Sunday, November 27, 2011

Rerun: Mozart, Genius, and Practice-Practice-Practice

A piece in today's NY Times, Sorry, Strivers: Talent Matters, takes issue with the conventional wisdom, endorsed by NY Times columnist David Brooks, that geniuses are made, not born. My 2009 piece below was faithful to Brooks' interpretation of genius (it's all about practice-practice-practice) while remaining skeptical of the idea that it's ONLY about practice-practice-practice.

Read on ...

Consider Mozart, who wrote his first symphony in utero and performed in his own rock opera at age five months, changing his own diapers (admittedly with mixed results) between acts. Clearly this is genius personified.

Not so fast, writes NY Times columnist David Brooks. Those early compositions of his were strictly kid stuff, and his performing skills as a child prodigy are highly over-rated. The Mozart you encounter in concert and opera halls is the product of an adult mind honed to a fine creative edge through years and years of unstinting effort.

Writes Brooks:

“What Mozart had, we now believe, was the same thing Tiger Woods had - the ability to focus for long periods of time and a father intent on improving his skills.”

Rather than some mystical divine spark or high IQ, genius may be as mundane as practice-practice-practice. Citing two new books - “The Talent Code” by Daniel Coyle and “Talent is Overrated” by Geoff Colvin - Brooks says it helps to have some kind of adult role model as a kid, say a novelist living in your town. Then you might dare imagine yourself writing your own masterwork. Armed with this ambition, you would start reading novels and literary biographies and thus attain a core knowledge of the field.

Mind you, it doesn't hurt if you have a bit more going for you than Lennie in "Of Mouse and Men."

Anyway, here you are - somewhere north of Lennie and south of Einstein - slowly building up your body of knowledge. Next thing, you're engaging in the intellectual equivalent of playing with your food, moving ideas around, divining patterns (excellent for the memory), and otherwise thinking like a novelist.

Then practice-practice-practice until your mind turns labored conscious skills into effortless unconscious ones. But the mind is sloppy, Brooks advises, and tends to settle for good enough. So, you practice your routines slowly. You break down your efforts into tiny parts and repeat-repeat-repeat until the brain internalizes a better pattern of performance.

At the right time, a mentor steps in who provides feedback, corrects your tiniest errors, and pushes you to tougher challenges. By now, your brain is programmed to understand and solve future problems.

According to Brooks, the primary trait is not genius. Rather, “it is the ability to develop a deliberate, strenuous and boring practice routine.” The hard wiring of our genes plays a part, but Brooks concludes, “the brain is also phenomenally plastic. We construct ourselves through behavior. As Coyle observes, it’s not who you are, it’s what you do.”

So back to Mozart. According to critics, as reported in Wikipedia, Mozart composed his "breakthrough work," his Ninth Piano Concerto, when he was 21. The concerto has been assigned a "Kochel listing" of 271, which implies a vast body of work that fell short before the composer hit his stride. Practice-practice-practice.

But for Mozart, good enough was not good enough. After forming a friendship with Franz Joseph Haydn and developing an appreciation for the Baroque masters, Mozart did the equivalent of changing his golf swing, which set the stage for the transcendent pieces by which we know him best.

"The Marriage of Figaro", "Jupiter Symphony", and his "Requiem" - among many others - are the work of a man in his thirties.

In short, geniuses are made, not born. Or are they? Certainly others have labored as long and hard as Mozart only to become industrious drudges lacking that - ahem - divine spark. Think Salieri.

So why don't we forget about outcome - we can't control whether we will end up geniuses or not. But we can control process - the art of constantly challenging and reinventing ourselves through practice-practice-practice. Do we have it in us to become Mozart? Who knows? Can we fashion our modest talents into something more formidable? Chances are you're doing it right now.

In today's NY Times piece, the authors cite a study that tracked intellectually gifted kids into adulthood. According the authors:

The remarkable finding of their study is that, compared with the participants who were “only” in the 99.1 percentile for intellectual ability at age 12, those who were in the 99.9 percentile — the profoundly gifted — were between three and five times more likely to go on to earn a doctorate, secure a patent, publish an article in a scientific journal or publish a literary work. A high level of intellectual ability gives you an enormous real-world advantage.

Tuesday, November 22, 2011

Rerun: Creativity - We Are Killing It Off; Hopefully There Will Be Enough Creative Thinkers Left To Rescue Us From the Disaster We Are Headed Into

 From August, last year ...

"I excelled at every subject just for the purpose of excelling, not learning. And quite frankly, now I'm scared."

High school valedictorian Erica Goldson (pictured here) had the guts to speak out. In an address to her graduating class, she spelled it out in a way that even the stupidest teacher in the audience could comprehend, if not accept:

Between these cinderblock walls, we are all expected to be the same. We are trained to ace every standardized test, and those who deviate and see light through a different lens are worthless to the scheme of public education, and therefore viewed with contempt.

She went on to say:

And now here I am in a world guided by fear, a world suppressing the uniqueness that lies inside each of us, a world where we can either acquiesce to the inhuman nonsense of corporatism and materialism or insist on change. We are not enlivened by an educational system that clandestinely sets us up for jobs that could be automated, for work that need not be done, for enslavement without fervency for meaningful achievement. We have no choices in life when money is our motivational force. Our motivational force ought to be passion, but this is lost from the moment we step into a system that trains us, rather than inspires us.

Coincidentally, last month Newsweek ran a cover feature, The Creativity Crisis, that reported that for the first time, measures of creativity in US school kids are way down. The implications are enormous. As Newsweek points out:

The potential consequences are sweeping. The necessity of human ingenuity is undisputed. A recent IBM poll of 1,500 CEOs identified creativity as the No. 1 “leadership competency” of the future. Yet it’s not just about sustaining our nation’s economic growth. All around us are matters of national and international importance that are crying out for creative solutions, from saving the Gulf of Mexico to bringing peace to Afghanistan to delivering health care. Such solutions emerge from a healthy marketplace of ideas, sustained by a populace constantly contributing original ideas and receptive to the ideas of others.

Ironically, as the rest of the world is moving beyond from the old "drill and kill" method of learning, the US is heading in precisely the opposite direction toward prepping students for acing standardized tests. Meanwhile, arts in the schools have been liquidated.

Creativity is not just about the arts. It's about generating original ideas, across all fields of endeavor. The creative process involves both "divergent" and "convergent" thinking. In the divergent phase, the brain is literally roaming the library stacks, gathering up books by the armload. A strong body of research suggests that creative individuals may have brains that are less than efficient at filtering out incoming information.

But we are easily overwhelmed by too much information, not to mention sensory input and emotion - which may explain much of mental illness. This is where the convergent phase comes in. The brain becomes ruthlessly efficient in weeding out irrelevancies and focusing only on the facts that matter. Finally, the brain needs to find associations between apparently unrelated facts and ideas to come up with an original solution.

In his outstanding 2009 book, "How We Decide," science writer Jonah Lehrer reports on what was going on in the minds of the flight crew of United Airlines Flight 232 from Denver to Chicago when one fine day over Iowa in 1989, the rear engine of their DC-10 exploded and took out all three hydraulic systems.

Without a functioning hydraulic system, Captain Al Haynes had no control of his plane. UA 232 was on the verge of flipping into a death spiral. Emergency procedures never anticipated a total loss of hydraulics. The manual had not provided for this contingency. The experts on the ground had no answers. Haynes and his crew were totally on their own.

As Lehrer reports, the first remarkable thing to happen was that Haynes and his crew fought back their panic. Haynes then did a mental scan of all the cockpit controls he could operate without hydraulic pressure. The list was a short one, and only one was useful - the thrust levers. But you couldn't steer a plane with thrust levers.

Or could you?

Haynes' DC-10 had two working engines. If he idled one while boosting the other - what they call differential thrust - in theory he could steer the plane. It was a crazy idea. No one had ever thought of it before, much less tried it. Lehrer notes that the pilots dealt with potential information overload only by focusing on the most necessary bits of data:

For instance, once Haynes realized that he could control only the throttle levers - everything else in the cockpit was virtually useless - he immediately zeroed in on the possibility of steering with his engines. He stopped worrying about his ailerons, elevators, and wing flaps.

Meanwhile, inside the brain, the prefrontal cortex took an abstract principle - the physics of engine thrust - and applied it "in an unfamiliar context to come up with an entirely original solution."

The brain at this convergent stage of creative thinking was uncompromisingly disciplined and rational. Without a strong "I" in the cockpit, mentally we are nothing more than flakes and fruitcakes. Likewise, without wide horizons in the divergent stage, we are mere industrious drudges unable to think our way outside of a paper bag.

Haynes and his crew managed to get UA 232 to an emergency landing strip. But they couldn't control the speed of the landing. The plane skidded into a cornfield and shattered into several sections, leaving 112 passengers dead but sparing 184 lives.

Meanwhile, in the US, our school system is gearing us to a crash landing. It is conditioning our young to become mere takers of tests and uncritical followers of received wisdom. Bound to the past, our next generation may lack the means to think our nation into the future, much less work its way out of our next round of current social, political, environmental, and economic jams.

Thank heaven, then, for boat-rockers such as Erica Goldson. "We are the new future and we are not going to let tradition stand," she told her graduating class. "Once educated properly, we will have the power to do anything ... We will not accept anything at face value. We will ask questions, and we will demand truth."

Ah, there is hope.

Thursday, November 17, 2011

The RIght Med for the Right Brain - Not There Yet

Yesterday’s piece, Brain Science and Recovery, ran through a list of some of my favorite psychiatric genes, which - quite ironically - may signal the end of psychiatry as we know it. The exercise sent me back to my old notes, from an eye-opening session at the NAMI Convention in Chicago in early July.

“Emerging Technologies to Improve Care,” read the name of the session in my program book. I waltzed in late, trying to shake myself awake, prepared to make a hasty exit.

“The way psychiatrists practice right now,” I heard one of the panelists say, “is all trial and error.”

Suddenly, I was wide awake. I flipped through my program for the name of the speaker -  Jay Lombard MD, chief scientific officer at a Norfolk company called Genomind. Its website says:

Many patients complain of mood disturbances, including depression and anxiety. However, despite the commonality of these complaints, there is significant biochemical heterogeneity regarding the etiology of mood disorders, which may account for the high rate of treatment failures or adverse side effects.

OK, here’s the English translation. A depression is not just a depression. There are many biological-environmental causes, which makes one-size-fits-all treatments such as antidepressants not only a joke, but lamentably bad medicine.

Dr Lombard reeled off some of the same genes I listed in yesterday’s piece. A quick review:

Serotonin transporter gene: Regulates serotonin reuptake. A variation results in a hyperactive amygdala that results in over-reaction to stimulae, with downstream anxiety, depression, and other conditions.

BDNF: Regulates cell maintenance and survival, neural growth and connectivity. A variation results in inefficiencies in these processes, leading to moodiness and anxiety.

COMT: Breaks down dopamine. A variation impacts signaling in a way that raises the risk of schizophrenia.

MAO-A: Breaks down dopamine. A variation results in a hyperactive amygdala and low-responding cortical areas, resulting in difficulties controlling impulses, leading to aggressive behavior.

In addition, Dr Lombard noted three more, namely:

DRD2: Antipsychotics bind to this receptor. A variation results in poor binding and a bad med response.

Methylfolic acid gene: Breaks down folic acid. A variation results in B vitamin deficiencies that may lead to depression.

Calcium channel gene: Regulates the intake of calcium into the neuron. A variation results in too much calcium which ramps up excitability, with risk of bipolar, schizophrenia, and treatment-resistant depression.

So -  maybe if we can pinpoint the actual physical malfunction that is contributing to our bad moods and behaviors, we can target our treatments accordingly. This would represent a quantum leap over our current mindset of throwing meds at diagnostic labels. 

Daniel Hoffman MD, president and chief medical officer at the Denver-based CNS Response, put it this way: “The world wants buckets of symptom clusters and it doesn’t work.” He quoted Thomas Insel, head of the NIMH to the effect that the DSM is 100 percent reliable but zero percent valid.

In other words, doctors may all be in agreement on what schizophrenia or bipolar may look like, but they may also be unanimously wrong. “Why we’re spending so much time on the DSM-5 is beyond me,” he went on to say.

Instead of symptom clusters, we need to be looking at neurological outcomes that correlate to specific parts of the brain. Otherwise, “we are doing harm.”

He wasn’t through. Citing STAR*D (which most unequivocally demonstrated the limited efficacy of antidepressants), he observed: “What Pharma told us about these meds didn’t pan out.”

Maybe you can see where this is going, real diagnostics based on bio-markers: A saliva kit to tease out problematic genes, a blood test to differentiate bipolar from schizophrenia, qEEG to read brain waves. All of these are just about ready for prime time. The biggest issue is getting the insurance companies to reimburse.

About one third of patients diagnosed with ADHD, said Dr Hoffman, don’t have the neuropathology for it. Kids with ADHD have very specific EEG patterns. But we don’t give up on the non-ADHD kid. In essence, we are looking for “the right drug for the right brain.”

What a novel thought.

Wednesday, November 16, 2011

Brain Science and Recovery - Knowledge is Necessity

My last two pieces - on psychiatrists behaving badly - diverted me from my true mission here at Knowledge is Necessity, namely providing food for thought in the quest of knowing thyself. A very key part of that is passing along any cool brain science stuff I happen to pick up along the way.

Brain science and ancient wisdom represent the crucial double helix in our getting well and staying well. After decades of guess-work psychiatry, researchers have finally figured out how to open up the hood and peer into the brain’s moving parts, and what they are finding out can be applied by us right now in our recovery. I have been shouting this from the roof tops for nearly ten years, and I have no intention of stopping.

My starting point this time is Barbara Oakley’s must-read 2007 “Evil Genes: Why Rome Fell, Hitler Rose, Enron Failed and My Sister Stole My Mother's Boyfriend.” Last week, in Figuring Out Human Behavior, I couldn’t hide my enthusiasm for Dr Oakley’s show-and-tell of the brain science, which paralleled a lot of my research and writing. For both of us, the focus was the serotonin transporter gene, perhaps the most-studied gene related to psychiatric disorders.

To recap: A glitch in this gene predisposes certain people to over-react to environmental stressors, which in turn makes them sitting ducks for depression and other conditions. The breakthrough work came out in the early 2000s, and makes an excellent teaching lesson for a number of points we all need to know, namely:
  • Our genes and our environment interact. We may not have any choice in changing our genes, but we can often choose to change our environments in a way that lets sleeping genes lie.
  • Genes are not deterministic, but they do predispose us to how we react to whatever life may throw our way.
  • Stress is the key driving force in mental illness. There are other factors, but stress is invariably complicit. A good deal of mental illness can be summed up as “stress vulnerability disease.”
  • Diagnostic categories useful to a point, but malfunctions in serotonin transport have been linked to anxiety, mania, depression, substance abuse, borderline personality disorder, and all manner of things that can go wrong. Likewise, malfunctions in other processes tend to have similar shotgun effects.
  • It is more helpful to think of genes switching on and off certain mechanical processes in the brain than “causing” a specific disease. Moreover, these processes work in the context of whole brain systems interacting with other brain systems, which may exacerbate or mitigate the effects of the equivalent of a tap not being able to shut off.
  • There are no “good” genes or “bad” genes. Inevitably, there are trade-offs. A gene variation that may predispose you to stress may also protect you from Alzheimer’s.
To give us a better understanding of the brain in action, it is useful to look at the impact of other genes. Of all things, Dr Oakley’s list and my list are virtually identical. This is no accident. Daniel Weinberger of the NIMH is Oakley’s main source. Likewise, he is mine. Dr Weinberger was part of the team involved in the breakthrough research into the serotonin transporter gene, and he and his NIMH colleagues have been involved with the following, as well:

Brain-Derived-Neurotrophic Factor (BDNF)

This protein is involved in brain cell maintenance and survival and encourages the growth of new neurons and neural connectivity. A “double-val” variation in this gene has been linked to stronger memory. The catch is those with the double-val are prone to more anxiety and moodiness and hostility, possibly due to a magnification of the serotonin transporter glitch. A “double-met,” on the other hand may offset the glitch.

Catechol-O-methyltransferase (COMT)

Mechanically, this gene breaks down dopamine and other neurotransmitters. The more slowly you metabolize dopamine (the “met” variation), the smarter you are. The unfortunate “val/vals” may be a bit less intelligent, with a slightly increased risk of schizophrenia, plus risk of antisocial behavior, and hyperactivity. The “val/mets” fall in between. The trade-off? Vals may be able to handle stress better than the mets and be more flexible to change.

Monamine Oxidase A (MAO-A)

This protein breaks down dopamine and other neurotransmitters. Low-functioning MAO-A has been linked to aggressive and antisocial behavior and substance abuse and more. Those with low-efficiency versions of this gene tend to display hyperactive amygdalae (involved in fight-or-flight) and low-responding orbitofrontal and cingulate cortices. In other words, the front end of the brain has problems turning down the alarm signals from the back end of the brain. Impulsive violence may be one result.

A breakthrough 2002 study found that maltreated kids with low-efficiency MAO-A developed significant antisocial problems while the high-efficiency MAO-A kids were better able to weather the storm.

Wrapping it Up

Don’t worry about understanding all the fine details. The purpose here is to simply display how the interplay between genes and environment affect thinking and feeling and behavior. We are a long way from definitive answers, but we are definitely looking ahead to what 2000 Nobel Laureate Eric Kandel describes as “the new science of the mind.”

We don’t have to wait for psychiatry to get with the program. As I said at the beginning, we can apply brain science to our own recovery right now. Dr Oakley makes it abundantly clear that our behaviors are far less governed by free will and reason than our over-sized egos would have us believe. But knowing that, we can intelligently take stock of our vulnerabilities and make the type of course corrections that allow us more control over our brains and, with it, our lives.

Be smart. Live well ...

Monday, November 14, 2011

Rebutting Whitaker: Not Such a Good Idea - Part II

On Saturday, I published a piece that said it is not such a good idea to claim to rebut (or for that matter refute or repudiate) Robert Whitaker and his 2010 book, “Anatomy of an Epidemic.” Not unless Whitaker happens to be a flat-earther making up his own facts.

The danger with framing a counter-argument in the form of a rebuttal is that you have to declare in advance that you are about to score a first-round knock-out. So, even if you win on points in 15 rounds you have lost. Earlier this year, Andrew Nierenberg of Harvard went for the knock-out, and disgraced himself and psychiatry in the process.  (See Part I and Part II to "Whitaker vs Quack Psychiatry.")

Rebuttals are hardly an impossibility, but you need to bring both your A-game and a measure of respect for the other side and all interested parties. For a stellar example, go to YouTube and view Robert Lustig’s masterful demolition of conventional and scientific wisdom concerning weight gain and obesity.

The most recent rebuttal claim on Whitaker came in the form of a confused two-part commentary by William Glazer MD on Behavioral Healthcare. In my previous piece, I showed how Dr Glazer most unambiguously failed in his claims that Whitaker’s thesis was “sensational” and “scientifically unsound.”

Would Dr Glazer have been more successful had he merely set out to knock holes in Whitaker’s arguments? Let’s examine the hole-knocking:

Whitaker advanced the novel proposition that psychiatric meds have caused an increase (rather than an expected decrease) in mental illness. Exhibit A in Glazer’s counter-argument were two authoritative population studies done ten years apart. The early 2000s data was virtually the same as the early 1990s data.

But Whitaker went a lot further back in his comparisons, digging into research from the sixties and earlier. Glazer’s comparing modern data to modern data was the equivalent of a cheap accounting stunt. This is where Glazer really sets his foot in it. In citing the mental illness prevalence data at 29 percent and 30 percent from both studies, Dr Glazer makes this extraordinary statement:

These figures hardly support the notion of an “epidemic” of mental illness, the assertion on which Whitaker rests his case, as well as the provocative title of his book.

No mental illness epidemic, Dr Glazer? Really? Let’s examine the threshold levels for what constitutes an epidemic. In 2003, the US Surgeon General declared: “We have an epidemic of childhood obesity.” How many kids were obese? Fifteen percent (triple the rate of forty years earlier).

Glazer is on far more solid ground when he takes issue with other population and disability figures Whitaker cites in his book, but this was already covered by Daniel Carlat in his two blog pieces earlier this year. (See my reviews: A Discussion at Last, and When Is Speculation Justified?) I, too, have expressed my concerns with Whitaker over this, but these hardly rate as rebuttals. Quibble all we want, we are still looking at an alarming 30 percent prevalence rate of mental illness, an epidemic.

Now we get to the meat of Whitaker’s arguments, namely: 1) Prolonged antipsychotic use may result in a form of “rebound psychosis”; 2) In many cases, schizophrenia patients may do better not on meds; 3) Prolonged antidepressant use may set up “oppositional tolerance” that worsens the course of depression.

In numerous blog pieces, I cited Whitaker with moving violations for playing fast and loose with the evidence. In short, the studies Whitaker cites do not actually prove his claims. But they do support his claims. The scientific conversation is full of this type of discourse. Thus, support that is short of proof carries a certain level of scientific validity. So - can Glazer knock out the supports? Or will he choose instead to recycle Nierenberg personal insults? You guessed it:

“Mr. Whitaker needs a basic course on principles of epidemiologic research, specifically on the concept of ‘susceptibility bias.’”

This is the same Dr Nierenberg who in debating Whitaker miscited a longitudinal study as “restrospective.” Um - who needs the basic course?

Speaking of longitudinal studies, Glazer also repeats Nierenberg’s mischaracterization of an NIMH study as a 20-year study supporting the long-term effects of antidepressants. If there were such a study, then we might have some strong counter-evidence to the “oppositional tolerance" hypothesis that Whitaker advances. Yes, there was an NIMH study, but it merely investigated long-term illness outcomes, not long-term antidepressant use. The study does not say that patients were on antidepressants for 20 years, nor does it purport to make a finding based on long-term use.

Zen koan: If psychiatrists quote howling mistatements from fellow psychiatrists enough times, do the howling misstatements eventually become scientific fact?

Yes, apparently. In the words of Dr Glazer:

The knowledge base for psychiatric medications is evolving, but it has not come anywhere near the point where conclusions can be reached about whether they cause disability. Such a conclusion should rest in the hands of scientists, not reporters.

I could go on and on, rebutting Dr Glazer's rebuttals, but I have better things to do. Instead, I will leave the last word to someone who actually knows what she is talking about. Corinna West is actively involved in the recovery movement. In a blog piece entitled, It Feels So Great To Be Off Meds, she writes: 

I’m not anti-medication, but I am anti-bullshit. I know that medications truly help some people, and some people do well on them. Those people should feel free to continue using them. However, I think all people should be given honest information about psychiatric meds before being put on them. We should be told how hard they can be to get off, and that there is not a ton of research showing long term effectiveness for medications. We should be given the truth that the chemical imbalance theory has not proven to be true. We should be given help and support for getting back off the medications as soon as possible. This would be the best way to help the 40% of people that do not respond to any given medication and might actually be harmed by it. In our current system, people unhelped by medications are only given more medications as well as the message that they are doing something wrong if they’re not recovering.

Saturday, November 12, 2011

Rebutting Whitaker: Not Such a Good Idea

In Oct last year, I began a series of pieces based on Robert Whitaker’s shot heard ‘round the world, his 2010 book “Anatomy of an Epidemic.” Whitaker’s astonishing thesis is that psychiatric meds have been a contributing factor to the apparent global rise in mental illness.

Yes, we know our meds may make us worse rather than better, but this comes up in the context of side effects or trade-offs (such as weight gain and cognitive impairments). Whitaker goes a step farther in claiming that many of our meds actually worsen the very conditions they were meant to alleviate, namely:
  • Long-term antipsychotic use may bring on psychosis.
  • Long-term antidepressant use may bring on depression and affective instability.
  • Any kind of antidepressant use may turn those who never experienced mania in their lives into life-long bipolars.
In my initial series of blog pieces and numerous follow-ups, I took serious issue with Mr Whitaker’s fast and loose interpretation of the scientific evidence he cites in his book, not to mention his mindlessly unqualified endorsements of the antipsychiatry movement and his ill-informed cheap shots against advocacy groups that actually get off their asses and help people, such as NAMI (disclosure: I serve on the board of NAMI San Diego).

But I also concluded that Mr Whitaker had made the equivalent of a “case to answer,” a strong prosecutorial argument that demands an equally strong counter-argument from the other side. In other words, until psychiatry can present a convincing case of its own - on point, with strong scientific evidence - any fair-minded jury would have to decide in favor of Whitaker.

So, for right now, in the absence to date of any credible marshaling of the facts from psychiatry, Whitaker stands as the most authoritative voice on psychiatric treatment. A very sad state of affairs.

Yes, Daniel Carlat in two blog pieces (see my reviews: A Discussion at Last, and When Is Speculation Justified?) raised some thoughtful concerns, but he came across more like a woman (and in rare cases a man) on a first date wondering how to dress for the occasion. Andrew Nierenberg, one of psychiatry’s leading authorities on mood disorders, in a grand rounds debate, purported to “refute” and “repudiate” Whitaker, only to embarrass himself and his profession in a DSM-worthy display of disordered thinking and outrageous conduct. (See Part I and Part II to "Whitaker vs Quack Psychiatry.")

The latest criticism of Whitaker is in the form of a two-part piece (Part I and Part II) on "Behavioral Healthcare" by William Glazer MD. Dr Glazer runs his own consultancy, and has been affiliated with Yale and Harvard. Dr Glazer is a welcome voice to the conversation, but from the very beginning he sets up his counter-argument to fail.

“Rebuttal: Questioning the validity of ‘Anatomy of an Epidemic'”, reads the title to his first piece. “Whitaker's claims are ‘sensational’ but scientifically unsound,” reads the subheading.

So, to meet his own criteria in making his case, Dr Glazer would have to prove the falsity of Whitaker’s argument. Not only that, he would have to demonstrate that there is no scientific basis to Whitaker. The catch is that Whitaker is no mere flat-earther engaging in pseudo-science. His conclusions - as far-fetched as they may appear to someone considering the issue for the first time - are strongly grounded in findings published in mainstream journals, not to mention the observations of some of the leading experts in the field.

In addition, to shoot down Whitaker, Dr Glazer would have to marshal his own scientific evidence. This would involve citing studies that convincingly demonstrate the long-term efficacy and safety of numerous classes of psychiatric meds. You would think this would be a very easy mission to accomplish, but these studies simply do not exist. Here, for instance, is a key disclosure from the Depakote product labeling:

The effectiveness of valproate for long-term use in mania, i.e. for more than 3 weeks, has not been demonstrated in controlled clinical trials.

An older version of the labeling read:

The effectiveness of Depakote ER for long-term use in mania, i.e. for more than 3 weeks, has not been systematically evaluated in controlled clinical trials.

So here is the situation: We know it is common psychiatric practice to prescribe Depakote for long-term use in stable patients to prevent relapse or recurrence into mania. Yet the drug has only been successfully tested on a floridly manic group of patients for three weeks.

This is hardly an isolated example. Time and time again, in picking through the long-term data, (with the possible exception of lithium) all we come up with are the equivalent of 18-minute gaps in the tape.

Are we to conclude, then, that psychiatry is “scientifically unsound?” Yes, indeed, if we are to apply Dr Glazer’s extremely reckless terminology. I trust you get the point: The truth is certainly out there, but the facts are extremely hard to come by. The best we can do is make intelligent guesses based on the very limited information available to us.

In a sense, psychiatric treatment equates to meteorological forecasting - impressive in the short-term but highly problematic over the long-haul.  

So forget about rebutting Whitaker. Psychiatry is in no position to do that. The best it can do is interpret the same data in a way that helps all of us make informed decisions. I’m still waiting.

More to come ...

Friday, November 11, 2011

Rerun: This Veteran's Day

I run this every Veteran's Day and Memorial Day:

This Veterans Day:

Our men and women are returning from two wars. They have witnessed things and felt things that those of us who stayed home have no clue. Their brains have been overwhelmed, their psychic beings shaken to the core.

This Veterans Day:

Our soldiers may leave the battlefield, but they cannot leave their memories there. Very high percentages are returning home with PTSD, depression, and other mental illnesses. Even those without full-blown symptoms have issues to deal with. Others are ticking time bombs. Suicide will claim more of them than enemy gunfire. Many will attempt to cope by turning to alcohol and drugs.

This Veterans Day:

Many brave men and women have no clue what is about to happen to them. They served as heroes, but, like many who served in Vietnam, may wind up homeless. They may be remembered for their bravery, but we will cross the street to avoid them.

This Veterans Day:

It's not just about flags on graves. It's about serving the people who served our country.

This Veterans Day:

Resolve to do something tangible. Advocate. Donate. Get involved with one of the veteran's organizations. Get involved with a mental health group making an outreach to veterans. Do something. Then keep doing it.

This Veterans Day:

It's our turn now.


From Therese Borchard's Beyond Blue:
  • Almost one in three veterans returning from Afghanistan and Iraq confront mental health problems.
  • On an average day in this country, suicide claims another 18 veterans.
  • Approximately 30 percent of veterans treated in the veterans health system suffer from depressive symptoms, two to three times the rate of the general population.
  • More Vietnam veterans have now died from suicide than were killed directly during the war.
  • Approximately 40 percent of homeless veterans have mental illnesses.

Wednesday, November 9, 2011

Figuring Out Behavior

I have been writing about mental health since 1999, but only with any basic level of understanding since 2003. That year and the previous one were watershed ones in our understanding of how genes and the environment interact to influence human behavior, and I had the dumb luck to walk into a symposium to hear one of the key players explain what was going on as it was happeneing.

Daniel Weinberger is a brain scientist at the NIMH. Eavesdropping on brain scientists talking to each other is kind of like overhearing two women having a heart-to-heart coming out of the women’s room - totally unintelligible to outsiders. But this was a psychiatric conference  - the American Psychiatric Association annual meeting in San Francisco - and Weinberger compassionately dumbed down his talk. This way, I could almost understand it.

Years later, I would hear Dr Weinberger give a presentation to a room full of fellow brain scientists that included Nobel Laureate Arvid Carlsson and all I could understand were the prepositions.

In a study published in Science in 2002, Weinberger and a team of researchers scanned the brains of healthy individuals as they looked at pictures of scary faces. The scans revealed that those with a certain gene variation - a double short-allele combination to the serotonin transporter gene - lit up like a Christmas tree in a certain part of the brain. That part of the brain was the amygdala - fear central - that kicks off the fight-or-flight response.

As Dr Weinberger explained it, this may have been the first study to link genes to emotions. A few months after hearing the talk, Science published another study examining the same gene variation. This time a research team surveyed a population cohort in New Zealand for recent stressors (such as financial difficulties) in their lives. It turned out that the short-allele people who had experienced high stress suffered way higher rates of depression than the high-stress long-allele group.

(A year earlier, this same research group using similar methodology found a connection to a gene variation that acts on the enzyme MAO - involved in breaking down dopamine and serotonin - and antisocial behavior.)

So - picture me in 2003 as the light bulbs are starting to go off. We have a gene variation that appears to affect the brain in a certain way that makes some of us over-react to stressful situations. And one of the end results is depression.

No, the gene variation did not cause depression. In no way could this be called a depression gene. A stress gene, maybe. Depression was the downstream effect, perhaps just one of many possible downstream effects.

But if you looked at the gene in terms of pure mechanics, it was just a biological unit that switched on something in the brain - in this case the serotonin transporter inside the neuron. The serotonin transporter - or reuptake pump - sucks excess serotonin from the synapse - gap - between two neurons in preparation for another release of the neurotransmitter.

But if the gene responsible for efficient serotonin transporter function isn't doing its job, we have the equivalent of a traffic jam. Bumper-to-bumper serotonin in the synapse. The new serotonin has trouble reaching its destination with its important chemical message.

That message may be trying to tell the other neurons in the brain to calm down, that the situation is OK. But if the message is tied up in traffic, the amygdala - fear central - may be the dominant voice in the brain, sending out a far more alarming message.

But wait - the meat inside our skull doesn’t just operate in a vacuum. It is reacting to what is going on around us. So, if the world out there is just fine, if our lives are just humming along, maybe it doesn’t matter that some rogue gene variation is messing with our serotonin traffic.

It’s amazing how long it took scientists to get this basic point. A PubMed search I did some years back revealed that researchers were hot on the trail of this gene variant at least as far back as 1992. They knew there had to be some mood disorder and other behavior connections somewhere, but the standard gene association studies came up empty.

Basically, to figure out how the gene variant affected behavior, scientists had to tickle it. Expose its owners to stress. As I heard Dr Weinberger explain three years later, this particular gene "impacts on how threatening the environment feels."

By now, the studies were coming in thick and fast. A totally new picture of how our genes and the environment interact and how this played out in the brain and affected behavior was beginning to emerge. The old diagnostic categories - useful to a point - were far too simplistic. So was our conception of biological psychiatry.

I have written on these studies many times, here on Knowledge is Necessity and elsewhere. What caused me to revisit the topic was picking up Barbara Oakley’s 2007 "Evil Genes" two days ago. (See my previous piece, Figuring Out Evil).

“If you ever want to know whether your tax dollars are being used for a good purpose,” she writes, “go take a look at the extraordinary work that the National Institute of Mental Health and other National Institutes of Health are doing in digging out the genetic bases of psychiatric illness.” Dr Weinberger is mentioned often.

It turns out that Dr Oakley and I shared very similar voyages of discovery. The studies I have cited here feature very prominently in her book. She also cites related studies that I have also referred to here and elsewhere, illustrating the vast complexity of the brain as it attempts to simultaneously grapple with the genetic hand it has been dealt and the environment that turns these genes loose.

As I read her words, I found myself re-experiencing the thrill of my awakening that began eight years ago. Call it reverse post-traumatic-stress. The memories joyfully came flooding back. Naturally, I had to write about it.

Much more to come ...

Further reading on mcmanweb: Psychiatry's Big Bang

Tuesday, November 8, 2011

Figuring Out Evil

I just started reading Barbara Oakley’s 2007 “Evil Genes: Why Rome Fell, Hitler Rose, Enron Failed and My Sister Stole My Mother's Boyfriend.” Trust me, this is a must-read.

Dr Oakley is a bio-engineer, and in her past lives served as an Army private (who rose through the ranks), a translator aboard Russian trawlers, a radio operator at the South Pole, author, and a mom. What got her started on her new voyage of discovery was coming to terms with her deceased sister, Carolyn, who really did steal her mom’s boyfriend.

Chances are there is someone like Carolyn in your own family, probably at least two or three. At other times in your life, you’ve had to contend with abusive bosses, backstabbing colleagues, clients from hell, and other forms of human unpleasantness. Call me a proctologist - I’m forever dealing with assholes.

Dr Oakley’s term is “successfully sinister.” These are your classic Machiavellians, out for themselves at the expense of anyone unfortunate enough to cross their field of vision. It turns out that “high-Machs” correspond very well to sociopathy, psychopathy, and borderline, though it is not as simple as that. We tend to associate a sociopath, for instance, as someone who resides in a maximum-security prison, but his or her more successful counterpart could be running a Fortune 500 company or heading up a university department or leading a government.

These are your master schemers and manipulators, socially charming, charismatic, and smart, not prone to making mistakes, indifferent to your needs, willing to squash you like a bug with no remorse.

But then we have the people who don’t grow up to be CEOs or professors or dictators. They simply make your life miserable. People like Carolyn, who break their mother’s hearts. 

The human condition is complex, and psychiatric/psychological labels and descriptors can only take us so far, as Dr Oakley makes abundantly clear. But we all know what it’s like to be abused and violated and taken advantage of, not to mention recoil in the presence of evil. But, what, precisely, are we contending with?

Ah, that is the question.

Much more to come ... 

Monday, November 7, 2011

The Caveman and The Avocado: Figuring Out the Diet Paradox

I just blew up one of my old mcmanweb articles on eating right, and replaced it with a new one. Following is an edited extract:
A 2003 journal article concluded that "the combined decline in mental health and the disappearance of traditional diets in circumpolar peoples makes a direct connection between diet and mental health in these people a very real possibility."

So, should we return to the diet of our ancient ancestors? Funny you should ask.

The Caveman Diet

A Jan 10, 2010 article in the New York Times describes a small tribe of city dwellers eating as they imagine their paleolithic ancestors did. The emphasis is on grass-fed (preferably wild) meat and seafood, nuts (but not peanuts), and berries. No grains or legumes. Advocates of the diet (there are at least three books out there) insist these are the foods we were built to eat.

According to an article published in the New England Journal of Medicine in 1985, the "diet of our remote ancestors may be a reference standard for modern human nutrition."

Prior to the advent of agriculture some 10,000 years ago, males stood at five feet ten and a half inches (179 cm). With the advent of agriculture (and with it novel foods), males shrunk five inches. Granted, the life expectancy way back then was about 25 years, but Fred and Wilma Flintstone weren't dying of the things we are dying of today, and they probably weren't as depressed.

Vegan and Vegetarian Diets

The very opposite of the caveman diet would be ones involving strict or loose taboos on animal products. Strangely enough, although the caveman and the vegan have very different concepts of what type of food is good or bad for you (meat vs agriculture) both shun many of the same foods, such as dairy products and refined sugars.

The principle of vegetarianism dates back to ancient times, but its widespread practice is fairly modern, based in large part upon our regard for our fellow sentient beings. And, oh yes, vegan and vegetarian diets are good for you.

Agricultural produce looms large, and saturated fats are avoided. Smart use of legume and grain combinations easily provides the full range of protein normally found in meat and seafood.

The Mediterranean Diet

The catch to eating like a caveman or a vegan is most people find these diets very difficult to stick to. They also raise alarms over the elimination of entire food groups, such as meat and agricultural products. Eating like a Greek or Southern Italian peasant, on the other hand, involves far less extreme culinary course corrections.

Meat and agriculture share the same dish, along with dairy products such as yogurt. The emphasis is on meat and seafood in low quantities, supplemented with grains and legumes such as rice or lentils. Olive oil is the main source of fat, and wine serves as an antioxidant kick.

Various studies attest to the health and mental health benefits of the Mediterranean Diet.

The Atkins Controversy

The Atkins Diet has been around for some 40 years, but until about ten years ago it was considered a quack diet, completely at odds with medical received wisdom. But a funny thing happened: People kept losing weight on it, thereby challenging the prevailing notion that we should be eating more carbs and less meat.

The diet features such offerings as bacon cheeseburgers, but nothing made from flour and hardly any vegetables.

A June 7, 2002 Sunday NY Times article, What if It's All Been a Big Fat Lie? raises this paradox: Fat-free carbohydrates, which digest quickly, may make us hungrier and inclined to eat more while fatty meat, which takes longer to digest, may keep us sated and less prone to over-eating. Indeed, this was the prevailing expert opinion, well into the 1970s, before the great cholesterol scare.

Yes, a Porterhouse steak may raise cholesterol, but not all cholesterol is bad.

Meanwhile, as carb consumption increased over the 1980s and 1990s, so did the incidence of obesity. The reason may have to do with the way our bodies burn fuel. Carbohydrate consumption switches on insulin. Insulin helps burn carbs for energy and stores fat for fuel. When insulin levels are low, we burn our own fat (a starvation-like but possibly natural state called "ketosis"). Too many carbs in the diet means fat stays stored rather than gets burned. There is also a risk that raised insulin levels may lead to "insulin resistance" and artificial hunger cravings.

A 2005 study comparing the Atkins Diet to the Ornish Diet (vegetarian), Weight Watchers, and the Zone Diet (emphasizing carbs) over one year resulted in similar weight loss in all the groups. A 2010 study comparing low-carb to low-fat diets over two years yielded much the same result.

The Avocado

Perhaps no food represents dietary confusion more than the avocado. A medium-sized avocado contains 30 grams of fat, about the same as a quarter-pound burger. Fat also equates to mucho calories (about 250 for an avocado). Because of all this, the avocado is a forbidden fruit on many eating plans, including the Ornish Diet.

But a 20-oz Coke also clocks in the same calorie count as an avocado. Seriously, is an avocado to be equated to a Coke?

Likewise, is the fat in an avocado comparable to a burger? Most of the fat in an avocado is monosaturated, the kind that lowers cholesterol. Indeed, a 1996 study found bad cholesterol (LDL) levels dropped in avocado-eaters while good cholesterol (HDL) levels climbed.

Meanwhile, the avocado is low in carbs and nutrient-rich, with more potassium than a banana and loaded with vitamins and minerals and antioxidants. Moreover, we all need fat in our diet, and if you are avoiding meat the avocado represents an obvious healthy alternative.

A similar case can be made for nuts (peanuts are technically a legume, but we can include them here), high in fat and calories but loaded with good stuff.

Wrapping Up the Food Debate

The obvious lesson from all this conflicting information is how adaptable we are to very different types of diets. If a high vege regime doesn't suit us, for instance, we have other choices. The other lesson is that it seems that those who stick to their diets - or at least stay with some kind of cogent plan - experience at least moderate success, regardless of choice.

We also see an emphasis on eating healthy and natural foods in moderate portions and staying away from processed and refined foods. This comes into play especially when we prepare our own meals (every diet plan comes preloaded with home recipes) where we control the ingredients that go into our mouths.

Finally, we begin to realize that smart-power is as important as will-power. Opting for a high-fat, high calorie food, for instance, may be a smart choice. It may also be a very dumb one.

Be smart. Eat well, live well ...

Based on: You Are What You Eat

Also on McManWeb: Diet and Obesity * Sweet and SourSupplements and Natural Remedies * More on Supplements and Natural Remedies * Omega-3 for Depression