Energy restricted diets improve liver function(1) and habitual nut consumption has been associated with a lower prevalence of fatty liver(2). This study examined the effect of incorporating almonds in an energy restricted diet on liver health biomarkers. One Hundred and forty adults (42M:98F, 47.5 ± 10.8 years, BMI 30.7 ± 2.3 kg/m2) enrolled in a 9-month (9M) dietary intervention comprising 3 months (3M) weight loss (30% energy restriction) followed by 6 months (6M) of weight maintenance. Participants were randomly assigned to consume almonds (n = 68, AED) or isocaloric carbohydrate-rich snacks (n = 72, CRD) which provided 15% of total daily energy. At baseline (BL), 3M and 9M, fatty liver index (FLI) scores (0-100)(3) were calculated using body mass index (BMI), waist circumference (WC), fasting serum gamma-glutamyl transferase (GGT) and triglyceride (TAG) levels, and other liver health biomarkers were assessed by ultrasound (volume, visual appearance and elastography (a marker of stiffness due to fibrosis)). Intention to treat analyses were conducted using mixed effects modelling (fixed effects group and time, with participants as the random effect). Significant reductions from BL occurred over time (all p<0.001 for 3M and 9M) with no difference between groups (AED vs CRD, P>0.05) in BMI (3M: −2.44 ± 0.20 vs −2.32 ± 0.20, 9M: −2.83 ± 0.19 vs −2.81 ± 0.19 kg/m2), WC (3M: −8.04 ± 0.79 vs −7.00 ± 0.81, 9M: −8.72 ± 0.83 vs −9.14 ± 0.81 cm), TAG (3M: −0.24± 0.08 vs −0.22 ± 0.09, 9M: −0.37 ± 0.09 vs −0.21 ± 0.09 mmol/L), FLI score (3M: −23.8 ± 2.0 vs −17.6 ± 2.1, 9M: −23.8 ± 2.0 vs −17.6 ± 2.1), and liver volume (3M: −134.56 ± 38.30 vs −100.96 ± 37.25, 9M: −113.68 ± 37.42 vs −110.64 ± 35.47cm3). Significantly greater reductions occurred for AED compared to CRD at 3M and 9M in GGT (p = 0.003) (3M: −9.68 ± 1.93 vs −0.01 ± 2.00, 9M: −7.75 ± 2.06 vs −2.78 ± 2.15 IU/L) and liver visual assessment scores (p = 0.03) (3M: −0.58 ± 0.24 vs −0.45 ± 0.23, 9M: −1.33 ± 0.23 vs −0.50 ± 0.22). There were no significant changes in liver elastography over time or between groups. Energy restriction improved body composition and reduced the extent of fatty liver and liver size but did not change liver stiffness. The inclusion of almonds in an energy restricted diet demonstrated additional benefits to some liver health biomarkers providing support for almonds being incorporated into lifestyle interventions to improve liver function.

The metabolomic profile of a biofluid can be altered by dietary intake, exercise and disease processes and, thus provides an important tool for the study of many physiological processes. However, in addition to perturbation due to disease, the metabolomic profile of urine and plasma has also been shown to vary due to many intrinsic physiological factors such as age, sex, hormonal status and diurnal variation. Characterisation of this normal degree of variation in the metabolomic profiles of human biofluids is a necessary and important step in the development of metabolomics for use in nutrition-related research. The current review focuses on the impact of sex on the metabolomic profile. A number of studies have reported that sex impacts metabolites such as amino acids, lipids, sugars and keto acids. Furthermore, we examine the effect of the menstrual cycle on the metabolomic profile. Responses to dietary interventions can also differ between the sexes and highlighting this is important for the development of the field of precision nutrition.

This paper contributes to explaining the obesity epidemic and finding a potential remedy. We build a theoretical model of food consumption decisions that accounts for social influence. In our model, individuals’ rationality is affected by an endogenous social weight norm, which influences their calorie consciousness and perceived survival chances. Individuals are conformist, and the degree of conformism describes the extent to which individuals’ discounted utility is influenced by the social weight norm. With an endogenous social weight norm reflecting a heavier and heavier average body weight, we show that a high degree of conformism to the social norm could explain the obesity epidemic. In this environment, a government intervention decreasing energy density is ineffective at reducing steady-state body weight. This result could explain why this type of government dietary intervention seems to have had no effect on obesity, and suggests that the same type of intervention through the Food Stamps Program would be ineffective on its own. We also find that in the steady state, individuals can be overweight or underweight depending on their degree of conformism relative to the education they receive about the healthy weight. While education programs focusing on either diet or exercise have had moderate success, we show that focusing on healthy weight education could combat social influence and reduce obesity.

Strategies are needed to improve the dietary habits of children. The aim of the present study was to evaluate the effect of implementing a school food programme on the dietary quality of lunches consumed by school children aged 7–13 years compared with packed lunches brought from home. A secondary objective was to investigate if a possible effect would differ between the younger children and the older. A quasi-experimental study design with four intervention schools and four matched control schools was conducted. In total, 984 school children participated. Data on packed lunches were collected at baseline. At the 1st follow-up the children in the intervention schools were offered free school meals and at the 2nd follow-up children paid for their school meals. The control group had packed lunches at all measurements. A digital photographic method combined with a Meal Index of dietary Quality (Meal IQ) was used for dietary assessment. Multilevel modelling was employed for data analyses. The quality of dietary intake was improved when free school meals were offered (P = 0·004); if the school meals were paid for the use was limited and no difference in change in dietary quality was found (P = 0·343). The school food programme had no difference in effect according to age (P = 0·083). In conclusion, offering a free school meal had a positive effect on dietary quality of the lunches consumed by school children aged 7–13 years. No effect was measured when the school meals were not provided for free. The dietary effect did not depend on age.

This review evaluates evidence on dietary interventions for cancer survivors giving an overview of people's views and preferences for service attributes and provides a narrative review. After cancer, people often want to change their diet and there is a plethora of evidence why dietary optimisation would be beneficial. However, cancer survivors have different preferences about attributes of services including: place, person and communication mode. Randomised control trials have been reviewed to provide a narrative summary of evidence of dietary interventions. Most studies were on survivors of breast cancer, with a few on colorectal, prostate and gynaecological survivors. Telephone interventions were the most frequently reported means of providing advice and dietitians were most likely to communicate advice. Dietary assessment methods used were FFQ, food diaries and 24-h recalls. Dietary interventions were shown to increase intake of fruit and vegetables, dietary fibre, and improve diet quality in some studies but with contradictory findings in others. Telephone advice increased fruit and vegetable intake primarily in women with breast cancer and at some time points in people after colorectal cancer, but findings were inconsistent. Findings from mail interventions were contradictory, although diet quality improved in some studies. Web-based and group sessions had limited benefits. There is some evidence that dietary interventions improve diet quality and some aspects of nutritional intake in cancer survivors. However, due to contradictory findings between studies and cancer sites, short term follow-up and surrogate endpoints it is difficult to decipher the evidence base.

Public health authorities recommend all fertile women to increase their folate intake to 400 µg/d by eating folate-rich foods or by taking a folic acid supplement to protect against neural tube defects. In a previous study it was shown that folate-rich foods improved folate blood status as effectively as folic acid supplementation. The aim of the present study was to investigate, using NMR metabolomics, the effects of an intervention with a synthetic folic acid supplement v. native food folate on the profile of plasma metabolites. Healthy women with normal folate status received, in parallel, 500 µg/d synthetic folic acid from a supplement (n 18), 250 µg/d folate from intervention foods (n 19), or no additional folate (0 µg/d) through a portion of apple juice (n 20). The metabolic profile of plasma was measured using 1H-NMR in fasted blood drawn at baseline and after 12 weeks of intervention. Metabolic differences between the groups at baseline and after intervention were assessed using a univariate statistical approach (P ≤ 0·001, Bonferroni-adjusted significance level). At baseline, the groups showed no significant differences in measured metabolite concentrations. After intervention, eight metabolites, of which six (glycine, choline, betaine, formate, histidine and threonine) are related to one-carbon metabolism, were identified as discriminative metabolites. The present study suggests that different folate forms (synthetic v. natural) may affect related one-carbon metabolites differently.

DNA methylation is a key component of the epigenetic machinery that is responsible for regulating gene expression and, therefore, cell function. Patterns of DNA methylation change during development and ageing, differ between cell types, are altered in multiple diseases and can be modulated by dietary factors. However, evidence about the effects of dietary factors on DNA methylation patterns in humans is fragmentary. This study was initiated to collate evidence for causal links between dietary factors and changes in DNA methylation patterns. We carried out a systematic review of dietary intervention studies in adult humans using Medline, EMBASE and Scopus. Out of 22 149 screened titles, sixty intervention studies were included, of which 65% were randomised (n 39). Most studies (53%) reported data from blood analyses, whereas 27% studied DNA methylation in colorectal mucosal biopsies. Folic acid was the most common intervention agent (33%). There was great heterogeneity in the methods used for assessing DNA methylation and in the genomic loci investigated. Meta-analysis of the effect of folic acid on global DNA methylation revealed strong evidence that supplementation caused hypermethylation in colorectal mucosa (P=0·009). Meta-regression analysis showed that the dose of supplementary folic acid was the only identified factor (P<0·001) showing a positive relationship. In summary, there is limited evidence from intervention studies of effects of dietary factors, other than folic acid, on DNA methylation patterns in humans. In addition, the application of multiple different assays and investigations of different genomic loci makes it difficult to compare, or to combine, data across studies.

Advancing age increases the risk for diseases and health concerns like cognitive decline, constituting a major public health challenge. Lifestyle, especially healthy diet, affects many risk factors related to chronic diseases, and thus lifestyle interventions among older adults may be beneficial in promoting successful ageing. We completed a randomised 2-year multi-domain lifestyle intervention trial aiming at prevention of cognitive decline among 631 participants in the intervention and 629 in the control group, aged 60–77 years at baseline. Dietary counselling was one of the intervention domains together with strength exercise, cognitive training and management of CVD risk factors. The aim of this paper was to describe success of the intervention – that is, how an intervention based on national dietary recommendations affected dietary habits as a part of multi-intervention. Composite dietary intervention adherence score comprising nine distinct goals (range 0–9 points from none to achieving all goals) was 5·0 at baseline, and increased in the intervention group after the 1st (P<0·001) and 2nd (P=0·005) year. The difference in change compared with the control group was significant at both years (P<0·001 and P=0·018). Intake of several vitamins and minerals decreased in the control group but remained unchanged or increased in the intervention group during the 2 years. Well-targeted dietary counselling may prevent age-related decline in diet quality and help in preventing cognitive decline.

Plant sterols (PS) lower LDL-cholesterol, an established risk factor for CHD. Endothelial dysfunction and low-grade inflammation are two important features in the development of atherosclerosis. Whether PS affect biomarkers of endothelial function and low-grade inflammation is not well studied. The aim of the present study was to investigate the effect of regular intake of PS on biomarkers of endothelial dysfunction and low-grade inflammation. In a double-blind, randomised, placebo-controlled, parallel-group study, which was primarily designed to investigate the effect of PS intake on vascular function (clinicaltrials.gov: NCT01803178), 240 hypercholesterolaemic but otherwise healthy men and women consumed a low-fat spread with added PS (3 g/d) or a placebo spread for 12 weeks. Endothelial dysfunction biomarkers (both vascular and intracellular adhesion molecules 1 and soluble endothelial-selectin) and low-grade inflammation biomarkers (C-reactive protein, serum amyloid A, IL-6, IL-8, TNF-α and soluble intercellular adhesion molecule-1) were measured using a multi-array detection system based on electrochemiluminescence technology. Biomarkers were combined using z-scores. Differences in changes from baseline between the PS and the placebo groups were assessed. The intake of PS did not significantly change the individual biomarkers of endothelial dysfunction and low-grade inflammation. The z-scores for endothelial dysfunction (−0·02; 95 % CI −0·15, 0·11) and low-grade inflammation (−0·04; 95 % CI −0·16, 0·07) were also not significantly changed after PS intake compared with placebo. In conclusion, biomarkers of endothelial dysfunction and low-grade inflammation were not affected by regular intake of 3 g/d PS for 12 weeks in hypercholesterolaemic men and women.

Intrauterine growth restriction has been noted to adversely impact morbidity and mortality in the neonatal period as well as cardiovascular well-being in adolescence and adulthood. Recent data based on a wide range of ultrasound parameters during fetal and neonatal life has noted early and persistent involvement of the cardiovascular system. Some of these measures are predictive of long-term morbidities. Assessment of vascular mechanics is a new and novel concept in this population, and opens up avenues for diagnosis, monitoring and evaluation of the likely effectiveness of interventions. Prevention of these adverse vascular and cardiac outcomes secondary to fetal growth restriction may be feasible and of clinical relevance. This review focuses on growth restriction in humans with respect to cardiovascular remodeling and dysfunction during fetal life, persistence of functional cardiac impairment during early childhood and adolescence, and possible preventive strategies.

Whether supplemental Ca has similar effects to dietary Ca on vascular and bone markers is unknown. The present trial investigated the feasibility of applying dietary and supplemental interventions in a randomised-controlled trial (RCT) aiming to estimate the effect of supplemental Ca as compared with dietary Ca on vascular and bone markers in postmenopausal women. In total, thirteen participants were randomised to a Ca supplement group (CaSuppl) (750 mg Ca from CaCO3+450 mg Ca from food+20 µg vitamin D supplement) or a Ca diet group (CaDiet) (1200 mg Ca from food+10 µg vitamin D supplement). Participants were instructed on Ca consumption targets at baseline. Monthly telephone follow-ups were conducted to assess adherence to interventions (±20 % of target total Ca) using the multiple-pass 24-h recall method and reported pill count. Measurements of arterial stiffness, peripheral blood pressure and body composition were performed at baseline and after 6 and 12 months in all participants who completed the trial (n 9). Blood and serum biomarkers were measured at baseline and at 12 months. Both groups were compliant to trial interventions (±20 % of target total Ca intake; pill count ≥80 %). CaSuppl participants maintained a significantly lower average dietary Ca intake compared with CaDiet participants throughout the trial (453 (sd 187) mg/d v. 1241 (sd 319) mg/d; P<0·001). There were no significant differences in selected vascular outcomes between intervention groups over time. Our pilot trial demonstrated the feasibility of conducting a large-scale RCT to estimate the differential effects of supplemental and dietary Ca on vascular and bone health markers in healthy postmenopausal women.

Most human intervention studies have examined the effects on a subset of risk factors, some of which may require long-term exposure. The plasma proteome may reflect the underlying changes in protein expression and activation, and this could be used to identify early risk markers. The aim of the present study was to evaluate the impact of regular fish intake on the plasma proteome. We recruited thirty healthy men aged 40 to 70 years, who were randomly allocated to a daily meal of chicken or trout raised on vegetable or marine feeds. Blood samples were collected before and after 8 weeks of intervention, and after the removal of the twelve most abundant proteins, plasma proteins were separated by two-dimensional gel electrophoresis. Protein spots < 66 kDa with a pI >4·3 visualised by silver staining were matched by two-dimensional imaging software. Within-subject changes in spots were compared between the treatment groups. Differentially affected spots were identified by matrix-assisted laser desorption ionisation-time of flight/time of flight MS and the human Swiss-Prot database. We found 23/681 abundant plasma protein spots, which were up- or down-regulated by the dietary treatment (P< 0·05, q< 0·30), and eighteen of these were identified. In each trout group, ten spots differed from those in subjects given the chicken meal, but only three of these were common, and only one spot differed between the two trout groups. In both groups, the affected plasma proteins were involved in biological processes such as regulation of vitamin A and haem transport, blood fibrinolysis and oxidative defence. Thus, regular fish intake affects the plasma proteome, and the changes may indicate novel mechanisms of effect.

An increasing number of children are exhibiting features of the metabolic syndrome (MetS) including abdominal fatness, hypertension, adverse lipid profile and insulin resistance. Healthy eating practices during school hours may improve the cardiometabolic profile, but there is a lack of evidence. In the present study, the effect of provision of school meals rich in fish, vegetables and fibre on a MetS score (primary outcome) and on individual cardiometabolic markers and body composition (secondary outcomes) was investigated in 834 Danish school children. The study was carried out as a cluster-randomised, controlled, non-blinded, cross-over trial at nine schools. Children aged 8–11 years received freshly prepared school lunch and snacks or usual packed lunch from home (control) each for 3 months. Dietary intake, physical activity, cardiometabolic markers and body composition were measured at baseline and after each dietary period. The school meals did not affect the MetS score (P= 1·00). However, it was found that mean arterial pressure was reduced by 0·4 (95 % CI 0·0, 0·8) mmHg (P= 0·04), fasting total cholesterol concentrations by 0·05 (95 % CI 0·02, 0·08) mmol/l (P= 0·001), HDL-cholesterol concentrations by 0·02 (95 % CI 0·00, 0·03) mmol/l, TAG concentrations by 0·02 (95 % CI 0·00, 0·04) mmol/l (both P< 0·05), and homeostasis model of assessment-insulin resistance by 0·10 (95 % CI 0·04, 0·16) points (P= 0·001) compared with the control diet in the intention-to-treat analyses. Waist circumference increased 0·5 (95 % CI 0·3, 0·7) cm (P< 0·001), but BMI z-score remained unaffected. Complete-case analyses and analyses adjusted for household educational level, pubertal status and physical activity confirmed the results. In conclusion, the school meals did not affect the MetS score in 8–11-year-olds, as small improvements in blood pressure, TAG concentrations and insulin resistance were counterbalanced by slight undesired effects on waist circumference and HDL-cholesterol concentrations.

Metabolomic profiles were used to characterise the effects of consuming a high-phytochemical diet compared with a diet devoid of fruits and vegetables (F&V) in a randomised trial and cross-sectional study. In the trial, 8 h fasting urine from healthy men (n 5) and women (n 5) was collected after a 2-week randomised, controlled trial of two diet periods: a diet rich in cruciferous vegetables, citrus and soya (F&V), and a fruit- and vegetable-free (basal) diet. Among the ions found to differentiate the diets, 176 were putatively annotated with compound identifications, with forty-six supported by MS/MS fragment evidence. Metabolites more abundant in the F&V diet included markers of the dietary intervention (e.g. crucifers, citrus and soya), fatty acids and niacin metabolites. Ions more abundant in the basal diet included riboflavin, several acylcarnitines and amino acid metabolites. In the cross-sectional study, we compared the participants based on the tertiles of crucifers, citrus and soya from 3 d food records (n 36) and FFQ (n 57); intake was separately divided into the tertiles of total fruit and vegetable intake for FFQ. As a group, ions individually differential between the experimental diets differentiated the observational study participants. However, only four ions were significant individually, differentiating the third v. first tertile of crucifer, citrus and soya intake based on 3 d food records. One of these ions was putatively annotated: proline betaine, a marker of citrus consumption. There were no ions significantly distinguishing tertiles by FFQ. The metabolomic assessment of controlled dietary interventions provides a more accurate and stronger characterisation of the diet than observational data.

Few trials have evaluated the metabolic effects and health outcomes of lowering dietary n-6 PUFA. The objectives of the present paper were (1) to report the methods employed to lower dietary n-6 PUFA, while either increasing or maintaining n-3 PUFA intake and (2) to validate our methods with 24 h recalls and erythrocyte fatty acid analyses. A total of sixty-seven subjects were randomised to either (1) an average-n-3 PUFA, low-n-6 PUFA (L6) intervention designed to lower linoleic acid (LA; ≤ 2·5 % of energy (en%)) and arachidonic acid ( ≤ 60 mg/d), while maintaining an average US intake of n-3 PUFA or (2) a high-n-3 PUFA, low-n-6 PUFA (H3-L6) intervention designed to lower n-6 LA, while increasing the n-3 PUFA α-linolenic acid (ALA; ≥ 1·5 en%) and EPA+DHA ( ≥ 1000 mg/d). Pre- and intra-intervention nutrient intakes were estimated with six 24 h dietary recalls per subject. Both groups achieved the targeted reductions in dietary LA to ≤ 2·5 en% (median LA 2·45 (2·1, 3·1); P< 0·001). Intakes of n-3 PUFA did not change for the L6 group. Target increases in n-3 ALA (median 1·6 en%, (1·3, 2·0), P< 0·001) and EPA+DHA (1482 mg, (374, 2558), P< 0·001) were achieved in the H3-L6 group. Dietary changes were validated by corresponding changes in erythrocyte n-6 and n-3 fatty acid composition. Dietary LA can be lowered to ≤ 2·5 en%, with or without concurrent increases in dietary n-3 PUFA, in an outpatient clinical trial setting using this integrated diet method.

There is increasing interest in the potential chronic beneficial effects of dietary n-3 PUFA on the metabolic syndrome (MetS) and associated cardiovascular complications. We have recently established that increased dietary n-3 PUFA has a profound acute benefit on fasting lipids and the postprandial pro-inflammatory response in the JCR:LA-cp rat, a model of the MetS. However, it is unclear to what extent chronic dietary n-3 PUFA intervention can modulate the progression of end-stage metabolic and vascular complications. The present study aimed to determine the chronic effects of dietary n-3 PUFA supplementation on fasting and non-fasting dyslipidaemia, insulin resistance and vascular complications in the JCR:LA-cp rodent model. JCR:LA-cp rats were fed an isoenergetic lipid-balanced diet supplemented with 5 % n-3 PUFA (w/w) of the total fat (fish oil-derived EPA/DHA) for 16 weeks. Fasting and non-fasting (postprandial) plasma lipid profile was assessed. Hepatic and adipose tissue was probed for the expression of lipogenic proteins (acyl-CoA carboxylase (ACC), fatty acid synthase (FAS) and sterol regulatory element-binding protein-1 (SREBP-1)), while the activity of Jun N-terminal kinase (JNK) was assessed via Western blot to target phosphorylated JNK protein in primary enterocytes. The frequency of myocardial lesions was assessed by haematoxylin and eosin staining. Increased dietary n-3 PUFA improved both the fasting and postprandial lipid profiles (TAG, cholesterol and apoB48) in the JCR:LA-cp rat, potentially via the down-regulation of the hepatic or adipose tissue expression of lipogenic enzymes (ACC, FAS and SREBP-1). Rats fed the 5 % n-3 PUFA diet had lower (58·2 %; P < 0·01) enterocytic phosphorylated JNK protein and secreted less cholesterol (30 %; P < 0·05) into mesenteric lymph compared with the control. The chronic metabolic benefits of dietary n-3 PUFA may underlie the potential to reduce vascular complications during the MetS, including the observed reduction in the frequency (approximately 80 %) of late-stage 3 myocardial lesions.

Interventions to combat mild Fe deficiency in women of childbearing age may affect Zn nutriture. We used dietary and laboratory indices to assess change in Zn status during a 4-month partially blinded placebo-controlled Fe intervention in women with low Fe stores (serum ferritin < 20 μg/l and Hb ≥ 120 g/l) from Dunedin, New Zealand. Subjects aged 18–40 years were randomly assigned to three groups: dietary advice (diet group; DG; n 29), daily Fe supplement with meals (supplement group; SG; n 23; 50 mg Fe as amino acid chelate) and placebo (placebo group; PG, n 26). A validated semi-quantitative FFQ (SFFQ) was administered at baseline, and at 4, 8 and 15 weeks; fasting morning blood samples were assayed for serum Zn, alkaline phosphatase (ALP) and C-reactive protein at baseline, and at 4, 8, 12 and 16 weeks; hair Zn and taste detection thresholds by electrogustometry were measured at baseline and at 16 weeks. Intakes of flesh foods and vitamin C but not Zn or Fe increased, whereas phytate and phytate:Zn molar ratios decreased (all P ≤ 0·01) in the DG compared with the PG and SG, based on three SFFQ. Serum Zn increased in both the DG and PG (adjusted, P ≤ 0·002), so the between-group difference was not significant; the lack of a parallel rise in the SG was significant when compared with the PG (P = 0·02). ALP activity (but not hair Zn or taste acuity) followed a similar trend. In conclusion, Zn status was not improved compared with placebo by an Fe-based dietary intervention. However, a daily moderate-dose Fe supplement with meals appeared to lower Zn status in these young adult women.

The infant born small size for gestational age (SGA) has low bone mass. Since dietary arachidonic acid (AA) and DHA enhance bone mass in normal-birth-weight piglets the objective of the present study was to test for such benefits in the SGA piglet. In the present 15 d study, two levels of dietary AA and DHA (6:1 ratio of AA:DHA diets, 0·6:0·1 or 1·2:0·2 g/100 g dietary fat) v. a control diet were tested for effects on growth, fatty acid status, whole-body and regional bone mineral content (BMC) and metabolism in SGA piglets categorised as either very low birth weight (VLBW; ≤ 1·0 kg; n 12) or low birth weight (LBW; 1·1 to 1·2 kg; n 18). Differences in outcomes for each body weight category were detected using ANOVA with post hoc Bonferroni tests. Growth was not influenced by diet, yet the LBW piglets fed 0·6:0·1 AA and DHA as g/100 g fat had elevated BMC in the spine, whereas the VLBW piglets had higher BMC of the spine if fed the higher intake of AA and DHA. In both weight categories, the higher intake of AA and DHA lowered bone resorption relative to controls, whereas bone formation was unchanged. Tissue fatty acid concentrations reflected dietary AA and DHA, especially trabecular bone of VLBW piglets. Whether the enhanced lumbar spine BMC is due to enhanced Ca absorption and thus suppression of bone resorption remains to be established.