A systematic review of variations in circadian rhythm genes and type 2 diabetes.

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.

Genetics of caffeine and brain-related outcomes - a systematic review of observational studies and randomized trials.

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.

The efficacy of genotype-based dietary or physical activity advice in changing behavior to reduce the risk of cardiovascular disease, type II diabetes mellitus or obesity: a systematic review and meta-analysis.

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.

The impact of genetic variability on the relationship between caffeine and cardiometabolic outcomes: A systematic review.

The relationship between caffeine consumption and cardiometabolic health has been reported, however with heterogenous results. Discrepancies in study results may be due to inter-individual variability between study participants. This systematic review aimed to identify the impact of genetics on the relationship between caffeine consumption and cardiometabolic outcomes. Electronic databases (PubMed and EMBASE) were searched for studies published until July 2021. Selected studies were of both intervention and observational design and included (1) analysis of at least one of the selected cardiometabolic outcome (type 2 diabetes, glucose/insulin levels, cardiovascular disease [CVD], blood pressure [BP] or hypertension, and blood lipid and catecholamine levels), (2) adults aged 18-65 years, and (3) genetic analysis of individuals consuming caffeine. Seventeen studies were included: four randomised controlled trials and an interventional and quasi-experimental study, six population-based prospective cohort studies, three cross-sectional studies, and three case-control studies. CYP1A2 rs762551 and ADORA rs5751876 were associated with glucose response when caffeine was consumed with carbohydrates. CYP1A2 rs762551 moderated the association between coffee intake and hypertension. Moreover, ADORA2A rs5751876 and the ADRA2B I variants moderated the associations between caffeine and BP. Studies that investigated the effects of genetic variations on CVD and caffeine consumption reported equivocal findings (CYP1A2) or warrant replication (COMT, ADORA and TRIB1). Elucidating the extent to which these genes moderate the association between caffeine and cardiometabolic outcomes will enable caffeine consumption advice to be tailored to specific individuals to optimise health.

Nutrition knowledge, food choices and diet quality of genotyped and non-genotyped individuals during the COVID-19 pandemic.

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 (ß = .428, t = 4.822, p = <.001 and ß = -.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.

Association of adherence to the dietary approach to stop hypertension and Mediterranean diets with blood pressure in a non-hypertensive population: Results from Isfahan Salt Study (ISS).

BACKGROUND AND AIMS: Hypertension is among the major risk factors for cardiovascular events in the Iranian population. This cross-sectional study was designed to examine the association of adherence to the dietary approaches to stop hypertension (DASH) and Mediterranean (MED) dietary patterns with the distribution of blood pressure and pre-hypertension prevalence. METHODS AND RESULTS: This cross-sectional study was carried out in 1363 non-hypertensive adults. Adherence to the DASH and MED diets was calculated using a semi-quantitative food frequency questionnaire (FFQ). Hypertension was measured by the standard method. Multiple logistic regression was applied to obtain the odds ratio of pre-hypertension in the tertiles of MED and DASH dietary patterns. Compared to the lowest, participants with the highest adherence to the DASH dietary pattern had significantly lower systolic blood pressure (SBP) (111.3 ± 11.8 vs. 112.8 ± 12.5; P = 0.010) and diastolic blood pressure (DBP) (70.7 ± 9.2 vs. 71.8 ± 9.8; 0.042). There was no significant difference in the mean SBP and DBP among the participants across tertiles of MED or diet adherence. Higher scores of the DASH and MED diets were inversely associated with lower SBP after adjustment for all potential confounders (OR = -0.04, 95% CI = -0.29, -0.01, P = 0.039) and (OR = -0.04, 95% CI = -0.72, -0.02, P = 0.044), respectively. Also, DASH and MED dietary patterns was associated with reduced OR of pre-hypertension occurrence by 13% (OR: 0.87; 95% CI: 0.70-0.98; P for trend = 0.042) and 16% ([OR: 0.84; 95% CI: 0.69-0.97; P trend = 0.035), respectively. CONCLUSION: Adherence to the DASH and MED diets was inversely associated with the odds for pre-hypertension and SBP.

Red and processed meat consumption and risk of incident cardiovascular disease and mortality: Isfahan cohort study.

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.

Does personalised nutrition advice based on apolipoprotein E and methylenetetrahydrofolate reductase genotype affect dietary behaviour?

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.

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.

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.

Caffeine, exercise physiology, and time-trial performance: no effect of ADORA2A or CYP1A2 genotypes.

The aim of this study was to investigate the influence of ADORA2A and CYP1A2 genotypes on the physiological and ergogenic effects of caffeine. Sixty-six male cyclists were screened for ADORA2A and CYP1A2 genotypes; with 40 taking part subsequently in a randomised, double-blind, placebo-controlled study. Trial 1 was used to establish the oxygen uptake-power output relationship and maximal oxygen uptake. In trials 2 and 3, participants ingested 5 mg·kg-1 of caffeine or placebo 1 h before completing a submaximal incremental cycling test, followed by a time-trial (∼30 min). Relative to placebo, caffeine led to a significant reduction in time to complete the time-trial (caffeine: 29.7 ± 1.8 min; placebo: 30.8 ± 2.3 min); but there was no effect of genotype. During submaximal exercise, caffeine reduced mean heart rate by 2.9 ± 3.7 beats·min-1, with effects dissipating as exercise intensity increased. Caffeine also significantly reduced perceived exertion by 0.5 ± 0.8, and increased blood lactate by 0.29 ± 0.42 mmol·L-1, respiratory exchange ratio by 0.013 ± 0.032, and minute ventilation by 3.1 ± 6.8 L·min-1. Nonetheless, there were no supplement × genotype interactions. In conclusion, caffeine influences physiological responses to submaximal exercise and improves time-trial performance irrespective of ADORA2A or CYP1A2 genotypes. Novelty: Caffeine affects physiological responses at rest and during submaximal exercise independent of ADORA2A or CYP1A2 genotypes. Variability in the effect of caffeine on time-trial performance is not explained by ADORA2A or CYP1A2 genotypes.

Systematic Review and Meta-Analysis of Candidate Gene Association Studies With Fracture Risk in Physically Active Participants.

Background: Fractures are common in physically active populations and genetic differences may mediate injury risk. Objective: To meta-analyse the pooled results of candidate gene association studies with non-osteoporotic fracture risk in physically active humans. Methods: Systematic searching of databases returned 11 eligible studies published in English. Pooled odds ratios (ORs) with 95% confidence intervals (CI) were produced using allele contrast, recessive and homozygote contrast meta-analysis models to evaluate associations of risk alleles in the COL1A1 (rs1800012), COL2A1 (rs412777), CTR (rs1801197), ESR1 (rs2234693 and rs9340799) LRP5 (rs3736228), VDR (rs10735810, rs7975232, rs1544410, and rs731236) genes with fracture incidence. Results: Eligible study quality was generally low (7/11) and no significant overall effect was found for any genetic variant with any comparison model (p > 0.05). A trivial reduction in fracture risk was found for female participants with the COL1A1 Sp1 (rs1800012) T allele (OR = 0.48, 95% CI = 0.25-0.91, p = 0.03, d = -0.18). Conclusions: No overall effect was found from the pooled results of included genetic variants on fracture risk in physically active participants. The COL1A1 Sp1 rs1800012 T allele may reduce fracture risk in physically active females but further high-quality research with sex-specific analysis is required. Trial Registration: (PROSPERO; CRD42018115008).

The Association of Parental Genetic, Lifestyle, and Social Determinants of Health with Offspring Overweight.

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.

Genetic predisposition to salt-sensitive normotension and its effects on salt taste perception and intake.

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.

Salt-sensitive hypertension: mechanisms and effects of dietary and other lifestyle factors.

Salt sensitivity, which is an increase in blood pressure in response to high dietary salt intake, is an independent risk factor for cardiovascular disease and mortality. It is associated with physiological, environmental, demographic, and genetic factors. This review focuses on the physiological mechanisms of salt sensitivity in populations at particular risk, along with the associated dietary factors. The interplay of mechanisms such as the renin-angiotensin aldosterone system, endothelial dysfunction, ion transport, and estrogen decrease in women contributes to development of salt sensitivity. Because of their effects on these mechanisms, higher dietary intakes of potassium, calcium, vitamin D, antioxidant vitamins, and proteins rich in L-arginine, as well as adherence to dietary patterns similar to the DASH (Dietary Approaches to Stop Hypertension) diet, can be beneficial to salt-sensitive populations. In contrast, diets similar to the typical Western diet, which is rich in saturated fats, sucrose, and fructose, together with excessive alcohol consumption, may exacerbate salt-sensitive changes in blood pressure. Identifying potential mechanisms of salt sensitivity in susceptible populations and linking them to protective or harmful dietary and lifestyle factors can lead to more specific guidelines for the prevention of hypertension and cardiovascular disease.

The effect of nutrient fortification of sauces on product stability, sensory properties, and subsequent liking by older adults.

There are potential nutritional and sensory benefits of adding sauces to hospital meals. The aim of this study was to develop nutrient fortified sauces with acceptable sensory properties suitable for older people at risk of undernutrition. Tomato, gravy, and white sauce were fortified with macro- and micronutrients using food ingredients rich in energy and protein as well as vitamin and mineral premixes. Sensory profile was assessed by a trained panel. Hedonic liking of fortified compared with standard sauces was evaluated by healthy older volunteers. The fortified sauces had higher nutritional value than the conventional ones, for example the energy content of the fortified tomato, white sauce, and gravy formulations were increased between 2.5- and 4-fold compared to their control formulations. Healthy older consumers preferred the fortified tomato sauce compared with unfortified. There were no significant differences in liking between the fortified and standard option for gravy. There were limitations in the extent of fortification with protein, potassium, and magnesium, as excessive inclusion resulted in bitterness, undesired flavors, or textural issues. This was particularly marked in the white sauce to the extent that their sensory characteristics were not sufficiently optimized for hedonic testing. It is proposed that the development of fortified sauces is a simple approach to improving energy intake for hospitalized older people, both through the nutrient composition of the sauce itself and due to the benefits of increasing sensorial taste and lubrication in the mouth.

Hospital catering systems and their impact on the sensorial profile of foods provided to older patients in the UK.

Impaired sensorial perception is very common in older people and low sensorial quality of foods is associated with decreased appetite and dietary intake. Hospital undernutrition in older patients could be linked to sensorial quality of hospital food if the quality were low or inappropriate for older people. The aim of this study was to examine changes in the sensorial quality of different foods that occur as a result of the food journey (i.e. freezing, regeneration, etc.) in the most common hospital catering systems in the UK. A trained sensory panel assessed sensorial descriptors of certain foods with and without the hospital food journey as it occurs in the in-house and cook/freeze systems. The results showed effects of the food journey on a small number of sensorial descriptors related to flavour, appearance and mouthfeel. The majority of these effects were due to temperature changes, which caused accumulation of condensation. A daily variation in sensorial descriptors was also detected and in some cases it was greater than the effect of the food journey. This study has shown that changes occur in the sensory quality of meals due to hospital food journeys, however these changes were small and are not expected to substantially contribute to acceptability or have a major role in hospital malnutrition.

Intervention with fish oil, but not with docosahexaenoic acid, results in lower levels of hepatic soluble epoxide hydrolase with time in apoE knockout mice.

Long-chain n-3 PUFA from fish oil protect against death from CHD but mechanisms are not well understood. Preliminary results indicate that fish oil may affect the enzyme soluble epoxide hydrolase (sEH) and influence inflammatory pathways in a time-dependent manner. In the present study male apoE knockout (Apoe-/-) mice were randomised to three dietary groups receiving a high-fat high-cholesterol diet supplemented with 2 % (w/w) high-oleic acid sunflower-seed (HOSF) oil, DHA oil or fish oil. Livers and proximal aortas were collected on day 2 and on weeks 1, 2, 4 and 10 to determine hepatic sEH levels, hepatic fatty acid composition, hepatic proteome and atherosclerotic plaque size in the aortic root. Intervention with fish oil, but not with DHA, resulted in significantly lower levels of hepatic sEH levels with time compared with HOSF oil. DHA and fish oil caused differential regulation of thirty-five hepatic proteins which were mainly involved in lipoprotein metabolism and oxidative stress. All mice developed atherosclerosis without differences in plaque size between the three groups. Thus EPA may be responsible for lowering levels of hepatic sEH and both fish oil and DHA could beneficially affect lipoprotein metabolism and oxidative stress.

Long-chain n-3 polyunsaturated fatty acids: new insights into mechanisms relating to inflammation and coronary heart disease.

Evidence from observational studies, prospective cohort studies and randomized clinical intervention studies indicate that moderate doses of long-chain n-3 polyunsaturated fatty acids (LC n-3 PUFA) significantly decrease risk of fatal coronary heart disease (CHD). Higher doses and longer duration of intervention may also protect from non-fatal CHD events. The exact mechanisms through which LC n-3 PUFA has an effect on CHD are not well established but may include a decrease in fasting and postprandial triacylglycerol levels, a decrease in arrhythmias, modulation of platelet aggregation and decreased synthesis of pro-inflammatory agents. The mechanistic relation between LC n-3 PUFA and inflammation has attracted great interest, and in vitro studies have revealed that these fatty acids decrease endothelial activation, affect eicosanoid metabolism (including epoxygenation pathways) and induce inflammatory resolution. However, the effects of LC n-3 PUFA on established biomarkers of inflammation and endothelial activation in vivo are not strong. Consequently we need new and more sensitive and systemic biomarkers to reveal the effects of LC n-3 PUFA on localized inflammatory processes.

The response of human colonocytes to folate deficiency in vitro: functional and proteomic analyses.

Low folate intake is associated with colon cancer. We combined a proteomics and biochemical approach to identify proteins and pathways affected by folate deficiency in human colonocytes. Folate differentially altered activity and expression of proteins involved in proliferation [e.g., PCNA], DNA repair [e.g., XRCC5, MSH2], apoptosis [e.g., BAG family chaperone protein, DIABLO and porin], cytoskeletal organization [e.g., actin, ezrin, elfin], and expression of proteins implicated in malignant transformation [COMT, Nit2].