Archive for the ‘Pain Management’ Category

Acute Transverse Myelitis – A Clinical Manifestation of Lyme (That Nobody Has a Clue About Prevalence)

https://www.ncbi.nlm.nih.gov/pubmed/30622896

2018 Dec 29;15:e00479. doi: 10.1016/j.idcr.2018.e00479. eCollection 2019.

Acute transverse myelitis – A rare clinical manifestation of Lyme neuroborreliosis.

Abstract

Acute transverse myelitis (ATM) is a rare, potentially devastating neurological syndrome that has variety of causes, infectious being one of them. Lyme disease (LD) is the most common vector borne zoonosis in the United States (U.S.). While neurologic complications of LD are common, acute transverse myelitis is an exceedingly rare complication.

We present a case of a previously healthy 25-year-old man who presented with secondary erythema migrans, aseptic meningitis and clinical features of transverse myelitis including bilateral lower extremity motor and sensory deficits manifesting as weakness and numbness, urinary retention and constipation.

Despite negative serum antibodies against Borrelia burgdoferi, cerebrospinal fluid (CSF) was positive for Borrelia burgdorferi PCR.

Following treatment with methylprednisolone and ceftriaxone, he attained complete recovery apart from neurogenic bladder necessitating intermittent self-catheterization. We report rare manifestation of a common disease and emphasize the importance of considering LD in the differential diagnosis of acute transverse myelitis, particularly in residents of endemic areas.

__________________

**Comment**

Nobody has a CLUE about how often anything is occurring in Lyme/MSIDS, when testing misses over half of all cases and folks are commonly misdiagnosed or undiagnosed for years.  Again, because words mean things, and research has been used against patients for over 40 years, a more accurate statement would be, “This is the first recorded case of ATM caused by Lyme Disease.”  And remember, just because something isn’t on record doesn’t mean it hasn’t happened.  Important distinction.

According to https://myelitis.org/living-with-myelitis/disease-information/afm/

The predominant presentation is weakness that may affect the limbs, face, oral or eye muscle. Weakness varies greatly ranging from subtle to very severe. AFM may result in total paralysis, partial paralysis, or weakness of just one limb. The combination of paralysis and how individuals present are widely variable. The limbs or muscle structures of individuals with AFM appear weak, flaccid, or limp and are not spastic as seen in classic cases of transverse myelitis. Since it is markedly the gray matter of the spinal cord that is inflamed in individuals with AFM, sensory, bowel and bladder functions can remain intact, however there are individuals that have both upper and lower motor neuron involvement.

The enterovirus (EV-D68) has been suspect in many of these cases however, it has not been definitively proven that it is this particular virus that has caused the paralysis,(1) although several cases of AFM occurred at around the same time as an outbreak of the EV-D68 virus.(2)

There has been a spike in AFM:  https://madisonarealymesupportgroup.com/2018/10/19/rise-in-acute-flaccid-myelitis-cases-and-the-link-to-vaccinations/

Within the above link, you will learn there are numerous theories on what causes AFM including viruses & vaccinations.  Lyme/MSIDS patients often have viral involvement, and reactivation of Lyme has been documented after vaccinations:  https://madisonarealymesupportgroup.com/2017/12/02/scottish-doctor-gives-insight-on-lyme-msids/, as well as Bartonella:  https://madisonarealymesupportgroup.com/2016/04/24/gardasil-and-bartonella/

https://madisonarealymesupportgroup.com/2016/11/07/connection-of-acute-flaccid-myelitis-and-vaccinations/  In this article, James Lyons Weiler states:

The US press has been pushing a view of acute flaccid paralysis as a mysterious condition of unknown etiology (unknown cause). Checking the scientific literature, however, tells us that AFP is most often Guillain Barre Syndrome (GBS), a condition that appears on the National Vaccine Injury Compensation Program as a “Table Condition” – i.e., one that the US HHS has no defense against when parents file in the NVICP for compensation for GBS as a vaccine injury in their children.  https://madisonarealymesupportgroup.com/2018/12/07/acute-flaccid-paralysis-is-most-often-guillain-barre-syndrome/

GBS is also often a player with Lyme/MSIDS:  https://madisonarealymesupportgroup.com/2019/01/09/transverse-myelitis-guillain-barre-associated-with-bartonella/

https://madisonarealymesupportgroup.com/2017/07/14/clinical-association-lyme-disease-and-guillain-barre/  In Dr. Waisbren’s book, Treatment of Chronic Lyme Disease, the majority of his 51 cases of chronic Lyme had high EBV titers.  He also states,

“As will be seen in other cases, the Epstein-Barr virus may be a candidate for a co-infection associated with LD.”  

Waisbren often treated this co-infected patients that had EBV with 1000mg of Valtrex three times a day with good success.  He also used gamma globulin (4cc twice a week).

So Lyme/MSIDS patients are at the top of the list for AFM for numerous reasons.  Personally, I had a MRI at one point due to the excruciating pain in my spine and occipital headaches.  This pain was unrelenting.  Borrelia burgdorferi (Bb) loves the brain and spinal column.  Many viruses hang out in the spine.  The MRI showed nothing abnormal and I was sent home with the same pain I came with.  While I believe proper antimicrobial treatment to be imperative, what finally relieved this pain for me was MSM:  https://madisonarealymesupportgroup.com/2018/03/02/dmso-msm-for-lyme-msids/

Along with swelling in the spine, patients can have brain swelling as well.  Within one week, I met 3 Lyme patients with Chiari, another supposed “rare” condition:  https://madisonarealymesupportgroup.com/2016/04/02/chiari/  While Chiari is often caused by structural defects in the brain and spinal cord that occur during fetal development, it can also be caused due to injury, exposure to harmful substances, or infection. 

When you study the Bb organism, along with the numerous coinfections, spine and brain swelling makes complete sense and needs to be studied further:  https://madisonarealymesupportgroup.com/2016/02/13/lyme-disease-treatment/

There is so much research begging to be done, yet main stream medicine wants to wrap Lyme into a pretty box with a bow on top.  Again, if there is any box involved with Lyme/MSIDS, it’s Pandora’s.

 

 

LDN & CBD

 Approx. 1 Min

LDN Plus CBD

In this video Dr. Liptan explains the additive effects of CBD (cannabidiol) when taken with LDN (low dose naltrexone) in reducing neuroinflammation and fibromyalgia pain. CBD can also ease some of the side effects caused by LDN.

 

 Approx. 20 Min

CBD for Fibro Pt 1

Dr. Liptan explains the science of CBD, and its uses in the treatment of fibromyalgia. This video also covers:
  • The difference between THC and CBD
  • The effects of CBD on the body based on human and animal studies
  • CBD’s benefits for pain, muscle tension, arthritis, anxiety, insomnia, and adrenal fatigue

To purchase Dr. Liptan’s medical grade, lab tested CBD products visit https://www.fridabotanicals.com Dr. Liptan is also an author of:  “The FibroManual: A Complete Treatment Guide For You And Your Doctor” http://amzn.to/1XP7ZMV “The Fibro Food Formula” https://amzn.to/2rggeZt

**Comment**
I am not affiliated with any products nor do I make a red cent on anything related to this website or the support group; therefore, I can recommend the following product strictly from personal experience and use:  Lidtke CBD Gold:  https://lidtkecbd.com
We use the 2500mg plain.  While it’s $189.00, I only take 2-6 drops at night.  Definitely helps with sleep and pain.
cbd-gold-plain-2500mg
Their CBD Gold line of tinctures blends the full-spectrum CBD extract with supplements such as iodine, GABA, 5-HTP, L-tryptophan, and a whole-food complex of the vitamin C component. Besides, the Lidtke brand indicates that their manufacturing process is from non-GMO, herbicide and pesticide-free hemp for those seeking assurance on the possibility of additives.
We also take LDN.  You titrate up from 1.5mg.  Our ending dose is 4.5mg but some patients need higher dosages.  We found LDN helps our immune systems generally but specifically with better sleep and pain reduction.
Very informative documentary put out by the LDN Research Trust on Lyme/MSIDS.  Dr. Horowitz, Dr. Toups, Dr. Schweig, Dr. Windham, Dr. Holtorf, & Dr. Schwarzback, speak on everything from testing, to diet, to inflammation, and how LDN can help patients.

Widespread Inflammation in Brains of Those With Fibromyalgia

https://neurosciencenews.com/inflammation-fibromyalgia-9925/?

Widespread Inflammation in Brains of Those with Fibromyalgia

Summary: A new study reveals elevated glial activation in the brains of those with fibromyalgia.

Source: Mass General.

A study by Massachusetts General Hospital (MGH) researchers – collaborating with a team at the Karolinska Institutet in Sweden – has documented for the first time widespread inflammation in the brains of patients with the poorly understood condition called fibromyalgia. Their report has been published online in the journal Brain, Behavior and Immunity.

“We don’t have good treatment options for fibromyalgia, so identifying a potential treatment target could lead to the development of innovative, more effective therapies,” says Marco Loggia, PhD, of the MGH-based Martinos Center for Biomedical Imaging, co-senior author of the report. “And finding objective neurochemical changes in the brains of patients with fibromyalgia should help reduce the persistent stigma that many patients face, often being told their symptoms are imaginary and there’s nothing really wrong with them.”

Characterized by symptoms including chronic widespread pain, sleep problems, fatigue, and problems with thinking and memory, fibromyalgia affects around 4 million adults in the U.S., according to the Centers for Disease Control and Prevention. Previous research from the Karolinska group led by Eva Kosek, MD, PhD, co-senior author of the current study, suggested a potential role for neuroinflammation in the condition – including elevated levels of inflammatory proteins in the cerebrospinal fluid – but no previous study has directly visualized neuroinflammation in fibromyalgia patients.

A 2015 study by Loggia’s team used combined MR/PET scanning to document neuroinflammation – specifically activation of glial cells – in the brains of patients with chronic back pain. Hypothesizing that similar glial activation might be found in fibromyalgia patients as well, his team used the same PET radiopharmaceutical, which binds to the translocator protein (TSPO) that is overexpressed by activated glial cells, in their study enrolling 20 fibromyalgia patients and 14 control volunteers.

At the same time, Kosek’s team at Karolinska had enrolled a group of 11 patients and an equal number of control participants for a similar study with the TSPO-binding PET tracer. Since that radiopharmaceutical binds to two types of glial cells – microglia and astrocytes – they also imaged 11 patients, 6 who had the TSPO imaging and 5 others, and another 11 controls with a PET tracer that is thought to bind preferentially to astrocytes and not to microglia. At both centers, participants with fibromyalgia completed questionnaires to assess their symptoms. When the MGH team became aware of the similar investigation the Karolinska group had underway, the teams decided to combine their data into a single study.

a brain scan

The results from both centers found that glial activation in several regions of the brains of fibromyalgia patients was significantly greater than it was in control participants. Compared to the MGH team’s chronic back pain study, TSPO elevations were more widespread throughout the brain, which Loggia indicates corresponds to the more complex symptom patterns of fibromyalgia. TSPO levels in a structure called the cingulate gyrus – an area associated with emotional processing where neuroinflammation has been reported in patients with chronic fatigue syndrome – corresponded with patients reported levels of fatigue. The Karolinska team’s studies with the astrocyte-binding tracer found little difference between patients and controls, suggesting that microglia were primarily responsible for the increased neuro-inflammation in fibromyalgia patients.

“The activation of glial cells we observed in our studies releases inflammatory mediators that are thought to sensitize pain pathways and contribute to symptoms such as fatigue,” says Loggia, an assistant professor of Radiology at Harvard Medical School. “The ability to join forces with our colleagues at Karolinska was fantastic, because combining our data and seeing similar results at both sites gives confidence to the reliability of our results.”

Original Research: Open access research for “Brain glial activation in fibromyalgia – A multi-site positron emission tomography investigation” by Daniel S.Albrecht, Anton Forsberg, Angelica Sandström, Courtney Bergan, Diana Kadetoff, Ekaterina Protsenko, Jon Lamp, Yvonne C. Lee, Caroline Olgart Höglund, Ciprian Catana, Simon Cervenka, Oluwaseun Akeju, Mats Lekander, George Cohen, Christer Halldin, Norman Taylor, Minhae Kim, Jacob M. Hooker, Robert R. Edwards, Vitaly Napadowa, Eva Kosek, and Marco L.Loggia in Brain, Behavior and Immunity. Published September 14 2018.
doi:10.1016/j.bbi.2018.09.018

_________________
**Comment**
Many Lyme/MSIDS patients are initially diagnosed with fibromyalgia.
https://www.lymedisease.org/lyme-sci-fibro/  In this informative article you will read about how Rheumatologist, Dr. Miller, became a Lyme activist due to his daughter-in-law’s misdiagnosis of fibromyalgia.
He believes all patients who have been given a diagnosis of a neurodegenerative disease—including ALS, MS, lupus, and fibromyalgia—should be evaluated for Lyme disease.

Almost all of these diseases are accompanied by pain, fatigue, sleep issues, cognitive issues, headache, numbness and tingling.

And, according to a survey of over 4000 patients with Lyme disease,

“roughly 20% of those with chronic Lyme disease were initially misdiagnosed with a neurologic disease including MS, ALS, Parkinson’s and multiple systems atrophy.”

Dr. Miller’s 4-part Lyme series:  https://madisonarealymesupportgroup.com/2017/05/11/dr-al-miller-lyme-disease-series/

Interview with Dr. Miller:  https://madisonarealymesupportgroup.com/2017/10/13/dr-miller-a-new-perspective-on-lyme-disease/

 

 

Live Webinar – The Pain Solution With Dr. Bill Rawls

https://rawlsmd.com/webinars/pain-solution/

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The Pain Solution with Dr. Bill Rawls

The sensation of pain serves the vital purpose of signaling the brain that something is wrong and requires attention and healing. But when pain is chronic and seems to have no identifiable cause, the brain doesn’t know how to restore health — and neither do most medical experts.

Join a live webinar with best-selling author Dr. Bill Rawls, who has studied the causes and symptoms of fibromyalgia, chronic Lyme disease, and chronic fatigue syndrome extensively.

He’ll explore the underlying forces that drive chronic pain and natural ways to resolve them, so you’re not just managing pain, but overcoming it.

PLUS: Have your questions ready for a LIVE Q&A on chronic pain and related illnesses including fibromyalgia, Lyme disease, and chronic fatigue syndrome with Dr. Rawls.

  • Presented by Dr. Bill Rawls and Carin Gorrell
  • Tuesday, December 11
  • 8pm EST
  • Webinar can be viewed on any device

RESERVE MY SEAT »

In this webinar, Dr. Rawls will also discuss:

  • The causes, characteristics, and biology of different types of pain
  • How your microbial burden impacts levels of pain-causing neurotransmitters and hormones
  • How CBD (cannabidiol) moderates the endocannabinoid system to reduce pain
  • Additional natural remedies for addressing underlying causes of pain and delivering both immediate and long-term relief
  • The four primary lifestyle factors that amplify pain
  • Numerous insights and answers during the LIVE Q&A with Dr. Rawls

 

Medical Cannabis Superior to Opioids for Chronic Pain, Study Finds

http://www.greenmedinfo.com/blog/medical-cannabis-superior-opioids-chronic-pain-study-finds?

Medical Cannabis Superior To Opioids for Chronic Pain, Study Finds

“© [Nov 4, 2018] GreenMedInfo LLC. This work is reproduced and distributed with the permission of GreenMedInfo LLC. Want to learn more from GreenMedInfo? Sign up for the newsletter here http://www.greenmedinfo.com/greenmed/newsletter.”

Sufferers of chronic pain have been faced with a perilous decision—risk a crippling addiction to opioids or find a way to live with the pain. A new clinical study has focused on medical cannabis as an alternative to opioids, and the results may be a turning point towards a safe, plant-based option for easing pain

A new study published in the European Journal of Internal Medicine represents hope for millions of sufferers of chronic pain. Researchers at the Cannabis Clinical Research Institute at Soroka University Medical Center, and Ben-Gurion University of the Negev (BGU), found that medical cannabis can significantly reduce chronic pain without adverse effects, particularly among adults aged 65 and older. Use of cannabis, aka medical marijuana, was found to be both safe and effective for elderly patients experiencing pain because of another medical condition, such as cancer, multiple sclerosis, Parkinson’s disease, Crohn’s disease, ulcerative colitis, and post-traumatic stress disorder.

One of the head researchers in this study, Prof. Victor Novack, M.D., is a professor of medicine in the BGU Faculty of Health Sciences (FOHS), as well as BGU’s Chair in Internal Medicine. He also heads the Soroka Cannabis Clinical Research Institute. According to Prof. Novack, M.D.:

“Older patients represent a large and growing population of medical cannabis users, [yet] few studies have addressed how it affects this particular group, which also suffers from dementia, frequent falls, mobility problems, and hearing and visual impairments.”[1]

The study surveyed 2,736 patients aged 65 years and older, at the inception of medical cannabis treatment, and throughout the 33-month study period. Surveys indicated the most common reasons for using cannabis were pain (66.6%) and cancer (60.8%). Methods of ingestion included cannabis-infused oils and smoking or vaporizing the herb. After six months of cannabis therapy, researchers provided a follow-up questionnaire which sought to determine any changes to pain intensity and quality of life, as well as any adverse events that were experienced. 901 of the original respondents replied.

After 6-months of medical marijuana treatment (all statistics are +/-):

  • 94% reported an improved overall condition, and a 50% reduction in pain
  • 60% reported improved quality of life, from “bad” or “very bad” to “good” or “very good”
  • 70% reported moderate to significant improvement in their condition
  • 20% of respondents stopped using opioids or reduced their dose

Notably, the most common side effects reported were mild: dizziness (9.7%) and dry mouth (7.1%), a far cry from the high-percentage of opioid-related deaths that are linked to chronic pain.[2] BGU researchers believe that utilizing cannabis may decrease the use of other prescription medications, including opioids, and encourage further research into this plant-based alternative, especially as it relates to an aging population.

Chronic pain is a problem that affects an estimated 100 million Americans.[3] It is also one of the most significant public health problems in the United States, with an estimated cost to society of $560-$635 billion annually, an amount equal to about $2,000 for every person living in the U.S.[4] Meanwhile, the nation’s growing opioid epidemic sees 1 of every 550 chronic opioid users dying within three years of their first opioid prescription.[5] While natural alternatives to deadly opiates are rarely offered by medical doctors, medical marijuana may be the drug that bridges this senseless gap. Research is beginning to mount that shows more promise than the medical establishment can long ignore.

Neuropathy is a type of chronic pain that presents as tingling and numbness in the hands and feet, often due to nerve damage from complications of cancer or diabetes, among other causes. A 2017 meta-analysis of prior studies on neuropathy found that cannabis, particularly selected isolates called cannabinoids, can provide analgesic benefit in patients with chronic neuropathy. Cannabis can also be used as an adjunct to other pain therapies, potentially lowering the amount of dangerous synthetic medication that is required to relieve pain. A recent study on the Opioid-Sparing Effect of Cannabinoids found that when cannabinoids were administered with opioids, specifically morphine, nearly four times less morphine was needed to achieve the same analgesic effect. This presents further evidence for cannabis as a means of reducing cases of opiate dependency and death.

While the politics of cannabis are exceedingly complex, the truth of this miraculous plant is becoming increasingly obvious: it heals the human body. The fact that it does so without the need for a black-box warning of Serious Adverse Events ensures that cannabis is the future of medicine. While clinical studies in the United States have been impeded due to cannabis’s classification as a Schedule One Controlled Substance (meaning the substance has no medicinal value), other countries have taken the lead. A UK study seeking to reduce chronic pain in advanced cancer patients not fully relieved from use of opioids, found that a cannabis extract composed of THC (Tetrahydrocannabinol) and CBD (Cannabidiol), two of the active constituents in cannabis, reduced pain by more than 30% from baseline when compared with placebo, with no serious adverse effects.

Beyond the realm of chronic pain, cannabis has been shown to positively support individuals dealing with post-traumatic stress. It has demonstrated effectiveness at calming the often-debilitating side effects of inflammatory bowel disease, aka Crohn’s disease. Isolates from the cannabis plant have shown promise at treating “incurable” diseases such as Grave’s disease and brain cancer, and work better than traditional medications for Alzheimer’s disease. With so much evidence of profound medicinal value, legislation based on old systems of control will not long hold back the tide. There are simply too many health benefits to be obtained from the cannabis plant.

For additiona research on the medical benefits of cannabis, visit the GreenMedInfo database on the subject.



Resources

[1] https://www.sciencedaily.com/releases/2018/02/180213111508.htm

[2] Service Use Preceding Opioid-Related Fatality. Olfson, Wall, Wang, Crystal, Blanco. Am J Psychiatry. 2017 Nov 28:appiajp201717070808. doi: 10.1176/appi.ajp.2017.17070808.

[3] Institute of Medicine Report from the Committee on Advancing Pain Research, Care, and Education: Relieving Pain in America, A Blueprint for Transforming Prevention, Care, Education and Research. The National Academies Press, 2011. http://books.nap.edu/openbook.php?record_id=13172&page=1.

[4] IOM (Institute of Medicine) 2011. Relieving Pain in America: A Blueprint for Transforming Prevention, Care, Education and Research, Washington, DC; The National Academies Press.

[5] Gabapentin, opioids, and the risk of opioid-related death: A population-based nested case-control study. Gomes, Juurlink, Antoniou, Mamdani, Paterson, van den Brink. PLoS Med. 2017 Oct 3;14(10):e1002396. doi: 10.1371/journal.pmed.1002396. eCollection 2017 Oct.


 

 

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

“© [9/6/16] GreenMedInfo LLC. This work is reproduced and distributed with the permission of GreenMedInfo LLC. Want to learn more from GreenMedInfo? Sign up for the newsletter here http://www.greenmedinfo.com/greenmed/newsletter.”

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.

_________________

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.

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