By: Brian S. MH, MD (Alt. Med.)
Calcification is the process by which calcium salts accumulate in body tissues, where calcium is typically deposited in bones and and teeth. However, abnormal calcification can occur in soft tissues, including blood vessels, kidneys, and other organs, leading to significant health issues. While calcification is part of the body’s natural regulatory processes, it can sometimes signal disease, particularly when it occurs in blood vessels or other soft tissues.
Types of Calcification and How Each Occurs
There are two main types of calcification in the body:
Dystrophic Calcification: This form of calcification occurs in damaged or necrotic tissues. Calcium accumulates in the areas of cell injury or inflammation, commonly seen in atherosclerotic plaques, damaged heart valves, and areas of infection (Demer & Tintut, 2014).
Metastatic Calcification: This occurs in otherwise healthy tissues and results from an imbalance of calcium and phosphate levels in the blood. Conditions like hyperparathyroidism or chronic kidney disease often drive metastatic calcification, as these conditions lead to elevated calcium or phosphate levels (Giachelli, 2009).
Each form of calcification has a unique biochemical basis and occurs in different contexts of health and disease.
Calcification and Atherosclerosis
Atherosclerosis is a progressive condition in which fatty deposits, cholesterol, and calcium accumulate within the walls of arteries. Calcification in atherosclerosis generally occurs in the later stages of plaque development, transforming the plaque from a soft to a hardened structure (Libby, 2021). This calcified plaque can restrict blood flow or even rupture, leading to cardiovascular events.
Biochemical Reactions in Calcification and Atherosclerosis
Calcification within atherosclerotic plaques results from a series of biochemical processes:
1. Inflammatory Response: Damaged endothelial cells release inflammatory molecules, attracting immune cells that form foam cells. These foam cells contribute to the fatty core of plaques (Sorescu et al., 2004).
2. Mineralization: As plaques evolve, calcium and phosphate begin to accumulate. Vascular smooth muscle cells (VSMCs) also undergo phenotypic changes, adopting bone-like properties and actively depositing hydroxyapatite (the primary mineral in bone) into the plaque (Shanahan et al., 2011).
3. Stabilization through Calcification: The calcified plaque becomes more rigid and is considered less likely to rupture, though it can still restrict blood flow due to its bulk and rigidity.
Why Calcification Occurs in Atherosclerosis: The body may initiate calcification as a stabilization mechanism to reinforce damaged arteries. However, excess calcification can make arteries brittle, impairing elasticity and increasing the risk of cardiovascular complications (Libby, 2021).
The Role of Calcium Supplementation in Elderly Populations
Doctors commonly prescribe calcium supplements to older adults to prevent osteoporosis, as aging typically leads to decreased bone density. However, emerging research suggests that magnesium, which aids calcium metabolism, may be equally essential in elderly health. Magnesium supports calcium transport and prevents its excessive accumulation in soft tissues, thus maintaining a healthy balance that reduces the risk of abnormal calcification (Spence et al., 2019).
Prolonged Calcium Supplementation and Potential Health Risks
There is concern that prolonged calcium supplementation without adequate magnesium or vitamin K2 may increase calcification risks in soft tissues, particularly in arteries and joints:
Calcification in Joints and Extremities: Excess calcium can accumulate in joints and extremities, potentially worsening conditions like osteoarthritis by depositing calcium crystals in soft tissue (Shanahan et al., 2011).
Arterial Calcification without Atherosclerosis: Even in individuals without atherosclerosis, excessive calcium can lead to calcification in arteries, as studies indicate that excess calcium in the blood may deposit in vascular walls when regulatory mechanisms are overwhelmed (Moe & Chen, 2008).
Implications of Prolonged Supplementation
1. Increased Cardiovascular Risk: Prolonged supplementation may promote calcified atherosclerotic plaques or exacerbate existing plaques, as excess calcium contributes to plaque mineralization. This can result in reduced vascular flexibility and a higher likelihood of adverse cardiovascular events (Anderson et al., 2016).
2. Joint Health: Accumulation in joint spaces can exacerbate joint pain or degenerative joint diseases, indicating the need for careful management of calcium intake in susceptible populations (Demer & Tintut, 2014).
Does Prolonged Calcium Supplementation Worsen Existing Atherosclerotic Plaques?
For individuals with pre-existing atherosclerosis, high calcium intake may further mineralize these plaques, potentially increasing the risk of adverse events like heart attack or stroke. This is especially true if supplementation is not balanced with magnesium and vitamin K2, as these nutrients play protective roles by directing calcium away from soft tissues and into bones (Schurgers & Vermeer, 2000).
Guidance for Practitioners and Dietitians
Before recommending calcium supplements, practitioners should review a patient’s complete diet to ensure dietary calcium intake is assessed. Calcium-rich foods, such as leafy greens, dairy products, and nuts, are widely available and may suffice for most individuals. Additionally, an antioxidant-rich diet and balanced mineral intake are critical in maintaining bone and cardiovascular health without excessive reliance on supplements.
Conclusion
Calcification and calcium supplementation in aging populations present complex challenges. While calcium is essential for bone health, it must be balanced with other nutrients, especially magnesium and vitamin K2, to avoid unintended consequences like arterial and joint calcification. Practitioners should adopt a holistic view, considering patients' overall diet and lifestyle to ensure that calcium supplementation supports health without contributing to potential complications.
References
Anderson, J. J. B., Kruszka, B., Delaney, J. A. C., et al. (2016). Calcium intake from diet and supplements and the risk of coronary artery calcification and its progression among older adults: 10-year follow-up of the Multi-Ethnic Study of Atherosclerosis. Journal of the American Heart Association, 5(10), e003815.
Demer, L. L., & Tintut, Y. (2014). Inflammatory, metabolic, and genetic mechanisms of vascular calcification. Arteriosclerosis, Thrombosis, and Vascular Biology, 34(4), 715-723.
Giachelli, C. M. (2009). The emerging role of phosphate in vascular calcification. Kidney International, 75(9), 890-897.
Libby, P. (2021). The changing landscapes of atherosclerosis. Nature, 592(7855), 524-533.
Moe, S. M., & Chen, N. X. (2008). Mechanisms of vascular calcification in chronic kidney disease. Journal of the American Society of Nephrology, 19(2), 213-216.
Schurgers, L. J., & Vermeer, C. (2000). Determination of phylloquinone and menaquinones in food: Effects of food matrix on circulating vitamin K concentrations. Biochimica et Biophysica Acta (BBA) - General Subjects, 1475(1), 155-159.
Shanahan, C. M., Crouthamel, M. H., Kapustin, A., & Giachelli, C. M. (2011). Arterial calcification in chronic kidney disease: Key roles for calcium and phosphate. Circulation Research, 109(6), 697-711.
Sorescu, D., Weiss, D., Lassegue, B., et al. (2004). Superoxide production and vascular smooth muscle proliferation in atherosclerosis. Circulation, 109(5), 587-593.
Spence, J. D., Jenkins, D. J. A., & Davignon, J. (2019). Nutritional supplements and cardiovascular disease: Beyond fish oil, fiber, and plant sterols. Current Opinion in Lipidology, 30(1), 35-41.
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