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● Introduction

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● Authors

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● Your Story

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● TOC

Below are the sections of the guide linked directly. You will jump straight to what you select. Keep reading below if the first time to the guide.

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● Symptoms vs. Results

I’ve been on ketamine for six years. I have had 100% remission of rumination, depression, ideation, CPTSD, and almost all trigger situations non-stop. Ketamine has rebuilt my healthy synapses, neurons and relocated dendrites, so I can happily cope with life and now view the world through an objective lens showing love, support, compassion, and acceptance of me and who I am today.

Ketamine improves cognition, memory, and mental flexibility, so damage caused by depression has been healed completely. This results in mental clarity and an overall ‘lighter’ feeling. Depression was a heavy blanket that weighed me down, unmotivated. Hard to start and harder to finish. Ketamine made my mind quieter; I no longer cycle on intrusive thoughts. I am no longer obsessed with suicide. I no longer ruminate. Look to this page to see how ketamine improves the default mode network in our mind, quieting it and taking away cyclic or impulsive thoughts completely—the inner narrator quieted in my mind, which feels tranquil.

I love life and live every minute. I feel joy and happiness now, and I’m very content almost all of the time. These past six years have been the best of my life.

I knew ketamine was working for me with the first dose (no more ideation after the first dose). The depression lifted in the first few doses. Once the healthy synapses grew, I reinforced them. As I was triggered, I broke down trauma underneath and differentiated it from my new reality, rewiring them to no longer fire. Six + years in, I’m a completely different person that loves life in every way, and ketamine has been so successful I don’t feel like any other treatment is needed to feel better.

Being bipolar, I maintain a mood stabilizer, antipsychotic, stimulant, and sleep med, but I no longer need recreational drugs and several prescriptions I used to take.

It takes ketamine time to regrow synapses and relocate dendrites depression and PTSD Maladaptation creates. So, like many, I did feel worse before I felt better.

See: Feeling Worse When Starting Treatment

Emotional processing is complicated, significantly before the depression lifted and the new synapses developed and grew strong. They’re like muscles, and they need exercise to grow strong. So, the therapy was complex emotionally at first, and I cried a lot. Profuse sobbing. It was so cathartic though. To release all that lifted the weight of the world from my shoulders.

So, in summary, ketamine lifts rumination, depression, and ideation completely, and words can’t describe how good that feels. Incredible feeling. It also restructured my brain to appreciate these things and come healthily to the world.

I’m so happy now, consistently happy and healthy.

It’s why I wrote the guide and built the site. Ketamine made such a difference for me I’m getting the word out to everyone that it can help.

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● Treatable Mental Illnesses

If other antidepressants haven’t worked or cause unwanted sexual side effects (which is common), or you want to go straight to the best option IMHO, explore ketamine.

Ketamine has been proven in treatment-resistant depression, which requires multiple antidepressants to be tried first to indicate by most evidence-based practices. Do not self-diagnose. Only do diagnosis through a qualified health provider.

See: Treatable Mental Illnesses

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● Effectiveness by Mental Illness

Effectiveness Rating Legend

Survey Results

Thank you; every submission adds weight to our collected evidence!

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● Treatment Center

Treatment is done via ketamine clinic often, and telemedicine is an alternative. There are practices everywhere that specialize in ketamine.

Search Google for ‘ketamine providers near me’ or ‘ketamine telemedicine providers.’

Our site hosts a comprehensive provider directory, with a matrix by state in our Providers by State page.

With a clinic, expect a $350ish consult fee. Most do IVs, often $300ish to $700ish each, and standard practice is 6 to 8 IVs administered over two to three weeks. Telemedicine and some clinics also do troches (sublingual lozenges). Troches, by comparison, are $75-$90 for the equivalent of 4 IVs.

See: Optimal Dosing Frequency

More costs can be found in costs by route of administration.

Make sure your treatment center believes in patient education and patient self care. It’s key to know the dosages you are being given, and at what frequency.

Ketamine increases anesthesia tolerance across the board – so if one were to be in an ER, and about to undergo surgery they’d need to tell the ER what dose of ketamine they take, and at what frequency for the anesthesia to be adjusted appropriately (upward).

As I understand it, worst case scenario is you could be in emergency surgery and not sufficiently sedated – iow, sedated enough to be paralyzed, but not sedated enough to be unconscious. And then experience the surgery.

Which is unlikely I’m sure, but I know when I went in for a colonoscopy and gave them my doses and frequency they doubled the anesthesia. So definitely a remote possibility.

Many patients share the guide with their providers, and as a result are able to have more in-depth conversations with their providers about their course of treatment, the potential side effects, and other related concerns. Be sure you choose your provider carefully, and that you are well informed and educated about your treatment, and related protocols.

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● Administration

Typically, an IV series is done over two to three weeks, with injections Monday, Wednesday, and Friday, over two/three successive weeks, for example. This initial series of 6-9 (typically) infusions are called the “loading doses“.

I started with troches, did them for two months, then did my IV series of 6. I use a local provider overseen by a psych specialized in ketamine. I know many choose telemedicine, and there are several viable alternatives, however, do your research, as several get many bad reviews for poor support during the treatments. If we see enough negative feedback about a provider, we will annotate our provider directory to call that out.

At first, in my treatment, I found troches preferable to IV. No injection was involved. I could do them as I saw fit, go as deep for as long as I liked, and ensure I had a quiet, safe space for the experience. It’s essential to be in a safe space with limited (no) interruptions (outside of a friend/therapist, perhaps). Still, while you’re under the influence, you’re vulnerable, and avoiding trauma is essential (I’ll go into that more below).

Do not mix ketamine with water, like a bathtub, hot tub, or pool. Cognition can take a break while under ketamine, and drowning is a risk. Instead, find a comfy recliner, couch, or bed. It is anesthesia, and you will fall unconscious if the dose is too high.

Another reason I preferred troches to IV is because clinics do o2 stats and blood pressure checks, which negatively interrupt the experience – so you’ll be knee-deep in childhood trauma, and a nurse will bug you. Not ideal. If this is your provider’s practice, ask them to limit their interactions to before and after the dose is administered and has been completed. My practice changed its standard operating procedure for everyone upon this request.

Note that I say I used to prefer troches. So, ketamine at high doses can cause psychosis symptoms for me to occur intermittently. Since I’m bipolar, the last thing I want to do is reinforce my psychotic neural networks, so I have arranged a predetermined dose delivered by IV once every 3 months as my maintenance schedule. The IV is a lower dose, delivered over a longer window (2 hrs). This ensures I 1. do not become psychotic as the dose is controlled more tightly, and 2. that someone is there if I do become psychotic because some serious adverse events in my life have resulted from psychoses. I no longer trust myself to self-administer, so I’ve built a support network. The key takeaway here is to be careful with dosing, more is not better, and there is a point where you may do things you’re not aware of. Keep doses manageable to avoid that.

In the IV series, dosages are increased over the series to promote higher dissociation. This can be done with troches. However, heed the warning above, and please read carefully about the dosing below because more is not always better.

With IV administration, you can request magnesium alongside, which increases the effect and reduces hangover.

Ketamine can cause nausea in some people, so they can also administer Zofran, an antinausea drug.

You can supplement it with magnesium glycinate using troches or other non-IV methods. It is highly bioavailable and comes without the laxative effect of magnesium l-threonine. 400mg. An early morning dose on the day of your ketamine is recommended, although magnesium is good to take at 400mg daily.

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● Bioavailability

In regards to tooth enamel:

• Ketamine is acidic, with a pH of 3.5-5.5. Acidic substances below the critical pH of enamel (5.5) can erode enamel over time.
• However, the limited contact time with low concentrations used therapeutically is unlikely to cause significant enamel erosion.
• One study found no difference in salivary pH after intravenous ketamine administration. No clinical studies have directly evaluated the effects of long-term therapeutic ketamine use on dental enamel.
• Proper oral hygiene practices should prevent any minimal erosive effects of therapeutic ketamine use.

Overall, while more research is needed, there is no strong evidence currently that therapeutic ketamine under proper medical supervision degrades or erodes tooth enamel to a significant degree, especially with short-term use.

The nasal is even better at 1st pass digestion than under the tongue (more mucosa), resulting in a higher bioavailability than sublingual.

Intranasal administration of ketamine, by way of comparison, has a higher bioavailability of around 45-50%. This is because intranasal administration allows the drug to be absorbed directly into the bloodstream through the mucous membranes in the nose, bypassing metabolism in the liver.

You may want to consider getting a nasal dispenser. This can lower the risk of bladder damage, covered last in the guide. See Vitality Medical to Buy a Nasal Dispenser.

Racemic rapid dissolve tablets and racemic troches can be placed into warm saline, dissolved, and dispensed nasally with this device.

The suppository also has higher bioavailability than the sublingual due to more mucosa. Here, follow the same protocol to prepare RDTs or troches and inject rectally with a rectally appropriate syringe.

Suppositories generally avoid first-pass metabolism like nasal, IV, and IM. Suppositories can have variable absorption depending on the specific formulation and individual differences in absorption in the rectal mucosa. It is generally thought to be higher than oral, however.

So, all that said, always involve and follow your provider’s guidance in any variation to your prescribed treatment plan, including formulations and route of administration. Discuss any changes with them, and get approval to try a given technique. You need to understand your provider’s protocol for such approaches and protocols for infection mitigation.

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● Half-Life

• Ketamine has a relatively short half-life of around 2-3 hours. This means that after 2-3 hours, the plasma concentration of ketamine is reduced by half.
• However, the psychoactive effects of ketamine typically last 45-90 minutes when used at therapeutic doses. The effects wear off gradually.
• Ketamine is metabolized into norketamine with a longer half-life of around 12 hours. Norketamine is also psychoactive and can prolong the effects.
• Most guidelines recommend waiting 24 hours after using a therapeutic dose of ketamine before driving or operating heavy machinery. This allows time for the drug and metabolites to be sufficiently cleared from your system.
• Some experts say waiting 12-16 hours may be sufficient based on the short half-life, but 24 hours is a more conservative timeframe given the presence of active metabolites and individual variability in response.
• The effects of ketamine vary significantly between individuals based on factors like body size, liver function, other medications, etc. It’s best to be cautious when judging your ability to drive safely after ketamine.
• If you must drive sooner than 24 hours, be careful and attentive. Have someone else drive if you notice lingering effects like sedation, slowed reflexes, coordination issues, or altered judgment. Please don’t take any risks when it comes to driving safely.

In summary, a 24-hour wait is recommended after a therapeutic ketamine dose, but if driving sooner, take every precaution and avoid driving if any effects persist. The clearance time can vary.

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● Experience

To start, ketamine disables the perineuronal net, a protective system in the brain dealing with trauma. This is one of its greatest strengths, as by disabling the net, the mind becomes adaptable to how trauma is stored and the stimulus-response patterns of triggers. This comes with some risk, though, as when new trauma occurs within the window wherein the net is down, the trauma won’t be processed as normal, and the effects of that are unknown. Due to this, my advice is to avoid traumatizing yourself with the experience itself.

Disassociation is accomplishable via a moderate dose, so there is no need to wipe out your cognition (anesthetic dose) or ‘ego-die/khole‘. Some report therapeutic value in ego-death levels, and some research indicates reset of brain circuits and neural networks at those doses can be therapeutic. I have dosed at elevated levels and found benefit in understanding myself spiritually, yet there is some risk to my sanity. Know, however, that those doses are not required for ketamine to be effective, and they can be traumatic if you aren’t prepared for them.

Again, my guidance is to start low and work up. Trauma processing is best when your ego is present and lucid, which is lower doses than ego death. Start low and work up to it if you want to go as far as ego death. As you’ll see below, though, many of ketamine’s therapeutic aspects do not require this.

Ketamine at high doses recycles neural networks/resets brain circuits (aka neural fragmentation), so you may be out of it for a bit. Do not let it concern you — it’s a natural and transient part. Try not to go this high, but know it happens, and nothing to worry about. For more about this, you can read this Sheep on K for a good study. Research has shown the human brain doesn’t behave precisely similarly, but it should give you the gist.

See even more of Ketamine’s Action in the Brain.

Note that the flatlining of brainwaves shown is hypothesized to create a Near Death Experience (NDE) for some while undergoing the experience.

Again, trauma processing only requires a moderate disassociated dose. This keeps you mentally intact but opens memories from suppressed traumas and will surface the issues your mind needs help with. At these doses, ketamine exposes suppressed memories, triggers (stimulus/response), traumas, and thought patterns for modification. This is how it most effectively treats PTSD & CPTSD. At these doses, the recall on ketamine will be near perfect.

Dissociation provides new perspectives on problems, memories, and triggers — and each time you take ketamine, the view differs. This will give you much to think about and work on.

Do not try to make your mind focused. It will prove difficult. Trauma is processed in the background; you need not work on it consciously. You can, though, and as you understand triggers better, you can target them intentionally and rewire them to fire appropriately.

Ketamine collapses neural networks/brain circuitry and some brainwaves in no particular order and to varying degrees while enhancing other neural networks/brain circuits/brainwaves. This is a highly active field of study, with imaging of all nature being produced, and the terms are broad because there isn’t consensus on the exact mechanisms here.

See: Brainwave Changes

As a result, ketamine is unpredictable in that the same two doses will rarely have the same effects. Each time you take ketamine, the subjective experience and the nature of the trip will vary – some trips will be more vital and more profound, while others may not even induce visual or any mental effects. Each time you take ketamine results in a new point of view, however, and part of that variability is thought to stem from the variations in these collapses and resets. Again, theoretical.

Like many, I did feel worse before I felt better. Processing trauma was brutal, and I cried non-stop for a couple of days after each dosing for the first eight or so.

See: Feeling Worse When Starting Treatment

By starting with troches, I had already begun the formation of the new synapses and dendrites found in a healthy brain. I had pre-processed a lot already going into the IVs, so my IV series was anti-depressive and healing.

Those starting with IVs build the new synapses and dendrites with the first dose, and the growth happens 12-72 hours after a dose. In the beginning, the newly formed structures are weak and need a lot of reinforcement. The series of 6 IVs gives them lots of time to build out, and what you do during your series can affect how well they build out, and like a muscle, they need exercise. Do everything you can to be healthy. Therapy, yoga, walks, meditating, bonding with loved ones, processing emotions, letting them come and go. Learn mindfulness. This is key, and being present now is what gets rid of triggers.

Even though the first few doses may be difficult emotionally, your ideation (should you have any) will be removed with the first dose, so you won’t want to end your life. If you continue to ideate after the first dose (which happens rarely), it’s a sign of cyclic ideation caused by depression and may take a while longer to resolve as your networks build.

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● Transliminal Space

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● Near Death Experience (NDE)

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● Out of Body Experience

It’s important to note that OBEs are often associated with altered states of consciousness, such as near-death experiences, deep meditation, psychedelic substances, or certain sleep states. However, they can also occur spontaneously without any apparent trigger. The exact cause and nature of OBEs are still subjects of ongoing research and debate in the scientific community.

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● Super-Hearing

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● Neurological Growth
● Improved Cognition
● Neural Plasticity

Ketamine promotes (at least) three mechanisms through which your brain changes and heals: Neurogenesis, synaptogenesis, & dendrite relocation, regrowth, and extension (aka remodeling).

Neurogenesis –

Ketamine appears to increase the proliferation and development of new neurons from neural stem cells. It does this primarily by activating the mTOR (mechanistic target of rapamycin) pathway, which stimulates synaptogenesis and growth of new dendrites on developing neurons. Ketamine also seems to increase levels of BDNF (brain-derived neurotrophic factor), an important neural growth factor. The most prominent growth occurs in the hippocampus.

Synaptogenesis –

Research shows that ketamine rapidly increases synaptogenesis in the prefrontal cortex and hippocampus. It does this in several key ways:

• Ketamine increases brain-derived neurotrophic factor (BDNF). BDNF supports long-term potentiation – the strengthening of synapses based on patterns of neural activity. BDNF facilitates synaptic plasticity.
• Ketamine also activates the mTOR pathway. mTOR signaling promotes the translation of synaptic proteins needed to produce new synapses.
• The new synapse formation induced by ketamine occurs via the rapid synthesis of synaptic proteins like PSD-95, glutamate receptors, and synapsin. This leads to increased density and function of synapses.
• Ketamine also increases the number of mature mushroom-shaped dendritic spines, the sites where synapses form. This further enables synaptogenesis.

Dendrite Relocation, Regrowth, and Extension (Remodeling) –

• Ketamine increases brain-derived neurotrophic factor (BDNF) levels, which promotes dendritic remodeling and motility. BDNF activates pathways that allow dendritic spines and branches to become more mobile.
• The increased dendritic mobility induced by ketamine leads to elongation and branching of dendrites. This allows dendrites to sample a greater area to form new synapses.
• Ketamine also rapidly increases the turnover of dendritic spines, with the loss of certain spines and the growth of new ones. This reorganizes the dendritic network.
• Advanced microscopy techniques have shown dendritic spines redistributing within 30 minutes of ketamine treatment in rodent models.
• The new dendritic configurations allow neurons to form novel circuits and increase synaptic connectivity.

Inducing rapid relocation and rewiring of dendrites, ketamine can quickly remodel communication between neurons in brain regions involved in depression. This may help “reset” circuits that have become dysfunctional, restoring neural plasticity. The reconstitution of neural networks via dendrite reorganization is likely a key mechanism underlying ketamine’s robust and sustained antidepressant effects.

Note that Spravato has not shown the same effect. Again, this implies not rebuilding synapses as effectively, but speculative and not proven through research.

Neural plasticity opens during a dose and persists up to 72 hours afterward. Neural plasticity means your mind is open for conscious modification, and it’s as if your conscious and subconscious can discuss things and come to terms with one another.

Decide to change, accept, and love something; it will become solidified in your mind after the window closes. For instance, you can quit a substance and wake up the next day, not craving it.

The uses of this are manyfold, experiment and surprise yourself!

There is limited research available, but ketamine is also remarkably similar and thought superior to modern treatments for Alzheimer’s as well. Out of five hypothesized pathways for Alzheimer’s, ketamine shows improvements in four and uncertain effects in a fifth.

One of the leading theories in Alzheimer’s is that the dendric spines become complex and, as a result, require expensive metabolic processing. Ketamine reforms dendric spines, making them leaner and more efficient and attaching them to new locations on the synapses. This reduces the metabolic expense of the dendrite and is theorized to act as a precognitive agent against Alzheimer’s. I’ll add more info here as studies proceed.

See Alzheimer’s Disease for more recent updates here.

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● Metacognition

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● Fight or Flight Mode

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● Name Your Minds

Other minds could be clever, empathetic, optimistic, or pessimistic. Use your imagination. We all have many.

Encourage healthy minds and discourage your unhealthy ones.

Just speak to yourself inside, and when programming your mind, speak to it in your internal voice. Your executive center controls which mind speaks and which coping strategy gets used when (in the absence of a trigger kicking in the reptilian brain), so tell yourself what you want those minds to do, then remember and reinforce that. This is most effective when you reinforce this when you’re within the window of neural plasticity.

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● Deprogramming Triggers

Find the root, and repeatedly (like a mantra) tell yourself, “Now is different than then!” In the window of neural plasticity, your brain can be rewired to see today’s circumstances as an entirely different scenario, keeping the trigger from firing in the future.

In my therapy, I use my puppy dog as an anchor to the now. She wasn’t around when the triggers were formed, so I mindfully interact with her, hugging her and getting puppy kisses, thus rewiring my stimulus-response system to recognize her as a differentiator when looking to fire triggers. If she’s around, triggers aren’t appropriate. Doing this helped me greatly.

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● Doom Loops

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● Patches and Upgrades

Regardless, you’ll appreciate the mental clarity you get from recently recycled networks. And the new points of view.

I know It sounds odd, especially to someone completely new to ketamine. But once experienced, it is quite an apt description.

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● Dosing Levels

There is controversy in research around therapeutic doses. Some research indicates the therapeutic value in going through a ‘k-hole’ experience, while others have shown therapeutic value without that being necessary.

Some research shows ketamine disconnects a hyperconnected default mode network that ruminates, and it is unclear what dose is required to do that.

There is also the formation of new synapses and dendric spines in areas damaged by maladaptation 12-72 hours after dosing, which is also hypothesized to create some of the therapeutic effects – and in that case, it’s not required to wipe your cognition, ego die or ‘k-hole’.

So, while I think moderate doses to promote disassociation are helpful from a PTSD & CPTSD perspective (untangling triggers and divorcing the mind from the stimulus-response), it isn’t clear how high a dose is required to solve depression and regrow the synapses damaged by depression and maladaptation.

Again, studies have shown that ketamine takes down the perineuronal network, which protects the brain against trauma. Knowing this, it’s essential to ensure that the ketamine experience doesn’t traumatize you. At high doses, especially without any prior experience with ketamine, a khole (ego death) can be traumatizing. The lack of coherent thought and inability to remember yourself or aspects of your life can be scary.

For this reason, I recommend you start low and slowly work your way up in dosing, ensuring you stay within your comfort zone throughout treatment. This may result in smaller increases in doses than recommended or additional doses to reach the level of disassociation you find therapeutic. Many people have reported (and research is showing) that moderate dosing is very effective.

“I started at 0.5mg/kg but decided to try upping the dose a little because I was emotionally overwhelmed. It was like exploring an inner dreamscape, but I didn’t have the emotional regulation skills to process everything that was coming up. Someone on here suggested that I might be a little more comfortable with a little more distance. However, I still found 0.5mg/kg helpful in gaining insights and processing trauma. I felt terrific afterward, though. Happy and grounded after the first infusion.

At first, I tried upping it to 0.6mg/kg, which was a disaster. It became increasingly intense and a giant looping flashback of a traumatic event. I had enough control at the lower dose to bring in a friend or affect my experience. At 0.6mg/kg, I was just stuck. I didn’t get the same insights or symptom relief as I did at 0.5mg/kg.

My most helpful infusions (at 0.55mg/kg with magnesium over 40 min) were like exploring an inner dreamscape with safety and perspective. It wasn’t precisely revisiting past trauma but more like metaphorical visuals that gave me insights (watching my father drift away on a raft, seeing my mother frozen in time, passing through a portal, and turning into a bird with metal wings). It all made sense to me during the infusions or the integration work a few hours later. It was trippy but specific to my situation. I sobbed through most of my infusions and processed a lot. And the insights (e.g., I am more than what was done to me) felt like a light bulb turning on, like flipping a switch in my brain. I didn’t have to struggle to accept things I’d been working on in therapy forever; they just became true. I can still open my eyes and communicate at 0.55mg/kg; I don’t.”

For another view on the ketamine experience itself, read WhiskeyBravo’s story as he undergoes therapy and journals about his experiences.

Just be careful not to traumatize yourself, as those traumas are potentially severe with the perineuronal network being down.

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● Maintenance & Boosters

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●Ketamine as a Cure

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● Ketamine and THC

So, many providers recommend (and test) that THC not be present during treatment so those networks grow correctly. This is the right approach. That doesn’t mean you can’t imbibe some once you’ve grown out of the healthy net (mostly there after the series of six and a few boosters) but don’t train your new, healthy mind to be habituated on a drug.

There is good news here, though, ketamine makes quitting amazingly easy. It’s like it wants to. With one dose, you can stop, easy peasy. With the window of neural plasticity, you can decide to change a habit like that, and poof, like magic, it changes.

I know that’s not what some wanted to hear, and if they ask around, I’m sure they’ll find some that advocate THC while using ketamine. As I said, it’s controversial.

I quit THC personally, and now that my brain is healthy and reinforced, I also stopped drinking LSD, THC, DMT, mushrooms, caffeine, and several prescriptions that I no longer need. It turns out that baseline me is the version of me I like best. That’s a personal choice, of course, but I find my healthy mind is preferable to other altered states.

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● Spravato vs. Racemic Ketamine

See also Spravato vs. Racemic Ketamine for additional detail.

Update: See this recent study, which proves across 3299 patients that spravato is significantly less effective than racemic ketamine.

Spravato is esketamine aka the s-anomer of ketamine. Racemic ketamine is a mix of r and s isomers, targeting more receptors.

Advantages of Spravato:

• Clinically proven to treat treatment-resistant depression
• Approved by the FDA and VA for TRD treatment
• It can be cheaper than IV ketamine treatments
• It is often covered by insurance
• For some may be the only option – and it’s better than nothing
• Stronger disassociation than ketamine at equivalent doses

Disadvantages of Spravato:

• Not shown to improve cognition in limited testing
• Limited potential for dissociation
• It can be more expensive than ketamine troche, rapid dissolve tablets
• Limited dosing options per manufacturer recommendations
• Not shown effective, either clinically or anecdotally, for other mental illnesses than TRD.
• Nasal spray only
• Only approved to treat depression

Advantages of Racemic Ketamine:

• Flexible in form and dosage
• Available in more treatment centers
• No upper limit to disassociation dosages (they can be dosed more strongly)
• Cognitive benefits shown via correlated studies
• Treats a broader array of mental illnesses
• Some methods of administration are cheaper than Spravato

Disadvantages of Racemic Ketamine:

• Few clinical trials. Benefits are primarily shown through psychological tests and lots of patient and doctor reports.
• Limited backing studies
• Little FDA rigor
• IVs can be more expensive than Spravato

Note that dozens of people have done ketamine proper and Spravato, and they universally report that ketamine is far more effective across a broad spectrum of mental illnesses. A few (and clinical studies show) that Spravato is effective against TRD regardless of the cognitive or dissociative benefits. So far, only one person has reported Spravato being equally effective. I recommend trying ketamine if you have the option between ketamine proper and Spravato; ketamine will be cheaper, more flexible to dose, and by many reports, more effective across the board when people have taken both. Admittedly, though, it is largely anecdotal.

As studies proceed, I will add more info here. Spravato shows potential, and clinical evidence is sparse on the efficacy of racemic ketamine, whereas Spravato has more clinical evidence. Suppose you wish for a more reported effective path. In that case, racemic ketamine has more of a record of accomplishment and shows solid, consistent results for most across various mental illnesses. In contrast, Spravato has only been clinically proven for TRD and has few anecdotal reports of being effective in other mental illnesses.

Note that by way of comparison between IV ketamine and Spravato, especially if you have limited insurance coverage or are restricted by the VA, Spravato may well be the better choice and potentially cheaper. Choose your route of administration method carefully, as the costs vary, and Spravato is more expensive than many ketamine administration methods.

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● Recommendations

See also: Session Recommendations

Music

Play instrumental music. Part of this is you want to let your mind wander, to associate and disassociate freely. Music with words prevents this because it constrains you to a topic.

• ‘Ketamine Saved Me’ (Spotify) – very few uplifting words here and there.
• ‘Ketamine Infusion // Heart Opening‘ (Spotify)
• ‘Infusion‘ (Spotify)
• This is Enigma (Spotify).
• Subnautica Below Zero Soundtrack (Spotify).
• John Hopkins University Playlist (Spotify).

Eye Mask

• You’re going to want to maximize your mind’s eye. Block light so you can see mental imagery better.

Headset

• Ideally, something noise canceling. Note, at times, ketamine music can become atonal. Not unusual.

Red and Itchy Eyes

• If you have red or itchy eyes afterward, use antihistamine eyedrops.

See: Itchy Eyes

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● Ketamine Assisted Therapy

I have had times where I’ve been on lower doses of ketamine and talked through problems/traumas/events as they’ve come up, and interactively resolving the issues while on ketamine can be effective.

Lots of people have benefited from working with therapists alongside ketamine therapy. Reddit user u/awkwardflea said, “I got a ton out of doing integration works a few hours AFTER infusions. I know at least one other person with CPTSD on here who also found that beneficial and an infusion doc supporting the post-infusion integration work approach.

I never tried ketamine-assisted psychotherapy (KAP), but based on my experience with infusions, I don’t think I’d find it beneficial. Even with the lower dose, my experience is very internal. I would lose a ton trying to talk to someone during it. My ego is still intact, but it takes a backseat and lets my subconscious steer, if that makes sense, unless I open my eyes and try to fight the treatment.”

I agree with u/awkwardflea in terms of KAP. Even when in a coherent state, my mind is working so quickly and associating and disassociating so many disparate thoughts with each other, and delving into all the associations that underlie triggers, having to talk through it would get in the way – and that’s if I could hold my train of thought long enough to carry on a conversation.

Something important here to mention! PTSD patients have typical maladaptive behavior as a result of triggers. Learn about these PTSD maladaptive behaviors and work through them intentionally in your ketamine therapy.

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● Contraindications

Lamictal and Risperidone

Both potentially reduce the effectiveness of ketamine, according to this study: Ketamine and other depression meds.

I take both, and ketamine still worked 100%, but I need higher doses than others.

The interaction between lamotrigine (Lamictal) and ketamine is not fully understood, and the available literature provides mixed results. Here are some key findings from various studies:

1. A study titled “Modulatory Effects of Ketamine and Lamotrigine on Cognition: Emotion Interaction in the Brain” suggests that the effects of acute ketamine challenge are sensitive to modulation by pretreatment with lamotrigine, which inhibits glutamate release. However, the inhibition of glutamate release by pretreatment with lamotrigine did not influence ketamine’s subjective effects source.
2. Another case report titled “Failure of ketamine anesthesia in a patient with lamotrigine overdose” discusses a situation where ketamine failed to work as an anesthetic in a patient who overdosed on lamotrigine. The authors suspected an interaction between lamotrigine and ketamine, as lamotrigine reduces the glutamate release needed to mediate ketamine’s dissociative effects source.
3. A systematic review titled “Pharmacodynamic Interactions Between Ketamine and Psychiatric Medications Used in the Treatment of Depression” found that two out of five studies on lamotrigine indicated that the effects of ketamine were attenuated source.

These findings suggest that lamotrigine may potentially alter the effects of ketamine, possibly by inhibiting glutamate release. However, more research is needed to fully understand this interaction’s nature and implications.

Grapefruit Juice

There are reported interactions (as is common with grapefruit juice and other meds), but the exact effect caused is unclear.

Liver Interaction

• Rifampin, a tuberculosis drug that decreases ketamine
• St John’s Wort is a popular supplement for a variety of conditions that decreases ketamine
• Ketoconazole, an anti-fungal drug that increases ketamine
• Cimetidine (Tagamet), an acid reducer for heartburn and peptic ulcers that theoretically increases ketamine
• Orphenadrine (Norflex), a muscle relaxant, inhibits CYP2B6 and slows the breakdown of ketamine which increases the amount of ketamine in the body
• Dexamethasone, a common steroid, induces CYP2B6 and speeds up the breakdown of ketamine. This decreases the amount of ketamine left in your system to work.

Rapamycin

According to more recent reports, rapamycin appears to be a catalyst to ketamine, prolonging its anti-depressant effects. There are very few studies in this area – so make sure you look this up and speak with your provider about it, as it may be a way to improve the effectiveness of your therapy.

Immune System

In recent studies, ketamine has been shown to suppress aspects of the immune system. This is important because you may want to avoid sessions while sick or chronically ill.

Benzodiazepines

Ketamine and benzodiazepines (benzos) both have central nervous system depressant effects, so using them together can lead to enhanced sedation and respiratory depression. This increases the risk of unconsciousness and potentially overdose.

Gabapentin

Gabapentin and ketamine appear to by synergistic, with some reporting improved results when used in combination with one another. It has also been noted that they exacerbate side effects, however.

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● Ketamine and Psychosis

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● Ketamine Cystitis (Bladder Harm)

See also: Ketamine Cystitis (Bladder Harm)

Note, like much around ketamine therapy, this section is controversial and the most often criticized. Do your research and know my guidance is quite conservative, according to many. The way I see it, since the risk here is long-term damage to the body, it is much better to be safe than sorry, so I am conservative intentionally.

Most chronic bladder damage seen with ketamine results from abuse in recreational users.

Bladder damage potentially occurs from chronic exposure to ketamine metabolites, which damage the inner mucosa lining of the bladder. There may also be damage to interstitial tissue, microvascular changes, and autoimmune responses. Chronic contact with metabolites is hypothesized to result in submucosal edema, vascular ectasia, detrusor muscle inflammation, and fibrosis. Collectively, this is called ketamine cystitis (KC). Lower urinary tract symptoms were found in around 30% of ketamine abusers.

I’m told dosing at 200 mg a day, and lower has been shown to result in extremely low (no) incidents of KC. If your dose exceeds 200 mg daily for over a few days, consider a break to allow the bladder’s mucosal layer to heal.

The bladder’s internal lining is made out of exactly the same tissue as the inner lining of your cheek. Ketamine crystals and metabolites scratch away mucosal membranes. This is why troches and RDT can often cause a sloughing of cheek cells. Just like your cheek, the bladder can heal the mucosal membrane within it completely as long as it doesn’t become too damaged. KC begins when ketamine crystals and metabolites scratch the mucosal membrane so much that it becomes worn away and exposes the tissue underneath. Ketamine metabolites also damage the underlying tissue, but unlike the mucosal membrane, the underlying tissue can’t heal. By taking a break early and often, the bladder heals between sessions, preventing the long-term symptoms of KC.

See: Bladder Health and the Mucosal Layer

This amount taken varies by the route of administration, based on its bioavailability. IV and IM are the most bioavailable forms, so lower relative doses in those forms result in the same therapeutic value as higher doses in other forms. For example, 200mg of troches may only require 50mg via IV. For those experiencing or prone to bladder issues, using more highly bioavailable forms may mitigate the risk of KC onset.

Trends toward KC damage can be monitored interactively – signs of progression toward KC are bloody urine, cloudy urine, increased urinary frequency, urge incontinence, bladder pain, and dysuria (burning). If you find these early signs, taking a break is safest. The bladder can heal itself completely early on, so those symptoms should clear up within a month if caught early.

Outside of active bladder harm management, drinking a lot of water is recommended, diluting the ketamine metabolites and reducing potential damage. Drink a lot of water after your session, not before, as it’s unpleasant to get up to pee while in the middle of a dose.

• Ketamine cystitis: Its urological impact and management
• Illicit ketamine and it’s bladder impacts

Additionally, even though KC is not well understood, potential treatment programs may be available, and research in this area shows the potential to reverse chronic long-term symptoms.

“Treatment with the antifibrotic compound N-acetylcysteine alleviated the symptoms and pathological characteristics of KC, indicating that the antifibrotic capacity of MSC therapy underlies its benefits. Thus, this study, for the first time, shows that MSC therapy might help to cure KC by protecting against tissue fibrosis in a KC animal model and provides a foundation for clinical trials of MSC therapy.”

• Mesenchymal stem cells protect against the tissue fibrosis of ketamine-induced cystitis in rat bladder.

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● Disclaimer

See also: Site Disclaimer

Ketamine therapy can, at times, be challenging. Ketamine is not normally euphoric. Sometimes, subjective experiences with ketamine aren’t fun. Those sessions can be the most therapeutic, though. Whether it is a positive or negative experience, it benefits your psyche. The regrowth of healthy new synapses and dendrite spines will happen no matter the subjective experience.

Ketamine yields no results in 20% of people. I have read firsthand accounts of it not working. However, it worked great for me, and 80% of people responded well.

I am not a Dr, nor are the site collaborators. Dozens of providers have proofread us, and many use us as their patient primer, but nothing in this guide (or site) is to be taken as a substitute for legitimate medical advice from a qualified provider. This content is for informational purposes only. Ketamine research is constantly ongoing, and while we strive to keep current with recent advancements, our information may not always reflect the most recent study results. As a result, independently verify information through the sources provided and/or Google searches to ensure you review the most recent developments. Always consult a qualified provider about any changes to your treatment plan.

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