This is the last post in my mini-series on the Mandometer® Treatment. (Links to earlier posts here: Part I, Part II, and Part III). In this post I’m going to continue examining Bergh et al.’s reasons for why eating disorders are not mental disorders (#6-10). In my last post I omitted something important: I didn’t define mental disorders, but to avoid repeating myself, please see my comment on the topic here.
Bergh et al.’s reason #6 why EDs are not mental disorders:
Reason #6. Gender differences argue against an underlying mental health disorder. Women constitute more than 90% of eating disorder patients (Hoek & van Hoeken, 2003), but teenage males are more likely to have OCD than teenage females (Fireman, Koran, Leventhal, & Jacobson, 2001), and there are no differences in the prevalence of anxiety and anxiety-related disorders in male and female teens (Beesdo, Knappe, & Pine, 2009).
The ratio of women to men receiving treatment is NOT representative of the ratio of women to men struggling with an eating disorder. I think this is fairly obvious: Men who struggle with EDs face additional barriers in getting diagnosed (for one, our screening criteria are not optimized to identify male sufferers) and receiving treatment. (A good, short overview of the issue can be found in this open access article, “Eating Disorders in Men: Underdiagnosed, Undertreated, and Misunderstood“).
But even if men made up less than 10% of ED sufferers, so then what? And say they are more likely to suffer from OCD and other anxiety disorders.* So what?
Bergh et al. are implying that the gender ratios should be the similar because their underlying premise (see previous post) is that anxiety disorders cause/lead to EDs, thus, if men are more likely to have OCD/anxiety disorders, they should experience eating disorders more frequently. However, a high prevalence of anxiety disorders among patients with EDs does NOT mean that anxiety disorders lead to EDs and it does NOT mean that there should be a high prevalence of EDs among individuals with anxiety disorders (see confusion of the inverse).
Contrary to Bergh et al.’s unstated premise, no one is suggesting that OCD or other anxiety disorders cause or lead to eating disorders. They seem to be committing yet another logical fallacy here: the straw man fallacy.
*Funny thing. Most of the data I found seem to contradict Bergh et al. (not surprising if you’ve read my past posts!): Females are as/more likely than males to suffer from OCD and anxiety disorders, though findings vary substantially depending on the population studies, methods, sample size, and so on. (OCD: here, here, here, here, and here; Anxiety disorders in general: here, here, here, and here; lay description here).
Instead, young women respond differently to skipping a meal than young men. When the young men miss dinner, they respond by eating about 30% more during the next day. Young women, on the other hand, eat about 20% less the day after they missed their dinner (Zandian, Ioakimidis, Bergh, Leon, & Södersten, 2011).
Knowing that these authors tend to fudge, omit, or lie about findings of papers they cite (even their own papers!), I looked up the Zandian et al. (2011) study. They examined 13 women and 9 men. (They had 21 women who participated in another related, but separate experiment.) THIRTEEN and NINE.
Notice how they said, “about 30% more” and “about 20% less” in the blurb above? This is what they wrote in their abstract: “We found that women consumed 12% less food after fasting and that men ate 28% more food after fasting.”
I mean c’mon, they can’t even accurately describe their own findings from just two years prior? On its own, it seems like an honest mistake, but taken as a whole (see parts I-III), well, it spells out a different story I’ll get to in the end. (Did I mention 13 women and 9 men?) The work was supported entirely by the Mando Group AB which owns the Mandometer® Treatment.
One can see how a reduction of food intake can lead to a further reduction in food intake, thereby making some women more vulnerable to developing an eating disorder when they engage in dieting.
Riiiiight. So, if Bergh et al. are arguing that anorexia nervosa is solely or almost solely a physiological response to reduced food intake how the VAST, VAST majority of dieters and people who skip meals DO NOT develop anorexia nervosa? What’s up with that? Could it be that, *gasp*, genetic and neurobiological predispositions that are unique to particular individuals) are involved?
But moving on…
Reason #7. Studies of the mechanism underlying increased physical activity in those with eating disorders argue against an underlying mental health disorder. Foraging strategies that include increased activity are engaged in humans when food is restricted (McCue, 2012; Noakes & Spedding, 2012), and physical hyperactivity has long been recognized as a symptom of anorexia (Gull, 1874; Södersten et al., 2008).
Foraging? Really? We are comparing excessive exercise in eating disorders to foraging in low-food environments? Somehow it is hard for me to connect the foraging behaviours that my C. elegans worms exhibited in low-food environments (here’s a semi-relevant link for anyone who, like me, likes this awesome model system) to the rigid and compulsive (but low levels) of exercise I briefly engaged in during the initial phases of my eating disorder.
Increased physical activity greatly worsens their physiological status, given that they are also starving. Although this behavior appears to be consistent with a psychiatric disorder involving self-injurious behavior, there is an alternative explanation for this behavior.
Something tells me their alternative explanation isn’t going to be what I’m hoping for.
In particular, when individuals lose body weight, their surface area through which they lose heat is not as affected, but the biomass producing heat is much diminished. Moreover, body metabolism is suppressed in individuals who are restricting their food intake (Speakman & Mitchell, 2011). Patients with eating disorders therefore feel cold continually (Gull, 1874; Luck & Wakeling, 1980, 1982) and a primitive, yet effective method of thermoregulation in such circumstances is increasing physical activity.
Except most don’t. Do some? Of course, malnutrition and low body fat do that. Do all? No. For more on this please see my first post where I went into detail looking into the studies Bergh et al. cite to support their hypothermia-driven over-exercise hypothesis. (Short story: The studies they cite aren’t nearly as convincing as they lead you to believe.)
Besides, this discussion is ignoring an important and more prevalent eating disorder: bulimia nervosa. Many BN patients exercise excessively, but guess what: they are not underweight and many do not lose much (or any) weight.
On the other hand, if one provides warmth to either patients with eating disorders or to rats in an animal model of anorexia, one can prevent the increased physical activity (Bergh et al., 2002; Carrera et al., 2012; Gull, 1874; Gutiérrez, 2013).
It is true that rats do seem to run on their wheel less when they are provided with a heat pad. It is true that it may reduce physical activity in AN patients, too. This, surprisingly, was actually suggested in an independent study (i.e., different group of people from Bergh et al.). The open access article is here. It is not a totally out-there idea. If you are cold, heat is good. We move around to keep worm when we are cold. It makes sense. But what about bulimia nervosa patients?
Rather than being a psychiatric symptom, this behavior can therefore be understood as a normal physiological response to feeling cold and/or displaced foraging for food (Södersten et al., 2008).
I don’t know about you, but to suggest that excessive exercise in AN and BN is solely (or even mostly) driven by the desire to keep warm (or search for food?) seems, um, to dismiss the abundance of evidence we have for all of the other reasons individuals with eating disorders engage in excessive exercise. Nevermind that many AN and BN patients do NOT exercise excessively OR feel cold.
When my worms moved around on a plate without food, I don’t think they were thinking about losing weight, burning calories, or getting rid of the anxiety they felt for eating the last bit of their food. Rats and mice are more complex than worms, but not quite as complex as humans, to say the least.
Reason #8. Commonalities with the etiology [causes] and the treatment of obesity argue against an underlying mental health disorder. Just as anorexia and bulimia are generally thought to be the consequence of a complex mental disorder, obesity is often thought to be a consequence of a character flaw (Brownell et al., 2010). However, obesity appears to have the same etiology as anorexia and bulimia. That is when individuals skip meals, restrict their food intake, or speed through their meals, gut hormones are not available to limit food intake, and consequently, these individuals go on eating (Galhardo et al., 2012).
Bergh et al. are arguing for commonalities in causes for eating disorders and obesity. But hold on, weren’t they JUST saying above that when women skip a meal they eat LESS the next day?! But they just argued the opposite occurs in individuals with obesity: “these individuals go on eating.”
A small portion of those in this situation continue eating only little food slowly. The vast majority, however, simply gains weight. When we normalize food intake patterns for obese individuals in a manner similar to that used to treat anorexics and bulimics, their body weight is significantly reduced, and their health improves (Ford et al., 2010).
So they “normalized” eating in a group of obese adolescents and came to the conclusion that obese people should just eat less and they are obese because they eat too quickly. Now, I don’t know a lot about obesity, but something tells me it is a little bit more complex to treat than to tell people to eat less. Indeed, a recent study suggests that these messages might actually have the opposite effect.
Bergh et al. are completely ignoring gene-environment interactions. In both their discussion of EDs and obesity, they are ignoring the genetic and neurobiological predispositions that lead to particular behaviours in particular environments.
In writing, “the vast majority, however, simply gains weight,” they are ignoring the mountain of research that highlights the genetic and epigenetic factors that predispose some individuals to eat more and/or gain weight in an environment with ample food. Just like they are ignoring the same type of research that suggests some individuals are more likely to develop eating disorders when they restrict their caloric intake.
They are shifting the blame entirely on the individual. Keep in mind that saying genetic/epigenetic factors are involved DOES NOT mean *at all* that individuals are NOT able to recover/change their behaviours/lose or gain weight. It says nothing about treatment interventions and their efficacy. What it does is that it paints a more complex picture of causality.
Reason #9. The success of a therapy in which eating behavior is normalized in patients with eating disorders argues against an underlying mental health disorder. In the initial randomized clinical trial, we found that 88% of the patients went into remission, compared to 7% of the control patients (Bergh et al., 2002). In both the study with 168 patients (Bergh et al., 2002) and the current study with 1,428 patients, the estimated rate of full remission was 75%, with only 10% of the patients relapsing within 5 years and 0% mortality. These outcomes compare favorably with standard care treatments and could be implemented easily in clinics that treat these disorders, much to the benefit of their patients.
I discussed my issues with their study mainly in my second post. I addressed how the fact that behavioural interventions are successful DOES NOT negate that it is a mental disorder in my lengthy comment to CB here.
Bergh et al.’s 2002 paper is hilarious. I can write another essay on it but instead I’ll just show you something hilarious that immediately caught my eye. Their remission criteria included (among other things) that the individuals no longer met the criteria for an eating disorder. Reasonable, right?
Check out this results table (the kind of table that is missing from their 2013 study). So first, note how they wrote 168 patients: They show data only for FOURTEEN. That’s right, 14. You gotta wonder why they couldn’t, like every other study ever just include the rest of their sample in a simple table, right?
But here’s the kicker. In brackets is the range of the values (the lowest and highest). So if you look at what I highlighted, the range for BMI of individuals considered in remission for AN ranges from 15.4 to 19.9.
One possible explanation is that the participants were young, so a BMI of 15.4 might actually be a normal weight for someone who is like, say, 13. But they don’t mention average age of the entire sample. Besides, if they had very young patients, they should have switched to using percentage of expected body weight, which would normalize this data based on age.
Check out their table on the demographics/characteristics of their 168 participant sample:
Now I don’t know, maybe addition works differently in Sweden, but 19+13 doesn’t add up to 168. You can’t just cherry pick data to show sample characteristics in a study like this. It doesn’t work that way. You can’t say we studied 168 patients but we are just going to show you data for 14 of them, because like, the rest are the same so yeah, just trust us. Nah-uh.
Reason #10. A partially successful standard of care. Family therapy has become a standard therapy for anorexia that shares certain aspects with our treatment. In particular, this therapy treats anorexia by coaxing affected individuals to increase their food intake without psychiatric treatment. However, without an effective feedback system during meals, this approach does not improve the outcomes of most individuals with eating disorders, and only affords a small improvement in those few patients who are both very young and very mildly affected (Bergh et al., 2006; Eisler et al., 1997; 2000; Fisher, Hetrick, & Rushford, 2010; Lock & le Grange, 2005; Russell, Szmukler, Dare, & Eisler, 1987). At the same time, those patients do not reach a normal body weight, their psychiatric symptoms typically persist, and they are at an increased risk for developing bulimia (Bergh et al., 2006; Geist, Heinmaa, Stephens, avis, & Katzman, 2000; Robin et al., 1999). Indeed, there was no difference between the groups after a long-term follow-up, very much like the long-term outcomes from psychiatric care (Ben Tovim, 2003). Appropriately, the authors of the family therapy study concluded that their results could be “attributed to the natural outcome of the illness” rather than to the therapy (Eisler et al., 1997, p. 1025).
Wait, why are they citing Eisler et al (1997) or Ben Tovim (2003) opposed to the much better and more recent Lock & le Grange (2005) study? (I blogged about that study in depth here, the comments are worthwhile to read, too.) They are citing old research going: See, this thing is crappy but ignoring the recent and much better studies showing that it actually isn’t that crappy at all.
But more more importantly, as I said in my previous post, I fail to see how the argument that our treatment modalities are sub par (and no one is debating that) argues against eating disorders being mental disorders disorders.
FBT works for some. I’m sure Mandometer® works for some, too. Many, however (myself included), are able to recover without either of those, suggesting that there isn’t one path to recovery. One clear-cut, sure-fire way to recover. As I said before, my issue with Mandometer® isn’t so much that I think their idea of focusing on eating and reducing exercise is wacky. It most certainly is NOT. I very much agree with focusing on behavioural components initially. Absolutely.
Let me be absolutely clear:
My issue is not with the treatment as much as it is with their absurd lack of transparency in their methodology, in their statistical analyses, and in their data. My issue is the plethora of unsupported claims. My issue is that when you look at studies they cite to support their claims you find that they actually don’t support their claims at all. My issue is that they leave 378 patients unaccounted for in their 2013 study; the numbers simply do not add up. My issue is that Bergh et al. (2013) do not report ANY actual data about their remitted patients. None.
I have, personally, never seen anything quite like this in peer-reviewed literature to date.
Why is this a problem? I’ll let Gwyneth Owlyn explain, since she beat me to it in her comment on my last post:
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.
This is my takeaway too. This is the reason I spent four posts talking about the Mandometer® Treatment. Just because someone makes a claim, and just because that claim is published in a peer-reviewed journal, does not mean it is valid or true. It may not even mean that the peer-reviewers thought it was a good study (see last part of the comment).
Advertorials and other crap like that are nothing new, for more on these types of shady things, I highly recommend Carl Elliott’s White Coat, Black Hat: Adventures on the Dark Side of Medicine and, though dealing with slightly different issues, Ben Goldacre’s Bad Science: Quacks, Hacks, and Big Pharma Flacks (and Bad Pharma: How Drug Companies Mislead Doctors and Harm Patients). Now, before you have the urge to throw your hands up in a sign of defeat, I’d like to say that demanding more transparency from peer-review and from any clinical trials (whether they are run by pharmaceutical companies, companies like Mando Group AB, or academics in fancy institutions) is a much better approach than vilifying everything. We need peer-review. We just need it to be better.
Anyway, I’m happy to say I’m done talking about this Mandometer® stuff. Back to good research and science shortly! Andrea has two posts lined up that I’ve put on hold to write this mini series, so look forward to that.
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