CBD efficacy on nonmotor symptoms of Parkinson Disease anxiety & psychosis


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This is the last section of a review article Managing Psychosis in Parkinson Disease

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Results from preclinical and preliminary studies also suggest that cannabidiol (CBD) has therapeutic potential for nonmotor symptoms of PD.14 The multifaceted mechanism of action as an agonist of 5-HT1A, partial agonist of CB1 and CB2 receptors, and antagonist of the G-protein–coupled receptor GPR55 reverses the iron-induced epigenetic modification of mitochondrial DNA and the reduction of succinate dehydrogenase activity and decreases the levels of the pro-inflammatory cytokines IL-1β, TNF-α, IFN-β, IFN-γ, IL-17, and IL-6—all of which decrease pro-inflammatory mediators resulting in neuroprotective, anxiolytic, and antipsychotic effects.14

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“Several in vitro experiments have demonstrated promising neuro- protective effects of CBD in PD models. In one of these models, using PC12 and SH-SY5Y cells treated with MPP+ [1-methyl-4-phenylpyridinium], CBD increased cell viability, differentiation, and the expression of axonal [GAP-43] and synaptic [synaptophysin and synapsin I] proteins,” Ferreria-Junior and colleagues wrote,15 while acknowledging the paucity of studies that have addressed the biological bases for the purported effects of CBD on PD. “Double-blind, placebo-controlled, randomized trials with larger samples of patients with PD are needed to elucidate the possible effectiveness and mechanisms involved in the therapeutic potential of CBD in this movement disorder. This will also include the putative effects of CBD in preventing L-dopa–induced severe [adverse] effects and preventing PD progression.”

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The endocannabinoid system serves as an important filter of excitatory, inhibitory, and modulatory inputs that act at the midbrain and terminal regions to orchestrate DA neurotransmission by controlling DA cell body firing patterns, terminal release, and effects on postsynaptic sites in the striatum.16 Beneficial effects of CBD administration have been observed prior to or immediately after induction of PD-like symptoms in animal studies, which may suggest a preventive role rather than a therapeutic one.14 In an early open-label pilot study to evaluate the efficacy of CBD on nonmotor symptoms of PD in 6 patients with PDP, psychotic symptoms significantly decreased under CBD treatment, as evaluated by the brief psychiatric rating scale and the Parkinson psychosis questionnaire.17

 

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Psychiatric comorbidities prevalent in the majority of patients with PD are associated with more disease severity, impaired QOL, and increased use of healthcare resources, with longer hospital stays and re-hospitalizations adding to the total cost burden.

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The material on this site is for informational purposes only.

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It is not legal for me to provide medical advice without an examination.

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It is not a substitute for medical advice, diagnosis or treatment provided by a qualified health care provider.

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Low Dose Naltrexone for Pain


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From NPR: 

In Tiny Doses, An Addiction Medication Moonlights As A Treatment For Chronic Pain

 

Alex Smith

 

Lori Pinkley, a 50-year-old from Kansas City, Mo., has struggled with puzzling chronic pain since she was 15.

 

She’s had endless disappointing visits with doctors. Some said they couldn’t help her. Others diagnosed her with everything from fibromyalgia to lipedema to the rare Ehlers-Danlos syndrome.

 

Pinkley has taken opioids a few times after surgeries but says they never helped her underlying pain.

 

“I hate opioids with a passion,” Pinkley says. “An absolute passion.”

 

Recently, she joined a growing group of patients using an outside-the-box remedy: naltrexone. It is usually used to treat addiction, in a pill form for alcohol and as a pill or a monthly shot for opioids.

 

As the medical establishment tries to do a huge U-turn after two disastrous decades of pushing long-term opioid use for chronic pain, scientists have been struggling to develop safe, effective alternatives.

 

When naltrexone is used to treat addiction in pill form, it’s prescribed at 50 mg, but chronic-pain patients say it helps their pain at doses of less than a tenth of that.

 

Low-dose naltrexone has lurked for years on the fringes of medicine, but its zealous advocates worry that it may be stuck there. Naltrexone, which can be produced generically, is not even manufactured at the low doses that seem to be best for pain patients.

 

Instead, patients go to compounding pharmacies or resort to DIY methods — YouTube videos and online support groups show people how to turn 50 mg pills into a low liquid dose.

 

Some doctors prescribe it off-label even though it’s not FDA-approved for pain.

 

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For discussion of mechanism and case reports of the remarkable efficacy of this anti-inflammatory medication, use search function top left above small photo. Thankfully his insurer is covering the cost of the compounded capsules.

 
 
 
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The material on this site is for informational purposes only.

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It is not legal for me to provide medical advice without an examination.

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It is not a substitute for medical advice, diagnosis or treatment provided by a qualified health care provider.

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For My Home Page, click here:  

Welcome to my Weblog on Pain Management!

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Avoid opioid use in surgery to reduce postop pain


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Science for years has confirmed that opioids trigger inflammation and that creates pain. Trauma and surgery also create inflammation that leads to pain. How logical is it then to continue use of sufentanil for anesthesia when it is the most highly potent opioid 500 to 1,000 times stronger than morphine. Where is the logic in creating pain by using sufentanil as the anesthetic? A new one on the market will be 10,000 times stronger than morphine. Inflammation is not always easy to reset after you strafe the innate immune system with an opioid.

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Why is ketamine not used more often for surgical anesthesia when we know ketamine profoundly lowers the inflammatory response thus reducing pain more than ever. Studies for years have shown that even a small dose of ketamine reduces postop pain. This is not new.

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A study needs to be done comparing patients who receive no opioids. At least this study showed that when fewer opioids are used, pain scores are 37% lower than if more had been given. Patients given higher doses of opioid, had higher analgesic requirements postop. That increases the risk of persistent chronic pain and the tragic risk of addiction.

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Opioids inflict known lasting harm, pain and suffering, perhaps disability and addiction.

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Reduced opioid use in surgery linked to improved pain scores
Written by Brian Zimmerman

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After anesthesiologists at the University of Virginia Health System in Charlottesville began administering fewer opioids to patients during surgeries, patients’ self-reported pain levels dropped, according to a study led by three UVA anesthesiologists.
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For the study, the team examined 101,484 surgeries that took place in the UVA Health System from March 2011 to November 2015. During this time period, the amount of opioids administered via general anesthesia at the system was reduced by 37 percent.
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For the same time period, self-assessed patient pain scores recorded in post-op recovery units dropped from an average of 5.5 on a 10-point scale to an average of 3.8, marking a 31 percent improvement.

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One of the study’s leaders, UVA anesthesiologist Marcel Durieux, MD, PhD, said the impetus behind the pain score improvements is likely attributable to several factors. One, previous research has indicated opioids can ultimately make people more sensitive to pain. And two, the increased use of non-opioid painkillers like lidocaine and acetaminophen during surgeries at UVA was likely effective.

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….”There is very clear evidence that people can become opioid-dependent because of the drugs they get during and after surgery,” said Dr. Durieux. “I think that by substantially limiting opioids during surgery, we’ve made an important step in addressing that problem.”

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The material on this site is for informational purposes only.
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It is not legal for me to provide medical advice without an examination.

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It is not a substitute for medical advice, diagnosis or treatment provided by a qualified health care provider.

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Microbiome, Metabolome & Disease


 

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Many of us have followed the research in this field for health, happiness and well-being. Today’s questions and answers from an expert on microbiota in Reddit Science is of great interest and something I wanted on these pages for future reference. I sifted through the pages to condense the questions, leaving answers intact. AMA is short for Ask Me Anything. Where Professor Barrett’s  responses to questions are clear, I have omitted the questions; where not clear, questions are abbreviated and/or added. I am sure we would all like much more information on inflammation and the inflammasome, the gut and brain and health. Support science. Be careful of low quality journals and quackery. She says even some yogurts have no bacteria.

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Science AMA Series: I’m Kim Barrett, Professor of Medicine at the University of California, San Diego and Editor of The Journal of Physiology. This week, we published an issue on the microbiota [editorial free], so I thought it would be a great opportunity to discuss how our microbes influence our well being. AMA!

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This is her main message, again and again:

[–]Kim_Barrett

Eat a well-balanced diet, including cultured/fermented foods, and avoid excessive fat and processed carbohydrates..

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[–]Kim_Barrett

Thanks to both. There is a lot of epidemiological evidence for the health benefits of all of these fermented foods, which may deliver bacteria similar to probiotics as well as beneficial metabolites that have greater bioavailabilty. These foods have been consumed by humans for millennia but were less prevalent in the diet as society discovered refrigeration etc. But studies to actually prove efficacy and mechanisms of action remain in their infancy. This is an area where the National Center for Complementary and Integrative Health is placing a lot of emphasis for research funding.

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Q Nose/sinuses:

[–]Kim_Barrett

Yes, this is a less appreciated area but rapidly growing area of study. I definitely would encourage you to look at our special issue of the Journal of Physiology, which has short reviews on the oral, skin and vaginal microbiota. Our external cavities all have their own distinctive microbiotas, but in aggregate they may encode many of the same sorts of metabolic capacities as seen in the gut. The specific populations may also depend on the type of environment – for example, the bugs on your forearm are different from those on your forehead. Lots more work to be done.

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there is not a simple way currently of knowing about our microbiota’s composition, but general indices of gut health may give some clues. Likewise, finding effective probiotics may be a bit of a case of trial-and-error, but there is good epidemiological evidence for a beneficial effect of fermented foods like Kombucha.

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Q on IBS:

[–]Kim_Barrett 

Serotonin is a major controller of gut motility and sensation, and alterations in serotonin signaling have been documented in irritable bowel syndrome. The cells that make serotonin in the gut have been shown to express receptors for short chain fatty acids (SCFAs), which are major products of bacterial metabolism of undigested carbohydrates. Finally, some gut bacteria metabolize the serotonin precursoe, tryptophan, which in turn has implications for the production of appropriate gut levels of serotonin.

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Q:  Sometimes, when I am constipated, I can perceive a certain taste and smell that arrives internally. Have direct nerve connections between the bowel and the brain been identified? What role to microbiota play in perception of satiety? What is the importance of the neurological phenomenon vs the blood chemistry in controlling weight gain or loss?

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[–]Kim_Barrett 

Lots of nerve connections between the brain and gut, and gut nerve endings have been shown to sense bacterial metabolites. To the extent that the microbiota and their metabolites control the secretion of GI hormones, they clearly participate in satiety perception, but this still needs further study. And weight gain/loss is such a complex phenomenon, also encompassing societal and behavioral aspects, that the relative contributions of the factors you mention have not been worked out by any means.

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Good and bad may be too simplistic. A “good” bacteria may be bad for you if in the wrong place. As for substrates and products, this is probably too big of a topic to tackle right now, but I would direct you to the work of Eugene Chang at the University of Chicago who has done a lot of work in this area. Gut permeability is also clearly important. We have done work to show that certain commensal and probiotic species can tighten the gut barrier so that pathogens and toxic metabolites are less able to penetrate and initiate inappropriate inflammatory reactions and a vicious cycle of further weakening of the gut barrier.

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Q   Strong evidence correlates aberrations in gut diversity with certain diseases. Phylogentitcally speaking, it seems to matter more that the microbiome is diverse and less important which species are specifically there. The hypothesis being that the gut microbial metabolome is relatively stable, regardless of specific species present. http://go.nature.com/2iQLOu1

Q1 – Have clinicians started to take the next step, looking at disease correlations with perturbation of the microbial metabolome?

Q2 – If so, what have they found? Do probiotics replace those missing metabolic pathways?

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[–]Kim_Barrett 

Absolutely agree with your comments about the metabolome. However, most of this work at present is still in preclinical models, although there has been a lot of attention to the way in which metabolic pathways change after bariatric surgery, for example.

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Q:

When I was very young, I had a few instances of food poisoning visiting family in Mexico, I even contacted tuberculosis. I, of course, was given many antibiotics. I’ve had a lot of digestive issues since then, it was always a problem. I’m 36 now, and adopted a very low carb diet 3 years ago. During the initial transition, I had, to put it succinctly, severe dhiarrea. Like stuff was probably dieing off. And then, 4 months in, I had more energy, metal alertness, and general feeling of being present. And I no longer had crippling depression. From a completely anecdotal standpoint, I think that changing my diet also drastically changed my gut biome, and that, in turn, actually effected my brain function. It seems like what you’re research has shown is that this isn’t some woo-woo thinking, but an actual thing?

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Q does Kefir boost gut bacteria?

[–]Kim_Barrett

Yes, along with other related foods.

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Q are we discovering new categories of bacteria in the body?

[–]Kim_Barrett 

This was a big sticking point in the field initially since many of the bacteria cannot be cultured. Now they are identified by sequencing. The estimate is that healthy individuals harbor at least 1000 different species. Not to mention viruses, fungi, protea….we’re just getting started, and as you imply, the bioinformatics challenges are huge.

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[–]Kim_Barrett 

There’s quite a bit of evidence that mixtures of different bacteria are more effective than single bacteria. Perhaps they have complementary metabolic functions, or mutually help each other to colonize the gut.

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Q  research of healthy bacteria for auto immune disease?  Crohn’s disease?

[–]Kim_Barrett

Others are exploring a role in asthma.

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Q: studies in which obese mice had received gut flora from lean mice and subsequently lost weight, and vice versa. Does this imply that a microbial treatment for obesity in humans could be developed, and if so, is there any interest in this?

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[–]Kim_Barrett 

A lot of people are looking for just such a treatment!

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The material on this site is for informational purposes only.
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It is not legal for me to provide medical advice without an examination.

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It is not a substitute for medical advice, diagnosis or treatment provided by a qualified health care provider.

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Caffeine May Reduce Age-Related Inflammation, Stanford Aging Study


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Caffeine may be able to reduce inflammation.

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Inflammatory immune molecules increase as we age and are associated with mortality from all causes, Alzheimer’s disease, stiffening of arteries, hypertension and cardiac disease. Inflammation kills. Yesterday Stanford and colleagues from University of Bordeaux published results of a long term aging study of 114 patients in Nature Medicine (paywall):

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Expression of specific inflammasome gene modules stratifies older individuals into two extreme clinical and immunological states

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For nonscientists, see below. Caffeine may block inflammation. Adenosine and adenine are known to stimulate the inflammasome. Caffeine blocks the effect of adenosine.

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“They found that older people between the ages of 60 and 89 tend to ramp up production of immune molecules in a complex called the inflammasome. That’s a clump of immune proteins inside cells that activate one of the immune system’s big guns, called interleukin 1 beta or IL-1B. It’s an important molecule for fighting off infection, but too much of it for too long has been linked with chronic diseases like heart diseasecancer, and Alzheimer’s disease.

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Among the older people in the study, 12 of them made much more of these inflammatory molecules, and 11 people made much less. The less-inflamed group was also healthier, with lower blood pressure, more flexible arteries, and more relatives who lived past age 90.

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They also had lower levels of the breakdown products of DNA and RNA circulating in their blood, including one molecule called adenine, and another called adenosine — which is adenine attached to a sugar molecule. These molecules are known to stimulate the inflammasome, and lower levels of them could explain why this group was less inflamed. In fact, treating cells with these breakdown products made them churn out more inflammatory molecules, and made mice more inflamed, with higher blood pressure.

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HIGHER BLOOD LEVELS OF CAFFEINE CORRELATED WITH LESS INFLAMMATION

That’s where the caffeine comes in. Caffeine is known to block the effects of adenosine in the brain — that’s how scientists think it keeps us awake. So, the researchers suspected that it’s possible that it could block the effects of adenine and adenosine on immune cells, too, and reduce their ability to cause inflammation. According to a questionnaire, people in the less inflamed group consumed more caffeinated beverages like coffee, soda, and tea. In fact, higher blood levels of caffeine and other caffeine breakdown products correlated with lower production of inflammatory molecules like IL-1B.

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When the scientists treated cells with adenine and another molecule known to trigger the inflammasome, the cells that were soaking in caffeine produced far lower levels of inflammatory molecules. The researchers still haven’t fully explained how caffeine is interfering with inflammation. And the results aren’t enough to base any behavioral recommendations off of; but it’s comforting news for those of us who were already reaching for that second hit of caffeine, anyways.”

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Many articles on pro-inflammatory cytokines IL-1β, IL-6, and TNF-α are found in the setting of chronic pain and in depression:

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IL-1β is an essential mediator of the antineurogenic and anhedonic effects of stress.

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Depressed rodents shown to have inflammation, published by Yale and NIMH a few years ago.

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The material on this site is for informational purposes only.
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It is not legal for me to provide medical advice without an examination.

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It is not a substitute for medical advice, diagnosis or treatment provided by a qualified health care provider.

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This site is not for email and not for appointments.

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CRPS & All Patients – pills no help for this severe pain


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Yes, people with nerve pain, CRPS pain, any pain, and often those without pain have this. It can lurk for decades before pain is obvious. But find the right spot and you’ve got it. Doctors and patients fail to understand one of the worst disabling causes of severe pain. Pills, drugs fail to help, but doctors reflexively respond with pills because they often have no training in this. The slightest movement, a sudden flicker of being jarred and pain explodes up to a 9. Pain may catch you by surprise, you yelp, you can’t help it, and you stop instantly. It’s unbearable, the slightest jolt, the wrong angle, a split second. Some reach for a handful of pills, and cut back activity until they are completely unable to walk or move without fear. For others, no jolt or yelp, it just appears and silently gets worse without your knowing, until it manifests decades later and now you cannot function. You forget the incident that set it off.

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CASE

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Healthy 19 year old with pain on standing, walking, wanted a motorized wheelchair on first visit

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This young student had suddenly dropped out of UC Berkeley before the end of the quarter due to severe pain, difficulty walking. The only patient in 41 years of medicine who asked for a motorized wheelchair, was only 19, had no medical illness, no neurological deficit, no inflammatory markers, no injury, but unbearable pain on standing and walking.

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After four months of physical therapy, he was pain free and regained full function, out in the park running with his dog and his friends. Nineteen years old and able to live a normal life. It hurts like crazy. Physical therapy had to get out all the “snags” in muscle and fascia that prevented normal function and caused excruciating pain. There is no magic.

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CASE

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A grandmother with pain in both feet had not been able to stand for six long years. She loved cooking for family and grand kids, but was unable to stand to do anything. She could not walk. In less than two weeks of physical therapy, she was walking 1 to 2 miles a day and loving her life again. Depression vanished. Building her strength to walk more each day.

 

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Oh, need I explain that when you taper off opioid in a case like these, yes, they will have pain just from withdrawing the opioid – the body wants its opioid back and taper creates pain that may stay high for weeks even months, until the body stops klanging for its opioid and the psyche stops catastrophizing to figure out it can live without vegetating by sedating the brain. Each cell in the body goes wild for its opioid and does not want to give up its drug. The autonomic nervous system goes into overdrive, patients leave your practice to find any of hundreds of thousands of doctors for more opioid that perpetuate the desire to lie back and do nothing to trigger any slight jolt. Just narcotize the brain.

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CAUSE

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Stasis. Inactivity. Not moving. Immobilization. Sedentary muscle, just sitting, or in a cast or after knee surgery, bedridden. Stasis. Simply stasis. Muscles and fascia develop “knots” that you are not aware of until suddenly, the wrong jolt, the slightest move, and you freeze, screaming in pain. Prolonged sitting often causes hip flexion contractures. “Knots” can be felt in muscle,  tender points are highly localized. P.T. finds them and causes screaming pain to get them out. My own body has it now in several muscles, both thighs. It’s common. They’re quiet until you find them and mash them. It hurts like crazy to treat it, but that’s the only way to get this silent killer that takes lives. Pills do nothing. Blood curdling yelps and bruises appear during P.T. If you don’t do it, it gets worse. They are not always easy to find, not always a “knot” that can be felt, but zingers they are.

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HOW

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What’s in blood besides red cells, white cells, oxygen? Fibrin and collagen. If you cut yourself, fibrin instantly seals the bleed and forms a clot. The body then builds collagen, a major component of connective tissue. What had been soft tissue can turn into a tough fibrous matrix. Nutrients and oxygen cannot get to it. The “knots” must be properly and precisely released by a skilled physical therapist to find them all, to release them all.

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Just this week, a patient with back pain who quit P.T. early, told me she learned to reduce back pain in bed by placing pillows under the knees, two pillows. Perfect! to develop hip flexion contractures that prevent standing erect, thus throwing out the spine and soon a 3rd or 4th back surgery. Undiagnosed, untreated hip flexion contractures are surely one of the major causes leading to preventable spine surgery.

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Doctors don’t know how or perhaps don’t care to diagnose it.

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Pills do NOTHING to relieve it.

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There is no hope until the knots are undone.

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Compliance is crucial. We have a choice. But in 2003, W.H.O reported: 50% of people don’t comply w/ chronic disease management. Insurance denies medications, insurance limits physical therapy, you are left with rapidly increasing disability and a miserable hell that does not respond to pills of any kind, not even massive doses of opioids.

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STASIS – OBESITY

 

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Obesity leads to increasing stasis. Let’s not dwell on obesity in itself that causes inflammation and increases estrogen production in fat all over the body – that’s one of the reasons obese men develop breasts. Every woman knows estrogen can cause horrific disabling pain. The more fat we pack on is like adding estrogen producing ovaries all over the body. And fat cells remain hungry for 10 years before new ones arise. We take to walkers and wheelchairs instead of the obvious: lose weight, take pounds of fat off joints, muscles and spine, rid the system of excess pain-producing estrogen, and then work out the knots with physical therapy. Thin people get knots in muscle too but obesity and its load of estrogen is a big culprit.

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Motorized wheelchairs:  How many obese individuals are willing to lose weight, even when it means regaining life and use of body? You don’t have to pay money to eat less. Exercise helps but it is not the only way to lose weight, and people may eat more after exercise.

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Seize the day. Failure is not a healthy option but I’ve chosen favorite foods too often. Eat well, nothing between meals, limit protein to 4 oz of fish/chicken/meat or 8 oz dairy/legumes, one piece of fruit in AM with protein, add loads of veggies – 5 cups per day, the low glycemic veggies, one tablespoon oil/butter with each meal. Never skip meals. Plan ahead, carry your own food if you work away from home. Most of all, avoid anything that is high glycemic. Stomach will feel very full, but very eager at the time of next meal. You will find your mood is stabilized. Your joints will not bother you as much or not at all.  You will have more energy and less depression.

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If you are unsure what foods are considered high glycemic, use the old axiom for weight loss “if it’s white, don’t bite” with some exceptions such as cauliflower. Here is a link to a list of glycemic food levels to get you started.

 

 

 

 

 

 

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The material on this site is for informational purposes only, and is not a substitute for medical advice,

diagnosis or treatment provided by a qualified health care provider.

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Please understand that it is not legal for me to give medical advice without a consultation.

If you wish an appointment, please telephone my office.

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Ketamine Prescribed Since 1994 – My Experience


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Ketamine offers an opportunity for normal life unmatched by any medication I know of when given off-label for chronic treatment of intractable pain, treatment resistant depression, bipolar depression, juvenile bipolar disorder. It is one of the safest medications I have prescribed in 41 years of medicine. I have never seen anything more effective – it is not a cure, but remission is highly possible. Please refer to peer reviewed references since 2009 on this website on ketamine and depression or pain. Read elsewhere about street drugs, junkies, addicts and media headlines.

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Never Ketamine Alone

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Ketamine is short acting no matter how it is given.

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I never prescribe ketamine by itself – a fools errand; the religion of ketamine is like the religion of opioids. Decades of intractable conditions and chronic neuroinflammation require more than one short acting drug and usually require a multi-disciplinary approach. I work with psychologists or psychiatrists and other specialists when indicated.

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Entourage effect 

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DRUGS ARE LIKE POLITICIANS. A FAMOUS POLITICIAN MAY WALK UNRECOGNIZED, BUT WHEN YOU SURROUND HIM OR HER
WITH MANY PEOPLE, EVEN OF LESSER STATUS, THE POLITICIAN HAS A FAR MORE POWERFUL EFFECT.

Mechoulam

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1994 – I first prescribed IV when teaching cancer pain at MD Anderson Cancer Center.

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2001 – prescribed for outpatient care of chronic intractable pain

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2011 – prescribed for treatment resistant depression, bipolar depressed, juvenile bipolar/fear of harm phenotype often diagnosed as oppositional defiant disorder.

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2009 – writing about ketamine, neuro-inflammation and glial modulators on this site, with classic references to publications from the foremost peer reviewed journals, including low dose naltrexone, oxytocin.

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Dosing

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Depression, Bipolar Disorder, Juvenile Bipolar/FOH, treatment resistant – may need a dose only twice daily or every 3 days. The dose and frequency of use cannot be predicted – it is idiosyncratic – look up that word.

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Intractable pain – dosing and frequency of medications is very different than for depression.

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My work with these medications, these glial modulators, is too extensive to annotate on these pages. This website since April 2009 has references for context and guidance with active links to peer reviewed publications. Example:

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Clinical experience using intranasal ketamine in the treatment of pediatric bipolar disorder/fear of harm phenotype. D Papolos et al, J Affect Disord. 2013 May;147(1-3):431-6.

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RESULTS:

Ketamine administration was associated with a substantial reduction in measures of mania, fear of harm and aggression. Significant improvement was observed in mood, anxiety and behavioral symptoms, attention/executive functions, insomnia, parasomnias and sleep inertia. Treatment was generally well-tolerated.

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CONCLUSIONS:

Intranasal ketamine administration in treatment-resistant youth with BD-FOH produced marked improvement in all symptomatic dimensions. A rapid, substantial therapeutic response, with only minimal side effects was observed. Formal clinical trials to assess safety and efficacy are warranted.

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mTOR-Dependent Synapse Formation Underlies the Rapid Antidepressant Effects of NMDA Antagonists. R Duman et al, August 2010, Science, Science 2010 Aug: Vol. 329, Issue 5994, pp. 959- 964. [this article free with registration]
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ABSTRACT:

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We observed that ketamine rapidly activated the mammalian target of rapamycin (mTOR) pathway, leading to increased synaptic signaling proteins and increased number and function of new spine synapses in the prefrontal cortex of rats. Moreover, blockade of mTOR signaling completely blocked ketamine induction of synaptogenesis and behavioral responses in models of depression. Our results demonstrate that these effects of ketamine are opposite to the synaptic deficits that result from exposure to stress and could contribute to the fast antidepressant actions of ketamine.

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“The resulting protein synthesis and neuronal alterations in the medial prefrontal cortex are the opposite of those produced by chronic stress….”

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Read elsewhere about street drugs, junkies, addicts and media headlines.

If that is you, see an addictionologist, not me.

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Some medications can be drugs of abuse but every patient and every medication that I dispense is followed meticulously. If any sign of misuse or abuse, that unfortunate person is immediately discharged and referred elsewhere.

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It is not legal for me to give medical advice

unless you are my patient which means I have done a medical history and examination.

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I generally accept only those who have failed most or all known treatments, and only those who I feel I can help.

 

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I interview each patient before accepting.

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Any advertising below is not recommended or condoned by me.

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