Among the foods that represent a major source of dietary SFAs, dairy foods deserve consideration since they are largely consumed worldwide
[14] and contribute a relevant proportion to the global SFAs intake (i.e., one fifth in the USA, 17–41% in Europe)
[15]. A substantial reduction in the intake of dairy and a preferential consumption of low-fat products has been advocated as a strategy for CVD prevention, although evidence in this regard is scant and inconsistent. Dairy foods are a highly heterogeneous food group comprising foods with different biochemical composition, nutritional characteristics (i.e., fat, micronutrients, and salt content), preparation techniques (i.e., fermentation, pasteurization, processed by enzymatic procedures) which may all impact on their nutritional properties and metabolic effects. Partly due to this heterogeneity, the relationship of dairy consumption with cardiovascular diseases remains controversial. The large geographical variation of patterns of dairy food consumption, deeply rooted in sociocultural behaviors and, therefore, influenced by the background diet, further adds to the complexity of the relationship of dairy consumption with health outcomes.
It is therefore appropriate to evaluate the updated evidence on the relationship between dairy food consumption and CVD taking into account the available information on the specific food items included in the dairy food group; in particular, it is relevant to evaluate the impact of dairy foods on established and emerging cardiovascular risk factors in order to substantiate possible mechanisms trough which dairy foods may impact on CV health and differentiate population groups that might be more prone to their possible untoward effects.
Indeed, there is consistent evidence that a total consumption of dairy foods (i.e., including milk, cheese, and yogurt) up to 200 g per day has a neutral association with CVD risk, independent of whether full-fat or low-fat products are considered. As for specific dairy foods, a neutral association was found for milk, while fermented products—cheese and yogurt—were associated with a lower risk of total mortality and CV events. These results highlight the wide heterogeneity existing among dairy foods with regard to their association with CVD
[16]. This complexity is partly due to potential interrelated influences of different nutrients and non-nutrient bioactive compounds, as well as other food characteristics (i.e., fermentation physical features, processing and cooking procedures) which can modulate the bioavailability and the metabolic effects of nutrients and, consequently, their impact on health
[17]. By focusing on foods rather than on nutrients (namely SFAs) the present work is aligned with the most recent research on nutrition and health, which emphasizes food choices and dietary patterns above the nutrients composition of the diet as major determinants of health
[13][18]. This approach is also more suitable for the translation of the information into clinical recommendations, as it is more understandable to lay people.
Current nutritional recommendations for CVD prevention in adults are mainly informed by the evidence that SFAs, largely present in dairy, contribute to increasing plasma cholesterol levels which, in turn, increases CV risk; however, recent data indicate that not all SFAs have the same metabolic effects
[19][20][21].
The knowledge that different sources of SFAs have a different impact on CVD is not new. Early prospective studies indicated that the consumption of dairy fat (mainly milk and butter) was associated with an increased mortality from CHD
[22][23][24]; however, when cheese was included among the sources of dairy fat, the correlation coefficients were reduced and become less statistically significant
[24].
A subsequent study based on quantities of 40 food items available for consumption from the 1977 Food Balance Sheets (FBSs) of the Food and Agriculture Organization (FAO), relative to 40 countries, has investigated the relationship between a dietary lipid score that combined the intakes of cholesterol and saturated fat (Cholesterol–Saturated Fat Index, CSI) and CHD mortality
[25]. The results showed that in Finland CHD mortality was three to five times higher than in France, even though the CSIs of these two countries were almost the same; however, the quality of products consumed was different, since milk intake was 3.5 times greater in Finland than in France
[25].
The difference between milk and cheese in relation to CVD outcomes has been ascribed, among others, to the higher calcium content of cheese. On one hand, calcium might partly limit the absorption of SFAs
[24][26]; on the other hand, extracellular and intracellular calcium concentrations influence cell membrane potentials of excitable tissues, including the myocardium. In vitro and in silico studies have shown that cardiomyocyte calcium handling is a major determinant of excitation–contraction coupling
[27]. However, the clinical implications of these findings remain unclear. Results of human studies on the role of calcium in CV health are incoherent: while dietary calcium does not seem associated with the incidence of CVD, calcium supplementation is reported to increase the risk of MI
[28].
There is evidence that differences in the chain length of SFAs lead to different physicochemical properties and biological effects
[29]. The physical and nutritional structure of foods can further modulate their biological effects by influencing the digestion, absorption, and bioavailability of the various nutrients. This is particularly true for a complex food group such as dairy foods. For example, despite their high content in long-chain saturated fatty acids (60% of dairy fat), dairy products are an important source of potentially beneficial compounds, such as medium- and odd-chain saturated fats, natural trans fats, unsaturated and branched-chain fats, branched amino acids, vitamin K1 and K2, and calcium
[29]. Probiotics and bioactive compounds naturally contained in fermented dairy further increase the complexity of this food group, since their presence can influence the composition and function of the gut microbiota of the host, which in turn modulates the cardiometabolic risk
[21]. In more detail, the probiotics’ activity favors the intestinal epithelial integrity and reduces the low-grade inflammation due to metabolic endotoxemia; moreover, it modulates host microbiota composition, thus improving the energy homeostasis, the intermediate metabolism, and the insulin sensitivity
[29][30].
The relationship between the various categories of dairy products and cardiovascular disease is largely, though not completely, mediated by their impact on major CV risk factors. To further substantiate the findings on hard CV outcomes (i.e., fatal and non-fatal events), and investigate biologically plausible mechanisms through which dairy may impact on CVD risk, researcher have reviewed the available meta-analyses of RCTs exploring the effects of the various dairy foods (i.e., low/full-fat dairy, milk, cheese, yogurt) on major CV risk factors, namely: body weight/waist circumference, plasma glucose/glycated hemoglobin, insulin sensitivity, blood pressure, plasma lipids, subclinical inflammation.
For body weight/waist circumference, either total dairy foods or specific items showed a substantially neutral effect; very modest changes in weight or waist circumference were reported in some meta-analyses, but they were mainly driven by the energy content of the dietary intervention. In more detail, when the dietary intervention is performed without limitation in the energy intake, enhanced dairy consumption may lead to increased energy intake and weight gain
[31][32][33]. Conversely, dairy products may have modest effects in facilitating weight loss in the context of an energy-restricted diet
[31][34][32][33] and there is some suggestion that yogurt may be protective against long-term weight gain
[29].
A marginal or null effect of total or specific dairy foods has been reported on fasting glucose and glycated hemoglobin in population without diabetes. Dairy products contain variable amounts of sugar, which may explain the marginal and non-clinically relevant increase in fasting glucose reported by O’Connor et al.
[35]. Conversely, there are some indications that fermented dairy products added with probiotics might exert beneficial effects on fasting glucose and glycated hemoglobin. This is in line with the protective effect of yogurt consumption on the risk of developing type 2 diabetes reported by some authors
[17][36].
The evidence regarding insulin sensitivity and subclinical inflammation is scant and overall does not support a significant impact of this food group.
The effects of dairy on blood pressure have also been shown to be substantially neutral; notwithstanding, several studies have provided evidence for biologically plausible mechanisms through which dairy foods might lower blood pressure (i.e., calcium, vitamin D, potassium, and phosphorous content, bioactive small peptides effect, and probiotic activity)
[37]. Moreover, habitual dairy intake is associated with lower blood pressure levels in cross-sectional observational studies. Additionally, in the large randomized DASH trial dairy intake was associated with lower blood pressure; however, the dietary intervention included multiple dietary components besides low-fat dairy food (i.e., reduced total and saturated fat intake and increased consumption of vegetables and fruit), and therefore it is not possible in this entry to estimate the effects of each single intervention
[38].
The effects of dairy foods on plasma lipids have been extensively studied. The well-established knowledge that saturated fats in the diet increase serum cholesterol, which in turn leads to an increased risk of CVD, was the basis on which over time, guidelines for CVD prevention in the general adult population focused on the control of plasma LDL cholesterol, to be achieved, among others, by limiting dairy foods consumption and by substituting whole fat with low-fat products
[39]. Indeed, the evidence reviewed here does not support an adverse effect of moderate dairy food consumption (either low or full fat) on plasma lipids, and the literature on this topic is constantly growing. Notably, despite dairy fat consists of around 60% SFAs, they represent a mixture of various subtypes, with different effects on the lipid profile. For instance, besides long-chain SFAs with LDL-raising effect as lauric acid, myristic acid, palmitic acid and stearic acid, dairy fatty acids include (9.8%) medium-chain saturated fatty acids (MCSFAs) (between 6 to 12 carbons, i.e. 6:0 to 12:0), (31.9%) odd-chain SFAs (OCSFAs) (15:0, 17:0), (25%) monounsaturated and (2.3%) polyunsaturated fatty acids (18:1n-9, 18:2n-6 and 18:3n-3), branched-chain saturated fatty acids, and trace amounts of natural (ruminant) trans fats (i.e., trans-palmitoleic acid, 156–158 trans-16:1n-7)
[40][41].
Accordingly, a meta-analysis of five randomized controlled trials from Denmark, Norway, and Australia supports heterogeneous effects of dairy on lipid profiles depending on the type of food consumed
[42]. Indeed, in this paper, hard cheese compared to butter lowers total cholesterol by 5% and LDL cholesterol by approximately 6.5% despite a similar ratio of polyunsaturated/saturated fatty acids (P/S ratio); this indicates that the different effects of cheese and butter on plasma lipid levels in this meta-analysis cannot be due to the relative amounts of SFAs and PUFAs in the two diets. More probably, the different responses should be attributed to other dairy components or to the specific processing methods utilized for butter and cheese production.
In this regard, it is notable that dairy products enriched with probiotics have a clear hypocholesterolemic effect, since they can modify the gut flora by promoting bacteria strains able to ferment dietary fiber (non-digestible carbohydrates) from seeds, wholegrains, legumes, and vegetables, which are not metabolized or absorbed while passing through the upper gastrointestinal tract. Fiber fermentation leads to the production of short-chain fatty acids (SCFAs) that exert local and systemic effects, such as the inhibition of the hepatic cholesterol synthesis and the stimulation of liver cholesterol uptake
[43].
Furthermore, SCFAs, especially butyrate, can lower the plasma levels of pro-inflammatory markers (high-sensitivity C-reactive protein, TNF-α and IL-6) by acting at the gene expression level or by the activation of the MAPK pathway
[44].
In summary, by combining data on CV events and risk factors, this entry provides coherent evidence for a neutral effect of a moderate consumption of total dairy food on CVD irrespective of fat content. A beneficial effect of some specific items (i.e., fermented products and products added with probiotics), largely mediated through their effect on major CV risk factors—mainly lipids and subclinical inflammation—also emerges.