Original article Increased cardiovascular risks associated with familial inbreeding: a population-based study of adolescent cohort Mohd Fareed PhD, Mohammad Afzal PhD * Human Genetics and Toxicology Laboratory, Section of Genetics, Department of Zoology, Faculty of Life Sciences, Aligarh Muslim University, Aligarh, Uttar Pradesh, India article info Article history: Received 23 November 2015 Accepted 16 March 2016 Available online 24 March 2016 Keywords: Consanguinity Cardiovascular risks Hypertension Diabetes Public health abstract Purpose: Cardiovascular diseases are the leading cause of mortality and morbidity among humans worldwide. We aimed to estimate the effect of familial inbreeding on cardiovascular risks. Methods: The study was conducted during April 2014 through June 2014, and a total of 587 adolescent subjects (male ¼ 270, female ¼ 317; 1118 years of age) were recruited from ve Muslim populations viz., Gujjar and Bakarwal (n ¼ 130), Mughal (n ¼ 111), Malik (n ¼ 114), Syed (n ¼ 108), and Khan (n ¼ 124). Wrights path relationship method was used for calculating the coefcient of inbreeding (F). Anthropometric and physiological parameters were estimated using standard methods. Results: We observed higher mean values for major physiological traits among the inbred subjects in comparison with the non-inbred groups of ve different populations. Our study suggests that inbreeding and sex are the key factors affecting cardiovascular prole. Multivariate analysis of covariance revealed inbreeding as a major source of variation for cardiovascular risks, dominating over other factors causing greater variability in the physiological traits. The magnitude of cardiovascular risks shows an increase with the increase in the values of coefcient of inbreeding (i.e., from F ¼ 0.00 to F ¼ 0.125). The abnormal levels of systolic blood pressure (SBP; range 140e159 mm Hg) and fasting blood glucose (FBG; range 101e126 mg per dL) show persuasive increase with an upsurge in the homozygosity level (i.e., coefcient of inbreeding). Conclusions: Our comprehensive assessment presents the deleterious consequence of inbreeding on cardiovascular prole. This study can be used as fact-sheet for framing the heath policies and hence can play a vital role in genetic counseling strategies for transforming the public opinion regarding the practice of consanguinity and its associated risks. Ó 2016 Elsevier Inc. All rights reserved. Introduction Cardiovascular diseases (CVDs) are the leading cause of mortality and morbidity worldwide, accounting for over 17 million deaths per year. In the year 2008, 30% of all global mortality was attributed to the cardiovascular diseases. The incidence of death due to cardio- vascular diseases are found at higher frequency in low and middle income countries, and about 80% of all global deaths caused by cardiovascular diseases are observed among these countries. It has also been estimated that by 2030, over 23 million people will die worldwide from cardiovascular diseases each year [1]. Several epidemiologic studies have reported the major non- adjustment risk factors of CVDs such as gender, age, family history, and consanguineous marriage and/or inbreeding [2e4]. Genetic studies have led to the recognition of altogether new complex disease causing variants and lie focus on the association between poly- morphism and risk of coronary artery disease [5]. Gender is also considered as an untreatable and non-modiable risk factor. The male subjects are at greater risk of heart disease than a premeno- pausal woman [6]. Several studies have found a strong linear rela- tionship of the body mass index (BMI), waist circumference (WC) and skinfold thickness, waist to hip ratio (WHR) with various CVDs among Indian populations [7,8]. Ethnic differences in the different risk fac- tors for obesity, diabetes, and hypertension have been well docu- mented in different studies in adults and childhood populations [9e11]. The variables such as BMI and WC, WHR, and waist to height ratio have been found to be associated with adverse car- diometabolic risk prole in adolescents [12]. The pulse pressure (PP, The authors declare that they have no competing interests. * Corresponding author. Aligarh Muslim University, Department of Zoology, Hu- man Genetics and Toxicology Laboratory, Section of Genetics, Aligarh 202002, India. Tel: þ91-0571-2700920-3442. E-mail addresses: mohdfareedk@gmail.com (M. Fareed), afzal1235@rediffmail. com (M. Afzal). Contents lists available at ScienceDirect Annals of Epidemiology journal homepage: www.annalsofepidemiology.org http://dx.doi.org/10.1016/j.annepidem.2016.03.001 1047-2797/Ó 2016 Elsevier Inc. All rights reserved. Annals of Epidemiology 26 (2016) 283e292