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.
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