ED Science Stuff by Trisha Gura

Seeing Brains Develop

If eyes could see. Well, then what?

The answer may have implications in the brain's susceptibility to eating disorders.

Neuroscientist Pawan Sinha and his team at MIT launched the Prakash Project, named for the the Sanskrit word meaning ‘light.‘ At first, the project sought to cure blind children in India. It's a noble effort, given that India has the highest population of blind people, less than half survive to their third birthday and less than one percent are employable.

According to Sinha, who presented at the One Mind for Research Forum, his team screened 20,000 children and treated 700 of them for problems such as cataracts, which can be corrected by surgery. Now these 700 children can see. Sort of.

Their vision doesn't arrive, voilà, as with the Biblical character Bartimaeus. Instead, parts of vision develop, gradually. And in surprising ways. It's real science in real time with a humanitarian grounding. The results are blowing the minds of developmental scientists, including Nobel Laureates, who have asserted that blind children older than 5 - 10 years of age probably will never see again - surgery or not.

Studies show that blindness at birth creates profound deficiencies in the brain, defects which cannot be reversed by restoring sight - unless that correction occurs before certain "critical periods" of development. Researchers had thought the critical window, open only until about 5-8 years of age in children, was rigid. Once shut, the door to sight could not be reopened. In other words, the mind locks itself in.

The results echo studies of the role of hormones in the womb on the development of eating disorders. Research shows that boys with a twin sister were ten times more likely to get anorexia than boys with a twin brother. The reason may have to do with estrogen exposure in the womb. The hormone may bathe the brain of the developing fetus and influence its susceptibility to eating disorders. 

What this means is that like vision, the window to eating disorder development opens very early in development. And possibly reopens later in puberty.

In a study of pre-adolescent twin versus adolescent twins, researchers found that the genetic influences on disordered eating symptoms were minimal in pre-pubertal twins and substantial in twins who had begun puberty. Conclusion: puberty might be reawakening an early-seeded eating disorder.

How? That's the stuff of future studies. And knowing how will help to figure out how to close the brain to eating disorders either very early in life or later before adolescence.

It's the ultimate in prevention. Let's hope for more promising discoveries.

 

Are Anorexics like Geniuses?

When Kate Taylor asked me to write a chapter for Going Hungry: Writers on Desire, Self-Denial and Overcoming Anorexia, she pondered a connection between anorexia and intelligence. Her idea (one I had heard before) was that individuals who are prone to anorexia tend to be smart and high achievers. How else could a person successfully override such a primal impulse as hunger? Therefore, the disease might have a yin-yang character: on one side, self- achievement; on the other, self-destruction.

While the the concept of anorexia and exceptionalism has inspired debate and caution (because the notion gives anorexia a destructive mystique), I am intrigued by the concept that complex personality traits can link with environmental factors to define a group of people. For example, scientists have long been tantalized by the study of genius, which has its own yin-yang quality. Geniuses can be brilliant; Geniuses can be mad.

There’s been a shape-shifting to these genius studies. Researchers first defined genius by measures of intelligence or posterity, then genetics. (You had to be born with right genes to be a genius.)  More recently, New Yorker writer Malcolm Gladwell in Outsiders asserted that genius arises from not so much genes but rather a modicum of talent, a heap of hard work and a tide singular advantages.

Now, new studies are defining genius as a more precise constellation of nature and nurture factors. For example, one expects geniuses to be off-the-charts smart. And it is true that geniuses must possess sufficient intelligence to master the obligatory knowledge and skills in their field. However, in his book, Genius 101, psychologist Dean Simonton describes another signature genius-making trait that may matter as much, if not more than intelligence.

Simonton found that genius-level scientists who made the greatest impact scored highest on measures of openness to experience, defined as broad-mindedness that prods an individual to explore outside the box. The higher the impact, the more a scientist was engaged in avocations outside of science.  

This would seem a paradox: scientists should be slaving at the bench, not playing the violin or perfecting metal working, on the side. But Simonton shows that genius is linked to a process called “blind-variation and selective retention.” Simply, the mind receives input from all experiences. If left to percolate, those combine, blindly and at random, to fuel truly one-of-a-kind ideas that everyone wants to emulate. 

And that gets to the core of Simonton’s genius theory. 

Geniuses, he says, generate products that are highly original, useful and exemplary. And that gift is born out of extraordinary creativity, the kind that revolutionizes the whole domain and inspires future generations. Creativity as a foundation for genius helps one understand how the same term, “genius,” places Steven Spielberg in the ranks of Isaac Newton, Albert Einstein and Napoleon. Outstanding creativity, born out of an “open mind,” undergirds geniuses in disciplines as diverse as philosophy, politics, mathematics and music, Simonton says.

His arguments are bolstered by genetic findings. In 2009, psychiatrist Szaboles Keri discovered a polymorphism in the neurorulin 1 gene that was associated with creativity in people with extraordinary intellectual and academic performance. The gene affects neuronal development, synaptic plasticity, and glial functioning. Keri suggests that the gene variation may spur reduced cognitive inhibition in the prefrontal cortex. The less inhibition, the more truly original the idea. And the more the genetic seeding for genius.

Another, more obvious trait that breeds genius is “conscientiousness,” being painstaking and careful in accord with one’s conscience. Psychologist Angela Duckworth conducted a meta-analysis of “Big-Five” personality traits (those that blend to define any human being). Conscientiousness, more than any other, predicted genius. She then teased apart exactly what aspects of the trait were key and came up with “sub-traits” of industriousness, perfectionism, tidiness, refrainment from procrastination, self-control, cautiousness, task planning and perseverance. Refining this analysis, Duckworth for the first time came up with a new and highly predictive personality trait she labels, “grit,” defined as perseverance and passion for long-term goals. This makes sense. Geniuses must be born with talent but they also have to work at its mastery. Therefore geniuses are also endowed with the traits that foster and maintain the ability to focus and practice for years, if not decades.

But even intelligence, openness to experience and grit are not enough for genius to emerge. Those traits must be placed in a singular environment. One might expect that environment to be a stable household stocked with books, musical instruments and parents exemplary in role modeling of the domain of interest. And while studies do show that geniuses are more likely to come from homes that are intellectually or culturally stimulating, a 2010 meta-analysis details a host of developmental and social factors that also contribute. For example, disrupting events like orphanhood, parental abuse or stigmatizing disabilities can actually force an individual from a normal developmental path, breaking with convention and nurturing that originality component of genius. 

The same is true for positive disrupters like constant travel during childhood and varied exposure to new cultures and languages. This input harkens back to Simonton’s argument for blind variation. The more unorthodox or varied the upbringing, the more likely the fodder for truly original ideas. In fact, artists set in wild environments -- ones that effect blind variation -- achieve the highest levels of artistic genius. 

But wildness can go too far. Even before discovering neurorulin 1’s link to creative genius, Keri found the gene was linked to psychosis. In other words, one major root of genius is linked to madness. What might be the tipping point, genius or insanity, is environment. So, for example someone born with the polymorphism and raised in more “stable” environment might learn to check the impulse for inhibition – and stay sane. Another raised in chaos, might not. 

Another environmental influence toward nurturing genius, and perhaps the most intuitively clear, is what psychologist K. Anders Ericsson’s group at Florida State University labels “deliberate practice” -- defined as activities specially designed to improve performance to attain world-mastery. The activities are intensive, regular and must continue for at least 10 years. And geniuses must not only have the ability to perform at this level, they must also perform.

Overall, a genius, then, is an exquisite combination: consisting of the right genetic seeds to acquire the knowledge and skills to master a domain and spawn truly original and useful ideas and persevere through lots of practice. These seeds then must sprout in the right social and psychological setting at exactly the right time. It’s almost a one-off, which true geniuses really are. 

I would like to see similar studies that tease apart the precise constellation of factors that spur anorexia or bulimia nervosa. And then put them back together into a picture of cause and effect that helps us steer individuals at risk into a healthier way of expressing drive and achievement.

Image by Torley 

Give it Up

It’s a throwback with a comeback. 

A Colombian intimate apparel model named Natalia Paris wants to reinvent herself. According to the Atlantic, this blonde, babelicious, ex-girlfriend-of-a-former-Medellin-cartel-lieutenant has changed her “look.”  She got rid of her implants.

Why?

“Not getting any younger,” she says in the article.

Years ago, Natalia started a trend. She hit the spotlight with a new vision of Colombian beauty: silicone lips, busts and buttocks  - and blonde, really blonde. The whole girlfriend of a drug dealer thing. And Colombians were seduced.  

In the US, we might see it as a throwback to Al Capone and the mafia dons. But now the supermodel, whose mother gave her implants for her 18th birthday and who used them to invent “the golden girl of Medellin,” recently gave them up. 

Well, my interest is peaked. This is the sequel to the story of a pedestal woman. We don’t often hear what happens after a Bridget Bardot gets old. Does she pine for former days? Does she go mad? Or does she reinvent herself?

Natalia may be letting go of something, something bigger than her faux breasts. I see it as analogous to giving up an eating disorder in midlife. When I wrote, Lying in Weight, I learned that most women who had eating disorders in midlife, acquired them sometime earlier in their lives. Some had remained constantly ill since adolescence. Others had recovered and relapsed. Somehow midlife flips a trigger. 

What seems to happen is that the many and difficult transitions of midlife - from kids leaving home to divorce to menopause - force women into a tough life phase. Midlife is a bookend to adolescence, replete with similar tumult. But instead of growing up into adulthood, which can be bright and promising, midlife pushes people in quasi-denial. Into the realm of senescence, where our culture really struggles.

And yet in this phase of life, women do actually faced their demons. Some make heroic efforts at recovery and give up their eating disorders. These are wonderful stories of hope and self-forgiveness. One woman told me her motivation. “I realized that life is too short,” she said. “What was I going to be doing this at 60?”

Could age possibly teach the importance of health and other matters over appearance? Studies of women’s body satisfaction say, yes. With age, women’s self esteem can increase, even as their BMI increases. Women can place health over appearance. And judge it less harshly. 

It’s complicated, as all of life is, because while women gain wisdom, they also lose treasured aspects of youth. The give and take is part of the turbulence of midlife. But the message, I think, is that women can let go of their past compulsions, just as Natalia gave up her implants.

And while the change may be gradual or episodic - Natalia still works the camera like a ex-70‘s porn star - change is there, nonetheless. “I like to look more natural now,” she says. 

Indeed. If we all could relax more into our bodies - even just a little. 

Power Bars and Periods

There's good news today about an alarming trend in teenage female athletes. As many as a fourth of our daughters who participate in sports or strenuous exercise stop menstruating -- or don’t start -- compared with 2 to 5 percent in the general population. The phenomenon, known as hypothalamic amenorrhea is one part of the so-called "female athlete triad," which includes low energy availability, weak bones and menstrual disorders.

The reason for menstrual shutdown, particularly in athletes who are not thin enough to be diagnosed with anorexia nervosa, is not clear. But now medical researchers have found one major suspect in the mystery: the hormone leptin - and new hope for treatment. 

I wrote about leptin for years in the journal Science. It’s an appetite suppressor made by fat cells. This is why leptin, discovered in 1994, first generated widespread hype as an potential anti-obesity pill.  But researchers figured out that overweight individuals actually produced enough - if not too much leptin  - from too many fat cells. Adding more did not add up to more benefit. The problem with obesity and leptin is that the body’s receptors for the hormone stop responding, much like insulin receptors desensitize in type II diabetes. 

That disappointment led investigators to rethink leptin less as a marker of surfeit in the land of contemporary obesity and more as a counter to starvation in a prehistoric world plagued by famine, which is probably when leptin evolved.

Leptin signals the brain and body when it is experiencing an energy deficit. 

Low fat = low leptin 

The body, in turn, shuts down its monthly menstrual cycles. This is because the female body is wired to not have a baby when a woman and her clan are starving. And so our active girls as they kick their goals or erg their crew strokes and watch their diets, in essence, are hitting an evolutionary kill-switch that controls survival of the species.

NOT getting their periods is a serious thing. While my 15-year old, crew-loving daughter may not agree, studies show that lack of menses can lead to frightening bone loss at an age where girls need to build their bones to ward off osteoporosis later in life. 

That leads us to the recent study, a continuation of previous work. Researchers at Beth Israel Deaconess Medical Center (BIDMC) and Harvard Medical School pooled 20 college-aged women who’d lost their periods, mostly runners, and gave them a either a synthetic form of leptin or a sugar pill. Seven of 10 receiving leptin responded to the treatment during the 36-week trial. Four ovulated. The women taking synthetic leptin also showed higher levels of biochemical markers of bone formation compared with the control group.  

“Our findings now prove beyond any doubt that leptin is the missing link in women with significantly diminished body fat, and that this, in turn, results in numerous hormonal abnormalities,” says study investigator Christos Mantzoros, Director of the Human Nutrition Unit at BIDMC and Professor of Medicine at Harvard Medical School.

Beyond understanding the athletic triad problem, the study also raises hope for leptin supplements as treatment for girls and young women at risk. 

It's worth a shot. On the one hand, I do believe wholeheartedly that girls should be free to pursue their athletic dreams. At the same time, we should not forget to encourage our daughters to eat healthy and balanced and enough while being active. And get our girls treatment if they are struggling to keep the weight on or trying to dieting while engaging in competitive sports. 

Finally, work with their coaches not to push regimes that include, for example, weigh-ins for rowing - the lower the weight, the more the advantage. My daughter’s school has a policy that caps the low end of weight for placement in a boat. If she drops any lower, her placement does not change. And if she loses too much weight, they would bar her from participation in any sports.

I applaud these studies and hope for more. Beyond helping us to understand and treat a growing problem, it also highlights the vulnerability of girls and young women to eating disorders and helps foster the right thinking and behaviors for prevention.

The findings are reported today on-line in the Proceedings of the National Academy of Sciences (PNAS)

 

EDs: Who or What's to Blame

Several years ago, I received an email from a mother of a child diagnosed with anorexia. She asserted that the disease was caused by genes alone and that culture did not play a role. In response, I pulled several studies that testified to the the influence of societal mores on eating disorders. I told her what experts had told me -- that the disease was seeded by genes. But those seeds had to be sown on the fertile ground of environment in order to grow into the weeds of disease.

She became more vehement, and she and I agreed to disagree. Still, the conflict lingered in my mind.  

It led to my article for Scientific American Mind about the neurological roots of anorexia nervosa and my conviction that that this is a “both” rather than an either/or debate. 

It evolved into my understanding of the importance of it all; the question of cause becomes paramount when the conflict leaves the realm of abstraction and falls into the household of a parent, who learns that his or her child has an eating disorder. If the disease is purely genetic, then the parents are off the hook. Her genes made her do it. If anorexia or bulimia are environmentally-caused, well, then it must be her/my fault. 

If the disease is happening to you, then the debate is about blaming your biology versus blaming yourself.

And so what combination of nature and nurture sprouts the seeds?

I think we’ll be trying to answer that for a long time, probing with the help of more sophisticated studies. But rather than try to answer questions about cause, which is complicated and has been dealt with by many, I found an article that deals more with the psychology of the question of who or what to blame.

Shaun Nichols came out this month with an article about free will and whether we really have it. He says we all live with a philosophical conflict. On the one hand, we understand that we could be governed by determinism, where events happening now are programmed by the past such that they cannot happen in any other way. (Her genes made her do it. Nothing could have prevented this). On the other hand, we could be totally free agents with completely free will (She chose to do these bad behaviors. They must be her/my fault.) 

Whichever the philosophy, Nichols shows it changes - depending on the circumstances.  

His team told volunteers, Imagine that you live in a world in which “every decision is completely caused by what happened before the decision - given the past, each decision has to happen in the way that is does. Would it be possible for anyone to be morally responsible for his or her actions?”  

People said, no. A person is not morally responsible.

But if volunteers were told, “A man kills his family but he has a neurological condition. Do you think he should be blamed?” People tend to say, yes.  And the more people were made to feel negative emotions before rendering the verdict, the harsher the ultimate blame.

What this comes down to is context. In the abstract, people accept the idea that determinants, genes being one, could render a person exempt from responsibility for his or her actions. But when posed as a specific case, people are quick to point the finger. 

 The discrepancy might have to do with emotionality. When people are calm and collected, they can acknowledge that determinism precludes responsibility. But when faced with situations much closer to home, the desire is to blame the offender. 

 I think the real insight here is to understand that a person with an eating disorder is bound or determined, at least in part, by his or her genes. AND, at the same time, he or she is responsible for his or her actions, going forward. Determinism and moral responsibility can co-exist.

 But are eating disorders determined? 

 That’s a question for another blog. No doubt, we will continue to debate the contribution of genes versus environment to eating disorders, if nothing more than to help devise better prevention and interventions.  But it is also important to understand that our notion of blame is fluid. And that it all depends on the context, our perspective and our mood for the day.

Eating Disorder Unveiled?

She’s a bride-to-be, a princess-to-be and apparently losing weight. Kate Middleton’s recent appearance in Northern Ireland sparked a buzz about whether she’s slimming too many pounds before her April wedding.

Is the stress? Is it the diet? Is it the media following her around snapping photos of body parts and analyzing the girth of her calves?

Who knows? except Middleton. And thankfully, she is keeping mum. Apart from whether she has an eating disorder or simply pre-marital jitters, the chattering and twittering points a finger at almost has become an iconic prenuptial phenomenon. Brides-to-be are losing weight. And doing so to the extreme.

A survey of 272 engaged women found that more than 70 percent wanted to lose weight before their wedding day and more than a third were going the extremes to do so - taking diet pills, fasting and buying bridal gowns one or more sizes smaller than normally worn.

A second study of 879 Australian brides-to-be recruited from five bridal websites, showed a parallel trend. Nearly 75 per cent planned to exercise more and follow a 'healthy eating plan;' 35 per cent planned to cut fat or carbohydrates out of their diets; and on average, participants wished to lose over 18lbs by their wedding day.

They’re fueled by wedding-themed reality shows such as WEtv's hit “Bridezillas” and TLC's “Say Yes to the Dress.” And People magazine’s recent series that put six brides on a diet and a dogged them through a competitive, wedding day countdown.

Need I state the obvious: there’s a huge emphasis on appearance among brides-to-be and the need for a healthier bridal ideal? Or is it better to just shrug it off, knowing that most put the weight right back on anyway. What a waste of time, effort and money.

Getting "Pregnant" to Lose Weight

Here’s a shocker. Doctors and weight loss centers are prescribing human Chorionic Gonadotrophin (hCG), a hormone produced during pregnancy, as a weight loss aid. They serve it up to desperate dieters, as daily injections, in combination with a 500-calorie-a day meal plan. 

Are you kidding me? hCG is a PREGNANCY hormone. It’s made from the urine of pregnant mares.

Besides being really gross, the fad has little basis in science. Medical proponents argue that hCG, “tricks your body into a state of pregnancy; it burns off fat so the ‘fetus’ can get enough calories, but it protects muscle.” This thinking comes from an ancient paper, published in The Lancet in 1954, and a book by A.T.W. Simeons, a Roman doctor. He talks about “fat on the move” in the body and how the injection of only 125 units (of hormone) per day shaves off roughly one pound per day, for “even in a colossus weighing 400 pounds, when associated with a 500- Calorie diet.”

However, a 1995, Dutch study debunked the whole hCG scheme by analyzing 14 randomized clinical trials of the diet. The conclusion: “There is no scientific evidence that HCG is effective in the treatment of obesity;it does not bring about weight-loss or fat-redistribution,nor does it reduce hunger or induce a feeling  of well-being.”

What’s more, this it’s dangerous. According to a spokesman for the Food and Drug Administration, hCG carries risks of blood clots, depression, headaches and breast tenderness or enlargement. A patient on the hCG diet suffered a blood clot in the lungs.

Making matters worse, women who are far from obese are taking hCG: a 5’3”, 130-pound, soon-to-be bride wanted to slim down in time for her wedding. 

I can attest that this is not the way to go. I took shots of hCG 15 years ago as a successful, but grueling fertility treatment. The hormones made me feel miserable, bloated and depressed.  And I only suffered through a week of the injections. 

Meanwhile, the hCG companion diet, at 500 calories a day, echoes anorexia. Most people require 1,800 - 2,000 calories a day. And no good doctor weight-loss doctor advocates such an extreme.

So really, let’s get a grip on our obesity obsession. I’m really saddened by this approach and angered that it is being aided by physicians, however well-intentioned. Or, at a $1000 month for the consultation alone...maybe not so humanistic.

 

What Dieting Does to Your Brain

Post holidays, guilt flares. And it is all to common to watch the treadmills fill and the diet plans flow, as people try to shave off the results of indulgence.

But here’s a study that begs caution. Researchers have shown that dieting sensitizes the brain to stress, which in turn, prompts cravings for treats. These brain changes last long after the diet is over. (They become genetic.) And they entice even healthy individuals to binge -- and ultimately gain or regain weight.

In short, the diet backfires because stress of dieting overwhelms the dieter, forcing him or her to binge or comfort eat high-fat, high sugar foods.

Sound familiar?

The links between dieting, stress and binge eating are not new, especially in the world of eating disorders. But what is startling in this recent study is that mice who were forced to diet acquired brain and body changes and these reached their genes, in just three short weeks.

The center of this quagmire is stress. Dieting, while trying to ultimately achieve health in overweight individuals, is a form of stress on the body. Stress triggers the release of the hormone cortisol. The body, via cortisol, is fueling the blood with energy (in the form of sugar) as part of the fight-or-flight response. That is supposed to be short-lived. But pre-holiday stress, followed by post-holiday diet-stress, means chronic stress -- and chronically elevated levels of cortisol levels. Those ultimately makes even healthy individuals seek out rewards like high-fat, high-calorie foods

So the answer might be not to rush to the gym or the Adkins book to cope with winter blues or post-holiday rumination. Instead, look for better ways to cope with stress, yoga, meditation visits with friends, for example. And then, of course, seek out healthy eating. In the case of eating disorders, medications that target cortisol-related stress pathways might help individuals who suffer.

Diet Drug Defect: Part III

Having covered obesity research for more than a decade for the journal, Science, it is no surprise to me that yet another diet pill, called Qnexa, suffered defeat by the Food and Drug Administration on Thursday.

Qnexa is the third weight loss medicine to run afoul this month due to safety issues. First, the FDA forced the withdrawal of 13-year veteran, Meridia, because of concerns about heart attacks and strokes. Next came lorcaserin, which the FDA rejected last week because it caused tumors in rats.

That leaves only Xenical, approved in 1999, for long-term use in managing weight. And its effects are, at best, modest.

While drug developers now bemoan the lack of success in a huge market that should be roping in the cash (a third of Americans are obese and another third overweight), I argue that there is another side of the coin to consider. Once a diet drug is out, everyone will start taking it, not just people who are obese.  A recent study that high school-aged females' use of diet pills nearly doubled from 7.5 to 14.2 percent over the course of five years. By the ages of 19 and 20, 20 percent of females surveyed used diet pills.

Diet drug abuse is a tremendous problem with severe, sometimes fatal consequences. At the same time, diet drugs generally produce modest weight loss – only about 5 percent. And that is because the body bears a plethora of way to keep weight on.

Human beings evolved from Neanderthal days to guard against starvation – not obesity. This was to prevent death in times of famine. Therefore, messing about with the body’s system through extreme diets and synthetic drugs and culture-driven, unhealthy behaviors can have long term consequences. As the body tries to right itself from riding roller coasters of over and under-eating -coupled to bouts of intense physical activity or pill-popping - obesity and eating disorders are actuallly unwanted side-effects. You perturb the system too much, and it breaks. Diet pills, however beneficial to some, are extremely detrimental to others.

Therefore, I applaud the FDA for making sure that what does get out to market is safe. For those who are obese, I don’t believe losing 8-10 pounds is enough to justify the risk of a heart attack or cancer. For those who are not, a diet pill is…simply…dangerous.

Two Therapies Work: But Families Do it Better

Just out today:  Researchers found that individual therapy and family-based treatments both work for treating anorexia nervosa in teens. But adolescents in family-based programs are more likely to achieve full remission, gain weight faster and need less hospitalization.

The study tackles one of the most pressing questions about anorexia: which therapy works best? Treatments had not been examined scientifically. So no one could say without utter certainty which was the best route to recovery for teens.

Psychiatrist James Lock at Stanford took a stab at it. He led a team that randomly assigned 121 teens with anorexia (ages 12 to 18) to either an adolescent-focused individual therapy program, which focused on enhancing autonomy, assertiveness, identifying and defining emotions, and tolerating these feelings instead of numbing them with starvation; or a family-based treatment that promoted parental control of weight regain, while restoring healthy family functioning. 

At the end of treatment, both groups fared (by scientific standards) the same at achieving normal weight and an average score on an assessment of eating disorder symptoms. (A total of 42 percent of family-based treatment participants and 23 percent of adolescent-focused individual therapy participants achieved this definition of full remission.) 

However, those who underwent family-based treatment did better than the individual therapy group at the six- and 12-month follow-ups (40 percent vs. 18 percent after six months and 49 percent vs. 23 percent at 12 months). There seemed to bellower rate of relapse (10 percent) for family-based treatment versus 40 percent for adolescent-focused individual therapy, as well as more family-based participants achieving recovery. The family-based patients also gained weight faster and were hospitalized significantly less often.

The author’s conclusion: family-based treatment is superior, although teen-centered therapy remains an important alternative for families who would prefer an individual approach. “

Let’s see what happens when researchers compare family-based with other credible treatments, including cognitive behavioral treatment.

(Arch Gen Psychiatry. 2010;67[10]:1025-1032.)