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A Randomized, Placebo-Controlled Trial of Sertraline
in the Treatment of Night Eating Syndrome
John P. O’Reardon, M.D.
Objective: The authors assessed the effi-
placebo. Twelve subjects in the sertraline group (71%) were classified as having re- Kelly C. Allison, Ph.D.
sponded (CGI improvement rating ≤2, in-dicating much or very much improved) Method: Thirty-four outpatients diag-
Nicole S. Martino, B.A.
Jennifer D. Lundgren, Ph.D.
traline (N=17) or placebo (N=17) in an 8-week, double-blind, flexible-dose (50–200 CGI severity ratings, quality of life ratings, Moonseong Heo, Ph.D.
mg/day) study. A mixed effects linear re- Albert J. Stunkard, M.D.
Clinical Global Impression (CGI) improve- jects in the sertraline group (N=14) lost a ingestions, total daily caloric intake after placebo (N=14) (mean=–0.3 kg, SD=2.7).
Conclusions: In this 8-week trial, sertra-
quality of life ratings, and weight.
Results: Sertraline was associated with
night eating syndrome and was well toler- (Am J Psychiatry 2006; 163:893–898)
Night eating syndrome is an eating disorder charac- more common in obese persons than in nonobese per- terized by morning anorexia, evening hyperphagia, and sons and to increase in prevalence with increasing adipos- insomnia with awakenings followed by nocturnal inges- ity. In a Danish study (7), female obese subjects exhibiting tions (1, 2). In addition, mood is usually low (3), with a pat- night eating gained 5 kg over a 6-year period, whereas fe- tern of worsening in the latter half of the day (2). The core male obese subjects who did not engage in night eating feature of night eating syndrome appears to be delay in gained 1 kg. About half of individuals with night eating the circadian timing of food intake (4). Food intake is syndrome report that they were of normal weight before lower in the first half of the day and greater in the evening the syndrome developed, suggesting that night eating syn- and nighttime. Sleep is often disrupted in the service of drome may be an important pathway to obesity (8).
food ingestion. In the largest controlled study to date of There have been few reports on the treatment of night overweight and obese outpatients with night eating syn- eating syndrome. Case reports have suggested benefit from drome (4), energy intake in the first 8 hours of the day (6:00 a variety of strategies including d-fenfluramine (9), photo- a.m. to 2:00 p.m.) averaged only 575 kcal in night eating therapy (10), progressive muscular relaxation (11), and syndrome subjects (N=46) versus 1,082 kcal in a compari- topiramate (12). The first clinical pharmacotherapy trial son group (N=43), whereas energy intake in the last 8 (13) was a 12-week, open-label study of 17 subjects treated hours (10:00 p.m. to 6:00 a.m.) averaged 591 kcal in night with sertraline, a selective serotonin reuptake inhibitor eating syndrome subjects versus only 118 kcal in compar- (SSRI). A significant reduction of symptoms was seen in ison subjects. The total energy intake over 24 hours was obese subjects with night eating syndrome, with about half not different between the two groups.
(N=8) of the group responding to sertraline. Those respond- Night eating syndrome is of clinical importance because ers who achieved remission of night eating syndrome (N=5) it is associated with both obesity and psychological dis- also lost a significant amount of weight (–4.8 kg, SD=2.6).
tress. Its prevalence has been estimated at 1.5% in the gen- The present study sought to follow up this previous open- eral population (5) with a reported range of 8.9% (6) to label trial with a double-blind, randomized, placebo-con- 14% (3) in obesity clinics and rates of up to 27% in severely trolled trial. This time we also included a small number of obese persons (5). Night eating syndrome appears to be normal weight subjects with night eating syndrome to deter- SERTRALINE AND NIGHT EATING SYNDROME
mine if sertraline might relieve the distress associated with four tablets daily. Medication tolerance and adherence were re- Subjects were weighed at each visit and completed three self- report scales: 1) a night eating symptom scale, 2) the Beck De- pression Inventory, and 3) the Quality of Life Enjoyment and Sat-isfaction Questionnaire. The night eating symptom scale is a self- Subjects were recruited from a study that characterized the psy- report scale measuring the range and severity of night eating chological and behavioral aspects of night eating syndrome (4).
symptoms over the preceding week (13). It measures in a series of These patients were recruited through a combination of print ad- 13 items the degree of morning anorexia, evening hyperphagia, vertisements, TV programming, and a website. The characteriza- sleep disturbance, nocturnal eating episodes and associated tion study included 1) a structured clinical interview designed to as- cravings or compulsion to eat, and level and pattern of mood dis- sess the presence or absence of night eating syndrome, performed turbance. Each item is scored from 0 to 4, providing a possible by a trained clinician; 2) a 10-day sleep and food diary; 3) the Struc- range of scores from 0 to 52. The study physician recorded the tured Clinical Interview for DSM-IV (SCID) to assess the presence of number of nighttime awakenings (defined as when the subject past or current psychiatric disorders; and 4) the Eating Disorder Ex- got up out of bed for reasons other than solely to use the bath- amination to assess the presence of concomitant eating disorders.
room) and ingestions. The study physician also administered theClinical Global Impression (CGI) improvement and severity Participants
scales and the 17-item Hamilton Depression Rating Scale at each Eligible subjects were at least 18 years of age, met standard cri- visit. The Hamilton and Beck instruments were used to track teria for night eating syndrome according to the structured clini- changes in depressive symptoms. Outcome was categorized at cal interview, and had a body mass index (BMI) >18 kg/m2. Appli- week 8 on the basis of the CGI improvement rating, which ranges cants were excluded if they 1) were severely depressed (symptoms from 1 to 7. CGI improvement ratings were considered a primary in excess of the number required for DSM-IV diagnosis and mark- outcome measure, with a priori standards applied as follows: sub- edly interfering with occupational functioning or with usual so- jects with scores of 2 (much improved) were categorized as having cial activities or relationships); 2) had a lifetime diagnosis of bipo- responded, and those with scores of 1 (very much improved) were lar disorder or any psychotic disorder; 3) reported substance abuse or dependence within the preceding 6 months; 4) were cur- Evening hyperphagia was assessed by reviewing with the sub- rently taking psychotropic medications (including hypnotics); 5) ject the proportion of their daily caloric intake that occurred be- were working a night shift or swing shift schedule; 6) were in a tween the end of the evening meal and bedtime plus any noctur- weight reduction program; 7) had a current diagnosis of anorexia nal ingestions that occurred. As some subjects with night eating nervosa or bulimia nervosa (but not binge eating disorder); or 8) syndrome delay their evening meal considerably as part of the lacked awareness of their night eating episodes. The latter crite- circadian delay in the food intake rhythm, a cutoff of 8:00 p.m.
rion was used to exclude subjects with nocturnal sleep-related was used. Any food intake commencing after this time was con- eating disorder, a parasomnia in which nocturnal eating is ac- sidered to be caloric intake after the evening meal. The total ca- companied by a lack of awareness at the time and subsequent loric intake after the evening meal represents the sum of calories ingested between the end of the evening meal and bedtime plusany calories derived from nocturnal ingestions; it is expressed as Procedures and Measures
a percentage of total 24-hour calorie intake.
Baseline night eating syndrome symptoms were assessed as The Institutional Review Board of the University of Pennsylva- part of the characterization of night eating syndrome study (4).
nia approved the protocol. All subjects signed the informed con- Each subject collected data in a food and sleep diary during a 10- sent form after study procedures had been fully explained.
day 24-hour prospective monitoring period, with the first 2 days Data Analysis
discarded as practice days and the last day discarded because ofincomplete data. The diary included a record of all meals, snacks, Means and standard deviations of the outcome variables at and beverages consumed. Awakenings (during which the subject each time point were used for descriptive statistics as well as for got out of bed), nocturnal ingestions, as well as the timing of bed- the depiction of trends over the 8 weeks. The analyses were con- time and morning awakening were all recorded. A research dieti- ducted on an intent-to-treat basis for all subjects who completed cian analyzed diaries for caloric intake and macronutrient con- at least one follow-up visit after the baseline visit. The repeated- tent. Subjects were paid for the baseline diary data collection but measures outcome variables over the 8-week period were ana- not for participation in the treatment trial itself. Of the 65 subjects lyzed by a mixed effects linear regression model in the following with night eating syndrome who completed the diary assessment, form: outcome variable=intercept + group + week + group x week.
28 who were eligible to participate in the trial decided not to. Rea- The intercept was assumed to be random in order to take within- sons for not participating were inability to schedule (N=16), not subject correlations of the dependent variables into account for wanting to be in a placebo-controlled study (N=7), and not want- statistical inference. Group and time variables were taken as fixed ing a medication (N=5). This left a total of 37 subjects who entered and discrete; two-sided p<0.05 was considered significant. This the treatment trial. Three subjects attended the baseline visit but mixed effects modeling approach with available cases using a did not return for any subsequent visits, leaving a total of 34 sub- maximum likelihood method is valid in the presence of observa- jects whose data were included in the analyses.
Subjects were randomly assigned to 8 weeks of double-blind The effects of particular interest were the main group effect treatment with sertraline or placebo. Psychotropic agents other and the group-by-week interaction, with this interaction repre- than the study medication were prohibited during the study. The senting differences in trends of the outcome variables over time 8-week duration of the trial was based on the results of our earlier between night eating syndrome and comparison groups. Omni- 12-week trial. Subjects took tablets, identical in appearance, con- bus interaction significance tests are reported in the text. Post hoc taining either 50 mg of sertraline or placebo. Subjects com- testing of the main group effects at each time point on the out- menced with one tablet daily taken with the evening meal. Sub- come variables was followed by testing of the corresponding pa- jects were seen every other week for 30-minute visits at which rameter contrasts in the mixed effects model with Wald t tests. For time medication dosage could be adjusted up to a maximum of this purpose, we used a Bonferroni-corrected significance level O’REARDON, ALLISON, MARTINO, ET AL.
TABLE 1. Demographic and Clinical Characteristics at Baseline Among Subjects With Night Eating Syndrome Randomly As-
signed to 8 Weeks of Double-Blind Treatment With Sertraline or Placebo

Duration of night eating syndrome (years) Quality of Life Enjoyment and Satisfaction Questionnaire score a Obtained from self-report ratings of 13 items (score range=0–52).
0.05/4=0.0125 (correcting for the number of treatment visits after none of the three normal weight subjects in the placebo baseline), except when testing for correlations. Main group ef- fects at any week with p values lower than this corrected signifi- Figure 1 shows that the largest reduction in symptoms cance level were declared to be significant even if the overall maingroup or interaction effects were not significant.
occurred between baseline and week 2, indicating an early Three subjects who met criteria for binge eating disorder in ad- and robust effect of sertraline. Overall, a subject receiving dition to night eating syndrome were included as part of the sam- sertraline had a 30% chance of responding by week 2. Five ple. In line with recent evidence, binge eating disorder and night of the 12 who ultimately responded to sertraline had re- eating syndrome appear to be two distinct disorders rather than sponded as early as week 2, and four of these five achieved variable expressions of the same underlying psychopathology remission status by week 2. The lack of early improvement (15, 16). In this respect, binge eating disorder was treated as a co-morbid condition in night eating syndrome subjects and was not with sertraline did not preclude ultimate response, as 50% viewed as exclusionary for study participation. All three subjects of all responses occurred between weeks 4 and 8.
with binge eating disorder plus night eating syndrome were ran- The CGI severity scale is a further index of overall domly assigned to the placebo group. We tested for the signifi- change in night eating syndrome symptoms. The sertra- cance of binge eating disorder by including binge eating disorderstatus in the aforementioned mixed effects models. Binge eating line group had a reduction of two points in symptom se- disorder status did not have a significant effect on any of the out- verity, from 4.2 at baseline (moderate severity) to 2.2 at comes except for caloric intake after the evening meal. Thus, ca- endpoint (borderline ill), whereas there was a much more loric intake after the evening meal was the only variable for which modest reduction (from 4.2 to 3.4) in the placebo group binge eating disorder status was controlled. Pearson’s correla- tions were used to assess the association of changes at week 2with those at week 8 in the SSRI group. We used SAS v8.2 for sta- Night Eating Symptoms
Changes in night eating syndrome symptoms were sig- nificantly greater in the sertraline group, as assessed bynight eating symptom scores over the course of the 8-week Characteristics of the sertraline and placebo groups at baseline are presented in Table 1. No significant between- By week 8, the night eating symptom scores of the sertra- group differences for these variables were found.
line group had dropped by 18.1 points (57%) from a base-line score of 31.7 as compared with a reduction of only 5 CGI Ratings
points (16%) from a baseline score of 30.5 in the placebo The CGI improvement rating classified 12 of the 17 sub- group (F=8.0, df=4, 112, p<0.0001). A significant correlation jects receiving sertraline as having responded (score ≤2), was found between the change in night eating symptom and seven of these 12 achieved remission or complete res- scores from baseline to week 2 and the change from base- olution of night eating syndrome symptoms (F=6.7, df=4, line to week 8 for subjects receiving sertraline (r=0.68, p= 113, p<0.001). Of those receiving placebo, only three sub- 0.01), indicating that early improvement with sertraline was jects were classified as having responded (a response rate predictive of ultimate response. In addition, in terms of the significantly lower than that seen with sertraline [χ2=9.66, speed of response, the dose at first observed response in the df=1, p<0.002]), with one of the three placebo responders sertraline group was correlated with the week of response, achieving remission status. Of the three normal weight suggesting that those responding early improved at lower subjects in the sertraline group, two responded, while doses than those responding later (r=0.84, p<0.001). How- SERTRALINE AND NIGHT EATING SYNDROME
FIGURE 1. Changes in CGI Improvement Ratings and Night
FIGURE 2. Changes in Frequency of Awakenings and Noc-
Eating Symptoms Over the Course of the Study in Subjects
turnal Ingestions in Subjects With Night Eating Syndrome
With Night Eating Syndrome Randomly Assigned to 8
Randomly Assigned to 8 Weeks of Double-Blind Treatment
Weeks of Double-Blind Treatment With Sertraline or Pla-
With Sertraline or Placebo
estions –2
Noctur –6
vement R
CGI Impr 1
e in Number of
ting Symptom Scale 20
e in Number of
e on Night Ea 5
Chang –10
ever, the probability of response by the study endpoint at week 8 was not correlated with dose, indicating that doseper se was not an important predictor of ultimate response groups (F=4.7, df=1, 32, p=0.03). In post hoc testing, after adjustment for multiple comparisons, the difference at Ingestions and Awakenings
week 8 was not significant (t=–2.52, df=80, p=0.0137).
Figure 2 shows a significant reduction in the frequency Caloric Intake After the Evening Meal
of nocturnal ingestions in the sertraline group relative to Figure 3 shows that caloric intake after the evening meal the placebo group. The number of nocturnal ingestions in in the sertraline group fell by 68%, from 47.3% of total daily the sertraline group fell by 81% (from a mean at baseline of calories at baseline to 14.8% at week 8. In the placebo 8.3 per week [SD=8.5] to 1.6 [SD=2.6]) versus a fall of only group, caloric intake after the evening meal fell by 29.3%, 14% for the placebo group (from 6.4 [SD=4.9] to 5.5 [SD= from 44.7% at baseline to 31.6% at week 8 (F=3.5, df=4, 4.9] per week) (F=3.7, df=4, 80, p=0.01). Figure 2 indicates 106, p=0.009). Comparisons of individual time points were that the number of awakenings fell by 74% in the sertraline not significant (week 8: t=2.0, df=106, p=0.047).
group (from a mean of 8.8 per week [SD=8.6] to 2.3 [SD=4.7]) versus a fall of only 14% in the placebo group (from Weight Change
6.4 [SD=4.6] to 5.5 [SD=5.0]). This drop failed to reach sig- Among overweight subjects (N=14 in both groups), the nificance in the overall interaction effect (F=0.9, df=4, 80, sertraline group lost 2.9 kg (SD=3.8) versus 0.3 kg (SD=2.7) in p=0.40), but it yielded a difference in main effect between the placebo group (F=2.6, df=4, 63, p=0.06). The difference in O’REARDON, ALLISON, MARTINO, ET AL.
main effect for weight between groups at week 8 was signifi- FIGURE 3. Changes in Caloric Intake After the Evening Meal
cant (t=–2.7, df=63, p=0.009). The three normal weight sub- and Weight in Subjects With Night Eating Syndrome Ran-
domly Assigned to 8 Weeks of Double-Blind Treatment

jects receiving sertraline lost 1.2 kg compared with a gain of With Sertraline or Placebo
0.3 kg by the three normal weight subjects receiving placebo.
Mood Measures
Mood measures showed only a modest level of depressive symptoms in both groups at baseline (Table 1), and they did not differ over time (Hamilton score change: F=1.5, df=4,110, p=0.20; Beck score change: F=1.9, df=4, 100, p=0.10).
Change in night eating symptom scores in the sertraline group did not significantly correlate with reduction in de- e After Supper (%) 30
pressive symptoms as assessed with either the Beck De-pression Inventory (r=0.26) or Hamilton depression scale (r=0.08). When the two depression items were removedfrom the full night eating symptom scale, the score on the Caloric Intak
modified scale still correlated strongly with the full scale score (r=0.98, p<0.001), implying that change in depres-sive symptoms was not the principal driver of change in Quality of Life
In the sertraline group there was an increase in score on the Quality of Life Enjoyment and Satisfaction Question- naire, from 47.1 (SD=12.0) at baseline to 54.3 (SD=9.6) at week 8. Those receiving placebo remained essentially un- changed (mean=47.6 [SD=9.9] at baseline and 47.4 [SD= 7.3] at week 8; F=2.5, df=4, 108, p=0.045). No differenceswere noted at specific time points.
ight Chang
Dosing and Adverse Events
The mean daily dose of sertraline at study endpoint was 126.5 mg (SD=50.4). In contrast, the average dose of pla- cebo attained would have translated to 173.5 mg (SD= 40.0), indicating that dose was appropriately increased when a suboptimal response was observed (t=3.0, df=32, p=0.005). Sertraline was well tolerated, and no subject withdrew because of adverse events. Common side effects were mild and included dry mouth, fatigue, diminished li-bido, and sweating. Nausea as an adverse event was infre- evening meal dropped from 47.3% of total daily calories quent and transient (affecting two subjects receiving pla- consumed at baseline to 14.8% at week 8, thus approach- cebo and one receiving sertraline). There were two ing the normative levels of intake for obese comparison dropouts in the study, each related to lack of efficacy, one subjects without night eating syndrome found in our pre- from the sertraline group at week 6, and one from the pla- Consistent with the reduction in evening and nocturnal hyperphagia are the weight losses (about a pound a week), Discussion
which were similar to those in our earlier, open-label trial The results of this study, the first randomized, placebo- with sertraline (13). This finding is the more striking in controlled trial of sertraline in the treatment of night eat- that no advice or behavioral guidance regarding weight ing syndrome, are clear. Sertraline, an SSRI medication, loss was given. It suggests that sertraline may have a re- reduced the symptoms of night eating syndrome, and straining effect on the tendency to gain weight in persons most subjects (71%) met response criteria at the end of 8 weeks. The extent of improvement in core night eating Two patterns of improvement with sertraline were evi- syndrome symptoms was striking. The number of noctur- dent. Five subjects experienced an early and robust im- nal ingestions in the sertraline group was reduced by provement with sertraline, meaning that close to half of about 80% by study endpoint. The caloric intake after the those ultimately responding (N=12) exhibited this re- SERTRALINE AND NIGHT EATING SYNDROME
sponse after only 2 weeks of receiving active medication.
Improvement in the seven other responders occurred Received Feb. 11, 2005; revision received July 15, 2005; accepted Oct.
19, 2005. From the Department of Psychiatry, University of Pennsylvania.
more gradually, between weeks 4 and 8. The fact that there Address correspondence and reprint requests to Dr. O’Reardon, Depart- was only a weak, nonsignificant correlation between im- ment of Psychiatry, University of Pennsylvania, Rm. 4005, 3535 Market provement in depressive symptoms among night eating St., Philadelphia, PA 19104, (e-mail).
Supported by grants from the National Institute of Diabetes and Di- syndrome subjects receiving sertraline and improvement gestive and Kidney Diseases (R01 DK56735) and Pfizer Inc.
in night eating symptoms strongly implies that the im-provement with sertraline was independent of its antide-pressant effect.
Subjects receiving sertraline had experienced night eat- 1. Stunkard A, Grace WJ, Wolff HG: The night eating syndrome: a ing syndrome for a prolonged period of time (average du- pattern of food intake in certain obese patients. Am J Med1955; 19:78–86 ration of 17.6 years) before entering the study, but never- 2. Birketvedt GS, Florholmen J, Sundsfjord J, Osterud B, Dinges D, theless, four of the five fast responders achieved full Bilker W, Stunkard AJ: Behavioral and neuroendocrine charac- remission after only 2 weeks of sertraline treatment at a teristics of the night eating syndrome. JAMA 1999; 282:657– dose of 50 mg/day. This indicates that, despite chronicity 3. Gluck ME, Geliebter A, Satov T: Night eating syndrome is asso- of symptoms, a rapid and robust improvement is possible ciated with depression, low self-esteem, reduced daytime hun- for some night eating syndrome patients. A similar finding ger, and less weight loss in obese outpatients. Obes Res 2001; has been reported in another eating disorder, bulimia ner- vosa. When treated with the SSRI fluoxetine, a significant 4. O’Reardon JP, Ringel BL, Dinges DF, Allison KC, Rogers NL, Mar- tino NS, Stunkard AJ: Circadian eating and sleeping patterns in reduction was noted in both the binge eating and vomit- the night eating syndrome. Obesity Res 2004; 12:1789–1796 ing episodes after a single week of active treatment (17). It 5. Rand CS, MacGreggor AMC, Stunkard AJ: The night eating syn- is possible that the nocturnal ingestions in night eating drome in the general population and among postoperative syndrome, while not actual binges, share the psychologi- obesity surgery patients. Int J Eat Disord 1997; 22:65–69 6. Stunkard AJ, Berkowitz R, Wadden T, Tanrikut C, Reiss E, Young cal component of disinhibition with the binges of bulimia, L: Binge eating disorder and the night eating syndrome. Int J and that serotonergic medications such as fluoxetine and sertraline have the potential to quickly ameliorate the loss 7. Andersen GS, Stunkard AJ, Sorensen TIA, Petersen L, Heitmann of control present in both disorders.
BL: Night eating and weight change in middle-aged men andwomen. Int J Obes Relat Metab Disord 2004; 28:1338–1343 As indicated earlier, the core feature of night eating syn- 8. Marshall HM, Allison KC, O’Reardon JO, Birketvedt G, Stunkard drome appears to be a delay in the circadian timing of en- AJ: The night eating syndrome among nonobese persons. Int J ergy intake, with intake suppressed in the morning and in- creased in the evening and night. In an earlier study of 9. Spaggiari MC, Granella F, Parrino L, Marchesi C, Melli I, Terzano MG: Nocturnal eating syndrome in adults. Sleep 1994; 17:339– carefully monitored outpatients with night eating syn- drome and weight-matched comparison subjects (4), we 10. Friedman S, Even C, Dardennes R, Guelfi JD: Light therapy, obe- found dissociation between the sleep and eating rhythms sity, and night-eating syndrome. Am J Psychiatry 2002; 159: in the night eating syndrome group, with a delay in the 11. Pawlow LA, O’Neil PM, Malcolm RJ: Night eating syndrome: ef- food intake rhythm but not in the sleep rhythm.
fects of brief relaxation training on stress, mood hunger and The maintenance of normal circadian rhythms is the eating patterns. Int J Obes Relat Metab Disord 2003; 27:970– task of the suprachiasmatic nucleus of the hypothalamus, and serotonergic neurons are known to have inputs into 12. Winkelman JW: Treatment of nocturnal eating syndrome and sleep-related eating disorder with topiramate. Sleep Med the suprachiasmatic nucleus (18). It is possible that ser- traline may act by modulating suprachiasmatic nucleus 13. O’Reardon JP, Allison KC, Stunkard AJ: A clinical trial of sertra- function to restore a more normal food intake pattern in line in the treatment of the night eating syndrome. Int J Eat subjects with night eating syndrome. The suprachias- 14. Verbeke G, Molenberghs G: Linear Mixed Models in Practice: A matic nucleus may be a site of action in some individuals SAS-oriented Approach. New York, Springer, 1997, pp 222–233 for promoting a rapid improvement in night eating syn- 15. Allison KC, Grilo CM, Masheb RM, Stunkard AJ: Binge eating dis- order and night eating syndrome: a comparative study of dis-ordered eating. J Consult Clin Psychol 2005; 73:1107–1115 Limitations of this study include its short duration and 16. Allison KC, Stunkard AJ: Obesity and eating disorders. Psychiatr small size. Future studies of sertraline and other pharma- cotherapy agents in treating night eating syndrome should 17. Goldstein DJ, Wilson MG, Thompson JH, Potvin JH, Rampey AH determine if positive results are sustained over a longer Jr; Fluoxetine Bulimia Nervosa Research Group: Long-termtreatment of bulimia nervosa. Br J Psychiatry 1995; 166:660– term. If so, sertraline may be able to control both the core night eating syndrome symptoms and the obesity that is a 18. Miller JD, Morin LP, Schwartz WJ, Moore RY: New insights into frequent and distressing complication of the syndrome.
the mammalian circadian clock. Sleep 1996; 19:641–667



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