Prednisone can affect this through 3 different nutrient pathways: Potassium, Calcium, Selenium. This medication is commonly used for Inflammation.
Each nutrient below contributes to this impact through a different mechanism.
Potassium deficiency can progress from diffuse muscle weakness to flaccid paralysis, and in severe hypokalemia this paralysis may involve the diaphragm and other respiratory muscles, resulting in hypoventilation and acute respiratory failure. In these situations, patients often present with ascending weakness, areflexia, and shortness of breath or an inability to take a deep breath, and may require urgent ventilatory support while intravenous potassium is carefully replaced. Case reports and cohort data show that even admission potassium values just below the normal range are associated with a higher risk of needing mechanical ventilation in hospitalized patients, underscoring the importance of promptly recognizing and correcting hypokalemia before it reaches paralysis‑level severity.
Sobrosa P Sr, Ferreira Â, Vilar da Mota R, Couto J, Sousa L. Severe Hypokalemia and Respiratory Muscle Paralysis: An Atypical Manifestation of Primary Sjögren's Syndrome. Cureus. 2024 Dec 23;16(12):e76240. Alemu GK, Asfaw SA, Asres LS, Kassa BY. Severe Life-Threatening Hypokalemia Primarily Presented With Isolated Paralysis: Case Series From Ethiopia. Clin Case Rep. 2025 Jan 6;13(1):e70062. Pande AR, Rai N, Manchanda S, Srivastava A, Agarwal S, Srivastava IC, Awasthi A. The Critical Care Phenotype of Hypokalemic Paralysis: Etiology, Outcomes, and Predictors of Respiratory Failure in a Retrospective Cohort Study. Cureus. 2026 Feb 18;18(2):e103865. Gombar S, Mathew PJ, Gombar KK, D'Cruz S, Goyal G. Acute respiratory failure due to hypokalaemic muscular paralysis from renal tubular acidosis. Anaesth Intensive Care. 2005 Oct;33(5):656-8.
Low calcium levels overstimulate nerves and muscles, leading to muscle cramps, spasms, and twitching. More significant deficiency can cause tetany, a state of sustained, painful muscle contractions often with carpopedal spasms and tingling around the mouth, hands, and feet. In severe cases, untreated hypocalcemia may progress to breathing difficulties from laryngospasm, seizures, abnormal heart rhythms, and other potentially life‑threatening complications.
Agrawal A, Suryakumar G, Rathor R. Role of defective Ca2+ signaling in skeletal muscle weakness: Pharmacological implications. J Cell Commun Signal. 2018 Dec;12(4):645-659. Uday S, Högler W. Nutritional Rickets and Osteomalacia in the Twenty-first Century: Revised Concepts, Public Health, and Prevention Strategies. Curr Osteoporos Rep. 2017 Aug;15(4):293-302. Basma A. Dahash, et al. Rickets. StatPearls August 7, 2023. Seema M. Policepatil, et al. Hypocalcemic Myopathy Secondary to Hypoparathyroidism.Aloke A, Singh K. An Unusual Presentation of Multifactorial Hypocalcemia as Myopathy: A Case Report. Cureus. 2025 Jul 7;17(7):e87434.
When selenium status is chronically low, deficiency can produce a characteristic myopathy marked by skeletal muscle weakness and fatigue driven by impaired antioxidant defenses and damage to mitochondrial membranes and contractile fibers. Case reports in patients maintained on long‑term selenium‑deficient parenteral nutrition describe prominent proximal muscle weakness, elevated muscle enzymes, and biopsy findings of mitochondrial abnormalities that improve after selenium is added back. Because this selenium‑deficient myopathy tends to arise in the setting of chronic, severe deficiency, recognizing the pattern of otherwise unexplained weakness in high‑risk patients is important, since targeted selenium repletion can lead to meaningful functional recovery.
Hiroyuki Ishihara, et al. White muscle disease in humans: myopathy caused by selenium deficiency in anorexia nervosa under long term total parenteral nutrition. P.I. Mansell, et al. Journal of Neurology, Neurosurgery & Psychiatry 1999;67:829-830. Reversal of a skeletal myopathy with selenium supplementation in a patient on home parenteral nutrition. Clinical Nutrition. Volume 6, Issue 3, August 1987, Pages 179-183. Osaki, Y., Nishino, I., Murakami, N., Matsubayashi, K., Tsuda, K., Yokoyama, Y.-I., Morita, M., Onishi, S., Goto, Y.-I. and Nonaka, I. (1998), Mitochondrial abnormalities in selenium-deficient myopathy. Muscle Nerve, 21: 637-639. Chariot, P. and Bignani, O. (2003), Skeletal muscle disorders associated with selenium deficiency in humans. Muscle Nerve, 27: 662-668.
Some side effects may be linked to nutrient depletion caused by this medication.
Research has found that corticosteroids increased chromium excretion in patients after just three days. Chromium is an essential mineral that helps regulate blood sugar levels. This is important because corticosteroids themselves can raise blood sugar, contributing to diabetes. Evidence suggests that chromium supplementation improved fasting blood glucose levels in patients with steroid-induced diabetes.
Maintaining healthy potassium levels is important when taking corticosteroids. These medications can increase the amount of potassium the body loses through urine. Potassium is a vital mineral that helps muscles and nerves function properly. While short-term use of corticosteroids might not cause significant problems, studies suggest that with prolonged treatment, the body's ability to maintain proper potassium balance (homeostasis) can be affected.
Corticosteroids can lower calcium levels in the body. This is a double threat to bone health because corticosteroids themselves can weaken bones. Calcium is essential for strong bones, and a study showed that supplementing with both calcium and vitamin D3 helped prevent bone loss in people with rheumatoid arthritis taking corticosteroids. Supplementation with calcium should be considered during long term corticosteroid therapy.
Corticosteroids can increase the urinary loss of selenium elevating the risk for deficient levels. Selenium is a mineral that acts as an antioxidant, helping protect cells from damage. Studies have shown that rheumatoid arthritis patients taking high doses of corticosteroids tend to have lower selenium levels. This is concerning because low selenium intake is linked to osteoporosis, and selenium has been shown to play a role in bone protection in animal models of corticosteroid-induced osteoporosis. Supplementation with selenium should be considered during long term corticosteroid therapy.
Corticosteroids can increase the body's excretion of magnesium, potentially leading to a deficiency. This is concerning because magnesium plays a vital role in many bodily functions, including muscle and nerve function. Research suggests that magnesium supplementation alleviated corticosteroid therapy associated muscle atrophy. Supplementation with magnesium should be considered during long term corticosteroid therapy.
Research suggests corticosteroids can lower vitamin D levels in the body by increasing its breakdown. This is a concern because vitamin D plays a crucial role in bone health and the immune system, and corticosteroids themselves can weaken bones. A study found that calcium and vitamin D3 supplements helped prevent bone loss in the lower back (lumbar spine) and hip (trochanter) for people with rheumatoid arthritis who were on low-dose corticosteroids. Evidence suggests vitamin D may work synergistically together with corticosteroids to improve asthma treatment by boosting the effectiveness of corticosteroids or by overcoming resistance to these medications in some patients.