A study that attempted to replicate the “seminal” study that laid the foundation for psychiatry’s “serotonin theory” of depression, claiming a genetic- serotonin impairment underlying depression, has been debunked by the data from 14 similar studies claiming a genetic underpinning to depression.
The study, reported in The Journal of the American Medical Association, “found no evidence of an association between the serotonin gene and the risk of depression, no matter what people’s life experience was.” The real risk for depression is NOT BIOLOGICAL: Dr. Merikangas, the senior author said the findings show that “a major stressful event, like divorce, in itself raised the risk of depression by 40 percent.”
Dr. Kenneth Kendler, a prominent authority on psychiatry and human genetics at Virginia Commonwealth University, says that the new study “really takes the wind out of its sales” referring to the widely accepted claim that depression is linked to a genetic predisposition.
“I think what happened is that people who’d been working in this field for so long were desperate to have any solid finding,” Kathleen R. Merikangas, chief of the genetic epidemiology research branch of the National Institute of Mental Health and senior author of the new analysis, said in a phone interview. “It was exciting, and some people thought it was the finding in psychiatry, a major advance.”
Psychiatry is replete with invalid biochemical assumptions–that are, upon examination, contradicted by the data and life experience. But not before those false assumptions have spurred the use of extremely toxic, harmful interventions that have caused patients irreparable physiological and mental harm.
Indeed, the “chemical imbalance” theory is the cornerstone for prescribing serotonin boosting drugs for depression, and dopamine depleting drugs for schizophrenia. The literature is flooded with biased, scientifically invalid reports by psychiatrists who receive large sums of money from psychoactive drug manufacturers.
Serotonin-enhancing antidepressants have never been shown to be effective for most people the treatment of clinical depression–but they have caused serious toxicity–including serotonin syndrome which is often misdiagnosed and has a high risk of death–e.g., Libby Zion and Andy Warhol. See:Video about Yankee Scatman, Leslie Cohen, who died from undiagnosed serotonin syndrome http://www.youtube.com/watch?v=egfXW74LMi8
The other major unproven assumption underlies the use of neuroleptics (a.k.a. antipsychotics) to treat schizophrenia: the “dopamine theory” which assumes–again, without evidence–that schizophrenia is caused by high levels of dopamine which require life-long dopamine-depleting drugs. Among the dozens of severe adverse effects caused by both the old and new neuroleptics is Neuroleptic Malignant Syndrome, which has killed countless patients.
The myths crafted by psychiatry in collusion with drug manufacturers about the clinical superiority and cost-effectiveness of the atypical antipsychotics–which were deemed “very safe & effective” was shattered by the results of the NIMH-sponsored CATIE schizophrenia outcomes study, which documented the drugs’ intolerable effects and lack of clinical efficacy.
Indeed, the CATIE results forced psychiatry’s leading schizophrenia researchers to acknowledge that the drugs offered no improvement over the old cheap neuroleptics (at low doses) and they cause profound physical harm. Psychiatrists gave themselves a pass saying they were “beguiled” by the promise and industry’s aggressive marketing!
See: https://ahrp.org/cms/content/view/353/110/
However, empirical findings have not caused institutional psychiatry or its practitioners to change the failed, lethal, paradigm of care which remains welded to Big Pharma’s marketing agenda–the flow of cash continues to dictate psychiatry’s prescribing practices.
Worse still is that psychiatry in tandem with drug manufacturers have expanded the market for antidepressants and antipsychotics for healthy children whose physical and mental health are seriously harmed by these toxic drugs.
In light of the compelling indisputable evidence that there is no genetic predisposition for depression or other mental problems, there is no rationale for mental health screening initiatives–unless, we are prepared to rectify life’s adversities from children’s and pregnant women’s lives.
Question: Will the Obama administration put a stop to an ill conceived, and now thoroughly unsupportable policy of screening followed by drugging of children for presumed depression?
THE NEW YORK TIMES
June 17, 2009
Report on Gene for Depression Is Now Faulted
By BENEDICT CAREY
One of the most celebrated findings in modern psychiatry — that a single gene helps determine one’s risk of depression in response to a divorce, a lost job or another serious reversal — has not held up to scientific scrutiny, researchers reported Tuesday.
The original finding, published in 2003, created a sensation among scientists and the public because it offered the first specific, plausible explanation of why some people bounce back after a stressful life event while others plunge into lasting despair.
The new report, by several of the most prominent researchers in the field, does not imply that interactions between genes and life experience are trivial; they are almost certainly fundamental, experts agree.
But it does suggest that nailing down those factors in a precise way is far more difficult than scientists believed even a few years ago, and that the original finding could have been due to chance. The new report is likely to inflame a debate over the direction of the field itself, which has found that the genetics of illnesses like schizophrenia and bipolar disorder remain elusive.
“This gene/life experience paradigm has been very influential in psychiatry, both in the studies people have done and the way data has been interpreted,” said Dr. Kenneth S. Kendler, a professor of psychiatry and human genetics at Virginia Commonwealth University, “and I think this paper really takes the wind out of its sails.”
Others said the new analysis was unjustifiably dismissive. “What is needed is not less research into gene-environment interaction,” Avshalom Caspi, a neuroscientist at Duke University and lead author of the original paper, wrote in an e-mail message, “but more research of better quality.”
The original study was so compelling because it explained how nature and nurture could collude to produce a complex mood problem. It followed 847 people from birth to age 26 and found that those most likely to sink into depression after a stressful event — job loss, sexual abuse, bankruptcy — had a particular variant of a gene involved in the regulation of serotonin, a brain messenger that affects mood. Those in the study with another variant of the gene were significantly more resilient.
“I think what happened is that people who’d been working in this field for so long were desperate to have any solid finding,” Kathleen R. Merikangas, chief of the genetic epidemiology research branch of the National Institute of Mental Health and senior author of the new analysis, said in a phone interview. “It was exciting, and some people thought it was the finding in psychiatry, a major advance.”
The excitement spread quickly. Newspapers and magazines reported the finding. Columnists, commentators and op-ed writers emphasized its importance. The study provided some despairing patients with comfort, and an excuse — “Well, it is in my genes.” It reassured some doctors that they were medicating an organic disorder, and stirred interest in genetic testing for depression risk.
Since then, researchers have tried to replicate the gene finding in more than a dozen studies. Some found similar results; others did not. In the new study, being published Wednesday in The Journal of the American Medical Association, Neil Risch of the University of California, San Francisco, and Dr. Merikangas led a coalition of researchers who identified 14 studies that gathered the same kinds of data as the original study. The authors reanalyzed the data and found “no evidence of an association between the serotonin gene and the risk of depression,” no matter what people’s life experience was, Dr. Merikangas said.
By contrast, she said, a major stressful event, like divorce, in itself raised the risk of depression by 40 percent.
The authors conclude that the widespread acceptance of the original findings was premature, writing that “it is critical that health practitioners and scientists in other disciplines recognize the importance of replication of such findings before they can serve as valid indicators of disease risk” or otherwise change practice.
Dr. Caspi and other psychiatric researchers said it would be equally premature to abandon research into gene-environment interaction, when brain imaging and other kinds of evidence have linked the serotonin gene to stress sensitivity.
“This is an excellent review paper, no one is questioning that,” said Myrna Weissman, a professor of epidemiology and psychiatry at Columbia. “But it ignored extensive evidence from humans and animals linking excessive sensitivity to stress” to the serotonin gene.
Dr. Merikangas said she and her co-authors deliberately confined themselves to studies that could be directly compared to the original. “We were looking for replication,” she said.