|Year : 2022 | Volume
| Issue : 4 | Page : 116-123
Relationship between ABO blood group phenotypes and some cardiovascular risk factors among undergraduate students in Kano Nigeria
Isyaku Gwarzo Mukhtar, Abdulkarim Tsoho Abdullahi
Department of Human Physiology, Bayero University, Kano, Nigeria
|Date of Submission||17-Dec-2022|
|Date of Decision||27-Dec-2022|
|Date of Acceptance||28-Dec-2022|
|Date of Web Publication||22-Feb-2023|
Dr. Isyaku Gwarzo Mukhtar
Department of Human Physiology, Bayero University, Kano
Source of Support: None, Conflict of Interest: None
Background: Studies have linked ABO phenotypes to cardiovascular diseases (CVDs); however, data on the relationship between ABO phenotypes and CDV risk factors among healthy adults are lacking. Aim: To determine the relationship between ABO phenotypes and CVD risk factors among undergraduate students in Kano, Nigeria. Materials and Methods: This cross-sectional descriptive study recruited 150 participants. ABO phenotypes were determined using monoclonal antisera. Serum total cholesterol (TC), triglycerides (TG), and high-density lipoprotein cholesterolwere determined enzymatically, while low-density lipoprotein cholesterol (LDL-c) was calculated using the Friedewald equation. Blood pressure and anthropometric measurements were by standard protocols. Data were analyzed using SPSS version 23.0; P ≤ 0.05 was considered statistically significant. Results: Mean age of the participants was 23.12 ± 2.97 (17–31) years. The frequency of ABO phenotypes among the participants was: O (39.3%), B (26.0%), A (23.3%), and AB (11.3%). Non-O phenotypes had significantly lower systolic blood pressure (P = 0.050), higher TC (P = 0.023), TG (P = 0.003), and LDL-c (P = 0.050) compared to O phenotypes. Of the non-O phenotypes, A had significantly higher TC compared to B (P = 0.004) and O (P = 0.001); higher TG compared to O (P = 0.001); higher LDL-c compared to B (P = 0.001), AB (P = 0.042), and O (P = 0.006); heavier compared to B (P = 0.012) and O (P = 0.033); and higher hip circumference compared to B (P = 0.022). Conclusion: Non-O phenotypes, especially A phenotypes, had significantly higher mean serum lipids compared to O. ABO phenotypes should be considered in CVD risk stratification.
Keywords: ABO phenotypes, atherogenic index, cardiovascular disease, dyslipidemia
|How to cite this article:|
Mukhtar IG, Abdullahi AT. Relationship between ABO blood group phenotypes and some cardiovascular risk factors among undergraduate students in Kano Nigeria. Niger J Exp Clin Biosci 2022;10:116-23
|How to cite this URL:|
Mukhtar IG, Abdullahi AT. Relationship between ABO blood group phenotypes and some cardiovascular risk factors among undergraduate students in Kano Nigeria. Niger J Exp Clin Biosci [serial online] 2022 [cited 2023 Mar 24];10:116-23. Available from: https://www.njecbonline.org/text.asp?2022/10/4/116/370248
| Introduction|| |
Since their discovery in 1901, ABO blood group phenotypes have been associated with various disease conditions. One of such association that attracted much attention over the decades is the reported relationship between ABO blood group phenotypes and cardiovascular diseases (CVDs). Specifically, individuals with non-O blood phenotypes are said to be at higher risk for CVD than those with O.,,,,, While this association is thought to be mediated by the influence of the ABO system glycosyltransferase on circulating levels of von Willebrand factor and coagulation factor VIII, there is growing evidence pointing to a possible influence of serum lipid parameters, suggesting a possible link between ABO phenotypes and atherogenesis, the hallmark of some CVDs., Non-O blood phenotype is said to be associated with both prevalent and incident dyslipidemia and higher levels of serum total cholesterol (TC), low-density lipoprotein cholesterol (LDL-c), and nonhigh-density lipoprotein cholesterol (non-HDL-c). This observation has led to increasing interest in the study of the association of ABO blood group phenotypes and serum lipid parameters because of the role serum cholesterol, especially LDL-c, plays in the pathogenesis of atherosclerotic CVDs. However, the results of the association between ABO blood group phenotypes and serum lipid parameters have not been consistent. Similarly, most studies looking at the relationship between ABO phenotypes and modifiable CVD risk factors were conducted on participants who have already developed the disease rather than healthy populations at risk of the disease and where healthy participants are involved, they are mainly used as controls. Recently, attention has also shifted from the use of traditional serum lipid parameters to predict future CVD to the use of lipoprotein ratios called atherogenic indices (AIs). A number of studies have reported the superiority of these indices over individual serum lipid parameters in predicting future CVD.,,,,, There are many AIs being used to predict future CVD risk; however, the most common ones are the TC to HDL-c and LDL-c to HDL-c ratios. While the superiority of AIs in predicting future CVDs has been established, there are limited studies looking at the possible association between ABO phenotypes and TC/HDL-c ratio. The aim of this study was to determine the relationship between ABO blood group phenotypes and modifiable CVD risk factors, including TC/HDL-c ratio among undergraduate students in Kano, Nigeria.
| Materials and Methods|| |
Study design and sampling technique
The study is a descriptive cross-sectional study that was carried out at the Department of Human Physiology, Bayero University, Kano, Nigeria, from June to July 2021. The study population was made up of all undergraduate students of the Faculty of Basic Medical Sciences of the University. A multistage sampling technique was used to recruit eligible and consenting participants for the study. A comprehensive list of all the faculties in the university was obtained, and a simple random sampling technique was used to select one faculty. A systematic random sampling technique was then used to select participants to the desired sample size. Participants were initially briefly screened for a history of cardiovascular and other medical conditions through an oral interview. Participants found to be known patients of any of those medical conditions were not considered for inclusion in the study. Pregnant women and students older than 35 years were also excluded from the study. Specifically, participants with a history of hypertension, diabetes mellitus, stroke, heart disease, any endocrine disorder, and chronic kidney disease were excluded from the study.
Sample size determination
G*Power computer software (Heinrich-Heine-Universität, Düsseldorf, North Rhine-Westphalia, Germany). was used to calculate the minimum required sample size for the study. An effect size of 0.5, α level of significance of 0.05, and statistical power of 0.80 were used, which gave a minimum sample size of 102.
Ethical approval was obtained from the Research Ethics Committee of the Kano State Ministry of Health (SHREC/2021/2595 dated June 24, 2021), and all participants were required to sign an individual consent form after they were fully briefed about the study.
Sociodemographic information and clinical and cardiometabolic parameters of the participants were collected using a data capture form.
Measurement of anthropometric indices
Anthropometric indices were measured following standard protocol. Weight was measured using an Omron HN286 digital weighing scale (Kyoto, Japan) to the nearest 100 g with the participants standing erect, hands by the side, and wearing light clothing. Height was measured using a stadiometer with the participants facing forward and upward without shoes or cups. Waist and hip circumferences (HC) were measured according to the World Health Organization STEPwise protocol. Body mass index (BMI) was calculated as weight in kg divided by height in meter square (kg/m2), waist–hip ratio as waist circumference (WC) divided by HC, and waist-to-height ratio as WC divided by height.
Measurement of blood pressure and fasting blood glucose
Blood pressure was measured on the left arm using a mercury sphygmomanometer (Accoson™ Ltd., Ayrshire, UK) and Littmann's stethoscope (3M Littmann®, Minnesota, USA). Systolic blood pressure (SBP) was taken at the appearance of Korotkoff's sound, while its disappearance was considered diastolic. Fasting blood glucose (FBG) was measured by the glucose oxidase method after an overnight fast of at least 10 h.
Determination of ABO and Rh (D) blood groups phenotypes
ABO and Rh (D) blood group phenotypes were determined manually using potent monoclonal anti-A, anti-B, and anti-D reagents (Plamatec Lab. Ltd., Bridport, UK). The traditional tile agglutination method was used as described by Rawley and Milkins.
Determination of serum lipid parameters
Five mL of venous blood was collected from each participant between 9 and 10 am after an overnight fast of at least 10 h. Serum TC, triglycerides (TG), and HDL-c were determined by the enzymatic colorimetric method. Serum was extracted by first allowing the blood samples to coagulate and then centrifuged at 1000 g for 5 min. Reagents meant for each component of serum lipid from Randox laboratories Ltd., (Randox Laboratories Ltd., Crumlin, County Antrim, UK) were used to obtain a characteristic colored solution, the absorbance of which was measured by Ortho clinical Vitros DT60 II autoanalyzer (Diamond Diagnostics Inc., Holliston, Massachusetts, USA) at a wavelength of 560 nm. The final concentration of each parameter was calculated from the measured absorbance and concentration of the standard according to the manufacturer's instructions. Serum LDL-c was determined indirectly from the concentrations of serum TC, TG, and HDL-c using the Friedewald equation:
LDL-c = (TC − HDL cholesterol − TG)/5
Data were analyzed using the Statistical Package for the Social Sciences (IBM SPSS) version 23.0 (IBM, Armonk, New York, USA). One-way analysis of variance (ANOVA) with Bonferroni posthoc was used to determine the mean difference in cardiometabolic parameters between ABO phenotypes. An Independent t-test was used to compare means of cardiometabolic parameters between O and non-O phenotypes. Chi-square test of association was used to determine the association between categorical variables. Results were presented as frequencies, mean ± standard deviation, and P ≤ 0.05 was considered statistically significant.
Working definitions of some terms
Serum lipid abnormalities were defined based on the National Cholesterol Education Program Adult Treatment Panel III as follows: elevated TC >200 mg/dL; elevated TG >150 mg/dL; LDL-c >130 mg/dL; HDL-c <40 mg/dL in males and <50 mg/dL in females. BMI was classified according to the WHO classification into underweight (<18.5 kg/m2), normal (18.5–24.9 kg/m2), overweight (25.0–29.9 kg/m2), and obese (30 kg/m2 and above). WC and WHR were defined according to the International Diabetic Federation's consensus worldwide definition of metabolic syndrome. Blood pressure abnormalities were defined as SBP ≥130 mmHg and/or diastolic blood pressure (DBP) ≥85 mmHg (IDF, 2006). While FBG of <100 mg/dL, 100–125 mg/dL, and ≥126 mg/dL were considered normal, prediabetes, and diabetes, respectively. The atherogenic index was calculated as TC/HDL-c ratio. Details of the study protocol have been published elsewhere.
| Results|| |
One hundred and fifty participants were recruited for this study. The mean age of the participants was 23.12 ± 2.97 years (17–31 years). The majority of the participants were males (61.3%), Hausas (63.3%), studying BSc Human Physiology (42%), and in their 2nd year of study (33.3%) [Table 1]. The distribution of ABO blood group phenotypes of the participants is O (39.3%), B (26.0%), A (23.3%), and AB (11.3%). Similarly, 94.7% of the participants were Rh (D) positive [Table 2].
|Table 2: ABO and Rhe (D) blood groups phenotypes of the participants (n=150)|
Click here to view
When the participants were categorized into O and non-O phenotypes and mean cardiometabolic parameters between the two categories compared using independent t-test, non-O phenotypes had statistically significant lower SBP (mean difference = 3.834 mmHg, P = 0.050), higher TC (mean difference = 10.180 ml/dL, P = 0.023), TG (mean difference = 19.310 ml/dL, P = 0.003), and LDL-c (mean difference = 4.000 ml/dL, P = 0.050) compared to O [Table 3]. Similarly, when the mean difference in cardiometabolic parameters of the participants according to ABO blood categories was compared using one-way ANOVA with Bonferroni posthoc, A phenotypes had statistically significantly higher serum TC compared to B phenotypes (P = 0.004) and O phenotypes (P = 0.001); higher TG compared to O phenotypes (P = 0.001); higher LDL-c compared to B phenotypes (P = 0.001), AB phenotypes (P = 0.042), and O phenotypes (P = 0.006); heavier (weight) compared to B phenotypes (P = 0.012) and O phenotypes (P = 0.033); and higher HC compared to B phenotypes (P = 0.022). In contrast, A phenotypes had significantly lower AI (P = 0.019) compared to B phenotypes. There was no significant difference in mean values of the other cardiometabolic parameters between the ABO blood group categories [Table 3] and [Table 4].
|Table 3: Mean cardiometabolic parameters of the O and non-O phenotypes participants|
Click here to view
|Table 4: Mean cardiometabolic parameters of the participants according to ABO phenotypes|
Click here to view
When the various cardiometabolic parameters were converted into categories consisting of “normal” and “abnormal” categories and analyzed using Chi-square test of association, only AI categories were significantly associated with ABO blood group phenotypes (χ2 = 20.160, P = 0.003) [Table 5].
|Table 5: Association between ABO blood group phenotypes and some cardiovascular disease risk factors|
Click here to view
| Discussion|| |
This study examined the relationship between ABO blood group phenotypes and modifiable CVD risk factors including AI (TC/HDL-c) among undergraduate students in Kano, Nigeria. The distribution of ABO blood group phenotypes in this study is O> B>A>AB. This is similar to what we have reported from a cohort of prospective blood donors in this environment and is indeed consistent with the pattern found in northwest Nigeria. It is, however, in contrast to what has been reported from other geo-political zones of Nigeria, where the predominant pattern is O>A>B>AB. Genes coding for ABO blood group phenotypes is one of the most polymorphic genes with wide geographical and racial variations. The dominance of one phenotype over others in a particular geographical location or ethnic group may indicate an adaptive evolutionary trend to certain environmental factors over a period of time.
Non-O phenotypes in this study had significantly higher mean serum TC, TG, and LDL-c compared to the O phenotype. This is similar to what was reported by Chen et al. and MacDonald et al., In 6476 individuals undergoing coronary angiography, Chen et al. reported that those with non-O phenotypes had significantly higher serum TC, LDL-c, and non-HDL-c; and that 10% and 11% of the effects of non-O phenotype on coronary artery disease and myocardial infarction were respectively mediated by elevated serum LDL-c. In a cohort of 74,206 French women, MacDonald et al. found those with non-O phenotypes to have both prevalent and incident dyslipidemia compared to O phenotypes. When mean serum lipid parameters were considered among individual ABO phenotypes in this study, A phenotypes had significantly higher serum TC, TG, LDL-c, weight, and HC compared to either B, O or both phenotypes. This implied a higher CVD risk for A phenotypes compared to the rest. Indeed, a number of studies have reported a significant risk for CVD among A phenotypes compared to other phenotypes.,,,, Despite the relatively consistent reports of the relationship between ABO phenotypes and serum lipid parameters, Contiero et al. found no association between ABO phenotypes and serum TC, HDL-c, and LDL-c. We similarly did not find any significant difference in mean serum HDL-c between non-O and O phenotypes. Furthermore, we found no significant association between ABO phenotypes and lipid abnormalities when serum lipid parameters were classified into “normal” and “abnormal” categories and analyzed against ABO phenotypes using Chi-square test of association. This could be due to the relatively small sample size that might have affected subgroup analysis and also to the fact that the participants were drawn from an apparently healthy population.
Recently, attention has shifted from the use of individual serum lipid parameters in predicting CVD risk to the use of a combination of the parameters to calculate a ratio called atherogenic index. One of such ratio is the TC/HDL-c ratio. It is said to have greater CVD risk predictive value than individual lipid parameters; good in predicting coronary heart disease risk; and better in predicting incident CVD risk in women. For these reasons, we assessed the possible relationship between ABO phenotypes and TC/HDL-c ratio. A blood group phenotype had a significantly lower TC/HDL-c ratio compared to the B phenotype. Moreover when the TC/HDL-c ratio was converted into “low,” “moderate,” and “high” risk categories and cross-tabulated against ABO phenotypes using the Chi-square test of association, we found TC/HDL-c categories to be significantly associated with ABO phenotypes. Literature on the possible relationship between ABO blood group phenotypes and TC/HDL-c ratio is generally lacking, and this study is one of the extremely few that looked at it. Comparison is therefore not possible, and hence, this result should be interpreted with caution. Despite this limitation, this finding could provide baseline data for further studies.
The disproportionately high level of serum atherogenic cholesterol that is associated with non-O phenotype is said to play a role in the pathogenesis of atherosclerotic lesions and formation of fatty streaks in the blood vessels of these individuals, thus leading to the higher incidence and prevalence of atherosclerotic CVD among them.,,,
The relationship between ABO phenotypes and anthropometric indices in this study is mixed. While there was a significant difference in mean weight and HC among the participants, other anthropometric indices did not differ between the various phenotypes. Specifically, A phenotypes had significantly higher mean weight and HC compared to B phenotypes. There was, however, no association between ABO phenotypes and general or truncal obesity. In their study of 412 participants at Kwame Nkrumah University of Science and Technology, Kumasi in Ghana, Smith et al. reported no significant association between ABO phenotypes and BMI and weight. In a biracial study consisting of Caucasians and African Americans, The Bogalusa Heart Study, no consistently significant relationship was found between ABO phenotype and weight, height, and skinfold thickness among African Americans. They however reported significant associations between ABO phenotypes and weight and height among Caucasians. In another cohort of Bogalusa youths, Borecki et al. found a significant relationship between ABO phenotypes and anthropometric indices only in height, with B phenotypes being taller than non-B. The none significant relationship between ABO phenotypes and measures of obesity could be due to the low prevalence of obesity among the participants. Indeed, the mean BMI of the participants, which indicates general obesity, is within the normal range. The relationship between ABO phenotypes and measures of obesity in this environment, therefore, requires further clarification.
Hypertension is a well-established CVD risk factor. To assess the relationship between ABO phenotypes and hypertension, we looked at the mean difference in systolic, diastolic, and mean arterial blood pressure between O and non-O phenotypes and between the four ABO phenotypes. The O phenotype had significantly higher SBP than the non-O even though both mean values were within the normal limits. However, there was no significant difference in diastolic and mean arterial blood pressure between the ABO phenotypes; there was also no significant association between ABO phenotypes and hypertension. This is similar to what was reported by a number of previous studies., They both reported no consistent relationship between ABO phenotypes and systolic and diastolic pressure, especially among African Americans in Bogalusa, USA. However, Jawed et al. reported a significant association between ABO phenotypes and the prevalence of prehypertension among female medical students in Faisalabad, Pakistan. They found the O phenotype to be significantly associated with both SBP and DBP though only DBP remained significantly associated after logistic regression analysis. Similarly, Chandra and Gupta reported a higher prevalence of hypertension among B phenotypes compared to other phenotypes among blood donors in Iran. There seems to be therefore no consistent relationship between ABO phenotypes and indices of hypertension.
| Conclusion|| |
The findings of this study have highlighted a significant relationship between ABO phenotypes and various serum lipid parameters, weight, HC, SBP, and AI (TC/HDL-c) among healthy young undergraduate students in Kano Nigeria. Individual's ABO phenotype should therefore be considered when evaluating for CVD risk.
We acknowledge the management of the Faculty of Basic Medical Sciences of Bayero University, Kano, Nigeria, for granting us permission to conduct this study at the faculty. We also thank all the students that voluntarily participated in the study.
Financial support and sponsorship
Conflicts of interest
There are no conflicts of interest.
| References|| |
Wu O, Bayoumi N, Vickers MA, Clark P. ABO (H) blood groups and vascular disease: A systematic review and meta-analysis. J Thromb Haemost 2008;6:62-9.
Dentali F, Sironi AP, Ageno W, Turato S, Bonfanti C, Frattini F, et al.
Non-O blood type is the commonest genetic risk factor for VTE: Results from a meta-analysis of the literature. Semin Thromb Hemost 2012;38:535-48.
Chen Y, Chen C, Ke X, Xiong L, Shi Y, Li J, et al.
Analysis of circulating cholesterol levels as a mediator of an association between ABO blood group and coronary heart disease. Circ Cardiovasc Genet 2014;7:43-8.
Chen Z, Yang SH, Xu H, Li JJ. ABO blood group system and the coronary artery disease: An updated systematic review and meta-analysis. Sci Rep 2016;6:23250.
Pike MM, Larson NB, Wassel CL, Cohoon KP, Tsai MY, Pankow JS, et al.
ABO blood group is associated with peripheral arterial disease in African Americans: The Multi-Ethnic Study of Atherosclerosis (MESA). Thromb Res 2017;153:1-6.
Groot HE, Villegas Sierra LE, Said MA, Lipsic E, Karper JC, van der Harst P. Genetically determined ABO blood group and its associations with health and disease. Arterioscler Thromb Vasc Biol 2020;40:830-8.
MacDonald CJ, Madika AL, Severi G, Fournier A, Boutron-Ruault MC. Associations between smoking and blood-group, and the risk of dyslipidaemia amongst French women. Sci Rep 2021;11:14844.
Contiero E, Chinello GE, Folin M. Serum lipids and lipoproteins associations with ABO blood groups. Anthropol Anz 1994;52:221-30.
Millán J, Pintó X, Muñoz A, Zúñiga M, Rubiés-Prat J, Pallardo LF, et al.
Lipoprotein ratios: Physiological significance and clinical usefulness in cardiovascular prevention. Vasc Health Risk Manag 2009;5:757-65.
Mora S, Otvos JD, Rifai N, Rosenson RS, Buring JE, Ridker PM. Lipoprotein particle profiles by nuclear magnetic resonance compared with standard lipids and apolipoproteins in predicting incident cardiovascular disease in women. Circulation 2009;119:931-9.
Arsenault BJ, Després JP, Stroes ES, Wareham NJ, Kastelein JJ, Khaw KT, et al.
Lipid assessment, metabolic syndrome and coronary heart disease risk. Eur J Clin Invest 2010;40:1081-93.
Tohidi M, Hatami M, Hadaegh F, Safarkhani M, Harati H, Azizi F. Lipid measures for prediction of incident cardiovascular disease in diabetic and non-diabetic adults: Results of the 8.6 years follow-up of a population based cohort study. Lipids Health Dis 2010;9:6.
Nogay NH. Assessment of the correlation between the atherogenic index of plasma and cardiometabolic risk factors in children and adolescents: Might it be superior to the TG/HDL-C ratio? J Pediatr Endocrinol Metab 2017;30:947-55.
Sone H, Nakagami T, Nishimura R, Tajima N, MEGA Study Group. Comparison of lipid parameters to predict cardiovascular events in Japanese mild-to-moderate hypercholesterolemic patients with and without type 2 diabetes: Subanalysis of the MEGA study. Diabetes Res Clin Pract 2016;113:14-22.
World Health Organization. WHO STEPwise Approach to Surveillance (STEPS). Geneva, Switzerland: World Health Organization; 2008.
Rawley M, Milkins C. Laboratory aspects of blood transfusion. In: Bain BJ, Bates I, Laffan MA, editors. Dacie and Lewis Practical Haematology. London: Elsevier; 2006. p. 470-96.
Friedewald WT, Levy RI, Fredrickson DS. Estimation of the concentration of low-density lipoprotein cholesterol in plasma, without use of the preparative ultracentrifuge. Clin Chem 1972;18:499-502.
Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults. Executive summary of the Third Report of The National Cholesterol Education Program (NCEP) Expert Panel on detection, evaluation, and treatment of high blood cholesterol in adults (Adult Treatment Panel III). JAMA 2001;285:2486-97.
World Health Organization. Obesity: Preventing and Managing the Global Epidemic: Report of a WHO Consultation. WHO Technical Report Series 894. Geneva, Switzerland: World Health Organization; 2000. p. 252.
International Diabetes Federation. The IDF Consensus Worldwide Definition of the Metabolic Syndrome. Brussels, Belgium: IDF Communications; 2006.
Mukhtar IG, Muhammad SM, Yakasai BW, Salisu AI. ABO and Rh blood group phenotypes of Nigerian blood donors at Murtala Muhammad Specialist Hospital, Kano – A one year retrospective study. BJMLS 2018;3:48-53.
Anifowoshe AT, Owolodun OA, Akinseye KM, Iyiola OA, Oyeyemi BF. Gene frequencies of ABO and Rh blood group in Nigeria: A review. Egypt J Med Hum Genet 2015;18:205-10.
Babiak J, Rudel LL. Lipoproteins and atherosclerosis. Baillieres Clin Endocrinol Metab 1987;1:515-50.
Zhang H, Mooney CJ, Reilly MP. ABO blood groups and cardiovascular diseases. Int J Vasc Med 2012;2012:641917.
Biswas S, Ghoshal PK, Halder B, Mandal N. Distribution of ABO blood group and major cardiovascular risk factors with coronary heart disease. Biomed Res Int 2013;2013:782941.
Smith S, Okai I, Abaidoo CS, Acheampong E. Association of ABO blood group and body mass index: A cross-sectional study from a Ghanaian population. J Nutr Metab 2018;2018:8050152.
Fox MH, Webber LS, Thurmon TF, Berenson GS. ABO blood group associations with cardiovascular risk factor variables. II. Blood pressure, obesity, and their anthropometric covariables. The Bogalusa Heart Study. Hum Biol 1986;58:549-84.
Borecki IB, Elston RC, Rosenbaum PA, Srinivasan SR, Berenson GS. ABO associations with blood pressure, serum lipids and lipoproteins, and anthropometric measures. Hum Hered 1985;35:161-70.
Jawed S, Zia S, Tariq S. Frequency of different blood groups and its association with BMI and blood pressure among the female medical students of Faisalabad. J Pak Med Assoc 2017;67:1132-7.
Chandra T, Gupta A. Association and distribution of hypertension, obesity and ABO blood groups in blood donors. Iran J Ped Hematol Oncol 2012;2:140-5.
[Table 1], [Table 2], [Table 3], [Table 4], [Table 5]