There is evidence that a diet rich in fruit and vegetables reduces blood pressure (BP). Characteristically, the Mediterranean diet is rich in plant-derived foods and also in fat, but studies conducted in Mediterranean countries to relate diet to BP are scarce. We studied the association between fruit and vegetable consumption and BP in a cross-sectional analysis of 4393 participants in the Seguimiento Universidad de Navarra (SUN) Study, an ongoing dynamic cohort study in Spain. Diet was measured using a food-frequency questionnaire previously validated in Spain. Fat represented more than 37% total energy intake. Subjects were considered to have undiagnosed hypertension if they reported systolic BP ≥140 mmHg or diastolic BP ≥90 mmHg, and not a medical diagnosis of hypertension. The adjusted prevalence odds ratio of undiagnosed hypertension (upper v. lowest quintile) was 0·58 (95% CI 0·36, 0·91; P for trend 0·01) for vegetable consumption and 0·68 (95% CI 0·43, 1·09; P for trend 0·10) for fruit consumption. Comparing those in the highest quintile of both fruit and vegetable consumption with those in the lowest quintile of both food groups, the prevalence odds ratio was 0·23 (95% CI 0·10, 0·55; P=0·001), after adjusting for risk factors for hypertension and other dietary exposures. In a Mediterranean population with an elevated fat consumption, a high fruit and vegetable intake is inversely associated with BP levels.

A higher proportion of n-3 long-chain PUFA in tissue lipids has been associated with a lower risk of CVD and some cancers. Diet is an important predictor of n-3 long-chain PUFA composition; however, the importance of non-dietary factors such as sex and age is unclear. We measured the proportion of n-3 long-chain PUFA in serum phospholipid, cholesterol ester and TAG of 2793 New Zealanders 15 years or older who participated in the 1997 National Nutrition Survey to determine differences by sex and age. Women had lower proportions of EPA and docosapentaenoic acid in phospholipid, by 0·07 (P = 0·004) and 0·10 (P < 0·001) mol%, respectively, and a higher proportion of DHA by 0·16 mol% (P = 0·001) compared with men. Intake of fish fat did not differ between men and women. There was a positive association between age and the proportion of EPA and DHA in phospholipid (P < 0·001). The sex differences in EPA and DHA were similar at all ages. Similar sex and age differences in serum cholesterol ester n-3 long-chain PUFA were found; only age differences were found in serum TAG. Sex and age differences in n-3 long-chain PUFA occur in the general population. Men and women may need to be considered separately when examining the association between disease risk and biomarkers of n-3 fatty acids.

The extent to which maternal folate and vitamin B12 modulate infant birth weight is unclear. The present study investigated mothers in early gestation (mean 11·5 (sd 5·8) weeks) and neonates, at delivery. Erythrocyte (RBC) folate (mothers: n 683; neonates: n 614) and vitamin B12 (mothers: n 534; neonates: n 614) were measured. Data on smoking habits were available for 44 % of pregnancies (n 443). The relationship between vitamin levels and birth weight standardized for gender and gestational age was investigated, using linear regression and adjusting for possible confounding variables (maternal age, parity). Results are presented as standardized regression coefficients (b). Increasing maternal age was associated with elevated RBC folate (b 0·11 (95 % CI 0·08, 0·15), P<0·001; n 674) and smoking was associated with a decrease in maternal RBC folate (b −1·38 (95 % CI −1·92, −0·86), P=0·001; n 319). Neonatal RBC folate was predicted by maternal RBC folate (b 0·08 (95 % CI 0·04, 0·11), P=0·001; n 315) and maternal vitamin B12 (b 0·08 (95 % CI 0·01, 0·16), P=0·02; n 252). Smoking influenced maternal vitamin B12 status (b −0·88 (95 % CI −1·49, −0·27), P=0·005; n 231). Using univariate regression, smoking significantly influenced infant birth weight (b −2·15 (95 % CI −3·24, −1·04), P<0·001; n 437). However, the effect of smoking on birth weight was statistically non-significant when considered in a multivariate regression model, leaving maternal RBC folate as the only significant predictor of birth weight (b 0·25 (95 % CI 0·08, 0·42), P=0·005; n 145). These findings suggest that maternal folate status is an important determinant of infant birth weight. The combined effects of smoking and reduced RBC status on birth weight require further investigation.

Fish is an important source of energy, high-quality proteins, fat, vitamins and minerals. Within lipids, n-3 long-chain PUFA (n-3 LC PUFA), mainly EPA and DHA, play an important role in health promotion and disease prevention. In contrast to the potential health benefits of dietary fish intake, certain chemical pollutants, namely heavy metals and some organic compounds, contained in seafood have emerged as an issue of concern, particularly for frequent fish consumers and sensitive groups of populations. The present review summarises the health benefits and risks of fish consumption. n-3 LC-PUFA are key compounds of cell membranes and play an important role in human health from conception through every stage of human development, maturation and ageing. DHA has a major role in the development of brain and retina during fetal development and the first 2 years of life and positively influences neurodevelopment, mainly visual acuity and cognitive functions. n-3 LC-PUFA are also effective in preventing cardiovascular events (mainly stroke and acute myocardial infarction) especially in persons with high cardiovascular risk. By contrast, there is convincing evidence of adverse neurological/neurodevelopmental outcomes in infants and young children associated with methylmercury exposure during fetal development due to maternal fish consumption during pregnancy. Dioxins and polychlorinated biphenyls present in contaminated fish may also develop a risk for both infants and adults. However, for major health outcomes among adults, the vast majority of epidemiological studies have proven that the benefits of fish intake exceed the potential risks with the exception of a few selected species in sensitive populations.

1. Lee Index (weight (g0.33)÷ nasoanal length (mm)), density, body water and proportional weight of the gonadal fat pad were tested as estimates of body fat in a normal population of mice and a population which included obese mice.

2. In a normal population only body water and fat-pad weight correlated significantly with body fat.

3. In a population of normal and obese mice all four indices correlated significantly with body fat.

4. Lee Index had little advantage over weight: length as an estimate of body fat, and density did not correlate well enough to be used as a method of estimation.

5. Proportional weight of the gonadal fat pad is recommended as a simple reliable estimate of body fat in normal or obese mice.

Improvement of insulin resistance and inflammation is a basic strategy in the management of type 2 diabetes. There is limited evidence that prebiotics improve insulin resistance and inflammation. However, the ameliorating effect of resistant dextrin, as a prebiotic, on insulin resistance and inflammation in patients with type 2 diabetes has not been investigated so far. Therefore, the present study aimed to examine the effects of resistant dextrin on insulin resistance and inflammation in type 2 diabetic patients. In a randomised controlled clinical trial, fifty-five women with type 2 diabetes were assigned to two groups: the intervention group (n 30) and the control group (n 25). The intervention group received a daily supplement of 10 g resistant dextrin and the control group received a similar amount of maltodextrin as placebo for 8 weeks. Fasting plasma glucose (FPG), HbA1c, insulin, high-sensitivity C-reactive protein (hs-CRP), IL-6, TNF-α, malondialdehyde (MDA) and serum endotoxin concentrations were measured before and after the intervention. Data were analysed using SPSS (version 13). Paired and unpaired t tests and ANCOVA were used to compare quantitative variables after the intervention. Patients supplemented with resistant dextrin exhibited a significant decrease in fasting insulin (20·1 pmol/l, 22·8 %), homeostasis model assessment of insulin resistance (1·3, 24·9 %), quantitative insulin sensitivity check index (0·2, 7·2 %), IL-6 (1·4 pg/ml, 28·4 %), TNF-α (5·4 pg/ml, 18·8 %), MDA (1·2 nmol/ml, 25·6 %) and endotoxin (6·2 endotoxin units/ml, 17·8 %) concentrations than those supplemented with maltodextrin (P< 0·05). Decreases in FPG (0·05 mmol/l, 0·6 %), HbA1c (0·5 %, 9·6 %) and hs-CRP (2·7 ng/ml, 35·1 %) concentrations in the resistant dextrin group were not significant when compared with the maltodextrin group. In conclusion, resistant dextrin supplementation can modulate inflammation and improve insulin resistance in women with type 2 diabetes.

n-6 PUFA are well known for their critical role in many physiological functions and seem to reduce risks of CHD. However, some argue that excessive consumption of n-6 PUFA may lead to adverse effects on health and therefore recommend reducing dietary n-6 PUFA intake or fixing an upper limit. In this context, the present work aimed to review evidence on the link between n-6 PUFA and risks of CVD. Epidemiological studies show that n-6 PUFA dietary intake significantly lowers blood LDL-cholesterol levels. In addition, n-6 PUFA intake does not increase several CVD risk factors such as blood pressure, inflammatory markers, haemostatic parameters and obesity. Data from prospective cohort and interventional studies converge towards a specific protective role of dietary n-6 PUFA intake, in particular linoleic acid, against CVD. n-6 PUFA benefits are even increased when SFA intake is also reduced. In regards to studies examined in this narrative review, recommendation for n-6 PUFA intake above 5 %, and ideally about 10 %, of total energy appears justified.

Accurate dietary assessment is an essential foundation of research in nutritional epidemiology. Due to the weaknesses in current methodology, attention is turning to strategies that automate the dietary assessment process to improve accuracy and reduce the costs and burden to participants and researchers. ‘My Meal Mate’ (MMM) is a smartphone application designed to support weight loss. The present study aimed to validate the diet measures recorded on MMM against a reference measure of 24 h dietary recalls. A sample of fifty volunteers recorded their food and drink intake on MMM for 7 d. During this period, they were contacted twice at random to conduct 24 h telephone recalls. Daily totals for energy (kJ) and macronutrients recorded on MMM were compared against the corresponding day of recall using t tests for group means and Pearson's correlations. Bland–Altman analysis was used to assess the agreement between the methods. Energy (kJ) recorded on MMM correlated well with the recalls (day 1: r 0·77 (95 % CI 0·62, 0·86), day 2: r 0·85 (95 % CI 0·74, 0·91)) and had a small mean difference (day 1 (MMM −  recall): − 68 kJ/d (95 % CI − 553, 418 kJ) ( − 16 kcal/d, 95 % CI − 127, 100 kcal); day 2 (MMM −  recall): − 441 kJ/d (95 % CI − 854, − 29 kJ) ( − 105 kcal/d, 95 % CI − 204, − 7 kcal)). Bland–Altman analysis showed wide limits of agreement between the methods: − 3378 to 3243 kJ/d ( − 807 to 775 kcal/d) on day 1. At the individual level, the limits of agreement between MMM and the 24 h recall were wide; however, at the group level, MMM appears to have potential as a dietary assessment tool.

The objective of the present study was to investigate the postprandial metabolism of two starches with contrasting rates of hydrolysis in vitro. Characterized using the Englyst method of in vitro starch classification, C*Set 06 598 contained predominantly rapidly digestible starch and C*Gel 04 201 contained predominantly slowly digestible starch. Each test starch, naturally enriched with 13C, was fed to ten healthy female volunteers as part of a moderate fat test meal (containing 75 g test starch and 21 g fat), in a double-blind randomized crossover design. The metabolic response to each starch was measured after an overnight fast, in an acute 6 h study, before and after 14 d of daily consumption of 75 g test starch. During each acute study, blood samples were taken at 15 min intervals for the first 2 h and at 30 min intervals for the remaining 4 h. Breath 13CO2 enrichment was measured at the same time points and indirect calorimetry was performed for 20 min every 40 min immediately before and throughout the study. Significantly more rapid, greater changes in postprandial plasma glucose, NEFA and serum insulin concentrations were observed after consumption of the rapidly digestible starch. Breath 13CO2 output over the first 3–4 h rose rapidly then began to decline following consumption of the rapidly digestible starch, but plateaued for the slowly digestible starch. The 14 d adaptation period did not affect any of the glycaemic or lipaemic variables but there was a reduction in postprandial plasminogen activator inhibitor-1 concentrations. These data confirm that starches characterized as predominantly rapidly digestible versus slowly digestible by the Englyst procedure provoke distinctly different patterns of metabolism postprandially.

Gain in body weight over a number of years could be achieved through cumulative positive energy balances. These positive balances could come about through adjustments in the various components of energy expenditure or fuel utilization, together with shifts in food selection or eating patterns leading to adjustments in macronutrient intake. This means that many combinations of intake and expenditure could lead to a positive energy balance; these combinations can be called routes to body weight gain. However, these routes are difficult to trace by studying random samples of individuals. Previous investigations have found a clear association between high fat consumption and the occurrence of obesity, and although a high fat intake is a strong behavioural risk factor for weight gain, the relationship does not constitute a biological inevitability. Some normal-weight and lean individuals appear to eat a high-fat diet. To investigate reasons for this we have studied individuals initially defined by particular clusters of dietary characteristics related to fat and carbohydrate consumption. Habitual high-fat (HF) and low-fat (LF) consumers have been termed phenotypes. Various aspects of energy expenditure (physiological and behavioural) and energy intake were measured in these individuals with contrasting profiles. HF phenotypes had high intakes of fatty foods and an overall higher energy intake than LF. However, these groups of young adult males had similar BMIs and percentage body fat. The HF had a significantly higher resting metabolic rate (RMR) and a lower RQ, together with high plasma fasting leptin levels, and a higher sleeping heart rate. In HF individuals the physical activity level was somewhat lower and they had significantly more periods of sedentary behaviour than LF subjects. Although HF individuals appear to be more vulnerable to developing obesity, both phenotypes carry particular risk factors and protective factors for weight gain. The use of phenotypes has allowed the identification of different potential routes to weight gain. Different strategies are required to prevent age-related increase in body weight in these quite different individuals.

Previous studies in Australian children/adolescents and adults examining added sugar (AS) intake were based on now out-of-date national surveys. We aimed to examine the AS and free sugar (FS) intakes and the main food sources of AS among Australians, using plausible dietary data collected by a multiple-pass, 24-h recall, from the 2011–12 Australian Health Survey respondents (n 8202). AS and FS intakes were estimated using a previously published method, and as defined by the WHO, respectively. Food groups contributing to the AS intake were described and compared by age group and sex by one-way ANOVA. Linear regression was used to test for trends across age groups. Usual intake of FS (as percentage energy (%EFS)) was computed using a published method and compared with the WHO cut-off of <10 %EFS. The mean AS intake of the participants was 60·3 (sd 52·6) g/d. Sugar-sweetened beverages accounted for the greatest proportion of the AS intake of the Australian population (21·4 (sd 30·1) %), followed by sugar and sweet spreads (16·3 (sd 24·5) %) and cakes, biscuits, pastries and batter-based products (15·7 (sd 24·4) %). More than half of the study population exceeded the WHO’s cut-off for FS, especially children and adolescents. Overall, 80–90 % of the daily AS intake came from high-sugar energy-dense and/or nutrient-poor foods. To conclude, the majority of Australian adults and children exceed the WHO recommendation for FS intake. Efforts to reduce AS intake should focus on energy-dense and/or nutrient-poor foods.

The dual burden of malnutrition reportedly coexists in Malaysia; however, existing data are scarce and do not adequately represent the nutritional status of Malaysian children. The Nutrition Survey of Malaysian Children was carried out with the aim of assessing the nutritional status in a sample of nationally representative population of children aged 6 months to 12 years. A total of 3542 children were recruited using a stratified random sampling method. Anthropometric measurements included weight, height, mid-upper arm circumference, and waist and hip circumferences. Blood biochemical assessment involved analyses of Hb, serum ferritin, and vitamins A and D. Dietary intake was assessed using semi-quantitative FFQ, and nutrient intakes were compared with the Malaysian Recommended Nutrient Intakes (RNI). The prevalence of overweight (9·8 %) and obesity (11·8 %) was higher than that of thinness (5·4 %) and stunting (8·4 %). Only a small proportion of children had low levels of Hb (6·6 %), serum ferritin (4·4 %) and vitamin A (4·4 %), but almost half the children (47·5 %) had vitamin D insufficiency. Dietary intake of the children was not compatible with the recommendations, where more than one-third did not achieve the Malaysian RNI for energy, Ca and vitamin D. The present study revealed that overnutrition was more prevalent than undernutrition. The presence of high prevalence of vitamin D insufficiency and the inadequate intake of Ca and vitamin D are of concern. Hence, strategies for improving the nutritional status of Malaysian children need to consider both sides of malnutrition and also put emphasis on approaches for the prevention of overweight and obesity as well as vitamin D insufficiency.

This randomized, double-blind, placebo-controlled study was conducted to compare the effect of a 15-week weight-reducing programme ( − 2900 kJ/d) coupled with a calcium plus vitamin D (calcium+D) supplementation (600 mg elemental calcium and 5 μg vitamin D, consumed twice a day) or with a placebo, on body fat and on spontaneous energy/macronutrient intake. Sixty-three overweight or obese women (mean age 43 years, mean BMI 32 kg/m2) reporting a daily calcium intake < 800 mg participated in present study. Anthropometric variables, resting energy expenditure and spontaneous energy intake were measured before and after the 15-week programme. The calcium+D supplementation induced no statistically significant increase in fat mass loss in response to the programme. However, when analyses were limited to very low-calcium consumers only (initial calcium intake ≤ 600 mg/d, n 7 for calcium+D, n 6 for placebo), a significant decrease in body weight and fat mass (P < 0·01) and in spontaneous dietary lipid intake (P < 0·05) was observed in the calcium+D but not in the placebo group. In very low-calcium consumers, change in fat mass was positively correlated with change in lipid intake. During the weight-reducing programme, a calcium+D supplementation was necessary in female overweight/obese very low-calcium consumers to reach significant fat mass loss that seemed to be partly explained by a decrease in lipid intake. We propose that this change in lipid intake could be influenced by a calcium-specific appetite control.

The prevalence of obesity is reaching epidemic proportions in many industrialized countries. There is growing evidence that, even if the trigger of this epidemic is found in changes in the environment, genes are interacting with the environment to cause weight gain. Studies of twins reared apart indicate that approximately two-thirds of the variability in BMI is attributed to genetic factors. From prospective studies in Pima Indians we can ascribe 12 % of the variability in BMI to metabolic rate, 5 % to fat oxidation, and another probable 10 % to the level of spontaneous physical activity. These data indicate that at least 40 % of the variability in BMI is related to genetic factors involved in the regulation of food intake and/or volitional activity. This indicates that the most likely successful therapy for obesity may target pathways of the regulation of food intake. Similarly, an environment favouring engagement in physical activity should be promoted.

Many adult diseases, including type 2 diabetes, hypertension and cardiovascular disease, are related to low birth weight. The mechanistic basis of this relationship is not known. To investigate the role of fetal undernutrition, we used a rat model of maternal protein restriction in which dams were fed a diet containing 80 g protein/kg (v. 200 g/kg in the control group) throughout gestation and lactation. Offspring were born smaller than controls and in adulthood developed diabetes, hyperinsulinaemia and tissue insulin resistance. To determine possible mechanisms of fetal programming, circulating levels of several hormones were measured in maternal plasma at gestational days 14, 17 and 21 and fetal plasma at gestational day 21. Several differences were noted at day 14, when glucose concentrations in maternal and feto–placental blood were raised significantly (P=0·04 and P=0·0001 respectively); insulin levels in the low-protein (LP) dams were raised (P=0·04), prolactin levels were raised (P=0·047) and progesterone levels were reduced (P=0·02). Circulating 17β-oestradiol in the LP dams was raised by 35% over those of the controls from day 17 to day 21 (P=0·008). A significant decrease in maternal leptin levels (P=0·004) was observed at gestation on day 21. Neither oestradiol nor leptin levels were altered in the fetal circulation at day 21. Maternal and fetal corticosterone levels were comparable with control levels, suggesting that they do not initiate the programming effects in this model. Our present results suggest that maternal protein restriction imposes changes in maternal levels of glucose, insulin, prolactin, progesterone, oestradiol and leptin; these changes could influence the programming of eventual adult disease in the developing fetus.

Fibres with a range of abilities to perturb cholesterol homeostasis were used to investigate how the serum cholesterol-lowering effects of insoluble dietary fibres are related to parameters of intestinal cholesterol absorption and hepatic cholesterol homeostasis in mice. Cholestyramine, chitosan and cellulose were used as examples of fibres with high, intermediate and low bile acid-binding capacities, respectively. The serum cholesterol levels in a control group of mice fed a high fat/high cholesterol (HFHC) diet for 3 weeks increased about 2-fold to 4·3 mm and inclusion of any of these fibres at 7·5 % of the diet prevented this increase from occurring. In addition, the amount of cholesterol accumulated in hepatic stores due to the HFHC diet was reduced by treatment with these fibres. The three kinds of fibres showed similar hypocholesterolaemic activity; however, cholesterol depletion of liver tissue was greatest with cholestyramine. The mechanisms underlying the cholesterol-lowering effect of cholestyramine were (1) decreased cholesterol (food) intake, (2) decreased cholesterol absorption efficiency, and (3) increased faecal bile acid and cholesterol excretion. The latter effects can be attributed to the high bile acid-binding capacity of cholestyramine. In contrast, incorporation of chitosan or cellulose in the diet reduced cholesterol (food) intake, but did not affect either intestinal cholesterol absorption or faecal sterol output. The present study provides strong evidence that above all satiation and satiety effects underlie the cholesterol-lowering properties of insoluble dietary fibres with moderate or low bile acid-binding capabilities.

Bioavailability studies are vital to assess the potential impact of bioactive compounds on human health. Although conjugated phenolic metabolites derived from colonic metabolism have been identified in the urine, the quantification and appearance of these compounds in plasma is less well studied. In this regard, it is important to further assess their potential biological activity in vivo. To address this gap, a cross-over intervention study with a mixed fruit purée (blueberry, blackberry, raspberry, strawberry tree fruit and Portuguese crowberry) and a standard polyphenol-free meal was conducted in thirteen volunteers (ten females and three males), who received each test meal once, and plasma metabolites were identified by HPLC–MS/MS. Sulfated compounds were chemically synthesised and used as standards to facilitate quantification. Gallic and caffeic acid conjugates were absorbed rapidly, reaching a maximum concentration between 1 and 2 h. The concentrations of sulfated metabolites resulting from the colonic degradation of more complex polyphenols increased in plasma from 4 h, and pyrogallol sulfate and catechol sulfate reached concentrations ranging from 5 to 20 μm at 6 h. In conclusion, phenolic sulfates reached high concentrations in plasma, as opposed to their undetected parent compounds. These compounds have potential use as biomarkers of polyphenol intake, and their biological activities need to be considered.

A comparative, randomised, double-blind trial was performed in the medical departments of five hospitals to study the effects of regular consumption of short-chain fructo-oligosaccharides (sc-FOS) on the digestive comfort of subjects with minor functional bowel disorders (FBD). In step 1, 2235 subjects were questioned to assess the incidence and intensity of digestive disorders. In step 2, 105 of these patients diagnosed with minor FBD were randomised into two groups to receive either 5 g sc-FOS or 5 g placebo (sucrose and maltodextrins) per d over a 6-week period. The incidence and intensity of digestive disorders were assessed at the end of the treatment period (day 43) using the step 1 questionnaires. A quality-of-life questionnaire was also completed at the start and end of the treatment period to assess potential effects on well-being and social performance. In step 1, 44 % of the subjects questioned presented FBD, of whom 57·1 % suffered from minor FBD. In step 2, on day 43, the intensity of digestive disorders decreased by 43·6 % in the sc-FOS group v. a 13·8 % increase in the placebo group (P = 0·026). Symptoms were experienced less frequently by 75·0 % of subjects in the sc-FOS group, while 53·8 % of controls experienced no change (P = 0·064). Using the functional digestive disorders quality of life questionnaire, the discomfort item scores increased in the sc-FOS group (P = 0·031). However, expressed as change in quality of life (improvement, worsening or unchanged), daily activities were significantly improved in the sc-FOS group (P = 0.022). Regular consumption of sc-FOS may improve digestive comfort in a working population not undergoing medical treatment.

The effect of 16 d intake of 300 mg carotenoids/kg diet (β-carotene (βC), bixin (BX), lycopene (LY), lutein (LU), canthaxanthin (CX) or astaxanthin (AX)) on xenobiotic metabolizing enzymes in the liver, lung, kidney and small intestine of male Wistar rats was assessed. A control group received the basal diet (AIN-76) without carotenoids and a positive control group for enzyme induction received 3-methylcholanthrene (3-MC) at 666 mg/kg diet. Cytochrome P450 activity was assessed using the substrates ethoxyresorufin for P450 1A1, methoxyresorufin for P450 1A2, pentoxyresorufin for P450 2B1/2 and benzyloxyresorufin for P450 types 1A1/2, 2B1/2 and 3A. Glutathione-S-transferase (EC 2.5.1.18) and reduced glutathione status were assessed. Carotenoid uptake by the tissues was also determined. 3-MC and the carotenoids BX, CX and AX led to significant increases compared with control in liver, lung and kidney ethoxyresorufin-O-deethylation. Methoxyresorufin-O-demethylation activity was significantly increased in liver and lung by BX, CX and AX but only CX and AX significantly increased activity in kidney. Pentoxyresorufin-O-depentylation and benzyloxyresorufin-O-dearylation increased in liver of 3-MC-, BX-, CX- and AX-treated rats, but to a much lesser degree than for the other two substrates. Benzyloxyresorufin-O-dearylation in lung was significantly decreased by all carotenoids. Activities of any of the measured enzymes in the small intestine were undetectable in all treatment groups except the 3-MC group. Glutathione status was unaffected by any of the treatments. This is the first study identifying the carotenoids BX, CX and AX as inducers of rat lung and kidney xenobiotic metabolizing enzymes.

Carotenoid and vitamin C intakes, assessed by FFQ, have been positively associated with plasma concentrations in different populations. However, the influence of BMI on these associations has not been explored in detail. We explored in a cross-sectional study the relation between dietary carotenoid and vitamin C intakes, using a 135-item FFQ, with their plasma concentrations by BMI categories in 252 men and 293 women, 65 years and older. For men and women combined, significant (P < 0·05) Pearson correlations were observed between energy-adjusted dietary intakes and plasma concentrations (carotenoids adjusted for cholesterol) for: α-carotene 0·21, β-carotene 0·19, lycopene 0·18, β-cryptoxanthin 0·20 and vitamin C 0·36. Multiple linear regression analyses showed that the intake of carotenoids and vitamin C were significant predictors of their respective plasma concentration (P < 0·01), and that BMI was inversely associated with plasma concentration of carotenoids (P ≤ 0·01) but not with plasma vitamin C. In addition, we observed significant interactions between BMI and the intakes of α-carotene and lutein + zeaxanthin, and to a lower extent β-carotene, suggesting that these intakes in subjects with high BMI were not good predictors of their plasma concentration. The present data suggest that plasma carotenoids and vitamin C may be good markers of dietary intake in elderly subjects, but not so for α-carotene, β-carotene and lutein + zeaxanthin in obese subjects.