A brain disease AND (fill in the blank)

 

Schizophrenia
Schizophrenia (Photo credit: Alaina Abplanalp Photography)

 

Not addiction related, but a very interesting look at  new directions for treating and understanding schizophrenia.

 

The article opens by reflecting on where we stand with our attempts to understand the causes:

 

…the outcome of two decades of serious psychiatric science is that schizophrenia now appears to be a complex outcome of many unrelated causes—the genes you inherit, but also whether your mother fell ill during her pregnancy, whether you got beaten up as a child or were stressed as an adolescent, even how much sun your skin has seen. It’s not just about the brain. It’s not just about genes. In fact, schizophrenia looks more and more like diabetes. A messy array of risk factors predisposes someone to develop diabetes: smoking, being overweight, collecting fat around the middle rather than on the hips, high blood pressure, and yes, family history. These risk factors are not intrinsically linked. Some of them have something to do with genes, but most do not. They hang together so loosely that physicians now speak of a metabolic “syndrome,” something far looser and vaguer than an “illness,” let alone a “disease.” Psychiatric researchers increasingly think about schizophrenia in similar terms.

 

The author reports disenchantment with a simple biomedical model and offer three reasons.

 

First, disappointment with medication:

 

The first reason the tide turned is that the newer, targeted medications did not work very well. It is true that about a third of those who take antipsychotics improve markedly. But the side effects of antipsychotics are not very pleasant. They can make your skin crawl as if ants were scuttling underneath the surface. They can make you feel dull and bloated. While they damp down the horrifying hallucinations that can make someone’s life a misery—harsh voices whispering “You’re stupid” dozens of times a day, so audible that the sufferer turns to see who spoke—it is not as if the drugs restore most people to the way they were before they fell sick. Many who are on antipsychotic medication are so sluggish that they are lucky if they can work menial jobs.

 

Second, the genetics are much more complicated than was assumed:

 

The second reason the tide turned against the simple biomedical model is that the search for a genetic explanation fell apart. Genes are clearly involved in schizophrenia.

 

But:

 

The effort to narrow the number of genes that may play a role has been daunting. A leading researcher in the field, Ridha Joober, has argued that there are so many genes involved, and the effects of any one gene are so small, that the serious scientist working in the field should devote his or her time solely to identifying genes that can be shown not to be relevant.

 

Third, global research is revealing that culture and social factors play a much bigger role than previously understood:

 

The third reason for the pushback against the biomedical approach is that a cadre of psychiatric epidemiologists and anthropologists has made clear that culture really matters. In the early days of the biomedical revolution, when schizophrenia epitomized the pure brain disorder, the illness was said to appear at the same rate around the globe, as if true brain disease respected no social boundaries and was found in all nations, classes, and races in equal measure. … In recent years, epidemiologists have been able to demonstrate that while schizophrenia is rare everywhere, it is much more common in some settings than in others, and in some societies the disorder seems more severe and unyielding.

 

For example:

 

Schizophrenia has a more benign course and outcome in the developing world. The best data come from India. In the study that established the difference, researchers looking at people two years after they first showed up at a hospital for care found that they scored significantly better on most outcome measures than a comparable group in the West. They had fewer symptoms, took less medication, and were more likely to be employed and married.

 

The article closes with a few examples of alternative strategies from other countries. I’m sure it will provoke controversy, but seems increasingly hard to defend the status quo.

 

 

 

 

 

We’re not alone

Pat Deegan linked to a report on the state of treatment for schizophrenia for medicaid recipients.

Although there was some state-to-state variation in the findings, the study found that, while more than 90 percent of beneficiaries with schizophrenia or bipolar disorder received an evidence-based medication during the year, only 61 percent of those beneficiaries continuously refilled their prescriptions. Medication level monitoring was provided to about half of beneficiaries taking lithium or anticonvulsants, and screening for common side effects of antipsychotics was provided even less frequently. Only 30 percent of beneficiaries received any preventive physical health services. In some states, less than half of beneficiaries received psychosocial services. Overall, only 5 percent received all of the following: a continuous supply of evidence-based medications, medication level monitoring and screenings for medication side effects, and psychosocial services.

It sometimes seems that addiction treatment’s shortcomings get a lot of scrutiny (Our field definitely has a lot of room for improvement.), but I’ve always wondered how other medical treatment systems would fair under similar scrutiny. It’s sad to consider how much despair, stigma and secondary illness is generated by the failure of this system to consistently deliver treatment of the appropriate quality.

Following the evidence

Ouch:

Fluoxetine HCl 20mg Capsules (Prozac)
Fluoxetine HCl 20mg Capsules (Prozac) (Photo credit: Wikipedia)

Abstract: This paper raises the question about whether the data on the medications we call antidepressants justify the label of antidepressant. The authors argue that a true antidepressant should be clearly superior to placebo, should offer a risk/benefit balance that exceeds that of alternative treatments, should not increase suicidality, should not increase anxiety and agitation, should not interfere with sexual functioning, and should not increase depression chronicity. Unfortunately, these medications appear to fall short on all of these dimensions. Many of the “side effects” of these medications have larger effect sizes than the antidepressant effect size. To call these medications antidepressants may make sense from a marketing standpoint but may be misleading from a scientific perspective. Consumers deserve a label that more accurately reflects the data on the largest effects and helps them understand the range of effects from these medications. In other words, it may make just as much sense to call these medications antiaphrodisiacs as antidepressants because the negative effects on libido and sexual functioning are so common. It can be argued that a misleading label may interfere with our commitment to informed consent. Therefore, it may be time to stop calling these medications antidepressants.

From the conclusion:

If we do not call these medications antidepressants, what are some alternative labels that may better fit the existing data? The effect sizes for many of the “side effects” are larger than the antidepressant effect sizes. Using labels like antiaphrodisiac medications, agitation enhancers, insomnia inducers, suicidality inducers, mania stimulators, or gas busters obviously would not offer the same marketing appeal. Though tongue in cheek, we consider these possible labels to be more accurate than the commonly used label of “antidepressant.” It could be argued that the outcomes with the largest effect sizes should be offered as the primary label for a medication.

These guys are pretty sarcastic. And, their sarcasm is unlikely to be a conversation starter, but I suspect that there is more of this backlash to come.

It brings to mind a comment from a recent episode of On Being [emphasis mine]:

…individuals are hopelessly biased, they cannot perceive the truth by themselves.

Science is not just an individual activity. We expect our scientists, we exhort them, to be as objective as they can and a good scientist tries to do so very earnestly, but still fails. So therefore, there must be a social process that causes science to work to be a truth-discovering process.

This thing about scientific truth-discovery being a social process  puts it’s finger on something very important. It’s one of the things that so frustrating about hearing people tout evidence-based policies.

Consider the arguments for naloxone distribution. I’ve honestly got no quarrel with it, I just believe that it’s a woefully inadequate response. Of course it’s true that it’s an evidence based policy. I’m sure it saves lives. My problem is that advocates draw a straight line from this truth to universal implementation, AND anyone who balks is anti-science. The problem is that these advocates don’t ask what else we know to be true. For example, treatment also reduces overdose deaths. We fail to discuss what else improves this measure (overdose deaths), we also fail to discuss what other measures are important. If we have that conversation, then we can discuss why it sh0uld or shouldn’t jump to the top of the list without accusing others of being anti-science.

Another example are the evidence-based arguments that opiate substitution medications should be the front-line treatment for opiate addiction. To be sure, these medications reduce opiate misuse. However, there also exists a model, with evidence, that eliminates opiate use in 78% of patients over 5 years. Why not discuss that? Why not allow discussion of whether reduced opiate use is even a good measure? Or, the best measure?

This social aspect of truth-discovery is too often too exclusive. Of course, we can not and should not give equal standing to every goofball with a pet theory, but the points in the antidepressant paper above and the recent GSK scandal demonstrate that the current custodians of evidence are all too capable of leading us into policies based on something other than truth while scolding anyone who questions their evidence.

UPDATE: Just to clarify two things.

First, we’re not anti-medication, but we do believe that their benefits are overstated, the adverse effects are understated, that other methods are just as effective or more effective (And, provide additional benefits.) and that they too often constitutes risk management rather than real treatment.

Second, I see naloxone as first aid. I have no interest in interfering with access to first aid of any kind to anyone with any kind of physical crisis. However, first aid should be FIRST aid (Not last aid or only aid.), and meaningful treatment for the real problem should follow. I tend to bristle because these calls for naloxone programs never seem to include calls for access to treatment of adequate quality, intensity and duration following the overdose.

Coming of Age on Zoloft

An interesting take on anti-depressants from a writer who has benefited from them:

The mainstreaming of medication has bred confusion about what’s normal. In some sectors, we’ve grown so vigilant about the possibility of having a mental disorder that this vigilance becomes counterproductive, a source of anxiety in itself. Every negative emotion becomes a potential sign or symptom. I think people, particularly adults, should use medication if they wish, but I am concerned about the changing goalposts of what’s considered pathological. It’s nice to know that medication is available, but it’s also important not to lose sight of the comfort that can come from talking openly with each other, realizing that not every instance of feeling sad, or overwhelmed, or disappointed, or anxious, is a sign of something medically wrong.

With youth, I feel that a conservative approach to medication is best.

Partly that’s because of the way that getting a mental-health diagnosis can intersect with the adolescent search for self. Being diagnosed and using medication confers an identity, that of someone with a mental disorder. To an adolescent who is preoccupied with constructing an identity anyway, and looking for clues to who she is, that can be a big deal. Some adolescents feel that having a diagnostic label is clarifying and that it helps them. But others wrestle with it. They ruminate about what it means to be sick. They take that identity deep inside, and sometimes magnify it way out of proportion. A diagnosis event can have lasting, rippling consequences, and I think adults should be very cautious and careful before they impose a diagnostic label, or let a young person self-impose such a label, on what may be ordinary developmental struggles.

More thoughts on the use of antidepressants with kids. Here, she’s commenting on a piece in The Atlantic that discussed her book.

I think one thing that piece illustrated nicely is the potential difference between starting antidepressants as an adult and starting them young.

Kelly was saying, ‘Look, antidepressants help people; they helped me; they’re this wonderful thing, and I don’t understand why you people are trying to shoot holes in them.’ Kelly has a story that was similar to that of a lot of adults who start antidepressants: she was in therapy for years; therapy was helpful but notthat helpful; she went into crisis and finally overcame whatever inner resistance she had about trying antidepressants, and they were great — she wished she’d tried them sooner.

I very much respect that story, and many others have one like it. Part of what I’m on about in the book is that for people who start medication as teens, or even younger, the story is different. For them, using medication is often not their choice or not their idea. They don’t have the experience of trying other remedies for years and then reaching a point where they say, ‘You know what, these things aren’t working, this problem isn’t going away, and I’m going to take it seriously now and try something new.’ They haven’t necessarily had a chance to sort out what’s the turmoil of growing up and what might be deeper or longer lasting. Sometimes it’s very obvious that an adolescent is dealing with a real mental problem that goes way outside the realm of teen angst. But in other cases it isn’t always so clear. So for some of the people who start young, the narrative ends up not being one like Maura Kelly’s, of, ‘I had a problem, and then I used my own agency to find a solution, and it was wonderful.’ It’s more like, ‘Someone thought I had a problem, and this thing was given to me, and maybe it helped me or maybe it didn’t, sometimes it’s hard to tell, and if I stayed on it for years then I’ll never be quite sure, either what was the matter in the first place, or how I would have developed if I hadn’t taken this drug.’ It’s a singular experience, but it’s becoming more and more a hallmark of our time. That’s what I was trying to capture in the book.

One trend I find interesting is this. There was a time when anecdotes were used to attack antidepressants. The reaction of researchers and other advocates was that evidence should guide practice. Now, as the evidence has softened, we see many of these advocates using anecdotes to make their case. I’m not one to dismiss experiential knowledge, so this is just an observation.

Ritalin Gone Wrong

Ritalin

Not surprisingly, we get a lot of clients who have been diagnosed with ADD or ADHD. Many are concerned about suggestions to discontinue prescription stimulants.

This NYT opinion piece has gotten a lot of buzz over the last couple of days:

In 30 years there has been a twentyfold increase in the consumption of drugs for attention-deficit disorder. …

TO date, no study has found any long-term benefit of attention-deficit medication on academic performance, peer relationships or behavior problems, the very things we would most want to improve. …

But in 2009, findings were published from a well-controlled study that had been going on for more than a decade, and the results were very clear. The study randomly assigned almost 600 children with attention problems to four treatment conditions. Some received medication alone, some cognitive-behavior therapy alone, some medication plus therapy, and some were in a community-care control group that received no systematic treatment. At first this study suggested that medication, or medication plus therapy, produced the best results. However, after three years, these effects had faded, and by eight years there was no evidence that medication produced any academic or behavioral benefits.

Indeed, all of the treatment successes faded over time…

He draws these conclusions:

Our present course poses numerous risks. First, there will never be a single solution for all children with learning and behavior problems. While some smaller number may benefit from short-term drug treatment, large-scale, long-term treatment for millions of children is not the answer.

Second, the large-scale medication of children feeds into a societal view that all of life’s problems can be solved with a pill and gives millions of children the impression that there is something inherently defective in them.

Finally, the illusion that children’s behavior problems can be cured with drugs prevents us as a society from seeking the more complex solutions that will be necessary. Drugs get everyone — politicians, scientists, teachers and parents — off the hook. Everyone except the children, that is.