Obesity has become a new century, diseases of civilization, people are afraid of fat, such as the tiger. As everyone knows, extremes meet. The harmful effects of excessive consumption of fat is not self-evident, but edible fat and too little may not be a good thing. You know, fat is an essential nutrient is one of the seven, do not eat or eat too little is not enough.
fatty acid expert roundtable Key statements about fatty acids fatty acid expert roundtaBle key statements aBout fatty acids Background • Cardiovascular disease (CVD) remains a leading cause of death and disability. • Clinical guidelines and pharmaceutical development have focused on the reduction of LDL cholesterol (LDL-C) as a main goal for reducing CVD, but other lipoproteins, including HDL cholesterol (HDL-C), triglycerides, and LDL-particle size may also be important. • Saturated fatty acid consumption (grams or percent calories) increases LDL-C and HDL-C, but tends to lower triglycerides. • When substituted isocalorically for carbohydrate, any of the three classes of fatty acids (i.e., poly, mono, saturated) results in increases in HDL-C and decreases in serum triglycerides levels. • Dietary guidelines from the American Heart Association and other agencies recommend that <1%, with the remainder from monounsaturated and polyunsaturated fats. total fat account for <25-35% of total daily caloric intake; saturated fat, <7%; and trans fat, • A 2005 estimate of the average American diet found that trans fatty acid intake contributed 2.5% of total calories. • Changes in carbohydrate intake must be taken into account when considering the effect of changes in fatty acid metabolism in human physiology. considerations for replacing trans fats when a solid fat is required for food functionality and staBility • Trans fatty acids increase LDL-C and decrease HDL-C levels. • Public health officials and policy makers are recommending that trans fatty acids to be eliminated from the American diet. • Efforts to reduce or eliminate trans fatty acids in baked goods forces manufacturers to make one of several changes in food manufacturing: 1. Substituting saturated fat such as palm oil for trans fat 2. Substituting interesterified fat for trans fat 3. Substituting carbohydrate for trans fat • Each choice adds additional complexity to “improving” our manufactured food supply. • Finding a suitable fat with desirable functionality, taste and shelf life similar to a hydrogenated fat presents a challenge for food manufacturers. Solid fats (saturated fatty acids) are more readily adaptable for food preparation processes. • If half of trans fatty acids are replaced by polyunsaturated fat or monounsaturated fat, and half replaced with saturated fatty acids, it is expected that the saturated fat component in the diet will increase approximately 1 to 1.5% of total fat calories (composed of primarily palmitic and/or stearic acid). The overall public health goal in regard to trans fatty acids is to prevent adverse health effects associated with exposure to them. The preferred option would be to replace them with unsaturated fatty acids, or when necessary for structural or functionality purposes, a natural or modified saturate. A further consideration is that “healthier” baked goods with no trans fats should be consumed in the context of an overall diet containing fruit, vegetables, dairy products and grains. 1 fat replacement options for food manufacturers An example of replacing trans fatty acids with saturated fatty acids required for functionality might be formulated as follows: Medium Muffin With Trans Fat No Trans Fat Total Fat 10.3g 10.3g Trans Fat 0.7g 0g Saturated Fat 1.5g 2.2g Monounsaturated Fat 2.4g 2.4g Polyunsaturated Fat 5.7g 5.7g Currently available technology offers two major options: 1. Replace partially hydrogenated fatty acids with a saturated fatty acid that is mostly palmitic acid from natural fat(s). 2. Replace partially hydrogenated fat with a specifically designed, interesterified fat containing more saturated fatty acids made up mostly of stearic acid. The pros and cons of each of these choices are outlined in the table below. Fully Hydrogenated Issue Palmitic Acid Option Interesterified Stearic Trans Fatty Acid Acid Option Reasonable Evidence Naturally occurring Fully hydrogenated Partially hydrogenated saturated fatty acid Fatty acid is placed Fatty acid is placed Fat type Fatty acid is placed randomly at the 1,2 randomly at the 1,2 at the 1,3 position on and 3 position on the and 3 position on the triglyceride molecule triglyceride molecule triglyceride molecule Neutral to increase in Neutral to increase Increases LDL Effects on LDL LDL depending on level in LDL depending depending on level of intake on level of intake of intake Neutral to moderate Neutral to decrease Effects on HDL Decrease in HDL increase in HDL in HDL at high intakes 2 Fully Hydrogenated Issue Palmitic Acid Option Interesterified Stearic Trans Fatty Acid Acid Option Exploratory Evidence Effects on Relatively neutral to Tends to increase Increases ratio (typically) LDL: HDL ratio slight decrease in ratio ratio at high levels One study found increase One study found One study found in postprandial glucose Effect on postprandial increase in postprandial increase in postprandial (under the curve) more glucose (area under glucose (under the glucose(under the curve) than palmitic acid, but the curve) curve), but less than more than palmitic acid less than interesterified stearic acid and trans fat and trans fat stearic acid When combined with Increased fibrinogen, Increased fibrinogen Effect of high levels on myristic and lauric but at lower levels over control inflammatory markers acids has similar than stearic acid carbohydrate group effect as carbohydrates and control group Effect on myocardial Neutral effect Increases risk of MI Neutral effect compared infarction risk through compared to control compared to control to control fibrinogen increase a third option for food manufacturers—increase carBohydrate energy component A third option for replacing trans fatty acids (still within FDA guidelines for <0.5g TFA/serving) would be to reduce them to less than 0.5g without replacing the fat. Therefore, the carbohydrate and protein levels would not change, but they would represent a greater percentage of the total energy in the product. An example for a hypothetical muffin follows: Medium Muffin With Trans Fat No Trans Fat* Total Fat 10.3g 10g Trans Fat 0.7g 0.4g Saturated Fat 1.5g 1.5g Monounsaturated Fat 2.4g 2.4g Polyunsaturated Fat 5.7g 5.7g *Based on FDA labeling that states less than 0.5 g can be defined as “no trans fat” 3 key consensus statements • Where possible, the selection of oils or fats to replace trans fatty acids should favor polyunsaturated or monounsaturated fatty acids. • Where a solid fat is required for product taste and functionality, the only saturated fatty options currently available to replace trans fatty acids are palm oil or interesterified stearic acid. • Replacing trans fats with either palmitic acid or interesterified stearic acid is expected to reduce cardiovascular risk factors. • How future changes, including the introduction of fats from genetically modified crops and the availability of interesterified diets richer in stearic acid, will alter fatty acid consumption of consumers, and hence, cardiovascular risk, remains unclear. • Consumption of a variety of fats—including polyunsaturated (both omega-3 and omega-6), monounsaturated, and saturated fatty acids—is preferable to over-reliance on any one fatty acid. • A one-to-one exchange of saturated fatty acids for trans fatty acids is expected to raise the former to a level consistent with reduced cardiovascular risk (assuming no other shift in macronutrient composition or total amount of fats in the average diet). • Before any policies are made related to trans fatty acids and potential replacement fats, further interventional and observational studies should be completed to fully understand the tradeoffs inherent in the solution. references 1. Alberti KG, Eckel RH, Grundy SM, et al. Harmonizing the Metabolic Syndrome. A Joint Interim Statement of the International Diabetes Federation Task Force on Epidemiology and Prevention; National Heart, Lung, and Blood Institute; American Heart Association; World Heart Federation; International Atherosclerosis Society; and International Association for the Study of Obesity. Circulation. 2009;Epub Ahead of Print(Oct 5). 2. American Heart Association (AHA). Cardiovascular Disease Statistics. www.americanheart.org/presenter. jhtml?identifier=4478. 3. American Heart Association. Stearic acid. www.americanheart.org/presenter.jhtml?identifier=4747. 4. Baer DJ, et al. Dietary fatty acids affect plasma markers of inflammation in healthy men fed controlled diets: a randomized crossover study1–3. Am J Clin Nutr 2004;79:969 –73. 5. Denke MA and Grundy SM. Comparison of effects of lauric acid and palmitic acid on plasma lipids and lipoproteins. Am J Clin Nutr 1992;56:895-8. 6. Diet, Nutrition and the Prevention of Chronic Diseases. Report of a Joint WHO/FAO Expert Consultation. www. who.int/hpr/NPH/docs/who_fao_expert_report.pdf. World Health Organization, Geneva 2003. 7. Emken EA. Metabolism of dietary stearic acid relative to other fatty acids in human subjects. Am J Clin Nutr. 1994 Dec;60(6 Suppl):1023S-1028S. 8. Fabricatore AN, Wadden TA, Moore RH, et al. Predictors of attrition and weight loss success: Results from a randomized controlled trial. Behav Res Ther 2009; 47 (8), 685-691. 9. Feinman RD, Volek JS. Low carbohydrate diets improve atherogenic dyslipidemia even in the absence of weight loss. Nutrition & Metabolism 2006, 3:24. www.nutritionandmetabolism.com/content/3/1/24 10. Ford ES, Li C, Zhao G, Pearson WS, Capewell S. Trends in the prevalence of low risk factor burden for cardiovascular disease among United States adults. Circulation. Sep 29 2009;120(13):1181-1188. 11. Gidding SS, Lichtenstein AH, Faith MS, et al. Implementing American Heart Association pediatric and adult nutrition guidelines: a scientific statement from the American Heart Association Nutrition Committee of the Council on Nutrition, Physical Activity and Metabolism, Council on Cardiovascular Disease in the Young, Council on Arteriosclerosis, Thrombosis and Vascular Biology, Council on Cardiovascular Nursing, Council on Epidemiology and Prevention, and Council for High Blood Pressure Research. Circulation. Mar 3 2009;119(8):1161-1175. 12. Harvard www.health.harvard.edu/books/lowering_your_cholesterol.htm 13. High blood cholesterol: what you need to know. NHLBI. www.nhlbi.nih.gov/health/public/heart/chol/wyntk.htm. 14. Hu FB, Willett WC. Optimal diets for prevention of coronary heart disease. JAMA, 2002 Nov 27. 288;20:2569-2578. 15. Institute of Medicine, “Dietary Reference Intakes for Energy, Carbohydrate, Fiber, Fat, Fatty Acids, Cholesterol, Protein, and Amino Acids.” September 2002. Chapter 11: Macronutrients and Healthful Diets. 4 16. Jakobsen MJ, O’Reilly EJ, et al. Major types of dietary fat and risk of coronary heart disease: a pooled analysis of 11 cohort studies. Am J Clin Nutr 2009;89:1425-1432. 17. Judd JT, et al. Dietary cis and trans Monounsaturated and Saturated FA and Plasma Lipids and Lipoproteins in Men. Lipids 2002;37:123-131. 18. Katan MB, Zock PL, Mensink RP. Effects of fats and fatty acids on blood lipids in humans: an overview. Am J Clin Nutr 1994;60(suppl):1017S-22S. 19. Kellens M. Interesterification: process conditions. Society of Chemical Industry. 2000. www.soci.org/SCI/ publications/2001/pdf/pb82.pdf 20. Know your facts. American Heart Association. www.americanheart.org/presenter.jhtml?identifier=532. 21. Krauss RM, et al. Separate effects of reduced carbohydrate intake and weight loss on atherogenic dyslipidemia. Am J Clin Nutr 2006;83:1025-31. 22. Kris-Etherton P, et al. Dietary Stearic Acid and Risk of Cardiovascular Disease: Intake, Sources, Digestion, and Absorption. Lipids 2005; 40, 1193–1200. 23. Lockheart MS, Steffen LM, Rebnord HM, Fimreite RL, Ringstad J, Thelle DS, Pedersen JI, Jacobs DR Jr. Dietary patterns, food groups and myocardial infarction: a case-control study. Br J Nutr. 2007;98:380–387. 24. Mensink RM, et al. Effects of dietary fatty acids and carbohydrates on the ratio of serum total to HDL cholesterol and on serum lipids and apolipoproteins: a meta-analysis of 60 controlled trials. Am J Clin Nutr 2003;77:1146-55. 25. Mensink RP, Katan MB. Effect of dietary fatty acids on serum lipids and lipoproteins: a meta-analysis of 27 trials. Arterioscler Thromb 1992;12:911-919. 26. Mikkila V, Rasanen L, Raitakari OT, Marniemi J, Pietinen P, Ronnemaa T, Viikari J. Major dietary patterns and cardiovascular risk factors from childhood to adulthood: the Cardiovascular Risk in Young Finns Study. Br J Nutr. 2007;98:218 –225. 27. Rhee SK, et al. Desaturation and interconversion of dietary stearic and palmitic acids in human plasma and lipoproteins. Am J Clin Nutr 1997;65:451-8. 28. Schaefer EJ. Lipoproteins, nutrition, and heart disease. Am J Clin Nutr 2002;75:191-212. 29. Sundram K, Karupaiah T, Hayes KC. Stearic acid-rich interesterified fat and trans-rich fat raise the LDL/HDL ratio and plasma glucose relative to palm olein in humans. Nutrition & Metabolism 2007, 4:3. 30. The American Heritage® Stedman’s Medical Dictionary. Houghton Mifflin Company. http://dictionary. reference.com/browse/palmitic acid (accessed: October 20, 2008). 31. Westrate JA and Meijer GW. Plant sterol-enriched margarines and reduction of plasma total- and LDL- cholesterol concentrations in normocholesterolaemic and mildly hypercholesterolaemic subjects. European Journal of Clinical Nutrition (1998) 52, 334-43. 32. WHO, Cardiovascular Disease Prevention and Control. www.who.int. From International CVD Statistics. 33. van der Bom JG, de Maat MP, Bots ML, et al. Elevated plasma fibrinogen: cause or consequence of cardiovascular disease? Arterioscler Thromb Vasc Biol 1998;18:621–5. 34. Pedersen JI, Muller H, Seljeflot I, Kirkhus B. Palm oil versus hydrogenated soybean oil: effects on serum lipids and plasma haemostatic variables. Asia Pac J Clin Nutr. 2005;14(4):348-57. 5 addendum taBle Background • Baer DJ, et al. Dietary fatty acids affect plasma markers of inflammation in healthy men fed controlled diets: a randomized crossover study1–3. Am J Clin Nutr 2004;79:969 –73. - LMP diet, 8% of energy enrichment with saturated fatty acids as the sum of lauric (L), myristic (M), and palmitic (P) acids (ratio of L to M to P of 0.3:1.4:8.3); stearic acid (STE) diet, 8% of energy enrichment with stearic acid; trans fatty acid (TFA) diet, 8% of energy enrichment in TFAs (spectrum of trans 18:1 positional isomers similar to that in the US food supply). - Inflammatory Marker Data: In both stearic acid enriched diet and stearic acid/trans fat enriched diet fibrinogen increased. In stearic acid only, was 4.4% higher than control carbohydrate group. Consumption of the diet enriched in stearic acid resulted in higher concentrations of fibrinogen than did consumption of all other diets except the TFA/STE diet. Concentrations of plasma markers of inflammation after 5 wk of consumption of each diet: FIbRINOgEN diet mean (g/l) CHO (control) 2.74 OL 2.71 TFA 2.74 TFA + STE 2.75 STE 2.86 LMP 2.68 • van der Bom JG, de Maat MP, Bots ML, et al. Elevated plasma fibrinogen: cause or consequence of cardiovascular disease? Arterioscler Thromb Vasc Biol 1998;18:621–5. - Myocardial Infarction Risk: A rise in fibrinogen of 1 g/L was associated with a 45% increased risk (odds ratio adjusted for age, sex, and smoking, 1.45; 95% CI, 1.12 to 1.88). Lowering fibrinogen levels is not associated with a lower risk of myocardial infarction. • Sundram K, Karupaiah T, Hayes KC. Stearic acid-rich interesterified fat and trans-rich fat raise the LDL/ HDL ratio and plasma glucose relative to palm olein in humans. Nutrition & Metabolism 2007, 4:3. - One test fat rotation was based on palm olein (POL) and provided 12.0 percent of energy (%en) as palmitic acid (16:0); a second contained trans-rich partially hydrogenated soybean oil (PHSO) and provided 3.2 %en as trans fatty acids plus 6.5 %en as 16:0, while the third used an interesterified fat (IE) and provided 12.5 %en as stearic acid (18:0). - Effects on LDL: Dietary fat also affected absolute change in LDL-C, with the concentration after the PHSO being 7% greater than POL (P < 0.05). The IE diet effect was intermediate and not significantly different from either POL or PHSO. - Effects on HDL: After adjusting for multiple comparisons between dietary treatments, plasma HDL-C was significantly lower (p < 0.001) both during the PHSO (-8%) and IE (-9%) diet treatments compared to POL. - Effects on LDL:HDL ratio: The LDL-C/HDL-C ratio was similarly increased by the PHSO and IE diets, with differences being about 15% greater than the POL diet (P < 0.001). - Glucose Data: After four weeks on each test fat, the rise was 3% for POL, 9% for PHSO, and 22% for IE. 6 • Judd JT, et al. Dietary cis and trans Monounsaturated and Saturated FA and Plasma Lipids and Lipoproteins in Men. Lipids 2002;37:123-131. - The six diets were planned to vary by 8 en% as follows: diet CHO, 8.5 en% reduction in fat (approximately equivalent to 8 en% reduction in FA) replaced by digestible carbohydrate; diet OL, 8 en% enrichment in oleic acid; diet LMP, 8 en% enrichment with saturated FA as the sum of lauric (L), myristic (M), and palmitic acids (P) (LMP) with the ratio of L/M/P of 0.3:1.4:8.3; diet STE, 8 en% enrichment with stearic acid; diet TFA: 8 en% enrichment in TFA with a spectrum of trans 18:1 positional isomers similar to that in the U.S. food supply; and diet TFA|STE, a combined enrichment with 4 en% TFA and 4 en% STE. - Dietary fatty acid levels prior to enrichment were targeted at levels within the range of typical U.S. diets with the exception that saturated FA were to be about 10 en% with STE excluded. Otherwise, the diets before enrichment were targeted to have 2.5 en% STE, 4 en% linoleic acid, 10 en% OL, 10 en% LMP FA, and 2.5 en% other FA. Plasma Lipid, Lipoprotein Cholesterol, and Apolipoprotein Concentrations and Ratios of Total and LDL Cholesterol to HDL Cholesterol of 50 Adult Men After 5 wk Consumption of Each Dieta expressed as mg/dl Medium Muffin CHO OL TFA TFA/STE STE LMP Triglycerides 91b,c 78a 91b,c 94b, c 101c 86a,b Total Cholesterol 184a,b 179a 195d 194d 175b 193c,d LDL 119a,b 115a 131e 129d,e 121b,c 125c,d HDL 47b 48c 45a,b 46a,b 45a 51d Diets labeled with different roman superscripts are significantly different at P < 0.01. TC/HDL (ratio) 4.1b 3.9a 4.5d 4.4c,d 4.3c 4.0a,b 7
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