Friday, August 21, 2015

A New Kind of Twin Study and the Heritability Fraud

In my post on Psychology Today, "Scientific Fraud in the Nature versus Nurture Debate," I discussed the disturbing tendency of psychiatric researchers to use the term heritability as a synonym for genetic, which it certainly is not. The heritability statistic is a measure of phenotype, not genotype, meaning it is a measure of the final outcome of the influence of the interactions between genes and the environment on such things as certain personality characteristics or psychiatric symptoms.

The statistic is derived from twin studies in which fraternal and identical twins who were raised together are compared to each other and to those raised apart on various traits. It is not a measure of purely genetic influences but instead a measure of a mix of purely genetic influences plus gene-environment interactional influences. 

There is no way to tell how much of each is present in the statistic. The determination of heritability can also be manipulated in a number of ways, such as by setting the bar for saying that a symptom is present or absent at different levels.

Interestingly, a recent study employing a very different type of twin study has been getting a fair amount of press (Thalia C. Eley, Tom A. McAdams, Fruhling V. Rijsdijk, et. al., "The Intergenerational Transmission of Anxiety: A Children-of-Twins Study," American Journal of Psychiatry, 172 [7], pp. 630-637, 2015).

Rather than comparing twins with each other, the authors compared the children of twins with one another. The subjects were anxiety and a dimension of normal personality known as neuroticism - a measure of emotional reactivity. People with higher neuroticism scores tend to get more anxious and/or depressed in reaction to negative environmental stimuli, and remain dysregulated longer, than those with lower scores.

By comparing the extent to which correlations between children and their twin uncle/aunt (avuncular correlations) differ for monozygotic (identical) and dizygotic (fraternal) twin families, the authors were able to infer the extent to which genetic and environmental factors influence transmission from one generation to another. Children share a greater level of genetic influence with their uncle/aunt when in monozygotic families than when in dizygotic families.

Thus, if children resemble their uncle/aunt to a greater extent in monozygotic families than in dizygotic families, this implies a genetic influence on transmission of the trait of interest. In contrast, if these two sets of correlations are similar, and are significantly lower than the parent-child correlations, this is indicative of an environmental mode of transmission.

The results of the new study showed almost the opposite of the usual results of heritability studies on neuroticism: environmental factors came out very much more important than genetic ones! Living with one's parents was found to be far more influential than merely inheriting 50% of their genes.

It appeared that children and adolescents learned anxious behavior from their parents rather than inheriting a tendency towards it from their parents genetically.

Now, I must say that the authors used a statistical technique to come to their conclusion called "structural equation modeling"—of which I know absolutely nothing. So I am not able to say if the methodological techniques used in traditional twin studies yield more accurate results than those found in this type of study. This may, in fact, be a case of scientists being able to get the results they want to get through statistical manipulation of their study data.

And surely neuroticism must have some significant genetic component. Clearly, some people are naturally more high strung than others.

Nonetheless, I do know from the observation of blatantly obvious behavioral patterns within families and other social groups that anxiety can be highly contagious. Since as of now mental health professionals can't fix your genes but we can fix your relationships, I know on which factors therapists should focus the majority of their attention.

Tuesday, August 11, 2015

Performance versus Ability: Another Issue Frequently Ignored in Psychiatry Research

In previous posts, I have discussed some bizarre assumptions made in psychiatry research papers when the data is analyzed. I wrote about how, for example, differences in brain area size and functioning between different groups on fMRI scans are automatically interpreted as abnormalities.

Nassir Ghaemi, a blogger on Medscape with whom I have had some strong disagreements about borderline personality disorder and bipolar disorder, nonetheless had a great quote on this with which I wholeheartedly agree:
"All things biological are not disease, even though we can define disease in such a way that all diseases are biological. This matter is obvious once pointed out. A few assumptions,  which seem either patently true or very likely: all human psychological experience is mediated by the brain; each person only has one brain; therefore the brain will always be biologically changing as we have psychological experiences. Reading a blog post about the brain is a psychological experience. Having delusions from schizophrenia is a psychological experience. The first brain change does not reflect disease; the second does. So showing MRI changes with adult ADHD or borderline personality does nothing to demonstrate that those conditions are diseases. If you watch TV and play video games inordinately, you will have changes in your brain, and you might also develop clinical symptoms of ADHD. If you are repeatedly sexually abused, you will have changes in the brain, and you might also develop clinical symptoms of borderline personality. But those changes in the brain do not have the same causal role as the neuronal atrophy that happens with trisomy 21, or with schizophrenia, or bipolar illness..."

Another major nonsensical assumption that litters the psychiatric literature (the literature littering alliteration?) is that one can totally disregard the motivations of research subjects as well their past experiences and the environmental context in which they live when evaluating their performance on psychological tests. 

I mentioned an example of how this is utter nonsense in a previous post: The performance of African-Americans on IQ tests just might be related to the fact that for several generations Blacks who looked too smart were at high risk of being lynched. Do you think they are just as motivated as other folks to want to look smart on an IQ test which is being administered by White researchers?

What I have seen more and more lately, particular in the personality disorders literature, are studies that look at differences between various diagnostic groups on such issues as how much "impulsive aggression" they show, or how and how well they read the emotional state of ambiguous faces of strangers in photographs. When differences are found, once again the "lower" performing groups are just assumed to be "impaired" or "abnormal."

This, of course, confuses performance with ability. Without knowing anything about what the subjects in the experiments are motivated to do in their daily lives on any particular dimension for whatever reason, or what environmental contingencies they are worried about that may relate to the task at hand, it is literally impossible to say for sure whether any difference in their performance is related to what they would be able to do if those other issues were not operative.

Patients with borderline personality disorder, for example, grow up in families in which double messages are flying in all directions, and with parents who can switch from being over-involved to neglectful at the drop of hat. They are bound to have a higher index of suspicion about what facial expressions on strangers might mean than someone who grew up in a more consistent and predictable environment. If they did not, they would be morons.

Another major issue ignored in the literature is the difference between a research subject's real self versus their persona or false self in certain social situations. We all present different "faces" to the outside world depending on social context. Researchers who do not consider this must think that men, for example, present themselves exactly the same way around their children, their bosses, and their mistresses. Really?

With personality disorders, as I described in several previous posts, people play social roles designed to stabilize family homeostasis. These roles are merely a much more pervasive version of the different roles played by the above "normal" man interacting with different people. So someone with antisocial tendencies, for example, which are part of the role of avenger, are motivated to show more impulsive aggression than other people - on purpose - and have literally trained themselves to be like that. They do so habitually, automatically, and without thinking. Of course they will show more impulsive aggression in the experiment! Why wouldn't they? 

In fact, showing a lot of impulsive aggression might be considered to be part of the definition of antisocial behavior. The experiments therefore do nothing more than prove that anti-social people act habitually in an anti-social manner. Like, duh!

These types of results in no way indicate any "deficits," "deficiencies," or "abnormalities." One wonders how people who make these ludicrous assumptions ever manage to get through medical or graduate school.

Friday, August 7, 2015

Dr. Allen's Second Book Back in Print

My second book, Deciphering Motivation in Psychotherapy (which was originally going to be titled Ulterior Motives) is now available in paperback at a reasonable price on Amazon for the first time. It is actually my favorite of the ones I've written, but by far the least read.

It was out of print for a time, and then back out but at a ridiculous price. (A different publisher had bought out the original publisher, then re-published the book without even letting me know!)

It was meant for therapists but is written so lay people can understand it.

This book explains some basics about the theory behind Unified Therapy, including the core concept of dialectic causality.

The main topic is the use of language in dysfunctional family interactions, and how the true intentions and meanings of individuals who are being ambiguous or misleading can be discovered. If you want to see things that have been said to you repeatedly by difficult relatives in a whole new and surprising light, this is the book for you!

Friday, July 31, 2015

If Free Will Does Exist, How Often Do We Employ it in Our Daily Lives?

In my post of 7/31/10 I discussed a somewhat widely-publicized study published in 2008 in Nature Neuroscience, in which researchers using brain scanners could predict people's very simple decisions seven seconds before the test subjects were even aware of what their decision was. 

The concern raised at that time was whether some totalitarian government might start arresting people based on a determination of what they were going to do at some time in the future, like the precrime unit in the movie Minority Report.

This study still comes up in philosophical discussions of a different issue - whether people even really have free will at all, or if we are more like pre-programmed robots.

The decision studied in the experiment — whether to hit a button with one's left or right hand —may not be representative of complicated choices that are more integrally tied to our sense of self-direction. Regardless, the findings raise interesting questions about the nature of self and autonomy: How free is our will? Is conscious choice just an illusion?

"Your decisions are strongly prepared by brain activity. By the time consciousness kicks in, most of the work has already been done," said study co-author John-Dylan Haynes, a neuroscientist who was at the Max Planck Institute. Haynes updated a classic experiment by Benjamin Libet, who showed that a brain region involved in coordinating motor activity fired a fraction of a second before test subjects chose to push a button. Hayne's study showed a much large time gap between a decision and the experience of making it.

In the seven seconds before Haynes' test subjects chose to push a button, activity shifted in their frontopolar cortex, a brain region associated with high-level planning. Soon afterwards, activity moved to the parietal cortex, a region of sensory integration. Haynes' team monitored these shifting neural patterns using a functional MRI machine.

Taken together, the patterns consistently predicted whether test subjects eventually pushed a button with their left or right hand -- a choice that, to them, felt like the outcome of conscious deliberation. In fact, their decision seems to have been made before they were aware of having made a choice.

So does this mean the feeling and belief we have that we have free will is just an illusion?

Well possibly, but probably not. For one thing, as mentioned, the experiment may not reflect the mental dynamics of much more complicated and/or emotionally meaningful decisions. Also, the predictions were not 100% accurate. Might free will enter at the last moment, allowing a person to override a subconscious decision?

But there is a much bigger problem with drawing conclusions about free will from this type of experiment. We usually do not employ free will in the sense of making conscious choices when we engage in the vast majority of our usual daily activities. If individuals had to weigh the pro's and con's of their every move as they negotiated their lives, or if they had to stop and think about how to behave before doing the most routine activities, so much time would be spent on that that they would be nearly paralyzed. 

Most of our "decisions" are based on environmental cues which are processed subconsicously and which then trigger habitual behavior without requiring any thought on our parts at all. 

Through our life experiences, we all build mental models of our environment called schemas which then, when cued by environmental triggers, automatically kick in. Cues elicit a certain well-rehearsed repertoire of responses.

To understand this, think of your daily drive to work. Most drivers, while negotiating a familiar route, have at one time or another come to the realization that they had not been paying the least attention to what they had been doing for several minutes. Nonetheless, they arrived at their destination, with almost no recollection of any of the landmarks that they had passed.

Surely, we have the option to choose to make a turn that would take us away from our intended destination, but, under most circumstances, why would we waste our time even considering something like that?

A lot of predictable situations like this are handled on "automatic pilot." Gregory Bateson observed that ordinary situations and "constant truths" are assimilated and stored in deep brain structures, while conscious deliberation is reserved for changeable, novel, and unpredictable situations.

This does not mean, however, that rigid behavior cannot be overcome by conscious deliberation. In neurologically intact individuals, the more evolutionarily-advanced part of the human brain, the cerebral cortex, can override even the most reflexive of gross motor behavior.

So perhaps the brain processes described in this study are the ones that determine whether or not an individual goes on automatic pilot, or has to stop and think about potential unanticipated consequences. React in the usual habitual way, or re-assess? When it comes to pushing an inert button in a lab, the consequences for the subject are pretty predictable: there will not be any.

Unless the subject were purposely trying to foul up the experimenter's protocol, which would be a strange thing to want to do in an experiment with no social consequences to the subject, why would they extend brain energy in making a choice? They would not. They would just "go with their gut."

Therefore, from the data in this study alone, it is not possible to know which interpretation is correct: the experimenter's, or the one I just suggested.

Maybe you don't have free will, maybe you do. As I said in the earlier post, I am pretty sure I do.

Tuesday, July 21, 2015

Groupthink: How Even Scientists Con Themselves in Order to Fit In

In his brilliant book, The Righteous Mind, Jonathan Haidt argues convincingly that logic evolved in humans not to establish the truth about the world or to establish facts, but to argue for ideas that benefit the kin and ethnic groups to which we belong, as well as to maintain a good reputation within those groups. My colleague Gregg Henriques calls this the Justification Hypothesis: logic is used to justify our group norms.

Many of our beliefs are based not on facts or reason at all and in fact seem to be impervious to them. They are instead based upon either our groupishness (the opposite of selfishness). For almost all of us, it is generally more important for us to look right than to be right.

This type of reasoning appears at the level of the individual, where it is called defense mechanisms and irrational beliefs. It appears at the level of the family or kin group, where it is called family myths. It also exists at the level of cultural groups, where it is called theology. Or if it is not your particular brand of theology, then it is called mythology.

Another name for this phenomenon in general is groupthink. We cede the right to think for ourselves for the sake of our group, and we often try to discourage our intimates from thinking for themselves for the same reason.

Even scientists are not immune. So what are some of the mechanisms by which they do this to themselves and to other people? That is the topic of this post.

First, a brief review of some previous posts. As I described in one post, I realized a long time ago that the so-called defense mechanisms discussed by the Freudians and the irrational thoughts catalogued by cognitive therapists (CBT) had a purpose that was not only intra-psychic but interpersonal as well. 

Defense mechanisms are defined as mental processes initiated, typically subconsciously, to avoid ideas or impulses that are unacceptable to our value system, and to avoid anxiety. Another name for this is mortification. We may, for example, compulsively try to act in the opposite way that the unacceptable impulse would dictate (reaction formation), or displace our anger from one person onto another, safer one.

Their interpersonal purpose is to screen out beliefs and impulses that are threatening to the kin group, which is also why they are threatening to the individual within the kin group.

The irrational thoughts of CBT, which they attributed to humans being basically irrational, also functioned much like the defense mechanisms. If you, for example, "catastrophize" about what might happen if you indulged an impulse that your kin group does not approve of (by, say imagining the worst possible outcome of doing so), you will indeed scare yourself away from engaging in it. (Of course, the CBT folks reject the whole concept of defense mechanisms - I recall a somewhat sarcastic reply from cognitive therapy pioneer Albert Ellis when I brought this up at one of his talks).

On a related note, there are the logical fallacies that are enumerated by logicians and which are well known to members of college debate squads. An example is post hoc reasoning, which assumes wrongly that if event A is quickly followed by event B, then it is true that A caused B. I saw patients engage in many of these fallacies when confronted with the negative consequences of the behavior that seemed to be demanded of them by their families. So, I believe, the logical fallacies can also be used as defense mechanisms - specifically designed to avoid troublesome questions about cherished beliefs that on the surface are simplistic at best and preposterous at worst.

As mentioned above, scientists are not immune from groupthink and groupishness. In fact, they are as nearly as likely as anyone else to employ them. I witnessed many times in scientific debates how the debaters would subtly employ various techniques and mind tricks to silence critics of their studies or ideas.

A few examples among many:

a) Black-and-white, or all-or-none thinking. Biological psychiatrists seem to think that everything in the DSM diagnostic manual is a brain disease, whereas the anti-psychiatry folks believe that nothing is, and the listed diagnoses are all just alternate lifestyles, different ways of looking at the world, or reactions to trauma.

b) Arguments that advance the idea that, because many parts of the thinking of someone like, for instance, Freud, were totally off-base (like "penis envy" and his theories about homosexuality), that therefore ALL of his ideas were wrong (including such obviously real things as intra-psychic conflict and defense mechanisms).

c) Stating facts about the results of studies without describing certain contextual elements that put those facts in a different light. A great example I have already blogged about is how the leader of the National Institute on Drug Abuse spoke about experiments with monkeys showing them pulling a level to get cocaine until they died - while neglecting to mention that the animals were in solitary confinement with nothing else to do. When that was not the case, they behaved very differently.

d) Conflating the issue of how a phenomenon arises or what it means in the scheme of things with the issue of whether the phenomenon even exists at all. For example, CBT'ers would deny that the concept of resistance, a psychoanalytic idea that states that people are often highly invested in their psychological symptoms and resist change - is a real phenomenon. All the while, they failed to report in their case studies the high level of non-compliance with CBT homework assignments by their patients in treatment.

e) Grossly exaggerating the strength of certain research findings while completely ignoring the study's weaknesses and problematic assumptions.

f) Conflating another scientist's conclusion about the significance of a clinical anecdote with the description of the anecdote, and not considering what else the anecdote might mean.

g) Scientism: the idea that randomized placebo-controlled studies of something are the end-all and be-all of science, and that everything else is just anecdotal and not science at all. I answer those who make this argument by asking for volunteers for a randomized placebo-controlled study on whether parachutes reduce the incidence of deaths and injuries during falls from airplane flights. 

I also point out that scientism creates a problem when it is only a slight exaggeration to say that in order to study an important psychological phenomenon like self-deception with a large enough study sample and within a reasonable time frame, you would pretty much have to ask people about their opinion of themselves. Sorta defeats the goal of the study, doesn't it? So does this mean that therefore studying self-deception should be completely off limits to scientists? 

Scientists will often accuse other scientists of doing these things while doing them themselves. This is projection - another defense mechanism. These mental mechanisms are so pervasive in human beings that we are quite likely to find at least some of them in any scientific discussion. 

Discerning readers will no doubt find examples in which I do some of it in my posts on my blogs. 

Friday, July 10, 2015

Studies that Show Drugs are Ineffective are Often Deep-Sixed

The production and distribution of scientific information has, of late, frequently become a broken process. Richard Horton, editor of the pre-eminent medical journal The Lancet, recently observed, “The case against science is straightforward: much of the scientific literature, perhaps half, may simply be untrue. Afflicted by studies with small sample sizes, tiny effects, invalid exploratory analyses, and flagrant conflicts of interest, together with an obsession for pursuing fashionable trends of dubious importance, science has taken a turn towards darkness.”

This is a problem in all of science. When it comes to industry-sponsered science, industry employs well thought out and highly researched processes for inducing scientists, doctors, and the general public to buy into highly biased ideas that are good for the industry's bottom line. This of course is true for the pharmaceutical industry just as it is with oil companies and the like. 

Not to mention the worst and by far the most dangerous-to-your-health offender of all, the managed care health insurance industryGeorge Dawson does an superb job tearing them a new one on his blog. But this post is about the pharmaceutical industry, other scientists who do drug studies, and the politics of acceptance of studies by medical journals. 

A well-designed study - manipulation of study design is a 'hole 'nother issue - that tries to measure whether a drug is effective for treating certain symptoms or a certain condition can turn out, broadly, in two possible ways. The drug is either shown to be effective for the symptom or condition, or it is shown to not be, or to be not very. 

Any single study's result may be invalid due to a problem with the sample of subjects picked, which may be unrepresentative of the whole population of subjects exhibiting the particular condition or symptom under study. It can also be just a coincidence, what with the standard 5% chance of that being so. So in general positive results need to be replicated in several different studies before the US Food and Drug Adminstration (FDA) will approve the drug for public consumption.

But what happens if a drug company or academic scientists who are fighting to get their studies published so they can attain tenure submit for publication only the studies that seem to show that a drug works, and then does not submit the other studies that had a negative result? Well, of course then it looks to everyone like the evidence for the drug's efficacy is much stronger than it actually is.

It is also true that, even when a negative study is submitted for publication, the editors of journals often reject the manuscript. Editors seem to think that, when a study did not show a positive result, there is no reason to publish it, supposedly because it does not tell us anything. That's ridiculous, of course - negative studies can tell us what is not true, and are essential to good science. 

This bias against so-called "negative" studies happens all over science, by the way, whether studies are industry sponsored or not. I remember renowned biologist Stephen Jay Gould decrying this in a book from decades ago.

In order to deal with the problem of negative studies not seeing the light of day as it applies to drug studies, a 2007 U.S. Federal law required study authors to report the results of all of their clinical trials to a public website. The website is, which draws 57,000 visitors a day, including people who are confronting serious diseases and looking for experimental treatments.

The law was enacted also because of public concern that a failure to report negative results could harm participants in similar studies by failing to warn them of possible risks.

The Food and Drug Administration Amendments Act requires sponsors of most clinical trials to register and report their basic summary results within 1 year of either completing data collection for the primary outcome or of terminating. Failure to report study findings is supposedly punishable by sanctions including civil penalties of up to $10,000 per day and loss of funding.

So how are we doing? Not so good.

According to a widely reported story, a study from Duke University finds that five years after the reporting law took effect, only 13 percent of scientists running clinical trials had reported their results! The article about this study was published online in the New England Journal of Medicine.

Only 13.4% of investigators reported their results within 1 year, and only 38.3% reported their results at any time during the study period (N. Engl. J. Med. 2015;372:1031-9). Moreover, “despite ethical mandates, statutory obligations, and considerable societal pressure, most trials that were funded by the National Institutes of Health (NIH) or other government or academic institutions ... have yet to report results at, whereas the medical-products industry has been more responsive to the legal mandate,” the researchers explained.

Interesting that the pharmaceutical industry is doing somewhat (although not a whole lot) better than the NIH-funded scientists on this score.

At 1 year, the rate of reporting was 17.0% for industry-sponsored trials, 8.1% for NIH-funded trials, and 5.7% for other government- or academically funded trials. The corresponding rates of reporting at 5 years were only slightly better, at 41.5%, 38.9%, and 27.7%, respectively.

According to Clinical Psychiatry News, despite the regulation’s threat of penalties, no enforcement has yet occurred, the researchers noted, in part because this portion of the FDA Administration and Amendments Act is still under public discussion and hasn’t been finalized. 

Anyone who wants to contribute towards changing this situation can do so at

The lack of publication of negative studies is not the only strategy employed by big Pharma to bias everyone's impression of their drug's effectiveness study data. Some other tricks they employ include:
  • Publishing positive studies more than once by using journal "supplements."
  • Conducting a study at multiple locations and then publishing the results of the individual locations as if they were separate trials - and doing so selectively if that makes the drug look better.
  • Publishing different measures of drug efficacy at differnt times to give the impression that the results published later are from a new or different study.
  • Following study patients for longer and longer time periods and then publishing the results from each time period separately, again making it look like there was more than one study.
  • Publishing positive results in major or more prestigious journals and negative or neutral studies in more obscure journals.
  • Combining the results of multiple trials in ways that are more favorable than any individual study in its own right.

Let the buyer beware!

Tuesday, June 30, 2015

How Did I Learn About the Family Dynamics I Write About?

From Mark Anderson,

In my Psychology Today blogpost of 10/14/13, Don't Ask, Don't Tell, I discussed how patients in psychotherapy do not volunteer a lot of information about their family dynamics unless they are asked very specific questions - and often not even then until (and unless) they have formed a trusting relationship with their therapist. I mentioned the case of a patient who was smart enough to have been a Ph.D. candidate, came in complaining of anxiety, and did not think it relevant to tell me until months into therapy about the daily conversations with her mother that literally made her nauseous.

So, therapists who think that what they see and hear in the office is indicative of what is really going on in a patient's life may be sadly mistaken. For example, a woman may complain that her father is "controlling." The therapist should want to invite the father in at some point to see if this is accurate. Most do not. However, even if the therapist does this, both of them may then mislead him or her. 

The father may at first appear to be anything but controlling - telling the therapist about how he gives the adult daughter money to do whatever she wants without obvious restrictions, and never stopping her from doing anything she wants. What neither might mention, however, is that he always calls her incessantly on her cell phone whenever she goes anywhere!

When I was in training as a therapist during my psychiatric residency, psychoanalysis was the king of psychotherapy paradigms, and I was not taught about how to ask my patients about repetitive dysfunctional interactions with family of origin members occurring in the present. A lot of both analysts and CBT therapists seem to think that patients' problems reside entirely within the confines of their own heads, as if we are not social organisms at all.

When I write in my blogs about the types of family dysfunction that I have seen with my patients, a frequent criticism I get is that I am taking patients at their word, and that since patients often distort things, I am surely getting a distorted picture - which by implication must have led me to form distorted ideas about what actually is and has been taking place.

So how do I know that these patterns are real? Well, let me tell y'all how I discovered them. (Hey, I've lived in South now for over twenty years).

When I was a beginner as a therapist, I kept noticing that my patients usually did not respond to various interventions in the ways described in the psychotherapy literature. I would sometimes have some success with these interventions, but the results were often rather inconsequential. So in response I started reading about other paradigms one at a time, and each time, I would have the same experience. Perhaps I was not doing them right, but other therapists would tell me that they noticed the same limitations.

I somehow stumbled on a version of a therapeutic question that had, unbeknownst to me, first been proposed by Alfred Adler, one of the three founding fathers of psychodynamic psychotherapy. I had started to ask my patients why they were not employing the obvious solutions to their problems. If I could think of an obvious solution such as "why don't you just leave your abusive husband?" no doubt the patient has already thought of it, and has decided against it for some seemingly strange reason. 

When a therapist asks a question like that, the first answers he or she often gets in response is one described by Eric Berne. It goes something like, “Yes, I could do that but…” followed by some lame excuse for why they cannot do that. This is known as the game of Why Don’t You – Yes But.

I decided I would play my own version of the game that I called Why I Can’t – Yes But. Every time I heard a yes-but answer to my original question, I would counter with, “Yes, but you could handle that obstacle by doing [such and such].” This solution would of course also be yes-butted by the patient with another lame excuse - for which I would provide another obvious solution.

An example from my last book: one adult female could not seem to hold a job and always seemed to end up going back home to live with and depend upon on her abusive father and inadequate mother. I knew other relatives also lived in the home but I had no clue as to their significance. The patient was bright and had made it to the upper echelons of a sport that she liked to play, so I knew she was highly capable of holding a job. 

Every time she offered an excuse such as “I’m no good in school so I can’t learn new skills,” I would counter with my own yes-but. I went through a seemingly endless array of lame excuses in this manner, until finally she said, “If I’m not at the house, my father molests my niece.”

Whaaat??? She never thought to mention this before????  

So, a bit off guard, I said, “Have you thought about reporting him to child protective services?”  She replied, “Of course, but if I did that my mother would end up on the street because she cannot support herself." Her mother would suffer, and it would be all her fault. No doubt she would be blamed by the family.

Well, lessee. She could handle that obstacle to holding a job by…by…by…er, how exactly could she handle that problem? I had no answer. She could write her mother off, I suppose, but since when is caring about the survival of family members or her niece's safety a bad thing? This was a really devilish conundrum. As mentioned, I also wondered why she had not told me about this in the first place. That was the moment that I was first confronted by evidence that family members may be acting for altruistic motives rather than selfish ones, and that family problems might be incredibly difficult to solve.

I then found an easier way to get to this answer than playing a long game of yes-butting: the Adlerian question: What would happen if I could wave a magic wand and you suddenly got better and stayed better?

At first, patients would often answer with such non-answers, "I'd just find some other way to screw things up" or "I cannot even imagine what that would be like." I would not accept those "answers" and pressed on. Then I started getting the real answers. 

But were they really real? Was I just being fooled by my patients with distorted perceptions. Well, just so readers know, I do not just take them at their word.

I began to have conjoint sessions with the patients and their parents. I have had both the mothers of patients with BPD and their daughters with BPD as patients in individual therapy separately, some at the same time, on several occasions. As a psychotherapy supervisor, I have watched videotapes of the mother of a daughter with BPD in a session with one therapist and the daughter with another therapist describing the very same interactions.

Even more revealing, I have had patients who were sick and tired of being accused of distorting everything bring in audiotapes of phone conversations with their parents when the parents did not know they were being recorded. Illegal in some states to record, but not for me to listen to. I heard some of the most unbelievable things come out of their mouths.

In individual sessions, I listen very carefully to what the patients say and ask follow-up questions about anything that seems contradictory - when the patients with BPD are in "spoiler" mode (which is when they are distorting things, but sort of on purpose), they do that all the time. But knowing a few tricks of the trade, it's easy to get them to stop doing that.

One still needs a good theory in order to interpret the behavior that I had been observing. Luckily, as I started to try to make sense of the evidence before me, I came across some relevant ones. For example, there was Sam Slipp, who wrote about the dysfunctional family roles of savior, avenger, and go-between. And then there was family therapy pioneer Murray Bowen, who wrote about family emotional processes and the intergenerational transmission of dysfunctional family patterns.

So no, my ideas about family dynamics do not come just from listening to my patients alone.

Monday, June 22, 2015

Randomized Controlled Studies vs. Widespread Clinical Experience: the Case of Lamictal

There has been an increasing debate about whether doctors are using "evidence-based medicine" or instead are merely going by conventional wisdom or listening to pharmaceutical company sales pitches. Often, as I have discussed several times, the so-called "evidence base" consists of randomized controlled studies (RCT's), while clinical experience is written off as "anecdotal." 

An anecdote is a report of a single, or at most a few, specific incidents, such as a patients' seeming to get better after taking a medication, along with the interpretation of the event by an allegedly biased observer. Besides the fact that one or two cases may not be representative of a psychiatric condition, and that other causes for the observed effect have not been ruled out, the description provided by the source of the anecdote may be incomplete or incorrect. And his or her conclusion may be logical, or it may be fallacious in any of a variety of different ways.

Widespread clinical experience — or the clinical experiences of a wide variety of practitioners who are known to do careful diagnostic work-ups and to follow patients closely — is somehow also written off as "anecdotal," but this is just nonsense. 

First of all, as I discussed in a previous post, in psychiatry there are almost no objective diagnostic blood tests or direct measurements of brain function that can tease out the difference between neuropathology and normal neural plasticity in response to environmental factors. Therefore, conclusions drawn in RCT's are based entirely on the self-report data from subjects or by the potentially biased observations of the experimenters. They are just as much anecdotal as widespread clinical experience in that sense. 

Actually, widespread clinical experience is better than most RCT's in determining the efficacy of drugs. It employs a sample size far larger than all the RCT's on a treatment put together. Also, there are several important  limitations with RCT's.

In a paper by G. Parker and S. McCraw (Acta Psychiatrica Scandinavia, 2015: 1-10) about the drug Lamictal (lamotragine), they discuss the disconnect between the reported efficacy of a new psychotropic medication as quantified in RCTs and its actual effectiveness as observed in the 'real world' of psychiatric practice:

"Most commonly any such disconnect is one of degree, with the medication being progressively clinically judged as less or more effective. Less commonly, the medication may be judged to have a different therapeutic 'signal' than for its formal indication. Two examples of the latter are the selective serotonin reuptake inhibitors (SSRI's) which seemingly modulate emotional dysregulation as much as they have antidepressant propensities, and some atypical antipsychotic drugs having utility in augmenting antidepressant medications and in having mood stabilizing propensities rather than being confined to the management of psychotic conditions.

Any such disconnect can reflect multiple factors, as considered now in relation to antidepressant medications. An antidepressant's 'efficacy' is evaluated from RCTs with the 'control' treatment being either a placebo or a comparator drug. In such trials, the duration is often limited to several weeks, the sample constrained by inclusion and exclusion criteria (e.g. non-suicidal, no substantive co-morbid conditions) that do not hold in clinical practice, and which may, depending on recruitment strategies, be weighted to those with potentially spontaneously remitting and/or less severe conditions. 

RCT-evaluated efficacy may he overestimated using a lower-than-usual dose of any comparator medication, or underestimated if the antidepressant is prescribed at what might be later determined to be a suboptimal dose. Biases may emerge if the sponsoring developers provide data only on trials generating superior findings. "

Richard Horton, editor of the medical journal The Lancet, recently observed, “The case against science is straightforward: much of the scientific literature, perhaps half, may simply be untrue. Afflicted by studies with small sample sizes, tiny effects, invalid exploratory analyses, and flagrant conflicts of interest, together with an obsession for pursuing fashionable trends of dubious importance, science has taken a turn towards darkness.”

In studies used to evaluate medications for treatment of various mood disorders, there is another glaring problem: the use of inadequate and incomplete diagnostic evaluations of the subjects. I have written several posts about the nonsensical expansion of the diagnosis of bipolar disorder, in which researchers lump together Bipolar I with the bogus disorder Bipolar II. 

Readers of this blog know my attitude about the latter: In my practice since I started training, I have seen four patients who actually met the DSM criteria for this supposed disorder when they were interviewed carefully and followed closely, and all four responded to lithium, suggesting that they were just milder cases of Bipolar I. And most patients who were given that diagnosis by previous psychiatrists did not have bipolar disorder at all but had the mood instability characteristic of certain personality disorders. Some studies have shown this to be true.

Worse yet, some studies include patients diagnosed with unspecified bipolar disorder and "bipolar spectrum disorder."  Neither is defined clearly nor is there any agreement on exactly with what criteria these diagnoses are to be made. So the RCTS's are basically comparing apples to oranges.

This particular problem is not discussed clearly in the Parker and McCraw article. In fact, they conclude that the anticonvulsant drug Lamictal (lamotrigine) is probably not effective in bipolar I disorder, but probably is effective in bipolar II disorder - which probably means it may help the affective instability of patients with personality disorders. This puts this drug as a possible alternative to SSRI's, which the authors themselves note "... seemingly modulate emotional dysregulation."  Emotional dysregulation and affect or mood instability are basically the same thing.

(Combining SSRI's and a long acting benzodiazepine such as clonazepam is even more effective in "raising the bar" on the strength of environmental stimuli required to set off an episode of affect dysregulation, as well as in decreasing self-injurious behaviors like cutting. There are no RCT's on this combination for these symptoms; the drug companies won't do them because most of these drugs are generic and the drug companies probably know that it is effective but do not want docs to know this. However, widespread clinical experience by those doctors who know the difference between bipolar disorder and borderline personality disorder backs me up on this).

The history of the FDA approval for the drug Lamictal for bipolar disorder is bizarre. Its manufacturer first touted it as a treatment for the depressive episodes in bipolar disorder, although later studies showed it to be ineffective in the acute phase of bipolar depression. Then, when it got the FDA approval for psychiatric use, rather than being given the indication for prophylaxis for (prevention of) episodes of bipolar depression, it was given a general indication for bipolar disorder as a whole. This, even though there was zero evidence that it prevented episodes of mania, or that it was useful in acute mania.

In fact, most of the studies in bipolar disorder with the drug were based on a rather flawed outcome measure. The drug was found to delay, but not to prevent, the emergence of another bipolar episode. Whether the episode was a depressive episode or a manic episode was not specified in the majority of these studies!  

Furthermore, lithium — the standard prophylactic treatment—when used at the dosages which lead to the correct blood levels of the drug in patients who respond to and can tolerate it (about 80% of bipolar I patients) completely prevents the re-emergence of manic episodes. In those cases, the measurement "time until the next manic episode" would essentially be the patient's entire lifetime. 

Delaying episodes of bipolar disorder is better than having them more frequently, but why would you use a drug to do that when there is another drug that can prevent them from happening completely?

Friday, June 12, 2015

Why Does Psychotherapy with Patients With Personality Disorders Take So Long?

The type of psychotherapy I do with my patients who suffer from personality disorders is called Unified Therapy. It integrates ideas from all of the main schools of psychotherapy about both the causes and the treatment of significant and ongoing self-destructive as well as anxiety-producing and/or depressogenic behavior patterns. 

Briefly, it posits that the parents in the patient's family of origin experience ambivalence and emotional conflicts about the demands of certain family roles that they have learned are required of them. They learned these roles from their own families of origin. 

The roles were initially culturally determined. As a consequence of this ambivalence, they make contradictory demands on, and give double messages to, other members of the patient's family of origin about what is expected of them.

The ambivalence in the parents, in turn, is created by learned and ingrained family rules which became obsolete when the ambient culture changed quickly. In other words, the family rules lag behind changes in the requirements of the ambient culture.

The double messages are believed to reinforce (in the behaviorist sense and on a variable intermittent reinforcement schedule) the patient's intrapsychic conflicts and the resultant dysfunctional behavior. The patient's responsive behavior then simultaneously reinforces ambivalent, dysfunctional behavior in the rest of the family.

Most of the psychotherapy treatment protocols for significant personality disorders practiced today require long-term therapy, and my model is no exception. It usually takes between 70-120  sessions - sometimes more - which take place at a frequency of once every two weeks (most other therapy paradigms are based on weekly sessions). I wish I knew of a faster way to help these patients. If I could find one, please believe me, I would be the first to employ it.

So why does it take so long? 

The first reason is that, in the beginning of treatment, the therapist has to gain the trust of the patient. Most of these patients have been betrayed in one way or another by their own close family members - the very people whom they are supposed to be able to trust the most. Furthermore, they feel ashamed of both their own and their family's behavior.  

Even more important, they feel guilty if they don't keep the family's deep dark secrets to themselves.  

Given their experience, they would have to be idiots to trust a therapist - a complete stranger - right out of the box.

Even after they begin to open up, it also takes quite a while for the patient and therapist to understand what motivates all of the patient's family's bewildering behavior. Even figuring out the right questions to pose can be a challenge for the therapist. 

The reasons that problematic patterns exist usually involve historical events that have taken place over at least a couple of generations, and sometimes start even further back than that. Important historical events which might explain them better may not be discoverable because there are no longer any relatives alive who are old enough to know about them.

However, these are not the primary reasons for the length of therapy. The main reason is because personality disorders are not only highly complex and complicated, but extremely well ingrained into the brains of sufferers. As I have discussed in previous posts, behavioral reactions to the social environment are literally branded into the primitive part of their brains known as the limbic system over many years due to repetitive interactions with parents and/or other primary caretakers.

Patients may in some cases change their problematic behaviors fairly quickly over the short term, but the changes often do not last. Doing short-term interventions may seem to work if one does not follow the patient for very long, but these interventions work sort of like a fad diet. Those who go on fad diets lose a lot of weight quickly, but if you look at them a couple of years later, they usually have gained it all back. Often they gain back even more weight than they initially lost.  

Psychotherapy outcome studies that do not look at the frequency of certain behavior patterns and psychological symptoms two years after treatment has ended are highly misleading.

Dealing with family members who feed into the patient's self-destructive behavior, whether inadvertently or on purpose, leads to a whole new level of complexity. Their behavior patterns are also branded into their brains for the very same reasons! Not only that, but as family-systems therapists first pointed out decades ago, the whole group of family members automatically pushes back against someone attempting to change the old patterns. 

This is called family homeostasis. Everyone literally gangs up on the poor patient with invalidation of their new behavior. It is accompanied by the implicit instruction, "You are wrong, change back." I listed some of the ways this is done in a previous post.

Altering these dynamic family interactions is like a game of three dimensional chess, only with even more dimensions. Whenever I coach a patient on strategies concerning how to respond to a parent's problematic behavior, each move leads to a counter-move on the part of the parent which is designed to keep everything unchanged. 

These counter-moves do not necessarily occur immediately after the patient initially does what we have decided on in therapy sessions, but may occur suddenly at any time - often when least expected.

For therapy to work, the therapist and patient have to come up with a whole series of moves and responses in order to address each of the countermoves. Countermoves may also include a parent trying to rope in a third party - such as the other parent or a sibling. Sometimes the patient and I can figure out two or three of these moves in this game in advance, but not usually.

Furthermore, all of us have a seeming natural reluctance to discuss sensitive family dynamics with our parents and other primary attachment figures, so this whole process is usually interrupted by significant periods of time in which patients cannot seem to get their homework assignments done before the next session.

This type of therapy therefore requires a major investment of time and money and energy. It requires courage, nuance and subtlety as well. The alternative, however, is not only the continuation of the patient's personal misery, but the likelihood that dysfunctional patterns will be passed through to future generations of the patient's family.