Dr. Sarah Ravin - Psychologist | Eating Disorders |Body Image Issues | Depression | Anxiety | Obsessive-Compulsive Disorders | Self-Injury
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Dr. Sarah Ravin

Welcome to my professional blog. I am a Florida Licensed Psychologist and trained scientist-practitioner. In 2008, I received my Ph.D. in clinical psychology. A major component of my professional identity is staying informed about recent developments in the field so that I may provide my clients with scientifically sound information and evidence-based treatment. There is a plethora of information on the internet about Eating Disorders, Depression, Anxiety, Psychotherapy. Unfortunately, much of this information is unsubstantiated and some of it is patently false. It is my hope that by sharing my thoughts and opinions on psychological issues, with scientific research and clinical experience sprinkled in for good measure, I can help to bridge the gap between research and treatment.

Brain-Based Language and Eating Disorders (by guest blogger Carrie Arnold)

The following is a guest blog post from Carrie Arnold, science writer and blogger, who attended the International Conference on Eating Disorders with me earlier this month.

Language is a funny thing.

I’m a writer–every day, I see (and use!) the power of words to explain very esoteric subjects, to comfort a friend, and even to entertain. The language we use to talk about eating disorders is also important. It was refreshing to have a psychotherapist describe me not as “an anorexic,” but as “someone with anorexia.” Anorexia was a diagnosis. It wasn’t me.

The issue of language in eating disorders goes far deeper than whether or not to use anorexic or bulimic to describe someone. It cuts right to the heart of how we understand eating disorders and how we treat them. One of the sessions at the 2012 International Conference on Eating Disorders in Austin, Texas discussed the use of brain language in regards to eating disorders. Laura Collins, founder and executive director of FEAST, spoke about how the biological language can be empowering to parents and sufferers. Brett Deacon, a psychologist from the University of Wyoming, spoke of the power of the biopsychosocial model of mental illness, and the potential dangers of biological language. Anne Becker, an anthropologist and ED expert from Harvard University, talked about how language affects our perception of EDs. Lastly, Kelly Klump, a behavioral geneticist from Michigan State University, asked the crucial question: is it time for new language or new data?

First, a mini-history lesson. As neuroimaging techniques and other brain science has advanced in recent years, scientists studying mental illness have begun to use these tools to explore the biology of mental illness. Without these tools, researchers could only look at the psychosocial factors that contributed to mental illness, and they accumulated a mass of very important data on the subject. But neuroimaging and other techniques have allowed scientists to probe biological variations that might contribute to mental illness. Leading psychiatrists and psychologists like Tom Insel, director of the National Institute for Mental Health, have argued that these significant biological differences mean that “mental illness” should be renamed “brain disease.”

To some, a brain disease by any other name surely doesn’t smell as sweet. To me, the use of “brain disease” or, an alternative, “biologically-based mental illness” seems obvious. Depression, schizophrenia, and eating disorders affect the brain. That’s where they start. Deny that, and you may as well call them Big Toe Disorders or something equally ludicrous. If they’re not brain disorders, then what are they? I’m not asking a rhetorical question-I really would like an answer.

One potential answer that Dr. Deacon suggested was the biopsychosocial model. Mental illnesses are really biopsychosocial illnesses. Which is accurate. My problem with that term is that every disease, from eating disorders to cancer to diabetes, has biological, psychological, and social components. It’s like taking cows, sheep, goats, horses, dogs, and cats and putting them in a barn and trying to tell them apart by figuring out which have four legs.

I don’t know of anyone out there who can support the assertion that EDs are only biological. Genes matter, yes, but so does environment. Laura presented statements from families around the world that biological language like “brain disorder” gave them a way to move forward. Looking for blame didn’t really matter anymore. They could reframe their loved one’s behavior: instead of being a willful teen refusing to eat, they had a sick adolescent who wasn’t able to eat.

One of the main concerns with the biological language is the potential for stigma. If your genes caused your illness, then you’re screwed. After all, your genes are your genes, and they’re not changing unless you stand in front of some gamma rays. Which I wouldn’t recommend. Basically, then, it’s easy to see how biology would support the view of “Once an anorexic/bulimic, always an anorexic/bulimic.” Recovery was a hopeless endeavor.

While it’s true that you’re stuck with the genes you’re born with, your biology isn’t written in stone. To paraphrase biologist PZ Myers, biology isn’t rigid. It’s a bunch of squishy processes making do. Your genes don’t change, but their expression does. It’s a process known as epigenetics, whereby genes are regularly activated and silenced by various environmental factors. It’s entirely possible that the negative energy balance (that is, burning more calories than you’re consuming) that typically precedes anorexia activates genes that perpetuate the food restriction. It’s also entirely possible that nutritional rehabilitation silences these genes or activates other ones that help the brain and body return to normal.

The problem, then, isn’t with the biological language per se, but rather our culture’s generally abysmal level of scientific literacy. These concepts are difficult for even PhD scientists to understand. But as society’s awareness of the biological contributions to brain diseases/ mental illness grows, perhaps the understanding of the complex biology will improve as well. In fact, a study by Cindy Bulik and colleagues at UNC found that biological language actually decreased the stigma of anorexia, rather than increasing it.

Saying things like “brain disease” also doesn’t mean that the only solution is a pill. Although I do benefit from medication, I’m hardly a shill for Big Pharma. Psychotherapy remains one of the best ways to reliably change the brain long-term. Researchers found significant brain changes when a group of people with spider phobia underwent a course of cognitive-behavioral therapy. The authors conclude that “These findings suggest that a psychotherapeutic approach, such as CBT, has the potential to modify the dysfunctional neural circuitry associated with anxiety disorders. They further indicate that the changes made at the mind level, within a psychotherapeutic context, are able to functionally “rewire” the brain.”

At some point, however, all of this “language talk” makes me want to throw up my hands in frustration. Aren’t we just wasting loads of time playing at semantics? Call it Rainbows and Kittens for all I care!

Except that language really does matter. A recent study in the American Journal of Psychiatry found that people were significantly more likely to believe that someone needed treatment when they were diagnosed with social anxiety disorder versus social phobia. In the state of New Jersey, it was legal for health insurers to deny paying for anorexia treatment because it wasn’t a biologically based mental illness. A recent class action law suit caused this provision to be overturned and anorexia and bulimia treated on par with depression, bipolar disorder, and schizophrenia. Language matters, and it matters a lot.

The talk at ICED didn’t necessarily settle the matter, but then it wasn’t meant to. The most important thing was how it provided a better understanding of what we all mean when we say things like brain disease or biopsychosocial. What I mean when I say brain disease isn’t necessarily what other people mean. I know that talking about the biology of eating disorders doesn’t mean that environment is irrelevant as is psychotherapy. But that’s not necessarily what other people think. Perhaps what the field needs to do is clarify what their terms mean and how they use them in a sentence. Only then can we start to have a meaningful dialogue that will move the field forward.

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8 Responses to Brain-Based Language and Eating Disorders (by guest blogger Carrie Arnold)

  1. I always love your posts, Carrie, and this post (like all your blog posts) is very well researched and written.

    As for the term ‘brain disorder’ – to describe eating disorders (EDs); I hate it. My dislike of the term is both personal and academic.

    In terms of the latter, there is absolutely ZERO evidence that EDs are discrete, inherited brain disorders. Yes, they are biologically based; but they’re not brain based. There is no evidence that people who are vulnerable to developing EDs have a brain lesion, or specific and serious abnormalities in functioning before the onset of ED symptoms. EDs do not originate within in the brain. The illness seems to start with behavioural changes that influence energy balance, hormone levels, nutrient availability and appetite regulation. Various hormones and nutrients feedback on the brain and alter both its structure (e.g. grey matter shrinks in established AN) and neural activity. Thus, biological factors influence brain physiology.

    The very fact that brain physiology is altered in EDs is evidence that the person with the ED isn’t ‘choosing’ to behave in the self-destructive way that they do when they have an ED. It makes sense that EDs are described as ‘biologically based illnesses’; but not ‘brain disorders’. It is also important that treatment funders are aware that EDs are not ‘choices’.

    No research study has delineated the genes responsible for causing EDs as a whole, or EDs as defined categorically. Family studies suggest that EDs are familial; however, such studies also suggest that EDs, autism, anxiety disorders, depression and addictive disorders can run in families. It would seem more likely that the heritable characteristics relating to ED risk are temperament traits (e.g. anxiety) and cognitive processing style (e.g. poor set-shifting, detail-oriented focus). Some people with EDs have impulse-control difficulties, while others are over-controlled.

    From an ethical and personal perspective, I find the term ‘brain disorder’, to describe my own history of anorexia nervosa (AN) stigmatising. I exhibited a number of the ‘at risk’ traits and behaviours before the onset of AN – e.g. high anxiety, obsessionality, perfectionism, autistic traits and OCD. However, what tipped the balance and triggered my anorexic behaviours was trauma (serial bullying by peers + sexual abuse by someone outside of the family). These traumas caused me to hate myself, to have panic attacks and paranoid thinking. The latter wasn’t some ‘idiopathic brain fart’ that I was born with, but a neurological response to trauma. The thinking that underpinned my AN was not ‘I am too fat’, but ‘I fear looking sexual – in case I get raped again’.

    To have been told as as a teen struggling with both AN and PTSD that I had an inherent ‘brain disorder’ would have made me feel even more helpless and hopeless than I already felt. It was HUGELY invalidating to be told “you’re in a bad state today; have you taken your pills?” Of course, re-feeding and weight gain have been essential components in altering my brain physiology during recovery from AN; but there is absolutely no way that my AN was an inherited ‘brain disorder’.

    Some people may find the term ‘brain disorder’ to describe EDs empowering. I, for one, do not.

  2. To quote the late Senator Patrick Moynihan, we are all entitled to our own opinions, but not to our own facts. With due respect, it simply is not true that there is no evidence to support the “brain disease” hypothesis of AN. Below are links to two clips on the subject by Dr. Tom Insel, Director of the National Institutes of Mental Health. The second clip specifically addresses the issue of a lack of brain lesions, and why this should not be considered proof of the absence of brain-specific pathology.

    (1, shorter)
    http://youtu.be/wu6QaR_gO9I

    (2, longer, from keynote presentation at FEAST conference 2011)
    :http://youtu.be/CwqpM-dcHPk

  3. Thanks Morgan. I have watched these clips previously – before I wrote the comment above.

    There is no evidence that the brains of people with EDs develop differently – in contrast to autism and schizophrenia, for example. Sure, the brain of a person with an ED is functioning differently, but the disease doesn’t start off in the brain.

    Can you show me some evidence to support the hypothesis that the neurological development of the brains of people with EDs differs from that of people without EDs before the onset of sustained disordered eating?

    The very first video in particular, says nothing. Insel admits that we know very little of what is happening in the brain of people with EDs. That video can hardly be used as a defence for the theory that EDs originate in the brain, or are neurodevelopmental conditions.

  4. I’m not sure I understand the premise that a brain disorder must be a developmental brain disorder.

  5. If the term ‘brain disorder’, according to the language of Thomas Insel/NIMH, includes reversible brain ‘arrhythmias’ that may be elicited by environmental/interpersonal factors, then what’s the point of naming conditions such as EDs and PTSD as ‘brain disorders’? Such a term suggests that the disease originates in the brain, rather than being a CNS response to external cues and (e.g.) adrenal hormones at times of stress.

  6. Ian Frampton says:

    Dear Carrie, thanks for initiating this conversation, and to Extra Long Tail and Morgan for thoughtful contributions. Just to introduce myself to place my comments in context, I am a developmental neuropsychologist working in eating disorder research in the UK and Norway, who has had the pleasure of working with Julie, Morgan and colleagues at Kartini.

    I think that it might be helpful to couch this debate in terms of ‘risk factors’, rather than either/or. My view is that some forms of what we currently diagnose as Anorexia Nervosa are the final common pathway of an interconnecting series of cumulative risk factors including a specific genetic profile (we think noradrenergic) interacting with early epigenetic factors operating during pregnancy to confer a brain-based vulnerability to later environmental factors. None of these in isolation ’causes’ an eating disorder; it’s the exquisite interaction of these factors.

    The main problem for us brain proponents is that the neural risk factor isn’t a ‘lesion’ (or hole in the head) that will ever be imageable by even the most powerful MRI scanner. I think that this factor is an incredibly subtle alteration in a neural network that biases it to process information in specific ways. These could be the ‘at risk traits and behaviours’ you describe, Extra Long Tail.

    Our suggestion is that this neurodevelopmentally mediated underlying risk factor is a necessary, but not sufficient, predisposing element that makes some young people more vulnerable to later psychosocial/environmental triggers. The reason for being interested in this predisposing factor is that it might help us to understand the origins of eating disorders better, maybe even to develop new treatment approaches (including psychological therapies), as well as potentially to change the public perception of what ‘mental illness’ means; and possibly to support young people and their families who are facing the challenge of eating disorders.

    For more on all this, see: http://www.ncbi.nlm.nih.gov/pubmed/22326200

    With best wishes

    Ian

  7. Many thanks for your response Ian. I am actually a great fan of the research you do with Bryan Lask and Ken Nunn – and if you get the chance to read some of my blog, you will quickly see that I am opposed to the idea that AN is caused by popular culture, is some sort of ‘choice’, or is wilful behaviour. I emphasise the biological basis in many of my blog posts.

    I absolutely do not dispute the idea that an alteration of brain physiology is involved in mediating the symptoms of AN; however, I see little evidence to support the hypothesis that AN is a discrete inherited ‘brain disorder’, or that it always starts off in the brain. As yet there are no studies (please correct me if I am wrong…) that show the same unusual pattern of brain physiology you and your colleagues have observed in people with active AN (and some with AN who have recovered) BEFORE they developed symptoms of AN. It would be quite ethically challenging as well as expensive to scan the brains of a very large enough cohort (for adequate statistical power) of small children longitudinally, to investigate how their brains are developing and how their brains respond to external cues.

    One point I will make is that your brain-based model of AN is focused around disturbance/distortion of body image – which is presumed to trigger the behaviours of AN (?). Not all people with AN have this body image distortion. I certainly didn’t. When I had a BMI of 13, 14, 15, 16, 17, 18, (now >19), I could/can gauge my real shape. At BMI 13 I saw myself as emaciated/skeletal and I hated it. But I still felt compelled to restrict food and to over-exercise – because these behaviours attenuated my general anxiety.

    Nevertheless, on a personal level, I totally agree that I have always exhibited a particular information processing bias. Apart from anxiety and hypervigilance, which my mother observed in me as a baby, toddler and young child, I have always displayed superior attention to detail, alongside some difficulties with executive functioning. I was a subject for some of the studies conducted at IoP (KCL) in 2010, which examined information processing and compared such processing in individuals with AN, high-functioning autism and controls. My scores were very different to those of controls despite me having achieved a healthy weight. Therefore, I know that I have many of the risk factors for developing both AN and obsessive-compulsive behaviour patterns.

    However, the definite trigger for the onset of my anorexic behaviours at age 11 was trauma – and the thinking that underpinned my AN for the first few years was PTSD-related. I feared having a sexually mature body because I didn’t want to attract male attention and to be raped again. Thereafter, the behaviours of my AN became fixed and had no real ‘meaning’. I just felt compelled to do them; and if I didn’t do them I felt terribly anxious.

    So in summary: I entirely agree that to develop AN a person must possess a certain, inherent vulnerability. Research studies suggest that most people with AN have not been traumatised before they develop the illness. But if you were traumatised, and PTSD is intertwined with your AN, then it would be unhelpful if professionals were to ignore the PTSD and to invalidate your experiences – by informing you that you were ‘born that way’.

  8. The quantity and the type of eating depends up on the factors such as peer pressure, food availability, ethics in families, their own appetite, imitating role models, concerns about gaining weight, and psychological factors.

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