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Melissa A. Austin, PhD
University of Washington Seattle

Ronald M. Krauss, MD
University of California Berkeley

JAMA. 1995;273(2):115.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

To the Editor.

—We read with much interest the recent review article by Dr Slyper¹ summarizing the literature on small, dense low-density lipoprotein (LDL) as a risk factor for coronary heart disease (CHD). We wholeheartedly concur with his conclusion that "[u]nraveling the connection between dense LDL and atherogenesis will have important consequences for the treatment and prevention of coronary artery disease." However, his statement that "genetics has a limited influence on LDL phenotype" is incorrect. For example, recent results from a large study of female twins by Austin et al² demonstrated that one third to one half of the variation in LDL size is attributable to genetic influences, a statistically significant result. Findings from the National Heart, Lung, and Blood Institute³ male twin study are remarkably similar and fail to reach significance only because a statistical test with low power to detect genetic influences was used. Further . . . [Full Text PDF of this Article]

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