Tag: Behavioral Genetics
In his 2016 book The Gene: An Intimate History, cancer physician and researcher Siddhartha Mukherjee chronicled the initial idea of the gene, taking readers through the history of genetics up to the current “post-genome” period by interweaving science, social history, and his own personal narrative. In the process he documented some of the crimes of the eugenics movement and the monstrous atrocities committed by German National Socialism in the name of eugenics and biology, while noting the Nazi’s promotion of twin research. He also criticized aspects of intelligence testing and genetic theories of racial inferiority based on IQ tests. At the same time, Mukherjee supported and promoted many contemporary behavioral genetics positions.
Children exposed to SSRIs during pregnancy, a recent study shows, were diagnosed with depression by age 14 at more than four times the rate of children whose mothers were diagnosed with a psychiatric disorder but did not take the medication. Such reports are usually met, appropriately, with an outpouring of reassurances from clinicians who take care of pregnant women, who need to protect their emotional wellbeing in whatever way they can. From my perspective as a pediatrician specializing in early childhood mental health our attention must be on prevention.
The wealthy, and the institutions they finance and promote, look favorably upon research whose authors claim that economic disparities are rooted in biology, and are not harmful to humanity as a whole. But there are countless obvious real-world examples showing that political policies, social struggles, and public health programs, including those involving the adjustment of income differences, lead to improved health and well-being.
Psychiatry assumes that individuals who meet its vague criteria for anorexia nervosa have a disease, and the "disease-causing problem" resides in the genome. If we wish to understand what motivates individuals who systematically under-nourish themselves, however, we need to do two things: Abandon the empty, disempowering psychiatric labels, and recognize that it is through the uniqueness of each individual that we come to understand his or her perspective, and second, we need to sit down with the individual in a spirit of trust and collaboration, and listen to his or her concerns.
Antidepressants have been reported to cause a state called “akathisia,” where people feel extremely agitated and restless and may become preoccupied with thoughts of...
The March 3rd, 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.
Stephen Fry’s exploration of manic depression (in the current BBC series on mental health, ‘In the Mind‘) has drawn both praise (because of his attempts to destigmatize mental illness) and criticism (because he appears to have a very narrow biomedical understanding of mental illness). I have sent an open letter to the actor which challenges some of his assumptions about mental illness, and offers a very different understanding to that promoted in his recent television programme.
On January 27, 2016, a study1 was published online in the prestigious journal Nature that touted the possibility of discovering some potential biological origins of an "illness" called "schizophrenia" Subsequently, headlines across the world beamed excited proclamations of the latest breakthrough to occur in psychiatric research. The problem is, there is nothing profound about this study at all and, in fact, it is one of the least profound studies to emerge in the last few years on the topic of "schizophrenia." It ignores the robust support that has accumulated that undermines the genetic disease model of "mental illness" and the categorical understanding of experiences falling under the umbrella term "schizophrenia."
“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.
Although it is axiomatic in psychiatry that genetic factors are involved in bipolar disorder (manic-depression), and that they play a predominant role, there currently exists little if any scientifically acceptable evidence that bipolar disorder and other “affective disorders” are caused by disordered genes. Given almost 50 years of gene discovery claims that were not confirmed by replication attempts, we must assume by default that current gene finding claims are false-positive results as well. In the 1920s, pioneering psychiatric geneticist Ernst Rüdin decided against publishing his large family study of “manic-depressive insanity,” most likely because the results did not fit his theories of Mendelian inheritance, and failed to support his advocacy of eugenic policies.
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.
In a 2013 edition of the Journal of the History of Biology, Norbert Wetzel and I published an article on the Swiss-German psychiatric geneticist Ernst Rüdin (1874-1952) and his close colleagues, and how their work and crimes in the Nazi era have been discussed or ignored by contemporary psychiatric genetic writers and researchers. Here I would like to summarize the main points we raised in that article, and to make several additional observations. Whether Rüdin reluctantly aided and helped implement the “euthanasia” killing program in support of the war effort, or more likely, that he saw it as the crowning achievement of his decades of psychiatric genetic research based on racial hygienic (eugenic) principles, is an issue that may be decided in the future.
In 2000, behavioral geneticist Eric Turkheimer proposed "Three Laws of Behavior Genetics" based on what he saw as the “nearly unanimous results” of behavioral genetic studies of families, twins, and adoptees. However, critics have argued for decades that most behavioral genetic assumptions, models, concepts, “laws,” and “discoveries” do not hold up under critical examination. In 2015, a group of behavioral geneticists proposed an additional “Fourth Law of Behavior Genetics,” which states that behavioral characteristics are associated with many genes of small effect. Here I propose a “Fifth Law” of behavior genetics—actually, the only “law” one needs to know in order to properly understand this field.
The long-running debate on the validity of twin research recently resurfaced in American criminology, and has major implications for behavioral and medical twin research. Most twin researchers and their critics agree that reared-together monozygotic (MZ) twin pairs experience more similar environments than experienced by same-sex dizygotic (DZ) pairs, and we argue that the twin method is therefore unable to disentangle the potential influences of genes and environment on human behavioral differences, a conclusion supported by the failures of molecular genetic research.
A key psychiatric genetic concept is heritability. The concept was originally developed as a tool to help predict the results of selective breeding programs of farm animals,1 but has been extended in the past few decades as an indicator of the strength or magnitude of genetic influences on various psychiatric disorders and behavioral characteristics. Numerical heritability estimates have been a mainstay of the field of behavioral genetics, but here I would like to focus on problems with the heritability concept in psychiatry, while keeping in mind that most of the points made here and by previous critics apply to the use of heritability estimates in all areas of human behavior.
There seems to be no end to illogical and even comical “findings” from MZ-DZ twin method comparisons, where the original twin researchers argue that the greater behavioral resemblance of reared-together MZ (monozygotic, identical) versus same-sex DZ (dizygotic, fraternal) twin pairs demonstrates the “heritability” of the behavioral characteristic in question. Among these we find a twin study whose authors concluded in favor of a genetic basis for being a “born again Christian” (65% heritability), another that found important genetic influences on tea and coffee drinking preferences, and still another that found that the heritability of “loneliness in adults” is 48%.