Osteoporosis is a skeletal disease characterised by a chronic demineralisation of the bone tissue. Loss of calcium from long bones and the spine is particularly problematic because it structurally weakens the skeleton and increases the risk of fractures significantly. Osteoporosis takes decades to manifest as a disease, and because of this the causes can be difficult to identify particularly as they may be dietary in origin. The main focus of most research for osteoporosis has been based around understanding the role of calcium in bone demineralisation. For example, research published in the American Journal of Clinical Nutrition in 19891 investigated the effects of 1500 mg per day calcium as calcium carbonate on the bone mineral density of women over a 4 year period. The results showed some improvements in bone mineral loss, particularly in postmenopausal women, but overall the results were inconsistent. However, calcium does show some benefits, and generally these results are consistent with other research in the same area.
Therefore calcium supplementation appears to have some effects with regard bone mineral loss, but osteoporosis is clearly not a calcium deficiency in isolation. Investigating increased dietary calcium would seem logical based on the aetiology of osteoporosis involving mineral loss, particularly calcium. However, when it was realised that osteoporosis was characterised not be a deficiency of calcium, but an increase in calcium loss in the urine, it became clear that recommendations to increase calcium intakes would not prevent or reverse osteoporosis. A fact demonstrated in many human clinical trials. Another line of reasoning suggested that increasing dietary calcium may cause a decrease in parathyroid hormone, a hormone that causes bone resorption. However, results from studies investigating this theory have again been inconsistent, and results from such studies generally show that calcium can decrease parathyroid hormone, but that this does not result in consistent bone remineralisation.
The inconsistent results of calcium supplementation suggest that calcium may be part, but not all of the solution to the mineral loss seen in osteoporosis. It is often the case that when inconsistent results are seen that the actual aetiology is not fully understood and an unidentified variable is the root cause of the effect. It might be for example, that it is not calcium per se that is beneficial, but the form of calcium that is administered. However, more recent research indicates that calcium demineralisation is caused not by a calcium deficiency but instead by a decrease in plasma pH that result from too much animal protein in the diet. Animal protein increases the acidity of the blood by production of hydrogen ions following metabolism of certain amino acids, and in response osteoclasts mobilise mineral salts from the bones to neutralise the pH falls and maintain homeostatic levels. It is this chronically depressed blood pH that is now thought to cause demineralisation of the bones over a number of decades, leading to osteoporosis.
Plant foods are beneficial because they shift the pH back to normal. Plant foods do not result in the production of hydrogen ions following metabolism but instead increase production of potassium salts that can raise plasma pH. This prevents the resorption of bone by osteoclasts and decreases the calcium excretion seen in osteoporosis. Calcium in the diet is beneficial if it is in the calcium carbonate form, because when absorbed it can also neutralise plasma pH though the buffering of excess hydrogen ions. Other mineral salts would have the same effect, with sodium bicarbonate being particularly effective. This explains the inconsistent results seen in studies investigating calcium supplements and explains why researcher have been unable to find the route cause of osteoporosis by focussing myopically on dietary calcium intake. Like all systems in the body, the skeletal regulatory systems are incredibly complex and oversimplifying them to a simple calcium balance model is not helpful in understanding osteoporosis.
Dr Robert Barrington’s Comments: Osteoporosis research has a history that mirrors cholesterol research over the last 60 years. Both involved an over simplistic approach that did not follow normal scientific protocol. Observation of calcium loss from bones and cholesterol deposits in the arteries rightly require the investigation of dietary calcium deficiency or dietary cholesterol intakes, respectively. However, once observational science had shown that the relationship between the two parameters was not straightforward, other lines of inquiry should have been investigated. When a myopic obsession with a single line of inquiry developed, and a fanatical and single-minded approach using post hoc analysis to explain contradictory evidence ensued, all pretence at scientific observation was abandoned. Decades have been wasted chasing low intakes of dietary calcium as a cause of osteoporosis, when all along evidence suggested otherwise. Despite this research continues to investigate low calcium intakes as a cause of osteoporosis.
RdB
