There are insufficient studies of intake and CV calcification to draw firm parallels with the dietary risk factors for coronary artery disease (CAD), although in general the advice for prevention of calcification would also help prevent CAD. Nevertheless, a consistent theme throughout the nutrient intake studies is oxidative damage as a cause of CV calcification and CAD. Elevated lipid oxidation products and oxidised LDL are thought to be responsible for both atherosclerosis and mineralisation of vascular cells. Advanced glycation end products (AGEs), known to be elevated in diabetes, generate ROS when in contact with their receptor (RAGE) and induce VSMC calcification, which could be inhibited by antioxidants. Furthermore, homocysteine is a pro-oxidant, whose effect could be inhibited by antioxidants, while other compounds with antioxidant effect include vitamin K-hydroquinone, which can suppress lipid peroxidation, and MK4, which can inhibit oxidant-induced inflammation.
Although there are insufficient studies of intake or serum levels of nutrients to draw firm conclusions, in general transfats, disordered blood glucose and insulin, higher serum phosphate levels, oxidative stress and α-tocopherol supplementation should be avoided, while intake of long chain ω3 PUFAs, calcium, magnesium, vitamins B, D and K and antioxidants should be increased. In practice this amounts to avoiding sugar and processed foods and increasing oily fish, fruits and vegetables. Although animal studies have shown that many of the micronutrients discussed here may be effective in lowering or preventing CV calcification, there have been remarkably few clinical trials. In particular, it would be worth testing the effects of long chain ω3 PUFAs, magnesium and vitamin K.