There is More To Glucose Control Than Carbohydrates (4/?): Non-Carbohydrate Nutrients Blood for Glucose Management ➲ Calcium - Bone Builder + Fat Burner + Glucose Stabilizer?

Healthy due to calcium?
In the last three weeks we've already covered the effects of protein, fat and vitamin D in this series about the "non-carbohydrate" (micro-)nutrients which have an impact on your blood glucose levels (browse the previous installments).

With vitamin D as the topic of the last installment, it appears only logical to jump from vitamins to minerals and take a look at the "bone mineral" calcium, of which scientists have long believed that its management was the main, if not the only function of vitamin D.

In view of the fact that the word "calcium" did not even appear in last week's installment about the "sunshine vitamin", it may appear questionable, whether it would even be worth taking a closer look at the soft gray alkaline earth metal. As a SuppVersity reader who has read my previous articles about calcium, you will yet be aware that this would be as inappropriate as the shortsighted idea that the only function of 25OHD was to control the amount of calcium in your blood and bones.

There is more to calcium than bone health, but is glucose management part of the "more"?

There is in fact a plethora of studies to suggest that dietary calcium (specifically from dairy products; see Fumeron. 2011) and, in some cases, also supplements could have beneficial effects on the blood glucose levels of healthy and diabetic subjects (in some cases w/, sometimes w/out vitamin D supplementation; e.g. Pittas. 2007).
You can learn more about this topic at the SuppVersity

Proteins, Peptides & Blood Glucose

SFA, MUFA, PUFA & Blood Glucose

Vitamin D & Diabetes

Glucose Manager Calcium?

Read these ➲ while waiting

Fat to Blunt Insulin?
Vitamin D unquestionably is a top candidate for t One of those vitamin D + calcium studies was conducted by Joanna Mitri et al. in 2011. In their study, the researchers tested the effects of  2000IU vitamin D (cholecalciferol) in conjunction with 2x400 mg calcium per dayt on the pancreatic β cell function, insulin sensitivity, and glycemia in adults at high risk of diabetes. The marginal improvements in β cell function minimal attenuation of the rise in HbA1c Mitri et al. observed in the course of the 16 week study are yet by no means what study titles such as "Regulation of adiposity and obesity risk by dietary calcium: mechanisms and implications." (Zemel. 2002) would suggest.

The reasons for this discrepancy will yet become obvious, if we take a look at the results from well-controlled animal trials: While there is albeit inconclusive evidence that high calcium diets markedly inhibit lipogenesis, accelerate lipolysis, increase thermogenesis and suppress fat accretion and weight gain, and conclusive evidence that they can promote a modest energy loss through increased fecal fat excretion (Soares. 2010), papers that would confirm direct beneficial effects of calcium on glucose metabolism are rare: Even the often-cited effects Beaulieu et al. observed in a 1993 study are "vitamin D depenent", i.e. they occur only when the subjects are vitamin D depleted (interestingly, these observations were made in the absence of vitamin D supplementation; cf. Beaulieu. 1993).
Protein or calcium: Specifically in the case of the "dairy calcium" studies it's difficult, in many cases even impossible, to know whether the beneficial effects on blood glucose homeostasis are brought about by their high calcium and not by their high protein content and/or quality. Intervention studies with high calcium intake as a single variable, on the other hand, are scarce. It's thus most likely that it's the synergy of the two - a synergy you can get in concentrated form from dairy protein supplements (see box in the bottom line).
At least in the case of calcium supplements, the following examples from the contemporary scientific literature do thus not support the often-heard claim that calcium supplements would have beneficial effects on insulin sensitivity:
  • As an adjunct to an energy reduced diet, 1,000mg/day of supplemental calcium will have no effect on either insulin sensitivity or the changes in body composition (Shalileh. 2010).
I guess one of the most important reasons that the myth of the anti-diabetic effects of calcium supplements are so die-hard is the difference between the short and long-term effects of high calcium meals vs. diets:
  • Acutely, calcium supplements will have "beneficial" effects on the postprandial expression of hormones that are involved in the control of blood glucose, because it will augment the postprandial production of glucose-dependent insulinotropic peptide (GIP), glucagon-like peptide-1 (GLP-1).
    Figure 1: Difference in plasma GIP, GLP, insulin, glucose, lactate and NEFA levels after the ingestion of a standardized breakfast w/ 248mg vs. 1,239mg calcium (Gonzalez. 2013).
    As you can see in Figure 1, the downstream effects of isocaloric breakfasts providing 0.5 g carbohydrate/kg body mass (energy: 1,258 ± 33 kJ, 299 ± 8 kcal; protein: 11 ± 0 g; carbohydrate: 41 ± 1 g and fat: 10 ± 0 g) with either 248mg or 1,239mg of calcium on the blood glucose levels of the young, healthy, physically active study participants of the Gonzales study are negligible.
The increase in GLP-1 & Co is still not useless: On the contrary, it's not unlikely that ~150% increases in postprandial fatty acid oxidation and the protein sparing effects of dairy calcium Nicola Cummings et al. observed in a three-way cross-over study in which subjects were randomly provided breakfast meals either low in dairy Ca, high in non-dairy Ca (calcium citrate; see figure to the left, values expr. rel. to low CA), or high in dairy Ca are eventually triggered by said changes in GLP-1 & Co (Cummings. 2006).
  • In the long run, on the other hand, any beneficial effects on blood glucose management (if they occur at all) are probably "side effects" of the accumulating beneficial effects on lipid metabolism, body weight and energy balance of high calcium diets. It is furthermore not clear to which extend these benefits are eventually driven by additional / synergistic nutrients in dairy - the "calcium source of choice" in ~90% of the pertinent long(er) term studies.
If you take a look at the list of "high calcium" foods, which ranges from dairy (obviously), over broccoli, kale, water cress, peas, beans, almonds, brazil nuts, to sardines, salmon, apricots, and figs, it's actually no wonder that eating a diet that's naturally high in calcium is going to be beneficial for your glucose metabolism.

If, on the other hand, the addition of a bunch of calcium carbonate pills on top of the standard (obesogenic) Werstern diet, would protect you against diabesity, those 5% of the US population who are taking calcium or calcium containing supplements on a regular basis (Radimer. 2004) would have to be lean and insulin sensitive... needless to say that this is not the case, right?
Mind your total Ca intake if you use dairy protein: Unless you have been bamboozled into buying overpriced overprocessed specialty whey & casein products, the latter can easily provide you with a whopping 200mg (whey) and 500mg (casein) of calcium per serving... maybe another reason they help you to get and stay lean and insulin sensitive?
So what's the verdict then? When all is said and done, there are two fundamental conclusion you can take home from today's fourth installment of this series (browse the previous installments). The first one is that there is ample evidence that (a) a sufficient intake of calcium (800-1200mg total) is an important prerequisite for optimal glucose management and that (b) high calcium meals, due to their GLP-1-powered (learn more about GLP-1) thermogenic and "fat burning" effects are another valuable tools in your weight loss toolbox.

The second one, on the other hand, will probably sound less exciting to the supplement maniacs among the SuppVersity readers. Conclusion #2 is after all: If you are eating a whole foods diet with significant amounts of dairy and leafy greens in it, and consume a calcium containing mineral water (in Germany 90% of the tapwater qualifies as "mineral water), the use of supplements is at best useless, at worst detrimental to your health (think of the rumors about Ca supps and Prostate cancer, for example).
References: 
  • Beaulieu, Christine, et al. "Calcium is essential in normalizing intolerance to glucose that accompanies vitamin D depletion in vivo." Diabetes 42.1 (1993): 35-43. 
  • Cummings, Nicola K., Anthony P. James, and Mario J. Soares. "The acute effects of different sources of dietary calcium on postprandial energy metabolism." British journal of nutrition 96.01 (2006): 138-144.
  • Fumeron, Frédéric, et al. "Dairy consumption and the incidence of hyperglycemia and the metabolic syndrome results from a French prospective study, Data from the Epidemiological Study on the Insulin Resistance Syndrome (DESIR)." Diabetes Care 34.4 (2011): 813-817.
  • Gonzalez, Javier T., and Emma J. Stevenson. "Calcium co-ingestion augments postprandial glucose-dependent insulinotropic peptide1–42, glucagon-like peptide-1 and insulin concentrations in humans." European journal of nutrition (2013): 1-11.
  • Mitri, Joanna, et al. "Effects of vitamin D and calcium supplementation on pancreatic β cell function, insulin sensitivity, and glycemia in adults at high risk of diabetes: the Calcium and Vitamin D for Diabetes Mellitus (CaDDM) randomized controlled trial." The American journal of clinical nutrition 94.2 (2011): 486-494.
  • Pittas, Anastassios G., et al. "The effects of calcium and vitamin D supplementation on blood glucose and markers of inflammation in nondiabetic adults." Diabetes care 30.4 (2007): 980-986.
  • Soares, Mario J., and Wendy L. Chan She-Ping-Delfos. "Postprandial energy metabolism in the regulation of body weight: is there a mechanistic role for dietary calcium?." Nutrients 2.6 (2010): 586-598.
  • Shalileh, Maryam, et al. "The influence of calcium supplement on body composition, weight loss and insulin resistance in obese adults receiving low calorie diet." Journal of research in medical sciences: the official journal of Isfahan University of Medical Sciences 15.4 (2010): 191.
  • Zemel, Michael B. "Regulation of adiposity and obesity risk by dietary calcium: mechanisms and implications." Journal of the American College of Nutrition 21.2 (2002): 146S-151S.
Disclaimer:The information provided on this website is for informational purposes only. It is by no means intended as professional medical advice. Do not use any of the agents or freely available dietary supplements mentioned on this website without further consultation with your medical practitioner.