OBJECTIVE -The purpose of this study was to describe the development of the Diabetes Distress Scale (DDS), a new instrument for the assessment of diabetes-related emotional distress, based on four independent patient samples.RESEARCH DESIGN AND METHODS -In consultation with patients and professionals from multiple disciplines, a preliminary scale of 28 items was developed, based a priori on four distress-related domains: emotional burden subscale, physician-related distress subscale, regimen-related distress subscale, and diabetes-related interpersonal distress. The new instrument was included in a larger battery of questionnaires used in diabetes studies at four diverse sites: waiting room at a primary care clinic (n ϭ 200), waiting room at a diabetes specialty clinic (n ϭ 179), a diabetes management study program (n ϭ 167), and an ongoing diabetes management program (n ϭ 158).RESULTS -Exploratory factor analyses revealed four factors consistent across sites (involving 17 of the 28 items) that matched the critical content domains identified earlier. The correlation between the 28-item and 17-item scales was very high (r ϭ 0.99). The mean correlation between the 17-item total score (DDS) and the four subscales was high (r ϭ 0.82), but the pattern of interscale correlations suggested that the subscales, although not totally independent, tapped into relatively different areas of diabetes-related distress. Internal reliability of the DDS and the four subscales was adequate (␣ Ͼ 0.87), and validity coefficients yielded significant linkages with the Center for Epidemiological Studies Depression Scale, meal planning, exercise, and total cholesterol. Insulin users evidenced the highest mean DDS total scores, whereas diet-controlled subjects displayed the lowest scores (P Ͻ 0.001).CONCLUSIONS -The DDS has a consistent, generalizable factor structure and good internal reliability and validity across four different clinical sites. The new instrument may serve as a valuable measure of diabetes-related emotional distress for use in research and clinical practice. Diabetes Care 28:626 -631, 2005L iving with diabetes can be tough. In the face of a complex, demanding, and often confusing set of self-care directives, patients may become frustrated, angry, overwhelmed, and/or discouraged. Diabetes-related conflict with loved ones may develop, and relationships with health care providers may become strained. The risk of depression is elevated (1,2). As a result, motivation for self-care may be impaired. To investigate the nature and breadth of such distress, a number of self-report instruments have been developed, including the ATT39 (3), Questionnaire on Stress in Patients with Diabetes-Revised (QSD-R) (4), and Problem Areas in Diabetes scale (PAID) (5). These measures aim to tap the range of emotional responses to diabetes and to serve as screening measures for clinical and research use. The PAID has been the most widely used of the measures and has been recently translated into several other languages (6 -8). PAID scores have ...

Type 1 diabetes (insulin-dependent diabetes mellitus, IDDM) is a disease controlled by the major histocompatibility complex (MHC) which results from T-cell-mediated destruction of pancreatic beta-cells. The incomplete concordance in identical twins and the presence of autoreactive T cells and autoantibodies in individuals who do not develop diabetes suggest that other abnormalities must occur in the immune system for disease to result. We therefore investigated a series of at-risk non-progressors and type 1 diabetic patients (including five identical twin/triplet sets discordant for disease). The diabetic siblings had lower frequencies of CD4-CD8- Valpha24JalphaQ+ T cells compared with their non-diabetic sibling. All 56 Valpha24JalphaQ+ clones isolated from the diabetic twins/triplets secreted only interferon (IFN)-gamma upon stimulation; in contrast, 76 of 79 clones from the at-risk non-progressors and normals secreted both interleukin (IL)-4 and IFN-gamma. Half of the at-risk non-progressors had high serum levels of IL-4 and IFN-gamma. These results support a model for IDDM in which Thl-cell-mediated tissue damage is initially regulated by Valpha24JalphaQ+ T cells producing both cytokines; the loss of their capacity to secrete IL-4 is correlated with IDDM.