According to a recent fact sheet from the National Institutes of Health (NIH), older adults are at increased risk of magnesium deficiency. Factors that contribute to this are decreased Intestinal absorption of magnesium in older people and a greater excretion of it via the kidneys. In addition, the NIH Health and Nutrition Surveys found that older adults have lower dietary intakes of magnesium. The diseases to which the elderly are vulnerable, and some of the drugs used in therapy, also contribute to magnesium loss.
A lack of magnesium is also associated with osteoporosis. Bone health is supported by many factors, most notably calcium and vitamin D. However, some evidence suggests that magnesium deficiency may be an additional risk factor for postmenopausal osteoporosis. This may be due to the fact that magnesium deficiency alters calcium metabolism and the hormones that regulate calcium. In one study of older adults, a greater magnesium intake maintained bone mineral density to a higher degree than a lower intake.
Magnesium deficiency: Possible role in osteoporosis associated with gluten-sensitive enteropathy
Osteoporosis and magnesium (Mg) deficiency often occur in malabsorption syndromes such as gluten-sensitive enteropathy (GSE). Mg deficiency is known to impair parathyroid hormone (PTH) secretion and action in humans and will result in osteopenia and increased skeletal fragility in animal models. We hypothesize that Mg depletion may contribute to the osteoporosis associated with malabsorption. It was our objective to determine Mg status and bone mass in GSE patients who were clinically asymptomatic and on a stable gluten-free diet, as well as their response to Mg therapy. Twenty-three patients with biopsy-proven GSE on a gluten-free diet were assessed for Mg deficiency by determination of the serum Mg, red blood cell (RBC) and lymphocyte free Mg2+, and total lymphocyte Mg. Fourteen subjects completed a 3-month treatment period in which they were given 504-576 mg MgCl2 or Mg lactate daily. Serum PTH, 25-hydroxyvitamin D, 1,25-dihydroxyvitamin D and osteocalcin were measured at baseline and monthly thereafter. Eight patients who had documented Mg depletion (RBC Mg2+ < 150 microM) underwent bone density measurements of the lumbar spine and proximal femur, and 5 of these patients were followed for 2 years on magnesium therapy. The mean serum Mg, calcium, phosphorus and alkaline phosphatase concentrations were in the normal range. Most serum calcium values fell below mean normal and the baseline serum PTH was high normal or slightly elevated in 7 of the 14 subjects who completed the 3-month treatment period. No correlation with the serum calcium was noted, however. Mean serum 25-hydroxyvitamin D, 1,25-dihydroxy vitamin D and osteocalcin concentrations were also normal. Despite only 1 patient having hypomagnesemia, the RBC Mg2+ (153 + or - 6.2 microM; mean plus or minus SEM) and lymphocyte Mg2+ (182 plus or minus 5.5 microM) were significantly lower than normal (202 + or - 6.0 microM, P < 0.001, and 198 + or - 6.8 microM, p < 0.05, respectively). Bone densitometry revealed that 4 of 8 patients had osteoporosis of the lumbar spine and 5 of 8 had osteoporosis of the proximal femur (T-scores less than or equal to -2.5).
Mg therapy resulted in a significant rise in the mean serum PTH concentration from 44.6 + or - 3.6 pg/ml to 55.9 plus or minus 5.6 pg/ml (p < 0.05). In the 5 patients given magnesium supplements for 2 years, a significant increased in bone mineral density was observed in the femoral neck and total proximal femur. This increase in bone mineral density correlated positively with a rise in RBC Mg2+. This study demonstrates that GSE patients have reduction in intracellular free Mg2+, despite being clinically asymptomatic on a gluten-free diet. Bone mass also appears to be reduced. Mg therapy resulted in a rise in PTH, suggesting that the intracellular magnesium deficit was impairing PTH secretion in these patients. The increase in bone density in response to Mg therapy suggests that Mg depletion may be one factor contributing to osteoporosis in GSE.
Osteoporosis: Calcium and Magnesium
There are many forms of calcium supplements available. However, in order to be effective, calcium must be properly absorbed by the body. Look for chelated forms of calcium (calcium citrate, calcium lactate, or calcium gluconate) because it is the easiest form for most people to absorb. The recommended amount of calcium is 1000mg to 1500 mg per day. However, since your body can't absorb more than about 500 mg of calcium at a time, you should divide your doses and take them at different times of the day. Also, for maximum absorption, take your calcium supplements with food.
Magnesium is a mineral that plays an important role in maintaining healthy bones. It contributes to increased bone density and helps prevent the onset of osteoporosis. Most people do not get enough magnesium in their diets, especially if they eat large amounts of processed foods in which much of the magnesium is removed.
Since magnesium works closely with calcium, it is important to have an appropriate ratio of both minerals in order for them to be effective. A good rule of thumb is a 2:1 calcium-to-magnesium ratio. For example, if you take 1000mg of calcium, you should also take 500mg of magnesium.
The recommended amount of magnesium is 300mg to 500mg daily. As with calcium, chelated forms of magnesium are absorbed best by the body. Magnesium oxide is also available and is often less expensive, but it is poorly absorbed by the body. Since high doses of magnesium can cause diarrhea, you should divide your doses and take them with meals throughout the day.
You can also increase your intake of magnesium by eating magnesium-rich foods. Food sources that are high in magnesium include: brown rice, buckwheat, corn, legumes, seeds, whole grain cereals.