by Randy Cima, Ph.D.

A few weeks ago on 60 minutes, Leslie Stahl, my favorite reporter from the show, introduced us to Julia, the newest character on Sesame Street. Julia has autism.

Ms. Stahl interviewed producers and cast members from Sesame Street. She also spoke to parents with autistic children, and others who love them. It was an emotional segment, in a good way. Sesame Street intends to de-stigmatize children with autism, and everyone is proud.

I started watching 60 minutes and Sesame Street in the 1960's. Like most Americans, I learned to love, and trust, both shows. Coincidentally, during the same decade, I first became interested in autism.

Lloyd Nolan, a character actor from the 40’s, 50’,s and 60’s, was on the Johnny Carson show. He spoke of his “strange” 4 year-old son who had something called “autism.” I was captivated as he described in some detail the very odd behaviors of his son, Jay – and I’ve been captivated since.

Fifty years later, autism, Sesame Street, and 60 minutes converged in mid-March, 2017, with one reviewer of the show saying: “Sesame Street’s new Muppet Julia brought 60 Minutes viewers to tears.”

Brought me to tears too. For different reasons.

It’s Not So Easy Being Mean

Dear parents and other caretakers who love and protect and cherish these very unique children, I love them too.

For me, it’s a matter of temperament (See Keirsey’s brief portrait of this temperament in Notes). There is no biology to this, or genetics. These kids aren’t flawed or damaged. They aren’t disabled or disturbed or diseased either. That means they don’t need doctors, or their medicine. They do need our protection, because they are unique, and because they are so terribly misunderstood, and because someone is always trying to fix them. Some of their famous counterparts include Mozart, Spielberg, Cher, and Harpo Marx. There is much more about this, for a different place and time.

For now, parents and caretakers, and others who love these children as I do, please consider the following:

In 1983, the autism rate was 4.3 in 10,000

I know this is accurate. I was 38, in the profession for nearly 10 years, and I was in the final year of my Masters program (I received my Ph.D. about 4 years later). In the next 12 months I researched everything known at the time about autism, beginning with Leo Kanner. My research included Hans Asperger. I also did a year internship as a family therapist for 6 families with autistic kids (all boys). My Master’s thesis was titled: Autism and Other Self Defiling Phenomena. I was as informed about this very small population as anyone was at the time. Again, the incident rate was 4.3 in 10,000.

Keeping it simple, this means if there were 10,000 children randomly gathered in a large auditorium, we could expect to find 4 or 5 children who fit the description of autism in 1983.

In 2017, the autism rate is 1 in 68

Doing the math, that means the same auditorium with 10,000 randomly gathered children would now have about 150 children who fit the evolving, all inclusive description of autism. That’s an increase of 3500% - in 34 years.

How did that happen?

Is autism contagious? If so, how so? If not, how does it “spread?” Is there a virus or bacteria? Did something drastic happen to our water system in the last 4 decades? In the last 34 years, did the mercury just suddenly appear in the fish these children or their parents ate, that wasn’t there before? Did someone change the formulae for vaccines? Was there some other environmental catastrophe that triggered this incredible spike in the number of diseased children in that auditorium? By the way, these are some – not all – of the speculated “causes” of autism.

I’ve asked medical professionals who should know how this “epidemic” occurred, many, many, many times. They usually duck the question, or provide some form of psychobabble. I’m skilled at recognizing psychobabble.

So, can anyone from medicine explain this “epidemic,” please? Short answer? No. No one can. Long answer? No.

No one can.

So what really happened?

Psychiatry Happened

I’ve been awestruck, and demoralized, as the rate of autism has skyrocketed, without much fanfare. It’s been dramatic.

Take a look:

AUTISM RATE SINCE 1975

1975 – 1 in 5000
1985 – 1 in 2500
1995 – 1 in 500
2001 – 1 in 250
2004 – 1 in 166
2007 – 1 in 150
2009 – 1 in 110
2016 – 1 in 68

(SOURCE: Autism Speaks)

Why the "epidemic?” Because there has been an epidemic of diagnosers, armed with an ever-widening, all-inclusive diagnosis - nothing else.

The Psychiatric Process: Change the Definition

Autism was added to the 1980 edition of DSM III (Diagnostic Statistical Manual). This made it official. Autism became medical. It was called Infantile Autism disorder back then. There were six characteristics listed and each of the six had to be present to be diagnosed. Doctors mostly ignored what was then a very, very rare phenomenon. (See what Leo Kanner had to say about the rarity of autism in Notes)

By 1985, the rate was 1 in 2500.

In 1994, the DSM definition of Autism changed again, significantly. This is when I first became concerned. I knew what was coming. After a forty-year career – the last 25 as director of several mental health facilities for children - I’ve seen psychiatry do this as a matter of course.

Now there were 16 different symptoms, and only six of the 16 were needed to receive the diagnosis. As a result, the universe of diagnosable children grew exponentially. The game was officially rigged. The "epidemic" started.

By 1995, the rate was 1 in 500.

Enter ASD: The Final Solution

In 2013, DSM V was released. The diagnostic criteria for autism included these instructions to all professionals: "Individuals with a well-established DSM-IV diagnosis of autistic disorder, Asperger’s disorder, or pervasive developmental disorder (PDD) should be given the diagnosis of autism spectrum disorder."

There you have it. They "lumped" together all the symptoms of Asperger’s and PDD with "autism," and the population's diagnostic horizon multiplied - again. Now, any child who is a little too quiet, a little too distracted, a little too defiant, a little too introverted, can be on the “spectrum.” Also, because he can speak, doesn’t mean he isn’t on the “spectrum.”

By 2016, the rate is 1 in 68.

The Rest Is Easy for Psychiatry

Psychiatric scientists will argue for years, in the right journals, with academic vigor, about scientific studies that expose the real cause of autism. Is it genetic? There’s some “convincing” evidence. Is it the vaccine? Studies show a “link.”

What about a chemical “imbalance” in the brain? “There’s a correlation,” says the psychiatric scientist. By the way, psychiatry will neither offer, nor promise any cures. There’s a good reason for this. Psychiatry has a perfect record in this regard – 0 cures.

Will psychiatry ever find a “cause?” No, they won’t, for two reasons: (1) they never have, for any of the more than 400 disorders in DSM V and, (2) autism isn’t a disease, so a medical cause can never be found.

In the meantime, psychiatry will eagerly “treat the symptoms” with a variety of chemicals. Here’s what they’ve tried so far with these children:

• Adderall
• Ambien
• Anafranil (cloripramine)
• Clomipramine
• Clonazepam
• Desipramine
• Desyrel
• Dexedrine
• Dilantin (phenytoin)
• Dipiperon
• Fenfluramine
• Haldol (haloperidol)
• Imipramine
• Lithium
• Luvox (fluxovamine)
• Melatonin
• Naltrexone
• Periactin
• Piracetam
• Prednisone
• Risperdol (risperidone)
• Ritalin
• SSRI’s
• Tegretol
• Zoloft (sertraline)

Finally, psychiatry will caution all of us routinely, in eye-popping, fear invoking headlines, that the “epidemic” is worsening, again.

This is what the psychiatric medical model has to offer humanity, and it's 2017.

One More Thing to Consider

In 1957, Hollywood released "The Three Faces of Eve.” Based on a true story, the movie is about a young woman with three personalities. Joanne Woodward won an Academy Award for her portrayal of Eve. For a few years afterwards, there was a short-lived “outbreak” of multiple personality disorder reported by psychiatrists in America. A small industry was born, and then faded away. The “outbreak” ended.

If this movie was made in 2007 instead of 1957, there would be multiple personality websites, multiple personality theories, multiple personality medications, a slew of multiple personality books, multiple personality experts, and endless studies among medical professionals searching for the cause that would include genes, brain damage - maybe even vaccines - and a huge epidemic would still be growing. And, as usual, psychiatry would be ready to supply the chemicals, to treat the symptoms, while they look for the ever-elusive cause of multiple personalities.

This is, as far as I'm concerned, the genesis of modern day psychiatric "epidemics."

Like I Said – It’s not so easy being mean

The people at 60 minutes, and the actors and crew at Sesame Street, and the parents and professionals who know these children have unquestioned love and honest and pure intentions. They are assertively protective of these children, and they make sure they are informed.

From my perspective, it is a gut wrenching experience watching this tragedy unfold. I’ve known for forty years – as do many, many others – these kids need good teachers, not doctors. There isn’t a deficiency or – forgive us all – a “handicap.” (See what Hans Asperger had to say about “cure” in Notes.)

I’ll Be Watching Too

How will they portray Julia on Sesame Street?

Will she be unresponsive? Will she avoid eye contact? Will she be off to herself, isolated? Will she be portrayed as socially inept? Will she have difficulty making friends? Will she be fixated on an unusual object? Will she engage in various rituals? Will she become expressionless? Will she use peculiar phrases? Will she lack an interest in making friends? These are just some of the “symptoms” of children on the “spectrum.”

Will adults – professional and otherwise – be defending her behavior by explaining to everyone that Julia has a brain disorder and needs our understanding about her “challenges?”

Not without hearing from me, for what it’s worth.

Finally

To Ms. Stahl, to Oscar, to Big Bird, and all the others at Sesame Street, and to the parents and caretakers of these very special kids – we are on the same side. I love these kids too. I want to protect them too.

Lastly, dear Julia, your debut is loved and protected, and that’s a good thing. I can already tell, you’re going to be great. Everyone is watching.

Just be yourself.

~~~~~~~~~~~~~~~~~~~~~~~~~~
Notes

Kanner believed, and argued over his lifetime, that autism was rare. He must have noticed an initial “outbreak.” The John Hopkins psychiatrist “undiagnosed” – and sent home – 9 out of 10 children sent to his practice by other clinicians.

Asperger believed the "cure" for the most disabling aspects of autism is to be found in understanding teachers, accommodating employers, supportive communities, and parents who have faith in their children's potential.

Many people have read or are familiar with Kanner’s first 11 cases of autism. Less well known is the 30 year follow up for those 11 cases. Note the outcomes for the children left in hospitals. You can read it here.
~~~~~~~~~~~~~~~~~~~~~~~~~~

“Autism” from another point of view

“Composers are just as plentiful as the other Artisans, say nine or ten per cent of the population, but in general they are very difficult to observe and thus greatly misunderstood. Very likely the difficulty comes from their tendency not to express themselves verbally, but through their works of art. Composers are usually not interested in developing ability in public speaking, or even in the art of conversation; they prefer to feel the pulse of life by touch, in the muscles, in the eyes, in the ears, on the tongue. Make no mistake, Composers are just as interested as other types in sharing their view of the world, and if they find a medium of non-verbal communication-some art form-then they will express their character quite eloquently. If not, they simply remain unknown, their quietness leaving their character all but invisible.” Keirsey - (Please Understand Me II)

by Chuck Ruby, Ph.D.

A recent article in the Journal of Abnormal Psychology, also publicized in Science Daily, reports on the results of research that is attempting to develop a better way to classify mental disorders by using a dimensional rather than categorical approach. The system is called the Hierarchical Taxonomy of Psychopathology (HiTOP). While it might correct some of the shortcomings of the present Diagnostic and Statistical Manual of Mental Disorders (DSM) diagnostic system, it nonetheless falls short. Its weakness is three-fold: 1) as with the DSM, it still regards human struggles as pathology; 2) despite its use of dimensions, it still retains the main categorical challenge of determining normal from abnormal human experiences; and 3) the factor analysis statistical approach does not always account for all variation among individuals' experience of distress.

First and foremost, the HiTOP continues to use a medical model and invokes the term “psychopathology”. It must be remembered that this is figurative language at best and misinformation at worst. There is no evidence that anything psychological or mental can literally be pathological. If any “mental disorder” is shown to be caused by true brain pathology, then it would fall within the medical specialty of neurology. The HiTOP continues to perpetuate the scientifically empty hypothesis that existential human problems are illnesses. While it does use a dimensional approach in an attempt to recognize human diversity, it still couches those problems in language that implies illness (e.g., pathology, patient, symptoms, syndromes, clinical, illness, comorbidity, diagnostic, psychopathology, etiology, pathophysiology, etc.)

More over, the HiTOP might actually be increasing the extent to which natural human struggles are considered pathological, even more than the DSM. For example, it is said that “[d]imensions are psychopathologic continua that reflect individual differences in a maladaptive characteristic across the entire population (e.g., social anxiety is a dimension that ranges from comfortable social interactions to distress in nearly all social situations)." But how can “comfortable social interactions” be considered psychopathological (or even problematic) and entire dimensions of human experience be "psychopathologic continua"? This seems to be saying that all human activity can be considered pathological.

So in continuing to use the medical model, but absent any evidence of biomarkers that identify the putative pathology, the HiTOP remains a pseudo-medical endeavor and suffers the same weakness of the DSM. It claims pathology but it must rely on moral judgements, not science, to identify pathology. Given the lack of evidence of literal pathology, who determines whether something is maladaptive?

The researchers consider the HiTOP to be a project alongside the National Institute of Mental Health (NIMH) program called the Research Domain Criteria (RDoC) as promising dimensional alternatives to the DSM system. But the RDoC and HiTOP suffer from the same weakness: they fail to start with evidence of real pathology. Rather, they assume it. In the case of the RDoC, neurological concomitants of human distress are described as pathology. With the HiTOP, natural variation of human distress is considered pathological.

The HiTOP’s second weakness has to do with how the researchers use the dimensional model. They pass up an opportunity to use the factor analytic statistical approach to create a system of hierarchical continua with which to describe the intensity and types of distress outside a medical and pathology model. Such an approach is seen in the NEO Personality Inventory (NEO-PI-R), which is an instrument providing a measurement of five personality factors, each with six facets. It is one of the few psychological instruments that does not conjure up pathology.

To the contrary, the HiTOP retains a focus on distinguishing between abnormal and normal human experiences. Thus, despite using a dimensional approach, it still saddles itself with a categorical decision.  This is the exact opposite of what the HiTOP was intended to do. It is said, “[t]his quantitative approach responds to all aforementioned short- comings of traditional nosologies. First, it resolves the issue of arbitrary thresholds and associated loss of information.”  Really? If the task is to differentiate between normal and abnormal, there will always be the need to set an arbitrary threshold between psycho-normality and psycho-pathology.

This problem is manifest in the following statement: “A common concern with dimensional classifications is whether they are applicable to clinical settings, as clinical care often requires categorical decisions. Indeed, actionable ranges of scores will need to be specified on designated dimensions for such a classification to work effectively in clinical practice. Rather than being posited a priori, these ranges are straightforward to derive empirically, as is commonly done in medicine (e.g., ranges of blood pressure, fasting glucose, viral load, etc.).”

But how do we determine that point (or range) between normal and abnormal human experiences? In real medicine, that decision is based on the extent to which the pathological factor threatens the physical viability of the patient. We do not have that with “mental health” because none of the ranges or levels of "mental illness" affect the physical viability of people any more than other behaviors not typically considered pathological affect physical viability, such as high risk recreational pursuits and sports.

The problem with using dimensional tools to assess “illness” is that the assessors must arbitrarily determine the separation between abnormal (ill) and normal (healthy) without any scientific foundation to do so. It gets back to what I said earlier, the assessor will be making a moral judgement about how much distress is normal.

Lastly, like all research, the variation of human experiences of distress cannot be explained completely by factor analyses. In some research a sizable portion of the natural variation of human distress is unexplained. This can be a problem for the HiTOP, but it is difficult to determine as the authors do not report the specific statistics that would allow one to make that determination. For instance, the eigenvalues, loadings, and communalities of the factor analyses in studies used to construct the HiTOP are not given. There can be a substantial amount of the factor analytic data that isn’t accounted for by the dimensional model.

Also, factor analyses are dependent on the scales/instruments that are used in collecting the original data. Therefore, information that is not collected via these instruments is not considered. The factor analysis identifies the relationship between the variables assessed by the instrument. It doesn’t identify variables that are not assessed by the instrument. If there is an important variable that is overlooked by the original instruments, it won’t be included in the factor analysis. So, if the instrument only looks at variables consistent with a medical model, as is done here, then only medical model factors will result.

The HiTOP is the latest in a line of "newer and better" diagnostic systems. Even though it might offer a more realistic view of human variation, it nonetheless still suffers the same weaknesses as other attempts to classify the scientifically threadbare pathology model of human distress.

ISEPP's Executive Director, Chuck Ruby, Ph.D., was interviewed recently on WLJA radio's "Bedlam in America", hosted by Katherine Hine. Dr. Ruby discussed a variety of issues, including ISEPP's Open Letter to national professional organizations addressing the ethical problems with the DSM, psychologists' involvement in national security interrogations, and the limitations of psychological expertise, especially when it comes to dealing with violence in our society.

by Chuck Ruby, Ph.D.

A recent article in STAT addresses the poor track record of psychiatric drugs. But instead of concluding that the drugs or a flawed diagnostic system is the problem, the article focuses on the brain as the possible culprit in why the drugs don’t work.

It starts out with the story of Katie, who has been struggling for 20 years with visions and voices. My heart goes out to Katie in her life of struggle. But the article inhumanely and sterilely portrays her as merely a difficult patient. It notes that she has been homeless and hospitalized several times. But it never addresses the likely reason she was homeless: she’s been hospitalized and drugged several times. This would make her a shell of a human being without connection to her emotional world, which is where we find value, motivation, meaning, and the willingness to have faith in ourselves and others.

She is said to have finally found the right psychiatric drug after trying “just about every drug there is”. She is now taking Risperdal, one of the most dangerous of the psychiatric chemicals. It is said to “work well” for her. But this just means it put her into such a stupor that she isn’t concerned by the visions and voices anymore. But also, she is unlikely to be able to do anything else in an independent and functional way - thus the times of homelessness. Later in the article, she says, “With Risperdal, the voices don’t go away - but they get really quiet. They hardly bother me anymore.”

The author points out that it took Katie’s doctors 15 years to properly diagnose her condition, and even longer to find the right drug. Now why would it take 15 years to find a correct diagnosis? The DSM has been touted as a remarkable breakthrough as an objective and accurate psychiatric diagnostic tool. How could this be? The answer: The DSM is not, in fact, a valid diagnostic tool of real brain disease diagnoses. It is a catalogue of human problems in living, with fuzzy boundaries, similar to horoscope categories.

The article claims that while “scientists have made tremendous advances in decoding the genetics of physical illnesses, such as cancer, and developing precision therapies, treatments for mental health remain blunt tools.” The first part of this is true, but the reason mental health treatment tools are blunt is because “mental illness” (I’ll now dispense with the quotes but remember the term is figurative) is not an illness of the body that can be targeted for treatment. It is a metaphor that refers to personal, economic, political, spiritual, and existential dilemmas common to all people. If they keep looking for it in the body they will never find it. It would be like looking for evidence of heartbreak by examining the heart.

Nonetheless, psychiatry continues in blaming the brain. Psychiatric drugs are said to “work by blasting entire mechanisms in the brain, without addressing the specific chemical pathways that have gone awry.” In truth, medical science has never demonstrated mechanisms of the brain or chemical pathways to have “gone awry”. Again, they are looking in the wrong place. As another analogy, it would be like looking for the reason a driver is speeding by examining the engine.

With continued focus on the brain, the poor track record of psychiatric drugs and a 70% decline in drug company research is ostensibly “because the biological causes of mental illness are so complex. There hasn’t been much innovation in psychiatric medications in more than two decades.” This demonstrates the error. They keep looking and looking a the heart in order to find the causes of heartbreak, and they come up empty handed. True, the causes of mental illness are complex, but not complex bodily systems. The causes are complex human experiences.

So the search for biomarkers in the brain continues in order to help diagnose mental illness and to find treatments, with the often used comparison to the biomarker of increased blood glucose to diagnose diabetes. They hope such biomarkers will tell them “what’s gone wrong in the circuitry of a particular patient’s brain and offer clues for drug development — and, perhaps one day, even precision psychiatric therapies. But that’s far easier said than done.” Actually, that’s impossible. It’s impossible because they keep looking in the brain for defective circuits when decades of research has failed to give even a scintilla of evidence that the brain is what’s wrong. In most other areas of real scientific research the preponderance of evidence gathered dictates the direction of future research. In psychiatry, the research continues looking for proof the earth is flat, after years of evidence showing that it is spherical.

Then comes an absurdity. This article suggests that some biomarkers might not be physical. This is an oxymoron: biomarker by definition is about biology, which is physical. Voice analysis is an example given, but wouldn’t this just demonstrate not a biomarker, but one’s experience of emotional distress? The medically-scientifically-sounding quote, “Research suggests that voice analysis could give clues as to a patient’s mental illness, as certain sentence structures and cadences can objectively be linked to psychiatric disease” just means voice tone and structure are linked to distress. But more problematic about this, why not just listen to the meaning of what the person has to say? They are looking right past the issue.

But returning to biomarkers, a study is used to suggest an imbalance of free radicals could help diagnose schizophrenia. This is another absurdity. Free radicals increase when someone is under chronic stress. These aren’t biomarkers of schizophrenia, they are biomarkers of chronic distress. But would we really need to find biomarkers in order to conclude someone is distressed?

So the article turns to genes. One chair of psychiatry says, “As more genes are linked to various mental illnesses, the number of psychiatric biomarkers should increase.” Another misleading comment because no gene has ever been linked to mental illness.

In another frequently used tactic, the story of Alzheimer’s is presented to assuage those who are frustrated with the failure to find treatments for mental illness. It is said that the “physical characteristics of brains disordered by Alzheimer’s are well known, for instance, yet drug companies have failed for decades to come up with effective drugs, despite pouring hundreds of millions into research.” Throwing Alzheimer’s in here is a ploy, again to give a medical impression about mental illness. Alzheimer’s is a condition caused by real brain defects. There are no brain defects of mental illness.

The article then turns to illicit street drugs and their use as “treatment”. Aside from the fact that current illicit street drugs like cocaine and heroin were once prescribed as “medicines”, this line of research is silly. It is said that Ketamine is showing remarkable promise in treating depression. Psilocybin for anxiety and depression in terminally ill cancer patients. And MDMA, or ecstasy, for PTSD. Sure. And I use rum and coke to treat my workaholism. These drugs just like prescribed legal psychiatric drugs do no more treating than does alcohol.

Throughout this article, the language used and the allusions made give the impression that mental illness is about brain defects, when there is no evidence of that. It is repeated that brain mechanisms, circuits, and pathways are misfiring, awry, jarred, and strengthened. This is incredible as there is no evidence of any of it.

In closing out the article, the author notes that psychiatric drug prescription rates have increased substantially in the past two decades, with the rate of antidepressant use alone quadrupling, and with one in six Americans on some type of psychiatric drug. This should tell us something. Is the huge increase in drug prescription rates a sign of increasing prevalence of mental illness? Or that despite the use of these drugs, they don’t work? Or perhaps an even more parsimonious explanation: there is no illness to treat.

by Randy Cima, Ph.D.

In a February 17th story on NBC Nightly News entitled, Brain Scans Detect Signs of Autism in High-Risk Babies Before Age 1, Brian Williams reported the results of research on predicting autism. He characterized the research as “something surprising” and he said it might lead to better treatment for children “who haven’t even shown symptoms yet.” He summed up autism as a “neurological disorder that affects the ability to communicate and socialize.” Those terms “symptoms” and “neurological disorder” gnaw at me when the subject is autism.

The headline alerted me. I’ve seen headlines like this before. Here are a few of them:

• Could scans diagnose autism sooner? Images reveal how part of the brain differs in boys with the condition. Daily Mall, 2016.
• Brain Scans Can Identify Autistic Toddlers With Future Language Development Difficulties - MEDICAL DAILY, 2015.
• How Brain Scans Can Diagnose Autism With 97% Accuracy. 2014, TIME.
• Study: Brain scans detect early signs of autism - 2013 CBS Evening News.
• Brain Scans May Help Detect Autism - 2011, May, WEBMD.
• MRI Shows Differences in Autistic Brain - 2011, Sept, WEBMD.
• New brain scan to diagnose autism - 2010, August, BBC News.
• How Brain Scans Can Diagnose Autism With 97% Accuracy - 2010, December, TIME.

These were found after only a ten-minute Google search. There are more. As an exercise, I Googled “brain scan bi-polar.” I did the same for ADHD. You can see the results at the end of this article.

More than two decades ago, Dr. Peter Breggin, a nationally recognized psychiatrist, and critic of modern psychiatry, referred to brain scans as “brain scams.” They have not improved any since then. The science is primitive, and when used to predict or find ways to “treat” human behavior, it is useless.

Incidentally, this study about autism and a most recent study about ADHD were announced within days of each other (the ADHD study was also critiqued by ISEPP). The brain scans for autistic infants showed: “The brain volume of infants . . . grew faster in infants later diagnosed with autism, compared with those who did not receive a diagnosis. The ADHD brain scan study begins with this: People diagnosed with attention deficit hyperactivity disorder have smaller brain volume than those without the disorder. Too much brain volume, autism. Two little, ADHD. Within 24 hours of each other.

Funded by the NIH and Autism Speaks, the study was conducted by the Infant Brain Imaging Study Network (IBID). IBID is a consortium of 8 universities in the U.S. and Canada. Dr. Joseph Piven is the director. On February 15, 2017, IBID posted a press release touting “researchers from around the country were able to correctly predict 80 percent of those infants who would later meet criteria for autism at two years of age.” It is an impressive number. It was part of every reporter’s story.

But let’s look at the numbers to understand this claim better. The infants were “high risk” or “low risk.” “High risk” infants have an older sibling with autism, “low risk” do not. They scanned infants, while they slept (sedated), at 6 months, 12 months, and 24 months.

One group consisted of 117 infants with no family autism history. The second group consisted of 248 undiagnosed infants, who also had an autistic sibling. The third group included 70 infants already diagnosed with autism, who also had an autistic sibling. It’s the third group of 70 infants this study highlights.

Looking a little closer, “The brain growth analysis included only 15 of the 70 high-risk children diagnosed with autism,” noted Emily Willingham* in her review, because they were the only participants who had MRI at all three time points (ages 6, 12 and 24 months).” She also noted. “the study population was not large, especially considering the reductions in numbers for some analyses.”

“We now have this finding in these high familial risk infants that we can predict 8 out of 10 that we think will get autism,” says Dr. Piven, IBID’s Director, noted. He agrees the results need to be confirmed with a larger follow-up study. Thus, Dr. Piven’s IBID team has applied for funding from the NIH to do the study. So, Dr. Piven is accurate. The 80% number is for the 15 children used for the brain growth analysis.

This is modern psychiatric science practice. Replicant science means the same team of scientists is allowed to replicate and confirm their own findings, so numbers can be both accurate and misleading at the same time.

I became interested in autism in the late 1960’s. By 1982, as a working professional at the time, my Master’s thesis was Autism and Self-Defiling Phenomena. For a year, I researched everything known at the time about autism. During the same year, I was an intern therapist for 6 families with one of these unique children.

None of the theoretical explanations at the time of my research had anything to do with medicine. The rate of incidence was 4.3 per 10,000. Since psychiatry has intervened, the rate of incidence has increased to 1 in 68. If you already have one autistic child, psychiatry tells us, chances are 1 in 5 you will have another. These numbers are absurd on the face of it.

Reading studies is routine for me. Like the hundreds of brain scans that made headlines, nothing will come of this. The IBID team will be refunded, no new tools will be developed, no new scans that will be embraced by their colleagues, more “evidence” will be presented, more “possibilities” will be exposed, and, as always, “more study will be needed.”

Mostly though, nothing will come of this because autism isn’t a disease, disorder, disability, defect, dysfunction or anything else that can be “detected” by medicine.

Finally, on the Thinking Person’s Guide to Autism website there is a link "On Autism Orgs". Click on it at you find five tenets they adhere to, almost as a warning to other organizations. The first one is this:

"Support, not cure: autism is a naturally occurring human neurological variation and not a disease process to be cured. Medical or health issues that may accompany autism should be addressed independently."

Please repeat.

*Emily Willingham is a biologist, research scientist, writer, and science editor for Thinking Person’s Guide to Autism, and for the past 20 years, has written dozens about the “science” of autism.

More on purported brain scan "breakthroughs":

The results to follow took 20 minutes to find. You can do the same. Google “brain scan” and nearly anything else. Here’s a few suggestions: anxiety, depression, spouse abusers, sleep deprivation, PTSD, concentration problems, homosexuality, sex addiction, obsession, disorders of dreaming (nightmares), anorexia. You can come up with your own. As you will see, nothing is too ridiculous.

My personal favorite? This one: Location of Sense of Humor Discovered – Medscape, November 2000, here. "A small part of the frontal lobes appears critical to our ability to recognize a joke," said Dean K. Shibata, MD, principal investigator.

BI-POLAR

2015 - Bipolar disorder: New MRI imaging provides new picture, new insight.  https://www.sciencedaily.com/releases/2015/01/150106081217.htm

2014 - Bipolar disorder: brain scans show excitable pleasure response. http://www.medicalnewstoday.com/articles/279338.php

2013 - Is it Bipolar or Depression? New Brain Scan May Have the Answer. https://psychcentral.com/news/2013/09/29/is-it-bipolar-or-depression-new-brain-scan-may-have-the-answer/60060.html

2008 - Cognitive neuroscience and brain imaging in bipolar disorder. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3181872/

2006 - Finding Bipolar Disorder with MRI. https://www.technologyreview.com/s/405200/finding-bipolar-disorder-with-mri/

1999 - Brain Magnetic Resonance Imaging of Structural Abnormalities in Bipolar Disorder. http://jamanetwork.com/journals/jamapsychiatry/fullarticle/204822

ADHD

2017 - Brain differences in ADHD. https://www.sciencedaily.com/releases/2017/02/170216105919.htm

2016 - Can a Brain with ADHD Look Different? http://www.healthline.com/health/adhd/brain-scans

2015 - ADHD Patients' Brain Scans Showed This. http://www.webmd.com/add-adhd/childhood-adhd/news/20151215/adhd-patients-show-weaker-connections-in-brain-networks-tied-to-focus-study#1

2014 - Brain scans could save kids from ADHD misdiagnoses. http://www.wired.co.uk/article/adhd-scan-test

2013 - Reading the Brain: FDA Approves First Scan for Diagnosing ADHD. http://healthland.time.com/2013/07/16/reading-the-brain-fda-approves-first-scan-for-diagnosing-adhd/

2012 - ADHD and Stress in Children: Brain Scans. http://newideas.net/adhd-stress-children-brain-scans

2009 - Brain Scans Link ADHD to Biological Flaw Tied to Motivation. http://www.washingtonpost.com/wp-dyn/content/article/2009/09/21/AR2009092103100.html

2007 - Brain Matures a Few Years Late in ADHD, But Follows Normal Pattern. https://www.nimh.nih.gov/news/science-news/2007/brain-matures-a-few-years-late-in-adhd-but-follows-normal-pattern.shtml

2004 - Brain Imaging Data of ADHD. http://www.psychiatrictimes.com/adhd/brain-imaging-data-adhd

by Grace Jackson, M.D., Diplomate , American Board of Psychiatry and Neurology

I read with interest the February 18th Washington Post article (“Mental illness and heart disease are often found in the same patients”) by Dr. Nathaniel P. Morris, a physician in training at Stanford University’s psychiatry residency program. The article was correct about the bidirectional relationship between cardiac conditions and the phenomenological entity known as “clinical depression.” However, with the exception of one sentence (“older psychiatric drugs, such as tricyclic antidepressants, came with high-risk side effects on the heart”), the article overlooked the potential for most classes of psychiatric medication to cause or enhance cardiac problems. Equally striking, the article suggested that “newer generations of psychiatric drugs – such as selective serotonin reuptake inhibitors, may protect cardiovascular health.” Such a claim remains contestable, and a fact check is in order.

A thorough review of the medical literature (see sample abstracts, below) suggests that psychiatric drugs – particularly, antipsychotics and antidepressants -- remain a significant and controllable risk factor for coronary artery disease, sudden cardiac death, myocarditis, cardiomyopathy, arrhythmias (including pulseless electrical association), thromboembolic disease, stroke, transient ischemic attacks, and small vessel ischemia in the brain. Before any psychiatrist can act constructively as a consultant to other specialists, he or she must master the “target organ toxicities” associated with psychiatric and non-psychiatric pharmaceuticals.

While it was reassuring to read the empathic remarks of Dr. Morris, whose writings reflected a commendable sensitivity to the physical and emotional impact of the medical procedures which his patients had endured, I found myself frightened by possible inadequacies and omissions in his current training. I hope his empathy will be bolstered by unbiased instruction which must include the mortality and morbidity associated with all psychiatric drugs.

Sample abstracts:
-Epidemiol Psychiatr Sci. 2017 Feb;26(1):18-21. doi: 10.1017/S204579601600086X. Epub 2016 Nov 22. Antipsychotic drug exposure and risk of myocardial infarction. Barbui C1, Gastaldon C1, Papola D1, Ostuzzi G1.

It found nine studies and calculated that the odds (risk) for developing MI were 1.88-fold higher in antipsychotic users compared with individuals who had not taken antipsychotic drugs.

-Circulation. 2014 Jul 15;130(3):235-43. doi: 10.1161/CIRCULATIONAHA.114.008779. Epub 2014 May 16. Association between antipsychotic use and risk of acute myocardial infarction: a nationwide case-crossover study. Lin ST1, Chen CC2, Tsang HY2, Lee CS2, Yang P2, Cheng KD2, Li DJ2, Wang CJ2, Hsieh YC2, Yang WC2.

The adjusted odds ratio of AMI risk was 2.52 (95% confidence interval, 2.37-2.68) for any antipsychotics, 2.32 (95% confidence interval, 2.17-2.47) for first-generation antipsychotics, and 2.74 (95% confidence interval, 2.49-3.02) for second-generation antipsychotics.

-Arch Intern Med. 2004 Jun 28;164(12):1293-7. Antipsychotics and the risk of sudden cardiac death. Straus SM1, Bleumink GS, Dieleman JP, van der Lei J, 't Jong GW, Kingma JH, Sturkenboom MC, Stricker BH.

Current use of antipsychotics was associated with a 3-fold increase in risk of sudden cardiac death. Current use of antipsychotics in a general population is associated with an increased risk of sudden cardiac death, even at a low dose and for indications other than schizophrenia.

-Eur J Clin Pharmacol. 2017 Jan 9. doi: 10.1007/s00228-016-2187-x. [Epub ahead of print] Use of antidepressants and the risk of cardiovascular and cerebrovascular disease: a meta-analysis of observational studies. Biffi A1, Scotti L2, Corrao G2.

Use of SSRIs was associated with an increased risk of cerebrovascular disease (RRs, 1.24; 95% CI, 1.15 to 1.34), while the use of TCA was associated with an increased risk of acute heart disease (RRs, 1.29; 95% CI, 1.09 to 1.54).

-Neuropsychopharmacology. 2015 Dec;40(13):3027-35. doi: 10.1038/npp.2015.158. Epub 2015 Jun 10. White Matter Hyperintensity Accumulation During Treatment of Late-Life Depression. Khalaf A1, Edelman K1, Tudorascu D1, Andreescu C1, Reynolds CF1, Aizenstein H1.

Among all patients, there was as a significant increase in WMHs over 12 weeks (t(46)=2.36, P=0.02).

-Int J Cardiol. 2016 Jan 15;203:867-73. doi: 10.1016/j.ijcard.2015.11.032. Epub 2015 Nov 6. Antidepressant use and risk for mortality in 121,252 heart failure patients with or without a diagnosis of clinical depression. Brouwers C1, Christensen SB2, Damen NL1, Denollet J1, Torp-Pedersen C2, Gislason GH3, Pedersen SS4.

Patients with HF taking antidepressants had an increased risk for all-cause and CV-mortality, irrespectively of having clinical depression.

-Biomed Sci Instrum. 2015;51:400-6. The Effect Of Selective Serotonin Reuptake Inhibitors and Antidiabetic Drugs on Cardiomyocytes. Nelson SA1, Wilson GA, Tucci M, Benghuzzi H.

Cardiomyocytes were grown in a tissue culture environment and challenged with therapeutic concentrations of SSRIs alone or a combination of SSRIs and antidiabetic drugs. Intracellular markers for stress and cytomorphometric analysis indicated SSRIs and SSRIs in combination with antidiabetic drugs negatively impact the health of the cardiomyocytes with time in culture.

-Int J Cardiol. 2011 Jan 7;146(1):64-7. doi: 10.1016/j.ijcard.2010.01.006. Epub 2010 Feb 26. High mortality among heart failure patients treated with antidepressants. Veien KT1, Videbæk L, Schou M, Gustafsson F, Hald-Steffensen F, Hildebrandt PR; Danish Heart Failure Clinics Network.

In a Cox Proportional Hazard Model, pharmacologically treated depression was associated with a 49% increased mortality risk (Hazard ratio: 1.49, 95% confidence interval: 1.03-2.16) after adjustment for traditional confounders.

-Circ Heart Fail. 2009 Nov;2(6):582-90. doi: 10.1161/CIRCHEARTFAILURE.109.851246. Epub 2009 Sep 22. Prognosis in heart failure and the value of {beta}-blockers are altered by the use of antidepressants and depend on the type of antidepressants used. Fosbøl EL1, Gislason GH, Poulsen HE, Hansen ML, Folke F, Schramm TK, Olesen JB, Bretler DM, Abildstrøm SZ, Sørensen R, Hvelplund A, Køber L, Torp-Pedersen C.

Antidepressants were prescribed to 19,411 patients, and both TCA and SSRI were associated with increased risk of overall and cardiovascular death (TCA: HR, 1.33; CI, 1.26 to 1.40; and HR, 1.25; CI, 1.17 to 1.32; SSRI: HR, 1.37; CI, 1.34 to 1.40; and HR, 1.34; CI, 1.30 to 1.38, respectively). Coadministration of SSRI and beta-blockers was associated with a higher risk of overall and cardiovascular death compared with coadministration of beta-blockers and TCA (P for interaction <0.01). Coadministration of SSRIs and beta-blockers was associated with increased risk of overall death and cardiovascular death compared with coadministration of TCAs and beta-blockers.

-J Biochem Mol Toxicol. 2016 Sep 2. doi: 10.1002/jbt.21836. [Epub ahead of print]. Toxicity of lithium on isolated heart mitochondria and cardiomyocyte: A justification for its cardiotoxic adverse effect. Salimi A1,2,3, Gholamifar E1, Naserzadeh P1,3, Hosseini MJ4,5, Pourahmad J6.

Results revealed that Li+ induced a concentration- and time-dependent rise in mitochondrial ROS formation, inhibition of respiratory complexes (II), mitochondrial membrane potential (MMP) collapse, mitochondrial swelling, and cytochrome c release in rat heart mitochondria and also induced Caspase 3 activation through mitochondrial pathway, decline of ATP and lipid peroxidation in rat cardiomyocytes. These results indicate that the cardiotoxic effects of Li+ were initiated from mitochondrial dysfunction and oxidative stress, which finally ends in cytochrome c release and cell death signaling heart cardiomyocytes.

-Am J Emerg Med. 2015 Sep;33(9):1330.e1-5. doi: 10.1016/j.ajem.2015.03.023. Epub 2015 May 18. Acute cardiomyopathy precipitated by lithium: is there a direct toxic effect on cardiac myocytes? Anantha Narayanan M1, Mahfood Haddad T2, Bansal O3, Baskaran J4, Azzouz MS3, Akinapelli A3, Esterbrooks DJ3.

A patient with typical features of lithium toxicity including sinus bradycardia and junctional rhythm, who, in addition, presented atypical features with diffuse T-wave inversions, QT prolongation, and acute left ventricular systolic dysfunction with serum cardiac marker elevation.

-Drug Saf Case Rep. 2016 Dec;3(1):10. STEMI Secondary to Coronary Vasospasm: Possible Adverse Event of Methylphenidate in a 21-Year-Old Man with ADHD. Baumeister TB1, Wickenbrock I2, Perings CA2.

The case of a 21-year-old man diagnosed with ADHD who recently started therapy with Ritalin® Adult 20 mg for at least 3 days. Afterwards he presented with chest pain, elevated troponin and creatine kinase, and posterolateral ST elevations. A myocarditis was initially supposed. In the coronary angiography, signs of coronary artery spasm could be found. The echocardiography showed mild left ventricular dysfunction; no acute myocarditis could be found in the cardiac MRI and myocardial biopsy. The medication with methylphenidate was stopped, and after 12 days the asymptomatic patient was discharged from hospital.

-Case Rep Pediatr. 2015;2015:905097. doi: 10.1155/2015/905097. Epub 2015 Jun 28. Cardiac Arrest following a Myocardial Infarction in a Child Treated with Methylphenidate. Munk K1, Gormsen L2, Kim WY1, Andersen NH1.

A case with an 11-year-old child, treated with methylphenidate, who suffered cardiac arrest and was diagnosed with a remote myocardial infarction. This demonstrates that myocardial infarction can happen due to methylphenidate exposure in a cardiac healthy child, without cardiovascular risk factors.

But see:

-Atherosclerosis. 2014 Aug;235(2):496-502. doi: 10.1016/j.atherosclerosis.2014.05.918. Epub 2014 Jun 5. Anti-anxiety drugs use and cardiovascular outcomes in patients with myocardial infarction: a national wide assessment. Wu CK1, Huang YT2, Lee JK3, Jimmy Juang JM4, Tsai CT4, Lai LP4, Hwang JJ4, Chiang FT4, Lin JL4, Chen PC5, Lin LY6.

Anti-anxiety medications are independent associated with a decreased risk of cardiac mortality and heart failure hospitalization in patients after a new MI.

-J Cardiovasc Pharmacol. 1994 Jul;24(1):55-8. Antiischemic effects of intravenous diazepam in patients with coronary artery disease. Rossetti E1, Fragasso G, Xuereb RG, Xuereb M, Margonato A, Chierchia SL.

DZP significantly delays onset of exercise-induced myocardial ischemia in patients with coronary artery disease.

by Al Galves, Ph.D.

A careful reading of this CNN article about brain differences related to ADHD tells me that nothing in it will be very useful to human beings. The article reports on a study that finds that persons diagnosed with ADHD have smaller parts of the brain, which are related to the processing of emotions. How, pray tell, is this going to be useful to human beings?

We don’t have any psychotropic drugs or any forms of psychosurgery that can be used to improve the emotional processing of human beings. We have drugs and psychosurgery that can dull emotions or artificially enervate emotions but we don’t have any drugs or psychosurgery that can help people do a better job of learning from their emotions or using them in beneficial ways.

On the other hand, psychotherapy can and regularly does help people learn how to use their emotions in beneficial ways. And psychotherapy does this without causing the kind of harmful “side effects” that are associated with psychotropic drugs and psychosurgery.

Although it isn’t explicit in saying so, this article implies that ADHD is a result of smaller brain structures in areas that process emotions. There is no evidence of that being the case. All we have is a finding of correlation between smaller brain structures and ADHD. That is not evidence that such brain anomalies cause ADHD. It is merely a correlation, and a small one at that. Knowing what we know about the stress response in humans it is more likely that the behavior and state of being related to diagnoses of ADHD is causing the brain anomalies than the other way around.

Plus, as is typical of the claims in these studies, the claim is not supported by the data. The largest brain region difference reported in the study was with the amygdala. The difference between the ADHD and non-ADHD groups’ was a Cohen’s d of .19. But this is such a small difference in the group averages that the groups overlap so much that most people in the ADHD group don’t have the claimed smaller amygdala than those in the non-ADHD group. How can this be if the title reads, “Brains of those with ADHD show smaller structures related to emotion”? See the display below, which shows an even larger Cohen’s d of .20. The ADHD group would be the darker one.

In stating that ADHD is a neurodevelopmental disorder, the article tells an untruth. There is no scientific reason to believe that ADHD is a neurodevelopmental disorder. ADHD is diagnosed through observations of certain behavior, not brain scans. There can be many reasons for such behavior, including concern about being abused or mistreated at home, not being able to do the work being assigned in school, being bored in school, not caring about what is being focused on in school, being frightened by an abusive teacher, etc., etc., etc. Neurodevelopmental anomaly is only one of many explanations for the behavior associated with a diagnosis of ADHD, and it is a poor one. In order to call it a neurodevelopmental disorder, one must first show evidence of a neurodevelopmental defect, and that has not been done.

In closing, although the author of the article and the authors of the study may believe they have a finding which is useful to human beings, such is not the case.

by Mary Neal Vieten, Ph.D., ABPP

A February 8, 2017 article in Science Daily reports the results of mice research that suggests the chemical ketamine could make soldiers less reactive to the horrors of war. Besides the typical problems associated with translating animal research into human applications, any response to this line of inquiry must include a comment on SCIENCE as well as ETHICS.

In medical research scientific inquiry assumes that the ailment being cured as well as the treatment being offered, are tangible, identifiable things that can be scientifically distinguished from other things. Ketamine is a pharmaceutical, a thing, and distinguishable from other pharmaceuticals. Its powerful anesthetic effects also make it a popularly used recreational drug, under the names Special K, Cat Valium, and Vitamin K.

PTSD on the other hand, is a construct, not a thing, it is loosely defined, and it is the sum of its definition, a definition that is not isolated by science, but rather negotiated and voted into the DSM-5. No one will argue that there is no problematic response in people who are exposed to psychologically traumatic stimuli, however no one can argue that this is a distinguishable medical thing, separated from other things by objective medical/laboratory tests.

PTSD only requires that a sufferer complains of a specific set of predictable emotional responses, after being traumatized to a licensed listener, who agrees (diagnosis/label given) or disagrees (no diagnosis or another label given). Another listener may interpret the suffering differently, and apply no label or another label. Interpretation is subject to culture, religiion, values, the experiences of the listener - the list goes on. Scientifically determined categories of illness are not subject to this latitude: you either have a bacteria, virus, cancer, macular degeneration, fracture, or you don’t. All of this is to say, that PTSD is a construct, not an illness. Think of it like “peace” or “justice.” Everyone knows when they are there, and when they are absent, but they are still the sum of their definition, not objective things.

Using a potentially harmful pharmaceutical like ketamine that is known to be addictive, cause flashbacks, and a host of other undesirable effects to treat a loosely defined construct is not only unworthy of scientific inquiry, it is also unethical. Giving it to our military members for this purpose is unconscionable. Furthermore, even in the case that PTSD was an identifiable discrete illness, discrete from other illnesses, which it is not, the hallmark of PTSD is a person who is suffering because of something horrific that occurred.

We need to consider the ETHICS of injecting humans with a substance with the goal of preventing normal human suffering in the face of horror. If we succeed, what kind of human have we created? Ask yourself if you want to be or live next door to that creation.

by Chuck Ruby, Ph.D.

Including "Blue Monday" in the title of this article in The Sun and briefly mentioning it in the first few paragraphs is a way to grab the attention of readers. But in a bait and switch ploy, the bulk of this article reveals the real intention is to spread the propaganda that depression is an illness. Let me assure readers, depression is not a mental "illness".

In trying to distinguish depression from "common and totally normal" sadness, this article describes it as an "immense feeling of sadness that can last for weeks and maybe even months." So, we are told depression isn't just sadness, it is really, really sad sadness. Yet nowhere are we shown the evidence that it is an illness.

For decades, attempts have been made by the mental health industry to prove the brain-pathology basis of depression. Despite the billions of public dollars invested in this research, no such evidence of brain pathology has been discovered. The only thing this research has shown is that our experiences and behaviors are mirrored by changes in the brain. This is something we already knew. Yet, instead of giving up the search and redirecting those monies to more worthy research of real diseases, the mental health industry repeats the worn out pronouncement that discovery is just around the corner! Ironically, if such a discovery came, wouldn't depression then fall within the medical specialty of neurology, the real medical specialty that studies real brain illnesses?

We are also told in this article, "Some people think depression is trivial and not a genuine health condition. They're wrong - it is a real illness with real symptoms." This is the set up: present a false dichotomy straw man argument with those who believe depression is an illness on one side and those who think it is trivial on the other (I don't know of anyone who thinks it is trivial). This doesn't represent ISEPP's critique, nor many others' critiques, of the conventional medical model view of depression. It falsely categorizes those of us who say depression is not a real illness as people who think it is a trivial matter.

Nothing can be further from the truth, but it is the typical way those in power try to discredit organizations like ours and perpetuate the myth. ISEPP considers depression serious and potentially dangerous. But we see it for what it is: a natural and expected human reaction to intense emotional pain, not a sign of brain pathology. There is absolutely no evidence it is caused by real biological defects of the brain. Therefore, medical interventions, such as the prescription of chemicals and sending electrical currents through the brain, are not the answer.

In truth, depression is an insidious strategy adopted in an attempt to escape painful emotions. This is done in various ways such as remaining in bed, not answering the phone, not eating, not leaving the house, and generally trying to back out of life and to shut down. All these are attempts to sooth through escape.

The problem with the strategy of depression is that it doesn't work, other than in the very short term. Remaining in bed, for instance, can be very soothing. But once you wake up, your life is still there, and you might also now feel guilty and lethargic about having stayed in bed all day. As another example, turning down a social engagement provides immediate relief, but in the long run this can also lead to feelings of guilt and increasing social isolation. In short, the paradox of depression is that while it is intended to soothe, it actually adds more emotional pain to life, from which further and further attempts to escape are made, spiraling the person down into despair.

The answer to depression is in allowing emotions to be felt and "heard”, sometimes with the help of so-called professionals but sometimes just with the aid of an understanding friend. The process can be a long one, and it certainly isn't fixed by simplistic mechanical or chemical interventions. Emotions are how humans know what is important. The brain evolved to react to certain significant situations such as loss (sadness) and danger (fear). We experience these emotions when those things are happening and it is important to heed the messages, not avoid them.

This article is just one of thousands of others spread across the internet, which perpetuate the myth of mental illness. It is time to think critically about how basic human struggles have been inappropriately medicalized and subjecting people to the inhumane and harmful mental health industry.

by Chuck Ruby, Ph.D.

A recent CNN report is the latest in a long line of horrific shootings and the unfortunately misinformed and misunderstood calls to deny gun ownership to those with "psychiatric problems". NIMH estimates that around 1 in 5 adults are diagnosed with "psychiatric problems" each year. This doesn't include substance abuse "psychiatric problems" and it doesn't include children or teenagers. Further it only includes people who have been formally diagnosed and not those who choose to stay out of the psychiatric system (probably a good choice for them). Lastly, this is only an annual prevalence; each year additional people can be diagnosed, effectively increasing the number of those who have had "psychiatric problems". So if we were to deny all those people the right to have a gun, we're talking about a very large proportion of the population, and many of those calling on gun restrictions would be surprised to find out they are among those with "psychiatric problems".

The problem with gun violence is not "psychiatric problems". Research fails to show a relationship between a diagnosis of mental disorder and risk of violence. Mental disorder diagnoses are merely very loose ways to categorize people with various emotional and behavioral dilemmas. They do not map onto actual neurobiological illnesses that cause violence. There is no such illness. Problem yes, illness no.

But the important thing to remember about gun violence is that a diagnosis is not a way to weed out people who are at risk. There are fairly robust factors that increase one's risk of violence, but the ever-inclusive label of "psychiatric problems" is not one of them. You can see a summary of this issue here: https://psychintegrity.org/wp-content/uploads/2015/08/The-Role-of-Mental-Illness-in-Violent-Behavior-July-2-2014.pdf, which includes how conventional mental health treatment can increase the risk of violence, and in particular how psychiatric drug use can increase the risk as shown here: https://psychintegrity.org/wp-content/uploads/2015/08/White-Paper-Psychiatric-Drugs-and-Violence.pdf.

If we are serious about reducing violence, we should be focusing in the right direction instead of searching for a scapegoat.