Readers of my blog will know I'm a genius, a "very stable genius" in the immortal words of my hero Donald Trump. Readers of my blog will also know that when I call Trump "my hero," I'm making a joke in poor taste. I attend a weekly pub trivia contest at which I join forces with the rest of my team to answer questions like "Who was the eighteenth president of the United States?" and "What is the most common protein in the human body?" – questions to which I usually don't know the answer. Sadly, I lack a head for random facts. But in terms of critical thinking I think I can at least rival most people, once I've had enough time to process an issue. I have, I humbly submit, a profound need to get to the Truth even if it takes me a long time.
In tonight's post, I want to talk about the Dopamine Hypothesis of Schizophrenia and demonstrate that it is totally bullshit.
The Dopamine Hypothesis of Schizophrenia has been around a while. I believe it was the most popular explanation for schizophrenia eleven years ago, when I myself first became 'unwell', but has lost popularity in the decade since. My psychiatrist at the first or second appointment, back in 2007, explained my illness to me by telling me that I had suffered "a dopamine explosion" and put me on 2.5mgs of Risperidone. I didn't know what dopamine was, then, but did a little research in those first couple of months, finding, for instance, that dopamine was a neuro-transmitter, a chemical synthesised in the brain, and that it was involved in learning new behaviours. In the first three years of my treatment I often worried, sometimes to the point of having panic attacks, about what the drug might be doing to me, to my brain, to my hormones, to everything. I worry less about that now, although I still think it possible antipsychotics may gradually cause brain damage over the long term and still desperately want to get off them. Of course, the reason my psychiatrist told me I had suffered "a dopamine explosion" is because the Dopamine Hypothesis was then and is still now the justification for putting people on antipsychotics, even as it is being gradually discredited. Basically, this theory proposes that the cause of schizophrenia is an excess of dopamine (in the same way that depression is the result of a deficit in serotonin); consequently schizophrenics should be treated by drugs that reduce the amount of this chemical in the brain or, to be more accurate about what the drugs actually do, block the neuronal receptors that dopamine molecules attach to. The evidence for the hypothesis is the apparent success in reducing visible symptoms of so-called antipsychotics, which operate on the dopamine system, and, conversely, the way in which drugs like cocaine and metamphetamines, which have the opposite effect on the dopamine system, increasing dopamine levels, can cause psychosis.
So what is dopamine's function? The Wikipedia article on dopamine is full of arcane language (chemicals, organs and organelles in the brain, different types of brain cell) but, although dopamine's role is complex, its most important function seems to be related to motivation. It is involved in both 'wanting something' and 'enjoying that something when it's got'. Humans, like all animals, are goal-seeking machines. When we were hunter-gatherers, we would need to find food and consume food on a regular basis; dopamine appears to be involved in both a person's desire to get something and his or her pleasure in attaining his or her objective. Today it is relatively easy to obtain nutrients (we don't need to hunt mastodons anymore) but our goal seeking behaviour remains unchanged, expressing itself through other activities, such as sports and the playing of computer games. Every time we successfully navigate past the man-eating Venus Fly Traps in Super Mario Brothers or defeat the end-of-level boss, we experience that little dopamine rush. Nicotine breaks down into dopamine in the brain –which explains why people smoke and why when I don't have cigarettes I go out hunting for a person who will give me one. Dopamine encourages us to do stuff and to enjoy doing it when we do it.
Once we recognise that dopamine's main function is related to motivation and pleasure, the problem with the Dopamine Hypothesis of Schizophrenia becomes immediately apparent. I enjoy cigarettes – but I hated psychosis. There appears to be a contradiction. If the neurological basis of psychosis is an overproduction of dopamine, why is madness so unpleasant? Why do schizophrenics kill themselves? I can attest to the fact that psychosis is terrible and, as readers of my blog will know, my worst experiences of psychosis occurred while I was taking antipsychotic medication. Psychosis often expresses itself through catatonia and anhedonia; logically, then it simply cannot be the result of an excess of dopamine – assuming that dopamine is indeed related to goal-seeking behaviour.
And now we hit the crux of the matter.
How can a psychiatrist tell who is well and who isn't, which patient is dangerously psychotic and which is manageable? On the one hand she is presented with a patient who is voluble, excitable, and perhaps belligerent; on the other she is presented with a patient who is subdued, pliable, dull, who doesn't go on about crazy notions, and perhaps simply sits staring at the floor. The second is the one who is 'responding to treatment'. One dirty secret of the psychiatric profession is that psychiatrists are not interested in treating or curing patients; rather they are simply seeking to protect the commuinity from potentially violent or even criminal elements by sedating them, a kind of social hygiene, even, I think sometimes, a kind of eugenics. The other dirty secret is that, as I know from experience and from my observations of others, so-called antipsychotics do nothing to alleviate psychosis; they are, rather, simply tranquillisers that suppress behaviour without reducing psychotic symptoms such as voice-hearing and delusions at all. The supposed success of antipsychotics is of course adduced from the observed behaviour and reports of patients, and quiet patients seem better than noisy ones. I can remember when I was first put on Risperidone – I felt like a barrier had come down between me and the rest of the world. I could barely talk. If you, dear reader, submitted to a regimen involving high doses of Respiridone or Olanzapine, all you'd feel like doing is sitting in one place staring at a wall as well, until your brain adjusted or you liver learnt to efficiently remove the poison from your bloodstream. This, by the way, is the argument put forward by British psychiatrist Joanna Moncrieff – that the term 'antipsychotic' is a misnomer and that such drugs should rather be called 'major tranquillisers' as they once were. (Moncrieff is misrepresented in the Wikipedia article about her incidentally.) 'Antipsychotics', to put it simply, do nothing to alleviate psychosis but they flatten out behaviour by reducing motivation, by reducing neuronal sensitivity to dopamine. Logically, the reason why schizophrenics display blunted affect and anhedonia, why they have difficulty finding work or forming relationships, is probably the drugs, not the condition.
The apparent success of antipsychotics is only that, apparent. The Dopamine Hypothesis was invented to account for the apparently improved behaviour of patients taking antipsychotics rather than any improvement in their actual condition. Psychiatrists do not have access to patients' minds or to their lives outside of the consultation room. The Dopamine Hypothesis, under scrutiny, falls apart, and the only possible conclusion is that psychiatrists prefer sick but sedated patients to ones who are well but who forcefully point out that the psychiatric profession is stupid and crooked.
I find myself differing with consensus wisdom on many issues. Thinking that the claim antipsychotics are effective is a lie told to patients, patients' families, and to the public is one example – although Moncrieff and others think so too. I want to mention another divergence. Several years ago I wrote a post "On Evolution" in which I put forward, tentatively, an objection to Darwinian accounts of evolution. I identified the problem but I couldn't think of a solution. The problem is this: Darwinian accounts of Evolution presume evolution occurs gradually in almost imperceptible increments. In fact, evolution must occur in discreet steps – for speciation to occur, an individual must be born with a significant mutation, this mutation must be beneficial rather than detrimental, and another individual must be born with the same significant, beneficial mutation at the same time in the same vicinity for the two to breed. Their children must then breed incestuously with each other. All of this is enormously improbable but is the only logical way to marry speciation with Darwinian evolution. At the beginning of this year a solution occurred to me – in fact, it came to me in the form of a voice. For speciation to occur, a large number of individuals in a population must all be born with the same mutation at the same time. This view, which is in a sense mystical, puts me directly at odds with evolutionary biologists like Richard Dawkins and his theory of "The Selfish Gene". It suggests evolution is guided by a higher intelligence or collective soul. I hope that mentioning this second divergence doesn't make me seem flakey.
I'll finish this post by making an observation. I sometimes think readers only stumble over my bad posts. Do people read my good posts as well? I would like people to read my stories: "69", "A Refusal to Mourn" and "The Great God Pan". I would also like them to read the two latter posts about Janet Frame, "On 'The Sellout' and 'An Angel at My Table'" and "Jon Stewart, Janet Frame, and Katy Perry." It may be hard to find the best posts but I worry that those in the great world outside my apartment only ever find the bad ones. I hope that you do read the good ones as well. And I hope that in this post I made the point I was trying to make.
