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Bipolar Disorder – Missing the Point!

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.

Joanne Cacciatore’s Care Farm

12/14/2017        Uncategorized 0 Comments

Joanne Cacciatore's Care Farm


Take a look at the Yahoo Lifestyle article showcasing Joanne Cacciatore's Care Farm in Sedona, Arizona. Joanne's brainchild is a unique application of this model to helping people who are in the throes of bereavement. She helps people reconnect to the earth, animals, nature, and themselves while allowing the painful process of mourning to happen as it naturally does. This stands in stark contrast to the conventional and absurd method of trying to make the pain go away. Congrats Joanne!

Who are you and what are you doing here?

Who are you and what are you doing here?

So, you want to do the humanitarian thing, to treat people with respect, care, tenderness, empathy, understanding ? Good for you. Good for us. Good for ISEPP. Somehow, though, I think there is more to it than that.

I am an existential psychiatrist; we are a crusty lot. Our favorite subjects are:

Death
Isolation
Meaninglessness
Responsibility

 

You wonder why we need a drink at the end of the day?

“Yes, Mrs. Smith, you have a disease, an illness, a syndrome. We call  this condition  `being human`.” Some would say just “being,” but believe me (take care when someone starts his spiel with “believe me”) being human is special. I love dogs, cats, elephants, and Orca whales, but my best bet is they don’t think about the same things as I think about. OK, there is some overlap. They think about sex (at the appropriate time) and I think about sex any time. I think I am the center of the universe, all revolves around me and those creatures seem to share my self-centeredness. They do what they do to survive. So do I. Still, truly we humans are different. Why do I care about the Rohingya genocide in Burma or anti-women culture in Saudi Arabia? Why do I espouse such liberal taunts as “An injustice anywhere is an injustice everywhere?” Why do I care what is Dark Matter and Dark Energy? Why do I ask “why” so often? To be an existentialist is to take responsibility for my actions and my being even though I had nothing to say about “joining up” to life. Why do I seek meaning when clearly it is out of reach? Why am I capable of loneliness in a crowd? Why do I fear death in the midst of so much life?

Recently I read an interesting idea about cancer, the title of the article, “Why did God create cancer?” (Tedd Koren, Wise Traditions, Fall 2017, p 16, Vol 18, No. 3). The author gives a teleological explanation for cancer. Note: doctors are taught in medical school not to do this...not to think teleologically.  A teleological explanation  attempts to explain the purpose of a phenomenon rather than its cause. Koren’s argument:  malignancies are not the problem but the body’s attempt at a solution to cleansing the body of toxic substances such as pesticides and heavy metals. He cites Devra Davis’ work (“The Secret History of the War on Cancer”, NY, NY. Basic Books, 2001) which explicates the profoundly increased number of malignancies in toxic environments.  Dr. Davis also makes the case, unfortunately, that the so called War on Cancer actually followed the commercial interests of industry rather than the health of the populace. Also, Koren cites studies (Falck, F. Jr. et al. “Pesticides and polychlorinated biphenyl residues in human breast lipids and their relation to breast cancer. Arch Environ Health 1992; 47(2): 143-146. ) showing the heavy concentrations of toxins within cancers themselves. Oncologists miss the boat, he posits, as they focus on killing tumors which are the body’s filtering system. They should be focusing, instead, on detoxifying the person.

 ------
Are biological psychiatrists like oncologist? Kill, kill, kill?
------

Back to the original question, “Who am I, the existential psychiatrist, and what am I doing with this endeavor called “psychotherapy?” Perhaps we can think of psychotherapy as a kind of “filtering” system where the therapist in partnership with the patient filters out the toxicities within relationships: Interpersonal and intrapersonal  relations and the person’s relationship to his environment. The existential therapist also focuses on relationship to being itself. And, for good measure, the existential psychoanalyst focuses on relationship to the past.

Continuing with this metaphor: The biological psychiatrist is more like the current purveyors of oncology. The oncologist focuses on killing the tumor with toxic drugs, surgery, and radiation: slash, poison, burn. The biological psychiatrist attempts to kill symptoms with drugs and ECT. What I am positing is this:  The symptoms of mental and interpersonal anguish, depression, anxiety, delusions, hallucinations are the organism’s (the person’s) attempt to deal with, to cope with, to cleans, to filter, toxic-difficult conflict. The therapist is there to encourage and enhance this process, not kill it. We need more than empathy to do that. It also takes courage.

Spooky Language!

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

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.

Alternative History of the Native American Mental Health System

10/27/2017        Uncategorized 0 Comments

Watch ISEPP's David Walker speak about how the mental health industry has privileged "white" America and disenfranchised the native people who preceded the European invasion.

A New Treatment for Depression – Really?

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?

Breggin Fails in Court

Breggin Fails in Court


Remember folks, Peter Breggin is on our (ISEPP’S) side; so, when Peter fails, we fail. Or do we? How did we/he fail this time?


Commonwealth of Massachusetts vs Michelle Carter. Guilty of manslaughter


Michelle was found guilty of encouraging, coaxing, pushing her despondent boyfriend, Conrad Roy, to kill himself. Peter noted that in June of 2014, Michelle was actually encouraging Conrad to get psychological help, not kill himself. In fact she volunteered to go with him to work on her own problem, an eating disorder. She was then started on Celexa by her doc (she had been taking Prozac for years). By July 2014, a month into her new antidepressant treatment, Peter noted she had become -- transformed if you will -- apathetic, prone to bouts of mania, nightmares in which the devil told her to kill herself. In addition, according to the “Psychiatric Times,” September 2017, p. 13, Peter also testified:

[Carter] was enmeshed in a delusional system…really…a delusion where she’s thinking that it’s a good thing to help him die…[She] was unable to form intent because she was so grandiose that what she was doing was not to harm -- even though she was encouraging his suicide, her absolute intent was to help Conrad.

Well, the judge would have none of it. (Michelle chose not to have a jury trial.) When Michelle encouraged him to poison himself with carbon monoxide, there was no indication of an attempt to “help.”

This case bothers me. Although I am in Peter’s corner, railing against toxic substances poisoning the minds of vulnerable kids, I probably would have made the same judgment as Judge Lawrence Moniz. “The drug made me (her, him) do it!” is a slippery slope, particularly if you are of an existential bent as am I. We existentialists believe in personal responsibility. Note: Of all the drugs on the market, the drug causing the most violence is, you guessed it, alcohol. And alcoholic intoxication is not a defense in a court of law. 


So many culprits in this case


Yes, I know alcohol intoxication is quite different from taking a drug prescribed by an “expert.” When we drink alcohol, it is on our own recognizance.

But, isn’t it peculiar that pregnant women are warned that alcohol might be injurious to the health of the fetus but there is no black box warning indicating that alcohol might impair judgment, remove social inhibitions, lead to violent actions towards others or oneself?

What interests me is: WAS MICHELE EVER WARNED that Celexa could impair her moral judgment? How did the prescriber counsel her? Was she told that apathy was a possible effect? Most of all, the question is still open – where does personal responsibility end and professional responsibility begin? It is here that I am sympathetic to Judge Moniz’s decision. He is called upon to pass judgment on the person, not the system. There are so many culprits in this case: the careless prescribing physician; the corrupt pharmaceutical industry; distortions promulgated by the profession of psychiatry; the negligent families of each of these kids; society, with its futile dependence on pseudo-technical solutions to psychologic/spiritual problems. Michelle and Conrad were the end point of myriad influences. Conrad is dead. Michelle will do some jail time. Maybe she’s wiser. Are we?

Let’s clarify something. It is a mistake to think that patients always follow doctor’s orders. There are very persuasive accounts in the literature that the opposite is true, particularly when it comes to antidepressants.

Some examples:

  1. From Sawada, N et al. Persistence and compliance to antidepressant treatment in patients with depression: A chart review. BMC Psychiatry 2009:38. “In this retrospective chart review, 6-month adherence to antidepressants was examined in 367 outpatients with a major depressive disorder (ICD-10)… Only 161 patients (44.3%) [!] continued antidepressant treatment for 6 months.”
  2. From Warden D et al. Identifying risk for attrition during treatment for depression. Psychother Psychosom 2009:78:372-379. “The attrition rates in the first 12 weeks of treatment can be as high as 65% [!] in naturalistic setting (2,3,4) and 36% in clinical trials [5] and as many as 15% of the patients never begin a prescribed antidepressant [6].”
  3. From SansoneR.A. et al. in “Innovations in Clinical Neuroscience,” 2012. P41-46, “…approximately 50% of psychiatric patents and 50% of primary care patients prematurely discontinue antidepressant therapy…”

My sympathy goes out to Michelle and to Conrad’s family. I can’t explain why Michelle did not toss the drug down the drain, not wanting the effects that may have contributed to Conrad’s death. Often one’s desire to escape psychological pain has dire consequences. Is that what happened to Michelle Carter? “Die Conrad, I don’t want to feel your pain any more.”

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

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.

VA Damage Control: The VA Has Been Infiltrated!

This is an actual letter I mailed recently to help raise money for my veteran patient . Identifying information including the dog’s name, has been changed.


 

 

September 1, 2017

To Whom It May Concern:

Re: Skip Sullivan, Honorably Discharged Veteran
DOB: Too Young

VA’s Failure

Skip was referred to me by Sally H, Visiting Nurse for Veterans, Camp X, the South. He flew here to the Washington, DC area because he was informed by Colonel Sharon Z. founder of HELPFOR VETSUSA that I could help him.

Two deployments to Iraq, the deaths of a dozen comrades by enemy fire and by suicide, two suicide attempts himself, as well as musculoskeletal damage due to an enemy IED. You would think that would all be enough for him to deal with: psychological trauma, moral injury, the gut of war. No! His principle dilemma now is iatrogenic. Skip lost count after 40 different drugs had been prescribed for him over the last 7 years. When he arrived at my office on August 17, 2017, he was on high doses of nine different drugs all of which have had profound adverse reaction impact. Before arriving at the VA for medical care in 2010, his vision was perfect, now impaired. Before arriving at the VA he had normal GI functioning, now impaired. Before arriving at the VA, he had normal sexual functioning, now impaired. Before arriving at the VA, although in psychological turmoil, he had excellent cognitive function and could emotionally feel authentically, now, “I fake feeling. I know I’m supposed to feel but I can’t.” And he nods off in the middle of substantive discussion.

Skip flew 1500 miles from the MidWest because he could find no doctor with the will or the knowhow within the VA system to wean him. Be clear. Although I am an “expert,” I made it clear to Skip the complexity of dozens of psychotropic drugs interacting is BEYOND KNOWABLE. Without any guarantees, Skip and I have entered into a struggle, requiring daily monitoring and extraordinary help from his fellow vets, a different vet showing up each day to bring him along with Charlie, his companion dog, to my office since it would be dangerously foolhardy for him to drive himself.

What’s the big deal? Just stop the drugs! Well, stopping these drugs cold turkey would be inviting mortal danger. The body and all its systems, neurological, gastrointestinal, cardiovascular, adapt to the onslaught of these potent substances with a myriad of potential adverse reactions. Abrupt withdrawal would be like blowing up a dam, psychologically flooding – overwhelming the organism. It must be done slowly. Unfortunately, it is also painful. It takes courage, “I’m willing to put up with the pain if I can just be normal again.”

Why all the drugs? Thousands upon thousands of veterans are going through this. I believe the difficult answer to this question is that the VA has been infiltrated with self-defeating, and what I consider odious ideas about what it means to have suffered the damage of war battle. Pathologizing these returning warriors rather than accepting, hearing, understanding, and supporting their terror-filled experiences drives them further into misery, e.g., as soon as the idea of “suicide” is mentioned almost invariably the VA physician reaches for the prescription pad. And as the veteran experiences the first adverse reaction, the second drug is added, then the third, the fourth, etc. In time there is utter confusion about what is “real” and what is drug-induced. The chance then of finding a remedy becomes less and less.

So I will work with Skip this next year, seeing him frequently, daily when necessary, doing the necessary testing (e.g., he is probably Mg depleted as his GERD caused by one of his many drugs is being treated with yet another drug, a proton pump inhibitor (PPI), which potentially depletes this essential element. Note, he has been on this drug for more than six years while the recommended length of time to use PPIs is about three months!) and, most importantly working psychotherapeutically, existentially, spiritually as he comes to grips with war trauma. Ultimately, his goal is to help other vets. I believe he’ll do it.

Finally, Nurse Sally is paying for his treatment out of her own pocket. I am giving her some discount. This is a travesty! The government agency that has so poorly treated this veteran does not now take the responsibility of paying for the treatment that he had to seek out on his own. As an American, I feel shame and I am disheartened.

Sincerely,

Joseph Tarantolo, MD

Board Certified Psychiatrist