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Aboriginal vascular health and insights into atherosclerosis

Journal of Human Hypertension volume 30, pages 223–224 (2016)Cite this article

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Human beings, in their present genetic and phenotypic forms, have existed for a surprisingly short time compared with the Earth itself. Present estimates place our genome at roughly 40 000 years old, give or take a few 1000 years, or a mere 1000 or so generations.1 Within this evolutionary blink of an eye, it is extremely unlikely that major environmental adaptations to our genome have occurred. Thus, we find ourselves ill equipped to physiologically respond, in a favorable manner, to our contemporary health behaviors with respect to poor nutrition and suboptimal physical activity.

No matter how you choose to look at our present global health circumstances, it certainly seems we were intended to eat very little and to work very hard to obtain even that meager amount. And yet, the present reality in industrialized, mechanized societies is the polar opposite. We consume vast quantities of calorically high-dense foods and we need to only pick-up our phones to do it! This massive caloric imbalance leads directly to not only obesity, but also the generation of physiologically unmanageable quantities of free oxygen radicals, or the so-called reactive oxygen species (ROS), as the downstream effect of the obligate energy production driven by caloric intake itself. Left unchecked, ROS can contribute to pro-inflammatory microenvironments within many tissue beds, particularly the vasculature.2 This pathological vascular inflammation can, in turn, lead to increased oxidization of circulating low-density lipoprotein (LDL) cholesterol, with its subsequent absorption and sequestration in vascular cells. Once present, oxidized LDL triggers a cascade of immunologic and thrombotic responses that may ultimately give rise to the development and progression of atherosclerotic plaques.3 Thus, in purported first-world countries, and most second-world and emerging countries, the biological fault that leads to atherosclerosis and symptomatic vascular disease is not only a consequence of caloric excess but also an apparently genetically predetermined susceptibility to the development of pro-inflammatory, pro-thrombotic and pro-mitotic vascular environments.

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Authors and Affiliations

  1. Department of Cardiac Sciences, Cumming School of Medicine, University of Calgary, Calgary, Alberta, Canada

    J A Stone

  2. Cumming School of Medicine, University of Calgary, Calgary, Alberta, Canada

    J E Stone

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  1. J A Stone
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Correspondence to J A Stone.

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Competing interests

JAS has received speaking and Advisory Board honoraria from AMGEN, AstraZeneca, Boehringer-Ingelheim, Merck and Sanofi. JES declares no conflict of interest.

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JAS was involved in the original conception of this commentary, the original analysis of the article and in the drafting and review of the manuscript. JES was involved in the detailed analysis of the original article, background material research and in the drafting and review of the manuscript. Both the authors were involved in final editing and approval of the final version.

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Stone, J., Stone, J. Aboriginal vascular health and insights into atherosclerosis. J Hum Hypertens 30, 223–224 (2016). https://doi.org/10.1038/jhh.2015.54

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