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Relationship between bipolar illness and binge-eating disorders
Psychiatry Research 135 (2005) 165 – 170 www.elsevier.com/locate/psychres
Relationship between bipolar illness and binge-eating disordersB Carla E. Ramacciottia,T, Riccardo A. Paolia, Giovanni Marcaccia, Armando Piccinnia, Annalisa Burgalassia, Liliana Dell’Ossoa, Paul E. Garfinkelb a
Departments of Psychiatry, Neurobiology, Pharmacology and Biotechnology, University of Pisa, via Roma 67, 56126, Pisa, Italy b Centre for Addiction and Mental Health, Department of Psychiatry, University of Toronto, Toronto, Ontario, Canada Received 19 May 2003; accepted 6 April 2004
Abstract In this study we describe the frequency of eating disorders (EDs) in a group of bipolar (BP) patients. We evaluated a sample of 51 outpatients, diagnosed as having BP I disorder on the basis of the Structured Clinical Interview for DSM-IV (SCID). Each of these subjects was administered the Binge Eating Disorder Clinical Interview (BEDCI) to determine the presence of binge eating disorder (BED) or bulimia nervosa (BN). Of the 51 BP patients, 14 (9 BED, 5 BN) met criteria for an ED. Most patients developed binge eating coincident with the first episode of BP disorder or after the onset of it. This was true for those who developed BED as well as BN, and involved both manic and depressive phases. All BN patients were women (5/5), and family history of binge eating was present in 80% of BN subjects, but only in 22.2% of BED and 29.7% of non-ED BP patients. We found a high frequency of concordance between BP illness and binge eating problems in our sample of BP patients. Given the temporal sequence of the mood disorder, which generally preceded the ED, we suggest a model in which the ED evolves due to modulation of emotions with food, as well as use of medications to treat BP disorder that disrupt hunger and satiety mechanisms. Given differences in gender distribution and family history, cultural and familial influences may also be significant in the minority of BP binge-eating patients who develop BN. D 2005 Elsevier Ireland Ltd. All rights reserved. Keywords: Bulimia nervosa; Affective disorder; Family history; Mania; Depression
1. Introduction B An earlier version of this report was presented at a meeting entitled bDisturbo Bipolare e Comorbidita`: Strategie Cliniche e Terapeutiche,Q Bormio, Italy, March 12–16, 2001, and at the Second International Forum on Mood and Anxiety Disorders, Monte Carlo, November 28 to December 1, 2001. T Corresponding author. Tel.: +39 050 23751. E-mail address: [email protected] (C.E. Ramacciotti).
Questions have been raised about the relationship of eating disorders (EDs) to mood disorders (MDs) for over 25 years (Cantwell et al., 1977). Evidence for this relationship has been derived from the prominent affective symptoms in anorexia nervosa (AN) and bulimia nervosa (BN), frequent co-morbid affective syndromes (Garfinkel et al., 1995, 1996), and family
0165-1781/$ - see front matter D 2005 Elsevier Ireland Ltd. All rights reserved. doi:10.1016/j.psychres.2004.04.014
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history data (Piran et al., 1985), as well as investigations examining the course of the EDs (Toner et al., 1986). Much of this literature has focused on depression; there has been little understanding of the relationship between bipolar (BP) disorder and the EDs. What is also known is that people affected by BN share a high rate of comorbidity with BP disorder type II (Mury et al., 1995; Simpson et al., 1992; Sullivan et al., 1995). Kruger et al. (1996), conversely, examined BP patients (43 with BP disorder type I, 18 with BP disorder type II) and found 13% met DSM-IV (American Psychiatric Association, 1994) criteria for BED, and a further 15% exhibited a partial binge-eating syndrome. In the present communication, we describe a group of BP I patients and the frequency of EDs in this population. We decided to investigate this sample because affective symptomatology in these patients is generally so severe as to overshadow the possible underlying ED. Moreover, the overeating of BP patients is very often assumed to be a consequence of medications that can play a significant role in disrupting hunger and satiety mechanisms. We intended to investigate whether overeating is due mainly to medication or to affective symptomatology. We report a high frequency of concordance between BP I and ED, and given the temporal sequence of the mood disorder generally preceding the ED, we suggest a model in which the ED evolves due to modulation of emotions with food, as well as the use of medications that treat BP disorder, which disrupt hunger and satiety mechanisms. Given differences in gender distribution and family history, we suggest that cultural and familial influences are significant in the minority of BP binge-eating patients who develop BN.
2. Methods 2.1. Participants We evaluated a sample of 51 outpatients (29 males, age 40.9F2.4 years; 22 females, age 40.3F2.6 years). All were diagnosed as having BP I disorder by experienced clinicians using the Structured Clinical Interview for DSM-IV (SCID) (First et al., 1997). Each of these subjects was moreover administered the semistructured Clinical Interview for BED (BEDCI) (Spitzer et al., 1994) to determine the presence or
absence of BED in greater detail. The diagnosis of BN was made by clinicians experienced in treating these conditions, again using the BEDCI. The subjects were all ambulatory patients attending a mood disorders clinic at Santa Chiara Hospital, the primary teaching hospital of the University of Pisa. All patients were treated in a naturalistic fashion, with medications and dosages decided on the basis of clinical judgment. At various times, it was often necessary to use one or two mood stabilizers and atypical neuroleptics or antidepressants, as described for relapse prevention of BP disorder (Post et al., 1998). Patients had been ill for 13.7F9.4 years (range 1–43) at the time of assessment for this study. Demographic data were recorded for each subject, including age, sex, marital status, level of education, body mass index (present and highest ever), age of onset of binge eating, age of onset of BP disorder, family history of binge eating, and medications used to treat the mood disorder. These data were collected from a combination of direct inquiry and review of the patient’s record. After complete description of the study to the subjects, written informed consent was obtained. 2.2. Statistics The data were categorical in nature and were therefore subjected to chi-square analysis. The Kruskal–Wallis nonparametric test was used for the analysis of age and age of onset.
3. Results Of the 51 BP patients, 14 met criteria for an ED. Nine met DSM-IV criteria for current or lifetime BED. A further five patients met DSM-IV criteria for BN; of these, three were of the purging type and two non-purging (Table 1). Table 1 Sample of 51 bipolar (BP) patients BP patients without ED 37 (72.5%) BP patients with ED 14 (27.5%)
f
BP with BED current or lifetime 9 (17.7%) (3 BN-Purging Type, 2 BN-Non Purging Type) 5 (9.8%)
C.E. Ramacciotti et al. / Psychiatry Research 135 (2005) 165–170 Table 2 Onset of eating disorder (ED) in bipolar (BP) patients ED ED ED ED ED ED
after BP contemporary with BP before BP during a euthymic phase during a manic phase during a depressive phase
8 4 2 1 5 6
patients patients patients patient patients patients
3.1. Temporal sequence of the disorders In eight of the patients with an ED comorbid with BP disorder, the BP illness clearly preceded the BED or BN. In four others, the two disorders developed at approximately the same time; these patients recall the onset of the binge eating at some point in their initial mood episode. Two other patients felt their ED preceded the BP disorder. Four patients said their ED began during a manic episode, seven during a depressive period and one when euthymic (Table 2). Not surprisingly, all BN patients were women, in contrast to the other two groups of subjects. Of those with BED, six were male and, among the BP patients with no ED, 23 were male. The groups did not differ in level of education or marital status; however, as to the latter, there was a tendency for the non-eatingdisordered BP patients to have a higher rate of being married: 17 vs. 2 for BED and 0 for BN (Table 3). The three groups tended to have been ill for many years. The BP/non-ED group had an age of onset of 28.9F11.8. Corresponding figures for the BP/BED and the BP/BN groups were 25.9F7.4 and 19.0F4, respectively ( P = 0.037). At the time of the study, ages of the patients were 42.5F13.1 for BP/non-ED patients, 40.9F14.9 for the BP/BED patients, and 28.4F4.4 for the BP/BN group ( P = 0.053) (Table 3).
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Family history of binge eating in the patients was as follows: 80% of BN/BP patients, but only 22.2% of BED/BP patients and 29.7% of non-ED/BP patients reported that other family members binged on food ( P = 0.06) (Table 3). 3.2. Medications With regard to medications used to treat these patients, 40% had been treated with one mood stabilizer, 50% with two mood stabilizers, and 10% with three or more, at some point in their treatment at Santa Chiara. In addition, 50% of patients received antidepressants, and 50% of patients received antipsychotics. Of the 14 patients with a diagnosis of an ED, eight had received atypical antipsychotics, eight had received mood stabilizers, and six had received both. Four patients had been treated with a selective serotonin reuptake inhibitor. One patient had been treated with a typical antipsychotic agent.
4. Discussion We found a high frequency of binge-eating problems in a sample of people who were being treated as outpatients for BP disorder. These findings are similar to those of Kruger et al. (1996), who reported 28% of patients attending a tertiary care clinic for BP had either a full or partial BED. We have also examined the problem from the point of view of those being treated for BP disorder at a university hospital and, using standardized instruments and rigorous criteria, we found 18% to have BED and 10% BN. Most patients who developed binge-eating disorder did so coincident with the first episode of BP
Table 3 Differences in three subgroups of bipolar (BP) patients Demographic characteristics Gender distribution Marital status Age of onset Age at the time of the study Family history of binge eating
Bipolar patients with and without ED
Statistical significance
BP without ED
BP with BED
BP with BN
Male 23 (62.2%); female 14 (37.8%) Married 17 (45.9%); not married 20 (54.1%) 28.9 F 11.8 42.5 F 13.1 29.7%
Male 6 (66.7%); female 3 (33.3%) Married 2 (22.2%); not married 7 (77.8%) 25.9 F 7.4 40.9 F 14.9 22.2%
Male 0; female 5 (100%) Married 0; not married 5 (100%) 19.0 F 4 28.4 F 4.4 80%
v 2 = 7.3, df = 2, P = 0.025 v 2 = 5, df = 2, P = 0.08 v 2 = 6.6, df = 2, P = 0.037 v 2 = 5.9, df = 2, P = 0.053 v 2 = 5.6, df = 2, P = 0.06
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disorder or after the onset of it. This was true for those who developed BED as well as BN, and involved both manic and depressive phases. Strengths to this study include the fact that we used the BEDCI and SCID, state-of-the-art diagnostic instruments. These were administered by experienced clinicians who made all diagnoses. We also did not include partial syndrome cases; three cases were not included, although they had occasional episodes of binge eating. As was true of the study of Kruger et al. (1996), the patient population was heavily biased toward severity as it was obtained from a tertiary care facility. A further limiting factor to this research relates to our dividing the ED patients into BED and BN. It is not known whether this diagnostic distinction is valid; indeed, BED may be non-purging BN, or non-purging BN, at a particular phase of the disorder that waxes and wanes. There is some evidence that patients with BED experience excessive weight and shape concerns, as do those with BN, and they share the cognitive distortions of those with BN, thereby obscuring the distinction between these syndromes (Ramacciotti et al., 2000). This would have little bearing on our study, however, since the BN subjects here were largely of the purging type. The BP subjects in this investigation had all been extensively treated with a variety of medications— antipsychotic drugs, antidepressants, and mood stabilizers. These can play a significant role in disrupting hunger and satiety mechanisms, and may thereby induce weight gain. There is a substantial body of evidence that mood and eating behaviors are closely regulated by central serotonin pathways (Rosenthal et al., 1987; Schuman et al., 1987; Krauchi et al., 1990; Brezinski et al., 1990; Moller, 1992). It has also been suggested that an underlying serotonin deficiency is responsible for carbohydrate craving, which may subsequently facilitate serotonin synthesis in the brain (Moller, 1992). There is also evidence that excessive carbohydrate ingestion temporarily relieves depressive symptoms and may represent a form of selfmedication for some people with depression (Schuman et al., 1987; Moller, 1992). There may be differences here among obese versus lean people. Obese binge eaters have been shown to experience clinical improvement in depressed mood after consumption of carbohydrates, leading them to
repeatedly overeat, whereas lean subjects experience sleepiness, fatigue and deterioration in mood (Lieberman et al., 1986; Spring et al., 1983). This is consistent with the finding of high rates of depressive disorder among obese binge eaters, relative to others with obesity (Marcus et al., 1990, 1992; Ramacciotti et al., 2000). Several studies have also found that obese binge eaters were likely to favor carbohydrates in comparison to obese non-binge eaters (De Zwaan et al., 1993; Yanovski et al., 1992). If this literature is applied to the interpretation of the present study, it is possible that binge eating serves as a compensatory behavior during depression, modulating the mood of people with BP disorder. Some of the binge eaters in this study developed the behavior in the course of a manic episode. It is not clear whether binge eating resulted from the affective state or the medications used to treat it. Overeating could be an involuntary, adaptive strategy to cope with the overwhelming intense moods and poor impulse control of a manic state. Many people with BN binge in response to strong negative feelings, but feelings can be perceived as too intense, even if positive. It is known that the frequency of obesity in patients with psychotic disorders taking antipsychotic medications is higher than in the general population (McIntire et al., 2001) and that the use of the newer antipsychotic drugs is associated with increased fat mass (Elmslie et al., 2001). While studies suggest that up to 70% of body weight is genetically mediated, environmental factors also play critical roles (Yanovsky and Yanovsky, 1999; Mokdad et al., 1999). Most of the existing data describing mechanisms of antipsychotic-induced weight gain have emphasized changes in putative neurocircuits hypothesized to participate in increased energy intake (e.g. increased appetite) at the level of the lateral hypothalamus (Leibowitz, 1980; Jackson et al., 1997). Changes in food preference have also been shown—for example, higher intake of sucrose, leading to an excessive energy intake (Elmslie et al., 2001). Sedation could also be involved in this effect. Among antipsychotic agents, higher levels of weight gain are associated with the atypical drugs, especially with olanzapine (Simpson et al., 2001). One interesting aspect of these results relates to the different gender distribution of the binge-eating
C.E. Ramacciotti et al. / Psychiatry Research 135 (2005) 165–170
patients: two-thirds of the BED patients were male, while all five BN subjects were female. Also, the family history of binge eating was quite different in these two groups; 80% of the BN patients versus only 22% of those with BED had relatives with bingeeating behavior. While the sample is small, these data suggest subtle differences between the two, with the BN patients tending to have a more familial and culture-bound component to their disorder. Earlier epidemiologic studies have supported differential sex ratios between BED (2.5:1) versus BN (10:1) (Spitzer et al., 1993), suggesting the latter is much more influenced by the cultural emphasis on thinness for women. The present study confirms the earlier report of Kruger et al. (1996) that binge eating was common among a group of BP patients. The finding applied to both full syndrome BN and BED. This study extends the findings of the earlier one by demonstrating that the mood disorder generally preceded the eating disorder; and the onset occurred during both manic and depressive phases. Clinicians treating BP disorder should be alert to this association and provide nutritional and psychological support to those who begin to binge-eat. There may also be value in developing group psychoeducation programs for BP patients as a form of prevention.
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Garfinkel, P.E., Lin, B., Goering, P., Spegg, C., Goldbloom, D., Kennedy, S., Kaplan, A., Woodside, B., 1995. Bulimia nervosa in a Canadian community sample: prevalence and comparison of subgroups. American Journal of Psychiatry 152, 1052 – 1058. Garfinkel, P.E., Lin, B., Goering, P., Spegg, C., Goldbloom, D., Kennedy, S., Kaplan, A., Woodside, D.B., 1996. Should amenorrhea be necessary for the diagnosis of anorexia nervosa? Evidence from a Canadian community sample. British Journal of Psychiatry 168, 500 – 506. Jackson, H.C., Needham, A.M., Hutchins, L.J., Mazurkiewicz, S.E., Heal, D.J., 1997. Comparison of the effects of sibutramine and other monoamine reuptake inhibitors on food intake in the rat. British Journal of Pharmacology 121, 1758 – 1762. Krauchi, K., Wirz-Justice, A., Graw, P., 1990. The relationship of affective state to dietary preference: winter depression and light therapy as a model. Journal of Affective Disorders 20, 43 – 53. Kruger, S., Shugar, G., Cooke, R.G., 1996. Comorbidity of binge eating disorder and the partial binge eating syndrome with bipolar disorder. International Journal of Eating Disorders 19, 45 – 52. Leibowitz, S.F., 1980. Neurochemical systems of the hypothalamus: control of feeding and drinking behaviour and water– electrolyte excretion. In: Morgan, P., Panksepp, J. (Eds.), Handbook of the Hypothalamus, vol. 3. Marcel Dekker Inc., New York, pp. 299 – 438. Lieberman, H.R., Wurtman, J.J., Chew, B., 1986. Changes in mood after carbohydrate consumption among obese individuals. American Journal of Clinical Nutrition 44, 772 – 778. Marcus, M.D., Wing, R.R., Ewing, L., Kern, E., Gooding, W., McDermot, M., 1990. Psychiatric disorders among obese binge eaters. International Journal of Eating Disorders 9, 67 – 77. Marcus, M.D., Smith, D., Santellini, R., Kaye, W., 1992. Characteristics of eating disordered behavior in obese binge eaters. International Journal of Eating Disorders 3, 249 – 255. McIntire, R.S., Mancini, D.A., Basile, S.V., 2001. Mechanisms of antipsychotic-induced weight gain. Journal of Clinical Psychiatry 62 (Suppl. 23), 23 – 29. Mokdad, A.H., Serdula, M.K., Dietz, W.H., Bowman, B.A., Marks, J.S., Koplan, J.P., 1999. The spread of the obesity epidemic in the United States, 1991–1998. Journal of the American Medical Association 282, 1519 – 1522. Moller, S.E., 1992. Serotonin, carbohydrates and atypical depression. Pharmacology and Toxicology Suppl. 71, 61 – 71. Mury, M., Verdoux, H., Bourgeois, M., 1995. Comorbidity of bipolar and eating disorders. Epidemiologic and therapeutic aspects. Encephale 21, 545 – 553. Piran, N., Kennedy, S., Owens, M., Garfinkel, P.E., 1985. Affective disturbances in eating disorders. Journal of Nervous and Mental Disease 173, 395 – 400. Post, R.M., Denikoff, K.D., Frye, M.A., Dunn, R.T., Leverich, G.S., Osuch, E., Speer, A., 1998. A history of the use of anticonvulsants as mood stabilizers in the last two decades of the 20th century. Neuropsychobiology 38 (3), 152 – 166. Ramacciotti, C.E., Coli, E., Passaglia, C., Lacorte, M., Pea, E., Dell’Osso, L., 2000. Binge eating disorder: prevalence and psychopathological features in a clinical sample of obese people in Italy. Psychiatry Research 94, 131 – 138.
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Rosenthal, N.E., Genhart, M., Jacobsen, F.M., Skwerer, R.G., Wehr, T.A., 1987. Disturbances of appetite and weight regulation in seasonal affective disorder. Annals of the New York Academy of Sciences 499, 216 – 230. Schuman, M., Gitli, M.J., Fairbanks, L., 1987. Sweets, chocolate and atypical depressive states. Journal of Nervous and Mental Disease 175, 491 – 495. Simpson, S.G., al-Mufti, R., Andersen, A.E., DePaulo Jr., J.R., 1992. Bipolar II affective disorder in eating disorder inpatients. Journal of Nervous and Mental Disease 180, 719 – 722. Simpson, M.M., Goetz, R.R., Devlin, M.J., Goetz, S.A., Walsh, B.T., 2001. Weight gain and antipsychotic medications: differences between antipsychotic-free and treatment periods. Journal of Clinical Psychiatry 62, 694 – 700. Spitzer, R.L., Yanovsky, S.., Wadden, T., Wing, R., Marcus, M.D., Stunkard, A., Devlin, M., Mitchell, J., Hasin, D., Horne, R.L., 1993. Binge eating disorder: its further validation in a multisite study. International Journal of Eating Disorders 13, 137 – 153.
Spitzer, R.L., Yanovsky, Marcus, M.D., 1994. Binge Eating Clinical Interview (HaPI Record), Pittsburgh. Spring, B., Maller, O., Wurtman, J., Digman, L., Cozolino, L., 1983. Effects of protein and carbohydrate meals on moods and performance: interactions with sex and age. Journal of Psychiatric Research 17, 155 – 167. Sullivan, P.F., Bulik, C.M., Carter, F.A., Joyce, P.R., 1995. The significance of a history of childhood sexual abuse in bulimia nervosa. British Journal of Psychiatry 167, 679 – 682. Toner, B.B., Garfinkel, P.E., Garner, D.M., 1986. Long term follow up of anorexia nervosa. Psychosomatic Medicine 48, 520 – 529. Yanovsky, J.A., Yanovsky, S.Z., 1999. Recent advances in basic obesity research. Journal of the American Medical Association 282, 1504 – 1506. Yanovski, S.Z., Leet, M., Yanovski, J.A., Flood, M., Gold, P.W., Kissileff, H.R., Walsh, B.T., 1992. Food selection and intake of obese women with binge eating disorders. American Journal of Clinical Nutrition 56, 975 – 980.
Relationship between bipolar illness and binge-eating disordersB Carla E. Ramacciottia,T, Riccardo A. Paolia, Giovanni Marcaccia, Armando Piccinnia, Annalisa Burgalassia, Liliana Dell’Ossoa, Paul E. Garfinkelb a
Departments of Psychiatry, Neurobiology, Pharmacology and Biotechnology, University of Pisa, via Roma 67, 56126, Pisa, Italy b Centre for Addiction and Mental Health, Department of Psychiatry, University of Toronto, Toronto, Ontario, Canada Received 19 May 2003; accepted 6 April 2004
Abstract In this study we describe the frequency of eating disorders (EDs) in a group of bipolar (BP) patients. We evaluated a sample of 51 outpatients, diagnosed as having BP I disorder on the basis of the Structured Clinical Interview for DSM-IV (SCID). Each of these subjects was administered the Binge Eating Disorder Clinical Interview (BEDCI) to determine the presence of binge eating disorder (BED) or bulimia nervosa (BN). Of the 51 BP patients, 14 (9 BED, 5 BN) met criteria for an ED. Most patients developed binge eating coincident with the first episode of BP disorder or after the onset of it. This was true for those who developed BED as well as BN, and involved both manic and depressive phases. All BN patients were women (5/5), and family history of binge eating was present in 80% of BN subjects, but only in 22.2% of BED and 29.7% of non-ED BP patients. We found a high frequency of concordance between BP illness and binge eating problems in our sample of BP patients. Given the temporal sequence of the mood disorder, which generally preceded the ED, we suggest a model in which the ED evolves due to modulation of emotions with food, as well as use of medications to treat BP disorder that disrupt hunger and satiety mechanisms. Given differences in gender distribution and family history, cultural and familial influences may also be significant in the minority of BP binge-eating patients who develop BN. D 2005 Elsevier Ireland Ltd. All rights reserved. Keywords: Bulimia nervosa; Affective disorder; Family history; Mania; Depression
1. Introduction B An earlier version of this report was presented at a meeting entitled bDisturbo Bipolare e Comorbidita`: Strategie Cliniche e Terapeutiche,Q Bormio, Italy, March 12–16, 2001, and at the Second International Forum on Mood and Anxiety Disorders, Monte Carlo, November 28 to December 1, 2001. T Corresponding author. Tel.: +39 050 23751. E-mail address: [email protected] (C.E. Ramacciotti).
Questions have been raised about the relationship of eating disorders (EDs) to mood disorders (MDs) for over 25 years (Cantwell et al., 1977). Evidence for this relationship has been derived from the prominent affective symptoms in anorexia nervosa (AN) and bulimia nervosa (BN), frequent co-morbid affective syndromes (Garfinkel et al., 1995, 1996), and family
0165-1781/$ - see front matter D 2005 Elsevier Ireland Ltd. All rights reserved. doi:10.1016/j.psychres.2004.04.014
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history data (Piran et al., 1985), as well as investigations examining the course of the EDs (Toner et al., 1986). Much of this literature has focused on depression; there has been little understanding of the relationship between bipolar (BP) disorder and the EDs. What is also known is that people affected by BN share a high rate of comorbidity with BP disorder type II (Mury et al., 1995; Simpson et al., 1992; Sullivan et al., 1995). Kruger et al. (1996), conversely, examined BP patients (43 with BP disorder type I, 18 with BP disorder type II) and found 13% met DSM-IV (American Psychiatric Association, 1994) criteria for BED, and a further 15% exhibited a partial binge-eating syndrome. In the present communication, we describe a group of BP I patients and the frequency of EDs in this population. We decided to investigate this sample because affective symptomatology in these patients is generally so severe as to overshadow the possible underlying ED. Moreover, the overeating of BP patients is very often assumed to be a consequence of medications that can play a significant role in disrupting hunger and satiety mechanisms. We intended to investigate whether overeating is due mainly to medication or to affective symptomatology. We report a high frequency of concordance between BP I and ED, and given the temporal sequence of the mood disorder generally preceding the ED, we suggest a model in which the ED evolves due to modulation of emotions with food, as well as the use of medications that treat BP disorder, which disrupt hunger and satiety mechanisms. Given differences in gender distribution and family history, we suggest that cultural and familial influences are significant in the minority of BP binge-eating patients who develop BN.
2. Methods 2.1. Participants We evaluated a sample of 51 outpatients (29 males, age 40.9F2.4 years; 22 females, age 40.3F2.6 years). All were diagnosed as having BP I disorder by experienced clinicians using the Structured Clinical Interview for DSM-IV (SCID) (First et al., 1997). Each of these subjects was moreover administered the semistructured Clinical Interview for BED (BEDCI) (Spitzer et al., 1994) to determine the presence or
absence of BED in greater detail. The diagnosis of BN was made by clinicians experienced in treating these conditions, again using the BEDCI. The subjects were all ambulatory patients attending a mood disorders clinic at Santa Chiara Hospital, the primary teaching hospital of the University of Pisa. All patients were treated in a naturalistic fashion, with medications and dosages decided on the basis of clinical judgment. At various times, it was often necessary to use one or two mood stabilizers and atypical neuroleptics or antidepressants, as described for relapse prevention of BP disorder (Post et al., 1998). Patients had been ill for 13.7F9.4 years (range 1–43) at the time of assessment for this study. Demographic data were recorded for each subject, including age, sex, marital status, level of education, body mass index (present and highest ever), age of onset of binge eating, age of onset of BP disorder, family history of binge eating, and medications used to treat the mood disorder. These data were collected from a combination of direct inquiry and review of the patient’s record. After complete description of the study to the subjects, written informed consent was obtained. 2.2. Statistics The data were categorical in nature and were therefore subjected to chi-square analysis. The Kruskal–Wallis nonparametric test was used for the analysis of age and age of onset.
3. Results Of the 51 BP patients, 14 met criteria for an ED. Nine met DSM-IV criteria for current or lifetime BED. A further five patients met DSM-IV criteria for BN; of these, three were of the purging type and two non-purging (Table 1). Table 1 Sample of 51 bipolar (BP) patients BP patients without ED 37 (72.5%) BP patients with ED 14 (27.5%)
f
BP with BED current or lifetime 9 (17.7%) (3 BN-Purging Type, 2 BN-Non Purging Type) 5 (9.8%)
C.E. Ramacciotti et al. / Psychiatry Research 135 (2005) 165–170 Table 2 Onset of eating disorder (ED) in bipolar (BP) patients ED ED ED ED ED ED
after BP contemporary with BP before BP during a euthymic phase during a manic phase during a depressive phase
8 4 2 1 5 6
patients patients patients patient patients patients
3.1. Temporal sequence of the disorders In eight of the patients with an ED comorbid with BP disorder, the BP illness clearly preceded the BED or BN. In four others, the two disorders developed at approximately the same time; these patients recall the onset of the binge eating at some point in their initial mood episode. Two other patients felt their ED preceded the BP disorder. Four patients said their ED began during a manic episode, seven during a depressive period and one when euthymic (Table 2). Not surprisingly, all BN patients were women, in contrast to the other two groups of subjects. Of those with BED, six were male and, among the BP patients with no ED, 23 were male. The groups did not differ in level of education or marital status; however, as to the latter, there was a tendency for the non-eatingdisordered BP patients to have a higher rate of being married: 17 vs. 2 for BED and 0 for BN (Table 3). The three groups tended to have been ill for many years. The BP/non-ED group had an age of onset of 28.9F11.8. Corresponding figures for the BP/BED and the BP/BN groups were 25.9F7.4 and 19.0F4, respectively ( P = 0.037). At the time of the study, ages of the patients were 42.5F13.1 for BP/non-ED patients, 40.9F14.9 for the BP/BED patients, and 28.4F4.4 for the BP/BN group ( P = 0.053) (Table 3).
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Family history of binge eating in the patients was as follows: 80% of BN/BP patients, but only 22.2% of BED/BP patients and 29.7% of non-ED/BP patients reported that other family members binged on food ( P = 0.06) (Table 3). 3.2. Medications With regard to medications used to treat these patients, 40% had been treated with one mood stabilizer, 50% with two mood stabilizers, and 10% with three or more, at some point in their treatment at Santa Chiara. In addition, 50% of patients received antidepressants, and 50% of patients received antipsychotics. Of the 14 patients with a diagnosis of an ED, eight had received atypical antipsychotics, eight had received mood stabilizers, and six had received both. Four patients had been treated with a selective serotonin reuptake inhibitor. One patient had been treated with a typical antipsychotic agent.
4. Discussion We found a high frequency of binge-eating problems in a sample of people who were being treated as outpatients for BP disorder. These findings are similar to those of Kruger et al. (1996), who reported 28% of patients attending a tertiary care clinic for BP had either a full or partial BED. We have also examined the problem from the point of view of those being treated for BP disorder at a university hospital and, using standardized instruments and rigorous criteria, we found 18% to have BED and 10% BN. Most patients who developed binge-eating disorder did so coincident with the first episode of BP
Table 3 Differences in three subgroups of bipolar (BP) patients Demographic characteristics Gender distribution Marital status Age of onset Age at the time of the study Family history of binge eating
Bipolar patients with and without ED
Statistical significance
BP without ED
BP with BED
BP with BN
Male 23 (62.2%); female 14 (37.8%) Married 17 (45.9%); not married 20 (54.1%) 28.9 F 11.8 42.5 F 13.1 29.7%
Male 6 (66.7%); female 3 (33.3%) Married 2 (22.2%); not married 7 (77.8%) 25.9 F 7.4 40.9 F 14.9 22.2%
Male 0; female 5 (100%) Married 0; not married 5 (100%) 19.0 F 4 28.4 F 4.4 80%
v 2 = 7.3, df = 2, P = 0.025 v 2 = 5, df = 2, P = 0.08 v 2 = 6.6, df = 2, P = 0.037 v 2 = 5.9, df = 2, P = 0.053 v 2 = 5.6, df = 2, P = 0.06
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disorder or after the onset of it. This was true for those who developed BED as well as BN, and involved both manic and depressive phases. Strengths to this study include the fact that we used the BEDCI and SCID, state-of-the-art diagnostic instruments. These were administered by experienced clinicians who made all diagnoses. We also did not include partial syndrome cases; three cases were not included, although they had occasional episodes of binge eating. As was true of the study of Kruger et al. (1996), the patient population was heavily biased toward severity as it was obtained from a tertiary care facility. A further limiting factor to this research relates to our dividing the ED patients into BED and BN. It is not known whether this diagnostic distinction is valid; indeed, BED may be non-purging BN, or non-purging BN, at a particular phase of the disorder that waxes and wanes. There is some evidence that patients with BED experience excessive weight and shape concerns, as do those with BN, and they share the cognitive distortions of those with BN, thereby obscuring the distinction between these syndromes (Ramacciotti et al., 2000). This would have little bearing on our study, however, since the BN subjects here were largely of the purging type. The BP subjects in this investigation had all been extensively treated with a variety of medications— antipsychotic drugs, antidepressants, and mood stabilizers. These can play a significant role in disrupting hunger and satiety mechanisms, and may thereby induce weight gain. There is a substantial body of evidence that mood and eating behaviors are closely regulated by central serotonin pathways (Rosenthal et al., 1987; Schuman et al., 1987; Krauchi et al., 1990; Brezinski et al., 1990; Moller, 1992). It has also been suggested that an underlying serotonin deficiency is responsible for carbohydrate craving, which may subsequently facilitate serotonin synthesis in the brain (Moller, 1992). There is also evidence that excessive carbohydrate ingestion temporarily relieves depressive symptoms and may represent a form of selfmedication for some people with depression (Schuman et al., 1987; Moller, 1992). There may be differences here among obese versus lean people. Obese binge eaters have been shown to experience clinical improvement in depressed mood after consumption of carbohydrates, leading them to
repeatedly overeat, whereas lean subjects experience sleepiness, fatigue and deterioration in mood (Lieberman et al., 1986; Spring et al., 1983). This is consistent with the finding of high rates of depressive disorder among obese binge eaters, relative to others with obesity (Marcus et al., 1990, 1992; Ramacciotti et al., 2000). Several studies have also found that obese binge eaters were likely to favor carbohydrates in comparison to obese non-binge eaters (De Zwaan et al., 1993; Yanovski et al., 1992). If this literature is applied to the interpretation of the present study, it is possible that binge eating serves as a compensatory behavior during depression, modulating the mood of people with BP disorder. Some of the binge eaters in this study developed the behavior in the course of a manic episode. It is not clear whether binge eating resulted from the affective state or the medications used to treat it. Overeating could be an involuntary, adaptive strategy to cope with the overwhelming intense moods and poor impulse control of a manic state. Many people with BN binge in response to strong negative feelings, but feelings can be perceived as too intense, even if positive. It is known that the frequency of obesity in patients with psychotic disorders taking antipsychotic medications is higher than in the general population (McIntire et al., 2001) and that the use of the newer antipsychotic drugs is associated with increased fat mass (Elmslie et al., 2001). While studies suggest that up to 70% of body weight is genetically mediated, environmental factors also play critical roles (Yanovsky and Yanovsky, 1999; Mokdad et al., 1999). Most of the existing data describing mechanisms of antipsychotic-induced weight gain have emphasized changes in putative neurocircuits hypothesized to participate in increased energy intake (e.g. increased appetite) at the level of the lateral hypothalamus (Leibowitz, 1980; Jackson et al., 1997). Changes in food preference have also been shown—for example, higher intake of sucrose, leading to an excessive energy intake (Elmslie et al., 2001). Sedation could also be involved in this effect. Among antipsychotic agents, higher levels of weight gain are associated with the atypical drugs, especially with olanzapine (Simpson et al., 2001). One interesting aspect of these results relates to the different gender distribution of the binge-eating
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patients: two-thirds of the BED patients were male, while all five BN subjects were female. Also, the family history of binge eating was quite different in these two groups; 80% of the BN patients versus only 22% of those with BED had relatives with bingeeating behavior. While the sample is small, these data suggest subtle differences between the two, with the BN patients tending to have a more familial and culture-bound component to their disorder. Earlier epidemiologic studies have supported differential sex ratios between BED (2.5:1) versus BN (10:1) (Spitzer et al., 1993), suggesting the latter is much more influenced by the cultural emphasis on thinness for women. The present study confirms the earlier report of Kruger et al. (1996) that binge eating was common among a group of BP patients. The finding applied to both full syndrome BN and BED. This study extends the findings of the earlier one by demonstrating that the mood disorder generally preceded the eating disorder; and the onset occurred during both manic and depressive phases. Clinicians treating BP disorder should be alert to this association and provide nutritional and psychological support to those who begin to binge-eat. There may also be value in developing group psychoeducation programs for BP patients as a form of prevention.
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