Episode 135

Falling down the K-HoleTaking “Special K.”   Ketamine has quite the reputation as a recreational club drug.  But research is showing its promising potential as a treatment for severe cases of depression.

Jesse talks to Dr. Panos Zanos, Postdoctoral Researcher at the University of Maryland School of Medicine, (who has possibly the best name of any Smart Drug Smarts guest to date) about his research on ketamine and depression.

Medical and Recreational Uses

Ketamine was originally synthesized in a lab as a safe anesthetic and continues to be approved in many countries (including the US) for anesthesia and sedative use.  In the US, it’s classified as a Schedule III drug, meaning it has currently accepted medical uses, but carries a danger of abuse.

It’s the dissociative effects — feeling detached from the environment and users’ own selves, as well as experiencing sensory distortion — of ketamine that’s made it popular as a recreational club drug.  Users report feeling numb and serene, like they’re in another world or walking on clouds.  Important note:  while there’s no current evidence of any addiction potential, there’s certainly abuse potential.

A New Use For Ketamine:  Treating Depression

For sheer speed of efficacy, ketamine blows conventional antidepressant therapies out of the water.  Patients feel relief within two hours after a single ketamine injection, while traditional medicine can take up to three months to work.  It’s no surprise, then, that ketamine is often used as an emergency treatment in crisis situations to disperse suicidal thoughts.

But ketamine has potential as a long-term treatment as well.  The antidepressive benefits from one injection last up to two weeks. Multiple studies have confirmed these antidepressive effects.  Unfortunately, you’ll have to contend with all the side effects as well.  The dissociative effects of ketamine may become more pronounced and enduring with repeated treatment.  This is something that needs to be researched further — no one knows the long-term effects of persistent ketamine treatment.

How Does Ketamine Work?

There’s a lot we don’t know about ketamine yet, and it contains a shit ton (that’s the technical term) of substances, each with its own effect.  Here’s what we do know:

Once ketamine enters the body, the liver quickly breaks it down, creating metabolites (a chemical byproduct of the breakdown process), which stay in the body for up to a week.

Metabolites are responsible for the mood-boosting effects of ketamine, without all the side effects (anesthesia, dissociation).  Dr. Zanos’s recent research shows that a metabolite called (2R, 6R)-hydroxynorketamine is at least partially responsible for ketamine’s antidepressant benefits.

This is good news for depression sufferers, since if the active metabolites can be isolated, they can be used to treat depression without the ketamine high.

As for how ketamine metabolites lift depression, the jury’s still out, but a few likely theories have emerged.  Ketamine may work by…

  1. Increasing levels of glutamate, an excitatory neurotransmitter that may be linked to depression.
  2. Inhibiting NMDA receptors, a type of glutamate receptor.  NMDA receptors are a component of the glutamate pathway, involved in memory and cognition.  However, human trials of non-metabolite NMDA-receptor blockers were unable to replicate ketamine’s powerful antidepressant effects.
  3. Promoting the release of brain-derived neurotrophic factor (BDNF).  Depression damages neurons and synapses, while BDNF promotes neurogenesis and strengthens existing synapses.

Perhaps the most promising theory so far:  activation of AMPA receptors (another type of glutamate receptor).  Dr. Zanos’s recent research shows that, at least in mice, antidepressant effects depend on activating AMPA receptors.

Episode Highlights

0:22Ketamine and depression
1:40This Week in Neuroscience: Why We Sleep Badly on Our First Night in a New Place
4:24The audience interaction section
6:26Dr. Panos Zanos and his work with Ketamine
8:35Ketamine as an anaesthetic
9:45Recreational versus medical use
10:31Are there downsides with repeated use?
11:10Acute effects of ketamine
11:52Therapeutic uses
14:44The legality of ketamine in different parts of the world
16:38Which metabolites are pharmaceutically active?
17:44How was ketamine discovered?
18:16How ketamine treats depression
20:31Memory impairment
22:07Are there any contraindications?
23:37How long have scientists been researching ketamine as an antidepressant?
26:03Ketamine as an off-label therapeutic treatment
28:07Scheduling of ketamine in the U.S.
30:00Ketamine’s additive effects
32:40A first-hand account of ketamine treatment for depression
34:45Ruthless Listener-Retention Gimmick: Doctor’s Plan for Full-Body Transplants Raises Doubts Even in Daring China

PS:  You’ll be sad if you miss out on signing up for our weekly Brain Breakfast email.

Episode Transcript hideshow

— This Week in Neuroscience --

Jesse: So, odds are pretty good you've noticed that when you sleep in an unfamiliar environment, you often do not sleep as well.  This is kind of one of those, "Water is wet, sky is blue" observations that we all know.  But scientists actually have a name for this; this is called the First Night Effect, or FNE, because oftentimes it'll settle itself down and you'll kind of sleep normal after you've slept some place one night.  But trying to dig in a little bit further as to what's actually going on within the brain to cause the first night effect, sleep researchers at Brown University had healthy young adults come and sleep in an unfamiliar room where, yes, of course they had their brain scanned while they slept, and they did this on two nights spaced one week apart.  So, same people, same room, different nights, nights that weren't back-to-back because they knew that at least that first night they were going to probably have a crummy night's sleep and they didn't want the first crummy night's sleep to affect the second night's sleep, like more bounce back sleep or something like that.  So, they put six nights at home in their own bed in between and then had them come back on the eighth day for remeasuring how they slept. 

And actually what's going on is pretty interesting.  If you think of an old western movie where people are sleeping outside and they're in this dangerous environment, and one person stays up and stays on watch while the other people go to sleep in case something comes out of the wilderness and slits their throat while they're asleep, that is actually sort of analogous as to what goes on within any one person's brain when you're in a new environment on the first night.  And they did this experiment all with right-handed people, which is a little bit annoying because you'd kind of like to know if this swaps when it's lefties, but what they found is on that first night, the left half of the brain sleeps a lot less deeply.  The right half of the brain has a fairly normal night's sleep.  But it's almost like the left half stays up to keep watch on the environment while the right half gets some rest.  This is not what the researchers were expecting.  They were more or less expecting a degraded night's sleep across the entire brain.  But the results on that first night really seemed very lateralized. 

One of the perks of the job when you're a sleep researcher is you get to poke and prod people while they're trying to sleep and see if they wake up, and they can't really yell at you because that's part of why they're there.  And so the researchers did things like tapped people while they were asleep and played quiet, but not that quiet, noises to see at what volume they'd actually wake people up.  And not surprisingly, on that first night in a new environment, the left half of the brain would wake people up much more quickly at a smaller threshold level than if they'd already slept in that same location one night. 

So, how do you use this to your advantage?  If you need to get a really solid night's sleep, sleep somewhere where you've slept before.  If you need to travel somewhere and be sharp for a business presentation or something like that, add an extra day to your travel schedule, get there one night early so it's the day after your second night's sleep that you do anything where you really, really need to be on your best performance.  Now that researchers have identified part of the mechanism behind the first night effect, they now plan to try to identify whether certain types of insomnia might actually be caused by people that are experiencing something akin to the mechanism of the first night effect on every single night of their life, which would be a really interesting finding. 

-- Main Interview --

Dr. Zanos: Ketamine was initially started as an anesthetic, and it was like a safe anesthetic because it wasn't life-threatening and it wasn't a dose that would kill somebody.  So, they wanted something that would be a good anesthetic but with no life-threatening effects, and this is how ketamine started its progress towards clinical research.  As an anesthetic, ketamine, as I said, is kind of safe and has been widely used in most children, since ketamine has a dissociation effect and it's easier for a child to have this dissociation effect instead of a grown-up.  As a recreational drug, as generally all of the drugs that are abused and all of the drugs that are used as club drugs, ketamine has its own place there, and when people are using ketamine, they're feeling like dissociated from their body and they're feeling this high, they're like in another world.  But I know that it has abuse liability.  Still, nothing says that it has an addiction liability.  So, there is no evidence of ketamine being addictive. 

Jesse: On anesthetic vs.  recreational use, is that just a difference in dosage or is the route of administration different? 

Dr. Zanos: I think everything is different.  How ketamine is used in clubs, for example, some people will sniff it, some people will inject it intravenously.  And for the anesthetic part, it's mainly intravenously, and for recreational use, it's sniffed, and I think this is the main route of ketamine use. 

Jesse: When it's used anesthetically and it's injected, is that a localized anesthetic or does it generally affect the entire body? 

Dr. Zanos: It generally affects the body, a general anesthetic.  It can be used for surgeries, it can be used for small procedures.  For animals, for sure it's very well-used for surgeries and stuff.  But for humans as well, mostly, as I said, in children, but in adults, too. 

Jesse: For anesthetic useóhopefully people aren't getting anesthetized too oftenóbut are there particular downsides for repeated use for somebody that would be using it recreationally, say, on a semi-frequent basis?  What happens if somebody makes a habit of this? 

Dr. Zanos: There is no evidence of something specifically that happens.  It's not like morphine or cocaine that we know exactly their consequences and their withdrawal effects.  I'm sure that ketamine, using something that could change your brain pathways again and again and again, this will have some bad effects for sure.  However, there's nothing very evidenced that ketamine will induce something really, really bad. 

Jesse: And the acute effects that people feel when they take it short-term I guess in both cases, it comes on pretty quickly and is out of your system pretty quickly, too; it has a relatively short breakdown cycle, I guess. 

Dr. Zanos: The liver breaks down to different metabolites that break down products, and this starts very rapidly.  However, there was a paper from Carlos Zarate that shows that it's not so quickly.  Ketamine stays in the body for, I don't remember exactly the time, but stays for a good time, and also the metabolites stay, some of them, for a week in humans, which means that this drug has prolonged effects, at least in humans as I said, because in animal research this is not the case. 

Jesse: For the potential uses as a therapeutic for depression, what is the application like for that?  One thing that I read that was interesting actually was that it's sometimes used as like a short-term emergency antidepressant.  Like if somebody shows up in the hospital and feels like committing suicide right then and there, ketamine is sometimes used to immediately deal with the problem in a chemical way.  I know that probably in the studies that you're doing are looking at more long-term treatment.  Can you tell us about some of those differences in methodology? 

Dr. Zanos: Okay, first my studies are preclinical studies, and what we wanted to see is what can mimic ketamine's effects as a rapid-acting antidepressantóas you said, that it's an acute effectóand also its prolonged effects.  The important thing with ketamine is that it was shown that a single dose of ketamine has rapid antidepressant effects which ranges from like two hours after a single injection, and sometimes it lasts up to two weeks, which is impressive if we have in mind that the normal antidepressant, the conventional antidepressant therapies will need like three months at least to work, and this will be like in 30% of the people from which a high percent will just relapse back into depression.  So, ketamine has this rapid antidepressant effect, and that's why it's used in severe cases of suicidal thoughts, and ketamine has been shown to have anti-suicidal thoughts, so it prevents suicidal ideation.  Also it has this prolonged effect, which again it ranges between each person.  However, this is what I did initially to start with: we didn't do the intermediate doses to see how that works, which is very interesting, and I think in a clinic it started being examined in people and it shows that they can sustain the effects of ketamine.  However, you don't know if a molecule has so many different effects on the brain, because ketamine, unfortunately, let's call it a dirty drug, so it has so many other effects.  So, using that continuously, maybe it has a tolerance effect, maybe it has sensitization, but this was not shown.  Maybe there's so much difference that can change after prolonged use.  We can certainly say that the prolonged effects of a single administration is very promising for ketamine.  However, it has all of the side effects as well. 

Jesse: And the side effects are also prolonged. 

Dr. Zanos: The anesthetic effect, I cannot say that is prolonged.  This was like a very short-term anesthetic.  For the dissociative effect, if you use ketamine again and again, I suspect these will be prolonged effects and you will have some bad experiences for the person.  The addictive side effects, which I say that is mostly like abusive effects, these will be bad, yeah.  These will have prolonged effects and maybe it will affect health.  And starting with ketamine, people will continue with worse drugs of abuse; this is how it goes, usually. 

Jesse: I was looking at the scheduling and legality of ketamine in different countries, and it seems like it's all over the map.  Some countries, it's relatively easy for a person to get their hands on it, and I think in Australia it's actually a Schedule I narcotic, and in most countries it's somewhere in between.  But it seems like the jury's very much out on the level of public danger that it provides. 

Dr. Zanos: I would agree with that.  For clinical practices, anesthetic ketamine is used, and this is something that everybody knows.  However, for the treatment of depression, indeed, some countries have it off-label, and for some doctors to administer that, you have to pay a lot, I think.  But some countries do not allow ketamine as an antidepressant.  For example, I know for sure Cyprus in the European Union, it's not allowed; doctors cannot prescribe ketamine for depression.  It's been there for decades, however, it's not allowed.  I think it's good since nobody knows exactly what this will drug will induce after repeated administration, and also the route of administration is a little bit strange, for people to go to the doctor for an intravenous administration all the time.  Since only recently, there are studies showing that intranasal administration of ketamine has effects in humans, and this is only case studies.  Oral administration of ketamine has promise.  however we don't know how oral administration works since ketamine does not have the greatest oral bioavailability, meaning that ketamine enters the body, however it's been shown that we don't have ketamine levels after administration of ketamine orally.  So, you'll have some metabolites, yes, and not ketamine per se because it doesn't have oral bioavailability, which makes thinking how ketamine works in these peopleóif ketamine itself is not in the body, it's more evidence that something else is happening after ketamine administration except from ketamine itself. 

Jesse: You mentioned there being various metabolites.  Have we determined which of the metabolites are the ones that are pharmaceutically or psychologically active, or is that still sort of an open question? 

Dr. Zanos: The metabolites story of ketamine is very limited in research.  I would say that for depression, we are among the first ones testing this.  And there are so many metabolites of ketamine that obviously it's a little bit difficult to test everything.  We will, though; we have funding now that allows us to study all of these metabolites, at least the ones that are appearing in the body for longer.  And this is how we did that: we started from the metabolite that was in the highest concentrations in both humans and in animal research and we only tested these metabolites up to this point. 

Jesse: Is ketamine a naturally occurring compound, or is this something that was synthesized in the lab? 

Dr. Zanos: Ketamine is just synthesized, it's not an endogenous compound, unfortunately.  It would be good if it was endogenous and then stimulate something else to have it.  But no, it's not an endogenous compound, it's just synthesized. 

Jesse: How was it that it was discovered?  Was this just serendipity that it happened to come out of playing around with a bunch of organic molecular components, or was there some method to the madness that discovered it? 

Dr. Zanos: I'm sorry, but I'm not 100% sure.  What I suspect is that ketamine was discovered after knowing that a specific receptor, if you block this specific receptor in the brain, it induces anesthesia, this is how ketamine was discovered.  Because they wanted a safe anesthetic, and they developed ketamine to have these anesthetic effects. 

Jesse: For the antidepressant effects, do we know what's happening within the brain, what neurotransmitters are getting upregulated or downregulated that's producing the antidepressive effects? 

Dr. Zanos: So there are several theories on how ketamine works.  The main theory is that ketamine induces an increase in the glutamate neurotransmission.  Glutamate is a neurotransmitter that is everywhere in the brain.  So, increasing this glutamate release in the brain is thought to underlie the antidepressant effects of ketamine.  This is the main theory up until now.  However, there is no direct evidence, but there are other theories that, by blocking a specific receptor called the NMDA receptor, this by itself causes synaptic plasticity strength and this causes the antidepressant effects.  So, there are these main theories.  And also there are other theories that involve these two other theories, as I said.  Like BDNF release, or glutamate plus BDNF release, or some other neurotransmission changes in the brain that will induce antidepressant effects.  However, the exact mechanism, it is indeed not known. 

Jesse: Why is it that promoting neuroplasticity or BDNF, which is Brain-Derived Neurotrophic Factor, which is encourages the growth of new neuronsówhy would either of those affect depression?  That doesn't seem immediately obvious to me. 

Dr. Zanos: So in depression, we have a loss of synapses, we have a loss of neurons, we have neurons not working properly.  So, something that will promote neurogenesis, something that will promote synaptic strength, and something that will have neuroplasticity changes would definitely induce this antidepressant effect, and this is how scientists base this effect of ketamine on.  Because of the findings on depressed people, these are postmortem studies as well as some imaging studies showing changes in the strengthening of the synapses.  So, synaptic plasticity strength and BDNF that promotes neuronal growth, everything would have helped the antidepressant effects of ketamine.  And this is the impressive thing of ketamine: it can do a lot of stuff.  However, we have to limit the good stuff from the bad stuff that ketamine can do. 

Jesse: I've read at least a few reports of ketamine being used both as a date rape drug and also it being responsible for some pretty severe memory lapses.  Can you talk about either of those? 

Dr. Zanos: For memory, we have strong preclinical findings that shows that ketamine has some memory impairment effects.  However, we should mention that the doses that are used as an antidepressant are subanesthetic doses, and also these doses do not probably induce memory loss.  People are dissociated, yes.  So, as you inject the ketamine intravenously, people will have this dissociation effect and they might not remember, they might think that they do stuff that they don't actually do.  People actually have reported that they thought that this was an embarrassing moment when they were administered ketamine intravenously.  However, if you have a camera there, you will see that these people just sit on a chair and they don't do anything, they just sit thereówhich, for me at least, is not memory impairment.  The thing that we don't know is how ketamine administered long-term or in different routes, like samples in clubs, you don't know the dose that you get.  People would administer ketamine and then there are reports of people not remembering what they have done before.  This is the case with alcohol, as well; it depends on how much you'd drink.  So, ketamine has this effect presumably depending on the dose, on how you used it, andóI'm not sure about thisóbut also how clean it is, because in the clubs you don't know what you get. 

Jesse: Are there particular contraindications, people that should never be given ketamine for one reason or another because of what it's doing physiologically? 

Dr. Zanos: I have not read anything like that, I don't think that there is anything yet.  For every drug, there are always precautions where you have to make sure that you don't prescribe a drug in some specific people.  However, I have not heard or read anything specifically for ketamine since it still needs a lot of research to understand exactly what is happening.  However with the metabolism of ketamine, this is what we've shown, that the metabolites are basically safer than ketamine, and so far we have not seen any side effects with these metabolites.  This is how actually these metabolites did not make it into research until now, because they've shown very early, like in the 1980s, that ketamine and norketamine are the active compounds in using the anesthetic effects, while the metabolites that we have tested now for antidepressant effects do not induce anesthetic effects.  But this is a wrong conclusion from people saying that the active stuff is only ketamine since the other stuff does not induce anesthetic effects, it might induce something else.  This is what we've shown now, that these metabolites have promise for the treatment of depression.  Since ketamine, we believe, acts via these metabolites to induce at least the prolonged effects of ketamine, which is the most fascinating thing. 

Jesse: How long have the antidepressant effects of ketamine been something that science has been aware of? 

Dr. Zanos: I think it's just the lack decade now, the most important finding being Carlos Zarate's study showing that treatment of resistant major depressed patients show rapid antidepressant response, and this is prolonged.  And the important thing here is that this effect has been replicated again and again, which is rare in science.  So, this effect is established now: ketamine has rapid and prolonged antidepressant effects.  I believe this study was conducted in 2006 from the National Institute of Mental Health. 

Jesse: Antidepressant drugs are such big business, I mean just billions and billions of dollars spent every year on these things.  It's a little surprising to me that we've known that there's at least a rock to look under here for a decade and that it doesn't seem like this is a hotbed of research.  It doesn't sound like, given the potential breakthrough that another really effective antidepressant treatment would be found, I'm surprised there aren't more people looking into this. 

Dr. Zanos: I wouldn't say there are not a lot of people looking into this.  However, the finding of ours is one of the biggest findings since a completely different mechanism of how ketamine works as opposed to the main thought up until now that ketamine blocks the NMDA receptorÖ However, our study shows that ketamine might also work from another pathway that avoids the side effects.  So, the side effects were the most important limiting factors for ketamine, as you said, being researched.  People were afraid of just having especially over-the-counter ketamine for an antidepressant, or for doctors to administer that, how people have to go to the clinic and have the intravenous administration, which again limits its widespread use in clinics.  So, probably this has been not very active research, and since people believe that NMDA receptor antagonism is the mechanism, nobody would have believed until recently that something else happens when you give ketamine.  Because people started clinical and preclinical studies with other NMDA receptor antagonists that unfortunately do not have the ketamine antidepressant actions.  I can't say they don't have any antidepressant actions at all, but they do not share antidepressant actions of ketamine. 

Jesse: One of the things that I'm always sort of curious about is what illegal drugs that people assume are being used recreationally might actually be being used by people therapeuticallyóillegally, but therapeutically.  Like, is there any knowledge as to whether some people might be using ketamine as an off-label illegal antidepressant now, that we assume that ketamine is being used as a club drug but maybe it's not? 

Dr. Zanos: I think there are clinics that use ketamine for depression.  For example, I'm sure in the US we have some clinics that they do administer ketamine and it's actually very effective.  I don't know elsewhere how they do administer ketamine, but I'm sure there are clinics in the world.  I don't know how many people out there know that there are actually clinics doing that.  However, I think people administering ketamine off-label, since they would need a lot of money probably to have the ability to do so, probably I think it's something that would be somewhat expensive.  However, this is just my opinion.  I'm not sure exactly how much it might cost. 

Jesse: The drug isn't as expensive as the administration of having the medical personnel and things like that. 

Dr. Zanos: Yes, and you might need to go back and back and back since the maximum effect, which is not something short, however it's one to two weeks, and then what?  Then you might need another administration, another session.  So, you would need to pay again and again, and it's not an easy route of administration.  Maybe now that intranasal might have some more promise, which is much easierÖ And again, you cannot give something that has various side effects to somebody having it at home as an intranasal spray.  This is my opinion, as I said.  It's a little bit dangerous.  All the drugs generally have side effects, however the FDA, in order to approve that, it means having a lot of research and they have proof that the beneficial effects will be so above the side effects. 

Jesse: It's got to be worth the potential problems. 

Dr. Zanos: Yes.  I'm not sure this is the case for ketamine. 

Jesse: The scheduling of ketamine in the US is Schedule III, which I think is the same as heroin, for example; something that does have medical uses but is also recognized as being potentially dangerous. 

Dr. Zanos: Yeah, indeed it is recognized as an unsafe drugÖ And people try to find something else that mimics its effects.  There are some trials that show promise, however, still they're preliminary data.  And what the metabolites will have to do, and they will come into play, and it's easier for a metabolite of ketamine which does not show a side effect to go into an actual clinic, is that these metabolites are in the body of people for long now.  So we know that ketamine has these short-lived side effects, maybe some long-lived side effects.  However, the metabolites of ketamine are always there because people prescribe or administer ketamine for anesthetics, also for antidepressant effects, and we know that these metabolites are there.  So this makes it easier for the metabolites to be tested in humans, and this is a good thing.  Studies are now ongoing with the collaboration of the National Institute of Health, like toxicological studies, which are very, very important for a drug, and also some other background studies to show how this drug can be administered if it has oral bioavailability.  This is very, very important because, as you understand, it's much easier to have a drug as a pill that you can orally administer compared to intravenous administrations or even the intranasal administrationóI think it's much more important to have oral bioavailability.  And there are studies now ongoing, testing these parameters.  I want to be optimistic that in three years these will be tested in humans for treatment resistant depression. 

Jesse: The two potential mechanisms of action that we discussed for the treatment of depression, neither of them involved serotonin, or at least not directly.  Serotonin is kind of the first thing you hear when you talk about the benzodiazepines that are used so much for standard-of-care antidepressant effects today.  Is there reason to believe that ketamine and the benzodiazepines could be additive in their effects since they're probably working on different mechanisms of action? 

Dr. Zanos: This is indeed a possibility, and I think there's been some preclinical evidence of these additive effects.  Also, there is some evidence that when administered ketamine, and after the effect of ketamine, they were actually responsive to the classical monoamine-acting antidepressants.  However, this is not strong evidence; it's like some case studies.  Which might be the truth, actuallyóif this drug acts through different mechanisms, maybe this might be true.  However, there is evidence that long-term administration of the classical antidepressants induces this BDNF increase, which is believed to be one of the mechanisms of how ketamine works.  And also to have the synaptic strength after prolonged administration, to have neurogenesis as well, and so much other stuff that seems to have connection with the mechanisms of how ketamine worksÖ However, this has not been extensively researched.  What I can say is that there is preclinical evidence as well that ketamine may act via the serotonin system to increase the serotonin levels in the brain, and this is something that we should also test with the metabolites to see whether these metabolites actually treat your release of serotonin.  If that's the case, maybe ketamine and the metabolites may have double the mechanismóketamine acts via the glutamate and also the metabolites via glutamate, a double mechanism having increased glutamate as well as serotonin, or increased serotonin via indirect mechanisms involving glutamate as well.  These are very interesting questions that have to be answered. 

-- Ruthless Listener-Retention Gimmick --

Jesse: So, it's July 1st as we publish this episode.  I mention that because it's exactly three months after April 1st, when we had our April Fools episode.  This, however, is not April Fools, or if it is April Fools, it's because somebody's hoaxing me, not because I'm hoaxing you.  But according to the New York Times no less, there's a scientist in ChinaóI don't really know why it's relevant that he's in China, but they make a big deal of that in this articleóhis name is Dr. Ren Xiaoping of the Harbin Medical University, and he is planning to do something that sounds straight out of Mary Shelley's Frankenstein.  Apparently there are no lack of people that are signing up for this experimental procedure given that the alternative is essentially death; it's not like young healthy people are doing this.  But Dr. Xiaoping is going to be attempting a body transplant, which could also be called a head transplant.  Basically he's going to be taking a living head from a living person and trying to attach it to the bodyóthe functional bodyóof a recent cadaver.  So, exactly how it sounds, guillotine-style, chop off the head, put it on the body of a headless horseman-style body, stitch everything back together again, presto, there you go. 

Needless to say, this is raising some eyebrows in the biomedical community.  Yali Cong, a medical ethicist at Peking University, which I thought we said Beijing now instead of Peking, but it's written Peking here, so I'll say it that way.  But she said, "I don't want to see China's scholars, transplant doctors, and scientists deepening the impression that people have of us internationally.  That when Chinese people do things, they have no bottom line, that anything goes?"  Arthur L.  Caplan, a medical ethicist at New York University, also called out China.  He says, "I do not trust Chinese bioethical deliberation or policy.  Add healthy doses of politics, national pride, and entrepreneurship, and it is tough to know what is going on there?"  As for the doctor who's looking to perform the procedure, he says, "I've been practicing medicine for more than 30 years.  I've done the most complicated operations.  But compared to this one, there's no comparison.  Whether it's ethical or not, this is a person's life.  There's nothing higher than a life, and that's the core of ethics?" 

But ethics aside, the trickiness of the procedure is in the reconnection of the nerves in the central nervous system in the spinal cord between the living head and the cadaver body.  Reconnecting the blood vessels that flow between the head and the body, those are hoses when you get right down to it, and nothing that medical science hasn't been doing for many, many, many decades now.  But successfully reconnecting the huge number of nerve fibers inside the spinal column, that is where the rubber hits the road with this experimental procedure.  And whether you like the fact that they're trying this or hate the fact that they're trying this, that will be the really, really interesting part to see if they can get right. 

Written by Hannah Sabih
Hannah believes there's nothing 8 hours of sleep and some kale can't cure (yes, she's from California). She's an avid runner, reader, and traveler, who brings you the latest and greatest in neuroscience via our social media channels.
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