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Coronary heart disease population studies

R14. Rosengren, J., Wilhemsen, L., Erikssen, E., Risberg, B., and Wedel, H., Lipoprotein(a) and coronary heart disease A prospective case control study in a general population sample of middle aged men. BMJ 301, 1248-1251 (1990). [Pg.128]

Furthermore, polyphenolics present in wine, of which flavonoids are important components, have been suggested to be responsible of the so called French paradox, that is, the unexpectedly low rate of mortality from coronary heart disease in French population despite an unfavourable exposure to known cardiovascular risk factors such as high saturated fat consumption [19-21]. Epidemiological studies in USA [22] and Denmark [23] reported that moderate red wine drinkers had a lower risk of coronary artery disease than participants with no alcoholic beverage preference. However, controversial results about the antioxidant capacity of human serum after red wine consumption have been reported [24-27]. It is therefore uncertain whether wine constituents other than alcohol add to the cardioprotective effects of red wine. [Pg.570]

Tea is another important dietary source for flavonoids, In fact, about half of the flavonoid intake in western populations is derived from black tea. Tea was the major source of flavonoids in the Dutch [6,13] and Welsh studies [17]. Only a small number of studies investigated the association between tea consumption and cardiovascular disease risk. No association between tea consumption and cardiovascular disease risk were reported in Scottish men and women [28] and in U.S. men in the Health Professionals follow-up study [29]. However, in a Norwegian population an inverse association was reported between tea intake, serum cholesterol, and mortality from coronary heart disease [30]. Several studies reported that tea consumption did not affect plasma antioxidant activity [31] and hemostatic factors [32]. However, a recent prospective study (the Rotterdam study) of 3,454 men and women 55 years and older followed for 2 to 3 years, showed a significant, inverse association of tea intake with severe (> 5 cm the length of the calcified area) aortic atherosclerosis. Odds ratios decreased approximately 70 % for drinking more than 500 mL/day (4 cups per day). The associations were stronger in women than in men. However, the risk reductions for moderate and mild atherosclerosis were only weak or absent [33]. [Pg.570]

The Multiple Risk Factor Intervention Trial (Dolecek, 1992) included over 12,000 men over an 8-year period. The results showed that higher ALA intakes were associated with lower risks of death due to coronary heart disease and cardiovascular disease. Furthermore, a 28% reduction in risk of stroke was associated with a 0.06% increase in the ALA content of serum phospholipids (Simon et al., 1995). Other studies have since supported the association between ALA and reduction in stroke risk (Leng et al., 1999 Vartiainen et al., 1994). Vartiainen et al. (1994) followed a Finnish population of approximately 28,000 men and women over 20 years and found that a 60% reduction in mortality from stroke was associated with increased ALA consumption. In a study involving approximately 1,100 subjects, individuals suffering a stroke had significantly lower ALA concentrations in the red blood cell (Leng et al., 1999). [Pg.31]

Thrombomodulin mutations are more important in arterial diseases than in venous diseases. The thrombomodulin polymorphism, G—>A substitution at nucleotide position 127 in the gene, has been studied regarding its relation with the arterial disease. The 25 Thr allele has been reported to be more prevalent in male patients with myocardial infarction than the control population (25). Polymorphism in the thrombomodulin gene promoter (-33 G/A) influences the plasma soluble thrombomodulin levels and causes increased risk of coronary heart disease (26). Carriership of the -33A allele was also reported to cause increased occurrence of carotid atherosclerosis in patients less than 60 years (27). [Pg.548]

Oomen, C.M., Ocke, M.C., Feskens, E.J.M., van Erp-Baart, M-A.J., Kok, F.J., Kromhout, D. 2001. Association between trans fatty acid intake and 10-year risk of coronary heart disease in the Zutphen Elderly Study a prospective population-based study. Lancet. 357, 746-751. [Pg.636]

British Heart Foundation Statistics Database (1998). Coronary Heart Disease Statistics 1998. London British Heart Foundation Cappuccio FP (1997). Ethnicity and cardiovascular risk variations in people of African ancestry and South Asian origin. Journal of Human Hypertension 11 571-576 Connor MD, Walker R, Modi G et aL (2007). Burden of stroke in black populations in sub-Saharan Africa. Lancet Neurology 6 269-278 Coull AJ, Lovett JK, Rothwell PM et al. (2004). Population based study of early risk of stroke after transient ischaemic attack or minor stroke implications for public education and organisation of services. British Medical Journal 328 326... [Pg.13]

Jamrozik K, Anderson CA, Stewart-Wynne EG (1994). The role of lifestyle factors in the etiology of stroke. A population-based case-control study in Perth Western Australia. Stroke 25 51-59 Jespersen CM, Als-Nielsen B, Damgaard M etal. (2006). Randomized placebo controlled multicentre trial to assess short term clarithromycin for patients with stable coronary heart disease CLARICOR trial. British Medical Journal 332 22-27 Jorgensen HS, Nakayama H, Raaschou HO etal. (1994). Stroke in patients with diabetes. The Copenhagen Stroke Study. Stroke 25 1977-1984... [Pg.26]

An epidemiological study in a Finnish population indicated an association between moderate iron overload (measured by serum ferritin see Iron Proteins for Storage Transport their Synthetic Analogs) and increased incidence of coronary heart disease. This remarkable association has not been coirfirmed and further investigation will be necessary to determine whether excessive iron storage may relate to coronary heart disease. ... [Pg.3198]

Rhoads GG, Gulbrandsen CL, Kagan A. Serum lipoproteins and 144. coronary heart disease in a population study of Hawaii Japanese... [Pg.873]

It is now generally accepted that obesity is an independent risk factor for coronary heart disease, over and above its effect on blood pressure and serum cholesterol (Eckel 1997). A prospective 8-year follow-up study of 115,000 women who were initially free of heart disease demonstrated that those who were obese (BMI > 29) were 3.3 times more likely to develop serious heart disease than those who were not obese at the outset (Manson et al. 1990). Obesity is clearly a strong risk factor for coronary heart disease in middle-aged women 40% of the risk of developing coronary heart disease in this population can be attributed to obesity. [Pg.98]

Initial interest in cholesterol and Alzheimer s disease stemmed from a lengthy historical backdrop. One of the first studies hnking cholesterol to AD stemmed from an observation that senile plaques were quite prevalent in the brains of non-demented patients who had died from coronary heart disease [21], a population known to possess elevated cholesterol levels. Additional studies soon followed demonstrating that the ApoE4 allele of the ApoE cholesterol transporter was a major risk factor for AD [ 13 -16]. Is there a clear association between cholesterol and Alzheimer s disease ... [Pg.56]

The initial step in management is to modify the major risk factors for HID—hypertension, hypercholesterolemia, and smoking— and data from the Multiple Risk Factor Intervention Trial (MRFIT) show these interventions to be useful in patients with silent ischemia. In a subset of the study population that had abnormal baseline exercise ECG responses, the special intervention group had a 57% reduction in coronary heart disease death (22.2 of 1000 versus 51.8 of 1000) and a reduction in sudden death resulting from cessation of smoking and lowering of blood pressure and cholesterol when compared with the usual-care group. [Pg.285]

However, since reliable data on exposure levels were not available, it is impossible to establish a dose-response relationship or a NOAEL. In addition, coronary heart disease has a multicausal origin that is in part related to the saturated fat intake of the population and is also influenced by a large number of other risk factors such as smoking, other dietary habits, diabetes, and physical inactivity. A combination of two or more risk factors greatly increases the incidence of coronary heart disease, and therefore carbon disulfide may be a cofactor in the presence of other risk factors (WHO 1979). Another limitation with occupational studies reported from the viscose rayon industry is concurrent exposure to other chemicals such as hydrogen sulfide (Hemberg et al. 1970 Rubin and Arieff 1945 Swaen et al. 1994 Tolonen et al. 1979). [Pg.33]


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