Changes in atherogenic dyslipidemia induced by carbohydrate restriction in men are dependent on dietary protein source.

Previous studies have shown that multiple features of atherogenic dyslipidemia are improved by replacement of dietary carbohydrate with mixed sources of protein and that these lipid and lipoprotein changes are independent of dietary saturated fat content. Because epidemiological evidence suggests that red meat intake may adversely affect cardiovascular disease risk, we tested the effects of replacing dietary carbohydrate with beef protein in the context of high- vs. low-saturated fat intake in 40 healthy men. After a 3-wk baseline diet [50% daily energy (E) as carbohydrate, 13% E as protein, 15% E as saturated fat], participants consumed for 3 wk each in a randomized crossover design two high-beef diets in which protein replaced carbohydrate (31% E as carbohydrate, 31% E as protein, with 10% E as beef protein). The high-beef diets differed in saturated fat content (8% E vs. 15% E with exchange of saturated for monounsaturated fat). Two-week washout periods were included following the baseline diet period and between the randomized diets periods. Plasma TG concentrations were reduced after the 2 lower carbohydrate dietary periods relative to after the baseline diet period and these reductions were independent of saturated fat intake. Plasma total, LDL, and non-HDL cholesterol as well as apoB concentrations were lower after the low-carbohydrate, low-saturated fat diet period than after the low-carbohydrate, high-saturated fat diet period. Given our previous observations with mixed protein diets, the present findings raise the possibility that dietary protein source may modify the effects of saturated fat on atherogenic lipoproteins.

Reversal of small, dense LDL subclass phenotype by normalization of adiposity.

Excess adiposity and high-carbohydrate diets have been associated with an atherogenic lipoprotein phenotype (ALP) characterized by increased concentrations of small, dense low-density lipoprotein (LDL) particles (pattern B). We tested whether weight loss and normalization of adiposity could reverse ALP in overweight men with pattern B. After consuming a moderate-carbohydrate, high-fat diet for 3 weeks, pattern B and nonpattern B (pattern A) men were randomized to a weight loss (n = 60 and n = 36, respectively) or control weight-stable arm (n = 20 and n = 17, respectively). Men in the weight loss arm consumed approximately 1,000 fewer calories per day over 9 weeks to induce an average approximately 9 kg weight loss. In the control group, weight stability was maintained for 4 weeks after randomization. Weight loss led to the conversion of pattern B to pattern A in 58% of baseline pattern B men. Among men who achieved BMIs of <25 kg/m(2) (62% of pattern B men vs. 83% of pattern A men), 81% of pattern B men converted to pattern A. Weight loss was associated with a significantly greater decrease in small, dense LDL subclass 3b in pattern B relative to pattern A men. The lipoprotein profiles of pattern A men who converted from pattern B were comparable to those of men with pattern A at baseline. Conversion of LDL subclass pattern B to pattern A and reversal of ALP can be achieved in a high proportion of overweight men by normalization of adiposity.

Increased plasma concentrations of lipoprotein(a) during a low-fat, high-carbohydrate diet are associated with increased plasma concentrations of apolipoprotein C-III bound to apolipoprotein B-containing lipoproteins.

BACKGROUND: Low-fat, high-carbohydrate (LFHC) diets have been shown to increase plasma concentrations of lipoprotein(a) [Lp(a)] and of triacylglycerol- rich lipoproteins (TRLs). OBJECTIVE: We tested whether increases in plasma Lp(a) induced by an LFHC diet are related to changes in TRLs. DESIGN: Healthy men (study 1; n = 140) consumed for 4 wk each a high-fat, low-carbohydrate diet (HFLC; 40% fat, 45% carbohydrate) and an LFHC diet (20% fat, 65% carbohydrate). Plasma lipids; lipoproteins; apolipoprotein (apo) B, A-I, and C-III; and Lp(a) were measured at the end of each diet. In a second group of men following a similar dietary protocol (study 2; n = 33), we isolated apo(a)-containing particles by immunoaffinity chromatography and determined the concentrations of apo C-III in ultracentrifugally isolated subfractions of apo B-containing lipoproteins. RESULTS: In study 1, plasma concentrations of Lp(a) (P < 0.001), triacylglycerol (P < 0.001), apo B (P < 0.005), apo C-III (P < 0.005), and apo C-III in apo B-containing lipoproteins (non-HDL apo C-III) (P < 0.001) were significantly higher with the LFHC diet than with the HFLC diet. Stepwise multiple linear regression analysis showed that the association of changes in Lp(a) with changes in non-HDL apo C-III was independent of changes in body mass index, apo B, LDL cholesterol, and HDL cholesterol. Plasma lipid and lipoprotein changes were similar in study 2, and we found that both total apo C-III and the apo C-III content of apo(a)-containing particles were increased in a TRL fraction consisting predominantly of large VLDL particles [TRL-apo(a)]. CONCLUSIONS: The increase in plasma Lp(a) with an LFHC diet is significantly associated with an increase in non-HDL apo C-III. Enrichment of TRL-apo(a) with apo C-III may contribute to this dietary effect on Lp(a) concentrations.

Separate effects of reduced carbohydrate intake and weight loss on atherogenic dyslipidemia.

BACKGROUND: Low-carbohydrate diets have been used to manage obesity and its metabolic consequences. OBJECTIVE: The objective was to study the effects of moderate carbohydrate restriction on atherogenic dyslipidemia before and after weight loss and in conjunction with a low or high dietary saturated fat intake. DESIGN: After 1 wk of consuming a basal diet, 178 men with a mean body mass index (in kg/m(2)) of 29.2 +/- 2.0 were randomly assigned to consume diets with carbohydrate contents of 54% (basal diet), 39%, or 26% of energy and with a low saturated fat content (7-9% of energy); a fourth group consumed a diet with 26% of energy as carbohydrate and 15% as saturated fat. After 3 wk, the mean weight loss (5.12 +/- 1.83 kg) was induced in all diet groups by a reduction of approximately 1000 kcal/d for 5 wk followed by 4 wk of weight stabilization. RESULTS: The 26%-carbohydrate, low-saturated-fat diet reduced triacylglycerol, apolipoprotein B, small LDL mass, and total:HDL cholesterol and increased LDL peak diameter. These changes were significantly different from those with the 54%-carbohydrate diet. After subsequent weight loss, the changes in all these variables were significantly greater and the reduction in LDL cholesterol was significantly greater with the 54%-carbohydrate diet than with the 26%-carbohydrate diet. With the 26%-carbohydrate diet, lipoprotein changes with the higher saturated fat intakes were not significantly different from those with the lower saturated fat intakes, except for LDL cholesterol, which decreased less with the higher saturated fat intake because of an increase in mass of large LDL. CONCLUSIONS: Moderate carbohydrate restriction and weight loss provide equivalent but nonadditive approaches to improving atherogenic dyslipidemia. Moreover, beneficial lipid changes resulting from a reduced carbohydrate intake were not significant after weight loss.

Concordant lipoprotein and weight responses to dietary fat change in identical twins with divergent exercise levels 1.

BACKGROUND: Individuals vary greatly in their lipoprotein responses to low-fat diets, with some of this variation being attributable to genes. OBJECTIVE: The purpose was to test the extent to which individual lipoprotein responses to diet can be attributed to genes in the presence of divergent exercise levels. DESIGN: Twenty-eight pairs of male monozygotic twins (one twin mostly sedentary, the other running an average of 50 km/wk more than the sedentary twin) went from a 6-wk 40%-fat diet to a 6-wk 20%-fat diet in a crossover design. The diets reduced fat primarily by reducing saturated and polyunsaturated fat (both from 14% to 4%) while increasing carbohydrate intake from 45% to 65%. RESULTS: Despite the twins' differences in physical activity, the dietary manipulation produced significantly correlated changes (P < 0.05) in the twins' total cholesterol (r = 0.56); LDL cholesterol (r = 0.70); large, buoyant LDL [Svedberg flotation rate (S(f)) 7-12; r = 0.52]; apolipoprotein A-I (r = 0.49); lipoprotein(a) (r = 0.49); electrophoresis measurements of LDL-I (LDLs between 26 and 28.5 nm in diameter; r = 0.48), LDL-IIB (25.2-24.6 nm; r = 0.54), and LDL-IV (22-24.1 nm; r = 0.50); and body weight (r = 0.41). Replacing fats with carbohydrates significantly decreased the size and ultracentrifuge flotation rate of the major LDL and the LDL mass concentrations of large, buoyant LDL; LDL-I; HDL cholesterol; and apolipoprotein A-I and significantly increased concentrations of LDL-IIIA (24.7-25.5 nm) and lipoprotein(a). CONCLUSIONS: Even in the presence of extreme differences in exercise, genes significantly affect changes in LDL, apolipoprotein A-I, lipoprotein(a), and body weight when dietary fats are replaced with carbohydrates.