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Revisiting the Diet Heart Disease Hypothesis Paper

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White paper looking at the hypothesis that dietary fat leads to high cholesterol, which leads to cardiovascular disease and mortality. But does the research really show that saturated fat is really bad for you?

White paper looking at the hypothesis that dietary fat leads to high cholesterol, which leads to cardiovascular disease and mortality. But does the research really show that saturated fat is really bad for you?

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Revisiting the Diet Heart Disease Hypothesis Paper

  1. 1. Revisiting the Diet-Heart Hypothesis by Alexander J. Rinehart, DC, MS, CCN, CNS This article first appeared in the September 2013 issue of The Original Internist. Information on The Original Internist can be found at http://www.clintpublications.com Abstract: The diet-heart disease hypothesis has been hotly debated over the last few decades. The hypothesis rests on three assumptions: 1.) Intake of saturated fat causes high total cholesterol and low-density lipoproteins (LDLs) 2.) High total cholesterol and LDL are correlated with heart disease, and 3.) Therefore, high dietary intake of saturated fats causes heart disease. While the first two assumptions have strong support in the research literature, the third assumption has not been as well supported. In line with current dietary guidelines developed from the Diet-Heart Disease hypothesis, Americans have reduced their saturated fatty acid intake, and have subsequently increased their intake of processed Polyunsaturated Fatty Acids (PUFAs), and refined carbohydrates. However, new insights suggest that high intake of processed PUFAs, unnaturally occurring trans fatty acids (TFAs), and refined carbohydrates, may be more metabolically troublesome than high intake of saturated fats alone. Does Dietary Fat Cause Heart Disease? The Diet-Heart Disease Hypothesis makes three primary assumptions: 1.) Intake of saturated fat causes high total cholesterol and low-density lipoproteins (LDLs). 2.) High total cholesterol and LDL are correlated with heart disease. 3.) High dietary intake of saturated fats is correlated with high total cholesterol and LDL, and therefore, causes heart disease.
  2. 2. While the first two correlative assumptions have received wide support in the literature, recent meta-analysis has concluded that dietary fat is not significantly correlated with coronary heart disease or cardiovascular disease (1). It is just as well-known, yet less publicized, that saturated fat intake may also: ● Increase High Density Lipoproteins (HDLs) or "good" cholesterol ● Decrease Triglycerides ● Lower Lipoprotein(a) [Lp(a)], an independent marker of heart disease risk ● Improve the Total Cholesterol:HDL ratio, also a strong independent marker of heart disease risk(2; 3; 4; 5; 6; 7; 8) So while the last century of diet guidelines have focused on the correlation of saturated fat, LDLs, and Total Cholesterol with heart disease, eating a diet high in saturated fats may actually be heart protective. How so? While saturated fat intake undoubtedly increases LDLs and Total Cholesterol; its beneficial effect on other markers of heart disease may be more profound. The net "beneficial" effect may go against everything you have learned up to this point about saturated fats, cholesterol, and their proposed links to heart disease. The Diet-Heart Disease Debate The research community has largely ignored evidence with regards to the potentially healthy effects of saturated fats on Lp(a), HDL, and the Total Cholesterol:HDL ratio. Instead, much of the research has focused on saturated fat intake and its association with high LDLs. Since high LDLs are considered a risk factor for heart disease, researchers may have prematurely jumped to the conclusion that saturated fats are to blame. Our understanding of the connection between LDLs and Heart Disease has also adapted. We now know that different types of saturated fats and carbohydrates have differential effects on LDL size and particle number.
  3. 3. Heart disease is not necessarily associated with total LDLs, but it is definitely associated when there are numerous LDL's that are more "small and dense" in size. The "large and fluffy" LDLs may be heart protective (9). For instance, you may have high LDLs, but the majority of them may be of the protective, "large and fluffy" variety. On the other hand, you may have "normal" levels of LDLs, but the majority of them could be of the risky, "small and dense" variety. It is these findings that may help explain why 50% of 136,905 individuals hospitalized with coronary heart disease had "normal" levels of cholesterol, HDL, and LDL at the time of their hospitalization (10). Findings now suggest that total cholesterol, LDLs, and HDLs are not the most reliable indicators for heart disease risk. LDL particle number is now accepted as one of the strongest markers of heart disease risk - potentially even more than conventional markers like total cholesterol and LDLs (11). Saturated Fats and Heart Disease As discussed, an increase in saturated fat intake decreases the risk of heart disease, therefore; a decrease in saturated fat intake should also be associated with an increase in heart disease risk. What does the research say about this? In line with what you have been taught before, a decrease in saturated fat intake is associated with a decrease in LDLs. But as you now know, the story does not end there. Levels of healthy HDLs also decrease and unhealthy Lp(a) levels increase. When you choose to lower saturated fat intake, you have to balance the "improvements" in LDLs with the negative effects on HDLs and Lp(a) (12). Clinicians and researchers alike are now challenged with a broader picture of heart disease risk than what they have been taught over the last century.
  4. 4. The American Heart Association still recommends a diet that is comprised of only 7% or less calories from saturated fat (13); and interestingly, it has not given clear guidance as to what to substitute the saturated fats with. What happens when you substitute saturated fat intake with polyunsaturated fats or carbohydrates? Substituting Saturated Fats with Polyunsaturated Fats The research community has focused on the substitution of polyunsaturated fats (PUFAs) for saturated fats as a means of reducing heart disease risk based on the conventional diet-heart disease hypothesis. When you substitute PUFAs for saturated fats, heart disease risk does decline, but it is impossible to tell if the decline is because of adding more PUFAs to the diet, consuming less saturated fats, or combining the effect of adding PUFAs and reducing saturated fats. The correlation may also be due to unknown variables not yet considered (14; 15; 16). The underlying assumption is that PUFAs are associated with lower levels of LDLs and, therefore, are correlated with less incidence of heart disease. Generally, researchers have concluded that PUFAs are heart protective. As we know from my earlier discussion however, the widely accepted correlation between LDL levels and heart disease is not cut and dry - yet, researchers still make the assumption that LDLs are bad, citing the same correlative research articles over and over again. Again, the relationship is just a correlation, and the potentially healthy effects of dietary fats on HDL, Total Cholesterol:HDL and Lp(a) are still largely ignored. Complicating matters more, a recent meta-analysis reviewed that an increase in PUFA intake was associated with a 13.3% reduction in Total Cholesterol as expected; but the substitution of PUFAs for saturated fats was also associated with an increase in mortality. The authors proposed that the higher intake of PUFAs was associated with
  5. 5. increases in oxidized metabolites (which make up most of the fatty acids in oxidized LDLs). Nevertheless, their findings were counter to previous assumptions in the literature. The authors were careful to indicate that the trouble with PUFAs may be when they are consumed in refined and processed foods rather than when found naturally in whole foods such as nuts and vegetables (17). Excess dietary polyunsaturated fat is nearly impossible to achieve with a diet of whole foods. Oxidized LDLs are an often proposed cause of atherosclerosis. When you look at the composition of arterial plaques, they are predominantly comprised of oxidized polyunsaturated fats, not saturated fats. Substituting Saturated Fats with Carbohydrates: Without clear guidance as to what to substitute saturated fats with, most Americans have made up for their saturated fat intakes with carbohydrates, especially refined carbohydrates and added sugars (18). High intake of refined carbohydrates is associated with increased risk for type 2 diabetes and ischemic heart disease (19) When you substitute carbohydrates for saturated fat, little to no benefit is seen in reducing heart disease risk unless the carbohydrates added are unrefined and have a low glycemic index (20). Additional analysis reveals that when saturated fat intake is replaced with high- carbohydrate, high glycemic index foods, it is associated with a higher risk of a heart attack. When the opposite occurrs (substituting saturated fats with low glycemic carbohydrate foods) - it is associated with a lower heart attack risk (21). Researchers suggest that even if we decided that saturated fats are risky for heart disease, the effect of high intake of refined carbohydrates may cause even worse metabolic damage (22).
  6. 6. So it would appear that more focus should be placed on reducing refined carbohydrates, added sugar, and processed foods; and less focus should be placed on reducing intake of dietary saturated fats. LDLs, Cholesterol and Heart Disease There is no question that LDLs are associated with higher levels of heart disease. But as we've established, the story goes deeper when it comes to saturated fats and total cholesterol, LDLs, LDL size, LDL particle number, HDLs, Lp(a), Total Cholesterol:HDL ratio, and subsequent “net” risk for heart disease. First, cholesterol intake actually has little to do with cholesterol levels in the bloodstream. As intake increases, the body's natural production of cholesterol decreases. As the intake of cholesterol decreases, the body's production ramps up, increasing levels. Paradoxically, you can have elevated, potentially harmful levels of cholesterol due to not eating enough cholesterol. The research now suggests that saturated fat intake may have a greater beneficial effect on HDLs, Total Cholesterol:HDL, Lp(a), and LDL Particle Size and Particle Number. When you substitute saturated fat intake with refined carbohydrates and other processed oils high in PUFAs, you may actually be increasing your health risk. The Problem with Measuring Saturated Fat Intake When you think of typical, American foods, what do you think of? Hamburger and french fries, bacon and hash browns, pepperoni pizza... When research subjects fill out food frequency questionnaires, a check for "hamburger" is a check for saturated fat. But what do we eat hamburgers with? Typically a white, refined carbohydrate bun, along with a high sugar condiment like ketchup. Eating a
  7. 7. hamburger is not a simple categorization. The "white bread" and "condiment" parts tend to be ignored. Additionally, not all studies control for processed versus unprocessed meat as sources of saturated fat. One study did show an association between processed and unprocessed meat with stroke mortality, but the analysis was still assessed by a Food Frequency Questionnaire (FFQ) (23). FFQs do accurately reflect saturated fat intake, but the important grey areas are not taken into account. An additional study from the Journal of Nutrition made a really interesting observation, however. The researchers looked at total cheese intake and the use of butter in cooking which are both high sources of long chain saturated fats). They failed to find an association with heart attacks for both, but that was not the interesting part. When they controlled for "how" the butter was consumed, a new association appeared. When the butter was consumed on bread, it was positively associated with heart attack risk; when consumed by itself, no correlation was found (24). Bad News for Grains? In April 2013, the New York Times and other publications sent the media on a fury announcing a new proposed link between red meat and heart disease (25). The researchers found that those eating red meat were metabolizing its carnitine content into trimethylamine-N-oxide (TMAO). The study also showed a correlation between TMAO levels and heart disease risk (26). The media concluded that a new link between heart disease and red meat had been discovered, yet flaws in the association surfaced.
  8. 8. One of the highest natural sources of TMAO is fish. TMAO is actually the chemical that gives fish its "fishy" smell. Fish intake has largely been associated with heart disease protection. That was the first glaring problem with their analysis. The second problem took a little deeper analysis. The proposed mechanism for the conversion of carnitine to TMAO was the overgrowth of certain species of bacteria in the gut such as Prevotella. What might increase the level of Prevotella bacteria in the gut? A high-grain diet has been proposed at root cause for the overgrowth (27). The media could have just as easily reported that a new link was discovered between heart disease and grains, but the confirmation bias toward red meat and saturated fat was maintained in the coverage. The Skinny on Trans Fatty Acids Trans fatty acids (TFAs) comprise 2-5% of total fat in ruminant fats (from cows, goats, sheep, etc) but comprises 50-60% of total fat in partially hydrogenated vegetable oils. Naturally found TFAs differ from those found in partially hydrogenated vegetable oils because of the placement of the double bonds. The most common naturally occurring TFA is trans-vaccenic acid and is the precursor to conjugated linoleic acid (CLA or alpha-rumenic acid) (28). While CLA may still have a deleterious effect on lipid profiles like other trans fatty acids (29), it may also offer multiple beneficial effects for fat and bone metabolism, immune function, as well as risk of cardiovascular disease and cancer (30). It is generally considered a healthy fat when compared to the TFAs found in partially hydrogenated vegetable oils, but the research is still young. Dietary TFAs raise LDL cholesterol and total cholesterol, and lower HDL cholesterol (31). TFAs have also been reported to increase the stickiness of platelets in the blood (32) as well as levels of Lp(a) (33).
  9. 9. The news is troublesome as up to 70% of the vegetable oils used in foods like crackers, cookies, pastries, cakes, snack chips, candies and fried food are partially hydrogenated. Because of this, it is very difficult to assess TFA intakes among populations (28). Food companies are only required to list trans fat (TF) on the label if the TF content is more than 2g per serving. If the label reads partially hydrogenated fat in the ingredient list, but 0g of total TF, it is likely that the product contains TF, but less than 2g per serving. Estimates for American intake of TFAs range as high as 38.7g/day (28). Other possible adverse effects of TFAs include, but are not limited to:  Cognitive decline  Metabolic syndrome  Infertility  Compromised fetal development (33; 34) While TFAs naturally found in milk, cheese, and ruminant meats may be healthy, one might consider staying away from pastries, cookies, snacks, fried food, margarine, and other processed foods containing unnatural partially hydrogenated vegetable oils. Take-Aways From the Diet-Heart Disease Hypothesis 1.) Saturated fat and cholesterol may not cause heart disease. They may actually be heart protective. 2.) Be cautious of processed polyunsaturated fat (PUFA) oils that have been used to substitute saturated fats in our diet. PUFA-based oils may increase risk of vessel damage from oxidized LDLs. Be particularly careful when these oils are: ● Cooked at high heat ● Stored for long periods of time ● Exposed to long periods of air/light ● Partially hydrogenated/Hydrogenated
  10. 10. ● Consumed with refined, processed, high glycemic index carbohydrates 3.) Stay away from refined, processed, high glycemic index carbohydrates. In particular, white breads, refined grains, and added sugars. 4.) Stay away from TFAs found in margarine, pastries/baked goods, and partially hydrogenated/hydrogenated oils. Some natural trans fats such as conjugated linoleic acid (CLA) may offer health benefits. "The low-fat “diet–heart hypothesis” has been controversial for nearly 100 years. The low-fat–high- carbohydrate diet, promulgated vigorously by the National Cholesterol Education Program, National Institutes of Health, and American Heart Association since the Lipid Research Clinics-Primary Prevention Program in 1984, and earlier by the U.S. Department of Agriculture food pyramid, may well have played an unintended role in the current epidemics of obesity, lipid abnormalities, type II diabetes, and metabolic syndromes. This diet can no longer be defended by appeal to the authority of prestigious medical organizations or by rejecting clinical experience and a growing medical literature suggesting that the much-maligned low-carbohydrate–high-protein diet may have a salutary effect on the epidemics in question." ~Sylvan Lee Weinberg, MD, MACC, J Am Coll Cardiol (35) References 1. Siri-Tarino PW, Sun Q, Hu FB, Krauss RM. Meta-analysis of prospective cohort studies evaluating the association of saturated fat with cardiovascular disease. Am J Clin Nutr 2010;91(3):535-46. 2. Mozaffarian D, Micha R, Wallace S. Effects of coronary heart disease of increasing polyunsaturated fat in place of saturated fat: A systematic review and meta-analysis of randomized controlled trials. PLoS Med 2010;7(3):e1000252. 3. Muller H, Lindman AS, Brantsaeter AL, Pedersen JI. The serum LDL/HDL cholesterol ratio is influenced more favorably by exchanging saturated with unsaturated fat than by reducing saturated fat in the diet of women. J Nutr 2003;133(1):78--83. 4. Ginsberg HN, Kris-Etherton P, Dennis B, Elmer PJ, Ershow A, Lefevre M, Pearson T, Roheim P, Ramakrishnan R, Reed R, Stewart K, Stewart P, Phillips K, Anderson N. Effects of reducing dietary saturated fatty acids on plasma lipids and lipoproteins in healthy subjects: the Delta Study, Protocol 1. Arteriosclerosis, Thrombosis, and Vascular Biology 1998;18:441-449.
  11. 11. 5. Schaefer EJ, Lamon-Fava S, Jenner Jl, McNamara JR, Ordovas JM, Davis CE, Abolafia JM, Lippel K, Levy RI. Lipoprotein(a) levels and risk of coronary heart disease in men. the lipid Research Clinics Coronary Primary Prevention Trial. JAMA 1994;271(13):999-1003. 6. Hoenselaar R. Saturated fat and cardiovascular disease: the discrepancy between the scientific literature and dietary advice. Nutrition 2012;28(2):118-23 7. Lewington S, Whitlock G, Clarke R, Sherliker P, Emberson J, Halsey J, Qizilbash N, Peto R, Collins R. Blood cholesterol and vascular mortality by age, sex, and blood pressure: a meta-analysis of individual data from 61 prospective studies with 55,000 vascular deaths. Lancet 2008;372(9635):292. 8. Mensink RP, Zock PL, Kester AD, Katan MB. 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 trails. Am J Clin Nutr 2003;77(5):1146-55. 9. Siri-Tarino PW, Sun Q, Hu FB, Krauss RM. Saturated fat, carbohydrate and cardiovascular disease. Am J Clin Nutr 2010;91(3):502-509. 10. Sachdeva A, Cannon CP, Deedwania PC, Labresh KA, Smith SC Jr., Dai D, Hernandez A, Fonarow GC. Lipid Levels in patients hospitalized with coronary artery disease: an analysisof 136,905 hospitalizations in Get With The Guidelines. Am Heart J 2009;157(1):111-117. 11. Kathiresan S, Otvos JD, Sullivan LM, Keyes MJ, Schaefer EJ, Wilson PW, D’Agostino RB, Vasan RS, Robins SJ. Increased small low-density lipoprotein particle number: a prominent feature of the metabolic syndrome in the Framingham Heart Study. Circulation 2006;113(1):20-9. 12. Ginsberg HN, Kris-Etherton P, Dennis B, Elmer PJ, Ershow A, Lefevre M, Pearson T, Roheim P, Ramakrishnan R, Reed R, Stewart K, Stewart P, Phillips K, Anderson N. Arteriosclerosis, Thrombosis, and Vascular Biology 1998;18:441-449. 13. 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.
  12. 12. 14. Mozaffarian D, Micha r, Wallace S. Effects on coronary heart disease of increasing polyunsaturated fat in place of saturated fat: A systematic review and meta-analysis of randomized controlled trials. PLoS Med 2010;7(3):e1000252. 15. Siri-Tarino PW, Sun Q, Hu FB, Krauss RM. Saturated fat, carbohydrate, and cardiovascular disease. Am J Clin Nutr 2010;91(3):502-509. 16. Hooper L, Summerbell CD, Thompson R, Sills D, Roberts FG, Moore H, Smith DG. Cochrane Database Syst Rev. 2011;(7):CD002137. 17. Ramsden CE, Zamora D, Leelarthaepin B, Majchrzak-Hong SF, Faurot KR, Suschindran CM, Ringel A, Davis JM, Hibbeln JR. BMJ 2013;346:e8707. 18. Hu FB. Are refined carbohydrates worse than saturated fat? Am J Clin Nutr 2010;91(6):1541-1542. 19. Hu FB, Willett WC. Optimal diets for prevention of coronary heart disease. JAMA 2002;288(20):2569-78. 20. Nagata C, Nakamura K, Wada K, Oba S, Tsuji M, Tamai Y, Kawachi T. Total fat intake is associated with decreased mortality in Japanese men but not in women. J Nutr. 2012;142(9):1713-1719. 21. Jakobsen MU, Dethlefsen C, Joensen AM, Stegger J, Tiǿnneland A, Schmidt EB, Overvad K. Intake of carbohydrates compared with intake of saturated fatty acids and risk of myocardial infarction: importance of the glycemic index. Am J Clin Nutr. 2010;91(6):1764-8. 22. Hu FB. Are refined carbohydrates worse than saturated fat? Am J Clin Nutr. 2010;91(6):1541-2. 23. Bernstein A, Pan A, Rexrode KM, Stampfer M, Hu FB, Mozaffarian D, Willett WC. Dietary protein sources and the risk of stroke in men and women. Stroke 2012;43:637- 644. 24. Patterson E, Larsson SC, Wolk A, Åkesson A. Association between dairy food consumption and risk of myocardial infarction in women differs by type of dairy food. JN 2013;143(1):74-79. 25. Kolata G. Culprit in heart disease goes beyond meat's fat. The New York Times April 7 2013, http://www.nytimes.com/2013/04/08/health/study-points-to-new-culprit-in-heart- disease.html?_r=2& (accessed August 5, 2013). 26. Koeth RA, Wang Z, Levison BS, Buffa JA, Org E, Sheehy BT, Bi4rtt EB, Fu X, Wu Y, Li L, Smith JD, Didonato JA, Chen J, Li H, Wu GD, Lewis JD, Warrier M, Brown JM,
  13. 13. Krauss RM, Tang WH, Bushman FD, Lusis AJ, Hazen SL. Intestinal microbiota metabolism of L-carnitine, a nutrient in red meat, promotes atherosclerosis. Nat Med 2013;19(5):576-85. 27. De Filippo C, Cavalieri D, Di Paola M, Ramazzotti M, Poullet JB, Massart S, Collini s, Pieraccini G, Lionetti P. Impact of diet in shaping gut microbiota revealed by a comparative study in children from Europe and rural Africa. Proc Natl Acad Sci USA 2010 Aug 17;107(33):14691-6. 28. Enig MG. Know your fats: the complete primer for understanding the nutrition of fats, oils, and cholesterol. Silver Spring, MD: Bethesda Press, April 2000. 29. Wanders AJ, Brouwer IA, Siebelink E, Katan MB. Effect of a high intake of conjugated linoleic acid on lipoprotein levels in healthy human subjects. PLoS One 2010;5(2):e9000. 30. Dilzer A, Park Y. Implication of conjugated linoleic acid (CLA) in human health. Crit Rev Food Sci Nutr 2012;52(6):488-513. 31. Mensink RP, Katan MB. Effect of dietary trans fatty acids on high-density and low- density lipoprotein cholesterol levels in healthy subjects. N Engl J Med 1990;323(7):439-45. 32. Wahle KW, Peacock LI, Taylor A, Earl CR. Effect of trans fatty acids on platelet function. World Rev Nutr Diet 1994;75:183-6. 33. Kochan Z. Karbowska J, Babicz-Zielinska E. Dietary trans-fatty acids and metabolic syndrome. Postepy Hig med Dosw 2010; 64:650-8. 34. Bhardwaj S, Passi SJ, Misra A. Overview of trans fatty acids: biochemistry and health effects. Diabetes Metab Syndr 2011;5(3):161-4. 35. Weinberg SL. The diet-heart hypothesis: a critique. J Am Coll Cardiol 2004;43(5):731-33.

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