Is atherosclerosis fundamental to human aging? Lessons from ancient mummies

Bibliographic Collection: 
CARTA-Inspired Publication
Publication Type: Journal Article
Authors: Clarke, E.M.; Thompson, R.C.; Allam, A.H.; Wann, L.S.; Lombardi, G.P.; Sutherland, M.L.; Sutherland, J.D.; Cox, S.L.; Soliman, M.A.; Abd El-Maksoud, G.; Badr, I.; Miyamoto, M.I.; Frohlich, B.; Nur El-Din, A.H.; Stewart, A.F.; Narula, J.; Zink, A.R.; Finch, C.E.; Michalik, D.E.; Thomas, G.S.
Year of Publication: 2014
Journal: J Cardiol
Volume: 63
Issue: 5
Pagination: 329-334
Date Published: 05/2014
Publication Language: eng
Keywords: Aging, atherosclerosis, Coronary artery disease, Mummies, Paleopathology
Abstract:

Case reports from Johan Czermak, Marc Ruffer, and others a century or more ago demonstrated ancient Egyptians had atherosclerosis three millennia ago. The Horus study team extended their findings, demonstrating that atherosclerosis was prevalent among 76 ancient Egyptian mummies and among 61 mummies from each of the ancient cultures of Peru, the American Southwest, and the Aleutian Islands. These findings challenge the assumption that atherosclerosis is a modern disease caused by present day risk factors. An extensive autopsy of an ancient Egyptian teenage male weaver named Nakht found that he was infected with four parasites: Schistosoma haematobium, Taenia species, Trichinella spiralis, and Plasmodium falciparum. Modern day patients with chronic inflammatory disease such as rheumatoid arthritis, systemic lupus erythematosus, and human immunodeficiency virus experience premature atherosclerosis. Could the burden of chronic inflammatory disease have been a risk factor for atherosclerosis in these ancient cultures? The prevalence of atherosclerosis in four diverse ancient cultures is consistent with atherosclerosis being fundamental to aging. The impact of risk factors in modern times, and potentially in ancient times, suggests a strong gene-environmental interplay: human genes provide a vulnerability to atherosclerosis, the environment determines when and if atherosclerosis becomes manifest clinically.

Notes:

J Cardiol. 2014 May;63(5):329-34. doi: 10.1016/j.jjcc.2013.12.012. Epub 2014 Feb 28.

Author Address:

University of California, Los Angeles, CA, USA. Saint Luke's Mid America Heart Institute, Kansas City, MO, USA; University of Missouri-Kansas City School of Medicine, Kansas City, MO, USA. Al Azhar Medical School, Cairo, Egypt. Columbia St Mary's Healthcare, Milwaukee, WI, USA. Laboratorio de Paleopatologia, Catedra Pedro Weiss, Universidad Peruana Cayetano Heredia, Lima, Peru. Newport Diagnostic Center, Newport Beach, CA, USA. Saddleback Memorial, Laguna Hills, CA, USA. University of Cambridge, Cambridge, UK. National Research Center, Giza, Egypt. Cairo University, Cairo, Egypt. Institute of Restoration, Alexandria, Egypt. Mission Internal Medical Group, Mission Viejo, CA, USA. Smithsonian Institution, National Museum of Natural History, Washington, DC, USA. University for Science and Technology, 6th of October City, Egypt. University of Ottawa Heart Institute, Ottawa, Ontairo, Canada. Mount Sinai, New York, NY, USA. Institute for Mummies and the Iceman, European Academy, Bolzano, Italy. University of Southern California, Los Angeles, CA, USA. Miller Children's Hospital, Long Beach, CA, USA; University of California, Irvine, CA, USA. MemorialCare Heart & Vascular Institute, Long Beach Memorial, Long Beach, CA, USA; University of California, Irvine, CA, USA. Electronic address: gthomas1@memorialcare.org.

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