Adolescence: A Critical Period for Long-Term Tracking of Risk for Coronary Heart Disease?

Ovesen, Lars

doi:10.1159/000094294

Cited by 21 publications

(17 citation statements)

References 115 publications

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“…Despite these potential limitations, our findings lend some support to our biologically based hypothesis that nutritionally driven increases in sex steroid levels at puberty generate a lifelong less favourable HDL-cholesterol profile and body shape in boys while having the opposite effect in girls, without causing sex differences in precursors of diabetes 11 47…”

Section: Discussionsupporting

confidence: 68%

Does childhood meat eating contribute to sex differences in risk factors for ischaemic heart disease in a developing population?

Heys

Jiang

Cheng

et al. 2010

Journal of Epidemiology & Community Health

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Given the potential limitations of this study, especially the crude nature of the exposure and modest findings, the results should be considered as preliminary. However, they do lend support to the hypothesis that the male epidemic of premature IHD and sexual divergence in IHD rates that occur with economic development may be nutritionally driven in childhood. In elucidating the developmental origins of non-communicable chronic diseases, more attention should be focused on the sociohistorical context and the role of puberty.

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Section: Discussionsupporting

confidence: 68%

Does childhood meat eating contribute to sex differences in risk factors for ischaemic heart disease in a developing population?

Heys

Jiang

Cheng

et al. 2010

Journal of Epidemiology & Community Health

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“…growth hormone [70]–[75]. Lipids and central obesity track across the life course from adolescence [76]. We speculate that nutritionally driven increases in sex-steroids at puberty, manifested by earlier and more intense puberty seen in economically developed environments [77] but not in very poor environments [68], permanently increase sexual dimorphism in shape, HDL-cholesterol and ApoB with correspondingly increased IHD risk in men compared to women.…”

Section: Discussionmentioning

confidence: 92%

Growth Environment and Sex Differences in Lipids, Body Shape and Diabetes Risk

et al. 2007

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BackgroundSex differences in lipids and body shape, but not diabetes, increase at puberty. Hong Kong Chinese are mainly first or second generation migrants from China, who have shared an economically developed environment for years, but grew up in very different environments in Hong Kong or contemporaneously undeveloped Guangdong, China. We assessed if environment during growth had sex-specific associations with lipids and body shape, but not diabetes.Methodology and Principal FindingsWe used multivariable regression in a population-based cross-sectional study, undertaken from 1994 to 1996, of 2537 Hong Kong Chinese residents aged 25 to 74 years with clinical measurements of ischaemic heart disease (IHD) risk, including HDL-cholesterol, ApoB, diabetes and obesity. Waist-hip ratio was higher (mean difference 0.01, 95% CI 0.001 to 0.02) in men, who had grown up in an economically developed rather than undeveloped environment, as was apolipoprotein B (0.05 g/L, 95% CI 0.001 to 0.10), adjusted for age, socio-economic status and lifestyle. In contrast, the same comparison was associated in women with lower waist-hip ratio (−0.01, 95% CI −0.001 to −0.02) and higher HDL-cholesterol (0.05 mmol/L, 95% CI 0.0004 to 0.10). The associations in men and women were significantly different (p-values<0.001). There were no such differences for diabetes.ConclusionsGrowth in a developed environment with improved nutrition may promote higher sex-steroids at puberty producing an atherogenic lipid profile and male fat pattern in men but the opposite in women, with tracking of increased male IHD risk into adult life.

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“…From an etiologic point of view, this does not hinder the validity of our findings; in fact, it just emphasizes the need for public health interventions targeting young people. 26,27 Third, although we have adjusted our analyses extensively for several potential confounders, we cannot fully exclude the possibility of residual confounding. Fourth, although the use of local pulse pressure estimated by calibration of the distension waveforms 25 instead of brachial pulse pressure for the calculations of the carotid stiffness estimates constitutes a strength to our study, this method still may not optimally reflect the level of pulse pressure at the level of the carotid artery.…”

Section: Discussionmentioning

confidence: 99%

Carotid Stiffness in Young Adults: A Life-Course Analysis of its Early Determinants

et al. 2012

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Abstract-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. A rterial stiffness is an important cause of cardiovascular disease because of its contribution to systolic hypertension, left ventricular hypertrophy, and impaired coronary perfusion. 1-3 Arterial stiffness is primarily determined by aging and mean arterial pressure (MAP), 2,4 but other risk factors (RF) may also contribute, notably body fatness and/or a central pattern of fat distribution, 5-8 impaired glucose metabolism and insulin resistance, 2 poor cardiorespiratory fitness, 9,10 and dyslipidemia. 11,12 Recently, a systematic review suggested that the contribution to arterial stiffness of RF other than blood pressure (BP) was only modest, although this evidence was derived from cross-sectional studies only. 13 Therefore, a life-course rather than a single time-point approach to the study of (early) determinants of arterial stiffness is needed.The negligible, if any, role of RF other than BP on arterial stiffness was also emphasized in a prospective analysis conducted among men throughout middle age and older age. 14 However, some evidence suggests that arterial stiffness in adulthood has its roots early in life. Indeed, studies among the young have shown that greater levels of BP 15,16 and body fatness and/or a central pattern of fat distribution 5,15,17 measured in childhood/adolescence were as...

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Adolescence: A Critical Period for Long-Term Tracking of Risk for Coronary Heart Disease?

Cited by 21 publications

References 115 publications

Does childhood meat eating contribute to sex differences in risk factors for ischaemic heart disease in a developing population?

Does childhood meat eating contribute to sex differences in risk factors for ischaemic heart disease in a developing population?

Growth Environment and Sex Differences in Lipids, Body Shape and Diabetes Risk

Carotid Stiffness in Young Adults: A Life-Course Analysis of its Early Determinants

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