HoldsUp

Ronald Krauss

Children’s Hospital Oakland Research Institute

Ronald Krauss, M.D., is the director of atherosclerosis research at Children’s Hospital Oakland Research Institute and an adjunct professor at UCSF and UC Berkeley. His research focuses on lipid metabolism, having developed an assay to quantify low-density lipoprotein (LDL) particle size and concentration. His published work covers dietary effects on cardiometabolic disease and insulin sensitivity, statin responses, and the relationship between cholesterol regulation, genetics, and Alzheimer's disease.

38 claims checked on air: 2 context 2 overstated 33 supported 1 unverified 2 flagged

What they said on air - citing their own research

2 citing their own research

0:15:27supportedhightheir own paperDr. Ronald Krauss on LDL Cholesterol, Particle Size, Heart D

Genetic variants associated with high LDL are associated with increased heart disease risk, whereas genetic variants associated with HDL cholesterol levels are almost never associated with heart disease risk.

"genes associated with high LDL are associated with heart disease risk. That's a very important pathologic connection, because genes ultimately are the blueprint for our biology, and if the genes associated with high LDL are also associated with heart disease risk, it says that the LDL is really the causal agent. The genes associated with variation in HDL cholesterol have almost in every case not been associated with heart disease risk" (said at 0:15:27)

Extensive Mendelian randomization studies and human genetic analyses demonstrate that genetic variants associated with higher LDL cholesterol are consistently and causally associated with increased risk of coronary heart disease and myocardial infarction. In contrast, genetic variants that specifically raise or lower plasma HDL cholesterol (such as variants in LIPG or multi-SNP genetic risk scores specific to HDL-C) show no significant causal association with myocardial infarction risk, despite the inverse association observed in observational epidemiology.

0:33:58supportedhightheir own paperDr. Ronald Krauss on LDL Cholesterol, Particle Size, Heart D

Saturated fat intake increases large LDL particles rather than small, dense LDL particles in the majority of the population.

"we've shown that the form of LDL that increases with saturated fat is not the small LDL, but the large LDL. And in fact, that led me to question whether or not saturated fat was really an important factor in heart disease risk, because our studies did not show that it was increasing small LDL in the majority of the population." (said at 0:33:58)

Randomized dietary intervention studies and comprehensive reviews confirm that in the general population, increasing dietary saturated fatty acid intake predominantly elevates concentrations of large, buoyant LDL particles rather than small, dense LDL particles. A landmark crossover feeding trial by Krauss and colleagues showed that saturated fat intake was positively correlated with the mass of large LDL particles and inversely correlated with small, dense LDL particles. A state-of-the-art review in the Journal of the American College of Cardiology similarly concluded that while saturated fatty acids raise total LDL cholesterol, in most individuals this rise is driven by larger LDL particles rather than small, dense LDL subclasses.

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