Wednesday, April 16, 2014

Does Casual Pot Use Cause Brain Abnormalities?

First, I'll put all my cards on the table; I believe at most, marijuana should be legal, and at the very least decriminalized.

If you paid attention to lately, for the first time since the issue has been tracked, the majority of Americans think that marijuana should be legal. (1)

The federal government and the Justice Department think otherwise. So, how do you change public opinion? Two steps: 1) Pay for a study. 2) Lie about the results.

Pay close attention to the headline:
"Casual pot use causes brain abnormalities in the youn: study." (2)
The opening sentence: (2)
"Young, casual marijuana smokers experience potentially harmful changes to their brains, with the drug altering regions of the mind related to motivation and emotion, researchers found."

Here is one of the loud mouth authors: "'This study raises a strong challenge to the idea that casual marijuana use isn't associated with bad consequences,' Breiter said." (3)

If you're at all familiar with this blog, you'll know that one thing to watch out for is quoting someone not affiliated with the research.

From another article
"'This study suggests that even light to moderate recreational marijuana use can cause changes in brain anatomy,' said Carl Lupica, PhD, who studies drug addiction at the National Institute on Drug Abuse, and was not involved with this study." (3)

So of course, this was a rigorous, well controlled, experimental study, which shows a causal link between marijuana use and a change in brain structure, as well has highlighting the negatives of these changes.
"The team of scientists compared the size, shape, and density of the nucleus accumbens and the amygdala — a brain region that plays a central role in emotion — in 20 marijuana users and 20 non-users. Each marijuana user was asked to estimate their drug consumption over a three-month period, including the number of days they smoked and the amount of the drug consumed each day.  The scientists found that the more the marijuana users reported consuming, the greater the abnormalities in the nucleus accumbens and amygdala. The shape and density of both of these regions also differed between marijuana users and non-users." (3)

Nope, I was wrong. It was a correlation study. You wouldn't know that from the Yahoo! article (or any popular press article) by the use of the word "cause" in the lead title. Here's what we know from this study. The brains of a small sample of participants who casually smoke marijuana are different than non-smokers. Did marijuana cause these changes? maybe, maybe not. This study doesn't come close to showing that, but that doesn't stop people from saying it does.

When dealing with correlational research, always ask, what else could explain this result? One possibility may be that subjects' brains were different before they smoked marijuana. Maybe their nucleus accumbens or amygdala were already different and that made it more likely that they would use marijuana more than once. I'd be interested to know if the non-users ever smoked marijuana, since only a 3 month history was taken.

Fact is, this study doesn't address any of these possibilities. Instead, they take a non-generalizable study (very small sample size & limit age range) and turned it into anti-marijuana propaganda. So a big congratulations to the financial backers of this study: the National Institute on Drug Abuse, the Office of National Drug Control Policy, Counterdrug Technology Assessment Center, and the National Institute of Neurological Disorders and Stroke.

The sad part is, the media machine just regurgitates this garbage verbatim.

Saturday, June 23, 2012

Automaticity, the Stroop, and Human Behavior

Think back to when you learned to tie your shoelaces; you needed to think carefully through each step of the process. Probably, you made errors over the course of multiple attempts. Now you probably do not even think about the steps, but simply initiate a series of movements that proceed without any further influence. There are many behaviors that followed this same pattern of learning: reading, writing, typing, bicycling, piano playing, driving, etc. When a behavior no longer requires direct, deliberate thinking to perform, the behavior is automatized.

The amazing thing about automatized behaviors is that many people state that they do not consciously know how the behavior is performed, they just can do it. This is typically referred to as unconscious memory or implicit memory. For example, try explaining how to properly maintain your balance while riding a bike. Difficult, right?

In some instances, a behavior can be so over learned that we do it automatically. Or, in other words, we do it without thinking. A great example of this is reading. For literate people, it's impossible to not read. What I mean by that is, if a random word were to flash on the screen, you could not stop your self from reading it. Even if the word were flashed on the screen for a fraction of  second so that it only appeared as a blip, you would have a better than chance probability of identifying the correct word if it were presented again alongside another random word.

Not only can behaviors become automatized, some behaviors can be more automatized than others. And when you have automatized behaviors compete against each other, you get interference, or the slowing down of a behavior. This concept was best and most famously demonstrated in what is known as the Stroop effect named at J.R. Stroop.  In Stroop's classic experiment, participants were slower to properly identify the ink color when the ink was used to produce color names different from the color of the ink. That is, participants were slower to identify red ink when it spelled the blue. What makes this finding interesting is that participants are specifically instructed not to pay attention to the word names and simply report the color of the ink. However, this seems to be a nearly impossible task, as the word name seems to interfere with the participant's ability to report only the ink color.

Below is an example of the Stroop task. First read the color-matched words (trial 1) and then name the colors of the X's (trial 2) as quickly as you can. Note how quickly you're able to complete each task. For the third trial, try NOT read the word, but rather name the ink color in which the word is printed.

The difficulty you experience completing the third trial relative to the other two is interference. The automaticity of reading is eliciting a response that is different from the one that is required (naming the ink color) and therefore competes with the response that your suppose to make.

Aside from this being a cool demonstration of automaticity, did you know that you can use automatic behaviors to influences the behavior of others? In an experiment done by Langer and colleagues, it was demonstrated how compliant people will be with a small request as long as they heard what sounded as if they are being given a sound reason, even though no actual reason is given. In the experiment, an individual approached people standing in line to use a copy machine and presented one of three requests:

1. Excuse me. I have 5 pages. May I use the Xerox machine because I am in a rush? (sound reason)
2. Excuse me. I have 5 pages. May I use the Xerox machine? (no reason)
3. Excuse me. I have 5 pages. May I use the Xerox machine because I need to make some copies? (non-sound reason).

When given a request plus a sound reason (#1), 94% of subjects complied with the request. However, when given a request with no reason (#2), only 60% of subjects complied. But when given a request plus what sounds like a reason (#3), but actually wasn't a reason, the compliance rate jumped back to 93%!

What people were responding to was not sound reasoning, but to syntactical structure: a request followed by what should be a sound reason. Most of our behavior, it turns out, is automatic. That includes speaking and thinking. In other words, when we are doing something, we are doing it without occupying our minds. This means that our minds are often free to engage in other, higher order, and more meaningful activities; like watching TV.

Wednesday, June 20, 2012

Saccadic Masking, Chronostasis, and Concsiousness

Time. What is it? To some, Time is a kid-friendly news magazine characterized by info-graphics and colorful pictures. To others, Time represents a continuum of continued progress of events from the past, present, and future. While Time is indefinitely continuous, its rate can appear quite variable, at least to humans.

Below is a clock face with an active seconds hand. Focus your gaze on something nearby (e.g., something just above your CPU monitor) then shift your gaze to the clock and watch time elapse for 5 seconds. What you should notice is that the first second to elapse appears to take longer than the subsequent 4 seconds (It's subtle, you may have to try this a few times to notice the illusion).
If you did notice time lag, then you just experienced chronostasis. Chronostasis is the experience or illusion that occurs immediately after a saccade that appears to stop time momentarily. This occurs so much that every day we experience 40 minutes of chronostasis, though it goes entirely unnoticed.

So what's going here? When our eyes move, the image reflected on to the retina is also in motion. This creates 
motion blur (see picture at beginning of this post). A blurred image being utterly incomprehensible (and of no use) to us sighted humans, our brains have a mechanism to circumvent the blur an create a comprehensible image. This phenomenon is known as saccadic masking. During saccadic masking, the blur is suppressed, along with visual processing, and the gap in visual processing that should be experienced as your eyes move from on side to another. The brain then replaces the blur with an image of the very next thing that your eyes fixate on.  

This explains chronostasis experienced in the clock illusion. As you shift your gaze to fixate on the clock, instead of seeing a incomprehensible blur, the blur is supplanted with an image of the clock that your currently fixated. That's why that first second to elapse appears longer than all other subsequent seconds.

The process is depicted below:

The first figure depicts what actually occurs, but only our subconscious brain perceives. Figure two shows what what we actually see. If you imagine that point two is the image of the clock, our brain then fills in the time that had motion blur with the same image. 

If the brain is replacing a past image with a current image, does that mean what I'm seeing is not really in the present but the past? Yes, in fact, human awareness or what we experience as the "present" is actually the very recent past; more specifically our consciousness lags 80 milliseconds behind actual events. This is how saccadic masking and chronostasis are possible; before we become aware, our brain has to make sense of stimuli first, which takes just about 80 milliseconds.

As it turns out, saccadic masking and the 80 millisecond lag in awareness explain many of the visual illusions that many may already be aware of such as the moving snake illusion. As you move your eyes looking at the image below, the illusion of motion is apparent. If you fix your gaze on a black dot, the illusion of motion will cease. 
There are other phenomenon as it relates to time perception: Time passing more quickly as we age and time slowing down as we become scared. Of course, the latter phenomenon should not be confused with time dilation, which is an actual difference of elapsed time (as opposed to perceived difference) between two events as measured by observers moving relative to each other. 

Friday, January 27, 2012

Al Sharpton is an Idiot

America's Panacea for racial Freudian slips, Al Sharpton, had a "heated clash" with a Republican congressman whose identity isn't important since, if he actually agreed with Sharpton, he wouldn't have been on his program in the first place. 

What caused Sharpton to contort his face in such unnatural manner was the following exchange: 
Sharpton: "Is it fair that billionaires pay a lower tax rate than their own secretaries?" To which the Republican replied, "Well they actually don't, according to the IRS." 

Now, if two reasonable people were having this discussion, the conversation might proceed like this, Sharpton:
"Will you please show me the IRS data about which you speak? So I may correct myself"; Republican: "Sure Al; and would you like some motherfucking ice tea?" 

Reality turn out differently, "
Sharpton started to raise his voice and asked the question again. 'Is it fair? Is it fair?' Huelskamp continued to deny the accuracy of Sharpton's question. 'It's not true, Al.' Sharpton then said 'on the basis of the report—if the report is inaccurate, fine, you stipulate that—I'm asking you, is it fair? Is the arrangement fair, in your opinion?'" 

There is only one answer that Sharpton is willing to hear: NO! He's not interested in facts; notice how he continues to seek an answer even after granting that the statement "billionaires pay less than their secretaries" might be false. 

1. Warren Buffett's "secretary" is an idiot.
 Some time ago, Mr. Buffett claimed that his secretary made $60,000 and paid a 30% tax rate. Here's the problem with that: our income tax system is progressive, meaning that we pay higher tax rates as our income gets higher. As the table below shows, there are six tax brackets.

Let's say our income (husband and wife jointly filing) is $112,000. This would put us in the 25% bracket. If the U.S. had a flat rate tax system (and no deduction), we would pay 25 percent of $112,000 in income tax, or $28,000 
(a common misunderstanding of how the tax system functions). Under our tax system we pay 10 percent on the first $17,000, or $1,700. We then pay 15 percent on the next band of income up to $69,000, or $7,800. We then pay 25 percent on the marginal amount over $69,000, for another $10,750 in taxes. When we total the taxes paid on these three bands of income it comes to $20,250, for an average (or effective) tax rate of 18.8 percent. The national average is 11% 
(Note that effective tax rate is what was actually paid. It will always be lower than the marginal tax rate).

According to the bracket for single filers 
(let's assume Mr. Buffett's "secretary" is single), she would have paid $830 on the first $8,300 of her income (10%) and then she would have paid $3,255 for the remaining $21,700 of her income ($30,000 - $8,300). A total of $4,085 would have been paid for an effective tax rate of 13.6% (This does not include deductions and credits, which would have likely lowered her rate to 7%). Clearly Mr. Buffett needs to educate his "secretary" on how to file tax returns; after which, he should fire her.  

2. Who decides what is fair?

How Much Should the Top 1% Pay Before It's Considered Fair?

The top 1% of income earners (those with incomes of
 $343,927 in 2009) paid a larger percentage of the income tax (36.73%) than the bottom 90% combined (29.5%). Also in 2009, the top 1% earned 16.9% of the adjusted gross income (that's down from 20% before the recession). 

On the other side of the coin are the non-payers. 
A non-payer tax return is one filed by an individual or couple who, thanks to legal credits and deductions, owes nothing. In 2009, a record number of individuals (58 million) paid no income tax. That is, 42% of tax filers were non-payers. Only 0.3% (2009 data, table 1.1) of those non-payers earn more than $100,000. 

I'll repeat that since it's mildly important: 42% of the bottom 85% of income earners (i.e., <$100,000) paid no income tax.

Moreover, many of these non-payers also receive "refundable" tax credits even though they have no income tax liability. For millions of these non-payers, these refundable credits exceed their total payroll tax (i.e., social security, medicare, unemployment) contributions. In
 2008, more than a third of all tax returns resulted in complete nonpayment; that is, people got back every dollar that was withheld from their paychecks during the year. 

3. Raising Taxes on Wealthy Won't Fix Anything

Earlier, congress wanted to impose a 5.6% surtax on those with incomes above $1,000,000. According to the CBO, that tax would raise $450 billion over the next 10 years. That's 45 billion a year. Last year's deficit (fiscal year 2011) was 1.3 trillion, the second largest deficit of any nation in the history of the world. After you subtract 450 billion from 1.3 trillion you get 850 billion. If you cut out all non-defense discretionary spending you save $530 billion, leaving our deficit at $320 billion. Only after halving securing spending, will last year's deficit go away.

4. Stop Blaming the Bush Tax Cuts

The CBO broke "down the major components of the $11.8 trillion swing from surpluses to deficits over the ten year period 2002 to 2011."  Higher spending turns out to be the largest factor erasing those surplus projections.

As the chart above shows, the Bush Tax cuts have been declining in significance as a contributing factor to the annual deficits while increased spending and recent tax cuts (e.g., payroll tax cut) are larger contributing factors to annual deficits.

5. The Elephant in the Room
Mandatory spending is consumes 60% of the annual budget. That Social Security (761 billion), Medicare (468 billion), and Medicaid (269 billion). And last*, but certainly not least is Defense spending ($660 billion), which is not actually mandatory spending, although it should be since no one wants to touch it. 

Until people start focusing on reforming these programs and these programs alone, all other talk is a waist of time.   

The information is out there, all you have to do is let it in...

*All other mandatory spending programs combined (e.g., food stamps, unemployment) total over 600 billion. 

Friday, January 7, 2011

Koo Koo for Four Loko

Next time you watch your local news, remember this: News Media = Misses the Entire Point.

If you have not seen the news about the drink Four Loko being banned, I will bring you up to speed.

According to various we-have-nothing-else-to-report news organizations, the drink Four Loko is to some, a "blackout in a can" and to others, it is "cocaine in a can." Four Loko, through its "witch brew" mixture of alcohol and caffeine can, according to research (1a), cause a person to become a "wide-awake drunk," and thus impair a person's ability to judge his or her level of intoxication. The negative effects of this drink, which has predominately affected college students, are "spreading like a plague across the country." (1b, 1c).

In all, Michigan, Oklahoma, Washington, Utah, and New York have banned the drink. The FDA evaluated the situation and said that caffeine is an "unsafe food additive" (2). Because of this negative publicity, Fusion Projects has removed the caffeine content from their Four Loko brand.

However, even the removal of caffeine is not enough according to some experts (3). For some strange reason, all of these "experts" reside at Rutgers University:
"When consulted about the combination of caffeine and alcohol in one 24.5 oz. can, Rutgers U. nutritionist and registered dietitian Peggy Policastro explained the concoction’s effects on the body. 'The natural response of the body to alcohol is sleepiness and fatigue,' she said. 'When a stimulant such as caffeine is added, this response is blocked, allowing for the consumer to engage is riskier behavior for longer.'"
Here is an example of how the news covered this "controversy":

I've transcribed the more hyperbolic parts:

The created context is about the dangers of Four Loko (i.e., don't blame irresponsible teenage behavior)
Anchor: "Well, four teens are hospitalized in White Plains, and police say it's all because of a beverage that looks like an energy drink."
 Exaggerate the affects of the this witch brew (i.e., It's PCP in a can )
Field Reporter: "Cops and kids say just one can of Four Loko can make you do crazy things."
Cue expert, er, teenager who can attest to the affects of Four Loko
Dumb Teen: "I've seen people have half of it, and they're gone...and if you have a whole one, you're...way gone."
Cue inappropriate comparison to another beverage
Field Reporter: "That's because just one can of it has an alcohol content of 12% while the average mixed drink or beer has just 5%."(Note: Wine also has a 12% alcohol content)
Cue Morgan Rolland, a responsible teenager who has never drank Four Loko because "she's 19, and she's diabetic" (I bet she's a virgin too). Also note at the 50 second mark that there is a bunch of alcohol just behind her chair.
Dumb Teen: "I've seen a man get very drunk off just one, and he's like a hundred and like 95 pounds and he was gone."
Cue stupidity
Field Reporter: "What's more scary is that you can pretty much buy this anywhere, and in some stores, it's not even listed in the beer section."
 Just the Facts:

Four Loko is an alcoholic-energy drink marketed by Phusion Projects which contains alcohol, caffeine, taurine (which has no proven energetic affect), and guarana (a rich source of caffeine). In all, Four Loko has the equivalent of 80mg of caffeine (i.e., average cup of coffee). Depending on state law, Four Loko contains either 6%ABV (the equivalent of a Molson beer) or 12%ABV (equivalent to wine, 4). It comes in a 24.5 oz. can (the equivalent of a bottle of wine).

The Problem is Teenagers, Not Four Loko:
"The NIAAA states that approximately 599,000 college students in the United States get accidental alcohol-related injuries, such as alcohol poisoning. Half of them are under the legal drinking age of 21" (5).
"There are 1,742,887 drug-related ED visits nationwide and 7 percent involved alcohol only in individuals under the age of 21." (6).

"About four in five of all college students drink, including nearly 60 percent of students age 18 to 20." 
"Approximately two of every five college students of all ages—more than 40 percent—have reported engaging in binge drinking at least once during the past 2 weeks. However, colleges vary widely in their binge drinking rates—from 1 percent to more than 70 percent." 
"It is estimated that more than 696,000 students between the ages of 18 and 24 are assaulted by another student who has been drinking each year (430,000 of them by a college student under 21)." 
"About 11 percent of college student drinkers report that they have damaged property while under the influence of alcohol." 
"It is estimated that more than 97,000 students between the ages of 18 and 24 are victims of alcohol-related sexual assault or date rape each year (about half among students under 21)." 
"It is estimated that more than 400,000 students between the ages of 18 and 24 had unprotected sex as a result of their drinking and more than 100,000 students between the ages of 18 and 24 report having been too intoxicated to know if they consented to having sex each year" (7).
Fact of the Day: One's Belief that Alcohol Will Produce Relaxation, Sexual Desire, or Aggression Has More Effect on the Individual's Behavior than the Pharmacological  Effects of the Drug (8, 9, 10).

Thursday, August 26, 2010

How to Use a Journal Article to Advertise Your Product

From this Month's JAMA (1) "Cognitive Behavioral Therapy vs Relaxation With Educational Support for Medication-Treated Adults With ADHD and Persistent Symptoms" by Safren et al.

In order to use an article to advertise your product, first you'll need to chose a topic about which people are fairly ignorant and make yourself an expert on it:

Approximately 4.4% of adults in the United States have attention-deficit/hyperactivity disorder (ADHD).”

Writing Style Recommendation: If you use the word “approximately,” which means “near or around,” then don’t use a number with a decimal. That’s too much precision. Just say “approximately 4% of adults.”

The lead author is Steven Safren, Ph.D., ABPP. In case you’re wondering, those initials mean people have to refer to him as “doctor” and believe that he actually knows what he is talking about. Although adult ADHD is rather amorphous, Safren et al. have extensively researched CBT with adult ADHD. This gives Safren et al. a posteriori authority on the topic.

Second, you'll need to concoct a reason why you're conducting research:

…Medications have been the primary treatment; however, many adults with ADHD cannot or will not take medications while others show a poor medication response. Furthermore, those considered responders to medications may continue to experience significant and impairing symptoms. Thus, there is a need for alternative and next step strategies.

Reader Advisory: Don’t be fooled by this “need.” It’s not a real need, it’s a constructed need (hey look at this huge hole in the ground I created! It needs to be filled!). These authors are using the construct of ADHD and the failure of medication (to treat an arbitrary construct) to accomplish their own goal.

You can read the results in the abstract here (1) as they are only of secondary importance.

Here is the real importance of this article: “Cognitive behavioral therapy was delivered consistent with our manuals.”

The authors of this article are also the authors of these two books (2, 3). This journal article will serve as a marketing device for these manuals.

It works like this: First, they will give “talks” touting the results of this research.

I am going to show you a bunch of statistics that have no real world relevance…

Second, they will conclude that pointless discussion with…

Our manual is available in the literature section located in the lobby.”

Unfortunately, those manuals don’t contain actual cognitive and behavioral material. Sure, they use the jargon, but it’s not actual CBT.

Writing Style Recommendation: Add words to mundane terms, thus making them appear more important than they actually are.

Sessions were designed specifically to meet the needs of ADHD patients and included things like starting and maintaining calendar and task list systems

Anybody can use a calendar or task list, but only “doctors” can provide instruction on how to use a calendar system or a task list system.

Here's a beauty...

The first module focused on psycho-education about ADHD…

What’s the difference between psycho-education and regular education you ask?

If you read an ADHD article on webMD, that’s “education.” When a psychologist prints out that webMD article and hands it to you, that’s “psycho-education.”

Study CBT protocol (i.e., the important one)

Study Relaxation protocol (i.e., the unimportant one)

Other cutting edge cognitive behavioral techniques include “setting priorities” and “breaking large tasks into manageable steps.” Oh snap!

I argue that this is not CBT but rather a collection of common sense solutions to everyday organizational needs. However, Safren et al. refer to this as a particular “type of cognitive behavioral therapy,” which was successfully documented to be useful “as a next-step strategy for patients with ADHD…”

So you better go buy those books!

Safren SA, Sprich S, Mimiaga MJ, Surman C, Knouse L, Groves M, & Otto MW (2010). Cognitive Behavioral Therapy vs Relaxation With Educational Support for Medication-Treated Adults With ADHD and Persistent Symptoms: A Randomized Controlled Trial. JAMA : the journal of the American Medical Association, 304 (8), 875-80 PMID: 20736471

Friday, May 28, 2010

Cerebellar Agenesis: Life without a Cerebellum

Many people are familiar with the famous patient H.M., the man who, in an attempt to control his intractable epilepsy, underwent surgical resection of both his medial temporal lobes.

There is another patient who is less famous, known the by initials H.C. He died in 1939 when H.M. was just entering adolescence. Unlike H.M., this patient did not undergo radical resection surgery. In fact, he never underwent brain surgery at all. His contribution to neurology did not begin until after his death at the age of 76.

In what was supposed to have been a routine autopsy, H.C. was discovered to have had no cerebellum (see pictured brain above). H.C. had a very rare neurological condition known as cerebellar agenesis. When I was in graduate school, I was taught that the neuroplasticity of the brain was so remarkable, that even a child born without his or her cerebellum could grow-up to have no deficits and live a normal life. As it turns out, that was only partly true. H.C. was in fact, not without deficits. His tale is recounted briefly in two articles from the March 2010 issue of Brain:
"It was clear that there were indeed clinical signs included right external strabismus (i.e., misaligned eyes), slow and slurred articulation and an unsteady gait." (1)
However, he did live a "normal life":
H.C. "had employment, that he was able to work in a manual job and that his working life was not curtailed by his cerebellar agenesis." (1)
What is interesting about H.C. compared to H.M., is that H.C.'s agenesis was discovered only after he died. Very little clinical history about his life exists, making this story a great neurological detective case. Most of what is known about H.C. comes from hospital notes during his last years of life, just before he developed dementia:
"The social history describes him as 'single.' The notes contained a record of his assessment by a neurologist, Dr. Jacobson, who described him as 'a simple man with some hearing loss and slow slurred speech; he has a fair memory for recent and remote events concerning himself, but with limited general knowledge. There is no hallucination or delusions nor emotional defect. He is clean in his habits and able to attend to his person. He is able to get around unassisted." (1)
The human brain is estimated to have approximately 85 billion neurons (2). The cerebellum, which is typically 1/4 the size of the rest of brain, contains a full 50% of all our neurons. If you pay close attention to the image above, you will notice that, in addition to not having a cerebellum, H.C. was also missing his pons, the bulbous structure that is typically adjacent to the cerebellum and is responsible for arousal and alertness.

Many of the patients I have seen with cerebellar strokes typically have severe and irreversible deficits. While H.C. did have some cognitive and functional deficits, that he lived a full and functional life is nothing less than remarkable. His case is an example of how extraordinary the human brain actually is.

I encourage you to read more about the mysterious case of H.C. here.

Boyd, C. (2009). Cerebellar agenesis revisited Brain, 133 (3), 941-944 DOI: 10.1093/brain/awp265

Lemon, R., & Edgley, S. (2010). Life without a cerebellum Brain, 133 (3), 652-654 DOI: 10.1093/brain/awq030

Sunday, May 16, 2010

Detroit SWAT Team Kill 7 Year-Old Girl

There has to be a better way to do this....full story here.

UPDATE: As luck would have it, this particular raid was being filmed for a reality show known as "The First 48." Base on the footage, the family lawyer is alleging a cover up (1).

Friday, May 14, 2010

Draw Central Executives Day

May 20th has been declared "Everybody Draw Muhammad Day" (1). By now, many should be aware of the controversy surrounding South Park's 200th and 201st episodes.

Shortly after the airing of episode 200, a group known as Revolution Muslim posted the following message on their site:
"We have to warn Matt and Trey that what they are doing is stupid and they will probably wind up like Theo Van Gogh for airing this show...this is not a threat, but a warning of the reality of what will likely happen to them." (2).
Thereafter, the media got wind of this post and ran with it. All major news networks and outlets had something to say about this "controversy". A week later, the 201st episode aired. It was, against the wishes of Matt Stone and Trey Parker, heavily edited by the douche bags at Comedy Central/Viacom.

As a result of the ignorant and spineless actions by the douche bags at Comedy Central/Viacom, a self-proclaimed idiot (3) and artist, Molly Norris, declared May 20th to be "Everybody Draw Muhammad Day." She had created a poster showing many objects, such as a tea cup, claiming to be the likeness of Muhammad. She sent this poster to different media outlets, who took it seriously, and then it went viral.

Ms. Norris has since distanced her self from "Draw Muhammad Day" and suggested that we should draw Al Gore instead (4).

After reading and listening to the media, I decided to do some research. To me, all this "controversy" seemed a bit contrived. After all, this was nothing like the Danish cartoon hysteria. If you were paying attention at all, it appears that this "controversy" had fallen on deaf ears in the Muslim world (5).

The true extent of Muslim hysteria was this: one post, by one Islamic group, Revolution Muslim.

I read about the group on Wikipedia (6). It turned out to be an interesting read:
"The group of 5-10 by Yousef al-Khattab, born Joseph Cohen, an American Jew who converted to Islam in 2000 after living in Israel and attending an orthodox rabbinical school."
More about Joseph Cohen from :
"He was born and raised in the United States as a Jew, and holds both American and Israeli citizenship.   In the late eighties, Cohen embraced an ultra-orthodox interpretation of Judaism, and began attending a yeshiva (rabbinical school).  In 1998, Cohen hearkened to the Zionist call, and packed up his bags to relocate to the Israeli Occupied Territories where he became an Israeli settler.  As an ardent and extreme Zionist, Joseph Cohen fell in with the Jewish fundamentalist group Shas, an extreme right-wing political party that believes in flouting international law based on their religious beliefs.  Less than three years later, Cohen 'converted' to Islam, moved back to the United States, and founded the most radical Islamic group in the country." (7, 8)
A radical in one religion will be a radical in another religion.

Maybe, just maybe, it was not the Muslims who were over reacting, but rather, the American Media. Now many people across this country are angry, and on May 20th, people will take pencil to paper and draw the Prophet Muhammad.

Perhaps this anger is misplaced. After all, it was Comedy Central/Viacom that censored the cartoon. It was also Comedy Central/Viacom that censored people who criticized their spineless behavior (9). Perhaps the true enemies of free speech are the people responsible for actual censorship: the executives/lawyers at Comedy Central/Viacom.

Thursday, May 13, 2010

Woman Hospitalized Following Botched Raid

How many armed, anonymous, men does it take to give an old woman a heart attack? The answer:
"An elderly Polk County woman is hospitalized in critical condition after suffering a heart attack when drug agents swarm the wrong house. Machelle Holl tells WSB her 76-year-old mother, Helen Pruett, who lives alone, was at home when nearly a DOZEN local and federal agents swarmed her house, thinking they were about to arrest suspected drug dealers." (1)

Wednesday, May 5, 2010

There Are 40,000 of These Each Year

Here's what happened (1):
"SWAT team breaks into home, fires seven rounds at family's pit bull and corgi (?!) as a seven-year-old looks on.
They found a "small amount" of marijuana, enough for a misdemeanor charge. The parents were then charged with child endangerment.
So smoking pot = "child endangerment." Storming a home with guns, then firing bullets into the family pets as a child looks on = necessary police procedures to ensure everyone's safety.
Just so we're clear."

Transcranial Magnetic Stimulation: Does it Live Up to the Hype?

Repetitive Transcranial Magnetic Stimulation (rTMS) is a treatment for depression that was approved by the FDA in October of 2008 (1). Repetitive TMS involves a device (pictured right), which is noninvasive, that excites the neurons in the brain. When this done over the left dorsolateral prefrontal cortex (an area of the brain supposedly less active in depressed patients), brain activity increases. The major selling point is that it has very few side-effects compared to standard antidepressant treatment (most common effects are headache and tingling at the stimulation site).

The FDA approval of this device has been controversial (2). The initial study submitted to the FDA was rejected. The folks at Neurostar (the manufacturers of the device) did a post-hoc analysis of that data. They discovered that patients, who failed to respond to only 1 antidepressant, subsequently responded to rTMS greater than sham (27.3% versus 10.5%). Based on this analysis, the FDA approved rTMS for the treatment of MDD in patients who have failed only 1 antidepressant trial.

In this month's Archives of General Psychiatry, is an article titled "Daily Left Prefrontal Transcranial Magnetic Stimulation Therapy for Major Depressive Disorder" (3). This study was funded by the NIMH and is the first nonindustry funded multisite study of rTMS (though some of the researchers are paid consultants of the TMS manufacturer). It involved 190 people.

What supposedly separates this study from all others, is the sham treatment. One major criticism of the previous TMS research is that the sham treatment was not convincing enough to prevent unblinding (for example, sham did not cause scalp irritation or facial twitching). The researchers went to great lengths to develop a sham treatment which produced the similar physical sensations of rTMS to prevent unblinding.
(Click to Enlarge)

Unfortunately, approximately 50% of the active treatment group correctly guessed which treatment condition they were in. A full 66% of placebo participants correctly guessed their condition. In truth, the level of unblinding is not a whole lot different from standard antidepressant drug trials (since placebos are inactive). The patients, on average, were similar to the patients in the Neurostar post-hoc analysis. The participants failed 1.51 antidepressant trials. 
The primary outcome was remission, defined as a score of 3 or less on the HAM-D or 2 consecutive HAM-D scores less than 10 during phase 1 of the study. Phase 1 was three weeks in duration. Patients received rTMS once a day for 50 minutes (5 days a week).
(Click to Enlarge)
Unfortunately, the results were negative. During the three week period (the right side of the chart) only 6 patients (11%) met criteria for remission. The average drop in HAM-D score for active treatment was only 5 points (26 to 21). The researchers then extended the the length of phase 1 by two weeks. The number of patients who went into remission during this extension phase was 13 (14%). By increasing the length of the phase 1, they obtained statical significance. Sounds fishy to me, but at least they provide all the data.
Similar to the Neurostar analysis, those who did remit were less treatment resistance (i.e., failed only 1 antidepressant trial). The number needed to treat (NNT) was 12. That means, 12 people will need to be treated with rTMS before another person, who otherwise would have not remitted without intervention, finally does remit. That's not very good. However, that number is not far off from standard antidepressant drug trials.
Does rTMS have any practical value as a future treatment for depression? Based on these results, one will need to attend a 50 minutes session everyday (excluding weekends) for 3-5 weeks to see some sort of result. That is in stark contrast to attending psychotherapy 1-2 times a week or visiting a psychiatrist once every 4-6 weeks. As Daniel Carlat points out in his monthly report (1), each treatment session would cost approximately $400. Insurance companies do not currently cover this treatment (and probably never will). Moreover, the group of patients who did remit (i.e., those who failed only 1 antidepressant trial) is not very marketable. Odds are they will try a second antidepressant instead. According to the Star-D results, the odds of improvement are 30% on a second antidepressant compared to 14% of rTMS. Presently, rTMS just does not make economic sense.

George MS, Lisanby SH, Avery D, McDonald WM, Durkalski V, Pavlicova M, Anderson B, Nahas Z, Bulow P, Zarkowski P, Holtzheimer PE 3rd, Schwartz T, & Sackeim HA (2010). Daily left prefrontal transcranial magnetic stimulation therapy for major depressive disorder: a sham-controlled randomized trial. Archives of general psychiatry, 67 (5), 507-16 PMID: 20439832

Tuesday, May 4, 2010

Psychosis Among Substance Users

Psychosis among drug users is quite common. Often, it is difficult to determine which came first, substance use or psychosis. Frequently, they co-occur. In cases where drugs are causally related (i.e., substance-induced psychosis), the condition is typically transient with a duration of 1 month or less. In rare cases, the length of psychosis can last longer. And in even rarer cases, symptoms such as hallucinations can be permanent.

Psychosis can be associated with the use many legal (e.g., alcohol) or illicit substance such as stimulants (amphetamines and cocaine), cannabis, and hallucinogens. An article by Thirthalli and Benegal (1) reviews the evidence that these drugs can cause psychosis in nonpsychotic persons. 

The neurochemical effects of alcohol are complex. "Common knowledge" states that alcohol acts in a similar fashion to other sedatives (e.g., diazepam). In other words, it is an agonist of GABA receptors. In reality, the alcohol molecule is very simple. It has the ability to cross cell membranes (e.g., blood-brain barrier) easily and can exert its effects on the brain within minutes. Alcohol also influences the phospholipid bilayer that make up cell membranes. This ability has a widespread impact on normal cell functions and also enables alcohol to modify the action of many neurotransmitter systems, such glutamate, dopamine, and norepinephrine in addition to GABA.

Alcohol-induced psychosis can occur during different drug states such intoxication or withdrawal (e.g., delirium tremens, alcoholic hallucinosis). In general, the risk of psychosis is two-fold greater than in the general adult population.

Stimulants (click to enlarge picture; 2)
Cocaine and Amphetamines are widely known to lead to psychosis. The psychosis produced by both cocaine and amphetamines is similar to schizophrenia. The risk of psychosis from amphetamine use is quite high; greater than 70% in chronic users. Users who develop first episode psychosis use an average of 20 times years. Psychosis typically lasts for the duration the drug is in the system. However, it can last more than a month in more severe cases.

For cocaine, typically 50% of chronic users experience paranoia and hallucinations. Cocaine-induced psychosis has a stereotypical form; Users believe that their drug use is being watched and that they are being followed. This paranoia is typically accompanied by hallucinations. Cocaine-induced psychosis also shows sensitization; that is, psychosis becomes more severe and occurs more rapidly with continued use. Unlike amphetamine-induced psychosis, cocaine induced-persistent psychosis is very rare.

Cocaine has the highest affinity and binds most strongly to the serotonin (5HT)reuptake pump, followed by the dopamine (DA) reuptake pump, then the norepinephrine (NE) reuptake pump (FYI-Effexor is cocaine with a PG-rating; effexor's affinities are for serotonin, then NE, and then DA). Contrary to popular belief, amphetamines do not act by blocking the dopamine reuptake pump. Amphetamines are indirect agnonist of the catecholaminergic systems (i.e., dopamine and norepinephrine). First, amphetamines go inside the neuron and release both DA and NE from their vesicles into the cell cytoplasm (i.e., catecholamins are released inside the neurone). Second, The catecholamines are subsequently transported outside of the neuron by a reversal of the reuptake pumps. This results in a MASSIVE increase in synaptic DA and NE. Lastly, at higher doses, amphetamines inhibit catecholamine metabolism, leading to even higher concentrations in the synapse. 

There has been a boom in the current research of cannabis and psychosis. There appears to be a temporal correlation between early cannabis use and onset of schizophrenia. This association is stronger than for any other substance. Why the association exists is unclear. In general, cannabis has the same risk of inducing psychosis as alcohol (i.e., two-fold).

There are two cannabinoid receptors in the human body: CB1 and CB2. The CB2 receptor is not expressed in the brain, and is primarily found in the immune system. The CB1 receptor is typically found in the basal ganglia, cerebellum, hippocampus, and the cortex. CB1 receptors exist on the axon terminal instead of the post-synaptic cell. In others words, CB1 receptors are autoreceptors that can inhibit the release of many different neurotransmitters.

Many different drugs fall under this category: mushrooms, peyote buttons, and LSD, for example. Many hallucinogenic drugs are either synthesized by plants or are based on plant-derived compounds. The main active compound in peyote is mescaline, while psilocin in found mushrooms. LSD is actually a synthetic compound, but is based on a fungal alkaloid taken from ergot.

Hallucinogenic compounds have a catecholamine-like structure (most are similar in shape to serotonin). Hallucinogens are primarily 5-HT2a receptor agonists. While these drugs do not lead to dependence, withdrawal, or cravings, they still can lead to serious problems for some users. Some people experience acute anxiety or panic attacks in responses to the drugs' hallucinogenic effects. There is a disorder known as hallucinogen persisting perception disorder (HPPD), which is the fancy name for "flashbacks." The most severe reactions, of course, are psychotic breakdowns. However, similar to the above mentioned drugs, psychosis is typically transient. Most prolonged episodes of hallucinogen-induced psychosis involve individuals who have already been diagnosed with a psychotic disorder or who have manifested prepsychotic (e.g., prodromal) symptoms before taking these drugs.

In most cases, substance induced psychosis does not need medical treatment per se. It usually disappears when the drug's affects are gone. However, there are cases when treatment is necessary. Alcohol dependent individuals in withdrawal do need medical treatment because alcohol withdrawal can be lethal. Typically, sedatives (benzodiazepines) are the drugs of choice. For either cocaine or amphetamine induced psychosis, first or second generation antipsychotics are the drugs of choice because of their potent D2 receptor antagonism. In general, it is common for anyone presenting with psychotic symptoms to be prescribed antipsychotics. Occasionally, patients who are addicted to amphetamines will be prescribed antipsychotics in hopes that they will reduce the risk of subsequent psychosis or reduce euphoria, making the drug less reinforcing. Drugs that antagonize the 5HT2a receptor such as risperidone (or any second generation antipsychotic), ketanserin, and ritanserin have been shown to reverse hallucinogenic-induced psychosis.

In rare cases when psychosis persists, there are a few things to consider, such as, is their another cause for the psychosis? For example, does the person have schizophrenia or is there a physical cause for the psychosis (e.g., tumor, metabolic, etc)? Often times, doctors not knowing what to do, will double down on the antipsychotics. This is unlikely to work because the mechanism of action (D2 or 5HT2a blockade) does not necessarily increase with the addition of a second drug. Simply upping the does of the current drug should suffice. Side effects, however, are always additive. Antipsychotics with higher affinities for both D2 and 5HT2a receptors are preferable (e.g., risperidone).

Risk Factors
The risk factors for substance-induced psychosis are similar across all substances. Pre-morbid psychiatric history or a family history of schizophrenia put an individual at risk. Also, the longer a substance is consumed and the larger the quantities consumed are also risk factors. Polysubstance use or consuming drugs that contain other compounds increases the risk of psychosis too. Unfortunately, the research into the neurobiological and genetic underpinnings is substance-related psychosis are quite poor. A useful theory for substance-related psychosis which could lead to better acute treatment is lacking.

Thirthalli, J & Benegal, V. (2006). Psychosis Among Substance Users Current Opinion in Psychiatry