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Spotting the Tiger: Identifying Early Symptoms of Eating Disorders in Children for Timely Intervention

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In the powerful documentary, “Spotting the Tiger,” narrated by Oscar Award Winner Jamie Lee Curtis, the film emphasizes the importance of recognizing early warning signs of eating disorders in children. As we commemorate its 15th anniversary, the core message of this film remains just as relevant today: early detection of eating disorders in children is vital for successful treatment and long-term recovery.

In “Spotting the Tiger,” primary care providers, doctors, and therapists specializing in pediatric eating disorders reveal how even the most observant parents and medical professionals can miss subtle indications of conditions like anorexia nervosa. The film explains how these signs can often be concealed by the intricate nature of brain-based illnesses such as anorexia.

Genetic Factors and Eating Disorders: The experts in the film also discuss how eating disorders are predominantly genetic brain illnesses, rather than a result of poor parenting or the influence of the media’s obsession with physical appearance. While the media’s portrayal of beauty standards doesn’t help, it’s crucial to understand that parents don’t cause eating disorders, and children don’t choose to have them.

In the powerful documentary, “Spotting the Tiger,” narrated by Oscar Award Winner Jamie Lee Curtis, the film emphasizes the importance of recognizing early warning signs of eating disorders in children. As we commemorate its 15th anniversary, the core message of this film remains just as relevant today: early detection of eating disorders in children is…

In the powerful documentary, “Spotting the Tiger,” narrated by Oscar Award Winner Jamie Lee Curtis, the film emphasizes the importance of recognizing early warning signs of eating disorders in children. As we commemorate its 15th anniversary, the core message of this film remains just as relevant today: early detection of eating disorders in children is…

In the powerful documentary, “Spotting the Tiger,” narrated by Oscar Award Winner Jamie Lee Curtis, the film emphasizes the importance of recognizing early warning signs of eating disorders in children. As we commemorate its 15th anniversary, the core message of this film remains just as relevant today: early detection of eating disorders in children is…

We encourage you to watch “Spotting the Tiger” and learn more about the early signs of anorexia in children. By understanding the warning signs and contributing factors, we can take a more proactive approach to detecting and treating eating disorders. Share this essential film with your friends and family to spread awareness and promote early intervention.

Thank you!

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Spotting the Tiger: Identifying Early Symptoms of Eating Disorders in Children for Timely Intervention
Spotting the Tiger: Identifying Early Symptoms of Eating Disorders in Children for Timely Intervention 2

Are social media platforms making eating disorders in children worse?

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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.

Are social media platforms making eating disorders in children worse?
Are social media platforms making eating disorders in children worse? 4

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Breaking Science News: The Latest Genetic Study of Anorexia Nervosa

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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.

Breaking Science News: The Latest Genetic Study of Anorexia Nervosa
Breaking Science News: The Latest Genetic Study of Anorexia Nervosa 6

See Something, Say Something

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See something, say something is what the anti-terrorist watch tells us at the airport and in public spaces. When people take individual and collective responsibility for reporting whenever they see something potentially dangerous, something not right, it’s possible to prevent catastrophes.

 

An alert went out on the AED (Academy of Eating Disorders) listserv from Wendy Oliver-Pyatt, MD who had caught wind of a weight loss study recruiting subjects in Australia under the auspices of Children’s Hospital Westmead (Sydney) and Monash Medical Centre (Melbourne). The lead investigator is Professor Louise Baur; the Sydney Children’s Hospital Network Human Research Ethics Committee approved her proposal.

I did not respond in great detail on the listserv, except to protest children being dieted in general, as I had not yet seen the actual proposal. But now I have seen it.  For those of you who wish to read it in its entirety, here is the link.

First, let’s be clear, this is not a study for consenting adults which includes some teens, it is a study designed for children and adolescents. The youngest participants will be 13 and the oldest 17. They are looking for the equivalent of a 5% reduction in body weight in an adult or 0.12 point reduction in BMI z score in an adolescent. They say nothing about the sustainability of this weight loss, just that the fact of it will be considered a “successful endpoint”. We all know that dieting causes weight loss in the short term, but nearly always fails in the long term, so how is this progress?

The study lasts an entire year—which in my view is a very long time to starve a dog, much less a child. You have to have a BMI of between 30-45 to participate, which means that someone – likely several someones – has identified you as “fat” with all the psycho-social ramifications of that. A plethora of lab tests and frequent checks by a dietitian make it look medical, but I do not see pediatricians or adolescent medicine physicians referenced anywhere in the protocol. The dietitians are going to weigh the kids, but no one is checking their pubertal status, which matters a great deal when assessing growth and development; they measure their blood pressure but do not mention monitoring their menstrual status.

So if the teen-aged girls stop menstruating with weight loss and dietary restriction, would that still be a successful outcome?

Incredibly, the year-long study starts with all of the children being taken down to an 800 kcal a day, very low fat (less than 20%) diet consisting of “meal replacements”. Study authors think they will have an attrition rate over the year of 30% — I think it might be closer to 90% (run, children, run!). This painfully low level of initial food intake will last one month (4 weeks) for everyone, after which the subjects will be randomly assigned to one of two arms: the Modified Alternate Day Fasting arm and the Standard Hypocaloric Diet arm.  

In the alternate day fasting arm the children will eat 300-600 kcals/day for three non-consecutive days a week and a “healthy diet” not restricted in amounts for the others. The “healthy” bit means they will be “coached” to adhere to the Australian Dietary Guidelines which, if you look at them, state that one should only eat “small amounts of fats” and “mostly low-fat dairy.” Wow! Didn’t they get the memo?  Does anyone in the government actually follow the science as it evolves?  Children need fat to grow, or as one researcher points out: “Long-term dietary deprivation of (n-3) fatty acids results in measurable changes in the visual and neurological function of primates (Neuringer and Connor 1986).”  News flash: we are primates.

There are so many worrisome points (e.g., how does a 13 yr consent to this study?)  it is hard to know where to begin, and as I read on I found myself racing from one point to another, dizzy from the effort. Those children who were randomized to the non-fasting arm, or the “standard low calorie” arm as they put it, eat a diet consisting of 1434-1673 kcals/day at age 13 to 14 or 1673-1912 kcals/day for those 15 to17 years of age. Slim pickins! This so-called “healthy” diet is “high fiber” (> 30 gms/day), “moderate” carbohydrate and “moderate” protein, no mention made of dietary fat.

And the psychological “support”? Let’s remember these are kids and now they are very hungry kids who are already shamed by their size/weight and doubtless would blame themselves for any “failure” to comply. For support they see a dietitian at week 20, 26, 36 and then, as “additional support”,  receive an email, text or phone call lasting 10-15 minutes at weeks 18, 24, and 48.  

You have to ask: they receive support to do what?  Stick to the diet?

And don’t be fooled by a raft of psychological tests administered: the Body Appreciation Scale, the EDE-Q, and various quality of life questionnaires, self-esteem questionnaires and depression questionnaires. These are designed to help the study, not the kids, as it merely reports their symptoms, but cannot address them. Nor do I see a protocol for what to do should severe psychological distress arise as a result of the semi-starvation.

All of this is reason enough, in my view, to refrain from allowing your child to participate in a dieting experiment. Try it out on yourself for a month and see what I mean. Now imagine being a 13 year old kid who weighs 250 lbs and who has to live with hunger every day of their life for a full year, at school, on the playground and at home and who then, after all that, “successfully” weighs 237 lbs.

And here’s one more pressing reason not to allow it: it’s cruel.

So I have seen something, and I’m saying something: cease this madness and end this appalling and unethical experiment on children.  Please join me. Share this with your colleagues, friends, and elected representatives (if you’re in Australia). Let’s speak up and speak out.  And if the authors of this study believe we have misinterpreted their intentions, let’s have an open, respectful, scientific discussion about the merits, before a single child is enrolled.  Thank you.

Why We Limit Hyper-Palatable Foods for One Year

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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.