Sander L. Gilman is a distinguished professor of the Liberal Arts and Sciences as well as Professor of Psychiatry at Emory University, where he is also the Director of the Program in Psychoanalysis and the Health Science Initiative.  His new book, Obesity: The Biography, traces the history of obesity from the ancient Greeks to the present day, acknowledging that its history is shaped by the meanings attached to the obese body, defined in part by society and culture.  In the excerpt below we learn about “globesity”.

The view that fat spreads across the map, spread by chickens or by genetic transmission across generations, means that there could be populations free from obesity.  This fantasy of the Enlightenment physicians, of utopias where obesity could not exist because of the very nature of its inhabitants, their diet, the activities, reappears today with the public health model of globesity.  The “French diet” and the “Chinese diet” as cures for obesity: all assume populations without even the potential for obesity.  In 2001, the World Health Organization stated that there was a brand new pandemic of “globesity” sweeping the world.  What is labeled as “globesity” is in fact the more recent iteration of an obsession with bodily control and the promise of universal health.  Its modern iteration, however, comes with an unstated and complex history.  If, said the ancients, you would only eat well, sacrifice to the gods, and avoid beans, then your health would improve or simply never decline.  There have always been changes in eating patterns.  Perhaps in the twenty-first century these changes speed around the world more quickly than in the past.  But the notion of a world in decay due to the growth of girth carries with it odd and complex subtexts.  What the central implications of “globesity”?

“Globesity,” according a publication of the Pan American Health Organization in 2002, “places the blame not on the individual but on globalization and development, with poverty as an exacerbating factor.”  The focus on what have been called earlier in the twentieth century “disease of extravagance” postulates a model not so much of change but of invasion – a Gresham’s Law of Food in which the bad drives out the good.  It is a modern version of “degeneracy theory,” with the new assumption that the ills of the world are to be traced directly back to the developed world.  In this way it is a dietary version of the basic global warming thesis: developed nations destroyed their environment and now they are invading the rest of the world, corrupting it.  “Nature” was benign, even kind; now it has become threatening.  “Globesity” argues that inherently healthy eating practices have been corrupted by the expansion of development and the resultant poverty.  “Fat” is a product of globalization and modernity.  The utopian “undeveloped” world, in Enlightenment jargon, the world of the “noble savage,” is a world in which “diseases of extravagance” could not exist, as they are a reflex of a “civilized” model of exploitation and capitalism.  The “cure” for “Globesity” in the twenty-first century is “natural” or “slow” food as a prophylactic against obesity as well as illness…It is a return to the inherently “healthy” eating practices of the Edenic past.

Such views have a relatively long history.  The French food writer, Jean Anthelme Brillat-Savarin, could write as late as 1825 that “Obesity is never found either among savages or in those classes of society, which must work in order to eat, or which do not eat except to exist.”  But he provided a caveat: “Savages will eat gluttonously and drink themselves insensible when ever they have a chance to.”  This is very much in line with Immanuel Kant’s view of “savages” and alcohol use in his lectures on anthropology first held in 1772-3 and published in 1798.  Obesity, therefore, could be an illness of natural man as well as of civilization because of the “savages” weakness of will.  Christoph Wilhelm Hufeland (1762-1836), who was, as we have seen earlier, one of the first modern medical commentators on dieting, recognized this when he commented that “a certain degree of civilization is physically necessary for man, and promotes duration of life.  The wild savage does not live so long as man in a state of civilization.”

Bonnie Spring is a Professor of Preventive Medicine, Psychology, and Psychiatry and Behavioral Sciences Director of Behavioral Medicine, and Co-Program Leader for Cancer Prevention at Northwestern University. A Past President of the Society of Behavioral Medicine, she is board-certified in clinical health psychology. Dr. Spring’s most recent book is Smoking Cessation with Weight Gain Prevention, and in the  original post below, she reflects on her own struggle with giving up cigarettes and maintaining her weight.

“You’ve given me new hope.” So read the e-mail that arrived shortly after Parade Magazine published a story about my research showing that trying to manage weight gain while stopping smoking can help rather than hurt successful quitting. A steady stream of similar messages flowed in, taking my mind back to the days when I first started to study weight gain after quitting smoking. I still flinch at the memories. Faculty colleagues asked when I would switch to studying a real health problem – one with serious medical consequences. The reception was about as chilly at the National Institutes of Health. The words of a usually supportive program officer float back to me, “Oh come on…There’s only an average six to eight pound weight gain after quitting. That’s not a health problem – that’s a cosmetic problem. We’re in the business of studying threats to health – not insults to personal vanity!”

The physicians I spoke with weren’t much more helpful. They said things like, “Look, there’s no question that the much greater health risk comes from the smoking rather than the weight gain. The average person would have to gain about 100 pounds to offset the health benefit of quitting.” Indeed, medical practice guidelines conveyed a similar message. The U.S. Public Health Service Guideline on Tobacco Treatment encouraged physicians to tell patients not to worry about weight gain until they were fully confident and secure as non-smokers. The fear was that trying to manage both things at once – smoking and weight – would be overwhelming and would undermine the success of the quit attempt. Yet even though that guidance seemed right-minded and conservative, I watched it prompt my friends to make a life-threatening decision. Nor did I watch detachedly, because I was one of the many smokers who responded by making the same bad decision. Having to choose between being smoke-free and being slender felt like being crushed between a rock and a hard place. Yes, I cared about my long-term health and wanted very badly to quit. However, maintaining a slender, attractive appearance felt essential to sustain the social reinforcers that were vital to my quality of life. We can call it vain, irrational or disordered till the cows come home, but my priorities were certainly not unusual then or now. I continued to smoke.

Living out the truism that “research is me-search,” I began a series of treatment studies to test different ways to help smokers quit smoking without gaining weight. We already knew that ex-smokers gain weight especially because they eat more, but also because their metabolism slows down a bit. So I conducted a number of clinical trials using weight loss agents that are known to reduce food intake. Some of the drugs worked well in the short term. But as soon as patients stopped taking the medication, they gained weight, catching up to and sometimes surpassing the weight gain of patients who’d taken a placebo. Those studies convinced me that available medications were not a good long-term solution to prevent weight gain. I went back to the drawing board and began to experiment with cognitive behavioral interventions. The experimentation taught me enough to finally lick my own smoking habit without gaining weight. Eventually, the National Institutes of Health funded a clinical trial of 315 women who received smoking cessation treatment alone or the combined smoking and weight management treatment. Quitting smoking first and then beginning to self-regulate diet and exercise suppressed post-cessation weight gain. To our great surprise, given the ominous warnings in tobacco treatment guidelines, adding weight management to smoking cessation treatment didn’t compromise the quit attempt. To the contrary, it somewhat increased the likelihood that abstinence would be achieved. Fascinated by our findings, we culled the world research literature to learn whether others had found similar effects. Of the 779 articles we identified that used non-drug treatments to promote smoking cessation and prevent weight gain, 10 trials met our quality criteria. Meta-analyzing the responses of all 2027 participants included in those trials produced absolutely no evidence that combining smoking and weight control treatment produces any harm. From this expanded global purview, we observed again that combining smoking and weight treatment tends to improve both smoking cessation and weight control.

Indeed these findings do give new hope to the many smokers – now about 50% of women and 25-30% of men around the world – who say that fear of gaining weight discourages them from trying to quit. Providers no longer need to discourage their patients from pursuing two healthy goals – quitting smoking and managing weight. Smokers no longer need to hide their weight-related worries from their physicians. Clinicians have a new, non-drug treatment to help their patients to achieve both smoking cessation and weight management. We now know that striving for these two worthy outcomes isn’t going to do any harm and it’s likely to do some good for both quitting smoking and managing weight.

And now it’s time for me to go for a run, smell some fresh air, and come home to my snack of fruits and veggies.

Share your story with us below! What was the most difficult thing when YOU tried to quit smoking?

Neuroscientist Simon LeVay has served on the faculties of Harvard Medical School and the Salk Institute for Biological Studies, and is well-known for a 1991 study in which he reported on a difference in brain structure between gay and straight men. His forthcoming book Gay, Straight, and the Reason Why: The Science of Sexual Orientation examines the evidence that suggests sexual orientation results primarily from an interaction between genes, sex hormones, and the cells of the developing body and brain. In this original post, LeVay explains how he initially reacts to new reported findings in this field.

I often lecture on the topic of sexual orientation. When I do, I sometimes mention research on finger lengths: according to several studies, the index fingers of lesbians are slightly shorter than those of straight women, when measured with respect to the other fingers. As I describe this research, I invariably see audience members examining their own fingers, as if doing so might reveal something unexpected about their sexuality. I hasten to make clear that the findings on finger lengths are based on statistical analysis of data from hundreds or thousands of subjects—they can’t be used to assess the sexual orientation of any particular individual.

Yet I myself use the “me test” as a gut reaction to any reported findings in the field. Not to figure out whether I’m really gay—I’ve been confident on that score since puberty—but as a quick, involuntary assessment of whether I believe that particular finding or not. As a teenager, for example, I read Freud’s theory of how close-binding mothers and distant or hostile fathers drive their sons toward homosexuality. This seemed to correspond to my own childhood experience: I was my mother’s favorite son, whereas I got on badly with my father. So I thought Freud must have been right. Now I believe that the direction of causation is the reverse of what Freud imagined: “pre-gay” boys tend to elicit adoration or protectiveness from their mothers, but rejection from their fathers.

Recent research has focused on gender-related traits in gay people. There have been over ninety such findings in the last couple of decades, covering personality, cognitive traits, behavior, anatomy (including the finger-length studies), physiology, and brain organization. Most have reported that gay men are shifted in the feminine direction in some traits, whereas lesbians and bisexual women are shifted in the masculine direction. As each study appears, I can’t help asking: is it true for me? Gay men (like straight women) have higher verbal fluency than straight men—check! Gay men have lower visuospatial abilities that straight men—check! Gay men have slightly shorter arms—check! I seem to be a pretty stereotypical gay man in many of these traits. Most researchers interpret these findings in terms of a biological predisposition to become gay or straight—a predisposition that results from an interaction between sex hormones and the developing brain and body. I certainly buy into that.

Other evidence has pointed toward a genetic influence on sexual orientation. For one thing, gay people tend to cluster in certain families, as if genes running in those families are predisposing their members toward homosexuality. The “me test” authenticated that one: I have a gay brother.

Another set of studies, however, points in a direction that doesn’t quite gel with my own experience. Canadian researchers have reported a birth-order effect: gay men, they say, are more likely to be later-born in families than are straight men, and are more likely to have at least one older brother. I do have an older brother, but I also have three younger brothers, so I’m fairly early in birth order. And what’s more, my older brother is gay too, even though he’s first-born, whereas my younger brothers are not.

So it was difficult for me to accept the birth-order studies. But they’ve now been confirmed often enough to persuade me that they’re correct, at least in a statistical sense. Interestingly, this birth-order effect holds up even if the children are brought up separately, so it doesn’t seem to be caused by the social experience of having older brothers. Rather, the Canadian researchers believe that women’s immune systems ‘remember’ how many sons they’ve had, and this immunological memory affects prenatal brain development in later sons, predisposing them to be gay.

It’s natural for people to take account of own life experiences when considering explanations for traits such as sexual orientation, but this kind of thought process can be fallible. Some women believe that childhood molestation caused them to be lesbian, for example. Yet such molestation is shockingly common, so many lesbians will have a history of childhood molestation, just on a chance basis. In fact, statistical studies don’t support a causal connection between molestation and homosexuality in women (or in men, for that matter).

In other words, it’s best to keep an open mind about what factors led you to your own sexual orientation, whether it be gay, straight, or bisexual. In my research, I drop the “me test” and stick to the science. Even science is fallible, of course, but it has a way of correcting itself over time, in part because the personal prejudices of individual scientists tend to cancel each other out.

Christopher A. Kearney is a Professor of Psychology and Director of UNLV Child School Refusal and Anxiety Disorders Clinic, University of Nevada, Las Vegas. His new book, Helping Children with Selective Mutism and their Parents, provides information that can help readers better understand and combat selective mutism. In the excerpt below, Kearney provides some techniques to help children cope with their anxiety about speaking.

Breathing

A simple way to help children reduce physical feelings of distress is to teach them to breathe correctly.  Many children experience shortness of breath, breathe shallowly, or hyperventilate when upset.  Doing so actually makes the feeling of anxiety worse, so helping a child regulate breathing is important.  Have the child sit before you in a comfortable position.  Then ask the child to breathe in slowly through the nose (with mouth closed) and breathe out slowly though the mouth. As the child does so, encourage him to breathe deeply into the diaphragm (between the abdomen and chest and just below the rib cage.)  The child may need to push two fingers into the diaphragm to experience the sensation of a full, deep breathe.  The child can then breathe slowly out of his mouth.  Parents may even join the process to help their child practice at home.

For younger children such as Austin[age 6], you may wish to create an image during the breathing technique.  Austin could imagine blowing up a tire or pretend he is a large, floating balloon.  As Austin breathes in, he can imagine filling up with fuel and energy.  As he breathes out, he can imagine losing fuel and energy (or tension).  The child must come to understand the difference between feeling tense when the lungs are full of air and feeling more relaxed after breathing out.  The following breathing script adapted from Kearney and Albano (2007) may be helpful:

Pretend you are a hot air balloon.  When you breathe in, you are filling the balloon with air so it can go anywhere you want.  Breathe in through your nose like this (show for your child).  Breathe slowly and deeply – try to breathe in a lot of air!  Now breathe out slowly through your mouth like air leaving a balloon.  Count slowly in your head as you breathe out…1…2…3…4…5.  Let’s try this again (practice at least three times).

Key advantages of the breathing method are its ease, brevity, and portability.  The child can use this method in different stressful situations and usually without drawing the attention of others.  I recommend that a child practice this breathing method at least three times per day for a few minutes at a time.  In addition, the child should practice in the morning before school and during particularly stressful times at school.  Some children benefit as well by practicing this technique whenever they are around other people and an expectation for potentially speaking is present.  For example, a child could use the breathing technique prior to and during a church service.

Muscle Relaxation

Another method of helping a child reduce physical feelings of anxiety is progressive muscle relation (PMR).  Youths such as Austin are usually quite tense in different areas of their body, especially in the shoulders, face, and stomach.  Different methods of muscle relation are available, but a preferred one is a tension-release method in which a child physically tenses, holds, and then releases a specific muscle group.  For example, a child may ball his hand into a fist, squeeze as tightly as possible and hold the tension for 10 seconds, and then suddenly release the grip (try it).  When this is done two or three times in a row, people generally report feelings of warmth in the muscle as well as relaxation.

Muscle relaxation via tension-release can be done in different ways.  When I work with children, I use a relation script that covers most areas of the body.  I first ask the child to sit in a comfortable position and close her eyes.  I then read the script slowly and ask the child to participate.  You may wish to use the following script adapted from Ollendick and Cerny (1981) with a child:

(Speaking slowly and in a low voice) Okay, sit down, try to relax, and close your eyes.  Try to make your body droopy and floppy, as if you are a wet towel.  Take your right hand and squeeze it as hard as you can.  Hold it tight! (Wait 5 to 10 seconds.) Now let go quickly.  Good job.  Let’s do that again.  Take your right hand and squeeze it as hard as you can.  Hold it. (Wait 5 to 10 seconds.)  Now let go quickly.  See how that feels.  Nice and warm and loose.  Now take your left hand and squeeze it as hard as you can.  Hold it tight! (Wait 5 to 10 seconds.) Now let go quickly.  Good job.  Let’s do that again…

Now shrug your shoulders hard and push them up to your ears.  Make your shoulders really tight.  Hold them there.  (Wait 5 to 10 seconds.)  Now let go quickly.  Great.  Let’s do that again…

Now scrunch up your face as much as you can.  Make your face seem really small and tight.  Now hold it there.  (Wait 5 to 10 seconds.)  Now let your face go droopy.  Good.  Let’s do that again…

Now I want you to bite down real hard with your teeth.  Make your jaw really tight. Hold it there.  (Wait 5 to 10 seconds.)  Now open your jaw.  How does that feel?  Good.  Let’s try that again…

Let’s go to your stomach now.  Bring in your stomach as much as you can – make it real tight!  Press it against your backbone.  Now hold it there.  (Wait 5 to 10 seconds.)  Now let go quickly.  That feels betters.  Let’s try that again…

Okay, one more. Push your feet onto the floor real hard so your legs feel really tight.  Push hard! Now hold it.  (Wait 5 to 10 seconds.)  Now relax your legs.  Shake them a little.  Let’s try that again…

…I recommend that a child practice this script at least twice per day in the beginning of your intervention and then once or twice per day as he becomes more adept and independent.  In addition, the child could practice the method during times of the day when she feels most distressed…The idea is to replace anxious feelings with more relaxed ones so the child may feel more comfortable speaking.

Robert Freedman, MD, is Professor and Chair of Psychiatry at the University of Colorado and the Editor-in-Chief of the American Journal of Psychiatry.  His new book, The Madness Within Us: Schizophrenia as a Neuronal Process, is a discussion of these two aspects of the illness.  Freedman outlines the emerging understanding of schizophrenia as a neurobiological illness.  In the excerpt below we learn about the basic brain dysfunction in schizophrenia.

The earliest observers of how people with schizophrenia seemed to react to their environment noted a peculiarity in the ability of persons with schizophrenia to appear unaware of the environment and yet overly responsive to it.  Eugen Bleuler first developed the concept of an attentional dysfunction in schizophrenia in his essay on attention in schizophrenia…

Rachel not only hears voices but she hears noises as well, noises that her family members also hear but have learned to ignore.  She hears screaming all the time, and she sometimes wanders the neighborhood to find out who is screaming.  When my colleague Merilyn Waldo suggested to her that it might be traffic, she told us that her mother had said the same thing.  There is a busy corner near the front of her house, and there are always cars stopping and then accelerating away.  My wife and I experienced the very same perceptual abnormality ourselves on the night we brought our first son home from the hospital.  We put the baby to bed and tried to sleep ourselves, but I heard screaming.  I checked on the baby, and he was asleep.  Then my wife heard it too.  We checked again.  Then we listened at the door.  The screaming must be coming from another apartment, and we wondered if we should call the police to alert them to child abuse, but we knew that no other couples with babies lived in the building.  Finally, when the traffic on the highway in front of the building stopped at 2 a.m., we understood how two very anxious, hypervigilant new parents can misinterpret the world around them.

For Rachel, the problem is not a single stressful night.  It is a lifelong problem, which she has struggled with since she was a teenager, long before the onset of her illness at 28.  She could never concentrate at school.  The least noise captured her attention.  As she put it, “My mind has to be here, it has to be there, I can’t concentrate on anything.”  Unlike a typical child with attention-deficit disorder (ADD), whose attention is rarely captured, her attention was captured by everything, from the traffic squeaking to the refrigerator cycling on and off, to the neighbor’s ongoing argument next door.  As a result, she could concentrate on very little.

Paul, on the other hand, seems to be aloof in his environment.  When he was first ill and worried about snakes, I wondered if their voices arose out of noises around him in the dormitory.  He acknowledged that the noise of the dormitory was exquisitely painful, but he could not connect it to the snakes.  Now he seems withdrawn.  When I walk out to get him in the waiting room, he seems oblivious to the people around him.  He has constructed a psychological shell around himself, a solution many patients use to shield themselves from their otherwise overwhelming environment.

The most dramatic experience of the phenomenon of seeming to ignore the environment is catatonia, a rarely seen syndrome in schizophrenia today.  The patient gradually stops responding to environmental stimuli and then eventually stops moving altogether.  In the most advanced cases, the person suddenly freezes.  If he is moved passively, then he may retain the position into which he is moved, a symptom termed “waxy flexibility.”  These patients can often be drawn back to awareness by family members and sometimes even a familiar physician, which leads to the supposition that they may be faking their symptoms.  They are not, and it is sometimes shameful to watch medical personnel positioning them in uncomfortable poses or raising their arms over their faces to see if they will prevent their arms from hitting their eyes, a misguided attempt to uncover what they believe to be malingering.

Patients with catatonia have hyperactive electroencephalographic activity, consistent with the minds being quite active, rather than asleep or anesthetized.  They respond to barbiturates and benzodiazepines, drugs that are sedatives, with a paradoxical “awakening,” in which they resume normal movement.  This paradoxical response suggests that they have actively withdrawn from the world around them, perhaps to inhibit the response to stimuli.  When the barbiturate or benzodiazepine partially inhibits their brain’s responsiveness, they lose this withdrawal and temporarily resume normal interaction.  They often report that they were fully aware, indeed acutely hyper-aware, of their surroundings during the catatonia.  Catatonia takes several years to develop and most persons receive drug treatment before it becomes an obvious symptom.  I have occasionally seen it develop in patients from religious families who resist treatment and expend great effort to interact with their loved one, who is descending into deepening catatonia.  The otherworldly trance adds to the spiritual mystique of their loved one’s experience.

Rosalind D. Cartwright is Professor Emeritus of Rush University Medical Center’s Graduate College Neuroscience Division, and was chair of the College’s Department of Behavioral Sciences until 2008.  In her new book, The Twenty-Four Hour Mind: The Role of Sleep and Dreaming in Our Emotional Lives, Cartwright brings together decades of research into the bizarre sleep disorders known as parasomnias to propose a new theory of how the human mind works consistently throughout waking and sleeping hours.  In the excerpt below we learn how important it is to slow down and get the appropriate amount of sleep.

We live in a culture that values speed; fast foods, fast cars, fast service, and fast decisions.  All of this takes a toll.  Fast food is blamed for the epidemic of obesity, fast cars for motor vehicle accidents, and the wish for fast service and decisions for an increase in the general level of frustration when we are inevitably put on hold.  This “hurry up” lifestyle also has an impact on sleep – it has notably shortened the number of hours we as a society devote to it.  When sleep experts speak to general audiences, one question they are often asked is, “How can I spend less time sleeping?”  Those who ask this question tell us that sleep is a waste of time.  Not only is that notion wrong, but the attitude behind it is largely responsible for the increase of several major public health problems.

We now turn to those whose short number of sleep hours is troubling enough for them that they seek professional help.  This is not the case for all short sleepers; some manage to live productive lives and make significant contributions to society.  These are the ones who occupy the extreme left-hand tail of a normal distribution of average hours of sleep needed to feel rested.  Most of us will fall in the middle of that curve, needing between 7 and 9 hours, with an average close to 8.  Short sleepers average 5.5 hours.  Very few people are truly physiologically and psychologically healthy with only 5 hours of sleep on a nightly basis.  Those who, as adults, were 8-hour sleepers but can no longer get that much sleep are in trouble.  Some cannot get to sleep without a prolonged struggle, while others get to sleep but wake repeatedly.  Then there are those who wake too early and cannot get back to sleep.  Insomnia is a useful model to test the contribution of sleep to keeping us healthy in mind and body.

…

What is the definition of “short sleep”?  Sleep experts are reluctant to answer this question by giving a specific number of hours.  As noted, there is just too much variability among individuals in the amount of sleep it takes for them to accomplish the “rest and restoration” functions of sleep.  When we are getting “enough” sleep, we wake up feeling physically refreshed, in a reasonably good mood, and able to function well throughout the day without undue sleepiness.  All of us experience a down time around mid-afternoon, called the “circadian dip,” or sometimes known by the more colorful name, “circadian slump.”  This is when our internal body temperature drops, bringing on a natural tendency to feel sleepy enough for a midday siesta.  If you can get through this without falling asleep at your desk or in your car and then feel all right for the rest of the day, your number of sleep hours is right for you.

Another indicator of how much sleep is enough is the number of hours we sleep when sleep is unscheduled – that is, when we need not wake up at a set time, like on weekends and vacations.  Since we tend to go to bed later under these circumstances we also tend to sleep later, so it is not the hour at which we wake that makes the difference but how many hours we sleep when we can take our time.  If you sleep 2 or 3 hours more on weekend nights than you do during weeknights, you are probably not getting enough sleep on a regular basis.  This is what Bill Dement calls running a “sleep debt,” and this debt mus be paid back by extending your regular sleep schedule or by including some daytime naps.

A trend among American adults is to sleep fewer hours a night during the work week and to play catch-up on the weekends.  This is proof that many who report they are short sleepers actually can sleep longer, but do not by choice.  According to information about our sleep habits gathered periodically by the Centers for Disease Control and Prevention, the old 8-hour national average per night has dropped to 7.  Evidence that this is a real problem can be found in the push to develop new drugs to treat sleep troubles.  In addition to new sleeping pills, we now see new “stay awake” pills marketed to help keep us going even longer, to work more hours without experiencing a drop in the quality of our job performance.  For those who suffer from a neurological problem such as narcolepsy, one symptom of which is sudden abrupt sleep episodes that come without warning, these medications are a life-altering boon.  But for those who are healthy, the cost to our health of working longer hours by sleeping less is not worth the benefit.

Another alarming trend we see now is the misuse by adolescents and young adults of “stay-awake” prescription medications such as Ritalin, Adderall, and modafinil originally developed to treat attention-deficit hyperactivity disorder (ADHD).  More and more frequently these drugs are being used by young people to increase their focused attention.  Is this harmful?  Yes, if it interferes with the ability to get enough sleep, and for sure if the drug was not prescribed but is “borrowed” from someone else.

Some who sleep 6 or fewer hours argue that this is not by choice but by economic necessity, the result of having to work two jobs.  Data show that the use of stay-awake medicine is strongly related to shift work.  Daytime sleep is shorter and lighter than nighttime sleep and so less refreshing.  Those who report using stay-awake medications point out that there is simply too much to do in a 16-hour day, and that an 8-hour night is luxury they can no longer afford.  The economic need may be real but the price we pay for such a heavy sleep debt should be better understood.  It is especially important for physicians to understand the risks involved in aiding their patients to reduce sleep hours with a prescription, and it is up to sleep experts to offer some sensible alternatives…

Rom Harre is Emeritus Professor of Philosophy at Linacre College, Oxford, and Adjunct Professor of Philosophy at Georgetown University, Washington, DC. In his book, Pavlov’s Dogs and Schrodinger’s Cat: Scenes from the Living Laboratory, we get an enlightening look at the use of plants and animals–including humans–in scientific experiments. In the excerpt below we see how dogs were essential to figuring out heart transplants.

By coincidence, two men, one living in the seventeenth century and one in the twentieth, who both used dogs as models and whose work led to major breakthroughs in medicine bore the same name.  The first Richard Lower used dogs to perfect blood transfusion techniques, while the second Richard Lower used the same species of animals to perfect heart transplantation methods.

History, as presented in the media and so in popular belief, credits the beginning of heart transplantation techniques to Christiaan Barnard.  Digging a little deeper we come across the most successful practitioner of this art, Norman Shumway.  However, using dogs as experimental apparatus – as pilot plants- to perfect the surgical techniques required to carry out transplant operations on human beings.  Christiaan Barnard did forty-eight trial transplants with dogs before he undertook such an operation with a human being.  He acknowledges that what he uses ‘was a technique built on that developed by Shumway and Lower, who had experimented on more than 300 dogs… With their findings joined to mind there was little point in continuing to further sacrifice of animals.’

Richard Lower studied at the Medical School at Cornell but moved for his residency period to the University of Washington in the northwest of the United States.  One autobiographic snippet suggests that the American northwest suited his love of the outdoors.  Finding things not to his liking there he moved south to Stanford were he could qualify more quickly.  Working in very primitive conditions in the training section of the hospital he eventually met up with Norman Shumway and forged a remarkable partnership with him.

Norman Shumway (1923-2006) studied medicine at Vanderbilt University, moving on to a doctorate at the University of Minnesota in 1956.  He was appointed as a surgery instructor at Stanford University in 1958, where he remained for the rest of his career.  He seems to have been a somewhat paradoxical character.  Reticent and wary of publicity, yet he was famous for his witty and jocular conversation, particularly during the course of long and demanding surgical procedures.  The persistence with which he pursued his goal of successful himan heart transplantation suggests a dogged streak.

Lower began his experimental programme as an assistant to Shumway working on the techniques for open heart surgery, including the possibility of cooling a living heart so as to stop its beating.  Under this condition surgical repair would be greatly facilitated.  The heart could then be warmed up and restarted with a fibrillator.  Perhaps the heart could be removed completely from the patient’s body for delicate surgical work and replaced when the repair was done.  This is the procedure known as ‘auto-transplantation’.

Dogs were already in regular use at Stanford University Medical School for training surgeons.  …Lower and Shumway continued their use of dogs as experimental apparatus, pilot plants for the ultimate transfer of the techniques to the human case.  Despite his skill in surgery Lower was unable to achieve successful autotransplantation.  The reason was simple.  To remove the heart from the dog the aorta and pulmonary vessels had to be cut in such a way that there was sufficient length on each side of the incision for sewing the heart back in.  Lower simply could not manage to retain enough of the vessels on either side of the severing cut to meet this essential condition.  However, it then ocurred to him that in implanting a ‘homologous heart’ – one from another dog – the problem could be overcome.  By cutting the aorta of the first dog close to the heart a substantial section of the aorta remained in the cavity of the chest.  By cutting the aorta of the donor dog to leave a substantial length from the heart, enough ‘tubing’ was left to make successful suturing possible.  The same held for other cardiac blood vessels.  This technique proved to be entirely successful.  The first operation transplanting a heart from one dog to another was carried out in 1959.

The results of the project were reported in the Surgical Forum of 1960.  In the discussion section of the paper the authors report that the dogs died within a few days and at best survived for as much as three weeks.  The cause of death was found to be adverse immunological reactions rather than heart failure.  ‘If the immunological mechanisms of the host were prevented from destroying the graft, in all likelihood it would continue to function adequately for the normal life span of the animal.’  Lower carried out other experiments, include a bizarre xenotransplant, inserting a human heart into a chimpanzee.  A newspaper report described the result euphemistically: ‘the heart functioned until Lower euthanized the chimp and terminated the experiment.’

Lower eventually moved to Richmond, Virginia, where among his visitors was a South African surgeon, Christiaan Barnard.  Barnard also visited Shumway whom he had know previously at the University of Minnesota.  Back in Stanford it was not until 1967 that Shumway was ready to go ahead with confidence to a programme of human transplantations.  During the preceding eight years he had continued his use of the bodies of living dogs as the essential apparatus for his transplantation experiments.  It was a great surprise to him to learn that on December 23 his old acquaintance and recent visitor, Christiaan Barnard, had carried out a successful human heart transplantation operation on Louis Washkansky.  The use of the necessary immunosupprressing drugs left often the possibility of fatal infection.  Washkansky contracted pneumonia and died after only 18 days. After a few more operations Barnard abandoned his programme because the immunosuppresing drugs available at that time for preventing the rejection of the transplant also left the patient vulnerable to common and simple infections…

Shumway began his own programme of transplantations on 6 January 1968.  While his patients survived the operation for increasing lengths of time, and given immunosuppressing drugs, continued on the path to recovery, the life expectancy of the recipients of healthy hearts was subject to the danger of infections with which the damped immune system could not cope… All this changed when a new drug, ‘cyclosporine’, was introduced.  While suppressing the body’s efforts to expel the alien heart tissue it allowed resistance to common infections to remain robust.

Edna Foa is a Professor of Clinical Psychology in Psychiatry at the University of Pennsylvania and Director of the Center for the Treatment and Study of Anxiety.  Her most recent book, Prolonged Exposure Therapy for PTSD: Emotional Processing of Traumatic Experiences, was written with Elizabeth Hembree and Barbara Olaslov Rothbaum. The guide gives clinicians the information they need to treat clients who exhibit the symptoms of PTSD.  Recently Foa was name by Time Magazine as one of the most influential people in 2010.  Below she reacts to the honor.

My first reaction was that of disbelief when I learned that I had been selected for Time Magazine’s list of the 100 most influential people in 2010. I thought someone was pulling my leg. I called my husband and shared the news with him, he thought I was pulling his leg. My youngest daughter said: “get out of here, you must be joking”. But of course, we all know that the email was genuine. First, I was stunned. After all, I am not a rock star, not a head of state, not even a famous athlete. And then I was delighted. Isn’t it wonderful that someone at Time recognized the importance of the work we, clinical psychology researchers, do to help PTSD sufferers. I felt quite honored to represent our field.

As clinical scientists we know that we have a lot of powerful treatments. But we also are painfully aware of how difficult it is to make these treatments widely available. The treatments that we have for anxiety disorders are particularly efficacious and yet most clinicians do not deliver them. For many reasons it is hard to get mental health clinicians to adopt new treatments. As a result, countless individuals with anxiety and other disorders experience needless suffering that could be decreased or terminated via the application of the effective treatments we developed.

The cost of bad treatment reaches beyond individuals. Institutions and society as a whole suffer from what is a public health issue. For example, the VA, the military and insurance companies all have a stake in individuals receiving the most effective treatments for psychological disorders. And yet, there have been very few effective initiatives requiring practitioners to learn and deliver the best psychological treatments.

And so I hope that Time Magazine’s recognition of my work is in essence recognition of the tremendous importance of not only developing effective, evidence-based treatment, but more importantly, disseminating them among mental health professionals. The wars in Iraq and Afghanistan have brought home the awareness of how important it is to deliver effective treatments to the many soldiers who return from these wars with posttraumatic stress disorder (PTSD). I strongly believe that PTSD is not only a mental health disorder; it is also a societal problem. It is the responsibility of our society to help PTSD sufferers as a result of being injured at work, raped in our schools, physically assaulted in our streets, or experiencing the horror of war. We know that effective treatments for PTSD such as Prolonged Exposure (PE) can help patients regain their lives in as few as 10 sessions over the course of 5 weeks. It is no longer necessary for individuals with PTSD to suffer for decades. Recognition of our progress in knowing how to treat PTSD by Time and other media can play an important role in spreading the word about what clinical science has to offer.

I hope that Time’s recognition will help therapists to seek training in the effective treatments we developed and help patients to request them.

John Galbraith Simmons studied philosophy at Northwestern University, graduating with honors, and also holds a degree in developmental studies from Long Island University. His newest book, written with Justin Zivin, is tPA for Stroke: The Story of a Controversial Drug. The book, which will be published in November, looks at the history of tPA which can drastically reduce the long-term disability associated with stroke if it is administered within the first three hours after the event occurs. In the original article below Simmons looks at Beau Biden’s recent stroke.

Details around Beau Biden’s “mild stroke” on Tuesday, May 12, remain unclear, although his reported symptoms were paralysis, numbness, and headache. He and his family, and his political entourage, currently are limiting their contact with the press while portraying him as alert and in possession of “full motor and speech skills.” Stroke is a genuinely disorienting event, so some initial reluctance to disclose may be understandable — for now.

But Beau Biden, 41, may help put a public face on the larger issues around stroke, a disease much neglected in terms of public awareness. Stroke is the leading cause of adult disability and third leading cause of death (after the sum of cancers and heart attack) — and receives little attention relative to its importance. Most germane are two issues. First is whether Biden’s stroke was appropriately treated as an acute emergency. Second, but no less significant, is whether his stroke was ischemic (due to a blood clot or blockage) and if he received the FDA-approved drug for stroke, known as tPA.

At present, indications are that Biden or family members made the right call — which, for stroke signs and symptoms, always means 911. He was taken by ambulance to Christiana Care Health System, one of the largest hospital systems in Delaware. Christiana Care is a certified primary stroke center that would in effect insure that if he were eligible for treatment, and if tPA was appropriate, he would have received it. After suffering his stroke on Tuesday morning, Biden was later in the day transferred to Thomas Jefferson University Hospital in Philadelphia. No explanation for the transfer was forthcoming but reports continued to be positive for a full recovery.

tPA, which stands for tissue plasminogen activator, is the only approved treatment for ischemic strokes, which are caused by blood clots or blockages and account for about 85% of all strokes. A “clot-busting” drug, tPA is not difficult to administer but must be given within four and a half hours after symptoms start, and a computerized brain scan is first required to rule out a bleeding, or hemorrhagic, stroke. Although approved by the FDA for stroke in 1996, tPA has had a long and difficult road to widespread acceptance among physicians, while potential victims remain for the most part disturbingly unaware of it.

For the present, Beau Biden’s “mild” stroke is worthy of headlines because he’s young, the son of a U.S. vice president, and a rising political star in his own right. Although strokes are more common in older people, Biden’s problem is not rare.  But the genuine story, it may turn out, will be to enhance public awareness of stroke as a hyperacute event. From Biden and his family, we will be waiting to hear better and more detailed news.

Ancient Bodies, Modern Lives: How Evolution Has Shaped Women’s Health written by Wenda Trevathan, Ph.D., a Regents Professor of Anthropology at New Mexico State University, we learn about a range of women’s health issues.  Trevathan’s hypothesis is that many of the health challenges faced by women today result from a mismatch between how our bodies have evolved and the contemporary environments in which we live.  In the following excerpt, Trevethan draws from Jane Goodall’s observations of primates to illuminate how grandmothers, by virtue of being present in the family, contribute to the growth of prosperity of the grandchildren and the family unit as a whole.

Grandmothers and Reproductive Success

Most long-lived, group-living mammals have in their social groups as many as three generations present at any one time. Examples include elephants, whales and many primates. For primates who live in matrilocal groups, that usually means three generations of females: Infants, their mothers, and their grandmothers. A famous example comes from Jane Goodall’s studies of a Tanzanian chimpanzee social group in which Flo, her adult sons Faben and Figan, and her daughter Fifi lived together. Flo was a high-ranking female and her presence had a number of positive effects on her offspring. For example, Fifi was able to stay in the troop into which she was born, whereas the more typical pattern among chimpanzees appears to be for young females to leave their birth troops at maturity. By staying with her mother, Fifi was also able to rise to a high status. She began reproducing much earlier than most chimpanzee females and not only set the record for reproductive success at Gombe, but one of her sons became the largest male ever recorded at Gombe. Two of Fifi’s sons rose to high status in the dominance hierarchy and her daughter began reproducing much earlier than Fifi did. There is little doubt that grandmother Flo’s status had an effect on her daughter’s (and thus her own) reproductive success. There is no evidence, however, that Flo contributed directly to the care and feeding of her grandchildren, although it is true that she was not in good health at the time Fifi’s first infant was born in 1971.

Anthropologist Sarah Hrdy notes that despite her reproductive success, Flo serves as a good example of why having offspring at later ages may not be a good way to achieve this success or why “stopping early” might be selectively advantageous. Flo reproduced for the last time when she was very old and in poor health, but that infant did not live long. Goodall proposes that this last pregnancy was so draining for her that she was unable to mother her other young offspring, Flint, and when Flo died, Flint died also, even though he as at an age when he should have been able to survive on his own. In fact, if Flo had stopped reproducing after Flint, he probably would have lived, perhaps going on to sire another offspring and increasing Flo’s reproductive fitness through her grandchildren.

Similar evidence that the presence of grandmothers has positive effects on reproductive success comes from observations of a number of other primate species. Again, it is not usually resources and direct care that older female grandmothers provide; rather, they help to defend the infants from other troop members (including infanticidal males) whose behaviors endanger them. In fact, observers report that grandmothers will often act even more vigorously in defense of infants than younger kin. Grandmother Japanese macaques make a significant difference in survival of their grandchildren through the first year of life. Furthermore, females have much greater reproductive success if they have living mothers, even when those older females are still reproducing. Similar reports have come from studies of vervets, langurs and rhesus monkeys, as well as elephants. On the other hand, African Lions and olive baboons, while showing extensive caretaking by adults other than the mother (known as allomaternal care), do not seem to have their reproductive success influenced by the presence of grandmothers.

These descriptions of primate social groups with three generations of females are not very different from what is seen in traditional human societies and even in extended family households in health-rich nations like the United States. What is different, however, is that in most cases the grandmother is not only helping her own older children but she also provides care and resources to her grandchildren.

Another view of menopause focuses not on the mother and early termination of reproduction (the “long-lived mother hypothesis”) but on the grandmother who maintains health long after ceasing to reproduce. Known as the “grandmother hypothesis,” this proposal assumes that termination of fertility at about age 50 is a given, but that natural selection favored a long postreproductive period in women’s lives because by ceasing to bear and raise their own children, postmenopausal women would be freed to provide high-quality care for their grandchildren. In this scenario, older women “trade” their diminished chances of successfully raising an infant for enhanced opportunities to help raise their grandchildren. This is simply the continuation of a behavior that women have practices for most of their adult lives: providing food and care for children who have been weaned but who are not yet capable of getting their own foods in sufficient quantity and quality to survive. This continuity-of-care hypothesis also explains why so much of the focus on older people as alloparents is on grandmothers.

When the grandmother hypothesis was first proposed by Kristen Hawkes and her colleagues, it included supporting evidence based on their studies of the Hadza, a foraging population in Tanzania.  Among these people, when a woman gives birth, her time providing food for her older children is severely curtailed and remains lower than usual for several months.  During this time, the grandmother increases her foraging to make up for the reduction by the new mother.  Certainly her success is increased if she is still in good health and able to travel widely gathering food.  Thus, the argument is that natural selection not only favors termination of reproducing at about ago 50 and provisioning of older infants by grandmothers, but it also favors continued vigor and good health in the grandmothers until their own daughters cease reproducing and become provisioning grandmothers themselves.  Notably, this argument also proposes that matrilineal proximity would be favored as well, calling into question the assumption that early human social groups were patrilocal and that females dispersed at maturity.  Older women who provision their sons’ children would also increase their fitness, although certainty of kinship is higher through matrilines than through patrilines.

Robert Paarlberg is the B. F. Johnson Professor of Political Science at Wellesley College and Associate at the Weatherhead Center for International Affairs, Harvard University.  His new book, Food Politics: What Everyone Needs To Know, carefully examines and explains the most important issues on today’s global food landscape.  Politics in this area have become polarized and Paarlberg helps us map this contested terrain, challenging myths and critiquing more than a few of today’s fashionable beliefs about farming and food.  In the excerpt below we learn about the organic food.

Many who buy organic goods believe such foods are healthier than conventional foods because they contain more nutrients.  Others believe organic foods are safer to eat because they carry no pesticide residues.  Nutritionists and health professionals from outside the organic community tend to question both of these beliefs.

The strongest claim of superior nutrient content has been made by the Organic Center, an institution founded in 2002 to demonstrate the benefits of organic products.  In 2008, the Organic Center published a review “confirming” the nutrient superiority of plant-based organic foods, showing they contained more vitamin C and vitamin E and a higher concentration of polyphenols, such a flavonoids.  This review was rebutted, however, by conventional nutritionists who showed that the Organic Center had used statistical results that were either not peer reviewed or not significant in terms of human health.  Organic milk from cows raised on grass may indeed contain 50 percent more beta-carotene, but there is so little beta-carotene in milk to being with that the resulting gain is only an extra 112 micrograms of beta-carotene per quart of milk, or less that 1 percent the quantity of beta-carotene found in a single medium-size baked sweet potato.

Most certified health professionals find no evidence that organic foods are healthier to eat.  According to the Mayo Clinic, “No conclusive evidence shows that organic food is more nutritious than is conventionally grown food.”  European experts agree.  Claire Williamson from the British Nutrition Foundation says, “From a nutritional perspective, there is currently not enough evidence to recommend organic foods over conventionally produced foods.”  In 2009, the American Journal of Clinical Nutrition published a study, commissioned by the British Food Standards Agency, of 162 scientific papers published in the past 50 years on the health and diet benefits of organically grown foods and found no evidence of benefit.  The director of the study concluded, “Our review indicates that there is currently no evidence to support the selection of organically over conventionally-produced on the basis of nutritional superiority.”  The acidity of organic produce was found to be higher, which enhanced taste and sensory perception, but there was no difference for health.

The claim that organic food is safer due to lower pesticide residues is also suspect in the eyes of most health professionals. The Mayo Clinic says, “Some people buy organic food to limit their exposure to [pesticide] residues.  Most experts agree, however, that the amount of pesticides found on fruits and vegetables poses a very small health risk.”  Residues on food can be a significant problem in many developing countries, where the spraying of pesticides is poorly regulated and where fruits and vegetables are often sold unwashed, straight from the field.  Yet in advanced industrial countries, such as the United States, this risk is seldom encountered.  In 2003, the Food and Drug Administration analyzed several thousand samples of domestic and imported foods in the U.S. market-place and found that only 0.4 percent of the domestic samples and only 0.5 percent of the imported samples had detectable chemical residues that exceeded regulatory tolerance levels.

What are the tolerance levels?  The United Nations, through the Food and Agriculture Organization (FAO) and the World Health Organization (WHO), has established acceptable daily intake (ADI) levels for each separate pesticide. The ADI level is set conservatively at 1/100 of an exposure level that still does not cause toxicity in laboratory animals.  Moreover, actual residue levels in the United States on conventional foods are well below the ADI level.  For example, when FDA surveyed the highest exposures to 38 chemicals in the diets of various population subgroups, it found that for 4 of these 38 chemicals estimated exposures were less than 5 percent of the ADI level.  For the other 34 chemicals, estimated exposures were even lower, at less than 1 percent of the ADI level.  Carl K. Winter and Sarah F. Davis, food scientists at the University of California-Davis and the Institute of Food Technologies, conclude from these data, “[T]he marginal benefits of reducing human exposure to pesticides in the diet through increased consumption of organic produce appear to be insignificant.”

It is true that conventional foods are sometimes not safe to consume, but organically grown foods can also carry risks.  In 2006, bagged fresh spinach from a California farm in its final year of converting to organic certification was the source of E. coli infections in the United States that killed at least three and sickened hundreds.  In 2009, there were nine documented fatal episodes of salmonella poisoning from peanut butter and ground peanut products traced to peanut plants in Texas and Georgia, both of which had organic certification.

Edward Shorter is the Jason A. Hannah Professor of the History of Medicine endowed chair at the University of Toronto School of Medicine as well as a Professor of Psychiatry.  Max Fink has exensively contributed to the psychiatric community’s understanding of electroconvulsive therapy (ECT), pharmaco-electroencephalography (pharmaco-EEG), cannabis and the psychopathologies of catatonia, melancholia and mania.  Together they wrote, Endocrine Psychiatry: Solving the Riddle of Melancholia, which traces the enthusiasm of biological efforts to solve the mystery of melancholia and proposes that a useful, and a potentially life-saving, connection between medicine and psychiatry has been lost.  Below we have excerpted the preface which explains why endocrine psychiatry deserves a second look.

In the past hundred years, medicine has tried to acquire a scientific basis.  Age-old prejudices and pointless procedures have been discarded in controlled study after study.  Today, we take it for granted that the practice of medicine is evidence-based.

Yet in psychiatry the penetration of science has been imperfect.  The discipline has swung wildly from fashion to fashion – from asylum care to psychoanalysis to lobotomy to psychopharmacology -without having an underlying scientific rationale for doing so.  More than any other medical field, psychiatry has been guided by cultural preferences and political persuasions.  We vaguely dislike the notion of “locking up” people or of shooting volts of electricity through their brains; we have a natural enlightened tropism toward psychotherapy and the enhancement of human reason and against the madness of unreason.  None of these prejudices and preferences is in itself reprehensible, and all flow from a praiseworthy humanism.  But prejudices and beliefs are not science.  In a great disjunction, science and psychiatry have passed each other like two ships in the night.

Yet psychiatry cries out for science.  To be sure, we can gauge the neurochemistry of the brain and assess its structures with the devices of neuroimaging.  But the questions of clinical psychiatry are more complex than fluctuations in neurotransmitters or glucose uptake in the basal ganglia, where the brain gives up a few of its secrets.  Is there no other way to gain a window to the brain and gauge is activity in psychiatric illness?  Yes, there is.  Another system, the endocrine system, sets the biological rhythms of the brain and body.  Psychiatry was once fascinated with the endocrine system.  Today, the adrenal and pituitary glands, and the hypothalamus within the brain, have lost their charm and arouse little interest.

Simultaneously, psychiatry also said adieu to another familiar historical concept, melancholia, as a diagnosis of severe depression.  After the introduction of a new system of disease classification in 1980, the diagnosis of “major depression” – a heterogeneous assortment of varied illness entities and unhappiness states – swept in the field.  This is very interesting: At the same time that psychiatric interest in neurotransmitters such as serotonin quickened, the discipline embraced such new illnesses as “major depression” and “bipolar disorder.”  In understanding the seat of illness, there was a shift from the endocrine periphery to the neurotransmitter central, and in classification, there was a shift from such sturdy historical concepts as “melancholia” to the more faddish notions of “major depression” and “bipolar disorder.”  These two shifts are related.  In both, the profession of psychiatry walked away from solid, well-verified knowledge into a botanical maze of fashion, commerce, and politics.

Melancholia is a serious illness.  It involves the slowing of thought and mood, the absence of joy or pleasure in life, and profound changes in the body’s daily rhythms.  Max Fink and Michael Alan Taylor have defined it as “a recurrent, debilitating, pervasive brain disorder that alters mood, motor functions, thinking, cognition, perception and many basic physiological processes.”  This book makes the point that melancholia has a biology of its own that is heavily entwined with the endocrine system.  In coming to grips with the riddle of melancholia, psychiatry has this endocrine knowledge to draw upon, yet seldom does.  This is a failure of science and of clinical practice.

How did this failure happen?  Endocrine thinking in psychiatry rode a wave of great excitement in the 1970s and 1980s, and then it seeped away.  Few clinicians today are curious about cortisol or thyroid-releasing hormone, two hormones with intimate relationships to behavior.  While physicians might include assays of thyroid hormones when requesting laboratory tests, they are often incurious about the results unless a blood measure is wildly out of balance.  As for the complex interrelationships among hypothalamus, pituitary, adrenal gland, and the rest of it, that material is learned once during medical school and rarely considered again thereafter.

There is a price to be paid for this endocrine distaste, just as there is a price for the profession’s reluctance to contemplate convulsive therapy.  Melancholic illness, among the most serious of all psychiatric disorders, remains often imperfectly diagnosed and inadequately treated.  We try to deliver the best possible care of patients, yet patient care suffers when important guides to understanding illness and meliorating symptoms are left fallow.

This endocrine indifference is typical of a wider pattern.  A trail of discarded therapies and paradigms litters the history of psychiatry.  Some, such as lobotomy and pouring cold water on women with “hysteria,” will probably not again see the light of day.  Others, such as electroconvulsive treatment and using the brain’s electrical rhythms to study drug effects, have been prematurely cast aside – and urgently deserve a rebirth.  Our interest today in neurotransmitter levels and multicolor images of neuron-neuron interaction, on serotonin and dopamine, but cortisol may well offer a better marker of patients’ woes than the principle neurotransmitters.  This loss is particularly serious if the patients are melancholic.  In mood disorders, there are important markers that have unjustly fallen into desuetude.

…Endocrine psychiatry deserves a second look.

Barry S. Levy, MD, PHH, is an Adjunct Professor of Public Health at Tufts University School of Medicine and a consultant in occupational and environmental health.  Victor W. Sidel, MD, is Distinguished University Professor of Social Medicine at Montefiore Medical Center and Albert Einstein College of Medicine, and an Adjunct Professor of Public Health at Weill Medical College of Cornell University.  Together they edited, Social Injustice and Public Health, which looks at many aspects of social injustice and their relationship to public health. Major sections of the book focus on population groups affected by social injustice, areas of public health and medical care in which social injustice has an adverse impact, and approaches to the reduction and elimination of social injustice and its adverse effects on public health. In the excerpt below, from the essay “Nutrition” by J. Larry Brown, we learn about malnutrition’s effect in the United States.

While debate about the causes and remedies of hunger is conducted in the political arena, hunger itself is a public health issue.  The adverse consequences of chronic undernutrition, as well as the social sequelae, make hunger a critical problem for the nation.  Moreover, an increasing body of knowledge points to the problem of obesity as a health consequence frequently associated with inadequate income and even hunger.

In the United States, hunger presents quite differently than it does in developing nations. Protein-calorie malnutrition, or marasmas, and kwashiorkor, characterized by adequate calories but extreme protein deficiency, now occur in the United States only rarely.  Rather, hunger in this country typically takes the form of what the World Health Organization called “silent undernutrition.”  It is reflected in young children who are several pounds beneath the low end of the pediatric growth chart.  They may look simply like thin children, but a trained health professional will recognize that they are experiencing growth failure.  Although their symptoms are different from those of malnourished children in developing countries, they are, from a health perspective, in difficulty…

Because children grow and their height and weight gains are plotted on internationally used pediatric growth charts, they are perhaps the easiest population group in which to detect the consequences of inadequate nutrition.  Typically, youngsters who fall below the fifth percentile in weight or height for age on growth charts are candidates for further investigation.  To be certain, it is expected that normally 5 percent of any population would fall in this low end of the range; but in studies of low-income children, 10 to 15 percent do so.  This indicates that what is being observed is not normal genetic variation but rather a “human-made” outcome.  Moreover, this analysis is confirmed in the work of child development clinics in urban teaching hospitals across the United States, where children experiencing growth failure due to poverty are nursed back to health with appropriate nutrition.

While the relationship between inadequate nutritional intake and health status reflected in the height and weight of children is well established, scientific research in recent years has broadened our understanding of other insidious effects.  Direct links exist between inadequate food intake and a variety of poor developmental outcomes in children.  The health status of children from impoverished homes experiencing hunger and food insecurity is much worse that that of other children.  They get sick more often, have much higher rates of both iron-deficiency anemia and serious ear infections, and are hospitalized more frequently.

As a results, low-income children miss more days of school and are less prepared to learn when they do attend, making the relationship of food intake, health status, and learning far more poignant than previously understood.  Further exacerbating this interactive impairment of young bodies and minds are behavioral and emotional outcomes that accompany food deprivation.  Poorly nourished children have significantly higher rates of emotional problems, mental disorders, and withdrawn or disruptive behavior…

…Food deprivation is associated with considerable psychological and emotional distress in children.  In controlled studies, low-income children from households with inadequate food were more likely to exhibit impaired psychosocial functioning, including higher levels of anxiety, irritability, hyperactivity, and aggression.  In a national sample, children from food-deprived households manifested significantly higher levels of aggressive and destructive and withdrawn behavior.  Related outcomes apparently extend into the teenage years as well.  Two studies have shown that food-insufficient teenagers are more likely to have no friends and to exhibit both depressive disorders and suicidal behaviors.  Such efforts, not surprisingly, seem to be expressed in the educational environment as well.  Hungry children are much more likely to have had mental health counseling and to require special education services.

Nutritional status and cognitive function in children are strongly linked.  Children from food-insufficient households do not perform as well on academic achievement tests as do food-sufficient children.  In some studies, hungry children not only have higher rates of lateness and absence but also are more likely to have to repeat a grade in school.  For example, in two national studies of elementary school children, household food hardships were negatively correlated with school test results and achievement test results.  In another national study of kindergartners, children from food-deprived households not only entered school less prepared to learn mathematics but also learned less over the course of the year.

Food deprivation impairs cognitive function.  In a nutrient-deprived state, the body allocates energy (a) first to critical organ function, (b) then to height and weight gain, and (c) then to the role of the nervous system in one’s interaction with the environment, including listening to parents, dealing with peers, and learning.  If there is insufficient energy to enable a child to carry out the latter activities, cognitive dysfunction results.  Children from hungry and food-insecure homes are more likely to repeat grades, be absent or late, and be suspended from school.  The public health and economic implications of all this evidence are significant.

In general, low-income families know what constitutes a nutritious diet as well as the rest of the population.  Because limited income constrains their purchasing choices- for example, fresh fruits and vegetables typically are too expensive for them- their intake of required nutrients is significantly lower than both the Recommended Dietary Allowances (RDAs) and that of the general population.

Pregnancy is a period of significant risk from dietary inadequacy because a woman needs nutrient energy not only for herself but also fro the growing fetus.  Stores of maternal nutrients may be depleted, and maternal anemia can be one consequence.  The primary risk is borne by the fetus, including presmaturity (birth at less than 37 weeks’ gestation) and low birth weight (less than 2500 grams, or approximately 5.5. pounds).  Infants born too early of too small, or both, are not well equipped for extrauterine life.  Sequelae include respiratiory distress syndrome, weakening of the immune system, and long-term developmental problems.  The most paramount threat, however, is death, because low birth weight infants account for 75 percent of deaths to infants the first month of life (neonatal deaths).

David S. Wendler is Head, Unit on Vulnerable Populations, in the Department of Bioethics at the NIH Clinical Center. His work focuses on the ethics of research with individuals who cannot give informed consent. In his book, The Ethics of Pediatric Research, he looks at what appears to be an irresolvable dilemma: either we can protect pediatric subjects from exploitation, or we can protect pediatric patients from dangerous medicines, but not both. Wendler offers an original justification for pediatric research based on an in-depth analysis of when it is in our interests to help others. In the excerpt below we learn the history of pediatric research constraints.

The early history of pediatric research includes far too many examples of abusive research. One account maintains that: “The history of pediatric experimentation is largely one of child abuse.” In addition, many of the abuses cited by Henry Beecher in his famous 1966 article listing research abuses at prominent institutions in the United States included children, and a number of these studies focused on children specifically. Pappworth also cites many abusive studies involving children. There is inevitable debate over whether one or another of the cited examples in fact involved abusive research. What options did the children have? How are those options relevant to the appropriateness of the study in question? What impact did the study in fact have on the participating children?

Bracketing these questions, which largely are of historic interest, it is clear that many instances of unethical and abusive studies have occurred in the history of pediatric research. One of the earliest recorded cases of abuse occurred in 1892 when Albert Niesser, a medical professor at Breslau, gave serum taken from syphilis patients to unwitting individuals. Several of the recipients contracted syphilis, leading to public outcry and a government ruling, promulgated in 1900 and codified in the 1931 German guidelines, resulting in perhaps the first systematic regulations governing clinical research. These guidelines explicitly prohibit nonbeneficial research with children, as well as pediatric research that “in any way endangers the child.” It is difficult to imagine a research study that does not pose some risks to participating children. Seemingly innocuous surveys of health behavior, for instance, pose some chance of upsetting children. Even widely accepted pediatric research that offers a compensating potential for clinical benefit poses some chance of harm. In practice, then, these guidelines may prohibit essentially all pediatric research.

The German ruling of 1900 is one instance among many in which research guidelines were developed in response to a specific scandal. Most famously, in response to the horrific experiments perpetrated by the Nazis, the Nuremberg Code stipulates that participants’ consent is “essential” to ethical research. This approach, even more so than the German guidelines of 1931, appears to prohibit essentially all research with children. There is an obvious and very important virtue to this approach. If children are prohibited from being enrolled in clinical research, it will be difficult for investigators to exploit them in that context.

By the 1960s, increasing sentiment indicated that the Nuremberg Code needed to be modified in several important respects, especially to address the fact that it did not include a requirement that clinical research studies should be reviewed and approved by an independent ethics board. This requirement was included in the Declaration of Helsinki, promulgated by the World Medical Association in 1964, and intended to address the shortcomings in the Nuremberg Code. The Declaration of Helsinki also is based on recognition of the short-comings of attempting to protect individuals who cannot consent by excluding them from clinical research. This approach protects individuals in the short term but dramatically undermines investigators’ ability to identify better medical treatments for these groups. The Declaration of Helsinki attempts to protect individuals who cannot consent without excluding them from the potential benefits of clinical research by allowing them to be enrolled in clinical research based on the permission of an appropriate surrogate. This clause allows the enrollment of children in clinical research based on the permission of a legal guardian, typically the child’s parents.

The abuses perpetrated as part of the famous Tuskegee syphilis study were made public in 1972, 40 years after the study was initiated. The resulting outcry led to the formation of the U.S. National Commission, which was charged with evaluating the ethics of clinical research with humans and developing recommendations regarding appropriate safeguards. As part of its deliberations, the National Commission spend a good deal of time considering whether it can be acceptable to expose children to research risks for the benefit of others. These deliberations resulted in an entire volume dedicated to the ethics of pediatric research, including what are still some of the most important writings on the topic. These deliberations also produced a series of recommendations for the conduct of pediatric research, which became the framework for the existing U.S. regulations for research with children, one more instance in which scandal led to new regulations for clinical research.

Current Regulations

National regulations governing human subjects research are relatively recent. The U.S. federal regulations for clinical research are not yet 30 years old…

Unlike the early German regulations and the Nuremberg Code, current research regulations around the world attempt to allow important pediatric research while still protecting pediatric research participants. They try to achieve this balance by mandating specific safeguards, especially safeguards concerning risk level. The National Commission argued, and the framers of the U.S. regulations agreed, that what I am calling nonbeneficial pediatric research can be acceptable provided the risks are sufficiently low and several other safeguards are satisfied, including independent review and approval, and permission of the child’s parent or legal guardian…

The U.S. regulations, unlike most other regulations around the world, allow nonbeneficial pediatric research of greater risk in two circumstances. Review boards can approve nonbeneficial pediatric research when the risks are greater than minimal provided they are no more than a “minor” increase over minimal and several additional safeguards have been satisfied. In addition, the Secretary of the Department of Health and Humans Services (DHHS) may approve research that poses risks too great for review board approval following review by a panel of experts. In principle, if not in practice, these regulations would allow approval of nonbeneficial pediatric research that posed risks substantially higher than those average, healthy children face in daily life…

Dana C. Jack, EdD is Professor at Fairhaven College of Interdisciplinary Studies/ Western Washington University.  Her research examines women’s depression and anger in the U.S. and internationally, and qualitative research methods.  Alisha Ali, PhD is an Associate Professor in the Department of Applied Psychology at New York University.  Her research examines social influences on women’s depression, including the effects of emotional abuse, racism, and harassment.  Together, they edited Silencing the Self Across Cultures: Depression and Gender in the Social World.  The book offers evidence regarding why women’s depression is more widespread than men’s and why the treatment of depression lies in understanding that a person’s individual psychology is inextricably related to the social world and close relationships.  In the excerpt below, from the introductory essay by Jack and Ali, we learn about the Silencing the Self theory (STS), which details the negative psychological effects when individuals silence themselves in close relationships and how the authors created a scale to measure silencing in patients.

…STS theory is based on a longitudinal study of clinically depressed women’s descriptions of their experiences…, including their understanding of what led up to their depression.  The women detailed how they began to silence or suppress certain thoughts, feelings, and actions that they thought would contradict their partner’s wishes.  They did so to avoid conflict, to maintain a relationship, and/or to ensure their psychological or physical safety.  They described how silencing their voices led to a loss of self and a sense of being lost in their lives.  They also conveyed their shame, desperation, and anger over feelings of entrapment and self-betrayal.

Though this process feels personal to each woman, it is in fact deeply cultural.  A male-centered world tells women who they are or who they should be, especially in intimate relationships.  Self-silencing is prescribed by norms, values, and images dictating what women are “supposed” to be like: pleasing, unselfish, loving.  As I (Dana Jack) listened to the inner dialogues of depressed women, I heard self-monitoring and negative self-evaluation in arguments between the “I” (a voice of the self) and the “Over-Eye” (the cultural, moralistic voice that condemns the self for departing from culturally prescribed “shoulds”).  The imperatives of the Over-Eye regarding women’s goodness are strengthened by the social reality of women’s subordination – the experience of being a target of male violence, and the difficulties of financial dependence and poverty.  Women’s inner arguments about how they should act and feel revealed a divided self that results from self-silencing in an attempt to preserve relationships.  Inwardly, they experienced anger and confusion while outwardly presenting a pleasing, compliant self trying to live up to cultural standards of a good woman in the midst of fraying relationships, violence, and lives that were falling apart.

As I followed the negative self-evaluation (words like “no good” and “worthless”) in their narratives, it became clear that women’s self-judgment and behavior were guided by specific beliefs about how they should act and feel in relationships.  When followed, these self-silencing relational schemas create vulnerability to depression by directing women to defer to the needs of others, censor self-expression, repress anger, inhibit self-directed action, and judge the self against a culturally defined “good woman.”  In tandem with women’s wider social inequality, such beliefs can keep a woman entrapped in negating situations as she blames herself for the problems she encounters.

In order to measure self-silencing, I designed the Silencing the Self Scale…., a 31-item self-report instrument.  The STSS reflects the components of relational schemas held by depressed women.  The statements that comprise the scale came directly from the narratives of clinically depressed women, yet are gender neutral.  Respondents endorse each statement on a 5-point scale ranging from strongly disagree to strongly agree.  Four rationally derived sub-scales measure the relational schemas central to self-silencing, and each is understood as an interrelated component of the overall construct.  The subscales are considered to reflect both phenomenological and behavioral aspects of self-silencing:

1. Externalized Self-Perception assesses schema regarding standards for self-judgment and includes the extent to which a person judges the self through external standards.  For example, item #6 reflects seeing the self through others’ eyes: “I tend to judge myself by how I think other people see me.”  The last sentence on the STSS, item #31, reads, “I never seem to measure up to the standards I set for myself.”  Immediately following this item, the questionnaire instructs, “If you answered the last question with a 4 or 5 [agree or strongly agree], please list up to three of the standards you feel you don’t measure up to.”  This allows for continuing investigation  concerning the standards depressed individuals use to judge the self, including gender- and culture- specific standards.

2. Care as Self-Sacrifice measures the extent to which relationships are secured by putting the needs of others ahead of the needs of the self.  For example, if a women strongly endorses item #4, “Considering my needs to be as important as those of the people I love is selfish,” then that belief directs her vision of the hierarchy of needs within relationships; it guides behavior by directing how she should choose when her needs conflict with those of others she loves; and it provides a standard for negative self-judgment if she veers from its command.  Further, it can arouse anger as, following its dictates, she places her needs second to those of others, yet it also commands the repression of anger by purporting a moral basis for the suppression of her own needs.  It reinforces a woman’s low self-esteem by affirming that she is not as worthy or important as others, and finally, it legitimizes the historical and still prevalent view of women’s nature as essentially self-sacrificing and maternal…

3. Silencing the Self assesses the tendency to inhibit self-expression and action in order to secure relationships and to avoid retaliation, possible loss, and conflict.  Item #8 which is reverse-scored, reads, “When my partner’s needs and feelings conflict with my own, I always state mine clearly.”  The items in this subscale measure both behavioral and phenomenological aspects of self-silencing, as in item #30: “I try to bury my feelings when I think they will cause trouble in my close relationship(s).”

4. Divided Self measures the extent to which a person feels a division between an outer “false” self and inner self resulting from hiding certain feelings and thoughts in an important relationship.  In women, it appeared that the false self was characterized by a mode of relating through compliance to the partner’s wishes, and that the feelings hidden were oppositional or angry, challenging ones, as in item #16: “Often I look happy enough on the outside, but inwardly I feel angry and rebellious.”

The STS was validated in three groups of women in radically different settings: undergraduate women, mothers who abused drugs and were caring for young children, and a battered women’s shelter group.  Results demonstrated not only that STSS scores correlated with scores on the Beck Depression Inventory but also that STSS means varied with contexts in predicted ways.  Participants’ means in the three groups of women varies signifigantly from each other, with self-silencing highest among residents at battered women’s shelters, intermediate among mothers who abuse drugs, and lowest among undergraduate participants.  Across subsequent investigations, higher levels of self-silencing have been found to be associated with variables representing inequality, oppression, and other threats to self and relationships…

Bruno G. Breitmeyer, is a Professor of Psychology at the University of Houston.  In his new book, Blindspots: The Many Ways We Cannot See, we move from cataracts and color blindness through blindsight, acquired dyslexia, and visual agnosias.  Breitmeyer uses what we’ve learned about the limits of our sight to illustrate the limits of our ability to mentally visualize and our ability to reason, covering everything from logical fallacies to how our motives and emotions relentlessly color the way we see the world.  In the excerpt below we learn about one kind of blindness, caused by Vitamin A deficiency.

Even if we are blessed with caring parents and a stimulating environment during infancy and childhood, uncontrollable environmental factors can cause or promote visual deficits in an otherwise healthy visual system.  Imagine the following.  It is March of 1797.  You are a settler living in the subarctic wilds near Hudson Bay in present day Quebec, Canada.  Your crop of winter squash was nipped in the bud by the early onset of the harshest winter you have yet experienced.  It lingers into spring, by which time you have depleted your larder’s store of dried halibut and Arctic cod.  For some time your dietary mainstay has been nothing but the wild rice and the dwindling rations of dry beans you purchased late last fall.  Although high in carbohydrates, protein, and several of the B vitamins, these foods do not support your dietary needs for Vitamin A.  You have noticed some minor visual problems during your daytime activities; however, at night, your vision has deteriorated dramatically to the point where you do not dare to leave the immediate vicinity of your dwelling.  You are wondering whether or not you are suffering from some kind malady that will leave your vision permanently impaired.  By July, after you have feasted on plenty of fish harvested from the bay and on ripe berries gathered in the wild, you are relieved to find your vision has returned to normal.  Although you could not have known it, you were suffering from avitaminotic nyctalopia, a type of night blindness, during the prior winter.  It was caused by a prolonged (but fortunately temporary) vitamin A deficiency in your diet.

Vitamin A is known to play an important role in the regeneration of the rod photopigment, rhodopsin.  Rhodopsin molecules are “bleached” when they react with photons of light, rendering them inert to further stimulation by light.  If, due to a chronic dietary Vitamin A deficiency, bleached rhodopsin molecules are not restored to their prior unbleached photoreactive state, nocturnal vision eventually deteriorates to dysfuctional levels.  Epidemics of such night blindness have been known to occur in regions where the availability of plants or animal food sources containing vitamin A was drastically reduced.  For example, it have been common in parts of Southeast Asia where rice is the staple food.  Fortunately, avitaminotic nyctalopia can be readily treated by increasing dietary vitamin A.

However, dietary night blindness can occur even when food sources rich in vitamin A are plentiful.  Imagine the next sad scenario.  You have been a closet alcoholic for several years.  Besides the spider angianomas that give the tip of your nose a ruddy and friendly glow, you recently have noticed an increase of fatigue, an intolerable itch has been building up in your torso and arms, and you no longer wear your favorite pair of boots due to the swelling of your ankles and lower legs.  In addition, you have noticed that you have difficulty driving at night – even when you are sober.  Troubled, you go to your doctor and are diagnosed with cirrhosis of the liver.  What you did not know is that vitamin A deficiencies can result from this disease, as well as from other liver diseases such as hepatitis, and that night blindness can be a symptom of it.  Like avitaminotic night blindness, it too can be treated.  However, since the effects of cirrhosis are not reversible, you must treat your night blindness with (massive) daily doses of vitamin A to compensate for the permanent loss of normal liver function, recalling with regret a wise saying you read years ago: Rum makes for a great servant, but a bad master.

Julio Torres, Intern

Carol S. North and Sean H. Yutzy edited the sixth edition of Goodwin and Guze’s Psychiatric Diagnosis, which provides an overview of major psychiatric disorders, covering the definition, historical background, epidemiology, clinical picture, natural history, complications, family studies, differential diagnosis, and clinical management of each disorder.The excerpts bellow recount the place in history of panic disorders and phobias, and hysteria —what’s fascinating about both histories is the cultural emphasis in women as bearers of these disorders.  In both cases, earliest observations (even in their most primitive, often inaccurate form) dealt almost exclusively with women and were constantly paired with superstitions of the time. The trend articulates the phenomenon of sexism in early psychological research.

Panic Disorder and Phobias

My cheek is cold and white, alas!

O lift me from the grass!

I die! I faint! I fall!

…

My check is cold and white, alas!

My heart beats loud and fast.

Percy Bysshe Shelley,

The Indian Serenade

It has been suggested that Shelly was having a panic attack when he wrote these lines. If so, he probably would have called it something else. In the nineteenth century, “anxiety reactions’ referring to fainting—which was fashionable among women in the era—were called “vapors.” Modern patients with panic disorder also sometimes faint—probably from hyperventilating. In Victorian times the prototype of a refined young woman was a “sooner, pale and trembling, who responded to unpleasant or unusual situations by taking to the floor in a graceful and delirious maneuver, in no way resembling the crash of an epileptic”… A Jane Austen heroine found one social situation “too pathetic for the feelings of Sophie and myself. We fainted alternately on a sofa.” Overly tight corsets may have been responsible for some of the fainting. A nineteenth-century physician, Dr. John Brown, cured fainting by “cutting the stay laces, which ran before the knife and cracked like a bow string”…

One of the first medical terms to describe anxiety disorders was “neurasthenia,” defined by an American physician, G.M. Beard, in 1869… Neurasthenia broadly included patients with hysteria, obsessional illness, and anxiety disorders, as well as hypochondriacs and swooners… The term “anxiety neurosis” was first used by Freud in 1895. It was not until 1980 that the concept of neurosis was dropped form American Psychiatric Association general nomenclature, and the term “panic disorder” replaced the older term “anxiety neurosis” as the disorder’s official name… Panic disorder was later subdivided into two types, with and without agoraphobia…, a distinction that still holds today.

The term phobia originates from the name of a Greek god, Phobos, whose likeness was painted on masks and shields for the purposes of frightening the enemy… The word phobia first appeared in medical terminology in Rome 2,000 years ago, when hydrophobia was used to describe a symptom of rabies. Hippocrates also described cases of phobic fears.

During the nineteenth century, the term phobia appeared increasingly in descriptions of morbid fears, beginning with syphilophobia, defined in a medical dictionary published in 1848 as “a morbid dread of syphilis giving rise to fancied symptoms of disease.” Later authorities compiled a long list of phobias, naming each Greek and Latin terms after the object or situation feared. Thus, as Nemiah pointed out, “the patient who was spared the pangs of taphaphobia (fear of being buried alive) or ailurophobia (fear of cats) might yet fall prey to belonphobia (fear of needles), siderodromophobia (fear of rail-ways) or triskaidekaphobia (fear of thirteen at table), and pantaphobia was the diagnostic fate of that unfortunate soul who feared them all”…

Somatization Disorder (Hysteria)

The concept of hysteria, which probably originated in Egypt, is at least 4,000 years old. The name hysteria has been in use since the time of Hippocrates. The original Egyptian approach to hysteria was perhaps the most fanciful. Believing that physical displacement of the uterus caused the varied symptoms; physicians treated the patient by trying to attract the “wandering uterus” back to its proper site. Sweet-smelling substances were placed in the region of the vagina to attract the errant organ; unpleasant materials were ingested or inhaled to drive it away from the upper body…

Although Egyptian and Greek physicians applied the diagnosis whenever they believed that unusual symptoms were caused by a displaced uterus, the available records do not provide explicit diagnostic criteria. This state of affairs persisted, although various speculations about pathogenesis have been offered over the centuries… In particular, witchcraft, demonology, and sorcery were associated with hysteria in the Middle Ages… Mysterious symptoms, spells, and odd behaviour were frequently considered manifestations of supernatural, evil influences. Hysterical patients were sometimes perceived as either the active evil spirit (witch, sorceress, or demon) or as the passive victim of such an evil being, Since the Middle Ages there have been speculations of many kinds about the cause of hysteria. Such speculations have included ideas about neurological weakness, neurological degeneration, the effects of various toxins, and disturbances of what Mesmer called “anima magnetism.”

Hysteria became Freud’s central concern during the early years of psychoanalysis … That interest had developed while Freud was working in Paris with Charcot, who was treating hysteria with hypnosis. The psychoanalytic concept of conversion was an ego defense mechanism, referring to unconscious conversions of “psychic energy” into physical symptoms, ultimately led to the identification of conversion symptoms with hysteria in a psychoanalytic practice. Many psychoanalysts considered hysteria a simulation of illness designed to work out unconscious conflicts, partially through attention-getting and “secondary gain,” a term that refers to the possible advantages of illness such as being sympathy and support, including financial support, from relatives and friends and being excused from various duties…

Health Behavior Change and Treatment Adherence: Evidence-based Guidelines for Improving Healthcare, by Leslie Martin, Kelly Haskard-Zolnierek and M. Robin DiMatteo, synthesizes the results from more than 50 years of empirical research, resulting in simple, powerful, and practical guidance for health professionals who want to know the most effective strategies for helping their clients to put long-term health-relevant behavior changes into practice.  In the original post below, Leslie Martin Professor of Psychology, LaSierra University., looks at Michelle Obama’s fight against obesity.

Michelle Obama is taking on America’s obesity problem—starting with kids. But health behaviors are notoriously difficult to change, and food-related modifications are especially challenging because they require adjustments in an area that we are forced to encounter multiple times each day. Going “cold turkey” from food is simply not possible—we have to eat! And exercise—well, we don’t have time, it’s not fun—the excuses come easily. Michelle, along with the rest of us, needs some tools with which to address this obesity problem.

While not magical, the three-factor model is both simple and powerful. A review of decades of research on adherence and health behavior change reveals that three components must be in place in order for individuals to successfully adopt and maintain the healthy behaviors to which they aspire. First, people must have information—they have to really understand what it is that they need to do, and why. Second, people must be motivated—they have to want to make the change (sometimes this stems from a good understanding of their medical issue and the repercussions associated with failing to make changes, but there are many other potent motivators). Third, people need strategies—barriers will be encountered and obstacles will arise, so plans must be in place for dealing with these. Making healthy behavior rewarding in the short term, even if the ultimate goal will take much longer to accomplish, is also an important strategy; and many others, all solidly grounded in empirical research, are outlined in our book.

The Information-Motivation-Strategy model is relevant to a whole host of health behaviors, not just weight management. It emphasizes the pivotal role that provider-patient communication plays at each stage in the process and recognizes that there is no single strategy that works for everyone—instead tailored, multifaceted approaches work best. Despite its strengths, there is nothing high-tech or expensive about the IMS model, which makes it especially compelling as we strive to improve the quality and efficiency of our healthcare systems.

David E. Klein is Associate Chair and Associate Professor, Department of Politics, University of Virginia. Gregory Mitchell is Professor of Law and E. James Kelly, Jr.-Class of 1965 Research Professor, University of Virginia School of Law. Together they edited, The Psychology of Judicial Decision Making, which is part of the American Psychology-Law Society Series. The book maps ways of incorporating key concepts and findings from psychology into the study of judging. Together the essays will foster a better understand how judges make decisions, and open new avenues of inquiry into influences on judicial behavior. In the excerpt below, from the introduction, we learn a little about why combining the study of law and psychology is beneficial.

Over the years, psychologists have devoted uncountable hours  to learning how human beings make judgments and decisions.  Legal scholars and political scientists have expended immeasurable intellectual energy trying to understand why those particular human beings who sit on courts act as they do in presiding over and deciding cases.  It might seem obvious that fertile intellectual ground lies at the intersection of these disciplines, and certainly some scholars have seen it this way.  As far back as 1930, Jerome Frank drew on contemporary psychology to explain judging in his Law and the Modern Mind. And yet, nearly eighty years on, the area under active cultivation is quite small.  To be sure, psychological concepts crop up in studies of judicial behavior from time to time, but it would be difficult to name a score of published studies that have relied extensively on current ideas and evidence in psychology to generate major theoretical propositions about judging.  This is party because students of judicial behavior traditionally have not engaged deeply with scholarship in psychology, but only partly; it is also the case that psychologists have tended not to focus on the kinds of questions that would be most helpful for understanding what professional judges do….

The study of judicial decision making has indisputably made great strides in recent years, through the labors of hundreds of scholars from political science, law, economics, and other disciplines.  Nevertheless, one could argue that there remains a lack of both depth and breadth to our understanding of what judges do. Even where scholars can make consensual and successful predictions of a judge’s behavior – for example, that Justice J will vote for the conservative position in case C – they will often disagree sharply about exactly what happens in the judge’s mind to generate the predicted result.  (Does Justice J vote conservatively in a conscious effort to further his policy preferences, in an unconscious effort to do so despite a sincere desire to be guided by legal texts, or as a result of a method of interpretation that is independent of his ideology?)  And as soon as we move beyond ideology, we enter areas where good predictions are much harder to come by.  How will a judge’s decision on a motion, verdict, or appeal be affected by precedents, the presence of an amicus curiae brief or oral argument by the defendant’s attorney, the preferences and arguments of other panelists on a collegial court, the opinions of the local bar, the presentations of expert witnesses, other demands of the judges’ time?  Why will it be affected that way?  Some of these questions have been the subject of excellent scholarly analysis, but none have received definitive answers.

Naturally, various methodological difficulties unrelated to psychology have hindered attempts to study judging, and as scholars devise creative new ways to measure previously intractable concepts, observe hidden behaviors and influences, and design studies so as to control for more confounding factors, our understanding of judging will continue to improve.  Still, anyone who has ever tried to choose fairly between serious competing legal arguments must have been struck by the depth, complexity, and mysteriousness of the mental processes involved in the evaluation.  It is hard to see how we can hope to achieve a profound understanding of the far more complex and difficult undertaking we call judicial decision making without a close analysis of these underlying mental processes.

Thinking about the intersection of psychology and judicial decision making can do more than help us answer questions that have long troubled scholars; it can also point us toward equally exciting but less explored questions.  To give just a few examples: What does it mean to judge well?  Are some circumstances, personalities, or cognitive styles more conducive to good judging than others? Do most judges posses special reasoning skills that other people lack?  Do judges care what other people think about them, and, if so, how does this affect their decision making?  When different motivations come into play at the same time, which have the most influence on judges’ behavior, and why?…

Anthony D. Pellegrini is Professor of Educational Psychology at the University of Minnesota.  His book, The Role of Play in Human Development, examines the role of different forms of human play in terms of its phylogenetic history, its ontogenetic development, and possible functions, suggesting that human play represents one way in which experience shapes development.  In the excerpt below we learn about the importance of imaginary play.

The transition from solitary to social pretend play is a hallmark of the preschool period, reflecting children’s relatively sophisticated social cognitive and linguistic development… because social pretend play involves, by definition, the communication and coordination of abstract meaning between people, the possibility for ambiguity and the subsequent breakdown of social interaction around a pretend theme is relatively high.  This state of affairs is why social pretend play has been afforded such an important role in the ontogeny of children’s theory of the mind (e.g., Leslie, 1987).  With both social pretend play and theory of mind, children are concerned with others’ intents and beliefs.  Also in both theory of mind and social pretend play research, the role of the close adult-child relationship, such as the mother-child relationship, is central to children’s developing ability to understanding others’ intentions…

There is also a very good biological reason for mothers to spend time in joint interaction with their infants and children.  Mothers are “motivated” to spend time and energy on their offspring because they represent a major genetic investment.  Her offspring contain 50% of her genes, and the mother wants to maximize the survival and reproduction of her offspring, and her genes… Therefore, mothers not only invest in protecting and provisioning their offspring, but also in tutoring them in the skills necessary to maximize the offspring’s survival and reproduction.  Mother-child playful interactions are part of this process…

The offspring, too, have an interest in maintaining a close relationship with their mothers, providing their mothers are responsive to their needs.  That is, offspring depend on mothers for protection and provisioning, and they try to maximize the resources they extract from their mothers… This dynamic relationship of interdependence is enacted in the mother-child attachment relationship.  This relationship is developed in social pretend play and forms an important base of children’s representations of other social relationships.  This developmental progression has been documented in a series of studies by Carolee Howes (1992) and her students.  According to Howes, children’s social pretend with mothers begins at around 12 to 15 months of age when children take pretend play actions outside their functional context (i.e., decontextualization), such as pretending to drink from an empty cup.  In a mother-child interaction context, mothers will structure pretend scenarios to maximize children’s participation…, because the child is now capable of responding to its mother’s pretend initiations, often by watching, complying with, and imitating those acts.  To maximize children’s participation, mothers monitor their children’s behavior closely, being particularly vigilant around pretend behavior; they look at children closely and smile after children’s pretend play acts…  In this way children learn to recognize pretend play actions as distinct from non-pretend interactions, and they also come to realize the value of this sort of behavior in social interactions.  Mothers may also “correct” a child’s inappropriate response.  For example, if a child does not respond to the offer of a cup of tea, the mother might ask, “Aren’t you thirsty?”

By contrast, if this same decontextualized play act were initiated in the presence of a peer, there would be a lower likelihood that it would elicit a response.  If there was a response from a peer, however, it would probably take the form of the peer looking or smiling at the child, or imitating the actions…, not extending it as done by the mother.  In other words, peer play partners are expressing an interest in the play initiation, but they may not have the skills to extend the interaction more explicitly like adults do.  Even if this rather low level of interest is expressed, however, children come to recognize that pretend acts have social value (i.e., they are reinforced) and will be likely to continue.

Between 16 to 24 months of age, and as discussed above, children’s pretend play acts become yet more decontextualized, to the extent that they are no longer centered on the child: Children’s pretend acts can be directed at another person…  In the presence of a peer, children of this age are more likely than younger children to try to enlist each other in pretending, and if successful, to enact, or imitate, pretend acts similar to the initiation…, though children’s relatively low social cognitive and linguistic skills limit the degree to which pretend play can be extended beyond this rudimentary level.  For example, Child A may initiate a pretend act in the presence of Child B, such as moving a car around the floor saying “Brrmmmmmmm.”  Child A looks at Child B when this is completed and recruits Child B by handing over the toy car, and Child B then moves it across the floor, too…

By the end of their second year of life, children’s pretend play acts become more integrated into longer behavioral scripts with both their mothers and their peers.  In the mother-child dyad, it is not infrequently the case that the child initiates a script, such as changing a doll’s diaper.  Mother typically supports and extends these actions with prompts more for detailed enactments; for example, “Do we have more diapers?”  “How do you know she needs to be changed?”  Finally, at the end of this period, mothers encourage children’s independent pretend play…

…Important for the development of young children’s symbolization-processing involved in both pretend play and language is the realization that their imitations of adults’ actions and language can be used to solve social problems.  Thus, they recognize that adults are using gestures and vocalizations to get something done (i.e., recognizing adults’ intentions), and they use those same strategies to attain a goal.  Children come to realize that adults use symbols, language, and gestures to direct their attention.  Tomasello and colleagues… label this cultural learning.  Correspondingly, by the second year of life, children recognize adults’ intentionality when adults and peers extend children’s ability to understand that others have different views of situations and symbols than they do.

These descriptions of mother-child interaction in pretend play are also similar, at a general level, to that proffered by attachment theory, such that securely attached children and their mothers interact in a synchronous fashion.  The evolutionary roots of attachment theory, of course, provide an explanation to the motivation question.  Mothers and children alike are motivated to maximize children’s survival.  Building on this, I suggest a more differentiated, behavioral ecological, explanation for mothers’ willingness to invest in her children.  Recall, mothers would be more willing to invest in their children, and consequently spend more time interacting with their children and at more intensive levels, in ecologies that are relative abundant.  In this sort of niche it pays off, in terms of inclusive fitness, to invest more resources in fewer children… In less abundant and more severe ecologies, mothers try to maximize fitness by investing less in individual children and maximizing the number of offspring.  The result of each of these strategies translates into children being securely and insecurely attached, respectively.  Each attachment style, in turn, impacts the way in which children interact with their peers.

Julio Torres, Intern

George J. Annas is William Fairfield Warren Professor at Boston University, Chair of the Department of Health Law, Bioethics and Human Rights at Boston University School of Public Health, and professor in the Boston University School of Law. In his book, Worst Case Bioethics: Death, Disaster and Public Health, Annas explores how fear of worst case scenarios impacts bioethics through examples ranging from healthcare to bioterror. In the excerpt bellow, Annas dissects the former by means of analyzing metaphors and how they inform and impact the American healthcare phenomenon.

The first thing most Americans think about healthcare is not death and disaster. We’re good at denial. Nonetheless, the fragmented non-system we use for healthcare is based primarily on responding to the life-threatening risks of death. It is focused on saving lives and curing or stabilizing diseases, and only secondarily on disease prevention or improving quality of life. Nor is it not just death prevention at the end of life; death, in the form of risks, underlies medicine from the point of view of both patients and physicians from the moment of birth, even from the moment of conception. Death is personal; disasters affect populations. It is not uncommon to portray American healthcare itself as a disaster. At least since World War II, we have sought to reform a system that is itself widely viewed in disaster imagery, perhaps the most popular being that out healthcare system is a “train wreck.”

A good example is President Lyndon Johnson’s response to what he described as the “bombshell” Medical proposal to go along with his proposed Medicare plan. He explained his support for both proposals to Wilbur Cohen, the person who would take the lead in drafting them (with Wilber Mills) for his administration. He told Cohen the story about the railroad giving an intelligence test for switchmen. The question was:

“What would you do if a train was coming east going sixty miles per hour, and you looked over your shoulder and another one was coming the west going sixty miles an hour?” …and the fellow said, “I’d go get my brother.” And he said, “Why would you get your brother?” And he said “Because he hasn’t ever seen a train wreck.”

The image of a train wreck can be used to mobilize action, but train wreck imagery can be overwhelmed by other metaphors mobilized to resist reform. As I write this chapter, the House and Senate have each reported bills out of committee, but have yet to debate them. President Obama is committed to increasing health insurance access for Americans, but the longer he and his allies delay endorsing a specific plan, the less likely its success becomes, because financial stakeholders in present system will have time to find ways to frustrate meaningful reform.

Lawrence Brown has suggested that the metaphor blocking health reform to date is the “safety net,” which includes emergency departments and community health centers, because this imaginary net is seen as protecting even the uninsured from major health disaster. Similarly, William Sage has observed that we have yet to identify a health systems metaphor with traction. Metaphors referencing two struggling American industries, automobiles (“So you want Chevrolet or Cadillac coverage?”) and airlines (as a metaphor for patient safety), have, for example, failed to capture the public’s imagination.

Shortly after the demise of President Bill Clinton’s healthcare plan, I suggested that both the military and the market metaphors in American medicine had become counterproductive, and that they should be replaced by the ecological metaphor. This has not happened (at least not yet), and the Obama administration has continued to cling to the mast of the Clinton’s 1993-94 framing of the healthcare financing reform debate as shipwreck again threatens us. Of course, it is not just a replacement metaphor we need, but one that can help us confront and modify the major characteristics of American healthcare.

The inspiration for American healthcare is perhaps best embodied in Damien Hirst’s 2007 diamond-encrusted platinum human skull. The skull was cast from that of an 18th-century man; the original teeth are retained and the skull is coated with 8,600 diamonds. Hirst calls the diamond skull “For the Love of God” and says he was inspired by similarly jeweled Aztec skulls. As a metaphor, the skull displays all four of what I take to be the most enduring and problematic characteristics of American healthcare (and that of America itself): it was wasteful, technologically driven, individualistic, and death-denying. Nonetheless, skulls are not inspirational, even diamond frosted one, and this one has a strange allure that may subvert rather than promote reform. We need a plan more than we need a metaphor, but a plan without a metaphor is unlikely to be politically (or even economically) viable. What should it be?

Martin Benjamin is Professor Emeritus of Philosophy at Michigan State University.  Joy Curtis, R.N., is Professor Emerita of Nursing and Ombudsman Emerita at Michigan State University.  Together they wrote, Ethics in Nursing: Cases, Principles, and Reasoning, 4th edition.  The book provides a useful introduction to the identification and analysis of ethical issues that reflects both the special perspective of nursing and the value of systemic philosophical inquiry.  In the post below we learn about the history of the nurse-doctor relationship.

During the earliest period of nursing history, nursing and medicine developed independently and had little contact until recognition of the medical value of bedside nursing brought them together in the late nineteenth century.  With the development of the modern hospital came the introduction of the trained nurse, and patters of relationships in hospitals developed that affect current nurse- physician relationships.  Physicians developed the medical staff, but as a part of that staff, they were not employed by, subordinate to, or responsible to the hospital administration.  Physicians could and did, however, issue orders directly to nurses.  The nursing staff’s position was quite different from that of the medical staff.  Nurses were employed by, subordinate to, and directly responsible to the administration.  Thus, nursing developed under the dual command of physicians and hospital administrators.  The two lines of authority severely limited and complicated the decision-making role of a hospital nurse.

The Nightingale plan for nursing schools, which included instruction in both scientific principles and practical experience, appeared in the United States in 1873.  Unfortunately from American nursing, the schools had no endowment or financial backing, and hospitals quickly seized the opportunity to gain inexpensive student nurse labor.  Nursing education was essentially an apprenticeship, and, as late as the 930s, student nurses received little formal instruction in some hospitals.

Under the dominance of male doctors and administrators, schools of nursing grew, and they were not noted for encouraging nurses to think critically and for themselves.  Students entered nursing schools already expecting that women would defer to men, and therefore, that nurses would defer to doctors.  Adding to the traditional subordination of nurses to physicians, nursing school faculties often culled out overly questioning and rebellious students.  The students’ socialization and education taught them to be deferential.  Many diploma schools included the study of textbooks such as L. J. Morison’s Steppingstones in Professional Growth, published in a revised edition in 1965, which tells the student to cultivate loyalty, prudence, willingness, and cooperation since the physician has the right to expect such qualities.  Further, the nurse must follow orders and uphold the physician’s professional reputation.  Expected by society and trained by the nursing school to act as subordinates, most nurses behaved acordingly.

Yet tradition and nursing education alone cannot be blamed for the dominance of physicians and the deference of nurses.  In the late 1970s, Beatrice and Philip Kalisch argued that a physician who seems himself as an independent, omnipotent man with mystical healing powers relates to coworkers as he does to patients and therefore insists that nurses and other health care providers serve him in his “so-called captain of the ship role.”

The relegation of nursing to the subordinate position in the nurse-physician relationship limited collaboration between the two professions.  Empirical studies showed that physicians were at the center of the decision-making process and that nurses carried out those decisions.  In 1968, psychiatrist Leonard Stein described nurse-physician relationships in terms of a doctor-nurse game in which a nurse must appear to be passive.  In this game any suggestion a nurse makes to a doctor must be masked in such a way as to seem as if it were his idea, and a doctor may not openly seek advice from a nurse.  The historical legacy of nurse-physician relationships, while affecting specific nurses and doctors in various ways, gives decision-making power to a doctor and requires passivity (or biting one’s lip) of a nurse.  If a nurse and physician deviate from this pattern, the exchange of information and recommendations must occur in such a way that the doctor still appears to lead, the nurse to follow.

A study published in 1985 reports, among other things, that the “doctor-nurse game” described by Stein nearly 20 years earlier was still being played.  A resident interviewed for the study commented:

I have seen nurses, who really knew a lot more than an intern, kind of gently guide him [the intern] into making the right decision…They make some very good decisions and make some very helpful suggestions sometimes..It is like trying to guide the ship without actually taking hold of the wheel…There are nurses who are good at that.

A nurse in the same study claimed:

You have to be careful whenever you talk to them [physicians] that you are not telling them what to do.  You have to talk to them in such a way that you are asking their opinion and work in what you want to say without being overbearing or threatening…make them think that the idea is partially in their mind too.

In 1990, Stein claimed most nurses had stopped playing the doctor-nurse game.  But the legacy of the traditional pattern of dominance and deference has continued.  In a 2005 study involving physicians’ and nurses’ perceptions of collaboration and communication, researches found a positive effect on those perceptions following three interventions: “institution of daily multidisciplinary rounds, addition of nurse practitioners, and appointment of a hospitalist medical director.”  Researches concluded, however, that “physicians reported improved collaboration with nurses, but nurses did not improved collaboration with physicians.”

The difference between physicians and nurses in their reports of a collaborative effort is striking.  Physicians may define or view collaboration in a different light than do nurses.  We did not specifically define collaboration for the survey, but it was distinct from communication on the survey.  Perhaps the physicians thought that collaboration implied cooperation and follow-through with respect to following orders rather than mutual participation in decision making.  Although communication is a necessary component, it alone is not sufficient to allow collaboration.  Possibly, communication styles differ between nurses and house staff, so that physicians perceive collaboration whereas nurses feel they (i.e., the nurses) are being ordered to do something.  A second possibility is that nurses did not feel comfortable “challenging” physicians by giving a different point of view.  Or, possibly the input the nurses gave was not valued or acted upon, and thus the interaction was not perceived by nurses as collaboration.

Until the relationship between doctors and nurses can be fully restructured so as to be more collaborative and morally egalitarian, nurses may still have to choose, on occasion between optimally serving their clients and playing the classic doctor-nurse game…

John C. Avise is Distinguished Professor of Ecology and Evolutionary Biology at the University of California, Irvine.  His new book, Inside the Human Genome: A Case For Non-Intelligent Design, tackles the philosophical question of why humans are imperfect on the genetic level if made by a Creator God.  In this excerpt, Avise asserts that evolution is not random (as Intelligent Design proponents argue) due to natural selection.

Advocates of Intelligent Design contend that complex biological features cannot arise by chance, the implication being that chance equates to sentient forces.  From a scientific vantage, however, the driving force of adaptive evolution–natural selection– is itself the antithesis of chance.  Hereditary factors that promote organismal survival and reproduction in a particular environment tend to be precisely those that proliferate across the generations and thereby come to characterize natural populations.  Whenever genetic variation and differential reproduction exist in nature (as they do in all known species), natural selection is inevitable, both logically and empirically.  Biological traits that emerge from this inexorable operation may have the superficial aura of intelligent artistry, but that appearance is illusory (under a scientific interpretation).  Natural selection can be a highly creative process (given a suitable supply of genetic variation to work from), but it is merely a mechanistic phenomenon– as inescapable and insentient as gravity.

This is not to say that evolution is devoid of important stochastic (i.e. chance) elements.  Natural selection can sift only among the genetic variants available for its scrutiny, and two of the three primary sources of genetic variability– de novo mutation and recombination– occur essentially at random with respect to forging adaptations.  The new mutations and recombinant genotypes that arise in each generation have no biased tendency to enhance either an individual’s genetic fitness (its reproductive success relative to other individuals) or the adaptive needs of a species.  In other words, favorable alleles and more fit genotypes have no known mutational tendency to arise disproportionately when needed.  In this important sense, the genetic fodder upon which natural selection acts can indeed be characterized as stochastic or chancy in origin.

The third source of population genetic variation entails a mixture of “chance and necessity.”  Apart from de novo mutations and recombinant genotypes, the genetic variety available for natural selection in any generation is also a function of historical circumstance, that is, of idiosyncratic genealogical outcomes that have been affected by both stochastic and directive evolutionary processes across all prior generations.  Evolution going forward can work only with the biological substrates–”ghosts of evolution past”– are not supernatural legacies, but instead they are real genetic lineages and real species that have been subjected for eons to the full panoply of evolutionary processes including natural selection (the directive agent of adaptive evolution) as well as idiosyncratic mutation, recombination, and genetic drift (stochastic forces in the sense described above).

The temporal nature of heredity also means that evolution is inherently a phylogenetic process, involving descent with modification.  So, for example, when two or more species share exquisite details in some complex biological feature (such as a long nucleotide sequence for a protein-coding gene), the usual evolutionary interpretation is that these species inherited copies of that trait from a shared ancestor.  The creationist explanation, by contrast, posits that God created such traits independently in each species, starting in each case from scratch.  At least at a superficial explanatory level, evolutionary and creationist scenarios both seem plausible, in principle, for complex traits that perform their functions well.  A more acid test comes from complex traits that are more harmful to their bearers.  …Many complex genetic traits (such as pseudogenes and mobile elements) that often are functionless or even detrimental to the organisms that house them are rampant in the genomes of vertebrate animals, humans included.  Did a Creator God repeat these apparent errors of genomic construction time and time again?  Or are such genomic flaws merely the footprints of phylogenetic history?

Evolutionary processes do not contrive complexity directly from nothing.  Natural evolutionary processes operate on genetic lineages much like homeowners work on their houses– by taking advantage of available construction materials to make individually small but sometimes cumulatively substantial alterations to previously existing structures and functions.  On occasion, fairly extensive renovations may occur rather quickly, but the norm–both for houses and biological lineages–is evolutionary gradualism in which renovated forms closely resemble their immediate predecessors and increasingly diverge from the preexisting entities after longer periods of time and impetus.  In the case of biology, fossils and molecular evidence indicate that most grand evolutionary transitions (such as from ancestral fishes to various derived groups of terrestrial vertebrates) require millions of years and involve many intermediate steps.

The analogy of natural selection to a homeowner can be carried to far, however.  A homeowner presumably has a longer-term plan or intent for her renovations, whereas natural selection renovates biological features without foresight.  The force of natural selection acts as if myopic, unable to perceive the longer-term consequences of its immediate decisions, which are based solely on the fit of available genotypes to current adaptive needs.

At any horizon in time, history-laden genetic lineages both facilitate and constrain what evolution might accomplish going forward.  Natural selection is facilitated in the sense that it need not re-contrive complex biological features ex nihilo in each generation; but it is also constrained because it must operate within the framework of the available (phylo)genetic materials that underlie the existing biological structures and functions in each evolved lineage.  This raises a key point germane to this book.  Evolutionary causation via natural processes leads to a biological expectation not shared by most versions of ID: a routine appearance of suboptimal organic design.

Neil Websdale, PhD is Professor of Criminal Justice at Northern Arizona University and Principle Project Advisor to and former Director of the National Domestic Violence Fatality Review Initiative.  His book, Familicidal Hearts: The Emotional Styles of 211 Killers, uncovers the stories behind 196 male and 15 female perpetrators of this shocking offense, situating their emotional styles on a continuum, from the livid coercive to the civil reputable.  Websdale attempts to answer to important questions, why do individuals kill their families and why does familicide appear to be on the rise? In the excerpt below Websdale looks at the role of emotion in familicide.

Familicide is one of the consequences of modern emotional formations.  It remains a mystery why many men, and in all likelihood a (much smaller) number of women, experience this insurgent array of emotions and yet do not commit familicide.  The insurgent array of negative emotions in the the familicidal hearts seems profoundly linked to the ways men and women live out various ideas about masculinities and femininities.  It is almost as if these gender prescriptions offered an all-too-important lifeline for social order.  This observation raises the question of whether some offenders “perform gender” as they commit familicide.  It is possible to argue that when Marcus Sims killed his estranged wife, Gloria, with his barbells, he was doing his version of manhood, his particular form of masculinity.  Sensing that Gloria had abandoned him for another man, Marcus temporarily discharged his unbearable sense of shame with humiliated fury.  Similarly, Mandy Miller, replaced in her husband’s life by another woman, stashed her bullets in her sewing basket, a place were her husband Andrew would not go.  She bided her time for several weeks, then wrote Andrew a letter reminding him of her contributions over the years, her child-rearing, her housework, and their lovemaking.  Unlike Marcus Sims, Mandy did not use violence or fly into a rage at her departing husband.  Her approach was more considered, her emotional style more subdued and civil, even reputable.  Mandy told him she wanted him to be proud of her modest achievements in the field of volunteer work.  Andrew moved on anyway.  As she committed familicide, did Mandy perform the gender work of the humiliated housewife and mother, rejected for another woman?

The insurgent array of emotions that plagues the lives of perpetrators of familicide reflects the way these offenders were unable to life up to the gendered cultural prescriptions of their day as breadwinners, lovers, fathers, mothers, wives, and nurturers.  It is probably no accident we see these killings (where data exist) in homes evidencing a traditional or conventional sexual division of labor, with women being principally responsible for child care and housework and men for primary breadwinning.  Perhaps it is among these nuclear family forms that we see the greatest potential for profound shame and painful disappointment about the seemingly inadequate performance of gender scripts.  It is the failure to fulfill one’s perceived responsibilities within intimate interdependencies that strikes me as particularly important.

The failure of offenders like Marcus Sims and Mandy Miller to maintain intimacy with their departing spouses robbed them of a mechanism that the modern self avails itself of for bolstering its own authenticity.  The appropriate living out of gender prescriptions identifies the self as lovable, deserving, and socially acceptable.  For Marcus and Mandy to lose this avenue of affirmation and social integration eroded their standing in their own and others’ eyes.  The familicidal hearts had to deal with the exacting demands of modern-hyper-individuality and the ever more elaborate calls to cultivate self-identity.  When contextualized against the rigors of these modern prescriptions for individuation, the attack on the precarious self-identity of the familicidal hearts proved catastrophic.

The power relations of the modern gender regime are a necessary although not sufficient condition for the perpretration of familicide.  Embedded in this wider exercise of power, modern nuclear families life provides a contextual framework  for familicide, one flush with innovative notions such as the self-made man, the breadwinner, the isolated and intensely nurturing mother, the increasingly dependent and precious child…

The AMA Manual of Style is the ultimate go to resource for writing articles as well as understanding ethical standards in medical and scientific publishing, and it is now available online.  In the article below, Phil Sefton, ELS, Senior Manuscript Editor at JAMA and a contributor to www.amamanualofstyle.com, looks at words coined backwards. This article first appeared on the AMA Manual of Style site.  Read related posts here.

“The patient was ventilated.”

“We decided to ventilate the patient.”

Such statements are commonly overheard in critical care units and other areas when clinicians discuss the care of a patient experiencing insufficient or absent respiration. Both statements use forms of ventilate in ways that—because they appear in this sense in the latest edition of Merriam-Webster’s Collegiate Dictionary—are correct and so may be used in medical journals. However, writers and editors have a valuable opportunity to ensure the continuing precision of the language through careful use of such terms and their variants, referred to as back-formations.

As discussed in the 10th edition of the AMA Manual of Style, “Back-formation is the creation of a new word in the mistaken belief that it was the source of an existing word” (see §11.3, Back-formations, in the AMA Manual of Style, p 407 in print). Back-formations are formed by the removal of a suffix (either a derivational suffix such as -ion or an inflectional suffix such as the plural -s) from a word that actually appeared first, changing its part of speech and forming a new word. Thus, the verb ventilate when used in the clinical sense may well be such a form, as suggested by its appearance in common use slightly later than the appearance of the noun ventilation (early 1900s vs 1890s, respectively).1 Interestingly, however, users of the English language had been busily back-forming for some time before that: ventilate as used in the closely related sense of exposing the blood to air, now obsolete or nearly so apart from its use in the study of physiology, likely also represents a back-formation that appeared some 50 years after ventilation as used in this sense (1660s vs early 1600s, respectively).2

Back-formation plays a valuable role in language evolution, producing neologisms that often subsequently enter common use. However, coining verbs through back-formation can result in medical jargon (see §11.4, Jargon, in the AMA Manual of Style, pp 408-409 in print) that is vague, depersonalizing, and sometimes downright comical in the images it can evoke. Taking the case in point, for example, what does “the patient was ventilated” mean, exactly? Was the patient perforated? Fitted with louvers? Left outdoors?

While it is commonly understood that the use of ventilated in this sense in spoken English denotes the use of a mechanical ventilator or other means of artificial respiratory assistance (eg, use of a bag-valve-mask apparatus), it typically refers to the former. However, in written materials, the use of mechanical ventilation should be explicitly reported when appropriate. In addition, eschewing the use of assistance altogether is perhaps advisable, and certain constructions (eg, “was” or “on” constructions) should be avoided if they lead to ambiguity such as that noted above. For example, “the patient was ventilated” and “the patient was placed on a mechanical ventilator” should be rewritten to read “the patient underwent mechanical ventilation.” In some instances, it might also be helpful to report additional information to clarify whether the intervention was invasive (ie, required endotracheal intubation, nasotracheal intubation, or tracheostomy) or nonvasive (eg, used a mechanical, sealed-mask approach such as BPAP [bilevel positive airway pressure]).

Writers and editors of medical information, then, should be vigilant when using terms coined through back-formation. Such terms should not be used if they do not appear in a current dictionary of reference. Those that do—eg, ventilated—may be used, but writers and editors should take care to ensure that they are not used in ways that are vague, depersonalizing, or unintentionally comical. Ultimately, however, a bit of back-formation is not a bad thing—for example, edit is a back-formation coined from editor.3—Phil Sefton, ELS

1. Ventilate. The Compact Oxford English Dictionary. 2nd ed. Oxford, England: Oxford University Press; 1991:2223.
2. Ventilation. The Compact Oxford English Dictionary. 2nd ed. Oxford, England: Oxford University Press; 1991:2223.
3. Back-formation. In: Hoad TF, ed. The Concise Oxford Dictionary of English Etymology. Encyclopedia.com Web site. http://www.encyclopedia.com. Accessed December 16, 2009.