Nuclear Genetics

As most readers are aware, it is widely believed that both within and without of psychiatry genetic factors play an important role in causing major psychiatric disorders such as schizophrenia, bipolar disorder, major depression, ADHD, autism, anxiety, and even post-traumatic stress disorder (PTSD). Twin studies provide the main pillar of support for this belief which is often, though mistakenly, presented as a scientific fact.

As the schizophrenia/psychosis recovery research continues to emerge, we discover increasing evidence that psychosis is not caused by a disease of the brain, but...

“The substantial hereditary component in schizophrenia,” a pair of researchers wrote in 1993, “is surely one of the two or three best-established facts in psychiatry.” But is it really? For mainstream psychiatry and psychiatric genetics, schizophrenia is “a severe mental disorder with a lifetime risk of about 1%, characterized by hallucinations, delusions and cognitive deficits, with heritability estimated at up to 80%,” or a “highly heritable neuropsychiatric disorder of complex genetic etiology.” Many commentators have challenged these claims, and some have challenged the concept of schizophrenia itself.

While a great deal of the excitement about advances in psychological treatments comes from the potential for research in neuroscience to unlock the secrets of the brain, many mental health experts would like to temper this enthusiasm. A special issue of the Behavior Therapist released this month calls into question the predominant conception of mental illnesses as brain disorders.

In a study released June 6, 2012 through the online journal Behavioral and Brain Functions, researchers from Japan acknowledge that "the results of association...

Research from the Semel Institute for Neuroscience and Human Behavior at USC finds that "The standard concept of genetic testing includes at least three...

The candidate-gene approach to depression goes unsupported and is likely based on bad science, new research finds.

Psychiatric molecular genetic research has failed to discover genes that underlie the major psychiatric disorders, the existence of which twin and adoption studies are assumed to have established. "Genome-wide complex trait analysis" (GCTA) was developed a few years ago as a means of solving what researchers call the "missing heritability" problem. One researcher believed that the new GCTA method would “drive a stake through the heart of” criticism of behavioral genetic theories and methods, and would finally put criticism of twin studies “to rest.” The opposite scenario appears to be playing out, however, as leading behavioral genetic and psychiatric genetic researchers struggle to prevent some recent negative GCTA findings and the obvious false assumptions underlying twin research from driving a stake through the heart of twin studies themselves.

The March 3^rd, 2016 edition of the Wall Street Journal featured an article by past President of the American Psychiatric Association (APA) Jeffrey Lieberman and his colleague, computational neuroscientist Ogi Ogas. The article was entitled “Genetics and Mental Illness—Let’s Not Get Carried Away.” In their piece, the authors started by expressing the belief that a recent study identified a gene that causes schizophrenia, and then discussed whether it is desirable or possible to remove allegedly pathological genes in the interest of creating a future “mentally perfect society.” The authors of the article, like many previous textbook authors, seem unfamiliar with the questionable “evidence” put forward by psychiatry as proof that its disorders are “highly heritable” In fact, DSM-5 Task Force Chair David Kupfer admitted that “we’re still waiting” for the discovery of “biological and genetic markers” for psychiatric disorders.

In this article I will attempt to debunk one of the great “scientific” smoke and mirrors shows of the past half century—the claim that stories of reunited separated MZ (monozygotic, identical) twin pairs indicate that heredity plays a major role in causing human behavioral differences. These stories, which are often used to sell the false ideology of genetic determinism, have entered the public imagination in a way that academic research results never could. Here I will show that these stories provide no evidence whatsoever that (as yet undiscovered) “genes for behavior” influence human behavioral development.

In recent months, two teams of researchers in the UK and the US published complementary findings about the epigenetic origins of schizophrenia that have scientific communities who indulge in ‘genetic conspiracy theories’ abuzz. While these results are intriguing, and no doubt involve pathbreaking research methodologies, this line of thought represents a decontextualized understanding both of the symptoms that are typically associated with schizophrenia, and their causes.

On November 12, 2013, Molecular Psychiatry published online Evidence That Duplications of 22q11.2 Protect Against Schizophrenia, by Rees et al. The print version was published last month – January 2014. The idea of a genetic mutation that would protect one from schizophrenia aroused a good deal of interest and enthusiasm. The paper has added some impetus to psychiatry's claim that the condition known as schizophrenia is a genetic disease. For this reason, I thought it might be helpful to take a closer look at the study.

More than forty thousand papers have been published using functional magnetic resonance imaging (fMRI) technology to explore the brain. A new analysis of the common...

Human behavioral genetics and its allied field of psychiatric genetics are in trouble, as unfulfilled gene discovery expectations during the “euphoria of the 1980s” have continued to the present day, leading to researchers’ “nonreplication curse” dysphoria of the 2010s. In my recent book The Trouble with Twin Studies: A Reassessment of Twin Research in the Social and Behavioral Sciences, I presented a detailed argument that genetic interpretations of the common “classical twin method” finding that reared-together MZ twin pairs resemble each other more (correlate higher) for behavioral characteristics than do reared-together same-sex DZ twin pairs are invalid because, among other reasons, the twin method’s crucial MZ-DZ “equal environment assumption” (EEA) is false.

A large and rigorous meta-analysis fails to find support for the gene-environment interaction theory of depression.

In the light of the much trumpeted claims that recent research has identified genes for schizophrenia, it is important to review the track record of this type of endeavor. Despite thousands of studies costing millions of dollars, and endless predictions that the genetics of schizophrenia would shortly be revealed, the field has so far failed to identify any genes that substantially increase the risk of developing schizophrenia.

Biologists found that exposure to antidepressants suppresses important survival behaviors in zebrafish, an effect that persisted across three generations and was found to be more severe for males.

According to a leading group of psychiatric genetic researchers, writing in 1999, “From the perspective of psychiatric genetics, the Human Genome Project is an immense factory producing and refining the tools we will need to discover the genes that cause mental illness.” A 2002 “speculative outline” by a group helping to revise the DSM envisioned a future DSM-5 practice of classifying disorders on the basis of "the patient’s genotype, identifying symptom- or disease-related genes, resiliency genes, and genes related to therapeutic responses and side effects to specific psychotropic drugs.” A dozen or so years ago, at least some of the DSM-5 architects believed that genes would at long last be identified and would be integrated into the next version of the DSM. As we know, this did not happen.

Attempting to locate the mechanisms of psychiatric disorder is a step in the wrong direction and fails to challenge potentially unjust social practices.

A recent commentary by Ganesan Venkatasubramanian and Matcheri Keshavan notes that efforts to identify biomarkers in people diagnosed with psychiatric disorders have been overwhelmingly...

A new study out of Yale University uses evolutionary biology to debunk the idea that there is a “normal” or “optimal” brain.

The National Institute of Mental Health (NIMH) is increasingly shifting its research emphasis toward attempting to uncover biomarkers for “mental diseases,” which may have dramatic consequences for research and training in clinical psychology. In an article to be published in next month’s Professional Psychology: Research and Practice, Marvin Goldfried outlines how the shift in funding priorities for psychological research is tied to the needs of pharmaceutical companies and the biological model in psychiatry.

Some researchers have been arguing to reclassify all psychiatric disorders as diseases of the brain and nervous system, similar to epilepsy or Parkinson's disease. Neuroimaging research, however, reveals that psychiatric disorders appear to be distinct from neurological disorders, according to a new study published in this month’s issue of the British Journal of Psychiatry.

Acknowledging that current depression treatments are failing many people, researchers from Michigan State and MIT have developed a new model for understanding how multiple psychological, biological, social and environmental factors contribute to depression.

A new study, published in the journal Molecular Psychiatry, found no link between genetics and the occurrence of depressive symptoms.