Putting JAMA Psychiatry and MIA to the Genetic Test

Defenders of psychiatry, who like to tell of “evidence-based” practices, regularly describe critics of psychiatry as “biased,” or of “cherry-picking” the data, or of how such criticisms arise from those who are “antipsychiatry,” and thus are motivated by a hostility toward the profession. Mad in America is often characterized in this way, and on a personal level, I have heard such comments since I published my first book on this topic (Mad in America in 2002.)

I mention this because a recently published “Viewpoint” in JAMA Psychiatry provides an ideal way to put this criticism to the test, and elucidate what we do.

Over the past ten years, we have published reviews of numerous peer-reviewed articles that have concluded there is little evidence that schizophrenia is a “genetic” disease, and that, in fact, genetics account for very little of the “risk” for being so diagnosed. On January 20 of this year, we published an MIA Report, written by Peter Simons, our front-page editor and long-time science writer, that provided an exhaustive review of the search for the genetic causes of schizophrenia, and the title neatly summed up the bottom line: “Searching for the Psychiatric Yeti: Schizophrenia Is Not Genetic.”

However, in the February 28 online issue of JAMA Psychiatry, Kenneth Kendler—who is one of the most prominent psychiatric researchers in the world—presents an argument that genetic research provides “robust” evidence that there are “causal pathways to psychiatric illness” in the brain. He writes:

Thus, you can see, in our MIA Report and Kendler’s piece, two discordant conclusions regarding research on the “genetics” of schizophrenia. And here is the opportunity: if we review the evidence that is present in each of these two publications, we can assess whether Mad in America readers—or JAMA Psychiatry readers—are being provided with the most robust, and up-to-date, review of the scientific literature.

The Journalistic Roots of Mad in America

As background to this question, it is important to understand the journalistic roots of Mad in America. Those roots go back nearly 25 years, back to when I published Mad in America, my first book on the subject. Knowing this history can help readers understand what we do, and why.

At that time, psychiatry was telling a story of great advances in understanding the biological causes of schizophrenia and of drug treatments for the “disease.” In Mad in America, I sought to see if that narrative of great scientific discovery was supported by the science.

The narrative of advance took flight in 1980, when the American Psychiatric Association published the third edition of its Diagnostic and Statistical Manual (DSM III). As Nancy Andreasen declared in her 1984 book The Broken Brain, the conception present in DSM III was that “the major psychiatric illnesses are diseases. They should be considered medical illnesses just as diabetes, heart disease and cancer are. The emphasis on this model is on carefully diagnosing each specific illness from which the patients suffers, just as an internist or neurologist would.”

Soon, the public began hearing about how the different disorders were caused by specific chemical imbalances in the brain. Depression was due to low serotonin, schizophrenia to too much dopamine, and ADHD to not enough dopamine. This was a story of diagnoses that had been proven to be brain diseases—the pathology of these major disorders had been found.

In 1995, the editors of the American Journal of Psychiatry wrote that DSM diagnoses had been “validated by clinical description and epidemiological data . . . The validation of psychiatric diagnoses establishes them as real entities.”

A few years later, APA president Carolyn Rabinowitz was even more emphatic. “Mental disorders are [now] recognized as real illnesses,” she said, adding that just “as cancer is highly treatable and can be cured, we are experiencing a similar success in psychiatry.”

All of this told of great medical progress. Prozac was introduced into the market in 1988, touted as a “breakthrough medication,” and other companies soon produced me-too SSRIs. Then, in the mid-1990s, atypical antipsychotics arrived on the market, which were also heralded as “breakthrough medications.” The new drugs were touted as medicines that “fixed the chemical imbalances that cause schizophrenia, depression and other major disorders,” and thus were “like insulin for diabetes.”

Here is how the Los Angeles Times described the therapeutic advance provided by the new atypical antipsychotics: “It used to be that schizophrenics were given no hope of improving. But now, thanks to new drugs and commitment, they are moving back into society like never before.”

Given the complexity of the human brain, this was a story of arguably the greatest advance in the history of medicine. The pathology of major disorders was now known, and researchers had produced drugs that “fixed” that pathology.

That was the story I was told in 1998, when I co-wrote a series for the Boston Globe on abuses of patients in research settings. The experts I interviewed, including future American Psychiatric Association president Jeffrey Lieberman, all told me that schizophrenia was due to a dopamine hyperactivity in the brain, and that antipsychotics, by blocking dopamine transmission, helped remedy that abnormality. Again and again, I heard the refrain “like insulin for diabetes.”

When I researched Mad in America, I investigated the truth of that story in a simple way. I sought to see if the scientific literature supported it. Here was the crux of that investigation:

• Was there evidence that the introduction of antipsychotics in asylum medicine in the 1950s had led to a marked improvement in outcomes for those diagnosed with schizophrenia?
• Was there evidence that schizophrenia had been validated as a discrete disorder?
• Was there evidence that it was due to a chemical imbalance in the brain?
• Was there evidence that the atypical antipsychotics were breakthrough medications that provided a dramatic upgrade over the first-generation antipsychotics?

I immersed myself in the scientific literature, starting with the introduction of antipsychotics into asylum medicine in 1955. The research record told of the following:

• There was no evidence that schizophrenia outcomes improved following the introduction of antipsychotics. Indeed, in a prominent study that addressed this question, researchers reported that psychotic patients treated in 1967 with antipsychotics relapsed more frequently than a similar cohort treated in 1947 and were much more socially dependent.
• With questions swirling about the merits of these drugs, the NIMH funded three studies in the 1970s that sought to assess the impact of antipsychotics over longer periods of time (one to three years.) All reported superior outcomes for the cohorts treated without antipsychotics, or with a selective-use model that minimized their use.
• As a result, leading figures at the NIMH worried that neuroleptics might be worsening long-term outcomes. Jonathan Cole, who had been the director of the NIMH’s Psychopharmacology Service Center, co-authored a paper titled “Maintenance Antipsychotic Therapy: Is the Cure Worse Than the Disease?” William Carpenter, who had conducted one of the three studies, raised the possibility that the drugs induced a change in the brain that made patients more biologically vulnerable to psychosis than they would have been in the “normal course” of the disease.
• Two Canadian researchers then provided a biological explanation for why that appeared to be so. Antipsychotics blocked dopamine receptors in the brain, and in response, the brain’s postsynaptic neurons, in an effort to maintain a homeostatic equilibrium, increased the density of their receptors for that molecule. Antipsychotics, they wrote, induced a “dopamine supersensitivity” that could lead to more frequent and severe psychotic symptoms.

That history told of how antipsychotics were not improving long-term outcomes for those diagnosed with schizophrenia or other psychotic disorders. Researchers were also failing to find evidence that schizophrenia was caused by a lesion in the dopaminergic system. In 1994, John Kane, a prominent schizophrenia researcher, confessed that “a simple dopaminergic excess model of schizophrenia is no longer credible.”

Finally, I used a Freedom of Information request to get copies of the FDA’s reviews of risperidone, olanzapine, and quetiapine (the atypical antipsychotics.) Those reviews told of how the clinical trials of the new drugs had been “biased by design” to make them look good in comparison to the first-generation antipsychotics. As such, the FDA reviewers concluded there was no evidence they were more effective or had fewer adverse effects than the older drugs.

As for schizophrenia being validated as a discrete disorder, Nancy Andreasen, who was then editor-in-chief of the American Journal of Psychiatry, aptly summed up the state of uncertainty in research circles at the close of the 1990s: “Someday in the twenty-first century, after the human genome and the human brain have been mapped, someone may need to organize a reverse Marshall Plan so that the Europeans can save American science by helping us figure out who really has schizophrenia or what schizophrenia really is.”

Mad in America presented readers with a “counter-narrative” that told of how psychiatry’s own research, which could be dug out from the research literature, did not support the story of great progress that psychiatry had been telling the American public ever since it published DSM III. There was an extraordinary gap between what the profession was telling the public and the story that was present in the research literature.

That was the journalistic principle present in Mad in America: my job was to make known the science, and document that gap between the science and the story being told to the public.

The Test of Mad in America

As might be expected, I did experience some harsh criticism from those within the psychiatric field after Mad in America was published. E. Fuller Torrey quickly turned to the Scientology slur, that it seemed that I had fallen under the influence of Scientologists. Another review called it one of the most “disingenuous books” ever written, stating that it was impossible to claim that antipsychotics had not dramatically improved the lives of those with schizophrenia.

As the book did provide a counter-narrative to the story of great advances in psychiatry, there were two possibilities that awaited. One was that new studies would be reported that validated the story of great progress that had been told to the public. Perhaps there would be new findings of dopaminergic lesions in the brain and evidence that the second-generation antipsychotics minimized the harmful effects of those lesions. And perhaps studies of the longer-term outcomes of schizophrenia patients would show that antipsychotic use led to much higher recovery rates.

The other possibility was that the science of the past would prove predictive of the science of the future, and the great advance story would finally come tumbling down, with leaders in the field acknowledging that to be so.

A quick review can tell which of those two possibilities came true.

1) The validity of DSM diagnoses

There is now widespread acknowledgement that research since 1980 failed to validate the diagnostic categories in the DSM. Such confessions have come from Allen Frances, who was the chair of the DSM-IV task force; Nancy Andreasen, editor-in-chief of the American Journal of Psychiatry, and former NIMH director Thomas Insel, among others. My favorite quote comes from Nassir Ghaemi, at the Tufts Medical School Department of Psychiatry, who wrote in 2013:

Former NIMH director Steven Hyman was equally succinct: The DSM is “totally wrong . . . an absolute scientific nightmare.”

2) The chemical imbalance theory of mental disorders

Although the public was stunned in 2022 when Joanna Moncrieff and colleagues reported that there was no good evidence for the low serotonin theory of depression, leading figures in American psychiatry, in their own textbooks and publications away from the public glare, had long since admitted that there was a lack of evidence that supported the chemical imbalance theory. Such declarations can be found in the American Psychiatric Association’s 1998 Textbook of Psychiatry, in Stephen Stahl’s 2000 Essential Psychopharmacology, in Steven Hyman’s 2001 book Molecular Neuropharmacology, in a 2010 paper by Eric Nestler, in a 2011 blog by NIMH director Thomas Insel, and, most famously, in a blog that same year by Ronald Pies, editor of Psychiatric Times. He wrote that the chemical imbalance “notion was always a kind of urban legend—never a theory seriously propounded by well-informed psychiatrists.”

The most succinct epitaph for this research came from Kendler, co-editor in chief of Psychological Medicine, in 2005: “We have hunted for big simple neurochemical explanations for psychiatric disorders and not found them.”

3) The superiority of atypical antipsychotics

Once olanzapine and risperidone came to market, studies that weren’t funded by the pharmaceutical companies quickly challenged the “better than the old drugs” claim. A 2000 review of 52 randomized trials concluded that “there is no clear evidence that atypical antipsychotics are more effective or are better tolerated than conventional antipsychotics.”  A  2003 review by researchers at the US Department of Veterans Affairs found that olanzapine did “not demonstrate advantages” compared with haloperidol in “compliance, symptoms, extrapyramidal symptoms, or overall quality of life.” Then, in 2005, the CATIE bombshell landed.

CATIE was a NIMH study that randomized schizophrenia patients either to one of four atypicals or to an older, low-potency antipsychotic, perphenazine. At the end of 18 months, there was no significant difference between the older drug and three of the four atypicals (olanzapine was seen as slightly better than perphenazine.) Even more worrisome, neither the new drugs or the old drug could be said to work, as 74% of the 1,432 patients were unable to stay on the medications to the end of the trial, mostly because of their “inefficacy or intolerable side effects.” All of this led two British researchers, Peter Tyrer and Tim Kendall, to write in Lancet of the “spurious advance of antipsychotic drug therapy.”

That piece was published in 2009. While the research community may finally have had the scales removed from their eyes, readers of Mad in America had long known of this “spurious invention of the atypicals.” The evidence was there all along in the clinical trial reports that had been submitted to the FDA by the makers of these drugs in the 1990s.

4) On the long-term impact of antipsychotics

As those elements of the “great advance” narrative fell apart, the field still remained insistent that antipsychotics provided a long-term benefit and were an essential treatment for those diagnosed with schizophrenia. That belief remains. The drugs “reduce the risk of relapse,” and maintenance treatment remains the standard of care.

However, the scientific literature continued to tell a different story.

There were two NIMH-funded research projects that most powerfully countered that mainstream belief. The first was the longitudinal study conducted by Martin Harrow and Thomas Jobe. In the late 1970s and early 1980s, they enrolled 200 psychotic patients, most of whom were suffering either a first or second episode of psychosis, into their study. At the end of 15 years, they still had 145 in their study: 64 with a diagnosis of schizophrenia and 81 with milder forms of psychosis. In 2007, they reported that the recovery rate at the end of 15 years was eight times higher for those off antipsychotic medication than for those on the drugs.

“I conclude that patients with schizophrenia not on antipsychotic medication for a long period of time have significantly better global functioning than those on antipsychotics,” Harrow told the audience at the 2008 annual meeting of the American Psychiatric Association.

The same was true for those with milder psychotic disorders. Those who stopped taking antipsychotics had significantly better outcomes. And perhaps most notable of all, those diagnosed with schizophrenia who stopped taking antipsychotic medication had better long-term outcomes than those with milder disorders who continued taking the drugs.

 

Over the next decade, Harrow and Jobe continued to document this disparity in outcomes related to antipsychotic use, and as they did so, they returned to the dopamine supersensitivity theory for why this might be so. “How unique among medical treatments is it that the apparent efficacy of antipsychotics could diminish over time or become ineffective or harmful,” they wrote in 2013. “There are many examples for other medications of similar long-term effects, with this often reoccurring as the body readjusts biologically to the medications.”

The other research project that so upset conventional wisdom was Nancy Andreasen’s MRI study, which charted changes in brain volumes in 542 first-episode schizophrenia patients. In 2003 and 2005, she reported that there was a “progressive reduction in frontal white matter volume” over time, and that this shrinkage was associated with a worsening of negative symptoms, functional impairment, and cognitive decline.

In those reports, she attributed this shrinkage to the disease, describing schizophrenia as a “progressive neurodevelopmental disorder” that antipsychotics unfortunately failed to arrest. However, a study in macaque monkeys had found that such shrinkage was drug-caused, and in 2011, Andreasen reported that the drugs indeed had this effect. The first-generation antipsychotics, the atypicals, and clozapine were all “associated with smaller brain tissue volumes,” and such shrinkage was dose-related, she wrote.

Her research powerfully revealed an iatrogenic process at work. Antipsychotics block dopamine activity in the brain and this leads to brain shrinkage, which in turn is associated with a worsening of negative symptoms, functional impairment, and cognitive function.

There are a number of other studies that could be cited today as evidence that antipsychotics worsen long-term outcomes and reduce recovery rates. Indeed, in 2013, Finnish investigators published a systematic review of historical recovery rates for schizophrenia patients, and their data showed that they had steadily declined since the introduction of antipsychotics, and notably so since the introduction of atypicals in the mid-1990s, with the recovery rate dropping to 6%, the lowest it has ever been.

The American Psychiatric Association and “thought leaders” in American psychiatry have mostly avoided addressing this research, or, if so, they have sought to discount it. However, in 2012, the British Journal of Psychiatry, in an editorial by Peter Tyrer titled “The End of the Psychopharmacology Revolution,” stated that the time had come to rethink the use of antipsychotics. He wrote:

Maryland psychiatrist Ann Silver, in a 2009 interview, summed up the change wrought by antipsychotics in this memorable way: “In the nonmedication era, my schizophrenic patients did far better than do those in the more modern era. They chose careers, pursued them, and married. In the [later] era, none chose a career, although many held various jobs, and none married or even had lasting relationships.

The Founding of madinamerica.com

It is not surprising that the story that American psychiatry told to the public during the 1980s and 1990s subsequently fell apart. There were never scientific findings that supported that tale of breakthrough discoveries and treatment, and it is difficult to maintain a false narrative forever.

After Mad in America was published, I wrote two other books of non-fiction, and then in 2010, I published Anatomy of an Epidemic. That book sought to investigate this question: How do psychiatric drugs affect the long-term course of major psychiatric disorders? The public assumption at that time was that they do provide a long-term benefit, and public belief in the chemical imbalance provided a reason that would be true.

However, the short answer to that question is that there is a coherent body of research findings related to four major disorders—schizophrenia, depression, bipolar, and ADHD—that tell of how the medications increase the likelihood that patients will become chronically ill and functionally impaired.

In that book, I also documented how findings that tell of harm done are never promoted to the public by psychiatry or included in psychiatry’s own textbooks. For instance, even today I have never seen any report of Harrow’s longitudinal findings in a major American newspaper.

That absence was a primary motivation for founding madinamerica.com. When Kermit Cole, Louisa Putnam, and I launched the website in January 2012, we wanted it to serve as a forum that would make such research known. We would provide reviews of research findings that weren’t being promoted to the public, and in this manner we would seek to provide the public with “informed consent.”

We have been at this for more than 10 years now, and our science coverage has grown such that we now provide five science reviews per week. We also publish in-depth reports on such scientific findings. You can search through our science archives, and you will find a wealth of research findings that have gone missing from the mainstream media: studies on the long-term outcomes of medicated patients; risks of using antidepressants during pregnancy and possible harm to fetal development; drug withdrawal findings; the lack of validity of DSM diagnoses; the STAR*D fraud; and so forth. The “evidence base” on these topics continues to collect and grow, and we now have a global audience for this information. We had around six million visitors last year, and we now have 15 affiliate “Mad in the World” sites, which increasingly republish our science reviews.

That is the story of what we seek to do with our science coverage. We strive to make known research findings that are missing from the mainstream media and yet need to be known.

Now we can turn to our reporting on the genetics of schizophrenia, which, as I wrote above, can serve as a test of our science coverage on this topic, with Kendler’s piece in JAMA Psychiatry as a foil for comparison.

Kendler’s Viewpoint in JAMA Psychiatry

Kenneth Kendler is the director of the Virginia Institute for Psychiatric and Behavioral Genetics, and a long-time editor of Psychological Medicine. He is known in particular for his research on the genetics of schizophrenia, and as the BJPsych Bulletin noted in 2020, he is the second most highly-cited psychiatric researcher in the world.

He also has been one who, in fact, has poked holes in the story of progress told to the public. As noted above, in 2005, he told of how the search for chemical imbalances in the brain had not born fruit. In a 2021 paper published in JAMA Psychiatry, he added his voice to those who had spoken of how the DSM diagnoses lacked validity.

In his February “viewpoint” published in JAMA Psychiatry, he addressed what he calls a “vexing” question in psychiatry: “Are Psychiatric Disorders Brain Diseases?”

Starting in the 19^th century, he writes, this involved looking for “detectable pathology in the brain.” As no such characteristic pathologies have been found for psychiatric disorders, Kendler argues that way forward for psychiatry is to “turn instead to a more modest but more tractable question—can we show that critical causal pathways to psychiatric illness occur in the brain?”

He then begins his argument with the assertion quoted at the beginning of this essay: “To proceed, I use the most robust empirical findings in all of psychiatry—that genetic risk factors impact causally and substantially on liability to all major psychiatric disorders.”

Kendler cites a 2020 book he co-authored, “How Genes Influence Behavior,” as the source for his assertion. However, in his essay, he also cites a 2022 article by the Schizophrenia Working Group of the Psychiatric Genomics Consortium, which opens with this declaration of fact: “Schizophrenia has a heritability of 60 to 80%, much of which is attributable to common risk alleles.”

With that “fact” as a starting point, Kendler lays out his argument. Many human genes, he writes, are “expressed only in specific tissues, and for a goodly number, only in the brain.” That, he explains, is the case with some risk genes for schizophrenia. In their 2022 report, the Schizophrenia Working Group found that there was an “elevation” in the expression of “schizophrenia-risk genes” in 11 brain tissues, but not in other parts of the human body. As such, Kendler concludes, the field can now “claim that the effect of the strongest known risk factor for schizophrenia—genetics—largely occurs in brain tissue.”

The discordance between Kendler’s viewpoint and our MIA Report is this: Has research shown that genetics is the strongest known risk factor for schizophrenia?

Mad in America on the Genetics of Schizophrenia

During the past decade, Mad in America has published reviews of a number of research findings regarding the genetics of schizophrenia. Peter Simons’ MIA Report was prompted by a recent paper by E. Fuller Torrey, in which Torrey—a prominent promoter of the concept that schizophrenia is a “brain disease”—compared the search for schizophrenia genes to a “wild goose chase.” Twenty-five years of genetics research, Torrey concluded, had failed to find any meaningful genetic associations, with high-profile initial claims of such findings regularly failing to be replicated in further investigations. “Schizophrenia does not appear to be a genetic disorder,” Torrey concluded.

In his MIA Report, Simons detailed Torrey’s review of the genetics research, and then also reviewed many of the research findings that can be found in our science archives on this topic. In particular, he cited studies that assessed the “impact” of risk genes on the likelihood of developing schizophrenia. Here are the principal articles he referred to:

2014: A study in Lancet Psychiatry found that environmental risk factors (i.e., perinatal brain insults, cannabis use, neurotrauma, psychotrauma, urbanicity, and migration) were a “major risk factor for early onset schizophrenia,” while “polygenic genome-wide association study risk scores did not have any detectable effects on schizophrenia phenotypes.”

2015: In Molecular Psychiatry, researchers concluded that “the current empirical evidence strongly supports the idea that the historical candidate gene literature yielded no robust and replicable insights into the etiology of schizophrenia.”

2017: In Biological Psychiatry, researchers concluded that “taken as a group, schizophrenia candidate genes are no more associated with schizophrenia than random sets of control genes.”

2019: Researchers reviewing “genome-wide association studies,” which have found statistically significant associations between large gene sets and a schizophrenia diagnosis, determined that these associations explained 2.28% of the risk that a person will be diagnosed with schizophrenia. That left other risk factors, such as the environment’s impact on biology, emotional trauma, and childhood experiences constituting nearly 98% of the risk. The study was published in Neuropsychopharmacology.

2020: In Schizophrenia Bulletin, researchers reported that sequencing the exome (a particular set of genetic information) provided no clinically relevant data for making a schizophrenia diagnosis. “The main conclusion of this investigation is a negative one,” they wrote. “The diagnostic yield for exome sequencing of known neuropsychiatric genes in this sample is about 1%.”

2020: Researchers from the Netherlands, writing in Schizophrenia Bulletin, reported that familial and environmental factors account for most of the risk of developing schizophrenia, and that genetics constitute a risk factor of about 0.5%

2021: A study of 50,000 people, which was published in the Journal of Affective Disorders, failed to find any genes that influenced mental illness. “The results obtained from this study are completely negative,” the authors wrote. “No gene is formally statistically significant after correction for multiple testing, and even those which are ranked highest and lowest do not include any which could be regarded as being biologically plausible candidates.”

The 2019 study published in Neuropsychopharmacology is of particular relevance here. The authors analyzed data sets produced by the Schizophrenia Working Group of the Psychiatric Genomics Consortium in order to quantify the impact the risk gene variants had on schizophrenia diagnoses. Here is an excerpt of our review of that study, which we published in 2019:

Thus, if you incorporate these findings into Kendler’s argument, you understand that while researchers may have found that there are polygenic variants that are associated with a schizophrenia diagnosis, these gene-mediated pathways in the brain have very little impact on increasing the risk that people will develop schizophrenia. Trauma, public health environments, and other environmental factors have been found to have the biggest impact on “liability” to a schizophrenia diagnosis.

Making Known the Little Known

It is well known that once a scientific finding is embraced as “fact,” a scientific or medical discipline will resist findings that challenge that fact. Cognitive dissonance sets in, and the newer findings are dismissed as flawed in some way, or simply ignored. While the discordant findings may be published, they will likely be given little attention by others, and the corrective they provide to the conventional belief is lost.

For instance, the 2019 study published in Neuropsychopharmacology has been cited only 23 times, with an altmetric score of 18—a low score that tells of it being little discussed. There have been 8,133 people who have “accessed” the article, and there is no account of any media coverage of it. In contrast, Kendler’s essay, which was published only 10 days ago, has an altmetric score of 205 and more than 8,400 have accessed it.

As far as I know, Mad in America is the only “media” that reported on the 2019 article in Neuropsychopharmacology, and our MIA Report is surely the first time the finding has been incorporated into a review article, meant to be accessible to lay readers, on the “genetics” of schizophrenia. Our report, I am pleased to say, has been accessed more than 74,000 times.

And here is why this is important: the corrective to the “fact” that schizophrenia is in large part a “genetic” disease leads to a reconceptualization of the nature of the disorder, and what treatments may be of most help. The genetics conception leads to a search for treatments that can, in some manner, counteract the impact of the “faulty” genes. The conception also suggests it is bound to be a permanent state—you can’t change a person’s genetic makeup when hundreds or thousands of genes are said to confer the increased risk. But if environmental factors confer most of the risk, then it is reasonable to develop treatments that are responsive to those factors. This conception also provides hope for a full recovery from an episode of “schizophrenia.”

As I wrote at the start of this essay, this review could provide a test of whether our science coverage provided readers with a more robust knowledge of the research on the genetics of schizophrenia than the conventional understanding present in the JAMA Psychiatry essay by Kenneth Kendler. And here is the bottom-line difference: Whereas readers of the JAMA Psychiatry essay would be reminded of the “fact” that hereditary factors account for 60% to 80% of the risk for developing schizophrenia, our readers are reminded that studies have found that these gene variants account for perhaps 2% to 3% of the risk.

That’s a notable difference, and that tells of our motivation for reporting on research findings that otherwise would go unnoticed by the general public, and, if truth be told, go unnoticed in most corners of the psychiatric community.