Calcium, why is it important?
Calcium is one of the essential macrominerals in our body, also known as a mineral that is needed in large amounts for our bodies to function optimally. Macro stems from the word for ‘large’ in Greek.
The European Food Safety Authority (EFSA) recognises that calcium contributes to blood, bones, energy production and cell division (1). In addition to the EFSA health claims, the British Nutrition Foundation suggests that the mineral benefits foetal growth and neurological function, may increase the survival rates of those with colon or breast cancer, particularly in combination with low intakes of fat, and has the potential to enhance weight loss (2).
Calcium in the blood
Calcium is absorbed from the food we eat via the lining of the bowel, before being stored in our bones. The mineral is highly regulated so as to not allow excess calcium into the bloodstream, which can cause hypercalcaemia. Normal blood calcium levels are generally between 2.1 mmol/L and 2.6 mmol/L. When this is too low, additional calcium is released from the bones into the blood. The bowel is then signalled to increase the absorption of calcium from food, and the kidneys get rid of less calcium through the urine.
Bone Health and cell division
More than 99% of the body’s calcium is stored in the bones and teeth. This calcium is removed in small amounts and replaced by new calcium stores, otherwise known as the ‘remodelling’ process. In order to retain bone strength, we require adequate calcium intake to replace the removed calcium. Building up calcium stores when young helps to maintain bone strength for life, as it works to prevent the body from taking too much calcium from the bones (4).
When calcium is removed from the bones and teeth, components of the mineral are used within the cell division process. This includes breakdown and reformation of the nuclear envelope (a layer that surrounds the nucleus of the cell), cell plate formation and the process of indenting the cell’s surface which initiates the process of cytokinesis. (5)
As with many other nutrients, Calcium contributes to normal energy-yielding metabolism. When calcium stores are low, hypocalcaemia can cause extreme fatigue. This is usually because the health of our bones, muscles and nerves are compromised. Low calcium stores can cause a loss of appetite, which means that the body receives even less energy.
One study found that pregnant women with an inadequate supply of calcium required supplementation of the mineral. The mother passes on nutrients to the foetus and in order to grow and develop, the foetus requires an adequate supply of calcium from the mother. The child-bearing age of women is currently increasing with time. However, since a mother’s calcium stores decrease with age, this increases the need for good calcium intake when pregnant.
In terms of growth, the foetus requires calcium to form its skeleton, just as with any person. By the time of labour, the foetus has formed 98% of its skeleton, containing approximately 30g of calcium. Studies show that there is a positive relationship between a mother’s calcium intake and the foetus’ femur and arm length (6).
Several studies indicate that increasing calcium intake can result in weight loss, such as in a study that reviewed an intake from 400mcg to 1000mcg of calcium per day (7). Another study found that when increasing calcium intake alongside reducing energy intake, more weight loss was seen with higher calcium intake (8). Calcium-rich foods also often contain high amounts of protein, a macronutrient which promotes satiety and, therefore, enhances weight loss.
In addition to weight loss, the mineral is required for optimal enzymatic activity of certain digestive enzymes. The gastrointestinal tract contains a calcium ion receptor which is believed to play a role in gastric acid secretion.
Neurological and muscular function
Calcium is also required for both neurotransmission and muscle contraction. Nerve and muscle cell membranes contain calcium channels which allow an influx of calcium when the cell is depolarised. Calcium takes part in the contraction of skeletal, cardiac and smooth muscle, controlling the interaction between thick and thin filaments in muscle fibres. In certain types of muscle, such as skeletal muscle, action potentials induce the release of calcium ions which can then bind to other molecules to cause change, contributing to the muscular contraction process (2).
European Food Safety Authority. (2016) EU Register of Nutrition and Health Claims Made On Food. Available at: http://ec.europa.eu/food/safety/labelling_nutrition/claims/register/public/?event=search
Theobald, H. E. (2005) ‘Dietary Calcium and Health’, Nutrition Bulletin, 30(1), p. 237 - 277. Available at: https://onlinelibrary.wiley.com/doi/pdf/10.1111/j.1467-3010.2005.00514.x
Cancer Research UK. (2018) Your Body and Calcium. Available at: https://www.cancerresearchuk.org/about-cancer/coping/physically/blood-calcium/your-body-calcium
National Institute of Child Health and Human Development. (2016) What is calcium & how does it build strong bones?. Available at: https://www.nichd.nih.gov/health/topics/bonehealth/conditioninfo/calcium
Hepler, P. K. (1994) ‘The role of calcium in cell division’, Cell Calcium, 16(4), p. 322 - 330. Available at: https://www.ncbi.nlm.nih.gov/pubmed/7820852
Hacker, A. N., Fung, E. B. and King, J. C. (2012) ‘Role of calcium during pregnancy: maternal and fetal needs’, Nutrition Reviews, 70(7), p. 397 - 409. Available at: http://www.chori.org/Principal_Investigators/King_Janet/Downloadables/6.pdf
Zemel, P.C., Greer, B., Dirienzo, D. et al. (2000) ‘Increasing dietary calcium and dairy product consumption reduced the relative risk of obesity in humans’, Obesity Research, 8(1), p. 118. Available at: https://onlinelibrary.wiley.com/doi/pdf/10.1111/j.1467-3010.2005.00514.x
8. Zemel, M.B., Thompson, W., Milstead, A. et al. (2004) ‘Calcium and dairy acceleration of weight and fat loss during energy restriction in obese adults’, Obesity Research, 12(1), p. 582–90. Available at: https://onlinelibrary.wiley.com/doi/pdf/10.1111/j.1467-3010.2005.00514.x