Beyond obesity, visceral adipose tissue (VAT) has emerged as an important predictor of chronic disease, but the role of diet quality patterns (DQP) in VAT development is not well defined. Therefore, we conducted a systematic review of how various DQP are associated with VAT via literature searches in PubMed and EMBASE. We included observational investigations in disease-free adults/adolescents that related DQP to VAT assessed by imaging methods. The studies were evaluated separately for a priori and a posteriori DQP and according to design differences. Study quality was assessed using the Risk of Bias in Non-randomised Studies of Interventions tool. Of the 1807 screened articles, thirty-five studies met the inclusion criteria. The majority of a priori indices, for example, the Healthy Eating Index, showed significant inverse associations with VAT, while only a small proportion of a posteriori patterns were related to VAT. Results did not differ substantially by the method of exposure and outcome assessment or between studies with (n 20) or without (n 15) body-size adjustment, but significant findings were more common in younger v. older individuals, USA v. other populations and investigations with moderate v. serious risk of bias. The heterogeneity of the existing literature limited the ability to quantify the magnitude of the associations across studies. These findings suggest that a high-quality diet, as assessed by a priori DQP, is generally inversely associated with VAT, but results for a posteriori DQP are less consistent. As associations persisted after adjusting for body size, diet quality may beneficially influence VAT beyond its association with obesity.

We describe a novel dietary assessment strategy to estimate usual food intake in the ongoing large-scale multi-center German National Cohort (GNC). The dietary assessment is based on three 24 h food lists (24h-FL) and a food frequency questionnaire (FFQ) enriched by information from the representative German National Nutrition Survey II (NVS II). The novelty of this dietary assessment strategy is based on separating the probability of food intake from daily consumption amounts. The probability of consumption is estimated from 24h-FLs used in the GNC. To estimate daily consumption amounts, the already collected data of the NVS II are used. The 24h-FL simplifies the question on food consumption for all foods asked to consumption or not and so the questionnaire can be completed in about 10 minutes, reducing the burden on study participants. As proof of concept, we applied the assessment strategy to pretest data collected in 2012 to 2013 to assess the feasibility of the instruments. In brief, the novel dietary assessment strategy comprises three steps. First, the individuals’ consumption probability is estimated by three 24h-FLs and one FFQ applying a logistic linear mixed model adjusted for characteristics of the participants. Second, person-specific daily consumption amounts are estimated from the NVS II applying a linear mixed model taking the characteristics of the participants into account. Third, usual food intake is estimated by the consumption probability multiplied by person-specific daily amounts. Usual intake of 41 food groups in 318 men and 377 women were estimated. Of those participants who completed the first 24h-FL, 84.4, and 68.5% completed the second and third 24h-FL, respectively. No associations were observed between probability to participate and lifestyle factors. The estimated usual food intake distributions were in a plausible range as shown by comparing the estimated energy intake to the energy needs approximated by estimated total energy expenditure. Total energy was estimated to be 2,707 kcal/day for men and 2,103 kcal/day for women. With a few exceptions, the estimated food-based consumption probabilities did not differ considerably between men and women. The differences in energy intake between men and women were mainly due to their differences in the estimated person-specific daily amounts. As a conclusion, plausible but not validated values for usual food intake were derived in the pretest study, so that the combination of three repeated 24h-FLs, an FFQ and person-specific daily amounts from an external source is a feasible strategy for dietary assessment.

High alcohol consumption is an important risk factor for chronic disease and liver degeneration. Paraoxonase (PON1) and arylesterase (AE) are functions of the enzyme paraoxonase, which is synthesised by the liver. Paraoxonase circulates in plasma bound to HDL and hydrolyses lipid peroxides, protecting lipoproteins against oxidative modification. It has been shown that excessive alcohol consumption leads to a reduction of serum PON1 and AE activities; however, studies investigating the association with low and moderate alcohol consumption are scarce. We investigated the cross-sectional association between alcohol consumption and serum activities of PON1 and AE using data from the population-based Bavarian Food Consumption Survey II survey. PON1 and AE activities were quantified in serum samples of 566 male and female study participants (aged 18–80 years), and dietary intake including alcohol consumption was estimated from three 24-h dietary recalls. The association between alcohol consumption and PON1 and AE activities was analysed using linear regression, adjusted for age, sex and socio-economic status. There was no strong association between alcohol consumption and enzymatic activities of PON1 and AE in the Bavarian population. PON1 activity was seen to be lowest in non-drinkers (0 g/d) and highest in people who consumed 15·1–30 g of alcohol/d. AE activity increased across alcohol consumption categories, with a mean maximum difference of 14 U/ml (Pfor linear trend 0·04). These associations were attenuated after adjustment for blood concentrations of HDL. The results of this study do not support the hypothesis that alcohol consumption is related to important alterations in PON1 and AE activities.

Circulating fetuin-A, a novel marker for hepatic fat accumulation, has been related to a higher risk of type 2 diabetes and cardiovascular diseases in a growing number of prospective studies. However, little is known about dietary determinants of fetuin-A concentrations in the general population. Therefore, we aimed to investigate the association between dietary intake of energy, energy-providing nutrients, alcohol and major food groups and plasma fetuin-A concentrations in the Bavarian Food Consumption Survey II. Dietary intake was assessed by three 24-h dietary recalls, and plasma concentrations of fetuin-A were measured in 558 adults (18–81 years). After multivariable adjustment for lifestyle factors and body fatness, higher energy intake was nonsignificantly associated with higher fetuin-A concentrations (per 2092 kJ/d (500 kcal/d) 3·7 µg/ml, 95 % CI –0·5, 7·8 µg/ml). There was no clear association between energy-providing nutrients and fetuin-A concentrations. Higher alcohol intake was associated with lower fetuin-A concentrations (Ptrend 0·003): mean fetuin-A concentrations were 324 (95 % CI 313, 335) µg/ml in non-drinkers, and with 293 (95 % CI 281, 306) µg/ml significantly lower in participants who drank ≥30 g alcohol per d. Mean fetuin-A concentrations decreased across quintiles of milk and dairy product intake (lowest quintile 319 (95 % CI 309, 330) µg/ml; highest quintile 304 (95 % CI 293, 314) µg/ml; Ptrend 0·03), and each 150-g increment in milk/dairy products per d was associated with 5·6 (95 % CI –9·6, –1·5) µg/ml lower fetuin-A. Dietary intakes of vegetables, meat or fish were not associated with fetuin-A concentrations. Because of the preventive potential of our findings, further exploration is warranted.

Whole-grain intake has been reported to be associated with a lower risk of several lifestyle-related diseases such as type 2 diabetes, CVD and some types of cancers. As measurement errors in self-reported whole-grain intake assessments can be substantial, dietary biomarkers are relevant to be used as complementary tools for dietary intake assessment. Alkylresorcinols (AR) are phenolic lipids found almost exclusively in whole-grain wheat and rye products among the commonly consumed foods and are considered as valid biomarkers of the intake of these products. In the present study, we analysed the plasma concentrations of five AR homologues in 2845 participants from ten European countries from a nested case–control study in the European Prospective Investigation into Cancer and Nutrition. High concentrations of plasma total AR were found in participants from Scandinavia and Central Europe and lower concentrations in those from the Mediterranean countries. The geometric mean plasma total AR concentrations were between 35 and 41 nmol/l in samples drawn from fasting participants in the Central European and Scandinavian countries and below 23 nmol/l in those of participants from the Mediterranean countries. The whole-grain source (wheat or rye) could be determined using the ratio of two of the homologues. The main source was wheat in Greece, Italy, the Netherlands and the UK, whereas rye was also consumed in considerable amounts in Germany, Denmark and Sweden. The present study demonstrates a considerable variation in the plasma concentrations of total AR and concentrations of AR homologues across ten European countries, reflecting both quantitative and qualitative differences in the intake of whole-grain wheat and rye.

The prevalence of obesity, defined as a BMI of ≥30·0 kg/m2, has increased substantially over previous decades to about 20% in industrialized countries, and a further increase is expected in the future. Epidemiological studies have shown that obesity is a risk factor for: post-menopausal breast cancer; cancers of the endometrium, colon and kidney; malignant adenomas of the oesophagus. Obese subjects have an approximately 1·5–3·5-fold increased risk of developing these cancers compared with normal-weight subjects, and it has been estimated that between 15 and 45% of these cancers can be attributed to overweight (BMI 25·0–29·9 kg/m2) and obesity in Europe. More recent studies suggest that obesity may also increase the risk of other types of cancer, including pancreatic, hepatic and gallbladder cancer. The underlying mechanisms for the increased cancer risk as a result of obesity are unclear and may vary by cancer site and also depend on the distribution of body fat. Thus, abdominal obesity as defined by waist circumference or waist:hip ratio has been shown to be more strongly related to certain cancer types than obesity as defined by BMI. Possible mechanisms that relate obesity to cancer risk include insulin resistance and resultant chronic hyperinsulinaemia, increased production of insulin-like growth factors or increased bioavailability of steroid hormones. Recent research also suggests that adipose tissue-derived hormones and cytokines (adipokines), such as leptin, adiponectin and inflammatory markers, may reflect mechanisms linked to tumourigenesis.