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Dr. Bob is Robert Hsiung, MD,
bob@dr-bob.orgShown: posts 1 to 4 of 4. This is the beginning of the thread.
Posted by Hugh on February 20, 2019, at 11:16:54
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.
Scientists at the Stanford University School of Medicine have discovered that ketamine works as an antidepressant at least in part by activating the brain's opioid system.
The finding overturns previously held beliefs that the drug's antidepressant effects stemmed solely from its impact on the glutamate system. These beliefs led to the widespread use of ketamine to treat depression and spurred the development of glutamate-blocking drugs for use as antidepressants.
The new finding also highlights the interaction between depression, pain and opioid addiction and presents an opportunity for clinicians to reframe treatment approaches for these three public health crises.
The research is believed to be the first to address how ketamine works in the human brain to provide relief from depression. A paper describing the work was published Aug. 29 in The American Journal of Psychiatry.
"Before we did the study, I wasn't sure that ketamine really worked to treat depression. Now I know the drug works, but it doesn't work like everyone thought it was working," said Alan Schatzberg, MD, the Kenneth T. Norris Jr. Professor of Psychiatry and Behavioral Sciences, who shares senior authorship of the paper with Carolyn Rodriguez, MD, PhD, assistant professor of psychiatry and behavioral sciences.
Complete article:
Posted by Hugh on February 22, 2019, at 10:59:34
In reply to Surprising finding about ketamine, posted by Hugh on February 20, 2019, at 11:16:54
This quote is from the Stanford article: "The authors say that revealing the role of the opioid system in the antidepressant effects of ketamine is critical in the effort to develop new antidepressants. For instance, glutamate receptor blockers may not have rapid antidepressant effects unless they also involve the opioid system, Williams said."
We might not have to wait years and years for these "new antidepressants" to be developed. There's a drug that's been available since 1984 that can activate the opioid receptors in the brain. That drug is naltrexone, and it was developed to treat addiction. At a high dose (50 mg), naltrexone blocks the effects of endorphins from opiates and alcohol, as well as blocking the endorphins that the body produces naturally. At a much lower dose (1.5-4.5 mg), it is used to treat a number of autoimmune diseases and some forms of cancer. Some people find low-dose naltrexone (LDN) helpful for depression. Taken at even lower doses, naltrexone could be even more effective as an antidepressant. Ultra-low-dose naltrexone (ULDN) doses are in the micrograms, nanograms, and even the picograms. At these extremely low doses, naltrexone activates the opioid receptors in the brain.
The following quote is from
"Cotreatment with ultra-low-dose naltrexone at 16.7, 20, or 25 ng/kg, but not at 10 or 200 ng/kg, induced a significant CPP after this 2-h delay. This finding implies that, whereas the rewarding effects of morphine have dissipated by 120 min postinjection, ultra-low-dose naltrexone may extend this effect."
In other words, an extremely low dose of naltrexone enhanced the effects of morphine, and prevented tolerance to it from developing. And it prevented dependence and addiction from developing. A higher, but still tiny, dose of naltrexone didn't have these beneficial effects.
Even if you're not taking opiates, you might benefit from taking ultra-low-dose naltrexone, since we all have naturally occurring opioids -- endorphins. An extremely low dose of naltrexone, taken every day, might improve your brain's response to your naturally occurring endorphins.
So if you aren't helped by 1.5 to 4.5 milligrams of naltrexone, try lowering your dose to micrograms. If that doesn't help, lower your dose to nanograms. If that doesn't help, lower it to picograms. Other than the naltrexone, all you need is distilled water to dilute it with and a calculator.
Naltrexone is water-soluble, so dissolve a 50-mg tablet in 50 ml of distilled water and use a medicine dropper to measure the dose. If refrigerated, liquid low-dose naltrexone will keep for several weeks.
Posted by sigismund on February 22, 2019, at 12:22:21
In reply to Re: Surprising finding about ketamine, posted by Hugh on February 22, 2019, at 10:59:34
So that might be similar to the logic with Targin?
https://www.nps.org.au/medical-info/medicine-finder/targin-10-5-mg-modified-release-tablets
Some of the naloxone is absorbed.
Posted by Hugh on February 24, 2019, at 14:00:17
In reply to Re: Surprising finding about ketamine » Hugh, posted by sigismund on February 22, 2019, at 12:22:21
From what I've read about Targin, it seems that the reason for adding naloxone is to prevent opioid-induced constipation.
I don't know if adding ultra-low-dose naltrexone (ULDN) to an opioid would have this effect. The addition of ULDN to an opioid prolongs the effects of the drug, and it helps to prevent tolerance, dependence, and withdrawal.
I don't think that people should try to treat their depression by taking opioids along with ULDN. I think that ULDN alone might work as an antidepressant by enhancing the effects of endorphins that the body produces naturally.
This is the end of the thread.
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