Ronald
M. Krauss Ronald
M. KraussAdjunct Professor, Department of Nutritional Sciences
University of California at Berkeley
Senior Scientist
Lipoprotein
and Atherosclerosis Group Leader
Head, Department of Molecular and Nuclear Medicine
Life
Sciences Division
Ernest Orlando Lawrence Berkeley National Laboratory
Donner Laboratory, Room 464
Ernest Orlando Lawrence Berkeley National Laboratory
One Cyclotron Road
University of California
Berkeley, California 94720
USA
Phone... +1 (510) 486-4277 or 6185
FAX... +1 (510) 486-5342
email... Ronald_Krauss@macmail.lbl.gov
Web... http://www.modernmedicine.com/modern/915.html
http://www.lbl.gov/Science-Articles/Archive/heart-healthy-diets.html
http://www.aaas.org/meetings/scope/program/pubsyn.htm#261.0
http://www.lbl.gov/lifesciences/OHER-abstracts/OHER-Abstracts-1996.html
Dr. Ronald M. Krauss received his Biology undergraduate degree (magna cum laude) from Harvard University, and medical degree (cum laude) from Harvard Medical School, then completed his internship and residency (internal medicine) on the Harvard Medical Service of Boston City Hospital. He then joined the staff of the National Heart and Lung Institute in Bethesda, Maryland, first as clinical associate and then as senior investigator in the Molecular Disease Branch. He has since held numerous appointments as director or head of various research programs, primarily at the Lawrence Berkeley National Laboratory of the University of California, Berkeley, and has received numerous research awards.
His research involves studies of genetic, dietary, and hormonal effects on plasma lipoproteins and coronary disease risk. He has published more than 200 scientific papers and reviews.
Dr. Krauss is board-certified in internal medicine, endocrinology and metabolism, and is a member of several societies, including the American Society for Clinical Investigation, the American Federation for Clinical Research, and the Federation of American Societies for Experimental Biology. He is a section editor of Current Opinion in Lipidology and Current Opinion in Endocrinology and Metabolism, and is on the editorial board of Journal of Lipid Research, Menopausal Medicine, Coronary Artery Disease: Index & Reviews, Endocrinology and Metabolism, and Preventive Cardiology.
Dr. Krauss is actively involved with the American Heart Association, serving as Chair of the Nutrition Committee, and participating in several boards, councils, and committees.
Insulin resistance is commonly associated with an altered plasma lipid profile characterized by a relative increase in triglycerides and reduction in high-density lipoprotein cholesterol (HDLC) concentrations (1). Although total low-density lipoprotein cholesterol (LDLC) concentrations are generally not elevated in this metabolic syndrome, there are changes in the composition of LDL particles that result in a shift to smaller, denser, and more cholesterol-depleted particles than are found in normolipidemic subjects. Particle size and buoyancy of the peak LDL species are strongly inversely correlated with plasma triglycerides, and positively correlated with HDLC concentrations (2, 3). There are weaker correlations of these LDL characteristics with insulin sensitivity, as assessed by glucose and insulin responses to a glucose load (4, 5), and by steady state plasma glucose concentrations during a glucose-insulin clamp (5). The significance of these correlations is further reduced after adjusting for plasma triglyceride concentrations (5), consistent with evidence that altered triglyceride metabolism is a primary determinant of the relationship between small, dense LDL and insulin resistance (6, 7).
In a substantial subset of the population (30-35% of men and 15-20% of post-menopausal women), the LDL particle profile is characterized by predominance of a distinct subclass of small, dense LDL, designated LDL-III (8). Studies in families have demonstrated that this trait, termed LDL subclass pattern B, is under the influence of at least 4 major genetic loci (9). Consistent with the metabolic determinants of LDL particle size described above, individuals with pattern B have higher plasma concentrations of triglycerides and apolipoprotein B, lower HDLC, and decreased measures of insulin sensitivity than subjects with predominantly larger LDL, subclass pattern A (5, 10). Both case-control (11) and prospective studies (12-14) have demonstrated that LDL particle size in the range found for pattern B subjects (<255-260 Angstroms) is associated with a several-fold increase in risk for coronary artery disease that is independent of total and LDL cholesterol, but in some studies the risk was no longer significant after adjustment for triglycerides (11, 13) or total/HDL cholesterol (12). In vitro observations have indicated that LDL containing predominantly LDL-III bind more readily to arterial proteoglycans (15) and are more rapidly oxidized than LDL from subjects with larger, more buoyant LDL (16). A pathologic role for the small, dense LDL phenotype is also suggested by the finding that coronary angiographic benefit in a multiple risk factor intervention trial was found in patients with small but not large LDL, despite similar reductions in LDLC concentrations (17). Collectively, these findings strongly suggest that small, dense LDL, along with related metabolic alterations, contribute significantly to the increased risk of atherosclerotic cardiovascular disease in subjects with insulin resistance.
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Version 2.1a(5), revised March 5, 1998