Peter C. Gøtzsche, MD

Editor’s Note: Over the next several months, Mad in America is publishing a serialized version of Peter Gøtzsche’s book, Critical Psychiatry Textbook. In this blog, he discusses how textbooks portray ADHD and schizophrenia as genetic disorders, despite the much stronger evidence for environmental factors in causing these experiences. Each Monday, a new section of the book is published, and all chapters are archived here.

Textbook authors are preoccupied with telling the students that psychiatric disorders are hereditary. Obviously, this gives the specialty prestige. It makes it look more scientific to claim that psychiatric disorders are in the genes and that they can be seen on a brain scan or in brain chemistry (see next chapter). But even if it were true, it would have no clinical consequences, as we cannot change our genes.

I shall explain in this chapter why the information in the textbooks about the causes of psychiatric disorders is generally highly misleading.

Illustration of dna strand unraveling, glowing bright blue against dark blue backgroundFirst, a sobering fact. Many billions of dollars have been spent by the US National Institute for Mental Health (NIMH) on finding genes predisposing to psychiatric diseases and on finding their biological causes. This has resulted in thousands of studies of receptors, brain volumes, brain activity, and brain transmitters.7-231

Nothing useful has come out of this enormous investment apart from misleading stories about what the research showed. This might have been expected from the outset. It is absurd, for example, to attribute a complex phenomenon like depression or psychosis or attention deficit and hyperactivity to one neurotransmitter when there are more than 200 such transmitters in the brain that interact in a very complex system we don’t understand.25

The main purpose of psychiatric textbooks is to educate future clinicians. They will not become better clinicians by believing what the textbooks say about heredity. They might in fact become poorer clinicians. If they convey to the patients that their disorder is hereditary, they might take away the patients’ hope of becoming normal again. The offspring could also be scared that they might one day come to suffer from a psychiatric disorder. When I was young, the narrative was that 10% of children with a parent with schizophrenia would become schizophrenic, and people were understandably worried that they might be next.

This is not a thing of the past. One of my colleagues, Danish filmmaker Anahi Testa Pedersen, got the erroneous diagnosis schizotypy when she became stressed over a difficult divorce. Many years later, she became enraged when she received a phone call from researchers who wanted to examine her daughter for any possible symptoms arguing that psychiatric disorders are hereditary.

If instead the psychiatrists focused on the environment the patients live in and the traumas they have experienced, there would be hope of recovery, as the environment can be changed and as the traumas can be treated with psychotherapy.

The textbooks did not pull any punches. They spoke of breakthroughs using genome wide association studies,16:27,16:209,17:308 but there are none. For schizophrenia and similar disorders, each of the several hundred genes identified contribute very little,18:94 and together, the many loci explain only about 5% of the so-called heritability.16:210 For ADHD, it was the same. Many different genes have been found, each of which contributes very little.18:229

Nonetheless, the psychiatrists propagated the myth of heritability. They did this by quoting twin studies, which are a very soft type of science that has produced unreliable results. The psychiatrists used what I have called the UFO trick.26 It is very common in science to mislead your readers this way, and it is all about not losing power and prestige and being forced to admit that you were wrong. If you use a fuzzy photo to “prove” you have seen a UFO when a photo taken with a strong telephoto lens has clearly shown that the object is an airplane or a bird, you are a cheat. When genetic studies have come up empty handed, there is no reason to pollute psychiatric textbooks with fuzzy articles about twin studies, and no reason to read about them.

The fundamental problem with twin studies is that hereditary and environmental factors cannot be separated, not even when some of the twins have been adopted and grow up in another family. The “equal environment assumption” is simply not tenable.27

The 1990 Minnesota Study of Twins Reared Apart (MISTRA) illustrates the issues. It is an influential piece of heritability research.28 Published in Science, it is heavily cited as one of five essential studies that examined monozygotic (MZA, or identical) twins who were considered to have been raised separately from each other. MISTRA focused on the intelligence quotient (IQ), and the researchers concluded that intelligence is highly heritable and that very little of it is due to upbringing or environment.

In 2022, 32 years later, this study was debunked.29 The MISTRA publications had left out critical data. When these data were included, MISTRA failed to demonstrate that IQ is hereditary.

One of the main problems was that the control group—reared-apart dizygotic (DZA, or fraternal) twins—was omitted from the publication. Obviously, if MZA twins have similar IQs, but DZA twins have not, it will lend credence to the notion that IQ is hereditary. The researchers wrote themselves in Science that using MZA and DZA twin pairs “provide the simplest and most powerful method for disentangling the influence of environmental and genetic factors.”

They even noted that this aspect of their research made it superior to previous research. So why did they not include the DZA data? They claimed that this was due to space limitations and the small sample size. None of this was correct, and the sample size was very large for such studies and more than sufficient.

The likely reason for the omission is that when the data from both sets of twins are included, there are no significant differences between the groups, and the whole argument therefore falls apart.29 If the average MZ correlation does not exceed the DZ correlation for a particular trait, a genetic influence hasn’t been demonstrated.

Amazingly, later publications from the MISTRA group even found that the fraternal twins were more similar than the identical twins, but the researchers dismissed this finding in a footnote, calling it “sampling variability.”28 This is likely correct but the researchers prevented critics from reviewing their data, ensuring that no one would be able to test whether their conclusions were warranted.

This looks like fraud. Here is a telling table with the correlations from the 2022 re-analysis of the data that had become available:

74 MZA pairs 52 DZA pairs P-value
Wechsler (WAIS) IQ correlations 0.62 0.50 0.17
Raven’s Progressive Matrices IQ correlations 0.55 0.42 0.18


There are many important limitations of twins reared apart studies, including:29

  1. Twins aren’t actually separated at birth. In these studies, 33% were separated after a year or more spent growing up together;
  2. 75% of the pairs of twins still had contact with each other while growing up;
  3. More than half (56%) were raised by a close family member;
  4. In 23% of cases, the twins ended up being raised together again at some point or lived next door to each other.

One of the most serious limitations of such studies is that the twins were not randomly selected or followed from birth. Instead, the participants were adults who had already reconnected with each other, noticed similarities, and decided to participate in a study demonstrating heritability. In many cases, these twins ended up in the study after already being promoted in the media as being remarkably similar. This means that the participants were a self-selected group of people who had found themselves similar, who had been in contact with each other, and were usually not fully raised apart.

With a few exceptions, the psychiatry textbook authors swallowed it all, without any critical reflections. Here are some examples of what the textbooks say:

For schizophrenia and similar disorders, the risk ratio is 50 times higher for an identical twin than for other people;16:207 the heritability is 80%18:94,19:225 but the concordance rate in monozygotic twins is only 50%.19:225 It defies reason how the heritability can be bigger than that found in monozygotic twins, which are 100% identical.

Another book mentioned that a Finnish study contradicted these results.17:41 According to the book, it found that adopted children with a parent with schizophrenia only had an increased risk if they were adopted into a dysfunctional family. The Finnish paper is difficult to read,30 but it clearly shows that it is important if there are mental health issues in the adopting family.

For affective disorders (depression and mania), the concordance was claimed to be 75% for monozygotic and 50% for dizygotic twins in one book,18:113 but only 33% was reported for depression in another book.16:261

For bipolar, 80% of the cases were explained by genetics;16:294 for autism and ADHD 60-90%;20:11,20:467,18:229,17:612 and for obsessive compulsive disorder (OCD) 50%.20:482

I do not deny that, to some extent, the way we think and behave are in our genes. During evolution, natural selection has favoured the survival of people who, in situations of danger or stress, behaved in a way that increased their chance of survival. Thus, personality traits are partly hereditary, and it is unsurprising that if a boy in a family is energetic and impatient, the chance that his brother is also energetic and impatient is above average, and both of them might get a diagnosis of ADHD.

This does not make ADHD hereditary, however. ADHD is not something that exists in nature and can be photographed like a giraffe or a cancer can. It is a social construct, which people, including psychiatrists, usually forget. One textbook noted, for example, that women with ADHD are hit harder than men by ADHD in adulthood.17:612 The ghost has come to life and is now a real thing that can hit people like a car.

We should abandon such misconceptions. I therefore avoid using the expression “people with ADHD” and say “people with a diagnosis of ADHD.”

One of the times I lectured for the organisation Better Psychiatry, a woman in the audience said: “I have ADHD,” to which I replied: “No, you haven’t. You can have a dog, a car, or a boyfriend, but you cannot have ADHD. It is a social construct.”

I explained it is just a label. People tend to think they get an explanation for their troubles when psychiatrists give them a name, but this is circular reasoning. Paul behaves in a certain way, and we will give this behaviour a name, ADHD. Paul behaves this way because he has ADHD. It is impossible to argue this way.

I often joked during my lectures that we also need a diagnosis for those children who are too good at sitting still and not make themselves seen or heard in class. This became true, with the invention of the diagnosis ADD, attention deficit disorder, without the hyperactivity.

From that day on, I have joked about how long we shall wait before we will also see a diagnosis for those in the middle. Then there will be a stimulant drug for everyone, and the drug industry will have reached its ultimate goal, that no one will escape being drugged.

Schizophrenia and related disorders

Since schizophrenia does not seem to be hereditary, I was interested in seeing what the textbooks said about environmental factors.

As causal factors, the textbooks noted prenatal complications, birth complications, neuro-infections,18:94 hashish,17:308 traumatic life events,16:207,16:232,17:329 acute stress,16:232 lithium poisoning, malignant neuroleptic syndrome, serotonin syndrome,16:78 and abstinences after alcohol, benzodiazepines and gamma-hydroxybutyric acid (fantasy, a drug of abuse).16:78

What is more interesting is what the psychiatrists did not mention. Psychosis pills can cause psychosis, known as supersensitivity psychosis or oppositional tolerance.4:45,31 The drugs decrease dopamine levels, and the number of dopamine receptors goes up to compensate for this. If the drugs are suddenly stopped, which patients often do because they tolerate them poorly, the response can be a psychosis. A psychosis can even develop during continued treatment because of this and may not respond to increased dosages.32 Depression pills33 and ADHD pills34 can also cause psychosis (severe mania is a psychosis) but this was not mentioned either in the textbooks.

Traumas play a major role for the development of psychosis, but the textbooks generally ignored this. A typical example is a textbook that claimed 80% hereditability of schizophrenia while there was no numerical estimate for the role of traumas.19:225 Only one textbook offered a risk estimate, which was a four times higher risk if the patient had suffered from physical or psychological abuse.16:207

The science is clear. A paper that analysed the 41 most rigorous studies found that people who had suffered childhood adversity were 2.8 times more likely to develop psychosis than those who had not (P < 0.001).35 The P-value is the probability of getting such a result, or an even larger number than 2.8, if there is no relationship, which in this case is less than one in a thousand. Nine of the ten studies that tested for a dose-response relationship found it.35

Another study found that people who had experienced three types of trauma (e.g. sexual abuse, physical abuse, and bullying) were 18 times more likely to become psychotic than non-abused people, and if they had experienced five types of trauma, they were 193 times more likely to become psychotic (95% confidence interval 51 to 736 times, which means that we are 95% confident that the true risk lies within this interval).36

Such data are very convincing unless you are a psychiatrist. A survey of 2,813 UK psychiatrists showed that for every psychiatrist who thinks schizophrenia is caused primarily by social factors there are 115 who think it is caused primarily by biological factors.37 Accordingly, one textbook noted that schizophrenia (and autism and ADHD) are neurodevelopmental disorders, characterised primarily by biological risk factors, and not primarily by psychosocial risk factors and stressful events in childhood.19:51

One textbook noted that the intelligence quotient (IQ) of patients with schizophrenia was about one standard deviation below normal, on average, and it attributed this to brain defects caused by the disease as well as sequelae in the form of impaired social contact and disturbed educational course.18:84

This is a considerable impairment of the intelligence. The normal quotient is 100 and one standard deviation below normal is 85. There were no references and no reflections if this result came from patients who had been treated with psychosis pills, in which case the low IQ could be a result of drugging the patients, making it difficult for them to think and concentrate.

I therefore investigated this. I googled IQ risk of schizophrenia, and the top record was all I needed.38 It was a study of 50,087 18-year-old males conscripted into the Swedish army who were followed up for 13-14 years. During this period, 195 of them had been admitted to hospital with schizophrenia. According to the abstract of the study, “The distribution of scores in those later diagnosed as suffering from schizophrenia was shifted in a downward direction, with a linear relationship between low IQ and risk. This remained after adjustment for potential confounders.” The authors concluded that “The results confirm the importance of low intellectual ability as a risk factor for schizophrenia and other psychoses.”

The abstract was dishonest and did not reflect what the study showed. In the main text, the authors wrote that “The positive predictive value for low IQ is poor with below average IQ (< 96) predicting only 3.1% of cases.” I don’t know where they got the 3.1% from, and in a table, the predictive values were much lower, e.g. 1.3% for those with an IQ below 74 and 0.6% for those with an IQ between 74 and 81, and also for those with an IQ between 82 and 89, and between 90 to 95.

The odds ratio for developing schizophrenia based on the IQ score was only 1.27 (1.19 to 1.36). This is a very small increase in risk, which, moreover, was inflated by confounders. The authors adjusted their analyses for socio-economic status, behavioural and school adjustment, drug abuse, urban upbringing, family history of psychiatric disorder and psychiatric disturbance at the time of testing. This led to notable reductions in the odds ratios for all four subscales of the IQ test, but the authors nonetheless claimed that the overall odds ratio was 1.28 after the adjustment. This seems to be a mathematical impossibility.

The authors did not report what the average IQ was for patients with schizophrenia but it was easy to calculate, as they showed a table with numbers in nine different IQ groups. The lowest was < 74 and the highest was > 126, but whether I used 70 and 130, respectively, for these extreme groups, or 65 and 135, I got the same result. The average IQ was 95, or very close to normal.

The textbook claimed that the average IQ was 85.18:84 This supports my suspicion that these patients were likely incapacitated by psychiatric drugs when they were subjected to the IQ test.

A final question bothers me. What did the textbook authors want to achieve by claiming that people with schizophrenia were dumb? What is the relevance of this for future clinicians? None. It is likely that such information will worsen the stigma these patients are exposed to in psychiatry.7:183

It is often assumed that biological or genetic explanations of mental illness increase tolerance towards psychiatric patients by reducing notions of responsibility and blame.39 The core assumption of anti-stigma programmes is that the public should be taught to recognise the problems as diseases, and to believe they are caused by biological factors like a chemical imbalance, brain disease, and genetic factors. However, studies have consistently found that this disease model increases stigmatisation and discrimination. A systematic review of 33 studies found that bio-genetic causal attributions were related to stronger rejection in most studies examining schizophrenia.39

The biological approach increases perceived dangerousness, and fear and desire for distance from patients diagnosed with schizophrenia because it makes people believe the patients are unpredictable.39-42 It leads to reductions in clinicians’ empathy and to social exclusion.43 It also generates undue pessimism about the chances of recovery and reduces efforts to change, compared to a psychosocial explanation. It is therefore not surprising that participants in a learning task increased the intensity of electric shocks more quickly if they understood their partner’s difficulties in disease terms than if they believed they were a result of childhood events.41

Many patients describe discrimination as more long-lasting and disabling than the psychosis itself, and it is recognised as a major barrier to recovery.40,41 Patients and their families experience more stigma and discrimination from mental health professionals than from any other sector of society, and there are good explanations for this. For example, over 80% of people with the schizophrenia label think that the diagnosis itself is damaging and dangerous, and some psychiatrists therefore avoid using the term schizophrenia.41

In contrast to the psychiatric leaders, the public is firmly convinced that madness is caused more by bad things happening than by genetics or chemical imbalances.41 This lucidity is remarkable, given that more than half the websites about schizophrenia are drug-company funded. The public also sees psychological interventions as highly effective for psychotic disorders (which they are, see Chapter 7), whereas psychiatrists opine that if the public’s mental health literacy isn’t improved, it may hinder acceptance of evidence-based mental healthcare (which means drugs).

As I shall explain later, the spending of enormous amounts of money—largely by drug companies—to teach the public to think more like biologically oriented psychiatrists has had these outcomes: more discrimination, more drugs, more harms, more deaths, more people on disability pension, and greater costs for society.


To see the list of all references cited, click here.


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.

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