U.S. Antidepressant Use Doubled in A Decade

The proportion of Americans using antidepressants in a given year nearly doubled from 5.8% in 1996 to 10.1% in 2005, according to a paper just published: National Patterns in Antidepressant
Medication Treatment
, by Mark Olfson and Steven Marcus.

That means about 15 million more Americans were medicated in '05 than a decade previously. A huge increase in anyone's book. But the doubling in antidepressant use is not the only interesting result in this paper. In no particular order, here are some other fun facts -

  • Women are twice as likely to use antidepressants as men (female 13.4% vs male 6.7% in 2005); the ratio was the same in 1996. Studies consistently find that Western women are about twice as likely to report suffering from depression and anxiety disorders as men are. But these kinds of studies rely on self-report so this could merely mean that women are more willing to talk about their problems. This data suggests that they also seek treatment about twice as often.
  • The peak age bracket for antidepressants is 50-64, with 15.5% yearly use. This is more than double the rate in the 18-34 bracket. This surprised me, maybe because of the influence of books like Prozac Nation (tagline - "Young and Depressed in America"). So, it looks like the increasing use of antidepressants is not because younger people, having grown up in the "Prozac Era", are more accepting of them.
  • Antidepressants are a white thing - 12.0% of whites take them vs. about 5% of blacks and Hispanics. But it would be interesting to see a regional breakdown here. Are blue-state or red-state whites more likely to be medicated?
  • Family income was not correlated with antidepressant use, but the unemployed were twice as likely to use antidepressants: 22% in '05. This might be because unemployment is bad for your mental health, or because mental illness is bad for your employment prospects. Or both.
  • One of the questions in the survey asked people to rate their own mental health. Over 90% of Americans said it as "good", "very good" or "excellent" - including 80% of antidepressants users. This really surprised me, and suggests that these drugs are being prescribed to people who are not, overall, very unwell.
  • The % of antidepressant users also using an antipsychotic drug rose from 5.5% to 8.9% in 2005. Given that the number of users also doubled, this means the number of Americans using an antipsychotic as well as an antidepressant increased by a factor of more than 3. This is worrying since antipsychotics are generally the worst psychiatric drugs in terms of side effects. While there is evidence that some of the newer antipsychotics can be of use in depression as an add-on to antidepressants, this is controversial and it's not clear that they're any better than the older alternatives, such as lithium.
Overall, this report verifies that antidepressant use has risen dramatically over the past several years. This is hardly news, but the magnitude of the increase is still startling.

What makes it especially interesting is that nothing much happened between 1996 and 2005 in terms of new antidepressants. A couple of new SSRIs, such as citalopram, were approved for sale in the US. But these drugs are very similar to Prozac (fluoxetine) which has been around since '87. Remeron (mirtazapine) hit the market in '96, but it's never been nearly as popular as the SSRIs.

So the change was a change in behaviour, a cultural or social phenomenon. For some reason, America decided to take more antidepressants. Books could be written on why this happened, and I hope they will be, because it's an important topic. But here's my personal take: the main reason why people are taking more antidepressants is that the popular concept of "depression" has become more broad. People have become more willing to label their experiences as "depression" and seek medical treatment. The notion that mental illness is extremely common - the one in four meme - is one aspect of this.

Finally, the inevitable caveats. The data here come from the Medical Expenditure Panel Surveys (MEPS) which were household surveys of "national probability samples of the US civilian noninstitutionalized population". This means that military personnel, the homeless, prisoners, and (presumably) illegal immigrants weren't included. And not everyone agreed to take part; the response rate was 70% in '96 but dropped to 60% in '05. On the other hand, the samples were extremely large (28,000 in 2005).

ResearchBlogging.orgOlfson M, & Marcus SC (2009). National patterns in antidepressant medication treatment. Archives of general psychiatry, 66 (8), 848-56 PMID: 19652124

Of Carts and Horses

Last week, I wrote about a paper finding that the mosquito repellent chemical, DEET, inhibits an important enzyme, cholinesterase. If DEET were toxic to humans, this finding might explain why.
But it isn't - tens of millions of people use DEET safely every year, and there's no reason to think that it is dangerous unless it's used completely inappropriately. That didn't stop this laboratory finding being widely reported as a cause for concern about the safety of DEET.

This is putting the cart before the horse. If you know that something happens, then it's appropriate to search for an explanation for it. If you have a phenemonon, then there must be a mechanism by which it occurs.

But this doesn't work in reverse: just because you have a plausible mechanism by which something could happen, doesn't mean that it does in fact happen. This is because there are always other mechanisms at work which you may not know about. And the effect of your mechanism may be trivial by comparison.

Caffeine can damage DNA under some conditions. Other things which damage DNA, like radiation, can cause cancer. But the clinical evidence is that, if anything, drinking coffee may protect against some kinds of cancer (previous post). There's a plausible mechanism by which coffee could cause cancer, but it doesn't.

Medicine has learned the hard way that while understanding mechanisms is important, it's no substitute for clinical trials. The whole philosophy of evidence-based medicine is that treatments should only be used when there is clinical evidence that they do in fact work.

Unfortunately, in other fields, the horse routinely finds itself behind the cart. An awful lot - perhaps most - of political debate consists of saying that if you do X, Y will happen, through some mechanism. If you legalize heroin, people will take more of it, because it'll be more available and cheaper. If you privatize public services, they'll improve, because competition will ensure that only the most efficient services survive. If you topple this dictator, the country will become a peaceful democracy, because people like peace and democracy. And so on.

These kinds of arguments sound good. And they invite opponents to respond in kind: actually, legalizing heroin is a good idea, because it will make taking it much safer by eliminating impurities and infections... And so the debate becomes a case of fantasizing about things that might happen, with the winner being the person whose fantasy sounds best.

If you want to know what will happen when you implement some policy, the only way of knowing is to look at other countries or other places which have already done it. If no-one else has ever done it, you are making a leap into the unknown. This is not necessarily a bad thing - there's a first time for everything. But it means that "We don't know" should be heard much more often in politics.

Schizophrenia: The Mystery of the Missing Genes

It's a cliché, but it's true - "schizophrenia genes" are the Holy Grail of modern psychiatry.

Were they to be discovered, such genes would provide clues towards a better understanding of the biology of the disease, and that could lead directly to the development of better medications. It might also allow "genetic counselling" for parents concerned about their children's risk of schizophrenia.

Perhaps most importantly for psychiatrists, the definitive identification of genes for a mental illness would provide cast-iron proof that psychiatric disorders are "real diseases", and that biological psychiatry is a branch of medicine like any other. Schizophrenia, generally thought of as the most purely "biological" of all mental disorders, is the best bet.

With this in mind, let's look at three articles (1,2,3) published in Nature last month to much excited fanfare along the lines of 'Schizophrenia genes discovered!' All three were based on genome-wide association studies (GWAS). In a GWAS, you examine a huge number of genetic variants in the hope that some of them are associated with the disease or trait you're interested in. Several hundred thousand variants per study is standard at the moment. This is the genetic equivalent of trying to find the person responsible for a crime by fingerprinting everyone in town.

The Nature papers were based on three seperate large GWAS projects - the SGENE-plus, the MGS, and the ICS. In total, there were over 8,000 schizophrenia patients and 19,000 healthy controls in these studies - enormous samples by the standards of human genetics research, and large enough that if there were any common genetic variants with even a modest effect on schizophrenia risk, they would probably have found them.

What did they find? On the face of it, not much. The MGS(1) "did not produce genome-wide significant findings...power was adequate in the European-ancestry sample to detect very common risk alleles (30–60% frequency) with genotypic relative risks of approximately 1.3 ...The results indicate that there are few or no single common loci with such large effects on risk." In the SGENE-plus(2), likewise, "None of the markers gave P values smaller than our genome-wide significance threshold".

The ISC study(3) did find one significantly associated variant in the Major Histocompatability Complex (MHC) region on chromosome 6. The MHC is known to be involved in immune function. When the data from all three studies were pooled together, several variants in the same region were also found to be significantly associated with schizophrenia.

Somewhat confusingly, all three papers did this pooling, although they each did it in slightly different ways - the only area in which all three analyses found a result was the MHC region. The SGENE team's analysis, which was larger, also implicated two other, unrelated variants, which were not found in other two papers.

To summarize, three very large studies found just one "schizophrenia gene" even after pooling their data. The variant, or possibly cluster of related ones, is presumably involved in the immune system. Although the authors of the Nature papers made much of this finding, the main news here is that there is at most one common variant which raises the relative risk of schizophrenia by even just 20%. Given that the baseline risk of schizophrenia is about 1%, there is at most one common gene which raises your risk to more than 1.2%. That's it.

So, what does this mean? There are three possibilites. First, it could be that schizophrenia genes are not "common". This possibility is getting a lot of attention at the moment, thanks to a report from a few months back, Walsh et al, suggesting that some cases of schizophrenia are caused by just one rare, high-impact mutation, but a different mutation in each case. In other words, each case of schizophrenia could be genetically almost unique. GWAS studies would be unable to detect such effects.

Second, there could be lots of common variants, each with an effect on risk so tiny that it wasn't found even in these three large projects. The only way to identify them would be to do even bigger studies. The ISC team's paper claims that this is true, on the basis of this graph:

They took all of the variants which were more common in schizophrenics than in controls, even if they were only slightly more common, and totalled up the number of "slight risk" variants each person has.

The graph shows that these "slight risk" markers were more common in people with schizophrenia from two entirely seperate studies, and are also more common in people with bipolar disorder, but were not associated with five medical illnesses like diabetes. This is an interesting result, but these variants must have such a tiny effect on risk that finding them would involve spending an awful lot of time (and money) for questionable benefit.

The third and final possibility is that "schizophrenia" is just less genetic than most psychiatrists think, because the true causes of the disorder are not genetic, and/or because "schizophrenia" is an umbrella term for many different diseases with different causes. This possibility is not talked about much in respectable circles, but if genetics doesn't start giving solid results soon, it may be.

Edit: I missed it at the time but the great Prof. David Colhoun wrote an extremely good piece about this study.

Purcell, S., & et Al (2009). Common polygenic variation contributes to risk of schizophrenia and bipolar disorder Nature DOI: 10.1038/nature08185

Shi, J., & et Al (2009). Common variants on chromosome 6p22.1 are associated with schizophrenia Nature DOI: 10.1038/nature08192

Stefansson, H., & et Al (2009). Common variants conferring risk of schizophrenia Nature DOI: 10.1038/nature08186

93% of Surveys are Meaningless

Over at Bad Science, Ben Goldacre decries an article about a spurious "study", lifted straight from a corporate press-release, in his own newspaper The Guardian:

On Monday we printed a news article about a “report” “published” by Nuffield Health, headlined “No sex please, we’re British and we’re lazier than ever”. “This is the damning conclusion of a major new report published today,” says the press release from Nuffield ... I asked Nuffield’s press office for a copy of the new report, but they refused, and explained that the material is all secret. The Guardian journalist can’t have read it either. I don’t really see how this “report” has been “published”, and in all honesty, I wonder whether it even exists, in any meaningful sense, outside of a press release.

Nuffield Health are the people who run private hospitals and clinics which you can’t afford....the Guardian gave free advertising to Nuffield, for their unpublished published “report”, which nobody even read, in exchange for 370 words of content. This is endemic, and it creeps me out.

The Telegraph also reprinted the press release; sorry, wrote an article drawing on the press-release amongst many other carefully-research sources. The other papers probably did too; I'm too lazy to check.

For you see, the alleged study found that British people are monumentally slothful: 73% of couples said that they are "regularly" too tired to have sex while 64% of parents say that they are always "too tired" to play with their children, and so on.

Yes, according to Nuffield Health, only one in three British parents ever play with their own children. The rest are always too exhausted. It's a wonder they found 2,000 people who were awake enough to answer their survey - although, as Goldacre says, maybe they didn't.

This "study" is, obviously, bollocks. It serves only as advertising for Nuffield Health's network of fitness centers, the benefits of which are helpfully listed at the end of the press release. That newspapers regularly reproduce press releases because they can't afford to pay journalists to fill the space any other way is well known nowadays. This is thanks mostly to Nick Davies and his outstanding book Flat Earth News which revealed, in great detail, just how bad things have got.

But the fact that this advert was published in the Health section of The Guardian, is more than just a symptom of the decline of British journalism. It also reflects the peculiarly British obsession with "surveys".

Even if the Nuffield data was fully published in a proper journal, and even it had been a survey of 200,000 people, it would still be meaningless. Asking people whether they are lazy is not a good way of finding out whether they are, in fact, lazy. All it can tell you is whether people think of themselves as lazy, which is very different. If you wanted to prove that British people really were lazy and getting lazier, you would have to look at actual indicators of activity like, say, gym membership rates, or amateur sports team participation, or swimming pool use, or condom sales if you really think people are too tired have sex, etc.

Yet surveys like this seem to be almost mandatory if you want to draw attention to your cause in Britain at present. You have to do one, and you have to massively over-interpret the results. The gay rights group Stonewall this week accused British football of being institutionally homophobic. Their basis for this claim was a survey of - guess - 2,000 football fans, finding, amongst other things, that

Only one in six fans said their club was working to tackle anti-gay abuse and 54% believed the Football Association, Premier League and Football League were not doing enough to tackle the issue.

This survey demonstrates, at best, that many football fans think British football is institutionally homophobic. It does not "Sadly demonstrate that football is institutionally homophobic", as a Stonewall spokesman said, unless you think that British football fans are infallible godlike beings.

I have nothing but sympathy for Stonewall, and they may well be right about homophobia in football. But their survey is meaningless. It's advertising, just like Nuffield Health's survey. Attentive Neuroskeptic readers will remember the case of "In The Face of Fear", yet another survey of about 2,000 people, claiming that Britain is in the grip of an epidemic of anxiety disorders (it's not) and serving as advertising for another well-meaning group, the Mental Health Foundation.

A large and growing proportion of British newspaper articles are essentially promotional material for some kind of company, charity, or activist organization. Honestly, newspapers should just go the whole hog and replace half their pages with paid adverts, and use the money earned to pay their journalists to actually do some journalism. There would only be half as much news, but it would at least be news.


The Neuroscience of Niceness

The Templeton Foundation is offering $4,000,000 to fund research into "Positive Neuroscience". The idea seems to be put some neuro into Positive Psychology. Aspiring neuroscientists are invited to submit proposals for

...projects that apply tools of neuroscience to positive psychological concepts in the following core areas:

Virtue, strength, and positive emotion: What are the neural bases of the cognitive and affective capacities that enable virtues such as discipline, persistence, honesty, compassion, love, curiosity, social and practical intelligence, courage, creativity, and optimism?

Exceptional abilities: What is special about the brains of exceptional individuals and what can we learn from them?

Meaning and positive purpose: How does the brain enable individuals and groups to find meaning and achieve larger goals?

Decisions, values, and free will: How does the brain enable decisions based on values and how can decision-making be improved? What can neuroscience reveal about the nature of human freedom?

Religious belief, prayer, and meditation: How do religious and spiritual practices affect neural function and behavior?

All good and important things, no doubt. But does neuroscience have anything to say about them?

It may not do. Neuroscience has nothing useful to say, for example, about driving a car. If you want to learn how to drive, you get in a car and practice. Now, there must be some biological processes going on in your brain as you to learn how to drive, but we don't understand them, and this doesn't stop us doing it.

So while there must be a "Car Neuroscience", it's irrelevant to cars. And the neuroscience of good and exceptional behaviour may be irrelevant as well, if good and exceptional behaviour is something you learn. Genius, as we know, is 99% perspiration. The answer to the question - "What is special about the brains of exceptional individuals" - may be, nothing.

In fact, there surely are neurological correlates of at least some exceptional abilities. For example, it is hard to deny that autism is a neurological condition, or that people with autism sometimes (although not always) show incredible "savant" abilities. Rain Man is fiction, but that kind of thing does happen.

But researching the neural basis of talent and achievement might not be as nice as you'd think. There are shades of phenology in the idea. Worse, if there's a "neural basis of the cognitive and affective capacities that enable virtues such as discipline, persistence, honesty, compassion..." etc, there are certainly going to be genes which affect the function of those neural circuits. If you discover the "good" genes, might you not start to wonder if society would be better off without the "bad" ones...?

Personally, I'm not too concerned by this kind of speculation. There are plenty of worse things happening in the world than hypothetical future eugenics programs. But many people do worry about this kind of thing: declaring something to be a kind of eugenics is a popular way of ending arguments. It's interesting that by stressing the positive, happy, niceness of their program, the Templeton Foundation feel able to propose something that, looked at from another angle, has deeply un-PC implications.


Psych Drug Acronyms Explained!

Modern psychiatry is an alphabet soup of acronyms. Sometimes it seems like there are almost as many as there are drugs. This can be confusing. So, here's a quick guide to what they really mean.

Please add any of your own in the comments!

SSRI - Sexual Stimulation Required Increased(*)
Also, Suicides? Suppress Report Immediately!(*)
Also, Stopped Suddenly - Regret Imminent?(*)

NRI - No Real Impact?(*)
Also, Nix Relevant Information(*)

NASSA (mirtazapine) - Never Again Slim; Sleep Alot.(*)
Also, Nighttime, And Strange Sights Abound(*)

TCA - The Classic Antidepressants(*)
Also, Toxicity - Cardiac Arrests(*)

ECT - Effective, Cheap Treatment(*)
Also Erases Childhood Thoughts?(*)

VNS - Very Nebulous Science(*)
Also, Very New Snakeoil?

fMRI - Future Marketable Research Initiative(*)
Disclaimer - The digs at SSRIs are probably unfair: in my experience, the withdrawal symptoms are mild and I think the claimed link to suicide is most likely a myth. But it's funny.

Science, Journalism, and Bug Spray

Watch out! The BBC report that -

Deet bug repellent 'toxic worry'
While The Telegraph are even more concerned -
Insect repellent Deet is bad for your nerves, claim scientists
This is in reference to a new paper about the widely-used insect repellent DEET. The BBC, as usual, performed slightly better than the Telegraph here. They included quotes from two experts making it clear that the research in question was preliminary and in no way proves that DEET is dangerous to humans. But they still ran the headline implying that DEET could be "toxic", which is the only thing most people will remember about the article. As you'll see below, this is quite misleading.

DEET is an insect repellant, generally used to prevent mosquito bites. You spray it on your skin, clothes, mosquito nets, etc. If you've ever been to a tropical country, you'll probably remember it. It has a distinctive smell, it stings the eyes and throat, and, most distressingly, it dissolves plastics. My watch fell off in Thailand because DEET ate through the strap.

That aside, DEET is believed to be safe, so long as you spray it instead of drinking it. Hundreds of millions of people have used it for decades. And it works, which means it saves lives. Mosquitoes spread diseases like malaria, yellow fever, Dengue, and plenty more. They can all kill you. This is why any health professional will advise you to use mosquito-repellants, preferably DEET-based ones, when visiting risk areas.

So it would be massive news if DEET was found to be dangerous. But it hasn't. What's been found is that, in animals and in test-tubes, DEET is a cholinesterase inhibitor. Cholinesterase is an enzyme which breaks down acetylcholine (ACh), a neurotransmitter. If you inhibit cholinesterase, ACh levels rapidly increase. This can cause problems because ACh is the transmitter that your nerves use to communicate with your muscles. As ACh builds up, your muscles don't stop contracting, and you suffer paralysis, until you can't breathe. This is how "nerve gas" works.

But we know DEET isn't a strong cholinesterase inhibitor, when used normally, because people don't get cholinergic effects after using it. The toxicity of cholinesterase inhibitors is acute. You get paralyzed, and suffer other symptoms like uncontrollable salivation, crying, vomiting, and incontinence. You'd know if this happened to you.

Cholinesterase inhibitors are not, as various media reports have said about DEET, "neurotoxic" , they do not cause "neural damage". They act on the nerves, but they do not damage the nerves. In fact people with Alzheimer's take them (in low doses!), as do people with the nerve disease myasthenia gravis.

So the fact that DEET can act as a cholinesterase inhibitor in the lab changes nothing. It's still safe, at least until evidence comes along that it actually causes harm in people who use it. You can't show that something is harmful by doing an experiment showing how it could be harmful in theory.

To be fair, there is one cause for concern in the paper - in the experiments, DEET interacted with other cholinesterase inhibitors, leading to an amplified effect. That suggests that DEET could become toxic in combination with cholinesterase inhibitor insecticides, but again, the risk is theoretical.

The media should never have reported on this paper. The science itself is perfectly good, but the results are completely irrelevant to the average person who might want to use DEET. They are of interest only to biologists. If people decide not to use DEET on the basis of these reports, they are putting themselves in danger. Others have noted that journalists almost always report on laboratory experiments like these as if they were directly relevant to human health. They're not.

Appendix: In one of the articles, an expert says that "I also would guess that the actual concentration [of DEET] in the body is much lower than they had to use in the study to see an effect in the mouse tissues." But we don't have to guess, we can work it out. DEET had detectable effects in mammalian tissues at a concentration of 0.5 millimole. A millimole is a unit of concentration; 1 millimole is 0.19 grams DEET per liter of water. (Molar weight of DEET = 191g/mole). The human body is 60% water by weight. A person weighs, say, 75 kg, which means roughly 50 liters of water. That means that to achieve the level of DEET used in this study, you would need to absorb into your body about 50 x 0.19 = 9.5 grams of DEET (assuming it was evenly distributed in your body).

That's a huge amount. But maybe it's not completely impossible, bearing in mind that DEET might be absorbed through the skin? Is there any data on DEET levels in humans? Yes. This paper reports on the development of a way of measuring DEET in human blood. This method could detect DEET at levels from 1 ng/mL to 100 ng/mL. I assume that the upper limit was chosen because no-one ever gets more DEET than that. 100 ng / mL = 100 micrograms / L = 0.52 micromolar = 0.0005 millimolar. That's 1000-fold too low, and that's the upper limit.

This was just a back-of-the-envelope calculation so please feel free to critique it, but, I find it reassuring.


ResearchBlogging.orgCorbel, V., Stankiewicz, M., Pennetier, C., Fournier, D., Stojan, J., Girard, E., Dimitrov, M., Molgo, J., Hougard, J., & Lapied, B. (2009). Evidence for inhibition of cholinesterases in insect and mammalian nervous systems by the insect repellent deet BMC Biology, 7 (1) DOI: 10.1186/1741-7007-7-47

I'm On K, You're On K

According to CNN, the kids in Hong Kong are all taking ketamine ("the horse tranquilizer") nowadays - although we're not given much in the way of statistics.

Ketamine is a fascinating molecule. On the street, it's a drug, naturally. High doses produce a state of dissociative unconciousness affectionately called the "K-hole", while lower doses have a sedative and mild hallucinogenic effect which goes well with dancing, allegedly. It's also used medically as an anaesthetic.

In psychiatry, ketamine is three things: a drug of abuse, an antidepressant, and a way to mimic schizophrenia. Or rather, there are people who think of ketamine as each of these things. It seems somewhat unlikely that it could be all three at once. You don't treat depression by causing schizophrenia, and people don't deliberately give themselves psychosis, even temporarily.

Yet a journal could publish a paper about using ketamine as a model of schizophrenia, and another paper about its supposed antidepressant effects a few pages later, and few people would bat an eyelid. This is because most researchers interested in schizophrenia wouldn't read the depression paper, and vice versa.

Partly this is because, like all scientists today, psychopharmacologists tend to stick to their own research niches. But it's also a symptom of the fact that no-one's job is to study ketamine, as such. We study diseases, rather than drugs, which can lead to theories which fly in the face of half of the evidence. (See this post for another example.)

The evidence that ketamine can treat depression essentially consists of one study from 2006 (ref) and a pilot study from the same group (ref), plus a handful of case reports. Zarate et al reported that a single injection with a moderate dose of ketamine (0.5mg/kg) had a dramatic antidepressant effect in a large proportion of depressed patients, and that this lasted at least a week in some cases.

This paper sparked a flurry of interest into ketamine and depression, with animal studies and brain scans galore trying to explain how it might work. Maybe ketamine does have an antidepressant effect. But if it does, it's a miracle drug, acting much faster than any other. You need to take Prozac for several days or weeks before feeling any benefit. A single injection does diddly-squat.

The dramatic benefits seen in this study may have been simply placebo effects: the patients expected to feel much better after taking this exciting new drug, so they said they did. The study was placebo controlled, true. When people got injections of salt water, they didn't report any benefit. In theory, it was double blind - neither the patients nor the doctors knew whether they were getting ketamine or water. But you'll know when you've been injected with 0.5mg/kg ketamine. You get high. That's why people take it. The study can't really be called double blind.

To their credit, Zarate et al did acknowledge this, and suggested that in future ketamine could be compared to another drug which produces noticeable effects. But they really should have done that to begin with. This is not a criticism of these researchers - what they did was par for the course in psychopharmacology. Unfortunately.

The idea that ketamine intoxication mimics schizophrenia (ref) is an interesting one, and it may well be a model of some of the symptoms. My only ketamine experience doesn't really fit with either the schizophrenia or the antidepressant theory, however. I was slightly depressed before I took it, and it made me feel much worse. I didn't hear any voices, though. On the other hand, a good friend became addicted to the stuff for several months, and still craves it. To each his own...

powered by Blogger