BUMC PROCEEDINGS 2000;13:139–143 1. Is atherosclerosis a disease affecting all animals or only certain animals? Atherosclerosis affects only herbivores. Dogs, cats, tigers, and lions can be saturated with fat and cholesterol, and atherosclerotic plaques do not develop (1, 2). The only way to produce atherosclerosis in a carnivore is to take out the thyroid gland; then, for some reason, saturated fat and cholesterol have the same effect as in herbivores. 2. Are human beings herbivores, carnivores, or omnivores? Although most of us conduct our lives as omnivores, in that we eat flesh as well as vegetables and fruits, human beings have characteristics of herbivores, not carnivores (2). The appendages of carnivores are claws; those of herbivores are hands or hooves. The teeth of carnivores are sharp; those of herbivores are mainly flat (for grinding). The intestinal tract of carnivores is short (3 times body length); that of herbivores, long (12 times body length). Body cooling of carnivores is done by panting; herbivores, by sweating. Carnivores drink fluids by lapping; herbivores, by sipping. Carnivores produce their own vitamin C, whereas herbivores obtain it from their diet. Thus, humans have characteristics of herbivores, not carnivores. 3. Is atherosclerosis genetic in origin? Infrequently. Although many physicians and the lay public believe that atherosclerosis is genetic, the evidence for that is slim. One way to define the genetic variety of atherosclerosis is by the presence or absence of low-density lipoprotein (LDL) receptors in the liver (3–5). Patients with homozygous familial hypercholesterolemia have no LDL receptors in the liver, and their total cholesterol levels from birth are usually >800 mg/dL. The frequency of this genetic defect is 1 in 1,000,000. Patients with heterozygous familial hypercholesterolemia have only 50% of the normal number of LDL receptors in the liver. These patients generally have total cholesterol levels about 300 mg/dL, and they generally die (without lipid-lowering therapy) in their 40s or early 50s. The incidence of this familial defect is 1 in 500. The rest of us apparently have normal numbers of LDL receptors in the liver. Of course, a few patients have genetic defects involving high-density lipoprotein (HDL) cholesterol and triglyceride production and uptake, but these individuals are relatively few in number (6). Thus, the genetic defect producing atherosclerosis occurs in no more than 1 in 200 and possibly as low as 1 in 400 or 500 persons. This means, of course, that most persons with atherosclerosis acquire it by the types of calories they consume. Twenty questions on atherosclerosis