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Chapter 2 Eating Disorders and Disordered Eating Behavior

Deborah Young-Hyman, PhD, CDE

Definition of Eating Disorders (ED) and Disordered Eating Behavior (DEB)

The American Psychiatric Association [APA] manual of mental health diagnoses (DSM-IV-TR 2000) (American Psychiatric Association 2000) defines disordered eating behaviors as caloric restriction, excessive exercise, use of laxatives and other forms of pharmacologic purging, binge eating, and, in patients with diabetes, intentional reduction or omission of insulin. DEB cognitions, which also contribute to diagnostic criteria, include preoccupation with weight and size and/or shape. Reflecting the predominant behavior type, major diagnostic categories of ED are anorexia, bulimia, and eating disorders not otherwise specified. Diagnosis of ED vs. DEB is based on the frequency of behavior and cognitions. When threshold frequency is documented, either by self-report or interview, behavior and cognitions reach the level of diagnosis (ED). Less frequent behaviors and cognitions are considered subclinical (DEB). Though behaviors vary, shared characteristics are that the person desires to control weight and change appearance, and the behaviors and cognitions interfere with other activities of daily living and are extreme. Concerns about shape and size drive maladaptive weight management behaviors. Behavioral criteria used in the general population are applied to patients with diabetes with the additional behavior of insulin manipulation (omission or reduction) (Crow 1998).

Patients with Diabetes: A Vulnerable Population

Patients with type 1 and type 2 diabetes have elevated rates of overweight and obesity (Liu 2009). Weight status is strongly associated with DEB in otherwise healthy individuals seeking weight loss and in individuals with type 1 diabetes (T1D), particularly young women (Neumark-Sztainer 2002a, Young-Hyman 2011b, Young-Hyman 2011c). Although there is evidence regarding weight concerns, elevated BMI, and increased rates of binge eating in patients with type 2 diabetes (T2D) (Pinhas-Hamiel 1999, Papelbaum 2005), evidence linking weight, weight concerns, and development of ED and DEB in patients with T2D is scarce.

Behaviors and attitudes such as dietary restraint, food preoccupation (such as carbohydrate monitoring and restriction), portion control, control of blood glucose through selective food intake, and programmed exercise are prescribed components of diabetes treatment and are the cornerstone by which good glycemic control is achieved (American Diabetes Association [ADA] 2007). These treatment behaviors can become DEB when they are used inappropriately for rapid weight loss, carried to excess, interfere with activities of daily living, and/or become a health risk (American Psychiatric Association 2000, Daneman 2002).

Ongoing treatment of diabetes exposes patients to situations known to be triggers for the development of DEB. These include: feeling a loss of autonomy because of the monitoring/reporting of food intake, physical activity, and blood glucose to family members; monitoring by and accountability to health care providers to maintain health and weight (Surgenor 2002); sequelae of the treatment regimen such as changes in attitudes about eating (Steel 1990, Anderson 2002); increased sense of vulnerability and loss of control as a result of altered self and body concept (Steel 1990, Wolman 1994, Erkolahti 2003); and weight gain after the initiation of insulin treatment (Larger 2005). Adhering to treatment may be a predisposing risk factor for the development of DEB in patients with diabetes independent of other psychological, familial, or societal influences (Colton 1999).

Although there remain questions about whether DEB is associated with poorer long-term metabolic control in patients with T1D (Affenito 1997a, Herpertz 1998a, Engstrom 1999, Peveler 2005), the presence of diagnosable ED and behavior categorized as subclinical DEB has been shown to be associated with an increase in complications: retinopathy (Rydall 1997), neuropathy (Steel 1987), transient lipid abnormalities (Affenito 1997b), increased hospitalizations for diabetic ketoacidosis (Rodin 1992), and poorer short-term metabolic control (Rodin 1992, Affenito 1997a, Meltzer 2001). Cross-sectional studies have shown associations between elevated A1C and the presence of diagnosable ED (Wing 1986, Affenito 1997a, Herpertz 1998a), subclinical DEB (Wing 1986), and intentional insulin omission (Jones 2006). Associations between DEB and the complications of T2D have not been extensively examined (Herpertz 1998b, Herpertz 2000, Herpertz 2001, Papelbaum 2005). Refusal to initiate insulin treatment by patients with T2D (psychological insulin resistance) (Davis 2006) may be driven, in part, by concerns about weight gain, but this is anecdotal and has not been systematically tested.

An assessment of DEB should be performed when weight gain, weight loss, and/or worsening glycemic control (including severe hypoglycemia and/or ketoacidosis) cannot be explained by disease processes, changes in care, medication or insulin regimen, a monitored weight-loss program, obvious noncompliance, or psychiatric morbidity, especially in young women (Daneman 2002).

Prevalence of Diagnosable ED and Subclinical DEB

Diagnosable ED has low prevalence in the diabetes population (Ackard 2008). There are varying estimates of the prevalence of diagnosable ED and DEB in individuals with T1D compared with healthy referent populations (Crow 1998, Engstrom 1999). Estimates range from 3.8% (Pollack 1995) to 31% in adolescent and young adult women with T1D (Polonsky 1994). Some studies have found similar rates to the general population and some higher, but assessment methods vary (Rodin 1986–1987, Steel 1989, Fairburn 1991, Peveler 1992, Striegel-Moore 1992, Crow 1998, Herpertz 1998a, Bryden 1999, Engstrom 1999, Meltzer 2001).

Subclinical DEB is increasing in all segments of the U.S. population and Westernized cultures, presumably associated with emphasis on the thinness ideal and concern about overweight/obesity. Prevalence rates of subclinical DEB may be underestimated because dieting behavior is common and there is a stigma attached to self-reporting DEB (Neumark-Sztainer 2002b). The prevailing belief is that the diagnosis of diabetes is associated with elevated rates of DEB when intentional reduction in insulin dose or omission is considered purging behavior to control weight, especially in women with T1D and in adolescent girls (Hudson 1983, Bubb 1991, Rodin 1991, Hockey 1993, Biggs 1994, Pollack 1995, Crow 1998, Affenito 2001). However, a recent study using a population-based healthy comparison sample did not show elevated rates of diagnosable ED in the cohort with diabetes (Ackard 2008).

Bulimic behaviors and insulin omission are the most commonly reported DEB in patients with T1D (Goebel-Fabbri 2008, Alice Hsu 2009), whereas caloric restriction/restraint and binging are more commonly reported by women with T2D (Herpertz 2001, Young-Hyman 2010). Rates of DEB in boys with diabetes have been shown to be considerably lower than those found for women (Meltzer 2001, Neumark-Sztainer 2002a) but may be increasing (Svensson 2003). Higher prevalence of T2D in minority populations could potentially be associated with increased rates of DEB but this relationship has not yet been demonstrated. Studies that compare occurrence of DEB in patients with type 1 versus type 2 diabetes show similar rates; however, types of behaviors reported differ. “Drive for thinness” and “body dissatisfaction” are more common in individuals with T2D. Intentional insulin omission (to cause glycosuria) is more common in patients with T1D (Herpertz 1998b, Herpertz 2001).

Among overweight young women attempting weight loss, both with (type 1) and without diabetes, weight status is a strong predictor of DEB (Striegel-Moore 1992, Vamado 1997, Arriaza 2001, Sherwood 2001, Neumark-Sztainer 2002b, Rodin 2002, Decaluwe 2003, de Man Lapidoth 2006, Shisslak 2006). In studies reporting BMI, type 1 cohorts have been significantly heavier than healthy control subjects, with average BMI above the normal range. Elevation in weight, independent of diagnosis, would in itself predict higher rates of DEB (Engstrom 1999, Jones 2006). However, few studies of diabetes cohorts have compared rates of DEB with healthy control groups matched for age, sex, and weight (Engstrom 1999, Colton 2004, Jones 2006). When subjects matched for BMI were used to compare overweight and obese patients having T2D with obese nondiabetic patients seeking weight loss and an obese nonclinical sample (Battaglia 2006), low levels of binge eating disorder were diagnosed overall (<5% in all groups). However, obese patients with diabetes had the lowest scores on the Eating Disorder Examination, but the highest scores on the Restraint scale (Mannucci 2002). Higher scores on the Restraint scale were attributed to treatment behaviors. Although there is robust documentation that behavior generally considered subclinical DEB using DSM criteria such as binge eating, purging (defined as intentional insulin omission), and caloric restriction are commonly reported by patients with diabetes (Fairburn 1991, Bryden 1999, Jones 2006), it is not known how much these reports reflect cognitions based on attempted adherence to the diabetes care regimen.

Weight gain consequent to good blood glucose control could be a driver of weight concerns (Meltzer 2001, Battaglia 2006) and is known to be a side effect of successful treatment (Steel 1990). Although the presumption is that DEB in this population is associated with elevated BMI levels, only one study stratified the diabetes cohort (both type 1 and 2 diabetes, men and women, age range 18–65 years) by weight status. Three percent of under- and normal weight women had a current ED, whereas 6.8% of the overweight and 10.3% of obese women reported DEB (Herpertz 1998b). These rates are similar to samples with equivalent BMIs seeking weight loss (Vamado 1997). A conflict may exist between the need to control weight and achieve good glycemic control (in patients with both T1D and T2D). In particular, young adult and adolescent women have been shown to use insulin omission specifically for weight control (Biggs 1994, Khan 1996). Fear of improved glycemic control “because I will gain weight” and diabetes-specific distress predict intentional insulin omission (Polonsky 1994). Although one goal of medical nutrition therapy (MNT) is to prevent weight gain (Nathan 2005), supervised weight management programs are not routinely available when weight gain occurs secondary to successful treatment with insulin.

Etiology of ED and DEB in the Diabetes Population: Psychiatric Symptoms, Regimen Compliance (or Noncompliance), or Physiologic Dysregulation

Primary risk factors for ED and DEB (in the nondiabetic population) are weight and size concerns, early eating problems and dieting, the presence of other forms of psychopathology, sexual abuse and other adverse life experiences, and low self-worth (Jacobi 2004). Except for weight concerns and depression, the relationships between these risk factors and occurrence of DEB in the diabetic population have received little attention.

Establishing the occurrence of DEB attributable to having diabetes and managing the disease is complicated by the paucity of studies that concurrently assess psychiatric symptoms, psychological adjustment to illness, and sequelae of the diabetes care regimen. Bryden et al. (1999) tracked BMI along with weight and shape concerns in adolescents and young adults with T1D; as both men and women became overweight, DEB increased. However, baseline and ongoing psychological status, independent of weight concerns, was not assessed. In contrast, Pollock et al. (1995) followed new-onset girls and boys with T1D (ages 8–13 years) from diagnosis for up to 14 years. The presence of DEB, compliance with medical regimen, and psychiatric symptoms were assessed, including weight concerns. Low rates of DSM-III diagnosable ED (3.8%) were found; however “youths with eating problems were nine times more likely to have had a psychiatric disorder than the rest of the patients” (p. 291). A recent study found that onset of insulin restriction in women with T1D was associated with fear of weight gain and problems with the self-management regimen (Goebel-Fabbri 2011). Problematic eating behavior specific to the diabetes care regimen appears to be part of a constellation of pervasive noncompliance associated with higher psychiatric morbidity or poorer adjustment to illness (Pollock 1995, Wilfley 2000, Pollock-BarZiv 2005, Goebel-Fabbri 2011).

Two studies demonstrated an association between psychiatric morbidity and DEB in patients with T2D independent of weight status. In one study, overweight and obese patients had more diagnosable ED, and patients with ED had significantly more anxiety disorders and trended towards being more depressed. In the second, DEB was also strongly associated with psychopathology such as depression, low self-esteem, and general psychopathology but not weight (Herpertz 1998b, Papelbaum 2005). Given the known comorbidity between emotional disorders (depression in particular) (Anderson 2001) and diabetes, and between emotional disorders and DEB in the healthy population (Telch 1998, Stice 1999, Stice 2000, Stice 2001, Stice 2002), DEB could be part of a constellation of poor psychological adjustment and/or poor adjustment to illness, which is comorbid with overweight and T2D (Herpertz 1998a).

Behaviors considered triggers for and pathognomonic of DEB are embedded in the diabetes treatment regimen (Bantle 2006). Lack of success with MNT can leave patients feeling out of control of both eating behavior and glycemia (Surgenor 2002). Feeling out of control of eating behavior, preoccupation with food, and calorie restriction are DSM-IV-TR diagnostic criteria for bulimia, binge eating disorder, and eating disorder not otherwise specified (American Psychiatric Association 2000). Primary criteria for binge eating disorder include subjective self-evaluation of repeatedly eating amounts of food in a short period of time that are “definitely larger than most individuals would eat under similar circumstances.” Making this subjective determination (when an amount of food is large or excessive) for an individual with diabetes could be attributable to failure to adhere to MNT prescription, especially in the context of treatment of hypoglycemia. Other possibilities exist for misattribution of adherent behavior as DEB (Polonsky 1999). As caloric restraint is prescribed as part of treatment, inaccuracies in judgment regarding appropriateness of food intake can occur in the context of carbohydrate counting, falling blood glucose level, misjudgment of the causes of symptoms (Johnson 2000, Hay 2003, Davis 2004), or excessive nutrition intake related to exercise.

Hormonal evidence for dysregulation of hunger and satiety in patients with diabetes suggests difficulty controlling food intake and consequent blood glucose levels. Further, nonphysiologic dosing of insulin impacts appetite regulation (Young-Hyman 2010). Hormonal dysregulation (including loss of endogenous insulin and amylin secretion) (Koda 1992, Kruger 1999), dysregulation of incretin production, which contributes to metabolism in the gut (Dupre 2005, Higgins 2007), complications of the disease such as gastroparesis (Parkman 2004), and fluctuations in blood glucose level, particularly hypoglycemia (ADA 2002), may predispose vulnerable patients to adoption of maladaptive weight management strategies (such as insulin manipulation) to control hunger and associated weight gain.

Measurement of ED and DEB

Most studies to date have used measurement tools standardized in the general population to establish the presence of ED and DEB in patients with diabetes. Questionnaires include but are not limited to the Eating Attitudes Test (EAT) 40 (Garner 1979) and EAT-26 (Garner 1982), Eating Disorder Inventory (EDI-3) (Garner 2004), the Bulimia Test - Revised (BULIT-R) (Thelen 1991), and the Eating Disorder Examination (EDE) (Cooper 1989), which is conducted in interview format. Evaluation tools include items about attitudes and behaviors that are embedded in the diabetes treatment regimen. For example BULIT-R items (“Do you feel you have control over the amount of food you consume?” and “I eat a lot of food when I’m not even hungry.”) could refer to the diabetes care regimen (the former by prescription of dietary restraint and the latter by a prescribed meal plan), carbohydrate to insulin ratio, and/or treatment for low blood glucose. Diabetes care providers identified more than twenty questions on the EDI-3 that could be answered in the context of treatment and endorsed independent of weight concerns (Young-Hyman 2010). When questionnaires standardized in healthy populations are used, scores may be elevated in patients with both T1D and T2D, due to the overlap in items which are diagnostic of disordered eating attitudes and DEB and prescribed as part of diabetes treatment (Daneman 1998). When questionnaires or interview techniques standardized in the nondiabetic population are used, it is recommended that questions be modified to address intent of behaviors, including insulin manipulation (Criego 2009). Some studies have expanded the EDE and SCID interview format to include such questions (Peveler 2005).

Two questionnaire exceptions were found: the Diabetes Eating Problems Survey (DEPS), created by Antisdel, Laffel, and Anderson (2001) and refined by Markowitz et al. (2010), and the AHEAD (Assessing Health and Eating among Adolescents with Diabetes) survey (Neumark-Sztainer 2002a). Both include questions regarding the adjustment of insulin specifically for the purposes of weight reduction, and both couch questions in terms of diabetes care and issues related to glycemic control and weight gain due to treatment (Antisdel 2001, Neumark-Sztainer 2002a). However, neither questionnaire has been validated in a clinical population with an independent diagnosis of ED. Findings from a study validating a questionnaire that assesses hunger and satiety in the context of diabetic care, the Diabetes Treatment and Satiety Scale (DTSS-20), suggest that patients with T1D routinely experience contradictory clinical situations (regarding blood glucose levels, usual MNT, and insulin dosing) during which they feel full, hungry, and/or out of control of food intake (Young-Hyman 2011a). It is speculated that the lack of appropriate hunger and satiety cues is related to hormonal dysregulation. (See section regarding physiologic dysregulation of appetite.)

To establish diagnosis of ED or document subclinical DEB, thorough evaluation in the diabetes population should include assessment of adjustment to illness, overall psychological status, weight and shape concerns, specific questions regarding maladaptive use of the insulin or medication regimen to lose weight, and reliability of proprioceptive cues regarding hunger and satiety in the context of blood glucose levels (Young-Hyman 2010).

Limitations of Current Research Findings

Gaps in research regarding the association of DEB and diabetes include: 1) assessment of DEB in the context of adherence to medical regimen and adjustment to illness; 2) understanding the contribution of insulin and medication dosing to feelings of hunger and satiety; 3) dietary prescriptions/medical nutrition therapy as potential sources of information/attitudes leading to feelings of loss of control over food intake; 4) need for appropriate comparison groups such as healthy-weight matched individuals seeking to prevent weight gain or weight loss, minority comparison groups, and other chronic disease groups with conditions affecting weight/metabolism; 5) incomplete psychological characterization of samples; 6) discrimination of preexisting/evolving psychopathology associated with noncompliance; and 7) the need to use diabetes-specific assessment tools.

Prior studies of the prevalence of DEB in individuals with diabetes have not systematically addressed issues of regimen intensity, responsibility taking for regimen decisions, expectations of health care providers for glycemic and weight outcomes, and eating cognitions associated with medical care. The contributions of diabetes treatment knowledge or regimen adherence to the prevalence or endorsement of DEB are not established. Very few studies were found to have monitored patients from the time of diagnosis to establish the relationships or chronology between psychological symptomatology (depression in particular), DEB, weight gain, or regimen adjustment to prevent weight gain. Studies in adult women have not taken into account use of hormones for birth control or hormone replacement therapy (HRT), which can cause excess weight gain and increase appetite (Abrams 1992, Gallo 2004, Gallo 2006). Last, no studies to date have simultaneously assessed physiologic markers of hormones and incretins contributing to dysregulation of hunger and satiety and symptoms of DEB in the context of diabetes care.

Recommendations for Screening and Care

DEB is accepted as a serious and potentially life-threatening comorbidity of diabetes, despite controversy about diagnosis and prevalence. No published randomized controlled intervention trials of treatment of DEB or ED with diabetes cohorts could be found. Therefore screening recommendations are derived from the extant literature, and treatment recommendations are adapted from DEB interventions with healthy populations (Kelly 2005, Goebel-Fabbri 2009).

If DEB is suspected, screening should be implemented as follows:

1. Use diabetes-specific measurement tools to distinguish between behavior that indicates regimen adherence versus DEB to control weight, independent of glycemic control goals (Goebel-Fabbri 2009, Young-Hyman 2011a).

2. Evaluate overall psychological adjustment to establish whether behaviors indicate DEB, psychiatric morbidity, and/or poor adjustment to the diagnosis and requirements of treatment regimen (noncompliance). Patients with known psychiatric morbidity should be screened for DEB when unexplained poor glycemic control, weight gain, and/or weight loss occurs (Kelly 2005).

3. Evaluate insulin and other medication dosing/amount and episodes of hypoglycemia as potential causes for lack of satiety and/or loss of control over food intake. Evaluate accuracy of internal cues indicating need for food or treatment (with medication) in the context of blood glucose level (Goebel-Fabbri 2009).

4. Evaluate potential contributions of dietary prescription and information (MNT) to attitudes and behaviors regarding food intake, including food preoccupation and self-evaluation of actual or subjective dietary restraint and binging (ADA 2007).

5. Assess patients’ expectations for achieving good glycemic control: at what cost to psychosocial adjustment, quality of life, eating behaviors, and weight.

If screening indicates DEB, formal evaluation and care should be implemented:

1. Refer for psychological/psychiatric evaluation. Once ED/DEB is established by questionnaire/interview, referral for treatment to a mental health professional familiar with the medical management of diabetes and treatment of DEB should be made (ADA 2007).

2. When treatment for DEB is begun, the treating professional as well as key individuals in the patient’s social support network in treatment (parents for children and teens, partners or close family/community members for adults) should be incorporated into the diabetes management team (Criego 2009).

3. Depending on severity of symptoms, medications (antidepressant and antianxiety) and hospitalization should be considered.

4. Routine monitoring of DEB symptoms at medical management visits is also an integral part of the ongoing treatment process so that appropriate adjustments to the diabetes care regimen can be made (ADA 2007, Criego 2009). Careful evaluation of the contribution of prescribed diabetes care behaviors, knowledge, intent of behavior, and glycemic and weight goals should be conducted. Incorporation of diabetes treatment personnel into the DEB treatment plan helps to ensure that the prescription for regimen behaviors can be adjusted as needed (Goebel-Fabbri 2009).

5. Use of cognitive behavioral therapy, interpersonal therapy, and integrative cognitive therapy with adjunctive pharmacotherapy to address significant psychiatric symptoms are recognized treatment approaches in the nondiabetic population and should be provided to those with diabetes. Based on successful intervention methods, treatment can be individually or group administered by a trained professional (usually a behaviorally trained psychologist, social worker, or dietitian) who is familiar with the treatment of both DEB and diabetes (de Zwaan 2004, Pike 2004, Tantleff-Dunn 2004, Peterson 2004).

6. Interventions should target specific maladaptive behaviors (such as manipulation of insulin or medication omission) to ensure health, and should target cognitions about body image, self-esteem, autonomy, interpersonal relationships, and disease self-efficacy, particularly control of glucose and weight, depending upon symptoms reported, to improve mental health. Recommendations follow procedures used in the general population but with the addition of self-management behavior, which needs to be addressed with the diabetes care team in the context of preserving glycemic control. If metabolic derangements (severe hypoglycemia and ketoacidosis) are found to be associated with DEB, metabolic derangements must first be stabilized via medical management (ADA 2007).

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Deborah Young-Hyman, PhD, CDE, is Professor of Pediatrics at the Georgia Prevention Center, Institute for Public and Preventive Health, Georgia Health Sciences University, Augusta, GA.