Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We studied relationships between shyness and health during a health screening survey of older adults (ages 50-88) living in an active retirement community in the southwestern United States (n = 232). As in previous studies of infants, older individuals with hay fever, insomnia and constipation were more shy than those without these problems. Shy persons overall showed higher sitting systolic blood pressure and a larger fall in orthostatic systolic blood pressure on standing; shy men had a greater prevalence of hypertension histories than did low-shy men. Shy subjects of both sexes had lower HDL cholesterol and higher triglycerides than did low-shy subjects; shy women tended to have higher LDL cholesterol than did low-shy women. In contrast with findings of elevated salivary cortisol in extremely inhibited children of both sexes, only shy women had higher 24 h urinary free cortisol excretion than did low-shy women; men showed the opposite pattern, possibly related to suppression of aggression. Shy men also tended to report a higher prevalence of thyroid disease history than did low-shy men (20% versus 6%). Notably, autoimmune thyroiditis has previously been linked with panic and depression, disorders which in turn have been associated with shyness. Taken together with previous work in shy children and their families, the data raise the possibility of (a) increased risk for arteriosclerotic vascular disease; and (b) increased risk of adrenal- and/or thyroid-related diseases in certain shy older adults.
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PMID:Vascular disease risk factors, urinary free cortisol, and health histories in older adults: shyness and gender interactions. 843 51

Trans fatty acids (t-FA) are geometrical isomers of unsaturated fatty acids that assume a saturated fatty acid-like configuration. Human diets contain t-FA derived from animal sources (e.g., dairy products and ruminant meats), but most are supplied by products containing industrially hydrogenated vegetable oils (e.g., margarines, shortenings and baked goods). Typical intake of t-FA in American diets has been estimated to be between 8-15 g/day, although wide variation exists between individuals. Human clinical studies since 1990 have revealed that relative to cis-monounsaturated fatty acids (i.e., oleic acid), t-FA increase total cholesterol (TC) and low density lipoprotein cholesterol (LDL-C), and tend to decrease high density lipoprotein cholesterol (HDL-C) concentrations. Additionally, t-FA tend to increase the atherogenic lipoprotein (a). Thus, t-FA induce an adverse plasma lipid profile (increased ratios of TC/LDL-C and LDL-C/HDL-C), which represents increased risk for coronary heart disease. The effects of t-FA on LDL-C and HDL-C appear to be directly related to intake and clinically measurable above 3%en as t-FA. The cholesterol-raising ability of t-FA is analogous to that of the 12-16 carbon saturated fatty acids, possibly reflecting increased LDL production or delayed LDL clearance. By contrast, t-FA are unlike the saturated fatty acids in their depression of HDL-C. Preliminary evidence suggests that at least part of their impact on lipoproteins reflects increased serum cholesteryl ester transfer protein activity, i.e., increased transfer of cholesteryl esters from HDL to LDL. Since the adverse effects of t-FA on human plasma lipids may be confined to specific isomers, future studies delineating their effects are warranted.
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PMID:Dietary trans-monounsaturated fatty acids negatively impact plasma lipids in humans: critical review of the evidence. 882 86

This open, prospective therapeutic trial studied the effects of regular moderate androgen supplementation on bone mineral density in eugonadal men with established osteoporosis, and collected data on the safety of androgen therapy used in this setting. 23 men, aged 34-73 years, with vertebral crush fractures and back pain, in whom secondary causes of osteoporosis had been excluded, were treated with fortnightly intramuscular injections of 250 mg testosterone esters (Sustanon 250(R)) for 6 months. Blood pressure was recorded monthly; fasting lipids, glucose, haematocrit, plasma viscosity, and testosterone levels were measured every 3 months. Psychological effects were assessed using the Hospital Anxiety and Depression Scale (HADS) and General Health Questionnaire (GHQ), together with questioning on libido changes. Principal outcomes measured were changes in bone mineral density at the hip and spine by dual-energy X-ray absorptiometry (DEXA) over the treatment period. 21 men completed the study period. Mean bone mineral density at the lumbar spine increased from 0.799 g/cm(2) to 0.839 g/cm(2) during treatment (p < 0. 001), a rise of 5% in 6 months. Bone mineral density at the hip did not change. There were significant, favorable changes in diastolic blood pressure (-4.7 mmHg, p < 0.01), serum triglyceride levels (-0.405 mmol/L,p < 0.01), and total cholesterol (-0.27 mmol/L, p < 0.05). Adverse changes included a fall in HDL cholesterol (-0.087 mmol/L, p < 0.05) and a rise in plasma viscosity which was significant at 3 months but not at 6 months. The expected rises in hematocrit (0.434 to 0.456) and FAI (0.504 to 0.887) occurred. We conclude that testosterone supplementation significantly increased bone mineral density in this heterogeneous group of men with idiopathic primary osteoporosis, without an overall adverse effect on cardiovascular risk factors. This treatment warrants further evaluation in a randomized, controlled trial.
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PMID:Androgen supplementation in eugonadal men with osteoporosis-effects of 6 months of treatment on bone mineral density and cardiovascular risk factors. 883 11

To evaluate the effects of short-term cholesterol-lowering treatment on myocardial effort ischemia, 22 patients with stable effort ischemia and mild to moderate hypercholesterolemia (low density lipoprotein [LDL] cholesterol 160 to 220 mg/dl) were randomly allocated at baseline (TO) in 2 groups. Group A included 12 patients treated with simvastatin 10 mg bid; group B included 10 patients treated with placebo. All patients underwent a treadmill electrocardiography (ECG) test; total cholesterol, HDL and LDL cholesterol, triglycerides, plasma, and blood viscosity were measured. All tests were repeated after 4 and 12 weeks. For 18 of the same patients (11 taking simvastatin, 7 receiving placebo), forearm strain-gouge plethysmography was performed at baseline and after 4 weeks, both at rest and during reactive hyperemia. At 4 and 12 weeks, group A showed a significant reduction in total cholesterol (p <0.05) and LDL (p <0.05), with unchanged HDL, triglycerides, blood, and plasma viscosity. Effort was unmodified, ST-segment depression at peak effort and ischemic threshold were significantly improved after 4 and 12 weeks (all p <0.05) with unchanged heart rate x systolic blood pressure product. A significant increase in the excess flow response to reactive hyperemia was detected in group A (p <0.03); group B showed no changes in hematochemical and ergometric parameters. These data suggest that cholesterol-lowering treatment is associated with an improvement in myocardial effort ischemia; this might be explained by a more pronounced increase of coronary blood flow and capacity of vasodilation in response to effort.
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PMID:Effects of short-term reduction in serum cholesterol with simvastatin in patients with stable angina pectoris and mild to moderate hypercholesterolemia. 885 79

This study compared the serum lipid concentrations in 100 patients with major depressive disorder (MDD) with those from 100 matched healthy controls. It was found that the serum total cholesterol concentration in patients with MDD (5.27 +/- 1.18 mmol/L) was significantly lower than the value (6.63 +/- 1.32 mmol/L) in sex-, age-, and weight-matched healthy controls. This significant decrease in serum cholesterol in patients with MDD was noted in both sexes and in all age groups. Patients with MDD, however, had significantly higher HDL cholesterol than matched controls. There were no statistically significant differences in serum concentrations of triglycerides, apolipoprotein (Apo) A1, Apo B, transferrin, and albumin between patients and controls. Clinical recovery of patients with MDD was accompanied by a significant increase in serum total cholesterol from 5.27 +/- 1.18 mmol/L to 6.12 +/- 1.2 mmol/L. These results suggest an association between low serum total cholesterol and depression in both sexes and at all age groups.
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PMID:Serum lipid concentrations in patients with major depressive disorder. 893 15

Previous studies have indicated the benefits of cardiac rehabilitation programs after major coronary artery disease (CAD) events. We studied 591 consecutive patients from two academic institutions before and after completion of a cardiac rehabilitation and exercise training program to determine the effects of this therapy on exercise capacity, indices of obesity, plasma lipid values, behavioral characteristics, and quality of life parameters. After cardiac rehabilitation, statistically significant improvements occurred in exercise capacity (+33%), percent body fat (-6%), body mass index (-1%), HDL-C (+5%), triglycerides (-9%), LDL-C/HDL-C (-6%), anxiety score (-39%), depression score (-35%), somatization score (-37%), and in all parameters of quality of life studied (total +14%). These data further support the ability of cardiac rehabilitation and exercise training programs to improve exercise capacity, plasma lipid values, obesity indices, behavioral characteristics, and quality of life parameters in a large cohort of patients who have had major CAD events.
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PMID:Effects of cardiac rehabilitation and exercise programs on exercise capacity, coronary risk factors, behavior, and quality of life in patients with coronary artery disease. 900 23

Tobacco smoking is the leading preventable cause of death in the United States and an important cause of CHD. The effect of smoking on the cardiovascular system and coronary risk factors is pervasive. Unfavorable effects include acute increases in blood pressure and coronary vascular resistance, reduction in oxygen delivery, enhancement of platelet aggregation, increased fibrinogen, and depression of HDL cholesterol. Smoking cessation reduces cardiovascular morbidity and mortality rates relatively rapidly, even among individuals who stop smoking only after the age of 65 or after developing the clinical manifestations of CHD including myocardial infarction. Behavioral smoking-cessation programs and nicotine-replacement therapy each have been demonstrated to be effective for the treatment of smoking. The most effective treatment currently available is to combine the two. Nicotine-replacement therapy is safe and effective in patients with stable coronary heart disease. Although the threat or diagnosis of CHD is a powerful stimulus to spontaneous smoking cessation, many smokers continue to smoke after events such as myocardial infarction or CABG surgery. Studies have demonstrated that physician advice to stop smoking, supplemented by brief counseling by a nurse and follow-up, dramatically increases the smoking-cessation rate of patients hospitalized with myocardial infarction and is highly cost effective. In the outpatient setting, physician advice and counseling is also effective in helping smokers with or without CHD to stop smoking. This article outlines a simple protocol that has been demonstrated to be effective for counseling smokers.
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PMID:Cigarette smoking and coronary heart disease: risks and management. 907 91

The present study was undertaken to study the effects of chronic treatment with lisinopril on the cardiovascular complications in streptozotocin (STZ) diabetic and deoxycorticosteroneacetate (DOCA) hypertensive rats. Injection of STZ produced severe glycosuria (> 2%), hyperglycemia, hypoinsulnaemia, polydypsia, polyphagia and loss of body weight. It also produced hypothyroidism, hypercholesterolaemia, hypertriglyceridaemia, hypertension, bradycardia and decreased left ventricular developed pressure (LVDP). Elevation in serum creatinine level and increased activity of liver enzymes were also found in STZ treated animals. DOCA by itself did not produce any change in blood glucose but reduced serum insulin levels in non-diabetic animals. However, in the diabetic group, DOCA reduced blood sugar levels. Treatment of STZ-diabetic rats with DOCA did not aggravate cardiac depression or hyperglycaemia. Treatment of rats with lisinopril (1 mg kg-1, p.o. daily for six weeks), in diabetic and diabetic hypertensive animals prevented STZ induced loss of body weight and hypertension, bradycardia and hypothyroidism. It also prevented STZ induced hyperglycemia and hypoinsulinaemia in both diabetic and diabetic hypertensive animals. There was a reduction in cholesterol, triglyceride, and LDL levels; the ratio between total cholesterol to HDL and LDL to HDL and an improvement in LVDP at higher filling pressure in diabetic as well as diabetic hypertensive animals. Treatment with lisinopril also prevented hypertrophy and elevated levels of serum creatinine, SGOT and SGPT in diabetic animals. In conclusion, the present data suggests that STZ-DOCA model may not be considered as the ideal model for the study of cardiovascular complications of combined treatment hypertension and diabetes. However, the present investigation presents a number of beneficial effects of lisinopril treatment in diabetic with or without hypertensive rats and it may be considered as one of the drugs of choice in treatment of hypertension when it is associated with diabetes mellitus.
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PMID:Effects of chronic treatment with lisinopril on cardiovascular complications in streptozotocin diabetic and DOCA hypertensive rats. 907 44

Recently, there have been some reports that changes in serum lipid composition may be related to suicide, major depression and immune-inflammatory responses. Findings from our laboratory suggest that major depression is accompanied by reduced formation of cholesteryl esters and perhaps by impairment of reverse cholesterol transport. The latter is reportedly accompanied by lower serum high-density lipoprotein cholesterol (HDL-C). The aim of this study was to examine whether (i) major depression is accompanied by lower serum HDL-C or by abnormal levels of serum total cholesterol, triglycerides, low-density lipoprotein-C (LDL-C) or vitamin E, (ii) suicidal attempts are related to lower serum HDL-C and (iii) there are significant associations between serum HDL-C and immune/inflammatory markers. A total of 36 subjects with major depression, of whom 28 patients showed treatment resistance, as well as 28 normal control subjects, had blood sampled for the assay of the above lipids, serum zinc (Zn), albumin (Alb) and flow cytometric determination of the T-helper/T-suppressor (CD4+/CD8+) T-cell ratio. In total, 28 depressed subjects had repeated measures of these variables both before and after treatment with antidepressants. Serum HDL-C and total cholesterol, as well as the HDL-C/cholesterol ratio, were significantly lower in subjects with major depression than in normal controls. Serum HDL-C levels were significantly lower in depressed men who had at some time made serious suicidal attempts than in those without such suicidal behaviour. Treatment with antidepressants for 5 weeks did not significantly alter either serum HDL-C or other lipid variables. Serum HDL-C levels were significantly and negatively correlated with the (CD4+/CD8+) T-cell ratio, and positively correlated with serum Alb and Zn. These results suggest that (i) lower serum HDL-C levels are a marker for major depression and suicidal behaviour in depressed men, (ii) lower serum HDL-C levels are probably induced by the immune/inflammatory response in depression and (iii) there is impairment of reverse cholesterol transport from the body tissues to the liver.
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PMID:Lower serum high-density lipoprotein cholesterol (HDL-C) in major depression and in depressed men with serious suicidal attempts: relationship with immune-inflammatory markers. 911 54

Serum total tryptophan and the five competing amino acids (CAA), i.e., valine, leucine, tyrosine, phenylalanine, and isoleucine were determined in 35 major depressed subjects of whom 27 with treatment resistant depression (TRD), and 15 normal controls. Twenty-five of the depressed subjects had repeated measurements of the amino acids both before and after antidepressive treatment. The following immune-inflammatory variables were assayed in the above subjects: serum zinc (Zn), total serum protein (TSP), albumin (Alb), transferrin (Tf), iron (Fe), high-density lipoprotein cholesterol (HDL-C), number of peripheral blood leukocytes, and the CD4+/CD8+ T cell (T-helper/T-suppressor) ratio. Serum tryptophan and the tryptophan/CAA ratio were significantly lower in major depressed subjects than in normal controls. The tryptophan/CAA ratio was significantly lower in patients with TRD than in patients without TRD and normal controls. There were no significant alterations in any of the amino acids upon successful therapy. There were significant correlations between serum tryptophan and serum Zn, TSP, Alb, Tf, Fe, and HDL-C (all positive), and number of leukocytes and the CD4+/CD8+ T-cell ratio (all negative). The tryptophan/CAA ratio was significantly and negatively related to the number of leukocytes and the CD4+/CD8+ T-cell ratio. The results suggest that (a) TRD is characterized by lower availability of serum tryptophan; (b) the availability of tryptophan may remain decreased despite clinical recovery; and (c) the lower availability of tryptophan is probably a marker of the immune-inflammatory response during major depression.
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PMID:Serotonin-immune interactions in major depression: lower serum tryptophan as a marker of an immune-inflammatory response. 922 8


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