The Influence of Parathyroid Hormone, Urea, Sodium Chloride, Fat and of Intestinal Activity Upon Calcium Balance

Aub, Joseph C.; Tibbetts, Dorothy M.; McLean, Regina

doi:10.1093/jn/13.6.635

Cited by 25 publications

(18 citation statements)

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“…However, two normal controls studied during three periods of constipation and four periods of diarrhea induced by cascara showed an average increase in weight of wet feces of 700 grams per period while the increase in fecal calcium excretion averaged but 50 mgm. per period (5). The increase in this case of hyperparathyroidism on magnesium ingestion is, therefore, ten times that found in these controls.…”

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confidence: 47%

“…The amount of soft tissue magnesium involved, as well as that which should accompany calcium storage in bone can be roughly calculated. The definite diminution of magnesium excretion in the first postoperative periods is not comparable to the dramatic total change in the calcium balance but is more than ten times as great as the amount to be expected from the calcium balance if the ratio in 1 These patients are also discussed in another paper (5). 503 The data accumulated during the second observation, therefore, represents the period of parathyroid overactivity.…”

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confidence: 95%

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Magnesium Metabolism in Health and Disease. Ii. The Effect of the Parathyroid Hormone

Tibbetts¹,

Aub²

1937

J. Clin. Invest.

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In this series of studies of the relationship between calcium, magnesium, and phosphorus exchange, the effect of the parathyroid hormone is obviously of primary interest. With the dramatic changes which occur in calcium metabolism, it might be anticipated that similar 'effects would be found in magnesium exchange, and that this might be evident in soft tissue as well as bone metabolism.Greenwald and Gross (1) found that thyroparathyroidectomy in dogs had practically no effect on magnesium excretion. A potent parathyroid extract, however, increased fecal magnesium but had no effect on the urinary excretion (2). After most of the data here recorded had been accumulated, there appeared a publication by Bulger and Gausmann (3), who stated that a loss of calcium is accompanied by a loss of magnesium in hyperparathyroidism and that retention of both accompanies postoperative recovery.Our data differ somewhat from these observations in untreated hyperparathyroidism. The total magnesium excretion in our three cases of parathyroid adenoma showed no great loss of magnesium. The balances varied; in only one case (G. M.) was there a negative balance, the other two showing a greater storage of magnesium than did our normal controls on a similar intake (4).However, when comparing the excretion in the same individual before and after parathyroidectomy we find that variations in magnesium do occur, as reported by Bulger and Gausmann (3). These variations are in the same direction though not of the same magnitude as the large changes in calcium excretion.The observations here reported were all made on patients on the same regime and approximately the same diets as our normal controls described in Paper I of this series (4). The same methods of analysis were also used. The case histories are appended.' Patient G. M. (Table I), a boy of 13, was in a serious toxic state because of an intensely overactive parathyroid adenoma. This condition was entirely relieved by operation. Very careful metabolic observations were made upon him before and promptly after the complete removal of his 11.8 gram parathyroid adenoma. A third observation on exactly the same routine was obtained three months after the operation. These studies were made with both high and low calcium diets in order to observe variations in absorption and excretion which these changes might produce, but no clear cut variation in magnesium metabolism was obvious. The slight changes in excretion were those to be anticipated from the increased magnesium ingestion necessitated by the change in diet.It is readily seen that immediately after operation there is a marked fall in urinary magnesium excretion and a less dramatic drop in the fecal magnesium. These changes, however, had partly disappeared three months after the operation, though the storage of calcium was then most dramatic. The variations of magnesium metabolism must be interpreted with due regard to changes in weight. Thus, during the pre-operative periods (I to V) and in the observation three months after his operati...

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confidence: 47%

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confidence: 95%

Magnesium Metabolism in Health and Disease. Ii. The Effect of the Parathyroid Hormone

Tibbetts¹,

Aub²

1937

J. Clin. Invest.

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“…In an early study it was noted that NaCl supplementation of two subjects with 30 g NaCl/d for 3 d increased urinary Ca excretion (Aub et al 1937). Since then, a number of short-term studies have shown that acute increases in dietary Na intake generally cause an increase in urinary Ca excretion in healthy subjects.…”

Section: S T U D I E S W I T H C O N T R O L L E D S O D I U M I N T mentioning

confidence: 99%

“…Dietary sodium intake has long been known to influence urinary calcium excretion in man (Aub et al 1937;Hills et al 1959) and animals (Walser, 1961 ;Massry et al 1967). However, up to the early 1980s Na was not included among dietary factors believed to influence Ca requirements or the pathogenesis of osteoporosis (Draper & Bell, 1979;Spencer et al 1982).…”

Section: Introductionmentioning

confidence: 99%

Sodium-Calcium Inter-Relationships with Specific Reference to Osteoporosis

Shortt

Flynn

1990

Nutr. Res. Rev.

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“…12,13 Studies suggest that urinary Ca decreases by 0.5 to 1.5 mmol (20-60 mg/day) for every 100 mmol (2300 mg) decrease in sodium ingested. 14,15 In the DASH-Na diet, low salt intake was associated with decreased urinary Ca excretion and significantly reduced bone turnover markers; calcium balance, a more robust indicator of bone health, was not measured. 16 Increases in either intravenous or dietary Na intake are linked to increases in hormones such as parathyroid hormone (PTH) 17 that are known to affect bone turnover.…”

Section: Introductionmentioning

confidence: 99%

No evidence that the skeletal non-response to potassium alkali supplements in healthy postmenopausal women depends on blood pressure or sodium chloride intake

et al. 2012

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BACKGROUND/OBJECTIVES:In vitro studies demonstrate that bone is degraded in an acidic environment due to chemical reactions and through effects on bone cells. Clinical evidence is insufficient to unequivocally resolve whether the diet net acid or base load bone affects breakdown in humans. Increasing dietary salt (sodium chloride, NaCl) mildly increases blood acidity in humans and in rats with increased sensitivity to the blood pressure effects of salt, whereas increased potassium (K) intake can decrease blood pressure. Blood pressure responses to NaCl or K may potentially be a marker for increased bone turnover or lower bone mineral density (BMD) in women at higher risk for osteoporosis and fracture. SUBJECTS/METHODS: We retrospectively analysed data from two data sets (California and NE Scotland) of postmenopausal women (n ¼ 266) enrolled in long-term randomized, placebo-controlled studies of the effects of administration of low-or high-dose dietary K alkali supplementation on bone turnover in relation to sodium or chloride excretion (a marker of dietary salt intake). Mean arterial pressure (MAP) was calculated from blood pressure measures, MAP was divided into tertiles and its influence on the effect of dietary NaCl and K alkali supplementation on deoxypyridinoline markers of bone resorption and BMD by DEXA was tested. Data was analysed for each data set separately and then combined. RESULTS: Percentage change in BMD after 24 months was less for California compared with North East Scotland (hip: À 0.6 ± 2.8% and À 1.5±2.4%, respectively (P ¼ 0.027); spine: À 0.5±3.4% and À 2.6±3.5%, (Po0.001). We found no effect of dietary alkali treatment on BMD change or bone resorption for either centre. Adjusting for the possible calcium-or potassium-lowering effects on blood pressure did not alter the results. CONCLUSIONS: Blood pressure responses to Na, Cl or K intake did not help predict a BMD response to diet alkali therapy.

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The Influence of Parathyroid Hormone, Urea, Sodium Chloride, Fat and of Intestinal Activity Upon Calcium Balance

Cited by 25 publications

References 35 publications

Magnesium Metabolism in Health and Disease. Ii. The Effect of the Parathyroid Hormone

Magnesium Metabolism in Health and Disease. Ii. The Effect of the Parathyroid Hormone

Sodium-Calcium Inter-Relationships with Specific Reference to Osteoporosis

No evidence that the skeletal non-response to potassium alkali supplements in healthy postmenopausal women depends on blood pressure or sodium chloride intake

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