Archive for February, 2010

Posted on February 24, 2010 - by David

A response to Dr. Sally Satel’s review of ‘The Loss of Sadness’

I was happy to see that Dr. Sally Satel commented on Monday’s post which linked to her WSJ article about the proposed revisions for the DSM-V. She posted a link to this article, written two years ago, which is actually a review of The Loss of Sadness: How Psychiatry Transformed Normal Sorrow into Depressive Disorder, by Allan Horwitz and Jerome Wakefield. Written from the perspective of a psychiatrist critical of the direction the field is moving in, it’s plenty more than a book review. Dr. Satel incorporates her own knowledge of the history of psychiatry and the difficulties of diagnosis and treatment as she considers the book’s contributions and shortcomings.

I realize that some of my criticisms are really directed at Horwitz and Wakefield, and I may be repeating some of things I wrote in my post on the Horwitz interview, but here goes anyway:

Satel gives some valuable history on the state of affairs in psychiatry during the 60’s and 70’s leading up to the publication of DSM-III. I’ll just say that Horwitz and Wakefield identify the publication of the DSM-III in 1980 with a shift towards symptom-based diagnosis which effectively eliminated considerations of context. The biggest problem they see resulting from this, (as the title of their book implies), is that the normal expression of sorrow in the wake of difficult life events is being diagnosed as depression. They believe this leads to unnecessary prescription of medication, inflated rates of mental illness, and a culture-wide loss of the ability to integrate hardship and sadness into a normal, healthy life.

The book seems to argue (as Horwitz stated in the contexts interview) that there are two types of real depression. 1. Depression that appears without cause or context, and 2. Depression which begins with an apparent cause or context but persists longer than appropriate with more severe symptoms than normal.

From Satel’s article:

In the classic form of uncaused depression — referred to in the pre-DSM-III days as endogenous depression or melancholia — symptoms arise mysteriously out of the blue when life is otherwise good. It seems clear that whatever biological mechanism that regulates mood has gone badly awry.

Yet clinical depression need not always have a spontaneous onset; it can also arise in the aftermath of loss. The important distinction between normal sorrow and major depression, the authors say, is that in the latter the symptoms triggered by circumstances eventually lose their contextual moorings. Either they persist long beyond the resolution of the stressful situation, or the point at which an otherwise healthy person would have adapted to a new condition; or they mutate into overt psychosis, suicidal impulses or actions, or physical immobilization. A patient in the pathological realm is beset by self-reproach and ruminations. He does not brighten when, say, a beloved grandchild visits, and he cannot imagine anything ever making him happy again.

While I would agree that this idea makes sense on the surface, I see a real problem. When someone reacts too strongly for too long to some loss or crisis, we might say something went wrong to make this person overly-sensitive to either loss in general, or the particular loss that was suffered. But this is still much different from depression which arises “mysteriously out of the blue when life is otherwise good.” Perhaps the way we look at context or what we consider “context” to mean  leads us to see symptoms arising from nowhere which actually do have an explanation outside of a brain malfunction.

The argument presented in The Loss of Sadness seems to rest on the claim that real depression is the same today as it was over 2000 years ago – that culture has changed our understanding of mental illness but mental illness itself (assumed to be biologically caused) has not changed. To me, this implies that “normal sorrow” should look similar between cultures and over time, with some differences that can be accounted for by cultural and historical context.

I believe this view obscures the dramatic cultural change that modernity brings. We may take it for granted that a certain type of loss is difficult and a cause for deep sadness, but to extend this response to all of history and humanity is ignorant.  (I think Ethan Watters chapter on PTSD in Sri Lanka is helpful in looking at cultural differences in response to tragedy). Sure, some depression might be easier for us (as modern people) to understand given the context or spark. But if our “normal responses” to loss closely resemble pathological states, perhaps Horwitz’s conclusion isn’t the only one that can be drawn.  The authors are saying we have pathologized normal human emotions, but perhaps our responses to “normal life events” have actually become more pathological. Of course, if the broad cultural changes that accompany the rise of modernity are not considered important and human emotions and attitudes (or even Western emotions and attitudes) are seen as historically consistent, then this second possibility doesn’t even show up on the radar.

The principles inherent in nationalism provide the basis for modern culture – the only form of consciousness most people reading this blog have ever known. As defined by Liah Greenfeld, “nationalism is a fundamentally secular and humanistic consciousness based on the principles of popular sovereignty and egalitarianism.” For this discussion, it is important to recognize two aspects of modern culture: 1. It’s openness gives individuals great freedom, but very little guidance in forming identity 2. It changes what we hope for and what we expect out of life, therefore changing the nature of what constitutes “loss” and interfering with our ability to accept loss. Consider the following from Greenfeld’s essay, Nationalism and the Mind:

The focus on the life in this world dramatically increases the value of this life to the individual and inevitably leads to the insistence on a good life, however defined. One is no longer expected to submit to suffering or deprivation, unless one has special reasons to do so, for the general reasons for such submission – the expectation of rewards in the beyond, transmutation and migration of the souls, the duty to serve witness to the glory of God wherever one is called, or the sheer impossibility to change one’s condition – no longer apply.

Moreover, in a self-sufficient world, changeable and shaped by people, suffering is generally believed to be man-made. Even natural disasters are likely to be so interpreted: a famine, an earthquake, or an epidemic are as often as not attributed to some human agent’s withholding of the needed but available resources or negligence; personal misfortunes, such as debilitating, life-threatening, and incurable illnesses are blamed on artificially-created environmental conditions (second-hand smoke, lead paint, etc.) or on doctors’ incompetence. None of these natural disasters, it is said, “have to happen”: they are no longer believed to be in the nature of things. Of course, the right to a life free of suffering is most clearly asserted when suffering is caused – as it is mostly, in modern societies — by social evils: war, economic or political conditions, competition for precedence, and so forth. Humiliation, rejection, thwarted ambition are felt as unjust – as contrary to expectations and thus resulting from illegitimate intervention of malicious others.

Greenfeld’s argument is that modern culture causes problems with identity formation which can lead to “biologically real” mental illness. She is therefore arguing that diseases like schizophrenia, bipolar, and depression are not as old as humanity, but really began appearing about 500 years ago with the rise of nationalism.

Her work proceeds from the view that culture- the symbolic process by which human ways of life are transmitted historically, is an emergent phenomenon, logically consistent with the laws of physics and biology, but nonetheless autonomous. This is absolutely critical. It is this first view which distinguishes Greenfeld from the many biologists and anthropologists who see human culture as dictated by biologically evolved brain mechanisms and natural selection.

For Greenfeld, the mind is the individualized cultural process, or “culture in the brain.” The individualized cultural process is therefore dependent upon, but not determined by, the biological functions of the brain. Just as organic brain damage can cause symptoms of mental illness- problems with thought, mood, and speech for example – Greenfeld believes that problems with the mind (problems with culture, that is) can lead to problems with brain function.

Obviously, all I can do here is prevent a bare-bones, unsupported version of Greenfeld’s theory and set in against the dominant view of the day. She is well along in the process of writing a book on this very subject and I look forward to its publication. Her work is not meant to go against, but to complement and elucidate research on the biology and genetics of mental illness. Genetic susceptibility probably goes a long way in explaining why only certain individuals experience mental illness, but it is important to acknowledge, (as Dr. Satel’ article does) that the extensive research to date hasn’t revealed a genetic cause of mental illness:

Psychiatry, alas, has a long way to go. “Although the past two decades have produced a great deal of progress in neurobiological investigations,” notes a recent paper written to guide preparation of the forthcoming DSM-V, “the field has thus far failed to identify a single neurobiological phenotypic marker or gene that is useful in making a diagnosis of a major psychiatric disorder or for predicting response to psychopharmacological treatment.” Indeed, almost all of the recent genetic findings are not specific. A particular gene associated with bipolar illness was later discovered to occur in people with schizophrenia. The same goes for almost every other major finding — leading to the current hypothesis that these various genes confer risk for psychopathology, but not for any specific kind.

Nevertheless, the dogmatic view that true, serious mental illnesses are caused by a problem in the brain hasn’t lost any steam. Satel writes:

As brain-based etiologies of classic serious mental illnesses, such as schizophrenia and bipolar illness, are uncovered, psychiatry will probably lose those diagnoses to neurology. Perhaps one day psychiatry will cater only to patients suffering from existential crises. But not anytime soon.

Dr. Satel seems to feel that as a psychiatrist, her job is not to figure out the exact nature and cause of mental illness, but to provide the best patient-care possible, and I guess I can’t argue with this.

… in his essay the weary Dr. Spitzer admitted that, “I doubt that clinicians will ever be very concerned with what illness itself is…. Concerns with defining medical or psychiatric illness or disorder are generally left to sociologists, psychologists, philosophers of science, and members of the legal profession.” This is deeply true. Front-line clinicians will not be joining the fray anytime soon. The academic debate over the evolutionary history of their patients’ woes is irrelevant to everyday practice.

I suppose that so far, academic attempts to define mental illness have been “irrelevant to everyday practice” because they haven’t resulted in any understanding of etiology or pathogenesis that could be translated into treatment and prevention strategies. But just because nothing has been solved so far, doesn’t mean a radical new approach might not prove to be more than added noise in the “academic debate.”

Satel concludes that “in the end, the most we can say about mental illnesses is that they are the result of various interrelated causes unfolding at different levels of explanation: biological (genetic or cellular), cognitive (information processing), and psychological (the generation of meanings in contexts).” I believe Greenfeld’s view of the mind as the individualized cultural process can help put together this causal puzzle that Dr. Satel describes. But this can only begin if we allow for the possibility that human experience is not determined by our biology. If we persist in the hope, (which I believe Satel holds), that we will one day grasp “how those swirling galaxies of neurons and molecules make us who we are, both in sickness and in mental health,” we will never stop “struggling in the dark.”

Thanks again to Dr. Sally Satel for the comment that sparked this post. You can read more of her writing here.

Posted on February 22, 2010 - by David

More on the DSM-V Changes

I regret how spotty my posts have been lately, but if I’m not writing something new every day the best thing I can do is point you to someone else’s work. With the proposed changes for the DSM-V being made public last week, there are plenty of opinions floating around on the internet. I found this op-ed piece from the Wall Street Journal by Yale psychiatrist Dr. Sally Satel interesting.

She points out that many of the proposed changes, (as well as the opposition to those changes), have more to do with stigma, labels, and identity issues than actual advances in the understanding of mental illness. Satel also mentions the common overlap in symptoms and diagnoses within individual patients, and underlines our relative ignorance as to how genes are actually related to mental illness:

The other problem that confounds psychiatry is how to draw boundaries around diagnostic categories, given that we rarely know the cause of mental illness at the neural level. Mental illnesses are the product of numerous genes that interact with one another, with the environment and also with experience. (A recent study by the National Institute of Mental Health found that 80 genes could be associated with bipolar disorder.) Add to this the miasma of social and personal encounters that impinge upon the genetically vulnerable individual—stress, poverty, family instability, drug or alcohol use, and so forth—and the causal mechanisms of any mental illness become staggeringly complex and elusive. Moreover, the “psychopathological pie,” as a colleague calls it, is rarely divided up as tidily as the manual implies. Patients often have symptoms that sprawl across several diagnostic categories. For example, half of kids who receive the diagnosis of bipolar disorder also have ADHD.

Of course, if you’ve been a regular reader of this blog you won’t be surprised that I take slight issue with her explanation of mental illness, (even though it might not be totally fair to judge her based on one sentence in a WSJ op-ed piece). The inadequacy of her own definition is made clear when she mentions that “80 genes could be associated with bipolar disorder,” but says nothing about how these genes “interact with each other.” Also, what is meant by “environment” and “experience” is unclear and could be taken in a variety of ways. She seems to offer a broad explanation for mental illness and demonstrates well that there major issues with the way we classify symptoms as disorders which often overlap, but like a good psychiatrists she still locates cause with genetics or “at the neural level.”

MindHacks has an extensive summary of the DSM-V changes with links to other major media coverage. I found his comments on the restructuring of the schizophrenia diagnosis and the addition of ‘psychosis risk syndrome’ particularly interesting. His article suggests that a lot of the more subtle changes are aimed at “de-freuding” the DSM. Definitely worth your time to check this out.

Posted on February 17, 2010 - by David

Anemia During Pregnancy: Another Trigger for Schizophrenia?

At the close of a 20 year long study, researchers from the University Hospital of Copenhagen claim that “children of mothers who had been diagnosed with anemia during pregnancy, most likely due to iron deficiency, had a significantly elevated risk of developing the mental disorder. ” You can check out the article where I first read about the findings, or look at an abstract of the research paper, published in the Schizophrenia Bulletin.

Once again, I find myself less than impressed with the analysis of the data gathered and the conclusions drawn. I quote the Reuters news article:

To further investigate this potential link, Srensen and colleagues analyzed the psychiatric outcomes of a large group of Danish children born between 1978 and 1998 — the biggest cohort in which the relationship has been examined. Each child was followed from age 10 until the onset of schizophrenia, death or the study’s closure on December 31, 2008.

Among 1,115,752 newborns, 17,940 (1.6 percent) were exposed to anemia in the womb. A total of 3,422 — including 41 from the exposed group — went on to develop schizophrenia, according to the report published in the journal Schizophrenia Bulletin.

After accounting for differences between the two groups and other relevant factors, including the parents’ ages and history of mental illness, exposure to anemia in the womb was associated with a 60 percent increased risk of schizophrenia in offspring during the 20 years of the study.

The researchers further concluded that 0.58 percent of schizophrenia cases (a total of about 20 diagnoses) could have been prevented had there been no cases of anemia among the mothers.

Now I don’t claim to be a statistician. I took two semesters of stat in college to fulfill my math requirement, and let’s just say my attendance wasn’t great. Still, I can’t seem to resist doing some of my own number crunching…

• 41 schizophrenics in the exposed group / 17,940 exposed to anemia = a prevalence rate for schizophrenia of approximately 0.2% for those exposed to anemia in the womb
• 3,422 total cases of schizophrenia – 41 exposed cases= 3381 schizophrenics not exposed
• 1,115,752 total children – 17,940 children exposed to anemia = 1,097,812 children not exposed
• 3381 / 1,097,812 = a prevalence rate for schizophrenia of approximately 0.3% for those not exposed to anemia in the womb

Obviously, 0.3% is greater than 0.2%, but after adjusting for potentially confounding factors, the researchers still arrive at the conclusion that “exposure to anemia in the womb was associated with a 60 percent increased risk of schizophrenia in offspring.” According to my best reading, this adjustment leaves them with only 20 cases of schizophrenia among those exposed to anemia which could not be attributed to some other factor. If the adjustments cut the number of the exposed cases in half, and they still determine that this group has a 60% greater risk of developing schizophrenia, then obviously the total number of schizophrenic cases they are working with has also been drastically reduced. It seems pretty bold to make this claim about increased risk on the basis of 20 cases, but my lack of statistical expertise probably renders me unqualified to make this judgment. Still, the simple fact that adjustment for confounding factors dramatically altered the size of the group is a little reminder of how many and how varied are the explanations for the cause of schizophrenia. Even if it’s true that about one half of one percent of all cases of schizophrenia can be attributed to iron deficiency anemia, does this really get us any closer to understanding the origins of this destructive mental illness?

A few last thoughts. According to my admittedly brief google research conducted this afternoon, iron deficiency is probably the most common nutritional deficit in the world, and I would assume that iron deficiency, (and therefore iron deficiency anemia), is more common in less developed parts of the world. So, if Iron Deficiency Anemia during pregnancy is a significant cause or contributor to the development of schizophrenia, then why aren’t the rates of schizophrenia higher in less developed countries? This line of reasoning would also suggest that rates of schizophrenia should have been higher centuries ago when diets were poorer and fewer resources were available, but it appears that this is not the case.

Posted on February 12, 2010 - by David

The Children Formerly Known as Bipolar

According to an article I read on Wednesday, a new diagnostic category is expected to be included in the upcoming DSM-V which may provide psychiatrists with an alternative to diagnosing the most troubled kids they see with bipolar disorder. The creation of the new diagnosis, called temper dysregulation disorder with dysphoria, seems aimed at dealing with concerns over the growing prevalence of the lifelong, stigmatizing bipolar label among children.

Back in the 90’s, thanks largely to the work of one Dr. Janet Wozniak, an assistant professor of psychiatry at Harvard, the bipolar diagnosis was stripped of one of its most defining characteristics as professionals puzzled over what to do with children with ADHD who were prone to particularly persistent and disruptive outbursts. The traditional definition of bipolar was closely tied to the presence of alternating periods of mania and depression, but these kids rarely if ever experienced the typical episodic fluctuations. In order to make the new use of the diagnosis stick, some argued that in children, the episodes might be very brief and occur many times throughout the day. Critics of the extended application complained that “there wasn’t good evidence that these kids grew up to be bipolar, and that if you looked backward at bipolar adults, they didn’t necessarily have these uncontrolled anger issues when they were young.” Nevertheless, the pediatric bipolar diagnosis quickly spread, and Wozniak maintains this is “because it made clinical sense.”

The article suggests that part of the shift to childhood bipolar diagnoses may have been related to a desire to treat this kind of behavior as a disease which could be dealt with via medicine. The only other diagnostic option seemed to be conduct disorder, which usually wasn’t treated with medication and seemed to imply a parental failure. Now, with TDD, the behavioral and mood problems can still considered a medical illness, but those diagnosed aren’t necessarily lumped into a category of people required to take drugs for the rest of their lives.

What really struck me when reading this article was how the language used to talk about this stuff makes it so plainly obvious that these psychiatrists and researchers really don’t know what it is they are dealing with. First of all, the shift in diagnosis in the 90’s had nothing to do with any breakthrough discovery about how the brains of children with behavior problems function. Basically, the symptom-based definition of a particular mental illness was revised or expanded to fit the troubling phenomenon that psychiatrists were observing. That is not how science is supposed to be done. To quote the article: “research psychiatrists worried that the children were being given a label that wasn’t right for them, and saddled with the sentence of a serious mental illness for the rest of their lives.” A label? Is it an illness, or just a label? Does the naming of the thing determine its nature? And if people have a serious illness of any kind, doesn’t it exist independently of any “sentence”?

I find it strange that the word ‘label’ is used over and over again and there’s all this talk about categories or diagnoses being created and changed in order to deal with stigma and avoid offending parents, and yet these psychiatrists believe that whatever it is they are talking about is unquestionably a problem with the brain. I mean, isn’t the reason they can’t decide what to call it that they can’t pin down what is actually happening with these kids? I can’t help but shake my head when I read that “it will be seen as a brain or biological dysfunction, but not as a necessarily lifelong condition like bipolar?” How exactly did they determine that this is a biological dysfunction? Is it just the assumption that if symptoms are severe and difficult to manage, it must be a brain malfunction?

The article ends with the following two paragraphs:

Of course there is no way to predict what practical effects creating the TDD category might have. For instance, Carlson points out that even if they are successful at changing the label that clinicians use, it could be that the kids all get the same medications as before. “They may get many of the same. Absolutely,” she says. “But the difference is going to be that you won’t have to take this for the rest of your life.”

Carlson doesn’t necessarily see this as a bad thing. She emphasizes that these children have very serious problems, and though there’s been trouble naming it, there’s clearly some sort of dysfunction in their brain. Shaffer agrees. “I don’t think anyone is arguing that these are perfectly normal children that get the label [bipolar] — far from it,” he says. “We’re saying these kids are very sick. But they probably don’t have bipolar disorder. And they probably do deserve a name that adequately describes what they’re doing.”

I’m not arguing that these kids are “perfectly normal,” but I do take issue with the idea that a team of psychiatrists can create a new category and say without any evidence that the problem they are attempting to describe has its root causes in biological dysfunction. Am I the only one who finds this approach both arbitrary and dogmatic? I believe these kids deserve more than a name that fits their symptoms. They deserve an approach directed at understanding the nature and cause of whatever it is they are suffering from.

We still have another 3 years to go before the DSM-V is published. It will be interesting to see if this the unofficial diagnosis comes into common use before then.

Posted on February 9, 2010 - by David

Allan Horwitz on the Medicalization of Depression

A few weeks ago a friend of mine sent me a link to a podcast interview with sociologist Allan Horwitz, author of a book called The Loss of Sadness which looks at the medicalization of depression. If you’re going to listen to the podcast, skip ahead to 4:51, where the interview (which lasts about 20 minutes) actually begins.

at 6:50 into the podcast, Horwitz says:

… In the current environment, genetic explanations are, one, given tremendous credibility, so if you can link things to genes that somehow makes it more important explanation than linking them to life histories or linking them to social circumstances… and that’s a cultural phenomenon, [there’s] no reality that they’re more important… And the second important phenomenon, which I also think is purely social, is that if phenomena are linked to gene it makes them seem as if they’re disorders whereas in fact there’s genes for perfectly normal personality dispositions or there’s probably genes that make us grieve when somebody close to us dies, certainly doesn’t mean bereavement is a disorder, but that the cultural valence of genes associates them with mental disorders..

At first, I was happy to hear someone point out that the prominence of genetic explanations of mental illness is a cultural phenomenon, not a reflection that they are actually more important than other perspectives. However, I got more and more confused as I considered what Horwitz actually says in this interview. Let’s just look at the above statement piece by piece.

1. It is a cultural phenomenon that genetic explanations of mental illness are given such prominence. Ok, check, I follow.

2. Linking phenomena to genes makes it seem as if they are disorders. Ok, I think I’m still with you, but are you telling me they have succesfully linked specific genes to mental disorders?

3. There are genes for behavior which we would consider normal, such as expressing grief when someone close to us dies. Wait, so are you saying there’s a gene for everything  I do? Have they even linked sarcasm in blog posts to genes?

Let’s look at another piece of the interview, at 12:36

Horwitz: Depression is probably one of the very few psychiatric illnesses that’s been recognized for thousands of years, so it’s certainly not something that’s a new condition. From the ancient Greek philosophers, through the renaissance period, through the early psychiatrists, even through Sigmund Freud and the DSM I and the DSM II  – it had always been a contextualized illness so that the people who become sad or even intensely sad in contexts where we would expect people to be sad – the loss of intimates, diagnoses of a serious physical condition, serious economic difficulties- these sorts of things were always clearly distinguished from the mental illness of depression, which either arises with no context or persists longer than the original context in which it arose or features extremely severe symptoms- vegetative symptoms, hallucinations and delusions, these sorts of things.

Interviewer: So you’re saying that there’s been this historical legacy of seeing depression as a pathology only when it doesn’t fit the context, when it doesn’t fit the situation.

Horwitz: Precisely, the symptoms are identical but one is contextually appropriate and the other is without cause or without reason.

Now I guess I’ll have to read his book to see if he gives evidence for his claim that depression has been recognized for thousands of years and has “always been clearly distinguished” from normal, “contextually appropriate” sadness. (I will point out that all the examples he rattles off are clearly part of Western culture). It’s a bit confusing that he says the symptoms of “the mental illness of depression” are more severe than expressions of normal sadness, and then later says “the symptoms are identical” but in some cases they are not contextually appropriate. I do get the point he is trying to argue- that social and other contexts should be taken into consideration when making a diagnosis of depression- but I’m don’t think he’s being very clear or convincing.

He is critical of the emphasis on genetic explanations of mental illness because it confuses normal reactions to life with disorders, but at the same time he claims that the “the mental illness of depression,” where the symptoms are severe and not contextually appropriate,  has been recognized for thousands of years. So his argument basically amounts to a claim that the prevalence of depression is greatly overestimated because context is no longer considered when diagnoses are made. But where does this leave us with regards to the real, true cases of depression? Apparently, context can help explain why some reactions aren’t disorders, but Horwitz says nothing about how cultural context can account for the phenomena which actually are disorders. In fact, Horwitz seems to inadvertently reaffirm the prominence of the biomedical/genetic account of mental illness. By essentially suggesting that  phenomena which can be explained by social and cultural contexts are not actually disorders, he places the true, severe, undeniable forms of mental illness in a category which only biology and medicine can touch.

Posted on February 6, 2010 - by David

Super Bowl XLIV: The American Obsession with Greatness

Winning is not a sometime thing; it’s an all the time thing. You don’t win once in a while; you don’t do things right once in a while; you do them right all the time. Winning is a habit. Unfortunately, so is losing.

There is no room for second place. There is only one place in my game, and that’s first place. I have finished second twice in my time at Green Bay, and I don’t ever want to finish second again. There is a second place bowl game, but it is a game for losers played by losers. It is and always has been an American zeal to be first in anything we do, and to win, and to win, and to win.

Every time a football player goes to play his trade he’s got to play from the ground up — from the soles of his feet right up to his head. Every inch of him has to play. Some guys play with their heads. That’s O.K. You’ve got to be smart to be number one in any business. But more importantly, you’ve got to play with your heart, with every fiber of your body. If you’re lucky enough to find a guy with a lot of head and a lot of heart, he’s never going to come off the field second.

Running a football team is no different than running any other kind of organization — an army, a political party or a business. The principles are the same. The object is to win — to beat the other guy. Maybe that sounds hard or cruel. I don’t think it is.

It is a reality of life that men are competitive and the most competitive games draw the most competitive men. That’s why they are there — to compete. To know the rules and objectives when they get in the game. The object is to win fairly, squarely, by the rules — but to win.

And in truth, I’ve never known a man worth his salt who in the long run, deep down in his heart, didn’t appreciate the grind, the discipline. There is something in good men that really yearns for discipline and the harsh reality of head to head combat.

“I don’t say these things because I believe in the “brute” nature of man or that men must be brutalized to be combative. I believe in God, and I believe in human decency. But I firmly believe that any man’s finest hour, the greatest fulfillment of all that he holds dear, is that moment when he has worked his heart out in a good cause and lies exhausted on the field of battle — victorious.

-Vince Lombardi

1913-1970

The trophy that bears the legendary coach’s name is up for grabs again this Sunday, when the New Orleans Saints and the Indianapolis Colts meet in Miami for Super Bowl XLIV. As often seems to happen with championship games, much of the media hype has reduced the match-up between the two teams to a match-up between two quarterbacks, Peyton Manning and Drew Brees.

Do a quick google search of “Peyton Manning” and you’ll probably notice two major topics: 1. The record-setting contract he’s expected to sign after the season comes to an end, and 2. Where he ranks among the all time great quarterbacks. Many believe that winning his second Super Bowl this Sunday would solidify his status as the best to ever play his position. Listing all of his achievements here would be a waste of space, but the quick rundown looks something like this:

• Started 192 consecutive games since he was drafted #1 in 1998
• 10 pro bowl appearances in 12 seasons
• 10 seasons with over 4,000 yards passing (NFL record)
• 4 time Most Valuable Player (NFL record)
• 9-8 postseason record
• MVP of Super Bowl XLI

So if there’s one man in the game who, to use Lombardi’s words, seems to “do things right all the time,” it’s Peyton Manning. But with all the talk about Manning’s career, it’s easy to lose sight of the season Drew Brees just had. Despite the fact that Manning took the MVP award, Brees arguably had a better year, throwing more touchdowns with fewer interceptions and setting an NFL record with his 70.6 completion percentage.

If there is one thing America loves more than the consistent greatness that Manning represents, it’s an underdog like Drew Brees and the New Orleans Saints. We’re talking about a team that took 20 years to finish a season with a winning record and 33 years to win a playoff game. They played the entire 2005 season away from home due to that Hurricane Katrina did to the Superdome. Now, 42 years after they entered the league as an expansion team, the Saints are playing in their first Super Bowl. Interestingly, before Brees came to town, Peyton Manning’s father Archie was New Orleans’ most memorable quarterback, giving the team 10 hard-fought but losing seasons as a starter from 1971-1981. And who happens to be the quarterbacks coach helping Drew Brees with his gameday decisions? Vince Lombardi’s grandson Joe, who at 28 is younger than Brees and many of the teams veteran players.

But back to Brees. Despite a stellar college career at Purdue where he set a number of Big 10 conference records, he wasn’t picked until the second round of the 2001 draft due to concerns about his size and arm strength, and played in only 1 game in that first season with the San Diego Chargers. He beat out Doug Flutie for starting job in 2002, only to have the Chargers take the football from him and hand it back to a forty year-old Flutie late in 2003. In 2004, the Chargers picked up quarterback Philip Rivers on draft day, casting serious doubt on Brees’ future in San Diego. Rivers’ reluctance to sign a contract before the season started gave Brees another shot, and he made it count, posting his best numbers to that point in his career and making it to the Pro Bowl. But in the last game of the 2005 season, Brees was left lying on the ground with a shredded shoulder, and his time with the Chargers was up. In 2006, he stepped onto the field with the Saints in the newly repaired Superdome and led them all the way to their first NFC championship game, but their season ended one game before the big one due largely to mistakes he made. Since then, Brees has continued to put up very impressive numbers, making the Pro Bowl in 3 of his 4 seasons with the Saints, and in 2008 he became only the second quarterback to throw for over 5,000 yards in a single season. If he’s able to lead the trophy-less Saints to Super Bowl victory tomorrow, Drew Brees could potentially add his name to that list of great QB’s which currently has Peyton Manning hovering near the top.

Of course, as a Philadelphia  fan who has for the past 10 years watched quarterback Donovan McNabb and coach Andy Reid lead the Eagles to 8 winning seasons and 5 NFC championship games, only to come up empty handed each time, I know well that winning the Super Bowl is the only thing that matters. McNabb holds almost every possible Eagles quarterback record, he has the second best TD-interception ratio of all time, (behind Tom Brady), and among active quarterbacks, only Brady and Peyton Manning have a higher win percentage. Statistically, McNabb is unquestionably in elite company, but he can’t seem to shake the accusations that he’s a guy who can’t get the job done when it really counts. Just as it seems that a team’s successes are often reduced to the performance of one individual, McNabb is a perfect example of how a team’s failures often fall squarely on the shoulders of their on-field leader.

I’ve rambled on about football for a while now, and it feels a bit unnatural to shift back to thoughts about national identity, but I’m wondering, with the individualistic nature of American identity, is it even possible for our obsession with greatness and victory to be expressed other than through obsession with individuals? Do we ever think of whole teams as our heroes? How often do we really remember the guy who came in 2nd place? And does the American dream of rags-to-riches explain our love of underdogs?

All I have to say is, Go Saints.

Posted on February 2, 2010 - by David

Fish Oil the Latest in Psychiatric Treatment?

This article summarizes the results of a study from the University of Melbourne, which suggests that the omega-3 fatty acids found in fish oil may help prevent psychosis in adolescents and young adults who have been identified as “at-risk.”

The study involved 81 individuals ages 13-25 “who met at least one of the following three criteria: having low-level psychotic symptoms; having transient psychotic symptoms; or having a schizophrenia-like personality disorder or a close relative with schizophrenia, along with a sharp decline in mental function within the past year.”

For 12 weeks, half the group was given fish oil capsules and the other half recieved placebo. Participants were then monitored for next 40 weeks. Only 2 of the 41 people given fish oil developed a psychotic disorder compared to 11 of 40 of the placebo group. The omega-3 group also “also showed significant reductions in their psychotic symptoms and improvements in function.” The researchers hope to replicate the findings in a multicenter trial involving 320 people.

Certainly, the lack of adverse side effects compared to the commonly used anti-psychotic medications would make this treatment a much preferred choice for patients. While these findings are definitely positive, it was a very small and relatively short-term study, so further research is obviously needed to determine the value of fish oil as a treatment or preventitive measure for serious mental illness. Also, this once again highlights how little is understood about what is happening in the brain of the schizophrenic patient. The article mentions some of the potential reasons this novel treatment may be effective:

There are a number of mechanisms through which omega-3s could protect the brain, Amminger said; they are a major component of brain cells. They are also key to the proper function of two brain chemical signaling systems, dopamine and serotonin, which have been implicated in schizophrenia. Fish oil also boosts levels of glutathione, an antioxidant that protects the brain against oxidative stress.

In the quest to understand the cause and progression of this illness, nearly every neurotransmitter and every part of the brain has been implicated in some way or another. While hopefully this study will lead to new ways of dealing with the symptoms of schizophrenia without the devastating side-effects of many commonly prescribed drugs, it seems to be another example of a “scientific” answer which amounts to, “this might work, and if it does, these might be some of the reasons why.”