Table of Contents
- 1 What is Calcium?
- 2 Calcitonin: The Thyroid Hormone for Calcium Regulation
- 3 Parathyroid Gland: The Calcium Connection
- 4 How Thyroid Disorders Affect Calcium Levels in the Body
- 5 In Brief
- 6 References:
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The thyroid gland produces three hormones that affect growth, metabolism, and cellular differentiation.
Two are most notable: thyroxine and triiodothyronine, deficiencies of which can lead to hypothyroidism, while excesses of such can lead to hyperthyroidism. (Click here if none of those terms make any sense!)
Although the thyroid gland is largely known for these, it produces another hormone that plays a huge role in calcium metabolism: Calcitonin.
Here you will learn more about this hormone, and how it fosters the dependent relationship of the thyroid gland and the mineral calcium.
What is Calcium?
The most plentiful mineral in the body, calcium is responsible for a variety of bodily functions, such as muscle movement, nerve transmission, hormone secretion, and vessel contraction/dilation, among many others.
Only 1% of the body’s calcium are used for the aforementioned functions, while the other 99% is stored in the teeth and the bones.
Calcium can be obtained through a variety of food products, such as cheese, milk, and yogurt. Vegetables such as broccoli, kale, and Chinese cabbage are rich in calcium as well.
Supplements in the forms of Calcium Carbonate and Calcium Citrate are also available for consumption.
Even with a low-calcium diet, no dire health effects can be felt in a short duration because of the body’s regulatory systems (to be discussed in detail below.)
But if a calcium-deficient diet is done for a prolonged period of time, osteopenia (low bone density) can develop, and this can lead to osteoporosis, which is characterized by brittle, weak bones.
Unfortunately, conditions such as kidney failure, removal of the stomach, and diuretic intake can lead to hypocalcemia, where blood calcium levels fall below the normal range of 2.1 to 2.6 mmol/L.
Symptoms of this disorder include cramps, convulsions, weakness, poor appetite, tingling sensation in the fingers and toes, and abnormal heart rhythms.
Hypocalcemia, if left untreated, can lead to unwanted complications (to say the least.)
Similarly, increased calcium levels in the body or hypercalcemia can also lead to a myriad of health problems.
Such can lead to the presence of calcium in the urine, kidney problems (stones), and calcification of the vessels and tissues.
Despite the health risks associated with deficient or excessive calcium in the body, regular intake of such is recommended largely because of its wide variety of health benefits. For one, it can reduce one’s risk of acquiring hypertension. Similarly, it can lower one’s risk of developing cardiovascular diseases because of calcium’s ability to reduce lipid absorption and promote lipid excretion.
Calcium has also shown some protective effects against colon and rectal cancers. Studies suggest that intake of low-fat dairy sources with high calcium levels is associated with a lower risk of developing the said malignancy.
Calcitonin: The Thyroid Hormone for Calcium Regulation
Responsible for the metabolism of calcium and phosphorous, calcitonin is produced mostly in the C-cells or the parafollicular cells of the thyroid gland.
Calcitonin is widely known to lower the levels of calcium in the blood. It does so by stopping osteoclast activity in the bone.
This then inhibits the release of calcium and phosphorous in the body.
It also works on the kidney by preventing the reabsorption of these two minerals in the kidney tubules, and instead excretes them into the urine.
Because of calcitonin’s action on the body, secretion of this hormone is usually brought about by increased levels of calcium in the body.
Likewise, calcitonin secretion is halted if there is a drop-in calcium levels in the body.
Parathyroid Gland: The Calcium Connection
Calcitonin alone cannot manage blood calcium levels successfully. It works with the hormones of the parathyroid glands, two of which are found behind the thyroid gland. These rice grain-sized glands release parathyroid hormone, which works like Calcitonin.
Apart from controlling the levels of calcium and phosphorous, the parathyroid hormone is also responsible for managing the body’s manganese levels. Over all, these are the effects that the parathyroid hormone exerts on the body:
- Promotes calcium breakdown in order to increase the levels of the said mineral in the bloodstream
- Stimulates the kidney’s secretion of calcitriol, which enhances the absorption of calcium, phosphorous, and magnesium in the intestinal system
- Prevents the excretion of calcium and magnesium in the urine
In stark contrast with Calcitonin, parathyroid hormone is released when calcium levels in the body are low. However, both hormones have to work hand in hand in order to keep the blood calcium in normal ranges.
Because of its effects on calcium regulation, diseases of the Parathyroid gland bring about derangements in blood calcium levels – effects of which bring about the noticeable signs of the disease.
Caused by the over-activity of any of the body’s four parathyroid glands, this disease is characterized by elevated levels of parathyroid hormone in the bloodstream.
There are two types of hyperparathyroidism, one is primary hyperparathyroidism where there is enlargement in one or more parathyroid glands. It can be caused by a benign growth (adenoma) or a cancerous one.
Any of these causes result in an excess of parathyroid hormone, which then leads to hypercalcemia or an increase in blood calcium levels. Surgery is usually recommended for this affliction.
Another disorder is secondary hyperparathyroidism, which results from a prolonged state of low calcium levels in the body. Because of the body’s compensatory mechanisms, this results to heightened levels of parathyroid hormone over time.
Usual culprits behind secondary hyperparathyroidism include severe calcium or Vitamin D deficiency, as well as chronic kidney disease.
Symptoms of hyperparathyroidism include:
- Osteoporosis (fracture-prone and fragile bones)
- Kidney stones
- Increased urination
- Fatigue or tiredness
- Abdominal, bone, or joint pain
- Nausea and vomiting
- Loss of appetite
- Illness with no apparent reason
If you have been diagnosed with hyperparathyroidism, your physician will prescribe you with any of the following medications:
- Calcimimetics, drugs that imitate calcium, thereby fooling the parathyroid glands to release lesser amounts of parathyroid hormone.
- Biphosphonates, drugs which prevent calcium loss in the bones, as well as lessen the degree of osteoporosis caused by the said condition.
- Hormone replacement therapy, prescribed for women who have osteoporosis and have already underwent menopause.
Unfortunately, untreated hyperparathyroidism can lead to a variety of complications. Apart from the worsening of osteoporosis and kidney stones, individuals suffering from this ailment can also develop cardiovascular diseases.
Infants of afflicted pregnant women, on the other hand, can develop neonatal hypothyroidism, a disorder characterized by low calcium levels in the body.
A reverse of the aforementioned disorder, hypoparathyroidism is characterized by low levels of parathyroid hormone, which results to low levels of calcium and increased amounts of phosphorous in the bloodstream.
This can be caused by accidental removal or damage to the parathyroid glands, radiation treatment on the face and neck, autoimmune diseases, hereditary causes, as well as sub-optimal magnesium levels in the body. Signs and symptoms of hypoparathyroidism include:
- Tiredness or weakness
- Anxiety or depression
- Coarse and dry skin
- Brittle nails
- Burning/tingling sensation in the lips, fingers, and toes
- Spasms and twitches around the mouth, throat, hands, and arms
- Muscles pains and aches
- Painful menstrual periods
Calcium and phosphorous supplements are prescribed to treat this condition. However, if symptoms are left uncured, spasms and the burning/tingling sensation can occur for a longer period of time.
Other complications that can develop include deformed teeth, fainting spells, seizures, kidney problems, and irregular heart rhythms.
Unfortunately, irreversible complications can occur following untreated hypoparathyroidism. These include cataracts, calcium deposits in the brain, delayed mental development and short stature in children of affected mothers.
How Thyroid Disorders Affect Calcium Levels in the Body
Indeed, the thyroid gland helps regulate the calcium levels in the body. For one, it produces the hormone calcitonin that works by decreasing the available amount of calcium in the bloodstream.
As such, when the thyroid gland is in a state of disarray, calcium concentrations in the body can be affected as well.
In a 2011 study by Dhanwal, it was determined that “Thyroid hormones have direct catabolic effect on bone mineral homeostasis, leading to increased bone mineral resorption and calcium loss through kidneys.”
This was traced back to the early days when thyroid drugs were not available yet. Hyperthyroid patients showed signs of what was known as “Hyperthyroid bone disease,” wherein bones were noted to be friable and easily fractured.
As such, it comes as no surprise that hyperthyroidism caused secondary osteoporosis in most cases.
Although this is the case, it was noted that symptoms dissipate once the person reaches a euthyroid (normal thyroid) state.
Whether the person was treated with surgery, medication or radiation, hypercalcemia usually subsides once hyperthyroidism has been corrected. This has been noted in the study made by Krolner, Jorgensen, and Nielsen. Results showed that hyperthyroid patients had 12.5% lesser bone mineral content compared to those who did not have the disease. However, the bone mineral content increased by 3.7% after a year of proper thyroid treatment.
Because of hyperthyroidism’s effects on the bones, diagnostic tools such as the Dual-Energy X-ray Absorptiometry or DEXA has been used to determine the underpinnings of bone disorders associated with the disease.
Apart from hyperthyroidism’s effect on the bones, it was also noted that most hyperthyroid patients have normal or pronounced calcium levels in the blood (hypercalcemia), and these have been correlated with their T3 levels.
Likewise, calcium excretion through the urine has also been noted, even if the person is on a low-calcium diet.
Relatedly, a decrease in parathyroid hormone secretion has also been seen in hyperthyroid patients. This has been attributed to the high levels of calcium in the bloodstream that inhibit the secretion of the said hormone.
While one would suspect that hypothyroidism’s effects on the bones would be opposite to that of hyperthyroidism, it is not the case. Similarly, both sides suffer from a case of brittle bones that easily fracture.
In a study by Begic-Karup et al, it was determined that 33 of the patients with serum calcium levels below 2.1 mmol/L were hypothyroid.
The fracture risk for hypothyroid patients exist before and after the diagnosis of the disease, and this is attributed to poor bone quality.
This occurs despite an increase in bone density – due in part by the release of parathyroid hormone, which is stimulated because of the decreased levels of calcium in the bloodstream.
Sadly, even if calcium supplements can help reverse bone demineralization, studies show that it can have a negative consequence on hypothyroid patients. Perhaps that is why most thyroid supplements do not include calcium.
According to Dr. Jerome Hershman, calcium can prevent the absorption of thyroxine, a drug used to cure an underactive thyroid. In most individuals, these are taken simultaneously in the morning – thyroxine before breakfast – and calcium after eating.
Hershman adds that to prevent untoward interactions between the two drugs, patients should take these medications at least 6 to 12 hours apart.
Calcium plays a vital role in many body processes.
As such, it is important that those with thyroid disorders be treated accordingly so as to prevent the harmful effects of resulting hyper- and hypocalcemia.
If you take Levothyroxine or other thyroid medications already, it would be best to avoid Calcium unless specifically instructed by your doctor.
Begic-Karup, S., Wagner, B., Raber, W., Schneider, B., Hamwi, A., Waldhausl, W., & Vierhapper, H. (2001). Serum calcium in thyroid disease. [Abstract]. Wien Klin Wochenschr., 15(113), 1-2. Retrieved October 18, 2017, from https://www.ncbi.nlm.nih.gov/pubmed/11233472.
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Krolner, B., Jorgensen, J. V., & Nielsen, S. P. (1983). Spinal bone mineral content in myxoedema and thyrotoxicosis. Effects of thyroid hormone(s) and antithyroid treatment. [Abstract]. Clinical Endocrinology, 18(5), 439-446. Retrieved October 18, 2017, from https://www.ncbi.nlm.nih.gov/pubmed/6603290/.
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