Ketamine has turned out to be a pretty effective treatment for episodes of severe depression, particularly when there is a risk of suicide; one reason is that it starts having an effect in hours instead of days or weeks like SSRIs do. See Jessica Gilbert's work over at NIH [1].
One of the big focuses of clinical neuroscience is to find features in the brain that will predict treatment responses (to cognitive behavioral therapy, anti-depressants, and so on).<p>The amygdala is, as is generally known, strongly associated with fear responses, or other negative emotional responses. The subgenual cingulate cortex has been associated with emotion regulation (e.g. down-regulating responses to negative stimuli). I believe that other treatment-prediction studies have found that connectivity between the subgenual cingulate and other brain regions like the amygdala predict treatment responses, so, their result is pretty consistent with the literature as far as I understand.<p>1. <a href="https://scholar.google.com/citations?user=bSXKfxkAAAAJ&hl=en&oi=sra" rel="nofollow">https://scholar.google.com/citations?user=bSXKfxkAAAAJ&hl=en...</a>
This is really cool, I think there is a huge opportunity for analysis like this to allow drugs that are currently off market because some small percentage have bad side effects but it works for others. If we can start knowing who drugs will work for and who they won't it could be a game changer for our existing drugs, let alone what we can create in the future
MDMA and psilocybin (magic mushrooms) and both in later stages of research and could be approved by FDA. From what information that I have read, one treatment of magic mushrooms can have a profound impact for one's life time. As I understand it, ketamine treatments don't last that long, so one needs to continue them. As far as magic mushrooms being toxic, they can't find a limit where it is toxic. The biggest problem as I understand it is that one might have a bad trip that could cause something like PTSD; so proper screening and preparation is needed.
Check out youtube videos: <a href="https://youtu.be/kxFTWk9lLDU" rel="nofollow">https://youtu.be/kxFTWk9lLDU</a>, <a href="https://youtu.be/smBMn-CV9KE" rel="nofollow">https://youtu.be/smBMn-CV9KE</a>, <a href="https://youtu.be/SwMHr43fTqE" rel="nofollow">https://youtu.be/SwMHr43fTqE</a>, <a href="https://youtu.be/NGIP-3Q-p_s" rel="nofollow">https://youtu.be/NGIP-3Q-p_s</a>
I dont understand why we arent looking into methoxetamine over ketamine. Or any of the derivatives with a stronger dose-response curve. DCK, O-PCE, etc. These all have similar chemical and psychoactive properties and the doses are orders of magnitude smaller ergo they dont completepy fuck your bladder up.
Most Ketamine users are unaware that even occasional usage can cause untreatable ulcerative cystitis, a.k.a. Ketamine Bladder Syndrome. Ketamine thins the urothelium while increasing the collagen to smooth muscle ratio and exacerbating interstitial fibrosis. The syndrome is untreatable and causes serious problems down the line.<p>One promising <i>rat</i> study from 2015 shows that EGCG (epigallocatechin gallate) extracted from green tea has a protective effect on the bladder, reversing ketamine-induced damage to control levels. If you are taking ketamine for major depression or recreationally, taking EGCG before may prevent long-term bladder damage.<p>Summary from the study:<p>> "Objective<p>To investigate the protective effect of green tea epigallocatechin gallate (EGCG) on long-term ketamine-induced ulcerative cystitis (KIC) using a ketamine addiction rat model.<p>Materials and methods<p>Thirty Sprague-Dawley rats were divided into three groups which received saline, ketamine (25 mg/kg/d), or ketamine combined with EGCG (10 μM/kg) for a period of 28 days. In each group, cystometry and a metabolic cage micturition pattern study were performed weekly. Masson's trichrome study was done to evaluate the morphologic changes. Western blot analyses were carried out to examine the expressions of inflammatory protein [transforming growth factor-β (TGF-β)] and fibrosis proteins (fibronectin and type I collagen) in bladder tissues.<p>Results<p>Chronic ketamine treatment resulted in bladder hyperactivity with a significant increase in micturition frequency and a decrease in bladder compliance. These alterations in micturition pattern were accompanied by increases in the expressions of inflammatory and fibrosis markers, TGF-β, fibronectin, and type I collagen after long-term ketamine treatment. Masson's trichrome stain showed that ketamine treatment decreased urothelium thickness while increasing the collagen to smooth muscle ratio and exacerbating interstitial fibrosis. By contrast, simultaneous EGCG and ketamine treatment reversed ketamine-induced damage to almost control levels, showing the protective effect of EGCG.<p>Conclusion<p>This protective effect of EGCG may come from its antiinflammatory and antifibrotic properties."<p>[^1]: <a href="https://www.sciencedirect.com/science/article/pii/S1879522615004157?fbclid=IwAR3loLakNo0TV5xlboUqHsUDN8tDDOKN7O1z7WeqEvcrTLQoDxdnKu_IfhY" rel="nofollow">https://www.sciencedirect.com/science/article/pii/S187952261...</a>