Family history of cardiometabolic diseases and its association with arterial stiffness in the Malmo « Diet Cancer cohort Abd al-Hakim Fatehali a,b , Mikael Gottsa ¨ ter a,b , and Peter M. Nilsson a,b Objective: Arterial stiffening increases with age and is associated with increased cardiovascular risk. Several risk factors have been shown to predict the development of arterial stiffening; however, a positive family history (FHR) of cardiometabolic disease (CMD) and hypertension has not been extensively studied. We hypothesize that FHR of CMD plays a significant role in the development of arterial stiffening in offspring. Methods: We used data from the population-based Malmo ¨ Diet Cancer study (n ¼ 3056) examined in 1992– 1996 and again in 2007–2012. Several variables were analysed, including anthropometrics, carotid–femoral pulse wave velocity and FHR. The association between FHR of CMD and arterial stiffening in the offspring was analysed with analysis of covariance in SPSS. FHR was subdivided into three categories: family history for cardiovascular events (FH-CVEs), family history for diabetes mellitus type 2 (FH-DM2) and family history for hypertension (FH-HT). The first analysis of covariance-model was adjusted for age, sex, mean arterial pressure and heart rate; the second model additionally adjusted for self-reported medical history in the offspring. Results: Data indicated that FH-CVE (F ¼ 14.64, P < 0.001), FH-DM2 (F ¼ 18.57, P < 0.001) and FH-HT (F ¼ 13.92, P < 0.001) all significantly increased carotid– femoral pulse wave velocity levels. The results remained when additional adjustment was made for confounders and for self-reported CMD in the index participants, respectively, for FH-CVE (F ¼ 12.47, P < 0.001), FH-DM2 (F ¼ 7.62, P ¼ 0.006) as well as for FH-HT (F ¼ 7.30, P ¼ 0.007). Conclusion: These findings indicate that a FHR of cardiometabolic conditions and hypertension affects arterial stiffness in offspring independently of haemodynamic factors and self-reported CMD in the offspring without sex differences. Keywords: arteriosclerosis, cardiovascular, diabetes, family history, hypertension, offspring, pulse wave velocity, stiffness, vascular Abbreviations: AS, arterial stiffening; c–f PWV, carotid– femoral pulse wave velocity; CMD, cardiometabolic disease; CVD, cardiovascular disease; CVE, cardiovascular event; DM2, diabetes mellitus type 2; EVA, early vascular ageing; FH, family history; HT, hypertension; MAP, mean arterial pressure; MDC-CV, Malmo ¨ Diet Cancer study’s cardiovascular arm; OGTT, oral glucose tolerance test INTRODUCTION C ardiovascular diseases (CVDs) have in the past decades developed to become the most common cause of mortality in the Western world and cause millions of deaths every year [1]. The disease panorama is complex, multifaceted and is strongly associated with West- ern lifestyle, such as dietary habits and smoking. An illustra- tive example is that the risk of developing atherosclerosis is higher in the United States than in Japan, but Japanese immigrants to the United States gain, during their lives in the new country, a similar degree of risk as the majority population [2]. Other factors which affect the risk of devel- oping CVDs include genetics, risk factors (hypertension, hyperlipidaemia and diabetes) and a positive family history (FHþ) of CVD. Because of this public health problem, much effort has been invested in research in prevention, physiology and haemodynamic changes to increase our understanding of the multifaceted causality of CVD. In particular, research- ers have developed an interest in atherosclerosis as this is the main contributing cause for ischaemic heart disease, which is an important contribution to CVD mortality [3]. Factors such as hypertension, hyperlipidaemia, smoking, obesity, lack of physical exercise and FHþ (genetic and nongenetic aspects) have been thoroughly studied and much of the prevention programs of today revolve around limiting the clinical consequences of atheroscle- rosis [4]. Journal of Hypertension 2017, 35:000–000 a Department of Clinical Sciences, Lund University, Lund and b Department of Internal Medicine, Ska ˚ ne University Hospital, Malmo ¨ , Sweden Correspondence to Peter M. Nilsson, Professor, MD, PhD, Department of Clinical Sciences, Lund University, IM Nilssons gata 32, 2nd Floor, Lund, Sweden; Department of Internal Medicine, Ska ˚ ne University Hospital, S-205 02 Malmo ¨ , Sweden. E-mail: Peter.Nilsson@med.lu.se Received 16 December 2016 Revised 20 March 2017 Accepted 1 June 2017 J Hypertens 35:000–000 Copyright ß 2017 Wolters Kluwer Health, Inc. All rights reserved. DOI:10.1097/HJH.0000000000001457 Journal of Hypertension www.jhypertension.com 1 Original Article Copyright © 2017 Wolters Kluwer Health, Inc. Unauthorized reproduction of this article is prohibited.