Naltrexone in Low Dose Reduces Pain & Depression


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We’ve known LDN helps pain since the turn of the century. Stanford could really shake the research world if they trialed LDN for Major Depressive Disorder, not the depression that improves with less pain, or in Multiple Sclerosis clinics or the Parkinson’s or Inflammatory Bowel Disease clinics. Is it too much to ask for better quality clinical research, not just results of patients responding by click or touch on a computer touch pad?

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The astonishing promise of low dose naltrexone (LDN) research remains in its infancy since 1984, 33 years ago, when it was discovered to offer profound clinical relief for multiple sclerosis and other serious conditions. I have prescribed naltrexone in ultra low and low dose since 2003, and discussed its central anti-inflammatory glial modulating mechanisms in 2009:

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Low dose naltrexone, or LDN, has been prescribed “off label” for persons with many conditions including intractable pain, chronic fatigue syndrome, complex regional pain syndrome, RSD, Multiple Sclerosis, Parkinsons Disease, IBS, inflammatory bowel disease, autoimmune diseases and Crohn’s Disease to mention only a few. Low dose naltrexone is not a cure but may be potentially helpful for selected persons with these conditions. It appears to have little or no toxicity at this low dose – a few persons report transient insomnia, nausea or vivid dreams.

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The same year in 2009, soon after my post on LDN, Drs. Younger and Mackey of Stanford Pain Center reported a double blind study of low dose naltrexone in persons who had fibromyalgia more than 10 years and showed 30% improvement in pain and fatigue.

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In 2016, five Stanford authors including Dr. Mackey published a poster presentation. At least the 2009 study was double blind; not this one. It was open label.

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A novel glial cell inhibitor, low dose naltrexone, reduces pain and depression, and improves function in chronic pain: A CHOIR study

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Poster presented at: Annual Meeting of the American Pain Society; May 11-14, 2016; Austin, TX. Poster 418.

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Authors: K. Noon,  J. Sturgeon, M. Kao, B. Darnall, S. Mackey

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Stanford University Department of Anesthesiology, Perioperative, and Pain Medicine, Stanford, CA

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Funding received from NIH and the Redlich Pain Endowment

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NIH funding should lead us forward, not back to a single open label study. One would hope Stanford would do the larger study they recommended 7 years ago. This adds to the CV of five researchers, but

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  • does it help millions with chronic intractable pain?

  • does it add to the growing body of clinical LDN experience worldwide?

  • when will the mechanism and uses of LDN, the TLR4 receptor and the powerful innate immune system be taught by healthcare providers in academia, in practice, and in pharmacies, not just in basic science?

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The poster highlights the Stanford CHOIR Information Registry (discussed below), but provides almost nothing new despite the computing power of CHOIR that likely cost small fortunes. Patients are asked to enter clinic data into a convenient handheld click- or touch-based input device. What could be easier? We look forward to better studies from Stanford’s CHOIR devices and we long for the days when doctors publish better data that addresses the disabling pain, depression and needs of millions of our patients with chronic intractable pain.

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Stanford’s CHOIR Information System

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“We modified and implemented an existing, web-based system that administers computer-adaptive PRO questionnaires, called the Collaborative Health Outcomes Information Registry (CHOIR).  Next, we developed a messaging interface to send PRO results from CHOIR to the UF Health Epic EHR.

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The CHOIR system was developed at Stanford University by a team of informaticists and physicians who provided a no-cost license for our implementation. CHOIR utilizes a client-server architecture with web-based clinician and patient interfaces that use open source technologies, including jQuery mobile and Google Web Toolkit. Users can access CHOIR via web browsers on desktop or mobile devices. The primary patient user function is the completion of computer-adaptive PRO assessments using a click- or touch-based input device ( Figure 1 ).  Clinical user functions include registering patients to complete a PRO assessment, reviewing individual and summary PRO assessment results, longitudinal outcomes tracking, and clinical decision support through the aggregation of PRO result sets.”

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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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Spinal Cord Stimulators – comment on RSD


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Spinal Cord Stimulators 

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 Craig’s comment

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By no means do I mean to say that I or anyone else has better insight into how to treat pain, but I am against spinal cord stimulators [SCS’s] for treatment of pain due to CRPS, and possibly against use in other situations. I demand that the billions in profit they made be put into a retrospective and prospective study of damage caused by them in order for them to give full informed consent.

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I have 3 goals writing this.

  1. SCS’s

  2. Craig’s experience

  3. The Only Real Answer for severe pain, not damaging the system with opioids

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Informed consent is never given for spinal cord stimulators because it requires truth telling, something our corporations have been reluctant to do. Business ethics are not medical ethics, as we keep being reminded daily in the headlines.

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I enclose, below, a generously expressed and detailed comment by a man who had the patience to sit down and  write the painfully gory details so you can weigh-in on your decision whether to follow your pain specialist’s opinion to give you one. I don’t want anyone to feel suckered into choosing them and if I had pain I’ll admit I’d crave relief too. Anything. I’d be in line before the doors open.

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But if you have CRPS, spinal cord stimulators will create more pain. CRPS evolves unpredictably, by a will of its own. I know some very desperate patients with CRPS everywhere including face, mouth, gums, tongue, organs, trunk, limbs. Spinal cord stimulators will create more pain. Keep in mind, I don’t see the 5 year success stories even for lumbar disc pain. They don’t need me if they are pain free.

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But if you have CRPS and desperate need for pain relief because all else has failed — every known drug in highest possible doses of ketamine, propofol, opioids for weeks in ICU fail to even touch pain— there is one thing, and only one thing to do and I will set it out below. I just sent my recommendation to a patient with CRPS in extreme pain.

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My recommendation, below, is for patients who have nowhere else to turn.

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First I’ll mention the problems Craig encountered with SCS’s. He sent his comment to the opening page of this blog, so I will reproduce below. 

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I am currently undergoing a trial Medtronic SCS. I have had to have it reprogrammed 3 times since it was installed 5 days ago. I have had sensations and issues that I have addressed with my rep and my neurosurgeon. I get a severe headache when the unit is turned on. I get the constant feeling of having to urinate. I have current running through my testicles which they can not seem to program out and I am getting little pain relief. I have had to failed back surgeries, many failed injections and I have CRPS. The leads that were inserted when I was in the table covered my mid back and both legs. After I got to my feet and waited while they programmed the unit in another room. They came in and plugged it in and I no longer had coverage on the right side. My crps is in both legs, my hands, arms and face. The lyrica helped to tamp down some of the burning but I am in pain 24/7 and this was my last resort. I have scar tissue completely surrounding my S1 nerve. By the grace of God, I am on my feet, on crutches. I seem to get a look of disbelief when I tell them the unit is causing these issues or it’s not giving me the relief I was counting on. Relief, only to cause greater issues and pain. Is not relief to me. I can not wait to get this trial out of my back. I believe the leads slipped and that is why I am not getting the full coverage I had on the table. The issues I have had are as follows: severe headache, constant feeling of having to urinate, extreme joint pain, abdominal pain, sleeplessness, involuntary jerking, surges in current even when sitting still. Intense pain around the lead insertion site. Current uncomfortably running through my testicles, regardless of setting. It is my opinion there is still not a lot known about crps and I have read evidence of people have great success with these units. Everyone reacts differently. My body obviously creates a lot of scar tissue and my orthopedic surgeon created a fair amount herself. I can’t imagine even more or being forced into a chair for yet another unlucky decision. The medication helps and I have lived this far without the optimism that it would end soon. I had high hoed for this device but I don’t think it is right for me.

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One of my patients with CRPS was hospitalized for weeks with recurring unusual abscesses and required repeated surgery of hand and forearm. Even before surgery, she had failed opioids, failed ketamine, and was in ICU for weeks and weeks while the same medications were still given along with Propofol and IV Tylenol. Nothing helps her extreme pain.

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Anesthesiologists on staff in ICU threw everything they had at the pain for weeks. Most anesthesia pain doctors would have probably done what they did because that is the limit of tools we have.

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When you have hit the limit of benefit from opioids, ketamine, propofol, we have nothing else that treats pain with one exception: drug holiday.

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Stop all analgesics including Tylenol that destroys the liver as severely as cancer, the severity of which was newly discovered and published yesterday.

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The receptors for these analgesic drugs have up-regulated to such an extent they have caused the situation. Again, I stress, everything that was done during the ICU admissions would be done by any anesthesiology pain specialist. Those are the only tools. They cause the problem. The same for opioid induced hyperalgesia. We used to do it with Parkinson’s drugs in the 80’s.

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The only way to rehabilitate the up-regulation of all those receptors that have now exploded in numbers, immune to anything you throw at them, is stop the drugs.  Stop all of them for weeks, maybe months, years, no one knows, you are all the human guinea pig waiting to happen. But if we restart them, how long do we wait, how quickly will it again lead to this massive hyper-excitable state of pro-inflammatory cytokines that we know have gone wild, flooding the CNS. A flooded engine will not restart.

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Ketamine at least is known to reduce pro-inflammatory cytokines, but the system is too busy exploding, birthing new receptors that take over, and you’ve got a 55 car pile up. Well, more like millions I’d guess. No scientist here. Clnically, when can we resume something after a drug holiday, how soon and which drug? I’d avoid opioids because they create more pro-inflammatory cytokines. Choose ketamine, because they reduce pro-inflammatory cytokines, but if it works at all, stop it at first sign of tolerance, which is the need for increased dose. It becomes less effective. Walk a fine line, endure more pain because unless you do, it will no longer help. Opioids, analgesics of many kinds. 

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How do we get you through a drug holiday because we know withdrawing these drugs will trigger even more pain for possibly weeks until the system settles down?

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Pain storms, hurricanes

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This is complex regional pain syndrome where we see this insanity of pain storms. There is no other condition, unless several neuropathic pains in people with cancer, nowhere I have seen this type of pain in decades except CRPS – comparable to pain of subarrachnoid hemorrhage, blinding pain.

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No one has answers. None. One university does outpatient infusions of ketamine six hours daily for 8 to 12 weeks. Does it help? A small percentage. Outpatient, 6 hours daily, 5 days a week, staying at a hotel, 8 weeks.

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This is CRPS/RSD. No one has answers. It is futile to throw more of the drug in the system. That is my opinion. You have a choice and may choose otherwise. It is your body. You may stay on monthly opioids for decades, until you finally admit how poorly they work. A drug holiday is what we did in the 70s during my ancient training with Parkinson’s patients. They needed full 24-hour support. The American medical system has changed since then and those are not options currently available—cost.

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You need full psychological and psychiatric support.

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The Only Real Answer

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The country needs to invest $10 million to complete the clinical trials needed for an injectable, long-lasting interleukin 10 [IL-10], the anti-inflammatory cytokine. It already has full scientific and animal studies performed by and with the world’s foremost glial scientist at University of Colorado Boulder. Professor Linda Watkins has won awards from many countries. She has been the keynote speaker at the annual academy pain meetings for years. IL-10 can relieve pain for three months in animals that have intractable chronic neuropathic pain. This is not new —–NIH I’m looking at you to fund clinical trials. And those of you who care, do a Kickstarter to fund the clinical trials.

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This is the power of the innate immune system. NIH would rather fund research on the unknowns like stem cells rather than the known. It’s known for decades, NIH does not like to fund pain research. Glia are not all about pain. They are the innate immune system, the key to Alzheimer’s, neurodegenerative diseases, almost all known disease including atherosclerosis. It’s all about inflammation. We need the trials to stop giving drugs that cause inflammation, opioids —–CDC fiats are not as good as a drug that relieves pain, a drug that really works on mechanism. Where will the addicts go if the ER only has IL-10 for pain? That is one way to overspend on ER visits.  And NIH, please get us some real clinical research funding on how to use glia for our benefit. Get us some research on the entourage effect, combining medications to achieve relief especially for neuropathic pain.

Then bring on some crack negotiating teams from insurers to do some negotiation about pharmaceutical prices. Our new president has mentioned that.

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Please bring this to everyone’s attention. One way to get a grip on pain and/or depression is to build hope, help others, and energize behind a goal.

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Kickstarters work to raise tens of millions overnight. 

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IL-10 – animals have been shown to be pain free for three months, already proven in animal studies, by one of the world’s most widely acknowledged pain specialists Professor Linda Watkins, PhD. We need the final steps to fund the clinical trials in humans.

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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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Please IGNORE THE ADS BELOW. They are not from me.

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Pain Much Better off Opioids


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Patient disabled with CRPS/RSD markedly better after off opioids. The intense nerve pain began in his left ring finger eight years ago, not the dominant hand. Now he has pain everywhere below the neck. He has been bed-ridden for years.  Now his “bones feel like ice, freezing from the inside out and shaking.”

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Had been on Fentanyl patch 100 mcg/hr for years. Dose was lowered to 75 mcg/hr, then his pain specialist did an involuntary taper off in two short weeks. Both of those doses are far higher than the new CDC guidelines from 2016. Fentanyl is 100 times stronger than morphine.
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He says his pain is feeling much better off the opiates. He is quite surprised. On Fentanyl 100 mcg/hr patch, he rates his pain then as 6 to 8 on scale of 10.
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Pain is now  2 to 4 off opioids the last 3 to 4 weeks. Even the hands are not hurting as much..

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Initially after the abrupt taper, he spent 7 days in bed, then says he “started getting out a little bit, now hands are not hurting as much. Neuropathy even isn’t hurting as much.”

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I have seen several patients who said opioids caused pain, all over the body in places they never had pain before or since.

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Yes, clearly many are helped by opioids. But many are simply afraid to taper off. I understand this. The question then is, what will we do to treat pain? Most doctors have nothing else. Patients rightfully fear stopping opioids.

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We need to understand there is outstanding science that demonstrated years ago that opioids cause inflammation in the CNS (brain and spinal cord). Inflammation causes pain.

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Treat pain with glial modulators that relieve inflammation in the brain, neuroinflammation. These are off label and most of them must be compounded. Compounded medications are not covered by your insurance — thanks to pharmaceutical donations to congress.

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Cannabis (medical marijuana) can help some with spasm, pain, insomnia. Also not covered by your insurance — thanks to pharmaceutical donations to congress. But patients in New Mexico were able to get insurers to reimburse them for the cost of their medical cannabis.  Congress should allow dispensaries free access to banking systems and allow insurers to directly pay the cost for medical use. We all know the emperor has no clothes. Lets be real. Pain leads to desperate measures.

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Let me say right now, to all those who will send in comments attacking science, attacking me, attacking my clinical experience (my patient reports) on opioids, I will not post your attacks on these pages. I do prescribe opioids to select patients. I strongly believe all pain should be treated initially by glial modulators that relieve neuroinflammation before we begin causing pain and inflammation by ultimately having nothing else to turn to and then prescribe opioids. There is no better solution because pharma wants you on a drug for life. That’s money in the bank, forever, every single month for decades. It’s awful.

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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.

~~~~~

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

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Please IGNORE THE ADS BELOW. They are not from me.

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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.

~~~~~

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

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Steroids Corticosteroids Prednisone Cortisone Dexamethasone —Sensitize Microglia & Prime Glial Over-Responsiveness


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Glucocorticoids prime later immune &

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glial over-responsiveness that

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 induces cellular damage/stress in the brain

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The permissive role of glucocorticoids in neuroinflammatory priming: mechanisms and insights.

Frank MG, Watkins LR, Maier SF.
Curr Opin Endocrinol Diabetes Obes. 2015 Aug;22(4):300-5. doi: 10.1097/MED.0000000000000168. Review.
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“In light of these findings, we propose a model of glucocorticoid-induced neuroinflammatory priming whereby stress and glucocorticoids induce cellular damage/stress in the brain, the products of which prime the NLRP3 inflammasome. “
PMID: 
26087336 

Free PMC Article

Select item 255593332.
Barrientos RM, Thompson VM, Kitt MM, Amat J, Hale MW, Frank MG, Crysdale NY, Stamper CE, Hennessey PA, Watkins LR, Spencer RL, Lowry CA, Maier SF.
Neurobiol Aging. 2015 Mar;36(3):1483-95. doi: 10.1016/j.neurobiolaging.2014.12.003. Epub 2014 Dec 11.
PMID: 
25559333 

Free PMC Article

Select item 254331703.
Fonken LK, Frank MG, Kitt MM, Barrientos RM, Watkins LR, Maier SF.
Brain Behav Immun. 2015 Mar;45:171-9. doi: 10.1016/j.bbi.2014.11.009. Epub 2014 Nov 26.
PMID: 
25433170 

Free PMC Article

Select item 244854914.
Frank MG, Hershman SA, Weber MD, Watkins LR, Maier SF.
Psychoneuroendocrinology. 2014 Feb;40:191-200. doi: 10.1016/j.psyneuen.2013.11.006. Epub 2013 Nov 27.
PMID: 
24485491 

Free PMC Article

Select item 234590265.
Frank MG, Watkins LR, Maier SF.
Brain Behav Immun. 2013 Oct;33:1-6. doi: 10.1016/j.bbi.2013.02.004. Epub 2013 Mar 1. Review.
PMID: 
23459026
Select item 220412966.
Frank MG, Thompson BM, Watkins LR, Maier SF.
Brain Behav Immun. 2012 Feb;26(2):337-45. doi: 10.1016/j.bbi.2011.10.005. Epub 2011 Oct 24.
PMID: 
22041296
Select item 219074187.
Hains LE, Loram LC, Taylor FR, Strand KA, Wieseler JL, Barrientos RM, Young JJ, Frank MG, Sobesky J, Martin TJ, Eisenach JC, Maier SF, Johnson JD, Fleshner M, Watkins LR.
J Neuroimmunol. 2011 Oct 28;239(1-2):53-60. doi: 10.1016/j.jneuroim.2011.08.011. Epub 2011 Sep 9.
PMID: 
21907418 

Free PMC Article

Select item 215361238.
Loram LC, Taylor FR, Strand KA, Frank MG, Sholar P, Harrison JA, Maier SF, Watkins LR.
Brain Behav Immun. 2011 Oct;25(7):1408-15. doi: 10.1016/j.bbi.2011.04.013. Epub 2011 Apr 23.
PMID: 
21536123 

Free PMC Article

Select item 212569559.
Frank MG, Watkins LR, Maier SF.
Brain Behav Immun. 2011 Jun;25 Suppl 1:S21-8. doi: 10.1016/j.bbi.2011.01.005. Epub 2011 Jan 21. Review.
PMID: 
21256955
Select item 1964707010.
Frank MG, Miguel ZD, Watkins LR, Maier SF.
Brain Behav Immun. 2010 Jan;24(1):19-30. doi: 10.1016/j.bbi.2009.07.008. Epub 2009 Jul 30.
PMID: 
19647070

Select item 1738382611.

Stress-induced glucocorticoids suppress the antisense molecular regulation of FGF-2 expression.

Frank MG, Der-Avakian A, Bland ST, Watkins LR, Maier SF.
Psychoneuroendocrinology. 2007 May;32(4):376-84. Epub 2007 Mar 26.
PMID: 
17383826

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

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Glia regulate glucose & metabolism – diabetes, obesity, Alzheimers – will change treatment


 

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Sugar has a stronger effect on our brains than we even realised, study finds

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The complete opposite of what scientists thought.

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From publication today in Cell

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Astrocytic Insulin Signaling Couples Brain Glucose Uptake with Nutrient Availability

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Quoting from the Sciencealert report:

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“German scientists have discovered that our brains are actively taking in sugar from the blood stream, overturning the long-held assumption that this was a purely passive process.

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Even more surprising, they also found that it’s not our neurons that are responsible for absorbing all that sugar – it’s our glial cells, which make up 90 percent of the brain’s total cells, and . . .

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Not only does the find go against conventional wisdom on how our brains respond to sugar intake, it also shows how cells other than our neurons can actively play a role in controlling our behaviour.

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Astrocytes – which are a specialised form of glial cell that outnumber neurons more than fivefold – have long been thought of as little more than ‘support cells’, helping to maintain the blood-brain barrier, carry nutrients to the nervous tissue, and play a role in brain and spinal cord repair.

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But we now have evidence that they also play a role in human feeding behaviours, with researchers finding that their ability to sense and actively take in sugar is regulating the kinds of appetite-related signals that our neurons send out to the rest of the body. 

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And we’re not talking about a little bit of sugar here: the human brain experiences the highest level of sugar consumption out of every organ in the body. 

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“Our results showed for the first time that essential metabolic and behavioural processes are not regulated via neuronal cells alone, and that other cell types in the brain, such as astrocytes, play a crucial role,” explains study leader Matthias Tschöp from the Technical University of Munich.

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“This represents a paradigm shift and could help explain why it has been so difficult to find sufficiently efficient and safe medicines for diabetes and obesity until now.”

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Tschöp and his team decided to investigate how the brain decides to take in sugar from the blood – and how much – because this is directly related to our feelings of hunger.

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. . .The team used positron emission tomography (PET) scans to observe how insulin receptors act on the surface of the brain’s astrocytes. Insulin is a hormone produced by the pancreas to allow the body to use or store sugar (in the form of glucose) from carbohydrates in the food we eat.

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They found that if these receptors were missing on certain astrocytes, it would result in less activity in the neurons that are responsible for curbing food uptake, called proopiomelanocortin neurons. 

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Not only that, but they found that astrocytes missing insulin receptors actually became less efficient over time in transporting glucose into the brain – particularly in a region of the hypothalamus that sends out signals that you’re full, or satiated.

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So it looks like glial cells, not the neurons, are the true ‘gate-keepers’ for how much sugar our brains absorb, and we now know that sugar has such a powerful influence on them, they’re seeking out sugar, rather than just passively absorbing it.

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A better understanding of how this works could change everything about how we treat obesity in the future.”

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References to whet the appetite:

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Kleinridders, A., Ferris, H.A., Cai, W., and Kahn, C.R. Insulin action in brain regulates systemic metabolism and brain function. Diabetes. 2014; 63: 2232–2243

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De Felice, F.G. and Ferreira, S.T. Inflammation, defective insulin signaling, and mitochondrial dysfunction as common molecular denominators connecting type 2 diabetes to Alzheimer disease. Diabetes. 2014; 63: 2262–2272

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Ferreira, S.T., Clarke, J.R., Bomfim, T.R., and De Felice, F.G. Inflammation, defective insulin signaling, and neuronal dysfunction in Alzheimer’s disease. Alzheimers Dement. 2014; 10: S76–S83

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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.

~

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

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Complex Regional Pain Syndrome in Remission 6 years


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 Complex Regional Pain Syndrome

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Celebrating six years of complete remission

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Why ketamine should never be used alone

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I first posted her case here. 

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For years, pain below both knees was 8 to 9 on scale of 10, “like I had swallowed a fire burning.”

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She was unable to stand or walk for more than 4 years before seeing me. This week, I again saw this very healthy athletic RN who at almost 70 of age is very youthful, very energetic. She failed IV ketamine given first by Dr. Schwartzman daily for one week, then boosters for 8 months.

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After 8 months of ketamine, then no response at all. None. 

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That’s when I prescribed other glial modulators and rational polypharmacy that brought CRPS into remission. Then very very slowly tapered off all but one, leaving only low dose naltrexone (LDN) for the last 8 years. Zero pain. None. Hiking, working, fully active.

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When used in conditions with known neuro-inflammation, rats or human, LDN is a one of the most powerful, most effective glial modulators I have ever seen clinically in my patients in the last 15 years.

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Until proven otherwise clinically, LDN should be taken lifelong in those cases.

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This website is not for email.

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The advertising is not approved by me and

unrelated to anything on these pages.

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

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