Effect of an American Heart Association diet, with or without weight loss, on lipids in obese middle-aged and older men.

Forty-two obese [body mass index (kg/m2): 30 +/- 5; weight: 92.9 +/- 10.1 kg] men aged 60 +/- 9 y were recruited to determine the effects of an American Heart Association (AHA) diet, with and without weight loss, on lipoprotein lipids. All subjects entered a 3-mo, weight-maintaining AHA diet followed by either a 9-mo weight-loss (AHA + WL, n = 28) or a 9-mo AHA plus weight-maintenance (AHA + WM, n = 14) intervention. Baseline diets were high in fat (35 +/- 6% of energy) and cholesterol (380 +/- 158 mg/d), and low in dietary fiber (18 +/- 5 g/d). The 3-mo AHA diet resulted in an 11% decrease in plasma triacylglycerol (1.83 +/- 0.15 to 1.47 +/- 0.08 mmol/L, P < 0.05), a 16% decrease in plasma cholesterol (5.39 +/- 0.96 to 4.56 +/- 0.91 mmol/L, P = 0.0001), a 17% decrease in high-density-lipoprotein (HDL) cholesterol (1.09 +/- 0.23 to 0.91 +/- 0.18 mmol/L, P = 0.0001), and a 14% decrease in low-density-lipoprotein (LDL) cholesterol (3.47 +/- 0.83 to 2.98 +/- 0.78 mmol/L, P = 0.0001) The AHA + WL group lost 9.8 +/- 4.3 kg (P < 0.001, n = 28) and further reduced plasma triacylglycerol by 17% (P < 0.05), total cholesterol by 4% (P < 0.05), LDL cholesterol by 7% (P < 0.05), and significantly increased HDL cholesterol by 15% (P < 0.05) when compared with their 3-mo AHA-intervention values. These changes were significant (P < 0.05) when compared with the AHA + WM group, in whom lipoprotein lipids did not change.(ABSTRACT TRUNCATED AT 250 WORDS)

Magnesium homeostasis: conservation mechanism in lactating women consuming a controlled-magnesium diet.

This study was undertaken to determine whether lactating women consuming a low-magnesium diet compensate for magnesium secreted into breast milk by decreasing urinary magnesium losses. Six lactating (L) women, six nonlactating (NL) women (75 +/- 5 and 61 +/- 5 d postpartum, respectively), and seven never-pregnant (NP) women were studied while consuming a constant magnesium intake of 8.97 +/- 0.01 mmol/d for 20 d. After a 5-d stabilization period on the controlled diet, 24-h urine and fecal samples were collected for the next 15 d. The L women excreted significantly less (P < 0.01) urinary magnesium (2.10 +/- 0.35 mmol/d) than the NP women (3.45 +/- 0.37 mmol/d). No significant differences were detected in mean apparent magnesium absorption among the three groups of women, because of large individual variations of fecal magnesium and small sample size. L women apparently compensated for magnesium losses in breast milk (1.04 +/- 0.06 mmol/d) by reducing urinary magnesium losses (1.38 mmol/d) when consuming 8.97 mmol Mg/d.