The occurrence of dyslipidaemia, which is an established risk factor for cardiovascular diseases, has been attributed to multiple factors including genetic and environmental factors. We used a genetic risk score (GRS) to assess the interactions between genetic variants and dietary factors on lipid-related traits in a cross-sectional study of 190 Brazilians (mean age: 21 ± 2 years). Dietary intake was assessed by a trained nutritionist using three 24-h dietary recalls. The high GRS was significantly associated with increased concentration of TAG (beta = 0·10 mg/dl, 95 % CI 0·05–0·16; P < 0·001), LDL-cholesterol (beta = 0·07 mg/dl, 95 % CI 0·04, 0·11; P < 0·0001), total cholesterol (beta = 0·05 mg/dl, 95 % CI: 0·03, 0·07; P < 0·0001) and the ratio of TAG to HDL-cholesterol (beta = 0·09 mg/dl, 95 % CI: 0·03, 0·15; P = 0·002). Significant interactions were found between the high GRS and total fat intake on TAG:HDL-cholesterol ratio (Pinteraction = 0·03) and between the high GRS and SFA intake on TAG:HDL-cholesterol ratio (Pinteraction = 0·03). A high intake of total fat (>31·5 % of energy) and SFA (>8·6 % of energy) was associated with higher TAG:HDL-cholesterol ratio in individuals with the high GRS (beta = 0·14, 95 % CI: 0·06, 0·23; P < 0·001 for total fat intake; beta = 0·13, 95 % CI: 0·05, 0·22; P = 0·003 for SFA intake). Our study provides evidence that the genetic risk of high TAG:HDL-cholesterol ratio might be modulated by dietary fat intake in Brazilians, and these individuals might benefit from limiting their intake of total fat and SFA.

Dietary fat is a major energy source and an essential nutrient that supports healthy growth and development in young children(1). Despite the important role of dietary fat in early childhood, our understanding of fat intake trends during this period is limited, particularly among Australian children. Insufficient evidence has led to the establishment of an Adequate Intake (AI) for infants aged 0-12 months in Australia, while no recommendation is available for children ages 1-5 years. This study aimed to comprehensively describe fat intake and major food sources in young Australian children. The data of children at ages 9 months (n = 393), 18 months (n = 284), 3.5 years (n = 244), and 5 years (n = 240) from the Melbourne InFANT Program were used(2). At each time point, child dietary intake data were collected via three 24-hour recalls. Food measurement booklets were utilised to estimate food portions. Food groups and nutrient intakes per day were calculated using the 2007 AUSNUT Food Composition Database. Daily energy (kJ/d) and fat (g/d) intake, the contribution of fat to total energy intake, and key food sources of fat intake were calculated. Descriptive statistics (mean and SD) were used to summarise all data. The mean daily energy intake increased from 3490 kJ/d at 9 months to 5889 kJ/d at 5 years. The mean (SD) fat intake (g/d) was 33.7 (8.0) (Australian AI is 30 g/d) at 9 months, 37.5 (9.5) at 18 months, 44.6 (13.4) at 3.5 years, and 49.0 (15.1) at 5 years. The WHO/FAO recommends that total fat intakes should constitute a minimum of 35% of energy (%E) for children aged 6-24 months, gradually reducing to a range of 25% to 35 %E for children aged 2 to 5 years(3). Notably, 40% of children at 9 months, 76% at 18 months, 14% at 3.5 years, and 12% at 5 years had fat intakes below the WHO/FAO recommendations. In contrast, 24% of children at 3.5 years and 28% at 5 years exceeded the recommendation. At 9 months, the primary source of fat was formula/breastmilk, while at later ages, the major sources were milk/milk products, cakes/cookies, and breads/cereals. The proportion of fat from discretionary foods, such as cakes/cookies, processed meats, butter, oil or fat spreads, increased with age. The percentage of total fat from fish, nuts, and seeds was low, contributing <4 %E at all time points. The study highlights a significant proportion of children exceeding or falling below fat intake recommendations. Moreover, the results suggest low consumption of healthy fat sources such as fish, nuts, and seeds. The study findings will contribute to the refinement of fat recommendations in young Australian children and contribute to interventions that aims to improve fat intakes.

This study aimed to investigate the association between individual and combinations of macronutrients with premature death, CVD and dementia. Sex differences were investigated. Data were utilised from a prospective cohort of 120 963 individuals (57 % women) within the UK Biobank, who completed ≥ two 24-h diet recalls. The associations of macronutrients, as percentages of total energy intake, with outcomes were investigated. Combinations of macronutrients were defined using k-means cluster analysis, with clusters explored in association with outcomes. There was a higher risk of death with high carbohydrate intake (hazard ratios (HR), 95 % CI upper v. lowest third 1·13 (1·03, 1·23)), yet a lower risk with higher intakes of protein (upper v. lowest third 0·82 (0·76, 0·89)). There was a lower risk of CVD with moderate intakes (middle v. lowest third) of energy and protein (sub distribution HR (SHR), 0·87 (0·79, 0·97) and 0·87 (0·79, 0·96), respectively). There was a lower risk of dementia with moderate energy intake (SHR 0·71 (0·52, 0·96)). Sex differences were identified. The dietary cluster characterised by low carbohydrate, low fat and high protein was associated with a lower risk of death (HR 0·84 (0·76, 0·93)) compared with the reference cluster and a lower risk of CVD for men (SHR 0·83 (0·71, 0·97)). Given that associations were evident, both as single macronutrients and for combinations with other macronutrients for death, and for CVD in men, we suggest that the biggest benefit from diet-related policy and interventions will be when combinations of macronutrients are targeted.

The effects of macronutrient intake on obesity are controversial. This research aims to investigate the associations between macronutrient intake and new-onset overweight/obesity. The relationship between the consumption of carbohydrate and total fat and obesity was assessed by the multivariable Cox model in this 11-year cohort, which included 6612 adults (3291 men and 3321 women) who were free of overweight and obesity at baseline. The dietary intake was recorded using a 24-h recall method for three consecutive days. Moreover, substitution models were developed to distinguish the effects of macronutrient composition alteration from energy intake modification. During 7·5 person years (interquartile range 4·3, 10·8) of follow-up, 1807 participants became overweight or obese. After adjusting for risk factors, the hazard ratio (HR) of overweight/obesity in extreme quintiles of fat was 1·48 (quintile 5 v. quintile 1, 95 % CI 1·16, 1·89; Ptrend = 0·02) in women. Additionally, replacing 5 % of energy from carbohydrate with equivalent energy from fat was associated with an estimated 4·3 % (HR 1·043, 95 % CI 1·007, 1·081) increase in overweight/obesity in women. Moreover, dietary carbohydrate was inversely associated with overweight/obesity (quintile 5 v. quintile 1, HR 0·70, 95 % CI 0·55, 0·89; Ptrend = 0·02) in women. Total fat was related to a higher risk of overweight/obesity, whereas high carbohydrate intake was related to a lower risk of overweight/obesity in women, which was not observed in men.

Fatty acid taste (FAT) perception is involved in the regulation of dietary fat intake, where impaired FAT is associated with increased fatty food intake. There are a number of FAT receptors identified on human taste cells that are potentially responsible for FAT perception. Manipulating dietary fat intake, and in turn FAT perception, would elucidate the receptors that are associated with long-term regulation of FAT perception. The present study aimed to assess associations between diet-mediated changes to FAT receptors and FAT perception in humans. A co-twin randomised controlled trial was conducted, where each matching twin within a pair were randomly allocated to either an 8-week low-fat (LF; <20 % energy fat) or an 8-week high-fat (HF; >35 % energy fat) diet. At baseline and week 8, fungiform papillae were biopsied in the fasted state and FAT receptor gene expressions (cluster of differentiation 36 (CD36), free fatty acid receptor 2 (FFAR2), FFAR4, G protein-coupled receptor 84 (GPR84) and a delayed rectifying K+ channel (K+ voltage-gated channel subfamily A member 2; KCNA2)) were measured using RT-PCR; and FAT threshold (FATT) was assessed using three-alternate forced choice methodology. Linear mixed models were fitted, adjusting for correlation between co-twins. Intake was compliant with the study design, with the LF and HF groups consuming 14·8 and 39·9 % energy from fat, respectively. Expression of FFAR4 increased by 38 % in the LF group (P = 0·023; time–diet interaction P = 0·063). ΔFFAR4 (Δ, week 8–baseline) was associated with Δfat intake (g) ( = −159·4; P < 0·001) and ΔFATT ( = −8·8; P = 0·016). In summary, FFAR4 is involved in long-term diet-mediated changes to FAT perception. Manipulating dietary fat intake, and therefore FFAR4 expression, might aid in reducing taste-mediated passive overconsumption of fatty foods.

Body mass and fat intake are multifactorial traits that have genetic and environmental components. The gene with the greatest effect on body mass is FTO (fat mass and obesity-associated), but several studies have shown that the effect of FTO (and of other genes) on body mass can be modified by the intake of nutrients. The so-called gene–environment interactions may also be important for the effectiveness of weight-loss strategies. Food choices, and thus fat intake, depend to some extent on individual preferences. The most important biological component of food preference is taste, and the role of fat sensitivity in fat intake has recently been pointed out. Relatively few studies have analysed the genetic components of fat intake or fatty acid sensitivity in terms of their relation to obesity. It has been proposed that decreased oral fatty acid sensitivity leads to increased fat intake and thus increased body mass. One of the genes that affect fatty acid sensitivity is CD36 (cluster of differentiation 36). However, little is known so far about the genetic component of fat sensing. We performed a literature review to identify the state of knowledge regarding the genetics of fat intake and its relation to body-mass determination, and to identify the priorities for further investigations.

Dietary fat intake is correlated with increased insulin resistance (IR). However, it is unknown whether gene–diet interaction modulates the association. This study estimated heritability of IR measures and the related genetic correlations with fat intake, and tested whether dietary fat intake modifies the genetic influence on type 2 diabetes (T2D)-related traits in Chinese child twins. We included 622 twins aged 7–15 years (n 311 pairs, 162 monozygotic (MZ), 149 dizygotic (DZ)) from south-eastern China. Dietary factors were measured using FFQ. Structural equation models were fit using Mx statistical package. The intra-class correlation coefficients for all traits related to T2D were higher for MZ twins than for DZ twins. Dietary fat and fasting serum insulin (additive genetic correlation (rA) 0·20; 95 % CI 0·08, 0·43), glucose (rA 0·12; 95 % CI 0·01, 0·40), homoeostasis model of assessment-insulin resistance (Homa-IR) (rA 0·22; 95 % CI 0·10, 0·50) and the quantitative insulin sensitivity check index (Quicki) (rA −0·22; 95 % CI −0·40, 0·04) showed strong genetic correlations. Heritabilities of dietary fat intake, fasting glucose and insulin were estimated to be 52, 70 and 70 %, respectively. More than 70 % of the phenotypic correlations between dietary fat and insulin, glucose, Homa-IR and the Quicki index appeared to be mediated by shared genetic influence. Dietary fat significantly modified additive genetic effects on these quantitative traits associated with T2D. Analysis of Chinese twins yielded high estimates of heritability of dietary fat intake and IR. Genetic factors appear to contribute to a high proportion of the variance for both insulin sensitivity and IR. Dietary fat intake modifies the genetic influence on blood levels of insulin and glucose, Homa-IR and the Quicki index.

To investigate whether obese women can compensate for sucrose added to the diet when it is given blind, rather than gaining weight or exhibiting dysfunctional regulation of intake, in the present study, forty-one healthy obese (BMI 30–35 kg/m2) women (age 20–50 years), not currently dieting, were randomly assigned to consume sucrose (n 20) or aspartame (n 21) drinks over 4 weeks in a parallel single-blind design. Over the 4 weeks, one group consumed 4 × 250 ml sucrose drinks (total 1800 kJ/d) and the other group consumed 4 × 250 ml aspartame drinks. During the baseline week and experimental weeks, body weight and other biometric data were measured and steps per day, food intake using 7 d unweighed food diaries, and mood using ten- or seven-point Likert scales four times a day were recorded. At the end of the experiment, the participants weighed 1·72 (se 0·47) kg less than the value predicted by the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) model; the predicted body weight accounted for 94·3 % of the variance in the observed body weight and experimental group accounted for a further 1·1 % of the variance in the observed body weight, showing that women consuming sucrose drinks gained significantly less weight than predicted. The reported daily energy intake did not increase significantly, and sucrose supplements significantly reduced the reported voluntary sugar, starch and fat intake compared with aspartame. There were no effects on appetite or mood. Over 4 weeks, as part of everyday eating, sucrose given blind in soft drinks was partially compensated for by obese women, as in previous experiments with healthy and overweight participants.

Dietary fat intake in childhood may influence the risk for developing chronic diseases. The objective of the present study was to examine secular trends in the parameters of fat intake between 2000 and 2010 in a sample of German children and adolescents (n 808) participating in the Dortmund Nutritional and Anthropometric Longitudinally Designed (DONALD) Study. Dietary data from 4380 3 d weighed dietary records were analysed using repeated-measures regression to determine time trends in fat quantity, i.e. the intake of total fat, and in fat quality, i.e. the ratios of SFA, MUFA and PUFA. In young children (2–3 years) and in adolescents (13–18 years), total fat intake remained stable over time, but decreased by 0·08 % of total energy (%E) per year in 4–12-year-old children. In 2010, median fat intake was at the upper end of the recommendations. SFA intake decreased slightly in 2–3- and 4–12-year-old children by 0·09 and 0·05 %E per year, respectively. MUFA and PUFA intakes remained stable in all the age groups except in adolescents. Here, PUFA intake decreased initially, but increased between 2005 and 2010. In 2010, only between 3 and 18 % of the respective age groups had an intake of SFA or PUFA within the recommendations. In conclusion, fat quantity and quality did not change substantially between 2000 and 2010. Fat quality, in particular, needs to be improved, since a large percentage of our sample did not meet the recommended intakes for SFA and PUFA.

There is general agreement that exercise-induced energy expenditure is not entirely compensated for at the next meal or over the following 24 h, but inter-individual variability is high. The role of ‘fatness and fitness’ in this variability has never been assessed. Therefore, eighteen non-obese male subjects aged 22·2 (sd 2·0) years were selected and separated into a ‘high-fatness and low-fitness’ (Hfat/Lfit, n 9) and a ‘low-fatness and high-fitness’ (Lfat/Hfit, n 9) group, according to three criteria: maximal oxygen uptake; weekly hours of physical activity; fat mass index. At 1 h before lunch, they were subjected to 60 min of exercise on a cycle ergometer (70 % VO2max), or stayed at rest. Then, they self-reported food intake in diaries until the next breakfast. Intake at lunch was not different between conditions, but was higher after exercise than after rest over the 24 h, leading to a significant but partial mean level of compensation of 49·8 (sem 16·5) and 37·8 (sem 24·6) % for the Hfat/Lfit and Lfat/Hfit groups, respectively. Energy compensation at lunch and over the 24 h were strongly correlated (r 0·76, P< 0·001). Both groups consumed more fat and protein after exercise than after rest over the 24 h, but the percentage of energy derived from fat increased only in the Hfat/Lfit group (2·1 (sem 0·6) %, P= 0·026). Thus, the energy cost of an aerobic exercise session was partially compensated over the next 24 h independently of the ‘fatness and fitness’ status, but ‘high-fat and low-fit’ individuals compensated more specifically on fats.

The reduced contribution of physical activity to daily energy expenditure and the accessibility to high-fat foods have put an excessive burden on energy balance, resulting in an increase in the prevalence of obesity throughout the world. In this context, fat gain can be seen as a natural adaptation to deal with a fattening lifestyle, since the hormonal adaptations that accompany fat gain favour the readjustment of energy expenditure to energy intake. Intense physical activity would also seem to facilitate the regulation of energy balance, since it increases the energy cost of exercise, increases post-exercise energy expenditure and the potential of skeletal muscles to utilize lipids, and also favours a decrease in post-exercise intake. Moreover, the effects of intense exercise seem to be mediated by an activation of sympathetic nervous system activity that seems to be specific to skeletal muscle. It is also important to manipulate macronutrient composition in order to reduce fat intake, because unhealthy food habits can favour overfeeding and thus overcome the energy deficit caused by regular physical activity. Under free-living conditions, the combination of vigorous activity and healthy food practices can amount to a substantial weight loss which is comparable with that of other non-surgical approaches to treat obesity.

The aim of the present study was to investigate the interaction between the angiotensin-converting enzyme 1 (ACE) I/D polymorphism and energy and macronutrient intakes on adiposity-related phenotypes among toddlers and preschoolers. A representative sample of 2374 Greek children aged 1 to 5 years old was examined (Growth, Exercise and Nutrition Epidemiological Study in preSchoolers (GENESIS)). Dietary and anthropometric (i.e. BMI, waist circumference (WC)) assessments were carried out using standard procedures. DNA samples were obtained from 2102 children and were genotyped for the ACE I/D polymorphism. Among the entire population, 17 % were ‘at risk of overweight’ and a similar percentage were ‘overweight’. The frequencies of the II, ID and DD genotypes were 16, 46 and 38 %, respectively. Significant interactions were found between the ACE I/D polymorphism and total energy intake on WC (P = 0·004 for interaction) and the ACE I/D polymorphism and protein intake on BMI and being overweight (P < 0·05 for interaction). Furthermore, it was found that the ACE I/D polymorphism may modify the effect of fat intake on WC and BMI, but this interaction disappeared after adjustment for additional potential confounders. Stratified analyses revealed that total energy is correlated with WC and protein intake is associated with BMI and being overweight only among carriers of the D-allele (i.e. DD or ID genotypes). These results suggest that the ACE I/D polymorphism may act as a modifying factor in the response of adiposity-related phenotypes to diet.

Epidemiological studies conducted thus far have mainly used a single-nutrient approach which may not be sufficient in detecting diet–cancer relationships. The aim of the study was to examine the association of a food pattern based on explained variations in fatty acid intake by means of reduced rank regression with breast cancer risk. Study participants were female subjects (n 15 351) of the European Prospective Investigation into Cancer and Nutrition (EPIC)-Potsdam Study free of cancer at baseline and with complete dietary and outcome information followed for an average of 6·0 years. Among those, 137 incident cases of invasive breast cancer were identified. We identified a food pattern characterized by low consumption of bread, and fruit juices, and high consumption of processed meat, fish, butter and other animal fats, and margarine explaining >42 % of total variation in fatty acid intake (SFA, MUFA, n-3 PUFA, n-6 PUFA). Intake of all four fatty acid fractions was positively associated with the pattern score. Adherence to this food pattern adjusted for covariates was associated with a two-fold risk (hazard ratio 2·00; 95 % CI 1·30, 3·09) of breast cancer comparing extreme tertiles of the pattern score. There was no evidence of effect modification by menopausal status, overweight status and use of hormone replacement therapy, respectively. In conclusion, a food pattern characterized by high-fat food choices was significantly associated with increased risk of breast cancer. Given that the food pattern was high in all fatty acid fractions, we found evidence for total dietary fat rather than for specific fatty acids to be associated with breast cancer risk.

Undernutrition among hospitalized patients is highly prevalent. In contrast, the obesity pandemic is increasing in prevalence among all, including cardiology patients. The dietary challenge during hospitalization is to provide a healthy diet that stimulates the appetite and is suitable for both patients at risk of undernutrition and of cardiovascular events. The aim of the present study was to compare energy and macronutrient intake between a conventional hospital menu (Fixed) with a concept providing free serving hours and ad libitum intake à la carte (Free) among cardiology patients. The comparison was done between concepts for all lean (BMI < 25 kg/m2) and overweight and obese (BMI ≥ 25 kg/m2) patients and subgroups. Food intake was registered during a 3-week period on Fixed for forty-eight randomly selected patients and later by two similar time periods on Free1 for twenty-eight and Free2 for thirty-seven other patients. Free compared with Fixed increased the energy intake – but not above requirement – among the obese only (P < 0·001; Free v. Fixed). This was explained by an increase in the relative fat intake of 50 % (P < 0·001) and 37 % (P < 0·001) for Free1 and Free2 respectively. During Free1, the relative fat intake correlated positively with BMI (r 0·6; P < 0·01), and the relative carbohydrate intake negatively with BMI (r − 0·7; P < 0·01); the same pattern was seen during Free2, although insignificant. We conclude that the introduction of an ad libitum à la carte kitchen (Free) to cardiology patients slightly increases the average nutritional intake, but contains a potential health hazard for overweight cardiovascular patients, due to the selection of high-fat dishes and decreased carbohydrate intake. This emphasises the need for improvement in fat sources and in dietary advice when an ad libitum concept is applied during hospitalization.

Both jurisdictions of Ireland have high rates of chronic degenerative diseases, particularly of the cardiovascular system, and Irish migrants have worse health profiles, often lasting at least two generations. The influence of socio-demographic variation over the life course, and what role diet plays, has not been well researched in epidemiological terms. There is a long history of an unusual Irish diet. Estimated dietary fat intake (% total energy intake) in 1863 was only 9, but had reached 30 in 1948 and 34 in 1999. Conversely, carbohydrate intake has fallen steadily over 150 years. From 1948 onwards household budget survey data illustrate patterns of increasing urbanisation and socio-economic gradients in food availability. The National Survey of Lifestyles, Attitudes and Nutrition, (n 6539, 622 % response rate) provides clear evidence of inverse social-class gradients in intake of fruit and vegetables and dairy products and in reported patterns of healthy eating. Median carbohydrate and vitamin C levels are higher among social classes 1-2 and mean saturated fat intake is lower. International comparisons indicate a continuing, if narrowing, north-south gradient across Europe. Data from the Boston-Ireland study suggest a crossover in both dietary intake patterns and risk of heart disease in Ireland and the USA in the 1970s. Contemporary comparative data of middle-aged Irish and American women demonstrate patterns of diet intake and inactivity consistent with the modern epidemic of obesity and non-insulin-dependent diabetes. Thus, dietary variations within and between countries and over time are consistent with chronic disease patterns in contemporary Ireland.