A systematic review of the effect of dietary and nutritional interventions on the behaviours and mental health of prisoners.

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.

The Associations Between Bitter and Fat Taste Sensitivity, and Dietary Fat Intake: Are They Impacted by Genetic Predisposition?

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 (rs = -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.

Regulator of G-Protein Signalling 9: A New Candidate Gene for Sweet Food Liking?

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.

Prevalence of disordered eating, eating disorders and risk of low energy availability in professional, competitive and recreational female athletes based in the United Kingdom.

Eating disorders (ED), disordered eating (DE) and low energy availability (LEA) can be detrimental to health and performance. Previous studies have independently investigated the prevalence of ED, DE or LEA; however, few combined methods have identified risk within female athletes. The aim of this study was to identify the prevalence of ED, DE and LEA in UK-based female athletes and investigate whether associations exist between age, competition level and primary sport. The Female Athlete Screening Tool (FAST) and Low Energy Availability in Females Questionnaire (LEAF-Q) were used in a cross-sectional study design. A total of 112 responses eligible for analysis were received. A total of 16%, 44% and 53% of female athletes were at risk of ED (FAST: >94), DE and LEA, respectively. Competition level (recreational, competitive or professional athletes; fishers, p ≤ 0.05) influenced and was a predictor of FAST (R2 = 0.076, F(1,110) = 10.067, p ≤ 0.05, variance inflation value; VIF = 1.0) whereas age influenced (age: H(2) = 13.128, p ≤ 0.05), and was a predictor (R2 = 0.144, F(2,109) = 9.170, p ≤ 0.05, VIF = 1.0) of LEAF-Q. A positive correlation was observed between FAST and LEAF-Q scores (R = 0.496, p ≤ 0.05). Age and competition level may be predicting risk factors of ED/DE and LEA within female athletes; however, further research is required to support the findings of this present study.

Dietary Intake and TCF7L2 rs7903146 T Allele Are Associated with Elevated Blood Glucose Levels in Healthy Individuals.

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. R2 = 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.