Temporal patterns of hunger and fullness ratings and related cognitions in anorexia and bulimia

Appetite, 1991, 16, 219-237

Temporal Patterns of Hunger and Fullness Ratings and Related Cognitions in Anorexia and Bulimia KATHERINE A. HALMI and SUZANNE R. SUNDAY Cornell University Medical College

Hunger and fullness during an experimental liquid meal were evaluated by ratings in 84 eating-disordered patients, including three diagnostic subgroups, and in 19 controls who were normal in weight and eating healthily. Anorectic-restrictors had lower hunger ratings and higher fullness ratings than controls. The same tendency was present in anorectic-bulirnics. These ratings were relatively unaffected by treatment. Anorectic-restrictors had longer meals than the anorectic-bulimics and normal-weight bulimics. The anorectic-restrictors also tended to eat more slowly than did the bulimic patients. These groups did not, however, differ in amount consumed. At the end of the experimental meal, the anorectic-bulimics were more preoccupied with thoughts of food and anorectic-restrictors had a lower urge to eat, as compared with the controls. Hunger and fullness ratings were negatively correlated for all diagnostic groups; however, these correlations were less pronounced for the eating disorder groups. The eating-disordered patients had predominantly “abnormal” patterns of hunger and fullness curves, indicating a confusion of these concepts.

INTRODUCTION Hunger and satiety ratings result from integrating cognitive sets involving beliefs about and attitudes towards the nutritional content of food and signalling from internal physiology (gastrointestinal afferents, peptide hormones, metabolism). Both sources of information, as well as sensed dietary characteristics, affect eating behavior via neurotransmission. Booth (1982) postulated that underlying the culturally derived attitudes that influence food intake is a process of nutritional hedonic conditioning, whereby the nutritional functions of a food are related to its sensory characteristics, and thus its conceptual identity. Blundell (1987) similarly pointed out that the capacity to control nutrient intake to meet bodily needs requires specialized mechanisms to harmonize relevant information from the internal and external environments. It has seemed reasonable to suspect that patterns of these integrative perceptions of hunger and fullness would differ between underweight anorexia nervosa patients who exclusively starve and those who alternate severe starving with binge eating, and again between anorectics and normal weight bulimics. Further, each eating disorder group would be expected to differ from normal weight “healthy” eating persons.

This study was supported by National Institutes of Health and Mental Health Grants-5K02MHOO516, SROl-MH43314-02 and lROl-DK40961-OlAl. We wish to acknowledge the fine technical assistance of Angela Puglisi. Reprint requests should be sent to Dr Katherine A. Halmi, New York Hospital-Cornell Medical Center, 21 Bloomingdale Road, White Plains, NY, 10605, U.S.A. 0195-6663/91/030219+ 19 SO3@0/0

0 1991 Academic Press Limited

220

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AND S. R. SUNDAY

Robinson (1989) reported lower hunger ratings and higher fullness ratings after a meal in anorectic patients as compared with controls. He did not, however, find differences in the ratings between bulimics and controls. In a previous pilot study in which eating disorder patients and control persons tracked hunger and fullness before, during, and after an experimental liquid meal, the generated curves showed distinct differences between the subgroups of eating disorder patients and control persons (Owen et al., 1985). It has been suggested (Bruch, 1969) that anorectics may not be aware of or may not respond to internal stimuli associated with eating in a manner similar to controls. If that were the case, one might expect anorectic patients to be less influenced by internal cues associated with eating and more dependent on external visual cues to determine food intake. Owen and his colleagues attempted to examine this by testing their subjects under two conditions: one with the liquid meal reservoir visible to the subject and one with the reservoir hidden from view. Although they did not find differences between the two conditions, the number of subjects was too small for definitive resolution of the issue of the importance of external cues. A subsequent larger study with the same design as Owen et al. (1985) used group analyses to determine that underweight anorectics started and ended the meal with lower hunger and higher fullness levels than normal weight bulimics and healthy controls and that these ratings changed little at post-treatment testing (Halmi et al., 1989). This paper also reported differences in psychological variables among the groups. These differences normalized somewhat with treatment. The analyses presented in that paper did not characterize entire hunger and fullness curves, nor did they depict the differences in individual hunger-fullness curve patterns among the diagnostic subgroups. They did not specifically test for differences between the covered and uncovered conditions. Finally, the analysis of the effects of treatmentcombined patients who received drug therapy with those who did not receive such treatment. In the present study, both group and individual analyses in the eating disorder subgroups and healthy controls were carried out over the complete hunger-fullness curves and on other cognitions related to eating. These analyses tested the hypothesis that the disturbed eating behavior in anorectics and bulimics is strongly related to disturbances in hunger and fullness ratings. More specifically, we postulated that anorectic subjects would demonstrate decreased levels of hunger and increased levels of fullness throughout the entire testing session. Since the anorectic patients had previously been severely restricting their intake, we also expected those subjects to consume less food during the test meal compared with controls. Clinical observations of bulimics suggested that these persons may experience a more rapid rebound of hunger following a meal. Binge eating behavior also suggests an impairment in achieving sufficient satiety or fullness to end the meal. Thus, we postulated that bulimics would have differences in both hunger and fullness ratings compared to normal controls. Since bulimics have difficulty in controlling food intake and anorectics have excessive control over food intake, it seemed reasonable to expect these patients to differ in eating-related cognitions such as urge to eat, preoccupation with food, satisfaction at the end of the meal, and willpower needed to stop eating. The relationships of these latter ratings to hunger and fullness ratings were analyzed to

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determine the possible impact of such cognitions on the integrated concepts of hunger and satiety. In order to determine the dependence of eating-disordered patients, especially anorectics, on external cues for deciding the amount of food to consume, we tested for differences in food intake between two conditions, one with the food reservoir visible to the subjects and the other with it hidden from view.

METHODS

Subjects Twenty-nine anorectic-restrictors (AN-R, those who restrict intake and/or exercise but do not binge and purge), 25 anorectic-bulimics (AN-B), 30 normal weight bulimics (NW-B), and 19 normal weight controls (C) with no history of an eating disorder, obesity, substance abuse or a psychiatric illness were tested. All subjects were female. All eating disorder subjects met DSM-IIIR criteria for anorexia nervosa and/or bulimia nervosa and were inpatients on the eating disorder unit at Cornell Medical Center-Westchester Division. Controls were obtained from the local community and were paid $10 per testing session. Control subjects were 20.61 (SEM + 0.78) years of age and had body mass indices (BMI = weight in kg/height’ in m) of 20.81 (kO.47) at the first testing and 21.25 (f0.59) at the second testing. The clinical characteristics of each of the patient groups appear in Table 1. Significant differences between these groups were present in pretreatment BMI and percent of ideal body weight, lowest body weight as a percent of ideal weight, binge frequency, use of laxatives, vomiting behavior, and abuse of drugs. AN-R were younger at treatment and had a shorter duration of illness than the other two diagnostic subgroups. Although both anorectic groups (AN-R and AN-B) did show a significant increase in BMI with treatment, they were still significantly below NW-B at posttreatment testing. There were no significant differences in percent with suicide attempts or in Beck Depression scores between the patient groups. Eating disorder subjects were tested within 10 days of hospital admission and were retested after treatment but before hospital discharge. Patients were not allowed to binge and purge during the pretreatment testing and, if patients were not consuming sufficient calories, they were given a minimal caloric intake to prevent further weight loss. No patients were receiving drug therapy at pretreatment testing. The posttreatment testing was conducted at least 4 weeks after weight restoration for the anorectics and at least 4 weeks after establishing normal eating with no binging or purging for the bulimics. Controls were tested at similar time intervals. At posttreatment testing, all patients were consuming the amount of calories necessary to maintain their individual body weight range-a range of 1.14 kg* target weight. Therefore, patients were receiving different amounts of calories, but their intake of calories was standardized for maintenance of their target weight range. Procedure Meal testing occurred at lO.OOhrs following an overnight fast from midnight. Subjects were provided with a liquid breakfast meal of Sustacal, a nutritionally

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balanced food containing 1 kcal/ml and 24% of calories from protein (calcium caseinate, soy protein isolate, sodium caseinate), 21% of calories from fat (partially hydrogenated soy oil), and 55% of calories from carbohydrate (sucrose, corn syrup). The food was delivered directly into the mouth through a straw with a rate of intake controlled by the subject via a button which operated a small peristaltic pump. This procedure required no sucking by the subject. Participants were instructed to consider the meal their breakfast and to eat as much as they wished. Every 2min subjects made ratings on lOO-mm lines (visual analog scales; VAS) anchored on hunger or fullness; these ratings began 8 min before the meal, continued throughout the meal and for 12 min following the meal. Immediately after the meal, subjects rated satisfaction on VAS. At this time, subjects also answered three additional questions concerning their urge to eat, their preoccupation with thoughts of food, and the willpower they required to stop eating the meal using five-point ratings (1 = none, 5 = extreme). Four testing sessions were conducted, two prior to treatment and two after treatment. Within each treatment condition, during one meal the food reservoir was visible to the subject thus allowing her to see the amount of unconsumed food (uncovered condition); during the other meal the food reservoir was hidden from the subject (covered condition). The order of meal-type presentation was randomized. For a variety of reasons, including unexpected early departure from the hospital and scheduling conflicts, not all subjects participated in all test situations. Among the

TABLE

Clinical characteristics

Pretreatment, N Age at treatment Duration of illness (years) Pretreatment BMI” Pretreatment weight as % ideal Highest weight as % ideal Lowest weight as % ideal Binge Frequency per Month % Who have used laxatives to control weight % Who have used vomiting to control weight % With history of drug abuse % with suicide attempts Beck Depression score Posttreatment, N Posttreatment BMI

1

ofeating

disorder patients

AN-R

AN-B

NW-B

P

29 18.87* 1.13 2.65kO.50 15.45kO.60

25 21.67kO.92 5.17kO.72 16.13kO.43

30 22.27* 1.14 5.22f0.96 20.29 f 0.41

0.037* 0.029* <0.001*

72.36+ 1.59 103.16 f 4.40 67935f 1.98

79.17k2.18 100.95k4.32 66.75 + 2.26

100.87+ 1.89 112.85f2.78 82.28 f 2.05

<0401* NS <0.001*

73.05k21.51

73.48k 10.10


0.07 f 0.05 19.35

77.78

70.00

<0.001**

12.90

92.59

100~00

<0.001**

3.45 20.69 23.48 f 3.03 25 19.47kO.30

24.00 40.00 26.68 + 2.86 21 19.42kO.14

36.67 33.33 22.35 f 2.73 20 20.62 f 0.36


All means are f SEA4 ’ BMI = Bode Mass Index (Weight in kg/height’ in rnj * =p < 0.05 as determined by a;alysis of variance ** =p
0.001*

HUNGER AND FULLNESS IN EATING DISORDERS

223

AN-R, 29 participated in the pretreatment uncovered condition (Pre-Uric), 26 in the pretreatment covered condition (Pre-Cov), 24 in the post-treatment uncovered condition (Post-Uric), and 19 in the post-treatment covered condition (Post-Cov). Numbers of subjects in these tests for the other groups were as follows: Pre-UncAN-B=25, NW-B=30, C= 19; Pre-Cov-AN-B=21, NW-B=21, C= 19; PostUnc-AN-B = 22, NW-B = 21, C = 11; Post-Cov-AN-B = 19, NW-B = 17, C = 11.

Data Analysis An ANOVA on amount consumed in the pretreatment covered and uncovered conditions was conducted to examine the effects of visual food cues. Since the “covered” experimental meal was relevant only to the hypothesis that eliminating visual cues would affect the amount of food consumed, all other statistical analyses were conducted only for the “uncovered” experimental meal. Additional ANOVAs to assess diagnostic effects were conducted under the pretreatment uncovered condition for: amount consumed, meal duration, rate of eating, and postmeal hunger change. The latter variable measured the total increase in hunger ratings during the 1Zmin postmeal period and was included to assess the presence of a rapid hunger rebound, A MANOVA was conducted on postmeal cognitions (satisfaction and the three Likert questions) for the pretreatment uncovered condition. Following all ANOVAs and MANOVAs, pairwise comparisons were performed with alpha levels corrected using the Bonferroni procedure. Before- and after-meal hunger and fullness ratings were comparable across subjects since these ratings were completed at exactly the beginning and end of the meal by each patient. Making the ratings within the meal comparable across subjects was more complex. Looking across each 2-min interval during the meal was not feasible since some subjects had 4-min meals and others had 40-min meals. To control for the effect of varying meal length, within-meal hunger and fullness data were computed for each subject from ratings at certain percentages of the total meal duration. For subjects with meals of four or more minutes (all but O-2 subjects per group in each condition), hunger and fullness ratings at 50% of the total meal duration were computed. For subjects in the pretreatment uncovered condition with meals of 8 min or more (group sizes were: AN-R = 24; AN-B = 15; NW-B = 17; C= 15), ratings at 25%, 50%, and 75% of total meal duration were computed. A MANOVA examining hunger ratings (at the start of the meal, midway through the meal, at the end of the meal, and 12min after the meal) was conducted for the pretreatment uncovered condition. Similarly, a MANOVA on fullness ratings was also conducted. Pairwise comparisons were performed with corrected alpha levels. For the pretreatment uncovered condition, Pearson correlations were conducted between the questions assessing cognitions at the end of the meal, and Beck Depression Scores and several cognitive and meal variables. For the two groups of bulimic subjects only, correlations between binge frequency and several cognitive and meal variables were computed. Correlations between pretreatment percent of ideal body weight and several cognitive and meal variables were performed for the anorectics (AN-R and AN-B). Backward elimination stepwise multiple regressions were conducted with amount consumed and with satisfaction at the end of the meal entered as separate dependent

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variables. This procedure allowed an examination of the inter-relationships between variables; for example, how amount was affected by hunger and fullness variables. In addition to group analyses, we also examined various aspects of individual meal patterns. Booth (e.g. 1989) has argued for the need to examine the strength of association between concepts which seem to be related-such as hunger and fullness. To assess the relationship between hunger and fullness, Pearson correlations were computed between the two ratings during the pretreatment uncovered condition for each subject. Resulting r values were analyzed across groups using an ANOVA. Hunger and fullness curves were graphed for each subject for the pretreatment uncovered condition (e.g. Figure 4). Three patterns of hunger and fullness curves were categorized: 1) hunger and fullness curves intersected once during the meal; 2) no intersections of these curves; and 3) multiple intersections or a single intersection occuring outside of the meal. A chi-square analysis was performed on the curve patterns in each diagnostic group. Additional chi squares were conducted to examine group differences for subjects who never felt hungry (VAS hunger never reached 35 mm throughout the test session). Twenty-six of the 67 eating disorder patients who were tested both pre- and posttreatment were receiving drug treatment (phenothiazines, tricyclics, cyproheptadine, anticonvulsants, or phenothiazines and tricyclics) during the post-treatment test. Those patients who required pharmacological treatment were distributed among the diagnostic groups so that of the AN-R, two received a phenothiazine, three received a cyproheptadine, and one received a phenothiazine plus a tricyclic; of the AN-B, five received a phenothiazine, two received a tricyclic, and four received a phenothiazine plus a tricyclic; of the NW-B, two had a phenothiazine, four had a tricydic, one had an anticonvulsant, and two had a phenothiazine plus a tricyclic. Of the three eating disorder subgroups, AN-R had the lowest proportion of subjects which required drug therapy. Many classes of drugs appear to affect food intake (e.g. tricyclics as reported by Paykel et al., 1973). Since there was not sufficient numbers of patients within the diagnostic subgroups receiving each type of drug, subjects who were treated with drugs were dropped from the analyses to assess treatment effects. Therefore, in addition to the control subjects who were retested, only eating disorder patients who had not received drug therapy were included in the pretreatment/post-treatment analyses. Treatment effects (uncovered condition only) were examined by performing MANOVAs on hunger ratings, fullness ratings, and end of meal cognitions, and ANOVAs on amount, duration, rate, and postmeal hunger change (similar to the analyses done on the pretreatment uncovered condition data). Again, pairwise comparisons were also conducted with alpha levels corrected using the Bonferroni procedure.

RESULTS

Covered vs. Uncovered Condition

Figure 1 presents the amount consumed by subjects who were tested in both the pretreatment covered (no visual cues) and uncovered (visual cues) conditions. There were no significant effects of diagnosis, F(3,83) =0.05, covered vs. uncovered,

HUNGER

AND FULLNESS

400

IN EATING

DISORDERS

1

Pre-treatment I

3501

IXXXI

Covered

225

Uncovered

300

50 0

AN-R

/l/=26)

AN-B

(/Y-21)

NW-l3(N=21)

I

Cc)ni .ol

FIGURE1. Mean amount consumed with standard errors in the pretreatment covered (no visual cues) and uncovered (visual cues) conditions.

F( 1,83) = 1.19, nor the interaction of the two, F(3,83) = O-70. Additionally, comparing the two conditions within each diagnostic group also yielded non-significant effects. Diagnostic Effects - Pretreatment Uncovered Condition

There were no significant differences between the four diagnostic groups in amount consumed, F(3,99) = 0.32. Although the ANOVA of meal duration was nonsignificant, F(3,99) = 3.55, p = 0.076, there was a significant difference between AN-R and the two bulimic groups, F( 1,99) = 10.54, 0.008. AN-R had significantly longer meals (mean f SEM = 16.21 f 2.08 min) than did AN-B (9.84 f 1.21 min) and NW-B (10.4+_ l-31 min). The meal duration for control subjects was 12*95(+ 1.45) min. The ANOVA of rate of eating was also not significant, F(3,99) = 2.13; however, the difference between AN-R and NW-B approached significance, F(1,99) = 5.67, =0*076. NW-B had a slightly higher rate (28.51 k2.41) than did AN-R (20.46+ 3.0). AN-B and C had intermediate rates of 25.47 (f 2.18) and 22.17 ( f 2*08), respectively. The mean satisfaction rating and the Likert ratings for urge to eat, preoccupation with thoughts of food, and willpower needed to stop eating the Sustacal meal in the pretreatment uncovered condition appear in Figure 2. The MANOVA yielded significant effects of diagnosis [F(3,94) = 2.66, p = O-051and diagnosis by postmeal rating (Wilks’ 3,= O-83, F(9,224) = 2.00, p = 0.04). AN-R and NW-B were not significantly different from C. AN-B were significantly different from C overall (Wilks’ I = 0.82, F(4,91) = 4.93, p = 0.004); AN-B were significantly more preoccupied with thoughts of food than were C (F(1,94) = 8.10, p=O*O2). Abhough the overall difference between AN-R and NW-B only approached significance (Psdjusted= 0*072), AN-R did have a significantly lower urge to eat than NW-B @adjusted=0.004). For AN-R, the four postmeal cognitions were not correlated. Among AN-B, urge to eat and satisfaction were negatively correlated (r= -0.57, padj”s(ed=0’017). For Psdju&d

Padjustcd

=

K. A. HALMI AND S. R. SUNDAY

226

0 AN-R -AN-B

,3 E

(n=27) (n=251

ESI NW-B IControl

b29) (n=19)

t

Urge to eat

Wil Ipower

needed

to stop eating

0

Satisfaction

at end of meal

FIGURE2. Cognitive responses at the end of the meal for the pretreatment conditon where the food reservoir was visible (uncovered).

NW-B, urge to eat and preoccupation with thoughts of food were positively -0.019) as was preoccupation with thoughts of food correlated (r = + O-54, and Willpower to stop eating (r= +0’49, PadjUsted = 0.05); their correlation between urge to eat and satisfaction approached significance (r = - Oe47,padjusted= O-07). Only urge to eat and preoccupation with thoughts of food were correlated among the controls (T= + 0.62, Padjusted- 0.037). When the diagnostic groups were combined, the following significant correlations were found: urge to eat and preoccupation with thoughts of food (r= +0.34), urge to eat and willpower needed to stop eating (r = + 0.29) urge to eat and satisfaction (r = - 0.34). Figure 3 presents the hunger and fullness ratings across the test session for the pretreatment uncovered condition. As can be seen, hunger ratings are considerably lower and fullness ratings are considerably higher throughout the test session for the AN-R than for the NW-B and the C. Although not as pronounced, the same tendency (especially for fullness ratings) was also apparent for AN-B as compared with NW-B and C. The analysis of hunger ratings before, during, immediately after, and 12 min after the meal revealed a significant effect of diagnosis [F(3,96) = 5.84, p < OGIl]. ANB and NW-B were not significantly different from C. AN-R were different from C 0.0361; univariate F tests revealed signifimilks A= 0.87, F(4,93) = 3.42, cant differences at all points but 12 min after the meal. The MANOVA of fullness ratings again showed a significant effect of diagnosis [F(3,96) = 10.63, p < O*OOl]with no differences between NW-B and C. Although AN-B were not significantly different -0.159), their fullness ratings at 50% of the meal duration from C overall were significantly higher than C ratings (&djuSted- 0.012). AN-R were significantly P&justed

-

Padjusted=

@adjuslcd-

227

HUNGER AND FULLNESS IN EATING DISORDERS Pretreatment

uncovered Hunger

80

Y k

condition

ratings

60

w

AN-R

(n=29)

b--A

AN-8

(n=25)

M

NW-B

(n-30)

m

C (n=19)

& F 2 ti40
0

-8

-6

-4

-2

0

25

50

Fullness

75

100 t2

t4

t6

t8

+I0

i-12

ratinas

80

‘2 2 B z II

60

;

40

ci >’ 20

0

-8

-6

Pre-meal

-4

-2 (min)

0

25

50

75

% Meal duration

M

AN-R

(N=28)

M

AN-B

(N=25)

M

NW-B

(/l/=30)

@--cl

C (N=l9)

100 t2

t4

+6

Post-meal

t8

+I0

+I2

(mln)

FIGURE 3. Mean visual analog scale hunger and fullness ratings at 2 min intervals before the experimental meal, during the meal at 0, 25, 50, 75, and 100% of the total meal duration, and at 2-min intervals after the meal. Both graphs depict data from the pretreatment condition where the food reservoir was visible (uncovered).

different from C overall [Wilks’ A= O-77, F(4,93) = 6.87, p c 0*003] and at each of the four time points. The ANOVA of the increase in the VAS hunger rating in the postmeal period was not significant [F(3,99) = l-82, p N.S.]. None of the three eating disorder groups were

different from controls (C mean = 10.77 + 2.51). Although not significantly different, AN-R (with a mean change of 6.13 k2.02) tended to have a smaller increase than did NW-B (with a mean change of 15.03 + 3.69).

228

K. A. HALMI AND S. It. SUNDAY

The pretreatment relationship between hunger and fullness within each subject by diagnostic condition was assessed by an ANOVA of the resulting individual r scores. The means (f standard errors) were as follows: AN-R = -0.72 ( f 0.06), AN-B = -0.65 ( f 0.08), NW-B = -0.72 ( + O-05), C = - 0.85 ( f 0.04). Although there was no significant overall effect of diagnosis [F(3,99) = 1.55, p=N.S.], eating disorder subjects (AN-R+ AN-B+NW-B) had significantly lower r values than did controls [F( 1,99) = 3.93, p = 0*05]. Therefore, it appears that although hunger and fullness are negatively correlated for all groups, they are less highly correlated for eating disorder subjects than for controls. A backward elimination stepwise multiple regression was performed for the pretreatment uncovered condition with satisfaction at the end of the meal as the dependent variable and all other end of meal variables (hunger, fullness, urge to eat, preoccupation with thoughts of food, willpower needed to stop eating), in addition to amount consumed, postmeal hunger change, and diagnosis entered as predictors. The overall correlation was 0.48 (N =98, p=O-002), and these variables accounted for 23.3% of the variance in satisfaction. Amount consumed, end of meal hunger and fullness, and postmeal hunger change all accounted for negligible amounts of the variance (less than 1%). Diagnosis, preoccupation with thoughts of food, and willpower to stop eating accounted for small amounts of variance (3*2%, 3.4%, and 3.9%, respectively). Urge to eat accounted for the largest percentage of the variance, 11.8% (r = - 0.34, p = 0.001). Therefore, only urge to eat contributed considerably to the satisfaction felt at the end of the meal; the less the urge to eat, the more satisfied subjects felt. A backward elimination stepwise multiple regression with amount consumed entered as the dependent variable and hunger and fullness at the beginning and end of the meal; end of the meal satisfaction, urge to eat, willpower to stop eating, and preoccupation with thoughts of food; postmeal hunger change; diagnosis; and meal duration entered as predictors was also performed. All of these predictors together accounted for 40.6% of the variance in the amount consumed (r = 0.64, p
229

HUNGER AND FULLNESS IN EATING DISORDERS

the regression line appears in Figure 5. As can be seen, anorectics displaying abnormal hunger-fullness curve patterns tended to ingest rather small amounts of food, while many of the anorectics with normal patterns ingested very large quantities of food. These correlations were not significant among NW-B or C. The frequency analysis of hunger ratings throughout the pretreatment uncovered test session appears in Table 3. Significantly more AN-R never felt hungry (VAS always below 35 mm) and fewer anorectics felt at least a moderate amount of hunger at some point during the test session as compared to all other groups. To test whether subjects who had subnormal or low hunger responses or who had abnormal curve patterns showed other evidence of perceptual confusion or displayed a general denial response, we looked at the Interoceptive Awareness (IA) subscale of the Eating Disorder Inventory (EDI, Gamer et al., 1983) and the raw L, F, and K scale scores of the MMPI, two inventories that were given to all patients at the time of admission to the treatment program. The IA score was chosen because it relates to one’s awareness of internal states (especially emotional). The three validity scores from the MMPI were chosen because they reflect denial and reluctance to disclose feelings or attitudes (Dahlstrom et al., 1972). We examined correlations between responses and curve patterns in the pretreatment uncovered condition with the IA subscale score and multiple regressions between responses and curve patterns with the raw L, F, and K scale scores of the MMPI. Both correlations with IA score were nonsignificant. The backward elimination stepwise multiple regression between hungerfullness responses and L, F, and K scores and between curve patterns and L, F, and K scores also revealed no significant relationships. The regressions with all three predictors entered were both non-significant and accounted for only 9.6% of the variance in the hunger-fullness responses and 6.4% of the variance in the curve patterns. Across diagnosis, the correlations between Beck Depression Scores and the end of meal cognitions revealed a significant relationship only between depression and preoccupation with thoughts of foods (r = 0.3 1, Padj”sted= 0.039). Among the emaciated subjects (AN-R and AN-B), there were no significant correlations between percent of ideal body weight pretreatment and the following variables: amount consumed, hunger at the start of the meal, fullness at the start of the meal, urge to eat at the end of the meal. For bulimic subjects only (AN-B and NW-B), monthly binge frequency was positively correlated with Beck Depression score (r=0.35, padjusted

TABLE 2 Frequency of hunger-fullness curve patterns pretreatment uncovered condition Normal 1 Intersection during meal AN-R (N = 29) AN-B (N = 25) NW-B (N = 30) Controls (N = 19) x2= 1849, p = 0.006, df = 6 *“=p
df= 1

7 8 10 10

Abnormal

No intersection 16* 6 4 5

Other 6 11 16 4

230

K. A. HALMI AND S. R. SUNDAY

100

c

Anoretic-restrlctor

zP-7Ot 60 50 40 30 20 :

M

(70 cc

Fullness Meal

Pre

A--A

Hunger I

AA_

-8

-4

4

0

8

100

16

I2

Bulimic

20

24

28

32

i

(50 cc)

I

90

-4

0

12

8

Control

(33?

I6

20

24

28

cc)

70 60 50 40

;A

LA,!

r

-8

-4

0

4

8

I2

I6

20

24

Time (min)

FIGURE4. Hunger and fullness curves before, during, and after the experimental meal for three individual subjects in the pretreatment uncovered condition.

HUNGER AND FULLNESS IN EATING DISORDERS

231

1100

0

1000

0

900 -

W

800 700 600 -

0 0

500 400 300 200 IOOO-

Mnrmnl Hunger/fullness

curve patterns

FIGURE5. Amount consumed during the experimental meal is shown for subjects who displayed “abnormal” or “normal” hunger and fullness curve patterns.

= O-018). Monthly binge frequency was also positively correlated with urge to eat at the end of the meal for the bulimics (r = O-34, padjusted= 0.021). Treatment Effects for Drug-free Subjects-Uncovered

Condition

Tables 4 and 5 present the pre- and post-treatment meal related responses for all subjects who were tested on both occasions and did not receive pharmacological therapy. The ANOVA of amount consumed revealed non-significant effects of treatment and diagnosis by treatment interaction. None of the four groups showed a significant change with treatment, Similar results were found for rate of eating. There was a significant treatment effect for meal duration [F(1,47) = 4.53, p = 0.0391, however, the interaction between diagnosis and treatment was not significant. All groups had shorter meals at the post-treatment testing. The postmeal cognitive meal responses did not change significantly with treatment, nor did this lack of treatment

TABLE 3

Frequency of hunger ratings throughout test session pretreatment uncovered condition Hungry at some point

Neutral

(at some point VAS> 65) AN-R (A’= 29)

AN-B (N = 25) NW-B (N = 30) Controls (IV= 19) x2=14.30,p=0.026, df=6 l=p
6

10 17 11

Never hungry (VAS always < 35)

7 8 7 5

16* 7 6 3

Before meal hunger During meal hunger End of meal hunger After meal + 12 min hunger Before meal fullness During meal fullness End of meal hunger After meal + 12 min fullness

TABLE 4

10-50 + 33.94 f 64.06 f 76.63 +

8044 f 5.00

8.75 + 3.50 50.69 + 8.55 75.59k4.61 86.94 + 4.20

84.69 &-5.26

264 6.50 5.01 5.77

46.63 f 6.78 28.38 f 4.29 11.19f2.61

31.38k7.21 13.59f3.36 6.00_+ 1.89

Anorectic-restrictors (N= 76) Pre Post

82.00 + 7.01

7.3Ok3.03 45.90+ 10.15 67.65k6.16 86.10f7.48

29.70 & 8.29 21.1Ok5.46 2.80 + 164

78.90f6.91

15.6Ok6.72 29.1Ok7.14 62.30 + 6.26 78.50 & 6.72

48.30 + 8.78 23.75 & 5.33 16.60f6.66

Anorectic-buhmics (N=lO) Pre Post

77.73 + 5.59

14xKlk4.50 27.18k8.32 49.86k6.31 78.09 + 7.53

50.46k11.42 39.50 + 8.26 15.00 &-5.20

69.91 f 8.03

19.36k5.88 9.9 1 + 2.47 40.36k6.45 68.27 + 9.37

72.73k7.71 51.14k7.50 23.82 f 7.57

Normal weight-bulimics (N=ll) Pre Post

Pre

72.73 k4.48

23.00 f 6.07 23.36 + 6.67 50.18+6.36 78.55 f4.29

Post

76.09 &-4.92

17.27k4.32 26-27 f 6.90 50+0 + 5.50 71.82 f 7-38

64.45 + 7.38 41.00*5.71 22.91& 6.20

Controls (N= 11)

56.82 f 7.55 3846 f 7.54 16.46+4&l

Pre- and post-treatment hunger and fullness ratings for eating disorder and control subjects

3 2;

p z

8 tn

g

L

?c

Amount consumed 337.5Ok65.85 Meal duration 17.38k3.11 Postmeal VAS hunger change 7.02 & 344 Postmeal VAS satisfaction 68,96_+ 7.28 Postmeal urge to eat 1.22kO.13 Postmeal preoccupation with thoughts of food 2.17f0.32 Postmeal willpower needed to stop eating 1.56f0.19 178.5Ok28.08 8.60* 1.12 7.69 + 4.24 71.95k6.93 1.46f0.21 2.82kO.42 164kO.31

6.68& 1.74 70.81 k4.91 1.56f0.15 1.72f0.24

1.28+0.14 1.27kO.14

164kO.24

15-77 &-8.93 53.12f8.08 164*0.20

210.50+43.07 9.40 * 0.99

Anorectic-bulimics (N = 10) Pre Post

252.81k57.50 10.25+ 1.30

Anorectic-restrictors (N=16) Pre Post

1.55 + 0.28

2.27 f 0.27

16.08k7.81 62.18+11+)4 1.91 kO.25

281.82f56.70 12.36k2.51

1.36kO.15

1.73 f 0.27

13.08 + 6.47 66.65k8.88 164kO.28

361.82k92.97 11.46fl.46

Normal weight-bulimics (N=ll) Pre Post

1.27kO.14

1.82+0.23

13.57+ 3.97 54.87 f 6.38 1.73f0.24

Post

1.27-10.14

1.46kO.16

9.65 + 4.76 54.62+6+71 l&I&-O.20

270.46k40.07 9.46 + 0.94

Controls (N=ll)

23864k32.57 12.55 + 1.73

Pre

TABLE 5 Pretreatment and post-treatment meal and cognitive variables in eating disorder and control subjects

234

K. A. HALMI AND S. R. SUNDAY

effect differ between the diagnostic groups. Although not significant, AN-R did tend to have more urge to eat after the meal post-treatment, and AN-B did tend to feel less preoccupied with thoughts of food and less satisfied at the end of the meal post-treatment. The MANOVA of VAS hunger ratings showed a significant effect of treatment [F (144) = 18.13, p < O*OOl]and a significant interaction of treatment by hunger rating lVVilks’ L = 0.78, F(3,42) = 3.86, p = 0*016]. There were no significant interactions between treatment and diagnosis nor were there any significant changes across treatment within any of the diagnoses. All groups had higher hunger ratings during the post-treatment test, especially during the earlier portion of the meal session. There was also a significant treatment effect for VAS fullness ratings [F( 144) = 8.60, p=O*OO5].Subjects felt less full during the post-treatment test. For fullness ratings, there were also no significant interactions between treatment and diagnosis nor were there significant changes across treatment for any of the four diagnostic groups. With respect to the ANOVA of postmeal VAS hunger change, there were no significant effects nor were there any changes across treatment for the four groups.

DISCUSSION

The results of the present experiment indicate that there are differences in hunger and fullness ratings and in other meal and cognitive variables between persons with anorexia and bulimia and control subjects. Many of the differences, however, would not be apparent if hunger and fullness responses were not monitored numerous times throughout the meal. Additionally, an analysis of individual patterns of hunger and fullness responses revealed information not evident in the more traditional group analysis. The measurement of many meal and cognitive variables also demonstrated that the relationship between many of these variables differs between controls and the three subgroups of eating disorders. It is of special interest that there were no significant differences in amount consumed in the two experimental meals-when the reservoir of food was visible and when it was hidden from view. Since eating-disordered patients are so preoccupied with the amount of food that they consume and may be more influenced by external than by internal cues related to eating (Bruch, 1969), we had expected the addition of visual cues to reduce intake. In this experimental procedure with a liquid meal, the visual cues were relatively unimportant. Although there were no differences in amount consumed between our four groups, there was a tendency for the anorectic-restrictors to eat more slowly and to have longer meals than the bulimics. This is consistent with clinical observations and published reports concerning these patients (e.g. Robinson er al., 1988). Meal duration and rate of eating did not change significantly with treatment for these groups. Robinson et al., (1988) also failed to find a change in meal duration following weight restoration in their anorectic patients. Also in accordance with clinical observations, there were differences between the eating disorder groups in cognitions at the end of the experimental meal. For example, the anorectic-restrictors reported a lower urge to eat compared with the bulimic patients. An earlier study (Halmi et al., 1989) showed that the feeling of urge to eat was very strongly related to after-meal hunger, accounting for 22% to 42% of the variance. The current analyses produced a reassuring consistency, in that

HUNGER

AND FULLNESS

IN EATING

DISORDERS

235

anorectic-restrictors had the lowest hunger ratings and the lowest urge to eat at the end of the meal. It was somewhat surprising that the relationships between the postmeal cognitions varied among the four diagnostic groups. The cognitions were most inter-related for the normal weight bulimics. As urge to eat increased in these subjects, so did their preoccupation with thoughts of food and their feelings of a luck of satisfaction; as their preoccupation with thoughts of food increased, so did the level of willpower needed to stop eating. Urge to eat was also positively correlated with monthly binge frequency for the bulimic subjects, thus indicating that patients who engage in very frequent binging may alter their urge to eat even after their binging has ceased. Binge frequency was also associated with depression in these subjects. Bulimic patients who binged the most were also the most depressed. Since increased carbohydrate intake may in part increase brain serotonin (Wurtman et al., 1989) and decreased brain serotonin function is associated with depression (Coccaro et al., 1990), it is reasonable to hypothesize that bulimics’ binge eating may be adaptive behavior to correct a physiological deficit-low brain serotonin. A physiological state of hyposerotonergic function may well contribute to the bulimics’ urge to eat. Interventions that diminish serotonergic neurotransmission or receptor activation have been shown to increase food consumption (Leibowitz & Shor-Posner, 1986; Blundell, 1986). Cerebral spinal fluid studies (Kaye et al., 1984) and serotonin neuroendocrine challenge tests (Brewerton et al., 1986) have provided some indirect evidence for hyposerotonergic functioning in bulimics. For all patients, subjects who were most preoccupied with thoughts of food were also the most depressed. Across all groups of subjects, the feeling of satisfaction at the end of the meal was accounted for predominantly by the urge to eat. That is, the less urge to eat the more satisfied the subjects felt. The anorectic-restrictors had the least urge to eat and were the most satisfied after the meal. This depressed urge to eat by the anorectic-restrictors may reflect a mild hyperserotonergic state. A pharmacological intervention of a serotonin antagonist, cyproheptadine, has been shown to effectively increase caloric intake and weight gain in the anorectic-restrictor patients (Halmi et al., 1986). The variation in the amount consumed among our subjects was accounted for primarily by how hungry the subjects were when they began their meals and by the duration of the meal. The other meal and cognitive variables, surprisingly, did not account for very much variability in total food consumption. Group analyses of hunger and fullness levels before, during, immediately after, and 12 min after the experimental meal showed anorectic-restrictors to have lower hunger and higher fullness ratings compared with control persons (Figure 3). This finding is consistent with that reported by Robinson (1989). Although we did not measure gastric emptying in our patients, it is unlikely that differences in gastric emptying could explain our results. Robinson reported that hunger and fullness ratings did not differ in anorectic patients with slowed emptying as compared with those showing fast emptying. Additionally, Robinson et al., (1988) reported delayed emptying only in anorectic patients who were self-selecting their diets (and presumably continuing to restrict intake). Their inpatient subjects, with monitored and controlled food intake, displayed normal gastric emptying. Holt et al., (1981) did not find differences in gastric emptying within 10 min of meal ingestion in anorectic patients compared with controls. Since hunger and fullness responses were assessed

236

K. A. HALMI AND S. R. SUNDAY

only for a 12min postmeal period for our patients, it is unlikely that differences in gastric emptying would explain the differences in hunger and fullness ratings found in these patients. There was no effect of treatment on these ratings of hunger and fullness (Table 4), again suggesting that gastric emptying (and emaciation) did not underlie the differences in the ratings. The intriguing question is-just how set are these hunger and satiety perceptions? Retesting the anorectic-restrictors after they have maintained a normal weight for 1 year should provide evidence whether the lower hunger and higher satiety preceptions are a state or trait phenomenon. The normal weight bulimics and, to a lesser extent, the anorectic-bulimics did not differ significantly from the controls in the group analysis of hunger and fullness ratings; however, the hunger and fullness curve patterns of these individual subjects often indicated a confusion of the perceptions of hunger and satiety. Group analyses of hunger and fullness levels were not sufficient to capture this confusion. Examination of the individuals’ hunger and fullness curves showed that three hunger and fullness curve patterns emerged across all subjects (Figure 4). In general, control subjects began the test session hungry and not full. After they began their meal they felt less hunger and more fullness, with these two ratings intersecting at some point during the meal. Controls ended their meals feeling full and not hungry; this state was maintained during the postmeal period. The eating disorder patients had predominantly “abnormal” patterns. Anorectic-restrictors generally displayed a pattern in which hunger and fullness curves did not intersect; hunger was very low (for many never reaching 35 mm on the 100mm VAS) and fullness was high throughout the test session. This is especially interesting since these emaciated patients were fasted for 10 h and had not been permitted to severely restricted intake in the days immediately preceding the test meal. The hunger and fullness ratings in the normal weight bulimics often intersected many times during the test session or intersected in the premeal or postmeal period. It may be that the binging altered these patients’ responses of “normal” hunger and satiety to meals by physiological changes, or blunted and distorted the hunger and satiety sensations (a cognitive alteration), or produced a combination of physiological and cognitive alterations expressed by the disturbed hunger and satiety perceptions. It should be noted that these responses were to a liquid meal that contained the same proportion of macronutrients for all subjects and in all testing conditions. Since there is evidence of norepinephrine and dopamine dysregulation in anorexia nervosa (Kaye et al., 1984) and serotonin dysregulation in bulimia (Brewerton et al., 1986; Kaye et al., 1984) it is reasonable to suspect that these patients will respond discriminately to different proportions and amounts of macronutrients. The integrating processes of hunger and satiety, reflecting different cognitive sets and different internal milieus (neurotransmitter dysregulation), should produce distinguishing hunger and fullness curves across varying macronutrient proportions and eating disorder subgroups. We are currently investigating such responses. During the emaciated state, those anorectics who admitted to feeling hungry and not full were the patients who consumed the greatest amounts. This relationship was not present after weight restoration, nor was it present in normal weight bulimics or controls. In this experimental condition, it appears that the acknowledgement of hunger in the emaciated state was associated with responding to physiological needs. The disturbances in hunger and satiety perceptions in the eating disorder patients seemed to be sui generis and not related to other areas of perceptual confusion (Interoceptive Awareness on the EDI), or denial as measured by the L, F and K scales

HUNGER AND FULLNESS IN EATING DISORDERS

237

of the MMPI. These findings emphasize that the disturbed eating in eating disorder patients cannot be dismissed as merely reflecting an underlying psychodynamic turmoil. There is accumulating evidence that the aberrant eating behavior is directly influenced by disturbance of the integrating processes of hunger and satiety perceptions, based on cognitive sets and external and internal cues, all of which can be measured and subjected to experimental perturbations for characterization.

Blundell, J. E. & Hill, A. J. (1987) Nutrition, serotonin, and appetite: Case study in the evolution in a scientific idea. Appetite, 8, 183-184. Booth D. A. (1982) How nutritional effects of foods can influence people’s dietary choices. In L. M. Barker. (Ed.) The Psychobiology of Human Food Selection: pp. 67-85. Westport, CT: AVI Publishing Co., Inc. Booth D. A. (1989) How do eating disorders work? (1989) In L. H. Schneider, S. J. Cooper, & K. A. Halmi (Eds.), The Psychobiology of Human Eating Disorders. (Vol. 575), pp. 466 47 1. New York, Annals of The New York Academy of Sciences. Brewerton, T., George, D. & Jimerson D. (1986) Neuroendocrine response to L-tryptophan in bulimia. American Psychiatric Association, 224-225. Bruch, H. (1969) Hunger and instinct. Journal of Nervous and Mental Disease, 149, 91-114. Coccaro, E. F., Siever, L. J., Owen, K. R. 8c Davis, K. L. (1990) Serotonin in mood and personality disorders. In E. F. Coccaro & D. L. Murphy (Eds.), Serotonin in Major Psychiatric Disorders. Washington, D. C.: American Psychiatric Association. Dahlstrom, W. G., Welsh, G. S. & Dahlstrom, L. E. (1982) MMPZHandbook-VI. Minneapolis, Minnesota. University of Minnesota Press. Gamer, D. M., Olmsted, M. P. & Polivy, J. (1983) Development and validation of a multidimensional eating disorder inventory for anorexia nervosa and bulimia. International Journal of Eating Disorders, 2, 15-35. Halmi K. A., Eckert, E., LaDu, T. & Cohen, J. (1986) Anorexia nervosa: treatment efficacy of cyproheptadine and amitriptyline. Archives of General Psychiatry, 43, 177-18 1. Halmi, K. A., Sunday, S., Puglisi, A. & Marchi, P. (1989) Hunger and satiety in anorexia and bulimia nervosa. In L. H. Schneider, S. J. Cooper, & K. A. Halmi (Eds.), The Psychobiology of Human Eating Disorders, (Vol. 575), pp. 431-445. New York. Annals of the New York Academy of Sciences. Holt, S., Ford, M. J. & Heading, R. C. (1989) Abnormal gastric emptying in primary anorexia nervosa. British Journal of Psychiatry, 139, 550-552. Kaye, W. H., Ebert, M. H. & Gwirtsman, H. E. (1984) Differences in brain serotonergic metabolism between non-bulimic and bulimic patients with anorexia nervosa. American Journal of Psychiatry 141, 1598-1601. Kaye, W., Ebert, M. H. & Raleigh, L. (1984) Abnormalities in CNS monoamine metabolism in anorexia nervosa. Archives of General Psychiatry, 41, 350-355. Leibowitz, S. F. and Shot--Posner, G. (1986) Brain serotonin and eating behavior. Appetite, 7, 1-13.

Owen, W. P., Halmi, K. A., Gibbs, J. Jc Smith, G. P. (1985) Satiety responses in eating disorders. Journal of Psychiatric Research, 19, 279-284. Paykel, E. S., Mueller, P. S. & DeLaveragne, P. M. (1973) Amitriptyline weight gain in carbohydrate craving: A side-effect. British Journal of Psychiatry, 123, 501-507. Robinson, P. H. (1989) Perceptivity and paraceptivity during measurement of gastric emptying in anorexia and bulimia nervosa. British Journal of Psychiatry, 154, 400-405. Robinson, P. H., Clarke, M. & Barrett, J. (1988) Determinants of delayed gastric emptying in anorexia nervosa and bulimia nervosa. Gut, 29,458-464. Wurtman, R. J., O’Rourke, D. & Wurtman, J. (1989) Nutrient imbalances in depressive disorders: Possible brain mechanisms. In L. H. Schneider, S. J. Cooper, & K. A. Halmi (Eds.), The Psychobiology of Human Eating Disorders, (Vol. 575), pp. 75-85. New York: Annals of The New York Academy of Sciences. Received

1 May 1990, revision 2.5 October

1990