Recent studies (Bolland et al. 2008 and 2011; Li et al. 2012) have reported a possible association between calcium supplementation and increased risk for cardiovascular events (e.g. heart attacks). However, several researchers (Abrahamsen et al. 2011; Nordin et al. 2011) have pointed out flaws in the design of these studies and indeed questioned how the cardiovascular events themselves were determined.
It is known that large doses of supplemental calcium (such as taking 500 mg at a time) can cause spikes in blood calcium levels. This increased level of calcium in the blood stream can last for several hours and the concern is that these spikes could contribute to calcification of blood vessels and the increased risk for heart attacks and stroke. The problem with this theory is that the research that links calcium supplementation to increased cardiovascular risk includes individuals who only recently started taking supplemental calcium. In other words, the subjects in the studies who had heart attacks had only been taking supplemental calcium for short periods of time--too short in fact for there to have been any substantial contribution to calcification of blood vessels.
Calcification occurs slowly over long periods (years) of time. So the question is--could there be another explanation that would explain this link? Is there some other mechanism other than the calcification of blood vessels that could link calcium supplementation to increased cardiovascular risk? The answer to this question is important because with no physiological mechanism currently known that links supplemental calcium to heart attacks, it is impossible to determine risk and reach any final conclusion.
To maintain overall health we must keep our blood calcium levels between 9.0 and 10.1 mg/dl. Too little or too much calcium in the blood can lead to serious symptoms and even death. But can short term spikes in blood calcium cause problems? Can short term spikes lead to dangerous contractions of the heart, tightening of blood vessels, and, initiate cardiovascular events? If so, what is the physiological mechanism behind this chain of events?
In the most recent issue of the Journal of Bone and Mineral Research, researchers from Australia designed a study to determine exactly that. What, if any, physiological mechanism could possibly explain the connection between acute rises in blood calcium and heart attacks? In this proof of concept study, Burt et al. (2013) gave 25 subjects (all over the age of 50) 1,000 mg of oral calcium citrate and then evaluated them for changes in blood markers and specific cardiovascular function parameters linked to cardiovascular risk.
The researchers "found no significant change in PWV [pulse wave analysis] following calcium citrate administration. Carotid-femoral PWV is considered the gold standard measure of arterial stiffness"...
"PWV is a consistent predictor of fatal and nonfatal cardiovascular events in a range of subject populations, independent of other cardiovascular risk factors." "The failure to find a significant change in PWV suggests an acute serum calcium-mediated increase in arterial stiffness does not explain the reported increase in cardiovascular events with calcium supplements."
"Contrary to our hypothesis, we found a reduction in median Alx [augmentation index is an indirect marker of arterial stiffness] of about 10% following calcium citrate administration"...
..."if maintained long-term, [this reduction in Alx] would be associated with about a 30% reduction in relative risk of cardiovascular events." [In other words, if this 10% reduction in Alx as a result of the calcium supplementation was continued long term, there would be a 30% reduction, not increase, in risk for heart attacks.]
The authors concluded, "It is highly unlikely that there will ever be a randomized-controlled trial of sufficient size and duration to conclusively determine the effect of calcium supplementation on cardiovascular risk. Lacking these data, assessment of the effect of calcium supplements on plausible physiologic mechanisms that could underlie an increase in cardiovascular risk will greatly enhance the final interpretation of the above studies."
"Unfortunately, our study neither confirms nor refutes the safety of calcium supplementation. However, our findings do demonstrate that the rise in serum calcium following supplement administration does not acutely exert an adverse effect on these parameters of cardiovascular function."
The take home message from all of this research is not that calcium supplementation should be avoided but rather, excessive intake should be used with caution. How many times have we heard, "all things in moderation"? In addition to the superior bioavailability of the OsteoNaturals' calcium products OsteoSustain (160 mg/tab) and OsteoMineralBoost (140 mg/tab), the amount of calcium in each tablet is substantial but not overwhelming to the body. When taking these products one or two tablets at a time and spacing them out throughout the day, they provide optimal benefit to the skeleton but without excessive spikes in blood calcium.
The other important factor to remember is that when taking calcium supplements you should also make sure you are consuming adequate amounts of bio-available magnesium (NOT magnesium oxide!), vitamin D and vitamin K (OsteoSustain and OsteoStim). This is extremely important because these nutrients help your body fully utilize calcium and deposit it where it belongs--into the skeleton--and not into soft tissues where it could cause harm.
Burt et al. 2013. Acute effect of calcium citrate on serum calcium and cardiovascular function. JBMR 28(2):412-418.
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