Depression: PET Scan or Scan Pet?

The medical specialty of psychiatry has been the news quite a bit lately.  Last month, the National Institute of Mental Health withdrew their support of the new Diagnostic & Statistical Manual 5 of Mental Disorders which has been called the Bible of psychiatry.  Earlier this spring, a psychiatric hospital here in Las Vegas was accused of "patient dumping", that is the discharge of patients w/mental illnesses to places where they have no family or friends for support.

On a more upbeat note, I wanted to point out a small short randomized trial published early online two days ago in JAMA Psychiatry (aka Archives of General Psychiatry) in which the authors concluded that positron emission tomography (PET) scan was potentially useful in determining those whose depression might improve as a result of escitalopram vs cognitive behavioral therapy.  Currently, it's near impossible to predict who will respond to which antidepressant drug.  At most one in three will respond to the first choice.  Of the remaining two thirds, another one third will respond to the second choice.  Of those remaining, another third will respond to the third choice (after failing to respond to the first two).  But some will improve with cognitive behavioral therapy.  The difficulty lies in determining who will respond best to what.

So here you have a study of just 67 men & women followed for 24 weeks total.  However, of that group, only 38 had interpretable PET scans upon which the authors based their conclusions.  But you have to admit, the differences in imaging between responders & non-responders was like night & day.  More importantly, we still haven't developed a way to determine who will respond to escitalopram vs citalopram vs sertraline vs paroxetine vs fluoxetine vs cognitive behavioral therapy.  Don't get me started because dosing might make a difference along with the number of CBT sessions; perhaps longer or shorter sessions at more or less frequent intervals.

For now, this study, while it made the press, is just an interesting theory.  It's very doubtful that any insurer will pay for this test, not at least for the foreseeable future.  It's less expensive to just go thru a series of trials & errors.  Which is a sad commentary on how we treat our mentally ill (see "patient dumping" above).

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Long Work Hours & Lack of Sleep

You want hazard pay (don't we all?).  You work long hours and you don't get enough sleep (doesn't this apply to each of us?).  But how do you convince your boss that you need (not just want) more pay to compensate for the additional risks engendered by your efforts?

Well, in a meta-analysis of 12 studies published in this month's issue of the American Journal of Epidemiology, the authors found that working long hours (defined as >10hrs/d) was associated with a 40% increase risk of heart disease in 4 prospective studies and 143% increase risk in 7 case-control studies.  With the addition of a single cross-sectional study, the authors assessed risk in 22,518 participants in widely different types of research studies.  But the important point is that the studies all have similar conclusions.

But while these are but observational or epidemiologic studies capable only of helping to develop hypotheses but not at generating proof of cause & effect, it does give one pause to think about why this relationship exists and what can be done to prevent the proof from getting stronger.

On the other hand, if long work hours leads to insomnia & inadequate sleep, it might reflect in performance issues as noted in a survey of 4,991 employees as published in this month's Archives of General Psychiatry.  In fact, insomnia-related errors rang up an average of $32,062 compared to $21,914 for non-insomnia related accidents w/projected costs of $31.1B due to insomnia in the States.  Hmmm . . . on second thought, perhaps I shouldn't mention this study?  And when did I miss my bedtime again?

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Biomarkers Not Linked to MCI's Conversion into Alzheimer's Disease

We started off the year full of promise in our quest for some way to diagnose Alzheimer's disease when studies demonstrated the promise of florbetapir and plasma beta amyloid.  However, in a retrospective case control study published yesterday in the Archives of General Psychiatry, the authors concluded that biomarkers were of no benefit in predicting the conversion of 116 patients with mild cognitive impairment (MCI) to Alzheimer's disease (AD) compared to 204 controls w/MCI who did not convert to AD over a 2 year period of time.  

Instead, cognitive testing accounted for 50% of the conversion from MCI to AD, which is why, in my presentation, I recommend testing cognitive function each and every time a patient comes in for an evaluation, even if it's unrelated to his/her MCI.  I figure the more data points the better.  Of course, measurement of middle temporal lobe cortical thickness also helped in predicting conversion of MCI to AD.  However, cognitive testing is a heck of a lot cheaper when you're talking about following millions of patients.  Just something to think about in our current dysfunctional medical system . . . And thank you to my colleague, Dr. Sandy H, for pointing out this study!

Cannabis Use: Is It Really Safe?

No, I don't condone the use of illicit substances.  But I do find it curious as to how some are considered licit while others are illicit.  For instance, we know that there are very few benefits to the use of tobacco (are there any at all?) compared to all the down sides from its use, yet it's still sold legally here.  Alcohol is trickier since many studies demonstrate some benefit when consumed in moderation.  However, there's a very visible minority that enjoys their alcohol in excess to the detriment of others.  That's where I draw the line because when your business becomes my business, it's no longer a matter of individual rights & freedom.

Any way, I digress.  I wanted to review a meta-analysis (study of studies) published this month in the Archives of General Psychiatry  looking at the recreational non-medicinal use of cannabis (marijuana).  More importantly, I wanted to see if the authors reported any downside to the use of cannabis since most recreational users state that it causes no harm.  Turns out that cannabis users had an earlier psychotic break than non-users, almost 3 years earlier.  Alcohol and other substances did not play a role in onset of psychosis.

Ironically, in my previous life, exactly 3 short years ago, I wrote two posts regarding the use of marijuana, the first on February 5, 2008 and the second on February 18, 2008, the latter in response to some input from colleagues.  Concordant with my posts, an earlier analysis in the Lancet also concluded that use of marijuana increased the risk of psychosis later on in life.

Of course, one could always argue for an associative effect rather than causal in nature.  But the authors of this month's study concluded that the current evidence support a causal relationship.  In other words, use of marijuana increases one's risk of (earlier) psychosis.  So think twice before you light up!

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Part 3

Brain Volume vs Antipsychotics: Does Size Matter?

We've known for quite some time that there's a long list of side effects associated with taking antipsychotic medications, ranging from uncontrollable movements to diabetes and weight gain.  You can now add loss of brain volume to that list, at least in patients with schizophrenia.

In a study published this week, the authors followed 211 patients with schizophrenia who received on average 3 scans of their brains over the ensuing 7+ years of observation.  They concluded that those who were adherent with their antipsychotic regimen, especially larger doses for longer periods of time, had a notable loss of brain volume, compared to those who were less adherent.

But as the joke goes, does size matter?  We can't be too sure since the authors didn't include cognitive assessment in their study.  Given the option, I'd prefer to maintain my brain size.  What's worrisome to me is the increasing use of antipsychotics beyond schizophrenia and bipolar affective disorder.  New indications include depression unresponsive to traditional antidepressants alone while I've seen too often off-label use as a sedative-hypnotic to treat insomnia.  Even before this study, I wasn't convinced that this class of pharmaceuticals should be used for chronic insomnia.  Now, I'm even less inclined.

Vitamin D vs Depression: Associative or Causative?

So, did you all enjoy Black Friday?  My wife went out last night to run with the bulls, or in this case, her girlfriends, to go shop all the post-Thanksgiving sales.  If you notice an improvement in the local economy, y'all can thank them for doing their part. 

As for me, I've been putting in some late nights/early mornings trying to fix up my website, take care of legal paperwork required to start my practice, and read, read, read.  Thus, I've been spending more time indoors than out.  Less sun exposure leads to lower vitamin D.  And now, lower vitamin D may be associated with risk of depression!

I mention this because in a study published earlier this month, the authors performed a cross-sectional analysis of 7,970 participants of the National Health and Nutrition Examination Survey (NHANES III) with age range 15-39 years old.  Using standardized depression scales, they concluded that those with 25OH vitamin D <50 nmol/L (20ng/mL)  were more likely to be depressed than those with 25OH vitamin D >75nmol/L (30ng/mL). 

Interesting, you say.  But this isn't really a new finding.  A prospective study from May 2008 came to similar conclusions after evaluating a cohort of 1,282 participants 65-95 years old and concluding that a reduction of 14% in vitamin D was associated with an increase risk of depression.  And an earlier cross sectional study of 80 participants from December 2006 came to similar conclusion.

However, just as with the chicken and the egg, it's not always clear whether the relationship is associative in nature or causal.  For instance, vitamin D could be low because patients are too depressed to go outside.  But a smaller study published in July concluded that those euthymic women with lower baseline vitamin D were more likely to become depressed in 3-6 years.  So we have 3 studies demonstrating an association and 1 study raising the question of cause & effect.  To hedge my bets since I'm predominantly indoors these days, I supplement my solar-induced manufacture of vitamin D with appropriate vitamin D directed by regular laboratory analysis of my 25OH vitamin D.