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Title: Clock genes explain large proportion of phenotypic variance in systolic blood pressure and this control is not modified by environmental temperature

Author
item DASHTI, HASSAN - Jean Mayer Human Nutrition Research Center On Aging At Tufts University
item ASLIBEKYAN, STELLA - University Of Alabama
item SMITH, CAREN - Jean Mayer Human Nutrition Research Center On Aging At Tufts University
item LAMON-FAVA, STEFANIA - Jean Mayer Human Nutrition Research Center On Aging At Tufts University
item Lai, Chao Qiang
item ARNETT, DONNA - University Of Alabama
item SCHEER, FRANK - Harvard University
item JACQUES, PAUL - Jean Mayer Human Nutrition Research Center On Aging At Tufts University
item TUCKER, KATHERINE - University Of Massachusetts
item ORDOVAS, JOSE - Jean Mayer Human Nutrition Research Center On Aging At Tufts University

Submitted to: American Journal of Hypertension
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 5/13/2015
Publication Date: 1/1/2016
Citation: Dashti, H., Aslibekyan, S., Smith, C.E., Lamon-Fava, S., Lai, C., Arnett, D.K., Scheer, F., Jacques, P.F., Tucker, K.L., Ordovas, J.M. 2016. Clock genes explain large proportion of phenotypic variance in systolic blood pressure and this control is not modified by environmental temperature. American Journal of Hypertension. 29(1):132-140.

Interpretive Summary: Daily fluctuations in human blood pressure (BP) are known to be regulated by the human internal clock, however few studies have shown associations between clock genes regulating the human internal clock and BP. In addition, BP also shows seasonal variation as a result of fluctuations in environmental temperature. Therefore, we are first interested in examining whether seasonal variation in temperature influences BP in two population-based cohorts, Genetics of Lipid Lowering Drugs and Diet Network (GOLDN) and the Boston Puerto Rican Health Study (BPRHS) cohorts. Next, we are interested in investigating whether clock genes (a total of 18 genes involved in controlling the human internal clock) also play a role in differences in BP. In the GOLDN population, we observed that each additional 1 degree C increase in environmental temperature was associated with 0.18 mm Hg lower systolic and 0.10 mm Hg lower diastolic BP. Similar results were seen in the BPRHS for systolic BP only. In addition, we observed that clock genes explained some of the observed differences in systolic BP in GOLDN, but not in the BPRHS. The role of clock genes in influencing BP was not influenced by seasonal variation in environmental temperature. In conclusion, we identified that the genes involved in regulating the human internal clock also influences systolic BP. Also, although differences in BP were observed across seasons with different environmental temperatures, the link between clock genes and BP was still observable across seasons.

Technical Abstract: BACKGROUND: Diurnal variation in blood pressure (BP) is regulated, in part, by an endogenous circadian clock; however, few human studies have identified associations between clock genes and BP. Accounting for environmental temperature may be necessary to correct for seasonal bias. METHODS: We examined whether environmental temperature on the day of participants assessment was associated with BP, using adjusted linear regression models in the Genetics of Lipid Lowering Drugs and Diet Network (GOLDN) (n=819) and the Boston Puerto Rican Health Study (BPRHS) (n=1,248) cohorts. We estimated phenotypic variance in BP by 18 clock genes and examined individual single- nucleotide polymorphism (SNP) associations with BP using an additive genetic model, with further consideration of environmental temperature. RESULTS: In GOLDN, each additional 1 degree C increase in environmental temperature was associated with 0.18mm Hg lower systolic BP [SBP; beta +/- SE= -0.18 +/- 0.05mm Hg; P=0.0001] and 0.10mm Hg lower diastolic BP [DBP; -0.10 +/- 0.03mm Hg; P=0.001]. Similar results were seen in the BPRHS for SBP only. Clock genes explained a statistically significant proportion of the variance in SBP [VG/VP +/- SE=0.071 +/- 0.03; P=0.001] in GOLDN, but not in the BPRHS, and we did not observe associations between individual SNPs and BP. Environmental temperature did not influence the identified genetic associations. CONCLUSIONS: We identified clock genes that explained a statistically significant proportion of the phenotypic variance in SBP, supporting the importance of the circadian pathway underlying cardiac physiology. Although temperature was associated with BP, it did not affect results with genetic markers in either study. Therefore, it does not appear that temperature measures are necessary for interpreting associations between clock genes and BP.