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Continued Controversy Over Saturated Fat Intake and Cardiovascular Health
Several reviews were published recently that offered different viewpoints about the relationship between intake of saturated fatty acids (SFA), which increases
low-density lipoprotein cholesterol (LDL-C) and
apolipoprotein (Apo) B,
and cardiovascular health.1-6
In response to these papers, Kevin C. Maki, PhD, along with two of his colleagues, Carol F. Kirkpatrick, PhD, MPH, RDN and Mary R. Dicklin, PhD, prepared a commentary that was published in Journal of Clinical Lipidology in which they discussed the viewpoints and proposed tentative conclusions about SFA intake and atherosclerotic cardiovascular disease (ASCVD) risk.7
Briefly, the two sides of the argument are
1) that SFA intake should be minimized based on evidence that replacing SFA with unsaturated fatty acids, particularly polyunsaturated fatty acids (PUFA), reduces ASCVD events vs.
2) that the quality of the evidence base is weak and there are few data to support an ASCVD benefit from reducing SFA intake in healthy populations.
Furthermore, some have disagreed about the atherogenicity of the type of LDL-C that is increased by consuming SFA, i.e., cholesterol carried in larger, more buoyant particles.8 There is, however, general agreement that a cardioprotective dietary pattern that emphasizes the quality of foods is more important than specific nutrients and that the food matrix in which SFA are consumed likely affects their impacts on ASCVD risk factors.6
Data from randomized controlled trials (RCTs) of SFA and cardiovascular risk are, unfortunately, somewhat limited and often difficult to interpret due to the small size, relatively short duration, and time at which the trials were conducted, i.e., prior to current dietary practices and in populations with different prevalence of important risk factors, such as smoking and obesity.
Nevertheless, meta-analysis results are suggestive of cardiovascular benefit by reducing SFA intake,9
and in their review of the data an Expert Panel organized by the American Heart Association in 2017 concluded that replacing a portion of daily SFA in the average American diet with unsaturated fats (PUFA and monounsaturated fatty acids [MUFA]) as part of a healthy dietary pattern would be expected to reduce ASCVD risk.10
There is a larger body of evidence from observational studies examining the relation between SFA and cardiovascular outcomes.
Based on these data, modeling substitution of 5% of energy from SFA with 5% of energy from MUFA was associated with 15% lower ASCVD risk,
replacement with PUFA was associated with 25% lower risk, and
replacement with carbohydrate from whole grains was associated with 9% lower risk.11
Results from well-designed feeding trials have shown that decreasing SFA intake to amounts less than those consumed in an average American diet reduces LDL-C and Apo B concentrations to degrees that would be expected to reduce risk of ASCVD if maintained for an extended duration.
For example, if 5% of total daily energy from SFA was replaced with PUFA, this would be expected to lower LDL-C by 10.6 mg/dL, which could potentially reduce coronary heart disease risk by as much as 18%, if maintained for decades.12,13
Some have suggested that the possible benefits of lowering LDL-C by decreasing SFA intake are overestimated, since there is a preferential reduction of larger, more cholesterol-rich LDL particles, rather than smaller, more dense LDL particles that have a stronger association with ASCVD risk.8
However, the authors of the commentary cited evidence to support their position that this LDL subspecies shift does not downgrade the benefit of reducing SFA intake.
The association of LDL size loses statistical significance when adjusted for Apo B or LDL particle concentration.14
Furthermore, statin therapy preferentially reduces larger LDL subspecies
while also reducing ASCVD risk, and
patients with familial hypercholesterolemia have primarily large, buoyant LDL particles, but are also at high risk of ASCVD.15
There are several additional biologically plausible biomarkers and pathways that could be related to an association between increased SFA intake and increased ASCVD risk, such as:
1-inflammatory markers,
2-hemostatic factors,
3- Apo C3 production,
4-cardiac rhythms,
4- membrane fluidity, and
5-high-density lipoprotein function,
but the authors of the editorial concluded that additional clinical research is needed regarding these as potential mediators before firm conclusions are appropriate.7
The results from RCTs examining LDL-C and Apo B as biomarkers of ASCVD,
the limited evidence base from RCTs of dietary interventions in which ASCVD outcomes were evaluated, and
findings from prospective observational studies are in alignment with regard to the adverse effects of SFA on ASCVD risk relative to unsaturated fatty acids.
Thus, the authors concluded that, in their view, the evidence supports the current recommendation to limit SFA intake to <10% of total dietary energy for the general healthy population, and to limit it further in patients with hypercholesterolemia.16
