte dosis van minimaal 1,5 mg.en maximaal 4,5 mg. in te nemen vlak voor het slapen gaan. En deze dosis schijnt dan aldus onderstaande informatie ervoor te zorgen dat er een blokkade optreedt die ervoor zorgt dat er geen kankercellen worden gevormd. Interessant lijkt me de vergelijking met melatonine, ook een middel dat te maken heeft met ons slaapritme en productie van een bepaalde stof. Maar doe dit nu puur als leek en vraag uw arts hiernaar als u er wat mee wilt. Zie verderop ook een paar abstracts van studies bij dieren die ingespoten zijn met menselijke kankercellen.

Dr. Bihari maakt ook melding van een vrouw die leed aan gemetasteerde kwaadaardige huidkanker (melanoom). Deze vrouw leek heel snel te sterven en dr. Bihari gaf via haar dochter deze vrouw als laatste poging tot genezing de lage dosis naltrexone. Negen maanden later zou deze vrouw volledig genezen zijn. Of dat allemaal waar is weet ik niet natuurlijk. Wat me wel opvalt is dat de verhalen over de patiënten niet mooier zijn gemaakt dan ze blijkbaar zijn. Zie verder op deze pagina.  Ook de gevallen waar het niet werkt worden netjes genoemd en beschreven. En dan nog blijkt er een indrukwekkend aantal patiënten wel baat gehad te hebben met de naltrexone. Zeker als waar zou zijn dat de meeste patiënten echt uitbehandeld waren toen ze eraan begonnen. Op dit moment probeert dr. Bihari een aantal klinische studies goedgekeurd door de FDA van de grond te krijgen of het hem al is gelukt weet ik eerlijk gezegd niet. Wel zijn er al een aantal dierstudies bekend die hoopvolle resultaten melden. Maar lees deze introductie in het Engels en kijk zelf op de site, waar beschreven staat wat lowdosisnaltrexone in een kankerbehandeling kan betekenen. Het is naar zeggen non-toxisch, maar er wordt wel gewaarschuwd dat het een negatief effect kan hebben op bepaalde medicijnen, dus voor wie dit wil gaan uitproberen consulteer a.u.b. eerst uw arts. En vraag vooraf informatie bij Dr. Bihari. Zie zijn website.

Background
Before it was first used to treat cancer, LDN had been in use in the treatment of HIV/AIDS. A double-blinded placebo-controlled trial in 1986 showed significant immune system protection from HIV in a group of patients given the active drug. The development of LDN was based on several biological facts. One was the fact that naltrexone, which had been licensed in 1984 as an adjunct in treating heroin addiction, has the ability to induce increases in the endorphin levels in the body. Another was the fact that endorphins are the primary supervisors or (homeostatic) regulators of the immune system, representing 90% of immune system hormonal control. Ninety percent of the day's endorphins are produced by the pituitary and adrenal glands between 2a.m. and 4a.m.

Dr. Bihari and his colleagues then showed that endorphin blood levels averaged less than 25% of normal in people with AIDS. These facts all provided the background for the discovery of the value of LDN in HIV/AIDS. The nocturnal production of endorphins allowed Dr. Bihari and his colleagues to experiment with small doses of naltrexone taken at bedtime in order to jump-start endorphin production. They found that LDN increased endorphin production when taken at bedtime in doses of 1.5mg to 4.5mg. Doses lower than 1.5mg had no effect on endorphin production. Doses higher than 4.5mg produced no more of an endorphin boost, but did block endorphins for significantly longer, thereby reducing the benefit of increased endorphin levels.

During the course of the placebo-controlled trial of LDN in people with AIDS in 1986, a friend of Dr. Bihari's (M.B.) called him when she discovered that she was experiencing an exacerbation of non-Hodgkin's lymphoma which had gone into remission five years earlier after treatment with chemotherapy. Because of her awareness of the decreased likelihood of a long-term remission with a second round of chemotherapy, she called to ask if his AIDS drug might help her cancer. A recently published study of human lymphoma transplanted into mice suggested that it might. In this study, all of the mice in an untreated group died of lymphoma. A second group of mice was pre-treated with a single injection of beta-endorphin before the lymphoma transplant. Half of this second group did not get ill with lymphoma. The other half of these mice did, but with a much more slowly growing tumor and a much prolonged life span compared with that of the non-pre-treated group.

Dr. Bihari agreed to treat M.B. with LDN, and used the three golf-ball-sized tumors in her groin as markers of response. All three shrank and disappeared over the next six months. M.B. stayed on LDN and had no further exacerbations of her malignancy. She died six years later in her mid-seventies from her third heart attack.

Several months later, Dr. Bihari, while in Paris to present the LDN AIDS results at an International AIDS Conference, met a woman (C.P.) in her early forties who was quite ill with metastatic malignant melanoma. This had spread from a malignant mole on her arm to her brain, which showed four metastases on C-T scan. Her speech was slurred, her balance and handwriting impaired, and she suffered from headache and recent memory impairment. Her oncologist in Paris said the malignancy was untreatable, and believed that she had perhaps three to six months of life remaining. On his return to New York, Dr. Bihari shipped LDN to C.P.'s daughter, who started the patient on it. Nine months later, with all neurological signs and symptoms having cleared, C.P. had a repeat C-T scan that showed no residual tumor.

C.P. remained on LDN for the succeeding 12 years, stopping it without her family's knowledge in late 1999. Until that time, she had remained in complete remission, without any recurrence of her malignancy. Eight or nine months after stopping LDN she developed nodules under her skin and began to cough up blood. A C-T scan of the chest showed multiple metastatic lesions. Biopsy of one of the subcutaneous nodules confirmed recurrence of malignant melanoma. Dr. Bihari shipped LDN to the patient's family and she resumed it in early 2000. Eight months later, the nodules in the skin had cleared and a repeat C-T scan of the chest showed no residual tumor. She appears to be, once again, in remission.

Over the years encompassed by these two cases, 1986 to 1999, Dr. Bihari focused his research energy on the study of LDN's effect on immune function and on immunological approaches to the treatment of HIV/AIDS. In 1999, however, conversations with three small pharmaceutical companies revealed some interest in the development of LDN, with a goal of getting FDA approval for immune-related diseases including cancer. With this development possibility, Dr. Bihari decided to revisit the potential value of treating cancer with LDN.

Dr. Bihari began an informal private-practice-based evaluation of the effects of LDN with a variety of types of cancer in February 1999. He had seen positive results with a handful of patients with cancer during the preceding 14 years, while developing the drug as an immune modulator for HIV/AIDS. The drug was compounded by pharmacists in 3mg capsules and taken once a day at bedtime. Most patients have recently had their LDN dose increased to 4.5mg daily. It is nontoxic and has no side effects. Its only interaction with other drugs is with narcotics (such as morphine, Demerol and Percocet), which it briefly blocks


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