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Objectives To investigate whether adherence to a Mediterranean dietary pattern during adolescence and early adulthood affects arterial stiffness in adulthood, and the extent to which any such association may be attributed to a beneficial impact of this diet on cardiovascular disease risk factors such as blood pressure, central fatness and dyslipidaemia. Setting The Amsterdam Growth and Health Longitudinal Study. Design and subjects We compared longitudinal levels of adherence to a Mediterranean dietary pattern (a MED score with range 0-9) during adolescence and adulthood (two to eight repeated measures obtained between the ages of 13 and 36) between individuals with different levels of arterial stiffness in adulthood. The study population included 373 (196 women) apparently healthy adults in whom properties of the carotid, brachial and femoral arteries were assessed using ultrasonography at 36 years of age. Results After adjustments for potential confounders, individuals with stiffer carotid arteries (defined on the basis of the most adverse tertile of, for instance, the distensibility coefficient) had lower a MED scores (−0.32, 95% CI −0.60; −0.06) and were less likely to have adhered to this dietary pattern ( aMED score ≥5, odds ratio 0.69, 95% CI 0.50; −0.94) during the preceding 24 years compared with those with less stiff arteries. Differences in a MED scores were already present in adolescence and were only in part explained by the favourable associations between the Mediterranean dietary pattern and other cardiovascular disease risk factors (up to 26%), particularly mean blood pressure (up to 19%). Conclusions Promoting the Mediterranean diet in adolescence and early adulthood may constitute an important means of preventing arterial stiffness in adulthood. [ABSTRACT FROM AUTHOR]

Background/Aims: Monitoring overweight prevalence and its trends in Dutch youth is frequently based on self-reported data. The validity of self-reported data especially in young adolescents is not sufficiently known. The purpose of this study is to study the validity of self-reported height and weight in 12- to 13-year-olds, to identify sociodemographic correlates and to explore whether correction factors can be developed to estimate the prevalence of overweight in youth. Methods: 5,525 12- to 13-year-old pupils in the Rotterdam area filled in a confidential questionnaire on health topics, including their height and weight. In a sub-sample of 499 pupils both self-reported and measured height and weight were available. Results: Self-reported data led to a considerable underestimation of Body Mass Index and consequently the prevalence of overweight. Underestimation was higher in pupils who regarded themselves as more fat, were of non-Dutch origin and in lower education levels. Conclusion: Self-reported height and weight appeared to be inappropriate to estimate the overweight prevalence in 12- to 13-year-olds, unless the figures were adjusted. Using adjusted self-reported BMI on an individual level is questionable. Actual measurements of height and weight are necessary to draw up valid correction formulas in new samples. Copyright © 2006 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

Abstract Background High levels of cardiopulmonary fitness (VO2 max) are associated with reduced risk of cardiovascular morbidity and mortality, but little is known to what extent this is related to the effects of cardiopulmonary fitness on atherosclerosis and arterial stiffness. Moreover, the time course of these relationships needs to be elucidated. We sought to investigate (i) the cross-sectional relationship between VO2 max and carotid atherosclerosis and carotid and femoral arterial stiffness at age 36, as well as (ii) the relationship between VO2 max during adolescence (13–16 years) and the same arterial properties at age 36 (prospective analyses). Design Cross-sectional analyses consisted of 351 subjects (183 women) and the prospective analyses of a subpopulation of 154 subjects (79 girls). Arterial properties were assessed noninvasively by ultrasound imaging; VO2 max was measured with a maximal running text on a treadmill with direct measurements of oxygen uptake. Results After adjustment for confounding by other known risk factors, current and adolescent levels of VO2 max were independently associated with carotid intima-media thickness (β = -0·288, P = 0·004 and β = -0·381, P = 0·012) in men, and with the diameter of the femoral artery (β = 0·375, P < 0·001 and β = 0·252, P = 0·026, respectively) in both sexes. Current levels of VO2 max were positively associated with the compliance of the carotid and the femoral arteries (β = 0·186, P = 0·023 and β = 0·183, P = 0·033, respectively), and with the distensibility of the carotid (β = 0·162, P = 0·047) but not the femoral artery. Conclusion We conclude that cardiopulmonary fitness is associated with large artery properties at age 36, and that the roots of this association may already be present in adolescence. [ABSTRACT FROM AUTHOR]

Objectives: The aims of this study were to investigate (i) associations between uric acid and prevalent cardiovascular disease (CVD), ankle-arm blood pressure index (AAIx) and carotid intima-media thickness (CIMT) in the total population and in predefined subgroups according to glucose metabolism status and (ii) the extent to which these associations are explained by low-grade inflammation., Methods: Cross-sectional analyses were conducted among 530 individuals [60.6% men, mean age 58.9 years (s.d. 6.9), 52.6% normal glucose metabolism (NGM)] at increased risk of CVD from the Cohort of Diabetes and Atherosclerosis Maastricht study. A low-grade inflammation score was computed by averaging the z-scores of eight inflammation markers [CRP, TNF-α, IL-6, IL-8, serum amyloid A, intercellular adhesion molecule 1 (ICAM-1), ceruloplasmin and haptoglobin]., Results: After adjustment for traditional CVD risk factors, plasma uric acid (per s.d. of 81 μmol/l) was associated with CVD in individuals with NGM [odds ratio (OR) = 1.66, 95% CI 1.06, 2.58] but not with disturbed glucose metabolism (DGM) (OR = 0.81, 95% CI 0.55, 1.19, P interaction = 0.165). Uric acid was associated with CIMT in the total population (β = 0.024, 95% CI 0.007, 0.042) and slightly more strongly in individuals with NGM (β = 0.030, 95% CI 0.006, 0.054) than DGM (β = 0.018, 95% CI -0.009, 0.044, P interaction = 0.443). There was no association between uric acid and AAIx in any group (P interaction = 0.058). Uric acid was associated with low-grade inflammation in the total population (β = 0.074, 95% CI 0.013, 0.134, P interaction = 0.737). Adding low-grade inflammation to the models did not attenuate any of the associations., Conclusion: The associations for uric acid with CIMT, and with CVD in NGM only, were not explained by low-grade inflammation. A difference in the strength of the associations between individuals with NGM and DGM was suggested., (© The Author 2014. Published by Oxford University Press on behalf of the British Society for Rheumatology. All rights reserved. For Permissions, please email: journals.permissions@oup.com.)

Background: Cardiovascular disease (CVD) is characterized by slow progressive atherosclerosis and arterial thrombotic events, leading to occlusions. Whether either of these presentations is more likely in patients with a genetic predisposition for CVD is still unknown. We suggest that a genetic predisposition for CVD is related to recurrent events of the same nature., Methods: We retrospectively investigated 275 patients with premature CVD and divided them in two groups according to their first event: an arterial thrombotic event or stable atherosclerosis. We used a Cox proportional-hazards model to estimate the effect of a positive family history for CVD on recurrent events of the same nature. This was tested in the entire cohort and in patients with coronary artery disease only., Results: Patients with a first arterial thrombotic event and a positive family history had a threefold increased risk for a recurrent event of the same nature, compared to patients with a negative family history (hazard ratio 3.00, 95% confidence interval 1.32-6.81); p < 0.05). In contrast, a positive family history was not associated with an increased risk for a recurrent stable atherosclerosis (hazard ratio 0.98 (95% confidence interval 0.59-1.63). These findings were similar analysing the patients with coronary artery disease only. Additional adjustments for other risk factors did not change these associations., Conclusions: Patients with a first premature arterial thrombotic event and a positive family history for CVD have an increased risk for a second event of the same nature. This might be due to unknown hereditary mechanisms leading to recurrent acute events.

Aims/hypothesis: This study aimed to investigate the associations of plasma levels of the pro-inflammatory cytokine high-mobility group box 1 (HMGB1) with incident cardiovascular disease (CVD) and all-cause mortality in patients with type 1 diabetes., Methods: We prospectively followed 165 individuals with diabetic nephropathy and 168 individuals with persistent normoalbuminuria who were free of CVD at study entry and in whom levels of HMGB1 and other cardiovascular risk factors were measured at baseline., Results: During the course of follow-up (median, 12.3 years [interquartile range, 7.8-12.5]), 80 patients died, 82 suffered a fatal (n = 46) and/or non-fatal (n = 53) CVD event. After adjustment for age, sex, case-control status and other risk factors, patients with higher levels of log(e) HMGB1 had a higher incidence of fatal and non-fatal CVD and all-cause mortality: HR 1.55 (95% CI 0.94, 2.48) and HR 1.86 (95% CI 1.18, 2.93), respectively. Further adjustments for differences in markers of low-grade inflammation, endothelial and renal dysfunction and arterial stiffness did not attenuate these associations because plasma levels of HMGB1 were not independently associated with these variables., Conclusions/interpretation: In patients with type 1 diabetes, higher levels of plasma HMGB1 are independently associated with a higher risk of all-cause mortality and, to a lesser extent, with a higher incidence of CVD. Larger studies are needed to ascertain more definitely the role of HMGB1 in the development of vascular complications in diabetes.

Objectives: to compare the incidence of recurrent falls in older people with and without diabetes, and to examine diabetes- and fall-related risk factors explaining the increased risk of recurrent falls associated with diabetes., Methods: population-based cohort study of 1,145 (85 with diabetes) community-dwelling participants, aged ≥65 years, from The Longitudinal Aging Study Amsterdam (LASA). Falls were assessed prospectively (every 3 months) during a 3-year follow-up period. Incidence of recurrent falls was estimated with Poisson regression analyses. The associations between diabetes and time to recurrent falls, defined as at least two falls occurring within a 6-month period, and the potential explanatory role of several risk factors herein, were analysed with the use of Cox-regression models., Results: during a mean follow-up of 139 weeks, 30.6% of the individuals with and 19.4% of the individuals without diabetes fell recurrently [incidence rate of 129.7 versus 77.4 per 1,000 persons-years, respectively, HR = 1.67 (95% CI: 1.11-2.51)]. Adjustments for potential confounders did not change the increased risk associated with diabetes [HR = 1.63 (1.06-2.52)]. Factors that partly explained this increased risk were: greater number of medication, higher levels of pain, poorer self-perceived health, lower physical activity and grip strength, more limitations in ADLs, lower-extremity physical performance and cognitive impairment. Altogether, these variables accounted for 47% of the increased risk of recurrent falls associated with diabetes [adjusted HR = 1.30 (0.79-2.11)]., Conclusion: fall prevention efforts targeting the factors identified above may need to be incorporated into the care and treatment of older individuals with diabetes.

Cardiovascular risk factors affecting arterial stiffness in adulthood may develop at different critical periods earlier in life. We examined whether the trajectories, from adolescence to young adulthood, of blood pressure, body fatness and fat distribution, blood lipids, cardiorespiratory fitness, and heart rate determined levels of arterial stiffness in young adults. We investigated 373 apparently healthy adults in whom cardiovascular risk factors were repeatedly examined between the ages of 13 and 36 years and carotid stiffness estimates were obtained at the age of 36 years. Differences in the mean levels and the trajectories of risk factors throughout the 24-year longitudinal period between subjects with different levels of carotid stiffness at age 36 years were analyzed with generalized estimating equations. Compared with individuals with less stiff carotid arteries, those with stiffer carotid arteries at the age of 36 years were characterized from ages 13 to 36 years by greater levels of and steeper increases in blood pressure and central fatness, independently of each other and other risk factors. These increases were already present in adolescence, preceded the development of poorer levels of blood lipids, cardiorespiratory fitness, and heart rate, which were evident during adulthood only, and explained to a great extent the deleterious association between these risk factors and carotid stiffness at the age of 36 years. Multiple and intertwined mechanisms involved in the pathogenesis of arterial stiffness have their origins in early life. Blood pressure and central fatness have a pivotal role herein and should be specifically targeted to prevent arterial stiffening and its cardiovascular sequelae.

Background: Central fatness is associated with higher arterial stiffness, a mechanism that may explain adiposity-related increases in cardiovascular disease risk. In contrast, peripheral fat and lean masses may counteract such adverse effects, but evidence of this contention, as derived from longitudinal studies at the general population level, is lacking., Objective: The objective was to investigate the associations between changes in central (ie, trunk) fat mass, peripheral (ie, limbs) fat mass, and lean masses with changes in arterial stiffness., Design: A longitudinal study in 277 (145 women) healthy adults was conducted. Body composition (dual-energy X-ray absorptiometry) and arterial stiffness estimates (ultrasound imaging) were measured repeatedly at the ages of 36 and 42 y., Results: Changes (per 10 kg) in trunk fat mass were positively associated and changes in peripheral fat mass were inversely associated with carotid Young's elastic modulus (in 10(3) ⋅ kPa) [β = 0.14 (95% CI: 0.02, 0.25) and -0.16 (-0.30, -0.01), respectively] and carotid-femoral pulse wave velocity (in m/s) [β = 1.54 (0.02, 3.07) and -1.46 (-3.48, 0.56), respectively]. Individuals in whom trunk fat increased and peripheral fat decreased over the 6-y follow-up (33% of the study population) had the steepest increases in these stiffness estimates. Notably, these changes were accompanied by minor increases in body weight, which remained within the limits of the normal range throughout., Conclusions: Increases in trunk mass and decreases in peripheral fat mass are associated with accelerated arterial stiffening. These findings emphasize the importance of assessing regional changes in body composition, because it may enable identification of individuals with an unrecognized increased cardiovascular disease risk.

Background: Complement C3, a central component of the innate immune system is increased in subjects with obesity and type 2 diabetes and is a novel risk factor for cardiovascular disease. We hypothesized that the strong association between insulin resistance and circulating amounts of C3 may be related to hepatic fat accumulation -independent of central obesity itself and of a general low-grade inflammatory response., Research Question: To what extent is the association between insulin resistance and C3 explained by plasma levels of alanine aminotransferase (ALT) as a surrogate of hepatic fat accumulation., Methods: Cross-sectional analyses conducted in the Cohort on Diabetes and Atherosclerosis Maastricht (CODAM) study. Analyses were restricted to subjects with none-to-moderate alcohol consumption (n = 453, 61·4% men). Multiple linear regression analyses were used to investigate the association between HOMA2IR (main determinant) and circulating complement C3 (main outcome), and the mediating role of ALT herein. All analyses were adjusted for age, sex, presence of type 2 diabetes mellitus or heart disease, use of medication, smoking, alcohol consumption, waist circumference and inflammation., Results: Insulin resistance (estimated as HOMA2IR) was strongly associated with circulating C3 (standardized regression coefficient β 0·40 [95% CI: 0·30; 0·49]) and also with ALT (β 0·44 [0·34; 0·54]), both adjusted for the above-mentioned covariates. The association between HOMA2IR and C3 was attenuated after further adjustment for ALT (β decreased to 0·34 [0·24; 0·44])., Concluding Remarks: Plasma ALT can explain 14·2% of the strong association between insulin resistance and circulating concentrations of complement C3, independent of central obesity and general inflammation., (© 2010 The Authors. European Journal of Clinical Investigation © 2010 Stichting European Society for Clinical Investigation Journal Foundation.)

Background: It remains unclear whether the impact of habitual physical activity (HPA) differs for central vs. peripheral arterial stiffness, both of which are detrimental to cardiovascular health. We investigated the associations of lifetime HPA of different intensities on brachial and femoral stiffness in young adults, and compared these with those previously obtained for the carotid artery in the same study population., Methods: Prospectively measured data (eight repeated measures between ages 13 and 36 years) on HPAs, and other lifestyle and biological variables, were retrieved for 373 subjects in whom stiffness of the brachial and femoral, as well as the carotid, arteries was assessed at age 36 years. Generalized estimating equations were used to examine the differences in time spent in HPAs (min/week) across sex-specific tertiles of the brachial and femoral distensibility (DC) and compliance (CC) coefficients., Results: After adjustment for potential confounders, subjects in the highest (more compliant) vs. those in the lowest tertiles of the brachial and femoral CCs (less compliant) at age 36 years had spent on average more time in vigorous (+21.2 (95%CI:2.0; 40.4) and +24.4 (5.0; 43.8), respectively) but not in light-to-moderate HPAs throughout the longitudinal period. These differences were explained by 28 and 62%, respectively, by vigorous-HPA-related favorable impacts on other cardiovascular risk factors. No such associations were observed for the brachial and femoral DCs, however., Conclusions: Lifetime vigorous, but not light-to-moderate, HPA is favorably associated with brachial and femoral compliance, but not DC. Altogether, these and our previous findings thus suggest generalized vigorous-HPA-related adaptations, although of different nature, throughout the arterial tree.

Objective: The association between obesity and cardiovascular disease and venous thromboembolism might, at least partially, be explained by a hypercoagulable state. The extent to which body fat mass and its distribution contribute to a hypercoagulable state is unknown. In this study, we investigated the association between body composition and thrombin generation and evaluated the potential mediating role of low-grade inflammation., Methods and Results: We studied 586 individuals from the Hoorn Study (mean age, 69.7 ± 6.5 years, 298 women) in whom body composition was assessed by whole body dual-energy absorptiometry. Thrombin generation was measured using the calibrated automated thrombogram. Multiple regression analyses showed a positive association between total body fat and thrombin generation in women but not in men. In addition, detailed analyses of regional body composition showed that central but not peripheral fat mass was associated with greater thrombin generation and that there was a trend toward an inverse association with peripheral lean mass. The reported positive associations were partially attenuated by low-grade inflammation, however., Conclusions: Body fat mass, in particular a central pattern of fat distribution, is associated with higher levels of thrombin generation in elderly women but not in men. This association may partially be explained by adiposity-related low-grade inflammation, but this hypothesis needs to be further investigated in mechanistic/prospective studies.

Background: The association between low birthweight and increased blood pressure in later life has repeatedly been confirmed. Increased arterial stiffness may be an underlying mechanism for this phenomenon. This study investigated whether birthweight was related to blood pressure and local and regional arterial stiffness., Methods: In 281 subjects (161 women), with a mean age of 36, blood pressure was measured. The diameter, distension, and local pulse pressure of three large arteries were measured simultaneously using ultrasound imaging. Local and regional arterial compliance and distensibility were calculated. Information on birthweight was retrieved with a questionnaire., Results: Linear regression analyses showed a 3.3 mmHg lower systolic blood pressure (SBP) and a 1.8 mmHg lower diastolic blood pressure (DBP), per 1kg higher birthweight. These associations were statistically significant after adjustment for adult weight. Birthweight was significantly and positively related to carotid arterial compliance (P = 0.050), but less so to brachial (P = 0.114) and femoral arterial compliance (P = 0.058). However, after adjustment for adult height, the strength of these associations decreased. Birthweight was not related to arterial distensibility. The association between birthweight and arterial compliance could only partly explain the association between birthweight and blood pressure., Conclusions: Lower birthweight is related to increased blood pressure, and increased arterial stiffness. However, the latter relationship can only partly explain the association between birthweight and blood pressure. Therefore, mechanisms other than arterial stiffness contribute to the birthweight-blood pressure relationship.