A little forewarning, the following article contains some deep nutrition science, may I advise viewers with a nervous disposition to look away now? I have, in places tried to soften the science and in laymans terms describe the physiologic processes that are occurring without reducing its integrity, we all love science don’t we. I’ve also included some practical examples to make things a little easier on the eyeball.

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 calciumintakes may actually enhance fat loss when combined with moderate energy restriction (Zemel et al. 2005). 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.

Ok so we have a hypothesis, now lets look at the mechanisms by which 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 thee and me. It appears 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 agoutimouse 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 is also responsible for the redistribution of body fat to the abdomen through the stimulation of cortisol. Increased dietary calcium would also suppress 1,25-dihyroxy vitamin D levels, thus supposedly inhibiting adiposity and promoting weight loss (Zemel, 2009).

Fig.1: Role of dietary calcium in influencing fat oxidation. Source: Jawadwala, R. (2011) Dietary Calcium – A potential ergogenic aid? Chapter in Duncan M. J. (Ed.) Trends in Human Performance Research.

Ok, so if you survived that section I congratulate you. But basically:

Low calcium diets increase calcitriol (1,25-dihydroxy vitamin D)
Increased calcitriol increases calcium influx into the fat cell
Intracellular calcium results in a decrease in thermogenesis and lipolysis (breakdown of fat cells), and reciprocal stimulation of lipogenesis (creation of fat cells).
Increased calcitriol also increases body fat distribution in the abdomen, with the aid of cortisol.
Thus increasing dietary calcium can lower intracellular calcium, increasing fatty acid synthase.
Increased dietary calcium also stimulates lipolysis, the breakdown of fat cells.

Now I must add that this mechanism has been confirmed in rats, research is yet to confirm this in humans.

So we have the hypothesis and a potential mechanism, now lets look at the existing evidence from well-controlled intervention studies that explored the 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 & 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 randomized, 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 (1000mg/day-1) diet increased diet induced thermogenesis over two successive meals, and more significantly the mean 1-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 5-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). Further, calsium 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 totaling 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.

We now have a hypothesis, we have a mechanism and we also have some conclusive support from well-constructed, well-controlled human studies, now lets make some concluding suggestions and some practical recommendations.

Existing evidence suggests chronic (>7-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 10-years of age. Practically speaking the greatest source 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 the calcium in milk and diary products is much better absorbed than the calcium in spinach and/or watercress as these plants have high oxalate content, which is insoluble (Gueguen & 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.

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References

Abreu, S., Santos, R., Moreira, C., Santos, P., Vale, S., Soares-Miranda, L., et al… (2013). Relationship of milk intake and physical activity to abdominal obesity among adolescents. Pediatric Obesity,[ahead of print].
Barba, G., Troiano, E., Russo, P., Venezia, A., & Siani, A. (2005). Inverse association between body mass and frequency of milk consumption in children. British Journal of Nutrition, 93, 15 – 9.
Bolland, M., Avenell, A., Baron, J., Grey, A., MacLennan, G., Gamble, G., & Reid, I. (2010). Effect of calcium supplements on risk of myocardial infarction and cardiovascular events: meta-analysis. British Medical Journal; 341: c3691.
Bortolotti, M., Rudelle, S., Schneiter, P., Vidal, H., Loizon, E., Tappy, L., & Acheson, K. (2008). Dairy calcium supplementation in overweight or obese persons: It’s effects on markers of fat metabolism. American Journal of Clinical Nutrition, 88, 877 – 885.
Gueguen, L., & Pointillart, A. (2000). The bioavailability of dietary calcium. Journal of the American College of Nutrition, 19, 119 – 136.
Gunther, C. W., Lyle, R. M., Legowski, P. A., James, J. M., McCabe, L. D., McCabe, G. P.,… & Teegarden, D. (2005). Fat oxidation and its relation to serum parathyroid hormone in young women enrolled in a 1-y dairy calcium intervention. American Journal of Clinical Nutrition, 82, 1228 – 1234.
Jawadwala, R. (2011) Dietary Calcium – A potential ergogenic aid? Book chapter in Duncan M. J. (Ed.) Trends in Human Performance Research. New York: Nova Science Publishers.
Melanson, E., Donahoo, W., Dong, F., Ida, T., & Zemel, M. (2005). Effect of low- and high-calcium dairy-based diets on macronutrient oxidation in humans. Obesity Research, 13, 2102-2112.
She Ping-Delfos, W., & Soares, M. (2011). Diet induced thermogenesis, fat oxidation and food intake following sequential meals: Influence of calcium and vitamin D. Clinical Nutrition, 30, 376 – 383.
Soares, M. J., Ping-Delfos, W. C. S., & Ghanbari, M. H. (2011). Calcium and vitamin D for obesity: a review of randomized controlled trials. European Journal of Clinical Nutrition, 65, 994-1004.
Zemel, M. B., Shi, H., Greer, B., Dirienzo, D., & Zemel, P. C. (2000). Regulation of adiposity by dietary calcium. The Journal of the Federation of American Societies for Experimental Biology, 14, 1132-1138.
Zemel, M.B., Richards, J., Milstead, A., & Campbell, P. (2005). Effects of calcium and dairy on body composition and weight loss in African-American adults.Obesity Research,13,1218–1225.
Zemel., M. (2009). Proposed role of calcium and dairy food components in weight management and metabolic health. The Physician and Sportsmedicine, 37,29 – 39.

About the author

Bio: Matt holds a BSc (Honours) degree in Sport & Exercise Science, an MSc in Nutrition Science. Through his own Performance Nutrition business, Nutrition Condition, he delivers frequent Health & Wellbeing Workshops to corporate and personal clients advising on how best to develop a sound, scientifically structured nutrition programme free from fads and marketing bias. Nutrition Condition also delivers Performance Nutrition services to professional athletes.

Matt can be contacted on matt@nutritioncondition.com or at www.nutritioncondition.co.uk

For regular updates follow Matt on Twitter @mattNCUK.

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