In the News

It’s All Settled Now! Antidepressants Work. Or Do They?

9/5/2017        In the News 4 Comments

by Chuck Ruby, Ph.D.


A recent Medscape Psychiatry article announced the results of a "mega-analysis" study of the effectiveness of antidepressants vs. placebo. The lead researcher boldly claims "I think, once and for all, we've answered the SSRI question." There are many follow on assertions just as brazen, but just as misleading. Here are a few:

"...SSRIs work. They may not work for every patient, but they work for most patients. And it's a pity if their use is discouraged because of newspaper reports."

"The finding that both paroxetine and citalopram are clearly superior to placebo...when not producing adverse events, as well as the lack of association between adverse event severity and response, argue against the theory that antidepressants outperform placebo solely or largely because of their side effects...."

"...our results indirectly support the notion that the two drugs under study do display genuine antidepressant effects caused by their pharmacodynamics properties."

"And we did have an impressive, robust difference between active drug and placebo...."

These statements sound impressive. But the effect sizes between the SSRI and placebo groups in the study demonstrate that the difference between the groups is nearly meaningless. The reported effect sizes ranged from .31 to .49. See the graphic representation below which shows an effect size of .5:

The dark blue group would represent the people who took the SSRIs. The light blue represents the placebo group. One can see that the average level of depression for the SSRI group is less than that of the placebo group.

But look at how much the two groups overlap. Given the range of effect sizes in the study, 80-88% of the two groups would overlap. This means many people in the placebo group did better than people in the SSRI group, and many people in the SSRI group did worse than the people in the placebo group! With this in mind, how could the above claims of SSRI superiority be justified? They can't.

This bold sounding announcement that the question has been finally settled about SSRIs' superior effectiveness is typical of those who continue to support the medical model of human suffering. They use statistics to obscure practical and clinical significance. Looks good in medical journals and unless one understands the basics of statistical analyses (in most cases, the effect size is the telling number), it sounds good in media reports too.

The article mentions Irving Kirsch, Ph.D., who has critiqued the use of SSRIs (as have many others). Dr. Kirsch rightly points out another little known issue with studies like these. Not only is a placebo effect likely just because someone knows they are taking a substance (and they think it is the SSRI), but also because those taking the real SSRI will notice the psychoactive effects of the real chemical, and this will enhance the placebo effect. So, one would expect a small effect size difference between the SSRI and placebo group based on this alone. This is exactly what the study shows. Dr. Kirsch cautions that we should weigh this small, meaningless, effect with the potentially harmful side effects of taking these and other drugs to quell human emotional struggles, typically in combinations with other psychoactive drugs.

These above issues make this announcement weak. The study is far from demonstrating that SSRIs, or any other psychoactive drug, is an effective way to address the meaning-laden and personal struggle we call depression.

Religion – Is It All In The Brain?

8/9/2017        In the News 2 Comments

by Chuck Ruby, Ph.D.


A recent study in Neuropsychologica about veterans and brain trauma is a prime example of how medical model thinking and nomothetic research design and analysis wrongly imply: (1) that meaningful human experiences can be best understood by looking at the brain; and (2) that differences between research groups as identified by statistical tests, mean that the class of people in one group share a common characteristic different from the class of people in the other group(s). Unfortunately for the authors of the study, this is not true.

First, the follow quotes from the study reveal how meaningful human experiences are falsely reduced to brain structures:

“…religious beliefs are critically represented in the anterior frontal lobe.”
“…fundamentalist religious beliefs arise from the integrated processing and computations in a distributed brain network….”
“…a vmPFC lesion induces increased fundamentalism.”
“…religious beliefs are partially dependent on correct functioning of the PFC.”

None of these statements are accurate. We’ll never find religious beliefs inside the skull and brain activity does not give rise to religious belief, even though religious belief cannot happen without brain activity. Religious belief, in addition to a plethora of other kinds of meaningful human experiences, can only be understood by understanding the individual person, and even that changes over time. Further, given that they are individuals, people are inescapably nuanced, complex, and unique in terms of the factors that interact and lead up to any one particular characteristic, such as religiosity.

It is true that damage to an area of the brain necessary for a person to have a certain opinion, belief, conviction, or feeling can change the person’s experience of those things. However, especially in the case of highly meaningful things, like religiosity, such changes occur more often not because of damage to those areas but because of experiential changes in living. This study never takes this into account: that veterans who have suffered TBI had more severe and meaningful experiences (both during the trauma and post-trauma) than those who hadn’t suffered TBI. How did those experiences, and not brain damage, affect their turn toward religious fundamentalism?

Regarding the second issue, there was a statistically significant difference in fundamentalism scores between the group of veterans who suffered damage to the ventromedial prefrontal cortex and the group with damage to the prefrontal cortex but outside the ventromedial and dorsolateral regions. Yet, the Cohen’s D was only .71. This means the two group distributions of fundamentalism scores overlapped around 73%.

Given this amount of overlap of groups, it does not justify the researchers’ claim that, “…participants with vmPFC lesions reported greater fundamentalism.” or “[p]atients with vmPFC lesions scored higher in fundamentalism than patients without PFC lesions….” Neither of these claims represents the data. In fact, a large number of people in the ventromedial group had lower fundamentalism scores than the other group, and vice versa, contrary to the claim. If damage to that region increases religious fundamentalism, it should apply to all of them.

Moreover, the amount of variance in the data explained by the ventromedial lesions was only 1%. That means 99% of the observed variance in fundamentalism data among the participants was due to something other than the lesions. In fact, this study found that openness (9.7%) and cognitive flexibility (4.6%) explained far more variance in the data than did the lesions. This suggests a person’s subjective understandings of the world, separate from brain injury, are more important in understanding religiosity. And note that even with all of the studied variables included, only about 18% of the variance was explained; 82% was unexplained. This is the important statistic. Much of what people do can't be explained by using medical model, nomothetic approaches. It is important to understand one person at a time.

Despite the above, the “moral of the story” according to the authors is how damage to brain structures affects one’s religious fundamental beliefs. This perpetuates a medical model of humanity that reduces meaningful experiences to sterile brain activity, and it stereotypes people without even a minimal amount of justifying evidence.

ADHD Causes Car Accidents?

6/14/2017        In the News 3 Comments

by Chuck Ruby, Ph.D.


The results of a study, published in JAMA Pediatrics, claims that ADHD causes an increased risk of automobile crashes. I'll explain why this is a trivial conclusion. What's more, it is absurd that the authors suggest more research into “the specific mechanisms by which ADHD influences crash risk to develop effective countermeasures.” ADHD is not a disorder that causes anything. ADHD is a label that describes a constellation of behaviors. To say it is a disorder that causes an increased risk of crashes is like saying walking is a disorder that causes an increased risk of moving.

If we look at the definition of ADHD contained in the DSM, we find that it consists of an arbitrary checklist of items about not paying attention and not inhibiting impulses. It has nothing to do with brain dysfunction. There are no laboratory tests to detect it. It has nothing to do with pathology in the person. It describes people who do not pay attention, not people who can’t. It is written in the language of medicine and to the untrained eye, it seems to be talking about a brain disorder, when in fact there is nothing mentioned about the supposed disorder and no medical evidence ever presented that demonstrates its pathological basis, and thus why there is no lab test for it.

And yet the announcement of this study will worry parents of children who have been labeled with this mythical disorder. They will fear when their children start to drive and wonder if driving privileges should be contingent on their children being in psychiatric “treatment” consisting of daily stimulant drug doses. The already bloated departments of motor vehicles across the country might even see this and similar studies as reason to implement new rules and programs about monitoring or denying driver’s licenses to people “with ADHD”.

But if we brush away all the medical-sounding and misleading language, we are left with a trivial study. In short, its results are saying that people who don’t pay attention while driving are at increased risk of having accidents. Aren’t we already able to make that assumption? When we don’t pay attention, we don’t notice things. It doesn’t take a scientific study to tell us this. And it doesn't need the creation of a disorder.

In addition, there are basic statistical issues with this study that further trivialize it. When comparing the driving records of people “with ADHD” and people who have not been given that diagnosis, the study concluded, “…the crash hazard among newly licensed drivers with ADHD was 36% higher.” In the first place, this is inaccurate. The wording makes it sound that people “with ADHD” are more dangerous on the road than people without that diagnosis. But the statistics used in studies like this one are based on group averages, not individuals. In this study, the average number of accidents for the group of ADHD people was claimed to be 36% higher than the average number of accidents in the non-ADHD group. Graphically, this would look something like the following display of two normally distributed (bell curved) groups. The horizontal axis represents the number of accidents and the height of the curve is the number of people with that number of accidents. The dark group would be the people without a diagnosis of ADHD and the lighter color group would be those “with ADHD”.

 

One can easily see with this graphical representation that even though the average (indicated by the vertical line) number of accidents of the ADHD group is higher than the non-ADHD group, many people in the ADHD group have less accidents than many people in the non-ADHD group. The reverse is also true: many people in the non-ADHD group have more accidents than people in the ADHD group. The reason the researchers say there is a 36% increased crash hazard among ADHD drivers is only because the average number of crashes is higher than the average number of crashes for the non-ADHD group. Still there a many ADHD people with less accidents than people with no diagnosis.

This is because the 36% increased risk of accidents is minimal. As an example, ADHD males in this study had a 13% risk of having an accident within 6 months after getting their driver's license. On the other hand, non-ADHD males only had a 9% risk. Even though this is only a 4% absolute difference in risk, the relative difference is a 44% increased risk when compared to non-ADHD males. Using the relative difference in risk makes it sound more important than it really is.

As an aside, it is interesting to note that the researchers had the diligence to test whether stimulants prescribed to the ADHD people had any effect on accident risk. One might think that taking a daily dose of Ritalin, which is chemically similar to cocaine, could negatively affect driving skill. But, the researchers found that it didn’t. But this begs the question, then, of what value are the stimulants? If those ADHD people who were prescribed stimulants had the same accident risk as those who hadn’t been prescribed stimulants, but who were still diagnosed with ADHD, that suggests the conventional stimulant drug treatment is useless in increasing attention and, in this study, in reducing accident risk. This is not good news for the advocates of drug treatment.

In short, this study is trivial because it is saying that people who don't pay attention while driving are at a higher risk of having accidents. This is a "duh!" conclusion. Nonetheless, the authors mislead away from this simple fact of life and give the impression that a disorder called ADHD causes those accidents. Recommending further study to identify the "specific mechanisms by which ADHD influences crash risk" is absurd. It is absurd because there are no mechanisms of ADHD. It is tantamount to saying we want to find the specific mechanisms of inattention. What would those be? Inattention is inattention and it can be problematic. But even worse, the authors talk about developing "countermeasures" to this inattention. Those so-called countermeasures are very likely going to be just further authoritarian and inhumane attempts at control, not because they would be focused on reducing accidents, but because they would be focused on "treating" a mythical disorder.

The Latest In A Long Line of Bogeymen?

5/22/2017        In the News 5 Comments

by Chuck Ruby, Ph.D.


A recent article in Health News From NPR asks the question: "Is 'Internet Addiction' Real?" Other than the possible minimizing effects of using quotes around the term, this article does nothing but reify a concept in a very misleading and potentially dangerous way. It adds to a long line of others that perpetuate the myth of mental illness, and in particular the recent technological phenomenon of social media over the Internet.

This article is an example of how mental health professionals are notorious for over-complicating human behavior. Instead of focusing on real life problems teens face in an increasingly compliance oriented and superficial world, they obsesses about what is the correct “disorder”. Then the “disorder” is the focus of investigation instead; meaning that something is wrong with the teen. To quote the DSM, it is “…a dysfunction in the individual.” It is the dysfunction “in” that causes the behavior. And this leads to meaningless questions as posed in the article, like “when does an obsession become an addiction?” Would it be better to think of these professionals having a “diagnosis addiction”?

In actuality, there is no dysfunction “in the individual”. There is a challenge over how, when, why, and to what extent technology is used and what things are considered popular and of value to teens. Internet and other IT technology is going to stay with us and probably get even more complex. My great grandmother once told me how terrible the invention of the telephone was. Up until then people would write letters to each other. After the telephone, she feared they wouldn't write to each other anymore. Instead, they would become impersonal and spend too much time on the telephone. Her fears panned out. But was that an addiction at work?

Much of the description of Naomi’s behavior in this article is attributed to her “addiction” to the internet. But it actually just describes typical teen turmoil in their attempts to navigate that line between separation and belonging. But once a scapegoat like “addiction” is identified all sorts of problems can be attributed to it. The article actually points this out when it notes she also had to deal with how to become popular among her peers, how to cope with her parents’ discord, how to handle less then perfect academic performance, and how to cope with the death of her grandmother. These are all quite typical challenges of adolescence.

The overall flavor of this article reminds me of the alarmist quality of “Reefer Madness”, a 1930’s film that demonized marijuana, and implied that it led to all sorts of antisocial and dangerous behaviors. The psychologist at her $10,000 a week “treatment” facility said, “these teens are using smartphones and tablets…for the same reasons others turn to hard drugs - to numb what is really going on inside.” Really? Is that what doctors in the 1800’s would have said about my great grandmother’s prediction about telephone use?

The problems facing teens are significant and they can be very serious. But it is not because they “have” an “addiction” to anything. It is because they are faced with the most difficult set of social circumstances any teenagers throughout history have had to face before now. They struggle with the means of instantaneous gratification, the ever-increasing demand of consumerism, the age-old longing to belong, and how to meet parental expectations.

The term “addiction” is merely short hand for “a strong urge to do something because that something is enjoyable in the short term, but causes problems in the long term.” There is no need to reify it as if it is an entity that invades people and causes them to do things. In fact, it could easily be argued that talking about it and treating it as if it were some alien entity calling the shots is harmful and perpetuates the problem.

ADHD? A Food Deficit?

5/17/2017        In the News 1 Comment

by Elizabeth Szlek, LMHC, CGP


On April 9, 2017, an article appeared on the website, “The New American”. The writer, Joe Wolverton II, J.D., tells the story of a seven-year-old boy who was taken away from his family by Child Protective Services because his school decided he was “mentally unstable”. The parents of Cameron Maple, of Lebanon, Ohio, were instructed to take him to a hospital so that his disorder could be diagnosed. When the parents demurred, the state stepped in and placed the child in protective custody, citing “health neglect” against the parents, since they would not comply with the psychological evaluation recommended by the school administration.

This situation is wrong on many levels. There is no such thing as “ADHD” as a literal neurobiological disease that can be diagnosed and treated. With this in mind, it is regrettable this child was ripped from his parents’ home because a nonexistent “ADHD” was suspected. I think that something else could be going on. There could be a real bodily dysfunction that is being overlooked in many of these unfortunate children who are being labeled “mentally ill”. They could simply be malnourished.

There are many books out there written on the topic of “ADHD”, but as a Nutritional Therapy Practitioner and a Gut and Psychology Syndrome (GAPS) Practitioner, I have a different take on a possible answer to the question, “What is ADHD?” We know that a child’s brain requires nutrient-dense foods for proper development. This means things like eggs, cod liver oil or other fish oils, butter, liver, beef, lard, and a host of other fatty foods. The brain, of course, is largely made up of fats. When the proper fats are lacking or deficient, the brain does not function properly. We would say the child is malnourished.

How does a child with these nutritional deficiencies behave? They are not able to manage their behavior very well, and are apt to appear fidgety and unfocused. They lack the self-control they need to fit into social situations, like school, effectively. They have trouble controlling their moods, as well, and often seem inappropriate in their responses to the environment.

Children who are properly nourished, are much more able to control their behavior, to stay on task, and they suffer less from negative moods, like anxiety and anger. Their bodies can create the neurotransmitters their brain needs to calm themselves down and be happy, because they are eating the proper amino acids and other micronutrients their bodies need to do so.

A study done in Norway in 2013 showed that children who ate a diet largely consisting of processed sugary foods, and lots of starches like bread and buns, pizza and the like, were far more apt to exhibit either internalizing behaviors like worry, sadness and anxiety or externalizing behaviors like tantrums, hyperactivity and aggression.

On the other hand, children who ate lots of cheese, fish, vegetables and eggs showed fewer such symptoms. The point is, a child’s diet affects behavior and moods, either for good or ill, and diet is an important factor in this.

Another thought is that when a child develops his or her own diet, choosing starchy and sugary foods over anything else, it is likely that they are suffering from small intestinal bacterial overgrowth (SIBO). We know that if candida albicans, a fungus/yeast, takes over the small intestine, it is capable of sending messages to the brain instructing the person to eat more sugar and starch, its favored foods.

Thus, you have children who will preferentially eat these foods, to the exclusion of the healthier vegetables, meats, eggs, yogurt and other raw and fermented foods. This becomes a vicious cycle, eating the wrong foods, and being reinforced from the gut to continue to do so. Many parents despair of ever seeing their children take a bite of a vegetable. This is gut dysfunction, and when this situation continues for too long, intestinal permeability, or “leaky gut” appears. Toxins, produced by bacteria, or other toxic wastes, can leak into the bloodstream, and past the blood-brain barrier and into the brain, causing disordered thinking.

If some of you recall, ADD or ADHD used to be called “Minimal Brain Dysfunction”. It would be wonderful to get back to that concept, and apply the cure: Proper nutrition and healing the gut. Then, we could look forward to complete remission of that real dysfunction!

Elizabeth Szlek is the Director of The Door Counseling Center of Yorkville, NY. She is a Licensed Mental Health Counselor, a Nutritional Therapy Practitioner and a Certified GAPS Practitioner. She can be reached at (315) 768-8900 or at door@thedoorcounselingcenter.com.

Here Comes Julia!

4/5/2017        In the News 0 Comments

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)

A Replacement for the DSM?

4/2/2017        In the News 0 Comments

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 Director Interviewed

3/11/2017        In the News 0 Comments

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.

Looking In All The Wrong Places

2/24/2017        In the News 0 Comments

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.

Here We Go Again: Pseudo-Science and Autism

2/22/2017        In the News 0 Comments

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:

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