Introduction
Cardiovascular diseases (CVDs) are a class of heart- or blood-vessel diseases (Mendis, Puska, and Norrving, 2011). CVDs include coronary heart disease (CHD) known as Ischemic heart disease (IHD), myocardial infarction (MI), generally known as heart attack, stroke, rheumatic heart disease (RHD), cardiomyopathy, and other heart disease (Mendis et al., 2011; Celermajer, Chow, Marijon, Anstey & Woo, 2012). CVD cause nearly 34% of deaths in the UK (Nichols et al., 2012) and is still the foremost cause of deaths in the world (WHO, 2012). In developing countries, the rapid increase in cardiovascular mortality is largely due to the impact of modern behaviours including lifestyles without exercises, smoking and dietary patterns. Several risk factors, like obesity, hypertension, diabetes and dyslipidemia, have led to CVD. (Helfand et al., 2009). In addition, dietary factors and lifestyle habits are more important when developing CVD (Khosravi-Boroujeni, 2012). Numerous studies have outlined the role of dietary habits in the development of metabolic syndrome (Khosravi-Boroujeni, 2012; Esmaillzadeh, A., Boroujeni, & Azadbakht, 2012). Low density lipoprotein cholesterol (LDL-C) may be increased by consuming foods high in saturated fat, thus increasing the risk of CVD. Some studies (Artaud-Wild et al., 1993; Tholstrup, 2006) have indicated that dairy fats can cause an increase in CHD mortality because it contains a high saturated fatty acid content. Therefore, the European Countries’ and the American Heart Association Dietary Recommendations suggest a reduction in saturated fat intake and recommends only dairy products that are low in fat content (Lichtenstein et al., 2006; Perk et al., 2012).
Cheese is a highly nutritious fermented dairy product eaten by many people across the world and typically part of the Mediterranean diet (Hinrichs, 2004). It is a rich source of calcium in the diet, with approximately 360 mg of calcium per 50 g of hard cheese (Rozenberg, 2016) that can suppress heart disease by affecting plasma lipid levels (Jacqmain et al., 2003), lower blood pressure (Jorde and Bonaa, 2000) and adiposity (Loos et al., 2004; Zemel and Miller, 2004). To preserve bone safety for people who are lactose intolerant, cheese can be a healthy substitute for milk. In contrast, cheese is capable of contributing to increased low-density lipoprotein cholesterol (LDL-C), an apparent cardiovascular disease (CVD) risk factor due to the presence of high saturated fatty acid (SFA) in its composition (Mihaylova, 2012). Given the global consumption of cheese, a small increase or decrease in the risk of disease could have a significant implication on public health. Therefore, when it comes to cardiovascular health, it is important to emphasise whether eating it is healthy. Over the last two decades, much attention has been paid to the possible effects of cheese consumption on cardiovascular health, but there are limited studies examining explicitly the impacts of cheese on cardiovascular health (Elwood, Pickering, Givens, and Gallacher, 2010). Although dairy products are expected to contribute to the occurrence of metabolic diseases and CVDs due to the presence of saturated fats and cholesterol in them, there is inconsistency in the outcome of various studies. This review summarizes existing evidence on the inffluence of cheese intake on the risk of CVD. The arrangement is based on disease types. Additionally, possible mechanisms are discussed as to how cheese could affect the risk of CVD.
Review of Literatures
Outcomes from many studies assessing the relationship between CVD risk and cheese intake have been reported. Bonthuis et al. (2010) conducted a population based study in Australia and found no statistically significant relationship between the intake of full-fat cheese and CVD mortality (p-trend=0.63) in about 1,520 adults that were observed over 14.4 years. However, another study by Sonestedt et al. (2011) that involves 26,445 adults from the Swedish Malmö Diet and Cancer cohort and followed for 12 years indicated the consumption of cheese to be significantly correlated with the risk of CVD, but the role may differ between the genders as different outcomes were identified for both men and women. There were 2,520 cases of CVD found during the years of follow up. In females, cheese intake was linked with a lower risk of CVD (p-trend=0.03), but that was not the case in males (p-trend=0.98). They noted that lower relative validity of men’s cheese consumption in comparison to women could lead to such disparities, and that the results’ discrepancies could be explained by differences in gender or unidentified confounding variables. The results of a reduced CVD risk are consistent with the findings of a correlation and a prospective study that indicates a negative association between cheese and metabolic syndrome, a risk marker of CVD (Fumeron et al., 2011; Hostmark and Tomten, 2011). Additionally, few intervention studies suggest that cheese fat does not raise the concentration of LDL cholesterol relative to the same quantity of butter fat (Nestel, Chronopulos, and Cehun, 2005). Cheese is high in saturated fat and should therefore increase the concentration of cholesterol. Many efforts have been made to elucidate the mechanisms underlying the effects of cheese on cholesterol. Hjerpsted and Tholstrup reviewed the possible mechanisms in a recently accepted paper. They hypothesised that the cheese matrix, it high protein level or the fact that cheese is a fermented product could influence cholesterol levels. Calcium was also listed as a possible mechanism, but it seems more impossible to be a sole explanation unless there are some unexplained mechanisms by which calcium can influence cholesterol levels (Hjerpsted and Tholstrup, 2016).
Gramenzi and colleagues in 1990 found no association in 287 cases and 649 controls between the intake of cheese and the likelihood of acute Myocardial Infarction (MI) (Gramenzi et al. 1990). Tavani et al. subsequently noted that although statistical findings were not significant (p for trend = 0.153), the correlation between cheese consumption and non-fatal acute myocardial infarction was negative (Tavani et al., 2002). However, a much deeper result that confirmed the detrimental effect of cheese consumption was released a year later in a Costa Rican study. The study involved 485 non-fatal incidents of acute MI and 508 controls and it was discovered that intake of 1.4 portions (where a portion equals 28g) of cheese a day was linked with a triple increased risk of acute MI relative to those who did not eat cheese (Kabagambe et al., 2003). Contrary to these results, an inverse association between the intake of cheese and myocardial infarction was reported by Kontogianni et al. (2006) who found a 53% and 23% decrease in the risk of non-fatal acute coronary syndrome in the case of white and yellow cheese compared to no consumption. Biong et al. also reported in a Norwegian study that there was a reduced risk of MI with an increase in the rate of cheese consumption when adjusted for age and sex (Biong et al., 2008). In addition, a prospective case-control study that included 444 cases of myocardial infarction and 565 controls was undertaken by Warensjo et al. with the main objective of exploring the association between milk fat biomarkers (15:0 and 17:0) and the risk of MI and was nested in the Northern Sweden Health Disease study. The study also explored the relationship between the cheese consumption and the risk of myocardial infarction (Warensjo et al., 2010). Increased cheese consumption in both men and women were inversely correlated with the myocardial infarction (p-trend=0.025 and p-trend=0.005, respectively). However after multivariate modifications, the results (p-trend=0.31 and p-trend=0.36, respectively) were no longer significant.
Furthermore, a large prospective case cohort research was carried out in the Netherlands (Goldbohm et al., 2011), with 120,852 participants being monitored for 10 years. The sub cohort included 4,646 participants and 3,234 IHD cases and 1,054 stroke cases. The authors of this study did not report any correlation between the intake of cheese and stroke or Ischemic Heart Disease (IHD) mortality. The prospective study conducted by Snowdown, Philips and Fraser (1984) that included 25,153 members of Seventh Day Adventist and carried out for 21 years supported the findings of Goldbohnm et al., as they also found no correlation between cheese intake and fatal IHD. However, and contrary to the above results, in a prospective study of 10,802 vegetarians, flexitarians and non-vegetarians observed for an average of 13.3 years, Mann et al. (1997) found a growing trend for IHD with improved cheese consumption (except cottage cheese) in participants eating cheese five or more occasions a week relative to those eating cheese less than once a week.
Cheese intake has been found to be inversely associated with Coronary Heart Disease (CHD). Gartside et al. (1998) confirmed this in a prospective study where 1,958 out of 5,811 participants suffered from CHD during 16 years of follow-up (OR=0.88, p=0.002). The results according to the authors seem strange, as increased consumption of cheese indicates increased consumption of saturated fat and cholesterol, which is supposed to raise CHD occurrences. However, the results were backed by a study using data from the Nurses’ Health Survey (Iso et al., 1999). The major goal of the research was to study the effect of potassium, calcium and magnesium consumption on stroke risk in 85,764 women observed over 14 years. The outcome of the study showed an inverse association in the consumption of hard cheese and risk of stroke in women who ate cheese once or more a day compared with those who basically have never eaten cheese.
In Sweden, Larsson et al. carried out a prospective study involving 74,961 participants of both genders, monitored for an average of 10.2 years to explore the relationship between dairy food consumption and stroke. Low-fat dairy products were shown to be inversely correlated with stroke risk (RR=0.88; 95% CI: 0.80–0.97; p-trend=0.03). In addition, cheese was found to be inversely correlated with stroke risk (RR=0.86; 95% CI: 0.78–0.94; p-trend=0.02). However, these results became statistically insignificant after adjusting them for multiple factors (RR=0.91; 95% CI: 0.81–1.01; p-trend=0.11) (Larsson, Virtamo, and Wolk, 2012). Contrary to the findings of Larsson et al., Qin et al. recently explored singly the effect of dairy products on CVD risk, which include CHD and stroke. Interestingly, the cheese consumption was strongly linked with a considerably lower risk of stroke (4 studies; RR 0·91; 95 % CI 0·84, 0·98) and CHD (7 studies; RR 0·84; 95 % CI 0·71, 1·0) (Qin et al. 2015). In addition, an important correlation between cheese intake and stroke mortality was confirmed by Praagman et al. (2015), while CHD mortality was not affected. A probable justification for the apparent positive effects of cheese consumption on the risk of CHD and stroke could be a significantly high amount of calcium that is present in cheese, which increases the saponification of SFA in the intestine, making it resistant to digestion resulting in less fat absorption, as indicated by increased excretion of faecal fat. (Nestel et al., 2005; Lorenzen and Astrup, 2011). This mechanism is reinforced by the findings of a prospective cohort study, where it was found that the use of calcuim content as a confounder in the analysis diminished the predicted inverse association between cheese intake and CHD (Louie et al., 2013). Also, a meta-analysis of randomised control trials (RCTs) examining the effect of calcium from dairy and dietary supplements reported that a rise in intake of calcium from dairy by 1241mg/d led to a rise of 5·2(1·6–8·8)g/d in faecal fat (Christensen et al., 2009).
Limitations to the Studies
Ultimately, and while further research is required to clarify the mechanisms at work, the weight of available evidence point to the conclusion that there is no negative association between cheese consumption and CVD risk and mortality and that cheese could have beneficial impacts on the risk of CVD by mitigating cholesterol concentration. However, the variations in designs of study make difficult to compare their results. The study type, selection of participants, number of subjects, years of observation and monitoring, CVD type (e.g. CHD or Stroke), number of cases, the portion sizes, the dietary questionnaire, modifications, geographical region etc. may all influence the results. Asides the aforementioned factors, the type of cheese consumed may also influence the results as it is a complex food item in that the milk used in the production may vary depending on the source (i.e. animal type), the variations in methods of cheese production, the fat content, the strains of bacteria used, and the duration of ripening vary based on the cheese. It is worth noting that the limitation to many of the studies included in this review is that the primary objective of the study was not to investigate the effect of cheese consumption on the risk of CVD. Still, they were included in the review to show some of the existing evidence regarding cheese and CVD risk.
Dietary Guidelines, Recommendations and Conclusion
Current dietary recommendations, including the including the UK Food Standards Agency’s Eatwell plate, the US Dietary Guidelines for Americans, and the UK and US Dairy Councils, advise three dairy servings a day, with a focus on non-fat or low-fat dairy products (Food Standards Agency, 2001; US Department of Health and Human Services and US Department of Agriculture, 2005). Additionally, the American Heart Association and the British Heart Foundation advise to minimise the risk of cardiovascular disease by reducing the consumption of foods that have a high content of saturated fat and cholesterol, including dairy products that are high in fat (Krauss et al., 2000; British Heart Foundation, 2004).
These guidelines are predominantly established on early nutrition research that showed a strong correlation among dietary saturated fat, high level of cholesterol in the blood, and elevated risk of CVD. Nevertheless, the nutritional content of dairy products and their biologically active components are significantly different and more recent work emphasises the importance of concentrating on food product as a whole (i.e. the food matrix) rather than individual nutrients, like saturated fat (Thorning et al., 2017; Pfeuffer and Watzl, 2018). Infact, the body of recent evidence suggests that full-fat dairy products, specifically cheese and yoghurt, have no deleterious effects on blood lipid profile, insulin sensitivity and blood pressure as formerly postulated based on their saturated fat and sodium content; they also don’t increase the risk of cardio-metabolic disease and could actually prevent type 2 diabetes and CVD (Nestel et al., 2013; Soerensen et al., 2014; Lordan, and Zabetakis, 2017; Koskinen et al., 2018). Although the exact mechanisms underpinning these effects are not explicit and further study is needed to respond to potential confounding variable and to gain a better understanding of how the mechanisms of action will impact on health, it is becoming more and more apparent that the dietary advice to limit saturated fat in the diet so as to minimise the risk of cardiovascular disease is becoming obsolete. Thus, the recommendation that full-fat dairy be limited or removed from the diet may not be an optimal approach to reduce the risk of cardiovascular disease and should be revised in light of current evidence. Also, the major dietary guideline that recommended reducing the consumption of dietary SFA to under 10 % of the total energy to in order to mitigate the risk of CVD (WHO, “Fats and fatty acids in human nutrition’, 2008; EFSA ‘Dietary reference values for fats’, 2010) is still valid, but eliminating cheese and other dairy products from our diet is obviously not an evidence-based approach to achieve this goal.