Gene Theory for Depression Is Now Discredited
Thursday, 18 Jun 2009
ALLIANCE FOR HUMAN RESEARCH PROTECTION
A Catalyst for Public Debate: Promoting Openness, Full Disclosure, and Accountability
http://www.ahrp.org
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: http://www.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.
Quetion: 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?
Contact: Vera Hassner Sharav
veracare@ahrp.org
212-595-8974
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.
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