This is Part III of my mini-series on the Mandometer® treatment. In my first post, I wrote about the history and rationale of the Mandometer® treatment. In my second post, I evaluated a recent study published by the creators of Mandometer® (Bergh et al., 2013); I wanted to see whether their data supported their claims (spoiler alert: it didn’t). In this post, I’m going to focus on the first five of Bergh et al.’s ten reasons why eating disorders are not mental disorders (or something like it, anyway).
If it seems like I have a personal vendetta against Cecilia Bergh & Co/Mandometer®, rest assured that I most certainly do not. I just don’t like bad science, misleading claims, and snake oil. As I mentioned in my first and second posts, I actually like many of the components of the Mandometer® treatment. (For example, I agree that weigh restoration (when applicable) and normalization of eating are crucial, primary components of ED treatment.) I just thought I’d take the opportunity to illustrate how critical we have to be when evaluating claims — even if those claims come in form of peer-reviewed literature from PhDs and MDs affiliated with respected institutions.
Before launching into their list, Bergh et al. begin by claiming that ED treatment is far from standardized and often includes therapies that have not been shown to be effective for EDs. I whole-heartedly agree. I’ve written about this issue myself (Most notably in this post: Should Insurance Companies Cover Residential Treatment for Eating Disorders?).
But Bergh et al.’s lengthy list of therapies “used by different ED clinics as part of what can be considered standard care” includes therapies like “post-traumatic stress disorder therapy,” “sexual abuse counselling,” “drug therapy,” “trauma therapy,” and “traumatic incident reduction therapy.”Now I don’t know about you, but I have yet to come across a hospital that provided “sexual abuse counselling” or “post-traumatic stress disorder therapy” to their eating disorder patients regardless of whether or not they actually experienced sexual abuse or suffered from PTSD.
But I’m getting distracted. Here’s Bergh et al.’s first reason why eating disorders do not have an “underlying mental health disorder.” (I’m not sure what they mean by “underlying.” Do they mean eating disorders aren’t caused by another mental disorder? Or do they mean eating disorders aren’t mental disorders? Whatever they mean, I think this lack of clarity is purposeful: When things are murky, it is easier to spin them whichever way you want.)
Reason #1: The failure of psychotherapy argues against an underlying mental health disorder. The poor long-term remission rate for patients with eating disorders using interventions aimed at treating their psychiatric symptoms (reviewed in the Introduction) suggests that these symptoms are not the cause of their eating disorder.
Wait, what?Simpler explanations include (among others) that current psychotherapy interventions are (i) insufficient by themselves and/or (ii) not yet well developed.
Bergh et al.’s unstated premise is that psychotherapy cures all (or even most) mental disorders. Thus, since it “failures” to cure EDs, EDs must not be mental disorders!
Think about medical conditions like cancer, cardiovascular diseases and metabolic diseases. We know varying amounts of the causes of these illnesses. Sometimes we even know the exact cause of a disease but it doesn’t mean our current treatments are sufficient to cure it. Why? Because treatments may be (i) insufficient by themselves, (ii) not specific enough for a particular person’s biological make-up, (iii) initiated too late, (iv) not well-developed, and so on. But is anyone seriously arguing that just because chemotherapy, radiation therapy, and surgery fail to cure many (most?) forms of cancer that cancer is not a medical condition?
And by the way, psychotherapy doesn’t “fail” at treating eating disorders. Is it good enough? Not even close. Would I consider it evidence-based? Hardly. But it doesn’t “fail.”
A recent study comparing the long-term efficacy of interpersonal psychotherapy (IPT), cognitive behavioural therapy (CBT), and specialist supportive clinical management (SSCM) for adults with anorexia nervosa found that overall 49% of patients showed good outcome after ~6.5 years, and 64% of patients treated with IPT had good outcome at follow-up. Was it a small study? Yes, it was, but it is not the only one.
And for bulimia nervosa, CBT is the most evidenced-based treatment to date, with IPT also showing good results. For a short and recent review on psychological treatments for eating disorders, check out the review by Kass et al. (2013).
Are these remission outcomes adequate? No, not even close. But it is not failure. (And they are comparable to the results Bergh et al.’s results.)
Reason #2. The failure of pharmacotherapy argues against an underlying mental health disorder. The failure of psychoactive medication, which may be effective in alleviating psychiatric symptoms in other groups of patients, in treating eating disorders (reviewed in the Introduction), provides additional evidence that psychiatric disease does not cause eating disorders.
Wait, what? First of all, psychiatric drugs are generally crap. Why? Because the field is young and the brain is really, really, really, REALLY complicated. And also because similar behavioural and cognitive patterns may be caused by different underlying mechanisms in different people, so the same drug won’t work for everyone. We don’t have good medications for anxiety disorders and depression – so, do Bergh et al. argue that anxiety disorders and depression are not mental health disorders either? Expecting pharmacotherapy to cure eating disorders when we don’t even have drugs to cure diseases where we know exactly what’s causing the disorder/disease is a tall order.
Would anyone argue that the failure of chemotherapy to cure all/most cancer argues against an underlying medical condition? Or that the failure of pharmacotherapy in treating epilepsy, Huntington’s disease, cystic fibrosis, and AIDs argues against them being medical conditions? No, no it doesn’t.
Drug development is a lengthy process, and given that pharmaceutical companies are pulling out of developing drugs for mental disorders (see here and here), the “failure” of psychotherapy to treat eating disorders doesn’t and won’t mean much.
And by the way, pharmacotherapy doesn’t “fail” at treating eating disorders, it doesn’t “fail” at treating bulimia nervosa, anyway: 60mg of fluoxetine (Prozac) has been shown to be effective in greatly reducing symptoms in a subset of BN patients (see here, here, here, and here).
Reason #3. The vulnerability of women athletes argues against an underlying mental health disorder.
Wait, why? Are women athletes are somehow immune to mental health disorders?!
Although women athletes are 10 times more likely than nonathletes to develop eating disorders, they do not have an elevated incidence of psychiatric disorders (Berry & Howe, 2000; Johnson, Powers, & Dick, 1999; Kirk, Kusum, & Hildy, 2001; Martinsen & Sundgot-Borgen, 2013). Rather, these individuals are often in a state of negative energy balance due to their high level of activity and their situation may well mimic that of individuals who are in a similar state due to dieting. Their caloric deficit thereby places them at great risk of developing an eating disorder.
Given that Bergh et al. have a tendency to cite papers that do NOT support their claims (as I learned when writing Part I), I thought I’d fact check the four studies cited to support the claim that women athletes are TEN TIMES more likely than non-athletes to develop EDs:
1. Berry & Howe, 2012: The authors asked 46 female, college-level athletes to fill out questionnaires about eating patterns, anxiety, self-esteem, and so on. They were not assessed for eating disorders and most importantly: they were NOT compared to non-athletes.
2. Johnson, Powers, & Dick, 1999: Like the study above, Johnson et al. did NOT have a control group, so we CANNOT compare rates of eating disorders among athletes and non-athletes. Nonetheless, they found that 1.1% of female athletes met the criteria for bulimia nervosa and 0% met the criteria for anorexia nervosa.
3. Kirk, Kusum, & Hildy, 2001: This one is my favourite. Kirk et al. assessed the prevalence of EDs between female college-level athletes and non-athletes, they found, and I quote, “Although female nonathletes had somewhat higher average scores on the Eating Attitudes Test 26, the proportion at risk for disordered eating was not different in the 2 groups. There was no significant difference among female athletes in different sports.”
4. Martinsen & Sundgot-Borgen, 2013: These authors did find a difference: EDs were ~3x more prevalent in athletes versus non-athletes in this study ( 7.0% to 2.3% overall and 14% to 5.1% for females).
So, from the 4 studies Bergh et al. cite in support of 10x more, we get: one study with 46 female college athletes and no information on eating disorder prevalence for that study; one study that, though it didn’t have a control group, found rates of eating disorders to be less than the prevalence of AN and BN in females; one study that found no differences between female collegiate athletes and nonathletes on disordered eating symptoms; and a final one that found that EDs were a bit less than 3x more prevalent in college level athletes.
Ten times more? Hmm… the data Bergh et al. cite to support their claim seems to fall way short.
But let’s go with the (almost) THREE TIMES more, just for the sake of my argument.
Why exactly does this suggest it is not a mental disorder? Bergh et al. write: “Their caloric deficit thereby places them at great risk of developing an eating disorder.” Exactly.
Caloric deficit in and of itself is NOT an eating disorder, but it places individuals at a greater risk of developing an eating disorder. Why are athletes more likely to develop EDs? Presumably because they are more likely to diet and focus on their weight, because you know, they are athletes.
But then why is it that the majority of female athletes do NOT develop eating disorders? Presumably many are controlling their weight and dieting. Because caloric deficit is not enough, in and of itself, to cause an eating disorder. Genetic and neurobiological factors also matter; these traits and characteristics are not disordered in and of themselves, but in concert with environmental factors (like a weight-based sport), may lead to the development of an ED
Reason #4. Starvation studies argue against an underlying mental health disorder. Starvation of healthy men induces a full complement of mental health symptoms seen in anorexia (Keys, Brozek, Henschel, Mickelsen, & Taylor, 1950). When individuals try to lose weight rapidly by semistarvation, they show the same psychiatric symptoms seen in both men who were being starved and in anorexics (Robinson & Winnik, 1973). Moreover, the return to normal eating patterns obviated their psychiatric symptoms.
This seems like a valid point on the face of it, right? But these studies do not argue against an underlying mental disorder, they argue that some symptoms of anorexia nervosa are the result of malnutrition and starvation. No one argues that this isn’t the case; researchers commonly list this as a limitation to their research studies (whenever it is applicable, anyway). We know that anxiety, depression and obsessionality tend to increase as restriction and weight loss increase. This is uncontroversial.
But Bergh et al. fail to mention something crucial: Those healthy men were starved because they participated in a study. They were starved. In other words, they were NOT starving themselves the way individuals with anorexia nervosa do. This is a crucial difference.
Studies of sensory deprivation in healthy individuals induces hallucinations and delusions. Does this suggest that patients with schizophrenia who may also experience hallucinations and delusions do not have an underlying mental health disorder? No, I don’t think so.
Reason #5. Studies of comorbidities argue against an underlying mental health disorder. Kaye, Bulik, Thornton, Barbarich, and Masters (2004) suggested that young women who go on to develop eating disorders previously have had obsessive– compulsive disorder (OCD) that makes them vulnerable to eating disorders. However, only 7% of those individuals in their study who developed anorexia previously had OCD symptoms (Södersten & Bergh, 2006; Södersten et al., 2006a; 2006b; Zandian et al., 2007)
Note that Bergh et al. just cite themselves in support of the “only 7% of those individuals in their study who developed anorexia nervosa previously had OCD symptoms” (Zandian et al., 2007 is also part of the Sodersten and Bergh group). How does that make sense? What do Bergh et al.’s studies have to do with Kaye et al.’s 2004 paper?
Anyway, 7%? Try 41%. This is directly from Kaye et al.’s 2004 abstract:
About two-thirds of the individuals with eating disorders had one or more lifetime anxiety disorder; the most common were obsessive-compulsive disorder (OCD) (N=277 [41%]) and social phobia (N=134 [20%]). A majority of the participants reported the onset of OCD, social phobia, specific phobia, and generalized anxiety disorder in childhood, before they developed an eating disorder.
People with a history of an eating disorder who were not currently ill and never had a lifetime anxiety disorder diagnosis still tended to be anxious, perfectionistic, and harm avoidant. The presence of either an anxiety disorder or an eating disorder tended to exacerbate these symptoms. . . .
The prevalence of anxiety disorders in general and OCD in particular was much higher in people with anorexia nervosa and bulimia nervosa than in a nonclinical group of women in the community. Anxiety disorders commonly had their onset in childhood before the onset of an eating disorder, supporting the possibility they are a vulnerability factor for developing anorexia nervosa or bulimia nervosa.
Sodersten & Bergh wrote a response to Kaye et al’s study here. You can check it out. It is a good passage to read if you want to test your knowledge of logical fallacies (I literally laughed out loud at the “If OCD causes AN” part. Who is claiming that?).
In case you are wondering what’s wrong with their response. Let me explain: They say there were 94 patients with AN. Actually, there were 97 (94 were females). So it is 35% of 97, not 94 that had OCD. But then they say “23% had OCD before they had anorexia nervosa.” Wrong. Oh so Wrong. 23% of the ENTIRE SAMPLE — including those with anorexia nervosa, bulimia nervosa, and diagnoses of both, 673 individuals in total — had OCD prior to onset. Overall, 42% of the entire sample had one or more anxiety disorder before onset of an ED. I don’t know where the 12% drop out is coming from. The closest thing I could find is that those with EDNOS (around 10%) were excluded from all analyses because they were such a small group, compared to the others.
Godart et al (2006) provide a much more worthwhile analysis of the Kaye et al. paper in their commentary. You can find it here.
Anyway, Bergh et al. continue:
and only 11.3% of 815 patients with an anxiety disorder, including OCD, had an eating disorder (Sallet et al., 2010).
This is irrelevant. Although they don’t say it outright, Bergh et al. are implying that a higher prevalence of anxiety disorders (why do they focus on OCD?) in a population with eating disorder means that there should be an equal prevalence of eating disorders in a population with anxiety disorders. Actually, Bergh at al. are making a conditional probability fallacy (the inverse fallacy). One, anxiety disorders are more prevalent than eating disorders, and two, very simply, we can think of it this way: the presence of an anxiety disorder increases the risk for the development of an ED but additional factors are required.
Further on, when a dimensional (rather than a categorical) approach to determining whether there are relationships between eating disorders and specific symptoms of OCD, panic, depression, and general distress showed a zero-order correlation with anorexia (Wu, 2008). Moreover, the drugs that can treat OCD are ineffective in the treatment of eating disorders (Walsh et al., 2006; Zhu & Walsh, 2002).
Ignoring the first part because I don’t want to get too technical (but you can read more on dimensional vs. categorical approaches here) and skipping to the second: So what? One: Eating disorders are different from OCD. Eating disorders are different from anxiety disorders (see above). Two: Antidepressants help many individuals with bulimia nervosa (again as mentioned above). Three: So-called “drugs that can treat OCD,” do NOT improve or just PARTIALLY improve symptoms in ~40-60% of patients (Kellner, 2010; open access); nothing spectacular. Bergh et al. don’t mention they are spectacular, but the underlying assumption is that they are effective. PTSD, GAD, OCD, panic disorder, social anxiety, specific phobias are all types of anxiety disorders: Should we assume that what works to treat one should treat the other, and if it doesn’t, then they are not mental disorders or anxiety disorders or something?
Some have argued that the persistence of anxiety related disorders after weight gain supports the notion that these symptoms underlie the eating disorders (Kaye et al., 2004), but a more likely explanation is that these individuals have not actually recovered from the disorder.
It is certainly possible that the persistence of anxiety disorders after weight gain suggests that the individuals have not actually recovered from the disorder. I agree that this is probably the case for some.
But hold on: Weren’t Bergh & Co arguing that eating disorders (and associated anxiety, depression and obsessionality components) are simply the result of calorie restriction and excessive exercise? (See Part I and Part II for more details on those arguments). And weren’t they arguing that resumption of normal eating, weight, and exercise patterns is sufficient to treat EDs?
So then the fact that some individuals who are weight-restored and menstruating still exhibit anxiety disorders doesn’t so much argue that they are not actually recovered from the disorder (though I agree this may be the case) as much as it suggests that Bergh et al.’s hypothesis that weight-restoration and normalization of eating patterns is enough to treat an ED and its comorbidities is actually not the whole story.
If they are not actually recovered but they are weight-restored, eating well, and don’t fit the DSM-IV/5 diagnosis, what do Bergh et al. suggest is necessary for further recovery, particularly given that they eschew psychotherapy and pharmacotherapy (see Part I)?
In providing evidence for reason #5, Bergh et al. are focusing on within-subject and/or retrospective studies (that is, studies that assess something in the same individual at different time points, or retrospectively). But what about family studies?
Eating disorders are considerably more prevalent among relative of ED patients than among relatives of healthy controls. More interestingly, relatives of individuals with EDs are also more likely to have disorders that are highly comorbid with EDs (even in the absence of an ED) than relatives of healthy controls. These studies can’t delineate the role of genetics and the environment (since families share both), but they provide additional evidence that these disorders have overlapping risk factors and/or causes (for an open access review on this topic, see Berrittini, 2014; see also Lilenfeld et al. 1998, Strober et al. 2000).
And in other news, perhaps I should consider a career in fact checking. But jokes aside, I’ll publish the final part of this mini-series tomorrow, covering Bergh et al.’s reasons 6 through 10 why eating disorders are not mental disorders (or “don’t have an underlying mental disorder,” whichever). I hoped to cover all 10 in one post but as you can see, I got a little carried away. Skepticism: It is fun! If I omitted references somewhere, made a mistake, or didn’t explains something sufficiently, let me know.
References
Bergh C, Callmar M, Danemar S, Hölcke M, Isberg S, Leon M, Lindgren J, Lundqvist A, Niinimaa M, Olofsson B, Palmberg K, Pettersson A, Zandian M, Asberg K, Brodin U, Maletz L, Court J, Iafeta I, Björnström M, Glantz C, Kjäll L, Rönnskog P, Sjöberg J, & Södersten P (2013). Effective treatment of eating disorders: Results at multiple sites. Behavioral Neuroscience, 127 (6), 878-89 PMID: 24341712
So, are you saying that every eating disorder does stem from a mental health disorder? That doesn’t feel right in my own case. I can certainly say that I was mentally dysfunctional, but I would put that down to the way I was brought up and consequent warped views of reality. I have found my way out of that.
Hi Natasha,
Good question. I’m glad you asked because I didn’t have space to go into detail about that and took it out of the post.
I’m not saying that eating disorders stem from mental disorders: I am saying that they *are* mental disorders.
A mental disorder (or illness, or psychiatric disorder) simply refers to patterns of thinking, behaving, or perceiving that are dysfunctonal and/or distressing, and that are not, as Wikipedia puts it, “developmentally or socially normative.”
Wikipedia actually has a good definition:
“A mental disorder or psychiatric disorder is a mental or behavioral pattern or anomaly that causes distress or disability, and which is not developmentally or socially normative. Mental disorders are generally defined by a combination of how a person feels, acts, thinks or perceives. This may be associated with particular regions or functions of the brain or rest of the nervous system, often in a social context. . . . In many cases, there appears to be a continuum between mental health and mental illness, making diagnosis complex.”
I liked this, too:
“In DSM-IV, each of the mental disorders is conceptualized as a clinically significant behavioral or psychological syndrome or pattern that occurs in an individual and that is associated with present distress (e.g., a painful symptom) or disability (i.e., impairment in one or more important areas of functioning) or with a significantly increased risk of suffering death, pain, disability, or an important loss of freedom. In addition, this syndrome or pattern must not be merely an expectable and culturally sanctioned response to a particular event, for example, the death of a loved one. Whatever its original cause, it must currently be considered a manifestation of a behavioral, psychological, or biological dysfunction in the individual.”
(Source; also has a good discussion on the pros/cons of the actual terms and their implications.)
I don’t want to focus too much on the words (“mental” or “psychiatric”, “illness” or “disorder”). The point is that it refers to behaviours and/or thoughts that impair functioning. That is it, really. That’s the disorder/illness part. The “mental” or “psychiatric” part refers to the fact that this impairment occurs in the nervous sytem, as opposed to say a kidney disorder or a cardiovascular illness. It is mental because it has to do with thoughts and behaviours.
So yes, all eating disorders are mental disorders. The two crucial components that are highlighted in the quotes above are:
One: What we consider a disorder is largely socially constructed and is *not* static. There are no hard and fast rules. Behaviour occurs on a contiuum. While we may not agree where to draw the line between eating disorder, disordered eating, and normal eating (we may not even agree on the defintions of those), we do agree that differences exist. Things always get murky in the middle — regardless of the mental disorder, really — but further away from the murkiness most people can agree that a given pattern of behaviours and/or thoughts is either more-or-less normal or dysfunctional and disordered.
Two: The term “mental disorder” says NOTHING, ABSOLUTELY NOTHING, about causality, illness course, or outcome. Noooothing. Just like you can have a single-gene genetic disorder (e.g., cystic fibrosis) on the one hand and a viral disease contracted from the environment on the other. Calling eating disorders mental disorders to me is like calling hypertension a cardiovascular disorder. Eating disorders are mental disorders becase they are disorders of the nervous system. Hypertension is a cardiovascular disorder because it is a disorder of the cardiovascular system.
The causes of eating disorders, and other mental disorders, are complex but there’s no doubt that they — ALL of them — result from a mix of genetic and environmental components. In your case, you migth have had a dysfunctional upbringing but that would not have been enough to cause an eating disorder; just like dieting is not enough to cause an eating disorder, after all, only a few of those who diet develop an eating disorder.
Just like in the case of anxiety disorders: Only a subset of individuals exposed to the same environmental event develop PTSD. Why? We don’t know fully but lots of research suggests that genetic and epigenetic factors are at play (see here for a recent, open access review on the topic), making some individuals more vulnerable to develop PTSD than others after exposure to *same* event. Having a diagnosis of an anxiety disorder, such as PTSD, doesn’t mean it is forever. People can recover. But it is a mental disorder because it is a dysfunctional/detrimental pattern of behaviour and/or thought.
So, yes, all eating disorders are mental disorders. This doesn’t say anything about causality, and it certainly says NOTHING about causality for any single individual, and it also says nothing about illness course and outcome. It does NOT mean the disorder is forever or is incurable.
I fear that the hesitation for some to call them mental disorders is the result of the stigma (and misunderstanding) associated with the term “mental disorder/mental illness/psychiatric disorder.” That’s something that we, as a society, need to fix.
I’m continually amazed by how much time, work, and energy you put into this blog, Tetyana. Thank you so much for such a full answer. That’s really helped me to understand what was going on with me.
Aw, thank you! I’m so glad to hear that. I love doing this! It helps me improve my communication skills, I think (hope).
The point Bergh and colleagues are making is that eating disorders are behavioral disorders, not mental disorders. They argue, therefore, that the best treatments target behaviors, primarily eating behaviors and physical activity behaviors, not “mental” processes or “thinking” patterns. There is strong evidence to support their approach. Generally, behavioral treatments are more successful than treatments that target cognitive or emotional processes.
Many of your criticisms of Bergh’s argument are misleading. I won’t go into all the details. An example, however, is your refutation of the authors’ claim that women athletes are 10 times more likely than nonathletes to develop eating disorders. This claim is based on the data from Martinsen (2013), which found that 14% of the female athletes surveyed had symptoms of an eating disorder. In the general population, on the other hand, the percentage of people with eating disorders tends to be closer to 1% or 2% — about 1/10 of 14%. We can quibble over the details, but the point stands that eating disorders are more common among athletes than among nonathletes. The only difference between the two groups would appear to be patterns of physical activity, not psychiatric characteristics.
In earlier posts, you claim that the Mandometer data doesn’t support Bergh’s conclusion that Mandometer treatment resulted in a remission rate of 75% within 12.5 months. This conclusion was calculated on the basis that there were 1,428 individuals in the study. 462 of the 1,428 were “censored” from the results because, in most cases, they were still in treatment. This left 966 patients who were evaluated. 105 of the 966 withdrew, 124 of the 966 were treatment failures, and 737 of the 966 met the criteria for remission.
737/966 = 76%. Therefore, the authors of the study correctly stated that “the estimated rate of remission for this therapy was 75% after a median of 12.5 months of treatment.” These results are impressive. As the authors conclude, Mandometer is a promising treatment model compared to traditional treatments. Further research is warranted.
Saying that something is a behavioural disorder and not a mental disorder is like saying it is leukaemia, not cancer. Behaviour is, believe it or not, controlled by the nervous system. Mental disorders, as I said above, are dysfunctional patterns of thought, perception, AND/OR behaviour. There’s no evidence for mind-body dualism in neuroscience. A behavioral disorder, even if you want to argue that eating disorders are just behavioural disorders, still counts as a behavioural disorder. Please read DSM’s definition of mental disorder above (in my response to Natasha). Or you can just Google “mental disorder definition”: I bet almost all of them will include dysfunctional behavioural patterns in their description. The ones that won’t will probably be the really short, couple of word descriptions.
What I love about all of your responses (taken as a whole, not just this one) is your arrogance. You seem to think that just because of your experiences as a father of a daughter who had an eating disorder, you are suddenly an expert on everyone else’s experiences. Guess what: You are not. I am usually calm and composed on this blog, but I am getting tired of your dismissive nature with regard to my own and others’ real, lived experiences of having an eating disorder. Nevermind your tendency to ignore the mountain of good, pertinent research thus far that clearly suggests eating disorders include dysfunctions in both thought and behaviour. Perhaps your daughter didn’t experience dysfunctional thoughts. Perhaps she was misdiagnosed: perhaps it was just a diet gone too far. Perhaps it wasn’t. I don’t know. But eating disorders are NOT diets gone too far. Eating disorders may develop from a diet gone too far, but an eating disorder is different, it becomes different.
Your point on behavioural treatments being more successful than those targeting cognitive and emotional processes DOES NOT NEGATE that eating disorders are mental disorders. Many individuals learn to behave differently to their emotional and cognitive experiences: They learn to NOT binge/purge or restrict in response to an aversive emotional experience, for example. That doesn’t mean their emotional or cognitive patterns are “normal” (by which I mean, typical of majority). The dysfunctional behaviours are the result of, in most cases, inability to deal constructively with negative affect or emotional states in general (regardless of whether the states themselves are “normal” or not). Behaviour is a very, very important component of ED treatment. Huge. But it is not the only one. Behaviour is also much easier to evaluate in treatment studies than cognition and emotion: It is easier to weigh someone, to count how many times they binge/purge, than to evaluate their emotional processes. It is also easier to lie and say you feel fine. How many readers who’ve had ED’s lied to parents, professionals, and others, telling them they are “fine”, especially when they “look” fine?
You also purposely ignore data that doesn’t support your conclusion (classic tactic): 60mg of Prozac is effective in significantly reducing bingeing/purging for a large subset of bulimia nervosa patients, as I mentioned above. What does that say about your claim that EDs are just behavioural disorders?
Christopher, please stop being so dismissive not only about the experiences of those with eating disorders but about all the other research that doesn’t support your already-made conclusion. Bergh et al. have not done original research suggesting that EDs are just behavioural disorders, and if I missed something, let me know, but it still won’t outweigh the hundreds of papers, by researchers like Janet Treasure, Walter Kaye, Cindy Bulik, and Kate Tchanturia to name a few, clearly suggesting that eating disorders are not just a physiological outcome of starvation and exercise. If they were, then everyone who diets and exercises would be at risk. But we know that only a subset of those who diet and exercise develop eating disorder: There is more, much more, to it than just caloric restriction and exercise. Keyes’ studies show that some symptoms we see in AN are due to starvation, that is true, but again, not all. We have plenty of evidence to suggest this. I’ve said this many times over, but I guess it bears repeating.
With regard to your comment about Martinsen: You clearly do not understand the purpose of control experiments. Their control data show 5%. This is why controls are important. Also, 1-2% is likely looking only at one ED. We should be combining AN and BN *at least*. We can’t just take statistics DERIVED USING VERY DIFFERENT MEASURES and compare them. This is why so many meta-analyses suck, because they do that. You can’t take Bergh et al.’s 75% and compare it to studies that used intention to treat analyses: BECAUSE THEY USED DIFFERENT MEASURES. It is like comparing how many km you ran with how many miles someone else ran and going, “I ran 5km and you ran only 3.2 miles, so ha, I ran more than you.” It doesn’t work that way. I also love how you ignore the findings from the other 3 studies that Bergh et al. cite. Why’d they cite them if they don’t support their own point?! Just for fun? To increase their friend’s h-indexes? I don’t get it.
With regard to the Mandometer stats, I’m not sure if you looked at their supplemental data but this is NOT how they derived the 75%. I already wrote about this in previous posts. I chuckled at the “in most cases”, oh yeah? Where does it say that? They don’t mention any numbers.
Christopher, if you’d like to continue commenting on this website, I would appreciate that you stop dismissing the lived experiences of others base solely on your experience as a father of someone who had an eating disorder. I am very happy your daughter recovered. I know nothing about her or her experiences, and nothing about yours. Nothing applies to every single person. (Except perhaps that we were all born and we will all die.) It doesn’t mean you have to go around and tell everyone else that just because your experience was different that theirs are invalid.
Like I said, saying something is a behavioural disorder but not a mental disorder is like saying it is leukaemia but not cancer.
I just want to comment as a former patient of the Mandometer clinic in Stockholm, without however doubting any of your extended (and very impressive!) research. I appreciate the work and passion you put into these three parts of your review and thank you for sharing it.
To me, Mandometer treatment was truly amazing. However, I haven’t been through any other specialized treatments to compare, my previous experiences with clinics, hospitals, doctors and psychotherapists were traumatic. I am from Athens, Greece, where (especially back then) there was no special treatment for anorexia, so my parents were desperately looking for anything that could keep me alive and get me back to life pretty much. They randomly found out about Mandometer and they managed to take me to Sweden where I was admitted to the clinic (2007). I won’t get into too many details, I could never support my thoughts with any statistic or scientific proof, I just want to write about my experience.
I was forced into this treatment (by my parents), as most people dealing with eating disorders, the idea of it and any treatment was terrifying what I least wanted. I was also under 18 and suddenly found myself in Sweden instead of studying for the final exams of high school. However, the Mandometer staff was sweet and caring. They took good care of me, they treated my with respect and kindness which I so needed, after a while, both the staff and the other patients felt like a family. The treatment required a lot of work and was really tough for me, considering that I did not want it! But it worked. When dealing with anorexia, you need to have control, over your life and over your meals.
In the clinic, the way of gaining back that control was through making steps forward in the treatment, in a way that was logic and felt right. For instance, I wasn’t allowed to have any physical activity at first, because my situation made it dangerous for me (I was really underweight then), but I was encouraged to do so when my body got a little stronger. We planned small trips to Stockholm with other patients and staff, I moved to the hotel of the clinic (a different floor of the same building), I started taking meals out of the usual schedule. Little steps that gave me the feeling that I was earning my life back. Each patient had a “case manager” to help them deal with the treatment and plan it together. Mine, was really sweet, supportive and always there for me. Never felt like dealing with professionals who were just doing their job, it felt warm and honest.
Reading the review, I was getting the feeling that the treatment was probably unfortunately presented. Maybe less scientific terms should have been used and less theories. The important part for me is that no matter how they name it, I support their approach on the eating disorders, the general approach which claims that they should be treated as physical and not mental disorders. Again, without being able to scientifically support my thoughts, just because of what I have experienced, I believe that a good treatment has to first take care of the body (and soul) and when the patient is strong enough, to slowly return to their usual activities and lifestyle, with some psychological support.
Thank you again for your review and I hope you find my post somewhat useful.
Hi Lena,
I am glad you found success with Mandometer. I am not surprised at that. As I said in either this post or some of the other posts I did on Mandometer, I think some of the treatment methods they use are good and evidence-based. I am skeptical of the shoddy data they used in their papers and the unsubstantiated (or flat out incorrect) claims. Whenever people cite a study and say it said one thing but it really said something else, I think that should ring alarm bells. Have you read my other posts?
I don’t understand your claim that EDs should be treated as physical as opposed to mental disorders. I think there might be a misunderstanding here with what you mean by that. What you described as part of your treatment sounds very much rooted in behaviorism — an approach to treat cognitive and behavioural disorders. Eating disorders ARE mental disorders because they involve changes in cognition and behaviour that are maladaptive to the individual.
Mandometer sounds like it would work for individuals with no/limited comorbidities.
Thank you.
I was looking forward to reading your installments on this published material and am, of course, thoroughly (as expected) satisfied.
Just curious, Behavioral Neuroscience got any explanation for a peer review process that failed to notice that some 378 patients went missing?
At present, I would suggest the takeaway (and not a particularly shocking one to me) is that the APA-published Behavioral Neuroscience journal allows for those with proprietary for-profit programs who are keen to disprove criticisms that their program might lead to fatalities; will fail to provide for remission; and may not be something that could be globally marketed, to present information akin to an advertorial.
Although I expect everyone who might be combing these comments is familiar with the term, an advertorial is an advertisement that is usually formatted and written to look exactly like journalistic content. The material reads as though there has been some journalistic due diligence to investigate and confirm the information and ‘facts’ within the ‘article’, but it is merely company-produced promotional material in its entirety.
Presumably some peer-reviewed journals now offer papertorials to their readership.
I wholeheartedly support you Tetyana in your pointing out all the data gaps and it’s a very, very important thing to flag — the data appear in a prestigious and ostensibly peer-reviewed journal precisely because the proprietary owners of Mandometer are seeking validation that will allow for them to market the program in such a way that a mere wave of the hand towards the published materials will be sufficient to sway many a compromised patient and his or her terrified family.
FBT has RCT, replicated peer-reviewed and published 5-year remission rates (actual, not estimated). And to reinforce that FBT and Mandometer are not at all interchangeable: the third tenet of FBT treatment specifically includes the development of a healthy adolescent identity (FBT is directed at treatment for children and adolescents only). Such development necessarily includes various and appropriate psychological treatment modalities be applied to the patient as well as his or her family — it is simply not embarked upon until such time as the patient has rectified the impairments resulting from starvation.
It appears as though the Mandometer owners have missed, or perhaps were unable to generate, an opportunity to develop a body of evidence such that Mandometer might have become an alternative evidence-based approach to recovery beyond FBT.
And as for the behavioural/mental/neurological camps…sigh. Ethan Watters has pointed out: “Americans, for some reason, find it particularly difficult to grasp that mental illnesses are absolutely real and culturally shaped at the same time.” [The Problem With Psychiatry, the ‘DSM,’ and the Way We Study Mental Illness, June 3, 2013]
If eating disorders were just the result of starvation itself, then the entire group of subjects within the Minnesota Starvation Experiment would have required blankets and automatic devices weighing their food in order to recover and “normalize eating behaviours”, never mind those who have survived famine at anytime throughout history.
If the behaviour of restricting food intake alone were responsible for its perseverance, then there would have to be a near 100% success rate for weight loss by way of dieting.
The fact that starvation impairs brain function is beyond dispute. But the suggestion that re-feeding alone will resolve an active restrictive eating disorder flies in the face of mountains of really solid clinical data.
The patterns of thinking, behaving and perceiving that underpin an inability to remit and/or a propensity to relapse are utterly distinct from the neurological impairment that is due to starvation itself.
I am just repeating what you have already stated above (and not as well as you either).
In any case, I much appreciate the time you took to unpack the data and pseudo-data because a lot is at stake in our credential and epaulette driven society.
In light of how much our dependence on illustriousness, prestige, scientific elitism, and attitudes of “one could not possibly understand in the absence of highly specialized education and training” are being increasingly undermined with outright fraud rife throughout the scientific community and their journals, those who can call slipping standards out should be doing so and I commend you for doing so.
Cheers! I’m off to turn the heat on because I run hypothermic in the absence of any eating disorder 😉 Gwyneth.