That calcium is involved in the proper regulation of body weight is now well established in the scientific literature and this topic has been extensively reviewed1,2,3,4. While the inverse association between calcium and body weight is fairly well reported, the mechanism by which calcium may influence weight gain is less well understood. Dairy is an important sources of calcium, and some evidence suggests that additional factors in diary products such as conjugated linoleic acid, may also have an influence on the inverse association seen in epidemiological studies. Much of the positive research regarding calcium and weight management in humans has come as secondary outcomes of trials originally looking at bone health. The effects of calcium on the weight of laboratory animals is well documented, but animal studied should always be viewed with caution due to different physiological responses.
Calcium paradox disease describes the phenomenon of raised cytosolic Ca2+ levels in certain key tissues, in relation to a fall in dietary calcium. As calcium intakes fall, parathyroid hormone (PTH) is released from the parathyroid gland, which increases expression of 1-α-hydroxylase in the kidney. The conversion of 25-hydroxyvitamin D [25(OH)D] to 1,25-dihydroxyvitaminD [1,25-(OH)2D] is catalysed by 1-α-hydroxylase, and so as PTH concentrations rise, circulating concentrations of 1,25-(OH)2D rise concomitantly. The 1,25-(OH)2D then causes a rise in plasma calcium by increasesing absorption, decreasing excretion as well as allowing the resorption of calcium from bone. Plasma levels of PTH and 1,25-(OH)2D are therefore inversely associated with plasma levels of calcium. High levels of PTH and 1,25-(OH)2D, as might be seen with a chronic low intake of calcium, paradoxically raise intracellular levels of Ca2+. In the case of adipose tissue, high levels of cytosolic Ca2+ stimulate de novo lipogenesis and inhibit lipolysis (here).
However, there is another aspect of chronic low dietary calcium intakes that has not been extensively researched. Calcitonin is another hormone involved in the regulation of calcium, and as calcium plasma levels rise, calcitonin is released from the thyroid gland to allow increased excretion of calcium from the kidney and decreased resporption of calcium from bone. Calcitonin levels can rise rapidly up to 3-fold in response to calcium in the gut, and may act as a satiety signal in the central nervous system. Animals injected with calcitonin decrease their feeding behaviour and humans injected with calcitonin show rapid decreases in body weight. Low levels of calcium therefore turn off this satiety signal by reducing calcitonin levels, which increases energy intake. It is possible that this is a regulatory mechanism to ensure further calcium intake through increased food intake. Low calcium intakes could therefore contribute to obesity via multiple mechanisms.
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