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Gene and environmental interactions according to the components of lifestyle modifications in hypertension guidelines

Abstract

Risk factors for hypertension consist of lifestyle and genetic factors. Family history and twin studies have yielded heritability estimates of BP in the range of 34–67%. The most recent paper of BP GWAS has explained about 20% of the population variation of BP. An overestimation of heritability may have occurred in twin studies due to violations of shared environment assumptions, poor phenotyping practices in control cohorts, failure to account for epistasis, gene-gene and gene-environment interactions, and other non-genetic sources of phenotype modulation that are suspected to lead to underestimations of heritability in GWAS. The recommendations of hypertension guidelines in major countries consist of the following elements: weight reduction, a healthy diet, dietary sodium reduction, increasing physical activity, quitting smoking, and moderate alcohol consumption. The hypertension guidelines are mostly the same for each country or region, beyond race and culture. In this review, we summarize gene-environmental interactions associated with hypertension by describing lifestyle modifications according to the hypertension guidelines. In the era of precision medicine, clinicians who are responsible for hypertension management should consider the gene-environment interactions along with the appropriate lifestyle components toward the prevention and treatment of hypertension. We briefly reviewed the interaction of genetic and environmental factors along the constituent elements of hypertension guidelines, but a sufficient amount of evidence has not yet accumulated, and the results of genetic factors often differed in each study.

Hypertension is the most influential risk factor for cardiovascular disease (CVD) [1]. Recent evidence has suggested that hypertension is also associated with common non-CVD such as dementia and renal dysfunction [2]. Risk factors for hypertension consist of lifestyle and genetic factors. Family history and twin studies have yielded heritability estimates of blood pressure (BP) in the range of 34–67% [3]. The collective effect of all BP loci identified through genome-wide association studies (GWAS) accounted for only ~ 3.5% of BP variability [4]. The most recent paper of BP GWAS has identified 901 SNPs with BP and explained about 20% of the population variation of BP [5]. An overestimation of heritability may have occurred in twin studies due to violations of shared environment assumptions, poor phenotyping practices in control cohorts, failure to account for epistasis, gene-gene (G × G) and gene-environment (G × E) interactions, and other non-genetic sources of phenotype modulation that are suspected to lead to underestimations of heritability in GWAS.

The recommendations of hypertension guidelines in major countries consist of the following elements: weight reduction, a healthy diet (dietary patterns characterized by a high consumption of fruit, vegetables, whole grains, legumes, seeds, nuts, fish, low-fat dairy, and a low consumption of meat and sweets), dietary sodium reduction, increasing physical activity, quitting smoking (including avoiding passive smoking), and moderate alcohol consumption (Table 1) [6,7,8]. The hypertension guidelines are mostly the same for each country or region, beyond race and culture [9]. In this review, we summarize gene-environmental interactions associated with hypertension by describing lifestyle modifications according to the hypertension guidelines.

Table 1 Comparison between three major lifestyle modifications in the hypertension guidelines

Gene-sodium interaction

The INTERSALT study indicated an association between overdose salt intake and high blood pressure [10]. The Dietary Approaches to Stop Hypertension (DASH) study showed that sodium intake restrictions from a high level to an intermediate level and from an intermediate to a low level reduced both systolic blood pressure (SBP) and diastolic blood pressure (DBP) [11]. In a pooled analysis of data, lowering sodium intake was shown to be best-targeted at individuals with hypertension who consume high-sodium diets [12]. On the basis of these results, hypertension management guidelines recommend the following: salt intakes of < 5 g/day in Europe [6], < 6 g/day in Japan [8], and sodium intake of < 1500 mg/day (salt intake of < 3. 81 g/day equivalent) in the USA [7].

Salt sensitivity is an increase in BP in response to excessive dietary salt intake, and it is associated with genetic and environmental factors. Salt sensitivity is more frequently observed in hypertensive than normotensive subjects, in colored races than in Caucasians, and in older than in younger subjects [13, 14]. When gene-sodium interactions are studied, the investigations must consider the race and age group of subjects.

A cross-sectional study in Korea indicated that the mutant alleles of CSK rs1378942 and CSK-MIR4513 rs3784789 had the strongest protective effects against hypertension in the subjects in the middle group of the 24-h estimated urinary sodium-potassium excretion ratio (Table 2) [15]. In a cross-sectional study in China, Li et al. showed that the interaction for CLGN rs2567241 was associated with the sodium intake’s effects on SBP, DBP, and mean blood pressure (MBP), the impact of UST rs13211840 on DBP, and the effect of LOC105369882 rs11104632 on SBP through the examination of an SNP [16]. Also, genome-wide gene-based interactions with sodium identified MKNK1, C2orf80, EPHA6, SCOC-AS1, SCOC, CLGN, MGAT4D, ARHGAP42, CASP4, and LINC01478 which were associated with at least one BP variable. In Chinese Kazakh women, an interaction of ACE genotype and salt intake on hypertension was observed [17].

Table 2 Review for interaction of gene and salt intake on hypertension

In a Japanese population, the interaction between salt consumption and NPPA rs5063 (Val32Met) showed a significant association with SBP [18]. In a general Japanese population, a high sodium intake strengthened the association of AGT T174 M [19] and ADD1 G460 W (only women) [20] polymorphisms with hypertension and SBP levels, respectively. Another cross-sectional study showed that CYP3A5 variants might be a determinant of salt sensitivity of BP in Japanese men [21]. A case-control study in Taiwan showed that GNB3 C825T polymorphism might increase the risk of hypertension among individuals who consumed a high-sodium diet [22]. Adamo et al. reviewed studies of gene-salt interaction [23], but most of those studies might have been subject to error due to their small sample sizes. Studies of gene-environmental interactions require large sample sizes as they involve the grouping of genes and environmental factors.

Gene-healthy diet interaction

The DASH diet study showed no significant BP lowering in the control group, and the fruits/vegetable group, but SBP and DBP lowering were observed in the DASH diet group [24]. In a meta-analysis of 17 randomized controlled trials, significant reductions of 4.3 mmHg in SBP and 2.4 mmHg in DBP were observed in healthy dietary patterns, including the DASH diet, Nordic diet, and Mediterranean diet, all of which include the high consumption of fruit, vegetables, whole grains, legumes, seeds, nuts, fish, and dairy and a low consumption of meat, sweets, and alcohol [25]. These foods or combinational foods contribute to the prevention of high blood pressure.

A 2-year-randomized intervention trial revealed significant interactions between the Neuropeptide Y (NPY) rs16147 SNP and dietary fat intake in relation to changes in SBP and DBP (Table 3) [26]. The gene-diet interactions appeared only in hypertensive patients. During the 2 years of intervention, the subjects with C allele had greater reductions in SBP and DBP in response to a low-fat diet but had greater increases in SBP and DBP in response to a high-fat diet. NPY is implicated in the regulation of BP, and NPY pathways in the hypothalamus are sensitive to dietary fat. Animal experiments indicated that fat intake and NPY activity in the hypothalamus are inversely correlated [27].

Table 3 Review for interaction of gene and healthy diet on hypertension

A Korean genome and epidemiology study showed that a higher omega-3 (ω-3) polyunsaturated fatty acid (PUFA) intake was significantly associated with a more pronounced BP decrease over time in subjects with the CYP4F2 433VV genotype, although there was no association between ω-6 and ω-3 PUFA intakes, ω-6/ω-3, and changes of BP [28]. A meta-analysis of interventional studies showed that the intake of fish oil caused a decrease in BP in hypertensive patients [29].

In a study of Japanese men, the Met allele of COMT Val158Met was associated with higher BP and a higher prevalence of hypertension in the high-energy intake group but not in the low-energy intake group [30]. There was no difference in body mass index (BMI) between the low- and high-energy intake groups. The underlying mechanism of these results remains unclear.

In a Southern European study, there was an interaction between the NOS3 rs1799983 polymorphism and dietary saturated fatty acid and monounsaturated fatty acid that influenced DBP levels [31]. Martins et al. showed that nitric oxide synthase (NOS) activity was increased in an unsaturated high-fat diet group. The expressions of endothelial NOS (eNOS) and inducible NOS (iNOS) were also increased in the unsaturated high-fat diets group [32]. These changes may be involved in gene-dietary interactions.

Gene-alcohol interaction

Alcohol consumption is higher among East Asian men compared to Western men, but the consumption of alcohol by Western women is higher than that among East Asian women [33]. Approximately half of East Asians are found to be aldehyde dehydrogenase (ALDH) deficient, which accounts for a phenomenon called the ‘Oriental flushing syndrome.’ ALDH deficiency poses an increased risk of high BP [34].

In a study of middle-aged Finnish men, the apolipoprotein E phenotype significantly influenced the BP increasing effect of alcohol consumption (Table 4) [35]. A cross-sectional study of a Chinese population showed a significant interaction between the CYP11B2 genotype [36] and DNA methylation (CpG1 methylation) of the ADD1 gene promoter [37] and alcohol consumption on the risk of hypertension. In addition, the Stanford Asia-Pacific Program for Hypertension and Insulin Resistance (SAPPHIRe) study showed that ALDH2 genetic variants were associated with progression to hypertension in a prospective Chinese cohort [38]. In a cross-sectional study of 5724 Japanese participants, ALDH2 rs671 significantly and synergistically influenced the subjects’ drinking behavior and influenced the level of BP independently of the amount of alcohol consumption [39], but not in another study, in a case-control study of 532 Japanese patients, there was no significant interaction between the ALDH2 genotype and alcohol consumption overall or in Japanese male patients: this study may have had insufficient power to detect the interaction [40].

Table 4 Review for interaction of gene and alcohol intake on hypertension

A genome-wide analysis of the effect of SNP-alcohol interactions on BP traits showed 1 significant and 20 suggestive BP loci by exploiting gene-alcohol interactions in a study from the Framingham SNP Health Association Resource [41]. The CHARGE Gene-Lifestyle Interactions Working Group has systematically shown the gene-alcohol interaction on BP in a recent and extensive meta-analysis across multiple ancestries, conducting a large two-stage investigation incorporating joint testing of main genetic effects and single nucleotide variant (SNV)-alcohol consumption interactions [42]. The study identified and replicated 54 BP loci in European ancestry and multi-ancestry meta-analyses.

Gene-smoking interaction

According to the Global Burden of Disease Study 2015, central and eastern Europe and southeast Asia had a higher prevalence of smoking than the global average for men, and western and central Europe had a higher prevalence of smoking than the global average for women [43]. The population-attributable fractions of coronary heart disease caused by smoking among men and women were higher in the East Asian region than in the Western Pacific region [44].

In a rural Chinese population, the cigarette smoking index and ACE gene showed a low exposure-gene effect on essential hypertension with interaction indices (Table 5) [45]. In an eastern Chinese Han population, gene-environment interactions between rs1126742 and smoking were associated with an increased risk of essential hypertension [46]. A case-control study showed the association of KCNJ11 gene polymorphisms and BP response to the antihypertensive drug irbesartan in non-smoking Chinese hypertensive patients [47]. As a genome-wide study, the Framingham Heart Study identified 7 significant and 21 suggestive BP loci by gene-smoking interactions in an analysis of 6889 participants [48].

Table 5 Review for interaction of gene and smoking on hypertension

The further genome-wide research was proposed to examine African American participants in the Hypertension Genetic Epidemiology Network (HyperGEN) research, and testing the association in African American participants from the Genetic Epidemiology Network of Arteriopathy (GENOA) study [49]. The results suggested that NEDD8 rs11158609 and TTYH2 rs8078051 were associated with SBP including the genetic interaction with cigarette smoking, although these two SNPs were not associated with SBP in a main genetic effect model.

Gene-obesity interaction

Globally, the prevalence of overweight or obesity for adults increased from 28.8% and 29.8% in 1980 to 36.9% and 38.0% in 2013 for men and women, respectively, which were observed in both developed and developing countries [50]. The prevalence of overweight and obesity is rising among children and adolescents in developing countries as well, rising from 8.1% and 8.4% in 1980 to 12.9% and 13.4% in 2013 for boys and girls, respectively. A meta-analysis of 25 studies has estimated that as body weight decreased by 1 kg, SBP and DBP decreased by − 1.05 mmHg and − 0.92 mmHg, respectively [51]. Therefore, weight loss for obese people is an essential factor in lowering BP.

The Atherosclerosis Risk in Communities Study showed a significant interaction among the GNB3 C825T polymorphism, obesity status, and physical activity in predicting hypertension in African American subjects, and those who were both obese and had a low activity level with T allele were 2.7 times more likely to be hypertensive compared to non-obese, active C homozygotes [52].

The representative SNPs related to BMI are those in FTO and MC4-R loci. SNPs in FTO were associated with hypertension in different ethnic groups [53]. The Pima Indians in Arizona have the highest prevalence of obesity in the world, but a relatively low prevalence of hypertension and atherosclerotic disease [54]. The lack of increase in muscle sympathetic nerve activity with increasing adiposity and insulinemia in Pima Indians may explain this in part [55], but the reason why this population has a low tendency for hypertension despite the high prevalence of obesity and hyperinsulinemia are not yet known.

Gene-physical activity interaction

A meta-analysis that included 13 prospective studies suggested that there was an inverse dose-response association between levels of recreational physical activity and risk of hypertension [56]. A recent systematic review and meta-analysis of randomized control trials with a meta-regression of potential effect modifiers revealed that exercise was associated with a reduction in SBP of − 4.40 mmHg and in DBP of − 4.17 mmHg at 3–6 months after the intervention began [57]. Potential reasons for the association between physical activity and BP decreases are as follows. First, physical activity helps maintain appropriate body weight. Second, exercise decreases total peripheral resistance [58]. Physical activity has also been shown to improve insulin sensitivity [59], which increases high blood pressure via its effect in increasing sodium reabsorption and sympathetic nervous system activity [60]. An exercise habit can also help improve one’s other lifestyle habits. Individuals who exercise every day tend to focus on improving their lifestyle in other aspects of their daily lives.

In a cross-sectional study of African American women, SLC4A5 rs1017783 had a significant interaction with A allele and AA genotype by physical activity on SBP and DBP, respectively. In addition, SLC4A5 rs6731545 had a significant interaction with GA genotype by physical activity on both SBP and DBP. A study of Chinese children showed that interactions between a genetic risk score including ATP2B1 rs17249754, fibroblast growth factor 5 (FGF5) rs16998073 polymorphisms, and physical activity play important roles in the regulation of BP and the development of hypertension [61]. ATP2B1 is expressed in the vascular endothelium and regulates the homeostasis of cellular calcium levels, which is important in controlling the contraction and dilation of vascular smooth muscles [62]. The most commonly cited effect of FGF-5 is to promote angiogenesis in the heart. FGF-5 acts as an autocrine/paracrine mechanism of cardiac cell growth and as a cytoprotective mechanism against irreversible ischemic damage [63]. FGF-5 rs16998073 polymorphisms were significantly associated with hypertension risk in East Asians [64]. However, no evidence supports a role for this gene in the pathogenesis of hypertension.

Perspectives

In the era of precision medicine, clinicians who are responsible for hypertension management should consider the gene-environment interactions along with the appropriate lifestyle components toward the prevention and treatment of hypertension. The effects and contributions of other confounding and interaction factors such as race, age, other lifestyle habits (e.g., lack of sleep [65] and bathing [66]), and environmental factors (e.g., weather conditions [67] and air pollution [68]), stress [69], and social factors [70] must also be determined comprehensively.

We briefly reviewed the interaction of genetic and environmental factors along the constituent elements of hypertension guidelines, but a sufficient amount of evidence has not yet accumulated, and the results of genetic factors often differed in each study. The following requirements should be considered in future studies: (1) set of the reproducible environmental factor with simple and easy way; (2) consider the subjects’ race, gender, and age; (3) select research subjects so that bias is as small as possible; (4) use a risk score of the target disease including a simple dietary intake and physical activity questionnaire and examines genetic factors to improve the risk model; and (5) effectively provide hypertension management with precision medicine based on the components of appropriate lifestyle interventions in hypertension prevention guidelines for a cardiovascular disease model with the specific gene-environmental factors being studied.

The Genetic Epidemiology Network of Salt Sensitivity (The GenSalt) Study obtained novel implications regarding the association between BP responses to dietary sodium and potassium and hypertension and identifying an inverse relation between a BP genetic risk score and salt and potassium sensitivity of BP [71]. The UK Biobank data recently revealed 107 validated loci for BP, in a study that showed that BP which is 9–10 mmHg higher with an over twofold higher risk of hypertension (in a comparison of the top and bottom quintiles of the BP genetic risk score distribution) has potential clinical and public health implications [72]. Although the extent to which each gene contributes to BP is small, by incorporating the concept of a genetic risk score, the contribution of blood pressure has been shown by many GWAS. BP research will continue to contribute to future preventive medicine.

Conclusion

We summarize gene-environmental interactions associated with hypertension by describing common lifestyle modifications according to the recommendations of hypertension guidelines in major countries which consist of the following elements: weight reduction, a healthy diet, dietary sodium reduction, increasing physical activity, quitting smoking, and moderate alcohol consumption. We briefly reviewed the interaction of genetic and environmental factors along the constituent elements of hypertension guidelines, but a sufficient amount of evidence has not yet accumulated, and the results of genetic factors often differed in each study.

Abbreviations

ALDH:

Aldehyde dehydrogenase

BMI:

Body mass index

BP:

Blood pressure

CHARGE:

Cohorts for Heart and Aging Research in Genetic Epidemiology

CVD:

Cardiovascular disease

DASH:

Dietary Approaches to Stop Hypertension

DBP:

Diastolic blood pressure

eNOS:

Endothelial nitric oxide synthase

GENOA:

Genetic Epidemiology Network of Arteriopathy

GenSalt:

Genetic Epidemiology Network of Salt Sensitivity

GWAS:

Genome-wide association studies

HyperGEN:

Hypertension Genetic Epidemiology Network

iNOS:

Inducible nitric oxide synthase

INTERSALT:

International Cooperative Study on Salt, Other Factors, and Blood Pressure

MBP:

Mean blood pressure

NOS:

Nitric oxide synthase

PUFA:

Polyunsaturated fatty acid

SAPPHIRe:

Stanford Asia-Pacific Program for Hypertension and Insulin Resistance

SBP:

Systolic blood pressure

SNV:

Single-nucleotide variant

References

  1. Kokubo Y, Kamide K, Okamura T, Watanabe M, Higashiyama A, Kawanishi K, Okayama A, Kawano Y. Impact of high-normal blood pressure on the risk of cardiovascular disease in a Japanese urban cohort: the Suita study. Hypertension. 2008;52:652–9.

    CAS  Article  Google Scholar 

  2. Kokubo Y, Iwashima Y. Higher blood pressure as a risk factor for diseases other than stroke and ischemic heart disease. Hypertension. 2015;66:254–9.

    CAS  Article  Google Scholar 

  3. Hottenga JJ, Boomsma DI, Kupper N, Posthuma D, Snieder H, Willemsen G, de Geus EJ. Heritability and stability of resting blood pressure. Twin Res Hum Genet. 2005;8:499–508.

    Article  Google Scholar 

  4. Ehret GB, Ferreira T, Chasman DI, Jackson AU, Schmidt EM, Johnson T, Thorleifsson G, Luan J, Donnelly LA, Kanoni S, Petersen AK, Pihur V, Strawbridge RJ, Shungin D, Hughes MF, et al. The genetics of blood pressure regulation and its target organs from association studies in 342,415 individuals. Nat Genet. 2016;48:1171–84.

    CAS  Article  Google Scholar 

  5. Evangelou E, Warren HR, Mosen-Ansorena D, Mifsud B, Pazoki R, Gao H, Ntritsos G, Dimou N, Cabrera CP, Karaman I, Ng FL, Evangelou M, Witkowska K, Tzanis E, Hellwege JN, et al. Genetic analysis of over 1 million people identifies 535 new loci associated with blood pressure traits. Nat Genet. 2018;50:1412–25.

    CAS  Article  Google Scholar 

  6. Williams B, Mancia G, Spiering W, Agabiti Rosei E, Azizi M, Burnier M, Clement DL, Coca A, de Simone G, Dominiczak A, Kahan T, Mahfoud F, Redon J, Ruilope L, Zanchetti A, et al. 2018 ESC/ESH guidelines for the management of arterial hypertension. Eur Heart J. 2018;39:3021–104.

    Article  Google Scholar 

  7. Whelton PK, Carey RM, Aronow WS, Casey DE Jr, Collins KJ, Dennison Himmelfarb C, DePalma SM, Gidding S, Jamerson KA, Jones DW, MacLaughlin EJ, Muntner P, Ovbiagele B, Smith SC Jr, Spencer CC, et al. 2017 ACC/AHA/AAPA/ABC/ACPM/AGS/APhA/ASH/ASPC/NMA/PCNA guideline for the prevention, detection, evaluation, and management of high blood pressure in adults: executive summary: a report of the American College of Cardiology/American Heart Association task force on clinical practice guidelines. Hypertension. 2017;71(6):1269–324.

    Article  Google Scholar 

  8. Shimamoto K, Ando K, Fujita T, Hasebe N, Higaki J, Horiuchi M, Imai Y, Imaizumi T, Ishimitsu T, Ito M, Ito S, Itoh H, Iwao H, Kai H, Kario K, et al. The Japanese Society of Hypertension Guidelines for the Management of Hypertension (JSH 2014). Hypertens Res. 2014;37:253–387.

    Article  Google Scholar 

  9. Kokubo Y, Matsumoto C. Comprehensive lifestyle modification for hypertension and lifestyle-related disease under the new guidelines. In: Vasan RS, Sawyer DB, editors. Encyclopedia of cardiovascular research and medicine. Oxford: Elsevier; 2017. p. 651–8.

    Google Scholar 

  10. Intersalt: an international study of electrolyte excretion and blood pressure. Results for 24 hour urinary sodium and potassium excretion. Intersalt Cooperative Research Group. BMJ. 1988;297:319–28.

    Article  Google Scholar 

  11. Sacks FM, Svetkey LP, Vollmer WM, Appel LJ, Bray GA, Harsha D, Obarzanek E, Conlin PR, Miller ER 3rd, Simons-Morton DG, Karanja N, Lin PH. Effects on blood pressure of reduced dietary sodium and the dietary approaches to stop hypertension (DASH) diet. DASH-sodium collaborative research group. N Engl J Med. 2001;344:3–10.

    CAS  Article  Google Scholar 

  12. Mente A, O'Donnell M, Rangarajan S, Dagenais G, Lear S, McQueen M, Diaz R, Avezum A, Lopez-Jaramillo P, Lanas F, Li W, Lu Y, Yi S, Rensheng L, Iqbal R, et al. Associations of urinary sodium excretion with cardiovascular events in individuals with and without hypertension: a pooled analysis of data from four studies. Lancet. 2016;388:465–75.

    CAS  Article  Google Scholar 

  13. Sullivan JM. Salt sensitivity. Definition, conception, methodology, and long-term issues. Hypertension. 1991;17:I61–8.

    CAS  Article  Google Scholar 

  14. Luft FC, Miller JZ, Grim CE, Fineberg NS, Christian JC, Daugherty SA, Weinberger MH. Salt sensitivity and resistance of blood pressure. Age and race as factors in physiological responses. Hypertension. 1991;17:I102–8.

    CAS  Article  Google Scholar 

  15. Park YM, Kwock CK, Kim K, Kim J, Yang YJ. Interaction between single nucleotide polymorphism and urinary sodium, potassium, and sodium-potassium ratio on the risk of hypertension in Korean adults. Nutrients. 2017;9

  16. Li C, He J, Chen J, Zhao J, Gu D, Hixson JE, Rao DC, Jaquish CE, Gu CC, Chen J, Huang J, Chen S, Kelly TN. Genome-wide gene-sodium interaction analyses on blood pressure: the genetic epidemiology network of salt-sensitivity study. Hypertension. 2016;68:348–55.

    CAS  Article  Google Scholar 

  17. Wang Y, Zhang B, Hou L, Han W, Xue F, Wang Y, Tang Y, Liang S, Wang W, Asaiti K, Wang Z, Hu Y, Wang L, Qiu C, Zhang M, et al. Interaction of ACE genotype and salt intake on hypertension among Chinese Kazakhs: results from a population-based cross-sectional study. BMJ Open. 2017;7:e014246.

    Article  Google Scholar 

  18. Imaizumi T, Ando M, Nakatochi M, Maruyama S, Yasuda Y, Honda H, Kuwatsuka Y, Kato S, Kondo T, Iwata M, Nakashima T, Yasui H, Takamatsu H, Okajima H, Yoshida Y, et al. Association of interactions between dietary salt consumption and hypertension-susceptibility genetic polymorphisms with blood pressure among Japanese male workers. Clin Exp Nephrol. 2017;21:457–64.

    CAS  Article  Google Scholar 

  19. Iso H, Harada S, Shimamoto T, Sato S, Kitamura A, Sankai T, Tanigawa T, Iida M, Komachi Y. Angiotensinogen T174M and M235T variants, sodium intake and hypertension among non-drinking, lean Japanese men and women. J Hypertens. 2000;18:1197–206.

    CAS  Article  Google Scholar 

  20. Yamagishi K, Iso H, Tanigawa T, Cui R, Kudo M, Shimamoto T. Alpha-adducin G460W polymorphism, urinary sodium excretion, and blood pressure in community-based samples. Am J Hypertens. 2004;17:385–90.

    CAS  Article  Google Scholar 

  21. Zhang L, Miyaki K, Wang W, Muramatsu M. CYP3A5 polymorphism and sensitivity of blood pressure to dietary salt in Japanese men. J Hum Hypertens. 2010;24:345–50.

    CAS  Article  Google Scholar 

  22. Chen ML, Huang TP, Chen TW, Chan HH, Hwang BF. Interactions of genes and sodium intake on the development of hypertension: a cohort-based case-control study. Int J Environ Res Public Health. 2018;15

  23. Adamo KB, Tesson F. Gene-environment interaction and the metabolic syndrome. Novartis Found Symp. 2008;293:103–19. discussion 119-127

    CAS  Article  Google Scholar 

  24. Moore TJ, Conlin PR, Ard J, Svetkey LP. DASH (dietary approaches to stop hypertension) diet is effective treatment for stage 1 isolated systolic hypertension. Hypertension. 2001;38:155–8.

    CAS  Article  Google Scholar 

  25. Ndanuko RN, Tapsell LC, Charlton KE, Neale EP, Batterham MJ. Dietary patterns and blood pressure in adults: a systematic review and meta-analysis of randomized controlled trials. Adv Nutr. 2016;7:76–89.

    CAS  Article  Google Scholar 

  26. Zhang X, Qi Q, Liang J, Hu FB, Sacks FM, Qi L. Neuropeptide Y promoter polymorphism modifies effects of a weight-loss diet on 2-year changes of blood pressure: the preventing overweight using novel dietary strategies trial. Hypertension. 2012;60:1169–75.

    CAS  Article  Google Scholar 

  27. Belsky J, Pluess M. Beyond diathesis stress: differential susceptibility to environmental influences. Psychol Bull. 2009;135:885–908.

    Article  Google Scholar 

  28. Tagetti A, Ericson U, Montagnana M, Danese E, Almgren P, Nilsson P, Engstrom G, Hedblad B, Minuz P, Orho-Melander M, Fava C, Melander O. Intakes of omega-3 polyunsaturated fatty acids and blood pressure change over time: possible interaction with genes involved in 20-HETE and EETs metabolism. Prostaglandins Other Lipid Mediat. 2015;120:126–33.

    CAS  Article  Google Scholar 

  29. Geleijnse JM, Giltay EJ, Grobbee DE, Donders AR, Kok FJ. Blood pressure response to fish oil supplementation: metaregression analysis of randomized trials. J Hypertens. 2002;20:1493–9.

    CAS  Article  Google Scholar 

  30. Htun NC, Miyaki K, Song Y, Ikeda S, Shimbo T, Muramatsu M. Association of the catechol-O-methyl transferase gene Val158Met polymorphism with blood pressure and prevalence of hypertension: interaction with dietary energy intake. Am J Hypertens. 2011;24:1022–6.

    CAS  Article  Google Scholar 

  31. Goni L, Cuervo M, Milagro FI, Martinez JA. Influence of fat intake and BMI on the association of rs1799983 NOS3 polymorphism with blood pressure levels in an Iberian population. Eur J Nutr. 2017;56:1589–96.

    CAS  Article  Google Scholar 

  32. Martins MA, Catta-Preta M, Mandarim-de-Lacerda CA, Aguila MB, Brunini TC, Mendes-Ribeiro AC. High fat diets modulate nitric oxide biosynthesis and antioxidant defence in red blood cells from C57BL/6 mice. Arch Biochem Biophys. 2010;499:56–61.

    CAS  Article  Google Scholar 

  33. Zhou BF, Stamler J, Dennis B, Moag-Stahlberg A, Okuda N, Robertson C, Zhao L, Chan Q, Elliott P. Nutrient intakes of middle-aged men and women in China, Japan, United Kingdom, and United States in the late 1990s: the INTERMAP study. J Hum Hypertens. 2003;17:623–30.

    CAS  Article  Google Scholar 

  34. Takagi S, Baba S, Iwai N, Fukuda M, Katsuya T, Higaki J, Mannami T, Ogata J, Goto Y, Ogihara T. The aldehyde dehydrogenase 2 gene is a risk factor for hypertension in Japanese but does not alter the sensitivity to pressor effects of alcohol: the Suita study. Hypertens Res. 2001;24:365–70.

    CAS  Article  Google Scholar 

  35. Kauma H, Savolainen MJ, Rantala AO, Lilja M, Kervinen K, Reunanen A, Kesaniemi YA. Apolipoprotein E phenotype determines the effect of alcohol on blood pressure in middle-aged men. Am J Hypertens. 1998;11:1334–43.

    CAS  Article  Google Scholar 

  36. Pan XQ, Zhang YH, Liu YY, Tong WJ. Interaction between the C(-344)T polymorphism of CYP11B2 and alcohol consumption on the risk of essential hypertension in a Chinese Mongolian population. Eur J Epidemiol. 2010;25:813–21.

    CAS  Article  Google Scholar 

  37. Han L, Liu P, Wang C, Zhong Q, Fan R, Wang L, Duan S, Zhang L. The interactions between alcohol consumption and DNA methylation of the ADD1 gene promoter modulate essential hypertension susceptibility in a population-based, case-control study. Hypertens Res. 2015;38:284–90.

    CAS  Article  Google Scholar 

  38. Chang YC, Chiu YF, Lee IT, Ho LT, Hung YJ, Hsiung CA, Quertermous T, Donlon T, Lee WJ, Lee PC, Chen CH, Mochly-Rosen D, Chuang LM. Common ALDH2 genetic variants predict development of hypertension in the SAPPHIRe prospective cohort: gene-environmental interaction with alcohol consumption. BMC Cardiovasc Disord. 2012;12:58.

    CAS  Article  Google Scholar 

  39. Tsuchihashi-Makaya M, Serizawa M, Yanai K, Katsuya T, Takeuchi F, Fujioka A, Yamori Y, Ogihara T, Kato N. Gene-environmental interaction regarding alcohol-metabolizing enzymes in the Japanese general population. Hypertens Res. 2009;32:207–13.

    CAS  Article  Google Scholar 

  40. Hui P, Nakayama T, Morita A, Sato N, Hishiki M, Saito K, Yoshikawa Y, Tamura M, Sato I, Takahashi T, Soma M, Izumi Y, Ozawa Y, Cheng Z. Common single nucleotide polymorphisms in Japanese patients with essential hypertension: aldehyde dehydrogenase 2 gene as a risk factor independent of alcohol consumption. Hypertens Res. 2007;30:585–92.

    CAS  Article  Google Scholar 

  41. Simino J, Sung YJ, Kume R, Schwander K, Rao DC. Gene-alcohol interactions identify several novel blood pressure loci including a promising locus near SLC16A9. Front Genet. 2013;4:277.

    Article  Google Scholar 

  42. Feitosa MF, Kraja AT, Chasman DI, Sung YJ, Winkler TW, Ntalla I, Guo X, Franceschini N, Cheng CY, Sim X, Vojinovic D, Marten J, Musani SK, Li C, Bentley AR, et al. Novel genetic associations for blood pressure identified via gene-alcohol interaction in up to 570K individuals across multiple ancestries. PLoS One. 2018;13:e0198166.

    Article  Google Scholar 

  43. Collaborators GBDT. Smoking prevalence and attributable disease burden in 195 countries and territories, 1990-2015: a systematic analysis from the global burden of disease study 2015. Lancet. 2017;389:1885–906.

    Article  Google Scholar 

  44. Martiniuk AL, Lee CM, Lam TH, Huxley R, Suh I, Jamrozik K, Gu DF, Woodward M, Asia Pacific cohort studies C. The fraction of ischaemic heart disease and stroke attributable to smoking in the WHO Western Pacific and south-east Asian regions. Tob Control 2006;15:181–188.

  45. Xu Q, Wang YH, Tong WJ, Gu ML, Wu G, Buren B, Liu YY, Wang J, Li YS, Feng H, Bai SL, Pang HH, Huang GR, Fang MW, Zhang YH, et al. Interaction and relationship between angiotensin converting enzyme gene and environmental factors predisposing to essential hypertension in Mongolian population of China. Biomed Environ Sci. 2004;17:177–86.

    PubMed  Google Scholar 

  46. Zhang H, Jin L, Mu T, Fan Y, Zhang H, Zhu Y, Mao X, Li R, Tang S. Associations of CYP4A11 gene-gene and gene-smoking interactions with essential hypertension in the male eastern Chinese Han population. Clin Exp Hypertens. 2017;39:448–53.

    CAS  Article  Google Scholar 

  47. Jiang S, Venners SA, Hsu YH, Weinstock J, Wang B, Xing H, Wang X, Xu X. Interactive effect of the KCNJ11 Ile337Val polymorphism and cigarette smoking on the antihypertensive response to Irbesartan in Chinese hypertensive patients. Am J Hypertens. 2016;29:553–9.

    CAS  Article  Google Scholar 

  48. Sung YJ, de Las FL, Schwander KL, Simino J, Rao DC. Gene-smoking interactions identify several novel blood pressure loci in the Framingham heart study. Am J Hypertens. 2015;28:343–54.

    CAS  Article  Google Scholar 

  49. Taylor JY, Schwander K, Kardia SL, Arnett D, Liang J, Hunt SC, Rao DC, Sun YV. A genome-wide study of blood pressure in African Americans accounting for gene-smoking interaction. Sci Rep. 2016;6:18812.

    CAS  Article  Google Scholar 

  50. Ng M, Fleming T, Robinson M, Thomson B, Graetz N, Margono C, Mullany EC, Biryukov S, Abbafati C, Abera SF, Abraham JP, Abu-Rmeileh NME, Achoki T, AlBuhairan FS, Alemu ZA, et al. Global, regional, and national prevalence of overweight and obesity in children and adults during 1980-2013: a systematic analysis for the global burden of disease study 2013. Lancet. 2014;384:766–81.

    Article  Google Scholar 

  51. Neter JE, Stam BE, Kok FJ, Grobbee DE, Geleijnse JM. Influence of weight reduction on blood pressure: a meta-analysis of randomized controlled trials. Hypertension. 2003;42:878–84.

    CAS  Article  Google Scholar 

  52. Grove ML, Morrison A, Folsom AR, Boerwinkle E, Hoelscher DM, Bray MS. Gene-environment interaction and the GNB3 gene in the atherosclerosis risk in communities study. Int J Obes. 2007;31:919–26.

    CAS  Article  Google Scholar 

  53. Smemo S, Tena JJ, Kim KH, Gamazon ER, Sakabe NJ, Gomez-Marin C, Aneas I, Credidio FL, Sobreira DR, Wasserman NF, Lee JH, Puviindran V, Tam D, Shen M, Son JE, et al. Obesity-associated variants within FTO form long-range functional connections with IRX3. Nature. 2014;507:371–5.

    CAS  Article  Google Scholar 

  54. Saad MF, Knowler WC, Pettitt DJ, Nelson RG, Mott DM, Bennett PH. Insulin and hypertension. Relationship to obesity and glucose intolerance in Pima Indians. Diabetes. 1990;39:1430–5.

    CAS  Article  Google Scholar 

  55. Spraul M, Ravussin E, Baron AD. Lack of relationship between muscle sympathetic nerve activity and skeletal muscle vasodilation in response to insulin infusion. Diabetologia. 1996;39:91–6.

    CAS  PubMed  Google Scholar 

  56. Huai P, Xun H, Reilly KH, Wang Y, Ma W, Xi B. Physical activity and risk of hypertension: a meta-analysis of prospective cohort studies. Hypertension. 2013;62:1021–6.

    CAS  Article  Google Scholar 

  57. Williamson W, Foster C, Reid H, Kelly P, Lewandowski AJ, Boardman H, Roberts N, McCartney D, Huckstep O, Newton J, Dawes H, Gerry S, Leeson P. Will exercise advice be sufficient for treatment of young adults with prehypertension and hypertension? A systematic review and meta-analysis. Hypertension. 2016;68:78–87.

    CAS  Article  Google Scholar 

  58. Pescatello LS, Franklin BA, Fagard R, Farquhar WB, Kelley GA, Ray CA, American college of sports M. American College of Sports Medicine position stand Exercise and hypertension. Med Sci Sports Exerc. 2004;36:533–53.

    Article  Google Scholar 

  59. Henriksen EJ. Effects of acute exercise and exercise training on insulin resistance. J Appl Physiol. 2002;93:788–96.

    CAS  Article  Google Scholar 

  60. Corry DB, Tuck ML. Glucose and insulin metabolism in hypertension. Am J Nephrol. 1996;16:223–36.

    CAS  Article  Google Scholar 

  61. Xi B, Cheng H, Shen Y, Zhao X, Hou D, Wang X, Mi J. Physical activity modifies the associations between genetic variants and hypertension in the Chinese children. Atherosclerosis. 2012;225:376–80.

    CAS  Article  Google Scholar 

  62. Pande J, Mallhi KK, Sawh A, Szewczyk MM, Simpson F, Grover AK. Aortic smooth muscle and endothelial plasma membrane Ca2+ pump isoforms are inhibited differently by the extracellular inhibitor caloxin 1b1. Am J Physiol Cell Physiol. 2006;290:C1341–9.

    CAS  Article  Google Scholar 

  63. Cuevas P, Carceller F, Gimenez-Gallego G. Fibroblast growth factors in myocardial ischemia / reperfusion injury and ischemic preconditioning. J Cell Mol Med. 2001;5:132–42.

    CAS  Article  Google Scholar 

  64. Xi B, Shen Y, Reilly KH, Wang X, Mi J. Recapitulation of four hypertension susceptibility genes (CSK, CYP17A1, MTHFR, and FGF5) in east Asians. Metabolism. 2013;62:196–203.

    CAS  Article  Google Scholar 

  65. Kim JY, Yadav D, Ahn SV, Koh SB, Park JT, Yoon J, Yoo BS, Lee SH. A prospective study of total sleep duration and incident metabolic syndrome: the ARIRANG study. Sleep Med. 2015;16:1511–5.

    Article  Google Scholar 

  66. Zaccardi F, Laukkanen T, Willeit P, Kunutsor SK, Kauhanen J, Laukkanen JA. Sauna bathing and incident hypertension: a prospective cohort study. Am J Hypertens. 2017;30:1120–5.

    Article  Google Scholar 

  67. Goyal A, Aslam N, Kaur S, Soni RK, Midha V, Chaudhary A, Dhaliwal LK, Singh B, Chhabra ST, Mohan B, Anand IS, Wander GS. Factors affecting seasonal changes in blood pressure in North India: a population based four-seasons study. Indian Heart J. 2018;70:360–7.

    Article  Google Scholar 

  68. Dong GH, Qian ZM, Xaverius PK, Trevathan E, Maalouf S, Parker J, Yang L, Liu MM, Wang D, Ren WH, Ma W, Wang J, Zelicoff A, Fu Q, Simckes M. Association between long-term air pollution and increased blood pressure and hypertension in China. Hypertension. 2013;61:578–84.

    CAS  Article  Google Scholar 

  69. Dasgupta K, Quinn RR, Zarnke KB, Rabi DM, Ravani P, Daskalopoulou SS, Rabkin SW, Trudeau L, Feldman RD, Cloutier L, Prebtani A, Herman RJ, Bacon SL, Gilbert RE, Ruzicka M, et al. The 2014 Canadian hypertension education program recommendations for blood pressure measurement, diagnosis, assessment of risk, prevention, and treatment of hypertension. Can J Cardiol. 2014;30:485–501.

    Article  Google Scholar 

  70. Howard G, Cushman M, Moy CS, Oparil S, Muntner P, Lackland DT, Manly JJ, Flaherty ML, Judd SE, Wadley VG, Long DL, Howard VJ. Association of clinical and social factors with excess hypertension risk in black compared with white US adults. JAMA. 2018;320:1338–48.

    Article  Google Scholar 

  71. Nierenberg JL, Li C, He J, Gu D, Chen J, Lu X, Li J, Wu X, Gu CC, Hixson JE, Rao DC, Kelly TN. Blood pressure genetic risk score predicts blood pressure responses to dietary sodium and potassium: the GenSalt study (genetic epidemiology network of salt sensitivity). Hypertension. 2017;70:1106–12.

    CAS  Article  Google Scholar 

  72. Warren HR, Evangelou E, Cabrera CP, Gao H, Ren M, Mifsud B, Ntalla I, Surendran P, Liu C, Cook JP, Kraja AT, Drenos F, Loh M, Verweij N, Marten J, et al. Genome-wide association analysis identifies novel blood pressure loci and offers biological insights into cardiovascular risk. Nat Genet. 2017;49:403–15.

    CAS  Article  Google Scholar 

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Acknowledgments

We thank Drs Motoki Iwasaki and Taiki Yamaji for the valuable discussions.

Funding

This study was supported by grants-in-aid from Scientific Research A (grant no.17H01557 for Yoshihiro Kokubo) and Challenging Exploratory Research (grant no.17K1987 for Yoshihiro Kokubo).

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YK and SP conceived and wrote the paper. YI, KY, and AG contributed to the writing of the manuscript. All authors have reviewed the final version of the manuscript and approved to submit to your journal.

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Kokubo, Y., Padmanabhan, S., Iwashima, Y. et al. Gene and environmental interactions according to the components of lifestyle modifications in hypertension guidelines. Environ Health Prev Med 24, 19 (2019). https://doi.org/10.1186/s12199-019-0771-2

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Keywords

  • Gene and environmental interaction
  • Hypertension
  • Lifestyle
  • Epidemiology
  • Hypertension guideline