Kartini Clinic for Children and Families

Pediatric Eating Disorder Treatment Program

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Five Things Every Parent Should Know About Childhood Eating Disorders

February 28, 2017 by Julie O'Toole

1) Weight loss in children isn’t normal

Imagine you’re a parent of a bright, active 12 year old boy. He gets good grades and has lots of friends. He excels at sports. Then something changes; he begins to lose weight. At his last checkup his pediatrician registers a heart rate in the low 50s. He starts to withdraw, not doing many things he used to enjoy, with the exception of exercise. He now exercises with a new intensity.

His doctor tells you not to worry. “It’s just a stage”, she says. “Don’t make a big deal out if it, or you might make it worse. He has weight loss and a low heart rate because he’s an athlete.” But you have the nagging feeling that something’s wrong. What do you do?

For nearly two decades Kartini Clinic’s internationally recognized team of pediatricians and therapists has diagnosed and treated more than 3000 children from across the country and all walks of life. And we have seen presentations like the one described above hundreds of times.

Our message is always the same: weight loss in children is not normal and should be investigated immediately.

And weight loss shouldn’t be the only concern. Because children are still growing they need to gain weight. An interruption in their past rates of growth and development is a sign of potential trouble ahead. Your child’s growth chart is a critical diagnostic tool that can provide early warnings. Always review your child’s growth chart with their doctor and remember that averages don’t apply to individuals. What matters most for your child’s health should be based on their unique biology.

2) Children are not small adults

In the example above, with a daytime heart rate in the low 50s, this child’s overnight heart rate could be in the 40s. This is dangerous territory for a child. The American Academy of Pediatrics’ hospitalization guidelines recommend admission with a nighttime heart rate below 45, regardless of athleticism. Don’t be fooled into thinking that because Usain Bolt has a resting heart rate in the 40s, it’s OK for your child to do so.

Childhood is an essential period of growth and development, a time when critical biological systems form. Weight loss – or simply a failure to grow and develop normally – could signal a dangerous disruption to these processes.

3) Parents don’t cause eating disorders (and children don’t choose to have them)

This is our motto, and something we make clear to all families from day one. The scientific evidence is unambiguous. Parents don’t cause a child’s eating disorder, any more than they cause Type 1 diabetes or autism. These are both understood to be genetically inherited illnesses. So are eating disorders.

4) Eating disorders are brain disorders and run in families

How do we know this? Decades of research using twins separated at birth has firmly established the heritability of anorexia nervosa (the most thoroughly studied eating disorder) between 50% and 70%. By comparison, heritability of height is about 90%. This means your height is 90% dependent on your parents’ height. The other 10% comes from environment. Equally, anorexia’s high heritability rate implies that it’s largely a biological brain disease, passed from parent to child, but with a significant environmental component. But like many complex illnesses, we don’t yet know enough about what environmental “triggers” lead some who are genetically vulnerable to become ill.

5) If you think something’s wrong, get help

We always tell parents, ‘you are the experts in your child.’ If you think something’s wrong, don’t let your concerns be ignored, even by your pediatrician. Our colleagues in primary care are in a tough position; they don’t want to overreact. Furthermore, eating disorders are thankfully quite rare. However, most doctors don’t have training in diagnosing or treating them. But they do happen, especially to genetically predisposed children. It’s therefore critical to understand the specific risk to your child. A pediatric specialist’s evaluation is the best way to rule out an eating disorder.

Filed Under: Diagnosis, Eating Disorders, Evidence Based Treatment, General, Selective Eating

The Trouble With Accurate Eating Disorder Diagnoses

July 15, 2015 by Julie O'Toole

Almost anyone who works in a specialized field (such as pediatric eating disorders) spends a great deal of time thinking about diagnostic criteria for diseases and conditions.  This is true throughout medicine and psychiatry, of course:  is it type 1 or type 2 diabetes?  Is it autism or pervasive developmental disorder?  Is it bulimia nervosa or binge purge anorexia nervosa? Is it eating disorder not otherwise specified (EDNOS, a term no longer included in DSM-5) or anorexia nervosa?

As in other fields that deal with very young children, the patterns seen in adults can be present, absent, partly present, mostly absent… You get the idea.  Children with rheumatoid arthritis, for example, may have all or most of the symptoms that an adult with the same disease would have, or they might present completely differently (e.g. Still’s disease) and their symptoms change over time. Children are not miniature adults.

The problems of diagnostic accuracy have been well described, not least by Dr. Thomas Insel, director of the National Institutes of Mental Health (NIMH), who writes about the “gap between modern neuroscience and contemporary psychiatry.” This gap means that in the field of brain disorders we are still living in the era of the 1700’s, when the great biologist Linnaeus developed a system of taxonomy to classify all living organisms from their external characteristics. If the flower looked one way, the plant belonged in the pea family (Fabaceae), if somewhat differently, in the cabbage family (Brassicaceae), etc.  Since long before Linnaeus, physicians have classified diseases depending on the constellation of symptoms they could see with their eyes:  if the patient was driven to exercise, restricted their food intake severely, and believed themselves to be fat, despite all evidence to the contrary, they had anorexia nervosa, if they were not underweight, binged on large amounts of food and then, panicked, got rid of it by vomiting, they had bulimia nervosa, etc.  The human urge to classify, to organize, to arrange in patterns is strong and it has served us moderately well.  But classification based on external descriptors or symptoms is about to be blown apart by genetics, molecular biology and imaging technology.  Already the system of plant and animal classification developed by Linnaeus—amazingly still in use—has been altered by genetic information about the origins of living things.

Why does taxonomy matter?  Does it matter?  I would argue that it is in fact less important than the principles of treatment, especially in the world of pediatric eating disorders.  For example, whether a child has anorexia nervosa binge-purge subtype, or restricting varieties of ARFID is decidedly less important than recognizing that they need more food!  It does seems likely that prognosis could be different within and between diagnostic categories—for example, early onset anorexia nervosa may have a better or worse prognosis than ARFID.

Over the years I have become convinced that there are children, and especially teens, who have imitative forms of the condition we call anorexia nervosa (a brain disorder I hope we will one day see in neuroimaging).  These would be children/teens who refuse to eat for psychosocial reasons.  But which are which?  You can’t tell by looking, that is for sure.  And since the treatment is the same, it is of largely academic interest to try and tease this out.  Only time and longitudinal experience with their illness will tell, and trivializing the suffering of a child or that child’s parents by saying they have an “imitative” form, could do great harm.

So until we have that biological marker, that lab test, that brain imaging study, that gene assay, we are stuck with the simple observation of patterns.  Receiving treatment that works is more important than understanding why it works.

In the case of childhood eating and growth disorders we know what works: food and love.  So for now we’ll have to stick with that.

Filed Under: Anorexia Nervosa, Bulimia Nervosa, Diagnosis, Eating Disorders, Food Phobia, Genetics

The Promise of Personalized Medicine

September 4, 2014 by Julie O'Toole

Advances in medicine come in all shapes and sizes: vaccines, antibiotics, anti-virals, immune system boosters and reducers, technological changes and recently, the hope that faster, cheaper and more accurate genetic analysis can bring us the new approach to medicine and medications: personalized medicine.

As I have mentioned in a previous blog, a leading proponent of personalized medicine has been Dr Eric Topol, editor-in-chief of Medscape and director the Scripps Translational Science Institute.  Translational science is an important concept.  It means taking the bench sciences and research and translating them into actionable information for people who actually care for patients.  Dr Topol, himself a cardiologist, has written a great book on the subject called The Creative Destruction of Medicine.  Check it out.

At Kartini Clinic we are always searching for better ways to deal with medication for our patients.  We have often found it helpful to use the antipsychotic drug Olanzapine, in small doses, for the delusional fear of food and fat in anorexia nervosa.  It is the mainstay of our success with young patients with food phobia.  But we can’t use it in every patient, nor would we want to, and when we do use it we want to use it for the shortest period of time that we can.  For some patients Olanzapine is a game changer; for others it helps a little, and some seem to show little to no effect. And, of course, like all clinics which treat many patients with complex brain disorders, such as an eating disorder AND depression or an eating disorder AND obsessive compulsive disorder or an eating disorder AND anxiety, we have experience using the class of drugs called SSRI’s (Prozac, Paxil, Celexa, Lexapro, etc).  Once again, some patients respond brilliantly, some respond a little, and some seem to get no help at all.  Frustrating. So in thinking about medication and kids with eating disorders, we have piloted a few programmatic approaches to deal with safety and efficacy which, as far as we can tell, appear to be unique to Kartini Clinic.  As Dr Moshtael and I are both pediatricians, we tend to be conservative with medication.  Adult doctors seem to throw one medication after another at adults and see what sticks. “Just try it”, is often the motto.  We hate this approach and refuse to use it with our children, who, after all, have young, growing brains and are precious beyond telling to their parents.  So our general philosophy has been: “keep the formulary small and try to use one or at most two medications at a time”, “use no sleeping pills”, and “use no addictive drugs such as benzodiazepines to treat anxiety”.  We also say: “use the smallest dose that’s effective and for the shortest period of time you can.” Well, that’s all very well and good, but it’s not advanced science, it’s just a conservative approach to safety. A few years ago, when thinking about my own experience with tuberculosis and leprosy as a young doctor in the South Pacific, and gnashing my teeth over the fact that our young patients were often “non-compliant” with their medication, I hit on a game changing approach for us: “directly observed therapy”, such as is practiced for multiple drug-resistant TB.  Directly observed therapy means that a parent, in the case of our patients, (a community health nurse in the case of resistant TB in the Pacific islands and elsewhere) is placed in charge of all medication and gives it directly to the child every day “babybird style” directly into their mouth, followed by two sips of water and swishing the mouth.  Such directly observed administration follows our model of having parents in charge of food in family-centered treatment. Suddenly, safety and efficacy improved for our patients immensely.  Why don’t all doctors who treat children do it this way?  Well, for one, they don’t have the family-centered treatment approach that places parents in charge.  In the past, as a general pediatrician, I have seen adults abdicate control of insulin to their diabetic six year olds. Don’t get me started!  These are dangerous and important drugs, folks, be they insulin, metformin, Olanzapine, Prozac or anything else, and we must insure safety, at least for children.  These medications are too important to take for three days and forget on the fourth. So DOT BB S&Sx2  our shorthand for “directly observed therapy, baby-bird style, swish and swallow twice” has gone a long way towards ensuring stability and accuracy of dosing as well as reducing non-accidental overdose in teenagers, but it is still the shallow end of the pool. What is the deep end of the pool in personalized medicine?  Genetic testing.  And we have just begun to use it. A new firm called Genomind reached out to us about non-invasive (cheek swab or saliva) genetic tests which focus on testing for individual response to psychoactive medication.  To be certain that this was what it purported to be, I had myself tested first.  That way I could feel free to discuss the results, if any, with our families and my readers. The results?  I discovered that I carry a variant of the gene SLC6A4 which codes for “slow response, poor response and/or likelihood of adverse events with SSRI’s”.  Good to know! They further elaborate on my genetics, saying: “The serotonin transporter protein is a presynaptic transmembrane protein responsible for serotonin reuptake. The patient (me)  exhibits a variant of the serotonin transporter gene which the literature suggests may result in reduced reuptake of serotonin, less satisfactory response to SSRI-based treatments, and potentially a greater risk of adverse effects, compared to patients without this variant.” Citations are included for all of these assertions. They go on to say: “This variant has been associated in published literature with lower stress resilience and higher rates of PTSD”.  Well, I don’t know about lower stress resilience, as I have had a fair amount of stress to deal with in my life and have seemed fairly resilient, but it is true that my own father, obviously one of my closest genetic relatives, suffered from PTSD from severe combat experiences during WWII. Further, the study states, I have a variant of the 5HT2C gene which means I would be at high risk for the side effect of weight gain were I ever to use Olanzapine. (Glad not everyone carries this gene variant!)  I also have a deletion in the DRDR2 gene which means that Olanzapine would not only affect my weight metabolism, but it also likely would not work. Again, good to know. I fortunately have the normal MTHFR (no jokes, please) gene variant which means I would respond to drugs affecting the methylenetetrahydrofolate reductase system, such as Deplin, which we occasionally use in depression.  I have normal CY2D6 genes as well. Were this not the case I would likely metabolize psychotropic medications too rapidly and/or unpredictably, altering their response to them. We have been very excited about the possibilities of adding this personalized genetic information to our prescribing armamentarium.  It would be great to know in advance which drugs should or should not be expected to work in an individual patient.  This may turn out to be the ultimate weapon in increasing safety and efficacy and go a long way towards making sense out of who responds to medication for depression, anxiety and other brain disorders and who does not. We have just begun to test those patients whose parents wish it and whose insurance will cover it. Our patients and their parents are excited about the possibilities.  We are excited.  Targeted genetic testing is no doubt the future of personalized medicine.  And we, at Kartini Clinic, intend to embrace it.

Filed Under: Anorexia Nervosa, Diagnosis, Eating Disorder Treatment, Evidence Based Treatment, Family-based Treatment, Genetics, Medications

The Stigma of Mental Illness

July 17, 2014 by Julie O'Toole

Lots of ink is been spilled on the subject of the stigma associated with having an eating disorder.  And in order to discuss the subject sensibly we need to get a few terms straight. It was considered a giant step forward in our field when Dr. Thomas Insel, head of NIMH, began blogging, writing and speaking about the fact that all mental illnesses are brain disorders, and that anorexia nervosa in particular was a severe mental illness.  Prior to that it had been possible to trivialize anorexia nervosa as a psycho-cultural dysfunction, a “choice”, the result of family dysfunction, and/or attributed to reading too many fashion magazines.  Bulimia nervosa had even been described as “regurgitating the mother”.

A new era of understanding the brain has brought some clarity to the subject, but hasn’t really touched the issue of stigma. So, if eating disorders such as anorexia nervosa are severe mental illnesses, and by definition brain disorders, I think it seems clear that disorders of the brain should be no more stigmatized than disorders of the pancreas, disorders of the heart, or disorders of the liver.  As the pancreas produces insulin, the brain produces behavior, and this, I think, is what lulls us into believing that disorders of the brain are somehow “different”. What to do about the stigma? It is first important for us to examine our own role in furthering any stigma associated with eating disorders.  Let’s start with doctors. To be more specific, let’s start with psychiatrists.  It has long gone unchallenged that a higher level of “privacy” needs to be afforded psychiatrists, who, after all, deal with mental illnesses.  It is not uncommon for psychiatrists and other therapists to have waiting rooms that do not allow patients to see each other or to know who else might be waiting, they may even have separate entrances and exits for this purpose.  On the face of it that sounds good, but what’s the message? The message is that, contrary to a visit to a gynecologist, which certainly can involve information as sensitive as any psychiatric information, a visit to a psychiatrist needs to be kept “private” (read: secret). Your gynecologist might say hello to you in the grocery store, your psychiatrist will probably act as if they do not know you unless you acknowledge them first.  Again, what’s the message?  Psychiatric medical records are treated differently than other medical records.  On Epic, a widespread form of electronic medical record, even other doctors cannot access a patient’s psychiatric records without first “breaking the glass” to enter über-protected territory.  As long as we physicians continue to treat brain disorders differently than other disorders, we too are responsible for perpetuating the stigma. As parents we are naturally protective of our children.  It’s not uncommon for people to enter online forums anonymously, and the most cited reason for such anonymity, is to protect the privacy of their child. I think we must boldly ask ourselves, though, whether we are protecting our child’s privacy or we are somehow buying into the belief that mental illness is a “flaw” in our child, in our family, in ourselves.  Some families choose to conspire to keep the fact of their child’s eating disorder from their school, from their church, and even from their friends.  Occasionally even other family members are left out of the loop.  And while I completely sympathize with attempts to “control the message” at the time of initial diagnosis, I think that in the long run it will be critical to unambiguously send the message to our own family and our own children that there is no reason to feel stigmatized for having an eating disorder.  And that, in fact, to the contrary, we will fight this false belief together. As Pogo said “We have met the enemy, and he is us”. Only sunshine into the dark places will evaporate this unnecessary pain.

Once upon a time tuberculosis was a terribly stigmatizing illness.  Even now, when taking histories from some Southeast Asian families, it is common for the fact of a family member’s tuberculosis to be concealed.  It is medically unhelpful not to know who is vulnerable to what disease, but the stigma of TB was, and to a certain extent still is, far too great for many families to challenge.

With the evaporation of insurance denials based on “pre-existing conditions”, we no longer need fear that our child will not be able to get insurance if the fact of their eating disorder becomes known. With the many recent articles on the genetics of mental illnesses, the public statements reiterating that families do not cause eating disorders, and the air-clearing acknowledgment of eating disorders as brain disorders, we can finally begin to attack the stigma together. Let us not be that enemy.  For the sake of our children and all children, let’s find the courage — whether we are physicians, therapists, dietitians, parents, or patients — to cease contributing to the stigma, to stand our ground, to turn around and fight back.

Filed Under: Anorexia Nervosa, Diagnosis, Eating Disorders

Mixed Symptoms

April 3, 2014 by Julie O'Toole

Recently I was making our daily rounds at Randall Children’s Hospital and received a lesson from a very young patient of ours.  I say it over and over: “your patients are your teachers”, and it is really true.  I was first told this by Dr. Mizuo Tottori, pediatrician and mentor to many other pediatricians in Hawaii. And life itself has borne out the truth of it, again and again.

This particular little patient has anorexia nervosa and has done very well.  Her parents are competent and loving; but her illness is relentless and merciless. She had been in good remission until the latest bout of symptomatic resurgence.  The twist on the usual story has been the new emergence of “food phobia-like” symptoms along with the anorexic difficulties of eating at all.  She struggles to swallow and pools her saliva. Had presented like this initially, we would have made the diagnosis food phobia and consequently missed the early-onset AN, or at least for a while.  What we have discovered is the “magic food phobia dose” of Olanzapine (7.5 mg) seems to work as well for this mixed presentation as it does for pure food phobia (see also previous blogs).  For strict AN we don’t usually need this high of a dose.  Once we titrated our little girl up to 7.5 mg, her food phobia-like symptoms improved. So walking back to the office from making rounds, her sweet face in my mind’s eye, I began to think about diagnoses in general and hers in particular.  I tried to think of other medical situations where we have a “mixed diagnosis”. All diseases have a natural history.  Their natural history encompasses the totality of “how they act”, meaning what the onset is like (sudden, gradual, insidious), expected course of symptoms (rash, fever, weight loss, pain, appetite changes, sweats, etc., etc.), expected duration and course, etc.  Is it acute? Chronic? Does it wax and wane/remit and exacerbate? How does it respond to treatment? Is it fatal? Is it contagious? Does it burn itself out if the patient lives? For example, if you diagnose a patient with smallpox, we know something about the natural history of this illness: it is caused by the variola virus (therefore “contagious”), there is an incubation period of about 10-12 days (before skin symptoms appear) and a prodrome towards the end of that period involving high fever, back ache, and diarrhea. Then the characteristic rash appears, first in the mouth and then all over the skin: multiple raised spots which blister all at the same time before finally going away (often with severe scarring).  30-35% of people who acquired smallpox (when it existed on planet earth) died of it. So now you know its natural history.  You can see why it matters to know this, both to the treating doctor and — importantly — to the patient. But let’s say that, in the middle of a smallpox epidemic, you incorrectly diagnosed a patient with variola when what they really had was an infection with varicella (chickenpox).  Even if you could not do cultures or viral tests, you could likely tell that you had made a mistake by their differing, evolving natural histories.  Chickenpox is also contagious, with an incubation period similar to that of smallpox and a prodrome not entirely dissimilar either: nausea, loss of appetite, aching muscles, and headache.  If you were very experienced you might notice the lack of severe back pain.  But once the rash appeared you would know the difference: the chickenpox are pox at all different stages of blistering, redness and healing or rupture, not a mass of many pox all at the same stage, as is true for smallpox.  Ah hah!  They have a different natural history.  And to underscore why this is vital, almost no one will die of chickenpox. So are AN and food phobia like that?  Well, yes, in the sense that they have differing natural histories.  But how about a patient who shows features of both? To think about that, I need to think about more complex illnesses and nothing’s more complex than rheumatology…. Let’s say your patient has a strong family history of autoimmune disease (Hashimotos thyroiditis, type one diabetes, multiple sclerosis, etc.) and is suffering from joint pain, muscle inflammation, fevers, exhaustion and a strange thickening in the skin of the hands.  You first think scleroderma or lupus (SLE).  But then, they have features of rheumatoid arthritis and dermatomyositis… confusing.  After a period of watching their illness evolve and seeing how it responds (or doesn’t) to treatment, you decide they have “mixed connective tissue disease” (MCTD) with features of many autoimmune rheumatic illnesses, but a natural history somewhat different than any one of them.

Is AN with food phobia-features like this?  I believe it probably is.

Interestingly, MCTD does not seem to morph into SLE, for example, although they can share common diagnostic features.  Likewise, we do not have experience of food phobia morphing into anorexia nervosa; they seem to be independent illnesses, even when they both result in food avoidance. I guess the bottom line is that we clinicians are still stuck in the 19th century folks, that’s right — the 1800’s — where the primary tool we have at our disposal is basically observation of the natural history. We know what to do, what seems to work, but we are not sure why. The basic biology of childhood eating disorders is still almost entirely unelucidated (not to mention the genetics). And until they are, until genetics and biochemistry replace observation of natural history as our teachers, our patients retain that honor. In other words, Doctors, pay attention to your patients!

Filed Under: Anorexia Nervosa, Diagnosis, Eating Disorder Treatment, Food Phobia

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