The Promise of Low Dose Naltrexone Therapy

2009-01-22
 |  Health & Fitness
The Promise of Low Dose Naltrexone Therapy

Author: Elaine A. Moore

Publisher: McFarland

ISBN: 0786452587

Category: Health & Fitness

Page: 223

View: 390

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Naltrexone is an opiate antagonist drug developed in the 1970s and approved by the FDA in 1984 for opiate and drug abuse treatment. When used at much lower doses in an off-label protocol referred to as low dose naltrexone (LDN), the drug has been shown to halt disease progression in Crohn’s disease and certain cancers, to reduce symptoms in multiple sclerosis and autism, and to improve numerous autoimmune and neurodegenerative conditions, including Parkinson’s disease and amyotrophic lateral sclerosis (ALS). Grounded in clinical and scientific research, this book describes the history of naltrexone, its potential therapeutic uses, its effects on the immune system, its pharmacological properties, and how the drug is administered. It also lists fillers and compounding pharmacies, doctors who prescribe LDN, and patient resources, and includes interviews with LDN patients and researchers.

Advanced Therapeutics in Pain Medicine

2020-12-18
 |  Health & Fitness
Advanced Therapeutics in Pain Medicine

Author: Sahar Swidan

Publisher: CRC Press

ISBN: 9780429998263

Category: Health & Fitness

Page: 392

View: 820

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Chronic pain places a tremendous burden on both the patient and the healthcare system. The use of opioids to address pain has resulted in negative impacts. As practitioners work to undo the current opioid crisis, options to manage pain need a new approach. Advanced Therapeutics in Pain Medicine offers pioneering approaches to this intransigent problem providing a functional medicine approach toward treating pain. This book is dedicated to the advancement of non-opioid therapeutic options that offer real progress in reaching a future of better pain management. With an emphasis on pathophysiology, chapters review various types of pain and propose comprehensive treatment plans. These include manual therapies, novel pharmacologic and plant-based approaches, hormonal effects on pain pathways, as well as psychological and lifestyle interventions. Features · Written by a multi-discplinary team, the book provides clinicians with multiple non-opioid treatment considerations. · Enables practitioners to shift from a “one size fits all’ treatment approach toward individualized patient care. · Includes case studies to help educate the provider on how to implement treatment plans in practice. Written by a team of physicians, pharmacists, psychologists and researchers, this important book offers a much needed step forward in optimizing pain care and benefits practitioners who care for patients experiencing chronic pain.

Anti-Aging Therapeutics

2011-06-20
 |  Medical
Anti-Aging Therapeutics

Author: Academy A4M American

Publisher: eBookIt.com

ISBN: 9781934715062

Category: Medical

Page: 374

View: 146

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Proceedings of the American Academy of Anti-Aging Medicine's (A4M) Seventeenth World Congress on Anti-Aging Medicine & Regenerative Biomedical Technologies, Spring, Summer and Winter Sessions (2009 conference year). Also includes Anti-Aging Clinical Protocols, 2010-2011.

Modulation of the OGF-OGFr Axis Alters the Disease Course of Relapse Remitting Experimental Autoimmune Encephalomyelitis

2015
 | 
Modulation of the OGF-OGFr Axis Alters the Disease Course of Relapse Remitting Experimental Autoimmune Encephalomyelitis

Author: Leslie Hammer

Publisher:

ISBN: OCLC:927775294

Category:

Page:

View: 920

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Multiple sclerosis is a chronic autoimmune disease of the central nervous system and affects over 2.3 million individuals worldwide. The etiology of MS is unknown. However, epidemiological evidence suggests a combination of environmental and genetic factors. No cure exists for MS. Current FDA-approved therapies target limited aspects of the disease, are expensive, and have undesirable side-effects. Experimental autoimmune encephalomyelitis (EAE) is the most widely used animal model for MS. EAE is a CD4+ T cell disease that can be induced in mice through immunization with a myelin antigen, such as proteolipid protein (PLP139-151) in EAE susceptible mice like the SJL/J-strain. Modulation of the opioid growth factor (OGF)-opioid growth factor receptor (OGFr) axis, by administration of OGF or low dose naltrexone (LDN), in both chronic and/or chronic established EAE diminishes disease severity and reduces the histopathological damage associated with the disease. This holds promise for those patients who experience the progressive form of the disease; however, 85 percent of MS patients experience the relapse-remitting disease course. It is unknown whether OGF and/or LDN will be an effective treatment option for RR-MS patients. The central hypothesis is that modulation of the OGF-OGFr axis alters the course of relapse-remitting EAE (RR-EAE). The objectives of this research were to establish a working model of RR-EAE utilizing immunization of the SJL/J mouse with PLP139-151 and to assess the safety and efficacy of LDN or OGF when treatment is initiated at the time of induction or at the time of established clinical disease. Behavior and morphology of glia, macrophages, and neurons were evaluated, as well as the effects of treatment regiments on CD4+ T lymphocyte infiltration into the CNS.The first study established an animal model for relapse-remitting experimental autoimmune encephalomyelitis by immunization of SJL/J mice with PLP139-151. Treatment with OGF or saline was initiated simultaneously with immunization, and within 9 days, behavioral signs of RR-EAE were observed. OGF-treated RR-EAE animals had less severe clinical disease than mice receiving saline and exhibited 66% reductions in median cumulative disease scores, as well as prolonged periods of remission and diminished number and length of disease relapses. Neuropathological examination of lumbar spinal cord revealed reduced numbers of Iba-1 and CD3+ reactive cells, suggesting that OGF inhibited proliferation of microglia/macrophages and T lymphocytes, as well as decreasing the number of proliferating activated astrocytes (Ki67 and GFAP staining). Areas of demyelination and neuronal damage were markedly reduced after the 55-day observation period. The second study examined the therapeutic efficacy of OGF in an established RR-EAE model. Two days following establishment of clinical disease, treatment with OGF or saline was initiated, and mice were observed on a daily basis. OGF treated mice had markedly reduced clinical signs of disease over the course of 40 days. OGF treatment increased the incidence and lengthened the time of remissions relative to saline-treated mice with RR-EAE. OGF therapy also reduced relapses, and facilitated extended periods of mild disease. Neuropathological examination of lumbar spinal cord after 40 days of treatment revealed decreased numbers of Iba-1 and CD3+ reactive cells, suggesting that OGF inhibited proliferation of microglia/macrophages and T lymphocytes, as well as decreasing the number of proliferating activated astrocytes (Ki67 and GFAP dual labeled sections). Peptide treatment for 40 days diminished levels of demyelination in comparison to saline-treated mice with RR-EAE.The third study examined modulation of the OGF-- OGFr axis by low dose naltrexone (LDN) as a disease modifying therapy for established RR-EAE. After two days of clinical disease, mice received LDN or saline for 40 days. Mice were euthanized at study endpoints and spinal cords collected for neuropathological evaluation of glia, T lymphocyte infiltration, and demyelination. LDN treatment significantly reduced behavior scores across the 40 day observation period. The number of remissions was increased in LDN-treated groups relative to controls. A bimodal distribution of behavioral responses to LDN distinguished "responders" from mice considered "non-responders" that showed behavioral characteristics similar to saline-treated animals. More than 60% of the mice responding to LDN displayed several days of remission. LDN-treated mice also had reduced areas of demyelination and decreased numbers of macrophages/microglia and activated astrocytes, as well as reductions in spinal cord demyelination, relative to saline-treated controls. The fourth study examined whether OGF or LDN alter Th effector responses of CD4+ T lymphocytes within the CNS in established EAE. SJL/J mice were immunized with PLP139-151 and treated with OGF, LDN or saline after the second consecutive day of clinical disease. After five treatment days, EAE mice were euthanized and brains and spinal cords collected for intracellular staining. Mononuclear cells were stained were surface stained with anti-CD4, followed by intracellular and transcription factor staining with antibodies for IFN[gamma], IL-17, IL-4 and Foxp3 in order to assess the presence of CD4+ Th1, Th17, Th2, and Treg effector cells in the CNS. Flow cytometry analysis demonstrated that OGF and not LDN decreased CD4+ T lymphocytes present in the CNS of SJL/J mice with EAE at peak disease. However, modulation of the OGF-OGFr axis did not result in changes to CD4+ Th effector cell responses.In conclusion, the data from these studies demonstrate an active role for endogenous opioids in autoimmune diseases such as MS and EAE. Furthermore, these results support previous research indicating that modulation of the OGF-OGFr axis, through either exogenous OGF or intermittent blockade with LDN, can be safe and effective treatment options for EAE and MS. Of particular interest were the opposing effects of OGF and LDN on CD4+ T lymphocytes present in the CNS of established EAE mice, and the lack of effect on different effector cell subpopulations. These results add to the knowledge previously elucidated from studies using the chronic-EAE model, and have opened the door to ongoing research to discern the mechanisms behind OGF and LDN in animal models of EAE, and ultimately the pursuit of clinical trials on OGF and/or LDN for treating MS.

Buprenorphine

1995-03-02
 |  Medical
Buprenorphine

Author: Alan Cowan

Publisher: Wiley-Liss

ISBN: UOM:39015034206212

Category: Medical

Page: 326

View: 115

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Buprenorphine: Combatting Drug Abuse with a Unique Opioid Editors: Alan Cowan and John W. Lewis Scientists involved in the study of opioid pharmacology and drug abuse have long included among their goals the development of effective analgesics with reduced potential for abuse and dependence, and the development of effective pharmacological agents for the treatment of opioid abuse and dependence. Buprenorphine appears to have made an important scientific and clinical contribution on both of these fronts. In this timely volume, international experts describe the unusual chemical and biological characteristics which make this agent unique, from the opiate receptor, through animal pharmacology, to clinical uses, culminating in a discussion of the use of buprenorphine as a medication in the treatment of opioid abuse. Buprenorphine holds great promise as a significant addition to the therapeutic menu available to drug abuse therapists. Buprenorphine: Combatting Drug Abuse with a Unique Opioid will be indispensable to scientists and clinicians in pharmacology, neurobiology, psychiatry, neurology, and psychology, as well as to the wide spectrum of professionals involved in countering substance abuse.

Drugs for Pain

2003
 |  Medical
Drugs for Pain

Author: Howard S. Smith

Publisher:

ISBN: UOM:39015056258216

Category: Medical

Page: 552

View: 560

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DRUGS FOR PAIN is a new textbook designed to give readers an in-depth, comprehensive look at the pharmacologic armamentarium to treat pain. Its many experts/educators have deliberately presented material in a user-friendly style to appeal to a wide audience. The text covers traditional analgesics as well as state-of-the-art and future considerations. Additionally, the rationales for using different agents and how they each work are expounded on. Ediitor and authors from the top pain centers in U.S. Concise, practical manual Features charts and tables for quick access