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While atherosclerotic stroke affects millions of modern humans, it is unknown how often this disease occurs naturally in wild hominid populations. In a research setting, nonhuman primates are used in models of induced stroke in a background of chronic atherosclerosis and captive hominids are known to die of atherosclerotic disease, but atherosclerotic stroke appears to be a relatively unnatural event in wild hominid species. Two species of New World monkey (Lagothrix lagotricha and Aotus sp) display naturally ocurring hypertension and have a higher prevalence of stroke, although the evolutionary mechanisms or relation to human uniqueness for these findings have not yet been speculated.
Hypertension and hyperlipidemia are reliable predictors of atherosclerotic stroke. Both humans and chimpanzees are affected by hypertension, and hyperlipidemia occurs in captive chimpanzees and gorillas; however, atherosclerotic stroke is not associated with coronary heart disease or atherosclerosis in nonhuman primates. Thus it is speculated that while nonhuman primates experience atherosclerotic stroke naturally, it occurs to a lesser degree than in humans.
The difference in susceptibility between humans and hominids is less likely to be due to genetic differences since the genetic profile of human and chimpanzee hearts and livers (the main organs for atherosclerotic disease) are nearly identical. Genetic differences may explain differences in atherosclerotic stroke prevalence. In the prevailing theory, humans may have lost genes which enable adaptive traits, but which also cause a retrograde phenotype that increases susceptibility to atherosclerotic disease. In a less supported theory, humans may have recently acquired a gene that increases risk for atherosclerotic disease.
Given the ability to induce atherosclerosis in nonhuman primates; differences in atherosclerotic disease prevalence may significantly impacted by a modern high fat, high salt human diet which is shown to cause hyperlipidemia and hypertension in hominin species (precursors to atherosclerosis and thus increased susceptibility for stroke).
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