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From Departments of
* Nutrition and
Epidemiology, Harvard School of Public Health;
** General Medicine Division, Department of Medicine, Massachusetts General Hospital and Department of Medicine, Harvard Medical School;
the Channing Laboratory and
Division of Preventive Medicine, Harvard Medical School;
Department of Laboratory Medicine, Children’s Hospital and Department of Pathology, Harvard Medical School
2To whom correspondence should be addressed. E-mail: elopezga{at}hsph.harvard.edu.
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ABSTRACT |
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 TOP ABSTRACT SUBJECTS AND METHODSRESULTSDISCUSSIONLITERATURE CITED |
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KEY WORDS: • trans fatty acids • inflammation • endothelial dysfunction • Nurses’ Health Study
In prospective studies, trans fatty acid intake has been associated with higher risk of cardiovascular disease and type 2 diabetes mellitus (1–5). This relation can be explained by several mechanisms. Metabolic studies showed that trans fatty acid intakes above the population range of consumption raise LDL cholesterol, lower HDL cholesterol, and increase lipoprotein (a) and plasma triglyceride levels. Trans fatty acids can influence thrombogenesis through the eicosanoid synthesis pathway, and may also promote insulin resistance (6).
Increasing evidence indicates the important role of endothelial dysfunction in the development of cardiovascular disease and that dietary factors might influence cardiovascular risk through modulation of endothelial function (7). Recently, Mozaffarian et al. (8) found that intake of trans fatty acids was associated with plasma concentrations of biomarkers of systemic inflammation, but they did not evaluate their effects on endothelial adhesion molecules, which are markers of endothelial activation and dysfunction. In this study, we examined intake of trans fatty acids in relation to plasma concentration of biomarkers of inflammation and endothelial dysfunction, including C-reactive protein (CRP),3 interleukin-6 (IL-6), soluble tumor necrosis factor receptor (sTNFR-2), E-selectin, and soluble intercellular and vascular cell adhesion molecules (sICAM-1 and sVCAM-1, respectively) among apparently healthy women.
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SUBJECTS AND METHODS |
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TOPABSTRACTSUBJECTS AND METHODSRESULTSDISCUSSIONLITERATURE CITED |
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Blood collection and assessment of biomarkers. Blood was collected between 1989 and 1990. Women willing to provide blood specimens were sent instructions and a phlebotomy kit. Sodium heparin was used as an anticoagulant. Blood specimens were returned by overnight mail on ice, centrifuged (1200 x g, 15 min) on arrival to separate plasma from buffy coat and red cells, and frozen in liquid nitrogen until analysis; 97% of samples arrived within 26 h of phlebotomy. Quality control samples were routinely frozen along with study samples to monitor changes due to long-term storage and assay variability. All biomarkers were measured in the Clinical Chemistry Laboratory at Children’s Hospital in Boston. High-sensitivity CRP levels were measured by a high-sensitivity latex-enhanced inmunonephelometric assay on a BNII analyzer (Dade Behring). IL-6 was measured by a quantitative sandwich enzyme immunoassay technique (Quantikine HS Immunoassay kit) and sTNFR-2 by an ELISA kit utilizing immobilized monoclonal antibody to human TNFR-2 (Genzyme). Levels of E-selectin, sICAM-1, and sVCAM-1 were measured by Theyare ELISA (R&D Systems). The interassay CVs for each biomarker were: CRP, 3.4–3.8%; IL-6, 5.8–8.2%; sTNFR-2: 3.6–5.1%; E-selectin, 6.4–6.6%; sICAM-1, 6.1–10.1%; sVCAM-1, 8.5–10.2%. Processing times did not substantially affect concentration of the biomarkers (9).
Assessment of dietary intake.
In 1986 and 1990, a semiquantitative FFQ was mailed to participants. The FFQ included 116 food items with specified serving sizes that were described by using natural portions or standard weight and volume measures of the servings commonly consumed in this study population. For each food item, participants indicated their average frequency of consumption over the past year in terms of the specified serving size by checking 1 of the 9 frequency categories ranging from "almost never" to "
6 times/d." Detailed information about types of fat or oil used for frying, baking, and at the table, and the type, brand, and year of consumption of margarine was also collected. The average daily intake of nutrients was calculated by multiplying the frequency of consumption of each item by its nutrient content per serving and totaling the nutrient intake for all food items. Values for the total trans isomer fatty acid contents of foods were based on analyses by Enig et al. (10) and Slover et al. (11) and updated using data from the USDA, food manufacturers, and analyses of commonly used margarines, shortenings, and baked products performed at the Harvard School of Public Health (Department of Nutrition). We included the trans isomers of 16- and 18-carbon fatty acids. Nutrient intakes were adjusted for total energy intake by the residual approach (12). We calculated the means of nutrient intakes in 1986 and 1990 to represent long-term dietary consumption and to reduce measurement error.
Glycemic load was calculated for each food by multiplying the carbohydrate content of 1 serving by the food’s glycemic index value. We then multiplied this glycemic load value by the frequency of consumption and summed these products over all food items to produce the dietary glycemic load (13).
The reproducibility and validity of the FFQ were described in detail elsewhere (14). The questionnaire provided a reasonable measure of intake of total and specific types of fats compared with multiple 1-wk diet records. The correlation coefficients between the calculated dietary fatty acid intake from the FFQ and the proportion of the fatty acids in adipose tissue were 0.40 (P < 0.001) for total trans fats, 0.40 (P < 0.001) for polyunsaturated fats, and 0.16 (P > 0.05) for saturated fatty acids (15).
Assessment of other variables. Body weight and smoking status were assessed in 1990. BMI was calculated as weight (kg)/height2 (m). Physical activity was assessed in hours per week spent pursuing common leisure-time physical activities expressed as metabolic equivalent hours per week (MET-h/wk). Alcohol consumption was measured as mean intake (g/d) between 1986 and 1990 (16). Hormone therapy (HT) use was ascertained among postmenopausal women, who were classified as never, past, or current users in 1990.
Statistical analysis.
We used PROC GLM in SAS (17) to calculate adjusted geometric means and their 95% CI for the biomarkers according to quintiles of trans fat intake. We used the log-transformed biomarkers as the dependent variables. In multivariate models, we adjusted for age (
45, 46–50, 51–55, 56–60, 61–65, 66 y), BMI (<23.0, 23.0–24.9, 25.0–29.9, 30.0–34.9, 35.0 kg/m2), physical activity (<1.5, 1.5–5.9, 6.0–11.9, 12.0–20.9, 21.0 MET-h/wk), smoking status (never, past, current 1–14 cigarettes/d, current 15 cigarettes/d), alcohol consumption (nondrinker, <5.0, 5.0–10.0, >10.0 g/d), and intakes of monounsaturated, polyunsaturated, and saturated fatty acids (in quintiles). We performed sensitivity analyses, adjusting the models also for intake of fiber, cholesterol, total vitamin E, glycemic load (in quintiles), and for use of HT (premenopausal, never, past, current use). We also examined whether the associations were modified by body weight. In addition, we examined the effect of each type of trans fatty acid on the biomarkers.
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RESULTS |
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TOPABSTRACTSUBJECTS AND METHODSRESULTSDISCUSSIONLITERATURE CITED |
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We also performed analyses considering different types of trans fatty acids separately. The intake of oleic acid [t18:1(n–9)] appeared to be more strongly associated with the concentrations of biomarkers than trans palmitoleic acid [t16:1(n-7)] or trans linoleic acid [tt18:2(n-6)]. Trans oleic acid was positively related to levels of sTNFR-2 (P = 0.002), E-selectin (P = 0.001), sICAM-1 (P = 0.003), and sVCAM-1 (P < 0.001). Trans palmitoleic acid was inversely associated with levels of sTNF-R2 (P = 0.05), E-selectin (P = 0.05), sICAM-1 (P < 0.001), and sVCAM-1 (P = 0.02). Intake of trans-trans linoleic acid was positively associated with levels of sTNFR-2 (P = 0.006), E-selectin (P = 0.03), sVCAM-1 (P = 0.05), and marginally with sICAM-1 (P = 0.06). Finally, intake of cis-trans linoleic acid was positively associated with levels of E-selectin (P = 0.009) and marginally with sVCAM-1 (P = 0.08).
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DISCUSSION |
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TOPABSTRACTSUBJECTS AND METHODSRESULTSDISCUSSIONLITERATURE CITED |
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In a 3-y follow-up study, Ridker et al. (18) found that women who later developed cardiovascular events had baseline plasma levels of CRP 50% higher than those who were free of the disease at the end point. In addition, these women also had higher baseline levels of IL-6 and sICAM-1 (27 and 9%, respectively). In our study, we found that differences in concentrations of the biomarkers between extreme quintiles of trans fat intake are comparable to the differences in women with and without risk of developing cardiovascular events. Thus, the association between trans fat and biomarkers of inflammation and endothelial dysfunction could explain why the epidemiologic studies showed greater risk of developing cardiovascular disease than one would predict based solely on the effects of trans fatty acids on blood lipids (4).
The relevance of inflammatory and endothelial dysfunction biomarkers in the atherogenic process was suggested by several studies. CRP and IL-6 are markers of systemic inflammation and are independent predictors of cardiovascular disease in healthy women (18). Recent data suggest that CRP plays a direct role in atherogenesis (19). In addition, the soluble TNF receptor, which is induced by TNF and other cytokines, is an indicator of inflammatory processes (20) and has been associated with obesity and coronary heart disease (21,22). On the other hand, E-selectin, sICAM-1, and sVCAM-1 are surface and soluble cell adhesion molecules that are overexpressed when the endothelium encounters inflammatory stimuli. The relation between these adhesion molecules and cardiovascular disease has been established, i.e., patients with coronary heart disease had higher levels of E-selectin and sICAM-1 (23), and baseline plasma levels of sICAM-1 were predictors of myocardial infarction among apparently healthy men (24). Finally, sVCAM-1 was a predictor of a more advanced stage in the atherosclerotic process (25).
The biological mechanisms underlying the adverse effects of trans fatty acids on endothelial function are not clear. Trans fats are incorporated into endothelial cell membranes and thus could alter cellular and macromolecular components acting at the interface of the blood vessel wall. This could result in changes in the antihemostatic properties, altered vascular tone, hyperadhesiveness to blood leukocytes, and increased cytokine and growth factor production, all of which are characteristics of endothelial dysfunction (26).
In a recent study, trans fatty acids were found to impair endothelial function assessed by flow-mediated vasodilation (27). Because both the altered vasodilation and the increased production of inflammatory and adhesion molecules indicate endothelial dysfunction, these results are consistent with our findings. However, a high consumption of trans fatty acids might also impair endothelial function indirectly by reducing HDL cholesterol concentration (28), which in turn may trigger LDL oxidation (29). We did not adjust for plasma levels of HDL cholesterol in our analyses because we did not measure blood lipids. Nevertheless, adjustment for serum lipid concentrations only partly attenuated the association between intake of trans fats and sTNFR-1 and sTNFR-2 in a recent study of younger women (8), suggesting that the effect of trans fat on the endothelium is not entirely mediated by HDL cholesterol.
Another recent clinical trial found that the intake of 8% of energy in the diet from trans fatty acids at the expense of oleic acid or carbohydrate for 5 wk led to higher CRP and E-selectin levels (30). However, the effects were not observed at a lower level of trans fat (4% of energy). Our study suggests that long-term consumption of trans fat, even at lower levels, could be detrimental to endothelial function.
Adipose tissue is an important endocrine organ; adipocytes secrete a variety of bioactive proteins, including IL-6 and TNF-
(31). In a previous study of younger women, a positive association between trans fat and CRP was observed only among those with a higher BMI (8). However, we found that the effect of trans fatty acids on endothelial dysfunction was independent of BMI.
Although some evidence suggests that trans isomers of linoleic acid are more strongly related to risk of sudden cardiac death compared with trans isomers of oleic acid (32), intake of trans oleic acid was more strongly associated with plasma concentrations of biomarkers in our study. Trans oleic acid was the most abundant trans fatty acid in our population; thus, the different effects might be due to the higher proportion of trans oleic acid in the pool of trans fats rather than to their different biochemical characteristics.
Our study has several limitations. First, it is cross-sectional; therefore, we cannot infer causality from our results. Second, there is some degree of error in the measurement of food consumption as well as in biochemical measures, although the dietary questionnaire was shown to reflect long-term intake and the biomarker measures are reasonably stable over time. In addition, the use of the repeated measurement of food consumption enabled us to reduce within-person random error. Finally, changes in the trans fatty acid content of different foods over time might have resulted in errors in the estimation of trans fat intake (33). We minimized these errors by considering the brand and specific type of food when calculating trans fatty acid content.
In conclusion, our findings provide strong evidence that trans fatty acids adversely affect endothelial function, which might explain in part the association of these fatty acids with the risk of cardiovascular disease. These data lend further support for the recommendation to minimize the content of trans fat in the diet.
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FOOTNOTES |
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3 Abbreviations used: CRP, C-reactive protein; HT, hormone therapy; IL-6, interleukin-6; sICAM-1, soluble intercellular adhesion molecule 1; sTNFR-2, soluble tumor necrosis factor receptor 2; sVCAM-1, soluble vascular cell adhesion molecule 1.
Manuscript received 20 September 2004. Initial review completed 29 October 2004. Revision accepted 30 November 2004.
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LITERATURE CITED |
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TOPABSTRACTSUBJECTS AND METHODSRESULTSDISCUSSIONLITERATURE CITED |
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1. Willett, W. C., Stampfer, M. J., Manson, J. E., Colditz, G. A., Speizer, F. E., Rosner, B. A., Sampson, L. A. & Hennekens, C. H. (1993) Intake of trans fatty acids and risk of coronary heart disease among women. Lancet 341:581-585.[Medline]
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9. Pai, J. K., Curhan, G. C., Cannuscio, C. C., Rifai, N., Ridker, P. M. & Rimm, E. B. (2002) Stability of novel plasma markers associated with cardiovascular disease: processing within 36 hours of specimen collection. Clin. Chem. 48:1781-1784.
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16. Giovannucci, E., Colditz, G., Stampfer, M. J., Rimm, E. B., Litin, L., Sampson, L. & Willett, W. C. (1991) The assessment of alcohol consumption by a simple self-administered questionnaire. Am. J. Epidemiol. 133:810-817.
17. SAS/STAT (2001) Guide for Personal Computers, version 8.2 2001 Cary, NC.
18. Ridker, P. M., Hennekens, C. H., Buring, J. E. & Rifai, N. (2000) C-reactive protein and other markers of inflammation in the prediction of cardiovascular disease in women. N. Engl. J. Med. 342:836-843.
19. Blake, G. J. & Ridker, P. M. (2003) C-reactive protein and other inflammatory risk markers in acute coronary syndromes. J. Am. Coll. Cardiol. 41:37S-42S.
20. Aderka, D. (1996) The potential biological and clinical significance of the soluble tumor necrosis factor receptors. Cytokine Growth Factor Rev. 7:231-240.[Medline]
21. Hauner, H., Bender, M., Haastert, B. & Hube, F. (1998) Plasma concentrations of soluble TNF-alpha receptors in obese subjects. Int. J. Obes. Relat. Metab. Disord. 22:1239-1243.[Medline]
22. Benjafield, A. V., Wang, X. L. & Morris, B. J. (2001) Tumor necrosis factor receptor 2 gene (TNFRSF1B) in genetic basis of coronary artery disease. J. Mol. Med. 79:109-115.[Medline]
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31. Yudkin, J. S., Stehouwer, C. D., Emeis, J. J. & Coppack, S. W. (1999) C-reactive protein in healthy subjects: associations with obesity, insulin resistance, and endothelial dysfunction: a potential role for cytokines originating from adipose tissue?. Arterioscler. Thromb. Vasc. Biol. 19:972-978.
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