Supporting autonomy to motivate patients with diabetes for glucose control.

OBJECTIVE: We applied the self-determination theory of human motivation to examine whether patient perceptions of autonomy supportiveness (i.e., patient centeredness) from their diabetes care providers related to improved glucose control over a 12-month period. RESEARCH DESIGN AND METHODS: We conducted a prospective cohort study of patients with diabetes from a diabetes treatment center at a university-affiliated community hospital. Participants were 128 patients between 18 and 80 years of age who took medication for diabetes, had no other major medical illnesses, and were responsible for monitoring their glucose and taking their medications. The main outcome measure was a change in HbA1c values over the 12 months of the study RESULTS: Patient perception of autonomy support from a health care provider related to a change in HbA1c values at 12 months (P < 0.05). Further analyses showed that perceived autonomy support from the staff related to significant increases in patient autonomous motivation at 12 months (P < 0.05); that increases in autonomous motivation related to significant increases in perceived competence (P < 0.05); and that increases in a patient's perceived competence related to significant reductions in their HbA1c values over 12 months (P < 0.001). CONCLUSIONS: The findings support the prediction of the self-determination theory that patients with diabetes whose health care providers are autonomy supportive will become more motivated to regulate their glucose levels, feel more able to regulate their glucose, and show improvements in their HbA1c values.

Motivational predictors of weight loss and weight-loss maintenance.

Self-determination theory proposes that behavior change will occur and persist if it is autonomously motivated. Autonomous motivation for a behavior is theorized to be a function both of individual differences in the autonomy orientation from the General Causality Orientations Scale and of the degree of autonomy supportiveness of relevant social contexts. We tested the theory with 128 patients in a 6-month, very-low-calorie weight-loss program with a 23-month follow-up. Analyses confirmed the predictions that (a) participants whose motivation for weight loss was more autonomous would attend the program more regularly, lose more weight during the program, and evidence greater maintained weight loss at follow-up, and (b) participants' autonomous motivation for weight loss would be predicted both by their autonomy orientation and by the perceived autonomy supportiveness of the interpersonal climate created by the health-care staff.

Insulinopenic diabetes after rodenticide (Vacor) ingestion: a unique model of acquired diabetes in man.

A clinical syndrome, characterized by acute diabetic ketoacidosis associated with a toxic neuropathy, developed in five men who intentionally ingested a recently introduced rodenticide (Vacor) containing N-3-pyridylmethyl-N'-p-nitrophenyl urea (RH-787). A 7-yr-old boy, who accidentally ingested this poison, died within 14 h. Marked insulinopenia, without a reduction in glucagon levels, suggested a specific beta-cytotoxic effect, which was supported after autopsy in three cases by histopathologic evidence of extensive beta cell destruction. Lethal effects in rats prevented investigation of RH-787's diabetogenicity in vivo; however, studies in isolated rat islets confirmed a direct inhibitory effect, which was prevented by concomitant incubation with nicotinamide, suggesting a mechanism of action similar to that of streptozotocin. We detected islet cell-surface antibodies in two of four patients studied. These findings indicate that this nongenetic, acquired form of insulinopenic diabetes, which has persisted in the surviving patients for up to 3 yr, presents a unique opportunity to test in man the concept that hyperglycemia and the accompanying metabolic consequences of insulinopenia can induced diabetic microangiopathy in the absence of genetic predisposition.

Islet-cell-surface antibodies in juvenile diabetes mellitus.

Using an indirect immunofluorescence test on suspensions of viable, insulin-producing islet cells from rats, we found that 32 per cent (28/88) of insulin-treated patients with juvenile diabetes have islet-cell-surface antibodies in their circulation. These antibodies also occurred in four of nine children with glucose intolerance, in one of 24 healthy children and in nondiabetic children with thyroid disorders. In the diabetic children, the immunofluorescent reaction was inhibited by preadsorption of serum to islet cells but was little affected by preadsorption to rat hepatocytes or erythrocytes or to acetone powders of various rat tissues, including pancreas. These results show that organ-specific, nonspecies-specific antibodies reactive with the cell surface of the islet cells can be present in serum from diabetic children, and provide an approach to investigation of immunopathological aspects of diabetes mellitus.