Darlene M. Dreon

Changes in plasma lipids and lipoproteins in overweight men during weight loss through dieting as compared with exercise.

We studied separately the influence of two methods for losing fat weight on the levels of plasma lipids and lipoproteins in overweight sedentary men--decreasing energy intake without increasing exercise (diet), and increasing energy expenditure without altering energy intake (exercise, primarily running)--in a one-year randomized controlled trial. As compared with controls (n = 42), dieters (n = 42) had significant loss of total body weight (-7.8 +/- 0.9 kg [mean +/- SE]), fat weight (-5.6 +/- 0.8 kg), and lean (non-fat) weight (-2.1 +/- 0.5 kg) (P less than 0.001 for each variable), and exercisers (n = 47) had significant loss of total body weight (-4.6 +/- 0.8 kg) and fat weight (-3.8 +/- 0.7 kg) (P less than 0.001 for both variables) but not lean weight (-0.7 +/- 0.4 kg). Fat-weight loss did not differ significantly between dieters and exercisers. All subjects were discouraged from altering their diet composition; however, dieters and exercisers had slight reductions in the percentage of kilojoules derived from fat. As compared with the control group, both weight-loss groups had significant increases (P less than 0.01) in plasma concentrations of high-density lipoprotein (HDL) cholesterol (diet vs. exercise, 0.13 +/- 0.03 vs. 0.12 +/- 0.03 mmol per liter), HDL2 cholesterol (0.07 +/- 0.02 vs. 0.07 +/- 0.02 mmol per liter), and HDL3 cholesterol (0.07 +/- 0.02 vs. 0.06 +/- 0.02 mmol per liter) and significant decreases (P less than 0.05) in triglyceride levels (diet vs. exercise, -0.35 +/- 0.14 vs. -0.24 +/- 0.12 mmol per liter). Levels of total and low-density lipoprotein cholesterol were not significantly changed, relative to values in controls. None of these changes were significantly different between dieters and exercisers. Thus, we conclude that fat loss through dieting or exercising produces comparable and favorable changes in plasma lipoprotein concentrations.

Associations of diet and alcohol intake with high-density lipoprotein subclasses☆

Nutritional components from three-day records were studied in association with plasma high-density lipoprotein (HDL) cholesterol, serum HDL2-mass, serum HDL3-mass, and plasma HDL apolipoproteins A-I, A-II, and D concentrations in a cross-sectional survey of 77 adult males. Correlation and regression analyses revealed that the serum concentrations of HDL3 were strongly associated with the intakes of various nutrients, whereas serum HDL2 concentrations showed only weak nutritional associations. Carbohydrate intake correlated negatively with HDL3 concentrations, and alcohol intake correlated positively with serum concentrations of HDL3 and apolipoproteins A-I, A-II, and D. These associations remained significant when adjusted for cigarette smoking, adiposity, and aerobic fitness. HDL2 did not correlate significantly with alcohol intake, total carbohydrates, or starch. HDL-cholesterol concentrations showed two distinct regions of inverse association with intake of sucrose, one involving HDL3 with sucrose between 0 and 10 g/1,000 kcal and one involving HDL2 with sucrose above 25 g/1000 kcal. Alcohol, sucrose, and starch together accounted for 36% of the variance of HDL3 concentration, but less than 5% of the variance of HDL2 concentration. Thus, serum concentrations of HDL3 and HDL2 show different relationships to major dietary components.

The Effects of Polyunsaturated Fat vs Monounsaturated Fat on Plasma Lipoproteins: The Power of a Study-Reply

In Reply.— On our study of diet and high-density lipoprotein cholesterol subfractions, Dr Passey has focused on the negative low-density lipoprotein (LDL) cholesterol results. We designed our study with β error equal to .20 specifically to detect differences in highdensity lipoprotein cholesterol and cholesterol subfractions. We obtained significant differences for these variables and therefore think that the study groups were of sufficient size to report these positive results appropriately. While change in LDL cholesterol was not part of our primary hypothesis, clearly LDL cholesterol has a greater SE and greater differences would be needed with this sample size to obtain significance. With 80% power we could detect significance with an LDL cholesterol difference of 0.28 mmol/L, below which are levels we consider clinically insignificant. We consider the nonsignificant change in LDL cholesterol of 0.10 mmol/L to be of little clinical significance. We faithfully pointed out not only our P value but