| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
Original Research Communication |
1 From the Departments of Human Biology (RPM) and Methodology and Statistics (ADMK), Maastricht University, Maastricht, Netherlands, and the Wageningen Centre for Food Sciences and Division of Human Nutrition and Epidemiology, Wageningen University, Wageningen, Netherlands (PLZ and MBK).
2 Supported by Maastricht University, Wageningen University, and the Wageningen Centre for Food Sciences. 3 Reprints not available. Address correspondence to RP Mensink, Department of Human Biology, Maastricht University, PO Box 616, 6200 MD Maastricht, Netherlands. E-mail: r.mensink{at}hb.unimaas.nl.
 |
ABSTRACT |
|---|
 TOP ABSTRACT INTRODUCTIONMETHODSRESULTSDISCUSSIONREFERENCES |
|---|
Objective: The objective was to evaluate the effects of individual fatty acids on the ratis of total to HDL cholesterol and on serum lipoproteins.
Design: We performed a meta-analysis of 60 selected trials and calculated the effects of the amount and type of fat on total:HDL cholesterol and on other lipids.
Results: The ratio did not change if carbohydrates replaced saturated fatty acids, but it decreased if cis unsaturated fatty acids replaced saturated fatty acids. The effect on total:HDL cholesterol of replacing trans fatty acids with a mix of carbohydrates and cis unsaturated fatty acids was almost twice as large as that of replacing saturated fatty acids. Lauric acid greatly increased total cholesterol, but much of its effect was on HDL cholesterol. Consequently, oils rich in lauric acid decreased the ratio of total to HDL cholesterol. Myristic and palmitic acids had little effect on the ratio, and stearic acid reduced the ratio slightly. Replacing fats with carbohydrates increased fasting triacylglycerol concentrations.
Conclusions: The effects of dietary fats on total:HDL cholesterol may differ markedly from their effects on LDL. The effects of fats on these risk markers should not in themselves be considered to reflect changes in risk but should be confirmed by prospective observational studies or clinical trials. By that standard, risk is reduced most effectively when trans fatty acids and saturated fatty acids are replaced with cis unsaturated fatty acids. The effects of carbohydrates and of lauric acid–rich fats on CAD risk remain uncertain.
Key Words: Diet • fatty acids • carbohydrates • serum lipoproteins • coronary artery disease risk
|
INTRODUCTION |
|---|
|
TOPABSTRACTINTRODUCTIONMETHODSRESULTSDISCUSSIONREFERENCES |
|---|
|
METHODS |
|---|
|
TOPABSTRACTINTRODUCTIONMETHODSRESULTSDISCUSSIONREFERENCES |
|---|
We excluded studies that focused on very-long-chain (n-3) polyunsaturated fatty acids (PUFAs) such as fish oils. The effects of these oils have been reviewed elsewhere (12). Therefore, in this report, total PUFAs may be considered to equal the n-6 PUFAs with 18 carbon atoms (linoleic acid plus some 
-linolenic acid). We also excluded studies on medium-chain fatty acids, because there were too few to allow proper statistical analysis.
To convert them to serum values, plasma concentrations of total and HDL cholesterol were multiplied by 1.030 and those for triacylglycerols were multiplied by 1.029 (13). LDL-cholesterol concentrations were calculated (14). For the sake of uniformity, we also recalculated the ratio of total to HDL cholesterol and the LDL-cholesterol concentrations, even if they were reported by the authors of the report. Plasma values for apo B and apo A-I were also multiplied by 1.030 to convert them to serum values.
On average, dietary fat contains 96% (by wt) fatty acids; the other 4% is made up of glycerol and other lipids (15). For publications in which the intakes of the various fatty acid classes had been normalized to add up to 100% of total fat, we converted intakes back to true fatty acid intakes by multiplying them by 0.96.
Statistical analysis
Each data point consisted of the fatty acid composition of a particular diet (the independent variable) and the mean ratio of serum total to HDL cholesterol or the mean serum lipid or apolipoprotein concentration (the dependent variable) of a group of subjects, as obtained at the end of a dietary period. In all trials, fatty acids were exchanged for either other fatty acids or carbohydrates. Possible effects of protein and alcohol thus could not be estimated. The regression coefficients estimated in this way are the predicted change in the ratio of serum total to cholesterol or in the serum lipid or apolipoprotein concentrations when carbohydrate intake decreases by 1% of energy and that of a particular fatty acid increases by the same amount (16).
Two different models were used for SFAs and cis unsaturated fatty acids, and a third approach was used for trans fatty acids. The models used as dependent variables the absolute lipid or apolipoprotein concentrations during particular diets rather than changes induced by diet. Therefore, all models were corrected for the intrinsic concentrations to ensure that only within-study diet-induced differences were analyzed. The intrinsic concentration is a constant for a particular study. It reflects the mean estimated serum lipid or apolipoprotein concentration or their ratios that would result if this particular group of subjects consumed a standardized fat-free, high-carbohydrate diet. The intrinsic concentration is determined by such factors as genetic makeup, age, and body mass index and by such factors as the fiber, protein, or alcohol content of the background diet, which was constant within studies but differed between studies.
In the first model, the effects on a particular outcome of all fatty acids within a certain category—SFAs, cis monounsaturated fatty acids (MUFAs), or n-6 cis PUFAs—were estimated. Diets in which the fatty acid composition of a particular class of fatty acids diverged markedly from that in normal mixed diets were excluded. For example, Grande et al (17) specifically examined the effects of stearic acid on serum lipids. Because stearic acid is hypocholesterolemic compared with other SFAs (2), including this data point would have resulted in a biased estimate of the effect of a normal mixture of SFAs.
The second model estimated the effects of individual SFAs. The proportions of energy from lauric, myristic, palmitic, and stearic acids were used as independent variables, together with the sum of all cis MUFAs and the sum of all cis PUFAs. Diets rich in trans fatty acids were not included.
The validity of the regression models was examined in several ways (18). First, the influence of each separate observation (ie, trial or trial arm) on the estimated regression coefficients was assessed with the use of Cook’s distance to detect possible outliers. Our initial analysis showed that there were 1 or 2 observations with Cook’s distance > 0.3 that caused nonnormality of the residuals. Excluding these observations did not change our conclusions but resulted in normally distributed variables as indicated by the Shapiro-Wilk test (18) and narrower confidence intervals, a measure of the variability in dietary response between studies. Therefore, we decided to exclude from the final analysis observations with Cook’s distances > 0.3. Another source of errors in regression statistics can be collinearity—ie, correlations between supposedly independent variables (in this case, the various fatty acids). Collinearity can be quantitated as tolerance. For all models used, the tolerance for each fatty acid was 
0.22, which indicated that relation between the independent variables did not lead to inappropriate estimates of the regression coefficients. Finally, visual inspection of plots did not suggest a relation between residuals and predicted values or between residuals and the independent variables. This suggests that the differences between observed and predicted values (ie, the residuals) did not depend on the absolute serum lipid or lipoprotein of a trial or on the absolute intake of a particular fatty acid or class of fatty acids. All statistical analyses were carried out with PROC REG software, version 6 (19). Each study was represented by a dummy variable (the intrinsic concentration). The use of a random-effects model, which is frequently used in meta-analyses to correct for error within a study, was not possible, because it requires standard errors of treatment differences within studies, which generally were not given. Therefore, we could not differentiate within-study and between-study variability. However, the estimates of the regression coefficients in the present analysis would have been comparable with those of a random-effects analysis.
The effects of trans MUFAs were examined in a different way because the number of studies was too small for multiple regression analysis. For each single study, the difference in outcome variables between the trans diet and the control diet was adjusted for differences in the intakes of other fatty acids with the use of the results from the regression analysis described above. The effects of trans MUFAs relative to those of carbohydrates were calculated per 1% of energy, and the results from the various studies were then averaged.
|
RESULTS |
|---|
|
TOPABSTRACTINTRODUCTIONMETHODSRESULTSDISCUSSIONREFERENCES |
|---|
Classes of fatty acids
The number of diet data points included in the calculations varied from 102 for total:HDL cholesterol to 114 for total cholesterol concentration (Table 1
). In these diets, the mean intakes of fat, SFAs, MUFAs, and PUFAs were 34.3% of total daily energy (range: 4.5–53.0%), 10.2% of energy (2.2–24.4%), 13.5% of energy (1.5–39.8%), and 8.8% of energy (0.6–28.8%), respectively.
|
and Figure 1) showed that total:HDL cholesterol did not change if SFAs were replaced with carbohydrates, because total and HDL cholesterol decreased to a similar extent. The ratio decreased if SFAs or carbohydrates were replaced with cis unsaturated fatty acids. As shown in Figure 2, the observed and predicted values for total:HDL cholesterol were in excellent agreement.
|
|
). The effect was slightly but not significantly larger for PUFAs than for other fatty acids. This contrasts with the powerful triacylglycerol-lowering effect of n-3 PUFAs from fish (12), which is evidently not shared by linoleic acid, the major n-6 PUFA. Replacement of carbohydrates with SFAs did not change apo B concentrations. The cis unsaturated fatty acids, however, decreased apo B, and this effect was slightly stronger for PUFAs. SFAs and MUFAs increased apo A-I concentrations relative to carbohydrates. PUFAs did not significantly change apo A-I concentrations.
Individual saturated fatty acids
Intakes of individual SFAs were reported for 35 studies, yielding 91 data points. The mean intakes of lauric, myristic, palmitic, and stearic acids were 1.1% of total daily energy (0.0–16.9%), 1.3% of energy (0.0–14.3%), 6.2% of energy (1.0–19.9%), and 3.0% of energy (0.7–16.5%), respectively. The diet with the highest lauric acid intake, 16.9% of energy (42), was included in the model for total:HDL cholesterol but excluded from the models for total, LDL, and HDL cholesterol, because its Cook’s distance exceeded 0.3 (see Methods). The next highest lauric acid intake was 10.7% of energy.
Although lauric acid was the most potent total and LDL cholesterol–raising SFA (Table 2 and Figure 3), it actually decreased total:HDL cholesterol relative to carbohydrates. Thus, the cholesterol-raising effect of lauric acid is proportionally higher for HDL than for LDL. The ratio of total to HDL cholesterol was less affected by the other 3 SFAs, although it was somewhat more favorably affected by stearic acid than by myristic or palmitic acid.
|
|
0 mmol/L per % of energy for stearic acid. Replacement of the different SFAs with carbohydrates increased serum triacylglycerol concentrations to the same extent.
trans MUFAs
In the 8 studies that specifically examined trans MUFAS, the intake of trans MUFAs ranged between 0.0 and 10.9% of energy; these values include the trans fatty acid–free control diets in these studies. As shown in Table 3, trans 18:1 has the largest effect of all the fatty acids on total:HDL cholesterol. Furthermore, trans 18:1 does not increase HDL cholesterol or apo A-I concentrations relative to carbohydrates. Isoenergetic replacement of trans 18:1 constituting 1% of energy with SFAs decreased total:HDL cholesterol by 0.019; replacement with cis MUFAs, by 0.048; and replacement with cis PUFAs, by 0.054.
|
when mixed fat constituting 10% of energy in the "average" US diet (55, 83) is replaced with one particular fat source or with carbohydrates. For animal fats, we adjusted for the slight effects of dietary cholesterol on this ratio (84). The largest reduction is seen with unhydrogenated oils, such as rapeseed, soybean, and olive oils. Replacement of the average fat with stick margarines or butter would cause a small increase in the ratio, but, surprisingly, so would replacement with carbohydrates.
|
|
DISCUSSION |
|---|
|
TOPABSTRACTINTRODUCTIONMETHODSRESULTSDISCUSSIONREFERENCES |
|---|
Predicted effects on coronary artery disease risk
Epidemiologic studies suggest that a change of 1 U in total:HDL cholesterol is associated with a 53% change in the risk of myocardial infarction (9). We can use this figure and the coefficients in Table 1 to speculate about the effect of changes in fatty acid intake on the risk of CAD. The most clear-cut test of such speculations is provided by the clinical trials of dietary fat and heart disease. For the Finnish Mental Hospital Trial, our coefficients predict a decrease of 18% in the incidence of CAD in both sexes, compared with actual decreases of 44% in men (86) and 36% in women (87). For the Veterans Administration trial, the predicted and observed changes are 20% and 24%, respectively (88). Predicted effects are thus somewhat lower than observed effects, which suggests that dietary fatty acids also affect other risk factors for CAD. Epidemiologic observations, however, suggest a much larger effect of changes in the amount and quality of dietary fat and carbohydrates on CAD risk (89), and the possible reasons for this were discussed elsewhere (90, 91).
Effects of fatty acids and carbohydrates on serum lipids and lipoproteins
Our results suggest that isoenergetic replacement of SFAs with carbohydrates does not improve the serum total:HDL cholesterol. All natural fats contain both SFAs, which do not change this ratio, and unsaturated fatty acids, which lower it. As a result, even the replacement of dairy fat and tropical fats with carbohydrates will increase the ratio of total to HDL cholesterol (Figure 4). The products with the most favorable effect on this ratio are oils that are rich in cis unsaturated fatty acids, such as rapeseed, soybean, sunflower, and olive oils. The effects of the PUFAs, which in our analyses consisted mainly of linoleic acid plus some -linolenic acid, are more favorable than those of MUFAs such as oleic acid, but the difference is slight. Our study did not address the effects of n-3 PUFAs from fish. Their major effect on plasma lipids is to lower triacylglycerols (12), but their favorable effects on CAD mortality may also involve pathways other than plasma lipoproteins (92).
Apolipoprotein B and LDL particle size
There is evidence that not only the amount of cholesterol transported by LDL particles but also the size and density of these particles and their apo B content affect CAD risk (93). Effects of carbohydrates on apo B were less favorable than those of unsaturated fatty acids (Table 1), which may agree with the findings of studies in which high-carbohydrate diets not only increased triacylglycerol concentrations but also induced a shift toward smaller, denser LDL particles (93).
Individual saturated fatty acids
Lauric acid markedly increases cholesterol, whereas stearic acid lowers it somewhat when it is used to replace carbohydrates. However, the picture reverses if one looks at total:HDL cholesterol: both lauric and stearic acid are now more favorable than carbohydrates. Lauric acid—a major component of tropical oils such as coconut and palm kernel fat—has the largest cholesterol-raising effect of all fatty acids, but much of this is due to HDL cholesterol. As a result, lauric acid had a more favorable effect on total:HDL cholesterol than any other fatty acid, either saturated or unsaturated.
trans Fatty acids
The trans MUFAs were the most harmful macronutrient in terms of the ratio of total to HDL cholesterol. If trans MUFAs constituting 1% of energy are isoenergetically replaced with a 1:1:1 mix of carbohydrates, cis MUFAs, and cis PUFAs, then the ratio decreases by 0.04. This is equivalent to replacing SFAs constituting 1.8% of energy with such a mixture. If fat is replaced exclusively with carbohydrates, then the difference becomes even larger: isoenergetically replacing trans MUFAs constituting 1% of energy with carbohydrates has the same effect on this ratio as isoenergetically replacing SFAs constituting 7.3% of energy with carbohydrates (Tables 1 and 3). The US diet provides, on average, 2.6% of energy from trans MUFAs and nearly 13% of energy from SFAs (3), so that the total replacement of trans fatty acids in the diet with carbohydrates would have a greater effect on total:HDL cholesterol than would total replacement of SFAs. Therefore, even low concentrations of trans MUFAs in the diet should deserve attention as a target for efforts to lower CAD risk.
Consumption of trans fatty acids from partially hydrogenated oils is associated with the risk of CAD in observational studies. Unfortunately, the price, mouth-feel, and stability of such hydrogenated oils make them a favorite of manufacturers of fast foods (94). Palm oil is an acceptable alternative for the industry, and, in terms of the effect on total:HDL cholesterol, palm oil is still better than the partially hydrogenated vegetable oils used in the food service industry. However, unhydrogenated vegetable oils produce a much more favorable lipid profile than do either palm oil or hydrogenated oils, and they should be preferred.
The intake of trans fatty acids from ruminant fats including milk and cheese shows a less consistent association with CAD than does the intake of industrially hydrogenated fats. However, Oomen et al (95) found that the intakes of both ruminant and industrially produced trans fatty acids predicted a higher risk of CAD in the Zutphen Elderly Study. The intake of ruminant trans fatty acids can be kept low by a choice of skimmed dairy products and lean meat, in accordance with current guidelines.
Low-fat, high-carbohydrate diets and body weight
The unfavorable effect of carbohydrates on total:HDL cholesterol might be opposed by a favorable effect of carbohydrates on body weight, because low-fat diets may promote weight reduction. Isoenergetically replacing fat constituting 10% of energy with carbohydrates may reduce weight by 3 kg (96, 97). The data of Leenen et al (98) suggest that a weight loss of 3 kg may lead to a decrease of 0.24 in total:HDL cholesterol. If a high-carbohydrate diet reduces energy intake sufficiently to cause a 3-kg weight loss, then the effect on total:HDL cholesterol would be approximately equal that of isoenergetic replacement of SFAs constituting 10% of energy with cis unsaturated oils. This underlines the importance of weight management in the reduction of CAD risk. Unfortunately, the effects of low-fat diets on body weight over the long term are uncertain (99). The introduction of low-fat, high-carbohydrate foods in the United States does not appear to have reduced caloric intake; rather, carbohydrates seem to have been added to existing intakes. However, further studies on the long-term effect of high-carbohydrate diets on body weight are urgently needed.
Thus, it is not certain whether weight loss per se is a strong argument for replacing fat with carbohydrates. Without doubt, reducing the high prevalence of obesity should be a major public health target, but increased intakes of carbohydrates could be shown to be insufficient to counter the effects of low energy expenditure and high caloric intake that characterize modern societies.
Dietary fat and other risk factors
High-fat diets lower fasting triacylglycerol concentrations, which may reduce cardiovascular disease risk (85), but they also increase postprandial concentrations of triacylglycerol-rich lipoproteins, which are positively associated with CAD risk (100). In addition, the elevated factor VII coagulant activity that occurs during the postprandial phase of high-fat diets may predispose a person to coronary thrombosis (101, 102). Whether a high-fat diet or a high-carbohydrate diet changes insulin sensitivity or leads to the development of type 2 diabetes is still controversial (103). The final answer as to the overall effect of cis unsaturated fatty acids and carbohydrates on CAD risk can only be decided by long-term controlled clinical trials. Clinical trials have indeed shown that the replacement of SFAs and trans fatty acids with polyunsaturated oils reduces the incidence of CAD (104). The few trials that studied replacement of SFAs with carbohydrates were inconclusive (105, 106). Present trial data thus favor cis unsaturated fatty acids over carbohydrates.
Extrapolation to specific population groups and long-term effects
The number of studies of hyperlipidemic subjects who met our selection criteria was too limited for useful statistical analyses. We cannot be sure, therefore, whether the predictive coefficients for the effects of fatty acids will also apply to groups of patients with hyperlipidemia. However, persons with high baseline cholesterol concentrations are probably more sensitive to dietary changes than are persons with normal cholesterol concentrations (107, 108). Therefore, we think that our coefficients are also applicable to hyperlipidemic patients. If anything, the coefficients would underestimate the effect in persons with higher cholesterol concentrations, rather than overestimate it.
In one of our studies, we reported that the responses of total and LDL cholesterol to SFAs were slightly larger in men than in women (109). A sex effect could not be examined in the present meta-analysis because too many studies did not report separate data for men and women. Therefore, we may have slightly overestimated the effects of SFAs in women and underestimated those in men, and this issue certainly deserves further attention.
The studies included in our meta-analysis lasted between 13 and 91 d. This raises the question of whether the effects observed are transitory. However, long-term epidemiologic findings support our findings. For example, a life-long high intake of carbohydrates is associated with increased triacylglycerol concentrations (110), whereas the effects on total cholesterol of fatty acids in observational studies also agree with the trials analyzed here (111). This gives us confidence that the effects seen in our present meta-analysis are not transient.
Conclusions
The replacement of trans fatty acids with unsaturated fatty acids from unhydrogenated oils is the single most effective measure for improving blood lipid profiles. Even small amounts of unsaturated fatty acids have a major effect on the ratio of total to HDL cholesterol. The efficacy of replacing SFAs with carbohydrates depends on the effects on body weight in the long term, and that effect is uncertain.
Our results emphasize the risk of relying on cholesterol alone as a marker of CAD risk. Replacement of carbohydrates with tropical oils markedly raises total cholesterol, which is unfavorable, but the picture changes if effects on HDL and apo B are taken into account. The picture may change again once we know how to interpret the effects of diet on postprandial lipemia, thrombogenic factors, and other, newer markers. However, as long as information directly linking the consumption of certain fats and oils with CAD is lacking, we can never be sure what such fats and oils do to CAD risk.
The situation is much clearer for replacement of SFAs with cis unsaturated fatty acids. In that case, the effects on surrogate lipid markers (Tables 1 and 2), the epidemiologic findings (89), and the results of controlled clinical trials (104) all suggest that replacement of SFAs with cis unsaturated fatty acids reduces CAD risk. For trans fatty acids, the effect on lipid markers is strongly supported by prospective epidemiologic findings (95, 112). Studies such as ours can predict the effects of fats on plasma lipids, but they cannot determine whether a fat will cause CAD. Finally, it should be emphasized that our results may apply only to populationwide issues of lipid management and not to individual patients, whereas total:HDL cholesterol may not be useful for subjects with specific lipid abnormalities such as greatly decreased HDL- or increased LDL-cholesterol concentrations. In fact, this is true for any population-based study, and only a health care professional can ultimately determine the most appropriate (dietary) advice for any person. However, the effect of carbohydrates on total:HDL cholesterol justifies some caution in the application of high-carbohydrate diets to the prevention of heart disease.
|
ACKNOWLEDGMENTS |
|---|
|
REFERENCES |
|---|
|
TOPABSTRACTINTRODUCTIONMETHODSRESULTSDISCUSSIONREFERENCES |
|---|
-linolenic acid is as effective as oleic acid and linoleic acid in lowering blood cholesterol in normolipidemic men. Am J Clin Nutr 1991;53:1230–4.This article has been cited by other articles:
|
|
 |
|
  A. N. Hristov, M. Vander Pol, M. Agle, S. Zaman, C. Schneider, P. Ndegwa, V. K. Vaddella, K. Johnson, K. J. Shingfield, and S. K. R. Karnati Effect of lauric acid and coconut oil on ruminal fermentation, digestion, ammonia losses from manure, and milk fatty acid composition in lactating cows J Dairy Sci, November 1, 2009; 92(11): 5561 - 5582. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 T. Nishimoto, M. A. Pellizzon, M. Aihara, I. M. Stylianou, J. T. Billheimer, G. Rothblat, and D. J. Rader Fish Oil Promotes Macrophage Reverse Cholesterol Transport in Mice Arterioscler Thromb Vasc Biol, October 1, 2009; 29(10): 1502 - 1508. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 R. M. van Dam and W. C. Willett Unmet Potential for Cardiovascular Disease Prevention in the United States Circulation, September 29, 2009; 120(13): 1171 - 1173. [Full Text] [PDF]
|
|
|
|
|
|
R. K. Johnson, L. J. Appel, M. Brands, B. V. Howard, M. Lefevre, R. H. Lustig, F. Sacks, L. M. Steffen, J. Wylie-Rosett, and on behalf of the American Heart Association Nutrit Dietary Sugars Intake and Cardiovascular Health: A Scientific Statement From the American Heart Association Circulation, September 15, 2009; 120(11): 1011 - 1020. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 C. Perez-Ferrer, K. Lock, and J. A Rivera Learning from international policies on trans fatty acids to reduce cardiovascular disease in low- and middle-income countries, using Mexico as a case study Health Policy Plan., September 9, 2009; (2009) czp040v1. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 C. Puiggros, J. Sanchez, P. Chacon, P. Sabin, J. Rosello, R. Bou, and M. Planas Evolution of Lipid Profile, Liver Function, and Pattern of Plasma Fatty Acids According to the Type of Lipid Emulsion Administered in Parenteral Nutrition in the Early Postoperative Period After Digestive Surgery JPEN J Parenter Enteral Nutr, September 1, 2009; 33(5): 501 - 512. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. Schennink, W. M. Stoop, M. H. P. W. Visker, J. J. van der Poel, H. Bovenhuis, and J. A. M. van Arendonk Short communication: Genome-wide scan for bovine milk-fat composition. II. Quantitative trait loci for long-chain fatty acids J Dairy Sci, September 1, 2009; 92(9): 4676 - 4682. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. W. P. Koppe, M. Elias, R. H. Moseley, and R. M. Green Trans fat feeding results in higher serum alanine aminotransferase and increased insulin resistance compared with a standard murine high-fat diet Am J Physiol Gastrointest Liver Physiol, August 1, 2009; 297(2): G378 - G384. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 D. J. A. Jenkins, J. M. W. Wong, C. W. C. Kendall, A. Esfahani, V. W. Y. Ng, T. C. K. Leong, D. A. Faulkner, E. Vidgen, K. A. Greaves, G. Paul, et al. The Effect of a Plant-Based Low-Carbohydrate ("Eco-Atkins") Diet on Body Weight and Blood Lipid Concentrations in Hyperlipidemic Subjects Arch Intern Med, June 8, 2009; 169(11): 1046 - 1054. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 F. Nayeem, M. Nagamani, K. E. Anderson, Y. Huang, J. J. Grady, and L.-J. W. Lu Dietary {beta}-Tocopherol and Linoleic Acid, Serum Insulin, and Waist Circumference Predict Circulating Sex Hormone-Binding Globulin in Premenopausal Women J. Nutr., June 1, 2009; 139(6): 1135 - 1142. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. B Katan Omega-6 polyunsaturated fatty acids and coronary heart disease Am. J. Clinical Nutrition, May 1, 2009; 89(5): 1283 - 1284. [Full Text] [PDF]
|
|
|
|
 |
|
 E. E. Devore, M. J. Stampfer, M. M.B. Breteler, B. Rosner, J. Hee Kang, O. Okereke, F. B. Hu, and F. Grodstein Dietary Fat Intake and Cognitive Decline in Women With Type 2 Diabetes Diabetes Care, April 1, 2009; 32(4): 635 - 640. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
R. Corti, A. J. Flammer, N. K. Hollenberg, and T. F. Luscher Cocoa and Cardiovascular Health Circulation, March 17, 2009; 119(10): 1433 - 1441. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
P. M. Kgwatalala, E. M. Ibeagha-Awemu, A. F. Mustafa, and X. Zhao Influence of stearoyl-coenzyme A desaturase 1 genotype and stage of lactation on fatty acid composition of Canadian Jersey cows J Dairy Sci, March 1, 2009; 92(3): 1220 - 1228. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 F. M. Sacks, G. A. Bray, V. J. Carey, S. R. Smith, D. H. Ryan, S. D. Anton, K. McManus, C. M. Champagne, L. M. Bishop, N. Laranjo, et al. Comparison of Weight-Loss Diets with Different Compositions of Fat, Protein, and Carbohydrates N. Engl. J. Med., February 26, 2009; 360(9): 859 - 873. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. B. Katan Weight-Loss Diets for the Prevention and Treatment of Obesity N. Engl. J. Med., February 26, 2009; 360(9): 923 - 925. [Full Text] [PDF]
|
|
|
|
|
|
W. S. Harris, D. Mozaffarian, E. Rimm, P. Kris-Etherton, L. L. Rudel, L. J. Appel, M. M. Engler, M. B. Engler, and F. Sacks Omega-6 Fatty Acids and Risk for Cardiovascular Disease: A Science Advisory From the American Heart Association Nutrition Subcommittee of the Council on Nutrition, Physical Activity, and Metabolism; Council on Cardiovascular Nursing; and Council on Epidemiology and Prevention Circulation, February 17, 2009; 119(6): 902 - 907. [Full Text] [PDF]
|
|
|
|
|
|
C. Tyburczy, C. Major, A. L. Lock, F. Destaillats, P. Lawrence, J. T. Brenna, A. M. Salter, and D. E. Bauman Individual Trans Octadecenoic Acids and Partially Hydrogenated Vegetable Oil Differentially Affect Hepatic Lipid and Lipoprotein Metabolism in Golden Syrian Hamsters J. Nutr., February 1, 2009; 139(2): 257 - 263. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. Salas-Salvado, J. Fernandez-Ballart, E. Ros, M.-A. Martinez-Gonzalez, M. Fito, R. Estruch, D. Corella, M. Fiol, E. Gomez-Gracia, F. Aros, et al. Effect of a Mediterranean Diet Supplemented With Nuts on Metabolic Syndrome Status: One-Year Results of the PREDIMED Randomized Trial Arch Intern Med, December 8, 2008; 168(22): 2449 - 2458. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 A. L. Lock, F. Destaillats, J. Kraft, and J. B. German Introduction to the Proceedings of the Symposium "Scientific Update on Dairy Fats and Cardiovascular Diseases" J. Am. Coll. Nutr., December 1, 2008; 27(6): 720S - 722S. [Full Text] [PDF]
|
|
|
|
|
|
P. C. Elwood, D. I. Givens, A. D. Beswick, A. M. Fehily, J. E. Pickering, and J. Gallacher The Survival Advantage of Milk and Dairy Consumption: an Overview of Evidence from Cohort Studies of Vascular Diseases, Diabetes and Cancer J. Am. Coll. Nutr., December 1, 2008; 27(6): 723S - 734S. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
P. J. Nestel Effects of Dairy Fats within Different Foods on Plasma Lipids J. Am. Coll. Nutr., December 1, 2008; 27(6): 735S - 740S. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
W. A. van Staveren, J. M. Steijns, and L. C.P.G.M. de Groot Dairy Products as Essential Contributors of (Micro-) Nutrients in Reference Food Patterns: An Outline for Elderly People J. Am. Coll. Nutr., December 1, 2008; 27(6): 747S - 754S. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J.-C. Fruchart, F. M Sacks, M. P Hermans, G. Assmann, W V. Brown, R. Ceska, M J. Chapman, P. M Dodson, P. Fioretto, H. N Ginsberg, et al. The Residual Risk Reduction Initiative: a call to action to reduce residual vascular risk in dyslipidaemic patients Diabetes and Vascular Disease Research, November 1, 2008; 5(4): 319 - 335. [Abstract] [PDF]
|
|
|
|
 |
|
 I. Kralova Lesna, P. Suchanek, J. Kovar, P. Stavek, and R. Poledne Replacement of dietary saturated FAs by PUFAs in diet and reverse cholesterol transport J. Lipid Res., November 1, 2008; 49(11): 2414 - 2418. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 V. S. Retelny, A. Neuendorf, and J. L. Roth Nutrition Protocols for the Prevention of Cardiovascular Disease Nutr Clin Pract, October 1, 2008; 23(5): 468 - 476. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. Bingham, R. Luben, A. Welch, Y. L. Low, K. T. Khaw, N. Wareham, and N. Day Associations between dietary methods and biomarkers, and between fruits and vegetables and risk of ischaemic heart disease, in the EPIC Norfolk Cohort Study Int. J. Epidemiol., October 1, 2008; 37(5): 978 - 987. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
W. C Willett Commentary: Flawed study designs are not salvaged by large samples Int. J. Epidemiol., October 1, 2008; 37(5): 987 - 989. [Full Text] [PDF]
|
|
|
|
|
|
S. E. E. Berry, S. Tucker, R. Banerji, B. Jiang, P. J. Chowienczyk, S. M. Charles, and T. A. B. Sanders Impaired Postprandial Endothelial Function Depends on the Type of Fat Consumed by Healthy Men J. Nutr., October 1, 2008; 138(10): 1910 - 1914. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 R. M v. Dam, T. Li, D. Spiegelman, O. H Franco, and F. B Hu Combined impact of lifestyle factors on mortality: prospective cohort study in US women BMJ, September 16, 2008; 337(sep16_2): a1440 - a1440. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 A. J. Chicco, G. C. Sparagna, S. A. McCune, C. A. Johnson, R. C. Murphy, D. A. Bolden, M. L. Rees, R. T. Gardner, and R. L. Moore Linoleate-Rich High-Fat Diet Decreases Mortality in Hypertensive Heart Failure Rats Compared With Lard and Low-Fat Diets Hypertension, September 1, 2008; 52(3): 549 - 555. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
C. Zheng, C. Khoo, J. Furtado, K. Ikewaki, and F. M Sacks Dietary monounsaturated fat activates metabolic pathways for triglyceride-rich lipoproteins that involve apolipoproteins E and C-III Am. J. Clinical Nutrition, August 1, 2008; 88(2): 272 - 281. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. A. Bouattour, R. Casals, E. Albanell, X. Such, and G. Caja Feeding Soybean Oil to Dairy Goats Increases Conjugated Linoleic Acid in Milk J Dairy Sci, June 1, 2008; 91(6): 2399 - 2407. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. Schennink, J. M. L. Heck, H. Bovenhuis, M. H. P. W. Visker, H. J. F. van Valenberg, and J. A. M. van Arendonk Milk Fatty Acid Unsaturation: Genetic Parameters and Effects of Stearoyl-CoA Desaturase (SCD1) and Acyl CoA: Diacylglycerol Acyltransferase 1 (DGAT1) J Dairy Sci, May 1, 2008; 91(5): 2135 - 2143. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. F.G. Cicero, S. Nascetti, M. C. Lopez-Sabater, R. Elosua, J. T. Salonen, K. Nyyssonen, H. E. Poulsen, H.-J. F. Zunft, H. Kiesewetter, K. de la Torre, et al. Changes in LDL Fatty Acid Composition as a Response to Olive Oil Treatment Are Inversely Related to Lipid Oxidative Damage: The EUROLIVE Study J. Am. Coll. Nutr., April 1, 2008; 27(2): 314 - 320. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J.-M. Chardigny, F. Destaillats, C. Malpuech-Brugere, J. Moulin, D. E Bauman, A. L Lock, D. M Barbano, R. P Mensink, J.-B. Bezelgues, P. Chaumont, et al. Do trans fatty acids from industrially produced sources and from natural sources have the same effect on cardiovascular disease risk factors in healthy subjects? Results of the trans Fatty Acids Collaboration (TRANSFACT) study Am. J. Clinical Nutrition, March 1, 2008; 87(3): 558 - 566. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. B Keogh, G. D Brinkworth, M. Noakes, D. P Belobrajdic, J. D Buckley, and P. M Clifton Effects of weight loss from a very-low-carbohydrate diet on endothelial function and markers of cardiovascular disease risk in subjects with abdominal obesity Am. J. Clinical Nutrition, March 1, 2008; 87(3): 567 - 576. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
G. Bobe, J. A. Minick Bormann, G. L. Lindberg, A. E. Freeman, and D. C. Beitz Short Communication: Estimates of Genetic Variation of Milk Fatty Acids in US Holstein Cows J Dairy Sci, March 1, 2008; 91(3): 1209 - 1213. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. Raff, T. Tholstrup, S. Basu, P. Nonboe, M. T. Sorensen, and E. M. Straarup A Diet Rich in Conjugated Linoleic Acid and Butter Increases Lipid Peroxidation but Does Not Affect Atherosclerotic, Inflammatory, or Diabetic Risk Markers in Healthy Young Men J. Nutr., March 1, 2008; 138(3): 509 - 514. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. Tay, G. D. Brinkworth, M. Noakes, J. Keogh, and P. M. Clifton Metabolic effects of weight loss on a very-low-carbohydrate diet compared with an isocaloric high-carbohydrate diet in abdominally obese subjects. J. Am. Coll. Cardiol., January 1, 2008; 51(1): 59 - 67. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. T Merchant, L. E Kelemen, L. de Koning, E. Lonn, V. Vuksan, R. Jacobs, B. Davis, K. K Teo, S. Yusuf, S. S Anand, et al. Interrelation of saturated fat, trans fat, alcohol intake, and subclinical atherosclerosis Am. J. Clinical Nutrition, January 1, 2008; 87(1): 168 - 174. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 I. M. Singh, M. H. Shishehbor, and B. J. Ansell High-Density Lipoprotein and Dietary Fatty Acids Reply JAMA, November 21, 2007; 298(19): 2264 - 2264. [Full Text] [PDF]
|
|
|
|
|
|
Q. Sun, J. Ma, H. Campos, and F. B Hu Plasma and erythrocyte biomarkers of dairy fat intake and risk of ischemic heart disease Am. J. Clinical Nutrition, October 1, 2007; 86(4): 929 - 937. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
E. A Ruiz-Narvaez, P. Kraft, and H. Campos Ala12 variant of the peroxisome proliferator-activated receptor-{gamma} gene (PPARG) is associated with higher polyunsaturated fat in adipose tissue and attenuates the protective effect of polyunsaturated fat intake on the risk of myocardial infarction Am. J. Clinical Nutrition, October 1, 2007; 86(4): 1238 - 1242. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
I. M. Singh, M. H. Shishehbor, and B. J. Ansell High-Density Lipoprotein as a Therapeutic Target: A Systematic Review JAMA, August 15, 2007; 298(7): 786 - 798. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
P. Verhoef Homocysteine--an indicator of a healthy diet? Am. J. Clinical Nutrition, June 1, 2007; 85(6): 1446 - 1447. [Full Text] [PDF]
|
|
|
|
|
|
M.-P. St-Onge, I. Aban, A. Bosarge, B. Gower, K. D Hecker, and D. B Allison Snack chips fried in corn oil alleviate cardiovascular disease risk factors when substituted for low-fat or high-fat snacks Am. J. Clinical Nutrition, June 1, 2007; 85(6): 1503 - 1510. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
G. Bobe, S. Zimmerman, E. G. Hammond, A. E. Freeman, P. A. Porter, C. M. Luhman, and D. C. Beitz Butter Composition and Texture from Cows with Different Milk Fatty Acid Compositions Fed Fish Oil or Roasted Soybeans J Dairy Sci, June 1, 2007; 90(6): 2596 - 2603. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
R. H. Eckel, S. Borra, A. H. Lichtenstein, and S. Y. Yin-Piazza Understanding the Complexity of Trans Fatty Acid Reduction in the American Diet: American Heart Association Trans Fat Conference 2006: Report of the Trans Fat Conference Planning Group Circulation, April 24, 2007; 115(16): 2231 - 2246. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
Q. Sun, J. Ma, H. Campos, S. E. Hankinson, J. E. Manson, M. J. Stampfer, K. M. Rexrode, W. C. Willett, and F. B. Hu A Prospective Study of Trans Fatty Acids in Erythrocytes and Risk of Coronary Heart Disease Circulation, April 10, 2007; 115(14): 1858 - 1865. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
K. F Hilpert, S. G West, P. M Kris-Etherton, K. D Hecker, N. M Simpson, and P. Alaupovic Postprandial effect of n-3 polyunsaturated fatty acids on apolipoprotein B-containing lipoproteins and vascular reactivity in type 2 diabetes Am. J. Clinical Nutrition, February 1, 2007; 85(2): 369 - 376. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. T Merchant, S. S Anand, L. E Kelemen, V. Vuksan, R. Jacobs, B. Davis, K. Teo, S. Yusuf, and for the SHARE and SHARE-AP Investigators Carbohydrate intake and HDL in a multiethnic population Am. J. Clinical Nutrition, January 1, 2007; 85(1): 225 - 230. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. T. Flowers, A. K. Groen, A. T. Oler, M. P. Keller, Y. Choi, K. L. Schueler, O. C. Richards, H. Lan, M. Miyazaki, F. Kuipers, et al. Cholestasis and hypercholesterolemia in SCD1-deficient mice fed a low-fat, high-carbohydrate diet J. Lipid Res., December 1, 2006; 47(12): 2668 - 2680. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
K. Kuhnt, A. Wagner, J. Kraft, S. Basu, and G. Jahreis Dietary supplementation with 11trans- and 12trans-18:1 and oxidative stress in humans. Am. J. Clinical Nutrition, November 1, 2006; 84(5): 981 - 988. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
I. G.E. Zarraga and E. R. Schwarz Impact of Dietary Patterns and Interventions on Cardiovascular Health Circulation, August 29, 2006; 114(9): 961 - 973. [Full Text] [PDF]
|
|
|
|
|
|
A. H. Lichtenstein Thematic review series: Patient-Oriented Research. Dietary fat, carbohydrate, and protein: effects on plasma lipoprotein patterns J. Lipid Res., August 1, 2006; 47(8): 1661 - 1667. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
R. Clarke and S. Lewington Trans fatty acids and coronary heart disease BMJ, July 29, 2006; 333(7561): 214 - 214. [Full Text] [PDF]
|
|
|
|
|
|
R. N. Lemaitre, I. B. King, D. Mozaffarian, N. Sotoodehnia, T. D. Rea, L. H. Kuller, R. P. Tracy, and D. S. Siscovick Plasma Phospholipid Trans Fatty Acids, Fatal Ischemic Heart Disease, and Sudden Cardiac Death in Older Adults: The Cardiovascular Health Study Circulation, July 18, 2006; 114(3): 209 - 215. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 R. Estruch, M. A. Martinez-Gonzalez, D. Corella, J. Salas-Salvado, V. Ruiz-Gutierrez, M. I. Covas, M. Fiol, E. Gomez-Gracia, M. C. Lopez-Sabater, E. Vinyoles, et al. Effects of a Mediterranean-Style Diet on Cardiovascular Risk Factors: A Randomized Trial Ann Intern Med, July 4, 2006; 145(1): 1 - 11. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. Vega-Lopez, L. M Ausman, S. M Jalbert, A. T Erkkila, and A. H Lichtenstein Palm and partially hydrogenated soybean oils adversely alter lipoprotein profiles compared with soybean and canola oils in moderately hyperlipidemic subjects Am. J. Clinical Nutrition, July 1, 2006; 84(1): 54 - 62. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 H. A. Bischoff, H. B. Staehelin, and W. C. Willett The effect of undernutrition in the development of frailty in older persons. J. Gerontol. A Biol. Sci. Med. Sci., June 1, 2006; 61(6): 585 - 589. [Full Text] [PDF]
|
|
|
|
|
|
M. B Katan Alternatives to low-fat diets Am. J. Clinical Nutrition, May 1, 2006; 83(5): 989 - 990. [Full Text] [PDF]
|
|
|
|
|
|
R. M Krauss, P. J Blanche, R. S Rawlings, H. S Fernstrom, and P. T Williams Separate effects of reduced carbohydrate intake and weight loss on atherogenic dyslipidemia Am. J. Clinical Nutrition, May 1, 2006; 83(5): 1025 - 1031. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. Kraft, L. Hanske, P. Mockel, S. Zimmermann, A. Hartl, J. K. G. Kramer, and G. Jahreis The Conversion Efficiency of trans-11 and trans-12 18:1 by {Delta}9-Desaturation Differs in Rats J. Nutr., May 1, 2006; 136(5): 1209 - 1214. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
W.-H. Wu, Y.-P. Kang, N.-H. Wang, H.-J. Jou, and T.-A. Wang Sesame Ingestion Affects Sex Hormones, Antioxidant Status, and Blood Lipids in Postmenopausal Women J. Nutr., May 1, 2006; 136(5): 1270 - 1275. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
D. Mozaffarian, M. B. Katan, A. Ascherio, M. J. Stampfer, and W. C. Willett Trans Fatty Acids and Cardiovascular Disease N. Engl. J. Med., April 13, 2006; 354(15): 1601 - 1613. [Full Text] [PDF]
|
|
|
|
|
|
S. Tricon, G. C Burdge, E. L Jones, J. J Russell, S. El-Khazen, E. Moretti, W. L Hall, A. B Gerry, D. S Leake, R. F Grimble, et al. Effects of dairy products naturally enriched with cis-9,trans-11 conjugated linoleic acid on the blood lipid profile in healthy middle-aged men. Am. J. Clinical Nutrition, April 1, 2006; 83(4): 744 - 753. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
F. L Crowe, C M. Skeaff, T. J Green, and A. R Gray Serum fatty acids as biomarkers of fat intake predict serum cholesterol concentrations in a population-based survey of New Zealand adolescents and adults. Am. J. Clinical Nutrition, April 1, 2006; 83(4): 887 - 894. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. Lefevre and C. Champagne Reply to D Giugliano and K Esposito Am. J. Clinical Nutrition, April 1, 2006; 83(4): 921 - 922. [Full Text] [PDF]
|
|
|
|
|
|
T. Tholstrup, M. Raff, S. Basu, P. Nonboe, K. Sejrsen, and E. M Straarup Effects of butter high in ruminant trans and monounsaturated fatty acids on lipoproteins, incorporation of fatty acids into lipid classes, plasma C-reactive protein, oxidative stress, hemostatic variables, and insulin in healthy young men Am. J. Clinical Nutrition, February 1, 2006; 83(2): 237 - 243. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 A. D. Mooradian, M. J. Haas, and N. C. W. Wong The Effect of Select Nutrients on Serum High-Density Lipoprotein Cholesterol and Apolipoprotein A-I Levels Endocr. Rev., February 1, 2006; 27(1): 2 - 16. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. S. Itskowitz, J. L. Pollock, M. B. Katan, Y. Xie, N. O. Davidson, D. Ashen, and R. S. Blumenthal Low HDL cholesterol levels. N. Engl. J. Med., January 26, 2006; 354(4): 417 - 419. [Full Text] [PDF]
|
|
|
|
|
|
P. L. L. Goyens and R. P. Mensink The Dietary {alpha}-Linolenic Acid to Linoleic Acid Ratio Does Not Affect the Serum Lipoprotein Profile in Humans J. Nutr., December 1, 2005; 135(12): 2799 - 2804. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
L. J. Appel, F. M. Sacks, V. J. Carey, E. Obarzanek, J. F. Swain, E. R. Miller III, P. R. Conlin, T. P. Erlinger, B. A. Rosner, N. M. Laranjo, et al. Effects of Protein, Monounsaturated Fat, and Carbohydrate Intake on Blood Pressure and Serum Lipids: Results of the OmniHeart Randomized Trial JAMA, November 16, 2005; 294(19): 2455 - 2464. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
B. Fletcher, K. Berra, P. Ades, L. T. Braun, L. E. Burke, J. L. Durstine, J. M. Fair, G. F. Fletcher, D. Goff, L. L. Hayman, et al. Managing Abnormal Blood Lipids: A Collaborative Approach Circulation, November 15, 2005; 112(20): 3184 - 3209. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 T. J. Little, K. L. Feltrin, M. Horowitz, A. J. P. M. Smout, T. Rades, J. H. Meyer, A. N. Pilichiewicz, J. Wishart, and C. Feinle-Bisset Dose-related effects of lauric acid on antropyloroduodenal motility, gastrointestinal hormone release, appetite, and energy intake in healthy men Am J Physiol Regulatory Integrative Comp Physiol, October 1, 2005; 289(4): R1090 - R1098. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. A Thijssen and R. P Mensink Small differences in the effects of stearic acid, oleic acid, and linoleic acid on the serum lipoprotein profile of humans Am. J. Clinical Nutrition, September 1, 2005; 82(3): 510 - 516. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
P. Verhoef, T. van Vliet, M. R Olthof, and M. B Katan A high-protein diet increases postprandial but not fasting plasma total homocysteine concentrations: a dietary controlled, crossover trial in healthy volunteers Am. J. Clinical Nutrition, September 1, 2005; 82(3): 553 - 558. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. L. Fernandez and K. L. West Mechanisms by which Dietary Fatty Acids Modulate Plasma Lipids1 J. Nutr., September 1, 2005; 135(9): 2075 - 2078. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. L. Lock, C. A. M. Horne, D. E. Bauman, and A. M. Salter Butter Naturally Enriched in Conjugated Linoleic Acid and Vaccenic Acid Alters Tissue Fatty Acids and Improves the Plasma Lipoprotein Profile in Cholesterol-Fed Hamsters J. Nutr., August 1, 2005; 135(8): 1934 - 1939. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
P. T Williams, P. J Blanche, R. Rawlings, and R. M Krauss Concordant lipoprotein and weight responses to dietary fat change in identical twins with divergent exercise levels 1 Am. J. Clinical Nutrition, July 1, 2005; 82(1): 181 - 187. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. B. Keogh, J. A. Grieger, M. Noakes, and P. M. Clifton Flow-Mediated Dilatation Is Impaired by a High-Saturated Fat Diet but Not by a High-Carbohydrate Diet Arterioscler Thromb Vasc Biol, June 1, 2005; 25(6): 1274 - 1279. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
G. Bos, J. M Dekker, E. J. Feskens, M. C Ocke, G. Nijpels, C. D. Stehouwer, L. M Bouter, R. J Heine, and H. Jansen Interactions of dietary fat intake and the hepatic lipase -480C->T polymorphism in determining hepatic lipase activity: the Hoorn Study Am. J. Clinical Nutrition, April 1, 2005; 81(4): 911 - 915. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 K. Oh, F. B. Hu, J. E. Manson, M. J. Stampfer, and W. C. Willett Dietary Fat Intake and Risk of Coronary Heart Disease in Women: 20 Years of Follow-up of the Nurses' Health Study Am. J. Epidemiol., April 1, 2005; 161(7): 672 - 679. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
C. Bellido, J. Lopez-Miranda, L. M. Blanco-Colio, P. Perez-Martinez, F. J. Muriana, J. L. Martin-Ventura, C. Marin, P. Gomez, F. Fuentes, J. Egido, et al. Butter and walnuts, but not olive oil, elicit postprandial activation of nuclear transcription factor {kappa}B in peripheral blood mononuclear cells from healthy men Am. J. Clinical Nutrition, December 1, 2004; 80(6): 1487 - 1491. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. Desroches, M.-E. Paradis, M. Perusse, W. R. Archer, J. Bergeron, P. Couture, N. Bergeron, and B. Lamarche Apolipoprotein A-I, A-II, and VLDL-B-100 metabolism in men: comparison of a low-fat diet and a high-monounsaturated fatty acid diet J. Lipid Res., December 1, 2004; 45(12): 2331 - 2338. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
L. C. Tapsell, L. J. Gillen, C. S. Patch, M. Batterham, A. Owen, M. Bare, and M. Kennedy Including Walnuts in a Low-Fat/Modified-Fat Diet Improves HDL Cholesterol-to-Total Cholesterol Ratios in Patients With Type 2 Diabetes Diabetes Care, December 1, 2004; 27(12): 2777 - 2783. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J B. German and C. J Dillard Saturated fats: what dietary intake? Am. J. Clinical Nutrition, September 1, 2004; 80(3): 550 - 559. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M.-P. St-Onge, I. Janssen, and S. B. Heymsfield Metabolic Syndrome in Normal-Weight Americans: New definition of the metabolically obese, normal-weight individual Diabetes Care, September 1, 2004; 27(9): 2222 - 2228. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. U. Jakobsen, K. Overvad, J. Dyerberg, M. Schroll, and B. L. Heitmann Dietary Fat and Risk of Coronary Heart Disease: Possible Effect Modification by Gender and Age Am. J. Epidemiol., July 15, 2004; 160(2): 141 - 149. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
N. R. Matthan, F. K. Welty, P. H. R. Barrett, C. Harausz, G. G. Dolnikowski, J. S. Parks, R. H. Eckel, E. J. Schaefer, and A. H. Lichtenstein Dietary Hydrogenated Fat Increases High-Density Lipoprotein apoA-I Catabolism and Decreases Low-Density Lipoprotein apoB-100 Catabolism in Hypercholesterolemic Women Arterioscler Thromb Vasc Biol, June 1, 2004; 24(6): 1092 - 1097. [Abstract] [Full Text]
|
|
|
|
|
|
K. Meksawan, D. R. Pendergast, J. J. Leddy, M. Mason, P. J. Horvath, and A. B. Awad Effect of Low and High Fat Diets on Nutrient Intakes and Selected Cardiovascular Risk Factors in Sedentary Men and Women J. Am. Coll. Nutr., April 1, 2004; 23(2): 131 - 140. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. M. Mello, E. B. Rimm, and D. M. Studdert The McLawsuit: The Fast-Food Industry And Legal Accountability For Obesity Health Aff., November 1, 2003; 22(6): 207 - 216. [Abstract] [Full Text] [PDF]
|
|
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
) in serum lipids and lipoproteins when carbohydrates constituting 1% of dietary energy are replaced isoenergetically with saturated fatty acids (SFAs) (Carbohydrates 
SFAs), cis monounsaturated fatty acids (MUFAs) (Carbohydrates 
