In December 2006, New York City became the first city to ban the use of artificial trans fats at all city restaurants, a mandate that went into effect in July 2008. Since that time, NYC’s trans fat ban has been looked upon as a unique health model that other major cities, including Washngton, D.C. and Philadelphia, have also considered implementing. Recently, the states of California and Illinois have moved forward with legislation that will eventually ban the use of artificial trans fat in all restaurants, cafes, and movie theaters (1).
As knowledge about the true nature of fats has expanded, saturated fat has actually been found to be a healthy source of nutrition and essential to the proper maintenance of many body systems (2). In contrast, trans fat, which was initially thought to be a healthy source of unsaturated fat, has instead been linked to several diseases, including coronary heart disease (CHD), diabetes and even Alzheimer’s disease. This was not the given attitude even 20 years ago, when margarine was touted as healthy and lard was villainized.
Unsaturated fatty acids are found in two main configurations: trans (i.e., across) and cis (i.e., on the same side). These configurations are the result of carbon-carbon double bonds (C=C) within the skeleton of the molecule. If one were to look at a TFA molecule, one would see a relatively straight carbon chain due to the carbon atoms moving across the carbon double bond. Alternately, a cis fatty acid molecule would have more of a bent shape due to the adjoining carbon atoms moving away from the carbon-carbon double bond in the same direction (either up or down).
Carbon atoms are tetravalent; i.e., they can bind up to four different atoms. Hydrogen atoms, meanwhile, are monovalent because they can bind to only one additional atom. Carbon atoms typically bind to each other in a long chain to make up the skeleton of the fatty acid, with hydrogen atoms branching off the carbons like limbs. When the fatty acid contains a carbon-carbon double bond, it is called unsaturated, meaning that not all the carbon atoms are saturated with (bonded to) a maximum number of hydrogen atoms. The reason has to do with the following: if a carbon atom binds another carbon atom two times via a double bond, this leaves only two potential binding sites for the hydrogens instead of three. Alternately, if three carbon atoms are each double bonded to each other (C=C=C), the middle carbon atom cannot bind to any hydrogen atoms whatsoever because each of its four bonds are occupied by carbons. Such double bonds reduce the carbon atom’s potential to bind as many hydrogens as possible, a feature that distinguishes the fatty acid as unsaturated.
Trans fat is found both in nature and as a by-product of the chemical process of hydrogenation. In nature, trans fat is found primarily in the milk and fat of cows, sheep, and other ruminant animals. Conjugated linoleic acid (CLA) and vaccenic acid are two examples of natural trans fats, with CLA being both a trans and a cis fatty acid. Natural trans fat is found at a concentration of 2-5% in animal fat. Trans fat that results from the process of partial hydrogenation, where not all the carbon-carbon double bonds are removed from an unsaturated fat, is found primarily in frying oils, baked goods, margarine, spreads and shortening. This trans fat can easily make up to 40% of the total fat content of the aforementioned items (3). Elaidic acid is an example of a TFA, while oleic acid is an example of a natural cis fatty acid.
The process of hydrogenation was patented by Wilhelm Normann in 1902 and became a popular way to solidify liquid vegetable oils, particularly soybean oil. Margarine and shortening became two of the best-known foods produced almost exclusively by the process of partial hydrogenation, where a sufficient number of carbon-carbon double bonds are removed to make the oil a semi-solid. By forcibly adding hydrogen atoms (the essence of hydrogenation) to long carbon chains of unsaturated fats at very high temperatures, liquid oil becomes more saturated and solid. Removal of some (though not all) carbon-carbon double bonds via partial hydrogenation protects the now solid oil from rancidification, which is the process of free radical degradation of fatty acid double bonds. As a result, foods made with partially hydrogenated fats last longer. Partially hydrogenated fats also have superior baking qualities compared to butter and lard. All these advantages made partially hydrogenated fat quite popular, and because such manufactured fat was priced lower than natural fats like butter, it became a hit with consumers.
By 1940, however, studies were already indicating a link between partially hydrogenated fat and diseases such as cancer. Dr. Catherine Kousmine, a medical nutritionist, was convinced that the widespread consumption of partially hydrogenated oils after World War II was resulting in an increased rate of cancer in her patients. She opposed the use of all refined oils and proposed that only cold-pressed, virgin oils be consumed. Dr. Mary Enig, a nutritionist and researcher on the biochemical nature of fats and oils, published a report wherein she described a positive correlation between vegetable fat intake and cancer. Much of the vegetable fat being sold at that time consisted of partially hydrogenated oils, a major source of trans fat. This positive correlation between fat intake and cancer was not found when the main source of fat being consumed was animal fat such as beef tallow, lard and butter (4).
Cancer was not the only disease associated with a diet loaded with trans fat. CHD was another major issue. In 1976, The Nurses’ Health Study was launched and followed 120,000 nurses over 14 years. The results of this study were the following: for every 2% increase in trans fat calories, a nurse’s risk of developing CHD doubled. Conversely, reducing trans fat consumption by 2% reduced a nurse’s risk of developing CHD by over 50% (5). The increased risk of developing CHD as a direct result of trans fat consumption was due to two factors: cholesterol and a cytokine called C-reactive protein. Trans fat was found to raise low density lipoprotein, or LDL (the so-called “bad cholesterol”), yet also decrease high density lipoprotein, or HDL (the so-called “good cholesterol”). This raised the LDL/HDL ratio, in turn increasing a person’s CHD risk (6). C-reactive protein, which is an inflammatory cytokine often associated with heart disease, was found to be significantly increased in nurses who consumed a diet high in trans fat (7).
Correlations between other diseases and trans fat consumption have also been noted, including type II diabetes (8), liver dysfunction (9), depression (10) and Alzheimer’s disease (11). It is becoming more and more apparent that trans fat has a toxic effect on the body. However, there is yet no clear agreement as to what that toxic effect might consist of at the biomolecular level. Several hypotheses currently exist. One of the most prevalent hypotheses proposes that lipoprotein lipase, an esterase enzyme that catalyzes the breakdown of lipids, is incapable of recognizing TFAs (12). Because of lipase’s inability to recognize and break down TFAs, they remain in the bloodstream much longer than cis fatty acids, possibly leading to atherosclerosis. Other studies suggest that additional enzymes may also have difficulty with TFA metabolism; carnitine acyltransferase metabolizes the trans-9-octadecenoic acid substrate at roughly half the efficiency of its cis-counterpart (13).
While the actual biomolecular reason as to why TFAs are bad for one’s physical and mental health is still being worked out, the data do suggest that TFAs lead to disease and degeneration, possibly because these manufactured fats were never a part of our diet to begin with. As a result, we do not have the appropriate processing pathways to deal with these artificial fats. Clearly, much research still remains to be done to better understand how lipids are processed and used by the body and the effects they have on our biochemical, metabolic and signaling pathways.
2. Lard: It Does a Body Good!, by Halina Zakowicz
3. Trans: The Phantom Fat, by Margo Wootan, Bonnie Liebman, & Wendie Rosofsky
5. Hu, FB, Stampfer, MJ, Manson, JE, Rimm, E, Colditz, GA, Rosner, BA, Hennekens, CH, Willett, WC (1997). “Dietary fat intake and the risk of coronary heart disease in women” New England Journal of Medicine 337 (21): 1491–1499.
6. A Ascherio, Katan, MB; Zock, PL; Stampfer, MJ; Willett, WC (1999). “Trans fatty acids and coronary heart disease”. New England Journal of Medicine 340 (25): 1994–1998.
7. Lopez-Garcia, Esther; S; M; M; R; S; W; H (March 1, 2005). “Consumption of Trans Fatty Acids Is Related to Plasma Biomarkers of Inflammation and Endothelial Dysfunction”. The Journal of Nutrition 135 (3): 562–566.
8. A.P Simopolous (1994) Is Insulin Resistance Influenced by Dietary Linoleic Acid and Trans Fatty Acids? Free Radicals in Biology and Medicine 17:367-372.
9. Mahfouz M (1981). “Effect of dietary trans fatty acids on the delta 5, delta 6 and delta 9 desaturases of rat liver microsomes in vivo“. Acta biologica et medica germanica 40 (12): 1699–1705.
11. Morris MC, Evans DA, Bienias JL, Tangney CC, Bennett DA, Aggarwal N, Schneider J, Wilson RS (February 2003). “Dietary fats and the risk of incident Alzheimer disease“. Arch Neurol 60 (2): 194–200.
12. B.A.K. Zottorand B.L. Walker. (1989) “Relative hydrolysis of trans- and cis-triglyceride by rat mammary lipoprotein lipase“. Nutrition Research 9 (6): 679-683.
13. Ide T, Watanabe M, Sugano M, Yamamoto I. “Activities of liver mitochondrial and peroxisomal fatty acid oxidation enzymes in rats fed trans fat“. Lipids. 1987 Jan;22(1):6-10.