Like most parts of the body, bones undergo a continuous cycle of replacement and renewal. Existing components in the bone matrix break down, to be replaced by new ones; in youth, there is a near perfect balance in the process. The rate of renewal begins to slow down in early middle age, but in healthy adults the change in balance is negligible, at least until (in women) the menopause.
When this balance is more severely disrupted, so that bone minerals being lost are not fully replaced, the matrix loses density and strength, which can lead to fractures. These are most common in the hips, spine and wrists. Mild instances of low bone mineral density (BMD) are referred to as osteopenia; more severe instances are called osteoporosis.
In common with many diseases, medical opinion about the causes and treatment of low BMD changes over time as research reveals new knowledge.
At present, the most usual treatment is with bisphosphonate drugs such as alendronate and zoledronate, which are anti-resorptives – they slow down the rate at which existing bone components are removed from the matrix, thereby helping to maintain BMD. However, they don’t either cure or reverse osteoporosis. What has been known for a long time is that Vitamin D is important in routing calcium into bones, and Vitamin D deficiency can lead to both rickets and osteoporosis. Bisphosphonates are generally taken alongside a Vitamin D supplement. However, there is ongoing debate about how much Vitamin D is needed each day. Too much can lead to Vitamin D toxicosis, in which calcium, rather than being channeled into bone structure, is deposited in blood vessels and heart valve tissues. It’s likely that somewhere between 1000 and 2000 iu of Vitamin D, in foods or supplements, is about right as a daily intake for northern Europeans. (If in supplement form, cholecalciferol – D3 – is preferable to ergocalciferol, D2.)
At the time of writing, mainstream medicine is still catching up with new findings in the role of the gut, and in particular gut bacteria, in the regulation of mineral deposition. Vitamin K1 has long been known for its action in clotting, but Vitamin K2 is now known to play a crucial part in controlling Vitamin D’s management of calcium. K2 is readily available through diet, mostly in dairy products produced by animals fed on natural grass pasture. When they are digested, fermenting gut bacteria produce Vitamin K2 from these butters and cheeses and store one of K2’s metabolites, Menaquinone-7, in the liver, from where it is slowly released to work with Vitamin D. Essentially, K2 mediates the way that Vitamin D’s osteocalcin binds mineral to bone; with too little or no K2 the bone lacks mineral. At the same time, K2 directs calcium towards bone and away from arterial walls.
However, if the diet does not include grass fed dairy products – most dairy animals are now grain fed – or if the gut bacteria are for some reason impeded or absent, production of K2 does not take place, and disease such as osteoporosis can arise. One other natural food is a strong source of K2. Fermented soya bean is a dietary staple in parts of Japan, where it is called Natto, and when eaten regularly it can provide sufficient of K2’s Menaquinone-7 to support proper mineral deposition and restore the balance to bone’s replacement and renewal cycle.