PROTIP: When selling your snake oil treatment, try NOT to make wildly outrageous efficacy claims. But if you can’t resist that temptation, try to limit your hard-to-believe, eye-roll-inducing claims to your treatment — there’s no need to go further.
In this post, I’m going to give a brief history of the Mandometer® treatment and its apparent rationale. In the next one or two posts, I will do an analysis of the most recently study by the group that claims to show remission rates of 75% and relapse rates of only 10%. Sounds great, right? Well… we’ll see.
We suggest that the reason self-starving patients do not fit the DSM-IV criteria of anorexia nervosa is because there is in fact no psychopathological basis of the disorder … The DSM-IV offers no definition [of psychopathology], but it is reasonable to assume that a psychopathological basis of anorexia nervosa would be reflected in a behavioural or cognitive marker. There is, however, no need to refer to self-starvation and enhanced physical activity as a reflection of an underlying psychopathology.
We suggest therefore that analyses of self-starvation should focus on the reduced food intake and enhanced activity, since these are the only behavioral measures that consistently distinguish anorexia from other conditions. We also suggest that whatever additional behavioral or cognitive ephenomena ensue during the development of the illness, they emerge from those two initial behavioural markers [self-starvation and enhanced physical activity].
Just as the definition of psychopathology is unclear, so is the definition of a mental disorder. Again, the DSM-IV offers no definition, but it seems likely that “mental disorder” denotes a disorder that has a neurochemical cause or consequence. In anorexia nervosa, the neurochemical marker is the increased concentration of cortioctropin-releasing factor (CRF) in the cerebrospinal fluid and alterations in other neurotransmitters, probably secondary to the alteration in CRF. However, we see no reason to refer to this neuroendocrine alteration either as reflecting or caused by a “mental disorder” and suggest that in the absence of a psychopathology or clear idea of a specific mental disorder, it is more appropriate to refer to anorexia nervosa as self-starvation.
That was written in 1996 by Cecilia Bergh and Per Södersten in, surprisingly, Nature Medicine. Bergh and Södersten are the founders of Mandometer® and Bergh is currently its CEO.
The decision to label something as a mental disorder or not is not a scientific one, and as far as causality is concerned, it really doesn’t matter if we call something a mental disorder or just variation of normal behaviour (perhaps non-neurotypical behaviour). Regardless of the label, the behaviours/cognitions have underlying biological correlates in the brain that help explain why some people engage in those behaviours/cognitions while others don’t. For one, only a small proportion of individuals exposed to thin-promoting media develop anorexia and bulimia nervosa. (I don’t even want to touch on the notion of calling anorexia nervosa self-starvation.)
There is no question that the Diagnostic and Statistical Manual has a tendency to pathologize normal and non-pathological behaviour (homosexuality was in there until the 1973, gender dysphoria is still in there, and I’m not sure if caffeine withdrawal is worthy of a psychiatric diagnosis). The fact is that this actually support my point: the DSM is not scientific and decisions of what to include in it are influenced by societal factors. Furthermore, there is no doubt that starvation itself exacerbates psychopathology. And there’s no question that weight restoration and resumption of normal eating decreases some of those anxious, depressive, and obsessional thoughts (do I even need to cite things here?).
But whether you want to call it psychopathology or not (and frankly, I would prefer to call it non-neurotypical behaviour), there are risk factors to developing an eating disorder that go beyond exercise and dieting. There have to be for the simple reason that a lot more who exercise and diet who do not have eating disorders than those who do. This whole blog is practically dedicated to understanding why some individuals are prone to develop eating disorders and others aren’t.
And as for “behavioural and cognitive markers,” well, researchers are slowly getting there and I welcome you to browse the following categories: etiology (causes), neuroscience, genetics, psychology, and to a lesser extent, psychiatry, to get a sense of the state of the field. Saren’s two posts on endophenotypes and biomarkers might be a particularly good start: Part I and Part II. (Remember, though, that brains are complicated, studying humans is hard, and finding participants is rarely easy.)
In 1996, Cecilia Bergh and colleagues (including Per Södersten) published a letter in The Lancet describing a novel treatment for anorexia nervosa. In their letter, the authors describe how they successfully treated eight women (ages 14-23) with the assistance of a device called the Mandometer®. I’ll let them explain:
The patient eats from a plate placed on a balance and the weight loss of the plate is recorded by computer. At 1 min intervals a scale from none (0) to maximum (10) appears on a monitor and the patient records her perception of satiety. This device, Mandometer®, determines eating rate and satiety. A linear curve, steeper than that generated by the patient is then displayed on the monitor and the patient adapts her rate of eating, which emerges on the monitor during a meal, to the curve. Successive 20% increases in meal size and curve slope are presented. Similarly, the patient adapts her perception of satiety to less steep linear curves. Daily physical activity is monitored with the Actigraph, which records arm movements per 16 s, and the patient is taught to reduce her activity at the times of its peaks.
The device visualizes the ideal eating rate and the patient’s rate; patients are asked to adjust their eating to follow the ideal curve, thus training them to eating a “normal” pace.
In a follow-up study published in 2002, Bergh et al. provide more details about the other two crucial components of the Mandometer® treatment: supply of external heat and limited physical activity:
Supply of external heat. After each meal, the patients rested for 1 h in a room in which they could set the temperature at up to 40°C.
Physical activity. Anorexic patients were placed in wheel chairs or were allowed to walk slowly within the clinic. Bulimic patients were allowed to walk slowly for 30 min/day together with a member of the staff. Restrictions of physical activity were gradually reduced and, at time of remission, such restrictions were withdrawn.
The rationale for this is that hypothermia and physical activity are the results of self-starvation and should be treated because they maintain the disorder. The authors do not provide clear reasons for why treating hypothermia would be important for patients who are not underweight (bulimia nervosa, a proportion of eating disorder not otherwise specified (EDNOS) patients) except to say this in their 2002 paper:
From our perspective, psychopathology(20) is considered a consequence, not a cause, of starvation. Similarly, hypothermia(21) and a further increase in physical activity(22) emerge in the state of starvation.
Bulimics show all of the symptoms listed above [they listed more symptoms of AN in the text], including hypothermia(23) and physical hyperactivity(24), and a psychopathology similar to that of anorexics(2). Bulimics differ from anorexics mainly in that they eat excessive amounts of food in a short period and vomit and are of normal weight(25). However, dieting may be a risk factor for bulimia(26), anorexics often develop bulimia(2), and a subgroup of anorexics show bulimic eating behavior(25). Thus, while their physical appearance is different, the similarities between the two groups of patients are more conspicuous than the differences. There is no compelling reason, therefore, to believe that bulimia develops from a different cause than does anorexia. Consequently, it should be possible to treat both groups of patients similarly.
On a positive note, the treatment also focuses on restoring social life (at least in the 2002 paper), and I do think that’s a big positive. And I also think there’s benefit to having a sort-of monitor during meals — there have been many times where I wished I had someone tell me exactly how to eat and what amount as appropriate. But because Bergh et al. believe that psychopathology (like anxiety and depression) is a result of self-starvation, no individual or group therapy is provided at all. For the same reason, patients on any psychotropic drugs (like anti-depressants) are weaned off the drug in the initial stages of treatment.
I had no luck in finding an explanation as to why patients of normal or near-normal weight experience similar levels of psychopathology, given that they are not underweight and according to Bergh et al. these symptoms are the effects of self-starvation. But alas, perhaps it is because their eating is similarly also disordered?
But I want to go back to the hypothermia point.
Bergh and colleagues, in this and other papers, cite the same papers as evidence of hypothermia in AN and BN patients. I thought I’d check them out.
As evidence for the presence of hypothermia in AN, Bergh et al. cite a small paper by Wakeling & Russell (1970). Wakeling & Russell examined the regulation of body temperature in eleven AN patients, before and after refeeding. While they definitely found that thermoregulation was perturbed in AN patients and that their core body temperatures were lower than controls, they didn’t actually find much evidence for hypothermia.
Hypothermia is defined as a body temperature of below 35°C (or 95°F). Keep in mind, too, that how/where body temperature is measured is not an insignificant factor (see here, for example). The papers below seem to define hypothermia as <35.5°C or even <36.0°C, but given that all information I could find on hypothermia defines it as less that 35.0°C, I’m going to stick to it, though temperatures below 36.0°C are still noteworthy.
Wakeling & Russell (1970):
The temperature responses of the malnourished patients differed markedly from those of the control subjects […] the resting oral temperature of the patients was significantly lower, with a mean of 36.1° C compared with 37.05°C.
After refeeding, the mean body temperature of AN patients increased to 36.7°C, which was still significantly lower than in the healthy controls, but not exactly hypothermia.
What about hypothermia in bulimia nervosa patients? Citation #24 led me to this 1988 paper:
Marked hypothermia (<35.5°C) was noted in 52% of strict dieters and 33% of patients who vomit or purge, with temperatures as low as 34.0°C documented. Hypothermia was present to a lesser extent among inpatient bulimic adolescents (five had temperatures <36.3°C, with only one <35.5°C).
Looking at the data they provided in the paper reveals that none of the six BN patients had temperatures below 35.0°C, although 5 out of 33 AN patients did.
I had partial success when I looked for more recent and larger studies examining body temperature in patients with eating disorders.
In 2005, Miller and colleagues published a study of 214 women with anorexia nervosa, and unlike in the two studies above where the participants were inpatients, these women were outpatients and thus more representative of the general population of AN sufferers (average BMI was 16.8). The average core body temperature was 36.6°C , with a range (lowest and higher numbers) of 35.0 – 37.6°C. So, technically, none of the women had hypothermia. However, the authors of this paper defined as hypothermia as a temperature below 36°C, and by this definition, 22% of the participants fit the bill. So that’s roughly 1 in 5.
Okay, so what am I arguing here? Why am I going on this long rant about hypothermia? For one, the idea of keeping patients warm after meals is an important component of the Mandometer® treatment. This is from the Mandometer® website:
“In addition to normalizing eating behavior, the patient is kept warm to avoid excessive exercise to generate warmth and to decrease anxiety after meals.” (link)
“Some of the most important features of our treatment method are: We keep you warm in order to help you feel better. Hyperactivity decreases and body temperature increases by the patient’s resting in warmness. At the same time anxiety and compensation behaviours (activity, vomiting, laxative use) decrease or stop.” (link)
The idea, it seems, is that starvation-induced hypothermia leads to excessive exercise and anxiety in both AN and BN patients. Thus, I wanted to know how prevalent hypothermia is among AN and BN patients. Not really all that prevalent, it seems. Not enough, anyway, to explain the proportion of patients that engage in excessive exercise.
“Excessive exercise” is hard to define and statistics vary widely as a result (see here), but in the Miller et al. (2005) study, exercise was performed regularly by 75% of the participants (average of 5.9 hours a week), and this number does NOT include 5% of women whose exercise was restricted by their physicians, 2% who had injuries that prevented them from exercising and 13% who walked up to 10.5 hours a week.
This keeping-people-warm thing is not entirely ridiculous however, especially given that a temperature below 36°C is not exactly normal.
In 2012, there was a study by a group suggesting that keeping patients warm may reduce levels of physical activity. They didn’t actually show that keeping patients warm did that, but what they did show is that increasing ambient temperature was correlated with reduced physical activity in “semi-starved humans.”
Here’s the interesting part of all of this, though: That same year, the same group published the only study of the Mandometer® treatment that was headed by people other than Bergh and Södersten. It was a small randomized controlled trial–the only randomized controlled trial to compare Mandometer® to another treatment (as opposed to waitlist controls — which is what Bergh et al. did in their 2002 study). This is from the abstract:
After treatment 63% of the [Mandometer Treatment, MT] group and 85% of the [Treatment as Usual, TAU] group had reached a normal weight level and both MT and TAU showed a good outcome on the MROAS (75 and 71%, respectively). After two years more MT than TAU patients were still in treatment and more MT patients had relapsed. The outcome for both treatments in our study were similar and comparable with, if not better than outcome data of other AN studies. MT is not superior to TAU in outcome results and in relapse rate during the first two years following admission for AN treatment.
Don’t worry, Bergh et al. (2013) “explain” the reason for these findings in their latest study.
My second and frankly more important reason for this post is to illustrate that just because someone cites a study saying it supports this or that doesn’t mean that the study actually does. I wanted to use the hypothermia example to illustrate what Bergh and colleagues do repeatedly in their papers: They cite papers claiming the studies show X and Y but once you look deeper you find out that the evidence is often inadequate. More importantly, although peer-review is supposed to catch some of this kind of stuff, as you can see, it doesn’t always work. Indeed, while peer-review is one of the best bullshit-detectors we have (books, remember, are not peer-reviewed), it doesn’t work as well as most scientists and researchers would like to admit.
As an aside: The authors, refer to individuals with anorexia nervosa, bulimia nervosa, and EDNOS as “anorexics” and “bulimics” in almost all of the papers I’ve read by Bergh and Södersten. This is something I rarely see in the literature, unless I’m browsing through old papers, for the obvious reason that it is problematic to define individuals solely by a single medical or psychiatric diagnosis. It is one thing to do it in a title of a blog post (as I have, for brevity and search purposes), but it is another to do it in a peer-reviewed professional journal.
This turned out longer than I initially planned. In the next post I will look at the data and “statistical analysis” (if you can call it that) of the data from the recently published 2013 paper on the Mandometer® treatment, and my plan for the post after that is to critically examine the 10 reasons Bergh et al. (2013) list for why eating disorders are not mental disorders/do not have underlying psychopathology. (I’m not joking.)
Bergh C, & Södersten P (1996). Anorexia nervosa, self-starvation and the reward of stress. Nature medicine, 2 (1), 21-2 PMID: 8564826
Bergh, C., Eklund, S., Eriksson, M., Lindberg, G., & Sodersten, P. (1996). A new treatment of anorexia nervosa. The Lancet, 34, 611-612 DOI: 10.1016/S0140-6736(05)64824-6
Bergh, C., Brodin, U., Linberg, G., & Sodersten, P. (2002). Randomized controlled trial of a treatment for anorexia and bulimia nervosa. PNAS, 99 (14), 9486-9491 DOI: 10.1073/pnas.142284799
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