Former NIMH Director Writes of Crisis in Psychiatry

But, Dr. Steven Hyman also reports the “good news” of the latest never ending fraud eugenics claims for psychiatry’s bogus VOTED IN DSM “brain disorders” he debunks in the first part of this article. Dr. Jay Joseph has debunked all of the bogus gene claims of bio-psychiatry including the latest one touted by Dr. Hyman below on this web site and in his great books, THE MISSING GENE and THE GENE ILLUSION as have many others. Dr. Joseph has targeted psychiatry’s junk science in promoting heritability while demonstrating the nefarious right wing agenda behind such eugenics claims that existed when this horrific pseudoscience was invented in the 1930’s. The social control aspect of the schizophrenia stigma was apparent when the so called symptoms were changed to fit angry black men protesting racism as explained in the book, THE PROTEST PSYCHOSIS. It is well known that more blacks than other races continue to get this life destroying stigma. Also, studying the genes of those given bogus, unproven DSM stigmas with no evidence they exist or tests to prove anyone has them while also failing to take the effect of toxic drugs forced on such victims’ and their drugged genes or brains leaves much to be desired to say the least.

Such never ending pseudoscience that doesn’t even pretend to be credible is just another ploy to keep the never ending psychiatry/BIG PHARMA/government cartel global billion dollar gravy train going indefinitely while continuing to destroy countless lives in the guise of “mental health.”

From Dr. Hyman’s article:

Recent Advances

As long as we guard against renewed self-deception about what constitutes meaningful advances, there is good reason to feel optimistic about the long-term future of translational psychiatry—despite its palpable scientific challenges. My optimism is based partly on the extraordinary vitality of neuroscience and perhaps, even more important, on the emergence of remarkable new tools and technologies to identify the genetic risk factors for psychiatric disorders, to investigate the circuitry of the human brain, and to replace current animal models that have failed to predict efficacious new drugs that act by novel mechanisms in the brain. New ideas are, of course, central to scientific progress, but new tools can open up unexpected worlds and thus undergird the formulation of truly novel hypotheses. As brilliant as Galileo was, without advances in optics, he would not have observed the four moons of Jupiter that undergirded new models of the solar system.

Crucial to our better understanding moving forward is the clue that many psychiatric disorders run strongly in families. Based on family and twin studies, autism, schizophrenia, bipolar disorder, and attention-deficit/hyperactivity disorder are among the most common familial disorders. Far from having simple patterns of inheritance, we now know that psychiatric disorders result from the interaction of a very large number of genes—almost certainly hundreds—with different genetic pathways of risk in different families. To state this in another way, the aggregate influences of different subsets of risk-associated genes produce high likelihoods of autism, schizophrenia, or bipolar disorder in particular families (depending on which genes are involved). Moreover, different disorders such as schizophrenia and bipolar disorder share many risk genes but also have unshared risk genes.7 Finally, genetic risk is not fate: both chance and specific environmental factors operate in the context of a genetic risk background.

The ability to convincingly identify the many risk-associated genetic variants— some common in populations, others very rare—has proven necessary to study tens of thousands of patients and to compare them with roughly equal numbers of healthy individuals. Such an approach was simply not feasible until modern genomic technologies made it possible to determine genotypes (to use tools such as gene chips to identify specific variants in particular places in the genome) in an inexpensive and highly comprehensive manner and to sequence DNA rapidly, accurately, and cheaply. Although steady improvements in the technologies continue, the cost of DNA sequencing has declined approximately one million–fold over the last decade. Just over a decade ago, at the time of the human genome project, the cost of determining each “letter” in the genetic code was about one dollar; given that there are 3 billion such letters (or base pairs) in each human genome, the cost was $3 billion. The cost today of sequencing most stretches of DNA can be as low as $.07 for 1 million base pairs. As a result, we have gone from knowing about a handful of likely risk-associated genetic loci for schizophrenia in 2008 to approximately 75 by the end of 2012. As larger population samples are collected, progress is accelerating in the genetic dissection of schizophrenia, bipolar disorder, and autism.

A list of risk-associated genes does not guarantee an understanding of disease or of new therapies. One exciting recent development is the emerging recognition that genes involved in schizophrenia, bipolar disorder, and autism do not represent a random sample of the genome. Rather, the genes are beginning to coalesce into identifiable biochemical pathways and components of familiar neural structures. More excitement comes from the finding that a large number of risk-associated genes in autism, schizophrenia, and bipolar disorder code for proteins involved in the structure and function of synapses.

Our best hope is that the genetics will unfold over the next several years, due to the efforts of large international consortia that have formed to recruit and to study patients. As genetic clues accumulate, scientists are devising new ways to investigate their neurobiological functions and dysfunctions. One interesting development is to use stem cell technologies to complement the use of laboratory animals with human neurons engineered from skin cells of healthy subjects and from patients. The leading approach is to take a small skin biopsy from the arms of volunteers and to transform skin fibroblasts into neural progenitors and into neurons. Genetic engineering can then be used to add risk-causing mutations to “healthy” neurons and to reverse risk mutations in patients’ neurons. But it is still early in this new field, and it is not yet possible to engineer the specific kinds of neurons implicated in schizophrenia by postmortem studies.

This barrier is likely to fall soon. Whether or not engineered neurons or human neural circuits on a chip prove to be good systems for studying gene function, researchers will make substantial efforts to turn genetic clues into ideas for therapeutics. Many researchers hope that such efforts will help attract the pharmaceutical industry back to psychiatry by demonstrating new paths to treatment development. The emerging genetic results may be the best clues we have ever had to the etiology of psychiatric disorders. If other areas of medicine can guide us, there is enormous promise in deprioritizing existing drugs and old-fashioned animal-based assays as investigative tools and instead focusing on actual disease mechanisms identified by genetics. Technology has only recently begun to make this possible.

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