With the increasing popularity of dairy-free diets, Palaeolithic and other anti-dairy groups, and the rapidly growing fear of coronary artery calcification, dietary calcium intakes are decreasing rapidly.
Low calcium intakes not only have implications for bone health, recent evidence has indicated calcium may also regulate body fat content, where increased calcium intakes may actually enhance fat-loss when combined with moderate energy restriction.
It is interesting to note that a number of studies are now illustrating the fact that higher milk (a fantastic source of calcium at roughly 315mg per 250ml cup) intakes seem to have certain abdominal anti-obesity effects regardless of the individual’s physical activity (Abreu et al 2013). Reports have also indicated an inverse association between frequency of milk consumption and body mass in children (Barba et al 2005). Now this should be music to your ears, or your eyes, or both; such evidence clearly highlights the influence of dietary calcium intake on body fat content, thus bringing into question the logic of removing calcium rich foods, such as dairy, considering fat-loss is almost a universal goal.
HOW DIETARY CALCIUM MAY REGULATE BODY FAT CONTENT
Inadequate dietary calcium intakes are associated with increased body mass index and body fat content, suggesting dietary calcium intake may have certain anti-obesity properties. Various studies have demonstrated a key role of intracellular calcium in regulating adipocyte lipid metabolism; fat metabolism within fat cells to you and me. It appears that dietary calcium modulates circulating calcitriol (the active form of vitamin D), which in turn is responsible for the regulation of adipocyte intracellular calcium. Using the agouti mouse model, Zemel et al (2000) reported the influence of intracellular calcium on the accumulation of fat and obesity in these animals. The mechanism alludes that low dietary calcium intakes result in an increase in 1,25-dihydroxy vitamin D (calcitriol) which in turn stimulates calcium influx into the adipocyte (fat cell) (Fig.1). Increased dietary calcium via parathyroid hormone (PTH) chronically lowers intracellular calcium in the adipocyte. Thus either directly, or perhaps via insulin, intracellular calcium would regulate the expression of fatty acid synthase (FAS) – a key enzyme in the regulation of lipid (fat) deposition.
In addition, increased dietary calcium also stimulates adipose tissue lipolysis via its influence on cAMP production and thus the phosphorylation of hormone sensitive lipase (HSL). Intracellular calcium results in a decrease in thermogenesis and reciprocal stimulation of lipogenesis and inhibition of lipolysis (Fig.1), thus causing an expansion of adipocyte triglyceride stores. Increased levels of 1,25-dihydroxy vitamin D levels are also responsible for the redistribution of body fat to the abdomen through the stimulation of cortisol. Increased dietary calcium would also suppress 1,25-dihydroxy vitamin D levels, thus supposedly inhibiting adiposity and promoting weight-loss (Zemel 2009).
EFFECTS OF DIFFERING CALCIUM INTAKES ON BODY COMPOSITION AND FAT OXIDATION
A short-term calcium supplement study on mice revealed calcium intakes of 1.2% total energy lead to a 51% reduction in lipogenesis and a fivefold stimulation of lipolysis, resulting in a 29% decrease in body weight and a 36% decrease in fat mass (Zemel et al 2000). In human subjects, She Ping-Delfos and Soares (2011) also reported an acute dose of high calcium (543.2mg) at breakfast significantly increased whole body fat oxidation (p<0.02) and diet induced thermogenesis (p<0.01) when compared to a low calcium (248.2mg) breakfast.
In a randomised, controlled, crossover study conducted in a whole room calorimeter – the gold standard – Melanson et al (2005) reported a high calcium (~1,400mg/day-1 as dairy) diet suppressed calcitriol and resulted in a 30g/day-1 (270 kcal/day-1) increase in fat oxidation. Similarly, a high calcium (1,000mg/day-1) diet increased diet induced thermogenesis over two successive meals, and more significantly the mean one year change in whole body fat oxidation was greater in the high calcium group compared to low calcium group (<800mg/day-1) (Gunther et al 2005). However, from a critical perspective – because we must always report both sides of the argument – more recent evidence using abdominal subcutaneous microdialysis demonstrated that dietary calcium (~1,400mg/day-1 as milk mineral) for five weeks did not stimulate lipolysis, glycerol turnover or fat oxidation (Bortolotti et al 2008).
Some studies suggest that those with habitually low calcium (<600mg/day-1) intakes benefit more from increases in dietary calcium, meaning those individuals that currently avoid calcium rich foods are potentially missing out on a serious body composition aid. When calcium deficiency exists, the efficiency of calcium absorption is improved (Soares et al 2011). Furthermore, calcium supplements seem to augment fat oxidation to a greater degree than dairy calcium (Gonzalez et al 2012). This, despite the fact that dairy calcium appears to be more effective in weight and fat-loss trials, possibly owing to the synergistic effects of the bioactive components within dairy. Although interestingly, I must mention the fact that a meta-analysis of trials totalling 12,000 participants from 2010 found that calcium supplements increased the risk of myocardial infarction by 30% (Bolland et al 2010). But many of the clinical trials involved in this meta-analysis administered elemental calcium in dosages of over 1,000mg/day-1.
CONCLUDING SUGGESTIONS AND SOME PRACTICAL RECOMMENDATIONS
Existing evidence suggests chronic (>seven days) high calcium (~1,300mg/day-1) intake increases fat oxidation, which when combined with moderate energy restriction (-500kcal/day-1) may result in fat-loss (Gonzalez et al 2012). Interestingly, the high calcium intakes recommended here are almost in line with the current recommended dietary allowances for men and women, greater than ten years of age.
Practically speaking, the greatest sources of dietary calcium are dairy products, with milk, yoghurt and cheese among the richest of sources. Plant products, salts and mineral water also provide dietary calcium, although research conclusively shows that the calcium in milk and dairy products is much better absorbed than the calcium in spinach and / or watercress as these plants have a high oxalate content, which is insoluble (Gueguen and Pointillart 2000). Further, milk provides dietary calcium with “ensured absorbability”, as the many bioactive components within milk promote absorption and dairy products do not contain anything likely to inhibit intestinal absorption of calcium, such as phytates, oxalates, uronic acid or the polyphenols of certain plant foods.
Future research should aim to validate new evidence that fat oxidation is increased following acute Ca2+ intake and distinguish the long-term effects of a high Ca2+ diet on the rate of fat oxidation.
Article by Matt Jones, MSc Nutrition