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      7. feelings of worthlessness or excessive or inappropriate guilt (which may be delusional) nearly every day (not merely self-reproach or guilt about being sad)

      8. diminished ability to think or concentrate, or indecisiveness, nearly every day (either by subjective account or as observed by others)

      9. recurrent thoughts of death (not just fear of dying), recurrent suicidal ideation without a specific plan, or a suicide attempt or a specific plan for committing suicide

      B. The symptoms do not meet criteria for a Mixed Episode

      C. The symptoms cause clinically significant distress or impairment in social, occupational, or other important areas of functioning

      D. The symptoms are not due to the direct physiological effects of a substance (e.g., a drug of abuse, a medication) or a general medical condition (e.g., hypothyroidism)

      E. The symptoms are not better accounted for by bereavement, i.e., after the loss of a loved one, the symptoms persist for longer than 2 months or are characterized by marked functional impairment, morbid preoccupation with worthlessness, suicidal ideation, psychotic symptoms, or psychomotor retardation.

       Measurement of Depression

      Depressive symptoms may be adequately measured using self-report symptom inventories such as the Beck Depression Inventory-II (BDI-II) (Beck 1996), the nine-item depression scale of the Patient Health Questionnaire (PHQ-9) (Kroenke 2001), or the Center for Epidemiologic Studies Depression Scale (CES-D) (Radloff 1977). These measures vary in the number and content of items and may be used selectively for a variety of purposes (e.g., clinical screening, research). All have been developed for the general population (i.e., they are not diabetes specific) and have demonstrated acceptable levels of validity and reliability. For each measure, clinical cutoff scores that correspond to clinically significant and diagnosable depression have been developed and validated in psychiatric samples (Radloff 1977, Beck 1996, Kroenke 2001). The BDI has been specifically validated for use in patients with type 1 diabetes (T1D) and type 2 diabetes (T2D) (Lustman 1997a). It should be noted that the BDI-II and PHQ-9 gather specific information about suicidal ideation and/or intent and plan. These measures should be used in a setting where patient responses can be evaluated by providers immediately following completion and where follow-up evaluation of risk of self-harm and referral are available.

      Psychiatric interview protocols available for the assessment of depression range from semi-structured interviews such as the Schedule for Affective Disorders and Schizophrenia-Lifetime Version (SADS-L) and Structured Clinical Interview for the DSM-IV-TR (SCID) (Spitzer 1992, Williams 1992) to structured interviews such as the Composite International Diagnostic Interview (CIDI) (Robins 1988) and the Diagnostic Interview Schedule (DIS) (Helzer 1988) that can be administered and scored through computer interface (Erdman 1992). The DIS has been validated for use in patients with T1D and T2D (Lustman 1986). These interview protocols require expert training in psychopathology and interview assessment. A clinician version of the SCID (Spitzer 1992, Williams 1992) is available; however, these interviews are more commonly used in the context of clinical research protocols.

      Two measures have been created to measure diabetes-related distress: the Problem Areas in Diabetes (PAID) and Diabetes Distress Scale (DDS) (Welch 1997, Polonsky 2005, Fisher 2007). These measures show some shared variance with self-report depression questionnaires (Fisher 2007) as well as unique variance (Welch 1997, Hermanns 2006).

       Prevalence of Comorbid Depression and Diabetes

      The majority of studies have examined cross-sectional rates of MDD and/or depressive symptoms in samples diagnosed with T1D and T2D. Meta-analyses of the literature of prevalence rates of depression or depressive symptoms in patients with T1D have shown increased rates of depression in diabetes samples compared with nondiabetic control subjects (21.6 T1D vs. 11.4% nondiabetic) (Anderson 2001, Barnard 2006, Shaban 2006). Similarly, meta-analyses conducted on studies of depression in people with T2D have found increased rates of depression compared with nondiabetic control subjects (27 vs. 17.6%) (Anderson 2001, Ali 2006). Depression assessment methods and thresholds vary considerably in this literature as do rates of MDD and depressive symptoms (e.g., psychiatric interview protocols yield an average rate of depression of 11% compared with 31% in those using self-report questionnaires) (Anderson 2001). Psychiatric interviews provide greater diagnostic precision, and therefore lower prevalence rates, by permitting interviewers to determine the timing, origins, and alternative diagnostic explanations for individual depressive symptoms that may be endorsed by the patient (e.g., expectable bereavement vs. major depressive disorder). These distinctions are not made in self-report measures, so depressive symptoms attributable to any cause may be reported by respondents.

      Overall, rates of depression among patients with T1D and T2D are ~2 times greater than those in the general population (Anderson 2001) (see one exception: Pouwer 2003). Women with diabetes are 1.6 times more likely to report depressive symptoms than their male counterparts with diabetes, with one study finding a stronger association among younger women (<40 years) (Anderson 2001, Zhao 2006). Rates of depression among men with T1D have been shown to exceed those in nondiabetic comparison samples (Barnard 2006, Shaban 2006). The majority of studies have been conducted with white, middle-class samples; however, rates of depressive symptoms do not appear to vary considerably across diverse racial, ethnic, or international samples (Gary 2000, Grandinetti 2000, Fisher 2001, Roy 2001, de Groot 2006, Wagner 2006, Asghar 2007, de Groot 2007). Few studies have used well-controlled prospective designs.

      Well-controlled prospective longitudinal studies of the psychological characteristics of children and adolescents with T1D have shown mixed findings with regard to elevated rates of comorbid depression. Some studies have observed elevated rates (Kokkonen 1995, Kovacs 1997, Grey 2002), whereas others observed no differences in rates of depression compared to healthy control subjects (Jacobson 1997b). In one study, women with diabetes showed greater risk for depression recurrence than males with diabetes or psychiatric counterparts (Kovacs 1997). In a sample of youth (ages 10–21 years), men with T2D showed greater risk of self-reported depressive symptoms compared with men with T1D (Lawrence 2006). Depressive symptoms appear to increase the risk for worsened glycemic control, earlier-onset diabetic retinopathy, and increased adolescent hospitalizations and emergency department visits (Kovacs 1995, Stewart 2005, Lawrence 2006).

      Few studies have examined the naturalistic course of depression in adults with T1D and T2D. Depressive symptoms and affective disorders have been found to be highly persistent (e.g., 73–79% remain depressed) in prospective longitudinal investigations over 1–5 years follow-up (Lustman 1988, Peyrot 1999) with or without treatment. For example, a 5-year follow-up of patients enrolled in an 8-week antidepressant treatment trial found that 92% of patients experienced persistent or recurrent MDD, with 58% experiencing recurrence within 12 months of treatment (Lustman 1997c).

       Impact of Depression on Diabetes and Psychosocial Outcomes

      Depression has been found to be associated with worsened glycemic control and diabetes complications in diagnosed T1D and T2D samples. In a meta-analysis of 25 cross-sectional studies, small-to-medium effect sizes in the relationship between hyperglycemia and depressive symptoms were observed (Lustman 2000a). Recent cross-sectional studies have mirrored this finding among Hispanic adults (Gross 2004), children with T1D (Stewart 2005), and postmenopausal women with a lifetime history of MDD (Wagner 2007b). Prospective studies of changes in depressive symptoms have not shown depression to predict changes in glycemic control among ethnically diverse middle-age and older adults (Gary 2005, Trief 2006). Adherence to self-care behaviors does not appear to be a mediator between depressive symptoms and glycemic control among adults with T1D and T2D (Lustman 2005). A meta-analysis of 27 studies found medium effect sizes in the association between depression and worsened long-term diabetes complications (e.g., macrovascular disease, neuropathy, nephropathy, retinopathy, microvascular disease) in both T1D and T2D samples (de Groot 2001, Clouse 2003). Recent work examining the relationship of depression and diabetic neuropathy is consistent with these findings (Vileikyte 2005).

      There is accumulating evidence for negative outcomes associated with comorbid depression including:

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