Submitted to: Meeting Abstract
Publication Type: Abstract only
Publication Acceptance Date: 7/15/2006
Publication Date: 10/23/2006
Citation: Nielsen, F.H. 2006. Dietary magnesium deprivation decreases magnesium balance and urinary calcium excretion, increases sublingual cellular calcium and potassium concentrations, and decreases circulating neuropeptide Y and gluthathione concentrations in postmenopausal women [abstract]. 11th International Magnesium Symposium, October 23-26, 2006, Kashikojima, Japan. Program and Abstracts. p.O-13. Interpretive Summary:
Technical Abstract: An experiment was performed with the objective of determining whether a low dietary intake of magnesium impaired bone health other than through affecting parathyroid hormone and vitamin D action, and impaired cardiovascular health other than through affecting lipid metabolism. Eighteen postmenopausal women were recruited to participate and 13 women completed the 174-d experiment as designed. The women resided in a metabolic unit that provided a common environment for strict control of food consumption, weight, exercise, and data collection, and were fed a basal Western-type diet that provided about 112 mg Mg/d. Each woman consumed the basal diet supplemented with 100 mg Mg/d for the first 42 d, then the basal diet for 84 d, and finally the basal diet supplemented with 200 mg Mg/d for 48 d. Magnesium balance, which did not include surface or phlebotomy losses, approached zero during the 84-d magnesium deprivation period and was highly positive (50 mg/d) when dietary magnesium was about 300 mg/d. The 84-d magnesium deprivation induced biochemical changes suggesting a pro-inflammatory response and increased oxidative stress. Magnesium deprivation significantly decreased urinary calcium excretion. As a result, calcium balance was slightly higher when dietary magnesium was low than when dietary magnesium was about 300 mg/d. These findings suggest magnesium deprivation resulted in increased calcium retention. Some of the calcium apparently was retained intracellularly in soft tissue because magnesium deprivation also increased sublingual cellular calcium. The increased intracellular calcium may have altered the release of neuropeptides into the circulation because magnesium deprivation decreased neuropeptide Y, and apparently increased substance P (based on values from 7 women) in plasma. Increased white blood cell counts, decreased whole blood glutathione, and decreased plasma copper suggest that magnesium deprivation increased oxidative stress. Reports by other groups indicate that a moderate magnesium deficiency also induces soft tissue calcium retention, increases circulating pro-inflammatory neuropeptides, and increases oxidative stress in experimental animals. These biochemical changes have been associated with impaired bone and cardiovascular health in experimental animals. Thus, the findings from the described human experiment suggest that plausible low dietary magnesium intakes have functional and biochemical consequences related to impaired bone and cardiovascular health. Because a recent United States nutrition survey (NHANES 2001-2002) found that 5% of all women over the age of 19 yr consume 128 mg Mg/d or less, increased magnesium intakes may be beneficial to a significant number of women.