| Many individuals have been found to alter various behaviors in an attempt to adapt and cope with stressors and negative affective states. These behavioral changes often include poor health practice behaviors such as increased consumption of sweets, increased consumption of alcohol, reduced exercise, and fewer hours of sleep. These same behaviors are known risk factors for insulin resistance. Release of cortisol in response to chronic stress originating from both environmental and intrapsychic sources, has been shown to have deleterious effects upon both insulin sensitivity and mood.; An index for insulin resistance was created by adding measures of risk factors for insulin resistance. Logistic and linear regression analyses examined the relationship between depression and the subject's likelihood of being insulin resistant. Subjects likely to be insulin resistant were 9% (Odds Ratio = 1.09; 95% confidence interval = 1.02 to 1.16) more likely to be depressed than subjects unlikely to be insulin resistant after controlling for stress, social support, age, gender, and diagnosis of diabetes. Subjects with the highest possible insulin resistance index score of 15 were 222% more likely to be depressed than subjects with the lowest score of 5. The subject's number of hours of sleep per night, physical activity level, and to a lesser extent, alcohol consumption contributed toward the positive association between the insulin resistance construct and depression. BMI and sweets consumption either played very little part in this association or else detracted from it.; These results are consistent with findings that individuals with diabetes and cardiovascular disease are at greater risk of suffering from depression. The relationship between depression and insulin resistance is likely to be bidirectional. Individuals suffering from depression are more apt to engage in poor health practice behaviors that are risk factors for insulin resistance. Insulin resistance can contribute toward depressed mood by impairing insulin's ability to promote brain serotonin synthesis and to suppress the reuptake of norepinephrine and by increasing the pervasiveness of hypoglycemic reactions. |