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J. Tuomilehto

Bio: J. Tuomilehto is an academic researcher from National Institutes of Health. The author has contributed to research in topics: Population & Body mass index. The author has an hindex of 44, co-authored 107 publications receiving 11425 citations. Previous affiliations of J. Tuomilehto include University of Helsinki & King Abdulaziz University.


Papers
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Journal ArticleDOI
23 Oct 2002-JAMA
TL;DR: This meta-analysis of observational studies suggests that elevated homocysteine is at most a modest independent predictor of IHD and stroke risk in healthy populations.
Abstract: CONTEXT: It has been suggested that total blood homocysteine concentrations are associated with the risk of ischemic heart disease (IHD) and stroke. OBJECTIVE: To assess the relationship of homocysteine concentrations with vascular disease risk. DATA SOURCES: MEDLINE was searched for articles published from January 1966 to January 1999. Relevant studies were identified by systematic searches of the literature for all reported observational studies of associations between IHD or stroke risk and homocysteine concentrations. Additional studies were identified by a hand search of references of original articles or review articles and by personal communication with relevant investigators. STUDY SELECTION: Studies were included if they had data available by January 1999 on total blood homocysteine concentrations, sex, and age at event. Studies were excluded if they measured only blood concentrations of free homocysteine or of homocysteine after a methionine-loading test or if relevant clinical data were unavailable or incomplete. DATA EXTRACTION: Data from 30 prospective or retrospective studies involving a total of 5073 IHD events and 1113 stroke events were included in a meta-analysis of individual participant data, with allowance made for differences between studies, for confounding by known cardiovascular risk factors, and for regression dilution bias. Combined odds ratios (ORs) for the association of IHD and stroke with blood homocysteine concentrations were obtained by using conditional logistic regression. DATA SYNTHESIS: Stronger associations were observed in retrospective studies of homocysteine measured in blood collected after the onset of disease than in prospective studies among individuals who had no history of cardiovascular disease when blood was collected. After adjustment for known cardiovascular risk factors and regression dilution bias in the prospective studies, a 25% lower usual (corrected for regression dilution bias) homocysteine level (about 3 micromol/L [0.41 mg/L]) was associated with an 11% (OR, 0.89; 95% confidence interval [CI], 0.83-0.96) lower IHD risk and 19% (OR, 0.81; 95% CI, 0.69-0.95) lower stroke risk. CONCLUSIONS: This meta-analysis of observational studies suggests that elevated homocysteine is at most a modest independent predictor of IHD and stroke risk in healthy populations. Studies of the impact on disease risk of genetic variants that affect blood homocysteine concentrations will help determine whether homocysteine is causally related to vascular disease, as may large randomized trials of the effects on IHD and stroke of vitamin supplementation to lower blood homocysteine concentrations.

1,953 citations

Journal ArticleDOI
13 Feb 1999-BMJ
TL;DR: The highest death rates from coronary heart disease occurred in boys who were thin at birth but whose weight caught up so that they had an average or above average body mass from the age of 7 years.
Abstract: Objective: To examine whether catch-up growth during childhood modifies the increased risk of death from coronary heart disease that is associated with reduced intrauterine growth Design: Follow up study of men whose body size at birth was recorded and who had an average of 10 measurements taken of their height and weight through childhood Setting: Helsinki, Finland Subjects: 3641 men who were born in Helsinki University Central Hospital during 1924-33 and who went to school in Helsinki Main outcome measures: Hazard ratios for death from coronary heart disease Results: Death from coronary heart disease was associated with low birth weight and, more strongly, with a low ponderal index at birth Men who died from coronary heart disease had an above average body mass index at all ages from 7 to 15 years In a simultaneous regression the hazard ratio for death from the disease increased by 14% (95% confidence interval 8% to 19%; P Conclusion: The highest death rates from coronary heart disease occurred in boys who were thin at birth but whose weight caught up so that they had an average or above average body mass from the age of 7 years Death from coronary heart disease may be a consequence of poor prenatal nutrition followed by improved postnatal nutrition

1,161 citations

Journal ArticleDOI
TL;DR: Heritability for Type 1 diabetes was greater than that for Type 2 where both genetic and environmental effects seemed to play a significant role, according to computerized record linkage from death certificates, the National Hospital Discharge Register and the National Drug Register.
Abstract: We studied the cumulative incidence, concordance rate and heritability for diabetes mellitus in a nationwide cohort of 13,888 Finnish twin pairs of the same sex. The twins were born before 1958 and both co-twins were alive in 1967. Data on diabetes were derived through computerized record linkage from death certificates, the National Hospital Discharge Register and the National Drug Register. Records were reviewed in order to assign a diagnostic category to the 738 diabetic patients identified. Of these patients 109 had Type 1 (insulin-dependent) diabetes, 505 Type 2 (non-insulin-dependent) diabetes, 46 gestational diabetes, 24 secondary diabetes, 38 impaired glucose tolerance and 16 remained unclassified. The cumulative incidence of diabetes was 1.4 % in men and 1.3 % in women aged 28–59 years and 9.3 % and 7.0 % in men and women aged 60 years and over, respectively. The cumulative incidence did not differ between monozygotic and dizygotic twins. The concordance rate for Type 1 diabetes was higher among monozygotic (23 % probandwise and 13 % pairwise) than dizygotic twins (5 % probandwise and 3 % pairwise). The probandwise and pairwise concordance rates for Type 2 diabetes were 34% and 20% among monozygotic tiwns and 16% and 9 % in dizygotic twins, respectively. Heritability for Type 1 diabetes was greater than that for Type 2 where both genetic and environmental effects seemed to play a significant role.

657 citations

Journal ArticleDOI
02 Jul 1994-BMJ
TL;DR: An assessment of the data on the risk factors for ischaemic heart disease and mortality suggests that most of the decline in mortality from ischaemia heart disease can be explained by changes in the three main coronary risk factors.
Abstract: Objectives : To estimate the extent to which changes in the main coronary risk factors (serum cholesterol concentration, blood pressure, and smoking) explain the decline in mortality from ischaemic heart disease and to evaluate the relative importance of change in each of these risk factors. Design : Predicted changes in ischaemic heart disease mortality were calculated by a ligistic regression model using the risk factor levels assessed by cross sectional population surveys, in 1972, 1977, 1982, 1987, and 1992. These predicted changes were compared with observed changes in mortality statistics. Setting : North Karelia and Kuopio provinces, Finland. Subjects : 14 257 men and 14 786 women aged 30–59 randomly selected from the national population register. Main outcome measures : Levels of the risk factors and predicted and observed changes in mortality from ischaemic heart disease. Results — The observed changes in the risk factors in the population from 1972 to 1992 predicted a decline in mortality from ischaemic heart disease of 44% (95% confidence interval 37% to 50%) in men and 49% (37% to 59%) in women. The observed decline was 55% (51% to 58%) and 68% (61 to 74) respectively. Conclusion : An assessment of the data on the risk factors for ischaemic heart disease and mortality suggests that most of the decline in mortality from ischaemic heart disease can be explained by changes in the three main coronary risk factors.

488 citations


Cited by
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Journal ArticleDOI
TL;DR: Type 2 diabetes can be prevented by changes in the lifestyles of high-risk subjects by means of individualized counseling aimed at reducing weight, total intake of fat, and intake of saturated fat and increasing intake of fiber and physical activity.
Abstract: Background Type 2 diabetes mellitus is increasingly common, primarily because of increases in the prevalence of a sedentary lifestyle and obesity. Whether type 2 diabetes can be prevented by interventions that affect the lifestyles of subjects at high risk for the disease is not known. Methods We randomly assigned 522 middle-aged, overweight subjects (172 men and 350 women; mean age, 55 years; mean body-mass index [weight in kilograms divided by the square of the height in meters], 31) with impaired glucose tolerance to either the intervention group or the control group. Each subject in the intervention group received individualized counseling aimed at reducing weight, total intake of fat, and intake of saturated fat and increasing intake of fiber and physical activity. An oral glucose-tolerance test was performed annually; the diagnosis of diabetes was confirmed by a second test. The mean duration of follow-up was 3.2 years. Results The mean (±SD) amount of weight lost between base line and the end of ye...

10,178 citations

Journal ArticleDOI
TL;DR: This year's edition of the Statistical Update includes data on the monitoring and benefits of cardiovascular health in the population, metrics to assess and monitor healthy diets, an enhanced focus on social determinants of health, a focus on the global burden of cardiovascular disease, and further evidence-based approaches to changing behaviors, implementation strategies, and implications of the American Heart Association’s 2020 Impact Goals.
Abstract: Background: The American Heart Association, in conjunction with the National Institutes of Health, annually reports on the most up-to-date statistics related to heart disease, stroke, and cardiovas...

5,078 citations

Journal ArticleDOI
01 Jan 2011-Stroke
TL;DR: In this paper, the authors provided evidence-based recommendations for the prevention of future stroke among survivors of ischemic stroke or transient ischemi-chemic attack, including the control of risk factors, intervention for vascular obstruction, antithrombotic therapy for cardioembolism, and antiplatelet therapy for noncardioembolic stroke.
Abstract: The aim of this updated guideline is to provide comprehensive and timely evidence-based recommendations on the prevention of future stroke among survivors of ischemic stroke or transient ischemic attack. The guideline is addressed to all clinicians who manage secondary prevention for these patients. Evidence-based recommendations are provided for control of risk factors, intervention for vascular obstruction, antithrombotic therapy for cardioembolism, and antiplatelet therapy for noncardioembolic stroke. Recommendations are also provided for the prevention of recurrent stroke in a variety of specific circumstances, including aortic arch atherosclerosis, arterial dissection, patent foramen ovale, hyperhomocysteinemia, hypercoagulable states, antiphospholipid antibody syndrome, sickle cell disease, cerebral venous sinus thrombosis, and pregnancy. Special sections address use of antithrombotic and anticoagulation therapy after an intracranial hemorrhage and implementation of guidelines.

4,545 citations

Journal ArticleDOI
TL;DR: This work speculates on the reasons behind this large discrepancy between the expectations arising from proteomics and the realities of clinical diagnostics and suggests approaches by which protein-disease associations may be more effectively translated into diagnostic tools in the future.

4,062 citations

Journal ArticleDOI
TL;DR: Mendelian randomization provides new opportunities to test causality and demonstrates how investment in the human genome project may contribute to understanding and preventing the adverse effects on human health of modifiable exposures.
Abstract: Associations between modifiable exposures and disease seen in observational epidemiology are sometimes confounded and thus misleading, despite our best efforts to improve the design and analysis of studies. Mendelian randomization-the random assortment of genes from parents to offspring that occurs during gamete formation and conception-provides one method for assessing the causal nature of some environmental exposures. The association between a disease and a polymorphism that mimics the biological link between a proposed exposure and disease is not generally susceptible to the reverse causation or confounding that may distort interpretations of conventional observational studies. Several examples where the phenotypic effects of polymorphisms are well documented provide encouraging evidence of the explanatory power of Mendelian randomization and are described. The limitations of the approach include confounding by polymorphisms in linkage disequilibrium with the polymorphism under study, that polymorphisms may have several phenotypic effects associated with disease, the lack of suitable polymorphisms for studying modifiable exposures of interest, and canalization-the buffering of the effects of genetic variation during development. Nevertheless, Mendelian randomization provides new opportunities to test causality and demonstrates how investment in the human genome project may contribute to understanding and preventing the adverse effects on human health of modifiable exposures.

3,646 citations