The Trans-Fat Dilemma : Health VS Functionalities
by Kalyana Sundram & Yusof Basiron

Malaysian Palm Oil Council (MPOC), 2nd Floor Wisma Sawit, Lot 6, SS6 Jalan Perbandaran, 47301 Kelana Jaya, Selangor, Malaysia
E-mail: kalyana@mpoc.org.my, yusof@mpoc.org.my

Trans fatty acids (TFA) are produced when oils and fats containing unsaturated fatty acids are hydrogenated in the presence of a catalyst. Hydrogenation primarily increases the melting range of the unsaturated fats and thereby enables their incorporation into many solid fat formulations. When an unsaturated fat or oil is fully hydrogenated, all the unsaturated fatty acids are converted into their saturated analogues. Since unsaturation in most vegetable oils is largely 18-carbon fatty acids, namely oleic (18:1 n-9), linoleic (18:2 n-6) and linolenic (18:3 n-3), full hydrogenation of such oils would result in a steraic acid (18:0), high melting block of fat. Partial hydrogenation, in the presence of catalysts results in the formation of TFA. These are the geometrical isomers of unsaturated fatty acids containing at least one double bond in the trans configuration [1]. This trans configuration imparts physical properties including reduced fluidity of the fat thereby increasing its melting point. Thus partial hydrogenation of liquid oils has been the tool of choice to enable their use in solid fat formulations. Partial hydrogenation actually results in both cis and trans fatty acids, occurring anywhere between carbon 4 and carbon 16 of the fatty acid molecule with elaidic as a major isomer and smaller amounts of numerous other trans isomers occurring concurrently. Upwards of 20 different cis and trans geometrical isomers have been recorded following partial hydrogenation of vegetable oils. Small amounts of TFA occur naturally in dairy fat (butter) and meat as a result of bio-hydrogenation in the fore stomach of ruminant animals. TFA are present in foods containing traditional stick margarine, bakery and frying fats, vegetable shortenings, and vanaspati. They are widely distributed in the foods we consume. Estimates of trans consumption are very varied and this has been hampered by a lack of an accurate database to reflect their contents in common foods [1].

Nutritional Consequences of Trans Fatty acids

Since their introduction into the human diet and until the early 1990s, partially hydrogenated fats containing TFA were advocated as the preferred fatty acid base for solid fats, especially margarines. They were initially designed to replace butterfat and with advancements in our knowledge about the adverse impacts of saturated fatty acids (SFA) on cardiovascular disease (CVD) risk, TFA were made prominent as a safe alternative. Similar to other common fatty acids, TFA are efficiently absorbed in humans and completely catabolised to carbon dioxide and water. Variations in their geometrical configurations (relative to their cis fatty acids), melting behaviour and position of double bonds has no measurable effect on absorption efficiency. They are also incorporated into human adipose tissue and other organs just like cis fatty acids

The study of Mensink and Katan [2] suggested that trans increased total and low-density lipoprotein cholesterol (LDL-C) and decreased the beneficial high-density lipoprotein cholesterol (HDL-C) resulting in a less desirable TC/HDL-C ratio. Nearly a dozen other studies quickly fortified this finding, almost all reflecting increases in the atherogenic LDL-C and decreases in the beneficial HDL-C following the consumption of a TFA diet [1]. Invariably it was established that TFA could be worse than the SFA they were designed to replace in the first instance [1,3]. The Nurses Health Study [4] elucidated the effects of TFA using epidemiological data from 85.095 women, establishing an association between TFA and incidence of non-fatal myocardial infarction from coronary heart disease (CHD). A positive and significant association between trans and CHD was apparent. Foods that were major sources of trans including margarine and cookies also revealed a positive correlation. Relative risk for CVD was increased by 27% as a result of trans consumption [5]. These studies clearly established an association of TFA consumption with increased incidence and death from CVD and it was estimated that almost 80,000 deaths in the United States alone were associated with continued consumption of foods rich in TFA. Recent studies have implicated TFA not only with CHD [6] but also with increased risk and incidence of diabetes [7]. Dietary fat intake was evaluated for CHD risk [7] and type II diabetes in women. A 2% increase in TFA consumption relative to carbohydrate intake resulted in a relative risk score of 1.93 for CHD and 1.39 for type II diabetes. In comparison the score for SFA was significantly lower: 1.17 for CHD and 0.97 for type II diabetes. These findings served to highlight additional concerns about the safety of TFA in humans. Other concerns include adverse effects of TFA on cardiac arrhythmia and underlying implications for the developing fetus since TFA competes with essential fatty acids during fetal development. Based on these findings and a review of all available published literature relating to TFA, the Institute of Medicine (IOM) of the National Academies of Sciences, USA  [1] declared that there are no data available to indicate a health benefit from consuming TFA and an Adequate Intake, Estimated Average Requirement, and Recommended Dietary Allowance are not established for TFA. Resulting from this expert recommendation and the mounting evidence against TFA, there is currently an urgent race to reformulate many solid fats TFA-free.