2 resultados para etiology of insomnia

em Dalarna University College Electronic Archive


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Background: In light of the multifactorial etiology of fall-related hip fracture, knowledge of fall circumstances may be especially valuable when placed in the context of the health of the person who falls. We aimed to investigate the circumstances surrounding fall-related hip fractures and to describe fall circumstances in relation to participants' health and functional characteristics. Methods: The fall circumstances of 125 individuals (age >= 50 years) with hip fracture were investigated using semi-structured interviews. Data concerning participants' health (comorbidities and medications) and function (self-reported performance of mobility, balance, personal activities of daily living and physical activity, previous falls and hand grip strength) were collected via medical records, questionnaires and dynamometry. Using a mixed methods design, both data sets were analysed separately and then merged in order to provide a comprehensive description of fall events and identify eventual patterns in the data. Results: Fall circumstances were described as i) Activity at the time of the fall: Positional change (n = 24, 19%); Standing (n = 16, 13%); Walking (n = 71, 57%); Balance challenging (n = 14, 11%) and ii) Nature of the fall: Environmental (n = 32, 26%); Physiological (n = 35, 28%); Activity-related indoor (n = 8, 6%) and outdoor (n = 8, 6%); Trips and slips on snow (n = 20, 16%) and in snow-free conditions (n = 12, 10%) and Unknown (n = 10, 8%). We observed the following patterns regarding fall circumstances and participants' health: those who fell i) during positional change had the poorest functional status; ii) due to environmental reasons (indoors) had moderate physical function, but high levels of comorbidity and fall risk increasing medications; iii) in snow-free environments (outdoors) appeared to have a poorer health and functional status than other outdoor groups. Conclusions: Our findings indicate that patterns exist in relation to the falls circumstances and health characteristics of people with hip fracture which build upon that previously reported. These patterns, when verified, can provide useful information as to the ways in which fall prevention strategies can be tailored to individuals of varying levels of health and function who are at risk for falls and hip fracture.

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BACKGROUND: Epidemiological studies show that high circulating cystatin C is associated with risk of cardiovascular disease (CVD), independent of creatinine-based renal function measurements. It is unclear whether this relationship is causal, arises from residual confounding, and/or is a consequence of reverse causation. OBJECTIVES: The aim of this study was to use Mendelian randomization to investigate whether cystatin C is causally related to CVD in the general population. METHODS We incorporated participant data from 16 prospective cohorts (n ¼ 76,481) with 37,126 measures of cystatin C and added genetic data from 43 studies (n ¼ 252,216) with 63,292 CVD events. We used the common variant rs911119 in CST3 as an instrumental variable to investigate the causal role of cystatin C in CVD, including coronary heart disease, ischemic stroke, and heart failure. RESULTS: Cystatin C concentrations were associated with CVD risk after adjusting for age, sex, and traditional risk factors (relative risk: 1.82 per doubling of cystatin C; 95% confidence interval [CI]: 1.56 to 2.13; p ¼ 2.12 1014). The minor allele of rs911119 was associated with decreased serum cystatin C (6.13% per allele; 95% CI: 5.75 to 6.50; p ¼ 5.95 10211), explaining 2.8% of the observed variation in cystatin C. Mendelian randomization analysis did not provide evidence for a causal role of cystatin C, with a causal relative risk for CVD of 1.00 per doubling cystatin C (95% CI: 0.82 to 1.22; p ¼ 0.994), which was statistically different from the observational estimate (p ¼ 1.6 105 ). A causal effect of cystatin C was not detected for any individual component of CVD. CONCLUSIONS: Mendelian randomization analyses did not support a causal role of cystatin C in the etiology of CVD. As such, therapeutics targeted at lowering circulating cystatin C are unlikely to be effective in preventing CVD.