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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]

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]

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]

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. [ABSTRACT FROM AUTHOR]

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.