The role of dietary fats in cardiovascular disease (CVD) and many other disorders has been often discussed with general conclusions that this process is not simple, but rather a consequence of complex factors. Nevertheless, each group of fatty acids—SFAs, MUFAs, PUFAs and individual FAs—has a specific role in many biopathways and imbalance in their dietary intake could be result in many serious diseases. Coronary heart diseases (CHD) induce the biggest mortality worldwide. The major risk factors are contemporary lifestyle characteristic in physical training deficit, smoking, excessive food intake and wrong dietary pattern leading to overweight or obesity, high blood pressure, high level of total cholesterol, LDL cholesterol, and triglycerides [55]. In this section, statistical evaluation of impact of fat dietary intakes on CHD and CVD mortality in various countries is provided by using coronary heart disease (CHD) number and cardiovascular disease (CVD) mortality per 100,000 inhabitants and intakes of total fats, SFAs, MUFAs, and PUFAs of an adult in different countries. Data about CHD and CVD mortality were collected from the sources [56,57,58,59,60] and intakes of total fats, SFAs, MUFAs and PUFAs in different countries were used according to [61], all shown in Table 4.

As seen in Table 4, it could be concluded different intakes (% E_RDI) of total fats, SFAs, MUFAs and PUFAs in some European countries (the Czech Republic, Germany, Austria, Finland, United Kingdom, Norway, France and Greece), the USA, the Republic of South Africa, Australia with New Zealand, and Japan. Generally, a lower intake of SFAs was mostly in relation with a lower intake of total fat. The highest intakes of SFAs in some European countries and the USA could give evidence to popularity of hydrogenated fats intakes; similarly, the highest MUFAs intake in Greece is probably in connection with the Mediterranean dietary pattern characterized by high consumption of olive oil. Documented intakes of PUFAs are very heterogeneous in the range of 3.9%–8.0% E_RDI and are not in relation with number of CHD and CVD mortality in monitored countries. In accordance with data from Table 4, relatively high intakes of total fats were documented in global perspective study by Elmadfa and Kornsteiner [55] in Europe in the range of 28.5%–46.2% E_RDI, but also in Africa 13.1%–50.7% E_RDI, and America 25.7%–37.2% E_RDI. In the other continents—Asia and Australia—they were in the ranges of 11.1%–35.6% E_RDI and 32.5%–35.0% E_RDI, respectively. According to [55], the highest intakes of MUFAs 10.9%–22.3% E_RDI were also reported in Europe, further in Australia in the range of 11.8%–12.0% E_RDI, while the highest PUFAs intakes were 3.3%–11.3% E_RDI in Asia, which could be a consequence of typical cuisine patterns with high consumption of fish oil with the high content of PUFAs.

Relatively high number of CHD and CVD mortality has been found in some European countries, especially in the Czech Republic, Germany and Austria, with values exceeding three hundred events per 100,000 habitants. However, not only total fat intakes, but other factors, such as dietary pattern and stressful life style, and amounts and distribution of fatty acids could contribute to CHD and CVD mortality. The impossibility of recognizing direct relationships between total fats, SFAs, MUFAs and PUFAs intakes and CHD and CVD mortalities in different regions based on data from Table 4 is evident. Thus, in spite of the highest consumption of total fat in Greece, only a relatively low value of CHD and CVD mortality was documented. Similarly, the highest PUFAs intake in Austria did not correlate with the high number of CHD and CVD mortality.

In Figure 3, dependence of CHD and CVD mortality on total fats, SFAs, MUFAs and PUFAs intakes is demonstrated. In the case of MUFAs, two correlations were performed; in MUFAs 1 (correlation C) all monitored countries were included, while for MUFAs 2 (correlation E) it was created without data regarding Greece with a specific high consumption of olive oil, an abundant source of MUFAs. Statistical analyses using Spearman’s correlation have not confirmed the significant relationship between CHD and CVD mortalities and intakes (% E_RDI) of total fats, SFAs, MUFAs 1 and PUFAs in various countries. However, providing data from Greece were excluded, correlation E between MUFAs 2 intake and mortality showed even higher significance than correlation between SFAs and mortality. It is evident that direct dependence between factors mentioned above does not exist. The impact of specific fatty acids on disease incidence is very difficult to explain because of numerous factors including lifestyle as well as various functions and relationships between individual fatty acids in human biochemical pathways.

Results of prospective epidemiologic studies have proved the correlation between specific types of fats and risk of CHD, but no relationships with total fats [20,62]. High level of CHD and CVD mortality in Western countries has provoked general nutritional recommendations to reduce dietary intake of SFAs as cardinal prevention of these diseases. However, conclusions from other studies have indicated that dietary SFAs reduction itself cannot suppress the risk of CHD and CVD incidence and mortality and do not clearly support cardiovascular guidelines promoting high consumption of n-6 PUFAs and suggest reduced consumption of SFAs [63,64]. A complex solution is needed. Mostly, reduction of SFAs and TFAs with their simultaneous replacement by PUFAs could lead to reduction of the risk of CHD [61]. However, some argue that impact of excessive consumption of n-6 PUFAs on risks of CVD leads to fixing an upper limit of ideally about 10% E [65]. In another systematic analysis focused on global, regional and national consumption levels of dietary fats and oils in 1990 and 2010, great differences in fatty acids dietary intakes were also stated [66].

Moreover, reduction of one macronutrient in the diet has to be accompanied by an increase of another macronutrient to maintain the energy balance. Mostly, replenishment of energy after a decrease of fat intakes is accompanied with an increase of carbohydrate intakes. However, higher sugar levels in food do not prevent the increasing trend towards obesity and the second type of diabetes. Short-chain SFAs, e.g., from dairy fat and coconut oil, can influence gene expression via interactions with various G-protein-coupled receptors responsible for several hormonal responses, including insulin and leptin regulating overall energy metabolism in the human body [41]. Low-fat, high-carbohydrate diets are known to reduce HDL cholesterol and to raise triglycerides associated with increased CHD risk [40,55]. Further, cohort studies have showed an influence of different dietary composition on CHD risk. Replacing SFAs with PUFAs was inversely associated with the risk of CHD, whereas replacing SFAs with carbohydrates was not associated with CHD risk [67].

What is more, the study of almost 80 thousand women performed age-analyses and body mass index-analyses and proved the inverse correlation between polyunsaturated fat intake and CHD risk, while the trans-fat intake was associated with the raised risk of CHD. The strongest association was among women younger than 65 and also in women with the body mass index higher than 25 kg/m² [62]. Obesity and insulin resistance are both powerful predictors of CHD risk. Possibly, PUFAs can suppress the risk of CHD by improving both blood lipid levels and insulin resistance in overweight women, whilst TFAs may influence risk of CHD by its adverse effects on blood lipid levels [62,68].

Findings from many cohort studies are apparently inconsistent. Importantly, studies focused on the relationship between macronutrient intake and CHD have to be multifactorial as many environmental factors and personal conditions influence individual metabolic pathways. That is why the simple relationship between, i.e., total fats, SFAs and PUFAs intakes and the risk of serious diseases could not be determined.