Archive for the ‘Pain Management’ Category

Acupuncture Beats Injected Morphine For Pain: Groundbreaking Study

http://www.greenmedinfo.com/blog/acupuncture-beats-injected-morphine-pain-groundbreaking-study?

Acupuncture Beats Injected Morphine for Pain: Groundbreaking Study

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Acupuncture Beats Injected Morphine for Pain: Groundbreaking Study

An amazing new study has found that acupuncture, the ancient practice of using needles to stimulate bodily self healing, is more effective than intravenous morphine for pain. 

A truly groundbreaking study published in the American Journal of Emergency Medicine titled, “Acupuncture vs intravenous morphine in the management of acute pain in the ED,” reveals that acupuncture — one of the oldest techniques to treat pain — is more effective, faster in relieving pain, and with less adverse effects, than intravenous morphine.

The study was conducted over the course of a 1-year period at the Fattouma Bourguiba University Hospital in Tunisia, a tertiary care facility with over 100,000 Emergency Department (ED) visits per year.

300 ED patients with acute pain were included in the study: 150 in the morphine group (administered up to 15 mg a day) and 150 in the acupuncture group. The two groups were comparable in terms of age, sex, and co-morbidities, with the only significant difference being that there were more abdominal pain patients in the morphine group and more low back pain cases in the acupuncture group.

The striking results were reported as follows:

Success rate was significantly different between the 2 groups (92% in the acupuncture group vs 78% in the morphine group P b .01). Resolution time was 16 ± 8 minutes in the acupuncture group vs 28 ± 14 minutes in the morphine group. The difference was statistically significant (P b .01). The mean absolute difference in pain score between the 2 groups was 7.7. This difference is not clinically significant because the minimal clinically significant absolute difference reported by Todd et al is 13. In morphine group, the mean total dose of morphine administered was 0.17 ± 0.08 mg/Kg (Table 2).

The pain scale change from baseline at each time point in the 2 groups is shown in Figure. From the 5-minute time point, the acupuncture group reported significantly larger pain decrease compared with the morphine group. This difference persisted during the entire study period. Change of blood pressure, HR, RR, and oxygen saturation was not significant in both groups.

Overall, 89 patients (29.3%) experienced minor adverse effects: 85(56.6%) in morphine group and 4 (2.6%) in acupuncture group; the difference was significant between the 2 groups (Table 3). The most frequent adverse effect was dizziness in the morphine group (42%) and needle breakage in the acupuncture group (2%). No major adverse effect was recorded during the study protocol. (See Table 4.)”

In short, the acupuncture group saw a great pain-relieving effect, which occurred faster, with significantly less side effects.

A graph from the study showing the pain-decreasing differences between morphine and acupuncture

Discussion

Since 1996, the World Health Organization has recognized acupuncture as a safe and effective therapy for the treatment of a wide range of conditions, including pain and discomfort.1 Despite this, the use of acupuncture within the conventional standard of care is still exceedingly rare. A deep skepticism exists for therapeutic modalities that do yet have a clearly characterized mechanism of action, as defined through conventional biomedical understanding and terminology. Often, in lieu of this, its therapeutic effects are written off as merely “placebo.”

Placebo, however, is not as diminutive term as it may first seem.  The placebo effect actually reflects the deep power and regenerative capability of the body-mind to heal itself. And since its power translates directly into real, measurable improvements in terms of clinical outcomes, it does not matter if we fully understand “how” it works. Also, consider that “evidence-based” (EB) medicine not only depends entirely on clinical outcomes as final proof of an intervention’s efficacy, but also, the entire EB medicine model depends on “controlling” for the placebo effect, as it is already tacitly recognized as having immense power in influencing the outcomes in most interventions. And so, whether or not a fully known or plausible “mechanism of action” has been identified is secondary in importance to whether it works or not in clinical practice.

Acupuncture happens to be one of the most extensively supported alternative modalities, with clinical trial data supporting its value in over 100 different conditions. If you do a pubmed.gov search you’ll find over 6,700 published studies related to the keywords “pain” and “acupuncture.” You can view the primary literature we have gathered on the topic on the GreenMedInfo.com Acupuncture portal:

Clearly the new study reveals that acupuncture has a powerful role to play in pain management. With addiction to pain relieving drugs affecting millions around the world, acupuncture is perfectly poised to provide patients a time-tested, drug-free alternative. As you can see from the study’s graph, the adverse effects comparison is staggeringly in favor of acupuncture as the safer modality.

Finally, here are the study’s powerful conclusions:

Our study demonstrated that in patients with acute pain syndromes presenting to the ED, acupuncture is at least as efficacious and has a better safety profile than IV morphine. The results of this study suggest that acupuncture has a potential role in controlling acute pain conditions presenting to EDs and appears to be safe and effective. Future studies should be performed in international populations. “

References

1 World Health Organization. Acupuncture: review and analysis of reports on controlled clinical trials; 2002.

Disclaimer: This article is not intended to provide medical advice, diagnosis or treatment. Views expressed here do not necessarily reflect those of GreenMedInfo or its staff.

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More on pain management:  https://madisonarealymesupportgroup.com/2018/10/08/thc-vs-cbd-for-pain-the-differences-interactions/

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

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/

Enzymes:  https://madisonarealymesupportgroup.com/2018/03/05/how-proteolytic-enzymes-may-help-lyme-msids/

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.

References

  1. Center for Substance Abuse Treatment. Incorporating Alcohol Pharmacotherapies IntoMedical Practice. Treatment Improvement Protocol (TIP) Series, No. 49. Rockville (MD): Substance Abuse and Mental Health Services Administration; 2009.
  2. Kampman K, Jarvis M. American Society of Addiction Medicine (ASAM) National Practice Guideline for the Use of Medications in the Treatment of Addiction Involving Opioid Use.  J Addict Med. 2015;9(5):358-367.
  3. Sullivan MA, Garawi F, Bisaga A, et al. Management of relapse in naltrexone maintenance for heroin dependence. Drug Alcohol Depend.2007;91(0):289-329.
  4. Minozzi S, Amato L, Vecchi S, et al. Oral naltrexone maintenance treatment for opioid dependence.  Cochrane Database Syst Rev. 2011;(4):CD001333.
  5. Comer SD, Sullivan MA, Yu E, et al. Injectable, sustained-release naltrexone for the treatment of opioid dependence: a randomized, placebo-controlled trial.  Arch Gen Psychiatry.  2006; 63(2): 210-218.
  6. Low Dose Naltrexone (LDN) Pioneer Dr. Bernard Bihari Talks About His Life [Video]. YouTube.https://www.youtube.com/watch?v=x54Jccr8GT8. Published December 6, 2011. Accessed March 26, 2018.
  7. Bihari B. Low dose naltrexone in the treatment of HIV infection.  https://www.lowdosenaltrexone.org/ldn_hiv_1996.htm. Published September 1996.  Accessed March 23, 2018.
  8. Kokayi KB. Interview with Dr Bernard Bihari [transcript]. Global Medicine Review.  New York, NY: WBAI; September 23, 2003.  http://www.lowdosenaltrexone.org/gazorpa/interview.html. Accessed March 23, 2018.
  9. Bihari B. Bernard Bihari, MD: low-dose naltrexone for normalizing immune system function.  Altern Health Med. 2013;19(2):56-65.
  10. Bihari B, Drury FM, Ragone VP, et.al. Low dose naltrexone in the treatment of acquired immune deficiency syndrome. Oral presentation at the IV International AIDS Conference; June 1988: Stockholm, Sweden.
  11. Cha L, Berry CM, Nolan D, Castley A, Fernandez S, French MA. Interferon-alpha, immune activation and immune dysfunction in treated HIV infection. Clin Transl Immunology.  2014; 3(2):e10.
  12. Immunetherapeutics. Lodonal trial update: Nigeria.  https://www.immunetherapeutics.com/lodonal-clinical-trial/. Accessed March 23, 2018.
  13. Hindmarsh W, Tan L, Sankaran K, Laxdal V. Diurnal rhythms of cortisol, ACTH, and p-endorphin levels in neonates and adults.  West J Med. 1989;151:153-156.
  14. Sprouse-Blum AS, Smith G, Sugai D, Parsa D. Understanding endorphins and their importance in pain management. Hawaii Med J. 2010;69(3):70-71
  15. Poeaknapo C, Schmidt J, Brandsch M, Drager B, Zenk MH. Endogenous formation of morphine in human cells. Proc Natl Acad Sci U S A. 2004;101(39):14091-14096.
  16. Chalise U. The poppy plant: phytochemistry & pharmacology. Indo Global Journal of Pharmaceutical Sciences. 2015;5(1):58-65.17.

  17. Glattard E, Welters ID, Lavaux T, et al. Endogenous morphine levels are increased in sepsis: a partial implication of neutrophils. PLoS One. 2010;5(1):e8791.

  18. Yoshida S, Ohta J, Yamasaki K, et al. Effect of surgical stress on endogenous morphine and cytokine levels in the plasma after laparoscopic or open cholecystectomy. Surg Endosc. 2000;14(2):137-140.

  19. Brix-Christensena V, Tønnesena E, Sanchezb RG, Bilfingerc TV, Stefanod GB. Endogenous morphine levels increase following cardiac surgery as part of the anti-inflammatory response? Int J Cardiol. 1997;62(3):191-197.

  20. Daniel M, Martin AD, Carter J. Opiate receptor blockade by naltrexone and mood state after acute physical activity. Br J Sports Med. 1992;26(2):111-115.

  21. Gold MS, Dackis CA, Pottash AL, et al. Naltrexone, opiate addiction, and endorphins. Med Res Rev. 1982;2(3):211-246.

  22. Ludwig M, Zagon I, McLaughlin P. Serum [Met5]-enkephalin levels are reduced in multiple sclerosis and restored by low-dose naltrexone.  Exp Biol Med (Maywood). 2017;242(15):1524-1533.

  23. Gironi M, Martinelli-Boneschi F, Sacerdote P, et al. A pilot trial of low-dose naltrexone in primary progressive multiple sclerosis. Mult Scler.  2008;14(8):1076-1083.

  24. 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.

  25. Zhang JM, An J. Cytokines, inflammation and pain. Int Anesthesiol Clin. 2007;45(2):27-37.

  26. Carlson NG, Wieggel WA, Chen J, Bacchi A, Rogers SW, Gahring LC. Inflammatory cytokines IL-1 alpha, IL-1 beta, IL-6, and TNF-alpha impart neuroprotection to an excitotoxin through distinct pathways. J Immunol. 1999;163(7):3963-3968.

  27. Figiel I. Pro-inflammatory cytokine TNF-α as a neuroprotective agent in the brain. Acta Neurobiol Exp (Wars) . 2008;68(4):526-534.

  28. Olmos G, Lladó J. Tumor necrosis factor alpha: a link between neuroinflammation and excitotoxicity. Mediators Inflamm. 2014;2014:861231.

  29. Clark IA, Vissel B. Excess cerebral TNF causing glutamate excitotoxicity rationalizes treatment of neurodegenerative diseases and neurogenic pain by anti-TNF agents.  J Neuroinflammation. 2016;13(1):236.

  30. Parkitny L, Younger J. Reduced pro-inflammatory cytokines after eight weeks of low-dose naltrexone for fibromyalgia.  Biomedicines. 2017;5(2). pii: E16.

  31. Cheng F. OGF-OGFr Axis and its Inhibitory Actions on Cell Cycle Progression [master’s thesis]. State College: Pennsylvania State University; 2006.

  32. Liu XH, Huang DA, Yang FY, et al. A new cytokine: the possible effect pathway of methionine enkephalin. World J Gastroenterol. 2003;9(1):169-173.

  33. Zagon I, McLaughlin P. Opioid growth factor and the treatment of human pancreatic cancer: a review. World J Gastroenterol. 2014;20(9):2218-2223.

  34. Worley B, Zagon I, McLaughlin P. Opioid growth factor receptor (OGFR) expression is downregulated with progression of triple negative breast cancer. Int J Cancer TherOncol. 2015;3(4):347.

  35. Hammer L, Waldner H, Zagon I, McLaughlin P. Opioid growth factor and low-dose naltrexone impair central nervous system infiltration by CD4+ T lymphocytes in established experimental autoimmune encephalomyelitis, a model of multiple sclerosis. Exp Biol Med (Maywood). 2016;241(1):71-78.

  36. Donahue RN, McLaughlin PJ, Zagon IS. Low-dose naltrexone suppresses ovarian cancer and exhibits enhanced inhibition in combination with cisp latin.  Exp Biol Med(Maywood). 2011;236(7):883-895.

  37. Hesselink JM, Kopsky DJ. Enhancing acupuncture by low dose naltrexone. Acupunct Med. 2011;29(2):127-130.

  38. Rudd RA, Seth P, David F, Scholl L. Increases in drug and opioid-involved overdose deaths United States, 2010–2015. MMWR Morb Mortal Wkly Rep. 2016;65(5051):1445-1452.

  39. Younger J, Mackey S. Fibromyalgia symptoms are reduced by low-dose naltrexone: a pilot study.  Pain Med. 2009;10(4):663-672.

  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/

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

 

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/

 

 

 

Hotter Bodies Better at Fighting Disease

http://www.greenmedinfo.com/blog/hotter-bodies-better-fighting-disease

Hotter Bodies Better at Fighting Disease

Having a “hot body” has more benefits than ever before, thanks to new scientific findings on the role that elevated body temperature plays in helping fight infections and ward-off disease

A 2018 study examining the role that temperature plays in the body’s inflammatory response has demonstrated that the hotter our body temperature, the more effective our immune system becomes at fighting tumors, healing wounds, and fighting infections.

Researchers at the Universities of Warwick and Manchester in the UK recently published the paper entitled, Temperature regulates NF-κB dynamics and function through timing of A20 transcription,[1] in the Proceedings of the National Academy of Sciences of the USA. Acknowledging that inflammation is often accompanied by changes in body temperature, researchers sought to close the gap of information on how these phenomena may be linked.

Using an experimentation method incorporating mathematical modeling, researchers from the University’s Mathematics Institute partnered with biologists, infectious disease specialists, epidemiologists and other scientists to better understand these systemic interactions. These models were used to calculate cellular responses to inflammation, such as how small increases in body temperature affect specific genes, including keyinflammatory regulators.

Biologists focused on the actions of a protein called ‘Nuclear Factor kappa B’ (NF-κB). When inflammation markers are in the bloodstream, NF-κB proteins “switch on” by moving into and out of the nucleus of cells, turning genes on and off in response to inflammation. This cellular-signaling works on a biological clock, with cells activated for a period of time to respond to the perceived source of inflammation. A healthy NF-κB response allows the body to effectively suppress tumors and infections, and aids in rapid wound-healing. An uncontrolled NF-κB response is associated with inflammatory diseases such as psoriasis, rheumatoid arthritis, and Crohn’s disease.

Mathematical models were used to test the correlation of the rate of this NF-κB “clock” to changes in body temperature. Researchers discovered that if the body temperature is lower than normal, around 94℉, the NF-κB clock slows down. This has the effect of slowing the body’s response rate to wounds and infections. When the body temperature is higher than normal (>98.6℉), as in the case of fever, the NF-κB clock speeds up and continues to increase with each degree of uptick in body temperature. This increased physiological response to inflammation is associated with rapid wound healing, fewer and shorter infections, and even anti-cancer benefits.

Researchers correctly predicted that a protein called A20 holds a critical key in this process. When A20, the central gatekeeper in inflammation and immunity,[2] was removed from cells during experimentation, the NF-κB clock lost its correlative link with body temperature. This link helps explain why our bodies cycle through normal changes in body temperature (+/- 1.5 degrees) over the course of a 24-hour day.

Lead mathematician David Rand, Professor of Mathematics and member of the University of Warwick’s Zeeman Institute for Systems Biology and Infectious Disease Epidemiology, commented:

“The lower body temperature during sleep might provide a fascinating explanation into how shift work, jet lag or sleep disorders cause increased inflammatory disease.”

Researchers concluded that cellular response to inflammation may be “mechanistically and functionally regulated by temperature,” clearing the way for new drugs that control inflammation by more precisely targeting the A20 protein.

Professor Mike White, lead biologist from the University of Manchester, noted that these findings validate our understanding of why

influenza and cold epidemics tend to be worse in the winter when temperatures are cooler,” and that “mice living at higher temperatures suffer less from inflammation and cancer.” Said White: “These changes may now be explained by altered immune responses at different temperatures.”

Bring the Heat to Boost Immunity

Fever is a normal part of a healthy immune response that is often met by over-reaction. Fever is produced when we come into contact with toxins, E. coli bacterium, for example, that introduce pyrogens into the bloodstream. Pyrogens are toxins that infect the body and stimulate a fever-response. The immune system identifies pyrogens as threats, alerting the hypothalamus to signal the body to generate and retain heat in the form of a fever.

Medication designed to suppress a therapeutic fevercan do more harm than good. According to Harvard Medical School, an adult has a fever when his or her temperature exceeds 100.4℉. A fever is not considered medically urgent until it exceeds 104℉,[3] at which point measures should be taken to cool the body and seek immediate medical attention.

Pyrogens signal the immune system when a dangerous toxin has entered the bloodstream. But what about microtoxins that we are exposed to everyday? Persistent organic pollutants such as chemical fertilizers from agro-runoff are in the soil, air, and water of most places in America. Heavy metals loosed from the Earth by industrial operations become airborne and seep into soil and water tables. Plasticizers like phthalates are found in umbilical cord tissue and breast milk, and in the fat cells of most Americans. Most of us don’t get a fever every time we walk outside, but we should not mistake this apparent lack of bodily reaction for a lack of bodily harm.

“The dose makes the poison,” is more than just a colloquialism; it is a chemical reality that has allowed for questionable standards for public drinking water, mass-produced foods, and air quality in the United States. Until recently, medical science had essentially discounted the dangers of low-dose toxins. Difficulty with accurate testing methods, as well as the inability to affect rapid policy and procedural change, are among the reasons why scientists had left this question largely unexplored. Thankfully, this has changed in the last decade, and not a moment too soon: recent studies show that low-dose toxins can be among the most dangerous of all chemical exposures.[4]

In a landmark study released at the end of 2017,[5] scientists found that

“widely disseminated chemicals and pollutants…are proportionately more toxic at the lowest levels of exposure,” and “we will need to achieve near-zero exposures to protect public health.”

Other recent studies have shown that microdoses can and do impact health, including increased risk of neurodegenerative diseases,[6] hormonal disturbances,[7] and increased risk of cancers.[8] Since we can’t snap our fingers and make environmental toxins go away, a diligent approach to disease prevention includes enhancing our immune system and efficiently dumping toxins on a regular basis.

Thankfully, we don’t need to become sick with fever to reap the disease-fighting advantages of a body temperature boost. There are natural ways to hack our body heat that also speed detox—and are often downright enjoyable! Whether you patronize a health club or implement a DIY solution, here are three healthful therapies that will help you turn up the heat.

Break a Sweat

Your body has a powerful, natural system for detoxifying that doesn’t require you to suffer the discomforts of being under-the-weather. All you have to do is pick your favorite exercise and break a sweat! Sweating is one of mankind’s primary mechanisms for eliminating toxins and purifying the body. Sweating naturally raises body temperature, dumps wastes, and stimulates biochemical activity, including increased circulation of blood and lymphatic fluid.

A 2011 study published in the Archives of Environmental and Contamination Toxicology, observed that dangerous metals and petrochemicals were detected in the sweat of study participants that were not seen, or were seen in differing levels, in urinalysis and blood serum tests conducted on the same patients. This finding prompted researchers to call for “sweat analysis to be considered as an additional method for monitoring bioaccumulation of toxic elements in humans.”

You can induce a sweat with intense exercise or take a more leisurely approach through sunbathing. Sunbathing raises body temperature when photons penetrate the skin, stimulating production of Vitamin D and energizing the water in our cells. UV and radiant heat make H2O’s charge, polarity, and conductivity stronger, while blood, lymph, and other body fluids become thinner. This speeds circulation, moving oxygen-rich blood in, and waste products, out. Getting a deep, purifying sweat several times per week can greatly enhance the efficiency at which our bodies remove these everyday toxins.

Sauna Therapy

Another low-impact option for increasing body temperature is sauna therapy. Saunas can be enjoyed in many forms, including traditional dry sauna, steam sauna, and infrared sauna. In a dry sauna, humidity is kept between 10-20%, with temperatures reaching as high as 185℉. Body temperatures easily reach elevated levels during sauna, and can be safely sustained for around 15-30 minutes, for most individuals.

Dry or Finnish sauna is the standard in many countries and is widely regarded as a healthful way to purify and relax the body. But the benefits of sauna extend well beyond relaxation. A 2002 study introduced twenty patients suffering from chronic heart failure to daily, 15-minute dry sauna sessions. Results showed that 17 of the 20 patients had improved vascular and cardiac function after just two weeks of sauna therapy.

Wet or steam sauna has a different host of health benefits. Steam is healing for many respiratory ailments, and can deeply penetrate sore, aching muscles. Hot tubs can reach temperatures of 104℉, and for some, is a gentler way of achieving increased body heat. According to Harvard Health, “a study of 15 men with coronary artery disease showed that 15 minutes in a hot tub produced less circulatory stress than 15 minutes on a stationary bike.” Hot tubbing has also been shown to safely lower high blood pressure.[9]

Infrared saunas use warm, infrared heaters to emit light waved that are absorbed by the surface of the skin. In a 2010 study comparing infrared and steam saunas, researchers found that the sweat from the infrared sauna contained more bismuth, cadmium, chromium, mercury, and uranium. The steam sauna caused higher levels of arsenic, aluminum, cobalt, copper, manganese, nickel, lead, tin, thallium, and zinc to be excreted.

Whatever form of sauna you choose, you can achieve an even greater immunity boost by plunging into cold water in-between bouts of heat. This quick temperature shift agitates body fluids that have become stagnant from periods of inactivity and is great for enhancing circulation.

Thermotherapy

Therapeutic heating, or thermotherapy, applies to any form of therapy in which heat is applied to achieve physical improvement or relief from symptoms. Whether it’s applying a hot water bottle to an aching muscle group or taking a hot bath with Epsom salts, thermotherapy can achieve low-level increases in body temperature, and is a useful form of easy-to-render comfort and relief from aches and pains.

Heat wraps and pads are employed to great efficacy for treating muscle spasms, herniated disks, eye pain, and other types of musculoskeletal issues. A 2002 study found that warm paraffin wax baths were useful in improving range-of-motion in sufferers of rheumatoid arthritis.[10]Objective improvements were seen in ability to pinch fingers together, improved grip strength, and reduced pain and stiffness when compared to controls after four consecutive weeks of treatment. Treatments such as these can be a useful adjunct to traditional arthritis treatment and may allay the need for habitual pain medication.

Thermotherapy isn’t limited to mundane applications like heating pads—you can also find it in-use as a space-age, laser beam used to fight cancer. Intense heat is directed via infrared laser into the eyes of cancer patients, where it effectively heats and kills retinoblastoma tumor cells that form inside the eye.[11] Other low-level laser therapies are being employed for the treatment of chronic pain[12]and arthritis, with other therapeutic uses for laser currently under development.

References

[1]http://www.pnas.org/content/early/2018/05/09/1803609115/tab-article-info

[2]https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2659177/

[3]https://www.health.harvard.edu/diseases-and-conditions/fever-in-adults2

[4]https://doi.org/10.1371/journal.pbio.2003066

[5]IBID

[6]https://www.sciencedirect.com/science/article/pii/S2214750015300974

[7]https://www.ncbi.nlm.nih.gov/pubmed/23867546

[8]https://www.nature.com/articles/bjc2011489

[9]https://www.health.harvard.edu/staying-healthy/saunas-and-your-health

[10]https://www.cochrane.org/CD002826/MUSKEL_thermotherapy-heat-treatment-for-treating-rheumatoid-arthritis

[11]https://www.cancer.org/cancer/retinoblastoma/treating/thermotherapy.html

[12]https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4137223/

Disclaimer: This article is not intended to provide medical advice, diagnosis or treatment. Views expressed here do not necessarily reflect those of GreenMedInfo or its staff.

 

 

 

 

Rally for Recovery Saturday Wisconsin State Capital

Department of Health Services News Releases
September 21, 2018

Contact: Jennifer Miller/Elizabeth Goodsitt 608-266-1683

Rally for Recovery

Wisconsin Voices for Recovery hosts its annual Rally for Recovery at the State Capitol sponsored by DHS

WHO: Wisconsin Voices for Recovery
WHAT: Rally for Recovery
WHEN: Saturday, September 22, 2018 from 11 a.m. to 2 p.m.
WHERE: State Street Steps of the State Capitol, Madison

Key Activities:

11:00 a.m.: Performance by the Ho Chunk Drumming Circle

11-2 People sharing their stories of living in recovery
11:00 a.m. to 2:00 p.m.: Representatives of organizations supporting people in recovery will share resources, including a training on how to use naloxone, the opioid overdose reversal drug
11:30 a.m. to 11:45 a.m.: Media availability with DHS Director of Opioid Initiatives Paul Krupski (meet at the DHS table)
12:00 p.m. to 12:30 p.m.: Featured speaker Joseph Green, spoken word poet and motivational speaker
12:35 p.m. to 12:40 p.m.: Presentation of the Wisconsin Voices for Recovery Award to an organization that is helping people find long-term recovery
12:40 p.m.: Moment of silence for those who lost their lives before they could experience the promise of recovery
NOTE: DHS plans to broadcast portions of the program live on Facebook. Media are invited to use the videos and images posted on DHS social media: Facebook and Twitter.

Governor Scott Walker has proclaimed the month of September as Recovery Month in Wisconsin. For resources on recovery from mental health and substance use concerns, visit the DHS website.

https://www.wispolitics.com/2018/wisconsin-voices-for-recovery-rally-for-recovery-on-september-22/

“The 2018 Rally for Recovery is focused on encouraging social connectedness through partnerships and building a culture of resilience in order to build a stronger foundation against the current public health crisis,” said Wisconsin Voices for Recovery, Statewide Program Coordinator Jessica Geschke. “As the substance abuse and alcohol epidemic continues to grow, so do the number of those working together to strengthen and build recovery efforts for those individuals struggling with the disease of addiction. We have come together, recovering together, to bring unity and hope.”

The Rally for Recovery is Wisconsin’s largest celebration of National Recovery Month, which is observed every September. The Rally for Recovery provides an opportunity to share the successes of individuals in recovery, learn more about the recovery resources available in Wisconsin, and laud the efforts of treatment providers, peer supporters, and others who help individuals achieve wellness.

 

Prebiotics & Probiotics: Do They Really Work For Gut Health?

https://vitalplan.com/blog/do-prebiotics-and-probiotics-really-work-for-gut-health?utm_campaign=September+15+VP+newsletter%3A+Pre%2Fprobiotic

Prebiotics-and-Probiotics-for-Gut-Health

Prebiotics + Probiotics: Do They Really Work for Gut Health?

by Beth Janes | Posted September 12, 2018

Prebiotics and probiotics have been trending for a while now, but lately they’re getting even more attention — and showing up in more and more products, from packaged foods (pizza crust!) to topical skin-care products. It’s no surprise consumers are interested: As scientists learn more about the trillions of bacteria that inhabit our bodies and the role they play in our health, some have touted beneficial bugs as a cure-all for digestive distress and other health problems.

But there are still many unknowns among researchers, and a lot of questions and confusion among the rest of us about what prebiotics and probiotics are, and what exactly they can and can’t do, says Bill Rawls, M.D., medical director of Vital Plan. Here, he answers some of the questions he hears most often.

What’s the difference between prebiotics and probiotics?

“Prebiotics are types of fiber, such as inulin, that are known to promote the growth of healthy microflora in the gut,” Dr. Rawls says. In other words, prebiotics feed the good bacteria already living in your gut, which allows them to multiply, thrive, and better do their job of keeping you healthy.

Probiotics, on the other hand, are actual strains of friendly bacteria or yeast that populate your gut. Ideally, probiotics maintain or restore a healthy balance of microflora, either by keeping bad bacteria in check or giving a hand to the good bacteria so they can function and flourish.

What are the best sources of both?

For prebiotics, the best sources are vegetables, hands down, Dr. Rawls says. Certain veggies such as sunchokes, mushrooms, garlic, artichokes, dandelion leaves, onions, and chicory contain high amounts of inulin, but you needn’t be overly selective.

More than anything else, eating a range of vegetables will cultivate the growth of normal bacteria,” Dr. Rawls says. “Because it’s not just about feeding the good bacteria: All vegetable fiber helps ensure normal digestion and that you’re evacuating the gut properly and regularly, which prevents the buildup of harmful bacteria.”

As for probiotics, fermented foods such as sauerkraut, kimchi, kombucha, kefir, and yogurt are naturally rich sources of live and active cultures (as well as digestive enzymes, which may be equally important for normal digestion). “Humans have eaten lots of different kinds of fermented foods throughout our history, for many thousands of years,” says Dr. Rawls. “That’s where the original idea for probiotic supplements came from.”

Research also suggests real-food sources of probiotics may be more effective than probiotic supplements at maintaining a diverse and healthy gut microbiome, the collection of microbes that inhabit your digestive tract. That could be due to the bacteria themselves, or the fact that the foods also contain a plethora of other healthy nutrients, including prebiotics, Dr. Rawls says.

Can prebiotics and probiotics improve digestive symptoms?

Prebiotics do contribute to a happy, symptom-free gut in the sense that they serve as fuel for the good microbes that help keep the digestive process humming. So while on their own they don’t do much, you absolutely need prebiotics for gut microbiome support and healthy digestion. Natural foods are by far the best source — supplements aren’t necessary if you’re eating a healthy, balanced, and veggie-rich diet.

As for probiotics’ ability to improve digestive symptoms, the answer is possibly. Probiotic capsules seem to help most when they’re used short-term for acute GI upset (diarrhea, stomach cramps) from eating contaminated food, like a batch of chicken salad that sat out for too long, for example, Dr. Rawls says. They may also help protect your microflora while taking antibiotics, which kill off good bacteria along with the bad, or if you contract C. difficile, a dangerous bacterial infection that causes diarrhea and inflammation of the gut.

“Most probiotic supplements contain bacterial strains of lactobacilli or bifidobacteria, or a favorable yeast called saccharomyces boulardii,” Dr. Rawls says. “Those are the ones that seem to show the most benefit.”

As for other digestive conditions, it’s hit or miss, he says. “The gut contains 20,000-plus strains of bacteria, and bacterial counts in the trillions. A probiotic supplement may be just a drop in the bucket, so getting an effect can be really hard.”

Further complicating things is that the mix of bacteria in people’s guts varies widely — in fact, it’s probably unique to you, like a fingerprint. What’s more, your microbiome can change based on your diet or lifestyle, or due to illness, so what might work for one person with a certain condition or symptom might not won’t work for another, Dr. Rawls says.

In addition, while different brands may use the same species of bacteria (lactobacillus, for example), they usually contain slightly different strains. So unless human studies on that one specific strain or bacteria blend shows a benefit on your particular health concern, it’s difficult to know for sure whether it will help you.

For all those reasons, published research is also mixed. Some is promising; for example, one meta-analysis of 15 studies published in the World Journal of Gastroenterology reported that probiotic supplements reduced pain and symptom severity in those with irritable bowel syndrome compared with placebo.

But other research, especially in healthy adults, shows little benefit from taking probiotics. And in fact, it may even introduce new symptoms: One small study of 30 subjects, published in the journal Clinical and Translational Gastroenterology, showed that taking a lot of probiotics can result in symptoms like brain fog and bloating in those using them for GI complaints.

Still, many experts tend to agree that the supplements, when taken in moderate doses, pose little risk. “I think it’s fine if someone wants to try taking probiotics; the potential for harm is low,” Dr. Rawls says. “Some people — maybe 15 to 20 percent of folks – may even gain benefit from them long-term.”

The newest trend in probiotics is customized formulations that are said to be based on your unique microbiome needs. Companies develop them after testing your stool sample for different microbes, and then selecting probiotics they say you lack in your gut. “While it may be a step in the right direction, the science and technology have a long way to go before this is a viable option,” says Dr. Rawls.

If you want to try supplements, he suggests taking them daily for at least three months and keeping a journal to see if you notice any improvements. If you won’t remember to take them daily, however, don’t even bother. Because the strains of bacteria in supplements are not the same ones already living in your gut, it takes a few days for them to populate and build up in your gut, and then you must continue to deliver them via supplements to maintain any activity.

What are some alternatives to probiotics for microbiome balance?

Step one is eating a mostly plant-based diet that includes plenty of fermented foods. Getting plenty of sleep and exercise and keeping stress in check are also key, as too little sleep and activity and too much angst contribute to overgrowth of bad bacteria.

Beyond that, Dr. Rawls says herbs and botanicals are more reliably effective and beneficial than probiotic supplements in the long-term. A few to key ones to reach for:

  • Chlorella, a type of green algae, is thought to be one of the most nutrient-dense foods available. It contains chlorella growth factor (CGF), a complex of proteins, vitamins, and sugars that works with fiber in the GI tract to promote the growth of healthy intestinal flora. It also contains chlorophyll, a potent antioxidant that binds to toxins and helps remove them from the body. “Chlorella is known for detoxification, but I’ve found that it does wonders for promoting normal GI function,” Dr. Rawls says.
  • Berberine, a compound found in several bitter herbs and other plants that’s well known for helping to balance the gut microflora. It’s been used for centuries to address intestinal disorders and digestive problems. “Berberine works very nicely because it stays predominantly in the GI tract, isn’t absorbed, and it’s active against gut pathogens,” Dr. Rawls says. That helps tip the scales toward healthy bacteria, keeping the bad guys from taking over.
  • Andrographis is likewise known to help support a healthy microbiome, plus it offers immune system-supporting capabilities. Native to India, andrographis can help promote good bacteria in the gut for better total balance, Dr. Rawls says.

The bottom line: Keeping your gut microbiome balanced is vital for maintaining healthy digestion, promoting sleep and immune strength, and more – and natural approaches are the best way to achieve that balance, says Dr. Rawls. Feel free to give probiotic supplements a try if you like, but be sure to track your progress to make sure it’s worth the money. And know that supplementing with the right herbs and botanicals, along with eating plenty of natural sources of both prebiotics and probiotics, will likely deliver the results you seek much more quickly.

_________________

**Comment**

My LLMD has noticed a stark contrast in patients from when before he started using probiotics in their treatment regimen and after.  He states it’s important to use a reputable lab and a refrigerated probiotic/prebiotic with many strains.  Refrigerated ones should be “live” cultures.

In all the years we’ve been in and out of treatment with antibiotics, we’ve never had GI issues and much of that is do to a low/no sugar diet and good pre and probiotics.

 

Treating Pain With Magnetic Fields

https://www.medicalnewstoday.com/articles/322718.php?utm_source=newsletter&utm_medium=email&utm_country=US&utm_hcp=no&utm_cam

Treating pain with magnetic fields

Published
Scientists have designed a hydrogel loaded with magnetic particles and laboratory-grown neurons. By applying magnetic force, the researchers were able to reduce the pain signaling of the neurons.
hand holding magnet

 

In the United States, chronic pain is “the most common cause of long-term disability.”

According to the National Institutes of Health (NIH), over 76 million people in the U.S. — that is, approximately 1 in 4 people — have had an episode of pain that lasted for more than 24 hours.

Of these, 40 million have had severe pain. Such figures led the NIH to deem chronic pain “a major public health problem.”

In this context, the search for new, more effective pain management therapies is ongoing and of vital importance. Now, bioengineers from the University of California, Los Angeles (UCLA) have designed an innovative method that may succeed where other pain therapies have previously failed.

Researchers led by senior investigator Dino Di Carlo, a professor of bioengineering at UCLA, set out to investigate how magnetic force could be used to relieve pain.

The first author of the paper is Andy Kah Ping Tay, a postdoctoral researcher at Stanford University in California. The researchers published their findings in the journal Advanced Materials.

Magnetic force reduces neuronal pain signals

Tay and his colleagues designed a hydrogel using hyaluronic acid, which is a molecule uniquely capable of retaining water and that has key roles in skin moisture and skin aging. Additionally, hyaluronic acid can be found between the cells in the brain and in the spinal cord.

After creating this hyaluronic hydrogel, the scientists filled it with small magnetic particles. Then, they grew a type of brain cell — called dorsal root ganglion neurons — inside the gel.

Next, Tay and team applied magnetic force on the particles, which enabled the transmission of the magnetic field through the hydrogel and to the neural cells. By measuring the calcium ions in the neurons, the scientists were able to tell whether the cells responded to the magnetic pull — and they did.

Finally, the researchers steadily increased the magnetic force and found that doing so reduced the neurons’ pain signaling. In an attempt to return to a stable state, the brain cells adapted to the magnetic stimulation by decreasing their pain signals.

Our results show that through exploiting ‘neural network homeostasis,’ which is the idea of returning a biological system to a stable state, it is possible to lessen the signals of pain through the nervous system […] Ultimately, this could lead to new ways to provide therapeutic pain relief.”

Andy Kah Ping Tay

Prof. Di Carlo also comments on the results, saying, “Much of mainstream modern medicine centers on using pharmaceuticals to make chemical or molecular changes inside the body to treat disease.”

“However,” he adds, “recent breakthroughs in the control of forces at small scales have opened up a new treatment idea — using physical force to kick-start helpful changes inside cells. There’s a long way to go, but this early work shows this path toward so-called ‘mechanoceuticals’ is a promising one.”