Prolonged stress has long been shown to have major effects on the development of both type of diabetes mellitus, Type 1 and Type 2. Type 1 diabetes is an autoimmune disease that is characterized by the immune system attacking self-antigens. There is a failure or breakdown in immunological tolerance to allow this to happen. Prolonged physical or emotional stress can activate the hypothalamus-pituitary-adrenal (HPA) axis to induce production of the stress hormone glucocorticoid, causing abrupt thymus involution and result in escape of autoreactive T- cells. Though regulatory T-cells (Treg) are present in the circulation, they are unable to suppress the autoreative T-cells from initiating the destruction of -cells and the subsequent development of Type 1 diabetes. Stress also causes metabolic disturbances, including altered hepatic glucose metabolism, increased peripheral insulin resistance and hyperglycemia. Glucocorticoid is the potential contributor to the chronic hyperglycemia that results in insulin resistance and -cell dysfunction via the generation of oxidative stress which ultimately leads to the development of Type 2 diabetes."

Psychological stress has extreme adverse consequences on health. However, the molecular mechanisms that mediate and accelerate the process of aging due to stress hormone are not well defined. This review has focused on diverse molecular paths that come out in response to chronic psychological stress via releasing of excessive glucocorticoids (GCs), involved in the aging process. GCs suppress transcription of nuclear cell adhesion molecules which impair synaptic plasticity, memory formation, and cognitive ability. Again, GCs promote muscle atrophy by means of motivating ubiquitin proteasome system and can repress muscle protein synthesis by inhibition of PI3-kinase/Akt pathway. GCs also inhibit interleukin-2 synthesis through suppressing T cell receptor signal that leads to loss of T cell activation, proliferation, and B-cell activation. Moreover, GCs increase the expression of collagenase-3, RANK ligand, and colony stimulating factor-1 that induce bone resorption. In general, stress-induced GCs can play causal role for aging and age-related disorders.

Chronic Psychological stress has several adverse effects both on HIV- people and on HIV+ patient. When the HIV- people are concerned, stress makes them more susceptible to HIV infection. T-cells have CXCR4 receptor and Macrophage have CCR5 receptor which can bind with both glucocorticoid and catecholamine hormone. HIV has GP120 protein which has to bind with both CD4 and CXCR4/CCR5 receptor for its entry into the host cells. Mental stress increases glucocorticoid and catecholamine concentration in blood. When these stress hormones, glucocorticoid and catecholamine, bind with the CXCR4/CCR5 receptors, cAMP signaling pathway gets activated. This signal transduction pathway leads to the synthesis of more CXCR4 and CCR5 receptors by those cells, which in turn become more susceptible to HIV infection. Stress inhibits Th2 when the cell produces INF- as a response to viral attacks. So that other cells remain vulnerable to viral infection. When T-cell count is decreased in the blood, the body cannot protect itself from other opportunistic infectious pathogens. As a result progression of AIDS is increased."