![[Feedback]](/icons/banner/feedbackACT.gif){kind=icon}
![[For Subscribers]](/icons/banner/subscriberACT.gif){kind=icon}
![[Archive]](/icons/banner/archiveACT.gif){kind=icon}
![[Search]](/icons/banner/searchACT.gif){kind=icon}
![[Contents]](/icons/banner/tocACT.gif){kind=icon}
|
|
|
|
|
||
* Institute on Nutraceuticals and Functional Foods, Laval University, QC, Canada; Clinique romande de réadaptation, SUVA, Sion, Switzerland; ** Lipid Research Center, CHUL Research Center, QC, Canada; and College of Pharmacy, Touro University-California, Vallejo, CA
2 To whom correspondence should be addressed. E-mail: benoit.lamarche{at}inaf.ulaval.ca.
 |
ABSTRACT |
|---|
 TOP ABSTRACT SUBJECTS AND METHODSRESULTSDISCUSSIONLITERATURE CITED |
|---|
KEY WORDS: • diet • inflammation • lipoproteins
Accumulating evidence suggests that inflammatory processes are intimately involved in the pathogenesis of atherosclerosis and cardiovascular disease (CVD)3 (1). In support of this hypothesis, C-reactive protein (CRP) has been the subject of increasing attention in recent years due to results from cross-sectional and prospective studies that identified this acute phase reactant as an independent risk factor for CVD (2,3). Furthermore, studies reported that pharmacological treatments that reduce plasma CRP concentrations are associated with a reduced incidence of cardiovascular events (4,5). These results suggest that the cardioprotection ascribed to nonpharmacological interventions, such as dietary modifications, may be attributable, as least in part, to their effect on the inflammatory state.
An increasing number of studies recently investigated the effect of dietary modifications on this inflammatory marker. Reduced CRP concentrations were observed after different weight loss regimens, including rigorous dietary restrictions (6), the consumption of diets rich in soluble fibers (7) and (n-3) fatty acids (8), or diets with a low dietary glycemic load (9). The adoption of a prudent (10) or Mediterranean dietary pattern (11), both characterized by high intakes of fruits and vegetables, has also been associated with reduced plasma CRP concentrations.
Although large-scale association studies have provided insightful information on the dietary components most likely to affect chronic diseases, controlled dietary intervention studies indicated that diet responsiveness may vary among individuals. These variations may be attributed to genetic variability in the population (12); however, other factors including the baseline dyslipidemic state (13), the degree of obesity (14), and as suggested more recently, the inflammatory state (15–17) may also influence responsiveness to dietary manipulation. In a previous study that examined the extent to which variations in body composition may modulate plasma lipids and lipoproteins in response to the ad libitum consumption of a low-fat and a high monounsaturated fatty acid (MUFA) diet, we reported that the improvements in plasma lipids and lipoproteins after consumption of the low-fat diet were mediated in part by changes in body weight, whereas lipid changes induced by the high MUFA diet appeared to be independent of body weight changes (18). Therefore, in an attempt to further investigate the metabolic response induced by low-fat and the high-MUFA diets, we investigated the effect of these diets on plasma CRP concentrations and the extent to which the inflammatory status of the subjects at study onset may modulate the lipid and lipoprotein responses to the dietary interventions.
|
SUBJECTS AND METHODS |
|---|
|
TOPABSTRACTSUBJECTS AND METHODSRESULTSDISCUSSIONLITERATURE CITED |
|---|
Experimental design. Subjects were randomly assigned to either a low-fat control diet (25.8% of energy from fat) designed to be similar to the Step 2 diet of the AHA (now referred to as the Therapeutic Lifestyle Changes diet) or a high-fat diet, rich in MUFA (40.1% of energy from fat; 22.5% of energy from MUFA) that they consumed for 6–7 wk. Participants and staff performing laboratory measures were not aware of the dietary treatments. Participants were instructed to maintain their usual physical activity level throughout the study, but to refrain from intense physical exercise 3 d before blood draws at the beginning and at the end of the experimental period. Consumption of alcohol and vitamin supplements was also forbidden 1 wk before and during the experimental period. Body weights were monitored daily, whereas inflammatory markers, lipids, and lipoproteins were measured at the beginning and at the end of the experimental period.
Experimental diets. A 7-d cycle of menus was developed for each experimental diet; the meals were prepared daily in the metabolic kitchen and weighed in individual portions. The nutritional composition of the experimental diets was calculated with the Canadian Nutrient File database (Health Canada, Ottawa, 1997) and the Nutrition Data System for Research software (Nutrition Coordinating Center, Minneapolis, MN, Database version 4.03_30, 1999). The 2 experimental diets were formulated to have similar compositions, and differed mainly in the proportion of the food items/ingredients and, thus, macronutrients (Table 1).
|
Laboratory methods. At the beginning and end of the dietary intervention, blood samples were collected from fasting subjects (12-h fast) into tubes containing disodium EDTA. Samples were then immediately centrifuged at 4°C for 10 min at 1500 x g to obtain plasma, and were stored at 4°C until processed. Triglyceride (TG)-rich lipoproteins were separated by ultracentrifugation (d < 1.006 kg/L) of plasma in a 50.3 Beckman rotor, centrifuged at 93,000 x g (average), 4°C for 18 h. HDL cholesterol (HDL-C) was measured in the supernatant collected after heparin-chloride and MnCl2 precipitation of apolipoprotein B-containing particles in plasma (20). Plasma and lipoprotein cholesterol and TG were measured enzymatically (21) on a Technicon RA 500 (Bayer). Plasma CRP concentrations were measured by nephelometry (Behring Latex Enhanced on the Behring Nephelometer BN-100; Behring Diagnostic), using a highly sensitive assay as described previously (22). The interassay CV at CRP concentrations ranging from 1.0 to 10 mg/L was <5%. Distinct subpopulations of LDL particles in whole plasma were separated by size using nondenaturing 2–16% gradient gel electrophoresis, as described previously (19,23). Postheparin (60 IU/kg body weight) lipoprotein lipase (LPL) and hepatic lipase (HL) activities were measured after preincubation with SDS as previously described by Watson et al. (24).
Anthropometric and body composition measurements. Body weight and waist circumference were measured according to standardized procedures (25) at the beginning and at the end of the study period. Visceral adipose tissue accumulation was assessed by computed tomography, which was performed on a Siemens Somatom DRH scanner and analyzed as previously described (26).
Statistical procedures. Data were analyzed using SAS (version 8.2, SAS Institute). Differences among and between dietary groups were tested by the MIXED procedure for repeated measurements with adjustment for diet-induced variations in body weight for plasma total-C, VLDL-C, LDL-C, HDL-C, total TG, VLDL-TG, LDL peak particle diameter (LDL-PPD) and CRP. Fasting plasma TG, VLDL-TG, VLDL-C, and CRP concentrations were log-transformed to normalize their distribution before statistical analysis. Spearman's correlation coefficients were calculated to test for associations between baseline plasma CRP concentrations and changes in metabolic variables. During the course of the study, CRP concentrations of 4 subjects were >10 mg/L and they were excluded from statistical analysis (27). Therefore, results are presented for a total of 61 men. To divide subjects into low or high CRP subgroups, the relative risk categories described by the CDC and the AHA were used initially (low risk <1 mg/L, average risk 1–3 mg/L, and high risk >3 mg/L) (27). However, because the average- and high-risk subgroups responded similarly to the dietary intervention, their data were pooled. Values presented are means ± SD unless otherwise specified. Differences were considered significant at P < 0.05.
|
RESULTS |
|---|
|
TOPABSTRACTSUBJECTS AND METHODSRESULTSDISCUSSIONLITERATURE CITED |
|---|
|
|
|
|
|
|
DISCUSSION |
|---|
|
TOPABSTRACTSUBJECTS AND METHODSRESULTSDISCUSSIONLITERATURE CITED |
|---|
The body of literature reporting the effect of diet on inflammatory markers, especially CRP, is constantly growing. It was suggested that diets that reduced postprandial glucose and insulin would lead to lower plasma CRP concentrations (32). In a substudy from the Women's Health Study, women in the highest glycemic load category (the product of the glycemic index and the carbohydrate content of food) had a 9.4-fold greater risk of having plasma CRP concentrations higher than the CRP median value of the study population. Women characterized by the highest absolute intake of carbohydrates (CHO) had a 6.1-fold greater risk of having elevated plasma CRP concentrations than women consuming the lowest amount of CHO (9). Another study examined the effect of a low-fat/high-CHO diet incorporating plant sterols, soy protein, viscous fibers. and almonds on plasma CRP concentrations (33). Consumption of this intense ''Portfolio'' diet induced a 28.2% reduction in plasma CRP concentrations, which was similar to the 33.3% reduction in CRP induced by a diet very low in saturated fat plus 20 mg/d of lovastatin. The very low saturated fat diet alone induced a nonsignificant 10% reduction in CRP (33). Erlinger et al. (15) recently reported that the Dietary Approaches to Stop Hypertension (DASH) diet (27% fat, 6% saturated fat) consumed for 12 wk did not affect plasma CRP concentrations compared with a control diet (37% fat, 16% saturated fat). Finally, in a randomized study comparing the effects of a low-CHO diet and a conventional low-fat/high-CHO diet for 6 mo, Seshadri et al. (34) reported that both diets induced similar modest but nonsignificant reductions in plasma CRP concentrations. However, the authors also found that subjects with high CRP at baseline (>3 mg/L) experienced a greater decrease in CRP concentrations when consuming the low CHO diet (34). Our own data support these findings, although the difference in the CRP-response to the low-fat diet between the low CRP and high CRP subgroups was not significant (P = 0.09). Results from these previous studies suggest that the type of CHO consumed and the fiber content of the diet may be important aspects to consider in understanding the effect of low fat/high CHO diets on plasma CRP concentrations.
The concept that cardiovascular risk reduction related to the consumption of a Mediterranean diet generally rich in MUFA may be attributable in part to its anti-inflammatory effect is also rapidly emerging. Baer et al. (35) recently evaluated the role of dietary fats in altering the concentrations of inflammatory markers. Their results showed that plasma concentrations of IL-6 were significantly higher after consumption of diets high in trans fatty acids or the 12:0–16:0 saturated fatty acids (SFA) compared with a diet providing high amounts of oleic acid. However, when the high oleic acid diet was compared with the control CHO diet, the plasma markers of inflammation that were measured did not differ, including CRP (35), which is consistent with our results. We investigated the effect of 6 diets containing soybean oil, semiliquid margarine, soft margarine, shortening, traditional stick margarine, or butter as the major source of fat and found that increasing dietary trans fatty acids concentrations did not affect CRP concentrations (36). In a recent trial, free-living subjects with the metabolic syndrome were randomly assigned to either a Mediterranean-style diet or a prudent control diet (50–60% CHO, 15–20% protein, <30% total fat), which they consumed for 2 y. Compared with patients consuming the control diet, patients consuming the Mediterranean diet had significantly reduced serum concentrations of CRP, IL-6, IL-7. and IL-18 (29). Another study conducted in a Greek population also reported that greater adherence to a traditional Mediterranean diet was associated with lower plasma concentrations of CRP and IL-6 (11). On the other hand, there was no differential effect on CRP concentrations when a Mediterranean diet was compared with a high-fat diet in a controlled study in which all food was provided to the subjects for 90 d (37). Hence, not all studies found a reduction in inflammatory markers after consumption of a Mediterranean-style diet or a high-MUFA diet, likely due to the different study designs used. Indeed, in the 2 studies that reported a reduction in CRP concentrations, subjects had been following a Mediterranean diet for at least 2 y (11,29), which suggests that a minimal period of dietary changes may be required to modify concentrations of inflammatory markers, especially in healthy subjects.
Evidence suggests that infection and inflammation may unfavorably affect lipid and lipoprotein metabolism (38). In that regard, basal plasma CRP concentrations of individuals were identified as an additional potential modulator of the lipid-lipoprotein response in 3 dietary interventions (15–17). Erlinger et al. (15) reported in the DASH trial that subjects with plasma CRP above the median at study onset had smaller reductions in total and LDL-C and a greater increase in TG concentrations compared with subjects with lower baseline CRP concentrations. Similarly, Zhao et al. (16) demonstrated that subjects with higher CRP concentrations had a diminished cholesterol-lowering response to diets either high in linoleic acid (50% CHO, 15% protein, 35.7% fat) or 
-linolenic acid (50% CHO, 15% protein, 35.2% fat) compared with subjects with lower CRP concentrations (16). Recently, Hilpert et al. (17) conducted a study in which moderately hypercholesterolemic subjects consumed a low-fat diet with or without soy protein and found that regardless of the protein source, individuals with low CRP exhibited significant reductions in LDL-C and the LDL-C/HDL-C ratio, whereas those with high CRP had significant increases in LDL-C, the LDL-C/HDL-C ratio, apolipoprotein B and lipoprotein(a) compared with those consuming the run-in diet (17). Consistent with the findings from the DASH trial, we also found that consumption of a low-fat diet in subjects with high CRP concentrations led to increased TG concentrations, whereas those with low CRP had reduced concentrations of TG. Unlike results from previous studies, the present study could not demonstrate an effect of plasma CRP concentrations at baseline on cholesterol responsiveness to the low-fat diet. On the other hand, in the high-MUFA group, subjects with high CRP concentrations experienced a greater cholesterol-lowering response compared with subjects with low CRP baseline concentrations. These results suggest that low-grade chronic inflammation, as evidenced by plasma CRP concentrations, may render individuals more or less susceptible to respond favorably to a given dietary intervention.
Although they remain speculative, mechanisms underlying the differential effect of a low-fat and a high-MUFA diet on the lipoprotein/lipid response of individuals who have a high or a low inflammatory status may be suggested. First, it was shown that an increase in plasma concentrations of different inflammatory markers, such as CRP, was inversely associated with LPL activity (39) or mass (40,41). Our data do not support this hypothesis because there was no correlation between LPL activity and plasma CRP concentrations (data not shown). Second, inflammation was suggested to be associated with increased psychological or environmental ''stress'' (39). We therefore hypothesized that major dietary modifications in a context of a strictly controlled trial may be perceived as an additional physiological stress in individuals already exhibiting increased CRP concentrations at study entry, thus potentially explaining their less favorable response to certain therapeutic dietary interventions. Finally, polymorphisms in the promoters of the CRP gene that modulate its basal levels were discovered recently (42). These findings have led researchers to postulate in certain cases (39) and even demonstrate in others (42) that these genetic variations not only influence the basal but also the stimulated levels of inflammatory markers. Hence, a strictly controlled dietary intervention may represent a stimulus that could differentially affect individuals with different CRP polymorphisms.
In conclusion, the low-fat diet and the high-MUFA diet did not affect plasma CRP concentrations. However, baseline plasma CRP concentrations predicted the diet-induced changes in lipid and lipoprotein concentrations in men that consumed both experimental diets. Clearly, additional studies are warranted to identify the lifestyle interventions that have the greatest benefits in terms of CVD risk reductions in subjects with different inflammatory status. In addition, the extent to which CRP at baseline predicts the long-term response of plasma lipid concentrations to diet must be examined before this information is used in a clinical setting to optimize dietary recommendations made on an individual basis.
|
ACKNOWLEDGMENTS |
|---|
|
FOOTNOTES |
|---|
3 Abbreviations used: CHO, carbohydrates; CVD, cardiovascular disease; C, cholesterol; CRP, C-reactive protein; DASH, Dietary Approaches to Stop Hypertension; HL, hepatic lipase; LPL, lipoprotein lipase; MUFA, monounsaturated fatty acids; PPD, peak particle diameter; SFA, saturated fatty acids.
Manuscript received 29 September 2005. Initial review completed 16 November 2005. Revision accepted 3 January 2006.
|
LITERATURE CITED |
|---|
|
TOPABSTRACTSUBJECTS AND METHODSRESULTSDISCUSSIONLITERATURE CITED |
|---|
1. Libby P, Ridker PM. Inflammation and atherosclerosis: role of C-reactive protein in risk assessment. Am J Med. 2004;116: Suppl 6A:9S–16.
2. Ridker PM, Hennekens CH, Buring JE, Rifai N. C-reactive protein and other markers of inflammation in the prediction of cardiovascular disease in women. N Engl J Med. 2000;342:836–43.
3. Ridker PM. Clinical application of C-reactive protein for cardiovascular disease detection and prevention. Circulation. 2003;107:363–9.
4. Ridker PM, Cushman M, Stampfer MJ, Tracy RP, Hennekens CH. Inflammation, aspirin, and the risk of cardiovascular disease in apparently healthy men. N Engl J Med. 1997;336:973–9.
5. Jialal I, Stein D, Balis D, Grundy SM, Adams-Huet B, Devaraj S. Effect of hydroxymethyl glutaryl coenzyme a reductase inhibitor therapy on high sensitive C-reactive protein levels. Circulation. 2001;103:1933–5.
6. Tchernof A, Nolan A, Sites CK, Ades PA, Poehlman ET. Weight loss reduces C-reactive protein levels in obese postmenopausal women. Circulation. 2002;105:564–9.
7. Ajani UA, Ford ES, Mokdad AH. Dietary fiber and C-reactive protein: findings from National Health and Nutrition Examination Survey data. J Nutr. 2004;134:1181–5.
8. Pischon T, Hankinson SE, Hotamisligil GS, Rifai N, Willett WC, Rimm EB. Habitual dietary intake of n-3 and n-6 fatty acids in relation to inflammatory markers among US men and women. Circulation. 2003;108:155–60.
9. Liu S, Manson JE, Buring JE, Stampfer MJ, Willett WC, Ridker PM. Relation between a diet with a high glycemic load and plasma concentrations of high-sensitivity C-reactive protein in middle-aged women. Am J Clin Nutr. 2002;75:492–8.
10. Lopez-Garcia E, Schulze MB, Fung TT, Meigs JB, Rifai N, Manson JE, Hu FB. Major dietary patterns are related to plasma concentrations of markers of inflammation and endothelial dysfunction. Am J Clin Nutr. 2004;80:1029–35.
11. Chrysohoou C, Panagiotakos DB, Pitsavos C, Das UN, Stefanadis C. Adherence to the Mediterranean diet attenuates inflammation and coagulation process in healthy adults: The ATTICA Study. J Am Coll Cardiol. 2004;44:152–8.
12. Rubin J, Berglund L. Apolipoprotein E and diets: a case of gene-nutrient interaction? Curr Opin Lipidol. 2002;13:25–32.
13. Denke MA, Frantz ID, Jr. Response to a cholesterol-lowering diet: efficacy is greater in hypercholesterolemic subjects even after adjustment for regression to the mean. Am J Med. 1993;94:626–31.
14. Denke MA, Adams-Huet B, Nguyen AT. Individual cholesterol variation in response to a margarine- or butter-based diet: a study in families. JAMA. 2000;284:2740–7.
15. Erlinger TP, Miller ER III, Charleston J, Appel LJ. Inflammation modifies the effects of a reduced-fat low-cholesterol diet on lipids: results from the DASH-sodium trial. Circulation. 2003;108:150–4.
16. Zhao G, Etherton TD, Martin KR, West SG, Gillies PJ, Kris-Etherton PM. Dietary alpha-linolenic acid reduces inflammatory and lipid cardiovascular risk factors in hypercholesterolemic men and women. J Nutr. 2004;134:2991–7.
17. Hilpert KF, Kris-Etherton PM, West SG. Lipid response to a low-fat diet with or without soy is modified by C-reactive protein status in moderately hypercholesterolemic adults. J Nutr. 2005;135:1075–9.
18. Archer WR, Lamarche B, Deriaz O, Landry N, Corneau L, Despres JP, Bergeron J, Couture P, Bergeron N. Variations in body composition and plasma lipids in response to a high-carbohydrate diet. Obes Res. 2003;11:978–86.
19. Archer WR, Lamarche B, St Pierre AC, Mauger JF, Deriaz O, Landry N, Corneau L, Despres JP, Bergeron J, et al. High carbohydrate and high monounsaturated fatty acid diets similarly affect LDL electrophoretic characteristics in men who are losing weight. J Nutr. 2003;133:3124–9.
20. Moorjani S, Dupont A, Labrie F, Lupien PJ, Brun D, Gagné C, Giguère M, Bélanger A. Increase in plasma high-density lipoprotein concentration following complete androgen blockage in men with prostatic carcinoma. Metabolism. 1987;36:244–50.
21. Rush RF, Leon L, Turrel J. Automated simultaneous cholesterol and triglyceride determination on the AutoAnalyser II instrument. In: Barton EC, DuCros MJ, Erdrich MM, Golin JE, editors. Advances in automated analysis. Technicon International Congress 1970. Mount Kisco, NY: Futura Publishing; 1972. p. 503–507.
22. Pirro M, Bergeron J, Dagenais GR, Bernard PM, Cantin B, Després JP, Lamarche B. Age and duration of follow-up as modulators of the risk for the ischemic heart disease associated with high plasma C-reactive protein levels in men. Arch Intern Med. 2001;161:2474–80.
23. St Pierre AC, Ruel IL, Cantin B, Dagenais GR, Bernard PM, Despres JP, Lamarche B. Comparison of various electrophoretic characteristics of LDL particles and their relationship to the risk of ischemic heart disease. Circulation. 2001;104:2295–9.
24. Watson TD, Tan CE, McConnell M, Clegg SK, Squires LF, Packard CJ. Measurement and physiological significance of lipoprotein and hepatic lipase activities in preheparin plasma. Clin Chem. 1995;41:405–12.
25. Lohman T, Roche A, Martorel R. The Airlie (VA) consensus conference standardization of anthropometric measurements. Standardization of anthropometric measurements. Champaign, IL: Human Kinetics; 1988. p. 39–80.
26. Sjöström L, Kvist H, Cederblad A, Tylon U. Determination of total adipose tissue and body fat in women by computed tomography, 40K, and tritium. Am J Physiol. 1986;250:E736–45.
27. Pearson TA, Mensah GA, Alexander RW, Anderson JL, Cannon RO III, Criqui M, Fadl YY, Fortmann SP, Hong Y, et al. Markers of inflammation and cardiovascular disease: application to clinical and public health practice: a statement for healthcare professionals from the Centers for Disease Control and Prevention and the American Heart Association. Circulation. 2003;107:499–511.
28. Heilbronn LK, Noakes M, Clifton PM. Energy restriction and weight loss on very-low-fat diets reduce C-reactive protein concentrations in obese, healthy women. Arterioscler Thromb Vasc Biol. 2001;21:968–70.
29. Esposito K, Marfella R, Ciotola M, Di Palo C, Giugliano F, Giugliano G, D'Armiento M, D'Andrea F, Giugliano D. Effect of a Mediterranean-style diet on endothelial dysfunction and markers of vascular inflammation in the metabolic syndrome: a randomized trial. JAMA. 2004;292:1440–6.
30. Noakes M, Foster P, Keogh J, Clifton P. Very low carbohydrate diets for weight loss and cardiovascular risk1. Asia Pac J Clin Nutr. 2004;13:S64.
31. Nicklas BJ, Ambrosius W, Messier SP, Miller GD, Penninx BW, Loeser RF, Palla S, Bleecker E, Pahor M. Diet-induced weight loss, exercise, and chronic inflammation in older, obese adults: a randomized controlled clinical trial. Am J Clin Nutr. 2004;79:544–51.
32. Clifton PM. Diet and C-reactive protein. Curr Atheroscler Rep. 2003;5:431–6.
33. Jenkins DJ, Kendall CW, Marchie A, Faulkner DA, Wong JM, de Souza R, Emam A, Parker TL, Vidgen E, et al. Effects of a dietary portfolio of cholesterol-lowering foods vs lovastatin on serum lipids and C-reactive protein. JAMA. 2003;290:502–10.
34. Seshadri P, Iqbal N, Stern L, Williams M, Chicano KL, Daily DA, McGrory J, Gracely EJ, Rader DJ, Samaha FF. A randomized study comparing the effects of a low-carbohydrate diet and a conventional diet on lipoprotein subfractions and C-reactive protein levels in patients with severe obesity. Am J Med. 2004;117:398–405.
35. Baer DJ, Judd JT, Clevidence BA, Tracy RP. Dietary fatty acids affect plasma markers of inflammation in healthy men fed controlled diets: a randomized crossover study. Am J Clin Nutr. 2004;79:969–73.
36. Lichtenstein AH, Erkkila AT, Lamarche B, Schwab US, Jalbert SM, Ausman LM. Influence of hydrogenated fat and butter on CVD risk factors: remnant-like particles, glucose and insulin, blood pressure and C-reactive protein. Atherosclerosis. 2003;171:97–107.
37. Mezzano D, Leighton F, Martinez C, Marshall G, Cuevas A, Castillo O, Panes O, Munoz B, Perez DD, et al. Complementary effects of Mediterranean diet and moderate red wine intake on haemostatic cardiovascular risk factors. Eur J Clin Nutr. 2001;55:444–51.
38. Khovidhunkit W, Kim MS, Memon RA, Shigenaga JK, Moser AH, Feingold KR, Grunfeld C. Effects of infection and inflammation on lipid and lipoprotein metabolism: mechanisms and consequences to the host. J Lipid Res. 2004;45:1169–96.
39. Yudkin JS, Kumari M, Humphries SE, Mohamed-Ali V. Inflammation, obesity, stress and coronary heart disease: is interleukin-6 the link? Atherosclerosis. 2000;148:209–14.
40. Wallberg-Jonsson S, Dahlen G, Johnson O, Olivecrona G, Rantapaa-Dahlqvist S. Lipoprotein lipase in relation to inflammatory activity in rheumatoid arthritis. J Intern Med. 1996;240:373–80.
41. Kobayashi J, Tateishi S, Maruyama T, Kudoh A, Murano S. Marked reduction in serum high-density lipoprotein cholesterol concentrations in a woman with acute inflammation due to diabetic gangrene. Clin Chim Acta. 2003;335:33–8.
42. Brull DJ, Serrano N, Zito F, Jones L, Montgomery HE, Rumley A, Sharma P, Lowe GD, World MJ, et al. Human CRP gene polymorphism influences CRP levels: implications for the prediction and pathogenesis of coronary heart disease. Arterioscler Thromb Vasc Biol. 2003;23:2063–9.
This article has been cited by other articles:
|
|
 |
|
  M.-P. St-Onge, S. Zhang, B. Darnell, and D. B. Allison Baseline Serum C-Reactive Protein Is Associated with Lipid Responses to Low-Fat and High-Polyunsaturated Fat Diets J. Nutr., April 1, 2009; 139(4): 680 - 683. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J.-F. Mauger, J. Levesque, M.-E. Paradis, N. Bergeron, A. Tchernof, P. Couture, and B. Lamarche Intravascular Kinetics of C-Reactive Protein and Their Relationships with Features of the Metabolic Syndrome J. Clin. Endocrinol. Metab., August 1, 2008; 93(8): 3158 - 3164. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 L. F. Lien, A. J. Brown, J. D. Ard, C. Loria, T. P. Erlinger, A. C. Feldstein, P.-H. Lin, C. M. Champagne, A. C. King, H. L. McGuire, et al. Effects of PREMIER Lifestyle Modifications on Participants With and Without the Metabolic Syndrome Hypertension, October 1, 2007; 50(4): 609 - 616. [Abstract] [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]
|
|
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
