According to human research, the location of fat accumulation seems to play an important role in the induction of obesity-related inflammatory complications. To evaluate whether an inflammatory response to obesity depends on adipose tissue location, adipokine gene expression, presence of immune cells and adipocyte cell size of subcutaneous adipose tissue (SAT) and visceral adipose tissue (VAT) were compared between lean and obese cats. Additionally, the present study proposes the cat as a model for human obesity and highlights the importance of animal models for human research. A total of ten chronically obese and ten lean control cats were included in the present study. Body weight, body condition score and body composition were determined. T-lymphocyte, B-lymphocyte, macrophage concentrations and adipocyte cell size were measured in adipose tissue at different locations. Serum leptin concentration and the mRNA expression of leptin and adiponectin, monocyte chemoattractant protein-1, chemoligand-5, IL-8, TNF-α, interferon-γ, IL-6 and IL-10 were measured in blood and adipose tissues (abdominal and inguinal SAT, and omental, bladder and renal VAT). Feline obesity was characterised by increased adipocyte cell size and altered adipokine gene expression, in favour of pro-inflammatory cytokines and chemokines. Consequently, concentration of T-lymphocytes was increased in the adipose tissue of obese cats. Alteration of adipose tissue was location dependent in both lean and obese cats. Moreover, the observed changes were more prominent in SAT compared with VAT.

Little is known about the effects of combined micronutrient and sugar consumption on growth and cognition. In the present study, we investigated the effects of micronutrients and sugar, alone and in combination, in a beverage on growth and cognition in schoolchildren. In a 2 × 2 factorial design, children (n 414, 6–11 years) were randomly allocated to consume beverages containing (1) micronutrients with sugar, (2) micronutrients with a non-nutritive sweetener, (3) no micronutrients with sugar or (4) no micronutrients with a non-nutritive sweetener for 8·5 months. Growth was assessed and cognition was tested using the Kaufman Assessment Battery for Children version II (KABC-II) subtests and the Hopkins Verbal Learning Test (HVLT). Micronutrients decreased the OR for Fe deficiency at the endpoint (OR 0·19; 95 % CI 0·07, 0·53). Micronutrients increased KABC Atlantis (intervention effect: 0·76; 95 % CI 0·10, 1·42) and HVLT Discrimination Index (1·00; 95 % CI 0·01, 2·00) scores. Sugar increased KABC Atlantis (0·71; 95 % CI 0·05, 1·37) and Rover (0·72; 95 % CI 0·08, 1·35) scores and HVLT Recall 3 (0·94; 95 % CI 0·15, 1·72). Significant micronutrient × sugar interaction effects on the Atlantis, Number recall, Rover and Discrimination Index scores indicated that micronutrients and sugar in combination attenuated the beneficial effects of micronutrients or sugar alone. Micronutrients or sugar alone had a lowering effect on weight-for-age z-scores relative to controls (micronutrients − 0·08; 95 % CI − 0·15, − 0·01; sugar − 0·07; 95 % CI − 0·14, − 0·002), but in combination, this effect was attenuated. The beverages with micronutrients or added sugar alone had a beneficial effect on cognition, which was attenuated when provided in combination.

Previous studies have reported a close relationship between nutritional and functional domains, but evidence in long-term care residents is still limited. We evaluated the relationship between nutritional risk and functional status and the association of these two domains with mortality in newly institutionalised elderly. In the present multi-centric prospective cohort study, involving 346 long-term care resident elderly, nutritional risk and functional status were determined upon admission by the Geriatric Nutritional Risk Index (GNRI) and the Barthel Index (BI), respectively. The prevalence of high (GNRI < 92) and low (GNRI 92–98) nutritional risk were 36·1 and 30·6 %, respectively. At multivariable linear regression, functional status was independently associated with age (P= 0·045), arm muscle area (P= 0·048), the number of co-morbidities (P= 0·027) and mainly with the GNRI (P< 0·001). During a median follow-up of 4·7 years (25th–75th percentile 3·7–6·2), 230 (66·5 %) subjects died. In the risk analysis, based on the variables collected at baseline, both high (hazard ratio (HR) 1·86, 95 % CI 1·32, 2·63; P< 0·001) and low nutritional risk (HR 1·52, 95 % CI 1·08, 2·14; P= 0·016) were associated with all-cause mortality. Participants at high nutritional risk (GNRI < 92) also showed an increased rate of cardiovascular mortality (HR 1·93, 95 % CI 1·28, 2·91; P< 0·001). No association with outcome was found for the BI. Upon admission, nutritional risk was an independent predictor of functional status and mortality in institutionalised elderly. Present data support the concept that the nutritional domain is more relevant than functional status to the outcome of newly institutionalised elderly.

Consumption of fermented milk (FM) containing a probiotic, Lactobacillus gasseri SBT2055 (LG2055), previously showed a reduction in abdominal adiposity in a randomised controlled trial (RCT) using FM with 108 colony-forming units (cfu) of LG2055/g. However, whether the effectiveness is observed at lower concentrations, the recommended minimum or intermediate levels of probiotics (106 or 107cfu/g, respectively), remains to be examined. A multi-centre, double-blind, parallel-group RCT was conducted using 210 healthy Japanese adults with large visceral fat areas (80·2–187·8 cm2). They were balanced for their baseline characteristics and randomly assigned to three groups receiving FM containing 107, 106 or 0 (control) cfu LG2055/g of FM, and were asked to consume 200 g FM/d for 12 weeks. Abdominal visceral fat areas, which were determined by computed tomography, at week 12, changed from baseline by an average of − 8·5 % (95 % CI − 11·9, − 5·1; P< 0·01) in the 107 dose group, and by − 8·2 % (95 % CI − 10·8, − 5·7; P< 0·01) in the 106 dose group. Other measures including BMI, waist and hip circumferences, and body fat mass were also significantly decreased from baseline at week 12 in both groups; interestingly, the cessation of taking FM for 4 weeks attenuated these effects. In the control group, none of these parameters significantly decreased from baseline. These findings demonstrate that consumption of LG2055 at doses as low as the order of 108cfu/d exhibited a significant lowering effect on abdominal adiposity, and suggest that constant consumption might be needed to maintain the effect.

Sources of variation in nutrient intake have been examined for Western diets, but little is known about the sources of variation and their differences by age and sex among Koreans. We examined sources of variation in nutrient intake and calculated the number of days needed to estimate usual intake using 12 d of dietary records (DR). To this end, four 3 d DR including two weekdays and one weekend day were collected throughout four seasons of 1 year from 178 male and 236 female adults aged 20–65 years residing in Seoul, Korea. The sources of variation were estimated using the random-effects model, and the variation ratio (within-individual:between-individual) was calculated to determine a desirable number of days. Variations attributable to the day of the week, recording sequence and seasonality were generally small, although the degree of variation differed by sex and age (20–45 years and 46–65 years). The correlation coefficient between the true intake and the observed intake (r) increased with additional DR days, reaching 0·7 at 3–4 d and 0·8 at 6–7 d. However, the degree of increase became attenuated with additional days: r increased by 13·0–26·9 % from 2 to 4 d, by 6·5–16·4 % from 4 to 7 d and by 4·0–11·6 % from 7 to 12 d for energy and fifteen nutrients. In conclusion, the present study suggests that the day of the week, recording sequence and seasonality minimally contribute to the variation in nutrient intake. To measure Korean usual dietary intake using open-ended dietary instruments, 3–4 d may be needed to achieve modest precision (r>0·7) and 6–7 d for high precision (r>0·8).

The present study was aimed to validate two normalised short-form (SF) Mini-Nutritional Assessments (MNA) that contained either BMI (Taiwan version 1, T1) or calf circumference (CC; Taiwan version 2, T2) for rating the nutritional status of elderly Taiwanese. Both versions adopted Taiwanese anthropometric cut-offs, but T2 further had the BMI item replaced by CC. We compared the ability of the two SF in rating the nutritional status of 2674 elderly Taiwanese in the 1999 ‘Taiwan Longitudinal Survey on Aging’ with their respective full versions. We evaluated the agreement between the SF and full scales with weighted κ and performed Cox regression analysis for the follow-up 4-year mortality according to nutritional status rated at baseline. The results showed that the agreements between the respective SF and the full MNA were good (weighted κ: 0·679 for T1 and 0·667 for T2). Both SF performed well in predicting follow-up 4-year mortality relative to the full MNA. In conclusion, MNA-T1-SF and -T2-SF have good consistency with the full MNA and have quite comparable abilities in rating the nutritional status of elderly Taiwanese. Both SF versions appear appropriate for functioning as stand-alone units for rating the nutritional status of the elderly in community-living settings or the general population.

Inflammation mediates several chronic diseases. Micronutrients can act on inflammation, either through modulating cytokine production or by scavenging by-products of activated white cells. Identifying dietary patterns (DP) reflecting these mechanisms and relating them to inflammation is of interest. The objective of the study was to identify DP specifically associated with intakes of nutrients potentially involved in inflammatory processes in a middle-aged population and investigate long-term associations between these DP and C-reactive protein (CRP) status assessed several years later. Subjects included in the Supplementation in Vitamins and Mineral Antioxidants 2 cohort study, having available data on dietary assessment carried out in 1994–5 and CRP measurement in 2007–9, were included in the analysis. DP were extracted with reduced rank regression (RRR), using antioxidant micronutrients and PUFA as response variables. Associations between CRP measurements >3 mg/l and extracted DP were then examined with logistic regression models providing OR and 95 % CI. A total of 2031 subjects (53·2 % women, mean follow-up duration: 12·5 years) were included in the analyses. Of the four extracted DP, a DP with high loading values of vegetables and vegetable oils, leading to high intakes of antioxidant micronutrients and essential fatty acids, was significantly and negatively associated with risk of elevated CRP (OR 0·88; 95 % CI 0·78, 0·98). Conversely, a DP reflecting a high n-6:n-3 fatty acid intake ratio was positively and significantly associated with elevated CRP (adjusted OR 1·15; 95 % CI 1·00, 1·32). DP extracted with RRR provide support for further exploration of relationships between dietary behaviour and inflammation.

The purpose of the present study was to determine the effects of short-term supplementation with the free acid form of β-hydroxy-β-methylbutyrate (HMB-FA) on indices of muscle damage, protein breakdown, recovery and hormone status following a high-volume resistance training session in trained athletes. A total of twenty resistance-trained males were recruited to participate in a high-volume resistance training session centred on full squats, bench presses and dead lifts. Subjects were randomly assigned to receive either 3 g/d of HMB-FA or a placebo. Immediately before the exercise session and 48 h post-exercise, serum creatine kinase (CK), urinary 3-methylhistadine (3-MH), testosterone, cortisol and perceived recovery status (PRS) scale measurements were taken. The results showed that CK increased to a greater extent in the placebo (329 %) than in the HMB-FA group (104 %) (P= 0·004, d= 1·6). There was also a significant change for PRS, which decreased to a greater extent in the placebo (9·1 (sem 0·4) to 4·6 (sem 0·5)) than in the HMB-FA group (9·1 (sem 0·3) to 6·3 (sem 0·3)) (P= 0·005, d= − 0·48). Muscle protein breakdown, measured by 3-MH analysis, numerically decreased with HMB-FA supplementation and approached significance (P= 0·08, d= 0·12). There were no acute changes in plasma total or free testosterone, cortisol or C-reactive protein. In conclusion, these results suggest that an HMB-FA supplement given to trained athletes before exercise can blunt increases in muscle damage and prevent declines in perceived readiness to train following a high-volume, muscle-damaging resistance-training session.

Craving for chocolate is a common phenomenon, which may evolve to an addictive-like behaviour and contribute to obesity. Nepicastat is a selective dopamine β-hydroxylase (DBH) inhibitor that suppresses cocaine-primed reinstatement of cocaine seeking in rats. We verified whether nepicastat was able to modify the reinforcing and motivational properties of a chocolate solution and to prevent the reinstatement of chocolate seeking in rats. Nepicastat (25, 50 and 100 mg/kg, intraperitoneal) produced a dose-related inhibition of operant self-administration of the chocolate solution in rats under fixed-ratio 10 (FR10) and progressive-ratio schedules of reinforcement, measures of the reinforcing and motivational properties of the chocolate solution, respectively. The effect of nepicastat on the reinstatement of chocolate seeking was studied in rats in which lever-responding had been extinguished by removing the chocolate solution for approximately 8 d. Nepicastat dose-dependently suppressed the reinstatement of lever-responding triggered by a ‘priming’ of the chocolate solution together with cues previously associated with the availability of the reward. In a separate group of food-restricted rats trained to lever-respond for regular food pellets, nepicastat reduced FR10 lever-responding with the same potency as for the chocolate solution. Spontaneous locomotor activity was not modified by nepicastat doses that reduced self-administration of the chocolate solution and regular food pellets and suppressed the reinstatement of chocolate seeking. The results indicate that nepicastat reduces motivation to food consumption sustained by appetite or palatability. Moreover, the results suggest that DBH inhibitors may be a new class of pharmacological agents potentially useful in the prevention of relapse to food seeking in human dieters.

Previous studies have reported that polydextrose can reduce food intake; however, the optimal dose required to achieve this effect is currently unknown. The present study investigated the effects of consuming a range of doses of polydextrose on appetite and energy intake (EI) using a randomised within-subject, cross-over design. For this purpose, twenty-one participants (n 12 men, n 9 women) consumed an 837 kJ liquid preload containing 0 g (control), 6·3, 12·5 or 25 g polydextrose. Subjective appetite ratings were collected using visual analogue scales and an ad libitum test meal was served 90 min later. Participants recorded EI for the remainder of the day in a food diary. Test meal EI following the control preload (5756 (sem 423) kJ) was significantly higher than following the 6·3 g (5048 (sem 384) kJ), 12·5 g (4722 (sem 384) kJ) and 25 g (4362 (sem 316) kJ) preloads (P< 0·05), and EI following the 6·3 g preload was significantly higher than following the 25 g preload (P< 0·01). There were no differences in self-reported EI during the remainder of the day between the preloads containing the varying doses of polydextrose. Total EI (breakfast+preload+ad libitum test meal+remainder of the day) was significantly higher when the control preload was consumed (12 051 (sem 805) kJ) compared with either the 12·5 g (10 854 (sem 589) kJ) or 25 g (10 658 (sem 506) kJ) preload (P< 0·05). These differences in EI were not accompanied by corresponding differences in subjective appetite ratings. In summary, polydextrose effectively reduces subsequent EI in a dose-dependent manner.

The main objective of the present study was to determine the potential of n-3 and n-6 fatty acids or coenzyme Q10 (CoQ10) to alter serum prostate-specific antigen (PSA) levels in normal healthy men. A total of 504 healthy men with serum PSA level ≤ 2·5 ng/ml were recruited into the study. Serum PSA values were not segregated by decade of age. Participants were randomly assigned to a daily dietary supplement containing n-3 fatty acids (1·12 g of EPA and 0·72 g of DHA per capsule) (group 1, n 126), n-6 fatty acid (600 mg γ-linolenic acid (GLA) each capsule) (group 2, n 126), CoQ10 (100 mg per capsule) (group 3, n 126) or a similar regimen of placebo (group 4, n 126) for 12 weeks. Study medication was administered as two capsules to be taken twice daily. Serum levels of PSA, EPA, DHA, GLA, lipid profile and reproductive hormones were also measured. EPA treatment significantly reduced serum PSA level by 30·0 (95 % CI 25, 36) % (P= 0·004) from baseline. In contrast, GLA therapy significantly increased serum PSA concentration by 15·0 (95 % CI 11, 20) % (P= 0·02). CoQ10 therapy also significantly reduced serum PSA level by 33·0 (95 % CI 27, 40) % (P= 0·002). In multivariable analysis, serum values of PSA were strongly correlated with duration of EPA (r − 0·62; 95 % CI − 0·42, − 0·77; P= 0·003), n-6 (r 0·42; 95 % CI 0·31, 0·58; P= 0·02) and CoQ10 use (r − 0·77; 95 % CI − 0·56, − 0·87; P= 0·001). There were also significant correlations between serum values of DHA, EPA, GLA and CoQ10 and serum PSA levels. The present study demonstrates that dietary supplements containing EPA, GLA or CoQ10 may significantly affect serum PSA levels.

We have examined the associations between dietary glycaemic index (GI), substitutions of total, low-, medium- and high-GI carbohydrates for fat and the risk of CHD. The study consisted of 21 955 male smokers, aged 50–69 years, within the Alpha-Tocopherol, Beta-Carotene Cancer Prevention Study. The diet was assessed at baseline using a validated FFQ. During a 19-year follow-up, 4379 CHD cases (2377 non-fatal myocardial infarctions and 2002 CHD deaths) were identified from national registers. Relative risks (RR) and CI for CHD were analysed using Cox proportional hazards modelling, and multivariate nutrient density models were applied to examine the associations between the substitutions of macronutrients and the risk of CHD. Dietary GI was inversely associated with CHD risk: multivariate RR in the highest v. lowest quintile was 0·89 (95 % CI 0·81, 0·99). Replacement of higher-GI carbohydrates with lower-GI carbohydrates did not associate with the risk. Replacing saturated and trans-fatty acids with carbohydrates was associated with decreased CHD risk: RR for substitution of 2 % of energy intake was 0·97 (95 % CI 0·94, 0·99). On the contrary, replacing MUFA with carbohydrates was associated with an increased risk: RR for substitution of 2 % of energy intake was 1·08 (95 % CI 1·01, 1·16). We conclude that in the present study population, contrary to the hypothesis, a lower GI does not associate with a decreased risk of CHD. The associations of carbohydrates with CHD risk depend on the fatty acid composition of the diet.

Frailty is a state of decreased physical functioning and a significant complication of ageing. We examined frailty, energy and macronutrient intake, biomarkers of nutritional status and food insufficiency in US older adult (age ≥ 60 years) participants of the Third National Health and Nutrition Examination Survey (n 4731). Frailty was defined as meeting ≥ 2 and pre-frailty as meeting one of the following four-item criteria: (1) slow walking; (2) muscular weakness; (3) exhaustion and (4) low physical activity. Intake was assessed by 24 h dietary recall. Food insufficiency was self-reported as ‘sometimes’ or ‘often’ not having enough food to eat. Analyses were adjusted for sex, race, age, smoking, education, income, BMI, other co-morbid conditions and complex survey design. Prevalence of frailty was highest among people who were obese (20·8 %), followed by overweight (18·4 %), normal weight (16·1 %) and lowest among people who were underweight (13·8 %). Independent of BMI, daily energy intake was lowest in people who were frail, followed by pre-frail and highest in people who were not frail (6648 (se 130), 6966 (se 79) and 7280 (se 84) kJ, respectively, P< 0·01). Energy-adjusted macronutrient intakes were similar in people with and without frailty. Frail (adjusted OR (AOR) 4·7; 95 % CI 1·7, 12·7) and pre-frail (AOR 2·1; 95 % CI 0·8, 5·8) people were more likely to report being food insufficient than not frail people. Serum albumin, carotenoids and Se levels were lower in frail adults than not frail adults. Research is needed on targeted interventions to improve nutritional status and food insufficiency among frail older adults, while not necessarily increasing BMI.

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.

Few experimental data are available to support the notion that reducing night-time eating changes total daily energy intake (EI) or body weight in healthy adults. The present study primarily examined the short-term effect of night eating restriction (NER) on daily EI in healthy young men. It secondarily examined body weight and moods associated with NER. Using a cross-over design, twenty-nine men (20·9 (sd 2·5) years; 24·4 (sd 2·5) kg/m2) initiated a 2-week NER intervention (elimination of EI from 19.00 to 06.00 hours) and a 2-week control condition, counterbalanced and separated by a 1-week washout period. EI and macronutrient intake were assessed using computerised, multiple-pass 24 h food recalls, body weight via a digital scale and mood using the Profile of Mood States survey. Of the twenty-nine participants, twenty-seven (93 %) completed all aspects of the study. During the NER condition, the participants consumed less total energy per d than during the control condition (10 125 v. 11 146 kJ/d; F= 6·41; P= 0·018). During the NER condition, no energy was reported consumed between 19.00 and 06.00 hours; however, during the control condition, the energy intake of participants was 2920 (sd 1347) kJ/d between 19.00 and 06.00 hours. There was a significant difference in weight change between the NER ( − 0·4 (sd 1·1) kg) and control (+0·6 (sd 0·9) kg) conditions (F= 22·68; P< 0·001). Differences in total mood score or mood subscales between the NER and control conditions were not apparent (P>0·05). These findings provide support for NER decreasing short-term EI in healthy young men.

Evidence for cardioprotective effects of lycopene is inconsistent. Studies of circulating lycopene generally report inverse associations with CVD risk, but studies based on lycopene intake do not. The failure of dietary studies to support the findings based on biomarkers may be due in part to misclassification of lycopene intakes. To address this potential misclassification, we used repeated measures of intake obtained over 10 years to characterise the relationship between lycopene intake and the incidence of CVD (n 314), CHD (n 171) and stroke (n 99) in the Framingham Offspring Study. Hazard ratios (HR) for incident outcomes were derived from Cox proportional hazards regression models using logarithmically transformed lycopene intake adjusted for CVD risk factors and correlates of lycopene intake. HR were interpreted as the increased risk for a 2·7-fold difference in lycopene intake, a difference approximately equal to its interquartile range. Using an average of three intake measures with a 9-year follow-up, lycopene intake was inversely associated with CVD incidence (HR 0·83, 95 % CI 0·70, 0·98). Using an average of two intake measures and 11 years of follow-up, lycopene intake was inversely associated with CHD incidence (HR 0·74, 95 % CI 0·58, 0·94). Lycopene intake was unrelated to stroke incidence. The present study of lycopene intake and CVD provides supporting evidence for an inverse association between lycopene and CVD risk; however, additional research is needed to determine whether lycopene or other components of tomatoes, the major dietary source of lycopene, are responsible for the observed association.

Previous (mainly population-based) studies have suggested the health benefits of the elective, lifelong inclusion of whole-grain foods in the diet, forming the basis for public health recommendations to increase whole grain consumption. Currently, there is limited evidence to assess how public health recommendations can best result in longer-term improvements in dietary intake. The present study aimed to assess the impact of a previous 16-week whole-grain intervention on subsequent, elective whole grain consumption in free-living individuals. Participants completed a postal FFQ 1, 6 and 12 months after the end of the whole-grain intervention study period. This FFQ included inputs for whole-grain foods commonly consumed in the UK. Whole grain consumption was significantly higher (approximately doubled) in participants who had received whole-grain foods during the intervention (P< 0·001) compared with the control group who did not receive whole-grain foods during the intervention. This increased whole grain consumption was lower than whole grain intake levels required by participants during the intervention period between 60 and 120 g whole grains/d. Aside from a significant increase (P< 0·001) in NSP consumption compared with control participants (mean increase 2–3 g/d), there were no obvious improvements to the pattern of foods of the intervention group. The results of the present study suggest that a period of direct exposure to whole-grain foods in non-habitual whole-grain food consumers may benefit subsequent, elective dietary patterns of whole grain consumption. These findings may therefore aid the development of future strategies to increase whole grain consumption for public health and/or food industry professionals.

Intermittent energy restriction may result in greater improvements in insulin sensitivity and weight control than daily energy restriction (DER). We tested two intermittent energy and carbohydrate restriction (IECR) regimens, including one which allowed ad libitum protein and fat (IECR+PF). Overweight women (n 115) aged 20 and 69 years with a family history of breast cancer were randomised to an overall 25 % energy restriction, either as an IECR (2500–2717 kJ/d, < 40 g carbohydrate/d for 2 d/week) or a 25 % DER (approximately 6000 kJ/d for 7 d/week) or an IECR+PF for a 3-month weight-loss period and 1 month of weight maintenance (IECR or IECR+PF for 1 d/week). Insulin resistance reduced with the IECR diets (mean − 0·34 (95 % CI − 0·66, − 0·02) units) and the IECR+PF diet (mean − 0·38 (95 % CI − 0·75, − 0·01) units). Reductions with the IECR diets were significantly greater compared with the DER diet (mean 0·2 (95 % CI − 0·19, 0·66) μU/unit, P= 0·02). Both IECR groups had greater reductions in body fat compared with the DER group (IECR: mean − 3·7 (95 % CI − 2·5, − 4·9) kg, P= 0·007; IECR+PF: mean − 3·7 (95 % CI − 2·8, − 4·7) kg, P= 0·019; DER: mean − 2·0 (95 % CI − 1·0, 3·0) kg). During the weight maintenance phase, 1 d of IECR or IECR+PF per week maintained the reductions in insulin resistance and weight. In the short term, IECR is superior to DER with respect to improved insulin sensitivity and body fat reduction. Longer-term studies into the safety and effectiveness of IECR diets are warranted.

The present study was conducted to determine the association between fibre intake and insulin resistance in 264 women using a cross-sectional design. Insulin resistance was indexed using homeostasis model assessment of insulin resistance (HOMA-IR) (US formula: fasting insulin (μU/ml) × fasting glucose (mg/dl)/405 international formula: fasting glucose (mmol/l) × fasting insulin (μU/l)/22.5). Fibre and energy consumption were assessed using 7 d weighed food records. Fibre was expressed as g/4184 kJ (1000 kcal). Body fat percentage (BF%) was measured using the BOD POD, and physical activity (PA) was ascertained using Actigraph accelerometers (Health One Technology) worn for seven consecutive days. Women with high total fibre intakes (F= 4·58, P= 0·0332) or high soluble fibre intakes (F= 7·97, P= 0·0051) had significantly less insulin resistance than their counterparts. Participants with high insoluble fibre intakes did not differ from their counterparts (F= 0·7, P= 0·6875). Adjusting for either PA or BF% weakened the relationships significantly. Controlling for BF% nullified the total fibre–HOMA-IR link (F= 1·96, P= 0·1631) and attenuated the association between soluble fibre and HOMA-IR by 32 % (F= 6·86, P= 0·0094). To create dichotomous variables, fibre intake and HOMA-IR were each divided into two categories using the median (low and high). In women who had high soluble fibre intake (upper 50 %), the OR of having an elevated HOMA-IR level was 0·58 (95 % CI 0·36, 0·94) times that of women with low soluble fibre intake (lower 50 %). After controlling for all of the potential confounding factors simultaneously, the OR was 0·52 (95 % CI 0·29, 0·93). High fibre intake, particularly soluble fibre, is significantly related to lower levels of insulin resistance in women. Part of this association is a function of differences in PA and BF%.

Anaemia is prevalent in South East Asia and Fe deficiency (ID) is considered to be the main cause, but the role of subclinical inflammation in the aetiology is uncertain. In the present study, we determined the influence of inflammation on the biomarkers of Fe status in women and children, and herein, we discuss the proportion of anaemia associated with ID. As part of the 2006 Lao People's Democratic Republic (The Lao PDR) National Nutrition Survey, blood collected from 482 young children and 816 non-pregnant women was analysed. Plasma ferritin, transferrin receptor (sTfR), Hb, C-reactive protein (CRP) and α-1-acid glycoprotein (AGP) concentrations were measured. ID was assessed using ferritin concentrations ( < 12 (children) or < 15 (adults) μg/l), sTfR concentrations (>8·3 mg/l) and body Fe stores (BIS < 0). Elevated CRP (>5 mg/l) and/or AGP (>1 g/l) concentrations were used to categorise inflammation status in order to correct the Fe biomarkers for inflammation. Inflammation was present in 14 % of adults and 43 % of children. Anaemia was present in 37·6 % of both women (Hb concentrations < 120 g/l) and children (Hb concentrations < 110 g/l). Correcting ferritin concentrations for inflammation increased the prevalence of ID from 24·3 to 26 % for women and from 18 to 21 % for children (P< 0·001 for both). Ferritin concentrations were more helpful in detecting ID than sTfR concentrations or BIS, but regression analysis found that sTfr concentrations explained more of the variance in Hb concentrations in both women (20 %) and children (17 %) than ferritin concentrations (5 and 1·4 %, respectively). Nevertheless, the total variance in Hb concentrations explained was only 26 and 18 % in women and children, respectively, and other factors may be more important than ID in contributing to anaemia in The Lao PDR.