A Prospective Study of
            <i>Trans</i>
            Fatty Acids in Erythrocytes and Risk of Coronary Heart Disease

Sun, Qi; Ma, Jianchao; Campos, Hannia; Hankinson, Susan E.; Manson, JoAnn E.; Stampfer, Meir J.; Rexrode, Kathryn M.; Willett, Walter C.; Hu, Frank B.

doi:10.1161/circulationaha.106.679985

Cited by 215 publications

(176 citation statements)

References 37 publications

(51 reference statements)

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“…In contrast, the levels of trans-16:1 nÀ7 were not associated with higher CHD risk. The stronger results using measured TFA levels (Sun et al, 2007), compared with estimated TFA intake from dietary questionnaires (Willett et al, 1993;Hu et al, 1997;Oh et al, 2005) in the same cohort, suggest that inaccuracies (random error) in dietary questionnaire estimation may significantly attenuate the true association with CHD risk and/or that TFA in cell membranes may be a more proximate measure of their ultimate biologic effects than consumed TFA.…”

Section: Resultsmentioning

confidence: 97%

“…Nevertheless, because clinical trials often evaluate effects of higher doses of TFA over shorter durations of intake and in generally healthier individuals, the evidence for effects of habitual TFA consumption on serum lipids in observational studies is important. The relationships of erythrocyte TFA levels, a biomarker of dietary intake, and serum lipids were evaluated in 327 US women selected as controls in a nested prospective study of CHD events (Sun et al, 2007). After adjustment for age, smoking, body mass index (BMI), physical activity, alcohol intake, family history of myocardial infarction (MI) and fasting status at the time of blood draw, higher TFA levels (corresponding to a range of habitual TFA intake from 2.5 to 3.6 g/day) were associated with significantly higher LDL-C, lower HDL-C and a higher LDL-C:HDL-C ratio (each Po0.01).…”

Section: Resultsmentioning

confidence: 99%

“…Also in the Nurses' Health Study, a nested case-control study was conducted using measurement of TFA levels in plasma and red blood cells (Sun et al, 2007). The blood samples were collected in 1989-1990 while the women were generally healthy.…”

Section: Resultsmentioning

confidence: 99%

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Health effects of trans-fatty acids: experimental and observational evidence

2009

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Background/Objectives: 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). Subjects/Methods: 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. Results: The effects of TFA consumption on risk factors most consistently seen in both controlled trials and observational studies included adverse lipid effects (for example mlow-density lipoprotein cholesterol, khigh-density lipoprotein cholesterol (HDL-C), mtotal/HDL-C ratio), proinflammatory effects (for example mtumor necrosis factor-a activity, minterleukin-6, mC-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. Conclusions: 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.

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Section: Resultsmentioning

confidence: 97%

Section: Resultsmentioning

confidence: 99%

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Health effects of trans-fatty acids: experimental and observational evidence

2009

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“…The former may cause an overestimation of effects and the latter would cause its underestimation. For example, the use of objective biomarkers of TFA consumption (for example, erythrocyte membrane levels) (Sun et al, 2007) reveals stronger associations between TFA intake and CHD risk than the use of dietary questionnaires (Willett et al, 1993;Hu et al, 1997;Oh et al, 2005).…”

Section: Degree Of Adjustment Prospective Studymentioning

confidence: 99%

Quantitative effects on cardiovascular risk factors and coronary heart disease risk of replacing partially hydrogenated vegetable oils with other fats and oils

2009

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Background/Objectives: Reduced consumption of trans-fatty acids (TFA) is desirable to lower coronary heart disease (CHD) risk. In practice, partially hydrogenated vegetable oils (PHVO) that contain both TFAs and other fatty acids are the unit of replacement and could be replaced with diverse alternative fats and oils. We performed quantitative estimates of CHD effects if a person's PHVO consumption were to be replaced with alternative fats and oils based on (1) randomized dietary trials and (2) prospective observational studies. Subjects/Methods: We performed meta-analyses of (1) the effects of TFAs on blood lipids and lipoproteins in controlled dietary trials and (2) associations of habitual TFA consumption with CHD outcomes in prospective cohort studies. On the basis of these results and corresponding findings for saturated fatty acids (SFA), cis-monounsaturated fatty acids (MUFA) and cis-polyunsaturated fatty acids (PUFA), we calculated the effects on CHD risk for replacing 7.5% of energy from three different PHVO formulations (containing 20, 35 or 45% TFAs) with butter, lard, palm or vegetable oils. Results: In controlled trials, each 1% energy replacement of TFAs with SFAs, MUFAs or PUFAs, respectively, decreased the total cholesterol (TC)/high-density lipoprotein cholesterol (HDL-C) ratio by 0.31, 0.54 and 0.67; the apolipoprotein (Apo)-B/ApoAI ratio by 0.007, 0.010 and 0.011; and lipoprotein (Lp)(a) by 3.76, 1.39 and 1.11 mg/l (Po0.05 for each). We also included possible effects on C-reactive protein (CRP) of TFAs vs other fats from one trial. On the basis of these risk factor changes in controlled trials, CHD risk would be variably decreased by different fats and oils replacing 7.5% of energy from 20% TFA PHVO (CHD risk reduction: À2.7% (butter) to À9.9% (canola)); 35% TFA PHVO (À11.9% (butter) to À16.0% (canola)); or 45% TFA PHVO (À17.6% (butter) to À19.8% (canola)). In prospective cohort studies, each 2% energy replacement of TFAs with SFAs, MUFAs or PUFAs would lower CHD risk by 17% (95% confidence interval (CI) ¼ 7-25%), 21% (95% CI ¼ 12-30%) or 24% (95% CI ¼ 15-33%), respectively. On the basis of these associations in observational studies, CHD risk would be variably decreased by different fats and oils replacing 7.5% of energy from 20% TFA PHVO (CHD risk reduction: þ 0.5% (butter) to À21.8% (soybean)); 35% TFA PHVO (À14.4% (butter) to À33.4% (soybean)); or 45% TFA PHVO (À22.4% (butter) to À39.6% (soybean)). The demonstrated effects on TC/HDL-C, ApoB/ ApoAI, Lp(a), and CRP in randomized feeding trials together accounted for B65-80% and B50% of the estimated risk reduction for replacing PHVO with animal fats and vegetable oils, respectively, that would be calculated from prospective cohort studies. Conclusions: Effects on CHD risk of removing PHVO from a person's diet vary depending on the TFA content of the PHVO and the fatty acid composition of the replacement fat or oil, with direct implications for reformulation of individual food products. Accounting for the summed effects of TFAs on multiple CH...

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“…The TFA consumption increases the levels of fasting triglycerides as in comparison to the same amounts of MUFA and PUFA consumption (MOZAFFARIAN; CLARKE, 2009). In an observational study, it was found that the consumption of 2.6 to 3.6 g/day of TFA was associated with higher levels of LDL-C, lower levels of HDL-C, and higher LDL-C/HDL-C ratios (SUN et al, 2007). The mechanisms by which TFA promote these changes seems to be due to the increased activity of the protein carrier of cholesteryl esters (CETP), which may contribute to the increase in the production of LDL-C and low production of HDL-C when the TFA is consumed (van TOL et al, 1995).…”

Section: Trans Fatty Acidsmentioning

confidence: 99%