TRANS FAT BEGONE!
Perceptions of the health effects of trans fatty acids (TFA), particularly in the form of margarine, have undergone several changes during the past 10 years. What was once heralded as the healthy alternative to butter now assumes the role of coconspirator. In the 1990s, there was public health concern about epidemiological studies suggesting that high intakes of TFA may increase the risk of coronary heart disease. (1) However, a lot of studies still need to be done in order to confirm these results.
Trans fatty acids (TFA), unsaturated fatty acids with at least one double bond in the trans molecular configuration, are produced by partial hydrogenation of vegetable oils. This is a process that converts vegetable oils into semisolid fats, which have no known nutritional value. From the perspective of the food industry, partially hydrogenated vegetable oils are attractive because of their long shelf life, their stability during deep-frying, and their semi solidity, which can be customized to enhance the palatability of baked goods and sweets. While they occur naturally in meat from cows, sheep, and other ruminants (2), dietary trans fats are found primarily in margarines, vegetable shortening, prepared and packaged baked goods, chips and crackers, commercially prepared fried foods, and fast food and restaurant foods.
Epidemiological studies have shown a strong direct (positive) association between the intake of TFA and the risk of coronary heart disease (CHD), primarily accounted for by industrially produced TFA (IP-TFA). (3) It has been estimated that dietary TFAs from partially hydrogenated oils may be responsible for between 30,000 and 100,000 premature coronary deaths per year in the United States. (4) The meta-analysis study done by Mozaffarian and colleagues suggested that a 2% increase in the energy intake from TFA was associated with a 23% increase in the incidence of coronary heart disease. (5)
On the other hand, compared with the intake of IP-TFA, there was an absence of a higher risk of coronary heart diseases associated with the intake of TFAs from ruminants. It might be due to the lower levels of intake (typically less than 0.5 percent of total energy intake), different biologic effects, or the presence of other factors in dairy and meat products that balance any effects of the small amount of trans fats they contain. (5) Although each of these potential explanations deserves further investigation, the sum of the current evidence suggests that the public health implications of consuming trans fats from ruminant products are relatively limited.
Recent evidence on the relation between dietary TFAs and blood lipids has shown that TFAs increase low density lipoprotein (LDL) and reduce high density lipoprotein (HDL) cholesterol concentrations. Meanwhile, saturated fatty acids increase LDL and HDL cholesterol and unsaturated fatty acids decrease LDL and HDL cholesterol, polyunsaturated more so than monounsaturated. (3) Compared with equivalent changes in intake of saturated fats, intake of TFAs has a more adverse effect on the ratio of total cholesterol to HDL cholesterol concentrations. (5) As a result, the ratio of total to HDL-cholesterol rises markedly on diets high in TFAs; this ratio is a more powerful predictor of coronary heart disease than total or LDL-cholesterol alone. In several studies, TFAs also raise plasma triglycerides, and thus presumably very low-density lipoprotein (VLDL). (2) The mechanism of the rise in LDL and fall in HDL-cholesterol may involve cholesteryl ester transfer protein (CETP), a plasma protein that transfers cholesterol from HDL to LDL and VLDL. (6) However, it is not yet clear whether the increase in CETP observed on diets high in TFAs precedes the changes in LDL and HDL or follows them.
TFAs appear to affect lipid metabolism through several pathways. In vitro, TFAs alter the secretion, lipid composition, and size of apolipoprotein B-100 (apo-B-100) particles produced by liver cells. (7) Such alteration is paralleled to the decreased rates of LDL apoB-100 catabolism and changes in serum lipid levels. (2,6) TFAs also increase the cellular accumulation and the secretion of free cholesterol and cholesterol esters by liver cells in vitro. (8) TFAs may also increase the level of lipoprotein (a) levels relative to other fatty acids. Yet, the cellular mechanisms relating TFAs to inflammatory pathways and other nonlipid pathways are not well established.
Besides the adverse effects of TFAs on the lipid profile, high intake of TFAs can also affect endothelial function and biomarkers of inflammation, including C-reactive protein (CRP), interleukin 6 (IL-6), soluble tumor necrosis receptor 2 (sTNFR-2), E-selectin, and soluble cell adhesion molecules (s-ICAM-1 and s-VCAM-1). (9) As a result, it might partially explain why the positive relation between TFAs and cardiovascular risk is greater than what one could predict based solely on its adverse effects on lipids.
In addition, some observational and experimental studies showed that in type 2 diabetic patients who consumed diets enriched with TFAs, there was a significant reduction in insulin sensitivity that may lead to the developing clinical diseases. This might be explained by the greater fatty acid content of membrane phospholipids that increases insulin resistance. (10) However, the mechanisms involved in the long term effect of the TFAs intake on the insulin metabolism still remains unclear.
The 2005 Dietary Guidelines from the U.S. Department of Agriculture (USDA) suggest a total fat intake of 20-35% of daily calories, with the majority coming from unsaturated fats, <10% from saturated fats, and minimal amounts from TFAs. (11) While, dietary guidelines for disease prevention from the American Diabetes Association and the American Heart Association suggest a total fat intake that does not exceed 35% of total daily calories consisting primarily of unsaturated fats, <7% saturated fats, and minimal or <1% trans fats. (12,13)
With the scientific evidence associating TFAs intake with an increased risk of CHD, the U.S. Food and Drug Administration (FDA) issued a final rule that requires the declaration of the amount of TFAs present in foods, including dietary supplements, on the nutrition label by January 1, 2006. (14) In fact, Canada was the first country in the world to introduce the mandatory labeling of TFAs for pre-packaged foods. Mandatory addition of the content of saturated fats and TFAs to nutrition labels will enable customers to make healthier food choices that can lower LDL concentrations and reduce the risk of CHD and other vascular events.
In response to the growing evidence that industrially-made TFAs trigger heart diseases and other cardiovascular diseases, the food industry is working on ways to eliminate or greatly reduce TFAs in food products. Current efforts focus on four technological options: (i) modification of the hydrogenation process, (ii) use of interesterification, (iii) use of fractions high in solids from natural oils, and (iv) use of trait-enhanced oils. Challenges to the food industry in replacing TFAs in foods are to develop formulation options that provide equivalent functionality, are economically feasible, and do not greatly increase saturated FA content. (15) In Europe, TFA have been replaced with cis-unsaturates in soft margarines and they have been reduced also in industrial fats, but often by using palm kernel oils. (16)
Some major food chains have also chosen to remove or reduce the amount of TFAs in their products. KFC has begun its transition to TFAs free cooking oil – canola oil, starting November 2006. (17) Wendy’s announced in June 2006 plans to eliminate TFAs by switching to the new blend of corn and soy oil in its 6,300 US and Canadian restaurants, starting in August 2006. (18) The Walt Disney Company will also begin to eliminate added TFAs from food served at its Parks by the end of 2007 and from its licensed and promotional products by the end of 2008. (19)
Although there are still many questions that need to be answered when it comes to the effects of TFAs on human health, it is still highly recommended that we reduce the intake of TFAs in our diets to minimal amounts.
(1) Steinhart H, Rickert R, Winkler K. Trans fatty acids (TFA): analysis, occurrence, intake and clinical relevance. Eur.J.Med.Res. 2003 Aug 20;8(8):358-362.
(2) 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 trials. Am.J.Clin.Nutr. 2003 May;77(5):1146-1155.
(3) Lichtenstein AH. Thematic review series: patient-oriented research. Dietary fat, carbohydrate, and protein: effects on plasma lipoprotein patterns. J.Lipid Res. 2006 Aug;47(8):1661-1667.
(4) Zaloga GP, Harvey KA, Stillwell W, Siddiqui R. Trans fatty acids and coronary heart disease. Nutr.Clin.Pract. 2006 Oct;21(5):505-512.
(5) Mozaffarian D, Katan MB, Ascherio A, Stampfer MJ, Willett WC. Trans fatty acids and cardiovascular disease. N.Engl.J.Med. 2006 Apr 13;354(15):1601-1613.
(6) Ascherio A. Trans fatty acids and blood lipids. Atheroscler.Suppl. 2006 May;7(2):25-27.
(7) Mitmesser SH, Carr TP. Trans fatty acids alter the lipid composition and size of apoB-100-containing lipoproteins secreted by HepG2 cells. J.Nutr.Biochem. 2005 Mar;16(3):178-183.
(8) Dashti N, Feng Q, Freeman MR, Gandhi M, Franklin FA. Trans polyunsaturated fatty acids have more adverse effects than saturated fatty acids on the concentration and composition of lipoproteins secreted by human hepatoma HepG2 cells. J.Nutr. 2002 Sep;132(9):2651-2659.
(9) Lopez-Garcia E, Schulze MB, Meigs JB, Manson JE, Rifai N, Stampfer MJ, et al. Consumption of trans fatty acids is related to plasma biomarkers of inflammation and endothelial dysfunction. J.Nutr. 2005 Mar;135(3):562-566.
(10) Steyn NP, Mann J, Bennett PH, Temple N, Zimmet P, Tuomilehto J, et al. Diet, nutrition and the prevention of type 2 diabetes. Public Health Nutr. 2004 Feb;7(1A):147-165.
(11) Department of Health and Human Services and the U.S. Department of Agriculture: Dietary Guidelines for Americans 2005. Available online link Accessed on February 5, 2007.
(12) American Heart Association Nutrition Committee, Lichtenstein AH, Appel LJ, Brands M, Carnethon M, Daniels S, et al. Diet and lifestyle recommendations revision 2006: a scientific statement from the American Heart Association Nutrition Committee. Circulation 2006 Jul 4;114(1):82-96.
(13) Bantle JP, Wylie-Rosett J, Albright AL, Apovian CM, Clark NG, Franz MJ, et al. Nutrition recommendations and interventions for diabetes–2006: a position statement of the American Diabetes Association. Diabetes Care 2006 Sep;29(9):2140-2157.
(14) Moss J. Labeling of trans fatty acid content in food, regulations and limits-the FDA view. Atheroscler.Suppl. 2006 May;7(2):57-59.
(15) Hunter JE. Dietary trans fatty acids: review of recent human studies and food industry responses. Lipids 2006 Nov;41(11):967-992.
(16) Aro A. The scientific basis for trans fatty acid regulations-is it sufficient? A European perspective. Atheroscler.Suppl. 2006 May;7(2):67-68.
(17) KFC Canada (2006-10-30). KFC Canada phasing in zero grams trans fat menu in all 786 restaurants nationally early in the new year. Press release. Retrieved on 2007-01-18.
(18) Wendy’s (2006-06-08). Wendy’s Significantly Cuts Trans Fats — Switch to New Cooking Oil Under Way. Press release. Retrieved on 2007-01-18.
(19) Walt Disney Company (2006-10-16). The Walt Disney Company Introduces New Food Guidelines To Promote Healthier Kids’ Diets. Press release. Retrieved on 2007-01-18.