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

Asymptomatic or silent myocardial ischemia (SI) is frequent in coronary heart disease and its prognostic value is controversial. The aim of our study is to compare coronary atherosclerosis, left ventricular function and clinical out come of 110 patients with S.I. (A group) and 210 patients with stable angina (B group). The 320 patients were submitted: to symptom limited exercise stress-test with permanent electrocardiographic control by a Case 12-15 digitalized system with ST segment depression interpretation. A test was considered positive for ischemia if there was ST depression of > 1 mv in magnitude from baseline, persisting for 0.08 sec or exercise angina and ischemia: to selective coronarography by Seldinger technic, with left ventricular cineangiography in 2 incidences. A significant coronary stenosis was defined as > 50% reduction of luminal diameter; to medical treatment with betablockers (87.5% of patients), calcium inhibitors (12.5%), aspirin (90%) and nitrates; to regular medical surveillance. During the follow-up (42.4 +/- 5 months in mean) the number of deaths, myocardial infarctions, heart failure, unstable angina and revascularizations were analyzed. Patients of A group with S.I. had a high percentage of risks factors (diabetes mellitus 55%, nicotinism 85%, dyslipidemia 22.5%) and history of previous myocardial infarction in 33% of cases. There are not significant differences between severity and extension of coronary disease, or ventricular dysfunction in patients of A group or B. The percentages of deaths (2.10 versus 3%), acute myocardial infarctions (9.5 versus 8.5%), heart failures (2.72 versus 3%), surgical indications (14.7 versus 15.7%) are not significantly different between the 2 groups. In A group, 34% of patients were treated by angioplasty versus 40% of patients in group B (p < 0.02). S.I. has a bad prognostic and the clinical out come of coronary heart disease is not dependent of presence of angina during exercise testing and daily activities.
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PMID:[Prognosis of silent myocardial ischemia]. 803 89

Persons with chronic SCI have several metabolic disturbances. As a consequence of inactivity and the body compositional changes of decreased skeletal muscle with a relative increase in adiposity, a state of insulin resistance and hyperinsulinemia has been demonstrated to exist, associated with abnormalities in oral carbohydrate handling. Elevated plasma insulin levels in persons with SCI probably contribute to the cause of frequent dyslipidemia and hypertension. This constellation of metabolic changes represents an atherogenic pattern of CHD risk factors with many of the distinctive features of a cardiovascular dysmetabolic syndrome that is called syndrome X. Reduction in modifiable risk factors for CHD should decrease the occurrence of catastrophic cardiovascular events. There is evidence to suggest that endogenous anabolic hormone levels are depressed in a proportion of individuals with SCI. Depression of serum testosterone and growth hormone/IGF-I levels may exacerbate the adverse lipid and body compositional changes, reduce exercise tolerance, and have deleterious effects on quality of life. Because of immobilization, individuals with paraplegia have osteoporosis of the pelvis and lower extremities, and those with tetraplegia also have osteoporosis of the upper extremities. In addition, there is evidence to suggest that bone loss progresses with time in persons with chronic SCI. This may be caused by chronic immobilization per se or may be a consequence of adverse hormonal changes, including deficiency of anabolic hormones or deficiency of vitamin D and calcium with secondary hyperparathyroidism. Serum thyroid function abnormalities resembling the euthyroid sick "low T3 syndrome" have been reported in those with acute and chronic spinal cord injury. Depressed serum T3 and elevated rT3 in chronic SCI may be caused by associated illness. Current practice has been hesitant to treat abnormal serum thyroid chemistries associated with nonthyroidal illness. Recognition of metabolic abnormalities in individuals with SCI is vital as a first step in improving clinical care. The application of appropriate interventions to correct or ameliorate these abnormalities promises to improve longevity and quality of life in persons with SCI.
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PMID:Metabolic changes in persons after spinal cord injury. 1068 Jan 61

Obese patients are at an increased risk for developing many medical problems, including insulin resistance and type 2 diabetes mellitus, hypertension, dyslipidemia, cardiovascular disease, stroke, sleep apnea, gallbladder disease, hyperuricemia and gout, and osteoarthritis. Certain cancers are also associated with obesity, including colorectal and prostate cancer in men and endometrial, breast, and gallbladder cancer in women (1-6). Excess body weight is also associated with substantial increases in mortality from all causes, in particular, cardiovascular disease. More than 5% of the national health expenditure in the United States is directed at medical costs associated with obesity (7). In addition, certain psychologic problems, including binge-eating disorder and depression, are more common among obese persons than they are in the general population (8.9). Finally, obese individuals may suffer from social stigmatization and discrimination, and severely obese people may experience greater risk of impaired psychosocial and physical functioning, causing a negative impact on their quality of life (10).
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PMID:Obesity and its comorbid conditions. 1069 82

Obesity increases the risk of metabolic complications such as diabetes, dyslipidemia, systemic hypertension and cardiovascular disease. These are mainly responsible for the increased mortality of obese people. Other metabolic consequences of obesity are: gallstones, steatosis of the liver and the polycystic ovary syndrome. Beside the body mass index the distribution of body fat is important. Centralized obesity, as measured by the waist-to-hip circumference ratio (WHR), is associated with increased mortality and morbidity. Insulin resistance and hyperinsulinaemia seem to play a central role in the pathogenesis of this association. Obesity has not only metabolic complications. There is a relationship between obesity and impaired respiratory function. Furthermore is obesity a risk factor for osteoarthrosis of the knee, the hip and even the hand and for pulmonary embolism and venous thrombosis. Obesity can also lead to psycho-social problems such as depression, social discrimination and isolation.
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PMID:[Consequences and complications of obesity]. 1102 85

This study assessed psychosocial correlates of dyslipidemia, towards enabling improved tertiary prevention of macrovascular complications of diabetes mellitus (DM). We tested the hypothesis that psychosocial measures are related to high-density lipoprotein cholesterol (HDL-C) and triglyceride concentrations in a rural aboriginal population in British Columbia, Canada. Persons sampled were on-reserve registered Indians (n=198) with and at risk for Type 2 DM. Relationships between HDL-C and psychosocial variables were associated with glycemic status. For persons with diabetes and impaired glucose tolerance (n=44), quality of life and mastery were positively related (P<0.001), and depression inversely related (P<0.001), to HDL-C. An apparent lack of effect of behavior suggests the influence of emotional pathways involving autonomic-neuroendocrine axes. We recommend assessing mental health, and promoting mastery and diabetes quality of life through empowerment oriented diabetes management strategies, in negotiating culturally acceptable treatment of diabetic dyslipidemia for aboriginal people.
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PMID:Lipids and psychosocial status in aboriginal persons with and at risk for Type 2 diabetes: implications for tertiary prevention. 1131 42

In males, aging, health and disease are processes that occur over physiologic time and involve a cascade of hormonal, biochemical and physiological changes that accompany the down-regulation of the hypothalamic-anterior pituitary-testicular axis. As aging progresses there are relative increases of body fat and decreases in muscle mass. The increased adipose tissue mass is associated with the production of a number of newly generated factors. These include aromatase, leptin, PAI-1, insulin resistance, and the dyslipidemias, all of which can lead to tissue damage. Fatty tissue becomes the focal point for study as it represents the intersection between energy storage and mobilization. The increase in adipose tissue is associated with an increase in the enzyme aromatase that converts testosterone to estradiol and leads to diminished testosterone levels that favor the preferential deposition of visceral fat. As the total body fat mass increases, hormone resistance develops for leptin and insulin. Increasing leptin fails to prevent weight gain and the hypogonadal-obesity cycle ensues causing further visceral obesity and insulin resistance. The progressive insulin resistance leads to a high triglyceride-low HDL pattern of dyslipidemia and increased cardiovascular risk. All of these factors eventually contribute to the CHAOS Complex: coronary disease, hypertension, adult-onset diabetes mellitus, obesity and/or stroke as permanent changes unfold. Other consequences of the chronic hypogonadal state include osteopenia, extreme fatigue, depression, insomnia, loss of aggressiveness and erectile dysfunction all of which develop over variable periods of time.
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PMID:Aromatase, adiposity, aging and disease. The hypogonadal-metabolic-atherogenic-disease and aging connection. 1139 22

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

The stress system coordinates the adaptive responses of the organism to stressors of any kind.(1). The main components of the stress system are the corticotropin-releasing hormone (CRH) and locus ceruleus-norepinephrine (LC/NE)-autonomic systems and their peripheral effectors, the pituitary-adrenal axis, and the limbs of the autonomic system. Activation of the stress system leads to behavioral and peripheral changes that improve the ability of the organism to adjust homeostasis and increase its chances for survival. The CRH and LC/NE systems stimulate arousal and attention, as well as the mesocorticolimbic dopaminergic system, which is involved in anticipatory and reward phenomena, and the hypothalamic beta-endorphin system, which suppresses pain sensation and, hence, increases analgesia. CRH inhibits appetite and activates thermogenesis via the catecholaminergic system. Also, reciprocal interactions exist between the amygdala and the hippocampus and the stress system, which stimulates these elements and is regulated by them. CRH plays an important role in inhibiting GnRH secretion during stress, while, via somatostatin, it also inhibits GH, TRH and TSH secretion, suppressing, thus, the reproductive, growth and thyroid functions. Interestingly, all three of these functions receive and depend on positive catecholaminergic input. The end-hormones of the hypothalamic-pituitary-adrenal (HPA) axis, glucocorticoids, on the other hand, have multiple roles. They simultaneously inhibit the CRH, LC/NE and beta-endorphin systems and stimulate the mesocorticolimbic dopaminergic system and the CRH peptidergic central nucleus of the amygdala. In addition, they directly inhibit pituitary gonadotropin, GH and TSH secretion, render the target tissues of sex steroids and growth factors resistant to these substances and suppress the 5' deiodinase, which converts the relatively inactive tetraiodothyronine (T(4)) to triiodothyronine (T(3)), contributing further to the suppression of reproductive, growth and thyroid functions. They also have direct as well as insulin-mediated effects on adipose tissue, ultimately promoting visceral adiposity, insulin resistance, dyslipidemia and hypertension (metabolic syndrome X) and direct effects on the bone, causing "low turnover" osteoporosis. Central CRH, via glucocorticoids and catecholamines, inhibits the inflammatory reaction, while directly secreted by peripheral nerves CRH stimulates local inflammation (immune CRH). CRH antagonists may be useful in human pathologic states, such as melancholic depression and chronic anxiety, associated with chronic hyperactivity of the stress system, along with predictable behavioral, neuroendocrine, metabolic and immune changes, based on the interrelations outlined above. Conversely, potentiators of CRH secretion/action may be useful to treat atypical depression, postpartum depression and the fibromyalgia/chronic fatigue syndromes, all characterized by low HPA axis and LC/NE activity, fatigue, depressive symptomatology, hyperalgesia and increased immune/inflammatory responses to stimuli.
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PMID:Hypothalamic-pituitary-adrenal axis, neuroendocrine factors and stress. 1237 95

According to results of recent prospective studies depression is an independent risk factor of ischemic heart disease and should be considered together with such acknowledged risk factors as dyslipidemia, hypertension and smoking. Possible pathophysiological mechanisms of relationship between depression and ischemic heart disease are lowered heart rate variability and defects of physiological characteristics of platelets, depression also influences compliance to treatment and physicians recommendations. Depression negatively affects prognosis: mortality after myocardial infarction of patients with depression is 3-6 time higher than of those without depression. Incidence of depression is rather high and special investigation reveals its clinically significant symptoms in every fifth patient. Depression worsens clinical course of ischemic heart disease. Timely detection of depression is very important.
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PMID:[Depression--a novel risk factor of ischemic heart disease and predictor of coronary death]. 1249 75

The prevalence of obesity is increasing worldwide. In the United States, in 1999, 27% of adults had a body mass index >30 kg/m(2), almost double the prevalence of 20 years earlier. The estimated mortality from obesity-related diseases in the United States is approximately 300,000 annually and growing. In the future, mortality related to obesity is expected to exceed that of smoking. Numerous diseases are caused or made worse by obesity. These include type 2 diabetes; hypertension; dyslipidemia; ischemic heart disease; stroke; obstructive sleep apnea; asthma; nonalcoholic steatohepatitis; gastroesophageal reflux disease; degenerative joint disease of the back, hips, knees, and feet; infertility and polycystic ovary syndrome; various malignancies; and depression. Type 2 diabetes is perhaps the most visible obesity-related problem. Present in at least 14 million Americans, it leads to serious complications and premature death. It is largely caused by obesity, and is generally cured by weight loss. The quality of life of the obese is markedly reduced, and the costs to health care systems are great. Preventive programs have yet to affect the rising prevalence. An effective solution is needed.
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PMID:The extent of the problem of obesity. 1252 43


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