Archive for the ‘Inflammation’ Category

LDN: An Overview of Clinical Applications

https://www.dropbox.com/s/ltutmleuh0cw1mu/Low%20Dose%20Naltrexone%20-%20An%20Overview%20of%20Clinical%20Applications.docx?dl=0

Low Dose Naltrexone: An Overview of Clinical Applications

Following is an article from the Natural Medicine Journal: the journal of the American Naturopathic Association which provides an excellent review ofthe many clinical applications of Low Dose Naltrexone (LDN)

Reviewed applications include the following:

  • Anti-inflammatory activity
  • Regulation of the opioid growth factor
  • Autoimmune Conditions
  • Cancer
  • Depression
  • Dissociative Disorders and Post-Traumatic Stress Syndrome

As suggested in this review, LDN can provide an excellent therapeutic option for some of the health issues described.

The Uses of Low-Dose Naltrexone in Clinical Practice

Potential benefits for a wide range of conditions

By Timothy Schwaiger, ND, MA

Abstract

The purpose of this paper is to review low-dose naltrexone (LDN) for use in clinical practice. The known or theoretical mechanism of action of LDN, clinical research findings in relation to various medical conditions including pain, autoimmune conditions, cancer, and mood disorders will be discussed. Recommended doses and forms of LDN will also be summarized.

Introduction

Naltrexone, in oral form, was patented by Endo Laboratories in 1967 and approved by the US Food and Drug Administration (FDA) in 1984 for the treatment of opioid addiction.1 Referred to in early research as ENDO1639A, the drug would become what we know as naltrexone. In recent years, the use of buprenorphine and methadone have been recommended overnaltrexone to reduce undesirable side effects and/or counter the effect of morphine partly due to lack of patient compliance with naltrexone.2

The use of oral naltrexone for opioid addiction requires detoxification from the opioid drug and has been associated with low adherence and high level of relapse

back to opioid use after discontinuation of naltrexone.3,4 The typical daily oral dose of naltrexone is 50 mg but may vary depending on the addiction. An extended-release injectable naltrexone that only needs to be administered every 4 weeks is now available. This new method of naltrexone treatment produces better compliance rates in opioid-addicted individuals.5

Low-dose naltrexone was first used clinically in 1985 by Bernard Bihari, MD, a Harvard University physician and Director of the Division of Alcoholism and Drug Dependence, SUNY/Health Science Center at Brooklyn. He became the City Addiction Commissioner of New York in 1974 and continued working with drug addicts at the New York City Health Department and King’s County Hospital in Brooklyn, New York. Given his posts, he was steeped in the upcoming use of drugs such as methadone and naltrexone to treat addictions. He was aware of data indicating that naltrexone led to immune effects, an observation that was merely incidental to its approved use. In 1984, Bihari observed the therapeutic effects of the use of full-dose naltrexone (50 mg/dose) when given to heroin addicts. While naltrexone successfully blocked heroin’s ability to bind the opioid receptors, the complete blockage led to side effects so severe that the former addicts would not comply with continued use. Side effects such as severe anxiety, depression, irritability, and sleep disturbance hampered the adoption of naltrexone for long-term use.6

Meanwhile, while working for the Public Health Department in NewYork City in 1985, Bihari naturally became worried about the human immunodeficiency virus/acquired immune deficiency syndrome (HIV/AIDS) epidemic that was surfacing. He turned his research attention and his knowledge of naltrexone’s effect on the immune system in that direction. Realizing that naltrexone’s effects included increasing endorphins and that this raises immune competence he began research into the use of naltrexone for the HIV-positive (HIV+)/AIDS population. He began with testing innate endorphin levels in individuals with HIV+/AIDS and found they were low in endorphin production compared to patients who did not have AIDS.7

Unlike higher doses of naltrexone, LDN acts on β-endorphin receptors to stimulate the release of endorphins in the body. In an effort to find the minimal dose of naltrexone needed to raise endorphins, Bihari and his colleagues did a dose-ranging study comparing 50, 20, 10,5 and 3.0 mg of naltrexone.6  They found that while all of these doses raised endorphins equally, a dose as low as 1.0 mg had no effect on endorphins. He then compared various doses of LDN between 1.75 and 4.5 mg and verified that a dose of 3.0 mg of LDN increased levels of endorphins during the night and even throughout the next day.8,9 At the International AIDS Conference in 1988 Bihari reported fewer opportunistic infections in a group of AIDS patients using LDN as compared to the placebo group. He also found a reduction in the level of interferon-alpha (IFN-α) in those taking the LDN.10  Increased levels of IFN-α have been implicated in comorbidities in HIV patients such as vascular and kidney disease.11

In addition, patients with HIV infections often have reduced levels of CD4+ T cells. Bihari found that CD4+ T cells did not decrease in patients who received LDN, compared to the placebo group (who were not treated with LDN). These findings and other clinical trials led to the approval of LDN in April 2016 for management of HIV patients in the country of Nigeria by the National Agency for Food and Drug Administration and Control(NAFDAC),12  Nigeria’s equivalent to the US Food and Drug Administration (FDA).

The FDA has not approved LDN for use for any medical conditions in the United States at doses below 5.0 mg, so it is only available from compounding pharmacies.

Mechanism of Action

Several mechanisms of action of LDN have been reported in the literature. The following are 3 of the most prominent actions of LDN: 1) action on opioid receptors to increase release of β-endorphins; 2) ability to reduce pro-inflammatory cytokines and increase anti-inflammatory cytokines; and 3) regulation of the opioid growth factor (OGF)/opioid growth factor receptors (OGFr) axis.

Endorphin production and opioid receptor activation 

Bihari stated in his research that endogenous endorphins were released in the body between 2:00 am and 4:00 am; however, other research has shown that beta (β)-endorphins are released in healthy adults between 4:00 am and 10:00 am.13  Beta-endorphins bind to mu (μ)opioid receptors. This interaction between β-endorphins and μ receptors is thought to be responsible for the analgesic effects in the body.14  The word endorphin comes from the term “endogenous morphine.”  Endorphins are found in the human body originating from the amino acid L-tyrosine and the methyl group of L-methionine.15

Morphine, the drug, is the exogenous equivalent to our own endogenous opioids. Morphine is derived from the opium poppy plant Papaver somniferous and has been used for many years for its analgesic properties.16 Endogenous morphine has been found in the adrenal gland, and secretion from the liver has been shown to increase following physical stress such as sepsis and surgery.1719  In addition to increased levels of endogenous morphine following physical stress, levels of anti-inflammatory cytokines are released as a response to stresses such as surgery.

As mentioned, naltrexone in higher doses is classified as an opioid receptor antagonist and blocks the receptors to counteract the side effects of medication like morphine. Higher doses of naltrexone have also been shown to blunt the release of endorphins following physical activity.20  Unlike higher doses of naltrexone, LDN acts on β-endorphin receptors to stimulate the release of endorphins in the body.21  Low-dose naltrexone is still considered an opioid receptor antagonist, but only for a short duration, and research has shown that LDN increases levels of endogenous opioids.22  In addition, LDN stimulates the body’s own production of endorphins, even after the LDN is no longer in the system.

In a 2008 study, researchers found elevations in endorphins even 1 month after discontinuation of LDN doses of less than 5.0 mg.23  So, the analgesic effects attributed to LDN, in part at least,most likely come from its ability to stimulate β-endorphin release in the body.

Anti-inflammatory activity

The increase of β-endorphins to reduce pain levels is only one aspect of the use of LDN in pain management, especially when the source of the pain is related to aninflammatory process. It has been shown that LDN reduces inflammation by reducing multiple pro-inflammatory cytokines.24 Cytokines are chemical messengers, often made by immune cells, whose net effect can be to either increase or decrease immune function. The coordination of the immune system rests on the body’s ability to keep a balance between cytokines that promote inflammation and those that reduce it. Cytokines are produced by various cells in the body and are associated with the physiologic experience of pain.25  However, the cytokine system isn’t simple. For example, tumor necrosis factor alpha (TNF-α) is associated with both increased inflammation and neuroprotection when the body is presented with an insult such as nerve damage.26,27  Excess synthesis or upregulation of TNF-α is associated with certain conditions such as cerebral ischemia, Alzheimer’s disease, and atherosclerosis, and reducing levels of this cytokine may be of benefit in treatment.28,29

In an 8-week single-blinded pilot study using 4.5 mg of LDN each night, serum levels of numerous proinflammatory cytokines including interleukin (IL)-1, IL-2, IL-12, IL-18, interferon gamma (IFN-γ), granulocyte-macrophage colony-stimulating factor (GM-CSF), and TNF-α were significantly reduced when compared to baseline in patients suffering from fibromyalgia.30

Regulation of the opioid growth factor 

Low-dose naltrexone has been shown to upregulate the OGF/OGFr axis. Opioid growth factor is an opioid peptide also known as [Met5]-enkephalin. The name was changed to OGF due to the association of [Met5]-enkephalin with growth and cell proliferation. Cell growth cycles are classified as G1 (before DNA synthesis), S (DNA synthesis), G2 (before mitosis), and M (mitosis or cell division). OGF has been found to delay the G1/S phase of cell growth.31,32 In addition, there is evidence that the OGF/OGFr axis pathway is involved in the regulation of tumor growth.33  The use of LDN to regulate this pathway is of interest in cancer research and in the treatment of neurodegenerative diseases such as multiple sclerosis.34,35  In addition, research has shown that cell proliferation is altered when OGF binds tothe OGF receptors. When the OGF/OGFr axis pathway is upregulated, tumor growth may be decreased.36

The treatment of pain is a complex challenge and can benefit from an approach that includes attention to both biological and psychological aspects of a patient’s symptoms. Healthcare practitioners have multiple tools available when facing the challenge of pain management. Treating the symptoms of pain using LDN as a mono therapy does not always work; however, if the patient’s condition is highly inflammatory (eg, rheumatoid arthritis) using LDN can be extremely helpful by itself.37

Of course, the use of opioids in this country has risen to an unprecedented level. It was reported in 2016 that 90 individuals die of opioid overdose in this country each day.38  The model of using a low dose of an opioid antagonist such as LD

N is paradoxical. The benefit of using LDN for pain management has its foundations in the ability of this formulation to increase endogenous endorphins and decrease pro-inflammatory cytokines.  There have been several published articles on the use of LDN in patients suffering from fibromyalgia. In a 2013 placebo-controlled, crossover pilot study involving 31 women with fibromyalgia, a 4.5 mg dose of LDN at bedtime reduced daily pain levels (P=0.016) and improved mood (P=0.039) and overall reported quality of life (P=0.045). In this study, neither sleep nor fatigue improved.39 However, in a study conducted in 2009 by the same researchers, the same dose of LDN reduced pain levels and improved symptomsof fatigue (P=0.008) and stress (P=0.003) in 10 women with fibromyalgia.40

Autoimmune Conditions

Some of the more prevalent autoimmune conditions conducive to LDN therapy include rheumatoid arthritis (RA) and inflammatory bowel disease (predominately Crohn’s disease). Many autoimmune conditions present quite a challenge to physicians. Based on the scientific literature, LDN can offer a good option for those seeking pain relief along with a low side effect profile for some autoimmune conditions.

Rheumatoid arthritis is an autoimmune condition characterized predominantly by joint pain.  Although not always present, this condition is frequently associated with a positive rheumatoid factor (RF) and anticyclic citrullinated peptide (anti-CCP) antibodies. Proinflammatory cytokines such as TNF-α and some interleukins such as IL-1 are often associated with RA. Using TNF inhibitors has been an option for treatment; however, in patients for whom treatment is unsuccessful, researchers have found elevated T-helper type 17 (Th17) cells, which do not respond to this therapy.41  Inhibitors of TNF include medications such as adalimumab (Humira), etanercept (Enbrel), and infliximab (Remicade). Other options for treating RA include nonsteroidal anti-inflammatory drugs (NSAIDs) such as ibuprofen, steroids such as prednisone, disease-modifying antirheumatic drugs (DMARDs) like methotrexate, and biological agents like the TNF inhibitors. T-helper 17 cells are responsible for the production of IL-17, a proinflammatory cytokine. In general, Th1/Th17 type cells are considered pro-inflammatory and Th2/regulatory T cells (Tregs) are anti-inflammatory. T-helper 2 activity has been shown to be reduced in patients with RA.42  To further explore the effectiveness of LDN on inflammatory conditions, clinical trials are currently ongoing to study the effects of LDN on adults with osteoarthritis and inflammatory arthritis.43

Crohn’s disease is characterized by abdominal pain, severe diarrhea, fatigue, weight loss, and malnutrition. It is considered an autoimmune disease because of the presence of serum and mucosal autoantibodies acting against intestinal epithelial cells. Results from research using LDN on patients with Crohn’s Disease have been mixed.

In a 2014 article published in the Cochrane Data Base of Systematic Reviews, the authors stated that there was insufficient evidence to allow any firm conclusions regarding the efficacy and safety of LDN used to treat patients with active Crohn’s disease.44  This conclusion was based on 2 cited studies in which there was a significant positive clinical response; however, according to the authors of the Cochrane review, the number of remissions was not significant. In the one study mentioned, 25% of the 12 pediatric patients studied achieved clinical remission and 67% had a significant positive response to LDN therapy. In reviewing the actual study, which was called a pilot study, the authors conceded that the small sample size was a weakness. Also of note, the dose of LDN was based on body weight (0.1 mg/kg, up to 4.5 mg) and not a standard dose (eg, 4.5 mg).45  An adult study of the use of LDN on 17 patients with Crohn’s disease showed a 67% remission rate and a significant improvement in Crohn’s Disease Activity Index (CDAI) scores. In addition, both erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) levels were significantly reduced (P=0.03).46

Multiple sclerosis (MS) is an autoimmune disease that damages myelin, the protective sheath that covers nerve fibers. The most common type of MS is called relapsing-remitting because it cycles between periods of remission and active destruction. Because there is no cure for MS, the focus of treatment is to reduce inflammation and slow the progression of the disease.  Corticosteroids are used to reduce inflammation and a class of drugs known as disease-modifying therapies (DMTs) is used to try to slow the progression. Disease-modifying therapies include interferon beta (IFNB) 1-a and 1-b, glatiramer acetate (GA), mitoxantrone, natalizumab, fingolimod, teriflunomide, dimethyl fumarate, and alemtuzumab.47,48  Researchers have found that a larger number of IL-17 cells are found in the cerebrospinal fluid of patients suffering from MS compared to other noninflammatory neurological diseases. The inflammatory role of IL-17 cells is also important in Parkinson’s Disease and Alzheimer’s Disease.49  In addition, TNF-α, IFN-γ, and IL-1b have been shown to play a major role in neurodegenerative conditions, including MS.27

A retrospective study published in 2016 reviewed medical records from patients with relapsing-remitting MS who used either LDN only or LDN with glatiramer acetate, over a 10-year period (2006-2015). The study compared 3 parameters between the groups: laboratory values (e.g., kidney function, liver enzymes); time to walk a 25-foot course unassisted; and changes in the brain based on MRI.  Researchers concluded that there was no significant difference in the group that was treated with LDN alone vs those using the combination of LDN and glatiramer acetate.50  Even though there was no difference between the 2 groups, the authors concluded that LDN should be considered when treating MS patients because of the low cost. The average annual cost of LDN is around $212 per patient, while the annual cost of DMTs ranges from $41,078 to $53,032 per patient.  51

Cancer

To this author’s knowledge, there have not been any randomized clinical trials on the use of LDN as a monotherapy, or adjunctive therapy, for the treatment of cancer. However, there have been case reports, theoretical research, and in vitro studies.52,53  An in vitro study of triple-negative breast cancer (TNBC) cells revealed that the OGF/OGFr axis is diminished in these tumor cells. Since enhancing this pathway has been shown to have an inhibitory effect on cancer cells, LDN, which upregulates the OGF/OGFr axis, may offer some benefit in treating cancer such as TNBC.33  Triple-negative breast cancer is usually a more aggressive type of breast cancer with a poor prognosis. Because the cancer does not respond to hormone-based therapies, LDN is worth investigating for viability as an adjunctive therapy for TNBC.

In an attempt to determine the effects of modulating the OGF/OGFrc axis on cancer outcomes, researchers at Penn State College of Medicine studied the effects of infused OGF on patients with advanced unresectable pancreatic cancer and found that OGF increased survival time and, in 2 cases, resolved liver metastases.54  Another study looked at the use of OGF in patients failing standard chemotherapy for pancreatic cancer. Patients who received OGF therapy had a threefold increase in survival time compared to those who did not receive OGF therapy. In addition, patients on OGF therapy had significantly elevated blood levels of enkephalin after a month of treatment.55  Because LDN upregulates the expression of OGF and OGFr, these same researchers are exploring the use of LDN in the treatment of ovarian, pancreatic, and other types of cancer.56  There have also been 2 published reports (in 2006 and 2009) of long-term survival using LDN and infused alpha-lipoic acid in patients suffering from pancreatic cancer.52,53

In a study published in 2016, researchers compared standard doses of naltrexone with LDN on various genes involved in cell turnover. They found that genes responsible for apoptosis were upregulated by LDN but not by standard doses of naltrexone.57  In an in vitro study using ovarian cancer cells, investigators were able to demonstrate that LDN inhibited tumor growth when used with the chemotherapeutic agent cisplatin.35

Depression

There are no clinical studies evaluating the effectiveness of LDN as a mono therapy for depression. LDN has been studied, however, in patients with a history of using dopamine-enhancing medication for depression with history of relapse.  Many factors are involved in the relapsing of major depressive disorders, and trying to develop ways to prevent relapses is a challenge.58  In a small study of 12 individuals using dopamine-enhancing medications for depression, the addition of 1.0 mg of LDN 2 times a day for 3 weeks appeared to improve relapsing symptoms of depression. Scores on the Hamilton Depression Rating Scale fell, on average, from 21.2 (severe depression) to 11.7 (mild depression) in patients who were on LDN.59

Dissociative Disorders and Post-Traumatic Stress Syndrome

There is limited information, mostly from case studies, on the use of LDN for post-traumatic brain injury syndrome and post-traumatic stress syndrome. One published study looked at using 2.0 to 6.0 mg of LDN when working with individuals with a history of repetitive, prolonged childhood trauma such as sexual abuse or cruelty. According to the author of the study, WiebkePape, MD, most of the people suffered from dissociative disorder, which she described at the 2017 LDN conference as the act of shutting down or where the “brain goes blank.”  Of the 12 inpatients studied with LDN, most reported favorable benefits of taking LDN, including better regulation of traumatic memories and reduction of self-destructive impulses.60,61

Dosing Recommendations and Methods of Delivery

The recommended dose of LDN is typically 0.5 mg at bedtime for several weeks, followed by 0.5 to 1.0 mg incremental increases over a 1- to 3-month period. When using LDN for pain management, a thorough patient evaluation prior to each dosage increase is important. A thorough medical history including medications, nutritional supplements, and herbal formulas must be obtained before any LDN prescription. The decision to prescribe LDN as an adjunct to chemotherapy or other molecular or biologic agents for cancer treatment should be a joint decision that involves the prescribing physician, the oncologist, and the patient.

If a patient is at the typical maximum dose of 4.5 mg and symptoms return, the clinician should consider reducing or discontinuing LDN for 1 to 2 weeks, then reinitiating medication at a lower dose and building back up to a maximum effective dosage. When inflammatory markers are used to diagnose or follow a patient’s progress (eg, ESR, CRP) it is important to track these levels and correlate them with changes in symptomatology.

Oral use

Capsules and tablets can be prepared in any prescribed dose but the most common is 0.5 to 4.5mg, typically taken at bedtime. Be sure to ask the pharmacist what fillers are used because patients might be sensitive to such things as lactose. Also, the size of the capsule can vary from pharmacy to pharmacy and many patients prefer the smallest capsule available. Tablets are usually very small and well-tolerated by patients, but not all pharmacies distribute tablets. Liquids or sublingual preparations can be made for those who want or need to avoid using capsules or tablets. Typical solutions are a 1.0 mg LDN per 1.0 mL glycerol solution. Liquids are often preferred over capsules or tablets for young children, or adults with swallowing difficulties.

Most LDN is prescribed at bedtime; however, if patients report nightmares, then taking the dose in the morning can be an alternative. Vivid dreams are the most commonly reported side effect in clinical trials but this seems to decrease after a few nights. Another less common side effect is headaches, but these are reported as mild in severity.

No side effects of stomach ulcers, renal impairment, or interference with anticlotting medications have been reported in research.62

Summary

Considering its low cost and low side effect profile, LDN in oral form has potential clinical utility in the treatment of a wide variety of conditions including inflammatory diseases, fibromyalgia, neurological conditions, cancer, and mood disorders.

About the Author

Timothy Schwaiger, ND, MA, received his naturopathic degree from Southwest College of Naturopathic Medicine in Tempe, Arizona, and completed a two-year residency there in Family Medicine. Schwaiger recently served as Chief Medical Officer at Bastyr University in California before moving to Prescott, Arizona with his wife, Debra.  Schwaiger has been in practice since 1999 and loves being a naturopathic physician. He uses naturopathic modalities as well as an integrative approach to family care, pain management and cancer therapy.

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  40. Younger J, Noor N, McCue R, Mackey S. Low-dose naltrexone for the treatment of fibromyalgia: findings of a small, randomized, double-blind, placebo-controlled, counterbalanced, crossover trial assessing daily pain levels. Arthritis Rheum. 2013;65(2):529-538.

  41. Furst DE, Emery P. Rheumatoid arthritis pathophysiology: update on emerging cytokine and cytokine-associated cell targets. Rheumatology (Oxford). 2014;53(9):1560-1569.

  42. Larsen H, Muz B, Khong Tl, Feldmann M, Paleolo EM. Differential effects of Th1 versus Th2 cytokines in combination with hypoxia on HIFs and ang iogenesis in RA. Arthritis Res Ther. 2012:14(4):R180.

  43. National Institutes of Health. US National Library of Medicine. Low Dose Naltrexone for Chronic Pain from Arthritis (LDN-VA).  https://clinicaltrials.gov/ct2/show/NCT03008590.  Updated February 6, 2018. Accessed March 23, 2018.

  44. Segal D, Macdonald JK, Chande N. Low dose naltrexone for induction of remission in Crohn’s disease. Cochrane Database Syst Rev. 2014;(2):CD010410

  45. Smith JP, Field D, Bingaman SI, Evans R, Mauger DT. Safety and tolerability of low-dose naltrexone therapy in children with moderate to severe Crohn’s disease: a pilot study. J Clin Gastroenterol. 2013;47(4):339-345.

  46. Smith JP, Stock H , Bingaman S, Mauger D, Rogosnitzky M, Zagon IS . Low-dose naltrexone therapy improves active Crohn’s disease. Am J Gastroenterol. 2007;102(4):820-828.

  47. Loma I, Heyman R. Multiple sclerosis: pathogenesis and treatment. Curr Neuropharmacol. 2011;9(3):409-416.

  48. Gajofatto A, Benedetti MD. Treatment strategies for multiple sclerosis: when to start, when to change, when to stop? World J Clin Cases. 2015;3(7):545-555.

  49. Wu GF, Alvarez E. The immuno-pathophysiology of multiple sclerosis.  Neurol Clin. 2011; 29(2):257-278.

  50. Ludwig MD, Turel AP, Zagon IS, McLaughlin PJ. Long-term treatment with low dose naltrexone maintains stable health in patients with multiple sclerosis.  Mult Scler J Exp, Transl Clin. 2016;2:111.

  51. Hartung DM, Bourdette DN, Ahmed SM, Whitham RH. The cost of multiple sclerosis drugs in the US and the pharmaceutical industry: too big tofail?Neurology.  2015;84(21): 2185-2192.

  52. Berkson BM, Rubin DM, Berkson AJ. The long-term survival of a patient with pancreatic cancer with metastases to the liver after treatment with the intravenous alpha-lipoid acid/low-dose naltrexone protocol. Integr Cancer There. 2006;5(1):83-89.

  53. Berkson BM, Rubin DM, Berkson AJ. Revisiting the ALA/N (alpha-lipoic acid/low-dose naltrexone) protocol for people with metastatic and nonmetastatic pancreatic cancer: a report of 3 new cases.Integr Cancer Ther. 2009;8(4):416-422.

  54. Smith JP, Conter RL, Bingaman SI, et al. Treatment of advanced pancreatic cancer with opioid growth factor: phase I. Anticancer Drugs. 2004;15(3):203-209.

  55. Smith JP, Bingaman SI, Mauger DT, Harvey HH, Demers LM, Zagon IS.Opioid growth factor improves clinical benefit and survival in patients with advanced pancreatic cancer. Open Access J Clin Trials. 2010;2010(2):37-48.

  56. Donahue RN, McLaughlin PJ, Zagon IS. The opioid growth factor(OGF) and low dose naltrexone (LDN) suppress human ovarian cancer progression in mice. Gynecol Oncol. 2011;122(2):382-388.

  57. Liu WM, Scott KA, Dennis JL, Kaminska E, Levett AJ, Dalgleish AG. Naltrexone at low doses upregulates a unique gene expression not seen with normal doses: implicationsfor its use in cancer therapy.  Int J Oncol. 2016;49:793-802.

  58. Burcusa SL, Iacono WG. Risk for recurrence in depression. Clin Psychol Rev 2007;27(8):959-985.

  59. Mischoulon D, Hylek L, Yeung AS, et al. Randomized, proof-of-concept trial of low dose naltrexone for patients with breakthrough symptoms of major depressive disorder on antidepressants.  J Affect Disord. 2017;208:6-14.

  60. Pape W, Woller W. Low dose naltrexone in the treatment of dissociative symptoms [in German].  Nervenarzt. 2015;86(3):346-351.

  61. Pape W. A medication to stay in the present: treating dissociative symptoms in trauma-related disorders. LDN 2017 Conference. Portland, Oregon; September 22-24, 2017.

  62. Younger J, Parkitny L, McLain D. The use of low-dose naltrexone (LDN) as a novel anti-inflammatory treatment for chronic pain.Clin Rheumatol. 2014;33(4):451-459.

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More on LDN:  https://madisonarealymesupportgroup.com/2016/12/18/ldn/

https://madisonarealymesupportgroup.com/2018/07/16/low-dose-naltrexone-for-lyme-living-with-lyme-podcast/

https://madisonarealymesupportgroup.com/2017/06/12/ldn-reduced-pro-inflammatory-cytokines-in-fm-after-eight-weeks/

https://madisonarealymesupportgroup.com/2018/05/18/bullseye-low-dose-naltrexone-lyme-disease-documentary/

Category:

Inflammation, Lyme, Pain Management, research, Treatment

Study Shows Lyme/MSIDS Patients Infected With Many Pathogens and Explains Why We Are So Sick

**UPDATE May 2022**

This important article was retracted in Feb. 2022 due to:

The main method utilised in this study is an ELISA assay. An investigation by the University of Jyväskylä, Finland, has concluded that the patient selection and description in this Article, and in an unpublished report validating the methods used, do not justify the results presented. The Editors therefore no longer have confidence in the results and conclusions presented in this Article.

Please note that the scientists disagree with the retraction:

Kunal Garg, Leena Meriläinen, Heidi Pirttinen, Marco Quevedo-Diaz, Stephen Croucher and Leona Gilbert disagree with this retraction. Ole Franz did not respond to correspondence from the Editors about this retraction.

I can only surmise that ‘the powers that be’ are not happy with the attention this work has gotten and therefore want to erase it from history.

https://www.nature.com/articles/s41598-018-34393-9?fbclid=IwAR3k-zPy2rJu8OuFl3HHqJ0twLPJvQrxiIUALUs0T-BuuJ50_1VQVwcflIQ (Please see comment at end of article)

Evaluating polymicrobial immune responses in patients suffering from tick-borne diseases

Kunal Garg, Leena Meriläinen, Ole Franz, Heidi Pirttinen, Marco Quevedo-Diaz, Stephen Croucher & Leona Gilbert
Scientific Reportsvolume 8, Article number: 15932 (2018)   https://doi.org/10.1038/s41598-018-34393-9

Abstract
There is insufficient evidence to support screening of various tick-borne diseases (TBD) related microbes alongside Borrelia in patients suffering from TBD. To evaluate the involvement of multiple microbial immune responses in patients experiencing TBD we utilized enzyme-linked immunosorbent assay. Four hundred and thirty-two human serum samples organized into seven categories followed Centers for Disease Control and Prevention two-tier Lyme disease (LD) diagnosis guidelines and Infectious Disease Society of America guidelines for post-treatment Lyme disease syndrome. All patient categories were tested for their immunoglobulin M (IgM) and G (IgG) responses against 20 microbes associated with TBD. Our findings recognize that microbial infections in patients suffering from TBDs do not follow the one microbe, one disease Germ Theory as 65% of the TBD patients produce immune responses to various microbes. We have established a causal association between TBD patients and TBD associated co-infections and essential opportunistic microbes following Bradford Hill’s criteria. This study indicated an 85% probability that a randomly selected TBD patient will respond to Borrelia and other related TBD microbes rather than to Borrelia alone.

A paradigm shift is required in current healthcare policies to diagnose TBD so that patients can get tested and treated even for opportunistic infections.
Please see link for full article.  Snippets below:

Introduction
Tick-borne diseases (TBDs) have become a global public health challenge and will affect over 35% of the global population by 20501. The most common tick-borne bacteria are from the Borrelia burgdorferi sensu lato (s.l.) group. However, ticks can also transmit co-infections like Babesia spp.2, Bartonella spp.3, Brucella spp.4,5,6,7,8, Ehrlichia spp.9, Rickettsia spp.10,11, and tick-borne encephalitis virus12,13,14. In Europe and North America, 4–60% of patients with Lyme disease (LD) were co-infected with Babesia, Anaplasma, or Rickettsia11,15,16. Evidence from mouse and human studies indicate that pathogenesis by various tick-borne associated microbes15,16,17 may cause immune dysfunction and alter, enhance the severity, or suppress the course of infection due to the increased microbial burden18,19,20,21,22. As a consequence of extensive exposure to tick-borne infections15,16,17, patients may develop a weakened immune system22,23, and present evidence of opportunistic infections such as Chlamydia spp.24,25,26,27, Coxsackievirus28, Cytomegalovirus29, Epstein-Barr virus27,29, Human parvovirus B1924, and Mycoplasma spp.30,31. In addition to tick-borne co-infections and non-tick-borne opportunistic infections, pleomorphic Borrelia persistent forms may induce distinct immune responses in patients by having different antigenic properties compared to typical spirochetes32,33,34,35. Nonetheless, current LD diagnostic tools do not include Borrelia persistent forms, tick-borne co-infections, and non-tick-borne opportunistic infections.

The two-tier guidelines36,37,38 for diagnosing LD by the Centers for Disease Control and Prevention (CDC) have been challenged due to the omission of co-infections and non-tick-borne opportunistic infections crucial for comprehensive diagnosis and treatment39,40. Emerging diagnostic solutions have demonstrated the usefulness of multiplex assays to test for LD and tick-borne co-infections41,42. However, these new technologies do not address seroprevalence of non-tick-borne opportunistic infections in patients suffering from TBD and they are limited to certain co-infections41,42. Non-tick-borne opportunistic microbes can manifest an array of symptoms24,29 concerning the heart, kidney, musculoskeletal, and the central nervous system as seen in patients with Lyme related carditis43, nephritis44, arthritis45, and neuropathy46, respectively. Therefore, Chlamydia spp., Coxsackievirus, Cytomegalovirus, Epstein-Barr virus, Human parvovirus B19, Mycoplasma spp., and other non-tick-borne opportunistic microbes play an important role in the differential diagnosis of LD24,29. As the current knowledge regarding non-tick-borne opportunistic microbes is limited to their use in differential diagnosis of LD, it is unclear if LD patients can present both tick-borne co-infections and non-tick-borne opportunistic infections simultaneously.

For the first time, we evaluate the involvement of Borrelia spirochetes, Borrelia persistent forms, tick-borne co-infections, and non-tick-borne opportunistic microbes together in patients suffering from different stages of TBD. To highlight the need for multiplex TBD assays in clinical laboratories, we utilized the Bradford Hill’s causal inference criteria47 to elucidate the likelihood and plausibility of TBD patients responding to multiple microbes rather than one microbe. The goal of this study is to advocate screening for various TBD microbes including non-tick-borne opportunistic microbes to decrease the rate of misdiagnosed or undiagnosed48 cases thereby increasing the health-related quality of life for the patients39, and ultimately influencing new treatment protocol for TBDs.

Results
Positive IgM and IgG responses by CDC defined acute, CDC late, CDC negative, PTLDS immunocompromised, and unspecific patients to 20 microbes associated with TBD (Fig. 1) were utilized to evaluate polymicrobial infections (Figs 2–4). Patient categories included CDC acute (n = 43), CDC late (n = 43), CDC negative (n = 46), PTLDS (n = 31), immunocompromised (n = 61), unspecific (n = 31), and healthy (n = 177).

Polymicrobial infections are present at all stages of tick-borne diseases.

Microbes include Borrelia burgdorferi sensu stricto, Borrelia afzelii, Borrelia garinii, Borrelia burgdorferi sensu stricto persistent form, Borrelia afzelii persistent form, Borrelia garinii persistent form, Babesia microti, Bartonella henselae, Brucella abortus, Ehrlichia chaffeensis, Rickettsia akari, Tick-borne encephalitis virus (TBEV), Chlamydia pneumoniae, Chlamydia trachomatis, Coxsackievirus A16 (CVA16), Cytomegalovirus (CMV), Epstein-Barr virus (EBV), Mycoplasma pneumoniae, Mycoplasma fermentans, and Human parvovirus B19 (HB19V).

In Fig. 2A, 51% and 65% of patients had IgM and IgG responses to more than one microbe, whereas 9% and 16% of patients had IgM and IgG responses to only one microbe, respectively. Immune responses to Borrelia persistent forms (all three species) for IgM and IgG were 5–10% higher compared to Borrelia spirochetes in all three species (Fig. 2B). Interestingly, the probability that a randomly selected patient will respond to Borrelia persistent forms rather than the Borrelia spirochetes (Fig. S2) is 80% (d = 1.2) for IgM and 68% for IgG (d = 0.7). Figure 2A and B indicated that IgM and IgG responses by patients from different stages of TBDs are not limited to only Borrelia spirochetes.

In Fig. 3 sub-inlets, more than 50% of the patients reacted to only the individual Borrelia strains suggesting that Borrelia antigens are not cross-reactive. If patients were cross-reacting among antigens, a larger percentage of the patients would be seen with the combination of all three species (Fig. S2). These results provide evidence to suggest that the inclusion of different Borrelia species and their morphologies in current LD diagnostic tools will improve its efficiency.

Discussions
The study outcome indicated that polymicrobial infections existed at all stages of TBD with IgM and IgG responses to several microbes (Fig. 2). Results presented in this study propose that infections in patients suffering from TBDs do not obey the one microbe one disease Germ Theory. Based on these results and substantial literature11,15,16,17,27,49,50,51 on polymicrobial infections in TBD patients, we examined the probability of a causal relationship between TBD patients and polymicrobial infections following Hill’s nine criteria47.

An average effect size of d = 1.5 for IgM and IgG (Fig. 4A) responses is considered very large52. According to common language effect size statistics53, d = 1.5 indicates 85% probability that a randomly selected patient will respond to Borrelia and other TBD microbes rather than to only Borrelia. Reports from countries such as Australia27, Germany49, Netherlands11, Sweden50, the United Kingdom51, the USA15,16, and others indicate that 4% to 60% of patients suffer from LD and other microbes such as Babesia microti and human granulocytic anaplasmosis (HGA). However, previous findings11,15,16,27,49,50,51 are limited to co-infections (i.e., Babesia, Bartonella, Ehrlichia, or Rickettsia species) in patients experiencing a particular stage of LD (such as Erythema migrans). In contrast, a broader spectrum of persistent, co-infections, and opportunistic infections associated with diverse stages of TBD patients have been demonstrated in this study (Fig. 2). From a clinical standpoint, the likelihood for IgM and IgG immune responses by TBD patients to the Borrelia spirochetes versus the Borrelia persistent forms, and responses to just Borrelia versus Borrelia with many other TBD microbes has been quantified for the first time (Fig. S2).

Borrelia pathogenesis could predispose individuals to polymicrobial infections because it can suppress, subvert, or modulate the host’s immune system18,19,20,21,22 to create a niche for colonization by other microbes54. Evidence in animals55 and humans11,15,16,27,49,50,51 frequently indicate co-existence of Borrelia with other TBD associated infections. Interestingly, IgM and IgG immune levels by patients to multiple forms of Borrelia resulted in immune responses to 14 other TBD microbes (Fig. 4B). In contrast, patient responses to either form of Borrelia (spirochetes or persistent forms) resulted in reactions to an average of 8 other TBD microbes (Fig. 4B). Reaction to two forms of Borrelia reflected an increase in disease severity indicating biological gradient for causation as required by Hill’s criteria47.

Multiple microbial infections in TBD patients seem plausible because ticks can carry more than eight different microbes depending on tick species and geography56,57. Moreover, Qiu and colleagues reported the presence of at least 18 bacterial genera shared among three different tick species and up to 127 bacterial genera in Ixodes persulcatus58. Interestingly, research indicates Chlamydia-like organism in Ixodes ricinus ticks and human skin59 that may explain immune responses to Chlamydia spp., seen in this study (Fig. 2). Additionally, prevalence of TBD associated co-infections such as B. abortus, E. chaffeensis, and opportunistic microbes such as C. pneumoniae, C. trachomatis, Cytomegalovirus, Epstein-Barr virus, and M. pneumoniae have been recorded in the general population of Europe and the USA (Table S2). However, true incidence of these microbes is likely to be higher considering underreporting due to asymptomatic infections and differences in diagnostic practices and surveillance systems across Europe and in the USA. More importantly, clinical evidence for multiple microbes has been reported in humans11,15,16,27,49,50,51, and livestock55 to mention the least. Our findings regarding the presence of polymicrobial infections at all stages of TBD further supports the causal relationship between TBD patients and polymicrobial infections (Fig. 2). Various microbial infections in TBD patients have been linked to the reduced health-related quality of life (HRQoL) and increased disease severity39.

An association between multiple infections and TBD patients relates well to other diseases such as periodontal, and respiratory tract diseases. Oral cavities may contain viruses and 500 different bacterial species60. Our findings demonstrate that TBD patients may suffer from multiple bacterial and viral infections (Fig. 4). In respiratory tract diseases, influenza virus can stimulate immunosuppression and predispose patients to bacterial infections causing an increase in disease severity61. Likewise, Borrelia can induce immunosuppression that may predispose patients to other microbial infections causing an increase in disease severity.

Traditionally, positive IgM immune reaction implies an acute infection, and IgG response portrays a dissemination, persistent or memory immunity due to past infections. Depending on when TBD patients seek medical advice, the level of anti-Borrelia antibodies can greatly vary as an Erythema migrans (EM) develops and may present with IgM, IgG, collective IgM/IgG, or IgA62. This study recommends both IgM and IgG in diagnosing TBD (Figs 5 and S4–S6) as unconventional antibody profiles have been portrayed in TBD patients. Presence of long-term IgM and IgG antibodies have been reported in LD patients that were tested by the CDC two-tier system. In 2001, Kalish and colleagues reported anti-Borrelia IgM or IgG persistence in patients that suffered from LD 10–20 years ago63. Similarly, Hilton and co-workers recorded persistent anti-Borrelia IgM response in 97% of late LD patients that were considered cured following an antibiotic treatment64.

Similar events of persistent IgM and IgG antibody reactions were demonstrated in patients treated for Borrelia arthritis and acrodermatitis chronica atrophicans65, chronic cutaneous borreliosis66, and Lyme neuroborreliosis67. A clear phenomenon of immune dysfunction is occurring, which might account for the disparities in LD patient’s antibody profiles and persistence. Borrelia suppresses the immune system by inhibition of antigen-induced lymphocyte proliferation18, reducing Langerhans cells by downregulation of major histocompatibility complex class II molecules on these cells19, stimulating the production of interleukin-10 and anti-inflammatory immunosuppressive cytokine20, and causing disparity in regulation and secretion of cytokines21. Other studies have demonstrated low production or subversion of specific anti-Borrelia antibodies in patients with immune deficiency status22.

In the USA alone, the economic healthcare burden for patients suffering from LD and ongoing symptoms is estimated to be $1.3 billion per year69. Additionally, 83% of all TBD diagnostic tests performed by the commercial laboratories in the USA accounted for only LD70. Globally, the commercial laboratories’ ability to diagnose LD has increased by merely 4% (weighted mean for ELISA sensitivity 62.3%) in the last 20 years71. This study provides evidence regarding polymicrobial infections in patients suffering from different stages of TBDs. Literature analyses and results from this study followed Hill’s criteria indicating a causal association between TBD patients and polymicrobial infections. Also, the study outcomes indicate that patients may not adhere to traditional IgM and IgG responses.

__________________

**Comment**

For the first time, Garg et al. show a 85% probability for multiple infections including not only tick-borne pathogens but also opportunistic microbes such as EBV and other viruses.

I’m thankful they included Bartonella as that one is often omitted but definitely a player.  I’m also thankful for the mention of viruses as they too are in the mix.  The mention of the persister form must be recognized as well as many out there deny its existence.

Key Quote:  “Our findings recognize that microbial infections in patients suffering from TBDs do not follow the one microbe, one disease Germ Theory as 65% of the TBD patients produce immune responses to various microbes.”

But there is another important point.

According to this review, 83% of all commercial tests focus only on Lyme (borrelia), despite the fact we are infected with more than one microbe.  The review also states it takes 11 different visits to 11 different doctors, utilizing 11 different tests to be properly diagnosed.  https://www.news-medical.net/news/20181101/Tick-borne-disease-is-multiple-microbial-in-nature.aspx?

This is huge.  Please spread the word.

Category:

Babesia, Bartonella, Borrelia Miyamotoi (Relapsing Fever Group), Ehrlichiosis, Heart Issues, Inflammation, Lyme, Parasites, research, Rickettsia, Rocky Mountain Spotted Fever, Testing, Tickborne Relapsing Fever, Ticks, Viruses

Altering Human Genetics Through Vaccination

I’ve been sitting on this article for a while but with the push for gene-editing on mice and insects feel compelled to share it now while the iron’s hot.  To understand how this relates to Lyme/MSIDS, please see my comment at the end of the article.

https://worldmercuryproject.org/news/altering-human-genetics-through-vaccination/

June 28, 2018

Altering Human Genetics Through Vaccination

Children’s Health Defense Note: CHD has internal documents in which the FDA acknowledges that technology that allows for the creation of these new vaccines has outpaced their ability to predict adverse events. Shouldn’t our federal agencies be calling for a moratorium until we have that knowledge—especially since it is heavily reported that the CDC/FDA post-marketing surveillance systems are inadequate to pick up problems after licensure?

By Jon Rappoport, Contributing Writer, Children’s Health Defense

The National Institute of Allergy and Infectious Diseases (NIAID) has launched efforts to create a vaccine that would protect people from most flu strains, all at once, with a single shot.

Over the years, I’ve written many articles refuting claims that vaccines are safe and effective, but we’ll put all that aside for the moment and follow the bouncing ball.

Massachusetts Senator and big spender, Ed Markey, has introduced a bill that would shovel no less than a billion dollars toward the universal flu-vaccine project.

Here is a sentence from an NIAID press release that mentions one of several research approaches:

“NIAID Vaccine Research Center scientists have initiated Phase 1/2 studies of a universal flu vaccine strategy that includes an investigational DNA-based vaccine (called a DNA ‘prime’)…”

This is quite troubling, if you know what the phrase “DNA vaccine” means. It refers to what the experts are touting as the next generation of immunizations.

Instead of injecting a piece of a virus into a person, in order to stimulate the immune system, synthesized genes would be shot into the body. This isn’t traditional vaccination anymore. It’s gene therapy.

In any such method, where genes are edited, deleted, added, no matter what the pros say, there are always “unintended consequences,” to use their polite phrase. The ripple effects scramble the genetic structure in numerous unknown ways.

This is genetic roulette with a loaded gun. Anyone and everyone on Earth injected with a DNA vaccine will undergo permanent and unknown genetic changes…
Here is the inconvenient truth about DNA vaccines—
They will permanently alter your DNA.

The reference is the New York Times, 3/15/15, “Protection Without a Vaccine.” It describes the frontier of research—the use of synthetic genes to “protect against disease,” while changing the genetic makeup of humans. This is not science fiction:

“By delivering synthetic genes into the muscles of the [experimental] monkeys, the scientists are essentially re-engineering the animals to resist disease.”

“’The sky’s the limit,’ said Michael Farzan, an immunologist at Scripps and lead author of the new study.”

“The first human trial based on this strategy — called immunoprophylaxis by gene transfer, or I.G.T. — is underway, and several new ones are planned.” [That was three years ago.]

“I.G.T. is altogether different from traditional vaccination. It is instead a form of gene therapy. Scientists isolate the genes that produce powerful antibodies against certain diseases and then synthesize artificial versions. The genes are placed into viruses and injected into human tissue, usually muscle.”

Here is the punchline:

“The viruses invade human cells with their DNA payloads, and the synthetic gene is incorporated into the recipient’s own DNA. If all goes well, the new genes instruct the cells to begin manufacturing powerful antibodies.”

Read that again: “the synthetic gene is incorporated into the recipient’s own DNA.”

Alteration of the human genetic makeup.

Not just a “visit.” Permanent residence. And once a person’s DNA is changed, he will live with that change—and all the ripple effects in his genetic makeup—for the rest of his life.

The Times article taps Dr. David Baltimore for an opinion:

“Still, Dr. Baltimore says that he envisions that some people might be leery of a vaccination strategy that means altering their own DNA, even if it prevents a potentially fatal disease.”

Yes, some people might be leery.  If they have two or three working brain cells.

This is genetic roulette with a loaded gun. Anyone and everyone on Earth injected with a DNA vaccine will undergo permanent and unknown genetic changes…

And the further implications are clear. Vaccines can be used as a cover for the injections of any and all genes, whose actual purpose is re-engineering humans in far-reaching ways.

The emergence of this Frankenstein technology is paralleled by a shrill push to mandate vaccines, across the board, for both children and adults. The pressure and propaganda are planet-wide.

The freedom and the right to refuse vaccines has always been vital. It is more vital than ever now.

It means the right to preserve your inherent DNA.

The author of three explosive collections, THE MATRIX REVEALED, EXIT FROM THE MATRIX, and POWER OUTSIDE THE MATRIX, Jon was a candidate for a US Congressional seat in the 29th District of California. He maintains a consulting practice for private clients, the purpose of which is the expansion of personal creative power. Nominated for a Pulitzer Prize, he has worked as an investigative reporter for 30 years, writing articles on politics, medicine, and health for CBS Healthwatch, LA Weekly, Spin Magazine, Stern, and other newspapers and magazines in the US and Europe. Jon has delivered lectures and seminars on global politics, health, logic, and creative power to audiences around the world. You can sign up for his free NoMoreFakeNews emails here or his free OutsideTheRealityMachine emails here.

___________________

 

**Comment**

Frightening information, indeed, and reminiscent of Brave New World.

Hopefully regarding DNA based (gene-editing) vaccines, the evidence for harm is self-evident.

Regarding how this specifically could affect Lyme/MSIDS patients, the vaccine issue should STILL be self evident in the harm it could cause chronically/persistently infected people, but secondly, they are gene-editing mice and mosquitoes and releasing them into the wild in hopes of eradicating Lyme and Zika with unintended consequences:  https://madisonarealymesupportgroup.com/2018/10/11/new-england-scientists-explore-new-method-for-eradicating-lyme-disease/

In brief, gene editing has shown unintended consequences of mutations, enhancement of other pathogens, cancer in humans, and very real ethical issues. 

Lastly, while many think the only problem some have with aborted fetal tissue in vaccines is only an ethical one, I was told by people with far more experience than I, that putting human DNA from a certain gender into another human of a different gender, could also have unintended consequences – transgenderism.

Please read my entire comment at end of article within link.  This is scary business.  Please speak out in your sphere of influence.  

 

 

 

 

 

Category:

Activism, Genetic Mutations, Inflammation, Lyme, research, vaccines

THC vs. CBD for Pain: The Differences & Interactions

http://nationalpainreport.com/thc-vs-cbd-for-pain-the-differences-and-interactions-by-winston-peki-8837164.html

THC vs. CBD for Pain: The Differences and Interactions

Posted on September 9, 2018
By Winston Peki.
With the widespread legalization of medical marijuana, many people turn to the drug for a more natural pain relief method.

 

As a natural pain-relief drug, some experts consider cannabis more suitable for your body than the synthetic pharmaceuticals available.

The reasoning behind this is that the body can metabolize natural chemicals better than synthetic ones the same way it can digest natural foods better than processed ones.

Synthetic drugs, as with processed food, can create by-products, which remain as harmful toxins in the body, causing strain on the liver and kidneys. Some (medical) strains of cannabis also provide many health benefits, such as anti-oxidant, anti-depressant, anti-anxiety, pain-suppression, and anti-inflammatory effects.

Not only studies, but many users strongly support the pain-relieving properties of medical marijuana in anecdotal reports. Different types of strains, however, suit different pain conditions, so before diving into medical marijuana use, it’s important to understand the differences.

Let’s look at the difference between the strains of marijuana available, and what their effects are. With the information below, you can hopefully make an informed choice about whether it’s better to use a high-THC or high-CBD strain for your pain relief.

A Brief Overview of THC and CBD

Cannabinoids are the active ingredients specific to the cannabis plant, and they are the compounds primarily responsible for the healing effects. The two most effective and studied cannabinoids are tetrahydrocannabinol (THC) and cannabidiol (CBD).

There have been 70 cannabinoids identified to date, and there are several others currently being studied, such as cannabigerol (CBG) and tetrahydrocannabivarin (THCV).

They are not the only active ingredients, however, and some estimates predict a figure of over 120 active components in the plant. This richness in active compounds is one of the reasons experts consider it useful for treating several ailments.

It is worth noting that THC and CBD also only convert to an effective pain-relieving agent under heat, which is why smoking, vaporizing, or baking it is important.

Most cannabis oils and extracts, designed for direct consumption, haven’t undergone heat treatment. Without heat before ingestion, their effects may not manifest.

The Difference Between THC and CBD

Both THC and CBD contribute to the positive effects associated with marijuana. However, experts only link THC to the strong psychoactive effect known as getting high. This is one of the primary differences between the two components.

The Predominant Effects of High-THC Strains

THC is the primary psychotropic component in marijuana, that is the component responsible for an altered state of mood and perception. This effect makes THC attractive to recreational users.

But THC also contains strong anti-inflammatory and analgesic properties, so it has shown some success in the treatment of pain caused by inflammation, such as arthritis, and cancer.

THC relaxes the nervous system, which helps in spasm-related pain, such as multiple sclerosis. The altered mental state caused by THC can contribute to relieving severe pain in some cases in the same way medicine uses opiates to treat pain.

The Predominant Effects of High-CBD Strains

CBD has received recognition for its anti-carcinogenic qualities. Alongside the lack of feeling “high,” CBD has shown positive anti-inflammatory and pain relief effects. Clinical trials have proven links to suppressing pain receptors from some of the chemical reactions caused by CBD.

CBD has powerful anti-oxidant properties, which also help to support the immune system. Although not considered psychoactive, it can help with the depression, and anxiety sometimes a side-effect of chronic pain.

Cannabidiol Oil and Medical Supplements

Natural cannabis oil supplements are available in capsule and spray forms, as well as oils, which patients can smoke or consume orally. Patients should not confuse medical supplements with the synthetic pharmaceutical varieties, which mimic the effect of cannabis but are not natural. Medical supplements can be pure THC, pure CBD or, so called ‘full-spectrum products’ like CBD oil, which contain ALL the beneficial compounds found in the hemp plant.

The Effects of THC versus CBD in Pain Relief

More clinical trials have linked CBD to positive results for pain relief than THC.

For example:

Chronic Pain. A 2017 report concluded that there was substantial evidence that hih-CBD cannabis-based products are effective for treating chronic pain. Another, separate study published in 2012 in the Journal of Experimental Medicine, suggests that CBD use can lessen both pain and inflammation.

Digestive Pain. CBD has proven it also can help immensely as a digestive aid and digestive pain as well. Researchers have found evidence, as suggested in Cannabinoids for treating inflammatory bowel diseases: where are we and where do we go? that the endocannabinoid system, digestion and CBD have all sorts of interactions. While research involving CBD to treat digestive issues is still in its early beginnings, the experts believe it has the potential to help with all sorts of digestive issues which often come with pain.

Arthritis Pain. Arthritis, which literally means inflammation of the joints, is another condition that CBD oil may be very effective for. Research published in 2016 in the European Journal of Pain found a dramatic reduction in inflammation and signs of pain, without adverse side effects in rats with arthritis after the animals were given a topical gel that contained CBD for four days.

While some studies have shown positive effects of THC on pain relief, particularly for cancer-related pain, the side effects, like altered mental states, make it a less preferred cannabinoid to CBD. Although THC is more effective in muscle-spasm-related pain.

Interactions Between THC and CBD

When looking to reduce your pain, you don’t have to make a choice between THC and CBD. In fact, it could be wise to combine the two. Researchers have found that cannabis really is a synergistic shotgun in the sense that all the compounds in the cannabis plant interact with each other.

Although the exact mechanisms for these interactions remain unclear, the most effective cannabis-based pain treatments have been found to contain a combination of both THC and CBD. So, if your laws and regulations allow, go for a cannabis-based product which contains both compounds in good amounts. Just realize that THC can produce altered mental states, which can be dangerous while doing things that require proper hand-eye coordination like driving.

Choosing a Strain

There are a large range of chemical compositions within the high-THC and high-CBD varieties of cannabis. These can produce different medical effects.

To complicate the matter, the same product can have vastly different results in different people.

When looking for a natural herbal form of cannabis, the sativa strain (cannabis sativa) generally has a higher amount of CBD, whereas the indica strain (cannabis indica) contains more THC. However, due to crossbreeding this is not always reliable. Anecdotal evidence suggests that sativa is more energizing whereas indica is more of a relaxant. This observation may explain some differences that are not specific to the THC or CBD content and why many people prefer indica for pain relief. If you want therapeutic amounts of CBD, always go for a high-CBD strain, this can either be Sativa or Indica.

Conclusion

In medical use for pain relief, doctors prefer the CBD varieties of cannabis extract over THC, primarily due to their lack of side effects. Supplements combining CBD and THC, such as Sativix, have shown the best results in adults in clinical trials. Although experts prefer CBD because it has no side-effects, combining both CBD and THC might be the most effective way to treat pain.

Medical marijuana has fewer risks than other pain-relief medications such as codeine. It also offers more benefit while providing similar pain-relief effects. Since the reactions are incredibly variable and risks of any adverse effect are very low, it is best to discuss options for your pain management with a medical professional and begin with a small dose as a trial. Select the most suitable option for your needs, and let the results quickly manifest themselves.

Winston Peki is a marijuana enthusiast and vaporizer expert. Born and raised in Amsterdam He is the Founder of Herbonaut, an informative vaporizer and cannabis-based products site where you can find vaporizer reviews, CBD oil reviews and more.

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More on CBD derived from marijuana:  

https://madisonarealymesupportgroup.com/2018/06/14/caffeine-more-dangerous-than-cannabis/

https://madisonarealymesupportgroup.com/2015/05/19/marijuana-the-miracle-herb/

https://madisonarealymesupportgroup.com/2018/01/24/medical-marijuana-for-lyme-a-doctors-perspective/

https://madisonarealymesupportgroup.com/2017/01/23/nasem-report-on-cannabis/

https://madisonarealymesupportgroup.com/2017/10/05/marijuana-chronic-pain-q-a-with-dr-david-barton/

For more on Hemp-derived CBD (little to no THC):  https://madisonarealymesupportgroup.com/2017/09/28/cbd-for-pain/

https://madisonarealymesupportgroup.com/2017/10/19/november-madison-lyme-support-group-meeting/

https://madisonarealymesupportgroup.com/2017/11/14/hemp-oil-presentation/

More on other pain treatments:  

DMSO/MSM:  https://madisonarealymesupportgroup.com/2018/03/02/dmso-msm-for-lyme-msids/

LDN:  https://madisonarealymesupportgroup.com/2016/12/18/ldn/, https://madisonarealymesupportgroup.com/2017/06/12/ldn-reduced-pro-inflammatory-cytokines-in-fm-after-eight-weeks/

Magnetic Fields:  https://madisonarealymesupportgroup.com/2018/08/15/treating-pain-with-magnetic-fields/

Laser Therapy:  https://madisonarealymesupportgroup.com/2018/02/27/march-2018-support-group-laser-therapy/,  https://madisonarealymesupportgroup.com/2018/04/08/class-iv-laser-therapy/

Heat:  https://madisonarealymesupportgroup.com/2018/09/28/hotter-bodies-better-at-fighting-disease/

 

 

 

Category:

Activism, Herbs, Inflammation, Pain Management, research, Sleep, Treatment

He Got Schizophrenia. He Got Cancer. And Then He Got Cured.

https://www.nytimes.com/2018/09/29/opinion/sunday/schizophrenia-psychiatric-disorders-immune-system.html

He Got Schizophrenia. He Got Cancer. And Then He Got Cured.

A bone-marrow transplant treated a patient’s leukemia — and his delusions, too. Some doctors think they know why.
By Moises Velasquez-Manoff, science writer

CreditCreditJesse Jacobs

The man was 23 when the delusions came on. He became convinced that his thoughts were leaking out of his head and that other people could hear them. When he watched television, he thought the actors were signaling him, trying to communicate. He became irritable and anxious and couldn’t sleep.

Dr. Tsuyoshi Miyaoka, a psychiatrist treating him at the Shimane University School of Medicine in Japan, eventually diagnosed paranoid schizophrenia. He then prescribed a series of antipsychotic drugs. None helped. The man’s symptoms were, in medical parlance, “treatment resistant.”

A year later, the man’s condition worsened. He developed fatigue, fever and shortness of breath, and it turned out he had a cancer of the blood called acute myeloid leukemia. He’d need a bone-marrow transplant to survive. After the procedure came the miracle. The man’s delusions and paranoia almost completely disappeared. His schizophrenia seemingly vanished.

Years later, “he is completely off all medication and shows no psychiatric symptoms,” Dr. Miyaoka told me in an email. Somehow the transplant cured the man’s schizophrenia.

A bone-marrow transplant essentially reboots the immune system. Chemotherapy kills off your old white blood cells, and new ones sprout from the donor’s transplanted blood stem cells. It’s unwise to extrapolate too much from a single case study, and it’s possible it was the drugs the man took as part of the transplant procedure that helped him. But his recovery suggests that his immune system was somehow driving his psychiatric symptoms.

At first glance, the idea seems bizarre — what does the immune system have to do with the brain? — but it jibes with a growing body of literature suggesting that the immune system is involved in psychiatric disorders from depression to bipolar disorder.

The theory has a long, if somewhat overlooked, history. In the late 19th century, physicians noticed that when infections tore through psychiatric wards, the resulting fevers seemed to cause an improvement in some mentally ill and even catatonic patients.
Inspired by these observations, the Austrian physician Julius Wagner-Jauregg developed a method of deliberate infection of psychiatric patients with malaria to induce fever. Some of his patients died from the treatment, but many others recovered. He won a Nobel Prize in 1927.
One much more recent case study relates how a woman’s psychotic symptoms — she had schizoaffective disorder, which combines symptoms of schizophrenia and a mood disorder such as depression — were gone after a severe infection with high fever.
Modern doctors have also observed that people who suffer from certain autoimmune diseases, like lupus, can develop what looks like psychiatric illness. These symptoms probably result from the immune system attacking the central nervous system or from a more generalized inflammation that affects how the brain works.
Indeed, in the past 15 years or so, a new field has emerged called autoimmune neurology. Some two dozen autoimmune diseases of the brain and nervous system have been described. The best known is probably anti-NMDA-receptor encephalitis, made famous by Susannah Cahalan’s memoir “Brain on Fire.” These disorders can resemble bipolar disorder, epilepsy, even dementia — and that’s often how they’re diagnosed initially. But when promptly treated with powerful immune-suppressing therapies, what looks like dementia often reverses. Psychosis evaporates. Epilepsy stops. Patients who just a decade ago might have been institutionalized, or even died, get better and go home.
Admittedly, these diseases are exceedingly rare, but their existence suggests there could be other immune disorders of the brain and nervous system we don’t know about yet.
Dr. Robert Yolken, a professor of developmental neurovirology at Johns Hopkins, estimates that about a third of schizophrenia patients show some evidence of immune disturbance.
“The role of immune activation in serious psychiatric disorders is probably the most interesting new thing to know about these disorders,” he told me.

Studies on the role of genes in schizophrenia also suggest immune involvement, a finding that, for Dr. Yolken, helps to resolve an old puzzle. People with schizophrenia tend not to have many children. So how have the genes that increase the risk of schizophrenia, assuming they exist, persisted in populations over time? One possibility is that we retain genes that might increase the risk of schizophrenia because those genes helped humans fight off pathogens in the past.

Some psychiatric illness may be an inadvertent consequence, in part, of having an aggressive immune system.

Which brings us back to Dr. Miyaoka’s patient. There are other possible explanations for his recovery. Dr. Andrew McKeon, a neurologist at the Mayo Clinic in Rochester, Minn., a center of autoimmune neurology, points out that he could have suffered from a condition called paraneoplastic syndrome. That’s when a cancer patient’s immune system attacks a tumor — in this case, the leukemia — but because some molecule in the central nervous system happens to resemble one on the tumor, the immune system also attacks the brain, causing psychiatric or neurological problems. This condition was important historically because it pushed researchers to consider the immune system as a cause of neurological and psychiatric symptoms. Eventually they discovered that the immune system alone, unprompted by malignancy, could cause psychiatric symptoms.

Another case study from the Netherlands highlights this still-mysterious relationship. In this study, on which Dr. Yolken is a co-author, a man with leukemia received a bone-marrow transplant from a schizophrenic brother. He beat the cancer but developed schizophrenia.

Once he had the same immune system, he developed similar psychiatric symptoms.

The bigger question is this: If so many syndromes can produce schizophrenia-like symptoms, should we examine more closely the entity we call schizophrenia?

Some psychiatrists long ago posited that many “schizophrenias” existed — different paths that led to what looked like one disorder. Perhaps one of those paths is autoinflammatory or autoimmune.

If this idea pans out, what can we do about it? Bone marrow transplant is an extreme and risky intervention, and even if the theoretical basis were completely sound — which it’s not yet — it’s unlikely to become a widespread treatment for psychiatric disorders. Dr. Yolken says that for now, doctors treating leukemia patients who also have psychiatric illnesses should monitor their psychiatric progress after transplantation, so that we can learn more.

And there may be other, softer interventions. A decade ago, Dr. Miyaoka accidentally discovered one. He treated two schizophrenia patients who were both institutionalized, and practically catatonic, with minocycline, an old antibiotic usually used for acne. Both completely normalized on the antibiotic. When Dr. Miyaoka stopped it, their psychosis returned. So he prescribed the patients a low dose on a continuing basis and discharged them.

Minocycline has since been studied by others. Larger trials suggest that it’s an effective add-on treatment for schizophrenia. Some have argued that it works because it tamps down inflammation in the brain. But it’s also possible that it affects the microbiome — the community of microbes in the human body — and thus changes how the immune system works.

Dr. Yolken and colleagues recently explored this idea with a different tool: probiotics, microbes thought to improve immune function. He focused on patients with mania, which has a relatively clear immunological signal. During manic episodes, many patients have elevated levels of cytokines, molecules secreted by immune cells. He had 33 mania patients who’d previously been hospitalized take a probiotic prophylactically. Over 24 weeks, patients who took the probiotic (along with their usual medications) were 75 percent less likely to be admitted to the hospital for manic attacks compared with patients who didn’t.

The study is preliminary, but it suggests that targeting immune function may improve mental health outcomes and that tinkering with the microbiome might be a practical, cost-effective way to do this.

Watershed moments occasionally come along in medical history when previously intractable or even deadly conditions suddenly become treatable or preventable. They are sometimes accompanied by a shift in how scientists understand the disorders in question.

We now seem to have reached such a threshold with certain rare autoimmune diseases of the brain. Not long ago, they could be a death sentence or warrant institutionalization. Now, with aggressive treatment directed at the immune system, patients can recover. Does this group encompass a larger chunk of psychiatric disorders? No one knows the answer yet, but it’s an exciting time to watch the question play out.

Moises Velasquez-Manoff, the author of “An Epidemic of Absence: A New Way of Understanding Allergies and Autoimmune Diseases” and an editor at Bay Nature magazine, is a contributing opinion writer.

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**Comment**

This article is important on so many levels for Lyme/MSIDS patients as behavior/cognitive issues as well as immune-related issues are often present in those affected.  Killing pathogens is only one arm of treatment, that while important, is only part of the picture.  Detoxifying these pathogens as well as supporting the immune system is just as important.  Dealing with imbalances is a must.

Also noteworthy is the hyperthermia potential for Lyme/MSIDS as well as the impact of minocycline that while on it, schizophrenia patients completely normalized but when stopped their psychosis returned and how he prescribed the patients a low dose on a continuing basis.

Hmmmmm, the state medical board should come after him for overprescribing antibiotics….like they do Lyme doctors.

I personally found minocycline to be one of the most effective drugs I took.

Just for the record, I hate antibiotics, but they work.  I continue to be a human Guinea Pig and try many, many things, but nothing yet compares to antibiotics.  Recently an experienced Lyme practitioner in Wisconsin told me her patients do well off treatment for a year or two but then they suffer a relapse requiring a stint of antibiotics and/or herbs.  This has certainly been our experience as well.  

More on Mino:  https://madisonarealymesupportgroup.com/2017/06/04/minocycline-for-ms-and-much-more/

More on the Immune system and schizophrenia:  https://madisonarealymesupportgroup.com/2018/09/20/schizophrenia-breakthrough-identifies-importance-of-immune-cells/

Other brain abnormalities with Lyme/MSIDS:  https://madisonarealymesupportgroup.com/2018/07/03/lyme-meningoencephalitis-masquerading-as-normal-pressure-hydrocephalus/

https://madisonarealymesupportgroup.com/2018/03/17/how-ld-affects-your-brain-abc27-podcast/

https://madisonarealymesupportgroup.com/2018/08/25/neuropsychiatric-lyme-borreliosis-an-overview-with-a-focus-on-a-specialty-psychiatrists-clinical-practice/

https://madisonarealymesupportgroup.com/2018/08/01/risky-business-linking-t-gondii-entrepreneurship-behaviors/

BTW: t. gondii has been found in ticks (Ixodes ricinus), and these ticks also transmit Lyme and tick-borne encephalitis virus:  https://www.researchgate.net/publication/40846277_The_occurrence_of_Toxoplasma_gondii_and_Borrelia_burgdorferi_sensu_lato_in_Ixodes_ricinus_ticks_from_Eastern_Poland_with_the_use_of_PCR, and https://ecdc.europa.eu/en/disease-vectors/facts/tick-factsheets/ixodes-ricinus

https://madisonarealymesupportgroup.com/2018/02/20/mysterious-disease-where-the-body-attacks-the-brain-more-common-than-initially-thought/
https://madisonarealymesupportgroup.com/2017/10/01/panspandas-steroids-autoimmune-disease-lymemsids-the-need-for-medical-collaboration/  The story of Susannah Cahalan as well as the story of how a boy’s Lyme Disease Morphs into Autoimmune encephalopathy. It took 10 years and 20 doctors to find out 12-year-old Patrik had Lyme disease. Just 4 months later the doctors discovered he also has a condition where his immune system attacks his brain.

https://madisonarealymesupportgroup.com/2017/10/08/misdiagnosed-how-children-with-treatable-medical-issues-are-mistakenly-labeled-as-mentally-ill/

https://madisonarealymesupportgroup.com/2018/01/05/scary-side-of-childhood-strep/

https://madisonarealymesupportgroup.com/2017/12/01/guidelines-for-treating-pans-its-real/ “According to a Wisconsin specialist, 80% of his PANS/PANDAS patients have Lyme and other coinfections. This is important to know and tell others about, remembering that tick borne illness testing is abysmal. Getting to a specialist who understands this complexity is paramount. Another helpful tip is printing out and going through checklists with the children as discussing symptoms is quite helpful. Children aren’t experienced in this type of verbal specificity, so be patient and listen.

 

Category:

Activism, Detoxing, Hyperthermia, Inflammation, Psychological Aspects, research, Treatment