On February 28th, the New York Times reported the latest psychiatric disorder “gene finding” claim in an article entitled “5 Disorders Share Genetic Risk Factors, Study Shows,” The Times reporter described a study published online by the “Cross-Disorder Group of the Psychiatric Genomic Consortium” the same day in the high-impact British medical journal Lancet. The Cross-Disorder Group, led by psychiatric genetic investigator Jordan W. Smoller, claimed to have identified shared genes associated with five psychiatric disorders: autism spectrum disorder, attention/deﬁcit-hyperactivity disorder (ADHD), bipolar disorder, major depressive disorder, and schizophrenia.
As readers of my February 15th MIA posting are aware, we have seen thousands of such claims in psychiatry since the 1960s, and we have also seen that these claims do not survive replication attempts. But in typical Times reporting style its readers are told nothing of this history, even as reported in the Times itself. To cite a few examples for only one diagnosis, the Times reported (subsequently non-replicated) schizophrenia gene findings by scientists in 1988, 1997, 2002, 2006, and 2008.
Like most of the previous articles, the Times reported the Cross-Disorder Group researchers’ claims and opinions favorably, without even a hint of justified healthy skepticism. The author provided her readers with no reason to doubt that genes both exist, and have been discovered. Once again, there is every reason to believe that the Cross-Disorder Group findings will suffer the same fate as thousands of previous gene discovery claims in psychiatry. Given the decades-long track record of similar highly publicized yet non-replicated claims, we should assume that all gene discovery claims in psychiatry are false-positive findings until proven otherwise.
Mad in America hosts blogs by a diverse group of writers. These posts are designed to serve as a public forum for a discussion—broadly speaking—of psychiatry and its treatments. The opinions expressed are the writers’ own.
Dr. (Mr?) Joseph;
Is it Dr.? I ask because If you don’t have a PhD, you certainly deserve one.
Thank you so much for the work you do, and taking the time to post here.
With $16 Trillion in debt, and continually deepening, the last thing we need is for another Ernst Rudin to poke his head up and cry, “Eureka, We’ve Found It!” so Now, you people in Government (who pay us to Do this junk research) who are the actual Cause of it (debt), can Blame it on the folks with those defective genes who’ve dragged us down.
At some point, our Government is going to have to move beyond Talking about the debt to actually cutting spending, and those SSDI checks, junk medicine detention facilities, Real medical repair procedures for the damage Psychiatry inflicts, etc. etc. are going to be put on the block because it’ll be far more cost effective to just get rid of our genetic waste people.
He holds a doctorate: Jay Joseph, Psy.D.
IMO, he’s bright and a gift to MiA!
Thanks for the nice comments, and please feel free to address me by my first name.
I think your work and your writing is simply great, Jay. Thank you, as always. —Daniel Mackler
Thanks, Daniel. I think highly of you and your work as well.
Just the placebo effect of knowing you have this genetic marker might be enough to send one into psychosis. It would be nice to know how genetically screwed up we are so we don’t have to waste our time becoming successful. Could one go on psychotropic medications and SSI right at birth? 🙂
Thanks for the post.
Thank you for responding to our requests to clarify the latest bogus gene claims of psychiatry.
I noted that you said you were not going to get into epigenetics. Could you tell us why? I would appreciate your reconsidering that only in the sense that it appears this is a current area of fraud in psychiatry’s neverending claims of genes corresponding to their junk science DSM VOTED IN stigmas. Thus, it would be very helpful if you could debunk related false epigenetic claims and any others used to perpetrate the pseudoscience of biological psychiatry.
It strikes me as ludicrous that psychiatry could pretend to know who is more vulnerable to something like PTSD given their genes or even abuse history when there is no way that they could possibly know or compare every life stressor, abuse or other crisis that would contribute compared to those of others. Given their tendency to take ten to fifteen minutes to “slap on a diagnosis” per one psychiatrist, it does not seem likely that they would be willing or capable of discerning between their biological brain disorder pet theories and the environmental causes of PTSD. Also, it would most likely always be the victim’s fault for psychiatry to continue its role as the thought police for the latest social oppressor predators to deny their victims any justice or benefits as with the military and its PTSD victim while making BIG PHARMA profit centers out of their suffering.
Thank you again for sharing your very enlightening information. I am very grateful for your efforts and would welcome more explanation from you about these topics.
Thanks for your thoughtful post. I think it is best left to others more knowledgeable than I am about epigenetics to do the critique. But as I mentioned in a previous post, I may decide to look more closely at the topic in the future. The main fallback position in psychiatric molecular genetics currently is the “missing heritability” explanation of failed gene finding attempts, which I have written a lot about.
One potentially interesting subplot to this shared gene theory/myth is that this rather puts the nail in the coffin of the notion that these are all separate rareified disorders. As I commented to a friend, it leaves us with one unified disorder, lets call it unhapiness, and surely you can’t argue that this is purely caused by genes alone.
These genetic data cannot simultaneously be false positives propping up a failed theory (a myth) and be used to support a separate theory that all psychiatric disorders are the same. Logical consistency dictates that the data themselves are either valid or not.
I believe the conclusion of the study is not that schizophrenia, ADHD, Depression, etc are all basically the same, but that a similar process can confer risk for multiple disorders. These variants might underlie something like resilience so that when combined with environmental stressors (trauma) lead to a disorder which manifests differently depending on factors unique to the individual.
I don’t believe that anyone is claiming that any complex behavioral phenomena is “caused by genes alone”. Every reasonable person, including these scientists, would agree that the environment an individual is exposed to plays a profound role in the development of psychiatric disorders. The reverse position would be that hereditary factors play no role at all and that seems unlikely to me.
Oh, you’d be surprised how many “unreasonable” psychiatrists and doctors tell their clients that their disorder is entirely genetics and that nothing else but drugs will help (see Engineer’s post below). My son had experienced a severe emotional trauma a couple weeks before a routine doctor’s visit. On finding he had been briefly suicidal, she was prepared to prescribe antidepressants without once asking him what he was depressed about! I’ve seen it happen so often, I have come to believe that it’s a rare psychiatrist who even considers environmental stress relevant – mostly, they just hear the symptoms and prescribe.
This is fascinating to me, because if you think about it, which do we have more control over, our genetics or our environment? Obviously, the latter is much more readily changed, but we seem to be spending all of our time trying to change the one thing that we have the least influence over.
The search for genetic causes of psychiatric disorders is a complete waste of time. As you state, all this shows is that a certain genetic substrate may make a person more vulnerable to life stressors, which could lead to a wide variety of conditions. This substrate isn’t even identified as faulty genetically – it may well be an important set of survival traits that are simply not as compatible with the insane modern world we have to negotiate. If that’s the best they can come up with, they should hang up their test tubes and go home. Because while they are wasting their time, there are a ton of social issues, like poverty, warfare, gang violence, child abuse, domestic violence, authoritarian and abusive school settings, and on and on, that all could be changed if we worked on them together.
Let’s do research on things we can actually change!!!!
It has not been my experience that a lot of psychiatrists tell their patients that the difficulties they experience are purely genetic and that stress is not relevant. Regardless, the degree to which a properly diagnosed disorder (a psychiatric syndrome not a feeling) is genetic vs. environmental really doesn’t relate to whether a drug is the best course of treatment. They are dissociable issues.
The anecdote about your son is concerning because obviously it is critical to understand what happened to him in order to help him or to figure out if he is depressed. Even to make him feel heard and understood which could be therapeutic in and of itself. I would expect this of a primary care physician too, as you indicate is the case here, but psychiatrists are trained to do this. I suspect a psychiatrist would have done a better job.
Still, as important as it is to ask that type of question, it might also be irresponsible to fail to offer an anti-depressant medication. The correct course of action for this physician would have been to assess for acute suicidality, assess for a major depressive disorder and offer what is reasonable for that setting: perhaps an anti-depressant, perhaps referral to other resources psychiatric or psychological counseling depending on the individual’s personal desires and details of their case. The key word is offer. A physician’s job is to offer options and though many here reject medication, there are many others who desire medication and feel strongly that it has been helpful to them. I do not think the offering is wrong and I do not think it indicates that the condition was viewed as genetic or that stress/trauma was not an important contributor.
Regarding your second paragraph, remember that a medication does not change genetics. A medication changes the environment of the brain in a direct way. A physician may not be able to change a persons outward environment that much, so they may feel that the biggest change they can affect is through a medication.
I think there is somewhat of a misunderstanding of the potential value of research in psychiatric genetics. The point is not to label disorders as genetic in nature or pre-determined as seems to be the assumption. I think the point is to try to get a foothold on what is physically different in the brain of someone with severe depression, schizophrenia, etc. There are after all, people who suffer from quite severe forms of these disorders who have nothing obvious in their environment which would have caused them. As in other areas of medicine, an understanding of the mechanism of a disorder or syndrome is critical in identifying more effective ways to treat it. That has been the case with all other dysfunction in the body which leads to medical conditions, many of which can now be effectively treated. The brain is orders of magnitude more complicated than the heart for example, so it is taking longer and that sucks for people who are suffering.
I think it is a dangerous precedent though to decide that we should abandon research into the physical underpinnings of these disorders. Should we abandon research into Alzheimer’s disease? I think Alzheimer’s disease fulfills most of the same criteria here applied to psychiatric disorders. It involves the brain, it involves behavior/thinking/feelings, it is thought to be partly genetic and partly environmental, all the research has not yet lead to more effective treatments.
Not everyone fits into the same box in psychiatry, but for those that suffer from severe disorders, not easily written off as existential suffering, we owe it to them to gain a better understanding of these conditions as brain disorders. Psychiatric genetics has suffered a lot of failures, but I think refocusing efforts is a better strategy than abandoning the search for what has gone wrong in the brain. People forget that research is hard, especially so with the most complex problem of the most complex organ. These are the biggest scientific challenges that exist today.
Interesting. In my experience with (unfortunately) multiple psychiatrists and non-psychiatrists, they did not trouble to find out whether stress was a factor in my complaints.
All of my doctors were chosen for their excellent (and, as I found out, undeserved) reputations.
I was told on many occasions that my issue was a “chemical imbalance.” Prescriptions seemed reflexive and quite arbitrary — one internist told me “pick one, SSRIs are all the same.”
My conclusion is that no one should even attempt to discuss emotional problems with an M.D. They’re not selected or trained to be particularly empathetic. Feelings make them uncomfortable. Their fingers get itchy for their prescription pads no matter what. They hear you whining and — boom — you’re on meds for life.
ScottW, I disagree strongly that distinguishing genetic vs. environmental causes is not relevant to treatment.
Historically, emotional states aka “psychiatric symptoms” caused by environmental factors tend to resolve spontaneously within a short amount of time. They do not require invasive treatment such as psychiatric medication, with its many added risks.
One might say emotional distress is nature’s way of telling us to change our circumstances, not to take a pill.
You seem to have profound faith in the medical profession and psychiatry research, although the latter has been shown to have been distorted by commercial interests for the last 30 years. It’s not nearly in the same league as neurology research into Alzheimer’s. Have you read Robert Whitaker’s Anatomy of an Epidemic?
I have found plenty who say just that. As to my son, of course, he was depressed. He would have qualified for “major depressive disorder” if you wanted to diagnose him with something. But he was insulted that the person “offered” him antidepressants without even asking what was wrong. I hear from many who experience exactly the same from psychiatrists, to the point that I consider it the rule rather than the exception.
As to “brain disorders,” you continue to assume that a “disorder” such as “schizophrenia” exists as a distinguishable entity that has a physiological etiology of some sort. What evidence is there to support that? Every theory that’s been put forward so far has been shot full of holes by psychiatry’s own researchers who were dedicated trying to prove the theory correct. How do you know “schizophrenia” isn’t just a reaction, like a rash, to a variety of causes, some physical, some psychological, some existential? If there’s no physical way to distinguish those who “have” and “don’t have” schizophrenia, how do we know the sufferers have anything physiological in common? So far, the research suggests that what genes they may SOMETIMES have in common are just as common in different “disorders,” while many sufferers don’t have these genes at all.
And there are plenty of people diagnosed with “severe disorders” who would take strong exception to trying to say their conditions aren’t caused or triggered by “existential suffering” or trauma or childhood neglect or simply being sensitive to the horrid social conditions in the world they live in. Take the well-known but poorly-publicized fact that “schizophrenia” is far more common in urban areas than rural ones. Explain that in your “brain chemistry” model. Oh, right, the city badly affects their brain chemistry, triggering vulnerability to psychosis. Which means we treat their psychosis medically, rather than asking why cities make people mentally ill who would otherwise be healthy.
You also need to read about the “Open Dialog” approach, and about “Soteria House.” It should help you see that social support and caring can be incredibly effective in treating the most severe “mental illnesses,” far more effective than the crappy chemical treatment that’s helping kill people off 25 years earlier than their untreated peers.
If you haven’t read Whitaker’s book, read it. If you have, read it again with your mind open. He addresses almost everything you say here.
I stand by my contention. So far, genetic research has contributed almost nothing to the understanding and treatment of so-called “mental disorders.” I doubt it ever will. There may be a small segment of people who suffer depression or psychosis for a physiological reason. These should certainly be identified if they can, though genetics is a tiny fraction of the area of physiological causes to be studying. Given the results so far, I’d say the effort doesn’t merit the costs. Meanwhile, there are plenty of “experimental” treatments that are already proven to work better than drugs, which deserve lots of further research, but remain “experimental” because of lack of funding for research, and outright bias and prejudice by a system making billions off of drug sales.
There is much more benefit in changing the external environment. Messing with someone’s brain has so far proven ineffective, dangerous and often deadly. It’s time to invest in a different strategy.
Why would you give something to someone that doesn’t work any better than placebo and which has terrible side effects? Doesn’t make any sense to me.
In my experience, every time I wanted to tell my story to a psychiatrist when I was in the hospital most of them became very uncomfortable, started looking at their watches, and one of them asked me what I wanted her to do since her expertise was in prescribing the drugs and not in therapy! At least she was honest. Only one psychiatrist sat down and listened to what caused me to want to take my own life. You would think that this is what all of them would have wanted to know but instead, all they did was quickly prescribe the drugs! Go figure.
Steve, you so often express what are my thoughts exactly . We have so much control over “environment,” and yet that is not what is being focused on primarily. All of this searching for a genetic holy grail is taking resources away from what we can and direly need to be changing in the real world, right now. I cannot understand how searching for genes is viewed as more important than addressing the environmental factors which are admitted to be necessary for developing these problems. First of all, if they ever do find genes which are truly associated, it will not be a single gene, that much is clear – tt will involve many genes. Secondly, what are they going to do with that knowledge? Are they going to genetically manipulate all of those genes out of our human DNA? That can’t possibly be wise, can it? Or are they searching for genetic causality merely to defend what has been their stance and practice – their scientific credibility – for decades or more? I’m just wondering what the thought process and plan is in terms of what to do about these “conditions” if genetic predisposal is found. It just seems like so much blindess and eugenics-tinged fool-hardiness on the part of the scientific establishment.
Thanks for reminding us that there is nothing new or revolutionary in that study, and that it does not in any mean that genes for psychiatric disorders have been found.
But I diverge on why exactly the research article, and the nytimes report are misleading. I don’t think the findings of that specific research are a false positive. It is only the presentation that is mostly marketing talk for “continue to give us money because the research on genes is important”. But the real evidence collected is serious and is in fact matching MIA regular claims (that the role of genes in psychiatric disorders is at least orders of magnitude smaller than common beliefs).
When people claim to have “likely discovered the tip of the iceberg” (in their own words), it means they have only evidence for superficial conclusions. They basically confirmed they did not get evidence of a true “iceberg” (whether they still *believe* something is hidden underneath is less relevant that the admission they have no evidence for it).
That research actually confirms that the most significant and relevant genes ever found “confer only a small risk of psychiatric disease” (in their own words). I think that is a good study to use to support MIA claims.
While the authors are overall competent, they show their lack of understanding of statistical and mathematical meanings in promoting a very small p-value in the abstract out of context, while avoiding to mention the estimated range for the individual risk factors associated with that p-value.
I am glad research tools are so advanced that we can measure the statistical significance (at the population level) of risk factors that are themselves pretty insignificant, but it is wrong or stupid to only emphasize out-of-context the positive part of the result (that supports getting more grant money), without looking at the overall conclusion of that otherwise interesting genetic research. Since it would be surprising for any gene (or combination) to be absolutely mathematically neutral on any human characteristic (in a thought experiment where all other things are equal), finding statistical significance in the population is completely irrelevant if you don’t put a lower bound on the “effect sizes” that are in play.
Thanks for a great article.
My ex pdoc knew I had a hard upbringing, the child of alcoholic and dysfunctional parents and from that, he concluded that I was doomed to the same fate because of genetics. That’s how he kept me coming in every month, year after year after year- he had me believing I had a genetic disease and that I needed drugs for life rather than empathetic counseling and guidance. In fact, he refused to refer me for therapy. He said I would not be a good candidate for therapy. How can a doctor justify such a comment?
I left him a year ago this month. A locomotive could not drag me into another shrink’s office.
Congratulations to you for taking your life back in your own hands! It never ceases to amaze me how arrogant and dismissive and willing to decide people’s fates so many doctors are, both psychiatrists and regular medical doctors.
We all know that the great and powerful Oz is just a little man behind the curtain, making a lot of smoke and flim flammery.
The unreasoning belief in genetics seems to be psychiatry’s version of predestination.
Altostrata, you state that “psychiatric symptoms” that are caused by environmental factors tend to resolve spontaneously. Is that an admission that some psychiatric symptoms are not caused by environmental factors? What to do if it does not resolve spontaneously?
My only point above with that comment was that there is no a priori reason that a condition with genetic underpinnings need require medication. The best treatment for such a condition could still be psychological therapy. It just seemed we were conflating the two.
Not taking a pill is fine, it doesn’t mean no one should take a pill ever for symptoms that involve thought and behavior.
I will also say that it seems this whole debate is caught up in an antiquated version of the false nature vs. nurture dilemma. Nature and nurture are really not so separable. The environment has dramatic effects which change the expression of genes. It’s not about predetermination, it’s about trying to understand what is physically changed in the brain when there are severe symptoms out of the range of normal – like being acutely psychotic. Drug addiction changes the structure of the brain and it is because of exposure to the drug which is 100% environment. It doesn’t mean that nothing can be learned about addiction by studying genes.
I would challenge anyone to tell me why Alzheimer’s disease is fundamentally different than a psychiatric illness. Saying it isn’t even in the same ballpark doesn’t make it true.
Alzhimer’s does not tend to resolve on it’s own, neither do you tend to see dramatic increases in functining for people diagnosed with schizophreina within an hour (though it usually will not hold for more than a few hours, but with time will build up until it does hold) with good counselling. I’d say that is good evidence that so called schizophrenia is fundamentally different from Alzhimers.
Also there are identifiable bio-markers in Alzhiemers, non have been reliably found in schizophrenia.
Also, the same proceedures for helping someone get over bereavement or other psychological trauma help people who have a diagnosis of schizophrenia – not in every case but in the majority providing drugs are not used, or are used in low doses for a short a time as possible. Bertram Karom ran experiments two or thre decades ago of offering therapy to people who have diagnosis of schizophrenia and this is pretty much what his results were.
So that kind of challenges the idea that so called schizophrenia is an illness like Alzhiemers.
Hi Steve thanks for your comments.
[As to “brain disorders,” you continue to assume that a “disorder” such as “schizophrenia” exists as a distinguishable entity that has a physiological etiology of some sort. What evidence is there to support that?]
Everything has a physiological etiology, unless it is magic. Brain states give rise to feelings and behaviors. If you don’t believe there is a disordered correlate in the brain of someone who exhibits disordered thinking like psychosis then it sounds like you don’t believe that the brain gives rise to behavior.
[How do you know “schizophrenia” isn’t just a reaction, like a rash, to a variety of causes, some physical, some psychological, some existential?}
That is sort of what I think. If you have a rash and a dermatologist biopsies your skin they will find a physiological correlate of the process causing the rash. Many rashes look alike, but have different causes. Many things are called schizophrenia, but as you point out there are probably different entities with different causes.
[If there’s no physical way to distinguish those who “have” and “don’t have” schizophrenia, how do we know the sufferers have anything physiological in common?]
If it were as easy to biopsy the brain as the skin, we might have a way to determine those who have and don’t have schizophrenia. Even with the limitations of studying the brain there are measurable differences between those who do and don’t have schizophrenia. Those are not yet sufficient or available enough to use as diagnostic tools, but I think it is only a matter of time.
[You also need to read about the “Open Dialog” approach, and about “Soteria House.” It should help you see that social support and caring can be incredibly effective in treating the most severe “mental illnesses,” ]
I will look forward to reading about some of the things you mention. To be clear however, I have not said anything to the effect that social support and caring are not incredibly effective. In fact, I said and continue to feel the opposite.
[far more effective than the crappy chemical treatment that’s helping kill people off 25 years earlier than their untreated peers.]
I would also be interested to know why you think that if someone is treated for their psychiatric issues with medication they will die 25 years sooner than they otherwise would have.
[And there are plenty of people diagnosed with “severe disorders” who would take strong exception to trying to say their conditions aren’t caused or triggered by “existential suffering” or trauma or childhood neglect or simply being sensitive to the horrid social conditions in the world they live in.]
I didn’t say that. I only meant to say that not everyone has a clear traumatic event which could be expected to cause their psychiatric problems. To be clear again, I have not tried to downplay the significance of these types of environmental triggers, at all. None of this is inconsistent with there being a physiological basis to mental illness.
Finally, I agree with you that there are a range of techniques for studying the physiological basis of mental illness. Not everything is about genetics. Similarly there are many more theories than “brain chemistry” or “chemical imbalance” to explain mental illness. I never said anything about a “brain chemistry model”, I’m not specifically advocating these buzzwords which I can tell are viewed quite negatively.
I am saying that mental illness has a physiological basis whether it is a reaction to heritable factors or to environment. I am saying that although non-drug therapy may even be the most effective way of treating most mental illness at this time, we should not abandon the idea that medication can help people. (many people feel that medication has helped them and better medications could someday help a lot more people.)
Man, I never think I’m going to write this much, but then it just comes out…
To say that so-called psychiatric disorders have a biological basis because they occur in the brain, nervous system, and body — as all thoughts, feelings, senses, etc. do — is reductionism of the worst kind.
Yes, there must be a physiological basis for thoughts, feelings, senses, etc. But that does not mean there is a physiological disorder or disease underlying specific thoughts, feelings, senses, etc.
In fact, the “brain circuitry” proponents in psychiatry propose that disorder or disease underlies only those thoughts, feelings, senses, etc. of which they disapprove and have designated as “abnormal,” when they may not be abnormal at all.
Wow, thanks for taking the time for these thoughtful answers. It really helps me see where you’re coming from and where we agree, as well as why we might disagree.
You appear to be operating on a philosophical assumption that you believe to be obvious and unavoidable, namely, that “Everything has a physiological etiology, unless it is magic. Brain states give rise to feelings and behaviors.” I don’t buy that assumption myself. But I want you to see that it is an assumption and not a scientifically proven fact. All we know for sure is that biological changes correlate with changes in emotional state, but correlation is not causation.
Personally, I believe (and this is my assumption, not science) that thoughts and intentions give rise to brain states. I believe the brain and body give feedback to the entity running the show, and the physiological substrate of the body clearly determines a lot of what seems desirable/undesirable to the organism as a whole. But it’s pretty clear that we as beings can override even horribly negative feedback from the body if we have some overriding purpose that drives us hard enough. Many of these purposes seem to have no apparent survival value for the biological organism, but seem to have a lot of value for what I will call the spiritual being, whom I believe to be in charge, at least most of the time.
But that’s just me. There are lots of philosophies of causality out there. My objection to psychiatry is that it posits the primacy of physiological cause as an unavoidable truth, and castigates anyone who has another viable explanation, even when they don’t have any proof of their assertions as all.
Back to science. The 25 year earlier death rate is not something I made up. Read the following article for a taste of the issue, but this stuff is published in mainstream psychiatric journals as well. It’s not news: http://usatoday30.usatoday.com/news/health/2007-05-03-mental-illness_N.htm
As to “measurable differences” for those who do and don’t “have schizophrenia,” I have yet to see anything convincing on that ground. There was some big flap about loss of brain tissue, but more recent studies (Nancy Andreasen, for instance – see http://archpsyc.jamanetwork.com/article.aspx?articleid=211084) have shown that this appears to be a result of neuroleptic treatment rather than a characteristic of the “disease.” Besides which, why should we buy into the assumption, which you kind of agreed isn’t really true, that just because two people fit the subjective description of “schizophrenia,” they have the same thing “wrong” with them? If they don’t, then how is it possible or likely that “schizophrenics” will be biologically distinguishable from each other?
There are trained research psychiatrists who have opined that schizophrenia as a category should be done away with, because those who fit the criteria are too heterogeneous to study as a group. But that’s opinion again. There is no science that I know of that shows what “schizophrenics” have in common, besides hallucinations and delusions. If you have some studies, please share – I’d be interested.
Overall, I think we agree about a lot of things. I just want you to be careful not to make your assumptions into facts. What we KNOW is very limited, and to me, suggests that schizophrenia, or mental illness in general, is a pretty unhelpful concept. Between hazy and subjective definitions, and political and marketing forces, and the money to be made from choosing to believe certain things, the actual facts have long since been lost in the forest of bullshit. Whitaker really does bring us back to what is known. I think you should re-read his book. When it comes down to it, the most important result of good science is increased predicting ability and simplicity of your model. The fact that we’re killing people we’re trying to help, and making disabled people out of those who might otherwise recover, suggests that the current model is false and should be trashed. Not to say we shouldn’t ever do genetic research, or that no one should ever use psych drugs, but we need to spend our dollars on things that pay off. Pursuing a genetic cause of mental illness has not paid off, and never will. That last part’s my opinion, not a scientific fact, but the lack of effectiveness to date is pretty darned factual, as Jay has clearly demonstrated in his article.
Thanks again for your thoughtful and serious responses.
Hi ScottW. First of all I’ll say that I agree 100% with you when you say that “everything has a physiological etiology, unless it is magic”, but I think you draw the wrong conclusions from that premise.
I’ll try to be brief in this reply and only raise a couple of points rather than answering all your comments. I’ll also not take on your challenge to “tell me why Alzheimer’s disease is fundamentally different than a psychiatric illness”, even though I’m itching to do so, but that would make for an extremely long reply. I’ll tell you however in what way they are not different: in that we don’t know much about the etiology of either and in that we have effective treatments for neither.
I also agree very much with you that one thing is aetiology and another is treatment, so let’s looks at those two things separately. I will focus on schizophrenia as a case study because it is normally thought of as the most clear-cut case of a psychiatric condition with a strong genetic component in its etiology:
The question of whether schizophrenia’s etiology is genetic, environmental, epigenetic or multifactorial is important because, above all, it would not just sift the focus of treatment research but also open (or close) the door to prevention research. You cannot prevent a genetic condition (other than through eugenic practices) but you may be able to prevent an environmental condition. I see that you yourself are not a supporter of a crude genetic etiology of schizophrenia so I’ll skip that. I’ll also skip epigenetics for the sake of brevity and because I don’t think anything will come out of that – in any case you could say that it is a sub-type of multifactorial inheritance. So let’s look at multifactorial: shizophrenia as an inheritable disorder which results from the interaction between genes and environment. Of course at one level schizophrenia is an interaction between genes and the environment (what isn’t?) but in what sense would it be an inheritable disorder? The very notion of disorder, like disease, implies that it reduces the chances of survival of the organism, or in the case of a social organism such as ourselves, the chances of survival of the individual organism and/or its social group. That of course has very important implications from an evolutionary perspective, and particularly when it comes to the evolution and inheritance of genetic disorders or, most importantly for the case of schizophrenia, the evolution and inheritance of a “propensitiy” for a disorder – a genetically-determined “weaknesses”. We know already that whatever the genetic influence on schizophrenia might be, it hasn’t got a simple genetic architecture – there is no “single” gene coding for either the condition or the “propensity” – in fact, its architecture must be very complex or we would have identified it already. Now, when a disorder has such complex genetic architecture as schizophrenia should have (since we have more or less discarded all the simple options) it becomes increasingly difficult to consider it a disorder, since it is not possible to account for how such a complex genetic architecture could evolve in the face of negative natural selection (and all disorders are negatively selected unless they confer an advantage in certain environments, like sickle cell anemia-malaria). So what option do we have left? That the genetic component of schizophrenia is not a “propensity” or a “weakness” but a neutral or quite possibly advantageous trait which only becomes deleterious when exposed to particular environmental factors. I have used elsewhere the analogy of a gene that codes for better absorption of food: this gene would be advantageous and under normal conditions it is positively selected, but if the organism is exposed contaminated food the organism might develop a “disorder” while organisms who do not have this gene remain healthy. In the case of schizophrenia you might be looking for individuals who are more “sensitive”, who process certain signals like non-verbal language better than average, etc. But you are not looking for a “weakness” and there is not evidence at present to suggest that schizophrenia is multifactorial rather than 100% environmental – of course genes play a part in it, but not in the sense of there being a genetic “weakness”.
Now, I’m not saying that it is impossible that schizophrenia would turn out to be a multifactorial genetic disorder, that is still within the realm of possibility, but it would be a big surprise, it would go against everything we think we know about evolution and inheritance and against all the evidence (the real evidence) that we have so far. So why, one might ask, the insistence that it is a genetic disorder in one way or another? Because of a few twin-adoption studies that, quite frankly, are not worth the paper they are written on? Explain to me why all the research is directed towards the least likely etiological hypothesis of schizophrenia instead of into much more likely hypothesis. It is a big mystery to me unless you take into account very powerful commercial interests, a certain degree of ideological pressure (by which I mean mainly gay activism – since they have their own vested interests on the heritability of traits which reduce reproductive success), and the fact that it is a lot easier to obtain funding for neat genetic research that for more complex research into environmental factors.
Environmental factor are notoriously hard to pin-point, even when your common sense tells you that you are looking at it. Take trauma in connection to schizophrenia for example. A lot of “schizophrenics” have histories of childhood trauma, but not all. Or is it that they just don’t remember the trauma? And what is trauma exactly? Sexual abuse? Or simple a “double-bind” pattern of communication? A lot of people suffer childhood trauma and do not develop symptoms of “schizophrenia”, but how can you compare trauma with trauma? Even if you narrow it down to, say, sexual abuse, can you really compare two cases? Can you account for all the factors? Maybe the whole difference between two seemingly identical cases might be that in one the child had a dog that came to sit with him after the abuse took place whereas the other didn’t have a dog, or had a dog that didn’t come to sit with him. Research into environmental factors is notoriously difficult, but that doesn’t mean we shouldn’t even try it.
And I meant to be brief… I’m afraid I’ll have to cut it short without going into “treatment”. I’ll only say this about it: the question is not whether medication could help people with psychiatric “disorders”, but whether the actual medication that is currently in use does help or not. Or whether in fact it makes things worse. And I’d say that there’s enough evidence out there to say quite definitively that it does not work and that it does makes things worse. If you want to look at this evidence “Anatomy of an Epidemic” is indeed a good place to start. I’m not saying that people with schizophrenia or depression do not have a problem and that they don’t need “treatment” (I personally would prefer the word “help”), but I would very much question the treatment they are getting at the moment and the network of interests which support those treatments.
I will also add one last thing: if you look at enough studies into mental disorders you will begin to notice what cannot be describe as anything other than lies. Conclusions not supported by their own data, data excluded for no conceivable reason other than manipulating results, etc. Not one case or two, but many – I just posted one recent example in, “Preventing Depression: SSRIs for At-Risk Populations?”, nothing too dramatic, just the last one I have noticed myself. This is not a level playing field, and you should maybe ask yourself why isn’t it? If the “biological model” (and I agree that the word is very misleading, but you know what I mean) is right, why can’t they just let the data speak for itself?
There is a lot more I’d like to say, since you do raise some very interesting points, but I’m afraid I’ll have to stop here for now. Thanks for your comments – it is always good to hear a dissenting voice.
A small precision I wanted to make further into my reply before it grew too big. When I said I agree 100% with you that “everything has a physiological etiology, unless it is magic” I wasn’t being completely honest. I agree that everything has a physical etiology; physical, yes, but not necessarily physiological. The functioning brain is not a “brain in a jar”, it is part of a system of complex interactions which involves not just the body but, (at the very least) the entire material universe. The brain might be a “thing”, but the mind is a system, and when you are looking at “mental disorders” you have to think in terms of systems and interactions, not isolated “things”. But I don’t want to end up writing another monstrously long comment, so that’ll have to do.
Well said, Altostrata! In my opinion, “biological basis” is the most overused, least informative phrase in psychiatry. If we accept the reality that every aspect of human functioning is dependent on biological processes, then every thought, feeling, and behavior, including those listed as symptoms in the DSM, is in some sense “biologically-based.” Thus, describing a mental disorder as “biologically-based” is not really saying anything, at least not something everyone doesn’t already assume to be true. Yet, this phrase this is often used to support the disease model, as if biological basis is the equivalent to biological disease. It isn’t; the latter must be shown directly. And, as we all know here, it hasn’t been.
I appreciate your articles here. Thanks. It can be really difficult to know when apparent research findings are really relevant or whether they are just cleverly presented in a sort of scientific-babble that the uninitiated (including me!)can’t decipher. If you have a few minutes I would be interested in your thoughts/critique on this editorial I recently read. It claims there are 273 biomarkers for ‘schizophrenia’ http://www.currentpsychiatry.com/article_pages.asp?aid=11050
This actually supports just what I was saying above – if a “disorder”, and what you said, too. If there are 273 biomarkers for a “disorder,” and other “disorders” have some of the same biomarkers, how can we even call anything that heterogeneous a disorder at all? Or even identify it as an entity? There may be some percentage of these cases where there’s something actually wrong, but it’s not always the same thing, and many of the “cases” will not actually be disease states at all – simply normal genetic variations.
When a scientific theory leads to more complexity, it is generally very quickly discarded. Science should make things easier and simpler to understand. Schizophrenia is simply not a scientific concept. It’s a social construct, and the more we try to force it to be a “physiological” phenomenon, the more time we will waste and the more confusion we will generate.
Yes, this is the kind of article that gets my blood pressure up. On my very long post above (which by the way is riddled with typos, sorry) I talk about something similar, although I speak of genes or “genetic markers” and not of biomarkers which is a more general concept. But basically a similar idea applies, when it comes to biomarkers there’s such a thing as too many biomarkers. More is not better.
But to be honest that is not even the question with that article, which is a good example of the rubbish that gets published every day. When it says that “365 biomarkers for schizophrenia have been discovered” it means that studies which claim to have found an association between those biomarker and schizophrenia have been published in peer-reviewed journals. That doesn’t mean that anything has been “discovered”. These days people seem to think that getting your study published is a validation of your conclusions; well, it isn’t (and let’s not even talk about the integrity of some journals). We would have to look at all those studies which claim to have found a biomarker for schizophrenia (even the ones that have been “replicated at least 5 times”) and see what they really say – I’m pretty sure that after doing that we would go down from 365 biomarkers to somewhere around 0.
But what really makes me angry is that the article mixes markers for schizoprenia with “markers of drug response”, which half the time are markers of years of (enforced) drug abuse. Like for example prolactin, which is mentioned in the article: high prolactin is observed in “schizophrenics” so it becomes a biomarker for schizophrenia. No, actually hyperprolactinemia (high polactin) is CAUSED by antipsychotic drugs and so of course it is associated with people who have been given antipsychotics on a regular basis (i.e. “schizophrenics”).
The scary thing is that the article seems to be advocating blood tests to diagnose schizophrenia (probably in the absence of any clear symptoms). Are we approaching the days of “asymptomatic schizophrenia”?
Frankly, I think the best explanation for that article is probably to be found in Dr. Henry A. Nasrallah’s bank account.
Dear all – I have been eager to make a response to several comments, but have been tied up with work, please forgive the lag.
I wanted to say first of all that I’m generally impressed with the responses that I’ve received to my comments. Not only in the quality and thoroughness of the responses, but for the most part in how a dissenting viewpoint has been received. I didn’t expect this dialogue to last long, but here I find myself enjoying the discussion quite a bit and I appreciate that we’ve been able to find a fragment of common ground here and there. I suspect we will never reach agreement on some fundamental issues, but I didn’t start commenting just to stir things up, I’m really interested in understanding why so many of you think so differently about these issues. At the very least, perhaps we will come away with a more thorough understanding of each other. I’ll try to keep this brief and not comment on every point raised.
re: [“reductionism of the worst kind”]
I don’t see reductionism as a dirty word. It is just one of many ways of trying to discover how the natural world works. I would argue that it is by far the most effective way if you look at success in physics, chemistry, biology, etc and the way it has transformed our world. It is not the only way and some would argue that there are better ways or that at least there are better ways of understanding “psychiatric disorders” and I’m fine with that viewpoint which is I think what you are trying to say.
As an aside: I find myself struggling with terminology here. I feel that I keep using inflammatory terms: “psychiatric disorder”, “biological basis”, “mental illness”, “psychiatric symptoms”. I’ve tried pretty hard to avoid using “disease”, but come on I’ve got to use some word to describe what I’m talking about. I will do my best to avoid terms that are overused, but I suspect I will still say things that others feel the need to put in quotes… bear with me.
relatedly I will respond to Altostrata: [“brain circuitry” proponents in psychiatry propose that disorder or disease underlies only those thoughts, feelings, senses, etc. of which they disapprove and have designated as “abnormal,” when they may not be abnormal at all.”]
This is not just a problem with brain circuitry proponents. We can define a disorder however you want: typically it leads to some dysfunction in the person’s life and hopefully they themselves define it as a problem. Anyone who tries to help someone in any way will have to define what is a problem that needs addressing versus what is an acceptable variant of “normal” behavior. That is not to say I don’t appreciate the issue or that I don’t empathize with say members of the ADHD or autism communities that feel their brain architecture is a variant of normal with challenges and advantages and one to be celebrated in the name of neurodiversity. That seems reasonable to me and I have no desire to track them down and drug them up or anything like that I promise you. Then again I did just slip back into the assumption that those individuals are unique as a direct result of having a different type of brain than your average person and I know this is not widely accepted here. Forgive me, point stands. This all said though, I do maintain that wherever you draw the line there is a point at which people suffer quite severe dysfunction and suffering. I would call that a disease or a disorder. I hope that somewhere along that continuum you can agree with me, if you really don’t think that any behavioral state, no matter how extreme can be said to be abnormal or disordered then I fear we have reached the limit of this debate.
STEVE – thank you for your kind words and I appreciate your response.
[ want you to see that it is an assumption and not a scientifically proven fact. All we know for sure is that biological changes correlate with changes in emotional state, but correlation is not causation.]
I will grant you that my assumption is that all emotional states in human beings are caused or at least mediated through the brain. As you point out I cannot prove that with existing technologies and the limitations of human subjects research. However, it is not an uneducated assumption. Direct manipulation of neuronal activity in animals demonstrates that these alterations can causally influence a range of subtle behaviors. Further, humans who have lost specific parts of the brain lose specific abilities or have their behavior affected in distinct ways (see Phineas Gage) and manipulation of the brain activity of living humans during neurosurgery or with transcranial magnetic stimulation causes specific behaviors or emotional states. Taken together, to me these types of data indicate that if a disorder affects the brain it will/can cause psychiatric symptoms.
I am beginning to understand that some here view the brain as mediating these symptoms, but not causing them. I admit I’m still trying to come to a complete understanding of this idea. But I think it goes something like this: Things happen in the environment which induce a state or epiphenomenon in the complex system which is the brain and that affects behavior or symptoms. There is nothing “physically” wrong with the brain, though the brain is required for this to happen and the concept is consistent with a mechanistic world view. I’m sure I haven’t gotten it quite right for everyone’s taste, but I actually quite like this idea. In fact I suspect a lot of what are called psychiatric symptoms are operating in this manner – thank you for helping me to think more clearly about this idea.
That said, I still don’t think this is the only thing going on. I still think that brains are different from each other and that if a brain is constructed in a way that makes it highly probable to enter into one of these states it can be viewed as a physiological illness or disorder. For example, a young person who is prone to psychosis or schizophrenia or whatever you want to call it – maybe throughout their life their different brain manifests itself in subtle ways, as they get older something happens and they enter a state called a psychotic break and they are clearly suffering. No matter what you think is the best thing to do for this person, in many cases they will struggle with staying on the more functional side of that razor’s edge for a good part of their life. In a lot of cases (not all) I think it will turn out that there is a physical difference in how that person’s brain is constructed, maybe it will be subtle but I think that it is there. I don’t know what that form will take, I think there is evidence which supports this though I accept that for many here it will fall short of their standard of proof.
Another reason I think this is the following: That is how all other illness in the human body works to my knowledge. My observation is that for any complex system in the body I can point to an example where there are individuals who have either a congenital or acquired problem in the physical functioning of that organ which leads to disease. I am unaware of exceptions. The brain also has disease/disorders – I think many agree that there are neurological disorders for example. Strokes that cause paralysis, epilepsies which cause seizures, problems of brain formation that cause intellectual disability. Alzheimer’s which causes memory problems, difficulty with spatial navigation and personality changes. Huntington’s disease is an interesting case because it causes motor problems, but also an array severe psychiatric symptoms. It is by the way as close to 100% genetic as you can get – if you have the gene variant you will develop the disorder, though the severity can be quite variable. But I digress – The point is that in complex systems such as emotion, thought, motivation, etc. I have a hard time believing that there will not be physical dysfunction which leads to disruption of normal functioning. I think that this type of process causes some and in my opinion a lot of psychiatric illness (particularly in its more severe forms). Let’s be done with this topic though.
[“Back to science. The 25 year earlier death rate is not something I made up. Read the following article for a taste of the issue, but this stuff is published in mainstream psychiatric journals as well. It’s not news: http://usatoday30.usatoday.com/news/health/2007-05-03-mental-illness_N.htm“]
Steve, my original interpretation of what you were saying about a 25 years earlier death rate was that you were saying that treating a psychiatric disorder caused patient’s to die 25 years earlier than if they had not been treated. Perhaps I misunderstood. The article referenced here supports the idea that those with psychiatric illness die 25 years earlier than those without psychiatric illness. Many of these people were treated and it is unclear to what extent the drugs they were exposed to are responsible for this effect. Certainly the drugs, particularly long-term use of anti-psychotics, have the potential for many negative effects on health. This study does not directly address the influence of medication separate from the influence of having the psychiatric disorder in the first place. To determine that, you would have to compare treated vs. untreated patients with psychiatric illness controlling for factors like illness severity. I would be very interested to know the results of this study, but I am not convinced that it would come out the same way. Many of these medications could certainly cause someone to die younger, but so could the sequelae of untreated psychiatric illness (homelessness, poor access to healthcare, substance abuse, suicide). My assumption being that these would be more prevalent in those who were unmedicated, at least in the case of more severe disorders like schizophrenia. I don’t have data in front of me to support this at the moment I admit. My assumption is also that in specific types of cases medication is helpful, if even for acute stabilization. For example an acutely psychotic individual or an acutely manic individual, each at high short term risk of suicide or other dangerous behaviors. I know that many here will not agree that this is the case. To summarize my overall point though, I think one should be careful in interpreting the result of this study as indicating that psychiatric medications kill people 25 years before their time… I agree that medication side effects probably contribute, but the study does not demonstrate that medication is the prime driver of the effect.
[“There was some big flap about loss of brain tissue, but more recent studies (Nancy Andreasen, for instance – see http://archpsyc.jamanetwork.com/article.aspx?articleid=211084) have shown that this appears to be a result of neuroleptic treatment rather than a characteristic of the “disease.””]
This is a really great and I think important article, thanks for drawing my attention to it. This looks like a good study to me and it makes me think more carefully about the long term risks of antipsychotic treatment. I would however caution against over interpreting the results – even the author’s conclusion is that antipsychotics likely contribute to the tissue loss seen in those with chronic schizophrenia, not that this is the only reason there is tissue loss. In fact they state that there are differences in the volume of certain brain structures at the outset of treatment compared to controls, suggesting there is a difference in brain structure prior to treatment, though medication may hasten the process. A brief perusal of the literature around this issue indicates to me that there are a lot of conflicting studies about whether there is loss of brain tissue in schizophrenia that can be definitively dissociated from treatment with medication. I do not know the answer – but I have never thought of schizophrenia as a neurodegenerative condition anyhow so I’m not troubled if there is no loss of brain tissue. It is interesting that you point to an article by Nancy Andreasen though, as she is clearly a staunch supporter of the idea that there is a physical, physiological, biological, whatever cause in the brain for schizophrenia. It need not of course be loss of brain tissue.
Just a few key quotes from that article:
~”Antipsychotic medications are the mainstay of treatment because there is strong empirical evidence that these drugs reduce psychotic symptoms and relapse rates in schizophrenia patients.”~
~”Our results must be interpreted in the context of additional limitations. Identifying an association does not necessarily indicate a causal relationship. […] Even with the most sophisticated statistical methods, we may not be able to fully distinguish the potential confounding influences that illness severity or other sources of unmeasured variance could still have on the relationships between progressive brain volume reductions and antipsychotic treatment.”~
~”Are antipsychotic-associated GM and WM volume reductions “bad” for patients? The implicit assumption is that brain volume reductions are probably undesirable because patients with schizophrenia already have diffuse brain volume deficits at the time of illness onset.”~
~”Given that these medications have substantially improved the long-term prognosis of schizophrenia and that schizophrenia is a disease with significant morbidity, continued use of antipsychotics is clearly still necessary. However, our findings point toward the importance of prescribing the lowest doses necessary to control symptoms.”~
* Please understand that I am not trying to minimize the negative side effects of medication, these are serious issues, the medications are rife with problems and they can be quite dangerous. I do not think everyone should get medication or that those who do get it should stay on it indefinitely. I do not think the current medication are adequate and in some cases they may not work at all.
The clear exceptions in my mind are mood stabilizers and antipsychotics, particularly short term use in the acute patient. I would direct you to the writings of Kay Redfield Jamison (An Unquiet Mind) and Elyn Saks (The Center Cannot Hold). Each of these authors suffers from a psychiatric disorder, Bipolar and Schizophrenia respectively, and each has written about their struggles with exceptional thoughtfulness, power and intellect. Each believe very strongly in psychotherapy as a treatment modality and are far from across the board supporters of psychiatry – Yet each comes down unequivocally on the side of medication being essential in their recovery and ability to achieve long term stability.
[why should we buy into the assumption, which you kind of agreed isn’t really true, that just because two people fit the subjective description of “schizophrenia,” they have the same thing “wrong” with them?]
Like you said that’s not what I think. I also think anyone with a modestly nuanced view of the disorder doesn’t really think this. Schizophrenia (or any DSM category) is a pretty broadly cast net that is going to catch a broad set of entities with overlapping sets of symptoms. I would say it also almost definitely catches people who I would not categorize as having a disorder or a disease too. I’m sure I fit criteria for a number of disorders if criteria are strictly applied and I’m not the first to make this criticism. It is an unfortunately poor system for making diagnosis I admit. That said, while there are probably many different conditions being labeled as schizophrenia I expect that the number of basic problems in the brain that can cause a schizophrenia is not infinite. Also, it is not a meaningless category… Two people labeled with schizophrenia are probably more similar than they are to someone with autism for example. Schizophrenia may be too heterogenous a group to study I agree – that may be exactly the reason there is so much conflicting data… Perhaps a treatment is only effective for a small subgroup. I think that identifying subgroups and parsing schizophrenia into more uniform groups could really be critical and I know we hate genetics, but I think genetics could help with that aspect some day.
[” Whitaker really does bring us back to what is known. I think you should re-read his book.”]
I have not read it yet, but I’ve looked into it and I’ve decided that I will purchase and read this book.
MORIAS: Thanks also for your comments and appreciation for a dissenting voice. I hope that some of what I said above addresses parts of your comments. For the most part I’ll focus on what you said regarding heritability and evolutionary advantage vs. disadvantage.
[“You cannot prevent a genetic condition (other than through eugenic practices) but you may be able to prevent an environmental condition.”]
I’m assuming you meant something like ‘you can’t prevent a 100% genetic condition’? I see that you followed with a more nuanced discussion about gene-environment interactions. Just to clarify my position though: I see no reason why you cannot in theory prevent the development of a 100% genetic condition. I even have hope that one might be able to prevent the development of a disorder like Huntington’s or at least attenuate its severity. Plus, we are not talking about disorders that anyone (or at least not me) are calling genetic in that sense (I don’t think you are either). Nothing supports the idea that psychiatric illness is ‘predetermined’ and so I think it is very likely you could prevent it even if it is somewhat heritable.
[“Of course at one level schizophrenia is an interaction between genes and the environment (what isn’t?) but in what sense would it be an inheritable disorder?”]
If you agree that it is an interaction between genes and environment, how could it not be relevant which versions of genes you inherited? I really don’t understand the difficulty with conceptualizing schizophrenia as an at least partly heritable condition. I do of course give you credit for stating that it could be, but I still don’t understand why you think it is so clear that it is likely to be “100% environmental”. I mean even if it was 99% environment and 1% genetic, why is it so hard to give any credence to the idea that your genes play a role?
I’m not as well versed in why you think the twin studies are so flawed, but I gather that if I ask I will be redirected to the Whitaker book which is the namesake of this whole blog. I gather that it has to do with this equal environments assumption and the fact that identical twins experience more similar environments than fraternal twins. I further gather that this flaw is considered a central piece to the argument against an influence of genetics in psychiatric disorders. I don’t know enough about twin studies and its too late to get into this for me. Beside it seems that this particular aspect of the debate has been had out more than once already. Aren’t there any identical twin studies where they are separated at birth? (I don’t know)
I will say this though: In science there is no such thing as a perfect experiment, often and particularly in the case of something as difficult to study as human psychiatric disorders we have to look at the overall weight of the evidence and perhaps then go with our instincts in forming further hypotheses. Above all else it is most important that we apply the same standards of evidence to competing hypotheses. It follows that one cannot say something like the following: “the evidence is not airtight in support of genetic influences, there are always environmental confounders and this idea has not been unequivocally proven – Therefore it is likely that the alternative (that schizophrenia is entirely environmental) is correct” OR even that the two hypotheses are equal at that point. I still think that it is likely that heritable factors are relevant to the development of something like schizophrenia. At the very least I consider the idea that schizophrenia is 100% due to the environment to be as unlikely as that it would be 100% due to genetics, I just don’t think that these things work that way.
[“Explain to me why all the research is directed towards the least likely etiological hypothesis of schizophrenia instead of into much more likely hypothesis.”]
Again, I don’t understand why a combination of heritable factors and environment is in your mind “the least likely etiological hypothesis”.
[“Now, when a disorder has such complex genetic architecture as schizophrenia should have (since we have more or less discarded all the simple options) it becomes increasingly difficult to consider it a disorder, since it is not possible to account for how such a complex genetic architecture could evolve in the face of negative natural selection (and all disorders are negatively selected unless they confer an advantage in certain environments, like sickle cell anemia-malaria).”]
I do want to try to address your thinking here. First of all if you think it has such a complex genetic architecture (I agree that it does) – why is it so hard for you to believe that the versions of genes you inherit have an influence?
As regards whether it can still be a disorder, I don’t really get your thinking. If the only way genetically mediated disorders can exist is through conferring advantage in particular environment then we should have a lot fewer disorders, there is no malaria in the United States so by your thinking we shouldn’t have anymore sickle cell anemia or at least soon we shouldn’t? I don’t think so or at least I think we will have it for a while since the environment of the US isn’t really selecting against it that strongly. Type II diabetes is a disorder that has a complex genetic architecture but also depends critically on environmental factors. I’m not sure on what grounds you will disagree with me… Perhaps you will say that there is no evidence for a genetic contribution to diabetes, I don’t know. For that matter what is the evidence that anything is a heritable disorder? Regardless of how quantifiably heritable it is I suppose you can always say that there is some environmental factor that is not being controlled for which is actually confounding the experiment and causing the association.
Anyway, back to diabetes… I’m not saying that there cannot be an advantageous aspect to the individual genes that are inherited which underlie the disorder. Diabetes for instance is probably partly caused by sets of genes which were/are advantageous in times where food supply was limited. Those same genes do not confer a relative advantage when there is a McDonald’s on every other block selling super size meals for $5 and they probably help to cause diabetes. The genes are not well selected against at this point because there is good medicine which keeps you alive past the point of reproduction. I totally agree that genes underlying the complex architecture of schizophrenia could code for traits which have some advantage in particular environments. I also don’t remember saying “weakness” maybe I did and don’t remember it, not sure. There is also by the way a concept which I believe is called something like kin selection, meaning that the gene doesn’t have to help the particular organism it is in survive, it just has to help those around it with the same gene survive better so that on whole that gene is replicated. Wow… I’m getting way off track here and really doing a poor job on this point. Really need to get some sleep and I apologize for not doing this justice.
I’ll just say this: If you say there shouldn’t be any disorders with complex genetic contribution partially explaining their etiology then that should also apply to all the other disorders like that in other systems.
[“Research into environmental factors is notoriously difficult, but that doesn’t mean we shouldn’t even try it.”]
Yeah! I think we should definitely try it.
Thanks for reading, if you made it this far 🙂 It has really been helpful for me to write it and to help clarify my thinking on some of these issues. If anyone responds further I will be delighted.
I will read Mad in America OK? You’ve convinced me, so please don’t just say that I need to read this book as a response to my points.
Ok, then, you need to read “Anatomy of an Epidemic”.
Just joking, although, yes, you should read “Anatomy of an Epidemic” as well (perhaps more so than “Mad In America”). Also, if I can recommend another book, try “The Emperor’s New Drugs” by Irving Kirsch, it’s a very good and clear book and it gives a good sense of what is wrong with scientific research in psychiatry.
About twin studies, we are in luck! Jay Joseph has just posted a very good article about them on this site. I think it will answer a lot of your questions. He doesn’t go into adoption studies (the studies on identical twins separated at birth you refer to) but I hope he will write another article about those soon (yes, this is a humble request).
Regarding the point I was trying to make about the difference between a multifactorial genetic disorder and a disorder that is 100% environmental even though it is the result of the interaction between a genetic trait and the environment, perhaps I did not explain myself clearly. It isn’t easy to go into it in this format – it’s hard to be both clear and brief. Bear in mind that we are talking about evolution; about the development and transmission of a trait (or disorder) over thousands of generations – the time-scale is very “slow”.
Perhaps the easiest way to understand it is by looking at the practical consequences of what might otherwise sound like a mere play on words. For that I return to the “gene for food absortion” analogy which I used before. Imagine people with this gene, “G”, develop a disorder “D” because of their higher rate of absortion of nutrients also means they absorb more of the toxins in contaminated food. Imagine that scientists, who are convinced that disorder D is a multifactorial genetic disorder, identify gene G and say “this gene gives you a propensity to develop disorder D”, so they start giving everybody with gene G (whether they have been exposed to contaminated food or not) medication which somehow ameliorates the symptoms of intoxication but does not prevent intoxication if exposed to contaminated food.
The problem is that, on the one hand the medication itself is toxic and has brutal side-effects, often worse than disorder D itself, and, on the other hand, no effort is made to identify the toxin that is making people with gene G develop disorder D. Also, bear in mind that people without gene G who are exposed to the toxin in the food might not develop disorder D but will develop other less obvious disorders, disorder d1, d2…- the toxin affects everybody which comes into contact with it (scientists note this but erroneously conclude that D, d1, d2… have “overlaping genetic architectures”). Since no attention is given to the toxins in the contaminated food, and no attempt is made to remove them from the food supply, their concentration continues to increase so that now even people without gene G (people with a variant that gives them slightly lesser good nutrient absortion, “g1” and who up to now were developing disorder d1) begin to develop disorder D too. Of course, I forgot to mention that disorder D is actually a syndrome – a collection of symptoms of diverse severity depending on the amount of toxin consummed/amount of toxin absorbed… (at this point, if you are still thinking in terms of genetic disorders things get very complicated and nothing makes any sense anymore)
Now, would you say that gene G codes for a disorder? No, it doesn’t, in fact in normal circumstances it actually makes you healthier since you get more nutrition from the same food. Gene G is a good thing, it does not need to be medicated. Disorder D is an interaction between genes and environment but cannot be said to be a multifactorial genetic disorder; the toxins in the food are real toxins, they poison everybody, they affect everybody negatively – we are not talking about an allergy but a genuine intoxication.
I don’t know if this helps you understand how a disorder might be the result of the interaction between genes and environment and yet have a 100% environmental etiology. The “bad part” is wholly on the side of the environment, not on the side of the genes. I think this also holds for schizophrenia and other psychiatric disorders and that only this model is really consistent with evolutionary theory.
About kin selection and diabetes II, I won’t go into that, just to say that they don’t really apply. Diabetes II is not really analogous to psychiatric disorders and psychiatric disorders do not give any advantage to the group so kin selection is not a factor.
Enjoy “Mad in America” and “Anatomy of an Epidemic” and “The Emperor’s New Drugs”…
Oh, and of course people without gene G (or g1, g2,..) who have been exposed to very high levels of contaminated food will develop disorder D “for no apparent (genetic) reason”, whereas people with gene G who are not exposed to contaminated food will not develop disorder D or any other disorders – and people with gene G who are only exposed to small amounts of contaminated food might develop d1 or d2 instead of D.
You get the idea. Basically you have two variables, one genetic (toxin absorption), one environmental (toxin consumption), giving rise to a wide range of “disorders”
Toxin consumption/Toxin absorption = disorder type
If you try to look at the disorders as discrete entities things will get more and more complex until they become absurd – which is where I’d say psychiatry is at the moment. If, on the other hand, you look at the disorders as part of a continuum of various degrees of “intoxication”, everything falls into place.
What the “toxin” in question is in the case of psychiatric disorders is a more complex subject. I use “trauma” as a shorthand with a very inclusive (and so imprecise) meaning.
Oops I meant I will read Anatomy of an Epidemic, not the other one.
I’m going to try to keep this brief and to the point for the sake of my sanity. We are actually not that far apart in our understanding in some ways and I it seems we might be butting heads over semantics in some ways. However, there are other ways that you appear to be drastically misinterpreting my position and I believe drawing flawed conclusions.
In principal, your gene G and disorder D analogy looks OK to me. It could work that way.
You say, “this gene gives you a propensity to develop disorder D”, so they start giving everybody with gene G (whether they have been exposed to contaminated food or not) medication which somehow ameliorates the symptoms of intoxication but does not prevent intoxication if exposed to contaminated food.”
This is a gross mischaracterization of anything I’ve said. I don’t know who “they” are, but I have never proposed something like that. I am not saying that if you have whatever gene variant then you should get a medicine even if you don’t have symptoms. The disorders are not that simple and it won’t make sense to treat people in this manner.
You say, “at this point, if you are still thinking in terms of genetic disorders things get very complicated and nothing makes any sense anymore”
Just because things get very complicated, it does not follow that nothing makes sense anymore. It does not mean that the idea is wrong either, you note that the environmental influence is also complex, but you readily flatten it to a concept like trauma in order to discuss it or to the concept of a toxin in your analogy. That’s fine, it is what we have to do… Why don’t you have an issue with the complexity of how all the different variants of trauma affect all the diverse variants of disorders? Why is that concept not equally complex and therefore doesn’t make any sense and is therefore wrong?
Also, why should your analogy not be interpreted in the opposite direction? The exposure to the toxin leads to a propensity to develop disorder D, but only those with gene G actually develop the disorder, etc. This isn’t really exactly what I think, I’m just saying that we are talking about associations and the arrow of causality can not be determined with enough precision to say A CAUSES B over B CAUSES A. Really I’m totally fine with the way you set up the interaction of genes and environment in the analogy and if you read what I’ve written already you will clearly see that I have not said that I think heritable factors CAUSE schizophrenia, etc. I’ve said that they “contribute” to its development and this is also true in your analogy. Here is where I think this intellectual hula hooping is more about semantics than anything else.
I do think yours is the more extreme position though, because you steadfastly believe that the arrow of causation always originates in environment. My position is that sometimes it originates in the environment, sometimes it originates in the building blocks of brain (“genes” if you will), but vastly more often it is probably not as simple as one or the other. I’ve already given one example where it almost entirely originates in a gene, Huntington’s disease. If you have the Huntington allele you will develop a psychiatric disorder. I’m certain there is an equally extreme position on the environmental side where if you are exposed to X, 100% of the time you develop psychosis. Don’t get me wrong though, I think those are the extremes.
You seem to be under the impression that no gene variant can exist which is not fundamentally healthy for the organism. I apologize if I’m simplifying your stance, but something like this seems to be at the root of your ideas. What about the Huntington’s allele? How is that a good version of a gene to have? If it reduces reproductive fitness then YES, it should be selected against. However there are many ways in which it can stick around despite negative selection. I won’t get into all the ways that could operate, but suffice it to say “bad genes” (or at least unhealthy variants of good genes) do exist in the population. I gave you one example in Huntington’s and I can give you a dozen others off the top of my head. Mutated versions of genes also arise de novo at a certain rate in populations mind you, along with variations in the copy number of certain genes – this definitely causes disease. Just pointing out that the system does not need to indefinitely maintain unhealthy variants as they are introduced to the system.
You say, “Now, would you say that gene G codes for a disorder? No, it doesn’t, in fact in normal circumstances it actually makes you healthier since you get more nutrition from the same food.”
No it doesn’t code for the disorder in your example. I’ve never said anything so simplistic, except perhaps in my Huntington’s and even then I would not say something as obtuse as that it codes for the disorder. It codes for RNA. I’m not saying that your example can’t work, but its just one of a range of possibilities and I do not think it ALWAYS works that way. See above.
Regarding diabetes – I wasn’t trying to say kin selection explains diabetes, just that there are complex models of how genes can be selected for on a population basis. Forget about kin selection. Diabetes on the other hand… I do not see how you can say this has no role as an analogy. Diabetes in part probably works exactly like the analogy you proposed.
In your model: Gene G leads to better uptake of nutrition, but in an environment with the toxin has the “unintended” consequence of leading to higher toxin uptake leading to disorder D.
In my diabetes model: genes lead to the better uptake of nutrition in the environments where they were selected for, namely those with scant food resources. These genes are greedy and help suck up and store energy. Now put someone with those genes in an environment where you have the toxin. The toxin is easy access to cheap, high energy foods (McDonalds, soda, whatever). Now the genes lead to disorder D (D=Diabetes), those individuals store more fat, develop insulin resistance then high blood sugar then organ damage, etc. See anything about the Pima Indians or even look at the rate of diabetes in Mexican-Americans and this effect is obvious.
I’m not saying it is that simple. I’m saying that like psychiatric disorders, diabetes is extremely complex, it runs in families, twin studies would show heritability. We have not identified the genes involved, we cannot explain how they contribute to increased risk or even totally understand the environmental factors and how they contribute. We can certainly do a better job explaining diabetes than psychiatric disorders, but only because it is less complex and easier to study.
Maybe I can even give anyone diabetes no matter what genes they have if I feed them enough of these types of toxins… Just like your model. I’m not sure if you can give 100% of people diabetes that way or not, probably a lot. Can you give everyone schizophrenia with the right environment? I’m also not sure, but I’m not convinced you can. Either way, I think they are both disorders and not exactly the same, but similar enough to be instructive in terms of thinking about how these things work.
From the article and your post: ”Given that these medications have substantially improved the long-term prognosis of schizophrenia and that schizophrenia is a disease with significant morbidity, continued use of antipsychotics is clearly still necessary. However, our findings point toward the importance of prescribing the lowest doses necessary to control symptoms.”
This statement above is the one that we as a society and mental health system keep getting caught up on. When you read “Anatomy of an Epidemic,” you will see that the evidence does not support this claim, as often as you see it bandied about. The evidence suggests that, to the contrary, the “long-term prognosis” for schizophrenia is FAR BETTER in developing nations where psychotropic drugs are less available and less accepted. Whitaker also shows that the long-term prognosis for schizophrenia in this country was much better in the 1950s, BEFORE Thorazine and the ‘psychopharmacological revolution.’
He also shows that the BEST long-term prognosis for schizophrenia worldwide is in northern Finland, where they use an approach that considers psychotropic drugs as only an ancillary aid to a psychosocial intervention called “Open Dialog.” They are reporting functional social recovery rates (working, functional relationships, involved in normal community activities) of 80%! US rates are generally less than a 10th of that, with the huge majority of “schizophrenics” subsisting on SSI payments.
The statement I quoted above from the article is so generally accepted in the psychiatric community that to question it is akin to heresy. But the scientific evidence is mounting that it is not only false, but the opposite is true – long-term prognosis may actually be worsened by antipsychotics, even when they work to reduce symptoms in the short run.
READ THE BOOK!
Kay Redfield Jamison had a rather difficult childhood, her father was a pilot in the USA airforce. An industry where the psychological pressures on families not to upset Daddy, no matter how he behaves, is rather large. Her story could be interpreted as supporting the environmental cause of madness.
Her biography avoids self reflection. She idolises her parents, brother and sister. She avoids looking at her emotions or what gave rise to them as people overtaken by mania are apt to do. However this attitude does mean one is probably not going to resolve ones problems sufficiently enough to completely avoid mania and therefore might in prefernce take dangerous mind numbing medication.
Jamieson writes about therapy as a way of coming to terms with her, “illness,” not of uncovering the route of it and resolving her difficulties. Mania is about turning fear and distress into excitment by running around and doing things to avoid thinking about the difficulties in your life. It is probably an attitude that was learnt early on in life when overwhelmed by frightening events in ones family of origin.
I have a friend who has been manic 7 times. He is on drugs he does not like. I was talking to him about what was happening the first time he became manic. He was in dept and his boyfriend had just left him and this was when we lived in a much more homophobic culture than now. He started going to nighclubs and taking drugs and then it escalated and he did not sleep for three days and then he started thinking he was Jesus.
No one had asked him before what was going on before he became manic before despite using services for about 25 years. No one had asked him about his family or origin and how they treated him and how this might relate to his mania. It seldom happens in the mental health system. Yet when i ask these questions people often calm down, providing they can face thinking about these things, sometimes they can’t.
For more on this analysis of Jamieson and other aspects of psycho-social reasons for mania read the chapter on mania in Dorothy Rowe’s Beyond Fear. It’s one of my favourite books on mental health
By the way, you say “If you try to look at the disorders as discrete entities things will get more and more complex until they become absurd – which is where I’d say psychiatry is at the moment”
That is where psychiatry is at the moment I agree. It could go either way. I think we will be able to identify some discrete entities or at least categories which are similar enough to be meaningful. I can’t prove it yet, that is just what I think.
First, I owe you an apology. I was pressed for time in my reply yesterday and I’m afraid I was way too dismissive, particularly about diabetes II, something which has been niggling at me all day yesterday. I’m afraid I’m also pressed for time today, so again I’ll have to try to be brief, although I can honestly say that I would rather continue this conversation that do what I have on my desk… but I can only say a couple of things in reply to your thoughtful comments:
About diabetes II, I think you might be right, although not necessarily in the way you think – diabetes II might not be a multifactorial disorder either, but a 100% environmental (I’ll return to this is a moment – I assure you it isn’t just a difference in semantics).
Initially I just thought “diabetes II – probably autoimmune”, but if I’m honest with myself I was just avoiding the subject because, what do I know about the evolution of the immune system, autoimmune conditions or allergies? Not much, and I have to wonder why because it is a extraordinarily interesting area, so actually a big thank you for “forcing” me to think of this. One thing, though, about any possible analogy between diabetes II and psychiatric disorders (from a “clinical” rather than an etiological perspective, which I know is what we were discussing): insulin is not the “cure” but a very effective treatment for a symptom, hyperglycemia. The cure involves loss of weight, change of diet, etc. that in some cases can lead to complete recovery from diabetes II; you are cured when you don’t have diabetes II anymore, not when your sugar levels are under control. The cure is then to stop new “toxins” or “trauma” from entering the organism (change of diet) and give the organism a chance to heal (loss of weight) if damage has not yet become permanent. Of course insulin is a very effective treatment for hyperglycemia and the balance of benefit for the patient is as near perfect as you can hope for since it is not really a drug but you are redressing an imbalance (and I know that word immediately brings to mind SSRIs – for brevity I won’t touch on them other than to say please also read Kirsch’s “The Emperor’s New Drugs”).
Now, when it comes to schizophrenia the drugs in use are, as insulin for diabetes II, not a “cure” but a way to manage the symptoms. Well, so far so good, but we are not just talking about an abstract model, so we would need to look at those specific drugs and their balance of benefit for the patient. And that balance is a catastrophe – to be blunt, they do far more harm than good. Practically the only way in which they manage the symptoms of schizophrenia is in a “social” way, by making the schizophrenic “less of a problem” (a bit like methadone prescription – an analogous case in this sense). And in the meantime what of the cure? Or at the very least what of other strategies which might be far, far more successful at managing the symptoms to the point that the patient can remain medication free and far healthier than on any medication? Would you make no effort whatsoever to look at the role of diet and exercise in diabetes II and just be happy handing out insulin to an ever-increasing number of people? Except of course the “insulin” given to schizophrenics doesn’t really “rebalance their glucose” but just keeps them from complaining about it while in the process giving them half a dozen serious conditions as a side effect. I really encourage you to read some of the recovery (or even non-recovery) stories in this website and familiarize yourself with the “voice hearer” movement. What can I say? To me it is a source of unabated horror how the psychiatric profession (clinicians as well as researchers) simply dismiss recovery stories; how they simply refuse to look in that direction and refuse to even consider for example the connection between the content of a schizophrenic’s “delusions” with their life histories. If nothing else it represents a lack of scientific curiosity that shames the entire field.
Going back to multifactorial – 100% environmental: the question goes back to how a disorder evolves and is transmitted (although those two things are really just one) and how that sits with natural selection. Of course I’m not saying that “no gene variant can exist which is not fundamentally healthy for the organism” but I am saying that there is a threshold of complexity of genetic architecture beyond which a condition cannot possibly be seen as a disorder but must be considered as a trait – beneficial or at least neutral for the organism. You mention Huntington’s but of course Huntington’s has en extremely simple genetic architecture: autosomal dominant with bog-standard mendelian inheritance. And that is precisely the point, you can easily model how such a genetic disorder evolves and is transmitted and how natural selection lets it “slip through”. But schizophrenia has no simple genetic architecture (or we would have found it already) – in fact it must be so complex that we are not just talking about different genes at different loci but different loci on different chromosomes (again, if it wasn’t like this I think we would have found it already) . How would this complex architecture first develop and then be transmitted if it is a disorder – that is, it if it reduces survival/reproduction rates? And not only that, then we have to look at the incidence and distribution of schizophrenia across the globe – what kind of model would account for that pattern? There are also other considerations such as the fact that schizophrenia tends to develop relatively early in life (unlike for example Alzheimer’s) so that it would have a big impact on reproductive success “in the wild”. The only option which makes sense is that whatever genes might be associated with schizophrenia (if any, and I have my doubts that there really are any) the association is between a trait (a perfectly healthy type of human, if you like) and a deleterious environmental factor. If, as I said before, the “bad part” is wholly on the environment you cannot call that disorder multifactorial rather than environmental, even if there is an association to some genes – it would be like saying that my height is part of a multifactorial disorder because I keep hitting my head on a low door-frame to the point that I eventually develop brain damage; you don’t need to find ways of making me shorter or even find out what makes me tall or absent-minded (it might be interesting theoretically, but pretty useless from a clinical perspective), you just need to make a taller door-frame, put a cushion on the lintel or shout when you see me heading for the door. Or maybe you might find away to “cure” my absent-mindedness, but then that may be a fundamental part of my thinking process and by doing that you remove my ability to concentrate and find the solution to world hunger (I flatter myself a bit here). So, all in all, does it not make a lot more sense to concentrate on the environment?
What I am saying is that if (big if) any genes are associated with schizophrenia those genes are a valuable healthy variation – an asset to the individual and its group (in this case humankind); they will likely code for a slightly “different type of intelligence”, more attuned to certain stimuli (for example non-verbal communication, although this is only based on anecdotal evidence and probably completely off the mark).
A strategy on diabetes II should focus on avoiding overeating certain foods and exercising; similarly a strategy on schizophrenia should focus on finding the root causes (which are not the genes, in the same way that the root cause of diabetes II is not genetic since no matter what your genes are you won’t develop diabetes II if you have a healthy diet, etc). Where schizophrenia has already developed – or rather “voice hearing”, since we should really be talking in terms of specific symptoms rather than a dubious syndrome – then we should look at ways in which this symptom can be managed. And in this the evidence will show you that a combination of psychotherapy (the “talking” type) to treat underlying trauma coupled with learning strategies to accept and manage the voices (rather than suppress them) actually works, and very well. It makes people able to live fulfilling productive “normal” lives. Drug therapies on the other hand do not only not work but make things much much worse; they only work by making the patient “less of a problem”.
In closing I’ll say that of course I never suggested you yourself ever said “if you have whatever gene variant then you should get a medicine even if you don’t have symptoms”. Sorry if it read that way. But a lot of people are really suggesting this. “They” are Pzifer, Janssen… and a lot of researchers with a very keen interest in pushing an agenda of “preventive intervention” or “early detection”. I posted in this thread a link to one recent study pointing in that direction – just one of many. I could be wrong but I bet you (let’s say a one trillion dollar coin) that you are going to hear a lot more about psychiatric preventive interventions and about medicating people who have nothing wrong with them other than a particular combination of genes (or brain morphology or whatever) which some exceedingly questionable studies have associated to a higher risk of psychiatric disorders.
I hope you’ll stick around MIA – even if I might not always have the time to answer it doesn’t mean I’m not reading and taking things on board.
Oh! One more thing: sickle cell anemia – malaria. Yes, I am saying that in the absence of malaria in the US sickle cell anemia would eventually disappear. But only if you close down all hospitals (modern medicine messes up natural selection – not that I’m complaining, being rather “weak” myself ), revert to a hunter-gatherer culture and then wait, I don’t know, 50,000 years? Having said that, one thing is how a genetic disorder first develops and another whether it can remain in a population after the environmental conditions that made it possible disappear; that is an important point to keep in mind. The question still is, what is the etiology of schizophrenia (or PPD, or MDD, or BD, or OCD, or ADHD…)
for some reason I wrote “bog-standard mendelian inheritance” instead of “standard mendelian inheritance”. Why? Don’t ask me… we are a mystery unto ourselves…
ScottW wrote: “I think we will be able to identify some discrete entities or at least categories which are similar enough to be meaningful. I can’t prove it yet, that is just what I think.”
Yes, this is a matter of belief. Jay Joseph’s articles explain how history has proved this is unfounded. However, given the collapse of the “chemical imbalance” theory, psychiatry needs a scientific rationale, and millions of dollars are now being poured into genetic research and brain scans in psychiatry — all on the basis of belief, which becomes quasi-religious and impervious to evidence.
If you look at the vagaries of diagnosis in psychiatry, you will see why “discrete entities” are unlikely to be found. That high-tech research is being done on heterogenous populations because disorders are so sloppily defined. The results of the research are, therefore, chimerical — dependent of the biases of the researchers.