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Genetic predisposition to salt sensitivity and its effects on dietary salt taste perception and intake

Published online by Cambridge University Press:  24 November 2016

L. Pilic  and
Y. Mavrommatis
L. Pilic
Affiliation:
School of sport, health and applied science, St Mary's University Twickenham TW1 4SX, UK
Y. Mavrommatis
Affiliation:
School of sport, health and applied science, St Mary's University Twickenham TW1 4SX, UK
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Abstract

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Hypertension is one of the leading causes of cardiovascular diseases worldwide. It is largely a modifiable risk factor with dietary salt being one of the main contributors. Blood pressure (BP) response to dietary salt intake is not homogenous across population. This phenomenon is called salt sensitivity. Single nucleotide polymorphism (SNP) rs7571842 of the sodium-bicarbonate co-transporter (SLC4A5) gene has been particularly associated to salt sensitivity in Caucasian population, with A being the risk allele(Reference Carey, Schoeffel and Gildea1). In addition, genetic predisposition may affect dietary intake by altering taste perception(Reference Dotson, Babich and Steinle2). The aim of this ongoing study is to investigate whether genetic predisposition to salt sensitivity is associated to altered salt taste thresholds and habitual dietary salt intake.

To date, 13 participants (4 males, 9 females) have completed the study protocol. Salt taste detection (STDT) and recognition thresholds (STRT) were identified at baseline, using British Standards Institution (BSI) sensory analysis method (BS ISO 3972:2011). Habitual dietary salt intake was assessed with validated food frequency questionnaire (FFQ). DNA was extracted from stabilised saliva samples and genotyped using TaqMan® genotyping assay ID: C_197439_10 (Applied Biosystems, USA). Salt sensitivity was defined as the difference in mean arterial pressure (MAP) and systolic blood pressure (SBP) between 7-day low-salt (51·3 mmol/day sodium) and 7-day high-salt (307·8 mmol/day) diet. Dietary compliance was assessed based on 24-hour urinary sodium, potassium and creatinine excretion.

Fig. 1.

Example of an allelic discrimination plot for the SNP rs7571842 in the study population

BMI, Body mass index; DBP, Diastolic blood pressure

There was no difference in SBP (Fig. 2) or MAP (data not shown) response to dietary intervention between rs7571842 genotype groups. There was no correlation between salt sensitivity of BP, salt taste thresholds and habitual salt intake (data not shown) or a difference in salt taste thresholds and dietary salt intake between rs7571842 genotypes. In conclusion, genetic variation in the SLC4A5 gene is not associated to altered salt taste perception or intake.

Fig. 2.

SBP response to each diet by genotype status (participants with incomplete urinary samples excluded from the analysis)

References

1.Carey, RM, Schoeffel, CD, Gildea, JJ et al. (2012) Hypertension 60, 1359–66.10.1161/HYPERTENSIONAHA.112.196071Google Scholar
2.Dotson, CD, Babich, J, Steinle, NI (2012) Curr Nutr Rep, 1, 175–183.Google Scholar
Figure 0

Fig. 1. Example of an allelic discrimination plot for the SNP rs7571842 in the study population

Figure 1

Fig. 2. SBP response to each diet by genotype status (participants with incomplete urinary samples excluded from the analysis)