JA, Tennen H: History of major depressive disorder and diabetes outcomes in diet- and tablet-treated post-menopausal women: a case control study. Diabet Med 24:211–216, 2007b
Wagner J, Tsimikas J, Abbott G, de Groot M, Heapy A: Racial and ethnic differences in diabetic patient-reported depression symptoms, diagnosis, and treatment. Diabetes Research and Clinical Practice 75:119–122, 2006
Welch GW, Jacobson AM, Polonsky WH: The Problem Areas in Diabetes scale: an evaluation of its clinical utility. Diabetes Care 20:760–766, 1997
Williams JBW, Gibbon M, First MB, Spitzer RL, Davies M, Borus J, Howes MJ, Kane J, Pope HG Jr, Rounsaville B, Wittchen H-U: The Structured Clinical Interview for DSM-III-R (SCID) - II: multisite test-retest reliability. Arch Gen Psychiatry 49:630–636, 1992
Williams MM, Clouse RE, Nix BD, Rubin EH, Sayuk GS, McGill JB, Gelenberg AJ, Ciechanowski PS, Hirsch IB, Lustman PJ: Efficacy of sertraline in prevention of depression recurrence in older versus younger adults with diabetes. Diabetes Care 30:801–806, 2007
Zhang X, Norris SL, Gregg EW, Cheng YJ, Beckles G, Kahn HS: Depressive symptoms and mortality among persons with and without diabetes. Am J Epidemiol 161:652–660, 2005
Zhao W, Chen Y, Lin M, Sigal RJ: Association between diabetes and depression: sex and age differences. Public Health 120:696–704, 2006
Mary de Groot, PhD, is an Associate Professor of Medicine at the Indiana University School of Medicine in Indianapolis, IN.
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
