Trends in milk and dairy consumption

In the UK, current milk consumption is about 1·5 litres of milk per person per week, with the majority of this consumed as semi-skimmed milk (70 %) followed by whole milk (20 %) and skimmed milk (10 %). Over the past few decades, trends in milk and dairy product consumption have shown considerable variation (Fig. 1)^{( 7 )}. For example, consumption of whole milk has shown a dramatic decline since the 1970s from about 2·7 litres per person per week in 1974 to 0·3 litres per person per week in 2012 (Fig. 1(a)). In the early 1990s, the decline in whole milk consumption was partially replaced by semi-skimmed milk, consumption of which has remained fairly constant at about 1 litre per person per week over the last decade, while the intake of whole milk continues to decline. Fig. 1(b) shows the UK trends in consumption of other dairy products such as cheese, yoghurt and fromage frais, cream and butter. The trend for cheese and cream consumption has remained fairly constant at about 100 g and 20 ml per person per week for cheese and cream, respectively since the 1970s. In contrast, the trend for yoghurt and fromage frais consumption has increased significantly from the early 1970s with 33 ml per person per week to about 200 ml per person per week in 2012. The consumption of butter in the UK shows a similar downward trend as for whole milk, due, in part, to recommendations to reduce the amount of total and saturated fat in the diet, but also because of the increasing availability of other spreads.

Fig. 1.

Trends in milk, cheese, yoghurt and fromage frais, cream and butter purchase, 1974–2012. Source: AHDB Dairy.

The contribution of milk and dairy foods to nutrient intakes

Milk and dairy products are complex foods containing a number of different components. Table 1 shows the contribution of the dairy food group, which includes milk, cheese, yoghurt, butter, cream and fromage frais to energy and nutrient intakes in UK adults (age 19–64 years)⁽ Reference Bates, Lennox and Prentice ^{5 )}. It is clear that milk and other dairy products are important sources of a number of nutrients in the UK diet. Indeed, the dairy food group alone contributes more than the daily reference nutrient intake for vitamin B₁₂ and provides about 50 % of the recommended nutrient intake for calcium and phosphorus. Milk and dairy products are also the main source of iodine in the UK diet, contributing about 40 % of the recommended nutrient intake. Adequate iodine levels are important for both men and women throughout life, but particularly in women of childbearing age as iodine levels below recommendations during pregnancy have been associated with reduced cognitive outcome in their children⁽ Reference Bath, Steer and Golding ^{8 )}. Although dairy is an important contribution to iodine intake in the UK diet, there have been inconsistent reports of iodine concentrations in milk with a recent study showing a 30 % lower iodine concentration in organic compared with conventional milk⁽ Reference Payling, Juniper and Drake ^{9 )}. Therefore, although milk and dairy products are not an essential dietary component, they make an important contribution to the provision of key nutrients.

Table 1.

Energy and major nutrients provided by milk and dairy products to adults (age 19–64 years) diets in the UK

EAR, estimated average requirement; DRV, daily recommended value; RNI, reference nutrient intake.

Saturated fat from milk and CVD

Higher dietary SFA consumption is associated with increased risk of CVD, due primarily to the serum total cholesterol and LDL-C raising effects of SFA⁽ Reference Mensink, Zock and Kester ^{2 )}. The association between SFA and increased serum LDL-C has led to dietary recommendations worldwide for the restriction of SFA intake. Dietary recommendations by the FAO/WHO^{( 10 )}, UK dietary recommendations (Department of Health, 1991)^{( 11 )} and, dietary guidelines for Americans^{( 12 )} recommend intake of dietary SFA to <10 % of total energy intake. Despite these recommendations current SFA intakes in the UK are about 11·9 % of total energy⁽ Reference Bates, Lennox and Prentice ^{5 )}.

Milk and dairy products are the greatest contributor to dietary SFA in the UK diet, contributing about 27 % of SFA intake. As a result, guidance to reduce or eliminate dairy from the diet has been a common practice for CVD risk reduction. However, the evidence for the relationship between dairy consumption and CVD mortality does not support dairy restriction as an effective strategy for CVD reduction. It is important to recognise that we do not consume individual nutrients, but complex foods and diets that contain specific nutrients within various matrices. This can give rise to disparity between the biological effects of nutrients in different foods that may have contributed to the inconsistencies in the relationships of different SFA-rich foods and CVD mortality. Clear evidence for this comes from the Multi Ethnic Study of Atherosclerosis, in which different SFA-rich foods were shown to produce differential effects on CVD risk⁽ Reference de Oliveira Otto, Mozaffarian and Kromhout ^{13 )}. In 5209 subjects after a 10-year period (from 2000 to 2010). A lower hazard ratio (HR) for CVD was reported for every 5 g/d (HR 0·79; 95 % CI 0·68, 0·92) or 5 % of energy from dairy SFA (HR 0·62; 95 % CI 0·47, 0·82), whereas the equivalent intake of SFA from meat sources was associated with greater HR for CVD (HR for +5 g/d and a +5 % of energy from meat sources of SFA: 1·26; 95 % CI 1·02, 1·54 and 1·48; 95 % CI 0·98, 2·23, respectively)⁽ Reference de Oliveira Otto, Mozaffarian and Kromhout ^{13 )}. Furthermore, the substitution of 2 % of energy from meat sources of SFA with energy from dairy SFA was associated with a 25 % lower CVD risk (HR 0·75; 95 % CI 0·63, 0·91), suggesting that dairy foods containing SFA attenuated the detrimental association of SFA with CVD mortality. While this finding was attributed to the effects of other components within dairy foods, such as calcium, magnesium, bioactive peptides and proteins, it may also have been due to a difference in the relative proportions of different SFA between meat and dairy.

Further evidence for the beneficial association between dairy and CVD comes from an investigation of the association between plasma phospholipid fatty acids and incidence of CHD⁽ Reference Khaw, Friesen and Riboli ^{14 )}. In the present study, the enrichment of plasma phospholipid with even chain SFA: palmitic acids (C16:0) and stearic (C18:0), but not myristic (C12:0), was associated with significantly higher risk of CHD, while the odd chain SFA indicative of dairy consumption: pentadecanoic C15:0 and hexadecanoic acid C17:0 were associated with lower risk. These finding were corroborated by associations between similar circulating biomarkers of dairy fat and the incidence of stroke in US men (Health Professionals Follow-up Study n 51 529) and women (Nurses’ Health Study n 121 700)⁽ Reference Yakoob, Shi and Hu ^{15 )}. Odd chain fatty acids are found in milk and dairy products and result from bovine biohydrogenation⁽ Reference Vlaeminck, Fievez and Cabrita ^{16 )}. Their appearance in human plasma or tissue samples is now recognised as a specific biomarker of dairy intake, as man is unable to synthesise these fatty acids endogenously⁽ Reference Smedman, Gustafsson and Berglund ^{17 )}. These data support the prospective cohort data that suggest that milk and dairy products are not associated with detrimental effects on CVD risk.

Trans fatty acids and CVD

Other important fatty acids present in milk and dairy foods are TFA, which are synthesised via bacterial metabolism of unsaturated fatty acids in the rumen of cows⁽ Reference Lock and Bauman ^{18 )}. The intake of TFA from industrially hydrogenated vegetable oils (iTFA) has a negative impact on cardiovascular health⁽ Reference Mozaffarian, Katan and Ascherio ^{19 ,} Reference Brouwer, Wanders and Katan ^{20 )}. However, the association between ruminant TFA (rTFA) and CVD remains inconclusive⁽ Reference Gebauer, Chardigny and Jakobsen ^{21 ,} Reference Brouwer, Wanders and Katan ^{22 )}, with some studies showing a cardioprotective association⁽ Reference Mozaffarian, Katan and Ascherio ^{19 ,} Reference Jakobsen, Overvad and Dyerberg ^{23 )}. In an attempt to resolve conflicting reports, a systematic review and meta-analysis was undertaken by Bendsen et al. ⁽ Reference Bendsen, Christensen and Bartels ^{24 )} who reported that the relative risk (RR) for high v. low quintiles of total TFA intake (2·8 to approximately 10 g/d) was 1·22 (95 % CI 1·08, 1·38; P = 0·002) for CHD events and 1·24 (95 % CI 1·07, 1·43; P = 0·003) for fatal CHD. In addition, rTFA intake (0·5–1·9 g/d) was not significantly associated with CHD risk (RR 0·92; 95 % CI 0·76, 1·11; P = 0·36), although there was a trend towards a positive association for iTFA (RR 1·21; 95 % CI 0·97, 1·50; P = 0·09). The authors concluded that while iTFA may be positively related to CHD, rTFA were not, but the limited number of studies available prevented a firm conclusion on the critical importance of the source of TFA. In contrast to previous findings, a recent prospective cohort study by Kleber et al. ⁽ Reference Kleber, Delgado and Lorkowski ^{25 )} showed that total TFA content in erythrocyte membranes of 3259 participants of the Ludwigshafen Risk and Cardiovascular Health Study was inversely associated with adverse cardiac outcomes, while rTFA (trans-palmitoleic acid) was associated with reduced risk. In addition, erythrocyte membrane iTFA was associated with no increased risk of adverse cardiac outcomes⁽ Reference Kleber, Delgado and Lorkowski ^{25 )}. However, it is important to highlight that total TFA concentration in erythrocyte membranes in the present study population was relatively low compared with levels in other studies, and this may have been too low to observe an effect of TFA on CVD mortality. Furthermore, it has been suggested that the lack of an association between rTFA and CHD risk may be due to a lower intake from ruminant sources compared with iTFA⁽ Reference Bendsen, Christensen and Bartels ^{24 )}. Despite this controversy, there is little doubt that dietary iTFA are associated with increased CVD mortality⁽ Reference de Souza, Mente and Maroleanu ^{26 )}. In response there has been a substantial decrease in iTFA over the past 10–15 years, due to the voluntary action by the UK food industry^{( 27 )}. This has led to an increase in the relative proportion of rTFA in the UK diet, although the absolute intake of ruminant fat is unchanged, with the current mean population intake of total TFA (0·7 % food energy in adults)⁽ Reference Bates, Lennox and Prentice ^{5 )} below the recommended population maximum of 2 % of food energy intake^{( 11 )}. Although milk and milk products (including butter) contribute to 32 % of this intake⁽ Reference Bates, Lennox and Prentice ^{5 )}, current rTFA intake is not considered to be a major cause for concern with respect to cardiovascular health at a population level⁽ Reference Brouwer, Wanders and Katan ^{22 ,} Reference Tardy, Morio and Chardigny ^{28 )}. However, the impact of any increase in dietary TFA would need to be monitored.

Effects of milk and dairy foods on CVD risk: evidence from observational studies

The potential effects of milk and dairy consumption on CVD mortality would best be determined using adequately powered randomised control intervention studies, which have CVD events and CVD-related deaths as outcomes. However, for obvious financial and logistical reasons such studies have not been performed. The most informative data on the relationship between milk and dairy consumption and CVD is provided by long-term prospective cohort studies⁽ Reference Elwood, Pickering and Givens ^{29 )}.

Several influential reviews have focused on the impact milk and dairy food consumption and CVD risk, some of which have conducted meta-analyses of available cohort data (Table 2)⁽ Reference Elwood, Pickering and Givens ^{29 –} Reference Elwood, Pickering and Hughes ^{32 )}. Elwood et al. ⁽ Reference Elwood, Pickering and Hughes ^{32 )} conducted a meta-analyses of ten prospective cohort studies that examined the associations between milk and risk of IHD and stroke. Using a pooled estimate of the relative odds for IHD and stroke, the meta-analysis revealed no association with IHD (RR 0·87; 95 % CI 0·74, 1·03) and a significant inverse association for stroke (RR 0·83; 95 % CI 0·77, 0·90) in the subjects with the highest milk compared with those with the lowest intakes. These findings, together with a combined estimate of risk for both IHD and stroke (ten studies RR 0·84; 95 % CI 0·78, 0·90), suggested that consumption of milk was associated with a modest reduction in CVD risk. This work was extended by Elwood et al. ⁽ Reference Elwood, Pickering and Givens ^{29 )} to include nine prospective cohort studies of milk and dairy products and IHD and eleven studies for stroke. The meta-analysis indicated a 15 % lower RR for all-cause mortality (RR 0·85; 95 % CI 0·77, 0·98) and an 8 % lower overall RR of IHD (RR 0·92; 95 % CI 0·80, 0·99) in the subjects with the highest dairy consumption compared with those with the lowest intakes. Furthermore, a significant inverse association was observed for the risk of stroke (RR 0·79; 95 % CI 0·68, 0·91) in the subjects with the highest dairy consumption compared with those with the lowest intakes. These findings supported previous meta-analyses by Elwood et al. ⁽ Reference Elwood, Pickering and Hughes ^{32 )}, and support a reduction in IHD and stroke in subjects consuming the highest amount of milk and dairy products compared with the lowest intakes.

Table 2.

Summary of recent reviews and meta-analyses on milk or total dairy intake and risk of CVD

RR; relative risk.

In another meta-analysis of seventeen prospective cohort studies Soedamah-Muthu et al. ⁽ Reference Soedamah-Muthu, Ding and Al-Delaimy ^{30 )} showed a modest inverse association between milk intake and risk of overall CVD (four studies; RR 0·94 per 200 ml/d; 95 % CI 0·89, 0·99). However, milk intake was not associated with risk of CHD (six studies; RR 1·00 per 200 ml/d; 95 % CI 0·96, 1·04), stroke (six studies; RR 0·87; 95 % CI 0·72, 1·05) or total mortality (eight studies; RR per 200 ml/d 0·99; 95 % CI 0·95, 1·03). A recent meta-analysis by Qin et al.⁽ Reference Qin, Xu and Han ^{31 )}, which included a total of twenty-two prospective cohort studies, showed an inverse association between dairy consumption and overall risk of CVD (nine studies; RR 0·88; 95 % CI 0·81, 0·96) and stroke (twelve studies; RR 0·87; 95 % CI 0·77, 0·99). However, no association was found between dairy consumption and CHD risk (twelve studies; RR 0·94; 95 % CI 0·82, 1·07), which supports previous findings⁽ Reference Soedamah-Muthu, Ding and Al-Delaimy ^{30 )}. Qin et al.⁽ Reference Qin, Xu and Han ^{31 )} also investigated the association between individual dairy foods on risk of CVD, including stroke and CHD. Interestingly, cheese consumption was associated with a significantly reduced risk of stroke (four studies; RR 0·91; 95 % CI 0·84, 0·98) and CHD (seven studies; RR 0·84; 95 % CI 0·71, 1·0). Recently, Praagman et al.⁽ Reference Praagman, Dalmeijer and van der Schouw ^{33 )} also reported a significant association between cheese consumption and stroke mortality, although no impact on CHD mortality was found⁽ Reference Praagman, Dalmeijer and van der Schouw ^{33 )}. One possible explanation for the observed beneficial effects of cheese consumption on stroke and CHD risk may be the relatively high calcium content that increases saponification of SFA in the gut, rendering them resistant to digestion leading to increased faecal fat excretion⁽ Reference Nestel, Chronopulos and Cehun ^{34 )}. This mechanism is supported by the results from a prospective cohort study in which the observed inverse association between cheese consumption and CHD was attenuated when calcium content was used as a confounder in the analysis⁽ Reference Louie, Flood and Burlutsky ^{35 )}. Furthermore, a meta-analysis of randomised control trials (RCT) investigating the impact of calcium from dairy and dietary supplements estimated that increasing dairy calcium intake by 1241 mg/d resulted in an increase in faecal fat of 5·2 (1·6–8·8) g/d⁽ Reference Christensen, Lorenzen and Svith ^{36 )}.

Since publication of the meta-analyses above (Table 2), additional prospective cohort studies have been published. For example, the Rotterdam Study consisting of 4235 men and women aged 55 years and above showed that total dairy, milk, low-fat dairy, and fermented dairy were not significantly related to incident stroke or fatal stroke after a 17·3-year follow-up period⁽ Reference Praagman, Franco and Ikram ^{37 )}. In addition, the authors reported a significant inverse relationship between high-fat dairy consumption and fatal stroke (HR 0·88 per 100 g/d; 95 % CI 0·79, 0·99), but not incident stroke (HR 0·96 per 100 g/d; 95 % CI 0·90, 1·02). Total dairy or individual dairy foods were not associated with incident CHD or fatal CHD.

Contrary to these data and since these meta-analyses a study conducted by Michaelsson et al. ⁽ Reference Michaelsson, Wolk and Langenskiold ^{38 )}, reported that the milk intake was significantly associated with markedly higher total and CVD mortality and fracture risk in 61 433 Swedish women from the mammography cohort. This relationship was also observed in a cohort of 45 339 Swedish men, although the relationship was considerably weaker⁽ Reference Michaelsson, Wolk and Langenskiold ^{38 )}. However, the authors concluded that the study should be ‘interpreted with caution, due to the inherent possibility of residual confounding and reverse causation phenomena, which is often associated with observational study designs’. In addition, when this data were reanalysed, an inverse association was observed for the number of CVD deaths against milk consumption⁽ Reference Hellstrand and Michaëlsson ^{39 )}. These inconsistent findings between milk intake and CVD mortality observed with the same dataset require further investigation. Furthermore, since the study by Michaelsson et al. ⁽ Reference Michaelsson, Wolk and Langenskiold ^{38 )}, two further large prospective cohort studies have been published on the relationship between milk and myocardial infarction and IHD mortality in Japanese (n 94 980; 19 years follow-up)⁽ Reference Wang, Yatsuya and Tamakoshi ^{40 )} and Danish (n 98 529; 5·4 years follow-up)⁽ Reference Bergholdt, Nordestgaard and Varbo ^{41 )} populations, both of which reported no association with myocardial infarction or IHD.

The balance of current evidence, including meta-analyses of prospective cohort studies, indicates that milk and dairy products are associated with no detrimental effect on risk of CVD, with some evidence of a moderately protective effect of milk consumption. However, a further meta-analysis that includes all of the current prospective cohort data is required to confirm this and more studies are required to determine the effects of individual dairy products on CVD risk.

Differential impact of high- and low-fat dairy foods

There is no established nutritional benefit of whole-fat dairy consumption, except in children under 2 years, compared with lower fat alternatives. With respect to the latter, skimming milk fat to produce low-fat milk and dairy products is a common and an effective way of lowering SFA intake. However, there is currently no consensus on whether fat-reduced dairy foods are associated with a reduced risk of CVD⁽ Reference Benatar, Sidhu and Stewart ^{50 )} and studies in this area give inconsistent data, with few RCT that directly compare whole with low fat alternatives. Minimal benefit has been reported in a prospective study of 33 636 women, which suggested no significant differences between consumption of high- v. low-fat dairy products on risk of myocardial infarction⁽ Reference Patterson, Larsson and Wolk ^{51 )}. Furthermore, findings from a 12-month RCT concluded that in overweight adults inclusion of reduced-fat dairy foods had no impact on blood lipids, blood pressure (BP) and arterial compliance⁽ Reference Crichton, Howe and Buckley ^{52 )}. Moreover, a meta-analysis conducted by Soedamah-Muthu et al.⁽ Reference Soedamah-Muthu, Ding and Al-Delaimy ^{30 )}, showed that there was no significant difference between consumption of high-fat (RR 1·04; 95 % CI 0·89, 1·21) or low-fat dairy (RR 0·93; 95 % CI 0·74, 1·17) on CHD risk.

In contrast, data from the Nurses’ Health Study cohort illustrated that the associated RR of CHD varied according to the fat content of dairy foods with an estimated 20 % lower RR with low-fat dairy consumption (RR 0·80; 95 % CI 0·73, 0·87) compared with a 12 % higher RR with high-fat dairy consumption (RR 1·12; 95 % CI 1·05, 1·20)⁽ Reference Hu, Stampfer and Manson ^{53 )}. Furthermore, observational studies investigating the relationship between consumption of different types of dairy on cardio-metabolic risk factors have indicated that low-fat dairy consumption is an effective strategy to promote lower BP levels⁽ Reference Engberink, Hendriksen and Schouten ^{54 –} Reference van Meijl and Mensink ^{56 )}, circulating markers of inflammation⁽ Reference Esmaillzadeh and Azadbakht ^{57 )}, the ratio of total-C:HDL-C⁽ Reference Mensink, Zock and Kester ^{2 )} and LDL-C concentration⁽ Reference Kai, Bongard and Simon ^{58 )}, as well as aid in weight maintenance or reduction⁽ Reference Abargouei, Janghorbani and Salehi-Marzijarani ^{59 )}. Further evidence from well-controlled dietary intervention studies is required before a definitive conclusion can be drawn on the benefits of low- and high-fat dairy.

There have also been a number of studies suggesting that the specific milk proteins have differential effects on lipids. Whey (60 g/d for 12 weeks) has been shown to produce significant reductions in serum TAG and total and LDL-C in comparison with a casein control group⁽ Reference Pal, Ellis and Dhaliwal ^{60 )}. Furthermore, a significant decrease in the postprandial appearance of TAG after consuming a whey meal of 21 % compared to control and 27 % compared with the casein meals were reported⁽ Reference Pal, Ellis and Ho ^{61 )}. In addition to the specific dairy proteins, different dairy foods have been shown to have a range of lipid effects⁽ Reference Astrup ^{62 )}. It has been reported that cheese may have a differential effect on blood lipids compared with other dairy foods⁽ Reference Nestel, Chronopulos and Cehun ^{34 ,} Reference Tholstrup, Hoy and Andersen ^{63 ,} Reference Hjerpsted, Leedo and Tholstrup ^{64 )}, with prolonged ripening of cheddar cheese resulting in more pronounced lipid-lowering effects in a pig model⁽ Reference Thorning, Bendsen and Jensen ^{65 )}. A meta-analysis that included five of these RCT showed that when compared with butter intake, cheese consumption reduced LDL-C by 6·5 % (−0·22 mm/l; 95 % CI −0·2, −0·14) and HDL-C by 3·9 % (−0·05 mm/l 95 % CI −0·09, −0·02) but had no effect on TAG⁽ Reference de Goede, Geleijnse and Ding ^{66 )}. In addition, a recent RCT reported that consumption of 80 g/d of a high-fat cheese (27 % fat) compared with no cheese or 50 g/d of fat and salt-free cheese for 8 weeks resulted in no changes in total or LDL-C. Those in the high-fat cheese group with metabolic syndrome at baseline had significant reductions in total cholesterol (−0·70 mm/l) compared with control and a significantly higher reduction in TAG⁽ Reference Nilsen, Hostmark and Haug ^{67 )}. These data show that dairy products do not exert the negative effects on blood lipids which would be predicted solely from their SFA content, and highlights a need for additional studies before firmer conclusions can be made on the differential effects of dairy products on serum lipid and lipoprotein concentrations.

Overall, the current evidence presented in this section suggests that the fatty acid profile of milk may not be as detrimental for lipid risk factors as previously thought, and supports differential effects of dairy foods, particularly cheese.

Manipulating the fatty acid profile of milk

Modification of the fatty acid profile of bovine milk offers an alternate strategy for lowering the population's intake of SFA, by removing SFA from the food chain, while preserving the beneficial contributions that dairy products make to the protein and micronutrient content of the human diet⁽ Reference Shingfield, Bonnet and Scollan ^{68 )}. Partial replacement of milk SFA with cis-MUFA or cis-PUFA through supplementation of the cows’ diet with plant oils or oilseeds reduces synthesis of short- and medium-chain SFA by the bovine mammary gland, and increases the long-chain (>C₁₈) unsaturated fatty acid concentration in the milk⁽ Reference Givens, Shingfield, Williams and Buttriss ^{69 ,} Reference Glasser, Ferlay and Chilliard ^{70 )}. Inclusion of 49 g/kg of dry matter of rapeseed oil in the ruminant diet for a 28-d period increased cis-MUFA from 20 to 33 g/100 g fatty acids, while reducing SFA from 70 to 55 to 60 g/d fatty acids⁽ Reference Givens, Kliem and Humphries ^{71 )}. This feeding regimen inadvertently leads to increased concentrations of naturally produced rTFA, predominantly trans-linoleic acid (trans-18:1) and trans-MUFA, in the milk. However, despite this increase in rTFA, the consumption of the modified dairy products is not thought to have a major impact on CVD risk⁽ Reference Kleber, Delgado and Lorkowski ^{25 )}. In addition, cell culture studies have shown that rTFA has minimal impact on endothelial function and gene expression⁽ Reference Livingstone, Givens and Jackson ^{72 )}, although whether rTFA intake, through manipulation of the fatty acid profile of milk and dairy products to decrease SFA content, impacts on cardiovascular health, has yet to be determined.

Consumption of SFA-reduced milk and milk products, by feed modification has been shown to be beneficial to CVD risk, in healthy and hypercholesterolaemic populations when compared with conventional dairy products⁽ Reference Livingstone, Lovegrove and Givens ^{73 )}. Poppitt et al. demonstrated that consumption of 20 % energy daily as conventional or feed-modified SFA-reduced butter for a 3-week period resulted in significant reduction in both total cholesterol and LDL-C during the modified butter feeding⁽ Reference Poppitt, Keogh and Mulvey ^{74 )}. However, the evidence is relatively limited and the majority of studies have used butter only and relied on serum lipid levels as biomarkers of CVD risk. This knowledge gap is being addressed at the University of Reading with the RESET (Replacement of Saturated fat in dairy on total cholesterol) study investigating the impact of reducing SFA intake by using modified milk and dairy products on vascular function and CVD risk biomarkers, without limiting dairy product consumption. Milk that has a substantial proportion of SFA replaced with cis-MUFA will be collected from cows fed a diet supplemented with 1 kg/d of high-oleic sunflower oil. Cheddar cheese and butter will be produced from this milk and these dairy foods will be supplied to volunteers with increased CVD risk for a 12-week period in a randomised, crossover, double-blind, controlled study. The impact of these modified dairy products on fasted and postprandial vascular function, BP, lipids, insulin sensitivity and inflammatory biomarkers will be determined relative to typical commercially available products. The project, which started in late 2013, will provide unique evidence of the physiological effects of modified SFA-reduced dairy products, which could contribute to food-based dietary recommendations for CVD risk reduction.

Effects of milk and dairy products on blood pressure and arterial stiffness

Hypertension, defined as systolic BP ⩾ 140 mm Hg and/or diastolic BP of ⩾ 90 mm Hg, is one of the leading risk factors in the development of stroke, CHD, heart failure and end stage renal disease⁽ Reference Lawes, Vander Hoorn and Rodgers ^{75 )}. BP is modifiable by environmental and lifestyle factors, with diet as one of the most important mediators⁽ Reference Appel, Brands and Daniels ^{76 )}. The Dietary Approaches to Stop Hypertension trial demonstrated that a diet consisting of reduced total and SFA fats, high intakes of low-fat dairy products, and fruits and vegetables significantly lowered BP in normotensive and hypertensive individuals⁽ Reference Appel, Moore and Obarzanek ^{77 )}. Moreover, the magnitude of BP reduction was of greater magnitude after the diet rich in low-fat dairy products compared with the fruit and vegetable-rich diet, which omitted dairy products altogether⁽ Reference Appel, Moore and Obarzanek ^{77 )}. The findings from cross-sectional and prospective studies have shown an inverse association between consumption of dairy products, particularly low-fat varieties and risk of hypertension⁽ Reference Livingstone, Lovegrove and Cockcroft ^{48 ,} Reference Toledo, Delgado-Rodriguez and Estruch ^{55 ,} Reference van Meijl and Mensink ^{56 ,} Reference Pereira, Jacobs and Van Horn ^{78 –} Reference Soedamah-Muthu, Verberne and Ding ^{83 )}. These findings were confirmed in a meta-analysis by Soedamah-Muthu et al. ⁽ Reference Soedamah-Muthu, Verberne and Ding ^{83 )}, in which nine prospective cohort studies and a total of 57 256 participants, showed a reduced RR for hypertension (pooled RR 0·97; 95 % CI, 0·95, 0·99 per 200 g/d) and intake of total dairy⁽ Reference Soedamah-Muthu, Verberne and Ding ^{83 )}. A few RCT have examined the effects of dairy products on BP⁽ Reference van Meijl and Mensink ^{56 ,} Reference Stancliffe, Thorpe and Zemel ^{84 ,} Reference Maki, Rains and Schild ^{85 )}. For example, a randomised cross-over trial by Van Meijl and Mensink⁽ Reference van Meijl and Mensink ^{56 )} in thirty-five healthy overweight and obese men and women indicated that daily consumption of low-fat dairy products compared with carbohydrate-rich products for 8 weeks, significantly reduced systolic BP by 2·9 mm Hg. However, a recent study by Maki et al. ⁽ Reference Maki, Rains and Schild ^{85 )} observed no significant effects of consuming low-fat dairy products, compared with low-fat non-dairy products, on BP in sixty-two men and women with prehypertension or stage 1 hypertension⁽ Reference Maki, Rains and Schild ^{85 )}.

The impact of dairy foods on BP and other more novel markers of vascular health are becoming increasingly relevant. Increased central arterial stiffening is a hallmark of the ageing process and the consequence of many diseases such as diabetes, atherosclerosis and chronic renal failure. Arterial stiffness is also a marker for increased CVD risk, including myocardial infarction⁽ Reference Mitchell, Moye and Braunwald ^{86 )}, heart failure⁽ Reference Chae, Pfeffer and Glynn ^{87 )} and total mortality⁽ Reference Benetos, Safar and Rudnichi ^{88 )}, as well as stroke⁽ Reference Vaccarino, Berger and Abramson ^{89 )} and renal disease⁽ Reference Blacher, Guerin and Pannier ^{90 )}. Arterial stiffness is measured by pulse wave velocity and augmentation index, both of which are predictive of heart attacks and stroke ⁽ Reference Boutouyrie, Tropeano and Asmar ^{91 )} and all-cause mortality⁽ Reference Janner, Godtfredsen and Ladelund ^{92 )}. Pulse wave velocity measures the speed of propagation along the artery, whereas augmentation index is calculated from the BP wave form and is based on the degree of wave reflection. Significant relationships between dairy product intake and arterial pulse wave velocity have been shown in a cross-sectional⁽ Reference Crichton, Elias and Dore ^{93 )} and longitudinal⁽ Reference Livingstone, Lovegrove and Cockcroft ^{48 )} cohort studies. Livingstone et al. ⁽ Reference Livingstone, Lovegrove and Cockcroft ^{48 )} used data from the Caerphilly Prospective Study, based on 2512 men followed for a mean of 15 years and showed a significant inverse relationship between dairy product intake and augmentation index. The subjects in the highest quartile of dairy product intake (mean 480 g/d), excluding butter, had 2 % (P = 0·02) lower augmentation index compared with subjects with the lowest dairy intake (mean 154 g/d), whereas across increasing quartiles of butter intake there was no impact on augmentation index, but a significant increase in insulin, serum TAG and total cholesterol concentrations, and diastolic BP⁽ Reference Livingstone, Lovegrove and Cockcroft ^{48 )}.

The mechanisms by which milk and dairy products may reduce BP and arterial stiffness are unclear. It has been hypothesised that bioactive peptides released during milk protein digestion, dairy fermentation or industrially by enzyme or chemical treatments, may be involved in the relationship between dairy consumption and BP⁽ Reference FitzGerald, Murray and Walsh ^{94 ,} Reference Boelsma and Kloek ^{95 )}. It has been proposed that these bioactive peptides may inhibit the action of angiotensin I converting enzyme, thereby reducing blood levels of angiotensin, preventing blood vessel constriction, and modulating endothelial integrity. Ballard et al. ⁽ Reference Ballard, Bruno and Seip ^{96 )} showed that consumption of 5 g whey-derived peptide daily for a 2-week period significantly improved brachial artery flow-mediated dilation response⁽ Reference Ballard, Bruno and Seip ^{96 )}. A further study reported that although whey and casein exerted similar hypotensive effects, whey protein supplementation (60 g/d for 12 weeks) significantly reduced augmentation index compared with casein (60 g/d for 12 weeks)⁽ Reference Pal and Ellis ^{97 )}, an effect that requires confirmation. There is also evidence to suggest that certain peptides from milk proteins may modulate the release of vasoconstrictor endothelin-1 by endothelial cells, thus preventing an increase in BP⁽ Reference Maes, Van Camp and Vermeirssen ^{98 )}. Milk also contains a variety of other biologically active components such as calcium, potassium and magnesium that may exert impact on BP and arterial stiffness⁽ Reference Fekete, Givens and Lovegrove ^{99 )}.