We aimed to investigate the intricate interplay between genetic predisposition and lifestyle factors on stroke. We conducted a comprehensive genome-wide association study to identify the genetic variants linked to stroke in the participants who experienced a stroke event (cases; n 672) and those with no stroke history (non-stroke; n 58 029) in a large hospital-based cohort. Using generalised multifactor dimensionality reduction, we identified genetic variants with interactive effects and constructed polygenic risk scores (PRS) by summing up the risk alleles from the genetic variants. Food intake was measured with a validated semi-quantitative FFQ. No significant differences in stroke incidence were seen in demographic variables between the two groups. Among the metabolic indicators, only serum TAG levels were higher in males with stroke than those without stroke. The daily nutrient intake, dietary inflammation index, glycaemic index, dietary patterns, alcohol consumption, exercise and smoking did not display associations with the OR for stroke. The stroke-linked genetic variants were related to the IL-18 pathway. After accounting for covariates, the PRS derived from the 5-, 6- and 7-SNP models were positively associated with stroke chance with 2·5-, 2·9- and 2·8-fold. Furthermore, interactions between genetic predisposition and dietary components, including energy, carbohydrates, n-3 fatty acids and branched-chain amino acids (BCAA), that affected OR for stroke were observed. A high intake of energy, carbohydrates and BCAA and a low intake of n-3 fatty acids were positively associated with the chances of stroke occurrence. In conclusion, understanding the interaction between genetic variants and lifestyle factors can assist in developing stroke prevention and management strategies.

This study investigated whether long-chain n-3 PUFA (LC n-3 PUFA) given to pregnant rats fed a high-fat (HF) diet may prevent fetal programming in male offspring at adulthood. Six weeks before mating, and throughout gestation and lactation, female nulliparous Sprague–Dawley rats were given a chow (C) diet, HF (60·6 % fat from maize, rapeseed oils and lard) or HF in which one-third of fat was replaced by fish oil (HF n-3). At weaning, the three offspring groups were randomly separated in two groups fed C diet, or HF without LC n-3 PUFA, for 7 weeks until adulthood. Glucose tolerance and insulin sensitivity were assessed by an oral glucose tolerance test both at weaning and at adulthood. Insulin signalling was determined in liver, muscle and adipose tissue by quantification of the phosphorylation of Akt on Ser 473 at adulthood. At weaning, as at adulthood, offspring from HF-fed dams were obese and displayed glucose intolerance (GI) and insulin resistance (IR), but not those from HFn-3 fed dams. Following the post-weaning C diet, phosphorylation of Akt was strongly reduced in all tissues of offspring from HF dams, but to a lesser extent in liver and muscle of offspring from HFn-3 dams. However, it was abolished in all tissues of all offspring groups fed the HF post-weaning diet. Thus, LC n-3 PUFA introduced in a HF in dams partially prevented the transmission of GI and IR in adult offspring even though they were fed without LC n-3 PUFA from weaning.

Several countries have issued dietary recommendations about total and specific fatty acid (FA) intake for the prevention of CHD. For many years until today, controversies have existed especially about the deleterious effect or not of SFA, and the protective effect or not of n-3 PUFA, so that some authors have criticised these recommendations. There are many reasons for these controversies, including the different conclusions of prospective cohort studies compared with randomised clinical trials (RCT), and the contradictory conclusions of meta-analyses depending on the quality, number and type of studies included. The interrelationships between different FA in the diet make it difficult to analyse the specific effect of a particular class of FA on CHD. Furthermore, based on clinical practice and effectiveness of population-based prevention, it is very difficult at the individual level to assess in personal dietary intake the actual percentage and/or amount of SFA contained in each meal or consumed daily/weekly. In this critical narrative review, we try to answer the question of whether it would not be more relevant, in 2020, to promote dietary patterns, rather than FA intake recommendations. We critically analyse past and recent data on the association of FA with CHD, then propose that the Mediterranean diet and Japanese diet should be revitalised for Westerners and Asian populations, respectively. This does not exclude the usefulness of continuing research about effects of FA towards CHD, and accepting that what seems true today might be revised, at least partially tomorrow.

The present study aimed to evaluate the inflammatory response, oxidative status and fatty acid deposition in reproductive tissues of cats supplemented with the dried microalgae Schizochytrium spp. (Thraustochytriaceae) as a DHA source. Thirty-seven cats (males, n 21; females, n 16; 11·5 (sd 0·5) months of age) were divided by sex into five groups. Treatment diets contained algae biomass at 4·0, 8·0, 12·0 or 16·0 g/kg replacing poultry fat (n-6 source). Cats were fed the respective diet for 62 d and neutered on day 58. Blood samples were collected at the beginning of the experiment (day 1), before neutering (day 58) and 4 d after surgery (day 62) for analysis of inflammation and oxidative markers. Acute-phase protein levels were altered (P < 0·01) in the postoperative period, without any treatment effect (P > 0·05). PGE2 concentrations after surgery were reduced linearly (R2 0·8706; P = 0·002) with microalgal inclusion. Blood platelet count was reduced (P = 0·001) after the surgery regardless treatment, but it was higher in the DHA group compared with control (P < 0·001). The DHA deposition (testicles, R2 0·846; ovaries, R2 0·869) and the n-6:n-3 ratio (testicles, R2 0·859; ovaries, R2 0·955) in gonads had a pattern which fitted a quadratic model. DHA from Schizochytrium spp. modifies PGE2 response after the surgery in cats. The physiological roles of the DHA in the reproduction of cats were not investigated, but its gonadal deposition after supplementation was observed.

There is an increased use of vegetable oils containing n-6 fatty acids (FA) in aquafeeds, and several trials indicate that there might be an increased requirement of EPA and DHA for Atlantic salmon when they are fed higher dietary n-6 FA. With a limited supply of EPA and DHA for production of aquafeeds, it is important to know how to efficiently use these FA to maintain growth and health of the fish. In the present trial, three diets containing equal amounts of n-3 FA (about 7·7 % of total FA) and different n-6:n-3 FA ratios (about 1, 2 and 6), as well as one diet with n-6:n-3 FA ratio at about 1 but twice as much n-3 FA, were fed to Atlantic salmon. Despite constant dietary n-3, increasing dietary n-6 led to significantly reduced n-3 in tissue polar lipids. Interestingly, EPA was significantly reduced while DHA was not. Maintaining a stable n-3 content in the polar lipids when increasing dietary n-6 FA was only obtained by simultaneously increasing the dietary n-3 content and with this maintaining the same n-6:n-3 FA ratio. Polar lipid n-6 FA in tissues thus primarily reflected the dietary n-6:n-3 FA ratio and not the absolute dietary n-6 FA content. Neutral lipids, on the other hand, reflected the dietary absolute levels of both n-3 and n-6 FA. This study indicates that a better use of dietary EPA is achieved by keeping the dietary n-6:n-3 FA ratio low.

The omega-3 index, the percentage of EPA plus DHA in erythrocytes (measured by standardised analysis), represents a human body's status in EPA and DHA. An omega-3 index is measured in many laboratories around the world; however, even small differences in analytical methods entail large differences in results. Nevertheless, results are frequently related to the target range of 8–11 %, defined for the original and scientifically validated method (HS-Omega-3 Index®), raising ethical issues, and calling for standardisation. No human subject has an omega-3 index <2 %, indicating a vital minimum. Thus, the absence of EPA and DHA cannot be tested against presence. Moreover, clinical events correlate with levels, less with the dose of EPA and DHA, and the bioavailability of EPA and DHA varies inter-individually. Therefore, the effects of EPA and DHA are difficult to demonstrate using typical drug trial methods. Recent epidemiologic data further support the relevance of the omega-3 index in the cardiovascular field, since total mortality, cardiovascular mortality, cardiovascular events such as myocardial infarction or stroke, or blood pressure all correlate inversely with the omega-3 index. The omega-3 index directly correlates with complex brain functions. Compiling recent data supports the target range for the omega-3 index of 8–11 % in pregnancy. Many other potential applications have emerged. Some, but not all health issues mentioned have already been demonstrated to be improved by increasing intake of EPA and DHA. Increasing the omega-3 index into the target range of 8–11 % with individualised doses of toxin-free sources for EPA and DHA is tolerable and safe.

Marine n-3 fatty acids improve most of the biochemical alterations associated with insulin resistance (IR). Experimental models of dietary-induced IR in rodents have shown their ability (often at a very high dose) to prevent IR, but with sometimes a tissue specific effect. However, in a high sucrose diet-induced IR rat model, they are unable to reverse IR once installed; in other rodent models (dexamethasone, Zucker rats), they are inefficacious perhaps because of the severity of IR. The very low incidence of type-2 diabetes (T2D) in Inuits in the 1960s, which largely increased over the following decades in parallel to the replacement of their traditional marine food for a western diet strongly suggests a protective effect of marine n-3 towards the risk of T2D; this was confirmed by reversal of its incidence in intervention studies reintroducing their traditional food. In healthy subjects and insulin-resistant non-diabetic patients, most trials and meta-analyses conclude to an insulin-sensitising effect and to a very probable preventive or alleviating effect towards IR. Concerning the risk of T2D, concordant data allow us to conclude the protective effect of marine n-3 in Asians while suspicion exists of an aggravation of risk in Westerners, but with the possibility that it could be explained by a high heterogeneity of studies performed in this population. Some longitudinal cohorts in US/European people showed no association or a decreased risk. Further studies using more homogeneous doses, sources of n-3 and assessment of insulin sensitivity methods are required to better delineate their effects in Westerners.

The present study evaluated the interaction effects of n-3 fatty acids (from linseed oil (LSO), 0 v. 2·5, % DM basis) with rumen undegradable:degradable protein (RUP:RDP) ratios (low ratio (LR) 27:73; high ratio (HR) 38:62 based on crude protein %) in dairy calves’ starter diet. Forty-eight 3-d-old female Holstein dairy calves (41·5 kg of body weight (BW)) were allocated in a 2 × 2 factorial arrangements in the following treatments (n 12 calves/each): (1) no supplementation of LSO with LR (NLSO-LR); (2) no supplementation of LSO with HR (NLSO-HR); (3) supplementation of LSO with LR (LSO-LR) and (4) supplementation of LSO with HR (LSO-HR). The calves were weaned on day 53 of the experiment and remained in the study until day 73. Intake was not affected by LSO and RUP:RDP ratio. However, average daily gain (ADG) was improved with LSO supplementation. Feeding the HR diet increased ADG compared with the LR diet during the entire period. Final BW was greater in calves fed on the LSO than those fed the NLSO diet. Microbial protein production did not differ among treatments. Calves fed on LSO diets had greater feed efficiency than those which were not fed on LSO diets. The calves supplemented with LSO had greater wither and hip heights compared with the unsupplemented calves. The glucose, cholesterol, HDL and insulin concentrations increased in calves supplemented with LSO. In conclusion, the HR diet improved calves’ performance post-weaning; however, LSO could enhance growth performance of dairy calves during the pre-weaning period.

The aim of this study was to investigate the combined effect of n-3 fatty acids (EPA and DHA, at an EPA:DHA ratio of 150:500) and phytosterol esters (PS) on non-alcoholic fatty liver disease (NAFLD) patients. We conducted a randomised, double-blind, placebo-controlled trial. Ninety-six NAFLD subjects were randomly assigned to the following groups: the PS group (receiving 3·3 g/d PS); the FO group (receiving 450 mg EPA + 1500 mg DHA/d); the PS + FO combination group (receiving 3·3 g/d PS and 450 mg EPA + 1500 mg DHA/d) and the PO group (a placebo group). The baseline clinical characteristics of the four groups were similar. The primary outcome was liver:spleen attenuation ratio (L:S ratio). The percentage increase in liver–spleen attenuation (≤1) in the PS + FO group was 36 % (P = 0·083), higher than those in the other three groups (PS group, 11 %, P = 0·519; FO group, 18 %, P = 0·071; PO group, 15 %, P = 0·436). Compared with baseline, transforming growth factor-β (TGF-β) was significantly decreased in the three study groups at the end of the trial (PS, P = 0·000; FO, P = 0·002; PS + FO, P = 0·001) and TNF-α was significantly decreased in the FO group (P = 0·036), PS + FO group (P = 0·005) and PO group (P = 0·032) at the end of the intervention. Notably, TGF-β was reduced significantly more in the PS + FO group than in the PO group (P = 0·032). The TAG and total cholesterol levels of the PS + FO group were reduced by 11·57 and 9·55 %, respectively. In conclusion, co-supplementation of PS and EPA + DHA could increase the effectiveness of treatment for hepatic steatosis.

The fatty acid composition of chicken’s meat is largely influenced by dietary lipids, which are often used as supplements to increase dietary caloric density. The underlying key metabolites and pathways influenced by dietary oils remain poorly known in chickens. The objective of this study was to explore the underlying metabolic mechanisms of how diets supplemented with mixed or a single oil with distinct fatty acid composition influence the fatty acid profile in breast muscle of Qingyuan chickens. Birds were fed a corn-soybean meal diet supplemented with either soybean oil (control, CON) or equal amounts of mixed edible oils (MEO; soybean oil : lard : fish oil : coconut oil = 1 : 1 : 0.5 : 0.5) from 1 to 120 days of age. Growth performance and fatty acid composition of muscle lipids were analysed. LC-MS was applied to investigate the effects of CON v. MEO diets on lipid-related metabolites in the muscle of chickens at day 120. Compared with the CON diet, chickens fed the MEO diet had a lower feed conversion ratio (P < 0.05), higher proportions of lauric acid (C12:0), myristic acid (C14:0), palmitoleic acid (C16:1n-7), oleic acid (C18:1n-9), EPA (C20:5n-3) and DHA (C22:6n-3), and a lower linoleic acid (C18:2n-6) content in breast muscle (P < 0.05). Muscle metabolome profiling showed that the most differentially abundant metabolites are phospholipids, including phosphatidylcholines (PC) and phosphatidylethanolamines (PE), which enriched the glycerophospholipid metabolism (P < 0.05). These key differentially abundant metabolites – PC (14:0/20:4), PC (18:1/14:1), PC (18:0/14:1), PC (18:0/18:4), PC (20:0/18:4), PE (22:0/P-16:0), PE (24:0/20:5), PE (22:2/P-18:1), PE (24:0/18:4) – were closely associated with the contents of C12:0, C14:0, DHA and C18:2n-6 in muscle lipids (P < 0.05). The content of glutathione metabolite was higher with MEO than CON diet (P < 0.05). Based on these results, it can be concluded that the diet supplemented with MEO reduced the feed conversion ratio, enriched the content of n-3 fatty acids and modified the related metabolites (including PC, PE and glutathione) in breast muscle of chickens.

Limited availability of fish oils (FO), rich in n-3 long-chain (≥C20) PUFA, is a major constraint for further growth of the aquaculture industry. Long-chain n-3 rich oils from crops GM with algal genes are promising new sources for the industry. This project studied the use of a newly developed n-3 canola oil (DHA-CA) in diets of Atlantic salmon fingerlings in freshwater. The DHA-CA oil has high proportions of the n-3 fatty acids (FA) 18 : 3n-3 and DHA and lower proportions of n-6 FA than conventional plant oils. Levels of phytosterols, vitamin E and minerals in the DHA-CA were within the natural variation of commercial canola oils. Pesticides, mycotoxins, polyaromatic hydrocarbons and heavy metals were below lowest qualifiable concentration. Two feeding trials were conducted to evaluate effects of two dietary levels of DHA-CA compared with two dietary levels of FO at two water temperatures. Fish increased their weight approximately 20-fold at 16°C and 12-fold at 12°C during the experimental periods, with equal growth in salmon fed the FO diets compared with DHA-CA diets. Salmon fed DHA-CA diets had approximately the same EPA+DHA content in whole body as salmon fed FO diets. Gene expression, lipid composition and oxidative stress-related enzyme activities showed only minor differences between the dietary groups, and the effects were mostly a result of dietary oil level, rather than the oil source. The results demonstrated that DHA-CA is a safe and effective replacement for FO in diets of Atlantic salmon during the sensitive fingerling life-stage.

This study was performed to evaluate the effects of vitamin D and n-3 fatty acids’ co-supplementation on markers of cardiometabolic risk in diabetic patients with CHD. This randomised, double-blinded, placebo-controlled trial was conducted among sixty-one vitamin D-deficient diabetic patients with CHD. At baseline, the range of serum 25-hydroxyvitamin D levels in study participants was 6·3–19·9 ng/ml. Subjects were randomly assigned into two groups either taking 50 000 IU vitamin D supplements every 2 weeks plus 2× 1000 mg/d n-3 fatty acids from flaxseed oil (n 30) or placebo (n 31) for 6 months. Vitamin D and n-3 fatty acids’ co-supplementation significantly reduced mean (P = 0·01) and maximum levels of left carotid intima–media thickness (CIMT) (P = 0·004), and mean (P = 0·02) and maximum levels of right CIMT (P = 0·003) compared with the placebo. In addition, co-supplementation led to a significant reduction in fasting plasma glucose (β −0·40 mmol/l; 95 % CI −0·77, −0·03; P = 0·03), insulin (β −1·66 μIU/ml; 95 % CI −2·43, −0·89; P < 0·001), insulin resistance (β −0·49; 95 % CI −0·72, −0·25; P < 0·001) and LDL-cholesterol (β −0·21 mmol/l; 95 % CI −0·41, −0·01; P = 0·04), and a significant increase in insulin sensitivity (β +0·008; 95 % CI 0·004, 0·01; P = 0·001) and HDL-cholesterol (β +0·09 mmol/l; 95 % CI 0·01, 0·17; P = 0·02) compared with the placebo. Additionally, high-sensitivity C-reactive protein (β −1·56 mg/l; 95 % CI −2·65, −0·48; P = 0·005) was reduced in the supplemented group compared with the placebo group. Overall, vitamin D and n-3 fatty acids’ co-supplementation had beneficial effects on markers of cardiometabolic risk.

Intake of the plant-derived n-3 fatty acid α-linolenic acid (ALA) has been associated with anti-atherosclerotic properties. However, information on the association between ALA intake and development of peripheral artery disease (PAD) is lacking. In this follow-up study, we investigated the association between dietary intake of ALA and the rate of PAD among middle-aged Danish men and women enrolled into the Danish Diet, Cancer and Health cohort between 1993 and 1997. Incident PAD cases were identified through the Danish National Patient Register. Intake of ALA was assessed using a validated FFQ. Statistical analyses were performed using Cox proportional hazard regression allowing for separate baseline hazards among sexes and adjusted for established risk factors for PAD. During a median of 13·6 years of follow-up, we identified 950 valid cases of PAD with complete information on covariates. The median energy-adjusted ALA intake within the cohort was 1·76 g/d (95 % central range: 0·94–3·28). In multivariable analyses, we found no statistically significant association between intake of ALA and the rate of PAD (P = 0·339). Also, no statistically significant associations were observed in analyses including additional adjustment for co-morbidities and in sex-specific analyses. In supplemental analyses with additional adjustment for potential dietary risk factors, we found a weak inverse association of PAD with ALA intake above the median, but the association was not statistically significant (P = 0·314). In conclusion, dietary intake of ALA was not consistently associated with decreased risk of PAD.

Residents of Hong Kong have undergone a dietary transition from a traditional Chinese diet that is high in seafood to a more Western diet. This may have affected the nutritional composition of breast milk of Hong Kong mothers. The present study aims to investigate the relationship between the dietary pattern and the fatty acid profile of the breast milk of lactating women in Hong Kong. Seventy-three volunteering healthy Hong Kong lactating mothers participated in the study. Their dietary intakes were assessed by using a 3-d dietary record and FFQ. The mean n-3 fatty acid levels were approximately 0·4 % (EPA) and 0·9 % (DHA) of total fatty acids in the breast milk of lactating mothers who had exclusively breastfed their infants aged 2–6 months. Maternal dietary intakes of n-3 fatty acids were positively associated with their levels in the breast milk. The levels of maternal intakes of freshwater and saltwater fish, especially the consumption of salmon, croaker and mandarin, were significantly correlated with the content of DHA in breast milk. The present study is among the very few in the literature to determine the fatty acid profile of breast milk in Hong Kong populations and verify certain dietary factors that influence this profile. High levels of n-3 PUFA, especially DHA, were observed in the breast milk of Hong Kong lactating women. The findings may serve as a dietary reference for lactating mothers to optimise the fatty acid profile of their breast milk.

A more efficient utilisation of marine-derived sources of dietary n-3 long-chain PUFA (n-3 LC PUFA) in cultured Atlantic salmon (Salmo salar L.) could be achieved by nutritional strategies that maximise endogenous n-3 LC PUFA synthesis. The objective of the present study was to quantify the extent of n-3 LC PUFA biosynthesis and the resultant effect on fillet nutritional quality in large fish. Four diets were manufactured, providing altered levels of dietary n-3 substrate, namely, 18 : 3n-3, and end products, namely, 20 : 5n-3 and 22 : 6n-3. After 283 d of feeding, fish grew in excess of 3000 g and no differences in growth performance or biometrical parameters were recorded. An analysis of fatty acid composition and in vivo metabolism revealed that endogenous production of n-3 LC PUFA in fish fed a diet containing no added fish oil resulted in fillet levels of n-3 LC PUFA comparable with fish fed a diet with added fish oil. However, this result was not consistent among all treatments. Another major finding of this study was the presence of abundant dietary n-3 substrate, with the addition of dietary n-3 end product (i.e. fish oil) served to increase final fillet levels of n-3 LC PUFA. Specifically, preferential β-oxidation of dietary C18n-3 PUFA resulted in conservation of n-3 LC PUFA from catabolism. Ultimately, this study highlights the potential for endogenous synthesis of n-3 LC PUFA to, partially, support a substantial reduction in the amount of dietary fish oil in diets for Atlantic salmon reared in seawater.

In sows, n-3 fatty acids increase litter sizes, however, effects on gilt reproductive development have not been adequately studied. Moreover, not determined are effects of feeding n-3 fatty acids to sows on reproduction in offspring. The objective here was to determine effects of 4% dietary menhaden oil on growth and puberty in gilts farrowed by sows fed menhaden oil. Sows (n = 44) were assigned to: (1) control gestation and lactation diets, or (2) diets including menhaden oil. For primiparous sows only, total litter size and born alive were greater (P < 0.05) in females fed menhaden oil. Conversely, pigs from primiparous controls were heavier (P < 0.05) than pigs from primiparous sows fed menhaden oil (parity by diet interactions, P < 0.01). Diet did not affect (P > 0.20) other sow and litter characteristics. At weaning, 84 gilts from control- or menhaden oil sows were placed three gilts per pen and provided control diets or diets containing menhaden oil. Nursery and grow-finish feed intake and feed efficiency were similar (P > 0.21) for gilts from the different sows and weight gain was similar (P > 0.24) for gilts fed control or menhaden diets. Gilts fed menhaden oil tended to eat less in the nursery (1.18±0.08 kg v. 0.98±0.08 kg; P = 0.09) and overall (1.83±0.04 kg v. 1.72±0.04 kg; P = 0.06). Thus, overall feed to gain was greater (2.52±0.03 v. 2.33±0.03; P < 0.01) and nursery (2.12±0.04 v. 1.80±0.04; P = 0.10) and grow-finish (3.07±0.19 v. 2.58±0.19; P = 0.08) feed to gain tended to be greater, for control gilts. Age at puberty was greater (P = 0.02) for gilts from menhaden oil-fed sows (205.1±3.2 days) compared to gilts from controls (193.9±3.2 days) and tended to be greater (P = 0.09), for controls (203.5±3.2 days) compared to gilts fed menhaden oil (195.5±3.2 days). A tendency existed (P = 0.09) for greater follicular fluid in gilts fed menhaden oil, however, ovulation rate and ovarian, luteal and uterine weights were not affected by sow diet, gilt diet or the interaction (P > 0.23). Feeding gilts menhaden oil enhanced feed efficiency and hastened puberty onset. Gilts from sows consuming menhaden oil exhibited delayed puberty and retaining females from sows fed this feedstuff may be ill advised.

Supplementation with n-3 fatty acids can influence inflammation and markers of arterial stiffness that are increased in patients with rheumatoid arthritis (RA). However, it is unknown whether specific patterns of dietary fatty acid intake are similarly associated. In a longitudinal study, eighty-six RA patients reported their dietary intake and had arterial stiffness measured using the augmentation index (AIx) at baseline and 8 months. Latent profile analysis (LPA) was performed to characterise patterns of fatty acid intake using sixteen major fatty acids. Models for two to six profiles were compared using the Akaike and Bayesian information criteria. Associations between AIx and the profiles were adjusted for age, sex, disease activity, fish oil supplementation, medications, physical activity and socio-economic status. LPA identified five distinct profiles. Profile 1 subjects (n 7) reported significantly higher intake of palmitoleic acid (16 : 1), arachidonic acid (20 : 4n-6), EPA (20 : 5n-3), DHA (22 : 6n-3) and docosapentaenoic acid (22 : 5n-3) (P<0·001 for each) than profiles 2 (n 14), 3 (n 19), 4 (n 23) and 5 (n 23) and significantly higher grilled and tinned fish consumption. The AIx varied significantly across the five profiles (P=0·023); subjects in profile 1 had a significantly lower AIx than those in profile 3 (β=–7·2 %; 95 % CI –11·5, –2·9; P=0·001) who had the lowest reported intake of n-3 fatty acids. Fish oil supplementation was also independently associated with lower AIx (β=–4·15 %; 95 % CI –6·73, –1·56; P=0·002). A diet characterised by a higher reported intake of n-3 fatty acids, palmitoleic acid (16 : 1) and arachidonic acid (20 : 4n-6) is associated with a lower AIx in RA patients.

Newly diagnosed cancer patients are frequently found suffering from a metastatic disease, which poses additional challenges to the delivery of effective therapies. Chemotherapy and radiotherapy are associated with side effects which reduce tolerance to treatment and likelihood of tumour response. Identifying preventable factors of reduced response to therapy would translate into better care of cancer patients. Among other factors, malnutrition, as diagnosed by non-volitional weight loss, and cachexia, as revealed by sarcopenia, are universally recognised negative prognostic factors. Less certainty exists on the role of nutrition therapy in improving cancer patients’ body composition and clinical outcome. The reasons for the lack of convincing evidence are manifold, mostly related to the poor design of nutritional trials. Metastatic cancer patients should receive a quantitatively and qualitatively adequate diet, and in case of reduced tolerance of food, artificial nutrition is indicated. Most importantly, nutritional care should target the underlying mechanisms of reduced food intake/impaired anabolic response, and aim at minimising the impact of catabolic crisis, to maximise the recovery phase. The combined and early use of supplemental energies and proteins, as well as modulators of inflammatory response has been shown to improve nutritional status and may also benefit clinical outcome. When part of early palliative care, nutrition therapy improves cancer patients’ quality of life and may prolong survival at a fraction of the costs of developing new drugs.