Choice of Natural Or Modified Fats For Solid Fat Formultions: The Current Health Dilemma
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

Saturated Fatty Acids (SFA)

An important consideration is not all SFA are equal in their cholesterolaemic effects. Less certain is also the comparative hypercholesterolaemic behaviour of the different oils and fats that are often termed as saturated, yet contain significant amounts of both monounsaturated and polyunsaturated fatty acids e.g. palm oil [3]. Given the variance of fatty acids in the diet, interest in the biological effects of individual SFA on lipoprotein metabolism remains intense. The environment of individual fatty acids in the diet (inter-correlations with other SFA, PUFA and MUFA), their predominance in various oils and fats, the position occupied by individual fatty acids on the triacylglycerol (TAG) molecule and the percentage of SFA in the diet are all important variables modulating lipoprotein metabolism.

Predictive equations based on human trials have concluded that individual SFA differed in their cholesterolaemic potentials. Keys [4] who examined the hypercholesterolaemic nature of saturated fats assumed that lauric acid (C12:0), myristic acid (C14:0) and palmitic acid (C16:0) had equal cholesterol-raising properties. Hegsted et al. [5] found C14:0 to be more cholesterolaemic than C16:0 but C12:0 had little effect or no effect. Medium-chain fatty acids (C8:0-C10:0) and stearic acid (C18:0) were also considered as having little effect or were neutral. MUFA (predominantly oleic acid, C18:1) was speculated to be either neutral or half as potent as PUFAs in lowering blood cholesterol levels [6]. PUFAs, predominantly linoleic acid (C18:2) were estimated to have twice the capacity to lower blood cholesterol as SFAs had in raising them.
Meta-analyses have identified C14:0 as the most hypercholesterolaemic fatty acid and its potential has been variously assessed by investigators to be 4-6 times more powerful than C16:0. There is agreement that changes in TC are paralleled by changes in LDL-C and there is also similarity in their predictive coefficients [7]. In addition it was reported that TC:HDL-C ratio decreased with increasing saturation from C12:0 to C18:0.

A basis for comparing the capacity of individual fatty acids to modulate blood cholesterols levels was derived from regression coefficients developed through the use of predictive equations. This was calculated as 1% of energy equivalent to 6 g of carbohydrates or 2.7 g of fatty acid for an average man or woman consuming a total daily energy of 2400 kcal (10MJ) [8].  These analyses found C14:0 to be the most hypercholesterolaemic of the saturates. Though the analyses by Clarke et al. [9] found both C12:0 and C16:0 similar in their potential to raise blood cholesterol, the analysis by Mensink and Katan [8] found C16:0 to be more hypercholesterolaemic than C12:0. Both groups based their study on experiments conducted under metabolic conditions. Clarke et al’s [9] meta-analysis was based on 134 solid food experiments whereas Mensink et al. [8] worked with 16 studies. Other investigators also found C12:0 to be less hypercholesterolaemic than C16:0 [6].

Early clinical trials did not preclude to satisfactory predictive equations for the effects of individual fatty acids on HDL-C. This was because diet-induced changes in HDL-C were within a small range and within-person fluctuations from day-to-day were relatively large. There is now recognition that fats have the capacity to raise HDL-C. However, the degree to which HDL-C levels are raised is dependent on chain-length and saturation, with the SFAs being most potent, PUFAs the least and MUFA intermediate. Amongst the SFAs, C12:0 and C16:0 were shown to increase HDL-C [6] but opinion on C14:0 is divided between “…no effect” [6] and “…positive” [7,8].  Just as C18:0 is neutral towards TC levels, it appears to mediate no effect on HDL-C concentrations [7].