Objective: To examine the association of mid-life exposure to several psychiatric disorders with the development of late-life dementia. Methods: A matched case-control study using Western Australian state-wide hospital inpatient, outpatient mental health and emergency records linked to death records. Incident dementia cases (2000-2009) aged 65 to 84 years were sex- and age-matched to an electoral roll control. Records as far back as 1970 were used to assess exposure to medical risk factors before age 65 years. Candidate psychiatric risk factors were required to be present at least 10 years before dementia onset to ensure direction of potential causality. Odds ratios were estimated using conditional logistic regression. Results: 13, 568 dementia cases (median age 78.7 years, 43.4% male) were matched to a control. Depression, bipolar disorder, schizophrenia, anxiety disorder and alcohol dependence were found to be significant and independent risk factors for late-life dementia after adjusting for diabetes, heart disease, cerebrovascular disease and smoking risk factors. The effect of a history of depression, schizophrenia and alcohol dependency on dementia risk varied with age, being strongest for earlier onset late-life dementia and waning at older ages. Conclusion: Severe depression, anxiety disorder, bipolar disorder, schizophrenia and alcoholic dependency disorder treated by specialists in psychiatric facilities in mid-life are important risk factors for late-life dementia. These psychiatric conditions need to be considered in future studies of the risk and prevention of late-life dementia.
Abstract-A positive relationship between alcohol consumption and blood pressure (BP) is well-established but the relative effect of specific alcoholic beverages is controversial. This study aimed to determine whether red wine may improve vascular function and have less of an impact on blood pressure because of its high content of antioxidant vasodilator polyphenolic compounds. Healthy normotensive men entered a 4-period crossover study comparing in random order 4 weeks of control-abstinence with similar periods of daily consumption of red wine (375 mL; 39 grams alcohol), de-alcoholized red wine (375 mL), or beer (1125 mL; 41 grams alcohol). Ambulatory systolic BP and diastolic BP and heart rate (HR) were measured together with vascular function as assessed by flow-mediated dilatation (FMD) and glyceryl trinitrate-mediated (GTNMD) dilatation of the brachial artery. The systolic and diastolic BP and HR were not different between control-abstinence and de-alcoholized red wine. However, compared with control-abstinence, both red wine and beer increased awake systolic BP (2.9 and 1.9 mm Hg, respectively; PϽ0.05) and asleep HR (5.0 and 4.4 bpm; PϽ0.05). There were no specific effects of red wine, de-alcoholized red wine, or beer on FMD or GTNMD. Daily consumption of Ϸ40 grams alcohol as either red wine or beer for 4 weeks results in similar increases in systolic BP and HR. De-alcoholized red wine did not lower BP, and neither red wine nor de-alcoholized red wine influenced vascular function, suggesting that red wine polyphenolics do not have a significant role in mitigating the blood pressure-elevating effects of alcohol in men.
1. In spite of the dose-related effects of alcohol consumption to increase blood pressure, regular light to moderate alcohol intake appears to confer protection against both coronary artery disease and ischaemic stroke. In contrast, heavy alcohol consumption increases the risk of coronary artery disease and the risk of both haemorrhagic and ischaemic stroke. 2. Effects of alcohol consumption on endothelial cell function may be relevant to these disparate effects on cardiovascular outcomes. In in vitro animal studies, low doses of alcohol have been demonstrated to increase release of nitric oxide and augment endothelium-mediated vasodilatation, whereas higher doses impair endothelium-dependent relaxation responses. In contrast, chronic administration of alcohol to rats has generally been associated with tolerance to the acute inhibitory effects of alcohol on endothelium-mediated vasodilatation and may even result in augmentation of such responses. 3. The few human studies to date that have examined the effects of alcohol on endothelial function have focused on postischaemic flow-mediated dilation of the brachial artery (FMD). Although blunted FMD responses have been reported in alcoholic subjects, acute administration of alcohol or short-term interventions to reduce alcohol intake have had no effect to either improve or impair FMD. 4. Further studies in humans assessing acute and longer term dose-related effects of alcohol on endothelial function in both conduit and resistance vessels will be necessary if the relevance of the findings from in vitro and in vivo animal studies are to be understood in the context of the complex interrelationships of alcohol with cardiovascular disease.
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