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Salt sensitivity is an independent CVD and mortality risk factor, which is present in both hypertensive and normotensive populations. It is genetically determined and it may affect the relationship between salt taste perception and salt intake. The aim of this study was to explore the genetic predisposition to salt sensitivity in a young and a middle-aged adult population and its effects on salt taste perception and salt intake. The effects of Na loading on blood pressure (BP) were investigated in twenty normotensive subjects and salt sensitivity defined as the change in BP after 7 d of low-Na (51·3 mmol Na/d) and 7 d of high-Na diet (307·8 mmol Na/d). Salt taste perception was identified using the British Standards Institution sensory analysis method (BS ISO 3972:2011). Salt intake was assessed with a validated FFQ. DNA was genotyped for SNP in the SLC4A5, SCNN1B and TRPV1 genes. The subjects with AA genotype of the SLC4A5 rs7571842 exhibited the highest increase in BP (∆ systolic BP=7·75 mmHg, P=0·002, d=2·4; ∆ diastolic BP=6·25 mmHg, P=0·044, d=1·3; ∆ mean arterial pressure=6·5 mmHg, P=0·014, d=1·7). The SLC4A5 rs10177833 was associated with salt intake (P=0·037), and there was an association between salt taste perception and salt sensitivity (r s 0·551, P=0·041). In conclusion, there is a genetic predisposition to salt sensitivity and it is associated with salt taste perception. The association between salt taste perception and discretionary salt use suggests that preference for salty taste may be a driver of salt intake in a healthy population and warrants further investigation.

Sweet taste perception and preference play crucial roles in dietary habits and health outcomes. Understanding the genetic basis of taste thresholds and preferences can provide insights into individual differences in dietary behavior and susceptibility to metabolic disorders such as type 2 diabetes mellitus (T2DM). In Zambia, there is paucity of data concerning taste perception and preference in relation to genetics among diabetic and non-diabetic individuals. This study aimed to determine the relationship between the genotype and sweet taste thresholds, among individuals with and without T2DM in Zambia. A cross-sectional study was conducted among 89 adults at Livingstone University Teaching Hospital (42 non-diabetic and 47 diabetics). Saliva samples were used to determine the TRPV1 rs4790522, and TAS1R3 rs307355 genotype. We assessed sweet taste threshold and preference using a series of aqueous sucrose solutions. Demographic characteristics, anthropometrics, lifestyle factors, and dietary habits were collected using a structured questionnaire. Sweet taste threshold positively correlated with preferred concentration in both groups (p < 0.05). A higher proportion of PwT2D with elevated preferred sweet concentrations carried one or both homozygous risk alleles (77.8%, TT/AA). When compared to healthy controls, PwT2D had higher BMI, systolic and diastolic blood pressure, and pulse rate. They also exhibited higher taste thresholds but lower preferred concentrations, though this group was significantly older, potentially confounding results. These findings suggest taste perception and genetic variation may differ in PwT2D, highlighting the need for further research in Sub-Saharan African populations to inform personalized, cost-effective treatment strategies. However, studies with a larger sample size are required to validate our findings.

Salt impairs endothelial function and increases arterial stiffness independent of blood pressure. The mechanisms are unknown. Recent evidence suggests that there is a possible link between salt consumption and sodium buffering capacity and cardiovascular disease but there is limited evidence in the populations living in Sub-Saharan Africa. The aim of our study was to explore the relationship between erythrocyte sodium buffering capacity and sociodemographic, clinical factors, and self-reported salt consumption at Livingstone Central Hospital. We conducted a cross sectional study at Livingstone Central hospital among 242 volunteers accessing routine medical checkups. Sociodemographic and dietary characteristics were obtained along with clinical measurements to evaluate their health status. Sodium buffering capacity was estimated by erythrocyte sodium sensitivity (ESS) test. We used descriptive and inferential statistics to describe and examine associations between erythrocyte sodium sensitivity and independent variables. The median age (interquartile range) of the study sample was 27 (22, 42) years. 54% (n = 202) and 46% (n = 169) were males and females, respectively. The majority (n = 150, 62%) had an ESS of >120%. High salt intake correlated positively with ESS or negatively with vascular sodium buffering capacity. Self-reported high salt intake was associated with poor vascular sodium buffering capacity or high ESS in the majority of middle-aged Zambians living in Livingstone. The poor vascular sodium buffering capacity implies a damaged vascular glycocalyx which may potentially lead to a leakage of sodium into the interstitium. This alone is a risk factor for the future development of hypertension and cardiovascular disease. However, future studies need to validate vascular function status when using ESS testing by including established vascular function assessments to determine its pathophysiological and clinical implications.

Background/Objectives: Fat, a newly researched taste, has been associated with the cluster of differentiation 36 (CD36) gene, which codes for the CD36 receptor protein. The rs1761667 variant has been associated with fat taste sensitivity. Furthermore, umami is a well-established taste with known receptors. The combination of these tastes is common in food; nevertheless, they have not been extensively investigated together. This study aimed to assess whether CD36 rs1761667 is associated with food liking and the perception of fat and umami foods. Methods: Two studies were conducted: A field study on 235 individuals from Italy and a laboratory study on 49 individuals from the UK. Data includes demographics, anthropometrics, a food liking questionnaire or a fat and umami food flavour test, dietary intake assessment, and rs1761667 genotyping. Results: Study 1: The rs1761667 A-allele was associated with a reduced liking for fatty and umami foods in individuals with BMI ≥ 25. Study 2: The rs1761667 A-allele was associated with an increased intensity of the umami food samples, and a significant positive association of rs1761667 with BMI and DQS was found. Conclusions: This study is the first to address the potential links between rs1761667, fat, umami, diet, and BMI. Further research is required to confirm these findings.

Genotype-based dietary and physical activity advice can be delivered to young adults before unhealthy lifestyle behaviours or metabolic and physiological conditions have developed. The aim of the present study was to investigate the factors that influence the intention to adopt genotype-based personalised advice on diet and physical activity in young adults who perceive themselves to be a healthy weight versus those who perceive themselves to be overweight or obese. An online survey of 396 young adults (18–25 years) evaluated background factors (participant characteristics (including perception of body weight), psychological factors, belief composites) and constructs of the Theory of Planned Behaviour (TPB) related to the adoption of genotype-based personalised advice. The association between background factors and TPB constructs was assessed using multiple linear regression. The constructs of TPB predicted intention to adopt genotype-based personalised nutrition (P < 0.001, adj. R2 = 0.54; attitude: B = 0.24, subjective norm: B = 0.25, PBC: B = 0.45). Background factors including belief composites, health locus of control, gender, physical activity, and food choice motives of ‘health’, ‘price’, ‘familiarity’, ‘weight control’, and ‘convenience’ significantly added to models of TPB constructs related to the intention to adopt personalised advice (P < 0.05). The influence of background factors varied between TPB constructs and differed based on participants perception of their body weight. The study provides support for the use of the TPB in understanding the intention of young adults to adopt gene-based advice for dietary and physical activity behaviour. In addition to perceived body weight, the background factors identified should help to inform and modify the delivery of advice in behaviour change interventions that seek to use genotype-based personalised advice in young adult populations.

Background High dietary salt and a lack of reduced blood pressure (BP) at night (non-dipping) are risk factors for the development of hypertension which may result in end-organ damage and death. The effect of high dietary salt on BP in black people of sub-Saharan Africa living with HIV is not well established. The goal of this study was to explore the associations between salt sensitivity and nocturnal blood pressure dipping according to HIV and hypertension status in a cohort of adult Zambian population. Methods We conducted an interventional study among 43 HIV-positive and 42 HIV-negative adults matched for age and sex. Study participants were instructed to consume a low (4 g) dietary salt intake for a week followed by high (9 g) dietary salt intake for a week. Salt resistance and salt sensitivity were defined by a mean arterial pressure difference of ≤5 mmHg and ≥ 8 mmHg, respectively, between the last day of low and high dietary salt intervention. Nocturnal dipping was defined as a 10–15% decrease in night-time blood pressure measured with an ambulatory blood pressure monitor. Results The median age was 40 years for both the HIV-positive and the HIV-negative group with 1:1 male to female ratio. HIV positive individuals with hypertension exhibited a higher BP sensitivity to salt (95%) and non-dipping BP (86%) prevalence compared with the HIV negative hypertensive (71 and 67%), HIV positive (10 and 24%) and HIV-negative normotensive (29 and 52%) groups, respectively (p < 0.05). Salt sensitivity was associated with non-dipping BP and hypertension in both the HIV-positive and HIV-negative groups even after adjustment in multivariate logistic regression (< 0.001). Conclusions The results of the present study suggest that high dietary salt intake raises blood pressure and worsens nocturnal BP dipping to a greater extent in hypertensive than normotensive individuals and that hypertensive individuals have higher dietary salt intake than their normotensive counterparts. Regarding HIV status, BP of HIV-positive hypertensive patients may be more sensitive to salt intake and demonstrate more non-dipping pattern compared to HIV-negative hypertensive group. However, further studies with a larger sample size are required to validate this.

Introduction: Type 2 diabetes (T2D) is a leading cause of global mortality with diet and genetics being considered amongst the most significant risk factors. Recently, studies have identified a single polymorphism of the TCF7L2 gene (rs7903146) as the most important genetic contributor. However, no studies have explored this factor in a healthy population and using glycated haemoglobin (HbA1c), which is a reliable long-term indicator of glucose management. This study investigates the association of the genetic polymorphism rs7903146 and dietary intake with T2D risk in a population free of metabolic disease. Methods: T2D risk was assessed using HbA1c plasma concentrations and dietary intake via a validated Food Frequency Questionnaire in 70 healthy participants. Results: T allele carriers had higher HbA1c levels than the CC group (32.4 ± 7.2 mmol/mol vs. 30.3 ± 7.6 mmol/mol, p = 0.005). Multiple regression reported associations between diet, genotype and HbA1c levels accounting for 37.1% of the variance in HbA1c (adj. R 2 = 0.371, p < 0.001). The following macronutrients, expressed as a median percentage of total energy intake (TEI) in the risk group, were positively associated with HbA1c concentration: carbohydrate (≥39% TEI, p < 0.005; 95% CI 0.030/0.130) protein (≥21% TEI, p < 0.005, 95% CI 0.034/0.141), monounsaturated (≥15% TEI p < 0.05, 95% CI 0.006/0.163) and saturated fatty acids (≥13% TEI; p < 0.05, 95% CI 0.036/0.188). Conclusion: Carriers of the T allele showed significantly higher levels of HbA1c compared to non-carriers. Dietary intake affected T2D risk to a greater extent than genetic effects of TCF7L2rs7903146 genotype in a healthy population. The study focus on healthy individuals is beneficial due to the applicability of findings for T2D screening.

Background High blood pressure (BP) is associated with high-salt consumption especially in sub-Saharan Africa. Although the pressor effect of salt is viewed as a chronic effect, some studies suggest that a salty meal may increase BP immediately in some individuals, and that this effect may cause endothelial dysfunction. Therefore, the aim of our research was to study the immediate pressor response to oral salt (IPROS) and its determinants, with the expectation that a simple methodology may be devised to diagnose it in the clinic or in low-resource environments. Methods We conducted a time series trial at Livingstone Central Hospital. We present data in 127 normotensive participants who ingested 2 g of sodium chloride; their BP was monitored for 120 minutes in intervals of 10 minutes. Sociodemographic and clinical data were collected. Descriptive and inferential statistics were used for analyses of data. Results Median age was 30 years (interquartile range, 22–46 years) and 52% were female patients. An increase of ≥10 mmHg in mean arterial pressure (MAP), considered a clinically significant IPROS, was present in 62% of participants. Systolic BP 30 minutes after the salt load was a significant predictor of IPROS, avoiding the need to calculate MAP in the clinic setting. Conclusions We confirm the presence of an IPROS in a high proportion (62%) of otherwise normotensive participants. The average time course for this response was 30 minutes and its duration was sustained for the 120-minutes period of study in most of the participants. Prediction of IPROS by ∆SBP (change in systolic blood pressure) at 30 minutes allows for easy assessment of possible responder status in the clinic. Our data indicate that the IPROS to oral salt-loads in the range currently consumed by the Western world and African populations in single meals may increase the 24-hour BP load, which is a risk factor for hypertension and target organ damage. The relevance of our findings indicates the need to include dietary sodium assessment in the diagnosis, prevention, and management of high BP.

Hypertension is a major cause of cardiovascular disease and overall mortality. High dietary salt intake is one of the key risk factors for hypertension and in 2017, it was one of the three leading dietary risk factors for death and disability adjusted life years globally. Despite the efforts to change this behaviour, salt consumption still exceeds the recommendations. One of the main determinants of food intake, and potentially salt, is taste. Taste perception may be genetically determined, however research exploring the associations between genetics, salt taste perception and salt intake is scarce. This may be of special importance in younger adult populations where increased preference for salt is suggested. Therefore, the aim of this study was to explore the associations between genetics, salt taste perception (taste threshold and preference) and salt intake in young adults. This study was approved by the St Mary's University Ethics Sub-Committee. Forty-two participants (18–35 years, 67% female and 33% male) completed the study. Salt taste thresholds were identified using the British Standards Institution sensory analysis method (BS ISO 3972:2011) and preference for salty taste by asking participants how salty they usually prefer to eat their food using a Likert scale. Salt intake, expressed as mg sodium/1000 kcal, was measured using a five-step multiple pass 24-hour recall for one day of the week and one weekend day. Participants were genotyped for two genetic variants in the SCNN1B and TRPV1 genes, which code for ion channels expressed in taste cells. Multiple regression analysis was performed including SCNN1B and TRPV1 variants, salt taste threshold and preference as predictor variables and sodium intake (mg/1000 kcal) as the dependent variable. Statistical significance was set at p < 0.05. Participants were normal weight (Body Mass Index 23.8 ± 3.7 kg/m2), predominantly Caucasian with salt intake 7.5 ± 2.7 g per day, reflecting current intakes in the UK. Regression model including genetics, thresholds and preference for salty taste explained 54% of the variance (p = 0.028). In this model, TRPV1 variant rs8065080 [β = 422, confidence interval (50, 794), p = 0.030] and salt preference [β = 618, confidence interval (258, 978), p = 0.004] were indicated as predictors of sodium intake. These findings suggest that genetics and preference for salty taste may be drivers of salt intake in younger populations. If replicated, this information may in the future be used in designing more personalised approaches in changing this behaviour.

Purpose of ReviewTo provide a summary of current literature and propose potential mechanistic models to help us understand the role of HIV infection/antiretroviral therapy (ART), salt taste sensitivity (STS), and salt sensitivity of blood pressure (SSBP) in hypertension development.Recent FindingsThe epithelial sodium channel (ENaC) is the main protein/sodium channel for recognizing Na + in the tongue and mediates preference to low-medium salt concentrations in animals and humans. Considering the pressor response to oral salt in individuals with SSBP, poor STS may worsen blood pressure. Specific genetic variants in ENaC are linked to salt taste perception and hypertension. HIV infection, some ART, and specific antihypertensive drugs are associated with reduced STS and an increased liking for salty foods.SummaryPersons with HIV (PWH) on ART may have a decreased STS and are at a higher risk of developing salt-sensitive hypertension. Inflammation mediated by dietary salt is one of the drivers of poor STS and salt-sensitive hypertension among PWH.