Chuck Ruby, Ph.D.

Consumer Reports recently published an article reporting the results of research about how face-to-face interaction reduces the chance of depression in the elderly. There are two problems with this article.

First, the article makes it seem that elderly people are at higher risk of developing “mental illness”, in this case, depression. The problem with this is that the experiences they have as they approach the end of their lives, typically encountering health failures and the deaths of their peers, would reasonably lead to sadness and fear. Sometimes these emotions are so great that they trigger the shutting down of depression in an attempt to soothe. But this is natural, it is not an illness. It is also something I think most reading this article would already know.

Second, the article concludes with a call for screening. Screening for so-called “mental illnesses” is dangerous for two reasons: 1) it is well-known that such screening has large “false positives”; and 2) those identified by screening will then be subjected to the onslaught of the mental health industry, usually consisting of the prescription of toxic psychiatric chemicals that do nothing but sedate and chemically straightjacket.

In the case of low base rate occurrences, like depression, even the best and most precise screening tools will result in a large number of people who are not depressed nevertheless being identified as such. The screening is likely to cause concern in these non-depressed people, convincing them to see a doctor, effectively pulling them into that harmful psychiatric pipeline.

Those among us who are entering the final years will be helped with understanding and a meaningful, not medical, attempt to assuage the anguish.

by Matt Stevenson

Psychology Today reports the results of a study, For Depressed Teens, Therapy Shows No Edge Over Routine Care, concluding that psychotherapy doesn’t work with adolescents. But, this is an example of how the researchers stacked the deck by looking only at short term types of therapy. Such a model of research treats psychotherapy as if it were just another medical intervention that can be “applied”, rather than the interactive, relationship-dependent, and individualistic process that it is.

When people are depressed, there is a reason – usually it relates in large part to depressing events or difficult relationships in that person's life, which have often taken years to develop!

In this particular study, adolescents were only given a small handful of therapy sessions; to quote the article: “The median number of treatment sessions differed significantly between patients in the brief psychosocial intervention group (n=6 [IQR 4–11]), CBT group (n=9 [5–14]), and short-term psychoanalytical therapy group (n=11 [5–23]; p<0·0001), but there was no difference between groups in the average duration of treatment (27·5 [SD 21·5], 24·9 [17·7], 27·9 [16·8] weeks, respectively; Kruskal–Wallis p=0·238).”

Seeing someone 6, 8, or 10 times is likely to be modestly supportive during the limited timeframe the intervention is given, but it's nowhere near long enough to examine in depth the complex life experiences that may have led a person to feel depressed.

Forming a positive therapeutic alliance for a person in a difficult emotional state often takes 6-10 sessions or more on its own, before contributors to the feelings of depression are explored, which might in turn allow a person to gain insights and change their behavior in ways that really allow them to feel better. Thus, we should not be surprised that significant differences did not turn up in this particular study, since the intervention was likely not lengthy or intensive enough to allow significant differences to emerge.

An interesting contrast to this study lies in the meta-analyses of long-term psychotherapy (for 1 year or more) performed by Falk Leichsenring, Paul Knekt, and Barry Duncan:

For example, in Leichsenring's meta-analysis comparing long-term psychotherapies with shorter-term approaches, 96% of patients getting longer-term therapy felt and functioned better than patients in the shorter-term group. See specifics here:

http://jamanetwork.com/journals/jama/article-abstract/1028649

http://www.carlapulliam.com/web_documents/bjp_long-term.pdf

So in other words, more human help does tend to make a difference, regardless of the approach.

And in Barry Duncan's analysis of various kinds of therapy, about 80% of clients were better off with therapy than without, and this effect usually increased over longer periods of time. Interestingly, most therapy approaches did similarly well, suggesting that it's the quality of the relationship as perceived by the client that matters most. Supportive human relationships also provides benefits that can last without adverse side effects, so common in drug treatment:

https://www.amazon.com/Heart-Soul-Change-Delivering-Therapy/dp/1433807092/

So giving someone a handful of sessions of “general support”, “CBT”, or “psychoanalytic therapy” (the latter may be a misnomer for a short-term approach) may be about equally supportive over a few months, but it doesn't say much about the value of forming a longer-term helping relationship with an understanding professional or peer. Building a trusting relationship and making significant life changes that lead one to feel less depressed take time, as common sense should tell us.

Lastly, here is another study demonstrating that long-term intensive psychoanalytic therapy (over about 18 months) can make a dramatic difference for very disturbed depressed individuals:

http://www.riksforeningenpsykoterapicentrum.se/psykoterapi/forskning/Fonagy_et_al_2015_Tavistock_Adult_Depression_RCT.pdf

Maybe this type of approach should be tried with adolescents also?

by Al Galves, Ph.D.

In Medscape’s article on Depression and Suicidality, the section entitled “Etiology of Depression and Suicidality” contains statements that are not supported by scientific evidence. This section is based on ideology, not on science. It is based on the ideology of the Biopsychiatric Belief System.

The section places unsupported emphasis on the physiological factors associated with depression and greatly underplays the psychosocial factors associated with depression. It contains this statement: “A decrease in the functional balance of (serotonin and norepinephrine) causes certain types of depression”. This statement is not supported by scientific evidence. There may be evidence that depression is associated with changes in neurochemicals, but that is not evidence that the changing neurochemicals caused depression. This is an important distinction. Correlation is not causation.

Furthermore, if we have a research finding an association between depression and a change in neurotransmitters, proper scientific practice would be to be careful about making a determination of the meaning of such an association. There are at least three possible interpretations. One is that the change in neurotransmitters is causing the depression. A second is that the depression is causing change in neurotransmitters. A third is that the relationship between the neurotransmitter dynamics and the depression is so intertwined that it is virtually impossible to determine which causes which. Proper scientific practice would be to use parsimony in choosing an interpretation. In other words, we would base our interpretation on what is clearly known about other mind-body dynamics.

The most widely and deeply studied of such dynamics is the stress response. The stress response is a profound physiological dynamic that affects the entire body. That physiological dynamic is clearly caused by a psychosocial event – a perception of threat and a cognition that the threat is real and needs to be addressed. Thus, through the use of parsimony, we would choose the interpretation that the depression is causing the neurotransmitter changes.

This section of the Medscape article is also inappropriately certain about the current state of knowledge about neurotransmitter dynamics and depression. Many people with neurotransmitter changes do not experience depression. There is more serotonin in the stomach than in the brain, which throws a large monkey wrench into the relationship between serotonin and depression. There is no evidence of depression ever being reliably diagnosed through measurements of neurotransmitter levels in the brain.

The Medscape article erroneously downplays the association between psychosocial factors and depression. The following is evidence of such association: Persons who derive their sense of self-worth from social relationships are more vulnerable to depression after interpersonal loss than those who obtain self-esteem from other domains (Johnson and Roberts, 1995); women who use a ruminating style of thinking suffer more severely from depression than those who don’t (Lehmicke and Hicks, 1995); people who score low on self-esteem and high on stress are more likely to be depressed (Kreger, 1995); nursing home residents who had a bird in their room were significantly less depressed after being moved to a skilled rehabilitation facility than those who didn’t (Jensen, Cardello and Baun, 1996); persons who score high on a Self-Defeating Personality Scale are more likely to be depressed than others (McCutcheon, 1995); chronic pain sufferers are more likely to be depressed (Banks and Kerns, 1996); persons with more emotional strength and resiliency and a higher level of ego control are less likely to be depressed (Hirschfelt et.al., 1989); recovery from depression is facilitated by events that lessen ongoing difficulty or deprivation (Brown, Lemyre and Bifulco, 1992), and; psychotic depressed patients had significantly poorer pre-morbid functioning - particularly adolescent social functioning - than non-psychotic depressed patients (Sands and Harrow, 1995).

In short, this section of the article is ideology, not science.

References

Banks, S.R. and Kerns, R.D. (1996). Explaining high rates of depression in chronic pain: A diathesis-stress framework. Psychological Bulletin, 119: 95-110

Brown, G.W., Lemyre, L. and Bifulco, A. (1992). Social factors and recovery from anxiety and depressive disorders: A test of specificity. British Journal of Psychology, 161:44-54

Hirschfeld, R.M.A., Klerman, G.L., Lavori, P. et al. (1989). Pre-morbid personality assessments of first onset of major depression. Archives of General Psychiatry, 46:345-50

Jensen,J., Cardello,F., and Baun,M. (1996). Avian companionship in alleviation of depression, loneliness and low morale in older adults in skilled rehabilitation units. Psychological Reports 78, 339-348

Johnson, S.L. and Roberts, J.E. (1995). Life events and bipolar disorder: Implications from biological theories. Psychological Bulletin, 117(3), 443-449

Kreger, D.W. (1995). Self-esteem, stress and depression among graduate students. Psychological Reports, 76, 345-346

Lehmicke,N. and Hicks,R. (1995). Relationship of Response-set differences in Beck Depression Inventory scores of undergraduate students. Psychology Reports, 76, 15-21

McCutcheon, L.E. (1995). Further validation of the Self-Defeating Personality Scale. Psychological Reports, 76:1135-38

Sand, J.R. and Harrow,M. (1995). Vulnerability to psychosis in unipolar major depression: Is pre-morbid functioning involved? American Journal of Psychiatry, 152, 1009-1015

by Julie Greene

I cannot help but wonder why those who conducted this study about how Mental Disorders Predict Physical Disease and Vice Versa, reported at Medscape, considered patients who were treated for a particular condition a good base for study. My reasoning is that studying such patients means the researchers will not be able to distinguish which factor, the mental disorder itself (is it even an entity by itself?) or the treatment for mental disorder, caused the physical disorder.

Having taken psychiatric drugs myself in the past, I've noted that one the most universal set of side effects are called anticholinergic effects, also given a variety of nicknames by psychiatric practitioners due to their widespread occurrence. In brief, we patients experienced dry mouth, constipation, decreased sweating, drying out of the entire digestive tract, drying out of tear ducts, and consequences, both long-term and short-term of these effects. These secondary adverse reactions included dental carries and loss of teeth, acid reflux, risk of hyperthermia, overall poor digestion, serious ophthalmic reactions, worsening depression and malaise due to sluggish digestion and decreased desire to participate in vigorous exercise activities.

Antidepressants as well as other psychiatric drugs often given to depression sufferers cross the blood-brain barrier and go inside the nerve cells. This is the intent when giving a patient such a drug, to alter how nerve cells work. Does science even know if these drugs enter nerve cells outside the brain and wreak havoc, possibly causing chronic nerve pain such as Fibromyalgia? This would explain why almost all Fibromyalgia patients were previously or currently take antidepressant drugs or similar acting pharmaceuticals.

As for the relationship between eating disorders and seizures, likewise, eating disorders (or what appear to be such) can be brought on by pharmaceuticals. I myself suffered from an eating disorder for several decades. I noted that some pharmaceuticals cause unnatural and radical changes in weight and appetite, causing a patient to feel completely out of control of his body. Depakote, given for seizures, can cause rapid and extreme weight gain, and Topamax, also an anticonvulsant, can cause some patients to lose too much weight. Patients also reported to me changes in how food tasted, often an “odd metallic taste” to some foods, or suddenly losing their liking to foods they once enjoyed. Other times a drug could cause spontaneous vomiting upon exposure to certain sensual stimuli. I experienced this myself for about a week in reaction to a drug I was given many years ago. Most patients reported to me that prior to taking pharmaceuticals they did not have any issues with weight or food, or that their eating problems that they already had were compounded by the drugs they were given.

by Randy Cima, Ph.D.

Medscape online publishes yet another bold headline about the real cause of one of psychiatry’s cruelest invented diagnoses: “ADHD Likely Due to Genes, Not Parenting or Environment”. According to this study, children who don’t pay attention to adults and are always off task are victims of a mutated gene. At least, they conclude, ADHD is likely due to their self-selected mutated gene in one out of five participants in the study. (I added this one to my ever-growing long list of causes and cures I’ve collected over the years for ADHD. You can see 10 at the end*).

When I read a new study in psychiatry, I always begin at the same place:

Funding: Medgenics is the funder of this study. Founded in 2011 and recently added to the NASDAQ, Medgenics is one of many new drug companies formed to create and distribute their chemicals to treat genetic flaws, not brain flaws. Genetic psychiatry is the latest iteration of psychiatry’s failed science**.

Medgenics presented their results to AACAP in late October. Liza Squires, M.D., Vice President of Research & Development, announced the next phase of the study is being prepared. According to Dr. Squires, the company’s goal is “to develop a . . . product for this subpopulation . . . the first targeted therapy in any CNS disease . . .” Further, Dr. Squires proclaimed this study the “emergence of precision medicine."

And there you have it, dear customer. This is the one of the newest formulas drug companies use to make money for their stockholders. Keep an eye out for other “targeted therapy” and “precision medicine” studies.

How To Carve Out a Market in an Already Saturated Market: Maybe you wonder about the fuss this company makes out of a study that shows just 20% have this particular “gene mutation.” What about the other 80% who don’t, you ask? What’s the likely due for them? It doesn’t matter. Fortunately for psychiatry, their invented disorders can have multiple “causes,” to their financial advantage.

So, Medgenics is aggressively pursuing their business plan. The final results will be publicized as a newly discovered “sub-population” of ADHD children, requiring genetic treatment. Like magic, Medgenics financed the creation of new customers (the ”subculture”) for their soon to be created genetic repair chemicals (the medication), in order to fix their self-selected genetic mutation (the “likely due”).

Something is very wrong with this picture.

This Is Not Science: First clue? The headline. A legitimate scientist would never use the term “likely due,” unless you’re talking about earthquakes. That’s a marketing term used at the direction of corporate lawyers to avoid the term cause. That word – cause – has significant implications in court.

Instead, terms like association, correlation, relationship, interrelation, connection, interconnection, link, and others, are used because they are vague and subjective – and defensible in court. This study exposed me to one I hadn't seen before: “likely due.” Lots of wiggle room in “likely due.”

Second Clue? Confirmatory Findings, in bold. This is impossible in science. Any scientist, student or enthusiast understands that under no circumstances can a scientist confirm her own science. In this study, this scientist not only did so, her study found an increase of 100% of this sub-population from her prior study – the same sub-population she invented. That’s a remarkable increase. On the other hand, it sounds like good news for the investment team at Medgenics. Their market size doubled.

This process is an example of a marketing scheme, not science. Still, it begs the question: how is it possible that this type of scientific charade continues to be so successful - over and over and over again?

The Enduring Failure of Treatment: In the last half century, psychiatry has created more than 50 chemicals - just for ADHD. Alternatives include diet supplements and restrictions, hormonal medications, acupuncture, exercise, behavioral plans, talk therapy, and many, many, many more. Fame and fortunes have been made, and continue to be made, providing “treatment” for this lucrative, invented, destructive diagnosis.

Here’s the rub. None of them “work.” That’s why there’s always room for next years new batch of chemicals or procedures. Last years miracle cures failed too.

Then again, how could they work? There is no such disease, or disorder, or dysfunction, or disability, or deficiency, or disturbance. There is nothing medical about behavior, thus, medicine and medics are out of their element. Failure is unavoidable.

Science is for Sale in Psychiatry: I usually stop reading a new psychiatric study after learning a drug company supplies the cash – and they almost always supply the cash. Corporations rightly expect something in return for their often very large investments – or they won’t be using your “science” the next time they need a study to create some business.

In summary, as a long time mental health practitioner, I found nothing of interest and nothing of value from this psychiatric study. I must admit - I wasn’t surprised. I never am.

* I collect causes and cures of all of psychiatry’s false diseases (I call them Faults and Fixes). Here are ten for ADHD. There are many more: • Acetaminophen while pregnant: here • Dietary Factors (too much/too little: sugar, gluten, omega-3, food additives, GMO, etc): here • Abnormal brain iron levels: here • Pesticide: here • Smoking while pregnant: here • Pregnant women taking antidepressants: here • Smog: here • Marketing: here • Energy Drinks: here • Single Mothers: here

** Regarding the science of genetics, from the National Institutes of Health, 2012: “. . . In human behavior genetics, however, powerful new methods have failed to reveal even one bona fide, replicable gene effect pertinent to the normal range of variation in intelligence and personality. There is no explanatory or predictive value in that genetic information . . . The promises of the molecular genetic revolution have not been fulfilled in behavioral domains of most interest to human psychology.”

by Chuck Ruby, Ph.D.

A recent Medscape article reported the results of a study that concluded "...patients with depression can be subdivided into four biotypes defined by distinct patterns of dysfunctional connectivity in limbic and frontostriatal networks...." The study is complete with a litany of technical language and statistical analyses, along with very colorful charts and graphs, to once and for all prove that depression has biomarkers that can be used to diagnose and treat it.

But, all this fanfare obscures one important thing hiding in plain sight: Depression is not a real brain disease! Neither are any of the other 300 or so mental disorder categories. Depression is a natural and expected human reaction to emotional pain and at best is a metaphorical disease. It shouldn’t be treated as if it were a clinical or medical problem, and the people experiencing it shouldn’t be treated like patients. Yet this study is an example of how a curtain of complex technical and clinical jargon hides a reality that the devotees of this disease model of mental illness don’t want revealed. Let’s pull the curtain back and see what’s hiding behind it.

First, these kinds of studies come on the heels of the 2013 pronouncement by the Director of the National Institute of Mental Health (NIMH) that the still-in-use-today Diagnostic and Statistical Manual of Mental Disorders (DSM) is invalid and that a new diagnostic system needed to be developed from the ground up using brain scans to identify valid mental disorders rather than using symptom pictures. This study is an attempt to do just that. Yet the invalidity of the DSM is not the only problem here.

The bigger problem is that, as I said earlier, depression is not a real brain disease. The claim of disease is an a priori assumption, based on nothing. In this case “depression” is anointed as a disease at the outset (just because) and then it is discussed as if we all agree and that “biomarkers” can be used to diagnose it. But a “biomarker” is not the same as evidence of disease. The brain is “plastic”, in that it changes with use, and chronic use will result in more permanent change in both structure and activity levels. The fact that certain human experiences are accompanied by signature brain patterns merely reflects this fact. Such brain correlates of human behavior are not evidence of disease. Still, this concept of “biomarker” is used in order to give the impression of disease.

So given this, is it really that surprising to find different brain patterns in people who are having different types of depressive experiences? How is this a justification for describing those brain patterns as “abnormal connectivity”? The article also uses the phrases “reduced connectivity” and “hyperconnectivity” to give the same impression of dysfunction (disease). Similar to how the term “biomarker” implies disease when it really has nothing to do with disease, using the phrase “reduced connectivity” merely mean less activity, not some kind of defect in the connection between brain cells or circuits. And “hyperconnectivity” just means the particular brain areas are more active. This is linguistic sleight of hand, making it appear the brain activity in question is abnormal (diseased), when in fact, there is no such evidence of abnormality, dysfunction, or disease.

These kinds of studies will continue. But unless they come up with evidence (remember, we’re supposed to be scientific) of actual disease in the brain, the only thing they’ll demonstrate is that human activity affects brain patterns. But that is something we’ve known already for a long time. Of course, if they do find evidence of brain disease, we already have a medial specialty for that. It is called neurology.

by Frederick Ernst, Ph.D.

In a recent edition of the Wall Street Journal, Dr. Peter Kramer writes a defense of antidepressants and does a really nice job of convincing himself that what he is doing, prescribing drugs for people who are not ill, has merit. Unfortunately, he shared his thoughts with the Journal and, even more unfortunately, they published it.

The conclusions he has drawn are simply without merit. A science-informed reader would not have wasted time drifting past the first paragraph of this nonsense unless that reader was curious about the latest marketing-informed propaganda. So first, Dr. Kramer invents a new biochemical imbalance theory, one that not only has no support in science (like the one he’s trying to replace) but also has hardly even been mentioned in the literature of science. Brain resilience? This is a concept you can only find infrequently mentioned in connection with concussion or immune reaction. But according to Dr. Kramer, the “chemical properties of these drugs” (the SSRI’s) are inherently restoring resilience in the brain? (Please ignore here the evidence that these drugs are toxic and actually kill brain cells.)

“Little of the benefit comes from the classical placebo effect.” Says Dr. Kramer. He would be exactly correct if you believe more than 80% to be little. Drs. Joanna Moncrieff and Irving Kirsch should be invited to address this incredible statement! (see for instance http://www.contemporaryclinicaltrials.com/article/S1551-7144(15)30003-3/abstract). Further, Dr. Kramer exclaims, “I read the data with a doctorly eye.” That’s an interesting comment from a doctor identifying with a discipline that continues to wait for science to reveal validation of only one, a first, of its 350 so-called “mental” illnesses after 100 years of trying.

But, rest assured he will not abandon his authoritarian approach to the topic. He turns to a colleague to see if his experiences have been the same. And, of course, they both agree. Depression is getting better in those who are most depressed. Interestingly, and unintentionally, he provides the readers with a perfect example of why depression is not a brain disease that people wake up with one morning. Public health surveys (read, CDC science-based data) “are not fine-grained enough” so he turns to the ultimate science authorities… students and colleagues, and asks them what they see. And then, who does he describe as revealing evidence of this illness? Irma! A lady whose husband and daughter have died and, if things couldn’t get any worse, she now has heart disease. Sounds like an inexplicable endogenous depression to me. Clearly, one of her neurotransmitter systems has come down with something quite coincidentally following these three life events.

The lay public must be informed to understand that doctors are not trained as scientists. Skepticism is not promoted or even encouraged in the training of physicians and probably shouldn’t be. I certainly don’t want the surgeon for my emergency to be thinking about whether or not what he’s doing makes any sense. But of all medical specialties, psychiatry must be taught skeptically or it will never achieve the status of infectious disease medicine or cardiology, the leaders of science-based medicine.

A revolution in medical education is required for psychiatry to achieve the status of its peer disciplines. The foundational pillars of their discipline is marketing, with nearly unlimited underlying financial resources. Remove those dollars and this house of cards collapses under its own weight.

There simply is no science supporting these “treatments.” And, indeed, I will retract this statement in the most humiliating public way if any person on this planet can point to one study revealing that mental illness is an illness with a demonstrable underlying pathophysiology. Just one. Only one. Not much to ask. But as the subtitle of this article suggests, Dr. Peter D. Kramer has seen real benefits from antidepressants. That should be good enough for you.

All my sarcasm aside, the idea that human suffering and distress is a disease has not only long outlived any hoped-for usefulness, it has caused pervasive harm to our population. Mental illness portrayed as physical illness is a flawed idea based on a misconceived extension of metaphor resulting in irreparable harm to the world public. It’s time for a new paradigm and Dr. Kramer’s article is the exclamation point that I would add to the end of this sentence.

by Edward Dantes

Occasionally I stumble upon one of the dark side's websites (i.e. biological psychiatry), and usually find myself laughing or horrified or both. Today was no exception when I found this amusing article in the Psychiatric Times (http://www.psychiatrictimes.com/apa-2016-Schizophrenia/multidisciplinary-approach-first-episode-psychosis).

Here are a few quotes that stood out:

“To improve medication adherence, oral antipsychotic medication was transitioned to a long-acting injectable form.” - This Orwellian statement, so typical of out-of-touch psychiatrists who think they know what's best for “patients”, brings to mind Otsuka's new chip-implanted Abilify drug... it keeps giving me the thought that those aliens on Alpha Centauri are softening up the planet by drugging us all up in preparation for their invasion. Now what is that thought a symptom of?

“I will now review a case of a young man who came down with schizoaffective disorder...” - This made me laugh - poor guy, sounds like coming down with the common cold! I wonder what could cause someone to catch schizoaffective disorder? Is it airborne? Maybe it will become the new Zika or SARS... Hard to believe that psychiatrists are ignorant enough to use this type of language.

“A structured assessment of symptoms to clearly make a preliminary diagnosis and to be able to conclude on schizophrenia or psychosis..” - There are no symptoms of schizophrenia, because there is no such illness, nor is there a reliable or valid diagnosis named as such. To give psychiatrists credit, some of the more evolved ones are at least starting to tentatively admit that there is no singular schizophrenia and the disorganization and disorientation of psychosis is a continuum with many possible causes.

“The medical examination utilizing MRI imaging and laboratory blood tests is an important step in making the correct diagnosis so a young person is approached appropriately...” - What!? I guess psychiatrists are dreaming that they've come up with some way of using brain and blood scans to make valid diagnoses. Dream on. It's funny how serious sounding and clinical these psychiatrists try to make their terminology sound, when in fact what they are saying is absolute gibberish! There are no MRI imaging or laboratory blood tests that can be used in diagnosing.

The article creates a simulacrum of engaging and helping the person, but it's hard to effectively help when one is assuming the existence of a biologically-caused illness that just isn't there and drugging on that basis. As usual, in this article there is no discussion whatsoever of the lived experience of the case examples, no mention whatsoever of what the troubled person feels, wishes, hopes for, fears, or went through. Where is the humanity in the soulless, colorless T.S. Eliot-ian Wasteland of biological psychiatry?

It's such a shame that more US psychiatrists won't try Open Dialogue, learn about psychoanalytic or psychodynamic approaches, or other non-medical methods to helping people experiencing psychosis. Then their energy would be put toward something with a much better chance of understanding and helping. Meanwhile, more young people will be harmed by the lies about brain disease and the notion that they have to indefinitely take drugs that aren't even tested over the long term, and lead to a life time of disability and dependence.

by Chuck Ruby, Ph.D.

MIT Technology Review published a recent article entitled, "Military Funds Brain-Computer Interfaces to Control Feelings" describing research funded by the Defense Advanced Research Projects Agency (DARPA) that uses brain electrode implants to detect and prevent certain feelings and behaviors. The article says the goal is "to use brain implants to read, and then control, the emotions of mentally ill people". This is nothing less than Orwellian dystopia and brings to mind images of the 1970's novel and movie, The Stepford Wives. I have several questions.

One question to ask is how are we going to define “mentally ill people”? Just a quick look back over the changing, vague, and over-inclusive definitions of “mental illness”, to include the voting in and out of certain pet diagnoses, such as homosexuality, self-defeating personality disorder, asperger’s disorder, and attenuated psychosis syndrome, tells us that any unwanted behavior or experience can be dubbed “mental illness” depending on the desires of those in power. This usually means those on the diagnoses committees, heavily funded by pharmaceutical companies, and now with this line of research underway, the medical devices companies will soon chip in.

There have even been attempts to claim certain personal convictions such as liberalism, conservatism, and religiosity are signs of “mental illnesses”. Are we going to allow some authority to prevent us from having those convictions by identifying the brain circuits involved and zapping them?

Further complicating this is the dimensional rather than categorical reality of those things called “mental illness”. The problems addressed are human problems that everyone shares to varying degrees of severity. They aren't brain diseases. At what level of severity must one get to before being considered a candidate for this procedure? According to the article, these brain implants would only be considered for people who are truly debilitated and can’t be helped any other way. One psychiatrist involved in this research said, “This is never going to be a first-line option: ‘Oh, you have PTSD, let’s do surgery,’...It’s going to be for people who don’t respond to the other treatments.” Yeah right. We've heard that before.

Another question is whether these forms of "treatment" will be mandatory or voluntary. Given the poor track record our mental health industry has regarding the protection of human dignity and autonomy, I think I know the answer.

Well-intentioned as it may be, this research is a threat to us all. It conflates brain activation with lived experiences. The amygdala doesn't generate fear, people generate fear. The neurons in the amygdala just sit there and react as they are built to react when an adjoining neuron activates. They don't know what fear is. Fear is a meaningful human experience that tells us something may be a threat. Fear, as well as all other human emotions, are what make us human.

Considering the fact that there are nearly 100 billion neurons in the human brain and that feelings and behaviors involve several diverse areas of the brain in very complex ways, it is unlikely we are ever going to be able to achieve more than a crude approach to controlling people’s lived experiences and behaviors this way.

To save time and money, why don’t we just fit everyone with a shock collar at birth?

by Chuck Ruby, Ph.D.

Investigators from the French Land Transport Accident Investigation Bureau (French acronym BEA), which has been investigating the March 2015 Germanwings crash, have recently recommended that world aviation agencies require mental health workers report pilots whose mental heath condition "could threaten public safety". This is an alarming mistake. See the NBC story here: http://www.nbcnews.com/storyline/german-plane-crash/germanwings-crash-bea-investigators-urge-new-rules-about-reporting-mental-n537416.

One of the most robust findings of research is that mental health professionals are not good at predicting others' future violence or harmful actions. There are clear risk factors that increase a person's likelihood of doing so, but they do not enable us to predict whether the behavior will occur. The best we can do is manage those risk factors in order to reduce the chances. Complying with BEA's recommendations and putting mental health workers in the position of making predictions, will result in a huge false alarm problem, destroying people's lives in the process, and ironically causing those who would benefit the most from help with emotional problems avoiding such help.

Many occupations require employee background evaluations in order to determine continued psychological suitability and readiness for the job. In addition to airline pilots, other examples are law enforcement officers, employees working in national security programs, and nuclear power plant workers. The employers in these settings have a reasonable interest in knowing their employees can be trusted. And employers can understandably err on the side of caution by denying employment when possible problems exist. But requiring a psychological evaluation for a suitability determination and requiring mental health workers to report people to the authorities are two different things.

A mental health worker, most likely some type of counselor in this situation, has a fiduciary obligation to the person being helped. The relationship between the counselor and the client is paramount, and the confidential nature of the relationship is at the core of this trust. Requiring the counselor to report people who "could threaten public safety" places the counselor in an ethical double bind. If the counselor reports, she or he damages the relationship and harms the person. If the counselor fails to report and the person commits some act, the counselor becomes the target of legal and ethical censure.

Attempting to determine who "could threaten public safety" is impossible. This could actually mean anyone. How many times have uncharacteristic acts of violence been committed by people who never showed any warning? It would be easy to predict future harm when a client makes a statement about intent to harm a specific person(s), but how often does that actually happen? Hardly ever. Besides, there are already laws and guidelines in place that require counselors to warn of such clear cases.

But other than these clear cases, where does the counselor draw the line? How much of a risk is needed prior to warning? How do we quantify that? Must we use standardized instruments to assess the level of risk? How valid and reliable are those instruments? The answer is: not very. With behavior that happens infrequently among the population, any assessment of risk will necessarily have very high false positive results or false alarms. This is just a matter of statistics. Violent behavior is no exception. For instance, the FBI reported a .4% base rate of violent crime in 2013, and this includes all types of violence, not just murders and assaults (see https://www.fbi.gov/about-us/cjis/ucr/crime-in-the-u.s/2013/crime-in-the-u.s.-2013/tables/1tabledatadecoverviewpdf/table_1_crime_in_the_united_states_by_volume_and_rate_per_100000_inhabitants_1994-2013.xls). With such a low base rate occurrence, even the most accurate assessment instrument is doomed to result in extremely high false alarms. In other words, the great majority of those identified as potentially dangerous and reported by counselors to aviation authorities, will never commit a dangerous act. But being reported as at risk for such behavior can ruin their lives and damage the value of professional help.

The slope is slippery. For what other occupations will this kind of big brother monitoring apply? Should counselors be required to report police officers? Teachers? Bus drivers? Investment bankers? Physicians? Who would report the counselors?