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- Wormser, David, et al.
(författare)
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Adult height and the risk of cause-specific death and vascular morbidity in 1 million people : individual participant meta-analysis
- 2012
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Ingår i: International Journal of Epidemiology. - : Oxford University Press (OUP). - 0300-5771 .- 1464-3685. ; 41:5, s. 1419-1433
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Tidskriftsartikel (refereegranskat)abstract
- BackgroundThe extent to which adult height, a biomarker of the interplay of genetic endowment and early-life experiences, is related to risk of chronic diseases in adulthood is uncertain.MethodsWe calculated hazard ratios (HRs) for height, assessed in increments of 6.5 cm, using individual-participant data on 174 374 deaths or major non-fatal vascular outcomes recorded among 1 085 949 people in 121 prospective studies.ResultsFor people born between 1900 and 1960, mean adult height increased 0.5-1 cm with each successive decade of birth. After adjustment for age, sex, smoking and year of birth, HRs per 6.5 cm greater height were 0.97 (95% confidence interval: 0.96-0.99) for death from any cause, 0.94 (0.93-0.96) for death from vascular causes, 1.04 (1.03-1.06) for death from cancer and 0.92 (0.90-0.94) for death from other causes. Height was negatively associated with death from coronary disease, stroke subtypes, heart failure, stomach and oral cancers, chronic obstructive pulmonary disease, mental disorders, liver disease and external causes. In contrast, height was positively associated with death from ruptured aortic aneurysm, pulmonary embolism, melanoma and cancers of the pancreas, endocrine and nervous systems, ovary, breast, prostate, colorectum, blood and lung. HRs per 6.5 cm greater height ranged from 1.26 (1.12-1.42) for risk of melanoma death to 0.84 (0.80-0.89) for risk of death from chronic obstructive pulmonary disease. HRs were not appreciably altered after further adjustment for adiposity, blood pressure, lipids, inflammation biomarkers, diabetes mellitus, alcohol consumption or socio-economic indicators.ConclusionAdult height has directionally opposing relationships with risk of death from several different major causes of chronic diseases.
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| 4. |
- Hruby, Adela, et al.
(författare)
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Higher Magnesium Intake Is Associated with Lower Fasting Glucose and Insulin, with No Evidence of Interaction with Select Genetic Loci, in a Meta-Analysis of 15 CHARGE Consortium Studies
- 2013
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Ingår i: Journal of Nutrition. - : Elsevier BV. - 0022-3166 .- 1541-6100. ; 143:3, s. 345-353
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Tidskriftsartikel (refereegranskat)abstract
- Favorable associations between magnesium intake and glycemic traits, such as fasting glucose and insulin, are observed in observational and clinical studies, but whether genetic variation affects these associations is largely unknown. We hypothesized that single nucleotide polymorphisms (SNPs) associated with either glycemic traits or magnesium metabolism affect the association between magnesium intake and fasting glucose and insulin. Fifteen studies from the CHARGE (Cohorts for Heart and Aging Research in Genomic Epidemiology) Consortium provided data from up to 52,684 participants of European descent without known diabetes. In fixed-effects meta-analyses, we quantified 1) cross-sectional associations of dietary magnesium intake with fasting glucose (mmol/L) and insulin (In-pmol/L) and 2) interactions between magnesium intake and SNPs related to fasting glucose (16 SNPs), insulin (2 SNPs), or magnesium (8 SNPs) on fasting glucose and insulin. After adjustment for age, sex, energy intake, BMI, and behavioral risk factors, magnesium (per 50-mg/d increment) was inversely associated with fasting glucose [beta = -0.009 mmol/L (95% CI: -0.013, -0.005), P< 0.0001] and insulin (-0.020 In-pmo/L (95% CI: -0.024, -0.017), P< 0.0001]. No magnesium-related SNP or interaction between any SNP and magnesium reached significance after correction for multiple testing. However, rs2274924 in magnesium transporter-encoding TRPM6 showed a nominal association (uncorrected P= 0.03) with glucose, and rs11558471 in SLC30A8and rs3740393 near CNNM2showed a nominal interaction (uncorrected, both P = 0.02) with magnesium on glucose. Consistent with other studies, a higher magnesium intake was associated with lower fasting glucose and insulin. Nominal evidence of TRPM6 influence and magnesium interaction with select loci suggests that further investigation is warranted. J. Nutr. 143: 345-353, 2013.
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| 5. |
- Nettleton, Jennifer A., et al.
(författare)
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Meta-Analysis Investigating Associations Between Healthy Diet and Fasting Glucose and Insulin Levels and Modification by Loci Associated With Glucose Homeostasis in Data From 15 Cohorts
- 2013
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Ingår i: American Journal of Epidemiology. - : Oxford University Press (OUP). - 0002-9262 .- 1476-6256. ; 177:2, s. 103-115
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Forskningsöversikt (refereegranskat)abstract
- Whether loci that influence fasting glucose (FG) and fasting insulin (FI) levels, as identified by genome-wide association studies, modify associations of diet with FG or FI is unknown. We utilized data from 15 US and European cohort studies comprising 51,289 persons without diabetes to test whether genotype and diet interact to influence FG or FI concentration. We constructed a diet score using study-specific quartile rankings for intakes of whole grains, fish, fruits, vegetables, and nuts/seeds (favorable) and red/processed meats, sweets, sugared beverages, and fried potatoes (unfavorable). We used linear regression within studies, followed by inverse-variance-weighted meta-analysis, to quantify 1) associations of diet score with FG and FI levels and 2) interactions of diet score with 16 FG-associated loci and 2 FI-associated loci. Diet score (per unit increase) was inversely associated with FG ( 0.004 mmol/L, 95 confidence interval: 0.005, 0.003) and FI ( 0.008 ln-pmol/L, 95 confidence interval: 0.009, 0.007) levels after adjustment for demographic factors, lifestyle, and body mass index. Genotype variation at the studied loci did not modify these associations. Healthier diets were associated with lower FG and FI concentrations regardless of genotype at previously replicated FG- and FI-associated loci. Studies focusing on genomic regions that do not yield highly statistically significant associations from main-effect genome-wide association studies may be more fruitful in identifying diet-gene interactions.
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| 6. |
- Janszky, Imre, et al.
(författare)
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Daylight saving time shifts and incidence of acute myocardial infarction - Swedish Register of Information and Knowledge About Swedish Heart Intensive Care Admissions (RIKS-HIA)
- 2012
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Ingår i: Sleep Medicine. - : Elsevier. - 1389-9457 .- 1878-5506. ; 13:3, s. 237-242
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Tidskriftsartikel (refereegranskat)abstract
- Background: Daylight saving time shifts can be looked upon as large-scale natural experiments to study the effects of acute minor sleep deprivation and circadian rhythm disturbances. Limited evidence suggests that these shifts have a short-term influence on the risk of acute myocardial infarction (AMI), but confirmation of this finding and its variation in magnitude between individuals is not clear. less thanbrgreater than less thanbrgreater thanMethods: To identify AMI incidence on specific dates, we used the Register of Information and Knowledge about Swedish Heart Intensive Care Admission, a national register of coronary care unit admissions in Sweden. We compared AMI incidence on the first seven days after the transition with mean incidence during control periods. To assess effect modification, we calculated the incidence ratios in strata defined by patient characteristics. less thanbrgreater than less thanbrgreater thanResults: Overall, we found an elevated incidence ratio of 1.039 (95% confidence interval, 1.003-1.075) for the first week after the spring clock shift forward. The higher risk tended to be more pronounced among individuals taking cardiac medications and having low cholesterol and triglycerides. There was no statistically significant change in AMI incidence following the autumn shift. Patients with hyperlipidemia and those taking statins and calcium-channel blockers tended to have a lower incidence than expected. Smokers did not ever have a higher incidence. less thanbrgreater than less thanbrgreater thanConclusions: Our data suggest that even modest sleep deprivation and disturbances in the sleep-wake cycle might increase the risk of AMI across the population. Confirmation of subgroups at higher risk may suggest preventative strategies to mitigate this risk.
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| 7. |
- Pyshchyta, Ganna, et al.
(författare)
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Tea consumption, incidence and long-term prognosis of a first acute myocardial infarction : The SHEEP study
- 2012
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Ingår i: Clinical Nutrition. - : Elsevier BV. - 0261-5614 .- 1532-1983. ; 31:2, s. 267-272
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND & AIMS: Results of previous studies on tea consumption and incidence or prognosis of acute myocardial infarction (AMI) are conflicting. The aim of the present study was to examine the potential role of tea consumption in the previous 12 months in primary and secondary prevention of AMI. METHODS: We studied a total of 1340 individuals with a first non-fatal AMI and 2303 frequency matched control participants on age, gender and hospital catchment area including querying their tea consumption over the previous 12 months. The cohort of AMI cases was then followed for total and cardiac mortality and for non-fatal cardiovascular events with national registers over 8 years. Estimates of relative risks for a first AMI were based on odds ratios from unconditional logistic regression and Cox proportional hazards models were used to examine the prognostic importance of tea consumption in the cohort of cases. RESULTS: The prevalence of daily tea consumption was 20.5% among cases and 21.5% among controls. Tea consumption was associated with a lower risk for a first AMI with adjustment for matching criteria alone, with an odds ratio of 0.78 (95% confidence interval, 0.64-0.95) comparing those who consumed tea daily to those never consuming tea. However, in multivariable adjusted model there was no evidence for an association, the corresponding odds ratio was 1.08(0.86-1.36). There was also no association between tea consumption and cardiac mortality and non-fatal cardiovascular events, with a corresponding adjusted hazard ratio of 0.99(0.77-1.27). CONCLUSIONS: In this epidemiological study, greater tea consumption in the previous year was associated with a lower risk of AMI. However, a clear association between tea consumption and the incidence or prognosis of AMI was not demonstrated, probably because of tea drinkers having a healthier lifestyle.
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| 8. |
- Seshasai, Sreenivasa Rao Kondapally, et al.
(författare)
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Diabetes mellitus, fasting glucose, and risk of cause-specific death.
- 2011
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Ingår i: The New England journal of medicine. - 1533-4406 .- 0028-4793. ; 364:9, s. 829-41
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Tidskriftsartikel (refereegranskat)abstract
- The extent to which diabetes mellitus or hyperglycemia is related to risk of death from cancer or other nonvascular conditions is uncertain.
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