Calcium is an important determinant of peak bone mass in young adults because of its influence on skeletal development during growth. Attainment of maximum peak bone mass requires optimal positive balance between calcium intake and obligatory losses of calcium, primarily in urine and feces. Urinary excretion is an important determinant of calcium retention in the body. Accordingly, the purpose of this study was to evaluate the influence of various nutrients on urinary calcium excretion, and to assess their impact on bone mass of young females, aged 8-13 y, during early puberty. The study was conducted in 381 healthy white females in pubertal stage 2. From each participant we collected basic anthropometric measurements, a 3-d food record, blood, a 24-h urine sample, and bone mass measurements of the total body and forearm by dual X-ray absorptiometry. Urinary sodium was found to be one of the most important determinants of urinary calcium excretion: [urinary calcium (mmol/d) = 0.01154 x urinary sodium (mmol/d) + 0.823], whereas calcium intake had relatively little impact: [urinary calcium (mmol/d) = 0.02252 x calcium intake (mmol/d) + 1.5261]. Urinary calcium was much higher at a calcium intake of approximately 37.5 mmol/d (1500 mg/d), supporting the notion that calcium is a threshold nutrient. Calcium intake had a significant positive influence on the bone mineral content and density of the whole body and radius shaft whereas urinary calcium had a negative influence, presumably by reducing calcium accretion into the skeleton.(ABSTRACT TRUNCATED AT 250 WORDS)

Increasing emphasis is being placed on optimizing calcium intake during growth as a way to enhance peak bone mass. Although some studies in adults have shown that high calcium intake may negatively affect magnesium utilization, few data are available regarding the interaction of calcium and magnesium in healthy children. The purpose of our study was to measure the effect of calcium intake on magnesium balance in 26 adolescent girls (mean age 11.3 y) during a 14-d period. Subjects ate a controlled basal diet containing 667 mg Ca and 176 mg Mg. In addition to the basal diet, subjects were randomly assigned in a double-blind fashion to consume 1000 mg elemental Ca/d as calcium citrate malate or a placebo. Magnesium use did not differ between the low-calcium and high-calcium groups as measured by absorption (50% compared with 55%), urinary excretion (70 compared with 74 mg/d), and fecal excretion (88 compared with 79 mg/d). Accordingly, magnesium balance was not different in subjects consuming 667 or 1667 mg Ca/d and averaged 21 mg Mg/d for the whole study group. Magnesium balance was significantly correlated with magnesium intake (r = 0.511, P = 0.008) and magnesium absorption (r = 0.723, P < 0.001). Prediction intervals from the regression of magnesium balance on intake indicated that the current recommended dietary allowance of magnesium would result in magnesium balance > or = 8.5 mg/d in 95% of the girls. This value appears consistent with long-term accretion rates needed to account for the expansion of the total-body magnesium pool during growth. In summary, our observations support the adequacy of the current recommended dietary allowance for magnesium and indicate that alterations in magnesium utilization should not be anticipated in adolescent females consuming a high-calcium diet.

Fasting serum lipid levels, glucose tolerance, and immunoreactive insulin concentrations of 50 young patients with coronary heart disease (CHD) and 30 control subjects were evaluated to study the interrelationships of these metabolic factors. Abnormalities in one or more of these factors could be shown in 90% of the patients and 20% of the control subjects. Thirty-four of the 50 patients had elevated cholesterol or triglyceride levels, or both, 30 had abnormally elevated or delayed insulin responses after glucose, and 17 had abnormal glucose tolerance. A significant correlation existed between serum triglyceride and insulin concentrations. When insulin levels were reduced by phenformin, triglyceride concentrations fell toward normal.These findings indicate that carbohydrate, insulin, and lipid abnormalities are rather prevalent in patients with CHD. Excessive insulin secretion secondary to mild glucose intolerance probably induces hepatic synthesis of triglycerides and hypertriglyceridemia. Dietary alterations or pharmacological agents may help to control some of the metabolic abnormalities associated with premature CHD.

Glucose tolerance tests and immunoreactive insulin responses were analyzed in 203 subjects with abnormal glucose tolerance and in 298 nondiabetics. All subjects were grouped as obese (greater than 115 per cent of ideal body, weight) or lean. Those with an abnormal glucose tolerance test were further subdivided: (1) Normal fasting glucose and one or more abnormal subsequent values, and (2) elevated fasting glucose and an abnormal tolerance test. The "total mean glucose and insulin concentrations, expressed as the areas under the three-hour glucose tolerance curves, were compared in the six subgroups. Hyperinsulinism was found in obese nondiabetics as compared to lean nondiabetics. Mildly' impaired glucose tolerance in both obese and nonobese patients was associated with increased insulin levels compared to nondiabetics. Despite increased immunoreactive insulin levels in subjects with impaired glucose tolerance, the concentrations were less than expected for corresponding glucose levels during the early portion of the tolerance test. Decompensated diabetes, manifested by fasting hyperglycemia, was associated with absolute as well as relative deficiency of endogenous insulin. While definite trends in glucose-induced insulin responses could be determined in specific groups, there was marked individual variation. DIABETES i°: 458-64, June, 1970.

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