Depression is highly prevalent in haemodialysis patients, and diet might play an important role. Therefore, we conducted this cross-sectional study to determine the association between dietary fatty acids (FA) consumption and the prevalence of depression in maintenance haemodialysis (MHD) patients. Dietary intake was assessed using a validated FFQ between December 2021 and January 2022. The daily intake of dietary FA was categorised into three groups, and the lowest tertile was used as the reference category. Depression was assessed using the Patient Health Questionnaire-9. Logistic regression and restricted cubic spline (RCS) models were applied to assess the relationship between dietary FA intake and the prevalence of depression. As a result, after adjustment for potential confounders, a higher intake of total FA [odds ratio (OR)T3 vs. T1 = 1·59, 95 % confidence interval (CI) = 1·04, 2·46] and saturated fatty acids (SFA) (ORT3 vs. T1 = 1·83, 95 % CI = 1·19, 2·84) was associated with a higher prevalence of depressive symptoms. Significant positive linear trends were also observed (P < 0·05) except for SFA intake. Similarly, the prevalence of depression in MHD patients increased by 20% (OR = 1.20, 95% CI = 1.01–1.43) for each standard deviation increment in SFA intake. RCS analysis indicated an inverse U-shaped correlation between SFA and depression (Pnonlinear > 0·05). Additionally, the sensitivity analysis produced similar results. Furthermore, no statistically significant association was observed in the subgroup analysis with significant interaction. In conclusion, higher total dietary FA and SFA were positively associated with depressive symptoms among MHD patients. These findings inform future research exploring potential mechanism underlying the association between dietary FA and depressive symptoms in MHD patients.

The aim of this study was to examine the effect of three different fatty acid (FA)-rich meals enriched in either SFA, MUFA or PUFA on postprandial metabolic responses in premenopausal, normal-weight women. For this randomised, single-blind, crossover study, three high-fat (HF) meals rich in either SFA, MUFA or PUFA (65 % energy from fat; 35 % of participants’ total daily energy needs) were tested. For each visit, anthropometrics and RMR were measured following a 12–15 h fast. Then, participants consumed one of the HF meals, and respiratory gases were collected using indirect calorimetry for 3 h postprandially. Energy expenditure (EE) following a SFA-rich meal was significantly higher than a MUFA-rich meal (P = 0·04; η2 = 0·19), but SFA was not significantly different from PUFA. There was a trend towards significance in EE between PUFA and MUFA (P = 0·06). After adjusting for fat-free mass (FFM), there were no longer condition or time effects for EE, although FFM remained a significant predictor (P = 0·005; η2 = 0·45). There were no significant differences between conditions for dietary-induced thermogenesis or substrate oxidation. The relationship between fat mass (FM) and both total fat oxidation (r 0·62; P = 0·025) and total change in RER following a MUFA-rich meal was observed (r −0·55; P = 0·05). In conclusion, weight loss through increases in EE may be best achieved by increasing FFM rather than selection of FA type. Further, a relationship exists between FM and fat oxidation following a MUFA-rich meal, most likely due to an unidentified mechanism.

Cardio-metabolic risk (CMR) embodies a clustering of metabolic abnormalities that increase the likelihood of developing CVD in the large arteries of the heart, peripheral tissues and brain. These abnormalities share a common origin of insulin resistance, which manifests typically as excess visceral adipose tissue in the abdominal cavity, and within cells of key metabolic tissues (ectopic fat), including the liver, pancreas, heart and skeletal muscle. As expected, the increased risk of CVD that can be attributed to CMR factors is alarmingly high in overweight and obese populations, but this risk can be reduced by reversing many of the inappropriate diet and lifestyle behaviours that underlie its development. The Nutrition Society's 2018 Winter Meeting at the Royal Society of Medicine addressed the topic of the ‘Optimal diet and lifestyle for managing cardio-metabolic risk’, with the aim of providing mechanistic insights into the impact of macronutrients, dietary patterns and meal timing in key metabolic tissues. The 2-d programme concluded with a summary of its main outcomes, and an overview of their implications for dietary policy in the UK.

Dietary fatty acid (FA) composition may influence metabolism, possibly affecting weight management. The purpose of this study was to compare the effects of a 5-d diet rich in PUFA v. MUFA. A total of fifteen normal-weight men participated in a randomised cross-over design with two feeding trials (3 d lead-in diet, pre-diet visit, 5-d PUFA- or MUFA-rich diet, post-diet visit). The 5-d diets (50 % fat) were rich in either PUFA (25 % of energy) or MUFA (25 % of energy). At pre- and post-diet visits, subjects consumed breakfast and lunch test meals, rich in the FA for that 5-d diet. Indirect calorimetry was used for 4 h after each meal. There were no treatment differences in fasting metabolism acutely or after the 5-d diet. For acute meal responses before diet, RER was higher for PUFA v. MUFA (0·86 (sem 0·01) v. 0·84 (sem 0·01), P<0·05), whereas diet-induced thermogenesis (DIT) was lower for PUFA v. MUFA (18·91 (SEM 1·46) v. 21·46 (SEM 1·34) kJ, P<0·05). After the 5-d diets, the change in RER was different for PUFA v. MUFA (−0·02 (sem 0·01) v. 0·00 (sem 0·01), P<0·05). Similarly, the change in fat oxidation was greater for PUFA v. MUFA (0·18 (sem 0·07) v. 0·04 (sem 0·06) g, P<0·05). In conclusion, acutely, a MUFA-rich meal results in lower RER and greater DIT. However, after a 5-d high-fat diet, the change in metabolic responses was greater in the PUFA diet, showing the metabolic adaptability of a PUFA-rich diet.

TAG depleted remnants of postprandial chylomicrons are a risk factor for atherosclerosis. Recent studies have demonstrated that in the fasted state, the majority of chylomicrons are small enough for transcytosis to arterial subendothelial space and accelerate atherogenesis. However, the size distribution of chylomicrons in the absorptive state is unclear. This study explored in normolipidaemic subjects the postprandial distribution of the chylomicron marker, apoB-48, in a TAG-rich lipoprotein plasma fraction (Svedberg flotation rate (Sf>400), in partially hydrolysed remnants (Sf 20–400) and in a TAG-deplete fraction (Sf<20), following ingestion of isoenergetic meals with either palm oil (PO), rice bran or coconut oil. Results from this study show that the majority of fasting chylomicrons are within the potentially pro-atherogenic Sf<20 fraction (70–75 %). Following the ingestion of test meals, chylomicronaemia was also principally distributed within the Sf<20 fraction. However, approximately 40 % of subjects demonstrated exaggerated postprandial lipaemia specifically in response to the SFA-rich PO meal, with a transient shift to more buoyant chylomicron fractions. The latter demonstrates that heterogeneity in the magnitude and duration of hyper-remnantaemia is dependent on both the nature of the meal fatty acids ingested and possible metabolic determinants that influence chylomicron metabolism. The study findings reiterate that fasting plasma TAG is a poor indicator of atherogenic chylomicron remnant homoeostasis and emphasises the merits of considering specifically, chylomicron remnant abundance and kinetics in the context of atherogenic risk. Few studies address the latter, despite the majority of life being spent in the postprandial and absorptive state.

As obesity continues to be a global epidemic, research into the mechanisms of hunger and satiety and how those signals act to regulate energy homeostasis persists. Peptide YY (PYY) is an acute satiety signal released upon nutrient ingestion and has been shown to decrease food intake when administered exogenously. More recently, investigators have studied how different factors influence PYY release and circulating levels in humans. Some of these factors include exercise, macronutrient composition of the diet, body-weight status, adiposity levels, sex, race and ageing. The present article provides a succinct and comprehensive review of the recent literature published on the different factors that influence PYY release and circulating levels in humans. Where human data are insufficient, evidence in animal or cell models is summarised. Additionally, the present review explores the recent findings on PYY responses to different dietary fatty acids and how this new line of research will make an impact on future studies on PYY. Human demographics, such as sex and age, do not appear to influence PYY levels. Conversely, adiposity or BMI, race and acute exercise all influence circulating PYY levels. Both dietary fat and protein strongly stimulate PYY release. Furthermore, MUFA appear to result in a smaller PYY response compared with SFA and PUFA. PYY levels appear to be affected by acute exercise, macronutrient composition, adiposity, race and the composition of fatty acids from dietary fat.

The effect of arachidonic acid (ARA) intake on asthma risk is unclear. The objective of the present review was to systematically evaluate available observational studies on the relationship between ARA exposure and asthma risk in children and adults. A PubMed search was conducted on 22 October 2013 and seventy-three publications were checked against predefined criteria for eligibility. To identify additional eligible publications, potentially relevant articles were searched from bibliographies of articles on ARA and asthma. A total of 2924 citations were scrutinised. Finally, fourteen articles were included. A quality assessment was conducted based on the reporting and methodological quality. A meta-analysis was not conducted; therefore, a qualitative assessment is presented. Three high-, two medium- and ten low-quality studies were reviewed. Eleven studies, including two high- and two medium-quality studies, did not find a significant association between ARA exposure and asthma risk. In contrast, one high-quality study indicated a significant trend toward reducing asthma risk in children with decreasing maternal ARA intake (Ptrend = 0·025), and one low-quality study reported a significant trend of increasing asthma risk with higher blood ARA levels (Ptrend = 0·007). In two low-quality studies, asthma patients had significantly lower blood ARA levels than controls (both P < 0·05). These studies did not sufficiently demonstrate any relationships between ARA exposure and asthma risk because of the limited number of studies and their methodological limitations. They seem to suggest that ARA exposure is not consistently associated with asthma risk. Nevertheless, further evidence is required to prove or disprove the association.

Different dietary fat and energy subtypes have an impact on both the metabolic health and the intestinal microbiota population of the host. The present study assessed the impact of dietary fat quality, with a focus on dietary fatty acid compositions of varying saturation, on the metabolic health status and the intestinal microbiota composition of the host. C57BL/6J mice (n 9–10 mice per group) were fed high-fat (HF) diets containing either (1) palm oil, (2) olive oil, (3) safflower oil or (4) flaxseed/fish oil for 16 weeks and compared with mice fed low-fat (LF) diets supplemented with either high maize starch or high sucrose. Tissue fatty acid compositions were assessed by GLC, and the impact of the diet on host intestinal microbiota populations was investigated using high-throughput 16S rRNA sequencing. Compositional sequencing analysis revealed that dietary palm oil supplementation resulted in significantly lower populations of Bacteroidetes at the phylum level compared with dietary olive oil supplementation (P< 0·05). Dietary supplementation with olive oil was associated with an increase in the population of the family Bacteroidaceae compared with dietary supplementation of palm oil, flaxseed/fish oil and high sucrose (P< 0·05). Ingestion of the HF-flaxseed/fish oil diet for 16 weeks led to significantly increased tissue concentrations of EPA, docosapentaenoic acid and DHA compared with ingestion of all the other diets (P< 0·05); furthermore, the diet significantly increased the intestinal population of Bifidobacterium at the genus level compared with the LF-high-maize starch diet (P< 0·05). These data indicate that both the quantity and quality of fat have an impact on host physiology with further downstream alterations to the intestinal microbiota population, with a HF diet supplemented with flaxseed/fish oil positively shaping the host microbial ecosystem.

Vascular dysfunction is recognised as an integrative marker of CVD. While dietary strategies aimed at reducing CVD risk include reductions in the intake of SFA, there are currently no clear guidelines on what should replace SFA. The purpose of this review was to assess the evidence for the effects of total dietary fat and individual fatty acids (SFA, MUFA and n-6 PUFA) on vascular function, cellular microparticles and endothelial progenitor cells. Medline was systematically searched from 1966 until November 2010. A total of fifty-nine peer-reviewed publications (covering fifty-six studies), which included five epidemiological, eighteen dietary intervention and thirty-three test meal studies, were identified. The findings from the epidemiological studies were inconclusive. The limited data available from dietary intervention studies suggested a beneficial effect of low-fat diets on vascular reactivity, which was strongest when the comparator diet was high in SFA, with a modest improvement in measures of vascular reactivity when high-fat, MUFA-rich diets were compared with SFA-rich diets. There was consistent evidence from the test meal studies that high-fat meals have a detrimental effect on postprandial vascular function. However, the evidence for the comparative effects of test meals rich in MUFA or n-6 PUFA with SFA on postprandial vascular function was limited and inconclusive. The lack of studies with comparable within-study dietary fatty acid targets, a variety of different study designs and different methods for determining vascular function all confound any clear conclusions on the impact of dietary fat and individual fatty acids on vascular function.

A recent meta-analysis of prospective cohort studies has not found an association between dietary saturated fat intake and CHD incidence. This funnelled the discussion about the importance of the recommendation to lower the intake of saturated fat for the prevention of CHD. At the same time a document of the European Food Safety Authority has suggested that specific quantitative recommendations are not needed for individual fatty acids but that more general statements can suffice. In this review, we discuss methodological aspects of the absence of association between SFA intake and CHD incidence in prospective cohort studies. We also summarise the results of the controlled dietary experiments on blood lipids and on CHD incidence in which saturated fat was replaced by either cis-unsaturated fat or carbohydrates. Finally, we propose a nutritionally adequate diet with an optimal fatty acid composition for the prevention of CHD in the context of dietary patterns. Such diets are characterised by a low intake of saturated fat, and as low as possible intake of trans-fat and fulfil the requirements for the intake of n-6 and n-3 fatty acids. No recommendation is needed for the intake of cis-MUFA.

In recent years the intake of n-6 PUFA and trans-fatty acids (TFA) has increased, whereas n-3 PUFA intake has decreased. The present study investigated the effects of maternal diet high in n-6 PUFA, n-3 PUFA or TFA on glucose metabolism, insulin sensitivity and fatty acid profile in male offspring. Female weanling Wistar/NIN rats were randomly assigned to receive either a diet high in linoleic acid (LA), or α-linolenic acid (ALA), or long-chain n-3 PUFA (fish oil; FO), or TFA, for 90 d, and mated. Upon weaning, pups were randomly divided into seven groups (mother's diet-pup's diet): LA-LA, LA-ALA, LA-FO, ALA-ALA, FO-FO, TFA-TFA and TFA-LA. At the age of 105 d, an oral glucose tolerance test, adipocyte glucose transport and muscle phospholipid fatty acid composition were measured in the pups. All animals displayed normal insulin sensitivity as evidenced by similar plasma insulin and area under the curve of insulin after an oral glucose load. Maternal intake of n-3 PUFA (ALA or FO) resulted in higher n-3 PUFA in the offspring. Plasma cholesterol and NEFA were significantly higher in the TFA-TFA group compared with the other groups. Adipocyte insulin-stimulated glucose transport and adiponectin mRNA expression were lower in TFA-TFA and TFA-LA offspring compared with the other groups. While most mother-pup fatty acid combinations did not influence the measured variables in the pups, these results indicate that maternal intake of TFA led to an unfavourable profile in the pups through to the age of 105 d, whether the pups consumed TFA, or not.

Energy intake and expenditure tend on average to remain adjusted to each other in order to maintain a stable body weight, which is only likely to be sustained if the fuel mix oxidised is equivalent to the nutrient content of the diet. Whereas protein and carbohydrate degradation and oxidation are closely adjusted to their intakes, fat balance regulation is less precise and that fat is more likely to be stored than oxidised.

It has been demonstrated that dietary fatty acids have an influence not only on the fatty acid composition of membrane phospholipids, thus modulating several metabolic processes that take place in the adipocyte, but also on the composition and the quantity of different fatty acids in adipose tissue. Moreover, dietary fatty acids also modulate eicosanoid presence, which have hormone-like activities in lipid metabolism regulation in adipose tissue.

Until recently, the adipocyte has been considered to be no more than a passive tissue for storage of excess energy. However, there is now compelling evidence that adipocytes have a role as endocrine secretory cells. Some of the adipokines produced by adipose tissue, such as leptin and adiponectin, act on adipose tissue in an autocrine/paracrine manner to regulate adipocyte metabolism. Furthermore, dietary fatty acids may influence the expression of adipokines.

The nutrients are among the most influential of the environmental factors that determine the way adipose tissue genes are expressed by functioning as regulators of gene transcription. Therefore, not only dietary fat amount but also dietary fat composition influence adipose tissue metabolism.

The metabolic syndrome is a very common disease associated with an increased risk of type 2 diabetes mellitus (T2DM) and CVD. The clinical characteristics of the metabolic syndrome include insulin resistance, dyslipidaemia, abdominal obesity and hypertension. The diverse clinical characteristics illustrate the complexity of the disease process, which involves several dysregulated metabolic pathways. Thus, multiple genetic targets must be involved in the pathogenesis and progression of the metabolic syndrome. Nevertheless, the human genome has not changed markedly in the last decade but the prevalence of the metabolic syndrome has increased exponentially, which illustrates the importance of gene–environmental interactions. There is good evidence that nutrition plays an important role in the development and progression of the metabolic syndrome. Indeed, obesity is a key aetiological factor in the development of the metabolic syndrome. Understanding the biological impact of gene–nutrient interactions will provide a key insight into the pathogenesis and progression of diet-related polygenic disorders, including the metabolic syndrome. The present paper will explore the interactions between genetic background and dietary exposure or nutritional therapy, focusing on the role of dietary fatty acids within the context of nutrient regulation of gene expression and individual responsiveness to dietary therapy. Only with a full understanding of gene–gene, gene–nutrient and gene–nutrient–environment interactions can the molecular basis of the metabolic syndrome be solved to minimise the adverse health effects of obesity and reduce the risk of the metabolic syndrome, and subsequent T2DM and CVD.

Over the last 30 years it has become apparent that specific dietary fatty acids are capable of regulating, either directly or indirectly through various signal pathways, the expression of numerous genes, either positively or negatively. Such nutrient-gene interactions have important effects on cell metabolism, differentiation and growth, and ultimately on disease processes. The present review describes some of the more important fatty acid-gene interactions in relation to health and disease in mammalian species, and focuses on the underlying cell signal mechanisms, including various transcription factors, affected by fatty acids and some of their oxygenated derivatives, e.g. the eicosanoids. The review also attempts to clarify some of the complexities of the effects of fatty acids by suggesting a possible overriding regulation by the redox status of the cell. The latter will at least stimulate controversy in this exciting area of lipid research.

There is at present a justifiable debate as to the optimum level of total dietary fat which will reduce the risk of obesity without an elevation of plasma triacylglycerol or a depression of plasma HDL-cholesterol. Total plasma cholesterol and LDL-cholesterol levels are lowered and risk of fatal myocardial infarction is lowered when either saturated or trans-unsaturated fatty acids are replaced isoenergetically by either monounsaturated or polyunsaturated fatty acids. The triacylglycerol-raising and HDL-lowering effects of low-fat high-carbohydrate diets can be over-come with low intakes of n−3 polyunsaturated fatty acids and moderate exercise. Whilst a reduction in dietary fat is being attained in many countries, the reduction is uniform across all fatty acids, leaving dietary fat composition unchanged. The ability of low-fat diets to reduce cholesterol and cause a fall in body weight is not influenced by the carbohydrate ratio starch: sugars in the diet. However, weight-gain susceptibility to high intakes of dietary fat and the plasma cholesterol responsiveness to diet are considerably influenced by common genetic polymorphisms.

Quantitative dietary guidelines for fats were first issued in 1977 in the USA and these guidelines have changed little since then. In the UK only 14 % of the population achieve the dietary goal for fat (33 % energy) and only 3 % achieve the target (10 % energy) from saturated fatty acids. Analysis of the Dietary and Nutritional Survey of British Adults reveals that across quartiles of decreasing total fat intake, the actual fatty acid composition of this fat does not alter; i.e. when total fat is lowered, all fatty acid categories are equally lowered. This arises because 85 % of total fat and of each of the categories of fatty acids are provided by just five foods (milk, meat, cereals, spreads and vegetables). When total fat in the UK is lowered, the intake of polyunsaturated fatty acids is lowered. The problem is that if the intake of polyunsaturated fatty acids falls below a threshold of about 5 % energy, the cholesterol-raising properties of certain saturated fatty acids, e.g. myristic acid, are greatly augmented. In order to alter the balance of dietary fatty acids, more data are needed on food choices of those in the population achieving particular targets. These targets cannot be based on existing dietary goals, since so few people attain them. A new set of‘interim attainable dietary guidelines’, based on prevailing dietary intakes, must be the basis for establishing sensible food-based dietary guidelines.

Gender and dietary fatty acids are involved in the regulation of lipid metabolism, disturbances of which can lead to pathologies such as metabolic syndrome or CVD. Possible interactions between these factors were investigated in male and female hamsters fed diets rich in either saturated fatty acids (‘butter’ diet) or in α-linolenic acid (‘linseed oil’ diet). Gender effect predominated over the diet effect on cholesterol (CH) metabolism; compared to males, females exhibited lower concentrations of plasma total CH (−20%, P<0·001), LDL-CH (−40%, P<0·001) and HDL-CH (−16%, P<0·001), together with higher LDL receptor (+40%) and lower HDL receptor (−60%) hepatic content. Triacylglycerol (TG) metabolism was affected by diet above all: compared to animals fed the ‘butter’ diet, those fed the ‘linseed oil’ diet exhibited lower plasma (−23%, P=0·046) and liver TG (−20%, P=0·026) concentration which may result from both an increased β-oxidation (P<0·001), without any change in PPARα mRNA, and a decreased hepatic lipogenesis (P=0·023), without increased sterol response element binding protein 1c (SREBP1c) mRNA. The response to diet was much more pronounced in males than in females, without gender effect on the transcription level of PPARα and SREBP1c. Finally, the ‘linseed oil’ diet decreased the insulin resistance index (−80%, P<0·001) with a more marked effect in males, in relation to their higher hepatic PPARγ expression (+90%, P=0·012). In conclusion, in our model, the response of either TG or CH to dietary fatty acids is modulated differently by gender. The possible relevance of these interactions to dietary practice should be taken into account in man.