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.

Background: Sweet taste is partly modified by genetics. The rs35874116 single-nucleotide polymorphism (SNP) in taste receptor type 1 member 2 (TAS1R2) reduces the availability of a G protein-coupled receptor (GPCR), which binds to 'sweet' molecules. This might alter sweet taste perception, diet choices, and health outcomes. However, these findings, and other genes and pathways involved in sweet taste are yet to be identified. Therefore, a candidate gene study on TAS1R2 and a genome-wide association study (GWAS) exploring these outcomes were performed. Methods: TAS1R2 rs35874116, sweet perception, liking, diet, and health were investigated in two age- and sex-matched European cohorts (UK, n = 50/Italy, n = 235). Linear models were used to explore associations. The GWAS was performed with 2555 Italian participants. Associations with sweet food liking, food adventurousness (FA), reward dependence (RD), and health were explored. Results: The wildtype of TAS1R2 was associated with increased sweet taste and food liking (p = 0.049, β = 0.62, p = 0.038, β = 0.45), increased fibre consumption (p = 0.006, β = 7.95), and decreased HDL cholesterol (p = 0.025, β = −3.56). The GWAS identified rs58931966 in the regulator of G-protein signalling 9 (RGS9) gene. The minor allele was associated with decreased sweet food liking (p = 7.05 × 10 – 9, β = 0.3), a higher BMI (p = 0.007, β = 0.391), serum glucose (p = 0.013, β = 1.211), lower FA (p = 0.049, β = −0.065), and RD (p = 0.011, β = −3.840). Discussion: The TAS1R2 results show that taste receptor variations are associated with preference, diet, and health-related outcomes. TAS1R2 not reaching significance in the GWAS shows that sweet food liking is modified by pathways besides taste reception. RSG9 is expressed in the striatum, which is involved in the mesolimbic reward pathway, which is activated by sweet taste. RGS9 rs58931966 may moderate dopaminergic signalling in response to sweet foods via the negative regulation of G-protein signalling. This might explain why the minor allele was associated with reduced RD. The lower FA might decrease preference for bitter-tasting vegetables, which could explain the higher BMI and serum glucose. The FA and RD results provide evidence that food choice depends on psychological/biological interplay. These results show that sweet taste is modified by multiple pathways and genes, and variations can modify taste, diet, and health outcomes.

Unsaturated fatty acids (FAs) can influence various aspects of human biology (e.g., the immune system), and an excess of saturated fatty acids is associated with non-communicable diseases. The orosensory perception of FAs has been demonstrated and debated as a possible sixth taste. The Cluster of Differentiation 36 (CD36) gene codes for a membrane protein apically located in taste bud cells, which is considered a possible fat taste mediator. The single nucleotide polymorphism (SNP) rs1761667 (G>A) is associated with a reduced protein expression, possibly leading to fat taste hyposensitivity, but the results are controversial. Here, we investigate, in two European cohorts, rs1761667’s role on taste perception, food liking as an intake determinant, and diet-related traits. We analysed two cohorts from the UK (n = 49; 63% female) and Italy (Friuli Venezia Giulia (FVG); n = 235; 54% female). Data collected were taste perception and liking via actual foodstuffs in the UK; food liking, as evaluated by a questionnaire, in FVG; the rs1761667 genotype; and BMI as an indicator of non-communicable diseases. The effect of the SNP on the considered phenotypes was evaluated using linear regression models. In the UK, A-allele carriers showed higher perceived intensity (β = 0.99; p = 0.02) and reduced liking, although not significant (β = −0.30), from fat food sample; in the FVG cohort, we replicated the negative association between A-allele carriers and fat liking, specifically for “gorgonzola” cheese (β-value = −0.82; p = 0.03). These results align with the negative relationship seen between fat intensity and liking (cor = −0.2). Regarding other tastes, we found that A-allele carriers (UK) showed higher umami food perceived intensity (β-value = 0.89; p = 0.02) and reduced liking (FVG) for an umami food (“soy sauce”) (β value = −0.97; p = 0.02). Similarly, in the UK, the relationship between umami intensity and liking was negative (cor = −0.32). Considering effects on health status, we found that A-allele carriers (UK) showed an increased BMI (β-value = 2.02; p = 0.02). Our results show that the A-allele is associated with an increased perceived intensity and a decreased liking for fatty foods. In addition, a novel association was found between umami perception/liking and rs1761667. Further research is required to elucidate these observations and the possible effects on taste perception and dietary intake.

Prisoners experience a higher burden of poor health, aggressive behaviours and worsening mental health than the general population. This systematic review aimed to identify research that used nutrition-based interventions in prisons, focusing on outcomes of mental health and behaviours. The systematic review was registered with Prospective Register of Systematic Reviews on 26 January 2022: CRD42022293370. Inclusion criteria comprised of current prisoners with no limit on time, location, age, sex or ethnicity. Only quantitative research in the English language was included. PubMed/Medline, Web of Science, EMBASE, PsycINFO and CINAHL were searched, retrieving 933 results, with 11 included for qualitative synthesis. Studies were checked for quality using the revised tool to assess risk of bias in randomised trials or risk of bias in non-randomised studies of interventions tool. Of the included studies, seven used nutritional supplements, three included diet changes, and one used education. Of the seven supplement-based studies, six included rule violations as an outcome, and only three demonstrated significant improvements. One study included mental health as an outcome; however, results did not reach significance. Of the three diet change studies, two investigated cognitive function as an outcome, with both reaching significance. Anxiety was included in one diet change study, which found a significant improvement through consuming oily fish. One study using diet education did not find a significant improvement in overall mental resilience. Overall, results are mixed, with the included studies presenting several limitations and heterogeneity. Future research should aim to consider increased homogeneity in research design, allowing for a higher quality of evidence to assess the role nutrition can play in improving the health of prisoners.

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.

Objective: This study aimed to assess and comparatively analyse two menus from a Young Offenders Institution (YOI). One menu from 2019, and one from 2022, with the objective of identifying any improvements in meeting dietary guidelines. Design: Cross-sectional and comparative analysis. Setting: United Kingdom, a YOI in Northern England. Participants: YOI Menus. Results: Analysis of 30 dietary components identified that 25 exceeded the dietary guidelines (P < 0.05) for the 2022 menu, with five failing to meet the guidelines (P < 0.05). When compared to the 2019 menu, the 2022 menu showed improvements in saturated fat, sodium, and vitamin D. Despite the improvement, vitamin D levels remained below dietary guidelines (P < 0.01). Salt and energy content were reduced in the 2022 menu (P < 0.05); however, they were still above the dietary guidelines (P < 0.01). Free sugars were significantly above dietary guidelines for both menus, with no significant change between the 2019 and 2022 menu (P = 0.12). Conclusion: The 2022 menu has demonstrated progress in alignment with meeting dietary guidelines, particularly in reducing calories, fat, saturated fat, salt, sodium, and chloride, as well as increasing vitamin D. Despite improvements, calories, free sugars, salt, saturated fat, sodium, and chloride are still exceeding dietary guidelines, posing as potential health risks.

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.

Genetics plays an important role in individual differences in food liking, which influences food choices and health. Sweet food liking is a complex trait and has been associated with increased body mass index (BMI) and related comorbidities. This genome-wide association study (GWAS) aimed to investigate the genetics of sweet food liking using two adult discovery cohorts (n = 1109, n = 373) and an independent replication cohort (n = 1073). In addition, we tested the association of our strongest result on parameters related to behaviour (food adventurousness (FA) and reward dependence (RD) and health status (BMI and blood glucose). The results demonstrate a novel strong association between the Regulator of G-Protein Signalling 9 (RGS9I) gene, strongest single nucleotide polymorphism (SNP) rs58931966 (p-value 7.05 × 10−9 in the combined sample of discovery and replication), and sweet food liking, with the minor allele (A) being associated with a decreased sweet food liking. We also found that the A allele of the rs58931966 SNP was associated with decreased FA and RD, and increased BMI and blood glucose (p-values < 0.05). Differences were highlighted in sex-specific analysis on BMI and glucose. Our results highlight a novel genetic association with food liking and are indicative of genetic variation influencing the psychological–biological drivers of food preference. If confirmed in other studies, such genetic associations could allow a greater understanding of chronic disease management from both a habitual dietary intake and reward-related perspective.

Objective In 2021, centres across all seven NHS-England regions were selected to develop pilot clinics with the aim of treating children and young people (CYP) living with complications relating to excess weight (CEW). We led a process to develop core outcomes to enable the evaluation of these clinics. Methods A two-round Delphi process, virtual steering group meetings and two patient representation workshops were used to agree the most important outcomes for both clinicians/allied professionals and representative prospective service users. Results A total of 119 clinicians/allied professionals were invited to contribute to the Delphi process: 62 (52%) agreed and completed round 1 and 47 of these (76%) went on to complete round 2. Six young people (age range 13-17 years) and six parents were involved in two patient representation workshops and their experiences fed into virtual steering group meetings, via a representative. There were 44 outcomes assessed in round 1 and 21 outcomes assessed in round 2. There were 16 core outcomes selected: anthropometric, glucose tolerance/insulin resistance/type 2 diabetes, blood pressure, lipid profile, breathing problems, identification of aetiology, non-alcoholic fatty liver disease, idiopathic intracranial hypertension, anxiety, depression, self-esteem, quality of life, school attendance, dietary habits including disordered eating, exercise and activity habits. Conclusions Use of an online Delphi process, patient representation workshops and virtual steering group meetings has enabled the development of core outcomes for clinical obesity services with eight physical health, five mental health and three self-management outcomes. Further work is needed to develop outcome measures to complete a core outcome set. These will be used to guide the evaluation of novel regional clinics for the treatment of complications of excess weight.

Context Despite clear evidence that adherence to dietary and physical activity advice can reduce the risk of cardiometabolic disease, a significant proportion of the population do not follow recommendations. Personalized advice based on genetic variation has been proposed for motivating behavior change, although research on its benefits to date has been contradictory. Objective To evaluate the efficacy of genotype-based dietary or physical activity advice in changing behavior in the general population and in individuals who are at risk of cardiovascular disease (CVD) or type II diabetes mellitus (T2DM). Data Sources MEDLINE, EMBASE, PsycInfo, and the Cochrane Central Register of Controlled Trials (CENTRAL) were searched up to January 7, 2022. Randomized controlled trials of a genotype-based dietary and/or physical activity advice intervention that aimed to change dietary and/or physical activity behavior were included. Data Extraction Abstracts of 7899 records were screened, and 14 reports from 11 studies met the inclusion criteria. Data Analysis Genotype-based dietary or physical activity advice was found to have no effect on dietary behavior in any of the studies (standardized mean difference [SMD] .00 [-.11 to .11], P = .98), even when analyzed by subgroup: "at risk" (SMD .00 [-.16 to .16, P = .99]; general population (SMD .01 [-.14 to .16], P = .87). The physical activity behavior findings were similar for all studies (SMD -.01 [-.10 to .08], P = .88), even when analyzed by subgroup: "at risk" (SMD .07 [-.18 to .31], P = .59); general population (SMD -.02 [-.13 to .10], P = .77). The quality of the evidence for the dietary behavior outcome was low; for the physical activity behavior outcome it was moderate. Conclusions Genotype-based advice does not affect dietary or physical activity behavior more than general advice or advice based on lifestyle or phenotypic measures. This was consistent in studies that recruited participants from the general population as well as in studies that had recruited participants from populations at risk of CVD or T2DM. Systematic Review Registration PROSPERO registration no. CRD42021231147.

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.

Aims The NHS Long Term Plan (2019) committed to treat a further 1,000 children a year for severe complications related to their obesity in order to prevent children going on to require more invasive treatment in future. The objectives of this work were to: • Explore the evidence base to support the development of a framework outlining the ideal model of care for treating children and young people (CYP) with comorbidities related to severe obesity; • Develop clinics across England to meet the Long Term Plan commitment of treating 1,000 extra children a year; • Develop a core outcome set of metrics to develop the evidence base around the patient demographic and understand what works in terms of service provision. Methods From 2019 – 2021, a literature review of tier 3 weight management services was conducted in order to better understand the existing evidence-base for optimal service design. In areas where the evidence base was weak, subject matter experts were consulted. Existing commissioning arrangements for obesity services across the whole patient pathway (tier 1 to 4) were mapped. Finally, a national Delphi process was run amongst three stakeholder groups (physical health, mental health and patient voice) in order to seek consensus regarding a core outcome set. Results In 2021, a Framework for clinics to treat complications related to excess weight (CEW) was finalised, outlining a biopsychosocial model, delivered by a multi-disciplinary team. The Delphi process identified provisional physical and mental health outcomes to evaluate the clinics (body profile, glucose tolerance, blood pressure, lipid profile, obstructive sleep apnoea, identification of whether there is an underlying cause for the obesity, non-alcoholic fatty liver disease and idiopathic intracranial hypertension, anxiety, depression, self-esteem, quality of life and school attendance). Conclusion The Framework was used by national and regional commissioners to develop an expression of interest. In 2021 15 centres1across 7 NHS regions were selected to pilot clinics, and are currently preparing to start seeing patients. With over a million CYP now living with obesity, the CEW clinics are not designed to provide the solution to the obesity epidemic but will address the important problem of related disease in a minority of these children, and reduce burden on other paediatric specialties currently treating CEW who may lack the capacity/skill-sets to address lifestyle change. Specialist teams with inter-disciplinary input from dietetics, social care, psychology and others will offer holistic care to this vulnerable cohort. The service evaluation will support in understanding whether there is an optimal approach nationally. 1 1) Derriford Hospital, 2) Southampton University Hospitals, 3) Kent and Medway CCG, 4) East London (King’s College London Hospital and Bart’s Health NHS Trust), 5) West London (Great Ormond Street Hospital, University College London Hospital, Tavistock and Portman NHS Foundation Trust), 6) Addenbrooke’s Hospital, 7) Norfolk and Norwich University Hospitals, 8) Birmingham Women and Children’s, 9) Nottingham Children’s Hospital with Leicester Royal Infirmary, 10) Sheffield Children’s Hospital, 11) Alder Hey Children’s Hospital, 12), Manchester Children’s Hospital, 13) Royal Preston, 14) Leeds Teaching Hospital, 15) South Tees Hospital

Over the past decade, a potential sixth taste, fat taste ("oleogustus"), has been identified. Studies in adults and children of various ethnicities have demonstrated that both lifestyle and genetic factors may contribute to fat taste sensitivity (FTS). Data on females in the UK is limited. The aim of this study was to determine, using an ethnically similar, healthy, female cohort, whether known genotypes related to fat taste and dietary intake lead to differences in FTS. A cross-sectional study was carried out on a UK cohort of Caucasian females (32.7 +/- 11.4 years, 23.7 +/- 3.6 kg/m2). We report that FTS differed in individuals with differing genotypes; genotypes that have previously been associated with differences in dietary intake. Specifically, FTS was lower in rs1514175 Troponin I-Interacting Protein Kinase (TNNI3K) gene AA/AG genotype and was higher in rs6265 Brain Derived Neurotrophic Factor (BDNF) gene TT/CT genotype (both p < 0.05). We also report that participants in the rs1514175 TNNI3K AA/AG genotype group had a higher energy intake, total fat intake, and subsequently, higher monounsaturated fat and saturated fat intake when compared to the GG genotype (all p < 0.05). To our knowledge, this is the first study showing associations between genotypes that have been previously associated to dietary intake are also associated to FTS. Due to the heterogeneity of previous research and the infancy of fat taste research, further research is required on a larger, ethnically similar cohort.

Background Ibuprofen is used as first line therapy to close haemodynamically significant patent ductus arteriosus (PDA) but is associated with severe gastrointestinal and renal effects. Objectives The aims of this study were to determine the efficacy and safety of ibuprofen for pharmacological closure of PDA in preterm infants ≤29 weeks gestation. Methods Retrospective study between 2015–2019 at a tertiary centre. 82 infants ≤29 weeks gestation with a haemodynamically significant large PDA on echocardiogram were enrolled. Data was collected using an electronic patient record system. Results As shown in table 1, cohort had a median gestational age of 25+3 (range: 23+2 to 29+1), a median birth weight of 0.79kg (range: 0.39–1.25kg) and a median PDA diameter of 2.7mm (range 1.6–4.0mm). 70/82 infants completed their first course of ibuprofen, achieving full PDA closure in 25 patients (30.5%), partial closure in 29 (35.4%), and no closure in 24 (29.3%). 13/82 patients (15.9%) required a second course of ibuprofen, achieving full PDA closure in 3 patients (23.1%), partial closure in 1 (7.7%), and no closure in 9 (69.2%). Associated adverse effects were reported in 13/82 patients (15.9%). These were mainly gastrointestinal and included necrotising enterocolitis in 5/82, bowel perforation in 5/82, and a further 1/82 had an upper gastrointestinal bleed. 9 patients subsequently underwent surgical ligation of their PDA, and an additional 5 patients died prior to PDA ligation due to non-cardiac complications. Conclusions In our cohort ibuprofen was moderately efficacious in closure of PDA. Ibuprofen was generally well tolerated, although 13/82 infants (15.9%) were noted to have adverse effects. Whether these gastrointestinal adverse effects were the consequence of a persistent haemodynamically significant large PDA or the adverse effects of ibuprofen, or a combination of the two, is hard to say from our small cohort. A future prospective study should be planned to address this.

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/m(2)). 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 x 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.

Taste perception (sensitivity) may be determined by genetic variations in taste receptors and it affects food intake. Lower fat taste sensitivity is associated with higher dietary fat intake and body mass index (BMI). Recently, associations between bitter and fat taste sensitivity have been reported whereby bitter taste perception may be involved in textural perception of dietary fat. However, it is not clear if lower sensitivity to bitter taste would lead to an actual higher fat intake. Our objectives were to explore the associations between haplotypes in the bitter taste receptor TAS2R38, bitter taste sensitivity and fat intake and if bitter taste sensitivity is lower in individuals with higher BMI. Ethical approval was obtained from the St Mary's and Oxford Brookes University Ethics Committee. Eighty-eight healthy Caucasian participants (44% male and 56% female; mean BMI 24.9 ± 4.8 kg/m2 and mean age 35 ± 14 years) completed this cross-sectional study. Height and weight were measured and genotyping performed for rs713598, rs1726866, rs10246939 genetic variants in the TAS2R38. Haplotypes were determined with Haploview software. Participants rated the intensity of a phenylthiocarbamide (PTC) impregnated strip on the general Labelled Magnitude Scale (gLMS) to determine bitter taste sensitivity and were classified as bitter tasters and non-tasters. Dietary fat intake was calculated from the EPIC-Norfolk Food Frequency Questionnaire and expressed as % total energy intake. TAS2R38 haplotypes were associated with bitter taster status (P < 0.005). PTC ratings of intensity were negatively correlated with % saturated fat (SFA) intake (rs = −0.256, P = 0.016). %SFA and %total fat (rs = 0.656, P < 0.005) and %total fat and energy intake (kcal) (rs = 0.225, P = 0.035) were positively correlated. Normal weight participants rated PTC strips as more intense compared to overweight and obese participants (mean rank 53 vs. 41, P = 0.033). Bitter taste perception is determined by genetics and lower sensitivity to this taste is associated with higher intake of SFA. Lower bitter taste sensitivity in overweight/obese participants suggests that impaired bitter taste may be associated with an overall unhealthier and more energy dense dietary pattern. St Mary's and Oxford Brookes University.

Introduction: In the UK, the number of comorbidities seen in children has increased along with the worsening obesity rate. These comorbidities worsen into adulthood. Genome-wide association studies have highlighted single nucleotide polymorphisms associated with the weight status of adults and offspring individually. To date, in the UK, parental genetic, lifestyle, and social determinants of health have not been investigated alongside one another as influencers of offspring weight status. A comprehensive obesity prevention scheme would commence prior to conception and involve parental intervention including all known risk factors. This current study aims to identify the proportion of overweight that can be explained by known parental risk factors, including genetic, lifestyle, and social determinants of health with offspring weight status in the UK. Methods: A cross-sectional study was carried out on 123 parents. Parental and offspring anthropometric data and parental lifestyle and social determinants of health data were self-reported. Parental genetic data were collected by use of GeneFiX saliva collection vials and genotype were assessed for brain-derived neurotrophic factor (BDNF) gene rs6265, melanocortin 4 receptor (MC4R) gene rs17782313, transmembrane protein 18 (TMEM18) gene rs2867125, and serine/threonine-protein kinase (TNN13K) gene rs1514175. Associations were assessed between parental data and the weight status of offspring. Results: Maternal body mass index modestly predicted child weight status (p < 0.015; R2 = 0.15). More mothers of overweight children carried the MC4R rs17782313 risk allele (77.8%; p = 0.007) compared to mothers of normal-weight children. Additionally, fathers who were not Caucasian and parents who slept for <7 h/night had a larger percentage of overweight children when compared to their counterparts (p = 0.039; p = 0.014, respectively). Conclusion: Associations exist between the weight status of offspring based solely on parental genetic, lifestyle, and social determinants of health data. Further research is required to appropriately address future interventions based on genetic and lifestyle risk groups on a pre-parent cohort.

AbstractIntroductionObesity is an international epidemic. Worldwide, 1.9 billion adults are overweight, and 650 million adults are obese. Obesity has many chronic comorbidities, including diabetes and cardiovascular disease. Obesity's cause is positive energy balance involving environmental and biological factors.Genome-Wide Association Studies (GWAS) suggest that the A/T expression of Single Nucleotide Polymorphism (SNP) rs9939609 within the Fat-Mass and Obesity-Associated (FTO) gene significantly influences adiposity. The high-risk A allele is associated with increased Body Mass Index (BMI) (0.36kg/m2 per A allele) and a preference for increased fat and protein intake. FTO encodes for 2-oxoglutarate-dependant-nucleic-acid-demethylase, which is involved in energy homeostasis and lipolysis. Previous studies show that a high physical activity level (PAL) attenuates the increased BMI risks associated with the high-risk allele. However, results have been contradictory. This study aims to elucidate the links between FTO SNP rs9939609, PAL, BMI and food preference.MethodsAn observational cross-sectional study including 37 UK adults was performed. Participant height, weight and body fat% (BF%) (using Bioelectrical Impedance Analysis) were measured. A food frequency questionnaire was completed, a saliva sample was collected for DNA analysis and PAL was assessed using participants active hours.A two-way MANOVA was performed to determine differences in BMI and BF% between FTO rs9939609 genotypes and PALs. A Chi-squared test was performed to determine potential genotype associations with food preference.ResultsParticipant BMI was significantly higher in AA participants compared to AT (3.99kg/m2 ± 1.69, p = 0.027) and TT (3.7kg/m2 ± 1.73, p = 0.043) participants. Participant BMI was higher in low PAL participants compared to medium PAL participants (4.62kg/m2 ± 1.35, p = 0.002). Genotype did not significantly influence participant BF% (p = 0.281).A combination of PAL and genotype was significantly associated with BMI and BF% (p = 0.009). BMI was significantly increased in AA participants compared to TT participants (7.15kg/m2 ± 2.68, p = 0.013) and AT participants (8.15kg/m2 ± 2.77, p = 0.007) with low PAL. This difference was not seen as PAL increased.No significant associations were found between genotype and food preference (p = 0.717).DiscussionThis study suggests that combining genotype and PAL significantly influences BMI and BF%. Participants homozygous for the risk allele AA with low PAL have significantly higher BMI than AT/TT participants with low PAL. However, the obesogenic effects of the risk genotype are diminished as PAL increases. This suggests that PAL attenuates genetic predisposition for obesity associated with the FTO rs9939609 A allele. These results may be applied in obesity intervention programmes particularly for encouragement of genetically predisposed individuals.