آیا خویشتن داری غذایی معیار معتبر خویشتن داری غذایی هستند؟ اطلاعات بیولوژیکی و هدف رفتاری اضافی

Prospective studies find that individuals with elevated dietary restraint scores are at increased risk for bulimic symptom onset, yet experiments find that assignment to energy-deficit diet interventions reduce bulimic symptoms. One explanation for the conflicting findings is that the dietary restraint scales used in the former studies do not actually identify individuals who are restraining their caloric intake. Thus, we tested whether dietary restraint scales showed inverse relations to objectively measured caloric intake in three studies. Four dietary restraint scales did not correlate with doubly labeled water estimates of caloric intake over a 2-week period (M, r = .01). One scale showed a significant inverse correlation with objectively measured caloric intake during a regular meal ordered from an ecologically valid menu (M, r = −.30), but a significant positive relation that was qualified by a significant quadratic effect, to objectively measured caloric intake during multiple eating episodes in the lab (M, r = .32). In balance, results suggest that dietary restraint scales are not valid measures of dietary restriction, replicating findings from prior studies that examined objective measures of caloric intake.

Theorists have asserted that dieting increases risk for onset and maintenance of binge eating and bulimia nervosa (Fairburn, 1997, Huon, 1996, Levine and Smolak, 2006, Neumark-Sztainer, 2005 and Polivy and Herman, 1985). Dieting, or dietary restraint1, refers to intentional and sustained restriction of caloric intake for the purposes of weight loss or maintenance (Herman and Mack, 1975, Wadden et al., 2002 and Wilson, 2002). Dietary restriction must result in a negative energy balance for weight loss or a balance between intake and output for weight maintenance. Polivy and Herman (1985) argue that dieters’ chronic hunger increases the risk of binge eating and that a reliance on cognitive controls over eating leaves dieters vulnerable to uncontrolled eating when these cognitive processes are disrupted. Binge eating theoretically precipitates redoubled dietary restraint and the use of compensatory weight control techniques (e.g., vomiting), which may escalate into a binge–purge cycle (Fairburn, 1997). In support of this theory, prospective studies indicate that females with high versus low scores on dietary restraint scales are at greater risk for future onset of binge eating, bulimic symptoms, and bulimic pathology (Killen et al., 1996, Neumark-Sztainer et al., 2006, Stice et al., 1998 and Stice et al., 2008a) and increases in bulimic symptoms (Johnson and Wardle, 2005, Stice, 2001 and Wertheim et al., 2001). These studies primarily used the restraint scale (RS; Polivy, Herman, & Warsh, 1978) and the Dutch restrained eating scale (DRES; van Strien, Frijters, van Staveren, Defares, & Deurenberg, 1986). Given the consistency of these prospective findings, it is widely accepted that dieting plays a causal role in the onset of bulimic pathology (Fairburn, 1997, Levine and Smolak, 2006 and Neumark-Sztainer, 2005). Thus, eating disorder prevention programs often advise against dieting (e.g., Smolak et al., 1998 and Stewart et al., 2001), and some researchers have evaluated interventions that reduce dietary restriction and propose a moratorium on dieting (Bacon et al., 2002 and Polivy and Herman, 1992). In contrast to the results from prospective studies, randomized trials have found that assignment to weight loss diet interventions reduce binge eating and bulimic symptoms. Trials indicate that assignment to 5–6-month energy-deficit weight loss interventions, versus waitlist control conditions, resulted in significantly greater decreases in binge eating for overweight and obese women (Klem et al., 1997, Goodrick et al., 1998 and Reeves et al., 2001). Trials also indicate that assignment to 6-week energy-deficit weight loss interventions, versus waitlist control conditions, produced significantly greater decreases in bulimic symptoms among normal-weight adolescent girls and young women (Groesz and Stice, 2007 and Presnell and Stice, 2003) and women with bulimia nervosa (Burton & Stice, 2006). Participants in these interventions are instructed to reduce caloric intake and increase physical activity to achieve the negative energy balance necessary for weight loss. Further, assignment to a weight maintenance intervention that significantly reduced risk for weight gain and obesity onset over a 3-year period resulted in decreased bulimic symptoms and reduced risk for future onset of eating disorders in adolescent girls relative to assessment-only controls (Stice, Marti, Spoor, Presnell, & Shaw, 2008). Participants in this intervention were encouraged to bring their caloric intake into balance with their energy expenditure to avoid unhealthy weight gain. It is important to determine why these contradictory findings have emerged because they have opposing public health implications. If dieting causes bulimic pathology, interventions should attempt to decrease dieting. Yet, if dieting reduces bulimic symptoms and facilitates weight control, interventions should help individuals diet more effectively. The evidence that 45% of adolescent girls report dieting underscores the import of determining whether dieting has adverse effects (Neumark-Sztainer, 2005). One potential explanation for the inconsistent findings is that the dietary restraint scales used in the prospective studies are not valid measures of dietary restriction. The original dietary restraint scale was developed to identify individuals currently suppressing their weight through dietary restriction (Herman and Polivy, 2008 and Polivy et al., 1978). Other dietary restraint scales were developed to provide more valid measures for identifying people engaging in dietary restriction for weight control purposes (van Strien et al., 1986). If the scales used in the prospective studies do not identify individuals who are actually achieving the energy-deficit diet necessary for weight loss, it could explain why these studies produce findings that are discrepant from those emerging from experimental trials involving energy-deficit diets. That is, if the experiments are placing people on energy-deficit diets that result in documented weight loss, whereas the prospective studies are studying people who desire, but are not achieving an energy-deficit diet, it could explain why results from these two lines of research do not accord; the experiments are studying caloric deficit diets and the prospective studies are not. The evidence that people often under-report caloric intake, particularly those with elevated dietary restraint scores (Bandini et al., 1990, Lichtman et al., 1992 and Prentice et al., 1986), suggests this is a reasonable supposition. We conducted four studies that investigated whether five dietary restraint scales showed inverse correlations with directly observed caloric intake during single eating episodes (Stice, Fisher, & Lowe, 2004). We used caloric intake as the criterion because the original validity studies used self-reported intake as the criterion (French et al., 1994, Kirkley et al., 1988, Neumark-Sztainer et al., 1997, van Strien et al., 1986 and Wardle and Beales, 1987). All five dietary restraint scales were developed to assess intentional dietary restriction for the purposes of weight control: the RS (Polivy et al., 1978), three factor eating questionnaire-restraint scale (TFEQ-R; Stunkard & Messick, 1985), DRES (van Strien et al., 1986), eating disorder examination questionnaire-restraint subscale (EDEQ-R, Fairburn & Beglin, 1994), and dietary intent scale (DIS; Stice et al., 2004). These scales showed weak and generally non-significant correlations with objectively measured caloric intake during unobtrusively observed eating episodes across the four studies (M, r = −.07, range: −.34 to .20; Stice et al., 2004). For instance, the average correlation between three dietary restraint scales and observed caloric intake of students eating meals in dorm cafeterias was −.09. Our findings replicate results from other studies that examined objectively measured caloric intake during single eating episodes ( Epstein et al., 2004, Hetherington et al., 2000, Jansen, 1996, Ouwens et al., 2003, Sysko et al., 2007b and Wardle and Beales, 1987).