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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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:  

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Anger


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Anger at the failure of our medical system to support research and treatment of pain, anger at failure of the few currently available analgesics, anger at lack of interest or funding from Pharma – it requires at least $10,000,000 more to finish one important human treatment before submitting to FDA – that’s just one study. Pharma does not care, the price is peanuts to them. At one point, a company bought it, intending only to bury it. They do that for rheumatology treatments too, both the innate immune system and the adaptive immune system are being ignored. What could be more powerful than the immune system?

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Anger

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Anger at the failure of most medical organizations to discuss cannabis, medical marijuana. Training in cannabis is imperative.

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I am thrilled that Scripps Memorial Hospital Grand rounds in 10 days is a one hour lecture by the doctor who is head of HelloMD, national leaders in physician approval for medical marijuana, and in education.

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Anger at the destruction of the field of pain management. I posted on this two days ago, top left column. Anger at the greed in the medical system where pharma can buy whatever they want by sprinkling money at congress who will never ever ever do anything about the unholy prices of drugs. Certain elements in power will never stop trampling on the poor and the disabled. They will never treat the addicts. There is no will, they are paid off and nobody wants to help the disabled, the unwell, the poor. Not in  the U.S. Voters do not want to hear it.

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Anger says step back, surrender.

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There is nothing anyone can do. The swamp is exhausting, dirty, dangerous and black.

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I have tried 7-1/2 years to introduce a new paradigm. At various lifetimes in medicine, I have had funding, sat on boards of companies, and panels at FDA. I have witnessed the destruction of what it once was 43 years ago when I entered practice. A long and tortured history, but still the most exciting thing in the world is medicine, science. So what? They shut off the field of pain and are killing it. The world is the world. Always was, always will be. Lust and greed, says the sage. You cannot uncurl the curly tail of a pig, says the sage. Always was, always will be. Do your duty. You cannot escape it. But surrender to love.

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Surrender. Do what you can and surrender the results to the Infinite.

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Read these books:

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Dying to Get High, Marijuana as Medicine

by Wendy Chapkis and Richard J. Webb

NYU Press 2008

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From back leaf:

“How can a substance that is no mystery to half of all adults in the United States prompt such confusion and misrepresentation in the realms of law, medicine, and policy?…. Offering nuance in place of slogans, Dying to Get High tells an inspiring story of the tactics and philosophies of a little-understood health movement.”

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“A beautifully written account from the front lines of the struggle between a federal drug war complex determined to keep demonizing marijuana and the growing movement of patients and doctors who have found marijuana to be a valuable medicine.”

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“….. Provides a human element to the history, pharmacology, psychology, and politics of medical marijuana in a way that no other work has. I loved reading it.”

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Heroin Century

by Tom Carnwath and Ian Smith

Routledge Press, London

2002

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This is an extremely important, amazingly interesting, readable book for everyone.

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From back cover:

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Is heroin really dangerous? Or Is it just dangerous because it is illegal?

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Page-one 93,

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“The income of the drug barons is an annual $254 thousand million dollars, greater than the American defense budget.”

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Read this book. A page turner! Exciting! fast paced, awesome! mind boggling!

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And just because you might flash some anger to propel you to actually do something, don’t get stuck there. Be at peace. Work hard. Use your expertise. Surrender to the Infinite.

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While you are thinking about it, tell Congress to make pain management a mandatory course in more than the current 3% of medical schools, less then 30 hours in 4 years. Fund research and treatment of neuropathic pain such as CRPS, Complex Regional Pain Syndrome because it can be so disabling – the same neuropathic pain can occur from strokes. Don’t we deserve better? Not even cancer pain is taught, let alone grade schoolers who should be taught about the body, about addiction, drugs, sex. Teach all that opioids cause pain because they trigger inflammation in the immune system and that stimulates pain. The more opioid you give, the more the pain. Teach about the brain’s pleasure centers and addiction, how drugs and food and cigarettes work there and how addiction kills.

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Have a wonderful life all of you. There’s a lot of work to take up. You will meet great people. Can’t wait to see what a little anger will do.

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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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Comments are welcome.

This site is not for email, not for medical questions, and not for appointments.

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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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This site is not for email and not for appointments.

If you wish an appointment, please telephone the office to schedule.

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For My Home Page, click here:  Welcome to my Weblog on Pain Management!

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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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This site is not for email and not for appointments.

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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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Ketamine Consensus Statement for Mood Disorders Needed


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I just had a call from a student writing a paper on ketamine. Question #1: What % respond to ketamine.

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Why are we still asking this rather than treating with ketamine?

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3.7% of Americans are disabled with Major Depression, many for decades, or entire lives. Antidepressants may work on only 30%. It’s time we had a consensus statement on use and training of ketamine.

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Read Cornel West: Pity the sad legacy of Obama, before you read on.

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Pity the sad legacy of psychiatry. Even neoliberals fail to speak up, stuck in the dictates of the few. We’ve known for decades that ketamine is effective treatment. It can work in hours. IV ketamine clinics are popping up like Jack in the Boxes and will continue to increase in number.

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It is time to ask: Is IV the only way to administer? Is it cost effective? Do these doctors have the right training?

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We need a consensus statement from psychiatrists and from the American Academy of Psychiatry and Neurology on training in inflammation, the innate immune system and treatment with ketamine.

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Every psychiatrist and mental health specialist should be instructed in rationale, the innate immune system, glia, inflammation, addiction medicine, glial modulators (ketamine is only one), and how to look at the whole system, holistically, not just one more drug. Inflammation, diet, exercise, among these.

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A focus on Ketamine alone in treating a complex organ like the brain is incomplete. Think inflammation, brain, spinal cord, glial modulators, not just drugs, not just ketamine. Ketamine is potentially addicting, a schedule III drug. Evaluate a patient just as you do when prescribing opioids.

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Then we need consensus on its use for intractable chronic pain including RSD/CRPS.

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Why don’t schools teach anything on the human body and the immune systems rather than biology and cutting up frogs?

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 Data below is from National Institute of Mental Health:

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Major Depression Among Adults.

  • Major depression is one of the most common mental disorders in the United States.

  • The 12-month prevalence data for major depressive episode presented here are from the National Survey on Drug Use and Health  (NSDUH). Based mainly on the 4th edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-IV), in the NSDUH study a major depressive episode is defined as:

    • A period of two weeks or longer during which there is either depressed mood or loss of interest or pleasure, and at least four other symptoms that reflect a change in functioning, such as problems with sleep, eating, energy, concentration, and self-image.

    • Unlike the definition in the DSM-IV, no exclusions were made for a major depressive episode caused by medical illness, bereavement, or substance use disorders.

  • In 2015, an estimated 16.1 million adults aged 18 or older in the United States had at least one major depressive episode in the past year. This number represented 6.7% of all U.S. adults.

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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.

~~
This site is not for email and not for appointments.

If you wish an appointment, please telephone the office to schedule.

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