Ketamine Cystitis (Bladder Harm)

Ketamine cystitis (and other ketamine-provoked diseases) is:

• a severe and unmanageable risk for ketamine addicts
• a moderate and sometimes difficult-to-manage risk for occasional recreational ketamine users; and,
• a very low, easy-to-manage, risk for therapeutic ketamine patients.

Before proceeding with the topic of this article – ketamine cystitis – we also mention in passing that ketamine is believed to damage other parts of the urinary tract, the liver, and possibly the gall bladder. Much less is known about damage to these other organs. Bladder symptoms seem to be the first noticed. However, some recreational users report “k-cramps” or other symptoms without necessarily experiencing bladder symptoms. Generally, the precautions explained below should be helpful in avoiding serious damage to other organs. But we can’t have much confidence that green tea/EGCG or other supplements will be helpful for organs other than the bladder.

Naysayers conflate therapeutic ketamine patients with recreational users as a means of shutting down the conversation. This black-and-white rhetoric is analogous to naysayers using addiction risk to truncate a rational, comparative-risk analysis of therapeutic ketamine. This article is intended to present the facts, good, bad, and ugly, about ketamine cystitis risk and its management.

Ketamine cystitis is characterized by bladder inflammation and is typically associated with chronic and frequent ketamine abuse. Here, we use the word “abuse” judiciously. A recreational user who occasionally uses a small dose of ketamine for entertainment should not be construed to be “abusing” this drug. He probably does no harm to his own body nor to anyone else. Where is the abuse? To himself? To anyone else?

In therapeutic ketamine users for mental health, the risk of developing ketamine cystitis is considered low.

See: “Ketamine cystitis following ketamine therapy for treatment-resistant depression – case report.” Their conclusion: “To our knowledge, this is the first reported case of KIC in a patient receiving treatment-dose ketamine as part of their antidepressant therapy.” The publication date is January 2, 2024. https://pubmed.ncbi.nlm.nih.gov/38166893/

This conclusion is unduly optimistic. Nevertheless, it is indicative of how rare ketamine cystitis is reported among ketamine patients.

See: “Long-term safety and efficacy of sublingual ketamine troches/lozenges in chronic non-malignant pain management” https://pubmed.ncbi.nlm.nih.gov/34092024/

“. . . [A] retrospective review of 29 (n = 29) patients from a metropolitan tertiary pain service who have been receiving sublingual ketamine troches/lozenges between the period of 2012 and 2019. . . . There was a wide range of dosages used from 25 to 600 mg in divided doses. The duration of treatment ranged 2-89 months. . . . There were no reports of renal impairment, cystitis or hepatotoxicity.”

The doses and frequency of therapeutic administration are generally much lower than those frequently seen in recreational use. However, being aware of the potential risks, symptoms, and management strategies is still essential.

Symptoms of ketamine cystitis can include:

1. Urinary frequency and urgency
2. Dysuria (painful or difficult urination)
3. Hematuria (blood in the urine)
4. Suprapubic pain (lower abdomen, within the hips, in the intestines, bladder, and genitals)
5. Nocturia (excessive urination at night)
6. In severe cases, bladder shrinkage and decreased bladder capacity

To minimize the risk of bladder harm in therapeutic ketamine users and manage potential issues, take the following steps:

1. Keep well hydrated at dosing and throughout the day following dosing.
2. Use the lowest effective dose of ketamine and follow the prescribed treatment regimen. Reduce the frequency of dosing to that sufficient to maintain therapeutic benefits. Choose the most bioavailable form of administration, consistent with cost, availability, and transportation.
3. Patients must monitor themselves for urinary symptoms and signs of bladder irritation.
4. Patients must report any urinary symptoms promptly to their ketamine providers.
5. If ketamine cystitis is suspected, temporarily discontinue ketamine treatment and see a urologist for further evaluation.
6. Medications such as nonsteroidal anti-inflammatory drugs (NSAIDs) or anticholinergic agents may be used to manage symptoms.
7. See also the recommendations of the Interstitial Cystitis Association (ICA) at https://www.ichelp.org/

The evidence from urologists studying ketamine cystitis suggests that it is ketamine and its metabolites in the urine that irritate the bladder wall. If this is true (and this seems a reasonable theory), diluting and flushing the bladder contents should reduce exposure of the bladder wall to the irritating effects of ketamine and its metabolites. Nevertheless, reducing exposure does not eliminate exposure.

Timing of hydration needs to consider that you do not want to experience the urge to urinate during the one hour following taking a dose. You risk falling and injuring yourself while under the influence of ketamine. And even if you have a sitter to assist you, the urge to urinate and trip to the bathroom will interrupt the therapeutic flow of the ketamine dosing experience.

Avoid hydration in advance of taking your dose. Your body will process the liquid and fill the bladder before dosing, creating the urge to urinate while still under the effects of ketamine. Try hydrating moderately immediately before dosing so your bladder will begin filling during the one-hour dosing period. Then, you will be ready to urinate soon after the effects of ketamine are tapering off. Thereafter, hydrate aggressively throughout the day following your dosing.

Do not hydrate to excess. Excess hydration itself is very dangerous. Hydration aims to make a reasonable, healthful effort to reduce the effect of ketamine on the bladder without disrupting the flow of the ketamine experience, creating a risk of falling and certainly not running a risk of excess hydration.

Cystitis is an umbrella term encompassing a half-dozen manifestations of bladder irritation besides ketamine. It is notoriously difficult to treat. See Interstitial Cystitis Association (ICA) at https://www.ichelp.org/. Ketamine patients should take advantage of this organization’s research and advocacy.

The first thing to say about ketamine cystitis is that there is a rat study titled “The protective effect of green tea catechins on ketamine-induced cystitis in a rat model” _{(https://www.researchgate.net/publication/282316298_The_protective_effect_of_green_tea_catechins_on_ketamine-induced_cystitis_in_a_rat_model)} This report strongly indicates the use of green tea or EGCG supplements. It’s just one study, but it’s the best available.

It seems clear that every ketamine user should be aware of green tea and EGCG supplements as prophylactic to ketamine cystitis. We would advocate that every ketamine patient adopt a practice of regular consumption of green tea or taking a small dose of EGCG.

We assume that green tea/EGCG works by improving the health of the bladder. We do not assume that green tea/EGCG works by laying down a protective layer in the bladder before dosing nor by neutralizing ketamine in the bladder after dosing. Therefore, we recommend consuming green tea and EGCG as a regular routine practice every day of the week, not just before/after dosing.

In particular:

1. – Every patient with a history of urinary tract symptoms of any kind; and,
2. – Every patient prescribed a relatively higher quantity of ketamine, such as 800 – 1,000 mg per week.

Most of what we know about ketamine cystitis comes from reports of recreational users who routinely (several days a week) dose 1,000 mg or greater. Apparently, about 1/3 of such recreational users develop ketamine cystitis. The precision of this estimate is dubious. We don’t know, for example, if all (or nearly all) regular recreational ketamine users will eventually develop symptoms if they persist for enough years. Were this true, the 1/3 figure would be low. We don’t know if many recreational users discontinue ketamine promptly upon the appearance of symptoms and then never appear in urologists’ offices to be counted. What is perfectly clear is that the recreational user community routinely reports ketamine cystitis.

See: the study “Ketamine is associated with lower urinary tract signs and symptoms” _{https://www.sciencedirect.com/science/article/abs/pii/S0376871613000422} Bear in mind that the responders are presumptively predominantly recreational users with only a few therapeutic users. They report:

What to make of these – presumptively recreational – users’ reports of LUTS? How might it apply to therapeutic users who dose regularly but in much lower quantities? Very hard to say.

Suppose a wildly naive assumption that the erowid.org users’ health and lifestyle practices match those of therapeutic users except for ketamine use. Respondents who never used ketamine report a 24% incidence of LUTS. This figure is only a few percentage points below the 28-30% LUTS incidence of ketamine-using respondents. This interpretation suggests that LUTS is so commonplace that its appearance among ketamine users should not be seen as remarkable.

Reversing the wildly naive assumption, let’s suppose that the 24% of non-ketamine users reporting LUTS were users of a comparably bladder-irritating substance such as PCP. (See: https://tripsitter.com/psychedelics/arylcyclohexylamines/#Bladder_Damage.) That alternate interpretation suggests that LUTS is strongly associated with the use of drugs such as ketamine and PCP, known to irritate the bladder.

We wish the record were clear. E.g., perhaps a certain threshold of use, such as 7 grams per week over 7 months, marks the boundary between safety and heightened risk. Unfortunately, this simply isn’t the case. Everybody is different; some recreational users seem to tolerate high levels of ketamine use without developing symptoms. Conversely, some recreational users develop symptoms at doses much lower than those believed to be problematic. There is no clear-cut threshold of use to guide recreational users.

At this juncture of the discussion, we need to explain why this article on ketamine cystitis is not thoroughly documented. We wish we could reference numerous pertinent scientific articles on the subject. But, alas, this just isn’t possible.

All the scientific literature on ketamine cystitis is from urologists treating recreational users, typically those at the higher end of the quantity and frequency of usage spectrum. These articles consistently report that achieving satisfactory results from all the treatments is difficult. They consistently advocate complete discontinuation of ketamine use. Readers are invited to search the literature under the keywords “ketamine cystitis” and study the findings reported. Citations here would offer nothing more.

The most accessible article we’ve found is: Tsai, Y. C., & Kuo, H. (2015). “Ketamine cystitis: Its urological impact and management.” _{Urological Science, 26(3), 153-157. https://doi.org/10.1016/j.urols.2014.11.003 https://www.sciencedirect.com/science/article/pii/S1879522614001122?dgcid=raven_sd_recommender_email}

“The time of onset of LUTS after ketamine abuse ranged from a few days to a few years.² It is still unclear whether the ingested dosage directly related to the onset time of LUTS. However, it is clear that KC was rarely associated with the medical use of ketamine.²³ The clinical pictures of KC share many common clinical features with IC, thus, the IC questionnaire is the preferred one to record the lower urinary tract symptoms of KC.” [emphasis supplied].

We at KetamineTherapyForMentalHealth.com, are not particularly invested in treating advanced cases of ketamine cystitis. That would be vastly outside our scope. Instead, our focus is on alerting therapeutic users to the symptoms so that they may remain alert to possible onset. Moreover, we want to offer what we can in the way of suggestions that are apt to minimize the risks to therapeutic users.

In this regard, we cite the one rat study showing strong evidence of the protective effect of green tea and EGCG. It’s one study. Perhaps there will be more. As we identify others, we will include citations. One rat study is certainly not dispositive, but it’s what’s available. The cost and effort of adding green tea or EGCG to a therapeutic user’s diet seems to be justified by this single study. Numerous other ketamine users are likewise persuaded.

What can we learn from (what little we know) about ketamine cystitis in recreational users? Clearly, some such users are much more resilient than others. Or, to put it the other way round, some such users are much less resilient than others. It follows that the same diversity in resilience should exist among therapeutic users, dosing from 100 mg to 1,000 mg/week. There are apt to be a very few therapeutic users consuming low doses who are vulnerable to developing symptoms. How many?

The ketamine subReddits regularly publish anecdotes of ketamine patients reporting urinary tract symptoms. Not a lot; but enough to be concerned about. What should we make of these reports?

It’s difficult to tell. Urinary tract symptoms are commonplace. Women are particularly vulnerable to UTIs. It’s difficult to distinguish ketamine cystitis from a UTI (or other indication). Some people are highly vulnerable to urinary tract diseases. Males rarely get UTIs. So, if you are female and have symptoms, there is a fair likelihood that it’s something other than ketamine; but beware, the ketamine is apt to exacerbate the other condition. If you are male, the odds are that it’s the ketamine rather than a UTI. This is common-sense reasoning. There is simply no scientific literature about ketamine cystitis in therapeutic users that might offer support for this reasoning.

What should we suppose will happen to an individual who eventually will develop some urinary tract disease without ever taking ketamine? This individual’s destiny is written in his/her genetics, diet, lifestyle, etc. Now, introduce ketamine. Shall we suppose that the introduction of ketamine will:

1. Delay the onset of urinary tract symptoms?
2. Have no effect on when urinary tract symptoms manifest?
3. Accelerate the onset of urinary tract symptoms?

When the urinary tract symptoms appear, what will we blame? Ketamine? Or, the individual’s genetics, diet, lifestyle, etc.? Does it really matter what we blame? What do we do about it? This is the purpose of this article in KetamineTherapyForMentalHealth.com.

An excellent example is reported by u/wiserwhippingwheel in r/TheraputicKetamine. See: _{https://www.reddit.com/r/TherapeuticKetamine/comments/16jspf2/ketamine_troches_didnt_work_for_me/}. He started at 10 mg sublingual and titrated up to 40 mg for a few weeks when cystitis symptoms appeared. These are micro-doses. He writes:

Some advocates of ketamine therapy decry any discussion of the risk of ketamine cystitis when used for mental health therapy. They insist that there is insufficient clinical evidence of ketamine cystitis among therapeutic users to justify fear-mongering. We agree that there is insufficient evidence among therapeutic users. Nevertheless, there is some evidence. And for those few patients who manifest symptoms, there is cause for concern. And so we insist that this risk not be swept under the rug. It should be discussed so that patients take prudent precautions. This is our opinion and our policy in publishing this article.

You are free to scour the scientific literature on ketamine cystitis. You may satisfy yourself that you have found nothing to hint at the risk of ketamine cystitis in therapeutic users. If you conclude that lack of evidence is sufficient to put ketamine cystitis out of your consciousness, it is your choice. In our view, a lack of literature does not assure a lack of risk.

Just how great is this risk? It is extremely low. In one very large sample of mental health ketamine therapy users, there was a single plausible report of urinary tract symptoms associated with ketamine use. (This is an unpublished observation.) Not zero. One.

What is the statistical significance of this single report? Generally, it supports the conventional wisdom that the risk of urinary tract symptoms among therapeutic users is very low. Yet, each patient is an individual in his/her own right. And to vulnerable patients – especially those predisposed to urinary tract disease – the statistics are meaningless. If symptoms manifest, they are problematic.

This is why we advocate that ketamine patients consume green tea or take EGCG supplements as a regular practice.

Not all green tea or EGCG supplements are created equally. ConsumerLab.com published a report (_{https://www.consumerlab.com/reviews/green-tea-review-tea-bags-matcha-supplements/green-tea/?anchor=toppick-green&j=3271903&sfmc_sub=120068725&l=6547_HTML&u=37255818&mid=7276525&jb=14006&utm_medium=email&utm_source=exacttarget&utm_campaign=newsletter&utm_term=&utm_content=weekly_highlights_august_6_member_de_send#toppick-green}) evaluating 16 green tea products and 6 EGCG supplements. The report is behind a paywall for subscribers only, but an abstract of the report is available for non-subscribers.

They found that about a third of the products contained high levels of total EGCG and total catechins; a third had reasonable levels, and a third had negligible levels of these substances. One would do well to avoid products containing the lowest EGCG/catechins and prefer those containing the highest levels at reasonable costs.

Among caffeinated green teas, the following brands are interesting:

• Super Foods Matcha Green Tea Powder
• Trader Joe’s Organic
• Prince of Peace 100% Organic Green Tea
• Jade Leaf Organic Japanese Matcha
• Lipton Pure Green Tea
• Twinings of London Green Tea
• Super Foods Green Tea Powder.

Of the few decaffeinated brands, only Yogi GT Pure Green Decaf is interesting. Maybe Lipton Green Tea Decaffeinated.

Among the EGCG supplements, the following brands are interesting:

• Vitacost Green Tea Extract, and 
• NOW EGCg.

Most green tea products contain caffeine; the decaffeinated brands are harder to find. Presumably, there is no more reason to be concerned with the caffeine in a cup of green tea than in a cup of coffee. Green tea has less caffeine than coffee. A ketamine user pursuing a green tea regimen should consider decaffeinated green tea products preferable to caffeinated ones. In any case, it’s well understood that caffeine is a diuretic. It causes water to flush through the kidneys more rapidly and, consequently, less effective in hydrating the body.

It’s probably good advice to minimize, if not avoid, caffeine consumption. Likewise, consider whether any other drug or food/beverage one is taking is a diuretic. One might imagine that a diuretic will cause one to urinate any liquids he drinks sooner and flush the bladder more frequently, removing the ketamine-laden urine more effectively. This might be true. However, it’s at the expense of dehydrating the rest of the body. What the trade-off might be is hard to say. I’ve been advised to drink an extra cup of water for each cup of coffee. However, I have no idea whether that recommendation is adequate to overcome the diuretic effects of caffeine. And there is a limit on how much liquid I’m willing to drink each day.

Do not take more than 330 mg. of EGCG supplements per day. There is evidence of liver toxicity from consuming larger quantities. There seems to be no evidence of liver toxicity from consuming green tea. _{https://www.sciencedirect.com/science/article/pii/S0273230018300928}

A hybrid green-tea+EGCG-supplementation might be as follows. Drink green tea. Admittedly, the brand you use might not be high in EGCG and total catechins. You could consume a single capsule of an EGCG supplement at or below 330 mg each day. Alternatively, you could open the EGCG supplement capsule and pour a little of its contents into each cup of green tea you consume throughout the day. The EGCG supplement will be absorbed into your body in small increments throughout the day, not in a single “bolus” dose. And it is the “bolus” dosing of EGCG that seems to be somewhat toxic to the liver.

The Interstitial Cystitis Association (ICA) organization recommends the following additional supplements for patients suffering from cystitis (not ketamine cystitis in particular).

1. D-mannose
2. Vitamine D
3. Aloe Vera, particularly the product by Desart Harvest https://www.desertharvest.com/Super-Strength-Aloe/

Read what ICA has to offer its members and followers about cystitis in general. Again, nothing in the scientific literature either supports or refutes that ketamine cystitis has a close relationship to non-ketamine cystitis. It is merely reasonable conjecture that whatever non-ketamine users with cystitis have discovered might have some value to ketamine users.

See also: https://www.reddit.com/media?url=https%3A%2F%2Fpreview.redd.it%2Fgot-some-aloe-vera-how-do-i-use-it-to-help-with-protecting-v0-7npxtoshoz5d1.jpeg%3Fwidth%3D1284%26format%3Dpjpg%26auto%3Dwebp%26s%3D669ab9bf9434bd973b40c16bda2068af44c446b1

Apparently, BetterHealth advocates aloe vera as well. They also advocate: Chrondroitin Sulfate 600 mg daily at bedtime; Hyaluronic Acid 200 mg daily at bedtime; and, Prelief, an OTC medicine, 2 tablets before dosing.

As noted above for green tea/EGCG, we recommend a daily regimen of taking the foregoing supplements to promote bladder health consistently. We doubt that simply taking any of these supplements on dosing days is sufficient.

Desert Harvest claims:

“Desert Harvest Aloe Vera products are unique in that the high concentration of nutrients in our Super-Strength Aloe Vera preserves the glycosaminoglycans (GAG), which adhere to the bladder mucosal lining, preventing potentially irritating solutes in the urine from reaching the bladder wall.  Desert Harvest Super-Strength Aloe Vera naturally coats the bladder with a protective GAG layer without harsh chemicals or side effects.”

“Based on the recommended IC/BPS dosage of 3600 mg per day, many brands are not affordable in the long run, although they initially seem so. Some brands have so little Aloe Vera per capsule it would require you to take up to 72 capsules per day.”

If these claims are true, perhaps its aloe vera product helps to prevent ketamine from reaching the bladder wall. I.e., it has a prophylactic effect in addition to any analgesic effect. Desert Harvest further touts its product as superior for this purpose compared to other aloe vera products. See: _{https://www.desertharvest.com/why-desert-harvest-aloe-vera-vs-liquid-gel-and-other-brands.html}

Consumer Labs has a report _{(https://www.consumerlab.com/reviews/cranberry/cranberry/?anchor=uti-treatment&j=3320892&sfmc_sub=120068725&l=529_HTML&u=37941408&mid=7276525&jb=5006&utm_medium=email&utm_source=exacttarget&utm_campaign=newsletter&utm_term=&utm_content=quercetin_interaction_member_de_send#uti-treatment)} that offers the following:

“We now know that polyphenolic compounds in cranberries, such as flavonols, condensed tannins, phenolic acids (such as benzoic acid), and PACs (proanthocyanidins) limit the ability of E. coli bacteria that cause the infection to attach to the walls of the bladder and urinary tract and gain a foothold (adhesion).”

If this is true, then it is reasonable to speculate that cranberry limits the ability of ketamine to attach to the walls of the bladder.

Consumer Lab’s report strongly favored cranberry juices over capsules. Ocean Spray Pure Unsweetened Cranberry performed best, with R.W. Knudsen Family Just Cranberry a close second. Trader Joe’s 100% cranberry Juice and Lakewood Organic Pure Cranberry tied for third. For supplements, Theralogix Nutritional Science TheraCran One performed almost as well as the third-place juices.

Interestingly, ICHelp.org lists cranberry among the most bothersome foods. Perhaps the dichotomy is explained by ICHelp’s focus on treating an existing case of cystitis. Consumer Lab’s report indicates that cranberry has not proven helpful in treating UTIs; only as prophylaxis. Perhaps cranberry irritates an existing case of cystitis, whereas it promotes bladder health before cystitis attacks.

Here is our conjecture. Cystitis – in general – is a rare yet not an obscure disease. Therefore, a few percent of people are particularly vulnerable to cystitis.

There is ample evidence from the recreational user community that frequent ketamine use in high quantities triggers cystitis. There is ample evidence from urologists treating recreational users and non-ketamine-user cystitis patients that cystitis is difficult to treat successfully. A cup of green tea prevention is worth more than a pound of cure.

We are what we eat and drink. If this is true, there are apt to be components of our diet that make us more or less resilient to the causes of cystitis. We know ketamine is a cause; this much is indisputable. What causes cystitis in non-ketamine-using patients is unknown. Yet, it’s a reasonable conjecture that maintaining the health and resiliency of the bladder lining is probably helpful.

Green tea and EGCG support the health of the bladder lining. Why, we don’t know. It’s just what the rats are telling us. The cystitis community, patients, and their urologists conjecture that the aforementioned supplements seem to be helpful in treating serious cases of cystitis. It’s reasonable to conjecture that the operative mechanism is that these supplements promote the health of the bladder lining.

Therapeutic ketamine patients should, at least, be aware of these supplements. Some such patients will find that one or more of the following apply to their particular cases:

1. – The patient has a history of urinary tract infections or distress;
2. – The patient has been titrated up to a frequent and high dose of ketamine and has logged an extended course of ketamine treatment; or,
3. – The patient notices the onset of the first slight indications of urinary tract symptoms.

A patient finding her/himself in any such situation would be well advised to study the current recommendations of The Interstitial Cystitis Association (ICA) organization. https://www.ichelp.org/ Perhaps (this is merely conjecture on our part) prompt pursuit of ICA’s recommendations might enable therapeutic ketamine patients to keep urinary tract symptoms under control while pursuing ketamine therapy.

Or, such patients would be well advised to substantially reduce or suspend altogether ketamine usage for several weeks while undertaking the supplement regimes recommended by ICA; thereafter, when symptoms have disappeared, resuming ketamine at the prescribed or smaller doses or at longer intervals between doses.

We believe that the approach we advocate here is vastly superior to the alternatives:

1. Remaining ignorant of the risk of ketamine cystitis; or,
2. Waiting for symptoms to manifest severely enough to inspire an inquiry into the phenomena of ketamine cystitis.

A postscript: It seems reasonable to wonder the following. Suppose I take all the precautions to reduce the risk of cystitis. I’m taking all the supplements (green tea, EGCG, aloe vera, etc.), hydrating, and urinating frequently. Can I then use ketamine with impunity so long as I don’t notice any urinary tract symptoms? We believe the answer is ‘No!’.

There are reports, mostly from the recreational user community, of “k-cramps,” gall bladder, and, perhaps, liver symptoms. Therefore, there is reason to believe that ketamine damages organs other than the urinary tract. There is little reason to believe that the measures that seem protective of the urinary tract should also protect other organs. See the subReddit r/KetamineAddiction. If you think you can use ketamine with impunity, risk addiction, and deal with the consequences when you can’t stop ketamine, read up on your ghost of Christmas yet to come. You have been warned.

Accordingly, the guidance to minimize the quantity of consistent use is always controlling. If one’s usage is higher, one should look to a more bioavailable route of administration. While the bladder might be the most frequently affected organ, it is not necessarily the “canary in the mine” for your body.

1. Shahani, R., Streutker, C., Dickson, B., & Stewart, R. J. (2007). Ketamine-associated ulcerative cystitis: a new clinical entity. Urology, 69(5), 810-812. https://doi.org/10.1016/j.urology.2007.01.038
2. Chu, P. S., Ma, W. K., Wong, S. C., Chu, R. W., Cheng, C. H., Wong, S., … & Tse, J. M. (2008). The destruction of the lower urinary tract by ketamine abuse: a new syndrome? BJU International, 102(11), 1616-1622. https://doi.org/10.1111/j.1464-410X.2008.07920.x
3. Short, B., Fong, J., Galvez, V., Shelker, W., & Loo, C.K. (2018). Side-effects associated with ketamine use in depression: a systematic review. The Lancet Psychiatry, 5(1), 65-78. https://doi.org/10.1016/S2215-0366(17)30272-9