A Changing Perspective on Saturated Fat

The recent American Heart Association (AHA) position statement (Harris et al., 2009) and a new meta-analysis of 11 cohort studies (Jakobsen et al., 2009) reaffirmed that the body of clinical evidence indicates that a reduced risk of coronary heart disease (CHD) occurs upon replacement of dietary saturated fatty acids (SFA) with polyunsaturated fatty acids (PUFA). The AHA specifically recommends that the SFA intake equal less than 7% of total daily calories.

Despite the evidence-based position on the benefits of SFA reduction, are there metabolic consequences caused by replacement of dietary saturated fatty acids with protein, carbohydrate, or other kinds of fatty acids, thus resulting in lower saturated fatty acid consumption? If we were to examine the fatty acid composition of breast milk, do the innate saturated fatty acids that may be important for normal growth and development of infants provide insights into SFA and health relationships?

Saturated fatty acids represent early 40% of the total fatty acids in mature and preterm human milk throughout lactation (Fidler et al., 2000; Minda et al., 2004; Kovács et al., 2005; Bakor et al., 2007; Ribeiro et al., 2008). Palmitic (C16:0), stearic (C18:0), myristic (C14:0), and lauric (C12:0) acids represent about 95% of the SFA profile. There is little variation of the SFA profile among global regions. Some interesting etabolic functions of these fatty acids include the acylation of proteins (Rioux et al., 2002) and modulation of ceramide biosynthesis and sphingolipid metabolism (Beauchamp et al., 2007). These are two vital lipid components of cell membrane structure and appear to have roles in cell response to growth, stress, apoptosis, and possibly gene regulation (Beauchamp et al., 2007; Hartl et al., 2009).

The interpretation by health professionals over the course of the past four decades has been that total fat and saturated fat contribute to elevated LDL -cholesterol (LDL -C), one of several risk factors for progressive CHD (Mozaffarian et al., 2009). This diet-heart paradigm may be modified by other dietary components, such as n-3 fatty acids, trans fatty acids, types of carbohydrates, and foods including nuts, legumes, dairy products, fruits, and vegetables (Mozaffarian et al., 2005; Nestel, 2008; Kris-Etherton et al., 2009; German et al., 2009).

A meta-analysis of 60 controlled clinical trials suggests various dietary fats have different effects on LDL -C (Mensink et al., 2003). For example, short-term studies indicate stearic acid (3–4 en%) may have a neutral impact on LDL-C among normolipidemic subjects (Judd et al., 2002; Mensink et al., 2003; Thijssen & Mensink, 2005) and possibly lower LDL -C (Kris-Etherton and Yu, 1997). Interestingly, a 3-year study among postmenopausal women indicated that a greater risk of coronary atherosclerosis occurred when they consumed high carbohydrates vs high saturated fatty acids (3.5–16 en%) when following a relatively low-fat regimen (~ 25 en%) (Mozaffarian et al., 2004).

Another perspective on the SFA discussion, is that while some dietary interventions, such as the consumption of fruits and vegetables (Goldstein et al., 2006), may be associated with a reduced risk of stroke, there are several prospective studies that suggest low saturated fat intake may increase the risk of stroke, typically a small artery disease (Iso et al., 2001a; Iso et al., 2001b; Sauvaget et al., 2004). For example, among a Japanese population, the mortality risk from cerebral infarction was reduced by 62% among higher SFA (21 g/day) consumers vs lower SFA (7 g/day) consumers. These results are similar to those observed in the U.S Nurses’ Health Study (Iso et al., 2001). On the other hand, a study among health care professionals indicated an absence of any association between types of dietary fat and the risk of stroke in men (He et al., 2003).

The replacement of the three basic types of dietary fat—SFA, monounsaturated fatty acids (MUFA), and PUFA)—with carbohydrates appears to yield different effects on LDL -C (Mensink et al., 2003). Several prospective cohort studies suggest replacing dietary carbohydrates with different types of dietary fats have different effects on the relative risk of CHD (Mozaffarian et al., 2006; Jakobsen et al., 2009). However, it appears that the risk of CHD depends on the nutrient replaced. For example, the replacement of SFA with PUFA may lower the risk of CHD, while the replacement with MUFA seems to be neutral. Several reports suggest the replacement of SFA may not be effective in reducing the risk of CHD, particularly in individuals with elevated triglycerides or low HDL -C (Jakobsen et al., 2009) versus normolipidemic individuals.

As indicated by Westman (2009), there may be several aspects of SFA that deserve rethinking and further study. A composite of observational, cross-sectional, and prospective studies suggests that not all SFA have the same functions or effects on CHD risk factors.

As lower intake of SFA is prescribed, the impact on stroke risk deserves further consideration because of possible increased risk. Ultimately, it may be an individual’s underlying genetic profile that leads to more desirable responses relative to lower risk of cardiovascular heart disease and stroke. For example, APOA1 alleles (AA , GA, GG) respond differently to increased dietary PUFA due to a single nucleotide polymorphism at -75G/A.

Using data obtained from the Framingham Heart Study, Ordovas and co-workers (Ordovas et al., 2002) examined HDL-C levels over three dietary levels of PUFA (< 4%, 4–8%, > 8%) and correlated to specific genotypes. Their study indicated that increasing dietary PUFA elevated HDL -C in the AA (40%) > GA (20%) genotypes, while for the GG genotype, HDL -C was reduced (7%).

Individual genotypic expression contributes to the increase in the variability of the reported dietary intervention efforts. We know that altering people’s dietary habits to produce positive effects on health risks has been difficult. Perhaps it is not only personal dietary habits, but individual genes, that produce the increased risk and as such become the specific target to improve health.

Roger Clemens, Dr.P.H.,
Contributing Editor
Scientific Advisor, ETHorn, La Mirada, Calif.
[email protected]

Wayne Bidlack, Ph.D.,
Contributing Editor
Professor, California State Polytechnic University, Pomona
[email protected]