Archive for the ‘Pain Management’ Category

Sjogren’s Syndrome: Clinical Benefits of Low-dose Naltrexone Therapy

https://ldnresearchtrust.org/sites/default/files/sjogrens%20publication.pdf

Sjogren’s Syndrome: Clinical Benefits of Low-dose Naltrexone Therapy

Scott Zashin 1

1. Rheumatology, University of Texas Southwest Medical Center, Dallas, USA Corresponding author: Scott Zashin, szashin823@aol.com

 

Abstract

Sjogren’s Syndrome is a chronic autoimmune disorder that causes the inflammation of the lacrimal and salivary glands, resulting in dryness of the eyes and mouth. In addition, fatigue and musculoskeletal pain, often described as aching, is very common. Treatment directed toward alleviating the fatigue and pain associated with Sjogren’s is currently very limited. This report describes a case of a 47-year-old female with suspected Sjogren’s based on long-standing dry eyes, dry mouth, joint pain, fatigue, elevated measures of inflammation, and a positive rheumatoid factor. She failed standard therapy but improved clinically with low-dose naltrexone therapy.

Introduction

Low-dose naltrexone (LDN) is a unique compound that has pain-relieving and anti- inflammatory properties. Limited studies have shown benefit in helping relieve the pain in patients with fibromyalgia and improving disease activity in autoimmune conditions such as inflammatory bowel disease and multiple sclerosis. As a result, it seems reasonable that the medication might be useful in Sjogren’s Syndrome, an autoimmune condition that is associated with pain and inflammation.

Case Presentation

A 47-year-old female was diagnosed with Sjogren’s Syndrome six years ago by another rheumatologist, based on her history of eye and mouth dryness. She was found to have a negative rheumatoid factor at that time, but her sedimentation rate by modified Westergren (erythrocyte sedimentation rate, ESR) was recorded as low as 48 and as high as 61 (normal: less than 20 mm/h). Her C-reactive protein (CRP) was 1.74 (normal less than 0.80 mg/dl). Two years ago, she saw a second rheumatologist who agreed with the diagnosis of Sjogren’s Syndrome. At that time, her rheumatoid factor was now elevated at 69 IU/ml (normal: less than 14 IU/m/). Her antinuclear antibody (ANA) and Sjogren antibodies (SS-A and SS-B) were absent. Her anti-CCP antibody and 14.3.3 ETA protein were normal. Her ESR was 48 and her CRP was 1.42. Past medical history included a diagnosis of fibromyalgia. She also had a history of breast cancer that had been in remission for 20 years, a generalized seizure disorder, and elevated liver tests with normal biopsy. Additional medical issues included symptoms of neuropathy, anxiety, and depression. A prior sleep study did not reveal evidence of sleep apnea. She first came to see this author 18 months ago, seeking another opinion, with complaints of fatigue, severe musculoskeletal pain, as well as dryness of her eyes and mouth.

Her daily medications to help with her symptoms of Sjogren’s Syndrome and fibromyalgia included Lexapro, Restasis, meloxicam 15 mg, vitamin D3, magnesium, tramadol 100 mg daily prn, salagen 5 mg tid prn, and hydroxychloroquine 400 mg daily. Her exam demonstrated widespread trigger points affecting both sides of her body, above and below her waist. Her blood work was remarkable for an ESR of 37 and a CRP of 0.77. Her alanine aminotransferase (ALT) was 40 U/L (normal 6-29 U/L).

She elected to try low-dose naltrexone (LDN), which was compounded using a short-acting filler and started at 1.5 mg daily with instructions to increase the medication weekly by 1.5 mg. She came back to see me two weeks after starting the medication and was taking 3 mg daily. She stated that she felt terrific. Her lab was remarkable for a normal ESR of 25 and a CRP of 2.33. Her ALT was normal.

She was seen in follow-up 16 months ago and remained on 3 mg of naltrexone. She felt well but complained of neuropathic pain. Her ESR was now 20. CRP was not ordered. Her ALT was 31 U/L. She was seen in follow-up 14 months ago and remained on 3 mg of naltrexone and continued to feel well without stiffness or pain. She noted that, previously, it would take her all day to feel better. Her ESR remained at 20 and CRP was only minimally increased at 0.87.

She was then seen in follow-up 11 months ago with complaints of increased achiness. She had widespread tender points. She was given a short course of corticosteroids with symptomatic improvement in place of meloxicam. Naltrexone was increased on that visit to 4.5 mg. On the day of that visit, her ESR was 40 and CRP was 25.7 ( current normal value less than 8 mg/L). She was again seen in follow-up nine months ago, doing well on 4.5 mg of naltrexone. Hydroxychloroquine was discontinued a few weeks earlier due to a prolonged QTc interval. Her ESR was back down to 20 and CRP was down to 10.9.

Overall, the patient noted significant clinical benefit with her fatigue and pain within two weeks of starting low-dose naltrexone but no significant change in her dry eyes or mouth. She continues to do well on low-dose naltrexone four months after stopping hydroxychloroquine due to the electrocardiogram (EKG) abnormalities. While her symptoms improved, what is most interesting about this case is that her clinical improvement was associated with an improvement in her inflammatory markers.

Discussion

In the initial pilot study that used low-dose naltrexone in the treatment of fibromyalgia, the baseline sedimentation rate was a significant predictor of clinical response to LDN [1]. It was of interest to note that this patient’s dramatic clinical response to LDN correlated with an improvement in her ESR. It is postulated that low-dose naltrexone has a beneficial effect on the immune system due to the following mechanisms.

Low-dose naltrexone blocks mu-, delta-, and other opioid receptors. These receptors are present in the cells of the immune system. This inhibition may result in an upregulation of endorphins, which in addition to decreasing pain, may have a beneficial effect on the immune abnormalities by suppressing cell growth [2].

Low-dose naltrexone inhibits microglia activity. Microglia are immune cells in the central nervous system that, when stimulated, produce inflammatory products that may be associated with pain, fatigue, cognitive dysfunction (brain fog) sleep, and mood disorders. Low-dose naltrexone inhibits toll-like receptors that are found in microglia cells. As a result, the production of inflammatory substances declines with resulting symptomatic improvement [3- 4]. The inhibition of these toll-like receptors has been postulated to be responsible for the effectiveness of hydroxychloroquine, a standard therapy in diseases such as Sjogren’s Syndrome and systemic lupus.

Overall, LDN is well-tolerated. The 50 mg standard dose of naltrexone is Food and Drug Administration (FDA) approved in the treatment of alcohol dependence and for inhibiting the effects of opioids. Low-dose naltrexone is sometimes used to help alleviate the symptoms of patients with chronic conditions, including fibromyalgia [1], Crohn’s disease [5-6], and multiple sclerosis [7]. The use of LDN at this low dose and for these indications is considered “off-label” use. In other words, it has not undergone the rigorous testing needed to get the approval of the FDA. Side effects include but are not limited to vivid dreams (most patients take the medication in the evening, but morning dosing of the medication may help with this issue). Patients may experience a reduction in pain relief from narcotics for at least six to 24 hours after taking low-dose naltrexone. In addition, low-dose naltrexone should not be used in patients who are currently receiving opioid analgesics due to the possibility of acute opioid withdrawal. The medication should be avoided until it is felt that the narcotics are out of the patient’s system. Those patients taking thyroid replacement may require a lower amount of thyroid medication so periodic monitoring is indicated. The elevation of liver enzymes is a potential risk with naltrexone treatment but is not felt to be common with low-dose therapy. Other potential side effects may include but are not limited to gastrointestinal disturbances, such as stomach cramps and diarrhea, agitation, anxiety, flu-like symptoms, and headaches. The drug should be compounded with short-acting fillers, so calcium carbonate should be avoided. The most common starting dose is 0.5 mg daily in the evening and increased weekly up to a target dose of 4.5 mg. The drug can be started at higher doses. The drug should be stopped at a minimum of 24 hours prior to the time narcotics may be needed for pain relief for a scheduled surgical procedure. In my practice, I will ask patients to temporarily discontinue low-dose naltrexone 72 hours in advance of taking narcotics if the patient is new to therapy, to ensure pain relief [8-11].

Conclusions

Based on a Medline review, this is the first peer-reviewed case report of a patient with Sjogren’s Syndrome who was treated with low-dose naltrexone and obtained clinical benefits. As a result of this case, further study is needed to determine if low-dose naltrexone will subsequently prove to be a useful medication for treating Sjogren’s Syndrome.

Additional Information

Disclosures

Human subjects: Consent was obtained by all participants in this study. Conf licts of interest: In compliance with the ICMJE uniform disclosure form, all authors declare the following: Payment/services info: All authors have declared that no financial support was received from any organization for the submitted work. Financial relationships: All authors have declared that they have no financial relationships at present or within the previous three years with any organizations that might have an interest in the submitted work. Other relationships: I prescribe low dose naltrexone to patients in my medical practice.

References
  1. Younger J, Mackey S: Fibromyalgia symptoms are reduced by low-dose naltrexone: a pilot study. Pain Med. 2009, 10:663-672. 10.1111/j.1526-4637.2009.00613.x
  2. Wang D, Sun X, Sadee W: Different effects of opioid antagonists on μ-, δ-, and κ-opioid receptors with and without agonist pretreatment. J Pharmacol Exp Ther. 2007, 321:544-552.10.1124/jpet.106.118810
  3. 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, 33:451-459. 10.1007/s10067-014-2517-2
  4. Watkins LR, Hutchinson MF, Ledeboer A, Wieseler-Frank J, Milligan ED, Maier SF: Glia as the ‘bad guys”: implications for improving clinical pain control and the clinical utility of opioids. Brain Behav Immun. 2007, 21:131-146. 10.1016/j.bbi.2006.10.011
  5. Smith JP, Stock H, Bigaman S, Mauger D, Rogosnitzky M, Zagon I: Low-dose naltrexone therapy improves active Crohn’s disease. Am J Gastroenterol. 2007, 102:820-828.
  6. Raknes G, Simonsen P, Smabrekke L: The effect of low-dose naltrexone on medication in inflammatory bowel disease: a quasi experimental before-and-after prescription database study. J Crohns Colitis. 2018, 12:677-686.
  7. Gironi M, Martinelli-Boneschi F, Sacerdote P, et al.: A pilot trial of low-dose naltrexone in primary progressive multiple sclerosis. Mult Scler. 2008, 14:1076-1083.10.1177/1352458508095828
  8. Low dose naltrexone. (2018). Accessed: 2018: http://www.lowdosenaltrexone.org/.
  9. LDN Research Trust. (2018). Accessed: 2018: https://www.ldnresearchtrust.org/.
  10. Dickson, Windham, Smith, et al.: The LDN Book . Linda Elsegood (ed): Chelsea Green Publishing, White River Junction, VT; 2016.
  11. Moore E, Wilkinson S: The Promise of Low Dose Naltrexone Therapy. McFarland & Company Inc, Jefferson NC; 2009

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For an overview of Sjogren’s:  https://www.hopkinsrheumatology.org/rheumtv/sjogrens-syndrome-disease-overview/  (3 Min Video)  Please notice symptoms are quite similar to Lyme/MSIDS.  

Sjögren’s Syndrome is an autoimmune disease that is found primarily in women, where inflammation at the salivary and lacrimal glands causes dryness of the eyes and mouth. However, it’s also a systemic disease that affects the entire body, producing joint pain and fatigue, and damaging internal organs. As many as four million Americans suffer from Sjögren’s Syndrome, which often overlaps with other rheumatic diseases making it very common to misdiagnose or overlook. Unfortunately, many patients are not diagnosed on time, which makes it much more difficult to treat. In this video, the Director of the Jerome L. Greene Sjögren’s Syndrome Center, Dr. Alan Baer, discusses the symptoms and problems that many patients with Sjögren’s Syndrome face.

If you search the internet with the words Lyme & Sjogren’s, tons of blogs will pop up with people with both. There isn’t much if any science on the two, however. This is another problem with research in Lyme-land – nobody is studying the effects of Lyme triggering or in conjunction with other syndromes within the body.  A big problem.

Excerpt from The Lyme Book:  http://www.lymebook.com/beg_signs_symptoms.pdf

Lyme disease can trigger autoimmunity, so some people will present with rheumatoid arthritis, lupus, Sjogren’s, Hashimoto’s thyroiditis or any number of autoimmune diseases. It may not be that these diagnoses are incorrect; it may just be that the Lyme infection has unbalanced the immune system sufficiently to trigger the autoimmune mechanism. Where there is autoimmune disease with sufficient evidence of Lyme disease (either through lab work or clinically), treating the Lyme will often improve, if not eliminate, the autoimmunity.

The key concept to grasp here is that of underlying cause. Western medicine has somehow distanced itself from the quest for discovery of the underlying cause of illness. As is the case with bromyalgia or chronicfatigue syndrome, the diagnosis describes a set of symptoms but does not explain why they occur.

For more:  https://madisonarealymesupportgroup.com/2016/12/18/ldn/

https://madisonarealymesupportgroup.com/2018/10/30/ldn-an-overview-of-clinical-applications/

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/  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 Lyme/MSIDS patients.

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

https://madisonarealymesupportgroup.com/2019/01/16/ldn-cbd/

 

 

 

 

 

 

 

 

 

 

 

The Endocannabinoid System and the Important Role It Plays in Human Health

https://articles.mercola.com/sites/articles/archive/2019/02/10/endocannabinoid-system-role-in-human-health.aspx?

Published on Feb 5, 2019

Natural health expert and Mercola.com founder Dr. Joseph Mercola interviews Carl Germano, a board-certified nutritionist and phytocannabiniods expert, on how the endocannabinoid system influences human health.
February 10, 2019
By Dr. Mercola

STORY AT-A-GLANCE

  • Cannabinoid receptors in the human body were discovered in the 1990s, which in turn led to the realization that we make compounds in our body — endogenous cannabinoids — that influence these receptors
  • Endocannabinoid deficiency has been identified in people who have migraines, fibromyalgia, irritable bowel syndrome, inflammatory and neurological conditions and a variety of treatment-resistant conditions
  • While CBD has gained the most attention, CBD alone cannot fully support your body’s endocannabinoid system (ECS). You need the other phytocannabinoids and terpenes as well
  • Hemp has been outlawed in the U.S. since 1938. The latest Farm Bill, signed into law at the end of 2018, makes it legal again; hemp oil with full-spectrum phytocannabinoids may benefit a wide range of health problems
  • There’s an intimate relationship between your ECS and your omega-3 status. Omega-3 fats make your cannabinoid receptors more active, and are used as backbone structures to produce cannabinoids in your body

Hemp has been outlawed in the U.S. since 1938. Thankfully, the latest Farm Bill signed into law at the end of 2018 makes it legal. In this interview, board-certified clinical nutritionist and expert on phytocannabinoids, Carl Germano, discusses the exciting implications of this change.

Now, there’s a difference between cannabidiol (CBD) products made from hemp and those made from marijuana. While many mistakenly believe hemp and marijuana are interchangeable, they’re actually two different plants.

“Both are considered Cannabis sativa by genus and species, but that’s where the similarity ends,” Germano explains. “Hemp has been cultivated for many reasons for the past few thousand years — food, clothing, fiber and fuel. The plant itself contains naturally occurring active compounds called phytocannabinoids, of which CBD is just one of them.

Marijuana, on the other hand, has been cultivated for its primary phytocannabinoid, tetrahydrocannabinol (THC). While it has recreational value at small levels, it does have medicinal value.

Nevertheless, many decades ago, hemp got dumped into the definition of marijuana. Hemp was unjustly placed into the Controlled Substances Act (CSA), which kind of hampered its access, its ability to have U.S. farmers grow it, or to have even medical or academic institutions study it.

We’ve been in the Dark Ages for decades. Thanks to Israel and Europe, who’ve championed all the research, we’ve [discovered] the cannabinoid system in the body called the Endocannabinoid System (ECS).

Trump did sign a Farm Bill that finally deregulates hemp. It takes it out of the CSA … It gives the rights of farmers to grow it. It will open up the doors for academic and medical institutions to study it. It will give consumers access to [what is] probably the most important botanical we have on this planet.”

Why Whole Hemp May Be Better Than Isolated CBD

The hemp plant contains over 100 different phytocannabinoids, of which CBD is one. And while hemp has now been taken off the CSA, CBD is still under the jurisdiction of the U.S. Food and Drug Administration (FDA), which is responsible for the labeling of supplements and enforcing the Dietary Supplement Health and Education Act (DSHEA).

“With the passage of the Dietary Supplement Health and Education Act (DSHEA), you have several things against CBD. First, CBD was not in commerce prior to 1994, so it could not be grandfathered as a dietary supplement, yet hemp oil has been in commerce prior to 1994, so we’re OK there.

Secondly, DSHEA states that if you want to submit a new dietary ingredient application, you can do so and petition the FDA for an ingredient to be classified as a dietary supplement.

Well, if you were to do that today, you would get rejected immediately because the other part of DSHEA states that if Big Pharma takes a natural ingredient and makes a drug that gets approved, it’s hands-off to the dietary supplement industry.

GW Pharmaceuticals has two drugs using isolated purified CBD in it. Therefore, we’ve got several strikes against putting CBD on the front panel, calling it a dietary supplement, and I say, why bother? Because the story is much bigger than CBD, both clinically, scientifically and legally.”

Hemp oil is a food that happens to have CBD in it. But while CBD may not be legally advertised on the label, CBD-containing hemp products can be labeled as having phytocannabinoids — the class of compounds to which CBD belongs. While CBD has gained the most attention, CBD alone cannot fully support your body’s endocannabinoid system (ECS). You need the other phytocannabinoids and terpenes, which are very complementary to the phytocannabinoids, as well.

“Those of us in botanical medicine understand that the sum of all the parts of the plant is greater than any one single ingredient,”Germano says. “Let’s face it. There’s more than one ginsenoside in ginseng. There’s more than one curcuminoid in curcumin. There’s more than one isobutylamide in Echinacea. There’s more than one ginkgolide in ginkgo.

Well, there’s more than just one phytocannabinoid in hemp. Back in 2011, Dr. Ethan Russo in the British Journal of Pharmacology1 … wrote about the entourage effect of all the phytocannabinoids and terpenes needing to be present to give rise to full clinical, meaningful benefit …

While CBD may be the most dominant phytocannabinoid in hemp, the others are there in minor in number, but they are not minor in the body as they all participate in nourishing, supporting the ECS, which is the bigger story.”

Understanding Your ECS

While the discovery of the ECS is fairly recent, genetically it dates back over 600 million years.2Cannabinoid receptors in the human body were discovered in the 1990s, which in turn led to the realization that we make compounds in our body — endogenous cannabinoids — that influence these receptors.

It was also discovered that the ECS orchestrates communication between other bodily systems, such as your respiratory, digestive, immune and cardiovascular systems. The ECS does this via receptors found in every organ, including your skin.

“Your ECS is like the conductor of the orchestra. The orchestra are our organ systems. We cannot be healthy, we cannot be well if our ECS does not function well,” Germano says.

“Your body produces cannabinoids similar structurally to the cannabinoids found in cannabis. Your body feeds off of them. If you don’t produce enough to feed every single receptor, various conditions and various illnesses will ensue.”

Two Types of Endocannabinoid Receptors Have Been Identified

There are two primary ECS receptors: cannabinoid receptor type 1 (CB1) and cannabinoid receptor type 2 (CB2). While CB1 is typically thought of as being primarily in the brain and CB2 primarily in the immune system, both types of receptors are in fact found throughout your body.

One of the two cannabinoids your body produces is called anandamide — a nod to the word “ananda,” the Sanskrit word for “bliss,” as it attaches to the same CB1 receptors that THC attaches to. The other, 2-arachidonoylglycerol (2-AG), is found throughout your body.

“The ECS has been the subject of many scholarly textbooks … Quite frankly, this is something that should be taught from high school to college to medical school. Unfortunately, because of the stigma attached to cannabinoids … less than 13 percent [of medical schools in the U.S.] are teaching the ECS.

I say, ‘Are you insane? This is like saying that for the next 70 years we will not teach the cardiovascular system, as if it never existed.’ We now have to dismantle this medical travesty … The whole thing is about education. This is critical and crucial to our health and well-being.

We have to dismantle the stigma, and we have to start educating ourselves to understand that the ECS is probably one of the most important medical discoveries in quite some time. Understanding the enormity of this system and what it does and what it influences throughout the entire human body.”

Low Endocannabinoid Levels Result in Ill Health

With age, our bodies tend to become less efficient in creating the compounds needed for optimal health, and this holds true for anandamide and 2-AG as well. According to Germano, these two cannabinoids can actually be used as biological markers for certain illnesses and conditions.

Endocannabinoid deficiency has been identified in people who have migraines, fibromyalgia, irritable bowel syndrome, inflammatory and neurological conditions and a variety of treatment-resistant conditions. Germano also cites a paper3 in Translational Psychiatry, which found low anandamide levels are a statistically positive indicator for stress-induced anxiety.

They’ve also discovered there’s an intimate relationship between your ECS and your omega-3 status.4As it turns out, omega-3 fats make your cannabinoid receptors more active, and are used as backbone structures to produce cannabinoids in your body.

What do we see in people who have low omega-3 status? We see the same things we see in people who are endocannabinoid deficient: pain, inflammation, stress, anxiety, depression and so on. It is a perfect marriage between omega-3s and phytocannabinoids, which act like a multivitamin for the ECS.

But it doesn’t stop there. Look at bones … the reason we give post-menopausal women estrogen is because it influences the cells that build up bone, osteoblasts, and the cells that break down bone, osteoclasts. What does this have to do with the ECS?

We now know that if you stimulate the CB1 receptors, you start to stimulate the brain-to-bone communication by slowing down the brain from releasing bone-breaking compounds, like norepinephrine. Then when you stimulate the CB2 receptors, it increases osteoblasts, the bone makers, and decreases osteoclasts, the bone breakers.”

Top conditions associated with low cannabinoid levels include:
  • Pain, inflammation and inflammatory conditions
  • Stress, anxiety and insomnia
  • Ocular health
  • Bone health
  • Neurological conditions

“These are all conditions that can be suitably treated with phytocannabinoids,” Germano says. “These are conditions that we see in people who are endocannabinoid-deficient.”

Running Dramatically Boosts Anandamide Level

While runner’s high is typically attributed to the release of endorphins, running also dramatically increases anandamide in the body, and anandamide not only targets the CB1 receptor, but it also influences opioid and endorphin receptors. Not surprisingly then, the higher an individual’s anandamide level, the better they report feeling.

“That makes sense, because anandamide hits the receptors in the brain that are involved in reward and mood,” Germano says. “We also understand that the cannabinoids we produce are quite promiscuous.

They certainly touch the CB1 and CB2 receptors, but they [affect] other receptors as well, [such as] the 5-hydroxytryptamine (5-HT3) receptors, peroxisome proliferator-activated receptors (PPAR), gamma-aminobutyric acid (GABA) receptors, and receptors that control inflammation, pain, reward, anxiety and things of that nature.”

A paper5 published in PLOS ONE also details how various nutrients (such as omega-3 fats), drugs, exercise, chiropractic care, massage and acupuncture influence the function of your ECS.

Your Endocannabinoid System — A Key Player in Inflammation

Curcumin, boswellia, fish oil and quercetin are all well-recognized anti-inflammatory nutrients, but none can compare to what cannabinoids can do, Germano says, especially when the full spectrum is used.

As noted in a 2014 paper6 in Current Opinions in Clinical Nutrition and Metabolic Care, the ECS is an emerging key player in inflammation, because it’s intertwined with all of the inflammatory pathways, including the eicosanoid ones that omega-3 fish oils influence.

Germano also cites other research showing that targeting the ECS can ease both inflammatory and neuropathic pain, and describe how cannabinoids act as analgesics. According to Germano:

“You cannot contend with any inflammatory condition unless you’re supporting the ECS. They can be used interchangeably; phytocannabinoids along with curcumin and boswellia and fish oils would be remarkable, as they are complementary to each other by doing different things.

Again, we must address the ECS in any inflammatory condition, whether it be irritable bowel syndrome or injuries — even inflammation in the brain, which is one of the hallmarks of all neurological diseases. In 2003, the United States government got issued a patent on the neuroprotective effects of cannabinoids.

At that time, while the government has been telling us that phytocannabinoids are like lysergic acid diethylamide (LSD) and heroin — [meaning they] have no medical value — they go out and get a patent on the medical value.

But that was followed up, and there are many papers that talk all about the anti-inflammatory effects in the brain and in the nervous system, of these cannabinoids … There is nothing else like supporting the ECS with phytocannabinoids.”

Your Endocannabinoid System Also Plays a Key Role in Your Gut Health

You’re probably familiar with the fact that there’s a strong connection between not only your brain and your gut, but also your immune system. The importance of this triad in health and disease prevention cannot be overstated. Your gut not only is your largest immune organ, it’s also your second brain, containing hundreds of millions of neurons.

“We now understand how the gut is involved with communicating with the brain and the immune system, because it has brain cells and immune cells in it,” Germano says. In the middle of this trio is your ECS. It is actually the orchestrator of this tri-directional communication. According to Germano, researchers have also discovered the ECS controls:

  • Motility in the gut
  • Intestinal inflammation
  • Abdominal pain
  • Gut permeability
  • Tolerance to antigens

The ECS also reduces the activity of the stress pathways, including the hypothalamic-pituitary-adrenal (HPA) pathways. Anandamide, specifically, participates in the immunological response in the gut. What’s more, there’s also communication occurring between your endocannabinoid system and your gut microbiome (the bacteria in your gut).

Clinical Applications for Hemp Products

Again, a full-spectrum oil is actually far preferable to product in which CBD has been isolated. Germano cites a 2015 Israeli paper, which compared full-spectrum oil against isolated CBD, and found the full-spectrum oil was in fact clinically superior.

As for dosing, most of the literature demonstrates efficacy of CBD in the several hundred milligram range — but that is for “single magic bullet” isolated CBD. Preclinical studies and any clinicians are reporting that efficacy can be achieved with much lower doses when using a ful spectrum oil — some in the 10 to 25mg CBD range.

“Since CBD is the most dominant cannabinoid in hemp, when you extract oil from hemp, you do have much, much higher levels of CBD naturally in the oil as compared to the rest of the phytocannabinoid family. Providing 10 to 25 mg of CBD is the sweet spot for most conditions in the trade — especially when used with other synergistic ingredients …

People are responding quite remarkably, which [suggests] you don’t need a lot to jump-start the body’s ECS. Quite frankly, when we look at the bell-shaped curve with the isolates, the higher the dose, sometimes you decrease the effectiveness … When you use a full-spectrum oil and you’re getting the other important phytocannabinoid and terpene components, this is superior, and I’ll tell you why.

People have been focusing on CBD, which is the wrong message. It’s the myopic message. Think about it, CBD does not attach to the CB1 or CB2 receptors. If anything, CBD supports the CB1 receptors by preventing the breakdown of anandamide in our bodies and anandamide hits the CB1 receptor.

What about the CB2 receptor that controls inflammatory cycling, pain signaling, insulin sensitivity and bone building? CBD does nothing for that, so we need something of a CB2 agonist. A perfect partner to CBD would be another phytocannabinoid called beta caryophyllene. Luckily, the family of other phytocannabinoids in a full-spectrum oil contains other phytocannabinoids that complement to what CBD is not doing as well.

We must get off this single magic bullet bandwagon. We must appreciate the full gamut of all these phytocannabinoids as a whole, and that they complement each other, because CBD is not the answer to support the ECS as a whole.”

As with most things, too much can backfire. While CBD cannot kill you, using CBD isolate in too high amounts can reduce its effectiveness. Such problems are far less likely when using a full-spectrum oil.

“I don’t foresee anybody really overdosing on the standard dosages that we’re recommending,” Germano says. “Nor when we look at the data that’s been published, up to 1,500 mg of CBD chronically administered over time show that it was well-tolerated, minimal to no adverse reactions on physiological function, psychological functioning and other parameters in the body, including blood pressure. So, CBD is quite well-tolerated in humans.”

Hemp Oil for Sleep

Aside from inflammation and pain, another area where a full-spectrum hemp oil can be beneficial is to improve sleep and treat insomnia. Germano recommends using a full-spectrum oil in a dose that provides 25 mg of CBD.

“CBD at that range does a number of things. No. 1, it reduces excitability in the brain. It can reduce glutamate toxicity and any excitatory conditioning. Secondly, CBD is involved in various neurotransmitters that are involved with a normal sleep cycle.

While it has a calming effect and helps to establish a normal sleep cycle, it’s not necessarily a sedative. You can use it with melatonin. You can use it with lavender. You can use it with chamomile and passionflower, what have you. I would do that towards the latter part of the day, at least an hour or two before bedtime. Lower doses of CBD are more stimulating, so to speak, and more upregulating.”

How the New Law Can Improve Quality of Hemp Products

In the past, prior to the signing of the new Farm Bill, the leaf, flower and bud of the hemp plant could not be used in the production of CBD-rich hemp oil. The oil had to be pulled from the stalk and stem of the plant only — the less concentrated part. With the new law, all parts of the plant can be used, which will make processing easier and more economical, as the cannabinoids are more concentrated in the leaves, flowers and buds.

The law also makes it legal to grow hemp in in every state, so if you wanted to, you could grow it in your backyard. This is something I’m definitely considering, as you can easily juice the whole plant or add it to smoothies.

“Growing it for yourself would be wonderful,” Germano says. “It is a weed. It has a short period of harvest. It grows very rapidly — July, August and September. Yes, the whole plant can be used rather than just extracting the oils from it. All the phytocannabinoids and lipids are found in the oils, but the leaf can be juiced and put into smoothies as well …

In terms of growing and processing it, it’s a rather easy plant to grow, because it is a weed. When we talk about the raw plant, a lot of these cannabinoids are in their acidic form. CBD is in CBDA, cannabidiol acid, form. To convert it to its useable form, the acid has to be decarboxylated.

So, while you may benefit from a lot of the phytocannabinoids [in the raw plant], it’s going to be reliant on your body’s ability to process it from the acidic forms that are in there. Exposure to heat, light, moisture and air will decarboxylate a lot of them as well. The more you process it yourself, the more useable some of those phytocannabinoids will be.

[To process it], you can take the leaf, flower and bud. You can blend it and store it in the refrigerator. Over a day or two of exposure to heat, air, light and moisture, it’ll decarboxylate to some extent and you’ll benefit more from that. How much do you get? Appreciable amounts of CBD may be difficult with just juicing alone …

I don’t want to misquote myself and say the wrong thing, but probably an ounce or two [of raw plant] would do the trick as a healthy plant beverage. Again, you don’t need a lot to jump-start your body’s ECS. It’s not a numbers game. Small doses, you would definitely respond to.”

How to Identify a High-Quality Hemp Product

If you’re not growing your own, attributes to look for when shopping for a hemp product include:

Organic Kosher-certified
Non-GMO Verified pesticide and herbicide free
Full-spectrum phytocannabinoids Grown from certified seeds and not hybrids with marijuana

“I look for companies that are doing the right thing also. That is, they don’t mention CBD on the front panel or quantify it in the Supplement Fact box. Responsible companies talk about phytocannabinoids,” Germano says.

They talk about hemp oil. They talk about nourishing the endocannabinoid system. This is a superior story to just CBD. Those are the more reputable companies that are telling the right story, [and not just talking about] isolated CBD.”

More Information About Endocannabinoid System

Germano has written a book about the endocannabinoid system called, “Road to Ananda: The Simple Guide to the Endocannabinoid System, Phytocannabinoids and Hemp,” (www.roadtoananda.com) which is due out shortly. I am very proud to have written the forward to this book as it is a great resource. Definitely pick up a copy if you want to learn more about this fascinating topic.

“I’m ecstatic to announce that the person who wrote the introduction to the book is Raphael Mechoulam, the father of cannabinoid research and who was involved in the discovery of the endocannabinoid system.

He is well-known in the scholarly circles. There are certainly plenty of scholarly work out there, but we need to get this message, this story, which is enormous, out to the layman and practitioner out there who is really unaware still,” Germano says.

“I’ve been in this industry for over 35 years. I’m a clinical nutritionist by trade. I have not seen any natural compounds this clinically relevant since the inception of this industry. I can tell you that targeting the endocannabinoid system, supporting it, will dominate medicine and nutrition of the next couple of decades.

There are also topical applications for phytocannabinoids, because, again, our skin is one of our largest organs. It also has five to 10 times more cannabinoids in it than we have in our brain. The CB1 and CB2 receptors are there as well.

There are three targeted areas for topical applications. One, obviously, is pain and inflammation, because the CB2 receptors are there that control that. That is something that will blow away any of these compounds in the marketplace today for topical pain relief.

Then we know that certain cannabinoids strangle the sebaceous gland for acne. Certain cannabinoids also influence age spot development and antiaging. [There are] some very interesting things going on in the topical application area.

When we look at the global picture of what is the subcutaneous endocannabinoid system doing, it’s helping to maintain normal cell proliferation, differentiation and immune competence. Oncologists are going to be interested in that aspect.”

_________________

**Comment**

If you are a Lyme/MSIDS patient you should see yourself ALL over this article.  We struggle with pain, inflammation, gut issues (motility, permeability, antigen tolerance, pain/inflammation), neurological issues, & insomnia.  Many experience ocular & bone issues as well.  It will be interesting to observe the topical applications of this since so many have pain.

It’s quite amazing that our government has gotten away with pigeon-holing this wonderful plant into the same category as heroin and marijuana for decades.  Hopefully, we will see pricing begin to fall as currently, cost is high.

The article, and indeed everything I’ve read, stresses that full-spectrum CBD is crucial.

For more:  https://madisonarealymesupportgroup.com/2019/02/09/webinar-cbd-craze-health-or-hype/

My entire family has found CBD oil to help with both sleep and pain.  I give the brand we’ve had success with here:  https://madisonarealymesupportgroup.com/2019/01/16/ldn-cbd/  (I am not affiliated with ANY companies).  It is potent.  The company has other strengths as well.

Injection of Diabetic Drug Into Joints of Bb-Infected Mice Decreased Ankle Swelling & Immune Cell Recruitment

https://www.ncbi.nlm.nih.gov/m/pubmed/30700583/

Treatment of Borrelia burgdorferi-Infected Mice with Apoptotic Cells Attenuates Lyme Arthritis via PPAR-γ.

Hilliard KA, et al. J Immunol. 2019.

Abstract

Infection of mice with Borrelia burgdorferi causes an inflammatory arthritis that peaks 3-4 wk postinfection and then spontaneously resolves. Although the recruitment of neutrophils is known to drive the development of arthritis, mechanisms of disease resolution remain unclear. Efficient clearance of apoptotic cells (AC) is likely an important component of arthritis resolution. In this article, we show the number of AC increases in the joints of B. burgdorferi-infected mice around day 21 postinfection and peaks around day 28. Injection of AC directly into the ankles of B. burgdorferi-infected mice limited ankle swelling but had no effect on spirochete clearance or arthritis severity scores. In vitro, addition of AC to bone marrow macrophage cultures decreased B. burgdorferi-induced TNF-α and KC and increased IL-10. In addition, phagocytosis of B. burgdorferi and neutrophil migration to LTB4 were inhibited by AC. Exogenous AC caused an increase in peroxisome proliferator-activated receptor-γ (PPAR-γ) expression both in vitro and in vivo during B. burgdorferi infection. The PPAR-γ agonist rosiglitazone elicited similar changes in macrophage cytokine production and neutrophil migration as exogenous AC. Addition of the PPAR-γ antagonist GW 9662 abrogated the effects of AC in vitro. Injection of rosiglitazone directly into the tibiotarsal joints of B. burgdorferi-infected mice decreased ankle swelling and immune cell recruitment, similar to the injection of AC.

These results suggest that clearance of AC plays a role in the resolution of inflammation during experimental Lyme arthritis through the activation of PPAR-γ. PPAR-γ agonists, such as rosiglitazone, may therefore be effective treatments for inducing arthritis resolution.

________________

**Comment**

Apoptosis is programmed cell death without causing damage to other cells.  https://science.howstuffworks.com/life/cellular-microscopic/apoptosis.htm

apoptosis-diagram

When cells recognize viruses and gene mutations, they may induce death to prevent the damage from spreading.  In apoptosis the cell shrinks and sends out distress signals, which are answered by vacuum cleaners known as macrophages. The macrophages clean away the shrunken cells, leaving no trace.

Scientists are trying to learn how to modulate apoptosis, so that they can control which cells live and which undergo programmed cell death.  Many diseases and disorders are linked with the life and death of cells such as AIDS & Parkinson’s.  Decreased apoptosis can be a signal for lupus or cancer.

In the study above, they state that injecting the diabetic drug rosiglitazone (reduces blood glucose) into Bb infected mouse joints reduced swelling & immune cell recruitment similarly to injecting of apoptic cells.

Most interesting; however, is the admission that the injection of AC had no effect on spirochete clearance or arthritis severity scores.  

So the question becomes once again, is getting rid of inflammation/swelling the sole issue for those of us “chronically/persistently” infected or is spirochete clearance important?

I predict that while rosigliazone might help with inflammation and pain (like so many other substances), spirochete clearance is still important.  

This study begs the answer to what is causing persistent symptoms.  I think it also important to suggest it may be a number of factors and it may vary from patient to patient.

If there’s one thing I’ve learned about Lyme/MSIDS, it’s that it is highly variable & complex.

https://madisonarealymesupportgroup.com/2018/06/27/autophagy-finally-considered-for-disease-treatment/

What are the Similarities Between Autophagy and Apoptosis?  https://www.differencebetween.com/difference-between-autophagy-and-vs-apoptosis/#Autophagy%20vs%20Apoptosis%20in%20Tabular%20Form

  • Both result in programmed cell death.
  • Both are natural phenomena.
  • Both processes do not cause damage to other cells or cellular components.
  • Both are important in development and normal physiology.
  • Both are important in understanding the cellular basis of different pathological conditions including cancer and immune system related disorders.

 

Which Herbs For Inflammation?

https://www.medicalnewstoday.com/articles/324368.php?

Which herbs help reduce inflammation?

Many herbal remedies could have anti-inflammatory properties. However, the evidence to support the majority of these claims is lacking. Inflammation is the body’s primary defense mechanism against infections, wounds, and other forms of harm.

However, inflammation itself can be harmful in some cases. For example, many conditions can cause inflammation to remain elevated, resulting in tissue damage.

A range of anti-inflammatory drugs exist to help control inflammation in the body. However, they often have side effects and may not always be effective.

Natural compounds that are present in certain herbal remedies also have the potential to be anti-inflammatory. However, there is much less research in this area.

This article will list herbal remedies with the most evidence for their anti-inflammatory properties.

Turmeric

Anti inflammatory herbs

 

Turmeric typically comes in the form of a yellow powder from the root of the turmeric plant.

It contains a chemical called curcumin, which may have anti-inflammatory properties.

Several studies have shown that turmeric can help reduce inflammation and discomfort in people with arthritis.

It works by limiting the production of molecules called cytokines, which cause inflammation.

Researchers continue to investigate how curcumin affects inflammation in a range of other conditions, such as inflammatory bowel disease. Curcumin has the most substantial evidence base for its anti-inflammatory effects compared with other herbal remedies.

Turmeric is available in the form of capsules, tablets, teas, pastes, and extracts. Methods of taking turmeric will vary, depending on the intended use.

Ginger

Ginger, or Zingiber officinale, is a tropical plant that has long had a place in traditional medicines.

Ginger may have anti-inflammatory properties. There is evidence showing that many of ginger’s constituents can limit the production of cytokines and the activity of cyclooxygenase enzymes, which promote inflammation.

Research has found that the anti-inflammatory properties of ginger could be useful in treating several conditions, including arthritis and pain.

Ginger can be fresh or a dried root. It can also come in the form of tablets, capsules, and teas.

Green tea

Anti inflammatory herbs green tea

Green tea comes from Camellia sinensis leaves. Research has linked it to a variety of health benefits, such as aiding weight loss.

Green tea has anti-inflammatory properties that could underlie some of these specific health benefits.

For example, there is evidence to suggest that a component of green tea could disrupt processes that cause inflammation in the arthritis.

Other studies have found that green tea can have a positive effect on inflammation in people with metabolic disorders. Researchers suggest that it may drive these anti-inflammatory effects.

Green tea typically comes as a hot or cold drink. It is also possible to buy capsules, tablets, and creams that contain green tea.

Many other herbal remedies may also have anti-inflammatory properties. Examples include:

  • thyme
  • white willow bark
  • frankincense
  • resveratrol

However, there is not much research available on these remedies. Without this research, it is not possible to say with certainty whether these anti-inflammatory effects exist, or if they are effective treatment options for people with inflammatory conditions.

While a greater evidence base exists for the remedies in this article, the research in this area is still in the early stages.

For example, scientists have conducted many studies into the anti-inflammatory benefits of turmeric. However, the quality of these studies is not high enough to support the claim that turmeric can effectively reduce inflammation in humans.

It is also important to remember that studies in this area tend to use highly concentrated forms of these herbal remedies.

In some cases, certain compounds are isolated. One example of this is curcumin from turmeric. This means that the effects may differ when taking different forms of the remedy.

Risks

Anti inflammatory herbs doctor

  • gastrointestinal problems
  • liver problems
  • abdominal discomfort
  • heartburn
  • diarrhea
  • gas
  • sleep problems

It is also possible for these herbal remedies to interact with certain medications. For example, green tea can interact with certain beta-blockers such as nadolol.

It is important to discuss any herbal remedies with a doctor, who can advise further on drug interactions that may occur.

Summary

There is some evidence to support the claim that turmeric, green tea, and ginger have anti-inflammatory properties.

For people with inflammatory health conditions, consuming these herbal remedies could be useful for reducing inflammation.

However, more high-quality research will be necessary to confirm these effects. These herbal remedies are generally safe, but it is important to consult a doctor before taking them in conjunction with other types of medication.

_________________
Both DMSO & MSM are anti-inflammatory.  This in depth article explains their many uses – with recipes as well.
Both LDN and CBD are anti-inflammatory.

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/