Task 7 - The Diet Paradox PDF

Task 7 - The diet paradox Introductory chapters, Fairburn (2003), Polivy (2002) & Treasure (2010) Characteristics of eating disorders Most individuals who meet the criteria for one of the eating disorders "migrate" between them, meeting the criteria for 2 or more of the di...

Task 7 - The diet paradox Introductory chapters, Fairburn (2003), Polivy (2002) & Treasure (2010) Characteristics of eating disorders Most individuals who meet the criteria for one of the eating disorders "migrate" between them, meeting the criteria for 2 or more of the disorders at different times. Many individuals show behaviors and concerns typical of 1 or more of the eating disorders without meeting the full diagnostic criteria. Such individuals may be given the diagnosis of other specified feeding or eating disorder. Anorexia Nervosa Anorexia nervosa - a disorder in which people starve themselves with little or no food for long periods of time, yet remain convinced that they need to lose more weight. As a result, body weight is significantly below what is minimally normal for their age and height. Anorexic people have a distorted body image, often believing that they are disgustingly fat and need to lose more weight. They feel good and worthwhile only when they have complete control over their eating and when they are losing weight. Weight loss sometimes causes them to be chronically fatigued, yet they drive themselves to exercise excessively. Restricting type - people simply refuse to eat and/or engage in excessive exercise as a way of preventing weight gain. Eating is done just for survival and in response to pressure from others to eat Binge/purge type - people periodically engage in binge eating or purging behaviors (e.g. self-induced vomiting or the misuse of laxatives or diuretics). The difference with bulimia nervosa is that bulimic people are at normal weight or somewhat overweight. Anorexic people with the binge/purge type often do not engage in binges in which large amounts of food is eaten. Even if a small amount of food is eaten, the person feels as if she has binged and will purge the food. Whether weight is significantly low is determined by body mass index (BMI). Anorexia severity is mild if BMI >= 17kg/m2, severe if 15kg/m2 BED indiv iduals are discouraged from dieting, at least in the first phase of treatment, even if they are seriously overweight. This article is a review that explores to what extent dieting plays a causal role in BED. Restraint theory Restraint theory - people have set points for weight, and obese people have a higher set point than non -obese people. Restraint is a process of self-imposed food deprivation used to achieve a weight below one's physiological point. In other words, obese people who want to lose weight fight against normal biological processes. It has been hypothesized that eaters impose a diet boundary to regulate their eating in order to achieve weight-loss goals. This boundary consists of rigid cognitive rules & beliefs about allowed levels of food intake that override the physiological controls over food intake. This places an artificial limit on eating, which eventually causes feelings of physiological & psychological deprivation. When the boundary is transgressed, the attempt at dietary restraint is undermined and this leads to feelings of failure. At this point the individual loses control until he/she is uncomfortably full. Study: dieters are given a "diet-breaking" milkshake before participating in a taste test of ice cream. Both obese & normal -weight dieters ate more after being forced to break their diets than they did in situations not requiring that. This was explained as an overcompensation for prior caloric deprivation: an accumulation of stress between the physiological urge to eat and the resistance against this drive led to the melting away of the self-imposed restraint once the dietary restriction was broken. The 3-factor model Lowe's 3-factor model - dieting can affect current eating behavior through: 1. Accumulated effects of past cycles of dieting and overeating - this could be a vulnerability factor to future overeating, by impairing one's sense of hunger and satiety. 2. Current dieting practices - they may make people especially prone to eat when negative affect or low arousal (e.g. boredom) make it difficult to ignore the urge to eat. 3. Weight suppression - not discussed in this article because it is not relevant to examining dieting's role in the onset of BED. Dietary restraint in bulimia nervosa Dieting plays a causal role in the development of binge eating problems in individuals with bulimia nervosa. In women with bulimia, dietary restraint is correlated with severity of binge eating tendencies. Patients with bulimia always report that dieting preceded onset of binge eating. Psychopathology Page 7  Patients with bulimia always report that dieting preceded onset of binge eating. There is also evidence that dieting does not always precede binging in bulimia nervosa. Dieting history in BED Binge eating severity is related to the frequency of past dieting. Obese people with more severe binging behavior report that they began dieting at an earlier age and spent more of their lifet ime engaged in efforts to lose weight. Binge eating is also related to more frequent episodes of weight cycling and more extensive histories of yo -yo dieting. Studies looking at temporal onset of dieting and binge eating have found that only a minority of individuals with BED report that dieting preceded the onset of binge eating. Due to the methodological limitations (e.g. having to recall events from 10s of years ago), however, one cannot conclude definitively that dieting is not a significant contributor to binge eating problems in individuals with BED. This extensive past experience with dieting may contribute to the development of binge eating problems, as repeated attempts and failures at dieting along with weight cycling are hypothesized to result in an impairment of one’s sense of hunger and satiety and/or lower one’s self -confidence in his or her ability to diet successfully, which can lead to binge eating. Level of restraint in BED Levels of dietary restraint in people with BED depend on the measure of restraint that it used. Restraint scale Restraint scale - a 10-item self-report questionnaire used to assess weight fluctuations, degrees of chronic dieting, and related attitudes toward weight and eating. Studies using the Restraint Scale to assess levels of restraint in individuals with BED have found a strong positive correlat ion between level of dietary restraint and binge eating severity (r = 0.77). This scale confounds cognitive intent to restrain one's intake and actual behavioral success at dieting. 3-factor eating questionnaire The Cognitive Restraint subscale of the 3-factor eating questionnaire was designed to improve on weaknesses of the Restraint scale. However, it also confounds the cognitive intent with the actual dieting success. People with BED score low on this measure of restraint. Therefore, due to the confound, they either are not currently attempting to restrict their intake or they are attempting restraint and are not succeeding. Restraint subscale of the EDE (Eating disorder Examination) The Restraint subscale of the EDE measures restriction of food intake. Individuals with BED tend to score similarly to obese individuals without binge eating problems and lower than individuals wi th bulimia nervosa on this measure of restraint, Therefore, either they are not currently trying to restrict their intake at a level comparable to that of normal-weight individuals with bulimia or that they are restricting in ways not accounted for by the Restraint scale of the EDE. It is possible that this population uses more general strategies for controlling their intake, rather than the specific dietary rules mentioned in the interview. Cognitive factors scale The cognitive factors scale measures unrealistically high dieting standards. Binge eating is correlated with results on this scale, meaning that in some way or another, dieting is associated with strict , unrealistically high standards. Discussion Dieting has been hypothesized to play a causal role in BED, but a review of the literature highlights inconsistencies and a l ack of clarity in our understanding of the nature of this role. It cannot be ruled out that dieting plays a role in the etiology of BED, but research does not indicate that dieting is always a crucial factor or that it plays as much of a role in the development of BED as it does in the development of bulimia nervosa. Given concerns about the risks of obesity and the lack of solid evidence that dieting does play a causal role in BED, the de -emphasis on weight loss in the treatment of this disorder seems premature. Eating disorders need more experimental psychopathology - Jansen (2016) Introduction The lack of understanding mechanisms that cause, maintain and change eating disorders, currently is the biggest problem facin g the science of eating disorders. Treatment effectiveness for eating disorders is limited: many patients drop out, do not or barely benefit from treatment, bec ome chronic or soon relapse after an initial success. Therefore, the science of eating disorders (treatments) could benefit significantly from experimental studies into the mechan isms of maintenance and change of eating disorders, in order to improve existing treatments. Experimental Psychopathology (EPP) Psychopathology Page 8 Experimental Psychopathology (EPP) Experimental psychopathology - the experimental study of mental disorders in a laboratory setting, where variables that are assumed to be related to the appearance/disappearance of symptoms are manipulated. To understand which factors cause/maintain eating disorders, the manipulation of these factors in well -controlled experimental studies is preferably tested in healthy individuals. Due to ethical limitations, the psychological manipulations that are used in typical EPP research are quite weak imitations o f real causes, and also the effects are usually very weak imitations (i.e. mild symptoms of transient duration). The aim is not to model an entire disorder or to induce full-blown symptoms, but to test causation: does the activation of factor A lead to the occurrence of the (miniature) symptom B? Another way to determine the causal status of a factor is to reduce or remove the factor in analogue samples (nonclinical ind ividuals who show subclinical symptoms). If the factor is causal, the symptoms will reduce when the factor is removed. For example, inhibition training reduces 'go' associations and intake in chocolate cravers and mirror exposure increases body satisfaction in participants high in body dissatisfaction. Restriction of intake and food reward In anorexia, cross-sectional studies show that central reward systems in the brain function abnormally. This has been used to suggest that anorexia is a neurobiological disorder, but the studies are merely correlational, meaning that the differences between healthy controls and anorexic people may be a consequence of starvation. A recent study showed identical reward processing abnormalities in people who remitted from anorexia. However, remission was defined as weight restoration, which may not be sufficient for the recovery from an eating disorder. A more plausible hypothesis is that intentional starvation leads to abnormal brain reward activity. Brain reward systems are strongly influenced by mindset (top-down) processes. Mindset not only influences eating behavior but also one's physiological responding to food stimuli and actual nutrients. Healthy participants show increased activity in reward-related brain areas only when they focus on the taste of food pictures. Manipulations of mindset (training people to up-regulate, suppress or reappraise thoughts about taste of food) influence activity in brain reward and control centers, which are paralleled by self-reported eating desire. The relentless pursuit of thinness, rigid dieting and self-starvation in anorexia may be easier & more successful when there is a deliberate cognitive reappraisal of food which leads to a reduction of the positive incentive value of foods. Prolonged food exposure to tasty food cues (smelling) without reinforcement (eating) is a behavioral strategy that reduces reward activity in the brain. The habitual anorexic eating patterns may thus function as an effective extinction procedure. People with anorexia expose themselves to cues that usually signal intake while preventing actual intake, which will eventually lead to an extinction of appetitive responding. By reducing their reactivity to the temptation to eat, anorexic patients eliminate their primary motivation for eating, making it easier to restrict intake, and eventually impossible to eat. Extinction does not unlearn the existing association between exposure to tasty food and the pleasure of eating them. Rather, they create a new association. The original association still exists. If it is activated in a proper way, it is possible that appetitive responding will return. The fact that extinction is largely context-dependent may explain the huge relapse after clinical anorexia treatment - the eating schedule in a clinic may lead to a renewed appetitive responding but when the patient returns home (which is associated with abstinence), appetitive responding will be inhibited again. Restriction and binge eating Dieting is considered an important cause of binge eating. The evidence for that comes from retrospective clinical studies ass essing the chronology between dieting and binge eating, and laboratory studies. Binge eaters often report that eating a little bit of forbidden foods usually ends up in a binge. Lab studies have also shown that restrained eaters do not regulate their intake after their diets were broken by eating a higher-calorie preload or after another disinhibitor was introduced (e.g. alcohol, smelling tasty foods, and emotion manipulations). However, the conclusion that eating restraint causes binge eating, and eating disorders in general, is severely flawed becaus e restraint was never manipulated in existing experiments. Restrained and unrestrained eaters may differ in many respects, and all can be responsible for their differential response to a diverse range of disinhibitors. Furthermore, the often used self-report scales (e.g. Restraint Scale) are not valid measures of actual food restriction. Rather, they measure weight concerns and an intention to restrain intake. Study: self-reported restrained eaters ate significantly more than unrestrained eaters though they underestimated their intake and did not consider themselves overeating => there may be cognitive biases in self-reports of restraint and intake. Several studies have attempted to find out if calorie restriction was a real cause of overeating. Animal studies showed calorie restriction (20-30%) to be associated with greater longevity and better health. In humans, 6 months of calorie restriction beneficially affect measures of ageing and the prevention of age-related diseases. Calorie restriction lowers body weight & body fat, improves insulin and cholesterol levels, and cardiovascular markers, in ad dition to mood and quality of life. Experimental studies demonstrate to appetite increase during calorie restriction (25% energy deficit) when compared with a weight stable control group. There were no signs of eating disorder symptoms like overeating, binge eating, fear of fatness or purging. Clinical interventions in samples motivated to lose weight show that interventions that increase dietary restraint and calorie restriction result in weight loss, decrease overeating, binge eating and eating disorder symptoms. Therefore, a more plausible explanation for the association between dietary restraint and binge eating is that dieting follow s from overeating instead of the other way Psychopathology Page 9 Therefore, a more plausible explanation for the association between dietary restraint and binge eating is that dieting follow s from overeating instead of the other way around. The tendency to overeat follows from increased food cue reactivity, which can be both psychological and physiological responses to foods and cues that signal foods (cravings, salivation, reward activation etc.) Food cue reactivity is stronger in binge eaters and obese people compared to people without eating or weight concerns. These individual differences in food cue reactivity may follow from a genetic predisposition and/or conditional learning (when people learn that a cue or a context predicts the intake of highly rewarding foods, they will show (neuro-)biological reactivity and increased eating desires or food cravings in response to the cue or context). Therefore, binge eaters (BN & BED) and overeaters (obesity) could benefit from reduced appetitive responding (unlike anorexic patients who need to renew it). There are several clinical case studies that show that food cue exposure could be effective in the reduction of binge eating. Well-controlled studies found that cue exposure reduced eating in the absence of hunger of overweight and obese children and adults. Body overvaluation Current cognitive behavioral models of eating disorders argue that overvaluation of shape and weight (OSW) (self-worth that is predominantly or exclusively defined by one's body shape and weight and the ability to control them) is at the heart of any eating disorder. OSW has been indeed associated with the development, maintenance and relapse of eating disorders. Eating disorder patients tend to allocate more attention toward their self-defined unattractive body parts than to their self-defined attractive body parts. On the other hand, healthy controls focus more on their attractive body parts and less on their unattractive body parts. When looking at other bodies, the pattern is reversed. This has led to the conclusion that a healthy way of looking is opposite to what eating disordered patients do. The dysfunctional way of looking at their own bodies was suggested to maintain body dissatisfaction and eating disorder psych opathology. However, all the used data is correlational, making it impossible to draw conclusions about causality. This is why an experimental test of this causal hypothesis was done: Study: selective visual attention was induced in healthy female students toward their self-defined attractive or unattractive body parts. The participants whose attention was manipulated in a negatively biased way showed a significant decrease in body satisfaction as a consequence of the negative bias training. Study: a short positive bias training in healthy individuals scoring high on body dissatisfaction resulted in an increase in body satisfaction. These experimental findings demonstrate a causal relationship between selective visual attention and body dissatisfaction. Body dissatisfaction has been argued to be related to one's ideas about what other people would think. Study: healthy students were confronted with photos of their own body and bodies of other women. The bodies appeared randomly on a computer screen, and after clicking on them, another photo appeared. Experimental condition: the photo of one's own body was always followed by a photo of a smiling face while control bodies were followed by neutral or frowning faces. Control condition: smiling, neutral and frowning faces randomly followed the photos of all bodies. Body satisfaction increased significantly in the experimental condition while it did not change in the control condition. The intervention was also tested in a sample at high risk for the development of eating disorders. Weight and shape concerns decreased in the highly body dissatisfied sample, and the positive effects were maintained at a 12-week follow-up. Instability of eating disorder diagnoses: prospective study - Milos (2005) Method 192 women with a DSM-IV eating disorder (55 AN, 108 BN, 29 EDNOS) were followed up 12 months and 30 months after baseline evaluation. Eating disorders were diagnosed using the German version of the Structured Clinical Interview for Axis I of the DSM -IV, conducted by 4 psychologists (k = 0.8). At each follow-up assessment the procedure for making the eating disorder diagnoses was the same as that used at the baseline. Results Remission from an eating disorder Only 55 (28.6%) participants retained the same diagnosis across all 3 assessment points. 20.8%/31.3% were at remission at the 12/30-month follow-up, with EDNOS having the highest remission rates (31% and 52%), followed by bulimia (24% and 31%) and then by anorexia (9% and 22%). Only 13% of the sample were in remission at both assessment points. Migration between eating disorder diagnoses Migration between eating disorders occurred in 53% of the cases. 56% of anorexic patients retained the diagnosis at 12 months and 49% still had it at 30 months. Only 23% of anorexic patients retained their diagnosis at both reassessments. 51% of bulimic patients retained the diagnosis at 12 months and 37% still had it at 30 months. Only 29% of bulimic patients retained their diagnosis at both reassessments. 28% of EDNOS patients retained the diagnosis at 12 months and 31% at 30 months. Only 10% of EDNOS patients retained their diagnosis at both reassessments. Psychopathology Page 10  Only 10% of EDNOS patients retained their diagnosis at both reassessments. Marginally more anorexia nervosa cases changed to bulimia nervosa (20%) at either or both follow-up points than vice versa. 37% of the participants with a baseline diagnosis of anorexia or bulimia were given a diagnosis of EDNOS at either or both follow-ups. Stability of diagnosis was highest for anorexia, followed by bulimia and then by EDNOS. Illness duration and diagnostic stability Women who retained their diagnosis had a significantly longer eating disorder history at study entry than those who were in r emission at 30 months. Those with bulimia nervosa or EDNOS showed no association between eating disorder duration and either change in diagnosis or stable remission. Purging behavior 53.7% of participants with a baseline purging eating disorder received at some point (first and/or second follow -up) a non-purging diagnosis, whereas of 46 participants with a non-purging eating disorder at baseline 17.4%% subsequently received a purging diagnosis. Participants with a non-purging type of disorder at baseline had a significantly higher recovery rate (21%) than participants with a purging type of disorder. Discussion Diagnostic instability There were 3 main findings: Diagnostic stability was low. This was only in part due to remission. Although the overarching diagnosis of 'eating disorder' was relatively stable, there was considerable movement between the 3 specific eating disorder diagnoses. After excluding participants with a stable remission, changes between eating disorder categories of the restrictive and the b inge–purge type were frequent. Participants with a non-purging eating disorder had a higher recovery rate than those with binge –purge behavior. Eating disorders or eating disorder? The shared and distinctive psychopathology of anorexia nervosa, bulimia nervosa and EDNOS and the frequent movement of patien ts between the diagnoses, together with the fact that the average age at onset did not differ between them, strengthens the view that these disorders have so mu ch in common that they might be best viewed as a single entity. The current diagnostic scheme is limited, e.g. because minor changes in weight or eating behavior can result in a person rece iving an entirely different DSM-IV eating disorder diagnosis. Dissecting the core fear in anorexia nervosa - Murray (2016) The improvement of acquired fear does not operate only due to habituation processes (i.e. exposure to feared stimuli alone is insufficient to ensure long-term fear reduction). Rather, fear reduction operates more via mechanisms of inhibitory learning, where the violation of expected outcomes results in the new learning of nonthreat associations related to the original feared stimulus. Therefore, exposure therapies are now focused on maximally violating fear expectancies, instead of just aiming for habituation. Disentangling feared stimuli and feared outcomes in anorexia nervosa It is not clear if the fear of weight gain in anorexia is experienced as a feared outcome or as a feared stimulus/cue. Food as a material object is usually not a feared stimulus in anorexia. While many patients describe a variety of "fear foods" (usually calorie-dense foods) that are subjectively judged as more likely to result in weight gain, it is still unclear how much the magnitude of weight gain is deemed catastrophic. There is some clinical evidence that a small degree of weight gain in anorexia typically evokes a fear of continued, uncontrollable weight gain. Therefore, they may be a chained process in which consumption of foods (particularly ones associated with weight gain) leads to a fear of gaining any amount of weight, and small positive weight changes themselves stimulate a feared expectation of exponential weight gain. Another potential cue-outcome threat association in anorexia involves weight gain normalization as the stimulus and self -concept-related feared consequences as the outcome. Patients may fear that weight normalization will lead to intolerable affective states or violate their experience of themselves as highly controlled, unique, or adherent to culturally endorsed thin-body ideal. These hypothesized cue-outcome associations are not mutually exclusive. However, their relative magnitude & interactions may impact treatment efficacy, because it is unlikely that a uniform treatment approach will effectively violate all potential fear-based expectancies. The impact of this conundrum on treatment mechanisms If food consumption is the core fear stimulus and weight gain - the feared outcome, then the introduction of previous eliminated/feared foods together with the necessary weight gain may confirm the notion that these foods are indeed "dangerous", as weight increases. In this case, inhibitory learning may only start after achieving weight restoration, when feared food consumption will not necessarily result in further weight gain. Alternatively, if weight gain is the feared cue and negative self-related consequences are the feared outcome, then focusing on food and weight gain may not be an Psychopathology Page 11 Alternatively, if weight gain is the feared cue and negative self-related consequences are the feared outcome, then focusing on food and weight gain may not be an adequate exposure for violation of this fear. In this case, a broader treatment focus is warranted, where feared self-related consequences are violated. Individual differences in specific fears (e.g. of gaining weight or the negative self -image associated with it) may influence how well people holding these fears respond to treatment. It is important to separate what triggers the fear from what results from it. This way individualized treatments can be created for anorexic patients. Using exposure therapy without knowing exactly which fear-based expectations need to be changed might not be effective or could even be harmful. Can we live longer by eating less? A review of caloric restriction and longevity - Roth (2012) Prolonged caloric restriction improves longevity in yeast, nematodes, rodents and other lower animals. Calorie restriction in non-human primates has been shown to prevent age-related disease including diabetes, cancer, cardiovascular disease and brain atrophy. In rhesus monkeys, a younger outward appearance has been observed after 20 years of decreased calorie intake. Studies of caloric restriction and longevity in humans are still ongoing, however the impact of prolonged caloric restriction appears to be beneficial and has some possible anti-aging effects. Still, there is evidence that maintenance of calorie restriction in humans is difficult. Relation of successful dietary restriction to change in bulimic symptoms: A prospective study of adolescent girls - Stice (2006) Introduction Dieting has been proposed to increase risk for bulimia. A proposed mechanism is that it produces weight loss, which in turn may create a state of chronic hunger, especially if the weight loss leaves the dieter below a physiologically-defined set point of weight. The chronic hunger increases the risk to binge. Another proposed mechanism is that reliance on cognitive control over eating, instead of physiological cues, makes dieters vulnerable to uncontrolled eating when these cognitive processes are disrupted. Violation of rigid dietary rules may result in the abandonment of dietary restriction (abstinence violation effect!!!). Also, dieting may deplete tryptophan (serotonin precursor), which increases the likelihood of binge eating high-carb foods to restore tryptophan levels. Some have suggested that the effect of dieting on bulimic symptoms is mediated by negative affect and overvaluation of weight & shape, but virtually no experimental studies exist. Even though some studies provide support for the dieting theory of bulimia, some experimental findings seem incompatible with this theory: In RCTs, assignment to a low-calorie weight loss diet (1200kcal/day) results in significantly greater decreases in binge eating for obese & overweight adult women relative to wait-list controls. The authors conduct 2 experiments that investigate the effects of manipulations of dietary restriction on bulimic symptoms. Study 1 finds that assignment to a 6-week low-calorie weight loss diet resulted in greater decreases in bulimic symptoms in normal-weight school-recruited late adolescent young women relative to waitlist controls. Study 2 investigated whether a lower intensity diet weight maintenance diet has a different effect (because a prescribed low-calorie diet may be more restrictive than dieting practiced in the real world). This is the study conducted in the next paper (Stice, 2005), which I'm skipping - it's pretty straightforward. In this study, assignment to a weight maintenance diet resulted in greater decreases in bulimic symptoms and negative affect in normal-weight school- recruited adolescent girls over a 1-year period, relative to assessment-only controls. Although these experimental results seem incompatible with the dieting theory of bulimia, the prescribed weight loss diets ma y be qualitatively or quantitatively different than real-world diets. That's why the primary goal of the current study is to test if successful weight loss dieting in the real world is associated with increases or decreases with bulimic symptoms. Hypothesis: individuals who show successful dietary restriction will show greater decreases in bulimic symptoms over time than those not showing successful dietary restriction. Due to the low validity of dietary restraint scales, authors used decreases in objectively measured body mass to validate that girls with higher dietary restraint scores were actually engaging in weight loss dieting. A secondary aim of the current study is to test if successful dietary restriction is associated with increases or decreases i n depressive symptoms. Theory states that it increases depressive symptoms (e.g. due to tryptophan depletion), but RCTs show that diets decrease depressive symptoms. Hypothesis: successful dietary restriction is associated with declines in depressive symptoms. Method 496 adolescent girls participated in a structured interview assessing bulimia nervosa & symptoms of major depression (DSM -IV), had their weight and height measured at T1 and 3 annual follow-ups (Time 2 [T2], Time 3 [T3], and Time 4 [T4]). Successful dietary restriction was operationalized as high levels on a dietary restraint scale (above the median split on the Dutch Restrained Eating Scale) and a clinically meaningful decrease in body mass (10% reduction in BMI, after adjusting for age -related changes in BMI). Discussion As expected, moderately overweight school-recruited adolescent girls who showed successful dietary restriction showed significantly greater decreases in bulimic symptoms than did those who did not show successful dietary restriction. These findings are more ecologically valid than the experimental trials because participants did not undergo a prescribed weight control intervention. Reasons for the inconsistent results of prospective studies (after showing that it is not due to weight loss in the real worl d having different effects on bulimic symptoms Psychopathology Page 12 Reasons for the inconsistent results of prospective studies (after showing that it is not due to weight loss in the real worl d having different effects on bulimic symptoms than weight loss resulting from prescribed interventions): The usage of invalid dietary restraint scales, which do not correlate with objective measures of acute or chronic food intake. The possibility that most weight loss dieters do not enter a state of calorie deficit, but instead practice relative caloric restriction (i.e. eat less than they want to eat rather than what is necessary to induce a negative energy balance). The possibility that some unmeasured variable explains the relations between dieting and future bulimic symptoms (e.g. a chronic tendency towards caloric overconsumption that may lead to both self-reported dieting and eventual onset of bulimic symptoms). The fact that prescribed diets promote healthy dietary behaviors, while bulimic symptom onset may be caused by unhealthy diets. The fact that the relationship of dieting to bulimic symptoms is moderated by body mass or age: dieting in a normal-weight adolescent girl may produce effects on eating behavior that are different from dieting effects in overweight or obese individuals, who are probably in a state of positive energy balance. Post hoc analyses in this study revealed that the effect of successful dietary restriction on decreases in bulimic symptoms was significantly stronger for participants with higher initial BMI scores (p < 0.001). Contrary to expectations and the findings from weight loss treatment RCTs, successful dietary restriction was not associated with decreases in depressive symptoms. It may be that the effects of successful dieting on mood is more acute and not easily captured by the 1-year measure interval. Psychopathology Page 13