Dairy fat contains a high concentration of SFA and since dairy products are a considerable part of habitual diets, they have also generally been a target for restriction advice in order to reduce intake of saturated fat. Intake of saturated fat with chain length C12-C16 and tFA increases plasma LDL which is an independent risk factor for CVD. The presence of tFA in dairy fat increases the LDL/HDL linearly with dose and, theoretically, by lowering the tFA intake by 0.5% of energy, this might reduce the cardiovascular risk by 1.5-6%. Palmitic acid is the predominant fatty acid in milk fat and increases the LDL:HDL ratio more than lauric and myristic acids do. It can be calculated how much a change in SFA intake will affect the LDL cholesterol and the risk of developing CVD. By substituting 30 g of butter per day containing about 11 g of SFA with a margarine rich in unsaturated fatty acids containing 2.4 g of SFA, would reduce LDL cholesterol by 0.2 mmol/L and subsequently reduce the risk of CVD in the order of 6-10%. In light of this, the increase of 4.9 g/day SFA intake in the milk group in the study by Wennersberg resulted in a slight increase in LDL cholesterol of 0.1 mmol/L. In some cohorts with a rather high baseline intake of dairy fat, correlations between dairy intake and plasma cholesterol would therefore be scarce. However, dairy SFA is not only C12-C16, but around 25% is represented by short- and medium-chain fatty acids, which have the ability to affect the digestion of milk fat already in the stomach through digestion by gastric lipase and isomerization of fatty acids in the partially hydrolyzed TG. It is necessary to distinguish between the effects of butter and other dairy products, since butter increases plasma cholesterol, especially LDL cholesterol, more than other dairy products. Dairy fat raises both LDL and HDL cholesterol, but the evidence for a detrimental effect of high plasma LDL levels is stronger than the positive effects from an increased HDL concentration. Intervention studies that focus on reducing dairy fat intake and other studies as well, must be aware of the effect on HDL cholesterol, both regarding size and concentration, since a reduction in HDL size and concentration may not improve health or reduce CVD risks.
On the basis of controlled and randomized dietary intervention studies with different dairy products and recent meta-analyses of both epidemiological and controlled studies, the present approach to limit the intake of high-fat dairy products on behalf of low-fat products is unchallenged. A reasonable intake of cheese, low-fat and fermented milk reduced plasma cholesterol levels, mainly LDL cholesterol, in the order of 3-15% compared to butter or other high-fat dairy products, but not compared to nutrients containing more PUFA. The levels of milk components, e.g. MUFA, MCFA, and other polar lipids, have little individual impact on plasma cholesterol concentrations, but there are only few studies for consensus and no studies on concerted action of selected components. There is still no satisfactory explanation for the term 'milk factor,' although some unknown mechanism might yet be found in the interaction between calcium, proteins, lactose, and fatty acids.
