In the News

The Ideology of Depression and Suicide

12/25/2016        In the News 1 Comment

despair-513529_960_720by 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

Treatment Causing the Illness?

12/25/2016        In the News 0 Comments

allergy-18656_960_720by 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.

Psychiatry’s Cruelest Invented Diagnoses

12/23/2016        In the News 0 Comments

4bd6f881-a898-4829-8318-65e1b827d1acby 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.”

Hiding in Plain Sight: The Charade of Depression

12/20/2016        In the News 0 Comments

scanby 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.

 

Antidepressant Smoke & Mirrors

6/1/2016        In the News 10 Comments

Assorted collection of tablets and pills, some still in blister packaging, spread out on a white surface in an oblique angle viewby 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.

Psychiatry Misleads Again

5/31/2016        In the News 2 Comments

confusion

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.

Stepford Brains?

4/12/2016        In the News 3 Comments

BRAINby 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?

 

 

Dangerous Precedent

3/14/2016        In the News 4 Comments

mirror

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?

Attempt To End Stigma Increases It

2/17/2016        In the News 4 Comments

by William Schultz, Doctoral Student


Lena Dunham, a well-known actress, recently received attention and praise because of a collection of Instagram photos she publicly posted, which highlighted her emotional and psychological challenges (subsequently referred to as “mental illnesses”; although I think this and other medical terms are misleading, I’ll use them in this post just for clarity sake) and the medications she uses in response to those challenges. Her central message was that there should be “no shame” surrounding mental illnesses or the use of medications.[1] By “shame”, Dunham was referring to the stigma surrounding mental illnesses, which is pervasive and has a variety of negative effects, such as increasing distress and discouraging individuals from seeking help.[2] Due to the widespread, negative effects of stigma, mental health patients, mental health advocacy organizations, mental health professionals, researchers, celebrities, and politicians have communicated their commitment to ending stigma through psychoeducational campaigns.

For example, actress Glenn Close co-founded an organization called “Bring Change 2 Mind” whose purpose is to “end stigma and discrimination surrounding mental illness” through education. The method for combatting stigma endorsed by Dunham and Close appears to rely on explaining mental illnesses as brain diseases. For instance, the “facts” section of the Bring Change 2 Mind website states that “The fact is, a mental illness is a disorder of the brain – your body’s most important organ – and one in four adults experience mental illness in a given year, including depression, bipolar disorder, schizophrenia, and PTSD.”[3]

By asserting that mental illnesses are brain disorders, this approach highlights supposed brain defects as causes of mental illnesses. This, in turn, challenges the stigmatizing belief that mental illnesses are the result of some sort of moral failure or character weakness. The reasoning goes: You wouldn’t blame someone for being diagnosed with a physical disease to which they didn’t contribute. So why would you blame someone for their mental illness, since mental illnesses are really brain disorders to which they didn’t contribute?

This approach to stigma has been identified in research. For example, Corrigan et al. summarized the perspective described above when they wrote, “Moral models yield attributions that mental illness is onset controllable and persons with mental illness are to blame for their symptoms. Biological models are more consistent with attributions that mental illness is uncontrollable at onset.”[4] In other words, moral models suggest that individuals can control the development of their mental illness while biological models suggest they cannot. This is in line with Bring Change 2 Mind’s claim that “Like most diseases of the body…Mental illnesses are no one’s fault.”[5]

It seems to me that identifying and challenging stigma are excellent goals and I praise individuals and groups, like those mentioned above, for their efforts. However, I’m also concerned because I believe there are at least three important problems with this approach.

The first problem is the assertion that mental illnesses are “brain disorders” contradicts the scientific data and some important philosophic considerations underlying that data. To begin, consider what Thomas Insel, until recently the head of the National Institute for Mental Health, wrote near the end of 2015: “The problem is that even though there have been thousands of studies looking for biological markers of mental health problems such as depression or schizophrenia, none has proven clinically actionable. And, in truth, little has been replicable even in a research setting.”[6] Insel’s comments aren’t out of the ordinary. Congruent statements have been made by many mental health experts.[7] In sum: scientific research has not identified reliable biological pathologies causing mental illnesses. And it’s a plausible argument that if we’ve not identified biological pathologies, it’s a stretch to call mental illnesses “brain disorders” or “brain diseases.”

Perhaps it’s true that researchers may someday identify biological pathologies. Even if they don’t, at the least mental illnesses still involve or are mediated by the brain.[8] And as neuroscience continues to progress, it’s likely that more and more precise correlations between mental illnesses and brain structure and function will be discovered. But even these discoveries wouldn’t immediately justify understanding mental illnesses as brain disorders because a change in the brain is not synonymous with a brain disorder. Let me explain:

All mental phenomenon and behaviors are mediated by the brain. That is, everything changes our brain, from our developmental environment to stressful life events, falling in love, studying for an exam, meditating, and participating in psychotherapy.[9] So even if researchers reliably identified brain differences in individuals who experience, for example chronic anxiety, this does not lead to the conclusion that a disordered brain is causing the anxiety. It merely identifies that the brain changes in response to experiences. To illustrate this point, consider a study in which researchers identified that when individuals diagnosed with social anxiety are administered cognitive-behavioral psychotherapy, their distressful symptoms diminished and their brains changed.[10] Crucially, the mechanism involved in changing the brain was not primarily biological but psychological. In other words, it was not an individual’s disordered brain that was causing their symptoms, but their unhelpful beliefs and behaviors related to social situations.

An objection I’ve often heard to this sort of example is that even though the mechanism of change may be psychological, the change still occurs fundamentally at the biological level. This objection opens up a large discussion which I’ve explored elsewhere and can easily lead us off track (if it hasn’t already). [11] But before returning to discussing stigma, I’ll try to briefly explain an important aspect of my reply to this type of reductionist objection:

If fundamentality is what we are after, then mental illnesses aren’t “really” brain disorders but, instead, patterns of quarks (or quantum fields or whatever else physics identifies) interacting in particular ways. In fact, from this type of reductionist perspective, sciences such as “chemistry” and “biology” aren’t real: they’re useful fictions -- epistemological tools with pragmatic explanatory powers that scientists use until our understanding of physics becomes powerful enough to achieve our explanatory goals. So if we want to be scientific about mental illness, then we need to rely not on neuroscientists, psychiatrists, psychologists, and those who’ve experienced mental illness, but on physicists.

I hope you’ll agree with me that this sort of thinking doesn’t make a lot of sense. At the least, I think it’s important to note that many biological oriented researchers agree that this perspective isn’t comprehensive or functional. For example, Kendler argued “It is possible to study scientific questions from perspectives that are both too basic and too abstract” and this is why he thought it important to reject looking for “big, simple neuropathological explanations for psychiatric disorders” and instead accept that in “ways we can observe but not yet fully understand, subjective, first-person mental phenomena have causal efficacy in the world.”[12] In short: psychosocial factors are crucial to understanding the development of mental illnesses and approaches which emphasize only biological features, such as claiming that mental illnesses are brain disorders, overstate the current evidence and are deeply misguided.

Now that we’ve gotten muddy in that philosophical swamp…I want to return to the subject of combatting stigma and my two other concerns about approaches that emphasize brain deficits. My next concern is straight-forward: a significant body of evidence suggests that emphasizing bio-pathological etiologies of mental illness does not reduce stigma. For instance, Angermeyer et al. used a population-based study design to investigate “the question whether promulgating biogenetic explanations may help reduce the stigma attached to mental illness and, therefore, should be included into anti-stigma messages.” [13] They found that biogenetic explanations are linked to increased stigmatizing attitudes and, as a result, should be avoided in anti-stigma campaigns.

Their findings aren’t unusual. In fact, they’re typical. Similar outcomes are found in numerous studies and meta-analyses.[14] Even recent experimental studies suggest that biogenetic etiologies of mental illnesses increase perceived differentness – such as increased perceived incompetence and unpredictability – and do not reduce stigma as well as explanations which emphasize that mental illnesses may not be discrete diseases.[15]

When I first examined this evidence, I was perplexed. I wondered: if biological etiologies emphasize that individuals are not responsible for their mental illnesses – their genetics, brains, and/or chemical imbalances are – then why do biological etiologies not decrease, and often increase, stigma? Well, in short, the research strongly suggests that the reason is that stigma is not only comprised of responsibility. Schomerus et al. emphasized that while biological etiologies of mental illness are often associated with reduced levels of perceived responsibility and blame, these reduced levels can be “outweighed by the adverse effects mediated by perceived differentness and dangerousness, respectively” and similar findings are common.[16] These increased levels of perceived differentness and dangerousness can contribute to the negative effects of stigma that organizations like Bring Change 2 Mind are attempting to challenge. Thus, it seems to me that there’s good reason to rethink this strategy.

Finally, my third concern surrounding emphasizing brain deficits is that this way of thinking can have significant negative impacts on clinical outcomes. Within the past decade, a new area of research has explored the relationship between an individual’s beliefs regarding the etiology of mental illnesses and her or his treatment preferences and prognostic expectations. The research has consistently found that the greater an individual endorses a biological etiology of mental illness, the greater her or his prognostic pessimism. That is, they expect that their symptoms will persist at greater levels for longer periods of time. The proposed mechanism of this finding is that the greater an individual endorses biological etiologies, the greater she or he endorses “essentialist” views of her or himself – the view that an individual’s emotional and psychological states are largely determined by biological factors and that psychological and social factors are largely or completely impotent.[17] This prognostic pessimism is important because a clients’ expectancies to improve are an important contributor to their improvement – individuals who expect to do better, do better.[18] Thus, factors which contribute to individuals expecting to do worse – such as biological etiologies – can contribute to individuals doing worse.

So, given my concerns, where does this leave us? Unfortunately, with no quick and easy solution. Corrigan, Druss, and Perlick noted that “Advocates need to learn from the complex research on stigma change to implement programs that improve care seeking while not exacerbating other forms of discrimination.”[19] That’s not easy because mental illness and stigma are large, often complicated, subjects. At the least, though, I think it’s important to recognize that there are alternatives to biological etiologies of mental illnesses – such as psychosocial approaches -- which are congruent with the scientific evidence and may avoid promoting stigmatizing attitudes. That is, individuals who experience mental illness may be responding to harmful environments and/or lack the knowledge/resources to manage their lives in more adaptive ways. This perspective doesn’t reduce mental illnesses to brain disorders and it doesn’t imply that we should blame individuals for their mental illnesses. It seems to me that this is an approach worth considering.

[1] Holmes, L. (2016). Lena Dunham shuts down mental illness stereotypes in new photos. Retrieved from http://www.huffingtonpost.com/entry/lena-dunham-mental-illness-instagram_us_56a259b7e4b0d8cc1099cf59

[2] Corrigan, P. W., Druss, B. G., & Perlick, D. A. (2014). The impact of mental illness stigma on seeking and participating in mental health care. Psychological Science in the Public Interest15(2), 37-70.

[3] Bring Change 2 Mind (2016). The facts. Retrieved from http://bringchange2mind.org/learn/the-facts/

[4] Corrigan, P. W., River, L. P., Lundin, R. K., Wasowski, K. U., Campion, J., Mathisen, J., Goldstein, H., Bergman, M., Gagnon, C., & Kubiak, M. A. (2000). Stigmatizing attributions about mental illness. Journal of Community Psychology, 28(1), 91-102.

[5] Bring Change 2 Mind (2016). The facts. Retrieved from http://bringchange2mind.org/learn/the-facts/

[6] Insel, T. (2015). A different way of thinking. New Scientist, 227(3035), 5.

[7] Deacon, B. J. (2013). The biomedical model of mental disorder: A critical analysis of its validity, utility, and effects on psychotherapy research. Clinical Psychology Review, 33(7), 846-861; Fuchs, T. (2012). Are Mental Illnesses Diseases of the Brain?. Critical Neuroscience: A Handbook of the Social and Cultural Contexts of Neuroscience, 331-344; Graham, G. (2013). The Disordered Mind: An Introduction to Philosophy of Mind and Mental Illness. New York, NY: Routledge; Miller, G. A. (2010). Mistreating psychology in the decades of the brain. Perspectives on Psychological Science5(6), 716-743.

[8] Fuchs, T. (2011). The brain--A mediating organ. Journal of Consciousness Studies18(7-8), 196-221.

[9] Hunter, N., & Schultz, W. (2016). Brain scan research. Ethical Human Psychology and Psychiatry, 18(1), In press.

[10] Månsson, K. N., Salami, A., Frick, A., Carlbring, P., Andersson, G., Furmark, T., & Boraxbekk, C. J. (2016). Neuroplasticity in response to cognitive behavior therapy for social anxiety disorder. Translational Psychiatry, 6, e727, 1-8.

[11] Schultz, W. (2015). Neuroessentialism: Theoretical and clinical considerations. Journal of Humanistic Psychology, published online before print on December 3, 2015, doi:10.1177/0022167815617296.

[12] Kendler, K. S. (2005). Toward a philosophical structure for psychiatry. The American Journal of Psychiatry162(3), 433-440.

[13] Angermeyer, M. C., Millier, A., Kouki, M., Refaï, T., Schomerus, G., & Toumi, M. (2014). Biogenetic explanations and emotional reactions to people with schizophrenia and major depressive disorder. Psychiatry Research, 220(1), 702-704.

[14] Kvaale, E. P., Gottdiener, W. H., & Haslam, N. (2013). Biogenetic explanations and stigma: A meta-analytic review of associations among laypeople. Social Science & Medicine, 96, 95-103; Schomerus, G., Matschinger, H., & Angermeyer, M. C. (2014). Causal beliefs of the public and social acceptance of persons with mental illness: a comparative analysis of schizophrenia, depression and alcohol dependence. Psychological Medicine, 44(02), 303-314; Speerforck, S., Schomerus, G., Pruess, S., & Angermeyer, M. C. (2014). Different biogenetic causal explanations and attitudes towards persons with major depression, schizophrenia and alcohol dependence: Is the concept of a chemical imbalance beneficial?. Journal of Affective Disorders, 168, 224-228.

[15] Wiesjahn, M., Jung, E., Kremser, J. D., Rief, W., & Lincoln, T. M. (2016). The potential of continuum versus biogenetic beliefs in reducing stigmatization against persons with schizophrenia: An experimental study. Journal of Behavior Therapy and Experimental Psychiatry50, 231-237.

[16] Schomerus, G., Matschinger, H., & Angermeyer, M. C. (2014). Causal beliefs of the public and social acceptance of persons with mental illness: a comparative analysis of schizophrenia, depression and alcohol dependence. Psychological Medicine, 44(02), 303-314.

[17] Schultz, W. (2015). Neuroessentialism: Theoretical and clinical considerations. Journal of Humanistic Psychology, published online before print on December 3, 2015, doi:10.1177/0022167815617296.

[18] Constantino, M. J., Ametrano, R. M., & Greenberg, R. P. (2012). Clinician interventions and participant characteristics that foster adaptive patient expectations for psychotherapy and psychotherapeutic change. Psychotherapy, 49, 557-569.

[19] Corrigan, P. W., Druss, B. G., & Perlick, D. A. (2014). The impact of mental illness stigma on seeking and participating in mental health care. Psychological Science in the Public Interest15(2), 37-70.

ADHD Is Not a Disorder

2/9/2016        In the News 11 Comments

by Chuck Ruby, Ph.D.


“ADHD” is not a condition or disorder. It is a descriptive label given to people who are not interested enough in a particular topic that an authority figure says they should be. It is a moral judgement about what one ought to be interested in, how much, and when should that person be interested in it.

Yet, a recent article in the Washington Post entitled "ADHD in kids: What many parents and teachers don’t understand but need to know", like many others, continues to claim it is a “brain-based medical disorder”, a “neuro-behavioral disorder”, and “a type of mind, genetically transmitted”. These phrases are misleading and give the impression that ADHD is truly a neurological ailment, when in fact, there is no evidence of such an ailment. There is no research that shows the brains of people labeled ADHD are defective or in any other way pathological. Any “deficits” asserted by researchers are actually differences, not deficits. One would expect a child who has a history of paying attention very well to have a different looking brain than one who doesn’t. That’s what the brain does. It changes in structure and activity depending on how it is used over time. Those changes are not deficits. Further, the great majority of research fails to address the effect that the ADHD treatment of choice, stimulant drugs, have on the brain, making it difficult to determine what brain differences are true deficits created by long-term use of stimulant drugs.

It has been increasingly difficult over the years for psychiatry to explain why a child diagnosed with ADHD can sit for hours in rapt attention to a video game, when he is supposed to have a neurological deficit of attention. Instead of concluding from this that ADHD is actually a matter of the child’s willingness (not ability) to pay attention, this article demonstrates the typical response to that quandary. Linguistic gymnastics are used to re-describe ADHD, not as a neurological deficit per se, but as “wandering attention”, “inconsistency of attention”, or some other phrase that suggests a deficit of brain functioning, but without saying so directly. The concept of “self-regulation” has also been invoked as another linguistic fence-sitting tactic. Self-regulation merely means a person’s desire to bring behavior in line with societal expectations. But again, the idea is that there is a deficit of self-regulation, a contention which the evidence doesn’t support. So while no neurological deficit can be found, the believers in ADHD continue to suggest there is a deficit of attentional, disinhibition, or self-regulation capacity.

The announcement of the Mayo Clinic’s study, which found that girls diagnosed with ADHD have a “two-fold risk” of becoming obese, is also grossly misleading. Not only does it gives the impression that ADHD causes obesity, it also implies ADHD is a real and alarming disorder. In truth, the study simply shows a correlation between the behaviors that get one diagnosed with ADHD and weight control problems. This is something my grandmother would have known. The ADHD behaviors include a general failure to abide by societal expectations regarding self-regulation. It is logical to then assume those people who do not self-regulate according to societal expectations are likely to have similar failures of self-regulation in other areas of life, including eating behaviors. I cringe at the possibility of another study that compares ADHD kids who are prescribed stimulant drugs to “treat” the ADHD with those who are not. It would not be surprising in such a study to see that those not treated with stimulants were more obese than those treated. The conclusion? Treating ADHD reduces obesity. In fact, such a result would be what is expected for someone taking stimulant drugs - they lower appetite and induce weight loss.

The irony in this article is that although it markets ADHD as a real brain disorder, it inadvertently pulls back the psychiatric curtain a little so we can see what is really going on behind it. That is, it points out that ADHD is a label given to people who are not willing to fall in line with the status quo and who are interested elsewhere. Their creativity, vision, and inquisitiveness can lead to wonderful ideas and inventions. Perhaps there is a cost to such independence of thought, but that independence of thought is not a sign of brain deficit.