Calcium and vitamin D for obesity: a review of randomized controlled trials

Abstract

Obesity often coexists with low calcium intake and vitamin D insufficiency. There is emerging evidence of a role for these nutrients in the regulation of body weight. However, it is unclear whether increasing intakes of calcium and/or vitamin D during energy restriction, is a better strategy for weight and fat loss. We searched the literature from 2000 to date for randomized controlled trials (RCTs) on weight loss that had increased calcium or vitamin D per se, or in combination. Primary and secondary studies were included for this analysis. A total of 15 RCTs on calcium with or without vitamin D and seven on vitamin D alone met our criteria. Two studies reported that supplemental calcium significantly increased fat loss during caloric restriction by 1.8 and 2.2 kg, three found differences between 1 and 3.5 kg but were statistically nonsignificant, while nine trials were equivocal (±0.7 kg). The data on vitamin D supplementation during weight loss were too few to make firm conclusions. Current evidence from RCTs did not consistently support the contention that calcium and vitamin D accelerated weight or fat loss in obesity. There were studies that favoured the hypothesis but lacked the statistical power. There is a need for RCTs to examine the influence of vitamin D on body fat.

Introduction

Calcium accounts for 2–4% of gross body weight in mammals. Of this, more than 95% is present in bones and teeth and the remainder is either found in plasma bound to plasma proteins, or in extra-cellular fluid as ionic calcium concentration (Ca2+) (Weaver and Heaney, 2006). The latter is tightly regulated by parathyroid hormone (PTH), calcitonin and vitamin D. The physiological importance of calcium in human physiology is well established and is covered in this issue. There is growing evidence that poor calcium intake, inadequate vitamin D status, obesity and chronic non-communicable disease often cluster. This presents a paradigm that can be acted upon at the individual and population level, if causality of effect is secured.

A potential role for calcium in body-weight regulation came from observations that a high-calcium diet attenuated adipocyte lipid accretion and weight gain, during periods of overconsumption of an energy-dense diet (Zemel et al., 2000; Shi et al., 2001; Teegarden and Zemel, 2003; Zemel, 2003). Based primarily on the agouti mouse model, Zemel et al. (2000) proposed that intracellular calcium (iCa2+) held the key to fat deposition and obesity. According to their scheme, increases in dietary calcium would, via PTH, chronically lower iCa2+ in the adipocyte. Directly, or possibly via insulin, iCa2+ would then act to reciprocally regulate; a reduced expression of fatty acid synthase (FAS)—a key enzyme regulating lipid deposition—while stimulating adipose tissue lipolysis. An increased fat oxidation and thermogenesis through upregulation of uncoupling proteins could also account for the greater weight/fat loss following calcium (Zemel et al., 2000; Shi et al., 2001; Teegarden and Zemel, 2003; Zemel, 2002, 2003).

Dietary calcium has also been known to act at the level of the gastrointestinal tract to increase energy loss, through increased fecal-fat excretion (Figure 1) (Soares and Chan She-Ping-Delfos, 2010). These observations predate the calcium-body-weight hypothesis. A recent meta-analysis confirms that dietary calcium has a small but significant effect on fat excretion. However, the data on dairy calcium were more robust than non-dairy calcium, with intakes of 1200 mg/d resulting in an increased fecal-fat excretion of 5.2 g/d. Although not substantial, the latter could theoretically account for a weight loss of 2.2 kg over a year (Christensen et al., 2009).

Figure 1
figure1

A simplified scheme of the potential anti-obesity effects of calcium and vitamin D. PTH, parathyroid hormone; SNS, sympathetic nervous system; GI, gastrointestinal; FOR, fat oxidation rate.

Tordoff (2001) has hypothesized a ‘calcium appetite’ as the innate drive for calcium-rich food sources when faced with calcium depletion. Although confirmation comes from animal studies, this has proved difficult to demonstrate in humans, given the complex behavioural control of food intake in man. Nevertheless, the expectation would be that those with low calcium status somehow make inappropriate choices leading to increased energy intake, in their drive to meet their calcium requirements. Some indication for such effects comes from the observations that during weight loss, additional calcium (1200 mg/d) as a milk supplement attenuated subjective feelings of hunger and desire to eat, and resulted in a trend for a lower fat and energy intake (Gilbert et al., 2011). Suppression of hunger sensations by calcium has also been described during short-term weight loss (Kabrnová-Hlavatá et al., 2008). Our own observations through a sequential meal design indicate that calcium plus vitamin D acutely attenuated buffet meal intake, prolonged the inter-meal interval between buffet and dinner, and significantly reduced spontaneous 24-h food intake the following day (Chan She Ping-Delfos and Soares, 2011). Whether such potential roles for calcium on food and fat intake are mediated through resistin (Kabrnová-Hlavatá et al., 2008), ghrelin (Gilbert et al., 2011), leptin (Astrup et al., 2010) or by other gastrointestinal tract hormones controlling food intake, remain a fertile area of future research (Figure 1).

There are some issues with studies investigating the anti-obesity mechanism of calcium. These include the source used that is, dairy versus non-dairy, the formulation of the pharmaceutical preparation and the dosage administered. These facets of study design impinge on the effective dose absorbed and hence the ability to document metabolic versus gastrointestinal effects of calcium (Soares and Chan She-Ping-Delfos, 2010). Using milk or dairy product as a vehicle for increasing calcium, introduces milk bioactives, milk protein, probiotics, and in countries with mandatory fortification, vitamin D as well into the picture. It was therefore encouraging that despite these limitations, there was consistent evidence to support the stimulation of fat oxidation, following calcium alone or in combination with vitamin D (Soares and Chan She-Ping-Delfos, 2010). However, an increased thermogenesis and greater lipolysis were not always observed. Overall, there is good evidence to support many of the mechanistic pathways for an anti-obesity effect of calcium (Figure 1).

There is now a flurry of activity on the role of vitamin D in chronic disease and a meta-analysis on its role in type II diabetes is presented in this series. The active metabolite, 1, 25 (OH)2D3, independent of PTH, seems to modulate adipogenesis. This is achieved by inhibiting critical molecular components of adipogenesis, such as peroxisome proliferation (Duque et al., 2004). Hence, reduced vitamin D stores have the potential to cause excess differentiation of pre-adipocytes to adipocytes. Animal studies on VDR null mice strongly indicate a role for the vitamin in energy regulation (Wong et al., 2009). However, there is mixed evidence in humans to support a role in energy expenditure and fat oxidation (Boon et al., 2006; Teegarden et al., 2008). Could vitamin D hence modify insulin sensitivity and influence food intake (Figure 1) or is its action through improved calcium absorption and a reduction in PTH levels? One opinion is that the long-term suppression of PTH may hold the key to obesity prevention (McCarty and Thomas, 2003). A reduced activation of the sympathetic nervous system has long been implicated in the weight gain of both animals and man. Chronic lowering of PTH would then allow the sympathetic nervous system to normally stimulate thermogenesis and lipolysis. Validation of such a mechanism would be important to the management and prevention of obesity, as increases in vitamin D should complement increases in calcium, in suppressing PTH (Figure 1).

The last 10 years has seen an abundance of data from cellular, animal and epidemiological studies that have addressed the potential role of calcium and vitamin D in body-weight regulation. Consequently some reviews and meta-analyses have appeared in the literature, as evidence has become available (Barr, 2003; Shapses et al., 2004; Trowman et al., 2006; Dougkas et al., 2011). One area not specifically covered so far is whether calcium and vitamin D, per se or in combination, accelerate weight and fat loss during caloric restriction. The outcome is important to both clinical practice and strategies for public health, and forms the mainstay of this review.

Methods

We reviewed the literature from year 2000 to date, which directly and/or indirectly assessed the relationship between calcium, vitamin D and different measures of body fatness. Two researchers (WCSP-D and MHG) independently searched the literature for English language articles from databases including PubMed, Google scholar, ProQuest, Science Direct, Highwire Press and Wiley interscience. Keywords used for searching the articles were calcium, vitamin D, vitamin D supplementation, PTH, body fat, body weight, fat-free mass, fat mass, adiposity, fat distribution, body fat regulation, body mass index (BMI), weight loss and body composition. One researcher (MJS) screened all the papers and explored additional publications from the reference lists of obtained articles. Our main analysis included randomized controlled trials (RCTs) for weight loss that had manipulated calcium or vitamin D intake either through the diet or through supplementation. Studies that increased these nutrients through increasing serves of dairy were excluded, as that area has been recently covered in detail (Dougkas et al., 2011). The resultant 15 RCTs on calcium with or without vitamin D and seven on vitamin D alone are briefly described in Tables 1 and 2.

Table 1 Randomized controlled trials (RCTs) for weight loss investigating the effects of calcium with and without vitamin D on body fatness
Table 2 Randomized controlled trials on the influence of vitamin D on measures of body fatness

Discussion

Human evidence linking calcium with body-weight regulation first appeared as retrospective analyses of studies on bone mineral and hypertension (Zemel et al., 2000; Barr, 2003; Teegarden, 2003; Weaver and Heaney, 2006). Although some studies listed in Barr's review showed no significant benefit of increased calcium intake, others observed that dietary calcium, regardless of the source, negatively predicted changes in weight and fat mass (Davies et al., 2000; Zemel et al., 2000; Teegarden, 2003). Further calcium accelerated weight reduction on a calorie-restricted diet and attenuated weight gain when added to a diet without calorie restriction (Teegarden and Zemel, 2003; Lappe et al., 2004). These were retrospective analyses of clinical and observational studies and were not designed with body weight and composition as their primary endpoint (Davies et al., 2000; Zemel et al., 2000; Heaney, 2003; Teegarden, 2003; Drapeau et al., 2004; Loos et al., 2004). More recent analyses on a range of study designs by Shapses et al. (2004) and Trowman et al. (2006) conclude that there was no reason to expect a benefit of the nutrient on body weight. This is in contrast to the most recent meta-analysis by Dougkas et al. (2011) where a significant inverse relationship between calcium intake and BMI was obtained. The latter indicated that an 800-mg/d increase in calcium could reduce BMI by1.1 kg/m2. At a population level, such effects are not trivial (Heaney, 2003).

Randomized controlled trials (RCTs)

There is still some conjecture on whether calcium and vitamin D, alone or in combination, accelerate the effects of energy restriction on fat loss. In the studies in Table 1, the amount of caloric restriction varied between studies but was always a fixed kcal amount of each subject's baseline requirements. Except one (Cummings, 2006), all other trials had parallel designs comparing two to four arms (Table 1). Only three studies (Bowen et al., 2005; Cummings, 2006; Gilbert et al., 2011) used dairy-derived calcium while others used different formulations of a pharmaceutical preparation. The majority of studies were only on women. Further although all authors report the targeted kcals of energy restriction, it is not clear from the details provided by some, whether this was actually achieved on each arm of the trial.

According to the hypothesis increasing calcium intake during weight loss should result in greater fat loss and an attenuation of the loss in fat-free mass. From the tabled 15 RCTs that met our criteria, only two showed an effect of the nutrient. The results of Zemel et al. (2004) were the only clear cut example of a benefit a greater fat loss of calcium over placebo. Major et al. (2009) in an re-analysis obtained a significant effect of calcium plus vitamin D on weight and fat loss, with a significant time × treatment interaction (Major et al., 2007; Table 1). This indicated that the differences obtained increased over time in the treatment group. Riedt et al. (2007) investigated the effect of weight loss on bone metabolism and the protective effect of additional calcium. Their control group was on a weight maintenance diet and a 200-mg calcium supplement. Interestingly, they observed that during weight loss, higher calcium (1800 mg/d) was better than moderate calcium (1100 mg/d) in accelerating weight over time (time × intervention interaction, Table 1). However, differences in fat mass though sizeable (1.8 kg) did not achieve statistical significance.

There could be many reasons for a lack of treatment effect with calcium. There was a large range in calcium intake on control (350–701 mg/d) and treatment arms (850–1908 mg/d). Amount of energy restriction varied between trials from 1500 to 4500 kJ/d (there were smaller within trials variations). Higher calcium intake and greater weight loss per se are independently associated with reduced fractional and total calcium absorption (Cifuentes et al., 2004). This would reduce the metabolic effects of calcium on the treatment arm and contribute to between-trial differences. However, they would be offset by gastrointestinal tract mechanisms of calcium that promote energy loss through increased fat excretion (Figure 1). Threshold effects for both the processes can be expected but such data are not available as yet, so it is difficult to predict the net effect.

Zemel et al. (2009) have argued that selection of subjects with habitually low calcium intakes (usually <600 mg/d) is important, as they are most likely to benefit from the extra calcium. Other authors suggest a range of 600–800 mg/d above which effects of calcium may be anticipated (Major et al., 2009; Dougkas et al., 2011). All studies in Table 1 met the latter requirement, yet the majority did not detect differences in weight and fat loss. Monitoring compliance and determining adherers to the weight-loss program, is also crucial to the outcome measured. On the basis of these prerequisites, a re-analysis by Major et al. (2009) confirmed the beneficial effect of calcium plus vitamin D. Zemel et al. (2009), however, could only document the significant effects of increasing dairy intake over a control arm, but not the additional benefit of supplemental calcium; a facet they had observed earlier (Zemel et al., 2004). Potential effects of vitamin D through differences in intake between trial diets (supplemental or dietary) and through seasonal effects may also need to be considered, especially in those interventions of a long duration. Such information was lacking in many of the reported data.

During sustained negative energy balance, the body's switches its metabolism to counter the ensuing change in body weight. Calcium and vitamin D have many biological effects and in a situation such as weight loss, nutrient requirements will be directed towards vital functions at the expense of others. It is conceivable that the putative effects of calcium/vitamin D in a period of metabolic adaptation may then be masked, or too small to be detected. A quick tally of the direction and magnitude of differences suggests this to be true. In three trials, fat loss was marginally greater on the treatment arm by −0.21 to −0.6 kg (Major et al., 2007; Kabrnová-Hlavatá et al., 2008; Faghih et al., 2010), and in four studies treatment was marginally lower than control by +0.13 to +0.7 kg (Riedt et al., 2005; Cummings, 2006; Kabrnová-Hlavatá et al., 2008; Zemel et al., 2009), with two trials reported in Shapses et al. (2004) and those of Bowen et al. (2005) showing no net change. Another issue is the power to detect differences when they do exist. Zemel et al. (2004) detected a difference of 1.8 kg in fat mass, whereas Major et al. (2009) found a difference of 3.5 kg to be significant. This was in contrast to trials in pre-menopausal women where a 2.2 kg difference in fat loss (Shapses et al., 2004) and 1.8 kg in fat loss (Riedt et al., 2007) could not be detected; both in the direction of the hypothesis. Clearly, there is a need for consensus on subject characteristics and study execution/compliance, and the necessary statistical power if future trials are to advance this area.

Evidence for vitamin D in obesity

Cross-sectional studies

It is currently unclear to what extent poor vitamin D status is a consequence of obesity or is somehow, involved in its aetiology (Florez et al., 2007). Between 2000 and 2011 there have been over 15 cross-sectional studies that have assessed the relationship between vitamin D status and different measures of body fatness. Most of these studies have confirmed an inverse association between vitamin D and total body fat and regional (subcutaneous and visceral) adipose tissue, whether measured directly or from anthropometry (Arunabh et al., 2003; Kamycheva et al., 2003; Parikh et al., 2004; Snijder et al., 2005; Aasheim et al., 2008; Cheng et al., 2009; Kremer et al., 2009; Lenders et al., 2009; Moan et al., 2009; Moschonis et al., 2009; Freedman et al., 2010; Frost et al., 2010; Soares et al., Unpublished). Other cross-sectional studies suggest that individuals with higher PTH have higher body weight and/or BMI (Parikh et al., 2004; Bolland et al., 2005; Snijder et al., 2005; Alemzadeh et al., 2008; Lenders et al., 2009; Frost et al., 2010). One explanation is that the fat-soluble vitamin is sequestered in the expanded mass of adipose tissue, resulting in an apparently lower level (Wortsman et al., 2000). It is also possible that the overweight or obese are less likely to venture outdoors to engage in activity, and so their exposure to sunlight is low (Harris and Dawson-Hughes, 2007). If vitamin D is to have a causal role, then changes in vitamin status should be related to changes in weight status. This is not always seen after planned weight-loss interventions (Zittermann et al., 2009).

RCTs

It was therefore important to examine whether vitamin D supplementation during weight loss improved weight and fat change. We found only two studies that directly assessed the effects of supplementation with vitamin D3 on some measure of adiposity (Table 2). Sneve et al. (2008) and Zittermann et al. (2009) could not find any effect of supplementation with vitamin D3 on changes in body weight, waist-hip ratio or percent fat mass. Both studies were of a long duration (1 year) and achieved a 25(OH)D3 status >85 nmol/l.

Secondary studies

There were more than 15 studies carried out to explore the effects of vitamin D supplementation on endpoints like insulin resistance, glucose metabolism and endothelial function. The majority of these studies assessed body fatness, but neither report differences in the outcome nor provide raw data of adiposity measures. We briefly describe those four papers having adequate data in Table 2. In a recent study, supplementation with vitamin D led to significant improvement in insulin resistance over 6 months, but there was no effect on body weight (von Hurst et al., 2010). Nagpal et al. (2009) explored the short-term effects of mega doses of vitamin D on insulin sensitivity but did not observe changes in body fatness. Consistent with these studies, Jorde and Figenschau (2009) did not report any impact of supplementation on BMI or waist-hip ratio. Finally, Kim et al. (2006) administered vitamin D (2 μg intravenously) twice a week over 15 weeks and examined cardiac endpoints. No change in body weight or BMI was reported.

Indirect evidence

We found three studies that reported the impact of prevailing serum 25(OH)D on subsequent weight change. In the RCTs by Ortega et al. (2008) higher vitamin D at baseline (>50 nmol/l; mean value: 85.9±44.4) resulted in greater fat loss and preservation of lean tissue over 2 weeks. This was partially supported by a long-term RCT where higher vitamin D at 6 months (median for tertiles=14.5, 21.2 and 30.2 ng/ml) predicted greater weight loss at 2 years (Shahar et al., 2010). However, no other measure of fatness was reported in that study (Table 2). In contrast, the observational study of Forouhi et al. (2008) did not find any association between prevailing vitamin D status and waist circumference over a 4.5- or 10-year period. Overall there is good evidence for an inverse relationship between vitamin D and obesity; however, evidence for causality from RCTs is meagre.

Limitations

There are relatively few RCTs that have been primarily designed to uncover the potential of calcium or vitamin D alone, or in combination, to influence body fatness and its distribution during weight loss. There are many studies on bone density/dynamics during weight loss, where body composition was monitored. It remains to be determined whether primary versus secondary data contribute to systematic differences in trial outcomes. The evidence base currently available for the effect of vitamin D per se, is meagre. Future studies also need to address dose-response trials of sufficient duration, to examine whether threshold effects exist.

Conclusions

Currently available RCTs do not consistently provide evidence for an augmentation of weight or body-fat loss following calcium plus vitamin D. In part this may relate to the model of weight loss per se, as well as the statistical power to detect differences when they do exist. There are very limited RCTs data on vitamin D alone to enable any conclusion, however, cross-sectional studies consistently link low vitamin D to greater obesity. RCTs are accepted as the highest level of evidence for cause and effect relationships, but their execution and interpretation are far from easy. We have highlighted some issues in this area that need to be considered in future research.

References

  1. Aasheim ET, Hofsø D, Hjelmesaeth J, Birkeland KI, Bøhmer T (2008). Vitamin status in morbidly obese patients: a cross-sectional study. Am J Clin Nutr 87, 362–369.

    CAS  Article  Google Scholar 

  2. Alemzadeh R, Kichler J, Babar G, Calhoun M (2008). Hypovitaminosis D in obese children and adolescents: relationship with adiposity, insulin sensitivity, ethnicity, and season. Metab: Clin Exp 57, 183–191.

    CAS  Article  Google Scholar 

  3. Arunabh S, Pollack S, Yeh J, Aloia JF (2003). Body fat content and 25-hydroxyvitamin D levels in healthy women. J Clin Endocrinol Metab 88, 157–161.

    CAS  Article  Google Scholar 

  4. Astrup A, Chaput J-P, Gilbert J-A, Lorenzen JK (2010). Dairy beverages and energy balance. Physiol Behav 100, 67–75.

    CAS  Article  Google Scholar 

  5. Barr S (2003). Increased dairy product or calcium intake: Is body weight or composition affected in humans? J Nutr 133, 245S–248S.

    Article  Google Scholar 

  6. Bolland MJ, Grey AB, Gamble GD, Reid IR (2005). Association between primary hyperparathyroidism and increased body weight: a meta-analysis. J Clin Endocrinol Metab 90, 1525–1530.

    CAS  Article  Google Scholar 

  7. Boon N, Hul GBJ, Sicard A, Kole E, Van Den Berg ER, Viguerie N et al. (2006). The effects of increasing serum calcitriol on energy and fat metabolism and gene expression[ast]. Obesity 14, 1739–1746.

    CAS  Article  Google Scholar 

  8. Bowen J, Noakes M, Clifton PM (2005). Effect of calcium and dairy foods in high protein, energy-restricted diets on weight loss and metabolic parameters in overweight adults. Int J Obes (Lond) 29, 957–965.

    CAS  Article  Google Scholar 

  9. Chan She Ping-Delfos W, Soares M (2011). Diet induced thermogenesis, fat oxidation and food intake following sequential meals: Influence of calcium and vitamin D. Clin Nutr 30, 376–383. doi:10.1016/j.clnu.2010.11.006.

    CAS  Article  Google Scholar 

  10. Cheng S, Massaro JM, Fox CS, Larson MG, Keyes MJ, McCabe EL et al. (2009). Adiposity, cardiometabolic risk, and vitamin D status: the Framingham heart study. Diabetes 59, 242–249.

    Article  Google Scholar 

  11. Christensen R, Lorenzen JK, Svith CR, Bartels EM, Melanson EL, Saris WH et al. (2009). Effect of calcium from dairy and dietary supplements on faecal fat excretion: a meta-analysis of randomized controlled trials. Obesity Rev 10, 475–486.

    CAS  Article  Google Scholar 

  12. Cifuentes M, Riedt CS, Brolin RE, Field MP, Sherrell RM, Shapses SA (2004). Weight loss and calcium intake influence calcium absorption in overweight postmenopausal women. Am J Clin Nutr 80, 123–130.

    CAS  Article  Google Scholar 

  13. Cummings NK (2006). The Potential Role of Dietary Calcium in Obesity, Ph.D. Thesis, Curtin University of Technology. Retrieved 26 Feb 2011, from espace@Curtin database. From: http://espace.library.curtin.edu.au/R/?func=dbin-jump-full&object_id=17868&local_base=GEN01-ERA02.

  14. Davies MK, Heaney RP, Recker RR, Lappe JM, Barger-Lux MJ, Rafferty K et al. (2000). Calcium intake and body weight. J Clin Endocrinol Metab 85, 4635–4638.

    CAS  Google Scholar 

  15. Dougkas A, Reynolds CK, Givens ID, Elwood PC, Minihane AM (2011). Associations between dairy consumption and body weight: a review of the evidence and underlying mechanisms. Nutr Res Rev 15, 1–24, doi:10.1017/S095442241000034X.

    Article  Google Scholar 

  16. Drapeau V, Després J-P, Bouchard C, Allard L, Fournier G, Leblanc C et al. (2004). Modifications in food-group consumption are related to long-term body-weight changes. Am J Clin Nutr 80, 29–37.

    CAS  Article  Google Scholar 

  17. Duque G, Macoritto M, Kremer R (2004). 1,25(OH)2D3 inhibits bone marrow adipogenesis in senescence accelerated mice (SAM-P/6) by decreasing the expression of peroxisome proliferator-activated receptor gamma 2 (PPARγ2). Exp Gerontol 39, 333–338.

    CAS  Article  Google Scholar 

  18. Faghih S, Abadi AR, Hedayati M, Kimiagar SM (2010). Comparison of the effects of cows' milk, fortified soy milk, and calcium supplement on weight and fat loss in premenopausal overweight and obese women. Nutr Metab Cardiovasc Dis. Epub ahead of print. doi:10.1016/j.numecd.2009.11.013 (in press).

  19. Florez H, Martinez R, Chacra W, Strickman-Stein N, Levis S (2007). Outdoor exercise reduces the risk of hypovitaminosis D in the obese. J Steroid Biochem Mol Biol 103, 679–681.

    CAS  Article  Google Scholar 

  20. Forouhi NG, Luan JA, Cooper A, Boucher BJ, Wareham NJ (2008). Baseline serum 25-hydroxy vitamin d is predictive of future glycemic status and insulin resistance. Diabetes 57, 2619–2625.

    CAS  Article  Google Scholar 

  21. Freedman BI, Wagenknecht LE, Hairston KG, Bowden DW, Carr JJ, Hightower RC et al. (2010). Vitamin D, adiposity, and calcified atherosclerotic plaque in African-Americans. J Clin Endocrinol Metab 95, 1076–1083.

    CAS  Article  Google Scholar 

  22. Frost M, Abrahamsen B, Nielsen TL, Hagen C, Andersen M, Brixen K (2010). Vitamin D status and PTH in young men: a cross-sectional study on associations with bone mineral density, body composition and glucose metabolism. Clin Endocrinol 73, 573–580.

    CAS  Article  Google Scholar 

  23. Gilbert J-A, Joanisse DR, Chaput J-P, Miegueu P, Cianflone K, Alméras N et al. (2011). Milk supplementation facilitates appetite control in obese women during weight loss: a randomised, single-blind, placebo-controlled trial. BrJ Nutr 105, 133–143.

    CAS  Article  Google Scholar 

  24. Harris SS, Dawson-Hughes B (2007). Reduced sun exposure does not explain the inverse association of 25-hydroxyvitamin D with percent body fat in older adults. J Clin Endocrinol Metab 92, 3155–3157.

    CAS  Article  Google Scholar 

  25. Heaney RP (2003). Normalizing calcium intake: projected population effects for body weight. J Nutr 133, 268S–270S.

    Article  Google Scholar 

  26. Holecki M, Zahorska-Markiewicz B, Wiecek A, Mizia-Stec K, Nieszporek T, Zak-Golab A (2008). Influence of calcium and vitamin D supplementation on weight and fat loss in obese women. Obesity Facts 1, 274–279.

    CAS  Article  Google Scholar 

  27. Jensen LB, Kollerup G, Quaade F, Sørensen OH (2001). Bone mineral changes in obese women during a moderate weight loss with and without calcium supplementation. J Bone Miner Res 16, 141–147.

    CAS  Article  Google Scholar 

  28. Jorde R, Figenschau Y (2009). Supplementation with cholecalciferol does not improve glycaemic control in diabetic subjects with normal serum 25-hydroxyvitamin D levels. Eur J Nutr 48, 349–354.

    CAS  Article  Google Scholar 

  29. Kabrnová-Hlavatá K, Hainer V, Gojová M, Hlavaty P, Kopsky V, Nedvídková J et al. (2008). Calcium intake and the outcome of short-term weight management. Physiol Res 57, 237–245.

    PubMed  Google Scholar 

  30. Kamycheva E, Joakimsen RM, Jorde R (2003). Intakes of calcium and vitamin D predict body mass index in the population of Northern Norway. Journal of Nutr 133, 102–106.

    CAS  Article  Google Scholar 

  31. Kim H, Park C, Shin Y, Kim Y, Shin S, Kim Y-S et al. (2006). Calcitriol regresses cardiac hypertrophy and QT dispersion in secondary hyperparathyroidism on hemodialysis. Nephon Clin Pract 102, c21–c29.

    Article  Google Scholar 

  32. Kremer R, Campbell PP, Reinhardt T, Gilsanz V (2009). Vitamin D status and its relationship to body fat, final height, and peak bone mass in young women. J Clin Endocrinol Metab 94, 67–73.

    CAS  Article  Google Scholar 

  33. Lappe JM, Rafferty KA, Davies MK, Lypaczewski G (2004). Girls on a high-calcium diet gain weight at the same rate as girls on a normal diet: a pilot study. J Am Diet Assoc 104, 1361–1367.

    CAS  Article  Google Scholar 

  34. Lenders CM, Feldman HA, Von Scheven E, Merewood A, Sweeney C, Wilson DM et al. (2009). Relation of body fat indexes to vitamin D status and deficiency among obese adolescents. Am J Clin Nutr 90, 459–467.

    CAS  Article  Google Scholar 

  35. Loos RJF, Rankinen T, Leon AS, Skinner JS, Wilmore JH, Rao DC et al. (2004). Calcium intake is associated with adiposity in Black and White men and White women of the Heritage family study. J Nutr 134, 1772–1778.

    CAS  Article  Google Scholar 

  36. Major G, Alarie F, Doré J, Phouttama S, Tremblay A (2007). Supplementation with calcium + vitamin D enhances the beneficial effect of weight loss on plasma lipid and lipoprotein concentrations. Am J Clin Nutr 85, 54–59.

    CAS  PubMed  Google Scholar 

  37. Major G, Alarie FP, Doré J, Tremblay A (2009). Calcium plus vitamin D supplementation and fat mass loss in female very low-calcium consumers: potential link with a calcium-specific appetite control. Br J Nutr 101, 659–663.

    CAS  Article  Google Scholar 

  38. McCarty MF, Thomas CA (2003). PTH excess may promote weight gain by impeding catecholamine-induced lipolysis-implications for the impact of calcium, vitamin D, and alcohol on body weight. Med Hypotheses 61, 535–542.

    CAS  Article  Google Scholar 

  39. Moan J, Lagunova Z, Lindberg FA, Porojnicu AC (2009). Seasonal variation of 1,25-dihydroxyvitamin D and its association with body mass index and age. J Steroid Biochem Mol Biol 113, 217–221.

    CAS  Article  Google Scholar 

  40. Moschonis G, Tanagra S, Koutsikas K, Nikolaidou A, Androutsos O, Manios Y (2009). Association between serum 25-hydroxyvitamin D levels and body composition in postmenopausal women: the Postmenopausal Health Study. Menopause 16, 701–707.

    Article  Google Scholar 

  41. Nagpal J, Pande JN, Bhartia A (2009). A double-blind, randomized, placebo-controlled trial of the short-term effect of vitamin D3 supplementation on insulin sensitivity in apparently healthy, middle-aged, centrally obese men. Diabetic Med 26, 19–27.

    CAS  Article  Google Scholar 

  42. Ortega RM, Aparicio A, Rodríguez-Rodríguez E, Bermejo LM, Perea JM, López-Sobaler AM et al. (2008). Preliminary data about the influence of vitamin D status on the loss of body fat in young overweight/obese women following two types of hypocaloric diet. Br J Nutr 100, 269–272.

    CAS  Article  Google Scholar 

  43. Parikh SJ, Edelman M, Uwaifo GI, Freedman RJ, Semega-Janneh M, Reynolds J et al. (2004). The relationship between obesity and serum 1,25-dihydroxy vitamin D concentrations in healthy adults. J Clin Endocrinol Metab 89, 1196–1199.

    CAS  Google Scholar 

  44. Riedt CS, Cifuentes M, Stahl T, Chowdhury HA, Schlussel Y, Shapses SA (2005). Overweight postmenopausal women lose bone with moderate weight reduction and 1 g/day calcium intake. J Bone Miner Metab 20, 455–463.

    CAS  Article  Google Scholar 

  45. Riedt CS, Schlussel Y, von Thun N, Ambia-Sobhan H, Stahl T, Field MP et al. (2007). Premenopausal overweight women do not lose bone during moderate weight loss with adequate or higher calcium intake. Am J Clin Nutr 85, 972–980.

    CAS  Article  Google Scholar 

  46. Shahar DR, Schwarzfuchs D, Fraser D, Vardi H, Thiery J, Fiedler GM et al. (2010). Dairy calcium intake, serum vitamin D, and successful weight loss. Am J Clin Nutr 92 (Suppl 5), 1017–1023.

    CAS  PubMed  PubMed Central  Google Scholar 

  47. Shapses SA, Heshka S, Heymsfield SB (2004). Effect of calcium supplementation on weight and fat loss in women. J Clin Endocrinol Metab 89, 632–637.

    CAS  Article  Google Scholar 

  48. Shi H, Dirienzo DB, Zemel MB (2001). Effects of dietary calcium on adipocyte lipid metabolism and body weight regulation in energy-restricted aP2-agouti transgenic mice. FASEB J 15, 291–293.

    CAS  Article  Google Scholar 

  49. Sneve M, Figenschau Y, Jorde R (2008). Supplementation with cholecalciferol does not result in weight reduction in overweight and obese subjects. Eur J Endocrinol 159, 675–684.

    CAS  Article  Google Scholar 

  50. Snijder MB, van Dam RM, Visser M, Deeg DJH, Dekker JM, Bouter LM et al. (2005). Adiposity in relation to vitamin D status and parathyroid hormone levels: a population-based study in older men and women. J Clin Endocrinol Metab 90, 4119–4123.

    CAS  Article  Google Scholar 

  51. Soares MJ, Chan She-Ping-Delfos W (2010). Postprandial energy metabolism in the regulation of body weight: Is there a mechanistic role for dietary calcium? Nutrients 2, 586–598.

    CAS  Article  Google Scholar 

  52. Soares MJ, Chan She Ping-Delfos W, Sherriff J, Heidary D, Cummings NK, Zhao Y (2011). Vitamin D and parathyroid hormone in insulin resistance of abdominal obesity: cause or effect? Eur J Clin Nutr, e-pub ahead of print; doi:10.1038/ejcn.2011.111.

    CAS  Article  Google Scholar 

  53. Teegarden D (2003). Calcium intake and reduction in weight or fat mass. J Nutr 133, 249S–251S.

    Article  Google Scholar 

  54. Teegarden D, White KM, Lyle RM, Zemel MB, Van Loan MD, Matkovic V et al. (2008). Calcium and dairy product modulation of lipid utilization and energy expenditure. Obesity 16, 1566–1572.

    CAS  Article  Google Scholar 

  55. Teegarden D, Zemel MB (2003). Dairy product components and weight regulation: symposium overview. J Nutr 133, 243S–244S.

    CAS  Article  Google Scholar 

  56. Tordoff MG (2001). Calcium: taste, intake, and appetite. Physiol Rev 81, 1567–1597.

    CAS  Article  Google Scholar 

  57. Trowman R, Dumville JC, Hahn S, Torgerson DJ (2006). A systematic review of the effects of calcium supplementation on body weight. Br J Nutr 95, 1033–1038.

    CAS  Article  Google Scholar 

  58. von Hurst PR, Stonehouse W, Coad J (2010). Vitamin D supplementation reduces insulin resistance in South Asian women living in New Zealand who are insulin resistant and vitamin D deficient—a randomised, placebo-controlled trial. Br J Nutr 103, 549–555.

    CAS  Article  Google Scholar 

  59. Wagner G, Kindrick S, Hertzler S, DiSilvestro RA (2007). Effects of various forms of calcium on body weight and bone turnover markers in women participating in a weight loss program. J Am Coll Nutr 26, 456–461.

    CAS  Article  Google Scholar 

  60. Weaver CM, Heaney RP (2006). Calcium in Human Health. Humana Press Inc.: New Jersey.

    Google Scholar 

  61. Wong KE, Szeto FL, Zhang W, Ye H, Kong J, Zhang Z et al. (2009). Involvement of the vitamin D receptor in energy metabolism: regulation of uncoupling proteins. Am J Physiol Endocrinol Metab 296, E820–E8E8.

    CAS  Article  Google Scholar 

  62. Wortsman J, Matsuoka LY, Chen TC, Lu Z, Holick MF (2000). Decreased bioavailability of vitamin D in obesity. Am J Clin Nutr 72, 690–693.

    CAS  Google Scholar 

  63. Zemel M, Teegarden D, Van Loan M, Schoeller D, Matkovic V, Lyle R et al. (2009). Dairy-rich diets augment fat loss on an energy-restricted diet: a multicenter trial. Nutrients 1, 83–100.

    CAS  Article  Google Scholar 

  64. Zemel M, Thompson WG, Milstead AM, Morris KL, Campbell P (2004). Calcium and dairy acceleration of weight and fat loss during energy restriction in obese adults. Obesity Res 12, 582–590.

    CAS  Article  Google Scholar 

  65. Zemel MB (2002). Regulation of adiposity and obesity risk by dietary calcium: mechanisms and implications. J Am Coll Nutr 21, 146S–151S.

    CAS  Article  Google Scholar 

  66. Zemel MB (2003). Mechanisms of dairy modulation of adiposity. J Nutr 133, 252S–256S.

    Article  Google Scholar 

  67. Zemel MB, Richards JD, Milstead AM, Campbell P (2005). Effects of calcium and dairy on body composition and weight loss in African-American adults. Obesity Res 13, 1218–1225.

    CAS  Article  Google Scholar 

  68. Zemel MB, Shi H, Greer B, Dirienzo DB, Zemel PC (2000). Regulation of adiposity by dietary calcium. FASEB J 14, 1132–1138.

    CAS  Article  Google Scholar 

  69. Zittermann A, Frisch S, Berthold HK, Götting C, Kuhn J, Kleesiek K et al. (2009). Vitamin D supplementation enhances the beneficial effects of weight loss on cardiovascular disease risk markers. Am J Clin Nutr 89, 1321–1327.

    CAS  Article  Google Scholar 

Download references

Acknowledgements

MJS acknowledges Dairy Australia and Diabetes Australia for grants in the area of calcium, dairy and energy balance. No prior permission was necessary from these organizations before submission of this manuscript.

Author information

Affiliations

Authors

Corresponding author

Correspondence to M J Soares.

Ethics declarations

Competing interests

The authors declare no conflict of interest.

Additional information

Contributors: WCSP-D and MHG independently conducted the literature searches, assembled the initial tables and contributed to the writing of the manuscript. MJS planned the review, screened the evidence for inclusion, and wrote the manuscript.

Rights and permissions

Reprints and Permissions

About this article

Cite this article

Soares, M., Chan She Ping-Delfos, W. & Ghanbari, M. Calcium and vitamin D for obesity: a review of randomized controlled trials. Eur J Clin Nutr 65, 994–1004 (2011). https://doi.org/10.1038/ejcn.2011.106

Download citation

Keywords

  • calcium
  • vitamin D
  • weight loss
  • body fat
  • obesity

Further reading

Search