The propensity of saturated fat in the diet to raise LDL
cholesterol is what nutrition researchers have found so worrisome. In contrast, mono- and polyunsaturated fats tend to
lower LDL cholesterol, which is why the Dietary Guidelines
recommend replacing saturated fats in the diet with unsaturated fats. However, saturated fats also raise HDL cholesterol
more than any other type of fat, possibly mitigating the harmful effects of LDL cholesterol. Trans fats, the intended replacement for saturated fats, raise LDL cholesterol even more than
saturated fats, while lowering HDL cholesterol levels.
Total cholesterol levels in the blood do not always correlate well with a person’s risk for heart disease risk because
the measurement includes both LDL and HDL cholesterol. A
more sensitive and specific predictor is the ratio of total cholesterol to HDL cholesterol (total:HDL) (Kinosian, B., et al., J.
Investig. Med. 43:443–450, 1995). Mono- and polyunsaturated
fats lower total:HDL cholesterol, suggesting that they reduce
the risk of heart disease. In contrast, trans fats increase the
ratio, presumably increasing the risk of heart disease. However, because of their effects on both types of cholesterol
particles, saturated fats neither raise nor lower total:HDL cholesterol (Mensink, R. P., et al., Am. J. Clin. Nutr. 77:1146–1155,
2003), suggesting little or no effect on cardiovascular disease
risk (Fig. 2, page 349).
In the 1990s, Ronald Krauss, director of atherosclerosis
research at Children’s Hospital Oakland Research Institute in
Oakland, California, USA, and a practicing physician, discovered that the situation is even more complex than “good” and
“bad” cholesterol. Krauss developed a technique to separate
LDL cholesterol into different types of particles: large, buoyant particles and small, dense particles. As it turns out, the
small, dense LDL particles are more strongly associated with
cardiovascular disease risk than the large, buoyant particles
(reviewed in Berneis, K. K., and Krauss, R. M., http://dx.doi.
org/10.1194/jlr.R200004-JLR200, 2002). The small LDL particles
are more easily oxidized and more likely to trigger inflammation and plaque formation, leading to atherosclerosis.
Krauss has studied the effects of diet on these two LDL
subpopulations. “What we found is that the small, dense form
of LDL is raised by carbohydrates, and the larger form is raised
by saturated fat,” he says. “And so we started to wonder if the
dietary effects of saturated fat on LDL cholesterol could be
misleading in terms of heart disease risk.” Krauss notes that
because the larger particles contain more cholesterol, they
contribute more to the measurement of LDL cholesterol in the
blood than the smaller particles. Therefore, total LDL cholesterol measurements, commonly used by doctors to gauge heart
disease risk, could fail to identify the patients at highest risk.
Although methods for measuring specific types of LDL
are now commercially available, the tests aren’t widely utilized, says Krauss. “The testing is inexpensive, but it’s not well
known, and there’s a lot of controversy regarding its clinical
use,” says Krauss. “But for people who are concerned about
their heart disease risk, have other risk factors, or are considering treatments, it provides a much finer tool than the blunt
● Berneis, K. K., and Krauss, R. M. (2002) “Metabolic origins and clinical significance of LDL heterogeneity.” J.
Lipid Res., 43:1363–1379. http://dx.doilorg:10.1194/
● Blasbalg, T. L., et al. (2011) “Changes in consumption of
omega-3 and omega-6 fatty acids in the United States
during the 20th century.” Am. J. Clin. Nutr. 93:950–962.
● Chowdhury, R., et al. (2014) “Association of Dietary,
Circulating, and Supplement Fatty Acids with Coronary
Risk.” Ann. Intern. Med. 160: 398–406. DOI: 10.7326/
● Harcombe, Z., et al. (2015) “Evidence from randomised
controlled trials did not support the introduction of
dietary fat guidelines in 1977 and 1983: a systematic
review and meta-analysis.” Open Heart 2:e000196.
● Grootveld, M., et al. (2014) “Detection, monitoring,
and deleterious health effects of lipid oxidation products generated in culinary oils during thermal stressing episodes.” Inform 25:614–624.
● Keys, Ancel, ed. (1970) “Coronary Heart Disease in
Seven Countries.” Circulation 41(4 Suppl.):I 1–200.
● Kinosian, B., et al. (1995) “Cholesterol and coronary
heart disease: predicting risks in men by changes in
levels and ratios.” J. Investig. Med. 43:443–450.
● Menotti, A., et al. (1999) “Food intake patterns and
25-year mortality from coronary heart disease: cross-cultural correlations in the Seven Countries Study.”
Eur. J. Epidemiol. 15:507–515.
● Mensink, R. P., et al. (2003) “Effects of dietary fatty
acids and carbohydrates on the ratio of serum total
to HDL cholesterol and on serum lipids and apolipoproteins: a meta-analysis of 60 controlled trials.” Am.
J. Clin. Nutr. 77:1146–1155.
● Mozaffarian, D., et al. (2015) “Heart Disease and Stroke
Statistics—2015 Update. A Report from the American
Heart Association.” Circulation 131:434–441. DOI:
● Scientific Report of the 2015 Dietary Guidelines Advisory Committee. Downloaded from www.health.gov/
● Siri-Tarino, P. W., et al. (2010) “Meta-analysis of prospective cohort studies evaluating the association of
saturated fat with cardiovascular disease.” Am. J. Clin.
Nutr. 91:535–546. DOI: 10.3945/ajcn.2009.27725, 2010.
● Teicholz, Nina. The Big Fat Surprise: Why Butter, Meat
& Cheese Belong in a Healthy Diet. New York: Simon
& Schuster, Inc., 2014.
● World Health Organization, Fact Sheet No. 317, “
Cardiovascular Disease,” Updated January 2015. Downloaded from www.who.int/mediacentre/factsheets/
● Wright, J.D., and Wang, C.-Y. (2010) “Trends in intake
of energy and macronutrients in adults from 1999–
2000 through 2007–2008.” NCHS Data Brief, No. 49.
Downloaded from www.cdc.gov/nchs/data/databriefs/