Adipose tissue isomeric trans fatty acids and risk of myocardial infarction in nine countries: the EURAMIC study.
Department of Nutrition, National Public Health Institute, Helsinki, Finland. The Lancet
(Impact Factor: 45.22).
Dietary isomeric trans fatty acids-mainly produced by hydrogenation of oils-are suspected of increasing the risk of coronary heart disease. Dietary trans fatty acid intake is reflected in the fatty acid composition of adipose tissue. In an international multicentre study in eight European countries and Israel (EURAMIC), adipose tissue aspiration samples were obtained from 671 men with acute myocardial infarction (AMI), aged 70 years or less, and 717 men without a history of AMI (controls). The proportion of fatty acids, including isomeric trans monoenoic fatty acids with 18 carbon atoms (C18:1), was determined by gas chromatography. Although there were considerable differences between countries in mean (SD) proportion of adipose tissue C18:1 trans fatty acids, there was no overall difference between cases (1.61 [0.92]%) and the controls (1.57 [0.86]%). The risk of AMI did not differ significantly from 1.0 over quartiles of adipose C18:1 trans fatty acids: the multivariate odds ratio was 0.97 (95% CI 0.56-1.67) for the highest versus lowest quartile. After exclusion of subjects from Spanish centres because they had far lower proportions of adipose trans fatty acids than subjects from other countries, there was a tendency to increased risk of AMI in the upper quartiles of C18:1 trans; however, the trend was not statistically significant. Our results reflect considerable differences between countries in dietary intake of trans fatty acids but do not suggest a major overall effect of C18:1 trans fatty acids on risk of AMI. We cannot exclude the possibility that trans fatty acids have a significant impact on risk of AMI in populations with high intake.
Available from: onlinelibrary.wiley.com
- "Effects of TFAs on the cardiovascular system Most retrospective case-control studies and prospective cohorts have reported positive associations between the high consumption of TFAs (>3 g/d) and the risk to develop CVDs, a leading cause of mortality worldwide (Ascherio and others 1994; Aro and others 1995; Kromhout and others 1995; van de Vijver and others 2000; Chardigny and others 2008; Mozaffarian and others 2009). In fact, the consumption of TFAs corresponding to 2% TEI could increase the risk of CVDs to 23% to 25% (Oomen and others 2001; Mozaffarian and others 2006), suggesting that a necessary lower threshold TEI (that is, < 1%) shall be defined by the worldwide competent authorities for consideration by the global agroindustry (Menaa 2010; Menaa and others 2012). "
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ABSTRACT: Trans fatty acids (TFAs) mainly arise from 2 major sources: natural ruminal hydrogenation and industrial partial catalytic hydrogenation. Increasing evidence suggests that most TFAs and their isomers cause harmful health effects (that is, increased risk of cardiovascular diseases). Nevertheless, in spite of the existence of an international policy consensus regarding the need for public health action, several countries (for example, France) do not adopt sufficient voluntary approaches (for example, governmental regulations and systematic consumer rejections) nor sufficient industrial strategies (for example, development of healthier manufacturing practices and innovative processes such as fat interesterifications) to eliminate deleterious TFAs from processed foods while ensuring the overall quality of the final product (for example, nutritional value and stability). In this manuscript, we first review the physical-chemical properties of TFAs, their occurrence in processed foods, their main effects on health, and the routine analytical methods to characterize TFAs, before emphasizing on the major industrial methods (that is, fat food reformulation, fat interesterification, genetically modified FAs composition) that can be used worldwide to reduce TFAs in foods.
Journal of Food Science 03/2013; 78(3):R377-86. DOI:10.1111/1750-3841.12055 · 1.70 Impact Factor
Available from: nature.com
- "The EURAMIC Study. In this international multicenter study in eight European countries and Israel, trans-18:1 nÀ9 levels (but not other TFA isomers or total TFA) were measured in adipose tissue samples obtained from 671 men with acute nonfatal MI in 1991–1992 and 717 men without a history of MI (controls) (Aro et al., 1995). In overall analyses, adipose trans-18:1 levels were not significantly associated with risk of MI: the multivariable-adjusted odds ratio for the highest versus lowest quartile was 0.97 (95% CI ¼ 0.56–1.67). "
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ABSTRACT: Growing evidence indicates that trans-fatty acids (TFA) adversely affect cardiovascular health. As part of the World Health Organization (WHO) Scientific Update on TFA, we reviewed the evidence for effects of TFA consumption on coronary heart disease (CHD).
We searched Medline publications examining TFA consumption and CHD risk factors or outcomes, emphasizing results of studies in humans. We evaluated and synthesized evidence from both controlled feeding trials evaluating risk factors and long-term observational studies evaluating risk factors or clinical outcomes, each of which have complementary strengths and limitations, to enable the most robust and reliable inferences of effects.
The effects of TFA consumption on risk factors most consistently seen in both controlled trials and observational studies included adverse lipid effects (for example [upward arrow] low-density lipoprotein cholesterol, [downward arrow] high-density lipoprotein cholesterol (HDL-C), [upward arrow] total/HDL-C ratio), proinflammatory effects (for example [upward arrow] tumor necrosis factor-alpha activity, [upward arrow] interleukin-6, [upward arrow] C-reactive protein) and endothelial dysfunction. These effects were most prominent in comparison with cis unsaturated fats; adverse effects on total/HDL-C and endothelial function were also seen in comparison with saturated fatty acids (SFA). TFA may also worsen insulin sensitivity, particularly among individuals predisposed to insulin resistance; possible effects on weight gain and diabetes incidence require further confirmation. Five retrospective case-control studies and four prospective cohort studies demonstrated positive associations between TFA consumption and CHD events. A meta-analysis of prospective studies indicated 24, 20, 27 and 32% higher risk of myocardial infarction (MI) or CHD death for every 2% energy of TFA consumption isocalorically replacing carbohydrate, SFA, cis monounsaturated fatty acids and cis polyunsaturated fatty acids, respectively. The differential effects of specific TFA isomers may be important but are less well established. The available evidence indicates that trans-18:1 and particularly trans-18:2 isomers have stronger CHD effects than trans-16:1 isomers. The limited data suggest that the experimental effects of ruminant and industrial TFA are similar when consumed in similar quantities, but very few persons consume such high levels of ruminant TFA, and observational studies do not support adverse CHD effects of ruminant TFA in amounts actually consumed.
Controlled trials and observational studies provide concordant evidence that consumption of TFA from partially hydrogenated oils adversely affects multiple cardiovascular risk factors and contributes significantly to increased risk of CHD events. The public health implications of ruminant TFA consumption appear much more limited. The effects of specific TFA isomers require further investigation.
European journal of clinical nutrition 06/2009; 63 Suppl 2(Suppl 2):S5-21. DOI:10.1038/sj.ejcn.1602973 · 2.71 Impact Factor
Available from: uaemex.mx
- "Thomas et al. (1981) encontraron concentraciones elevadas de AGT en tejido adiposo proveniente de personas muertas por enfermedad coronaria. En otros estudios se observó una marcada disminución del colesterol de lipoproteínas de alta densidad (HDL) y un aumento de lipoproteínas de baja densidad (LDL) y proteína A (Aro et al., 1997; Khosla y Hayes, 1996; Katan et al., 1995). Lo anterior provoca un desbalance en el perfil lipoproteico que es compatible con un riesgo aterogénico aumentado y comparable al efecto del consumo excesivo de grasas saturadas (Lichtenstein, 2000; Hu et al., 1997; Khosla y Hayes, 1996). "
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