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Are social media platforms making eating disorders in children worse?

January 10, 2023 by Morgan O'Toole-Smith

At least one school district in Seattle thinks so. Seattle Public Schools (SPS) has filed a suit in US DIstrict Court alleging that “defendants [social media platforms such as Facebook, TikTok, Instagram, YouTube, and Snapchat] affirmatively recommend and promote harmful content to youth, such as pro-anorexia and eating disorder content.” Essentially it appears SPS is saying such content exacerbates eating disorder symptoms and undermines effective treatment.

Not surprisingly perhaps, the issue is complicated. First some medical facts: eating disorders are biological brain disorders that are highly heritable (estimates – based on twin studies and genome-wide analyses – are as high as 74%; as a reference, that heritability is similar to the heritability of height in humans is estimated around 80%). This means eating disorders run in families and are emphatically NOT lifestyle “choices”, volitional behaviors on the part of patients, the result of bad parenting or the effects of images on social media. Such theories and explanations were once common but have in recent years been completely debunked by rigorous scientific studies (see above).   

At Kartini Clinic we like to put it this way: parents don’t cause eating disorders and children don’t choose to have them. Period.

So what about the role of social media? 

Consider the following analogy: can a child develop type 2 diabetes (T2DM) from looking at pictures of cheeseburgers? I think most of us would agree this sounds implausible and not very scientific. That’s probably because we understand and acknowledge T2DM to be a biological condition caused by complex interactions of genetics and environment. Eating disorders such as anorexia are no different.

This is not to say social media messaging can’t do any harm, for example by triggering behaviors or making children feel worse about themselves, which in turn could undermine effective treatment. After all, SPS is not alleging that social media platforms cause eating disorders but rather that they are contributing meaningfully (and, crucially, knowingly) to the disease burden on children suffering from these potentially devastating and deadly illnesses. 

At Kartini Clinic we certainly do share these concerns, and we would wholeheartedly support efforts such as additional mental health professionals in schools, lesson plans and additional training for teachers  provided they are grounded in a scientific understanding of these illnesses. Ultimately the key is to ensure that eating disorders are diagnosed promptly and treated effectively using evidence-based practices (i.e. grounding diagnosis and treatment in physical medicine and using behavioral health interventions such as family-centered treatment: families are almost always part of the solution to treatment in children, not part of the problem). Could the social media companies do better? Certainly. Perhaps they could “pair” content of concern with objective information about the causes, symptoms and potential for effective, life saving treatment of eating disorders in children. Although they aren’t directly responsible for these terrible illnesses, social media platforms could be powerful allies in helping us address this problem more effectively.

Filed Under: Eating Disorders, Anorexia Nervosa, Diagnosis, Eating Disorder Research, Eating Disorder Treatment, Evidence Based Treatment, Family-based Treatment, Genetics, Recovery, Social Media

Breaking Science News: The Latest Genetic Study of Anorexia Nervosa

July 18, 2019 by Julie O'Toole

Since the founding of Kartini Clinic in 1998 we have operated under the assumption (then almost unheard-of) that anorexia nervosa is a biologically based, heritable human illness of the brain. For that reason we have always taken detailed family histories, and later in the early 2000’s began contributing towards what became a giant genetic study, and now at last reported on by lead author Cindy Bulik. On July 15th the results of the study were published in Nature Genetics: Genome-wide association study identifies eight risk loci and implicates metabo-psychiatric origins for anorexia nervosa (behind a paywall, unfortunately).

This is a major milestone in understanding the biology and heritability of this devastating illness. Kartini providers Dr. Julie O’Toole and Dr. Janiece Desocio are proud to have their names among the many on this paper. 

Dr. Bulik et al. have put together some summary talking points of the study. Please note some of the paradigm-busting comments:

“occurs in all racial and economic backgrounds and socioeconomic classes” and is “stable across time”, i.e. not a modern disease

“there is more to anorexia nervosa than just the psychological components…it is a metabo-psychiatric disorder” 

No longer is there any reason to view anorexia nervosa as a “choice”, a “result of flawed parenting” “a result of the oppression of women” or “caused by the media or bullying”

What is anorexia nervosa?

Anorexia nervosa is a life-impairing illness characterized by dangerously low body weight, an intense fear of gaining weight, and a lack of recognition of the seriousness of low body weight.

How common is anorexia nervosa?

The prevalence of anorexia nervosa is between ~1-4% in women and 0.3% in men and appears to be stable across time.

Who gets anorexia nervosa?

Anorexia nervosa does not discriminate. Although the most common age of onset is adolescence, anorexia nervosa can occur at any time of life, all sexes, genders, racial and ethnic backgrounds and socioeconomic classes.

What is a genome-wide association study (GWAS)?

A genome-wide association study involves scanning markers across complete sets of DNA, or genomes, of many people with a particular illness (such as anorexia nervosa) compared to controls. By identifying where differences in the genome lie, researchers can identify genetic variations associated with the illness. Once new genetic associations are identified, researchers can use the information to develop better strategies to detect, treat, and prevent the disease. Such studies are particularly useful in finding genetic variations that contribute to common, complex diseases, such as asthma, cancer, diabetes, heart disease and mental (brain) illnesses.

What is the Anorexia Nervosa Genetics Initiative (ANGI)?

Is an initiative of the Klarman Family Foundation who supported the largest single collection of samples from individuals with anorexia nervosa and controls ever performed. The study was based at the University of North Carolina at Chapel Hill and included researchers from Karolinska Institutet in Stockholm Sweden, Aarhus University, in Aarhus Denmark, Berghofer Queensland Institute for Medical Research, Brisbane Australia with assistance from the University of Otago in New Zealand. ANGI contributed 13,363 cases to the GWAS.

What are the details of the study? How many people participated?

A multinational group of more than 100 researchers combined data collected by the Anorexia Nervosa Genetics Initiative (ANGI) and the Eating Disorders Working Group of the Psychiatric Genomics Consortium (PGC-ED). The resulting data set included 16,992 anorexia nervosa cases and 55,525 controls of European ancestry from 17 countries across North America, Europe, and Australasia.

What were the main findings and results?

The GWAS identified eight genetic variants significantly associated with anorexia nervosa.

The genetic basis of anorexia nervosa overlaps with other psychiatric disorders such as obsessive-compulsive disorder, depression, anxiety, and schizophrenia.

Genetic factors associated with anorexia nervosa also influence physical activity, which could help explain the tendency for people with anorexia nervosa to be highly active even when acutely ill.

Intriguingly, the genetic basis of anorexia nervosa overlaps with metabolic (including glycemic), lipid (fats), and anthropometric (body measurement) traits, and, crucially, the study shows that this is not due to genetic effects that influence BMI. 

What does this mean for patients and families now?

It is helpful for patients and families to understand that there is a biological basis for anorexia nervosa. It is a perplexing and potentially fatal illness that is challenging to recover from and takes an enormous toll on individuals with the illness and their loved ones. These results offer hope that we may be on the right path to understanding the biology of the illness that may eventually allow us to develop novel therapeutics to treat this often intractable disorder.

Why call it a metabo-psychiatric disorder?

The panel of genetic correlations that we reported strongly suggest that there is more to anorexia nervosa than just the psychological component. The fact that we observed genetic correlations with a whole host of metabolic and anthropometric traits may explain some of the most perplexing aspects of anorexia nervosa such as: how can they reach such low body mass indices in the first place, how can they remain at such low body weights, why is it so hard for them to maintain a healthy body weight even after treatment, and why are our treatments inadequate to help them achieve full recovery? 

This could explain why adequate renourishment is so critical to long term recovery. Stopping treatment before reaching and maintaining a healthy BMI may destine someone with anorexia nervosa to relapse. 

Will there be gene-therapy for anorexia nervosa in the future? What’s next?

No and this is not the long term goal of this type of science. The goal of GWAS is to elucidate biology. Part of the reason that we have no medications that are effective in the treatment of anorexia nervosa is because the biology of the illness remains a mystery. We expect that hundreds and even thousands of genes will be implicated in risk for anorexia nervosa combined with environmental factors, meaning that anorexia nervosa is a classic “complex disease.” We hope that with increasing sample size, we will be able to identify underlying biological pathways that can give us insight into how these genes influence anorexia nervosa—and now we know to look not only at pathways that influence psychiatric factors, but also metabolic ones.

Future studies?

Even though almost 17,000 sounds like a large study, it is still small by GWAS standards. Our goal is to reach 100,000 anorexia nervosa cases with appropriate controls. Other psychiatric disorders have reached this milestone with intriguing results. We then need to do the same for the other eating disorders (bulimia nervosa, binge-eating disorder, and avoidant/restrictive food intake disorder-ARFID). We have a lot of work ahead and it will take a global effort to reach our goals.



 

Filed Under: Anorexia Nervosa, Eating Disorder Research, Genetics

The Role of Parents in Treatment

April 27, 2017 by Julie O'Toole

This post was originally published on December 16, 2015. 

kartini web 042712Possibly nothing has changed so much over the last ten years as the acceptance of parents’ role in the treatment of children and adolescents with eating disorders.

When I founded Kartini Clinic in 1998, “dysfunctional” parents were widely considered to cause eating disorders in general and anorexia nervosa in particular. Toxic and enmeshed mothers were commonly cited by therapists, doctors and lay people as the common denominator in these illnesses. In fact, eating disorders were not even considered illnesses as such, but more lifestyle choices, protests against puberty, against the suppression of women and girls– anything but brain based conditions. Many referring physicians, even pediatricians, would comment as they sent me their patient: “it’s no wonder she has anorexia, you should get a load of her mother.”

I’m proud of the fact that Kartini Clinic never accepted the “anorexogenic parent” as an explanation for these illnesses, and we created a family-based approach to treatment from the get-go. Today most everyone seems to have forgotten what it was like to be attacked by “the professionals” for the heresy of declaring that parents don’t cause eating disorders. Because of our belief that such an explanation (parental causation) made no biological sense, we were not surprised when “family based treatment” became popularized as the standard of care.

As a vocal booster of parental inclusion in all aspects of treatment I was, however, surprised when I began to receive reports from parents who told me they had been taken to task by other parents for seeking professional help when they “should be” re-feeding their child on their own.

One thing I have learned from experience is that there are many roles for parents in the healing of sick children, not just one role. And I have come to see that the single greatest disability a child could ever have is to grow up either without a parent or with one(s) who is/are not able to put the needs of their children first.

Parents are not saints. Mine weren’t. I’m not. And I’ll bet you aren’t either. Basically, parents are humans who have reproduced, which means that they have all the warts and bumps of people everywhere, with one distinguishing difference: the overwhelming majority of parents are their child’s biggest booster, most devoted fan club and deepest source of love and support. But parents can tire, get ill themselves, lose heart, get impatient, run out of steam and even die. To talk as if all parents are any one thing is to do a disservice to them. Some parents have a much harder row to hoe than others. Some are more fortunate, some are less so. Some have more severely ill children than others do. Outcome is not simply determined by parental virtue or hard work. For example, one of the implications of anorexia nervosa being a brain disorder is that outcome will be partially determined by a child’s own biology, the severity of their illness, the promptness of treatment and weight restoration, and the whole psychological and social environment within which they find themselves.

To illustrate the diversity of challenges some families face, I am going to outline a few.

Please remember that we have treated over 3000 children at Kartini Clinic, so if you think you recognize yourself in any of these vignettes, you are probably wrong. These vignettes do not include parents who have successfully re-fed their child at home and whose child is in good remission, because such parents would not be referred to us in the first place. Here are a few examples of those challenges:

  • A 15 year old girl who has had a bingeing and purging eating disorder for three years, without treatment.  Her father is a lawyer, her mother stays home. They have three other children, one of whom has a severe disability requiring tube feeding and many doctors appointments, so plenty of family stress and time constraints on both parents. They live near Kartini Clinic.

  • A 14 year old boy whose parents are divorced, who has restricting anorexia nervosa with a severe compulsive exercise component and is terribly malnourished.  Both parents work full time, father lives in another state and custody is in flux.  Because the legal issues are unresolved (it has been two years) Mom has not received any child support. She earns barely enough for their needs at her new job where she believes she has no family leave time — and certainly no paid family leave. She is convinced she cannot re-feed her son at home, as he defies her in almost all ways, and she needs to be at work.  She lives an hour and a half from Kartini Clinic.

  • A 16 year old girl from overseas with partially treated anorexia nervosa, whose parents tried Maudsley re-feeding with success when she was first diagnosed at age 13, but have not been able to get her to a weight where she can menstruate, and she has become more resistant and harder for them to manage. There is one Maudsley-style therapist in their region but she has “given up” on their daughter. They have two other children in school and some help from grandparents in their home country, but have flown 10 hours to get to us. Needless to say their health insurance is not valid in the US.

  • A 15 year old girl with severe bulimia nervosa and diabetes whose father died this year, whose mother has been in and out of rehab and whose grandparents live in another state.

  • A ten year old boy with two parents, both professors, who live three hours away and have two other children. They tried home re-feeding, but felt that “it was ruining their relationship with their son” as well as “severely straining their marriage” and “ruining the lives of their other children.”

  • An 8 year old boy with food phobia from across the country whose parents mortgaged their house to get treatment in Portland because all attempts (four or five in their home state) to get their child to eat again had failed.  Mom brought their son to Portland alone as Dad needed to keep working in the family business to maintain their health insurance and care for his elderly parents, who live with them.

  • An 11 year old girl whose mother, a nurse, took leave of absence from work to re-feed their daughter at home (despite father’s misgivings).  Father is a physician, they have no other children and live in Portland.  Despite everything Mom could do, their daughter gained, and then lost, weight in cycles they could not seem to control.  Mom sought the support of other parents who had been successful with home re-feeding, but is now feeling a failure and wants us to help her figure out how to go forward.

  • Twin 13 year old girls of undocumented parents from Mexico with severe weight loss of unknown origin.  The girls (born here) speak English, but their parents do not. Maternal grandmother and two maternal aunts have anorexia nervosa, from which one of them died.

Hats off to those parents who have done it themselves! But for those who need help (and those who don’t) let’s remember: the variety of human experience is very large, and those who have not been able to do home re-feeding can still be involved in a meaningful way in their child’s care — and should be. No parent should be made to feel like a failure if home re-feeding either did not work for them, or they felt it was never an option in the first place. The task will be to find a way for parents to be treated as critical team members while navigating their other challenges; after all, without their parents’ help and support, a child is unlikely to get well over the long term regardless  of treatment. In the end, children need to be able to return home, to learn to eat, love and live again within their own families and their own communities.

There is just more than one road that can lead us there.

Filed Under: Anorexia Nervosa, Eating Disorder Treatment, Eating Disorders, Family-based Treatment, Genetics

Why We Limit Hyper-Palatable Foods for One Year

September 22, 2016 by Julie O'Toole

dougnuts for web

When I was first introduced to the Minnesota Semi-Starvation Study (MSSS), published in 1950 by Ancel Keys and his team, I was overwhelmed by the sheer volume of data they were able to accumulate about the physical and psychological ramifications of semi-starvation in humans.

It was mind-blowing. Then I came across the graph on page 106 of the hardbound edition called “Over-all Changes in Body Weight in the Minnesota Experiment” with the subtitle: “Expressed as a percentage of the control value for the particular group of subjects”. I invite you to Google it.

The Y axis (the vertical one) of this remarkable graph showed “% of control weight achieved” (100% at the start of the study, before the subjects were dieted). On the X axis (the horizontal one) was the “number of weeks of the experiment,” which stretched out to 58, or one year and 1.5 months.

Over the course of the study, the subjects were fed a calorie-reduced diet designed to mimic war-time semi-starvation rations; the subjects’ body weights could be seen to drop to about 77% of “normal” by about week 24. So they were dieted for 24 weeks.

Thereafter came 12 weeks of “structured re-feeding,” which is what we do at Kartini Clinic — a process designed to give a healthy mixture of nutrients, but in a controlled fashion. Around the 12th week of re-feeding the subjects were allowed to eat “ad-lib” (or “intuitively” in the parlance of our day), with no content restrictions. This style of eating caused a very steep rise in the subjects’ rate of weight gain and resulted in them gaining 110% of their control weight. In other words, their weight went up higher than it had ever been before the diet.

The University of Minnesota published a video about this experiment 15 or so years ago. In it, they interviewed one of the “survivors” of this study, now an older man. He said that once they were allowed to eat what they wanted, they ate everything, often indulging in the sweets and desserts they had denied themselves during the period of semi-starvation. “We got fat” he said, and seemed to find it amusing. Following the above-referenced curve out to the 58th week of the study, though, you can see that the overeating appears to have subsided and the subjects’ weight to curve back down towards their normal weight — although they never really reached as low a weight as they had before they started dieting.

Taking a structured approach to refeeding at Kartini Clinic

OK, it may have amused some of the young men to “get fat,” but I reasoned that our patients (and their families) would not find this amusing at all. At Kartini Clinic, we are searching for the state of health that allows children to grow and thrive. And, in an effort to keep the growing body from “over-shooting the mark” with re-feeding and unnecessarily promoting binge eating (which appears to be common following semi-starvation and weight loss even in people who have never binged before), we decided to remove “hyper-palatable” foods for about a year encompassing weight restoration. Hyper-palatable foods are those with high sugar and fat content — neuroscientists’ definition, not ours.

If you look at Key’s graph, waiting a year to re-introduce these foods should take us out of the area of binge eating into more normally driven food intake. Simple, right?

I think that nothing that we have innovated at Kartini Clinic has caused us to be so roundly criticized as this suggestion that our patients avoid sweets during the initial phase of re-feeding. We immediately ran afoul of the “intuitive eating” proponents although, to date, no one has explained the medicine/science behind their objections. Ancel Keys’ research subjects did not have eating disorders and 12 weeks of ordered refeeding did not cause them to “fear foods” or to develop an eating disorder. Eventually, they went back to normal eating…a year plus later. That is our plan as well.

Once binge eating behavior starts, it’s hard to stop

In addition to studies about the bingeing and food seeking behavior that can follow dieting or restricting, there is also a plethora of animal studies specifically looking at bingeing and hyper-palatable foods. Bingeing in mammals is a product of gene-environment interactions. The “gene” part is how vulnerable to binge eating your brain is because of your genotype, the “environment” part is the food you are exposed to.

You cannot tell whether someone is binge-prone just by looking at them. From rat studies, we know that this tendency sometimes does not surface until puberty or later. In binge-prone rats “intake of just a morsel of PF [palatable foods] or simply the smell of PF is known to trigger relapses back to binge eating.”[1]

For those of you who like reading the science, Chapter 8 of the same text, by Michopoulos, Moore and Wilson, discusses the biology of diet choice and emotional feeding in times of stress, which will vary from one being to another. While brain chemistry causes these behaviors, they can appear to be lifestyle “choices” for which a patient is blamed.

Other authors (Ventura, Latagliata et al) note in their chapter on “Food Seeking In Spite of Harmful Consequences”: “…repeated stimulation of reward pathways through highly palatable food consumption may lead to neural adaptations that make consumption more compulsive.”

I ask you, why go there? In anorexia nervosa, simply refraining from adding hyper-palatable foods to our patients’ meal plans would seem to offer the possibility of a smooth return to normal eating. As we say: First do no harm, then innovate.

And as I say: Disagree? Show me the science.

 

[1] Animal Models of eating Disorders; Avena, N (Ed.); Humana Press 2013 ISBN 978-1-62703-103-5) page 8.

Filed Under: Anorexia Nervosa, Eating Disorder Research, Eating Disorder Treatment, Evidence Based Treatment, Genetics, Nutrition

Goodbye, Bryan

November 4, 2015 by Julie O'Toole

Anyone who knows me knows that I am no longer young. Yet I have teachers. My patients are my teachers and some of my colleagues are (still) my teachers. At this stage in the student/teacher relationship we often teach each other: we debate, we discuss, we disagree, we commiserate, we laugh.  As one of my general pediatrics colleagues told me the other day “what you do is hard; not everyone can love your patients”.  But I know someone who can and does — now, sadly, past tense could and did: Bryan Lask.

For those of you who knew him, you are weeping alongside me to have lost him. And Bryan did not go gently into that good night.  He did not want to go.  He had a mountain of research ideas for us to go over in the newly built Kartini Clinic conference room we had dedicated in his honor in March 2015.  He skyped about science and neurobiology and life with his most cherished colleague, the one he really admired and looked up to: Ken Nunn. He sat in the easy chair in his London flat — decorated with books, more books, and paintings — and read and wrote.  Wow, did he write!  He had just decided to have his genome analyzed through 23andMe after my husband Steve and he discovered their common ancestry and relatedness through the great Jewish diaspora that sent the Lasks to England and the Nemirows to Ellis Island.  He was endlessly curious. And like many of us, as he got older he got more interested in and connected to his ancestry and, in his case, his Jewish ancestry.  We talked a lot about that. Areligious as he was, his last text to me offered me the consolation of his wish for us to see each other one more time, to talk again, on another plane, in another existence.

Bryan was the quintessential scientist and researcher, but I know that his final thoughts were not with medicine.  They were surely with his family.  Health updates he sent to all of us, towards the end, were increasingly not about his health, but about his grandchildren: three little boys and one precious girl in whom he delighted with every breath he took.  And of course there were his own two sons and Judith.

One of the last things we did together as Steve and I travelled to London this spring to say goodbye to him — at his insistence — was go the theater. He loved the theater. And typical for this social and well-connected man, no sooner had we stepped into a little restaurant across from the theater than he was recognized by a man he had not seen in many years, with whom he had once been at school. Bryan was already in a lot of pain, it was hard for him to walk, but he drew himself up to his full height (not very tall) and chatted delightedly with this school chum who now knew of him only by his reputation.

For those of you who did not know him let me introduce Bryan Lask (1941-2015) and his work.  Bryan was a professor with an almost comical tail of titles behind his name:  Professor Bryan Lask, FRCPsych., FRCPCH, FAED, M.Phil., MB., BS., LRCP, MRCS, but he preferred to be called 'Bryan'.  Don’t get me wrong, despite the soft voice and cultured accent he was something of an authoritarian and commanded respect. He did not tolerate being ignored. He was Professor of Child and Adolescent Psychiatry at St George’s, University of London and Honorary Consultant Psychiatrist to South West London and St George’s Mental Health NHS Trust; he was Consultant Psychiatrist and Medical Advisor to Huntercombe Hospitals, in Maidenhead, Stafford, and Edinburgh, UK and Honorary Consultant Psychiatrist to Great Ormond Street Hospital for Children as well as Visiting Professor, University of Oslo, and Research Director, Regional Eating Disorders Service, Ulleval University Hospital, Oslo, Norway. Who could ignore all that?

Although in the early years of our friendship we argued a lot about the biological basis for eating disorders, as I was then far more convinced than he about the brain-based etiology, he came to be a leading proponent of research on eating disorders as brain disorders.  Together with Ian Frampton he wrote Eating Disorders and the Brain; with Ken Nunn and Tanya Hanstock  Who’s Who of the Brain; with his long-time collaborator Rachel Bryant-Waugh Eating Disorders of Childhood and Adolescence as well as Eating Disorders: A Parents Guide. He authored literally dozens and dozens of scholarly journal articles and was on the editorial board of several newer, more far-thinking journals in eating disorder research.

Bryan was an intrepid traveler and he loved Oregon.  What’s not to love, one might ask? A few years ago he flew in to Portland with six or seven young Norwegian graduate students in tow to “mine the data” Kartini Clinic has accumulated on children with anorexia nervosa. They all camped out at our house in the wine country, bunking together crammed into the guest house and on the couches in the living room, while the Professor had the bedroom of honor (which he — and we — called ‘his room’ from then on) and sun bathed in the rare summer sun looking out over the Cascade volcanoes.  The graduate students marveled at how we made our own bread and cooked at home (they had heard that Americans only ate fast food), they saw their first hummingbird.  Under Bryan’s supervision they set up headquarters in Steve’s painting studio, and plugged in a bank of computers which could talk to Kartini computers to extract their data on “seasonality of birth and its possible correlation to anorexia nervosa”.  Bryan kept them all on course, he was strict about quality control in data collection, he encouraged them to tell me their theories (about which I was sometimes skeptical, but politely interested). He was a great synthetic thinker and could draw many threads of ideas together in a way that could be examined objectively.  He kept everyone on task. I cooked.

Bryan’s son Gideon now owns a painting Steve did of him that summer: Bryan in a field of Oregon cornflowers. That is how we shall think of him.

The very last thing this man did for his Kartini colleagues, for me, was to send us a little girl with a rare and awe-inspiringly difficult diagnosis: pervasive arousal/withdrawal syndrome (PAWS). On his recommendation the family travelled to Oregon.  For a few months he helped guide her treatment.  He gave me the courage to treat her.  And then he was gone.  Her daily improvement, her nearly miraculous healing is now a testament to his inspiration.  She is quite possibly the last child he treated.  I hope she will live and thrive and one day know the gift of healing and where it started. Could there be a better epitaph?

Filed Under: Eating Disorder Research, Eating Disorder Treatment, Genetics

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https://www.youtube.com/watch?v=PVgVmDIXqHc
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The Kartini Clinic Difference

At Kartini Clinic we practice only evidence-based, family-centered eating disorder treatment. Our program is a multi-disciplinary medical and psychiatric treatment model rather than an exclusively psychiatric approach to eating disorder treatment.  read more »

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Contact Us

Tel: (971) 319-6800
Fax: (503) 282-3409

help@kartiniclinic.com

3530 N Vancouver, Suite 400
Portland, OR 97227

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Mon – Fri 9:00am – 5:00pm

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