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Mental Illness Again Implicated in Violence

8/28/2018        In the News 0 Comments

Mental Illness Again Implicated in Violence


David Katz, the Jacksonville shooter, is the latest in a long line of scapegoats for an apparent epidemic of violence. Just this past Sunday he opened fire at a e-sports tournament, wounding 10 and killing three, including himself. Katz' motives are still under investigation, but people are already implicating the bogeyman of mental illness. See CNN's reporting today - Jacksonville shooter had a history of mental illness and police visits to family home.

According to the report, Katz was prescribed "a number of psychiatric medications," including antidepressants and antipsychotics. He also was said to have seen "a succession of psychiatrists." These statements imply that Katz' a mysterious alien entity residing with him, called "mental illness," was the culprit. There is even current quibbling over what the "correct" diagnosis was.

A more reasonable explanation would be that Katz had been struggling with several real personal dilemmas, he wasn't infected with a nonsensical illness of the mind. Just one example is that he had to witness his parents' vicious divorce and custody battle over him. Instead of following the suggestion of his father for peer-based support group assistance during middle school, there was the default turn toward psychiatric treatment, as if there was something in him to truly treat via medical means.

If the treatment went as it typically does, this would have meant increasing focus on him as the problem, rather than his circumstances. Being subjected to a "succession of psychiatrists" means that one superficial attempt after another didn't work, so he was shuffled to the next psychiatrist in line. He likely felt the increasing sense of being misunderstood and persecute by those medical attempts to sedate him.

This is just the last in a long and continuing line of horrific episodes. It will continue. It will continue because the authorities are not looking at the causes of these events. They are trying to find a scapegoat. Three hundred years ago that scapegoat would have been witchcraft or demons. Now, it is the internal infection of "mental illness."

To make matters worse, the alleged treatment for that infection is typically to coerce the person into compliance. In other words, it is to get them to stop complaining about the problems (euphemistically called "symptoms reduction"). And the icing on the cake is that psychiatric drugging into a state of agitation clearly increases the chances of impulsive outbursts of violence. See ISEPP's White Paper on the link between psychiatric drugs and violence.

 

 

 

 

Genetic Language Smokescreen

2/10/2018        In the News 0 Comments

Genetic Language Smokescreen


Chuck Ruby, Ph.D.


The online magazine Science published a study titled "Shared molecular neuropathology across major psychiatric disorders parallels polygenic overlap," which purports to show genetic underpinnings of several mental disorders. It claims a breakthrough in understanding the genetic causes of these "disorders." 

I’m not a geneticist but my read of this research suggests it is another language smokescreen that obscures a simpler, more humane, and non-disease description of human problems. It is a way to continue on the charade of the myth of mental illness through a verbal sleight of hand trick. The genetic and medical terms used sound impressive (e.g., transcriptomic, phenotypes, pleiotropic) but they are euphemisms that refer to far more common, non-disease matters. Yet because they are used, they give the flavor of real disease.

Just a quick look at the study's abstract demonstrates this deceptive ploy:

"The predisposition to neuropsychiatric disease involves a complex, polygenic, and pleiotropic genetic architecture. However, little is known about how genetic variants impart brain dysfunction or pathology. We used transcriptomic profiling as a quantitative readout of molecular brain-based phenotypes across five major psychiatric disorders—autism, schizophrenia, bipolar disorder, depression, and alcoholism—compared with matched controls. We identified patterns of shared and distinct gene-expression perturbations across these conditions. The degree of sharing of transcriptional dysregulation is related to polygenic (single-nucleotide polymorphism–based) overlap across disorders, suggesting a substantial causal genetic component. This comprehensive systems-level view of the neurobiological architecture of major neuropsychiatric illness demonstrates pathways of molecular convergence and specificity.”

  • neuropsychiatric disease, polygenic, pleiotropic,architecture, dysfunction, pathology, transcriptomic, phenotypes, perturbations, dysregulation, polymorphism, and molecular convergence and specificity??

Now doesn't that sound impressive? I'm certain that most people will glaze over about half way through it and stop reading, and instead just accept the claims like this headline:

"Major mental illnesses unexpectedly share brain gene activity, raising hope for better diagnostics and therapies."

I’ve taken the time to wade through the abstract's wording and replace all that nifty medicaleze and substituting more common and humane terms:

"Behaviors have a genetic substrata. However, we don’t know how that substrata causes those behaviors. We examined cellular RNA activity to see how they varied across different types of behaviors. This showed differences and similarities among those behaviors, suggesting they have a genetic substrata.”

All this research says is there are genes being expressed as people experience the problems we call “mental illness” and that genetic expression is shared to some degrees across different types of problems, but also retains a degree of differences across those problems.

Didn’t we already know this?

Further, don't we already know that any human activity or experience is going to be represented by underlying gene expressions? What does that have to do with verifying something as an illness? Ans. Nothing. Looking from the outside, this smokescreen gives the impression of precision science identifying and confirming that mental illnesses are about genetic anomalies. But on the inside, once the smokescreen is blown away, it is merely pointing out that gene activity is going on during any human behavior.

 

Ignoring the Real World of Depression

1/9/2018        In the News 1 Comment

Ignoring the Real World of Depression


Chuck Ruby, Ph.D.


The Observer published a January 7th article by Johann Hari entitled, "Is Everything You Think You Know About Depression Wrong?" In it he questions the prevailing views about depression being caused by a chemical imbalance, among other things, such as the grief exception in the DSM5. One day later, Dean Burnett, identified as a "doctor of neuroscience," critiqued Hari in one called, "Is Everything Johann Hari Knows About Depression Is Wrong?" Dr. Burnett's piece addresses Hari's claims by, first, denigrating him, and then by basically claiming the bulk of what Hari said was either not true or that it is common knowledge and, thus, inconsequential. But there are some huge problems with Dr. Burnett's critique.

Whereas considering one's reputation is important in assessing an author's credibility, still the validity of the material is an independent matter. Disreputable people can claim valid facts. Ad hominem attacks are never helpful. Ending the opening section after having denigrated Hari with a comment to imply something like, "Let's see what he has to say anyway" ("...assume Hari has written this article with 100% good intentions and practices.") Dr. Burnett doesn't negate the preemptive negative effect of questioning his credibility.

Dr. Burnett avoids, as do most advocates of the medical model of human suffering, the big question: Is depression (and all other so-called "mental illnesses) a brain illness as supported by scientific evidence? Demonstrating biological underpinnings of depression obfuscates the issue. All things human are accompanied by biological underpinnings without being considered illness. Take for example hair color, height, temperament, athleticism, and cognitive ability. All these things are possible because of their biological underpinnings. But none are considered illnesses. It is only when we can scientifically demonstrate some lesion, malfunction, or defect in that biology that leads us to a conclusion of illness. For instance, we can demonstrate dangerous blood glucose levels with diabetes; detect damage to bones in a broken leg; and observe the ravenous onslaught of cancer. There is no such thing happening to the biology that underlies depression (or any other mental illness). Given this lack of evidence, medical treatment is not appropriate, and potentially dangerous.

And please don't counter with the worn-out "but things like chronic fatigue syndrome and restless leg syndrome don't have evidence of pathology either." First, you're right. But I question whether these "syndromes" are actually physiological illness, since they can be explained by other means. But second, this lack-of-evidence problem doesn't apply to a whole grouping of disease entities in real medicine. The so-called mental illnesses are all this way. Imagine if all pulmonary diseases were created without any evidence!

The chemical imbalance theory of mental illness does not need to be "challenged." One cannot challenge a theory that has no supporting evidence, other than to point out it has no supporting evidence. Science doesn't work by proving negatives; i.e., that there is no chemical imbalance. Those who assert the hypothesis are obligated to provide the evidence, and they haven't. There has never been any evidence presented that demonstrates a chemical imbalance (or any other bodily malfunction) causes depression or that depression is an illness. Keep in mind the term "imbalance": an imbalance vs. a balance must be demonstrated. Not just neurochemical changes that occur when a person is depressed. Neurochemical changes occur for every human experience and activity. And this empty theory has been going on since the 1950's when the drug industry and psychiatry stumbled upon chemical "cures." The convenience of this coincidence cannot be ignored.

Despite pointing out that Wikipedia outlines "several factors widely considered to be important" in depression, physicians, psychiatrists, and drug companies (at least as of last night when I watched the Abilify commercial) still encourage people to think it is a chemical imbalance. People don't go to Wikipedia for depression; they go to their doctor. Those of us in the business know first hand that those doctors tell people they have a chemical imbalance, sometimes for life, and sidestep "bio-psycho-social" factors as mostly irrelevant (actually, and not surprisingly, they do give some attention to the "bio-" part).

They also do not explain how drugs work, what they do, what they don't do, and the harmful effects of taking them, especially in combination with other drugs and over a long period of time. In my 20 years of doing this work I have never heard of even one example of such an explanation.

All this despite what NHS, NIMH, NAMI, CDC, or any other organizations may display on their websites and despite what faculty and students talk about in universities. The truth is that where the rubber meets the road it is explained as a chemical imbalance and pills are pushed, and the psycho-social part is just portrayed as an afterthought. The widespread belief in this chemical imbalance by the lay public attests to what they are being told.

While it is clear Hari's exaggerated use of depression being diagnosed one minute after the loss of a baby was intended for effect, any currently practicing psychotherapist, psychologist, psychiatrist, or physician knows full well that it doesn't take weeks of complaints before a person is diagnosed with depression. That can happen within minutes of walking into a doc's office for the first time and complaining about the so-called symptoms of depression. We who actually do this work on a daily basis hear about examples from the victims themselves. And the typical response by the doc is a prescription for antidepressants, or worse yet, benzodiazepines. "Oh, and yes, it would be a good idea to talk to someone."

It is not about what Dr. Burnett knows that is important. It is about what happens to that "average person” he talks about when they seek out help in real life. And what happens to them is a shame. That is why what he knows and what they know is wildly different, as he points out.

And, finally, people do not get depression in their brain. Depression is a meaningful dilemma that resides in experience. It is not a medical matter, nor a matter to be drugged, anymore than a rough day should be drugged with a stiff drink. But then, we don't consider stiff drinks as medicine and we don't think of bartenders as doctors.

Bipolar Disorder – Missing the Point!

12/25/2017        In the News 2 Comments

Bipolar Disorder - Missing the Point!


by Al Galves, Ph.D.


A recent study on bipolar disorder published at the International Journal of Epidemiology has problems. The biggest problem is it is not asking the most important question: How is bipolar disorder related to the desire and ability of people to live the lives they want to live? Bipolar disorder is a state of being characterized by certain subjective feelings and certain behaviors. If we assume that human beings are organisms which want to live their lives in enjoyable, satisfying ways, what does this state of being have to do with their ability or inability to do that?

The study is being done with apparent ignorance of the fact that human beings are meaning-making, desiring organisms who want to live their lives in certain ways and who, if they are unable to do so, are going to experience the states of being associated with all of the mental illness diagnoses. The study is missing its proper context. It is hanging in a kind of limbo. In the absence of a proper context, it is unlikely to be very useful to human beings.

I’m making an assumption here. I need to explicate it. I am assuming that human beings want to live enjoyable, satisfying lives. I’m also assuming that, in order to live satisfying and enjoyable lives, the great majority of human beings will have to be able to love the way in which they want to love and work (express themselves) in the way in which they want to express themselves. In the words of the positive psychologists, they will have to use the best part of themselves in the interest of something larger than themselves, have positive relationships with others and experience competence, achievement and mastery.

What evidence is there for these assumptions? What do human beings want in their lives? What are the roots of happiness? What are the ingredients of human well-being? What are the components of health? What are some of the factors with which health is associated?

I don’t have the answers to these questions. But I think these are the questions that need to be asked.

How does this relate to this study? This study is gathering information about people who have been diagnosed with bipolar disorder. It is comparing that information with similar information on persons who are not diagnosed with bipolar disorder or who have not been diagnosed with any psychiatric disorder. It is gathering information on the neurocognitive functioning of these people, their temperaments and personalities, their motivated behaviors, their life stories, their patterns of sleep and circadian rhythms and the outcomes and courses of their lives. It is also gathering information on biological factors – genetic components, the nature of the disease and nutrition.

But this data is being gathered in the absence of a useful context or an attempt to make meaningful sense of it. The authors say the etiology of bipolar disorder is unknown. But they don’t offer any hypotheses about what that etiology might be. And they don’t seem interested in exploring that question. It used to be that one of the psychologist’s jobs was to come up with a formulation of the case. What is going on with this person? This person is engaging in some bizarre, troubling and somewhat impairing behavior. What is the meaning of it? In what way may it be somehow functional? What can this tell us about what this person wants, how are they going about getting it and how they are reacting to the results they are achieving. These researchers aren’t asking these questions.

They also don’t seem open to the possibility that mania or depression might be somewhat functional for a person, might help a person have a useful experience or a desired experience, albeit bizarre and even impairing in some way. They are assuming that these states of beings are diseases and nothing more.

So the researchers find that there is a history of childhood trauma among the people diagnosed with bipolar disorder. They have suffered significantly more childhood trauma than the control group. But they don’t seem interested in wondering about how a history of childhood trauma would be related to the experiences and behaviors associated with bipolar disorder. Why might it be that people who have experienced childhood trauma would be subject to alternating mania and depression? How might we understand this in the context of people wanting to live satisfying and enjoyable lives? They also find that this history of childhood trauma is associated with a detrimental effect on inhibitory control and attention accuracy. This seems to fit with mania, to be somewhat of an explanation of the connection between what happened to this person as a child and being subject to manic episodes. But they don’t connect these dots.

I, for example, hypothesize that the manic episode is an attempt by an individual who has had a lot of pressure to be great and hugely successful but who is unable to do so, to experience the illusion of being great and successful. In other words it is an attempt to fake success and greatness or to have a faux experience of success and greatness.

The connections between childhood trauma and mania makes sense in this context. People who experience trauma in early life will likely have trouble managing their emotions and will have various kinds of trouble in interpersonal relationships. They will also suffer from cognitive deficits. The development of the brain in the first year of life is contingent on good attunement between mother and infant. We can assume that a child who is traumatized probably did not benefit from such attunement. So this child will suffer some cognitive and emotional deficits. Those deficits will make it difficult for him to be as successful in life as he might want to be. If a tremendous about of pressure is put on him to be successful, great, exalted, he might want to experience that kind of success and greatness. But the only way he will be able to do that is to go through a manic episode in which he can have the illusion of such greatness and success.

The researchers are not open to this connection between the states of being of mania and depression and the desire of people to live the kinds of lives they want to live and the inability to do that. Therefore, their efforts are unlikely to help human beings live the kinds of lives they want to live. Their considerations are too decontextualized from life, too divorced from what matters to human beings to be of much use.

Spooky Language!

11/4/2017        In the News 2 Comments

Spooky Language!


Chuck Ruby, Ph.D.


In 2001 the late irreverent comedian George Carlin used the phrase "spooky language" to describe the wording of the 10 commandments. I do not cite Carlin in order to debase religious beliefs as he did. I think spirituality and religion can be of immense comfort and contribute to a sense of meaningful well-being for some people. I mention Carlin's comedic use of the phrase only in order to apply it to a recent study by Schmitz and colleagues entitled, "Hippocampal GABA enables inhibitory control over unwanted thoughts". This study claims that brain activity is the key to understanding a person's intrusive thoughts. But the authors of this study use spooky language in order to obfuscate and mislead about what would otherwise be a more simple, yet still difficult, non-disease matter.

This study is peppered with the same spooky language as others reported throughout academic journals and the media that make the ontological mistake of conflating human experiences with the neurochemical happenings going on during those experiences, and of using this language in a way that implies those brain happenings are pathological, while no evidence is ever presented to support that assertion.

The mental health industry is replete with this mistake because it is an inevitable result of the medical model - assuming troublesome experiences are symptoms of brain dysfunction without evidence of such. If this assumption were true, it would make sense to pay attention to brain chemistry and functioning when those experiences occur.

For instance, when a person has a brain tumor in just the right place, she might experience the world differently and act differently than without the tumor. In this situation, neurologists are helpful medical specialists who can address this problem and possibly alter brain chemistry or surgically remove the tumor in order to fix the problem.

This is similar to how a mechanic would identify a faulty car part and repair or replace it. But absent an identifiable broken brain part, this model is inappropriate when dealing with individual experiences of intrusive thoughts. People are not cars and, as far as we know, cars do not have meaningful experiences they can complain about.

Consider just a few examples of spooky language in the Schmitz study and a more simple, straightforward (non-spooky) translation in parentheses:

"Intrusive memories, hallucinations, ruminations, and persistent worries lie at the core of conditions such as post-traumatic stress disorder, schizophrenia, major depression, and anxiety." (When people complain of persistent and intrusive thoughts we say they have a disease.)

"These debilitating symptoms are widely believed to reflect, in part, the diminished engagement of the lateral prefrontal cortex to stop unwanted mental processes, a process known as inhibitory control." (When people are experiencing intrusive thoughts, we notice a part of the brain becomes less active.)

"In individuals with schizophrenia, the severity of positive symptoms, such as hallucination, increases with hippocampal hyperactivity, as indexed from abnormally elevated resting blood oxygen-level-dependent (BOLD) activity, or increased regional cerebral blood flow, blood volume, or blood glucose metabolic rate." (When the severity of intrusive thoughts increases, we notice another part of the brain becomes more active.)

"Consistent with this view, animal models of schizophrenia show that disrupting GABAergic inhibition in the hippocampus by transgenic or pharmacological manipulations reliably reproduces hippocampal hyperactivity and volume loss, along with behavioral phenomena paralleling symptoms present in this disorder." (When we disrupt the natural workings of the brain it causes problems for the owner of the brain.)

"Together, these findings suggest that a deficit of GABAergic inhibition local to the hippocampus contributes to problems controlling a spectrum of intrusive memories and thoughts, although the pathogenesis of this deficit and its specific manifestations across disorders may vary." (When people experience intrusive thoughts, an area of the brain becomes more active, but we really aren't clear on this.)

"We hypothesized that GABAergic inhibition in the hippocampus forms a critical link in a fronto-hippocampal inhibitory control pathway that suppresses unwanted thoughts." (We think two areas of the brain change in activity level when people experience intrusive thoughts.)

I could go on and on. The point is that spooky language is often used in studies like this in order to mislead the reader into thinking something that isn't true; that being, scientific medical precision about a brain disease. Despite all the medical-sounding words and phrases, there is not one bit of real evidence ever presented that intrusive thoughts have anything to do with real brain health or illness. And, by the way, if such evidence were presented, this wouldn't be a matter for psychiatry. It would be a neurological problem to be addressed by neurologists and other real medical specialists.

All this study shows is that when people are having experiences (intrusive thoughts), their brains are working. The fundamental mistake is in conflating individual experiences with the workings of the brain during those experiences, and claiming that brain activity is therefore pathological.

Perhaps an analogy would help. What if we noticed that when people are lifting weights their level of muscular contraction and innervation simultaneously react in a particular way. Would we then conclude that lifting weights is a disease? Of course not. And we wouldn't say things like, "In individuals with weight lifting disorder, the severity of positive symptoms, such as muscular contraction, increases with motor and sensory cortex hyperactivity, as indexed from abnormally elevated resting blood oxygen-level-dependent (BOLD) activity, or increased regional cerebral blood flow, blood volume, or blood glucose metabolic rate." That would be preposterous.

Muscle contraction and changes in the sensory/motor cortex is not evidence of disease and it is not the same as the human experience of lifting weights. Likewise, hippocampal and prefrontal cortex activity is not evidence of disease and it is not the same as the meaningful human experience of intrusive thoughts.

That is another matter completely.

Another Spurious Correlation? – ADHD

10/30/2017        In the News 0 Comments

Another Spurious Correlation? - ADHD


by Chuck Ruby, Ph.D.


Are we seeing yet another spurious correlation peddled to the public as medical research? A study published at JAMA Pediatrics suggests that acetaminophen use during pregnancy causes ADHD. This study harkens back to the thalidomide controversy of the early 1960's, but instead of birth defects, the fear is that  a common over-the-counter drug may disrupt fetal brain development leading to ADHD. It has been reported to the general public here and here, among other outlets, not only causing fear among parents but also continuing to perpetuate the myth that ADHD is a real disease.

For now, let's set aside the fact that little evidence supports the neurobiological defect model of ADHD, the debunking of the Diagnostic and Statistical Manual of Mental Disorders (DSM), in which ADHD is listed as a disorder and is thus also invalid, and that ADHD makes no sense from a logical perspective. Let's instead get into the weeds of this study and consider a simpler explanation for the data showing a correlation between acetaminophen use during pregnancy and later ADHD.

This study was an analysis of over 64,000 mothers and their children  from the Danish National Birth Cohort from 1996 to 2002. The researchers gathered data regarding the mothers' acetaminophen use during pregnancy and the later incidence among these mothers' offspring of problems associated with hyperactivity. The study found that the offspring of mothers who took acetaminophen during pregnancy had higher rates of these problems.

However, the difference between offspring of mothers who used acetaminophen and those who didn't was quite small. Overall, the offspring of the mothers who took acetaminophen had a 13% increased risk of scoring moderately on the Strengths and Difficulties Questionnaire. A more detailed breakdown showed the offspring of the acetaminophen mothers had: 1) a 17% increased risk of hyperactivity; 2) a 14% increased risk of conduct problems; 3) a 5% increased risk of emotional problems; and 4) a 1% increased risk of peer problems. Interestingly, there was no difference in the scores of the childrens' prosocial behaviors (this is odd since one would expect someone diagnosed with a real neurological defect to lack prosocial behaviors too).

But these are relative risk statistics. If one looks at the absolute risk, the difference becomes even more meaningless. For example, using the largest risk ratio (# 1 above - hyperactive risk), the difference in risk was a matter of 5.7% vs. 4.3%. In other words, an offspring of a mother who took acetaminophen during pregnancy had a 5.7% risk of scoring greater than a 7 on the Strengths and Difficulties Questionnaire Hyperactivity Scale, in contrast to a 4.3% risk of scoring greater than 7 by the offspring of mothers who did not take the pain reliever.

This minimal difference in risk is even more diluted when looking at the confidence intervals for the risk ratios. For two out of the four risk ratios above (emotional problems and peer problems), the 95% confidence intervals included a risk ratio of 1, which would mean there is no difference in risk between the groups of offsprings. The other two risk ratios' confidence intervals came very close to including 1.

These forgoing measures were of "ADHD-like behaviors". Well, let's see what the risk of actually being diagnosed with ADHD (actually the researchers looked at those diagnosed with hyperkinetic disorder). For the offspring of mothers who took acetaminophen, there was  a 37% increased risk of being diagnosed. But again, a look at the absolute figures dilutes the practical significance of this risk ratio. The absolute risk difference in being diagnosed was around 1.5% for those mothers who took acetaminophen vs. 1% for the mothers who didn't. Hardly a matter of alarm or evidence of disease.

If there is any evidence that a drug causes fetal birth defects or neurological damage it should be taken seriously, regardless of the absolute risk. In the case of thalidomide, there was ample evidence that the toxic nature of the drug caused real defects. And, if acetaminophen is shown to cause real fetal defects, it should be treated similarly and prescribers and parents warned. But the resulting defect would not be called "ADHD" or "hyperkinetic disorder". The resulting defect would be more appropriately called a neurological disease, as would any other toxic chemical exposure, and fall under the bailiwick of the real field of medicine called neurology. The defect wouldn't be treated as ADHD and we certainly would not want to use toxic stimulant drugs to treat a real defect that was caused by another drug's toxic properties.

But this study was not looking at brain damage or defect. It was looking at the association between the incidence of acetaminophen use during pregnancy and the subsequent categorization of the offsprings' social problems using a set of checklists, not as having a neurological defect (no such defect has ever been demonstrated).

What would be a more simple interpretation of the results of this particular study? It is quite probable that parents who are more likely to resort to a pain reliever such as acetaminophen are also more keenly aware of bodily ailments, and more inclined to use chemicals to soothe those conditions instead of merely tolerating them. As these parents have children, they are also likely to transfer that concern and awareness to their children's ailments. 

Therefore, when these parents wonder about their children's hyperactive behavior and other social problems that are subsumed within the diagnostic criteria of ADHD, they would be more likely to see these issues as problematic and indicative of something going wrong rather than as within the normal range of childhood behavior. They would also be more likely to consider seeking out a pediatrician or child mental health professional. Due to the pressures to diagnose in order for health insurance to reimburse a professional's time, these children would then be more likely to receive ADHD (and other) diagnoses, in addition to being the target of symptom checklists such as the Strengths and Difficulties Questionnaire. This alone could easily account for the small correlation between acetaminophen use during pregnancy and the later identification of these problems in the offspring.

The biggest problem with this study is it perpetuates the misunderstanding of ADHD as a real neurological defect, in this case one that is caused by the hormonal disruption of acetaminophen.

A New Treatment for Depression – Really?

9/24/2017        In the News 0 Comments

A New Treatment for Depression - Really?


Chuck Ruby, Ph.D.


Pay attention to language! Here is a typical example of how language is used in mental health research in order to give the impression of medicine and disease, when in fact there is nothing medical or pathological about it. Yet, it is a linguistic smoke screen that obscures the real results.

JAMA Psychiatry recently published the results of a study that claims “whole-body hyperthermia” outperformed placebo in reducing the symptoms of depression. It sounds very clinical, medical, and based on an understanding of neuroscience. The study's lead paragraphs especially set the tone and give the impression of neuroscience at work. The researchers' conclude that hyperthermia "holds promise as a safe, rapid-acting, antidepressant modality with a prolonged therapeutic benefit." Isn't there a more direct way to say this?

If you take the time to dig into the weeds and see what this study is actually saying, it is quite commonplace. It is merely proposing that increased warmth can make people feel better. Didn’t we already know this? All the talk about brain structures and pathways activated during the process of warming is irrelevant, yet it is used to make depression sound like a matter of brain pathology and "whole-body hyperthermia" as medical treatment.

Beyond the critique of language, an examination of the data further question the value of this study.

To start off, the overall difference in depression between the "whole-body hyperthermia" group and the placebo group was minimal. At 6 weeks after treatment (the longest post-treatment assessment made), the hyperthermia group’s average score on the Hamilton Depression Rating Scale was about 12 and the placebo group’s average score was about 17. A Hamilton score of 12 is within the “mild” range and 17 is within the “moderate” range. The cutoff between mild and moderate ranges is 13-14. (For now let's ignore the issue of the 86% sensitivity and 92% specificity ratings of the Hamilton).

Added to the questionable meaning of these Hamilton score differences is the fact that the confidence intervals were quite large. For example, the 6 week difference in scores was 4.27. But the 95% confidence interval for this difference was 7.94 to .61. This means there is a 95% chance that the true difference between the groups’ scores was between 7.94 and .61, and a 5% chance the difference score was outside that range. Given that the cut off score between “mild” and “moderate” depression of the Hamilton is 13-14, claiming any practically significant difference between the hyperthermia group and placebo group is dubious.

Further, it must be remembered that the above Hamilton scores are group averages and they do not sufficiently account for the individuals’ scores. The two groups' score distributions overlap such that some in the placebo group did better than those in the hyperthermia group. At 6 weeks, the Cohen's d effect size between the groups was 1.66. At this value, about 40% of the two groups overlap. And remember, this is using the 4.27 Hamilton score difference, which is questionable given the large confidence intervals.

Finally, the placebo effect was greater for the hyperthermia group than placebo group. After the study, 94% of the hyperthermia group guessed correctly that they were in the experimental group, whereas only 71% of the placebo group thought they were receiving the experimental treatment. This would have artificially reduced the hyperthermia group's scores on the Hamilton based on the placebo effect alone.

Linguistic gymnastics are used in this and many other studies to give a medical model impression. More over, the very statistics reported ostensibly to justify a claim of superior treatment demonstrate the unconvincing nature of the results. Trivial effects, excessive confidence intervals, nomothetic washing away of individuality, and the placebo effect make this study of questionable use, other than to demonstrate that warmth can help some people feel better. How surprising is this?

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

9/5/2017        In the News 5 Comments

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


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 2 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.