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Jeffrey Dach, M.D. NewsLetter
Low Dose Naltrexone (LDN) by Jeffrey Dach MD
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Dear Friend or Colleague
The Only Drug that Can Reverse Narcotics Overdose
Imagine a drug addict slumped over from a lethal heroin overdose. He has shallow breathing and will die unless given prompt medical attention in the emergency room. If he is lucky enough to make the trip to the ER, the doctors will give him an IV injection of Narcan, the drug of choice to reverse narcotics overdose, waking the victim and snatching him from the jaws of death.
Narcan: FDA approved since 1984
Narcan, also called Naltrexone, has been FDA approved since 1984 for reversal of narcotics overdose. Narcan reverses the sedating effect of opiates by binding to the opioid receptors in the brain thus turning off the narcotic drug. Everyone uses narcan as it tends to come in handy. For example, narcan is available in the hospital operating room to wake up the patient after anesthesia.
Since I worked in the hospital for 25 years, and commonly used narcotics for sedation during interventional radiology procedures, I therefore developed an intimate knowledge of I.V. narcan which we used every once in a while to "bring back" a patient who had received a little too much sedation.
The surprising new information about narcan is that this commonly used drug has other very important uses, at a much lower dosage as an oral capsule taken before sleep. Medical scientists have been carefully studying its effect on the immune system, and its clinical benefits for a host of disease states for the past 20 years.
Low Dose Naltrexone, (LDN), How Does it Work?
The beneficial effect of low dose naltrexone, LDN, was discovered by Bernard Bihari, MD (1) (1A)
, a physician in New York City who found that a small dose (3 mg) of naltrexone taken as a capsule at bedtime blocks the opiate receptors in the brain for a few hours during sleep, which then stimulates the brain to increase production of endorphins over the next 24 hours. These endorphins then stimulate the immune system. Although Dr. Bihari did much of the early clinical work, Zagon did the groundwork with animal research studies at Pennsylvania State University (3-17).
LDN Cures Crohn's Disease, Breakthrough Publication
A recent publication in the Jan 2007 Journal of Gasteroenterology on the use of LDN in Crohn's Disease was the first breakthrough: (Low-Dose Naltrexone Therapy Improves Active Crohn�s Disease by Jill Smith MD)
Crohn�s disease is a severe inflammatory condition of the small bowel which can be difficult to treat. Not difficult for LDN however. Jill Smith, M.D. reported that two-thirds of her 17 Crohn�s patients went into remission, and 90% of the group had some benefit. Her article showed impressive colonoscopy photos before and after LDN treatment with complete clearing of the inflammatory changes in the bowel mucosa. Dr. Smith concluded that LDN therapy appears effective and safe in subjects with active Crohn�s disease. (2)
Other Conditions Which Benefit from LDN
The major therapeutic action of LDN is the restoration of normal endorphin production by the brain. This is beneficial for any condition in which there is a deficiency in endorphin production, such as autoimmune disease, cancer and HIV/AIDS. Bernard Bihari, MD, who discovered the LDN protocol, has used it in hundred of patients in the following categories:
LDN for Cancer
Bihari found LDN to be useful for cancers of the Bladder, Breast, Colon & Rectal Cancer , Glioblastoma, Lung Cancer (Non-Small Cell), Lymphocytic Leukemia (chronic), Lymphoma Hodgkin's and Non-Hodgkin's) Malignant Melanoma, Multiple Myeloma , Ovarian Cancer , Pancreatic Cancer, Prostate Cancer (untreated), Renal Cell Carcinoma, Uterine Cancer,
Bihari found LDN to be useful for Autoimmune and other Diseases:
According to Bihari, LDN treatment has benefited these diseases: ALS (Lou Gehrig's Disease), Autism Spectrum Disorders, Chronic Fatigue Syndrome, Crohn's Disease, Fibromyalgia, HIV/AIDS, Multiple Sclerosis (MS), Parkinson's Disease, Psoriasis, Rheumatoid Arthritis, Scleroderma, Systemic Lupus (SLE), Ulcerative Colitis, Wegener's Granulomatosis
LDN Has Virtually No Side Effects:
Occasionally, during the first week's use of LDN, patients may complain of some difficulty sleeping. This rarely persists after the first week. Should it do so, dosage can be reduced from 4.5mg to 3mg nightly.
Caution About Narcotics Withdrawal
Because LDN blocks opioid receptors throughout the body for three or four hours, people using narcotics pain pills such as Ultram (tramadol), morphine, Percocet, Duragesic, Oxycontin or codeine, should not take LDN until after complete withdrawal from their narcotic drugs. The use of LDN may induce narcotics withdrawal.
Although naltrexone is FDA approved, the LDN protocol is what is called "off-label use", and it is unlikely that any company will spend the millions needed to fund studies for FDA approval of the LDN protocol. However, off-label use of an FDA approved drug such as naltrexone is commonplace and widely accepted. The naltrexone capsules are inexpensive, about 20 dollars a month. The treatment is safe, with no adverse side effects.
Do you know someone who might benefit from LDN? Forward this newsletter to them with the button on the bar at the bottom of the page.
Thanks to Larry Frieders, the Compounder for bringing LDN to my attention, and for making low cost LDN capsules available to the public.
Regards,
Jeffrey Dach, M.D.
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4700 Sheridan, Suite T.
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954 983 1443
Dr. Dach will be on vacation August 6-13
Dr. Dach will be on vacation August 6-13, and the office will be closed, however, Dr. Judith Fine will be returning phone calls for messages left with the ansering service, and Dr. Dach will be available via email and phone while on vacation.
References:
(1)
Web site for low dose nalotrexone information.
(1A) Curriculum Vitae, BERNARD BIHARI, M.D. 29 West 15th Street New York, N.Y. 10011, (212) 929-4196
(2) 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.
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.
(3) Cancer Lett. 1983 Nov;21(1):89-94.
Opioid antagonists inhibit the growth of metastatic murine neuroblastoma.Zagon IS, McLaughlin PJ.
Naltrexone (NTX), an opiate antagonist, had an inhibitory effect on the growth of S20 Y neuroblastoma (NB) in A/Jax mice. Daily injections of 0.1 mg/kg NTX resulted in a 69% tumor take, 70% delay in time prior to tumor appearance, and a 60% increase in median survival time. Inoculation of NB in control mice resulted in 100% tumor take within 15 days. The pattern and incidence of metastases of NTX and control mice were similar. These results show that NTX has antineoplastic activity, and suggests a role for the endogenous opioid system in neuro-oncogenic events.
(4) Life Sci. 1983 Dec 12;33(24):2449-54.
Naltrexone modulates growth in infant rats.Zagon IS, McLaughlin PJ.
Naltrexone, a potent opiate antagonist, had both stimulatory and inhibitory effects on somatic growth in preweaning rats depending on dose. Daily injections of 50 mg/kg naltrexone, which blocked morphine-induced analgesia for 24 hr/day, resulted in increased body and organ weights, and acceleration in the appearance of physical characteristics and maturation of spontaneous motor activity. Naltrexone in a dosage of 1 mg/kg, which blocked morphine-induced analgesia for 4 hr/day, had the opposite effects. These results show that naltrexone can modulate growth, and suggest a role for the endorphins and opiate receptors in developmental events.
(5) Brain Res. 1999 Dec 4;849(1-2):147-54. Cloning, sequencing, expression and function of a cDNA encoding a receptor for the opioid growth factor, [Met(5)]enkephalin.
Zagon IS, Verderame MF, Allen SS, McLaughlin PJ.
Department of Neuroscience, The Pennsylvania State University, College of Medicine, 500 University Drive, Hershey, PA, USA. isz1@pus.edu
The native opioid growth factor (OGF), [Met(5)]enkephalin, is a tonic inhibitory peptide that modulates cell proliferation and tissue organization during development, cancer, cellular renewal, wound healing and angiogenesis. OGF action is mediated by a receptor mechanism. We have cloned and sequenced a 2.1-kilobase (kb) cDNA for a receptor to OGF (OGFr). The open reading frame was found to encode a protein of 580 amino acids, and eight imperfect repeats of nine amino acids each were a prominent feature. The protein encoded by this cDNA exhibited the pharmacological, temporal and spatial characteristics of the OGFr. Functional studies using antisense technology demonstrated an enhancement in cell growth. The molecular organization of the OGFr has no homology to classical opioid receptors. These results provide molecular validity for the interaction of OGF and OGFr in the regulation of growth processes.
(6) Int J Oncol. 2000 Nov;17(5):1053-61.
Opioid growth factor regulates the cell cycle of human neoplasias.Zagon IS, Roesener CD, Verderame MF, Ohlsson-Wilhelm BM, Levin RJ, McLaughlin PJ.
Department of Neuroscience and Anatomy, H-109, The Pennsylvania State University, College of Medicine, Hershey, PA 17033, USA. isz1@psu.edu
The native opioid growth factor (OGF), [Met5]-enkephalin, is a tonic inhibitory peptide that modulates cell proliferation and migration, as well as tissue organization, during development, cancer, homeostatic cellular renewal, wound healing, and angiogenesis. OGF action is mediated by the OGF receptor (OGFr). To investigate the target of OGF as to cell proliferation, the effects of excess OGF, and a deprivation of OGF-OGFr interaction by an opioid antagonist, naltrexone (NTX), were examined in 3 human cancer cell lines: pancreatic (BxPC-3), colon (HT-29), and head and neck (CAL-27). OGF exposure decreased growth, DNA synthesis, and mitosis, and increased the doubling time from control levels. FACS analysis revealed a marked increase in cells in the G0/G1 phase and compensatory reduction in cells in S and G2/M phases. Consistent with this observation, the percentage of labeled mitosis (PLM) analysis showed a notable increase in the time of the G0/G1 phase. Receptor blockade with NTX increased the rate of growth, length of DNA synthesis and mitotic phases, and decreased doubling time from control values. FACS analysis indicated an increase in the proportion of cells in S and G2/M phases, and a decrease in the number of cells in the G0/G1 phase. PLM evaluation demonstrated a shortening of the length of the S and G2 phases in the 3 cell lines, and decreases in the M and G0/G1 phases in some cancers. These results indicate that OGF action is directed at the G0/G1 phase, but interruption of OGF-OGFr interfacing has widespread repercussions on the cell cycle. The data on blockade of OGF-OGFr during log phase growth suggest a requisite escorting of the growth peptide and its receptor through the cell cycle.
(7) Cancer Lett. 1996 Mar 29;101(2):159-64.
Inhibition of human colon cancer by intermittent opioid receptor blockade with naltrexone.Hytrek SD, McLaughlin PJ, Lang CM, Zagon IS.
Department of Comparative Medicine, Pennsylvania State University, College of Medicine, Hershey 17033, USA.
Nude mice inoculated with human colon cancer (HT-29) and receiving 0.1 mg/kg naltrexone (NTX) beginning immediately after tumor cell injection exhibited a marked retardation in tumorigenicity. This dosage of NTX, which blocked opioid receptors for 6-8 h/day, resulted in a delay of 2.4-fold in tumor appearance compared to control subjects. At the time (10 days) when all control mice had tumors, 80% of the mice in the 0.1 mg/kg NTX group had no signs of neoplasia. Binding capacity, but not affinity, of [3H][Met5]-enkephalin was reduced 85% of control levels in tumor tissue from mice of the 0.1 NTX group. Plasma, but not tumor tissue levels of [Met5]-enkephalin were elevated (2.5-fold) in contrast to control values. These results suggest that daily intermittent opioid receptor blockade with NTX provokes the interaction of opioids and receptors in the interval following drug availability, with opioids serving to inhibit tumorigenicity of human colon cancer.
(8)
Cancer Lett. 1997 Jan 30;112(2):167-75.
Opioid growth factor (OGF) inhibits human pancreatic cancer transplanted into nude mice.Zagon IS, Hytrek SD, Smith JP, McLaughlin PJ.
Department of Neuroscience and Anatomy, Pennsylvania State University, Milton S. Hershey Medical Center, Hershey 17033, USA. iszl$@psuvm.psu.edu
Nude mice inoculated with human pancreatic cancer (BxPC-3) cells and receiving 5 mg/kg of opioid growth factor ([Met5]enkephalin; OGF) three times daily exhibited a marked retardation in tumorigenicity compared to animals injected with sterile water (controls). OGF-treated animals had a delay of 43% in initial tumor appearance compared to control subjects (10.6 days). At the time when all of the control mice had tumors, 62% of the mice in the OGF group had no signs of neoplasia. Tumor tissue excised from mice after 30 days was assayed for levels of [Met5]enkephalin and zeta opioid receptors. Tumor tissue levels of [Met5]enkephalin were 24-fold greater in OGF-treated mice than controls, but plasma levels of OGF were 8.6-fold lower in animals receiving OGF. Specific and saturable binding of radiolabeled [Met5]enkephalin to nuclear homogenates of pancreatic tumor tissue was recorded, with a binding affinity (Kd) of 10 nM and a binding capacity (Bmax) of 46.8 fmol/mg protein. Binding capacity, but not affinity, of [3H-Met5]enkephalin was reduced by 58% of control levels in tumor tissue from mice of the OGF group. OGF and the zeta (zeta) opioid receptor were detected in human pancreatic tumor cells by immuno-cytochemistry. These results demonstrate that an endogenous opioid and its receptor are present in human pancreatic cancer, and act as a negative regulator of tumorigenesis in vivo.
(9) Science. 1983 Aug 12;221(4611):671-3. Naltrexone modulates tumor response in mice with neuroblastoma.Zagon IS, McLaughlin PJ.
(10) Matthew, PM, Froelich CJ, Sibbitt WL, Jr., Bankhurst AD, Enhancement of natural cytotoxicity by beta-endorphin, J Immunol 130, pp.1658-1662, Apr 1983.
(11) Zagon IS, McLaughlin PJ, Naltrexone modulates tumor response in mice with neuroblastoma, Science 221, pp.671-3, Aug 12, 1983.
(12) Hytrek SD, McLaughlin PJ, Lang CM, Zagon IS, Inhibition of human colon cancer by intermittent opioid receptor blockade with naltrexone, Cancer Lett 101(2), pp. 159-64, Mar 29, 1996.
(13) Zagon IS, Hytrek SD, Lang CM, Smith JP, McGarrity TJ, Wu Y, McLaughlin PJ, Opioid growth factor ([Met5]enkephalin) prevents the incidence and retards the growth of human colon cancer, Am J Physiol 271(3 Pt 2), pp.R780-R786, Sep 1996
(14) Zagon IS, Verderame MF, Allen SS, McLaughlin PJ, Cloning, sequencing, expression and function of a cDNA encoding a receptor for the opioid growth factor, [Met(5)]enkephalin, Brain Res 849(1-2), pp. 147-54, Dec 4, 1999.
(15) Zagon IS, McLaughlin PJ., Opioid antagonists inhibit the growth of metastatic murine neuroblastoma, Cancer Letters 21, pp. 89-94, 1983.
(16) Zagon IS, McLaughlin PJ, Duration of opiate receptor blockade determines tumorigenic response in mice with neuroblastoma: a role for endogenous opioid systems in cancer, Life Sci 35, pp. 409-416, 1984.
(17) Zagon IS, McLaughlin PJ, Opioid antagonist modulation of murine neuroblastoma: A profile of cell proliferation and opioid peptides and receptors, Brain Res 480, pp. 16-28, 1989.
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Jeffrey Dach, M.D. TrueMedMD
Catalog of NewsLetters
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(1)
My Vitamins Are Killing Me by Jeffrey Dach MD !!!
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Stroke Prevention and Vitamin C by Jeffrey Dach MD
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Testosterone Risks and Benefits by Jeffrey Dach MD
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Medical School Days and SSRI Research by Jeffrey Dach MD
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Hypothyroidism Part One by Jeffrey Dach MD
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Guard Your Daughter from Gardisil, Virginia Tech Rampage Seung-Hui Cho by
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(12) Vitamin D Deficiency by Jeffrey Dach MD
(13) Andrew Weil AARP, and Human Growth Hormone HGH by Jeffrey Dach MD
(14) Michael Moore's SICKO by Jeffrey Dach MD
(15) Blood Pressure Pills for Hypertension, When to Treat? by Jeffrey Dach MD
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Catalog of Articles Published on Hank Barnes World,
You Bet Your Life, by Jeffrey Dach MD
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(1)
Lipitor and "The Dracula of Modern Technology" by Jeffrey Dach MD
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Prozac, Paxil and SSRI Drugs - Part One by Jeffrey Dach MD
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Prozac, Paxil and SSRI Drugs - Part Two by Jeffrey Dach MD
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The Origins of HIV by Jeffrey Dach MD
A Medical Article that I Published in 1980:
(7)
Dach J, Patel N, Patel S, Petasnick J. Peritoneal mesothelioma: CT,
sonography, and gallium-67 scan. AJR Am J Roentgenol. 1980 Sep;135(3):614
Jeffrey Dach, M.D.
Member of the Board of the American Academy of Anti-Aging Medicine
Board Certified by the American Board of Radiology
4700 Sheridan, Suite T
Hollywood Fl 33021
office phone 954-983-1443
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Sincerely Yours
Jeffrey Dach, M.D.
4700 Sheridan Suite T.
Hollywood, Fl 33021
954-983-1443
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Dr. Dach is Board Certified by the American Board of Radiology and a
member of the Board of the American Academy of Anti-Aging Medicine.
He has 25 years experience in the Memorial Hospital System as an
interventional radiologist. His current practice focuses on Bio-identical
hormone supplementation for men and women, menopause, andropause, HGH,
testosterone, natural thyroid and the use of natural substances rather
than drugs in the appropriate setting.
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