Saturated fatty acids

More than half of the milk fatty acids are saturated, accounting to about 19 g/l whole milk [9] (Table 1). The specific health effects of individual fatty acids have been extensively studied [10-13]. Butyric acid (4:0) is a well-known modulator of gene function, and may also play a role in cancer prevention [12]. Caprylic and capric acids (8:0 and 10:0) may have antiviral activities, and caprylic acid has been reported to delay tumour growth [11]. Lauric acid (12:0) may have antiviral and antibacterial functions [14], and might act as an anti caries and anti plaque agent [15]. Interestingly, Helicobacter pylori can in fact be killed by this fatty acid [16]. Another interesting observation is that capric and lauric acid are reported to inhibit COX-I and COX-II [17]. Stearic acid (18:0) does not seem to increase serum cholesterol concentration, and is not atherogenic [10,13].

It would appear, accordingly, that some of the saturated fatty acids in milk have neutral or even positive effects on health. In contrast to this, the saturated fatty acids lauric-, myristic-(14:0) and palmitic (16:0) acid have low-density lipoprotein (LDL)- and high-density lipoprotein- (HDL) cholesterol-increasing properties [13]. High intake of these acids raises blood cholesterol levels [13], and diets rich in saturated fat have been regarded to contribute to development of heart diseases, weight gain and obesity [4]. Association between consumption of milk and milk products and serum total cholesterol, LDL cholesterol and HDL cholesterol has been reported [18]. High cholesterol levels are a risk factor for coronary heart disease (CHD), with LDL cholesterol and a high ratio between LDL and HDL cholesterol enhancing the risk of CHD [19,20].

Several intervention studies have shown that diets containing low-fat dairy products have been associated with favourable changes in serum cholesterol [21-23]. However, milk fat consumption has been shown to have less pronounced effects on serum lipids than could be expected from the fat content [24,25]. To our knowledge epidemiological cohort studies does not show a higher risk for diseases in persons with high intakes of dairy fat, as also shown by Elwood et al. [26]; cohort studies provide no convincing evidence that milk is harmful. On the contrary, several studies have found a lack of association between milk consumption and CHD [27-30]. Two Swedish studies have shown that cardiovascular risk factors were negatively associated with intake of milk fat [31,32]. A Norwegian study suggests that intake of dairy fat or some other component of dairy products, as reflected by C15:0 as marker in adipose tissue may protect persons at increased risk from having a first myocardial infarction (MI), and that the causal effects may rely on other factors than serum cholesterol [33]. It has been shown that 34 grams dairy fat per day gives no negative effect on odds ratio for myocardial infarction [34]. As reported by Sjogren et al. [35], fatty acids typically found in milk products were associated with a more favourable LDL profile in healthy men (i.e., fewer small, dense LDL particles), and they concluded that men with high intakes of milk products had an apparently beneficial and reduced distribution of the harmful small, dense LDL particles [35].

A Canadian 13 year follow up study analysed plasma LDL sub fractions with different density, and showed that cardiovascular risk was largely related to accumulation of small, dense LDL particles [36]. The small, dense LDL particles are also reported to be associated with hypertriglyceridemia [37], insulin resistance [38], the metabolic syndrome and increased risk for CHD [39,40]. Saturated fatty acids increase the serum concentration of both LDL- and HDL cholesterol. In a metaanalysis of 60 selected trials Mensink et al. [13] reported that saturated fatty acids gave an unchanged ratio between total cholesterol and HDL cholesterol if carbohydrates replaced saturated fatty acids. It was shown by Hostmark et al. [41] that an index reflecting the LDL/HDL balance, ATH-index = (total cholesterol-HDL)*apoB/(apoA*HDL), improved the discrimination between controls and subjects with coronary artery stenosis. Unlike this, the distribution of total cholesterol was similar in controls and patients, as evaluated by coronary angiography. In keeping with these early results, in the INTERHEART case-control study on risk factors associated with myocardial infarction in 52 countries, an increase in apo B/apo A1 ratio was shown to be the strongest risk factor for myocardial infarction [5]. ApoB/apo A1 was found to be a stronger risk factor than total cholesterol alone, or ratio between LDL and HDL cholesterol (Yusuf, personal information).

Increased levels of C-reactive protein (CRP) have been associated with inflammation [42], and CRP is recognized as a risk factor for CHD and metabolic syndrome [42,43]. Fredrikson et al. [43] found, however, no significant association between CRP and intake of saturated fat. These studies are in agreement with others [44].

The increase in HDL cholesterol caused by the saturated fatty acids lauric-, myristic- and palmitic acid [13] has beneficial effects as the reverse cholesterol transport is increased [4]. HDL can also act as an antioxidant and prevent oxidation of LDL particles in the blood, and it may protect against infections and against toxins from microbes [45].