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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We examined whether the association of regional fat distribution with stress, defined in terms of vital exhaustion, and depression varies according to the total amount of body fat accumulation in healthy middle-aged men (n = 64). Regional fat distribution was measured using the waist-to-hip circumference ratio (WHR), and the total amount of body fat accumulation was measured using the body mass index (BMI). The results indicate that WHR in lean men was associated with characteristics contrary to those in moderately obese men. In lean men WHR tended to be associated with a high level of stress, while in moderately obese men an association was found with a low level of stress and a low level of depressive symptomatology. The present results support the suggestion that there is a difference between abdominal obesity at different degrees of generalized obesity, and they are likely to further our understanding about the differing risk for cardiovascular disorders posed by abdominal obesity in lean men compared to abdominal obesity in moderately obese men.
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PMID:Association of stress and depression with regional fat distribution in healthy middle-aged men. 773 33

This study determined the risk factors for exercise-induced silent ischemia (SI) in 281 apparently healthy volunteers aged 40 to 87 years and compared their risk factor profiles with those of 132 patients with overt coronary artery disease (CAD). SI (concordant exercise-induced asymptomatic ST-segment depression on electrocardiography and perfusion defects on tomographic thallium-201 scintigraphy) was detected in 37 of 225 men (16%), versus 2 of 56 women (4%, p < 0.05). The prevalence of SI increased with age from 6% in men aged < 55 years to 18% in men aged 55 to 70 years, and to 25% in men aged > 70 years (p < 0.001). Compared with the 118 men with concordant normal exercise electrocardiogram and thallium scan (normals), men with SI were older (p < 0.001), and had a higher waist-to-hip ratio (p < 0.005), higher plasma triglyceride levels (p < 0.001), and lower high-density lipoprotein (HDL) cholesterol levels (p < 0.001). In stepwise logistic regression analysis, age, waist-to-hip ratio, and HDL levels were independent predictors of SI in men. Compared with 108 men with overt CAD, men with SI were younger (67 +/- 2 vs 73 +/- 1 years, p < 0.001) but had similar plasma lipids and waist-to-hip ratio. Thus, older age, male gender, abdominal obesity, and reduced HDL levels--all well-established risk factors for overt CAD--were risk factors for exercise-induced SI in these asymptomatic volunteers.
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PMID:Risk factors for exercise-induced silent myocardial ischemia in healthy volunteers. 797 16

Obesity has now developed into a world-wide epidemic and is associated with large economic costs and prevalent diseases, particularly with central body fat distribution. Insulin resistance almost invariably occurs, and might be a major trigger for disease-generating mechanisms either directly or via generation of other disease precursors ("risk factors"). The hypothalamo-pituitary-adrenal (HPA) axis seems to be hypersensitive in abdominal obesity, a statement supported by increased responses to challenges from the adrenals to central regulatory centers. Furthermore, the feedback control by central glucocorticoid receptors, probably a secondary, functional consequence of an elevated HPA axis activity, because the receptor gene appears normal. Secretion of sex steroid and growth hormones is diminished, which might be consequence of elevated HPA axis activity. Hyperandrogenicity in women is probably of adrenal origin and another consequence of the sensitivity of the HPA axis. The endocrine abnormalities thus are periodically elevated cortisol and androgen (women) concentrations, as well as low secretions of gender-specific steroid and growth hormones. Since elevated cortisol, and low sex-steroid and growth hormone secretions, probably direct storage fat to visceral depots, the multiple endocrine abnormalities probably cause enlargement of these depots. Furthermore, these hormonal abnormalities most likely at least contribute to the creation of insulin resistance with additional effects of elevated fatty acids from central fat depots, which are sensitive to lipid mobilization agents. This chain of events indicates the central role of the hypersensitive HPA axis. Known causes of sensitization of this axis have been identified in subjects with abdominal obesity, including depression, anxiety, alcohol, and smoking. A common cause of HPA axis activation is perceived stress, with a depressive, defeatist, or "helplessness" reaction. In subjects with abdominal preponderance of body fat stores a number of psychosocial and socioeconomics handicaps have been identified, hypothetically predisposing to such reactions. In a primate model (monkeys), mild psychosocial stress is followed by identical psychological, endocrine, anthropometric, and metabolic abnormalities as in humans with abdominal preponderance of body fat stores, including early signs of diabetes and cardiovascular disease. These findings strongly support the interpretation that a stress reaction activating the HPA axis is involved also in the human syndrome. Interventions with normalization of the endocrine perturbations are followed by clear improvements of the multiple abnormalities in both clinical, experimental, cellular and molecular studies, suggesting that the pathogenesis of abdominal preponderance of body fat and its endocrine, anthropometric and metabolic abnormalities are indeed consequences of the endocrine abnormalities identified.
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PMID:Body fat distribution, insulin resistance, and metabolic diseases. 929 93

Abdominal obesity, anxiety, and depression have been found to cluster in several studies. To further characterize these associations, the following study was performed. In a population of 51-year-old men (N = 284), measurements of obesity (body mass index [BMI]) and body fat distribution (waist to hip ratio [WHR] and sagittal trunk recumbent diameter [D]) were analyzed in relation to dexamethasone (0.5 mg) inhibition of cortisol secretion, measured as salivary cortisol. Symptoms of anxiety and depression were defined by a validated questionnaire. Furthermore, testosterone, insulin-like growth factor-I (IGF-I), insulin, glucose, and serum lipid levels were measured. Twenty-five men (8.8%) had symptoms of anxiety and depression. BMI, WHR, and D correlated negatively with testosterone, except for BMI in the anxio-depressive (ADP) group. IGF-I showed no significant relationship. Furthermore, fasting insulin and the insulin to glucose ratio correlated positively and high-density lipoprotein (HDL) cholesterol correlated negatively with BMI, WHR, and D in the total study population and in the subgroups. Total and low-density lipoprotein (LDL) cholesterol showed no significant relationships. Correlation coefficients tended to be higher in ADP men. Dexamethasone inhibition showed a negative significant relationship with BMI (rho = -.47, P = .025), WHR (borderline, rho = -.37, P = .086), and D (rho = -.43, P = .046) only in the ADP group. Comparing the ADP group versus the group without anxio-depression (ADO) and high or low BMI (P = .008), WHR (P = .026), and D (P = .012) showed blunted dexamethasone inhibition only in ADP men with high anthropometric measurements. These findings suggest there is a subgroup with elevated BMI, WHR, and D in whom a blunted dexamethasone response is found associated with traits of anxiety and depression, conditions characterized by such an abnormality. The reason for the association might be insufficient control of cortisol secretion, followed by visceral fat accumulation.
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PMID:Endocrine and metabolic aberrations in men with abdominal obesity in relation to anxio-depressive infirmity. 978 19

The pathophysiology of abdominal obesity is unclear and controversial. Recent evidence now suggests that inadequate cortisol secretion is associated with abnormalities in glucose, insulin and lipid metabolism, including hypertension, bringing the importance of the hypothalamic-pituitary-adrenal (HPA) axis in the pathogenesis of abdominal obesity to the forefront. In addition, abnormal gonadal steroid concentrations and impaired plasma growth hormone levels accompany the abdominally obese state. Since the reproductive and growth axes are inhibited at many levels by various components of the HPA axis, increasing cortisol levels results in further depression of testosterone and growth hormone concentrations. Over the last decade, antidepressant (serotoninergic) drugs have proved useful as equalizers of HPA axis hyperactivity. Such therapy may interrupt the vicious circle of a hyperactive HPA axis leading to increasing abdominal obesity and endocrine perturbations that, in turn, leads to progressive accumulation of abdominal fat. Additionally, preliminary results indicate that serotoninergic agents decrease abdominal fat mass with improvements in related risk factors.
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PMID:The role of antidepressants in the treatment of abdominal obesity. 1086 53

We have previously shown that women with abdominal body fat distribution (A-BFD) have a hyperactive hypothalamic-pituitary-adrenal (HPA) axis. However, we did not consider the presence of anxiety and/or depression, common manifestations in obese subjects. Anxiety and depression may be associated with oversecretion of cortisol and could represent a confounding factor in the evaluation of the HPA axis in different obesity phenotypes. In this study nondepressed obese women with abdominal and peripheral (P-BFD) body fat distribution and a control lean group underwent a CRH/AVP stimulation test for ACTH and cortisol determinations. Moreover, all women underwent metabolic evaluation and had their urinary free cortisol (UFC) excretion measured. After the stimuli, ACTH and cortisol responded more in the A-BFD than in the P-BFD and control groups. A positive correlation was found between either ACTH area under the curve (r2 = 0.366; P = 0.003) or cortisol area under the curve (r2 = 0.378; P = 0.043) and the homeostasis insulin resistance index in all obese patients. Unexpectedly, A-BFD had significantly lower UFC per m2 values than P-BFD (P < 0.05). Lowered UFC excretion in the A-BFD group is in keeping with an increased cortisol clearance, which, in turn, may lead to HPA axis hyperactivity as an appropriate compensatory mechanism. On the other hand, other mechanisms, possibly central in origin, such as overdriving of the CRH-ACTH system to chronic environmental stress factors, may be involved in determining HPA overresponsiveness in abdominal obesity. In conclusion, this study suggests that women with the abdominal obesity phenotype are characterized by both central and peripheral alterations of the HPA axis activity.
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PMID:Abnormalities of the hypothalamic-pituitary-adrenal axis in nondepressed women with abdominal obesity and relations with insulin resistance: evidence for a central and a peripheral alteration. 1109 38

Women suffer more often from depression than males, indicating that hormones might be involved in the etiology of this disease. Low as well as high testosterone (T) levels are related to depression and well-being in women, T plasma levels correlate to depression in a parabolic curve: at about 0.4-0.6 ng/ml plasma free T a minimum of depression is detected. Lower levels are related to depression, osteoporosis, declining libido, dyspareunia and an increase in total body fat mass. Androgen levels in women decrease continuously to about 50% before menopause compared to a 20-year-old women. Androgen levels even decline 70% within 24 h when women undergo surgical removal of the ovaries. Conventional oral contraception or HRT cause a decline in androgens because of higher levels of SHBG. Hyperandrogenic states exist, like hirsutism, acne and polycystic ovary syndrome. Social research suggests high androgen levels cause aggressive behavior in men and women and as a consequence may cause depression. Higher androgen values are more pronounced at young ages and before and after delivery of a baby and might be responsible for the "baby blues". It was found that depression in pubertal girls correlated best with an increase in T levels in contrast to the common belief that "environmental factors" during the time of growing up might be responsible for emotional "up and downs". T replacement therapy might be useful in perimenopausal women suffering from hip obesity, also named gynoid obesity. Abdominal obesity in men and women is linked to type 2 diabetes and coronary heart diseases. Testosterone replacement therapy in hypoandrogenic postmenopausal women might not only protect against obesity but also reduce the risk of developing these diseases. Antiandrogenic progestins might be useful for women suffering from hyperandrogenic state in peri- and postmenopause. Individual dosing schemes balancing side effects and beneficial effects are absolutely necessary. Substantial interindividual variability in T plasma values exists, making it difficult to utilize them for diagnostic purposes. Therefore a "four-level-hormone classification scheme" was developed identifying when estradiol (E) and T levels are out of balance. (1) Low E-low T levels are correlated with osteoporosis, depression, and obesity; (2) high E-low T with obesity, decreased libido; (3) high T-low E levels with aggression, depression, increased libido, and substance abuse; (4) high E-high T with type II diabetes risk, breast cancer and cardiovascular risk. Testosterone delivery systems are needed where beneficial and negative effects can be balanced. Any woman diagnosed for osteoporosis should be questioned for symptoms of depression.
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PMID:The impact of testosterone imbalance on depression and women's health. 1195 93

Obesity and starvation have opposing affects on normal physiology and are associated with adaptive changes in hormone secretion. The effects of obesity and starvation on thyroid hormone, GH, and cortisol secretion are summarized in Table 1. Although hypothyroidism is associated with some weight gain, surveys of obese individuals show that less than 10% are hypothyroid. Discrepancies have been reported in some studies, but in untreated obesity, total and free T4, total and free T3, TSH levels, and the TSH response to TRH are normal. Some reports suggest an increase in total T3 and decrease in rT3 induced by overfeeding. Treatment of obesity with hypocaloric diets causes changes in thyroid function that resemble sick euthyroid syndrome. Changes consist of a decrease in total T4 and total and free T3 with a corresponding increase in rT3. untreated obesity is also associated with low GH levels; however, levels of IGF-1 are normal. GH-binding protein levels are increased and the GH response to GHRH is decreased. These changes are reversed by drastic weight reduction. Cortisol levels are abnormal in people with abdominal obesity who exhibit an increase in urinary free cortisol but exhibit normal or decreased serum cortisol and normal ACTH levels. These changes are explained by an increase in cortisol clearance. There is also an increased response to CRH. Treatment of obesity with very low calorie diets causes a decrease in serum cortisol explained by a decrease in cortisol-binding proteins. The increase in cortisol secretion seen in patients with abdominal obesity may contribute to the metabolic syndrome (insulin resistance, glucose intolerance, dyslipidemia, and hypertension). States of chronic starvation such as seen in anorexia nervosa are also associated with changes in thyroid hormone, GH, and cortisol secretion. There is a decrease in total and free T4 and T3, and an increase in rT3 similar to findings in sick euthyroid syndrome. The TSH response to TRH is diminished and, in severe cases, thyroid-binding protein levels are decreased. In regards to GH, there is an increase in GH secretion with a decrease in IGF-1 levels. GH responses to GHRH are increased. The [table: see text] changes in cortisol secretion in patients with anorexia nervosa resemble depression. They present with increased urinary free cortisol and serum cortisol levels but without changes in ACTH levels. In contrast to the findings observed in obesity, the ACTH response to CRH is suppressed, suggesting an increased secretion of CRH. The endocrine changes observed in obesity and starvation may complicate the diagnosis of primary endocrine diseases. The increase in cortisol secretion in obesity needs to be distinguished from Cushing's syndrome, the decrease in thyroid hormone levels in anorexia nervosa needs to be distinguished from secondary hypothyroidism, and the increase in cortisol secretion observed in anorexia nervosa requires a differential diagnosis with primary depressive disorder.
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PMID:Effect of obesity and starvation on thyroid hormone, growth hormone, and cortisol secretion. 1205 88

'Stress' embraces the reaction to a multitude of poorly defined factors that disturb homeostasis or allostasis. In this overview, the activation of the hypothalamic-pituitary-adrenal (HPA) axis and the sympathetic nervous system have been utilized as objective measurements of stress reactions. Although long-term activation of the sympathetic nervous system is followed by primary hypertension, consequences of similar activation of the HPA axis have not been clearly defined. The focus of this overview is to examine whether or not repeated activation of these two stress centres may be involved in the pathogenesis of abdominal obesity and its comorbidities. In population studies adrenal hormones show strong statistical associations to centralization of body fat as well as to obesity. There is considerable evidence from clinical to cellular and molecular studies that elevated cortisol, particularly when combined with secondary inhibition of sex steroids and growth hormone secretions, is causing accumulation of fat in visceral adipose tissues as well as metabolic abnormalities (The Metabolic Syndrome). Hypertension is probably due to a parallel activation of the central sympathetic nervous system. Depression and 'the small baby syndrome' as well as stress exposure in men and non-human primates are followed with time by similar central and peripheral abnormalities. Glucocorticoid exposure is also followed by increased food intake and 'leptin resistant' obesity, perhaps disrupting the balance between leptin and neuropeptide Y to the advantage of the latter. The consequence might be 'stress-eating', which, however, is a poorly defined entity. Factors activating the stress centres in humans include psychosocial and socioeconomic handicaps, depressive and anxiety traits, alcohol and smoking, with some differences in profile between personalities and genders. Polymorphisms have been defined in several genes associated with the cascade of events along the stress axes. Based on this evidence it is suggested that environmental, perinatal and genetic factors induce neuroendocrine perturbations followed by abdominal obesity with its associated comorbidities.
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PMID:Do stress reactions cause abdominal obesity and comorbidities? 1211 65

Depression is associated with an increased risk of developing cardiovascular disease and type 2 diabetes mellitus. Abdominal obesity is also a high risk factor for these diseases. Therefore, symptoms of depression and anxiety were examined in relation to abdominal obesity. A total of 59 middle-aged men volunteered for measurements with the Hamilton Depression Scale (HDS), the Montgomery-Asberg Depression Rating Scale (MADRS), the Beck Depression Inventory (BDI) and the Hamilton Anxiety Scale (HAS). These results were examined in relation to body mass index (BMI), waist/hip ratio (WHR) and sagittal abdominal diameter, a measurement of intra-abdominal fat mass, and metabolic variables. Men with WHR>1.0 (n=26) in comparison with men with normal WHR (<1.0, n=33) showed significantly higher sum scores in all the scales used. There were positive correlations between the sum scores of all the depression scales and the WHR or the sagittal abdominal diameter. BMI correlated comparatively weakly only with the HDS. The correlations with the WHR remained when the influence of BMI was eliminated, suggesting that obesity is less involved than centralization of body fat. Insulin and glucose were significantly related to the HDS. Morning cortisol levels were negatively related to the BDI and (borderline) to the MADRS, suggesting perturbations of the regulation of the hypothalamic-pituitary-adrenal axis. We conclude that men with abdominal obesity have symptoms of depression and anxiety.
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PMID:Depression and anxiety symptoms in relation to anthropometry and metabolism in men. 1242 56


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