Abstract-Development of hypertension has been linked to chronic low-grade inflammation. However, it is not known whether this connection is mediated by features of the metabolic syndrome or smoking, or their changes, which themselves have been linked to inflammation. We studied the predictive value of highly sensitive C-reactive protein (hs-CRP), smoking, and abdominal obesity to the development of hypertension in an 11-year follow-up of a population-based study cohort comprising 379 middle-aged normotensive men. During the follow-up, 124 men (33%) developed hypertension. Men with hs-CRP Ն3.0 mg/L were 2.8ϫ (95% confidence interval, 1.2 to 6.6) more likely to develop hypertension than with hs-CRP Ͻ1.0 mg/L even after adjustment for features of the metabolic syndrome, lifestyle factors, and their changes. Cigarette smoking was also associated with development of hypertension independently of inflammation and other confounders. Waist girth increased more in men who quit smoking than in other men. An increase in waist girth during follow-up strongly predicted incident hypertension. The decrease in smoking was not associated with a lower risk of hypertension in age-adjusted analyses. Hypertension is preceded by low-grade chronic inflammation in middle-aged white men independently of smoking or features of the metabolic syndrome. Furthermore, smoking may be a risk factor for hypertension. Although stopping smoking is beneficial with respect to health outcomes, the subsequent increase in weight and waist girth associated with smoking cessation may offset the decrease in the risk of hypertension that one may otherwise expect. Key Words: obesity Ⅲ smoking Ⅲ prospective studies Ⅲ insulin resistance C hronic low-grade inflammation seems to be an early feature of many chronic degenerative disorders, including atherosclerosis, abdominal obesity, and type 2 diabetes. 1-3 These disorders are also commonly associated with hypertension, which itself has also been linked recently to inflammation. The most compelling evidence comes from the Women's Health Study, in which C-reactive protein (CRP) as a marker of low-grade inflammation predicted the development of hypertension in a cohort of 20 525 female US health professionals during a follow-up of 7.8 years. 4 This effect was seen even in those with low baseline blood pressure levels and in those without other conventional cardiovascular risk factors, but no adjustment could be made for the presence of the metabolic syndrome, a possible mediator of this connection. 5 Smoking causes an acute rise in blood pressure, whereas the connection between chronic smoking and development of hypertension is still unclear. Smoking in its own right increases inflammation, 6 but smoking cessation may not reverse it. 7 Furthermore, stopping smoking commonly leads to weight gain. Weight gain is a well-established risk factor for hypertension. Moreover, weight gain and obesity, especially abdominal, appear to not only cause inflammation but may be preceded by inflammation. 8 Complicating the pictur...

Differences in methodology between national surveys make international comparisons difficult. Nevertheless, low-cost dietary interventions and the development of primary prevention strategies are needed to reduce the already existing public health problem of elevated TC in developing countries.

The study confirmed the tracking of SBP during childhood. Birth weight was inversely associated with SBP-15y. Family history of hypertension was not significantly associated with SBP during childhood.

The study evaluated the association of the insertion/deletion polymorphism of the angiotensin-converting enzyme gene (ACE I/D) with self-reported moderate-intensity leisure time physical activity (MILTPA), arterial blood pressure (BP) and history of hypertension (HT). A representative population-based sample of 721 middle-aged adults (358 women) from two areas of Finland was genotyped for the ACE I/D. After exclusion criteria were applied, 455 subjects (288 women) were selected for the analysis. The distribution of the ACE I/D genotypes did not differ significantly among frequent vs. nonfrequent MILTPA groups (chi(2) = 2.556; df = 2; P value = 0.279). The main predictors of BP were male gender, age, body mass index, and arterial pulse. Additionally, tobacco smoking and alcohol consumption also had a significant main effect on diastolic BP. HT was significantly more frequent in subjects with obesity, family history of cardiovascular disease, or lower educational level. As for BP, neither ACE I/D nor MILTPA was associated with HT. The study confirmed recent reports from population-based studies of no association between ACE I/D and physical fitness. The study also confirmed a lack of association between ACE I/D and BP or HT.