Cannabis, a few things you need to know


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PainWeek 2018 has a series of conferences in different cities. This weekend 10/13-10/14, it was in San Diego teaching pain management. 

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There was a talk on cannabis by a nurse practitioner from Stanford. I would add or highlight a few things.

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There are two species:

–Indica often said to help pain, sleep.

–Sativa more activating, for daytime use.

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Most are hybrids. Some people have opposite responses. It may be contraindicated for those with bipolar disorder. Those with multiple sclerosis may use it for spasticity. It can help depression but may cause anxiety, depression, paranoia, etc.

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The plant has 400 chemicals. More than 90 are cannabinoids. Two best known cannabinoids:

–THC is psychoactive.

–CBD has no psychoactive properties and does not make you high. In recent years, it has been found to help certain forms of epilepsy in children who are resistant to all known epilepsy medication.

–THCV has been said to prevent the munchies. Only one strain I know of has this cannabinoid, Durban Poison.

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It is not necessary to have THC for pain relief. Pain in some patients may respond to CBD alone.

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Tolerance does develop. It becomes less and less effective with use.

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Side Effects: the very worst is the munchies – deadly weight gain. Dry eyes and dry mouth can affect all, but for those with Sjogren’s Syndrome, it increases the risk of corneal transplants and loss of teeth that already exists and can be a serious problem. It can increase heart rate and blood pressure especially in those who have never used cannabis.

 

Update 10/19/18, cannabis may boost risk of stroke. The drug has system-wide effects therefor not limited to smoking it. Note that we have known it does increase heart rate and blood pressure, at least initially when starting use, but may develop tolerance to side effect with regular use – or not. The new study does not indicate how much cannabis these patients were using, their ages and blood pressure baseline and during use. Was their use conservative or were they overdosing, couch locked, less active than usual?

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  • Stroke increased by 15% among marijuana users between 2010 and 2014
  • Rates of stroke in non-cannabis users stayed constant over that time
  • Compounds in cannabis may cause blood vessels in the brain to narrow

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Rates of stroke among non-cannabis users didn’t change. However, rates among recreational users jumped by 15 per cent.

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“Avalon University researchers…analysed 2.3 million people between the ages of 18 an 84 who used cannabis recreationally and spent time in hospital from 2010-to-2014.

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Of these, 32,231 – 1.4 per cent – had a stroke.

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And 19,452 had an acute ischemic stroke (AIS), which occurs when blood supply to an area of the brain is suddenly cut off, leading to a loss of cognitive function.

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Over the four years, the rate of all strokes among marijuana users rose from 1.3 per cent to 1.5 per cent. And AIS increased from 0.7 per cent to 0.9 per cent.

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The research was presented today at the World Stroke Congress in Montreal.

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They scientists believe their findings ‘warrant further prospective studies to evaluate the marijuana-stroke association amidst legalisation of recreational use’.

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But the study contradicts previous research that suggests smoking cannabis can actually reduce the risk of stroke by boosting blood flow to the brain.

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Marijuana has also been linked to faster recovery post stroke.

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Stroke is the second leading cause of death and disability globally, with one person passing away from the condition every six seconds.

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Around 140,000 people die from stroke in the US and 32,000 in the UK every year.

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Leafly.com is a nationwide resource for locations where cannabis is legal, listing strains and dispensaries by zip code. For each local strain it shows a bar graph of EffectsMedical, Negatives. Negatives may include dry eyes, dry mouth, sleep, anxiety, paranoia, headache, etc. rated by buyers. For example, one strain may be rated 100% dry eyes, but only 50% dry mouth. Each strain is different. But dry eyes, dry mouth are the most common, always highly prevalent, whereas paranoia, dizziness, anxiety may be rated only 3%.

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FDA has approved 2 THC compounds available for medical use:

–Dronabinol (Marinol), schedule III drug. I have never seen a single person with cancer pain, HIV AIDS pain or chronic pain benefit. Instead they complain about it, including those who heavily used cannabis.

–Nabilone (Cesamet), a schedule II drug. I had it diluted 10 times for a healthy senior with intractable pain. He hallucinated for 12 hours after a tiny dose. I’ve never seen a plant do this.

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More research is greatly needed. It has primary effect on the immune system in brain and body including neuro-inflammation in the central nervous system and the skeletal cannabinoid system. It is anti-inflammatory. In the brain, the microglia makes and reabsorbs one of the endogenous cannabinoids made by the brain. Studies show cannabis can help pain but almost all of my patients who tried many many strains reported that it failed to help intractable pain. Others stopped due to side effects. But I have seen patients with intractable pain and treatment resistant migraine who responded to CBD alone.

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Use the search function top left above photo for previous posts on cannabis.

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Beware the munchies and weight gain. It can be deadly. That effect can be life-saving in cancer patients and end of life care.

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Urine drug testing does not always include cannabis. It may be present in urine for up to 2 months. Don’t even think about getting on a plane with cannabis.

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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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Ketamine’s effects tied to opioid system in brain


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Stanford announces:

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Ketamine’s antidepressive effects

tied to opioid system in brain

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“Ketamine’s antidepressive effects require activation of opioid receptors in the brain, a new Stanford study shows. The surprising finding may alter how new antidepressants are developed and administered in order to mitigate the risk of opioid dependence.”

 

 

…”The study enrolled adults with treatment-resistant depression, meaning their condition had not improved after multiple treatment efforts. Twelve participants received infusions of ketamine twice — once preceded by naltrexone, an opioid-receptor blocker, and once with placebo. Neither the study participants nor the researchers were told whether active drug or placebo was administered during each test. The researchers found that ketamine reduced depressive symptoms by about 90 percent for three days in more than half of the participants when administered with a placebo, but had virtually no effect on depressive symptoms when it was preceded by naltrexone.”

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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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Cannabidiol (CBD) FDA Approved for Epilepsy – May Help Pain, Mood – Costs Review


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Epidiolex from GW Pharmaceuticals, is a cannabidiol (CBD) recently approved by FDA for treatment of epilepsy. Others have found CBD helpful for pain, migraine, and mood disorders. CBD is one of the more than 80 known cannabinoids in the cannabis plant, the marijuana plant. It has no psychoactive effect, that means it does not make anyone “high”. But urine drug tests will be positive for marijuana and anyone may risk losing their job if their employer checks – some drug tests do not specify marijuana.

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Medications can be prescribed off-label by your doctor for conditions other than the FDA approved epilepsy in this case, and hopefully covered by healthcare insurance. Below are costs of the Epidiolex brand reviewed by O’Shaughnessy’s newsletter, the newsletter originally for California cannabis doctors.

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FDA approval means CBD now has accepted medical use and should be no longer classified as Schedule I, though the ruse will likely be continued by congress.

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GW Pharmaceuticals PLC said it plans to charge about $32,500 per patient annually in the U.S. for its new treatment for rare forms of epilepsy, the first prescription drug derived from the marijuana plant.

Chief Executive Justin Gover said in an interview Wednesday that the company set the price to be in line with other brand-name epilepsy drugs, such as H. Lundbeck A/S’s Onfi. He noted that the FDA designated the product an “orphan drug,” meaning it treats rare conditions, and that some other orphan drugs carry higher prices.

Out-of-pocket costs for patients taking Epidiolex could range from $5 to $10 a month for those in state Medicaid programs to as high as $200 a month for some private insurance plans, Julian Gangolli, president of the company’s North America unit, said on a conference call with analysts Tuesday. Uninsured patients may qualify for receiving the drug free.

Dr. Jacqueline French, chief scientific officer of the Epilepsy Foundation, said there are low-cost generic epilepsy drugs on the market, but many patients with the rare forms of the disease have already tried them and the drugs didn’t help much.

Dr. French said Epidiolex improved symptoms for many children in clinical trials, and she is happy the price isn’t significantly higher.

The company expects to make the drug available after the U.S. Drug Enforcement Administration assigns it a controlled-substance classification, a decision expected by late September. GW Pharmaceuticals will distribute the drug through specialty pharmacies that ship directly to patients and caregivers.

FDA approval of a CBD extract means that cannabidiol now has an acknowledged medical use and therefore doesn’t fit a key criterion of Schedule I status. DEA rescheduling is supposed to follow as day follows night. Logically, the DEA resked should apply to cannabidiol, the molecule. But fixisin.com says CBD will remain on Sked I, with an exception created for CBD in an FDA-approved pharmaceutical.”

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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.

~~

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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Memantine for Neuropathic Pain & Complex Regional Pain Syndrome, CRPS


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Neuropathic pain syndromes show an over-expression of NMDA receptors in the brain in animal models. Ketamine blocks the NMDA receptor. Another medication with the same mechanism, but in pill form is memantine. This report on six patients of the use of memantine for Complex Regional Pain Syndrome (CRPS) from 2007 in the Clinical Journal of Pain, six months after treatment with memantine, showed significant decrease in pain, improved motor symptoms and autonomic changes, and fMRI changes on the affected side improving, comparable to the unaffected side of the brain.

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It was approved for Alzheimer’s dementia gradually titrating to a dose of 28 mg/day, but for decades has been very useful off label for neuropathic pain including but not limited to CRPS, at a dose of 55 mg/day, and in recent years often prescribed for migraine.

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Ketamine is highly successful also for treatment resistant depression, and one patient, a psychiatrist disabled from the unfortunate triad of intractable neuropathic pain, migraine and treatment resistant depression, while slowly titrating to a dose of 55 mg/day, a process that takes almost 3 months, found depression relieved for the first time in decades at the dose of 35 mg. It was highly effective as one component of the multi-pronged approach for all three conditions.

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This life is a hard fact. We all need all the help, encouragement and positive attitudes we can get. Complex intractable pain and/or depression requires rational polypharmacy, selectively chosen based upon well known mechanisms, neurotransmitters, receptors, hormones, stress reduction, cognitive behavioral therapy, physical therapy, occupational therapy, nerve blocks, and spiritual understanding, etc. Several choices were summarized almost two years ago here.

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In my experience, memantine is very well tolerated with few if any side effects but covered by insurance only for mild to moderate dementia. Thus, not only is it highly challenging to treat neuropathic pain, but important to creatively meet the challenges of our backwards medical system that barely recognizes the needs of those with chronic pain.

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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.

~~

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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After Ketamine for pain, complaints of depression dropped in half & pain reports were lower


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KPBS Radio highlighted a new study today by UCSD School of Pharmacy

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San Diego Scientists Find Further Evidence A Club Drug Could Treat Depression

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In a new analysis published Wednesday in the journal Scientific Reports, UC San Diego researchers said millions of FDA side effect records reveal that people who took ketamine for pain relief reported lower rates of depression.

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“The occurrence of complaints about depression dropped in half after ketamine administration,” said UC San Diego Skaggs School of Pharmacy professor Ruben Abagyan, who led the study.

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The researchers focussed on the FDA’s Adverse Effect Reporting System, a database that tracks negative side effects among people who take various drugs. But the researchers were not primarily interested in bad outcomes.

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Instead, they looked for a positive outcome: declining rates of depression among people taking drugs not typically thought of as antidepressants.

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They found signs that other common drugs — including Botox, a pain reliever called diclofenac and the antibiotic minocycline — also reduced depression among patients in the FDA database.

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[minocycline is a glial modulator and it can prevent CRPS from spreading.]

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University of Miami psychiatry professor Charles Nemeroff wrote that the study was, “very interesting.”

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“The findings are of considerable interest. However the interpretation of the findings are key,” he wrote, saying it will be important to understand whether ketamine is directly treating depression or simply relieving pain, which can indirectly help people experience less depression.

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The UC San Diego researchers said they controlled for this variable by comparing people who took ketamine with those who took other pain medications. They said they still found a larger drop in depression among those who took ketamine.

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This is the open source (free) article in Nature with brief excerpts below:

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Population scale data reveals the antidepressant effects of ketamine and other therapeutics approved for non-psychiatric indications

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.Isaac V. Cohen, Tigran Makints, Rabia Atayee, Ruben Abagyan

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We found that patients listed in the FAERS database who received ketamine in addition to other therapeutics had significantly lower frequency of reports of depression than patients who took any other combination of drugs for pain (LogOR −0.67 ± 0.034) (Fig. 1c). This reduction in depression is specific to ketamine and is known to be much more rapid than current antidepressants, making this observed effect very promising for treatment of patients with acute depressive or suicidal episodes. These patients cannot afford to wait up to six weeks for reductions in their depressive symptoms. Pain reports were also significantly lower for ketamine patients (LogOR −0.41 ± 0.019) (Fig. 1c).

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The analysis of the whole FAERS database revealed several other unintentional depression reducing drugs among antibiotics, cosmeceuticals and NSAIDS (Fig. 2). Our data supported previous studies that observed the psychiatric polypharmacology of minocycline [my emphasis], a tetracycline antibiotic14 (Fig. 2). The NSAID, diclofenac [that has highest incidence of heart attack and cardiac arrhythmia of any NSAID], was also observed to have some antidepressant properties (Fig. 2). It is theorized that both of these drugs may accomplish antidepressant effects through an anti-inflammatory mechanism. Because of the antidepressant activity of several NSAIDs, we further separated the non-ketamine pain cohort. Ketamine patients were then compared to patients who received any other combination of drugs for pain excluding NSAIDs. It was observed that depression event rates remained low (LogOR −0.56 ± 0.035) (Fig. 2)..The reduction of depression rates in ketamine patient records makes a case for study of ketamine as a psychiatric drug. These results imply that ketamine may be further explored as a monotherapy or adjunct therapy for depression. It should also be noted that FAERS data revealed that ketamine use [may] lead to renal side effects and awareness and caution in patients with renal or hepatic impairment may be warranted (Fig. 1a and b). [my emphasis].

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As an important side note, we also evaluated efficacy and side effects with the use of ketamine for pain management. We found that patients who were on ketamine had reduced opioid induced side effects including constipation (LogOR −0.17 ± 0.023), vomiting (LogOR −0.16 ± 0.025), and nausea (LogOR −0.45 ± 0.034) than patients who received any other combination of drugs for pain indications (Fig. 1d). Our data supports ketamine’s opioid-sparing properties and alludes to the fact that patients may receive benefits of improved pain, reduced requirement of opioids, and ultimately less opioid reduced side effects.

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The results of this study support previous small scale studies’ conclusions that ketamine is a good monotherapy or adjunct therapy for depression. In clinical practice ketamine would be especially useful for depression because of the quick onset of its action compared to existing first line therapies. Regardless of the causative mechanism ketamine appears to have therapeutic potential for TRD. Further, the potential to reduce many of the most complained side effects of opioid treatment makes ketamine adjunct therapy for pain seem desirable.

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Overall, this study demonstrates that the therapeutic potential of ketamine can be derived from appropriate statistical analysis of existing population scale data. This study also outlines a methodology for discovering off label pharmacology of existing approved drugs. This method can be applied to other indications and may reveal new important uses of already approved drugs, providing reliable justification for new indications without large investments in additional clinical trials.

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FDA Adverse Event Reporting System. The FAERS database was created to support FDA’s post marketing surveillance on drugs and biologic therapeutics. It contains adverse reaction and medication error reports sent to the FDA through MedWatch, the FDA Safety Information and Adverse Event Reporting Program. Reporting is voluntary and is done by patients, family members, legal representatives, doctors, pharmacists and other health- care providers. If any party reports an adverse effect to the manufacturer, the manufacturer is legally obligated to forward the report to the FDA. Data is available online in quarterly format for AERS from the first quarter of 2004 to the third quarter of 2012 and for FAERS from the fourth quarter of 2012 to the first quarter of 2016.

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The study used over 8 million adverse event reports from first quarter of 2004 to the first quarter of 2016. All the quarterly files from 2004 to 2016 were combined into a master file which was used as the primary source for analysis. . . .

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Out of 8 million reports, 279,853 reports were used for analysis of ketamine in Fig. 1. Two cohorts for ketamine (K) patients and pain (P) patients with 41,337 and 238,516 patients respectively....

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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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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.

~~

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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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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