It's disturbing to me that consumers will ponder a menu for much longer than they will the side effects associated with their medications. And even those who do look up their medicine or ask their pharmacist still don't know that drugs can mug the body of nutrients, the very nutrients you need to stay healthy, to see clearly, have energy, keep you free of pain and maintain a happy mood.
Surprised? Most people are, and I can say that safely because I've been a pharmacist for 23 years, and I always get the same look when I tell people they need to "marry" their medicine with the right nutrient(s) to minimize or avoid (or reverse) side effects.
Don't believe me? Let's delve a little deeper into this.
Corticosteroids are medications used frequently this time of year and in the springtime for inflammatory conditions and disorders associated with a hyper-reactive immune response. Thus, corticosteroids are well-known for their anti-inflammatory and and immunosuppressant activity on the body. The most commonly-prescribed medications in this class include prednisone and hydrocortisone, and as an aside, these drugs are also classically used for various autoimmune disorders like lupus, multiple sclerosis and rheumatoid arthritis. Methylprednisolone is another corticosteroid that is sometimes used.
Corticosteroid treatment has been associated with many side effects. The most noted is increased loss of bone mineral density, causing a predisposition to osteoporosis. It is a proven fact that calcium is needed for healthy bones, and studies show that corticosteroids can suppress calcium absorption, as well as increase calcium excretion. In 1998, a study showed that low dosages (10 mg per day) of prednisone led to a reduction in osteocalcin, P1CP (Propeptide of Type 1 Procollagen) and alkaline phosphatase, as well an increase in the urinary excretion of calcium. Bone formation decreased, whereas resorption remained unchanged (or decreased slightly). Clearly, corticosteroids have a negative impact on bone metabolism. 
Corticosteroids also interfere with calcium through an indirect mechanism, by interfering with the body's ability to activate vitamin D and thus, increase risk of bone loss. Giving cortisone produces a decrease of net calcium absorption (under active transport conditions) via two different mechanisms: by depressing vitamin D-dependent calcium absorption and also by increasing vitamin D-independent calcium back flux. 
Calcium deficiency shows up with such symptoms as neuropathy (numbness or tingling in the hands and feet), convulsions, cardiac irregularities, bowel problems and osteopenia, as well as osteoporosis. Those last two lead to fractures in susceptible folks. People on corticosteroids would likely benefit from a high-quality form of calcium to replenish what the drug mugger stole.
Starting to believe me yet?
There is also evidence to suggest that corticosteroids may reduce serum magnesium levels. A study with 95 patients suffering from chronic airway obstruction displayed reduced magnesium levels after receiving long-term oral corticosteroid therapy. The amount of magnesium depletion was greater with prolonged usage.  Do you know what happens to you when you develop a deficiency of magnesium? It isn't pretty, but luckily it's easy to correct. Magnesium deficiency leads to constipation, body odor, insomnia, migraines or headaches, widespread body aches, weakness, chronic fatigue, nausea, cardiac arrhythmias of all sorts, and possibly a heart attack in severe cases. It causes depression, tearfulness, irritability, and suicideal ideation. It can contribute to pancreatic difficulties and diabetes. If you know of anyone who has been taking corticosteroids, either by mouth, or inhaled, and they have any of the symptoms related to calcium or magnesium deficiency, it's due -- at least in part -- to the drug-nutrient depletion effect, what I affectionately call the "drug mugger" effect.
The subject of mineral depletion and corticosteroid use is not limited to calcium and magnesium. There are studies to indicate that other minerals are affected by these medications. In fact, both animal and human studies point to a potassium depletion associated with steroid medications. [3, 4] According to the European Journal of Clinical Pharmacology, "Oral or parenteral administration of glucocorticoids (prednisone 5 to 2,000 mg/d) was a significant risk factor for hypokalaemic events."
Hypokalemia refers to the condition of low potassium. The hypokalemic effect appears to be dose-dependent and more significant with long-term usage of these medications. 
Zinc and copper are two other nutrients that are depleted during corticosteroid use treatment. This was first seen in a study in patients with RA (rheumatoid arthritis) in 1989. The mechanism by which this occurs appears to be due to enhanced urinary excretion of zinc and copper.  Plasma zinc levels are commonly reduced in this patient population, but the levels will plummet further with only 10 mg prednisone daily. In 1993, researchers who conducted a study published in Clinical and Experimental Rheumatology stated, "Conversely, plasma zinc was found to be lower in RA patients taking NSAIDs and/or steroids." This comment further supports the notion that corticosteroids may impact plasma zinc levels. 
Even though we do not thoroughly understand the mechanism of action by which selenium is depleted, there is a study from 1987 showing that corticosteroid use will significantly reduce selenium stores. It appears that the higher dosages of 20-60 mg prednisolone per day can suppress plasma selenium levels in some patients -- those with rheumatoid arthritis were the ones studied.  Selenium is an important mineral antioxidant that supports thyroid, prostate and immune system health.
Vitamin D may be affected by corticosteroid therapy. It is useful to include calcium and vitamin D supplements in the patient population taking these anti-inflammatory drugs to counteract steroid-induced osteoporosis. [8, 9, 10, 11, 12] A deficiency of vitamin D can exacerbate problems for those with autoimmune disorders, and low D reduces our ability to fight infections. Low D has also been tied to a higher incidence of many cancers, including those of the prostate and breast. 
In summary, the drug nutrient depletion effect is well-documented, even though most consumers do not know about it. The best thing to do is to ask your doctor about taking a supplement that contains all these minerals, so as to restore healthy levels of these minerals. Products such as Hawaiian Spirulina, Trace Minerals, and Multi-Mineral supplements are sold by various makers at health food stores worldwide.
For more information on drug nutrient depletion, read my book Drug Muggers, Which Medications are Robbing Your Body of Essential Nutrients and Natural Ways to Restore Them.
1. Lems WF, Van Veen GJ, Gerrits MI, Jacobs JW, Houben HH, Van Rijn HJ, Bijlsma JW. Effect of low-dose prednisone (with calcium and calcitriol supplementation) on calcium and bone metabolism in healthy volunteers. Br J Rheumatol. 1998 Jan;37(1):27-33.
2. Rolla G, Bucca C, Bugiani M, Oliva A, Branciforte L. Hypomagnesemia in chronic obstructive lung disease: effect of therapy. Magnes Trace Elem. 1990;9(3):132-6.
3. Widmer P, Maibach R, Kunzi UP, Capaul R, Mueller U, Galeazzi R, Hoigne R. Diuretic-related hypokalaemia: the role of diuretics, potassium supplements, glucocorticoids and beta 2-adrenoceptor agonists. Results from the comprehensive hospital drug monitoring programme, berne (CHDM). Eur J Clin Pharmacol. 1995;49(1-2):31-6.
4. Shenfield GM, Knowles GK, Thomas N, Paterson JW. Potassium supplements in patients treated with corticosteroids. Br J Dis Chest. 1975 Jul;69:171-6.
5. Peretz A, Neve J, Famaey JP. Effects of chronic and acute corticosteroid therapy on zinc and copper status in rheumatoid arthritis patients. J Trace Elem Electrolytes Health Dis. 1989 Jun;3(2):103-8.
6. Milanino R, Frigo A, Bambara LM, Marrella M, Moretti U, Pasqualicchio M, Biasi D, Gasperini R, Mainenti L, Velo GP. Clin Exp Rheumatol. 1993 May-Jun;11(3):271-81.
7. Peretz A, Neve J, Vertongen F, Famaey JP, Molle L. Selenium status in relation to clinical variables and corticosteroid treatment in rheumatoid arthritis. J Rheumatol. 1987 Dec;14(6):1104-7.8. Yeh JK, Aloia JF, Semla HM. Calcif Tissue Int 1984 Sep;36(5):608-614.
9. O'Regan S, Chesney RW, Hamstra A, Eisman JA, O'Gorman AM, Deluca HF. Reduced serum 1,25-(OH)2 vitamin D3 levels in prednisone-treated adolescents with systemic lupus erythematosus. Acta Paediatr Scand. 1979 Jan;68(1):109-11.
10. Chesney RW, Mazess RB, Hamstra AJ, DeLuca HF, O'Reagan S. Reduction of serum-1, 25-dihydroxyvitamin-D3 in children receiving glucocorticoids. Lancet. 1978 Nov 25;2(8100):1123-5.
11. Nuti R, Vattimo A, Turchetti V, Righi G. 25-Hydroxycholecalciferol as an antagonist of adverse corticosteroid effects on phosphate and calcium metabolism in man. J Endocrinol Invest. 1984 Oct;7(5):445-8.
12. Lund B, Andersen RB, Friis T, Hjorth L, Jørgensen FS, Norman AW, Sørensen OH.Effect of 1 alpha-hydroxyvitamin D3 and 1,25-dihydroxyvitamin D3 on intestine and bone in glucocorticoid-treated patients. Clin Endocrinol (Oxf). 1977 Dec;7 Suppl:177s-181s.
13. Lappe JM, Travers-Gustafson D, Davies KM, Recker RR, Heaney RP. Vitamin D and
calcium supplementation reduces cancer risk: results of a randomized trial. Am J
Clin Nutr. 2007 Jun;85(6):1586-91. Erratum in: Am J Clin Nutr. 2008
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