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Background/Objectives: The TAS1R2 SNP rs35874116 has previously been associated with sweet taste, diet, and health status, although never comprehensively in a single study. Also, associations between TAS1R2 and sweet taste might be body mass index (BMI)-dependent. Therefore, this study aimed to conduct a comprehensive investigation of rs35874116 and sweet taste intensity and liking, food liking, and diet and health status whilst considering BMI. Methods: Five-hundred and fifty-four participants were recruited. Linear regression models were used to explore rs35874116 associations with sweet taste intensity and liking, food liking, and diet and health status. A secondary analysis stratified participants by BMI <25/≥25 kg/m2. Results: The rs35874116 wildtype was associated with increased sweet taste intensity (p = 0.0345, B 1.29, SE 0.61) and liking (p = 0.021, B 0.25, SE 0.11). However, these associations only remained in BMI ≥25 individuals (intensity: p = 0.037, B 1.29, SE 0.61, liking: p = 0.008, B 0.46, SE 0.17). It was also associated with decreased diet quality (p = 0.03, B −0.27, SE 0.13) and reduced free sugar consumption but increased saturated fat consumption in BMI ≥25 individuals (free sugars: p = 0.0416, B −0.8, SE 0.38, saturated fat: p = 0.031, B 1.38, SE 0.62). There was no association with the mean liking score for sweet foods, although there were some associations with individual foods, which require further investigation. There were no associations with health status. Conclusions: This study revealed an association between the rs35874116 wildtype and an increased intensity and liking of the sweet taste and a corresponding worse overall dietary quality. This study adds to previous evidence regarding how associations between TAS1R2 and sweet taste are BMI-dependent. [ABSTRACT FROM AUTHOR]

The prevalence of obesity continues to rise, and public health dietary recommendations are not being adhered to. The transition to higher education is a period of risk for weight gain in young adults and has been demonstrated as a good time to initiate behaviour change. A genotype‐based personalised approach to dietary recommendations may motivate young adults to maintain or adopt positive dietary behaviours. The aim of the present study was to determine the efficacy of genotype‐based personalised dietary and physical activity advice on healthy eating motivation in young adults. Participants were young adults (n = 153), aged 18–25 years. Baseline measures (participant characteristics, height, weight, body mass index [BMI], body fat percentage [BF%], healthy eating motivation and physical activity) were collected. Participants were genotyped for a SNP in the FTO gene (rs99396090) and randomly allocated (stratified for genotype) to three different groups (1. Genotype‐based personalised advice: dietary and physical activity advice based on genotype, BMI and reported physical activity; 2. Non‐genotype‐based personalised advice: dietary and physical activity advice based on BMI and reported physical activity; 3. Control: no advice). A week after receipt of advice delivered via email, participants completed the healthy eating motivation questionnaire for a second time. Genotype‐based personalised dietary advice did not affect healthy eating motivation: when participants were analysed across the whole group (p = 0.417), when analysed according to those informed of a risk or non‐risk‐associated genotype (p = 0.287), or when analysed according to those with a BMI (>25 kg/m2; p = 0.336) or BF% (male >18%, female >31%; p = 0.387) outside the healthy range. There was also no significant difference in healthy eating motivation at 1‐week in the control or non‐genotype‐based advice groups. Genotype‐based personalised advice for the prevention of obesity did not affect healthy eating motivation in this group of healthy, young adults. [ABSTRACT FROM AUTHOR]

Background: Type 2 diabetes is a chronic disease that has severe individual and societal consequences, which is forecast to worsen in the future. A new field of investigation is variations in circadian rhythm genes, in conjunction with diet and sleep variables, associations with, and effects on, type 2 diabetes development. Objective: This systematic review aimed to analyse all current literature regarding circadian rhythm gene variations and type 2 diabetes, and explore their interplay with diet and sleep variables on type 2 diabetes outcomes. This review was registered with PROSPERO (CRD42021259682). Methodology: Embase and Pubmed were searched on 6/8/2021/11/8/2021 for studies of all designs, including participants from both sexes, all ethnicities, ages, and geographic locations. Participants with risk alleles/genotypes were compared with the wildtype regarding type 2 diabetes outcomes. Studies risk of bias were scored according to the risk of bias in non-randomised studies – interventions/exposures criteria. Results: In total, 31 studies were found (association n = 29/intervention n = 2) including >600,000 participants from various ethnicities, sexes, and ages. Variations in the melatonin receptor 1B, brain and muscle arnt-like 1 and period circadian regulator (PER) genes were consistently associated with type 2 diabetes outcomes. Conclusions: Individuals with variations in melatonin receptor 1B, brain and muscle arnt-like 1 and PER may be at higher risk of type 2 diabetes. Further research is needed regarding other circadian rhythm genes. More longitudinal studies and randomised trials are required before clinical recommendations can be made. [ABSTRACT FROM AUTHOR]

Context Although the stimulant and anxiogenic properties of caffeine are widely accepted, research on its specific effects on the brain remains controversial. Growing evidence shows that interindividual differences in caffeine response may be partly due to variations in genes such as CYP1A2 and ADORA2A, which have been used to identify individuals as "fast" or "slow" caffeine metabolizers and as having a "high" or "low" caffeine sensitivity, respectively. Objective The objective of this review was to identify, evaluate, and discuss current evidence on the associations between common genetic variants, caffeine consumption, and brain-related outcomes in humans. Data Sources PubMed and Embase databases were searched for relevant reports based on a predetermined search strategy. Data Extraction Reports of observational and experimental studies on healthy adults who underwent (a) genetic analysis for polymorphisms in genes associated with caffeine metabolism and effects and (b) measurements of brain-related effects such as anxiety, insomnia, and cognitive performance associated with the consumption of caffeine (habitual intake or supplementation) were included. Data Analysis Of the 22 records included, 15 were randomized controlled trials, 6 were cross-sectional studies, and 1 was a genome-wide association study. The main outcomes identified were cognitive performance (n = 9), anxiety (n = 7), and sleep disturbance/insomnia (n = 6). Polymorphisms in the CYP1A2 gene were associated with cognitive function, while variations in the ADORA2A gene were associated with anxiety and sleep disturbance. Conclusion The present review has provided evidence that variability in the CYP1A2 and the ADORA2A genes may modulate the association between caffeine and brain-related outcomes. Future studies are warranted to investigate the specific polymorphisms implicated in each brain outcome, which cognitive functions are particularly related to caffeine (simple vs complex), whether there are gender differences in anxiety effects, and how habitual caffeine intake may influence the acute effects of caffeine. Systematic review registration PROSPERO registration no. CRD42021257556. [ABSTRACT FROM AUTHOR]

Background: Severe obesity (body mass index ≥ 40 kg/m2) and non-communicable diseases, both influenced by diet, have been associated with COVID-19. Genotype-based personalised nutrition advice may improve nutrition knowledge and enhance behaviour change towards better diet quality compared with conventional recommendations. Aim: To investigate the nutrition knowledge, food choices and diet quality in genotyped and non-genotyped individuals during the COVID-19 pandemic. Methods: One hundred and twenty-three healthy UK adults were recruited using convenience sampling through social networks. The online questionnaire consisted of the General Nutrition Knowledge Questionnaire, the Food Choices Questionnaire, and the EPIC-Norfolk Food Frequency Questionnaire (FFQ). FFQ was used to calculate participant diet quality with the Diet Quality Index-International and socio-demographic and anthropometric data. Results: Median general nutrition knowledge, diet variety and diet balance scores were higher in genotyped compared with non-genotyped individuals (71.0 ± 11.0 vs. 61.0 ± 15.0, p = <.001, 18.00 ± 5.00 vs. 15.00 ± 5.00, p =.007 and 2.00 ± 4.00 vs. 0.00 ± 2.00, p =.025, respectively). Pooled sample multiple regression showed that health motive positively influenced while familiarity motive negatively influenced diet quality index scores (β =.428, t = 4.822, p = <.001 and β = –.356, t = –4.021, p =.001, respectively). Conclusions: Nutrition knowledge and diet quality indices of balance and variety were higher among genotyped compared with non-genotyped individuals; overall diet quality was similar between groups. This may be due to pandemic-specific factors, such as altered motives of food choice and availability. [ABSTRACT FROM AUTHOR]

Background: Dietary intake is linked to numerous modifiable risk factors of cardiovascular disease. Current dietary recommendations in the UK to reduce the risk of cardiovascular disease are not being met. A genotype-based personalised approach to dietary recommendations may motivate individuals to make positive changes in their dietary behaviour. Aim: To determine the effect of a personalised nutrition intervention, based on apolipoprotein E (ApoE, rs7412; rs429358) and methylenetetrahydrofolate reductase (MTHFR, rs1801133) genotype, on reported dietary intake of saturated fat and folate in participants informed of a risk genotype compared to those informed of non-risk genotype. Methods: Baseline data (n = 99) were collected to determine genotype (non-risk vs risk), dietary intake and cardiovascular risk (Q-Risk®2 cardiovascular risk calculator). Participants were provided with personalised nutrition advice via email based on their ApoE and MTHFR genotype and reported intake of folate and saturated fat. After 10 days, dietary intake data were reported for a second time. Results: Personalised nutrition advice led to favourable dietary changes, irrespective of genotype, in participants who were not meeting dietary recommendations at baseline for saturated fat (p < 0.001) and folate (p = 0.002). Only participants who were informed of a risk ApoE genotype met saturated fat recommendations following personalised nutrition advice. Conclusion: Incorporation of genotype-based personalised nutrition advice in a diet behaviour intervention may elicit favourable changes in dietary behaviour in participants informed of a risk genotype. Participants informed of a non-risk genotype also respond to personalised nutrition advice favourably but to a lesser extent. [ABSTRACT FROM AUTHOR]

To investigate the cardiovascular risks associated with red and/or processed meat intake in a large population-based cohort study in Iran. A total of 5432 participants from the Isfahan Cohort Study (ICS) were enrolled. Diet was assessed using a validated, 48-item food frequency questionnaire. Cox proportional hazards regression models were applied to calculate hazard ratios (HRs) for the CVD risk associated with red and processed meat intake. Median follow-up was 11.2 years. Compared to the first tertile, the highest tertile of red meat intake, either alone or in combination with processed meat was associated with a 50% reduced risk of stroke (95% CI: 0.31–0.77; 95% CI: 0.33–0.82, respectively), but increased risk of CVD mortality with corresponding HRs of 1.58 (95% CI: 1.06–2.35) and 1.47 (95% CI: 1.02–2.08), respectively. Red meat and red plus processed meat intake were inversely associated with stroke risk, but positively linked with CVD mortality. [ABSTRACT FROM AUTHOR]

A relationship between bitter and fat taste sensitivity, CD36 rs1761667 and TAS2R38 has been demonstrated. However, research is scarce and does not take diet into account. This study aimed to explore associations between genetics, fat and bitter taste sensitivity and dietary fat intake in healthy UK adults. A cross-sectional study was carried out on 88 Caucasian participants (49 females and 39 males aged 35 ± 1 years; body mass index 24.9 ± 0.5 kg/m2). Bitter taste sensitivity was assessed using phenylthiocarbamide (PTC) impregnated strips and the general Labeled Magnitude Scale. Fat taste sensitivity was assessed by the Ascending Forced Choice Triangle Procedure and dietary intake with a semi-quantitative food frequency questionnaire. Genotyping for rs713598, rs1726866, rs10246939, and rs1761667 was performed. Participants with TAS2R38 PAV/PAV diplotype perceived PTC strips as more bitter than groups carrying AVI haplotypes (AVI/AVI, P = 1 × 10−6; AVI/AAV, P = 0.029). CD36 rs1761667 was associated with fat taste sensitivity (P = 0.008). A negative correlation between bitter taste sensitivity and saturated fat intake was observed (r s = −0.256, P = 0.016). When combining the CD36 genotypes and TAS2R38 diplotypes into one variable, participants carrying both TAS2R38 AVI haplotype and CD36 A allele had a higher intake of saturated fat compared to carriers of CD36 GG genotype or TAS2R38 PAV/PAV and PAV/AAV diplotypes (13.8 ± 0.3 vs. 12.6 ± 0.5%TEI, P = 0.047) warranting further exploration in a larger cohort. [ABSTRACT FROM AUTHOR]

Research on caffeine and cognitive performance remains controversial. Variations in genes associated with caffeine metabolism and response such as CYP1A2, AHR and ADORA2A may account for variable findings.To investigate caffeine × gene interactions on cognitive performance in all key domains of cognition in healthy individuals.Participants completed a lifestyle and food frequency questionnaire and a cognitive test battery including validated tasks to assess the domains of social cognition, memory, attention and executive function. Genotyping was performed for AHR rs6968554, CYP1A2 rs2472297, ADORA2A rs5751876, ADA rs73598374 and APOE rs429358 and rs7412.Significant gene × caffeine interactions were observed for the domains of social cognition, (F2, 123 = 5.848, p = 0.004) and executive function (F2, 109 = 3.690, p = 0.028). ‘Slow’ metabolisers had a higher performance in social cognition compared with ‘fast’ metabolisers among high-caffeine consumers (p = 0.004), while ‘fast’ metabolisers had a higher performance in executive function compared with ‘slow’ metabolisers among moderate caffeine consumers (p = 0.002).The present findings suggest an association between genetic caffeine metabolism, habitual caffeine intake and cognitive function in the domains of social cognition and executive function. More research in naturalistic environments using larger cohorts is needed to confirm these findings to add to our understanding of how habitual caffeine may influence cognitive function based on individual genotype. [ABSTRACT FROM AUTHOR]