Hold the Patty, Not the Lettuce
2010; Lippincott Williams & Wilkins; Volume: 122; Issue: 9 Linguagem: Inglês
10.1161/circulationaha.110.971812
ISSN1524-4539
Autores Tópico(s)Fatty Acid Research and Health
ResumoHomeCirculationVol. 122, No. 9Hold the Patty, Not the Lettuce Free AccessEditorialPDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessEditorialPDF/EPUBHold the Patty, Not the LettuceProcessing Foods for Over a Quarter Century in the Nurses' Health Study Michael Miller, MD Michael MillerMichael Miller From the Departments of Medicine, Epidemiology and Public Health, University of Maryland School of Medicine, Baltimore, Md. Originally published16 Aug 2010https://doi.org/10.1161/CIRCULATIONAHA.110.971812Circulation. 2010;122:859–860Other version(s) of this articleYou are viewing the most recent version of this article. Previous versions: August 16, 2010: Previous Version 1 Nearly a century ago, Anichkov's keen experimental observations linking dietary cholesterol to accelerated atherosclerosis spawned an era of investigation assessing macronutrient intake in the development and progression of coronary heart disease (CHD).1 To this end, epidemiological studies identified total fat, saturated fatty acid, and trans fatty acid (TFA) intake as positively correlated with CHD risk,2 whereas intake of monounsaturated and polyunsaturated fatty acids was inversely correlated.3Article see p 876The epidemiological data are consistent with experimental studies supporting a mechanistic basis for these effects. Among these are acceleration of thrombus formation,4 downregulation of low-density lipoprotein receptor activity,5 impairment of high-density lipoprotein functionality6 and endothelial vasoreactivity,7 and modulation of proinflammatory signaling pathways after exposure to saturated fatty acid or TFA.8 Although the "definitive" diet-heart trial has yet to be undertaken,9 randomized clinical trial data in the aggregate have not been inconsistent with epidemiological studies; the most harmful dietary influences include TFA intake and a high glycemic load, whereas monounsaturated and polyunsaturated fatty acids and certain complex carbohydrates appear to confer cardioprotection.10 In this issue of Circulation,11 an updated analysis from the long-standing Nurses' Health Study provides additional insight into diet and CHD risk in women by departing from traditional dietary measures of fat and carbohydrate exposure. Rather, dietary protein sources were selected, because interchanging 1 protein for another would seemingly be easier to achieve in prescribing heart-healthy substitutions than more traditional and cumbersome methods that include calorie counting and isocaloric exchanges between fat and complex carbohydrates. Over an extended 26-year follow-up period, nurses who ate more than 2 servings of red meat daily (including processed meats) had an approximately 30% increased risk of CHD compared with those eating less than ½ serving of red meat daily. Similarly, the highest intake of red meat in relation to poultry and fish was also associated with the greatest risk. In evaluating the exchange of 1 dietary protein source for another, reduced CHD risk was observed when dairy, poultry, fish, or nuts were substituted for red meat.Although protein-protein substitution represents a novel approach in the dietary assessment of CHD risk, there are several caveats worthy of elaboration. First, because the authors chose to compare protein sources, the protein content per serving size should have been similar if not equal between comparators. Seemingly, this would have been implicit as a methodological consideration if true protein exchanges were to be made. Otherwise, it is difficult to appreciate whether we are truly comparing "apples to apples" or, in this case, red meat to other protein sources. For example, 1 serving of red meat such as a hamburger patty (75% lean) contains nearly 18 g of protein compared with 1 serving of canned fish (3 oz) that contains approximately 22 g. Adjustment for the higher content of protein in canned fish would also amplify baseline differences between red meat and canned fish in energy intake (195 versus 99 kcal), cholesterol (62 versus 26 mg), and trans fats (0.82 g versus undetectable), as classified in the US Department of Agriculture nutrient database,12 which in turn may have underestimated the true adverse effect of red meat consumption. The lack of such an adjustment was countered in part by the greater daily consumption of red meat as opposed to poultry and fish (third quartile 1.14 versus 0.24 and 0.14 servings/d, respectively). Another potential limitation in any long-term dietary follow-up study relates to ensuring that proper adjustments are made in the face of changing dietary patterns. In this regard, greater adjustments were made for chicken and fish vis-à-vis serving size portion (from 6 to 8 oz in 1980 to a range of 2 to 3 oz in 2002) than for beef and pork (from 6 to 8 oz in 1980 to 4 to 6 oz in 2002; see the online-only Data Supplement that accompanies the article by Bernstein et al11). On the basis of these adjustments, it may be more difficult to accurately interchange 1 (2 to 3 oz) serving of poultry or fish for 1 (4 to 6 oz) serving of beef or pork. Moreover, it is unclear whether or to what extent adjustments were made over the past 26 years in "unquantified" dietary sources (eg, a hamburger patty). This has become a prominent concern in the era of increased portion sizes that have contributed to the current obesity epidemic.13 For example, comparison between the original and largest size of a hamburger patty at McDonald's has increased 5-fold (precooked weight from 1.6 to 8 oz) during the past 50 years.14 Failure to adjust for changes in patty size and associated nutrient content among hamburger and other nonquantified food items may have also biased the follow-up results and CHD risk estimates. Finally, nurses who consumed the most red meat were also more likely to be hypertensive, smoke cigarettes, consume more TFA and total calories, and exercise less than their low-meat-eating colleagues. Although these confounders were adjusted for in multivariable analysis, leading a relatively unhealthy lifestyle may have been accompanied by additional exposures (eg, an increase in atherogenic remnant particles) or habits (eg, high glycemic load consumption) that were not captured in the model but that potentially compounded CHD risk.Notwithstanding the limitations inherent even among the most carefully executed long-term observational studies, several important findings stand out. In addition to the aforementioned low risk of CHD associated with poultry and especially fish consumption, there was a lack of increased risk associated with eggs, even if daily intake was low (ie, upper quintiles consumed less than 1 egg each day). Over the years, eggs have taken a beating, in part because the amount of cholesterol contained within an egg yolk is not insignificant (range of 150 to 250 mg, small to jumbo size).12 Yet, eggs are an excellent source of protein, relatively low in saturated fatty acid (1.2 to 2.0 g)12 and with undetectable TFA. Importantly, saturated fatty acid and TFA promote CHD to a greater extent than dietary cholesterol.15 Equally impressive was the inverse relationship between nuts and incident CHD. Although nut consumption at the upper quintile was modest (ie, less than ½ serving/d), a 32% lower risk of CHD was observed in nurses who snacked on a small packet of nuts (eg, walnuts, peanuts, almonds) daily compared with non-nibblers. This association, like that reported for egg consumption, reaffirms previous observations from the Nurses' Health Study,16,17 which now extends beyond a quarter century. In addition to their protein content, nuts are chock full of antioxidants, with hazelnuts, pecans, and pistachios being particularly rich in the flavonoid compound proanthocyanidin18 that is linked to improved lipid homeostasis, among other potential cardioprotective properties.19When the Nurses' Health Study originated, advertising jingles such as Burger King's "Have It Your Way" (ie, "hold the pickles, hold the lettuce …") were used to beef up hamburger sales. Now, more than a quarter century later, the current analyses reaffirm that a high intake of red meat, especially when processed meats are included, is associated with increased CHD risk. Moving forward, these data support a randomized clinical trial to determine whether "moderate" intake of lean red meat equivalent to poultry and fish (eg, up to 5 to 6 oz daily)20 affects CHD risk. Although this may be a difficult nut to crack, a carefully designed randomized study using isocaloric protein-protein substitutions is likely to yield new insights into the relationship between macronutrient intake and CHD. Until then, I'll take my eggs "over easy" (thank you), and please don't hold the pickles, lettuce, or even the occasional patty.The opinions expressed in this article are not necessarily those of the editors or of the American Heart Association.DisclosuresNone.FootnotesCorrespondence to Michael Miller, MD, Division of Cardiology, University of Maryland Hospital, 22 S Greene St, Room S3B06, Baltimore, MD 21201. E-mail [email protected] References 1 Schaefer EJ, Brousseau ME. Diet, lipoproteins, and coronary heart disease. Endocrinol Metab Clin North Am. 1998; 27: 711–732, xi.CrossrefMedlineGoogle Scholar2 Lichtenstein AH, Kennedy E, Barrier P, Danford D, Ernst ND, Grundy SM, Leveille GA, Van Horn L, Williams CL, Booth SL. Dietary fat consumption and health. Nutr Rev. 1998; 56: S3–S19.Google Scholar3 Hu FB, Willett WC. Optimal diets for prevention of coronary heart disease. JAMA. 2002; 288: 2569–2578.CrossrefMedlineGoogle Scholar4 Connor WE. The acceleration of thrombus formation by certain fatty acids. J Clin Invest. 1962; 41: 1199–1205.CrossrefMedlineGoogle Scholar5 Dietschy JM. Dietary fatty acids and the regulation of plasma low density lipoprotein cholesterol concentrations. J Nutr. 1998; 128: 444S–448S.CrossrefMedlineGoogle Scholar6 Nicholls SJ, Lundman P, Harmer JA, Cutri B, Griffiths KA, Rye KA, Barter PJ, Celermajer DS. Consumption of saturated fat impairs the anti-inflammatory properties of high-density lipoproteins and endothelial function. J Am Coll Cardiol. 2006; 48: 715–720.CrossrefMedlineGoogle Scholar7 Miller M, Beach V, Sorkin JD, Mangano C, Dobmeier C, Novacic D, Rhyne J, Vogel RA. Comparative effects of three popular diets on lipids, endothelial function, and C-reactive protein during weight maintenance. J Am Diet Assoc. 2009; 109: 713–717.CrossrefMedlineGoogle Scholar8 Mozaffarian D, Katan MB, Ascherio A, Stampfer MJ, Willett WC. Trans fatty acids and cardiovascular disease. N Engl J Med. 2006; 354: 1601–1613.CrossrefMedlineGoogle Scholar9 Stamler J. Diet-heart: a problematic revisit. Am J Clin Nutr. 2010; 91: 497–499.CrossrefMedlineGoogle Scholar10 Mente A, de Koning L, Shannon HS, Anand SS. A systematic review of the evidence supporting a causal link between dietary factors and coronary heart disease. Arch Intern Med. 2009; 169: 659–669.CrossrefMedlineGoogle Scholar11 Bernstein AM, Sun Q, Hu FB, Stampfer MJ, Manson JE, Willett WC. Major dietary protein sources and risk of coronary heart disease in women. Circulation. 2010; 122: 876–883.LinkGoogle Scholar12 USDA Nutrient Data Laboratory. USDA National Nutrient Database for Standard Reference. http://www.nal.usda.gov/fnic/foodcomp/search/. Accessed July 6, 2010.Google Scholar13 Ello-Martin JA, Ledikwe JH, Rolls BJ. The influence of food portion size and energy density on energy intake: implications for weight management. Am J Clin Nutr. 2005; 82: 236S–241S.CrossrefMedlineGoogle Scholar14 Young LR, Nestle M. Portion sizes and obesity: responses of fast-food companies. J Public Health Policy. 2007; 28: 238–248.CrossrefMedlineGoogle Scholar15 Eckel RH. Egg consumption in relation to cardiovascular disease and mortality: the story gets more complex. Am J Clin Nutr. 2008; 87: 799–800.CrossrefMedlineGoogle Scholar16 Hu FB, Stampfer MJ, Manson JE, Rimm EB, Colditz GA, Rosner BA, Speizer FE, Hennekens CH, Willett WC. Frequent nut consumption and risk of coronary heart disease in women: prospective cohort study. BMJ. 1998; 317: 1341–1345.CrossrefMedlineGoogle Scholar17 Hu FB, Stampfer MJ, Rimm EB, Manson JE, Ascherio A, Colditz GA, Rosner BA, Spiegelman D, Speizer FE, Sacks FM, Hennekens CH, Willett WC. A prospective study of egg consumption and risk of cardiovascular disease in men and women. JAMA. 1999; 281: 1387–1394.CrossrefMedlineGoogle Scholar18 Miller M. Preventive cardiology. In: Rosendorff C, ed. Essential Cardiology: Principles and Practice. Totowa, NJ: Humana Press; 2005: 801–827.Google Scholar19 Blade C, Arola L, Salvado MJ. Hypolipidemic effects of proanthocyanidins and their underlying biochemical and molecular mechanisms. Mol Nutr Food Res. 2010; 54: 37–59.CrossrefMedlineGoogle Scholar20 Lichtenstein AH, Appel LJ, Brands M, Carnethon M, Daniels S, Franch HA, Franklin B, Kris-Etherton P, Harris WS, Howard B, Karanja N, Lefevre M, Rudel L, Sacks F, Van Horn L, Winston M, Wylie-Rosett J. Diet and lifestyle recommendations revision 2006: a scientific statement from the American Heart Association Nutrition Committee. Circulation. 2006; 114: 82–96.LinkGoogle Scholar Previous Back to top Next FiguresReferencesRelatedDetailsCited ByMiller M, Stone N, Ballantyne C, Bittner V, Criqui M, Ginsberg H, Goldberg A, Howard W, Jacobson M, Kris-Etherton P, Lennie T, Levi M, Mazzone T and Pennathur S (2011) Triglycerides and Cardiovascular Disease, Circulation, 123:20, (2292-2333), Online publication date: 24-May-2011. August 31, 2010Vol 122, Issue 9 Advertisement Article InformationMetrics https://doi.org/10.1161/CIRCULATIONAHA.110.971812PMID: 20713894 Originally publishedAugust 16, 2010 Keywordsfollow-up studiescholesteroldietcoronary heart diseasefatty acidsEditorialsPDF download Advertisement SubjectsEpidemiology
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