Mechanism of action of Low Dose Naltrexone (LDN)
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1 Mechanism of action of Low Dose Naltrexone (LDN) Pradeep Chopra, MD Assistant Professor (Clinical) Brown Medical School, USA Director, Pain Management Center, RI, USA Copyright 2014 by Pradeep Chopra. No part of this presentation may be reproduced or transmitted in any form or by any means without written permission of the author 1
2 Disclosure and disclaimer I have no actual or potential conflict of interest in relation to this presentation or program Discussions in this presentation are for a general information purposes only. Please discuss with your physician your own particular treatment. This presentation or discussion is NOT meant to take the place of your doctor. Pradeep Chopra, MD 2
3 Introduction Training and Fellowship, Harvard Medical school Pain Medicine specialist with an interest in complex pain conditions Assistant Professor Brown Medical School, Rhode Island Pradeep Chopra, MD 3
4 Naltrexone Naltrexone is a reversible competitive antagonist at µ and ĸ receptors (opioid receptors) δ receptor antagonist to a lesser extent Its active metabolite 6-β-naltrexol is also reversible competitive antagonist at the µ and ĸ receptors Pradeep Chopra, MD 4
5 Naltrexone Plasma half life of Naltrexone is 6 hours Plasma half life of its active metabolite 6-βnaltrexol is 13 hours Naltrexone is almost fully eliminated in 24 hours. Full dose of Naltrexone is 50mg to 150mg per day Low Dose Naltrexone (LDN) is 1.75mg to 4.5mg Pradeep Chopra, MD 5
6 Low Dose Naltrexone Reversible competitive antagonism of Low Dose Naltrexone blocks the opioid receptor transiently This cause a positive feedback mechanism to increase production of endogenous opioids (endorphins) The levels of endorphin and enkephalin are raised persistently. Bourdette, Dennis. "Spotlight on low dose naltrexone (LDN)". US Department of Veteran Affairs. Archived from the original on 10 February Retrieved 14 May Novella, Steven. "Low Dose Naltrexone Bogus or Cutting Edge Science?". Retrieved 5 July
7 Low Dose Naltrexone LDN increases levels of endogenous opioid peptides, which: Promote healing Inhibit cell growth Reduce inflammation 7
8 Opioid Growth Factor [Met(5)]-enkephalin Pradeep Chopra, MD 8
9 Opioid Growth Factor (OGF) Opioid Growth Factor (OGF) also known as Metkephalin (Met5) Its an endogenous pentapepide OGF activates a specific receptor called Opioid Growth Factor receptor (OGFr). OGF and OGFr axis regulates cell growth in normal and abnormal cells 9
10 Opioid Growth Factor [Met(5)]-enkephalin The OGF regulates the OGFr (Opioid Growth Factor receptor). This combination regulates tissue growth, wound repair and inhibits certain cancers (pancreatic cancer, head and neck squamous cell carcinoma, Ovarian cancer) Clinically used to treat skin cancers and warts (Imiquimod) Zagon IS, Smith JP, McLaughlin PJ (March 1999). "Human pancreatic cancer cell proliferation in tissue culture is tonically inhibited by opioid growth factor". Int. J. Oncol. 14 (3): doi: /ijo PMID McLaughlin PJ, Levin RJ, Zagon IS (May 1999). "Regulation of human head and neck squamous cell carcinoma growth in tissue culture by opioid growth factor". Int. J. Oncol. 14 (5): doi: /ijo PMID Cheng F, Zagon IS, Verderame MF, McLaughlin PJ (November 2007). "The opioid growth factor (OGF)-OGF receptor axis uses the p16 pathway to inhibit head and neck cancer". Cancer Research 67 (21): doi: / can PMID Donahue RN, McLaughlin PJ, Zagon IS (March 2009). "Cell Proliferation of Human Ovarian Cancer is Regulated by the Opioid Growth Factor - Opioid Growth Factor Receptor Axis". American Journal of Physiology. Regulatory, Integrative and Comparative Physiology 296 (6): R doi: /ajpregu PMID Zagon IS, Donahue RN, Rogosnitzky M, McLaughlin PJ (August 2008). "Imiquimod upregulates the opioid growth factor receptor to inhibit cell proliferation independent of immune function". Experimental Biology and Medicine (Maywood, N.J.) 233 (8): doi: /0802-rm-58. PMID
11 Low Dose Naltrexone LDN blocks the opiate receptor intermittently The intermittent block increases production of OGF and OGFr by a positive biofeedback mechanism There is an increase in the number and density of OGF receptors 11
12 p16 and p21 cyclin dependent inhibitory kinases (CKI) p16 is a tumor suppressor protein that is encoded in the CDKN2A gene p21 CKI inhibits cyclin CDK1, CDK2 and CDK4/6 p16 and p21 is decelerate cell progression from G1 phase to S phase, acting as a tumor suppressor especially in cancers such as melanoma, oral, esophageal and cervical cancers. Entrez Gene: CDKN2A cyclin-dependent kinase inhibitor 2A (melanoma, p16, inhibits CDK4)". Nobori T, Miura K, Wu DJ, Lois A, Takabayashi K, Carson DA (April 1994). "Deletions of the cyclin-dependent kinase-4 12 inhibitor gene in multiple human cancers". Nature 368 (6473): doi: /368753a0. PMID
13 LDN and cell growth The effects of LDN are dependent on the OGF- OGFr axis. LDN upregulates OGF-OGFr at the translational level OGF-OGFr axis regulates cell proliferation by altering the G1/S phase of the cell cycle through the p16 and p21 cyclin dependent inhibitory kinases Metenkephalin production (OGF) stimulates p16 and p21 inhibitory pathways of cancer cell division R. N. Donahue, P. J. McLaughlin, I. S. Zagon. Low-dose naltrexone targets the opioid growth factor-opioid growth factor receptor pathway to inhibit cell proliferation: mechanistic evidence from a tissue culture model. Experimental Biology and Medicine, 2011; 236 (9): 1036 DOI: /ebm Pradeep Chopra, MD 13
14 Glia Pradeep Chopra, MD 14
15 Glial cells Glia constitute 70% to 80% of all cells in the Central Nervous System Perform immune surveillance under basal conditions Watkins, Hutchinson, Ledeboer, Milligan et al Brain Behav Immun 2007 Feb; 21(2):
16 Activated Glia When activated glia release a variety of substances (proinflammatory cytokines, chemokines, etc.) These substances in turn increase the excitability of nearby neurons Watkins, Hutchinson, Ledeboer, Milligan et al Brain Behav Immun 2007 Feb; 21(2):
17 Toll Like Receptors (TLR) TLR4 is predominantly expressed by microglia Its expression is upregulated under neuroinflammatory conditions. Opioids cause glial cell activation by acting on the TLR4 receptors leading to a cascade of proinflammatory cytokines Opioid antagonists (naloxone, naltrexone) block TLR4 signalling which in turn decreases glial cell activation, which decreases neuroinflammation Pradeep Chopra, MD 17
18 Briefly..Toll Like Receptor 4 The glial receptor that recognizes opioids is TLR4 This is the very same receptor that is activated in chronic pain Naltrexone inhibits TLR4 signalling suppressing chronic pain especially neuropathic pain Pradeep Chopra, MD 18
19 LDN and Immunity LDN blocks release of proinflammatory cytokines including Interleukins IL6 and IL12, TNFα, NF-ĸB (nuclear factor kappa light chain enhancer of activated B cells) Modulates T and B lymphocyte production Shift of immune response from TH2 to TH1 Pradeep Chopra, MD 19
20 Summary Reversible antagonism of the opioid receptors results in an increased production of endogenous opioids Upregulates the OGF-OGFr axis Blocks TLR signaling which decreases glial cell activation, decreases cytokines, decreases neuroinflammation Modulates T and B lymphocyte production Pradeep Chopra, MD 20
21 Summary LDN blocks release of pro-inflammatory cytokines including Interleukins IL6 and IL12, TNFα, NF-ĸB (nuclear factor kappa light chain enhancer of activated B cells) Regulates cell proliferation through the p16 and p21 cyclin dependent inhibitory kinases. Pradeep Chopra, MD 21
22 Thank you Pradeep Chopra, MD Pradeep Chopra, MD 22
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