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2 University of Göteborg, Gothenburg, Sweden; 3 Research Institute of Child Nutrition, 44225 Dortmund, Germany; and 4 Institute for Prevention and Nutrition, 85733 Ismaning, Germany
* To whom correspondence should be addressed. E-mail: envhealth{at}biofact.se.
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ABSTRACT |
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 TOP ABSTRACT IntroductionMaterials and MethodsResultsDiscussionLITERATURE CITED |
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Introduction |
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TOPABSTRACTIntroductionMaterials and MethodsResultsDiscussionLITERATURE CITED |
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A deficiency of minerals can arise from a suboptimal dietary intake. An evaluation of nutritional habits during human evolution demonstrates that diets introduced when farming commenced and when industrialization took place resulted in important changes in terms of an increased intake of grains and animal proteins, a lower intake of minerals, and a higher intake of sodium and simple sugars (5,6). These changes have become even more pronounced in today's city life and fast food consumption.
The consumption of animal protein, grain, and high amounts of milk increases the acidity of the body, whereas foods rich in minerals such as green vegetables and fruit increase the alkalinity (7). Generally, the Western diet induces a chronic, low-grade metabolic acidosis (8,9). Acidosis influences the homeostasis of calcium, partly due to the influence on renal mechanisms. A number of diet intervention studies have reported a relation between an increase in the body's acid load and an increase in renal calcium losses (10,11). This mechanism may also influence the homeostasis of magnesium. There are several studies indicating a number of similarities between renal handling of magnesium and calcium (12,13) suggesting that acid-base also has an effect on magnesium, similar to that of calcium. In children with distal tubular acidosis, metabolic acidosis has been found to block the reabsorption of magnesium in the tubuli and increase urine magnesium excretion (14). There are, however, no studies on the influence of acid-base status on renal magnesium excretion in a normal population of healthy individuals.
Regarding acid-base regulation, the elderly have a decreased renal function (9) that affects the capacity of the kidneys to excrete acid, leading to a lower blood pH and a reduced plasma bicarbonate concentration (15). In view of their generally lower intake of fruit and vegetables (9,16) they thus constitute a risk group for acid conditions and hence an increased secretion of calcium and possibly magnesium.
In this study, we investigated whether the urinary excretion of magnesium was related to acid conditions in terms of net endogenous acid production (NEAP) in healthy, elderly subjects.
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Materials and Methods |
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TOPABSTRACTIntroductionMaterials and MethodsResultsDiscussionLITERATURE CITED |
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From the population sample, 230 subjects were selected at random and contacted by letter, inviting them to join the study with the information that the purpose of the investigation was to evaluate their mineral homeostasis and acid-base conditions. From the selected sample, 112 subjects were willing to participate. They answered a questionnaire on previous and present disease. Exclusion criteria were kidney disease, diabetes, and a regular intake of medication and supplements that could influence the mineral homeostasis. Eight subjects who were taking medication that could influence the mineral balance and another 10 with serious illness were excluded.
Urine collection and analysis. Each subject collected a single 24-h urine sample and the aliquots were deep frozen immediately. They were instructed to retain their normal dietary habits during the urine collection, but dietary intake data were not collected. Dietary protein and potassium intakes were estimated from 24-h urinary nitrogen and potassium, taking average absorption coefficients (protein 75%; potassium 80%) into consideration (17,18). The urinary analysis comprised magnesium, potassium, and calcium quantified by flame atomic absorption spectrometry (12). NEAP was determined by measuring net acid excretion (NAE) according to established methods (8,19). For this, titratable acidity, ammonium, and bicarbonate were quantified and NAE was calculated as the sum of titratable acidity plus ammonium minus bicarbonate. Total nitrogen was measured by the Kjeldahl technique (Buechi 430 Digestor and Buechi Distillation Unit B-324).
Based upon the results from the urine analysis, 8 subjects were excluded because of inadequate urine sampling (subjects with creatinine <0.1 mmol · kg body weight–1 · d–1) and one person was excluded because of an outlier NAE value (–53.2 mEq/d). The final number of subjects in the study was thus 85.
Statistical analysis. All statistical analyses were carried out with SAS procedures (Version 8.2, Statistical Analysis System) with data presentation as means ± SD. Data analyses were carried out with Student's t test for comparison between males and females and Pearson's correlations and linear regression analyses with age and sex as covariates. Because calcium data were not normally distributed, they were logarithmically transformed before correlation or regression analyses were run. The magnesium excretion was further adjusted for potassium excretion using the residual method (20). Urinary potassium is a biomarker for dietary potassium intake (21). As dietary magnesium and potassium intakes are highly intercorrelated (22–24), their independent effects cannot be assessed appropriately using food frequency questionnaires (24). Hence, adjusting urinary magnesium for urinary potassium gives a proxy correction for magnesium intake.
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Results |
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TOPABSTRACTIntroductionMaterials and MethodsResultsDiscussionLITERATURE CITED |
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Discussion |
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TOPABSTRACTIntroductionMaterials and MethodsResultsDiscussionLITERATURE CITED |
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There are some methodological issues to consider. No measurements were made of dietary intake of magnesium and calcium. It is known, however, that the amount of urinary calcium is not related to dietary calcium (26). Furthermore magnesiuria is only weakly associated with dietary magnesium intake (12,27,28). Because food records do not allow a reasonable prediction of the absorption of divalent cations (12,26), dietary assessments of magnesium and calcium intake were not considered useful.
No analyses were made of calcium and magnesium in serum. Serum concentrations do not relate to urinary excretion because they are highly regulated by hormonally controlled tubular uptake mechanisms (22,29). Measurements of serum pH and bicarbonate were not made because determinations at one time point are inappropriate to assess overall daily acid load. The daily acid load is appropriately reflected by NAE (8).
The potential dietary influence of high or low magnesium intake on renal magnesium excretion was controlled for by adjusting for 24-h urinary potassium excretion, a biomarker for dietary potassium intake (23). Dietary potassium and magnesium intake are highly interrelated (24) because potassium-rich foods are usually magnesium-rich (30). In a study on young adults (Dortmund Nutritional and Anthropometric Longitudinally Designed study), the highest correlation coefficients among various mineral intakes were for dietary magnesium and dietary potassium, averaging around 0.85 (our unpublished data).
The urinary magnesium excretion was significantly associated with NAE, both before and after body surface area correction and also after adjusting for varying magnesium intakes with the biomarker potassium. When the regressions were run stratified by gender, this relation was significant for males but not for females. This is probably a reflection of lower NAE and magnesium excretion for females, partly due to their smaller body size (or BMI). At the same time, the relation to calcium for females was significant, suggesting that calcium excretion is less dependent on body size and more sensitive to alterations in acid-base-conditions than magnesium. The conclusion that the acid load could be a determinant of renal magnesium excretion is supported by results from animal experiments where alkalinization/acidification was found to regulate renal magnesium and calcium reabsorption proteins (13). However, our findings need to be tested in controlled intervention experiments in humans living in metabolic wards.
Whether the urinary excretion of magnesium is related to NEAP in other age groups as well, including children, needs to be examined in future studies. These are important in view of the potential influence of inappropriate dietary habits on the magnesium and calcium homeostasis and hence health status. The results also suggest that investigations on magnesium homeostasis should control for a possible acid-base dependent excretion of magnesium.
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FOOTNOTES |
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Manuscript received 8 March 2006. Initial review completed 14 April 2006. Revision accepted 22 June 2006.
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LITERATURE CITED |
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