Parathyroid glands are four tiny glands found in our neck right next to our thyroid gland. As part of our endocrine system, these glands produce parathyroid hormone (PTH). Along with vitamin D and calcitonin (a hormone produced by the thyroid gland), PTH regulates the calcium and phosphorus homeostasis in the bloodstream, a crucial process in bone growth and bone cell activity.
When these parathyroid glands are under-active, they have the challenge of producing enough PTH, resulting in a rare condition called hypoparathyroidism in which an individual may exhibit an abnormally low level of calcium (hypocalcemia), a high level of phosphorus (hyperphosphatemia), and sometimes low level of vitamin D and magnesium in the blood.
For those who have had a partial or complete thyroidectomy, please read this carefully: The most common cause of hypoparathyroidism is the accidental removal of the parathyroid glands due to thyroidectomy. Hypoparathyroidism can also be associated with low or high serum magnesium levels, autoimmune processes, intense radiation treatment in the neck area, congenital hypoparathyroidism, or other underlying disorders. In rare cases, it may occur as a genetic disorder.
HYPOPARATHYROIDISM OF RENAL DYSFUNCTION
Individuals with hypoparathyroidism are at risk of hypocalcemia and hyperphosphatemia. Not only the imbalance between calcium and phosphorus levels could cause a variety of symptoms, including weakness, nervousness, headaches, uncontrollable twitching, muscle cramps and spasms, and numbness and tingling around the mouth and in the fingers and toes. It could also have the following long-term severe health implications:
Too much phosphorus in the blood can pull calcium out of our bones, compromising bone density. In addition, even though conventional treatment with calcium and active vitamin D can maintain the serum calcium level, high doses of these treatments may sometimes be required, adding to the risk of long-term soft tissue calcifications. This puts patients at risk for various health conditions impacting different body systems, and kidneys are a major target organ for complications. A study with 100 hypoparathyroidism patients reported a substantial 40% who demonstrated chronic renal dysfunction between stages 3 and 5. One condition is nephrocalcinosis, known as an asymptomatic disorder where calcium deposition occurs in the kidneys and gradually progresses to renal abnormalities and renal insufficiency.
DIETARY STRATEGIES FOR MANAGING HYPOPARATHYROIDISM
Besides dietary strategies for maintaining a clean anti-inflammatory diet, it’s also beneficial to keep a relatively low phosphorus dietary intake.3 But there are a few challenges: First, it is challenging to limit phosphate intake while attempting to meet the recommended daily protein intake. Second, many foods, especially healthy ones, contain a decent amount of phosphorus, making it impossible to avoid all of these foods. Therefore, the approach of avoiding as many high-phosphorus-containing foods as possible is not practical. Instead, I recommend watching the phosphorus intake and only consuming those foods high in phosphorus in moderation.
Examples of high phosphorus-containing foods: dairy products, animal and organ meats, seafood, fish, legumes, soy, bran cereals, almonds, chocolate, soft drinks, and other beverage products.
Example of low phosphorus-containing foods: Most fresh fruits and vegetables contain a low amount of phosphorus, except for avocados, potatoes, pumpkins, and artichokes have a medium level of phosphorus content. There are some low- phosphorus grains, such as white rice, brown rice, and whole wheat.
In addition, there is another crucial dietary aspect to keep in mind:
There are three different sources of dietary phosphorus: organic phosphorus in plant foods with 20%–40% bioavailability, organic phosphorus in animal protein with 40%–60% bioavailability, and inorganic phosphorus from additives in processed food with 100% bioavailability.4. Needless to say, avoiding processed foods is a “no-brainer” principle, and the whole-food-based dietary approach should be the first-line approach.
Natpara has been the only PTH replacement therapy approved by the FDA for hypoparathyroidism. It’s a synthetic form of PTH, intended to be used in combination with Calcitriol (an active form of vitamin D) or vitamin D3 supplement and calcium supplement. Unfortunately, Natpara was recalled in 2019 in the U.S. With it being unavailable, endocrinologists would consider the use of Thiazide diuretics to help with reducing urine calcium excretion and increase renal calcium reabsorption.
I will now focus on discussing using calcium and vitamin D supplements to maintain calcium concentrations. The warning here is that it can be challenging to maintain the balance between providing adequate treatment to avoid hypocalcemia and avoiding over-treatment, increasing the risk of excess urinary calcium excretion and nephrocalcinosis. It’s recommended to keep the serum calcium level at the lower end of the normal lab reference range.
Here are some of my more detailed recommendations on the supplements:
Vitamin D3: 2,000 – 10,000 IU/day. This is highly individual, and I recommend closely monitoring serum vitamin D levels (both 25-hydroxy Vitamin D and vitamin D-1,25-Dihydroxy) regularly to ensure the levels are within optimal ranges.
Calcium Citrate or Malate: Citrate and Malate are the most absorbable forms of calcium supplements. The commonly used dosage is 1,000 – 1,200 mg/day. Again, it’s crucial to monitor the serum calcium level to ensure it stays at the lower end of the range.
Dealing with any chronic health issue is never easy. But if we can focus on getting our body what it needs rather than what makes it perfect, it may feel a lot easier.
Jenny Noland, MS, CNS, CNGS, CKNS, LDN, MBA
Functional Nutritionist in Eugene, Oregon
Board-Certified Nutrition Specialist
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Bilezikian JP. Hypoparathyroidism. J Clin Endocrinol Metab. 2020;105(6):1722. doi:10.1210/CLINEM/DGAA113
Levy I, Licht C, Daneman A, Sochett E, Harrington J. The Impact of Hypoparathyroidism Treatment on the Kidney in Children: Long-Term Retrospective Follow-Up Study. J Clin Endocrinol Metab. 2015;100(11):4106-4113. doi:10.1210/JC.2015-2257
Suki WN, Moore LW. Phosphorus Regulation in Chronic Kidney Disease. Methodist Debakey Cardiovasc J. 2016;12(4 Suppl):6. doi:10.14797/MDCJ-12-4S1-6
Umeukeje EM, Mixon AS, Cavanaugh KL. Phosphate-control adherence in hemodialysis patients: current perspectives. Patient Prefer Adherence. 2018;12:1175. doi:10.2147/PPA.S145648
Rubin MR. Recent advances in understanding and managing hypoparathyroidism. F1000Research. 2020;9. doi:10.12688/F1000RESEARCH.22717.1