Type 2 diabetes (T2D) and CVD are major causes of mortality and chronic morbidity. Whilst mortality from CVD has decreased they remain the largest cause of death in Europe and the prevalence of T2D is increasing rapidly. A consistent component of public health advice is to reduce intake of SFA to reduce CVD in particular, which implies limiting dairy food consumption. The prospective studies and randomised controlled trials included in this review show that for dairy foods at least, SFA are not consistently associated with CVD or T2D risk. For CVD the association with dairy foods is generally neutral despite dairy foods being the major source of SFA in many diets. This creates considerable doubt, at least for dairy foods, concerning the validity of the traditional diet-heart hypothesis which positively relates SFA intake to increased serum LDL-cholesterol and subsequent increased CVD. There is now emerging evidence to explain this which is highly relevant to dairy foods. These include the potentially counterbalancing effect of SFA-stimulated HDL-cholesterol and specific food matrix factors. In addition, SFA are associated with the less atherogenic large buoyant LDL particles and possible counterbalancing hypotensive effects of dairy proteins. Overall, dairy foods have either a neutral or beneficial association with CVD and T2D. Beneficial associations are seen for blood pressure and the reduced T2D risk linked to yoghurt consumption, a subject that needs urgent attention given the sharp rise in T2D prevalence in many countries.

Olive oil (OO) polyphenols have been shown to improve HDL anti-atherogenic function, thus demonstrating beneficial effects against cardiovascular risk factors. The aim of the present study was to investigate the effect of extra virgin high polyphenol olive oil (HPOO) v. low polyphenol olive oil (LPOO) on the capacity of HDL to promote cholesterol efflux in healthy adults. In a double-blind, randomised cross-over trial, fifty participants (aged 38·5 (sd 13·9) years, 66 % females) were supplemented with a daily dose (60 ml) of HPOO (320 mg/kg polyphenols) or LPOO (86 mg/kg polyphenols) for 3 weeks. Following a 2-week washout period, participants crossed over to the alternate treatment. Serum HDL-cholesterol efflux capacity, circulating lipids (i.e. total cholesterol, TAG, HDL, LDL) and anthropometrics were measured at baseline and follow-up. No significant between-group differences were observed. Furthermore, no significant changes in HDL-cholesterol efflux were found within either the LPOO and HPOO treatment arms; mean changes were 0·54 % (95 % CI (0·29, 1·37)) and 0·10 % (95 % CI (0·74, 0·94)), respectively. Serum HDL increased significantly after LPOO and HPOO intake by 0·13 mmol/l (95 % CI (0·04, 0·22)) and 0·10 mmol/l (95 % CI (0·02, 0·19)), respectively. A small but significant increase in LDL of 0·14 mmol/l (95 % CI (0·001, 0·28)) was observed following the HPOO intervention. Our results suggest that additional research is warranted to further understand the effect of OO with different phenolic content on mechanisms of cholesterol efflux via different pathways in multi-ethnic populations with diverse diets.

Epidemiological studies on the association between the low carbohydrate diet (LCD) score and CVD risk factors have limited and inconsistent results. Data are from the baseline survey of Community-based Cohort Study on Nervous System Diseases. A total of 4609 adults aged ≥ 18 years were included in the study. Dietary data were assessed using a validated semi-quantitative FFQ. Multivariable logistic regression analyses were used to estimate relationships of three LCD scores with low HDL-cholesterol, high LDL-cholesterol, hypercholesterolaemia, hypertriacylglycerolaemia, impaired fasting glucose (IFG), high blood pressure and hyperuricaemia after adjusting for potential confounders. A higher LCD score was negatively associated with low HDL-cholesterol (OR: 0·65 (95 % CI 0·50, 0·83), P = 0·0001) and IFG (OR: 0·65 (95 % CI 0·51, 0·81), P = 0·001) after the final adjustment. However, there are sex differences in this result. Males in the highest quintile of the animal-based or plant-based LCD scores showed a decreased risk of low HDL-cholesterol, and females in the highest quintile of the animal-based or plant-based LCD scores showed a decreased risk of IFG than those in the lowest quintile of the LCD scores. These results suggest that sex differences should be considered when using LCD to treat dyslipidaemia and reduce fasting blood glucose.

Se reduces cellular inflammation and lipid peroxides; therefore, its association with CVD and the metabolic syndrome (MetS) has been studied. We aimed to investigate the association between Se intake and the MetS and its parameters (high waist circumference, hyperglycaemia, high blood pressure, high TAG and low HDL-cholesterol) in Brazilian adolescents between 12 and 17 years old. This research is part of the Study of Cardiovascular Risks in Adolescents (ERICA), a Brazilian nationwide school-based study with regional and national relevance. We assessed: (1) socio-demographic data (sex, age, type of school and maternal education) using a self-administered questionnaire; (2) dietary intake using a 24-h recall applied for the whole sample and a second one applied to a subsample to allow within-person variability adjustment; (3) anthropometric data (weight, height, waist circumference) and blood pressure using standardised procedures; and (4) biochemical analyses (fasting glucose, TAG and HDL-cholesterol). Logistic regression was applied, basing the analysis on a theoretical model. Median Se intake was 98·3 µg/d. Hypertension and hyperglycaemia were more prevalent among boys, while a high waist circumference was more frequent in girls, and low HDL-cholesterol levels were higher among private school students. The prevalence of the MetS was 2·6 %. No association between the MetS and its parameters and Se intake was found. This lack of association could be due to an adequate Se intake in the studied population.

Currently, the prevention and treatment of CVD have been a global focus since CVD is the number one cause of mortality and morbidity. In the pathogenesis of CVD, it was generally thought that impaired cholesterol homeostasis might be a risk factor. Cholesterol homeostasis is affected by exogenous factors (i.e. diet) and endogenous factors (i.e. certain receptors, enzymes and transcription factors). In this context, the number of studies investigating the potential mechanisms of dietary fatty acids on cholesterol homeostasis have increased in recent years. As well, the cluster of differentiation 36 (CD36) receptor is a multifunctional membrane receptor involved in fatty acid uptake, lipid metabolism, atherothrombosis and inflammation. CD36 is proposed to be a crucial molecule for cholesterol homeostasis in various mechanisms including absorption/reabsorption, synthesis, and transport of cholesterol and bile acids. Moreover, it has been reported that the amount of fatty acids and fatty acid pattern of the diet influence the CD36 level and CD36-mediated cholesterol metabolism principally in the liver, intestine and macrophages. In these processes, CD36-mediated cholesterol and lipoprotein homeostasis might be impaired by dietary SFA and trans-fatty acids, whereas ameliorated by MUFA in the diet. The effects of PUFA on CD36-mediated cholesterol homeostasis are controversial depending on the amount of n-3 PUFA and n-6 PUFA, and the n-3:n-6 PUFA ratio. Thus, since the CD36 receptor is suggested to be a novel nutrient-sensitive biomarker, the role of CD36 and dietary fatty acids in cholesterol metabolism might be considered in medical nutrition therapy in the near future. Therefore, the novel nutritional target of CD36 and interventions that focus on dietary fatty acids and potential mechanisms underlying cholesterol homeostasis are discussed in this review.

The last few decades have witnessed a global rise in the number of older individuals. Despite this demographic shift, morbidity within this population group is high. Many factors influence healthspan; however, an obesity pandemic is emerging as a significant determinant of older people’s health. It is well established that obesity adversely affects several metabolic systems. However, due to its close association with overall cardiometabolic health, the impact that obesity has on cholesterol metabolism needs to be recognised. The aim of the present review is to critically discuss the effects that obesity has on cholesterol metabolism and to reveal its significance for healthy ageing.

Melatonin-rich and 1,8-cineole-rich extracts have been successfully obtained from yellow mustard (YM) and small cardamom (SC) seeds, respectively, employing green technology of supercritical CO2 (SC-CO2) extraction. Chemical profiling confirmed the presence of melatonin and 1,8-cineole and co-extractants in the respective extracts. Electron paramagnetic resonance spectroscopy attested strong antioxidant activities of the extracts foregoing pan-assay interference compounds involved in spectroscopic analysis. These extracts also exhibited synergistic efficacies greater than unity confirming antioxidant synergy among the co-extracted bioactives therein. To ascertain hypocholesterolaemic efficacies, these extracts were co-administered orally with Triton X (at the pre-optimised dose of 175 mg/kg body weight (BW)) to Wistar albino rats at doses of 550, 175 and 55 mg/kg BW. Serum total cholesterol levels in the rats were monitored on days 3, 7, 15 and 21. On day 21, total cholesterol level reduced appreciably by 49·44 % in rats treated with YM seed extract and by 48·95 % in rats treated with SC seed extract, comparable with atorvastatin-administered rats (51·09 %). Either extract demonstrated inhibitory effects on hepatic 3-hydroxy-3-methyl-glutaryl-CoA (HMG-CoA) reductase activity. A molecular docking exercise identified specific compounds in the extracts which possessed binding affinities comparable with therapeutically used HMG-CoA reductase inhibitors. In silico and in vivo studies concertedly concluded that the consortium of bioactive components in the extracts cannot be considered as invalid metabolic panaceas and therefore these ‘green’ extracts could be safely subjected to clinical studies as preventive biotherapeutics for hypercholesterolaemia. These extracts could be consumed per se as hypocholesterolaemic supplements or could be ingredients of new spice-based therapeutic foods.

Personalised nutrition is at its simplest form the delivery of dietary advice at an individual level. Incorporating response to different diets has resulted in the concept of precision nutrition. Harnessing the metabolic phenotype to identify subgroups of individuals that respond differentially to dietary interventions is becoming a reality. More specifically, the classification of individuals in subgroups according to their metabolic profile is defined as metabotyping and this approach has been employed to successfully identify differential response to dietary interventions. Furthermore, the approach has been expanded to develop a framework for the delivery of targeted nutrition. The present review examines the application of the metabotype approach in nutrition research with a focus on developing personalised nutrition. Application of metabotyping in longitudinal studies demonstrates that metabotypes can be associated with cardiometabolic risk factors and diet-related diseases while application in interventions can identify metabotypes with differential responses. In general, there is strong evidence that metabolic phenotyping is a promising strategy to identify groups at risk and to potentially improve health promotion at a population level. Future work should verify if targeted nutrition can change behaviours and have an impact on health outcomes.

Men have earlier first-time event of CHD and higher postprandial TAG response compared with women. The aim of this exploratory sub-study was to investigate if intake of meals with the same amount of fat from different dairy products affects postprandial lipoprotein subclasses differently in healthy women and men. A total of thirty-three women and fourteen men were recruited to a randomised controlled cross-over study with four dairy meals consisting of butter, cheese, whipped cream or sour cream, corresponding to 45 g of fat (approximately 60 energy percent). Blood samples were taken at 0, 2, 4 and 6 h postprandially. Lipoprotein subclasses were measured using NMR and analysed using a linear mixed model. Sex had a significant impact on the response in M-VLDL (P=0·04), S-LDL (P=0·05), XL-HDL (P=0·009) and L-HDL (P=0·001) particle concentration (P), with women having an overall smaller increase in M-VLDL-P, a larger decrease in S-LDL-P and a larger increase in XL- and L-HDL-P compared with men, independent of meal. Men showed a decrease in XS-VLDL-P compared with women after intake of sour cream (P<0·01). In men only, XS-VLDL-P decreased after intake of sour cream compared with all other meals (v. butter: P=0·001; v. cheese: P=0·04; v. whipped cream: P=0·006). Meals with the same amount of fat from different dairy products induce different postprandial effects on lipoprotein subclass concentrations in men and women.

Studies have shown that the reduction in serum TAG concentrations with long-chain n-3 fatty acid supplementation is highly variable among individuals. The objectives of the present study were to compare the proportions of individuals whose TAG concentrations lowered after high-dose DHA and EPA, and to identify the predictors of response to both modalities. In a double-blind, controlled, crossover study, 154 men and women were randomised to three supplemented phases of 10 weeks each: (1) 2·7 g/d of DHA, (2) 2·7 g/d of EPA and (3) 3 g/d of maize oil, separated by 9-week washouts. As secondary analyses, the mean intra-individual variation in TAG was calculated using the standard deviation from the mean of four off-treatment samples. The response remained within the intra-individual variation (±0·25 mmol/l) in 47 and 57 % of participants after DHA and EPA, respectively. Although there was a greater proportion of participants with a reduction >0·25 mmol/l after DHA than after EPA (45 υ. 32 %; P < 0·001), the mean TAG reduction was comparable between groups (–0·59 (sem 0·04) υ. –0·57 (sem 0·05) mmol/l). Participants with a reduction >0·25 mmol/l after both DHA and EPA had higher non-HDL-cholesterol, TAG and insulin concentrations compared with other responders at baseline (all P < 0·05). In conclusion, supplementation with 2·7 g/d DHA or EPA had no meaningful effect on TAG concentrations in a large proportion of individuals with normal mean TAG concentrations at baseline. Although DHA lowered TAG in a greater proportion of individuals compared with EPA, the magnitude of TAG lowering among them was similar.

CVD is common in older adults. Consumption of ‘meat’ (beef, pork, lamb, game, poultry, seafood, eggs) and dairy foods (milk, cheese, yoghurt) is encouraged in older adults as these foods provide protein and nutrients such as essential fatty acids, Ca, Fe, Zn and vitamins A, D and B12 required for healthy ageing. However, these foods also contain saturated fats considered detrimental to cardiovascular health. To determine the effect of their consumption on CVD risk we assessed associations between fat intake from ‘meat’ and dairy foods and serum cholesterol levels in 226 aged-care residents (mean age 85·5 years, 70 % female). Dietary intake was determined over 2 d using visual estimation of plate waste. Fat content of foods was determined using nutrition analysis software (Xyris, Australia). Fasting serum total cholesterol (TC), LDL-cholesterol and HDL-cholesterol were measured, and the TC:HDL-cholesterol ratio calculated. Associations were determined using random-effect models adjusted for CVD risk factors using STATA/IC 13.0. Total fat and saturated fat from ‘meat’ and dairy foods were associated with higher serum HDL-cholesterol levels, and dairy fat intake and number of servings were associated with a lower TC:HDL-cholesterol ratio. Every 10 g higher intake of fat and saturated fat from dairy products, and each additional serving was associated with a −0·375 (95 % CI −0·574, −0·175; P = 0·0002), a −0·525 (95 % CI −0·834, −0·213; P = 0·001) and a −0·245 (95 % CI −0·458, −0·033; P = 0·024) lower TC:HDL-cholesterol ratio, respectively. Provision of dairy foods and ‘meat’ in recommended amounts to institutionalised older adults potentially improves intakes of key nutrients with limited detriment to cardiovascular health.

The association between dietary patterns and CVD risk factors among non-Hispanic whites has not been fully studied. Data from 650 non-Hispanic white adults who participated in one of two clinical sub-studies (about 2 years after the baseline) of the Adventist Health Study-2 (AHS-2) were analysed. Four dietary patters were identified using a validated 204-item semi-quantitative FFQ completed at enrolment into AHS-2: vegans (8·3 %), lacto-ovo-vegetarians (44·3 %), pesco-vegetarians (10·6 %) and non-vegetarians (NV) (37·3 %). Dietary pattern-specific prevalence ratios (PR) of CVD risk factors were assessed adjusting for confounders with or without BMI as an additional covariable. The adjusted PR for hypertension, high total cholesterol and high LDL-cholesterol were lower in all three vegetarian groups. Among the lacto-ovo-vegetarians the PR were 0·57 (95 % CI 0·45, 0·73), 0·72 (95 % CI 0·59, 0·88) and 0·72 (95 % CI 0·58, 0·89), respectively, which remained significant after additionally adjusting for BMI. The vegans and the pesco-vegetarians had similar PR for hypertension at 0·46 (95 % CI 0·25, 0·83) and 0·62 (95 % CI 0·42, 0·91), respectively, but estimates were attenuated and marginally significant after adjustment for BMI. Compared with NV, the PR of obesity and abdominal adiposity, as well as other CVD risk factors, were significantly lower among the vegetarian groups. Similar results were found when limiting analyses to participants not being treated for CVD risk factors, with the vegans having the lowest mean BMI and waist circumference. Thus, compared with the diet of NV, vegetarian diets were associated with significantly lower levels of CVD risk factors among the non-Hispanic whites.

A major advantage of analyses on the food group level is that the results are better interpretable compared with nutrients or complex dietary patterns. Such results are also easier to transfer into recommendations on primary prevention of non-communicable diseases. As a consequence, food-based dietary guidelines (FBDG) are now the preferred approach to guide the population regarding their dietary habits. However, such guidelines should be based on a high grade of evidence as requested in many other areas of public health practice. The most straightforward approach to generate evidence is meta-analysing published data based on a careful definition of the research question. Explicit definitions of study questions should include participants, interventions/exposure, comparisons, outcomes and study design. Such type of meta-analyses should not only focus on categorical comparisons, but also on linear and non-linear dose–response associations. Risk of bias of the individual studies of the meta-analysis should be assessed, rated and the overall credibility of the results scored (e.g. using NutriGrade). Tools such as a measurement tool to assess systematic reviews or ROBIS are available to evaluate the methodological quality/risk of bias of meta-analyses. To further evaluate the complete picture of evidence, we propose conducting network meta-analyses (NMA) of intervention trials, mostly on intermediate disease markers. To rank food groups according to their impact, disability-adjusted life years can be used for the various clinical outcomes and the overall results can be compared across the food groups. For future FBDG, we recommend to implement evidence from pairwise and NMA and to quantify the health impact of diet–disease relationships.

CVD are the leading cause of death in women globally, with ageing associated with progressive endothelial dysfunction and increased CVD risk. Natural menopause is characterised by raised non-fasting TAG concentrations and impairment of vascular function compared with premenopausal women. However, the mechanisms underlying the increased CVD risk after women have transitioned through the menopause are unclear. Dietary fat is an important modifiable risk factor relating to both postprandial lipaemia and vascular reactivity. Meals rich in SFA and MUFA are often associated with greater postprandial TAG responses compared with those containing n-6 PUFA, but studies comparing their effects on vascular function during the postprandial phase are limited, particularly in postmenopausal women. The present review aimed to evaluate the acute effects of test meals rich in SFA, MUFA and n-6 PUFA on postprandial lipaemia, vascular reactivity and other CVD risk factors in postmenopausal women. The systematic search of the literature identified 778 publications. The impact of fat-rich meals on postprandial lipaemia was reported in seven relevant studies, of which meal fat composition was compared in one study described in three papers. An additional study determined the impact of a high-fat meal on vascular reactivity. Although moderately consistent evidence suggests detrimental effects of high-fat meals on postprandial lipaemia in postmenopausal (than premenopausal) women, there is insufficient evidence to establish the impact of meals of differing fat composition. Furthermore, there is no robust evidence to conclude the effect of meal fatty acids on vascular function or blood pressure. In conclusion, there is an urgent requirement for suitably powered robust randomised controlled trials to investigate the impact of meal fat composition on postprandial novel and established CVD risk markers in postmenopausal women, an understudied population at increased cardiometabolic risk.

Plasma apoB is a more accurate marker of the risk of CVD and type 2 diabetes (T2D) than LDL-cholesterol; however, nutritional reviews targeting apoB are scarce. Here we reviewed eighty-seven nutritional studies and present conclusions in order of strength of evidence. Plasma apoB was reduced in all studies that induced weight loss of 6–12 % using hypoenergetic diets (seven studies; 5440–7110 kJ/d; 1300–1700 kcal/d; 34–50 % carbohydrates; 27–39 % fat; 18–24 % protein). When macronutrients were compared in isoenergetic diets (eleven studies including eight randomised controlled trials (RCT); n 1189), the diets that reduced plasma apoB were composed of 26–51 % carbohydrates, 26–46 % fat, 11–32 % protein, 10–27 % MUFA, 5–14 % PUFA and 7–13 % SFA. Replacement of carbohydrate by MUFA, not SFA, decreased plasma apoB. Moreover, dietary enriching with n-3 fatty acids (FA) (from fish: 1·1–1·7 g/d or supplementation: 3·2–3·4 g/d EPA/DHA or 4 g/d EPA), psyllium (about 8–20 g/d), phytosterols (about 2–4 g/d) or nuts (30–75 g/d) also decreased plasma apoB, mostly in hyperlipidaemic subjects. While high intake of trans-FA (4·3–9·1 %) increased plasma apoB, it is unlikely that these amounts represent usual consumption. Inconsistent data existed on the effect of soya proteins (25–30 g/d), while the positive association of alcohol consumption with low plasma apoB was reported in cross-sectional studies only. Five isoenergetic studies using Mediterranean diets (including two RCT; 823 subjects) reported a decrease of plasma apoB, while weaker evidence existed for Dietary Approaches to Stop Hypertension (DASH), vegetarian, Nordic and Palaeolithic diets. We recommend using a Mediterranean dietary pattern, which also encompasses the dietary components reported to reduce plasma apoB, to target hyperapoB and reduce the risks of CVD and T2D.

A systematic review and meta-analysis of randomised controlled trials was undertaken to determine the effects of almond consumption on blood lipid levels, namely total cholesterol (TC), LDL-cholesterol (LDL-C), HDL-cholesterol (HDL-C), TAG and the ratios of TC:HDL-C and LDL-C:HDL-C. Following a comprehensive search of the scientific literature, a total of eighteen relevant publications and twenty-seven almond-control datasets were identified. Across the studies, the mean differences in the effect for each blood lipid parameter (i.e. the control-adjusted values) were pooled in a meta-analysis using a random-effects model. It was determined that TC, LDL-C and TAG were significantly reduced by −0·153 mmol/l (P < 0·001), −0·124 mmol/l (P = 0·001) and −0·067 mmol/l (P = 0·042), respectively, and that HDL-C was not affected (−0·017 mmol/l; P = 0·207). These results are aligned with data from prospective observational studies and a recent large-scale intervention study in which it was demonstrated that the consumption of nuts reduces the risk of heart disease. The consumption of nuts as part of a healthy diet should be encouraged to help in the maintenance of healthy blood lipid levels and to reduce the risk of heart disease.

Recent studies suggest that the ability to produce equol, a metabolite of the soya isoflavone daidzein, is beneficial to coronary health. Equol, generated by bacterial action on isoflavones in the human gut, is biologically more potent than dietary sources of isoflavones. Not all humans are equol producers. We investigated whether equol-producing status is favourably associated with risk factors for CHD following an intervention by dietary soya isoflavones. We systematically reviewed randomised controlled trials (RCT) that evaluated the effect of soya isoflavones on risk factors for CHD and that reported equol-producing status. We searched PubMed, EMBASE, Ovid Medline and the Cochrane Central Register for Controlled Trials published up to April 2015 and hand-searched bibliographies to identify the RCT. Characteristics of participants and outcomes measurements were extracted and qualitatively analysed. From a total of 1671 studies, we identified forty-two articles that satisfied our search criteria. The effects of equol on risk factors for CHD were mainly based on secondary analyses in these studies, thus with inadequate statistical power. Although fourteen out of the forty-two studies found that equol production after a soya isoflavone intervention significantly improved a range of risk factors including cholesterol and other lipids, inflammation and blood pressure variables, these results need further verification by sufficiently powered studies. The other twenty-eight studies primarily reported null results. RCT of equol, which has recently become available as a dietary supplement, on CHD and its risk factors are awaited.

Animal studies have suggested that Mn might be associated with some components of the metabolic syndrome (MetS). A few epidemiological studies have assessed dietary Mn intake and its association with the risk of the MetS and its components among Chinese adults. In this study, we assessed daily dietary Mn intake and its relationship with MetS risk among Chinese adults in Zhejiang Province using data from the 5th Chinese National Nutrition and Health Survey (2010–2012). A total of 2111 adults were included. Dietary Mn intake was assessed using 3-d 24-h dietary recalls; health-related data were obtained by questionnaire surveys, physical examinations and laboratory assessments. The mean intake of Mn was 6·07 (sd 2·94) mg/d for men (n 998) and 5·13 (sd 2·65) mg/d for women (n 1113). Rice (>42 %) was the main food source of Mn. The prevalence of the MetS was 28·0 % (590/2111). Higher Mn intake was associated with a decreased risk of the MetS in men (Q4 v. Q1 OR 0·62; 95 % CI 0·42, 0·92; Ptrend=0·043) but an increased risk in women (Q4 v. Q1 OR 1·56; 95 % CI 1·02, 2·45; Ptrend=0·078). In addition, Mn intake was inversely associated with abdominal obesity (Ptrend=0·016) and hypertriacylglycerolaemia (Ptrend=0·029) in men, but positively associated with low HDL-cholesterol in both men (Ptrend=0·003) and women (Ptrend<0·001). Our results suggest that higher Mn intakes may be protective against the MetS in men. The inverse association between Mn intake and the MetS in women might be due to the increased risk for low HDL-cholesterol.

The present study examined the effect of milk phospholipids (milk-PL) on lipid metabolism and on other risk factors for CVD, in comparison with milk fat (control) or soya phospholipids (soya-PL), respectively. Two double-blind parallel-group intervention trials were conducted in overweight or obese male subjects. In the first trial (trial 1), sixty-two men consumed milk enriched with either 2 g milk-PL or 2 g milk fat (control) for 8 weeks. In trial 2, fifty-seven men consumed milk enriched with either 3 g milk-PL or 2·8 g soya-PL for 7 weeks. In trial 1, milk-PL as compared with control reduced waist circumference but did not affect plasma lipids (total, HDL- and LDL-cholesterol, total cholesterol:HDL-cholesterol ratio, TAG, phospholipids), apoB, apoA1, glucose, insulin, insulin sensitivity index, C-reactive protein, IL-6, soluble intracellular adhesion molecule and total homocysteine (tHcy). Serum activities of alanine transaminase and aspartate transaminase were not changed. Activity of γ-glutamyl transferase (GGT), a marker of fatty liver, increased in the control but not in the milk-PL group, with a significant intervention effect. In trial 2, milk-PL as compared with soya-PL did not affect the above-mentioned parameters, but decreased GGT. Subjects with the methylenetetrahydrofolate reductase mutations CT and TT had 11 % (P < 0·05) higher baseline tHcy concentrations than those with the wild-type CC. However, genotype did not modulate the phospholipid intervention effect on tHcy. In conclusion, supplementation with milk-PL as compared with control fat reduced waist circumference and, as compared with both control fat and soya-PL, GGT activity.

CVD are the leading cause of mortality and morbidity worldwide. One of the key dietary recommendations for CVD prevention is reduction of saturated fat intake. Yet, despite milk and dairy foods contributing on average 27 % of saturated fat intake in the UK diet, evidence from prospective cohort studies does not support a detrimental effect of milk and dairy foods on risk of CVD. The present paper provides a brief overview of the role of milk and dairy products in the diets of UK adults, and will summarise the evidence in relation to the effects of milk and dairy consumption on CVD risk factors and mortality. The majority of prospective studies and meta-analyses examining the relationship between milk and dairy product consumption and risk of CVD show that milk and dairy products, excluding butter, are not associated with detrimental effects on CVD mortality or risk biomarkers that include serum LDL-cholesterol. In addition, there is increasing evidence that milk and dairy products are associated with lower blood pressure and arterial stiffness. These apparent benefits of milk and dairy foods have been attributed to their unique nutritional composition, and suggest that the elimination of milk and dairy may not be the optimum strategy for CVD risk reduction.