nificant decrease in perceived self-compe- arrythmogenic in patients with established tence. heart disease (Goldstein, 1995). This may ac-There is growing evidence that the physio-count for the fact that heart disease patients logical changes associated with depression who suffer from depression are more likely may also contribute heightened risk for pre-have died a cardiac death at 6-to 18-month mature physical morbidity (Vaillant, Orav, follow-up than are their nondepressed coun-Meyer, McCullough Vaillant, Ta-and mortality (Barefoot Shapiro, 1998). Cor-Winokur, Chang, Cooper-Patrick, Wang, & Klag, 1998; of insulin stimulate accumulation of visceral Glassman & Shapiro, 1998; Lee & Murray, fat, a highly metabolically active tissue that 1988; Murphy, Monson, Olivier, Sobol, & exerts profound effects on lipid metabolism, Leighton, 1987). In particular, it has been sug-coagulation, inflammation, and blood pres-gested that prolonged and recurrent dysreg-sure regulation. Decreased levels of growth ulation of the endocrine system that is associ-hormone and sex steroids, which have been ated with depression may play a role in the found among patients with melancholic de-development of medical illnesses such as os-pression, also lead to increased visceral fat de-teoporosis and heart disease (Barefoot Schroll, 1996; Chrousos & Gold, 1998; Glass- itself, significantly increases the risk of car-man part by leading to a loss of 1999). Hippisley-Cox, Fielding, and Pringle cardiac mass. Finally, excessive visceral fat (1998) showed that men with a history of de-leads increased secretion of PAI-l, a potent pression were 3 times more likely than age-inhibitor of clot dissolution and increased en-matched controls develop heart disease, dothelial inflammation, presumably accelerat-even when smoking controlled for. Glass-ing atherosclerosis (Reaven, 1995). man and Shapiro (1998) reported that, after In recent years, there have been a handful controlling for potentially mediating risk fac-of studies that have looked at the relation be-tors, men and women with depressive symp-tween depression and osteoporosis. Michel-tomatology were still more likely to develop son, Stratakis, Hill, Reynolds, Galliven, heart disease. Similarly, a prospective study Chrousos, and Gold (1996) demonstrated that by Anda, Williamson, Jones, Macera, Eaker, women with current or a past history of de-Glassman, and Marks (1993) showed that in-pression had reduced bone mineral density. dividuals with depressed affect or hopeless-More recently, Coelho, Silva, Maia, Prata, ness were at risk for heart disease after con-and Barros (1999) found higher rates of de-trolling for socioeconomic status, alcohol use, pression among women with osteoporosis, preexisting physical illness, and smoking. even after controlling for risk factors such However, there was evidence that smoking in-age, menopause, hyperthyroidism, calcium creased the risk for developing heart disease imbalance, alcoholism, smoking, anorexia among depressed persons. nervosa, drugs, diet, sunshine exposure, and Endocrine changes associated with melan-immobility. The cause of premature osteopo-cholic depression may partly account for its rosis patients with major depression has not association with heart disease. Hypersecretion been definitively determined. However, hy-of insulin triggers chronic SNS activation percortisolism has been associated with bone (Reaven, 1995), which profoundly deleteri-loss (Michelson ous to cardiac well-being. Excessive SNS ), and steroid-induced bone loss in activation increases heart rate and blood pres-patients receiving glucocorticoid treatment is sure and has an independent effect on decreas-well recognized (Lukert ing left ventricular compliance, a risk factor may be that steroids decrease bone formation for congestive heart failure (Gold sos, 1999). Moreover, increased NE secretion effects seem to be most pronounced in areas

DOI link for nificant decrease in perceived self-compe- arrythmogenic in patients with established tence. heart disease (Goldstein, 1995). This may ac-There is growing evidence that the physio-count for the fact that heart disease patients logical changes associated with depression who suffer from depression are more likely may also contribute heightened risk for pre-have died a cardiac death at 6-to 18-month mature physical morbidity (Vaillant, Orav, follow-up than are their nondepressed coun-Meyer, McCullough Vaillant, Ta-and mortality (Barefoot Shapiro, 1998). Cor-Winokur, Chang, Cooper-Patrick, Wang, & Klag, 1998; of insulin stimulate accumulation of visceral Glassman & Shapiro, 1998; Lee & Murray, fat, a highly metabolically active tissue that 1988; Murphy, Monson, Olivier, Sobol, & exerts profound effects on lipid metabolism, Leighton, 1987). In particular, it has been sug-coagulation, inflammation, and blood pres-gested that prolonged and recurrent dysreg-sure regulation. Decreased levels of growth ulation of the endocrine system that is associ-hormone and sex steroids, which have been ated with depression may play a role in the found among patients with melancholic de-development of medical illnesses such as os-pression, also lead to increased visceral fat de-teoporosis and heart disease (Barefoot Schroll, 1996; Chrousos & Gold, 1998; Glass- itself, significantly increases the risk of car-man part by leading to a loss of 1999). Hippisley-Cox, Fielding, and Pringle cardiac mass. Finally, excessive visceral fat (1998) showed that men with a history of de-leads increased secretion of PAI-l, a potent pression were 3 times more likely than age-inhibitor of clot dissolution and increased en-matched controls develop heart disease, dothelial inflammation, presumably accelerat-even when smoking controlled for. Glass-ing atherosclerosis (Reaven, 1995). man and Shapiro (1998) reported that, after In recent years, there have been a handful controlling for potentially mediating risk fac-of studies that have looked at the relation be-tors, men and women with depressive symp-tween depression and osteoporosis. Michel-tomatology were still more likely to develop son, Stratakis, Hill, Reynolds, Galliven, heart disease. Similarly, a prospective study Chrousos, and Gold (1996) demonstrated that by Anda, Williamson, Jones, Macera, Eaker, women with current or a past history of de-Glassman, and Marks (1993) showed that in-pression had reduced bone mineral density. dividuals with depressed affect or hopeless-More recently, Coelho, Silva, Maia, Prata, ness were at risk for heart disease after con-and Barros (1999) found higher rates of de-trolling for socioeconomic status, alcohol use, pression among women with osteoporosis, preexisting physical illness, and smoking. even after controlling for risk factors such However, there was evidence that smoking in-age, menopause, hyperthyroidism, calcium creased the risk for developing heart disease imbalance, alcoholism, smoking, anorexia among depressed persons. nervosa, drugs, diet, sunshine exposure, and Endocrine changes associated with melan-immobility. The cause of premature osteopo-cholic depression may partly account for its rosis patients with major depression has not association with heart disease. Hypersecretion been definitively determined. However, hy-of insulin triggers chronic SNS activation percortisolism has been associated with bone (Reaven, 1995), which profoundly deleteri-loss (Michelson ous to cardiac well-being. Excessive SNS ), and steroid-induced bone loss in activation increases heart rate and blood pres-patients receiving glucocorticoid treatment is sure and has an independent effect on decreas-well recognized (Lukert ing left ventricular compliance, a risk factor may be that steroids decrease bone formation for congestive heart failure (Gold sos, 1999). Moreover, increased NE secretion effects seem to be most pronounced in areas

nificant decrease in perceived self-compe- arrythmogenic in patients with established tence. heart disease (Goldstein, 1995). This may ac-There is growing evidence that the physio-count for the fact that heart disease patients logical changes associated with depression who suffer from depression are more likely may also contribute heightened risk for pre-have died a cardiac death at 6-to 18-month mature physical morbidity (Vaillant, Orav, follow-up than are their nondepressed coun-Meyer, McCullough Vaillant, Ta-and mortality (Barefoot Shapiro, 1998). Cor-Winokur, Chang, Cooper-Patrick, Wang, & Klag, 1998; of insulin stimulate accumulation of visceral Glassman & Shapiro, 1998; Lee & Murray, fat, a highly metabolically active tissue that 1988; Murphy, Monson, Olivier, Sobol, & exerts profound effects on lipid metabolism, Leighton, 1987). In particular, it has been sug-coagulation, inflammation, and blood pres-gested that prolonged and recurrent dysreg-sure regulation. Decreased levels of growth ulation of the endocrine system that is associ-hormone and sex steroids, which have been ated with depression may play a role in the found among patients with melancholic de-development of medical illnesses such as os-pression, also lead to increased visceral fat de-teoporosis and heart disease (Barefoot Schroll, 1996; Chrousos & Gold, 1998; Glass- itself, significantly increases the risk of car-man part by leading to a loss of 1999). Hippisley-Cox, Fielding, and Pringle cardiac mass. Finally, excessive visceral fat (1998) showed that men with a history of de-leads increased secretion of PAI-l, a potent pression were 3 times more likely than age-inhibitor of clot dissolution and increased en-matched controls develop heart disease, dothelial inflammation, presumably accelerat-even when smoking controlled for. Glass-ing atherosclerosis (Reaven, 1995). man and Shapiro (1998) reported that, after In recent years, there have been a handful controlling for potentially mediating risk fac-of studies that have looked at the relation be-tors, men and women with depressive symp-tween depression and osteoporosis. Michel-tomatology were still more likely to develop son, Stratakis, Hill, Reynolds, Galliven, heart disease. Similarly, a prospective study Chrousos, and Gold (1996) demonstrated that by Anda, Williamson, Jones, Macera, Eaker, women with current or a past history of de-Glassman, and Marks (1993) showed that in-pression had reduced bone mineral density. dividuals with depressed affect or hopeless-More recently, Coelho, Silva, Maia, Prata, ness were at risk for heart disease after con-and Barros (1999) found higher rates of de-trolling for socioeconomic status, alcohol use, pression among women with osteoporosis, preexisting physical illness, and smoking. even after controlling for risk factors such However, there was evidence that smoking in-age, menopause, hyperthyroidism, calcium creased the risk for developing heart disease imbalance, alcoholism, smoking, anorexia among depressed persons. nervosa, drugs, diet, sunshine exposure, and Endocrine changes associated with melan-immobility. The cause of premature osteopo-cholic depression may partly account for its rosis patients with major depression has not association with heart disease. Hypersecretion been definitively determined. However, hy-of insulin triggers chronic SNS activation percortisolism has been associated with bone (Reaven, 1995), which profoundly deleteri-loss (Michelson ous to cardiac well-being. Excessive SNS ), and steroid-induced bone loss in activation increases heart rate and blood pres-patients receiving glucocorticoid treatment is sure and has an independent effect on decreas-well recognized (Lukert ing left ventricular compliance, a risk factor may be that steroids decrease bone formation for congestive heart failure (Gold sos, 1999). Moreover, increased NE secretion effects seem to be most pronounced in areas