Clinical Utility of Weight Suppression in Bulimia Nervosa Treatment – Part II

In this post I will continue my discussion on weight suppression in bulimia nervosa (click here to read Part I). Just in case you happen to be reading the posts out of sequence, I will summarize the main points of that entry:

  1. Weight suppression is the difference between one’s current body weight and highest adult body weight.
  2. It has been found that individuals with BN are on average well below their highest historical weights (i.e. they are weight suppressed).
  3. Many studies have consistently found positive associations between WS and the onset and maintenance of BN symptoms.


Because most individuals with BN have undergone significant weight loss, this makes them susceptible to weight regain — much like obese individuals usually regain the weight they have lost. Indeed, evidence suggests that weight suppression predicts weight gain in individuals with BN during inpatient (Lowe et al., 2006) and outpatient treatment (Carter et al., 2008).

In contrast, other measures of weight history, such as highest or lowest body mass index (BMI) at current height and the difference between lowest weight and current weight, have failed to demonstrate consistent associations with disordered eating symptoms or weight gain (Butryn et al., 2011; Butryn et al., 2006; Carter et al., 2008), suggesting that weight suppression may be particularly salient (important) to the presentation and course of eating disorders – Wildes & Marcus, (2012)


  • Significant weight loss may result in a lower resting metabolic rate (Astrup, 1996).
  • As previously mentioned, individuals with BN tend to have reduced leptin levels, an important hormone that signals satiety. Such hormonal abnormalities could disrupt satiety cues and increase vulnerability to overeating (Wildes & Marcus, 2012).
  • Those highest in weight suppression may need to gain more weight to “reduce biobehavioural pressures maintaining the disorder” (Lowe et al., 2011). I’m thinking this could be linked to set point theory (refer here and here). Such individuals may thus possess a tendency to return to a weight influenced by genetic makeup, family history and/or individual history.

Hence, bearing in mind the relationship between (1) weight suppression and the onset and maintenance of BN symptoms, as well as (2) the relationship between weight suppression and weight gain, it is necessary to investigate whether weight suppression would hinder BN treatment outcome.


Study 1: Butryn et al. (2006) were the first to investigate — as far as I am aware of — weight suppression in 188 outpatients receiving cognitive-behavioural therapy (CBT). Participants who had dropped out of treatment had significantly higher levels of weight suppression than those who had completed treatment. Correspondingly, among those who had completed treatment, participants who continued to engage in binge eating or purging were higher in weight suppression than those who had abstained.

Study 2: Carter et al. (2008) attempted to replicate Butryn and colleagues’ findings (2006); 132 participants were similarly treated with CBT. They did not find that weight suppression played a significant predictor of treatment completion and treatment outcome among BN outpatients. The researchers hypothesised that this may be due to the fact that participants in their study had lower levels of weight suppression on average and were more similar to each other in their levels of weight suppression at pretreatment than were those in the study by Butryn et al. (2006). [This would make it harder to untangle the role of WS on treatment outcomes because if everyone has similar levels of WS, how can you tell whether higher levels of WS predict better or worse outcomes?]

Moreover, participants in the Butryn study may have been more concerned about the prospect of gaining weight over treatment, which could have negatively affected their response to treatment. Both studies also differed in their treatment approaches — Butryn and colleagues (2006) included normalisation of eating in their first phase of treatment, whereas Carter and colleagues (2008) addressed normalisation of eating within the context of identifying cues for binge eating and purging. Carter et al. thereby posited that their approach could have been less threatening for patients higher in weight suppression (2008). In sum, it is conceivable that individual and experimental differences accounted for the different findings.

Study 3: Given the inconsistencies in previous findings, Zunker et al. (2011) aimed to re-examine weight suppression in BN. Participants (128 adults) similarly received CBT. As in Carter and colleagues’ findings (2008), weight suppression in this study did not predict treatment completion or abstinence from binge eating or purging. (This study examined weight suppression in patients with binge eating disorder BED and the results were likewise non-significant.)

Zunker and colleagues pointed out that although weight suppression has already been defined as the difference between current and highest adult weight, it may not have been specific enough for both participants and experimenters. This could account for the inconsistent findings across studies. They therefore proposed that weight suppression be applied to “individuals with a current weight of 10 or more pounds below their maximum historic weight and whose age at maximum weight was at least 1 year earlier than their current age”.

Study 4: Finally and most recently, Dawkins, Watson, Egan, and Kane (2013) re-examined the relationship between weight suppression and treatment completion and outcome (abstinence from binging and purging at post-treatment) in a sample of 117 outpatients treated with Enhanced-CBT. Dawkins et al. found that weight suppression did not predict treatment completion outcomes and did not predict the likelihood of abstaining from binge eating and purging at post-treatment.


These findings are consistent with Carter et al.’s (study 2) and Zunker et al.’s (study 3)  findings but not with Butryn et al.’s (study 1) study. A possible reason could be due to the difference in sample size among the studies, as well as differences in style and length of treatment.

Another factor accounting for the inconsistencies could be moderators (definition: a variable that influences the strength of a relationship between two other variables; more information here and here) that have yet to be identified. Dawkins et al. did test several potential moderators such as parental history of overweight, childhood body shape, pretreatment BMI, and the difference between highest and lowest ever adult body weight but no moderator effects were apparent.


I am still of the opinion that the inconsistent results could be attributed to statistical, participant (e.g. number of participants as well as sample composition) and experimental (e.g. type of CBT delivered) differences.

Given that the investigation of weight suppression in eating disorder populations is rather new, all things considered, I believe that more time will be needed to:

  • Establish a standardized operational definition of weight suppression;
  • Identify moderator and mediator variables;
  • Construct a standardized treatment protocol

Additionally, I think that seeing as how weight suppression predicts weight gain during treatment as well as a longer time to achieve first remission, it is possible that weight suppression could hinder treatment.

Allow me to elaborate.

The fear of weight gain is in itself an obstacle to treatment for many individuals with bulimia nervosa (Carter et al., 2008; it is certainly an obstacle to treatment for anyone with an ED but I’m merely zooming in on BN seeing as it is the focus of this post). Specifically, as Butryn et al. suggested, people with BN who have once experienced a significantly higher weight may greatly fear the plausibility of weight gain, especially if highest past weight was overweight or obese (2006). Such fears would interfere with compliance with CBT for BN, which involves normalisation of eating patterns (Lowe et al., 2011). Furthermore, weight suppressed individuals may possess a biobehavioural profile that (dys)regulate weight and promote binge eating (as discussed above; Dawkins et al., 2013).

Plus, given that weight suppression has been associated with larger or more rapid weight gain during treatment, it is possible that individuals may be triggered to engage in compensatory behaviours or be psychologically and emotionally uncomfortable with the rate at which they are gaining (more so than those who are not as highly weight suppressed). Lastly, the faster rate of weight gain may mean that patients would have a shorter amount of time to adjust to their new body, potentially increasing risk of treatment dropout and/or relapse.

In sum, this is what a potential feedback cycle might look like (Butryn et al., 2011) — the perpetual dieting and/or compensatory behaviours needed to maintain a suppressed weight could sustain binge eating and purging. Also, considering that weight suppressed individuals are prone to weight gain (possibly due to reduced metabolic rate, increased overeating and/or hormonal abnormalities), this may result in greater dietary restriction. This weight gain could also lead to greater body dissatisfaction. Furthermore, since many individuals with BN were previously at a significantly higher weight, they may have an even greater fear of gaining weight. This would contribute to greater levels of dietary and compensatory behaviours.


Statistical VS Clinical (Practical) Significance

Regardless of the inconsistent results on whether weight suppression affects treatment outcomes, I propose that based on weight suppression’s strong, positive associations with the onset and maintenance of bulimic symptoms as well as weight gain during treatment, it has potential clinical utility.

Firstly, by gathering weight history information from patients at the start of treatment, clinicians could be informed about the course of the disorder. This is based on Lowe et al.’s finding that those high in weight suppression took a significantly longer time to achieve first full remission (2011). Secondly, as highly weight suppressed individuals may have more difficulty normalising their eating patterns, being aware of their weight suppression could allow for anticipation of this hurdle. Moreover, clinicians should prepare patients for the possibility of weight gain over time, that is, they should have realistic weight expectations (Carter et al., 2008; Lowe et al., 2011) in recovery.


  • Apart from identifying potential moderators, Keel and Heatherton also recommend that “studies could examine whether beliefs about the effects of disordered eating practices on weight or alterations in physiological processes that regulate eating and weight mediate associations between weight suppression and maintenance of bulimic symptoms” (2010).
  • To determine weight suppression values, highest adult weights were obtained by self-report. Considering that most individuals with eating disorders are acutely sensitive about their weight, their recalling of highest weight may be biased. Lowe et al. hence advocate that future studies should “collect a second source of data to check the validity of patients’ reports of highest historical body weights” (2006).
  • I suspect there could be a threshold that, once exceeded, will leave an individual more vulnerable to the various pathological symptoms associated with weight suppression. Lowe et al. (2011) found that individuals who were more significantly more weight suppressed took longer time to first full remission compared with women who were not as weight suppressed. A threshold of 25 lbs separated the upper WS tertile (i.e. those higher in weight suppression) from the lower tertiles. Perhaps the effects of weight suppression only become clinically important once weight suppression exceeds 20-30 lbs.


By determining the clinical significance of weight suppression, it could be used alongside BMI and % of IBW to measure illness severity and treatment response (Berner et al., 2013). This is especially important given the controversy surrounding BMI (read here and here) and ideal body weight (IBW). We simply need to identify more indices so as to achieve an acceptable level of reliability and validity with respect to evaluating treatment/recovery outcomes.


Butryn ML, Lowe MR, Safer DL, & Agras WS (2006). Weight suppression is a robust predictor of outcome in the cognitive-behavioral treatment of bulimia nervosa. Journal of Abnormal Psychology, 115 (1), 62-7 PMID: 16492096

Carter FA, McIntosh VV, Joyce PR, & Bulik CM (2008). Weight suppression predicts weight gain over treatment but not treatment completion or outcome in bulimia nervosa. Journal of Abnormal Psychology, 117 (4), 936-40 PMID: 19025238

Dawkins H, Watson HJ, Egan SJ, & Kane RT (2013). Weight suppression in bulimia nervosa: relationship with cognitive behavioral therapy outcome. International Journal of Eating Disorders, 46 (6), 586-93 PMID: 23606241

Zunker C, Crosby RD, Mitchell JE, Wonderlich SA, Peterson CB, & Crow SJ (2011). Weight suppression as a predictor variable in treatment trials of bulimia nervosa and binge eating disorder. The International Journal of Eating Disorders, 44 (8), 727-30 PMID: 20957701

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Jackie is a psychology undergraduate from Singapore. She ploughs through results sections of research articles so that you don't have to. Apart from eating disorders, she has a keen interest in anxiety and mood disorders. She aspires to become a clinical psychologist.


  1. Great post Jackie!

    That said, I’m not sure how much I buy this. I haven’t read any of these studies, but I have a couple of questions/thoughts:

    1. Did any of them look at the percentage of the participants that had lifetime diagnosis (or experience of) anorexia nervosa? Is there a difference between those with and without a history of AN?

    2. What’s the point/rationale of separating binge/purge AN types from BN when studying whether weight suppression has a role? (I don’t really see one, but maybe I’m not thinking hard enough.)

    3. The idea that WS would play a significant role strikes me as a hypothesis that’s derived from the Fairburn-esque/CBT model of bulimia nervosa and its maintaining factors. A model that, you know, certain has a lot of truths to it but, in my opinion, misses a lot of components too. I think it is more weight-centric than it needs to be and ignores other components of bingeing/purging that play a role in maintaining the behaviours.

    4. Is there a difference between the extent of WS between AN-BP and BN patients?

    Meh, I don’t know, I am not sold on this but I’m not sure to what extent that’s because of my own experiences with bingeing/purging(both AN-BP and BN), and where my experiences fit in when compared to other BN and AN-BP sufferers. I don’t know how generalizable they are because of how anxiolytic I find the whole process, because I tend to maintain or gain weight with BN, and because my starting weight is in the lower ranges of “normal” and I don’t have personal history with being overweight.

    I think what would matter here, if anything, is the extent of WS among those who binge/purge. Who cares if it is AN-BP or BN? Particularly if those with BN start at a higher weight, so then they might have lost the same amount as those who are in the AN-BP category. I don’t know.

    • Thanks, Tetyana! And thanks for the questions.

      1. A valid point! Only 2 studies had information on lifetime diagnosis/history of AN: Butryn et al. (24%) and Carter et al. (25%). I believe that the rest did not provide any information on the proportion of Ps with prior AN diagnosis. None of them compared those with and without a history of AN, unfortunately. I agree that it would have been useful to compare or even control for the history of AN in a multiple regression model/correlational analysis. I’d be curious to know your thoughts on the direction(s) of the results!

      2. Oh, I believe that the point of separating both groups is simply based on the evidence that patients with BN tend to report greater highest weights than do those with AN. Like I said, BN was first studied w.r.t. to WS, and I think researchers are finally catching up because Berner et al. investigated WS in AN and found that at admission, WS — independently of BMI — was positively associated with EDI-3 Bulimia Scores. It gets a little complicated when explaining the association between WS and bulimic symptoms at discharge but you can read the article here ( Anyway, Wildes & Marcus ( likewise found that even after controlling for AN subtype, higher levels of WS predicted bulimic symptoms during TX. So, the separation does seem a bit pointless in light of these recent findings. Of course, in all fairness, most of these studies on WS are typically obtained from a larger study investigating a TX so perhaps that’s why the separation is also warranted? Idk.

      3. I think it is related from the CBT for BN model. Yeah, I think models like CBT for BN or CBT-E (transdiagnostic) may be good but are definitely not perfect. Plus, in my opinion, it’s just really hard to come up with a general model for such a heterogeneous sample of patients. I believe that in due time, with more studies examining moderator and mediator variables, the models can be improved significantly.

      4. I’m going to have to equivocate. The two AN studies mentioned are very recent and I think no studies comparing WS in AN (specifically AN-BP) with BN have been published. It’s certainly something to think about. I think there may be a *statistical* significance but I think clinical significance-wise, it’s still a potentially important thing to address in TX for both groups. Gonna cut myself off before I start ranting/rambling about clinical significance, haha.

      Yep, that’s one of the issues arising from using the mean (and/or a normal curve) as a point of reference, I suppose.

      Exactly — it’s the extent of WS – not just those who binge/purge, regardless of diagnostic category – but within the context of the patient’s personal history (be it growth charts or familial history). Re: what you said about those with BN perhaps losing the same amount of weight as those in the AN-BP category, yes yes yes. I chose to write about this topic because I’ve always felt that it’s not just weight loss that matters but the degree of weight loss. Especially given the fact that a) studies on WS in AN are being conducted [hopefully that will lead to the comparison between AN-BP and BN and wouldn’t it be fascinating if there was no sig. differences in terms of WS between both groups?] and that the DSM has finally removed BMI from the AN diagnostic criteria…

  2. Actually you know, I think the threshold thing probably would be helpful in identifying the role of WS. Though I wonder if percent weight loss is a better way to measure than absolute weight lost.

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