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Amygdala connectivity predicts ketamine treatment response

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Re: Amygdala connectivity predicts ketamine treatment response

#12
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.

One promising rat 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.

Summary from the study:

> "Objective

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.

Materials and methods

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.

Results

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.

Conclusion

This protective effect of EGCG may come from its antiinflammatory and antifibrotic properties."

[^1]: https://www.sciencedirect.com/science/article/pii/S187952261...

Re: Amygdala connectivity predicts ketamine treatment response

#13
post #6

Earlier quoted context omitted.

Yes it is . The procedure wasn't really painful just uncomfortable and took about 20 minutes. I did it about 3 months ago I can't recall exactly. I was able to find a head and neck doctor that agreed to do it and did it for about 800$. 60 minutes made an episode about it that's when I first knew I had to try it There are 3 sites that they generally target but I just did right C6 .

Do you plan on repeating it?

You generally repeat it if your symptoms come back .

If it does then ya for sure

Re: Amygdala connectivity predicts ketamine treatment response

#14

Quoted post unavailable.

Ketamine is one of the most widely used emergency anesthetic for humans and has been approved for that use for decades. Ketamine use as an anti-depressant has been approved by the FDA for 3 years now. It is also part of the WHO list of essential medicines.

Re: Amygdala connectivity predicts ketamine treatment response

#15

Quoted post unavailable.

Ketamine is on the World Health Organization's list of essential medicines and is a primary anesthetic for infants, geriatric patients, and large areas of the developing world where access to general anesthetics is limited. It's also the field anesthetic of choice for situations where a patient has unknown allergens or is uncommunicative -- in the United States it's a standard issue medication for ambulances.

But, please continue with your misinformed and unfunny meme...

Re: Amygdala connectivity predicts ketamine treatment response

#16
post #12

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. One promising rat study from 2015 shows that EGCG (epigallocatechin gallate) extracted fro…

> even occasional usage can cause untreatable ulcerative cystitis, a.k.a. Ketamine Bladder Syndrome.

You'd have to stretch the definition of "occasional" to make this statement supportable. Clinical studies on the topic focus on chronic heavy users, whose usage far surpasses the dosing used by the median recreational user and typically persists for years. (In fact, most studies focus on recreational users who are using near-clinical levels, which is an order of magnitude more than the typical recreational dose, and doing so with regularity).

While it's possible that occasional use can cause issues, it's far from established fact, and the widespread usage of large doses of ketamine in inpatient settings for decades without reports of issues for those users would actually suggest otherwise.

Re: Amygdala connectivity predicts ketamine treatment response

#18
post #12

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. One promising rat study from 2015 shows that EGCG (epigallocatechin gallate) extracted fro…

> even occasional usage can cause untreatable ulcerative cystitis, a.k.a. Ketamine Bladder Syndrome. You'd have to stretch the definition of "occasional" to make this statement supportable. Clinical studies on the topic focus on chronic heavy users, whose usage far surpasses the dosing used by the median recreational user and typically persists for years. (In fact, most studies focus on recreational users who are usi…

> (In fact, most studies focus on recreational users who are using near-clinical levels, which is an order of magnitude more than the typical recreational dose, and doing so with regularity).

Is that so? For ambien it's the opposite, usually the recreational dosage can be a lot higher for some users than a clinical dosage (5 or 10mg)

Re: Amygdala connectivity predicts ketamine treatment response

#19

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 behavior…

This sounds really promising, but one thing that worries me is that ketamine is a sort-of painkiller (dissociative anesthetic). When heroin was first discovered, it was hailed as a wonder-drug, and it was also considered an effective treatment for severe depression. However, after some time, people realized that its addictive properties and high range of potential tolerance make it backfire pretty badly after a certa…

> one thing that worries me is that ketamine is a sort-of painkiller (dissociative anesthetic).

The fact that two drugs both can be used as an anesthetic doesn't tell you very much besides that, especially when comparing across different drug classes.

For example, cocaine and novocaine are both anesthetics that belong to the same drug class, and yet they have radically different risk profiles, despite both being commonly used in outpatient medical settings.

Ketamine is in a completely different category of drugs from cocaine and novocaine, which are also totally different from opiates.

It's a fallacy to assume that ketamine would be subject to the same issues as opiates just because both happen to be usable as anesthetics.

Re: Amygdala connectivity predicts ketamine treatment response

#20
post #18

Earlier quoted context omitted.

> even occasional usage can cause untreatable ulcerative cystitis, a.k.a. Ketamine Bladder Syndrome. You'd have to stretch the definition of "occasional" to make this statement supportable. Clinical studies on the topic focus on chronic heavy users, whose usage far surpasses the dosing used by the median recreational user and typically persists for years. (In fact, most studies focus on recreational users who are usi…

> (In fact, most studies focus on recreational users who are using near-clinical levels, which is an order of magnitude more than the typical recreational dose, and doing so with regularity). Is that so? For ambien it's the opposite, usually the recreational dosage can be a lot higher for some users than a clinical dosage (5 or 10mg)

> Is that so? For ambien it's the opposite, usually the recreational dosage can be a lot higher for some users than a clinical dosage (5 or 10mg)

Correct. What you are saying is true for almost all drugs: recreational doses are typically higher than clinical doses. Ketamine is the exception.

The recreational dose for a ketamine-naive user[0] is somewhere between 5-20mg. The clinical dose for depression is 86mg (not a typo), which is sometimes doubled, and the clinical dose for anesthetic purposes (which is what ketamine is mostly used for) is between 500mg-1g. The latter is IM injection, so it's also much more bioavailable than the first two (ie, the effective dose differential is even higher).

Of course, regular users develop a tolerance and heavy chronic users of ketamine can do more. But that's due to tolerance, not representative of the typical baseline recreational dose. (If they were to need ketamine for inpatient anesthetia, they would need absolutely massive doses for it to be effective).

It's hard to overstate how unusual ketamine is in this regard! It's very difficult to find an example of another drug that is frequently used both recreationally and clinically (by different groups of people) for which the standard clinical dose is 10x the standard recreational dose.

[0] "naive" is not a judgmental term; it's the clinical term used to describe a user who has no prior experience with the drug, or who has no baseline tolerance (ie, whose prior usage is far enough in the past that it is no longer relevant).

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