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Background: Inflammation contributes to atherogenesis. Dietary fats may be proinflammatory., Objective: The objective was to determine whether energy intake modulates the effects of low-fat, high-carbohydrate intakes on inflammatory markers., Design: Twenty-two healthy postmenopausal women with a mean (+/-SD) age of 61 +/- 11 y, who were not receiving hormone replacement therapy, were fed eucaloric diets to reduce their fat intake from 35% to 15% of energy. Next, the women consumed a 15%-fat ad libitum diet under free-living conditions. Serum highly sensitive C-reactive protein, interleukin 6, HDL serum amyloid A, and adiponectin concentrations were measured at the end of the eucaloric and ad libitum low-fat, high-carbohydrate intakes., Results: The eucaloric diet decreased adiponectin from 16.3 +/- 2.1 to 14.2 +/- 2.0 mg/L (P < 0.05) and increased triacylglycerol from 131 +/- 11 to 164 +/- 14 mg/dL (P < 0.01). The ad libitum low-fat diet caused 6 kg weight loss and decreased highly sensitive C-reactive protein from 4.3 +/- 0.6 to 2.5 +/- 0.5 mg/L (P < 0.01), decreased HDL serum amyloid A from 10.3 +/- 1.8 to 5.7 +/- 1.3 mg/L (P < 0.001), increased adiponectin from 14.2 +/- 2.0 to 16.3 +/- 1.7 mg/L (P < 0.05), and decreased triacylglycerol from 164 +/- 14 to 137 +/- 15 mg/dL (P < 0.05)., Conclusion: During the eucaloric phase, the low-fat, high-carbohydrate diet exerted unfavorable effects on the inflammatory markers. In contrast, the ad libitum low-fat, high-carbohydrate intake caused weight loss and affected inflammatory markers favorably. Thus, the energy content of a low-fat, high-carbohydrate diet determines changes in inflammatory markers.

Effects of a polyunsaturated fatty acid (PUFA)-rich diet were investigated in 17 polycystic ovary syndrome (PCOS) patients. After a 3-month habitual diet period, dietary fats were partly replaced with PUFAs for another 3 months. The PUFA-rich diet increased plasma linoleic acid from 28.36 +/- 1.00% to 33.76 +/- 1.08% (P < 0.002) and alpha-linolenic acid from 0.52 +/- 0.03% to 1.06 +/- 0.10% (P < 0.0001). Fasting glucose increased from 76 +/- 3 to 95 +/- 3 mg/dl (4.2 +/- 0.2 to 5.30.2 mmol/liter; P < 0.0001), and the area under the curve for glucose during oral glucose tolerance test increased from 421 +/- 34 to 503 +/- 31 mg/dl (23.4 +/- 1.9 to 27.9 +/- 1.7 mmol/liter; P < 0.001). Plasma insulin did not change either at fasting or during oral glucose tolerance test. Fasting plasma free fatty acids decreased from 0.596 +/- 0.048 to 0.445 +/- 0.058 mg/dl (P = 0.037), and ketone bodies decreased from 9.14 +/- 1.57 to 3.63 +/- 0.62 mg/dl (895 +/- 154 to 356 +/- 61 micromol/liter; P < 0.003). Plasma 15-deoxyprostaglandin J(2) tended to decrease (from 239 +/- 65 to 171 +/- 60 ng/ml; P = 0.053). Plasma testosterone, free testosterone, SHBG, dehydroepiandrosterone sulfate, LH, FSH, and urinary estrogen conjugates did not change. Urinary pregnanediol 3-glucuronide increased from 18.6 +/- 2.2 to 31.0 +/- 5.7 micro g/mg creatinine (P = 0.038). In conclusion, increased dietary PUFA intake can exert significant metabolic and endocrine effects in women with PCOS.

Objectives: To determine whether a very low-fat diet (<15% of energy intake) consumed ad libitum during an 8-month period can achieve weight loss of 5% to 10% of initial body weight while still providing adequate intakes of other essential nutrients., Design: Longitudinal, 8-month, ad libitum, free living, very low-fat diet trial., Subjects: Fifty-four of the sixty-four healthy postmenopausal women recruited completed the entire study (age 59+/-8 years, BMI=29.6+/-6.3). Twenty-four of these women used hormone replacement therapy, thirty women did not., Intervention: Weekly sessions aimed at teaching and reinforcing a very low-fat intake diet for eight months. MAIN: outcome measures Body weight, percent body fat, waist-to-hip ratio, resting energy expenditure, respiratory quotient, and nutrient intakes derived from 7-day food records at the beginning and at 2, 4, 6, and 8 months of the study. Statistical analysis performed Repeated measures analysis of variance and Tukey post hoc analysis were used to analyze significant differences in mean data (P<.05)., Results: Fat intake decreased from 33.2+/-7.5% to 11+/-4% over the 8-month intervention period (P<.00001). Weight loss was 6.0 kg+/- 4.2 kg (P<.000038), an 8% weight change, and decrease in percent body fat of 2.7%+/-0.2% (P< or =.000046). Weight correlated better with the self-reported fat intake (r=0.321, P<.01) than the energy intake (r=0.263, P<.05) at baseline. Fiber intake increased from 16 g+/-0.6 g to 23 g+/-0.2 g (P<.0005). All micronutrient intakes remained at or above preintervention ranges, except for a decrease in vitamin E intake from 8.1 mg+/-4.0 mg to 3.7 mg+/-1.1 mg (P<.0005) on the very low-fat diet and linoleic acid from 6.3%+/-1.5% to 2.5%+/-0.7% (P<.000001) with no significant reduction in linolenic acid. Hormone replacement was not associated with the amount of weight loss., Applications: This study demonstrates that adherence to a very low-fat diet consumed ad libitum causes weight loss in the 5% to 10% range and a reduction of body fat. These reductions, along with the observed decreases in fat intake, are associated with improved health outcomes. Because of the decreased vitamin E and n-3 fatty acid intake, emphasis on foods high in these nutrients may need to be encouraged for those consuming a very low-fat diet.

Hypertriglyceridemia is an independent risk factor for coronary artery disease (CAD) and is also commonly associated with other coronary risk factors, ie, small, dense low-density lipoprotein (LDL) particles and low plasma levels of high-density lipoprotein cholesterol (HDL-C). Dietary fat restriction is recommended for the prevention of nutrition-related cancers. Low-fat, high-carbohydrate intake can increase plasma triglyceride (TG) and decrease HDL-C. In general, plasma TG levels are inversely related to the particle size of LDL. We investigated the effects of dietary fat restriction on the concentration and particle size of plasma lipoproteins in 14 healthy postmenopausal women (aged 61 +/- 11 years). During a 4-month period of eucaloric controlled feeding, dietary fat was reduced stepwise from a habitual intake of 33% +/- 8% to 23% and then to 14% of daily energy. Changes in the plasma lipid level and particle size of very-low-density lipoprotein (VLDL), LDL, and HDL were determined at the end of each dietary phase. Increasing carbohydrate intake without weight loss was associated with an increase in plasma TG (1.86 +/- 0.30 v 2.47 +/- 0.37 mmol/L) and decreases in total cholesterol (5.82 +/- 0.25 v 5.40 +/- 0.21 mmol/L), LDL-C (3.07 +/- 0.18 v 2.61 +/- 0.21 mmol/L), HDL-C (1.42 +/- 0.1 v 1.24 +/- 0.1 mmol/L), and apolipoprotein (apo) A1 (5.14 +/- 0.25 v 4.61 +/- 0.36 mmol/L), whereas plasma apo B did not change. The particle size of VLDL increased (42.7 +/- 1.4 v 47.0 +/- 0.9 nm). However, there was no change in either LDL (25.1 +/- 0.2 v 25.3 +/- 0.2 nm) or HDL particle size. Although at each level of dietary fat intake LDL particle size correlated inversely with plasma TG and apo B, there was no relationship between the increase in plasma TG and LDL particle size. These results show that hypertriglyceridemia caused by a eucaloric high-carbohydrate intake is not associated with a decrease in LDL particle size. Therefore, carbohydrate-induced hypertriglyceridemia may not have the same atherogenic potential as genetic hypertriglyceridemias.