Phytosterol intake and dietary fat reduction are independent and additive in their ability to reduce plasma LDL cholesterol.

We studied the interrelationship of diet and plant sterols (PS) on plasma lipids, lipoproteins and carotenoids. Mildly hypercholesterolemic men (n = 13) and postmenopausal women (n = 9) underwent four randomized, crossover, double-blind, controlled feeding periods of 23 days each. The design consisted of two levels of PS (0 and 3.3 g/day) and two background diets having fat content either typical of the American diet (total and saturated fat at 33.5 and 13.2% of energy, respectively), or a Step 1 type of diet (total and saturated fat at 26.4 and 7.7% of energy, respectively). Plasma total cholesterol (TC), high density lipoprotein (HDL) cholesterol, low density lipoprotein (LDL) cholesterol, Apo A1 and Apo B were 4.3, 5.3, 4.5, 2.8 and 2.5% lower, respectively (P

Common leptin receptor polymorphisms do not modify the effect of alcohol ingestion on serum leptin levels in a controlled feeding and alcohol ingestion study.

We explored whether serum leptin response to alcohol ingestion was related to common leptin receptor gene polymorphisms, K109R (Lys109Arg), Q223R (Gln223Arg), S343S [Ser(T)343Ser(C)], and K656N (Lys656Asn), of reported physiologic significance during a controlled intervention. Fifty-three participants rotated through three 8-week treatment periods and consumed 0, 15 (equivalent to one drink), or 30 g (equivalent to two drinks) of alcohol (95% ethanol in 12 ounces of orange juice) per day, in random order. During the controlled feeding periods, all food and beverages including alcoholic beverages were prepared and supplied by the staff of the Beltsville Human Nutrition Research Center's Human Study Facility (Beltsville, MD), and energy intake was adjusted to maintain a constant weight. Blood was collected after an overnight fast on 3 separate days during the last week of each controlled feeding period and pooled for hormone analysis. Circulating serum leptin concentration was measured in duplicate by RIA and genotype analysis was done on DNA extracted from WBC using real-time PCR analysis amplification (TaqMan). Linear mixed models with a single random intercept reflecting a participant effect were used to estimate changes in serum leptin levels at 15 and 30 g of alcohol per day relative to 0 g of alcohol per day. No significant effects were found between common leptin receptor polymorphisms and serum leptin levels (P > or = 0.26).

Effects of alcohol on insulin-like growth factor I and insulin-like growth factor binding protein 3 in postmenopausal women.

BACKGROUND: Increased circulating insulin-like growth factor I (IGF-I) concentrations, frequently adjusted for IGF binding protein 3 (IGFBP-3), have been associated with increased risk of several types of cancer, including colon, prostate, and breast. Studies have suggested that alcohol may affect IGF-I or IGFBP-3; however, controlled feeding studies to assess alcohol's effects on IGF-I or IGFBP-3 have not been conducted. OBJECTIVE: To determine whether chronic, moderate alcohol intake affects serum IGF-I or IGFBP-3 concentrations, we performed a controlled, crossover feeding study. DESIGN: Fifty-three postmenopausal women were randomly assigned to consume 0 g (control), 15 g (one drink), or 30 g (2 drinks) alcohol daily for 8 wk and were rotated through the other 2 intake levels in random order. All foods and beverages were provided during the intervention. Individuals were monitored and calories adjusted to maintain constant weight, and serum was collected at the end of each diet period. RESULTS: Compared with the effects of 0 g alcohol/d, IGF-I concentrations were nearly unchanged by 15 g alcohol/d (0.8%; 95% CI: -3.2%, 3.5%) but decreased significantly by 4.9% (95% CI: -8.0%, -1.6%) with 30 g alcohol/d. IGFBP-3 concentrations significantly increased by 3.0% (95% CI: 0.4%, 5.6%) with 15 g alcohol/d but did not increase significantly with 30 g/d (1.8%; 95% CI: -0.9%, 4.5%). CONCLUSIONS: To our knowledge, this is the first published controlled diet study to find that in postmenopausal women, when weight is kept constant, alcohol consumption reduces the amount of serum IGF-I potentially available for receptor binding. These findings suggest that the effect of alcohol intake should be considered in studies of IGF-I, IGFBP-3, and cancer in postmenopausal women.

Effects of alcohol and menstrual cycle on insulin-like growth factor-I and insulin-like growth factor binding protein-3.

Alcohol ingestion and insulin-like growth factor-I (IGF-I) have been associated with increased breast cancer risk, the latter primarily in premenopausal women. We investigated whether alcohol ingestion altered IGF-I or its major binding protein (BP), IGFBP-3, in a controlled feeding study in premenopausal women. We also determined whether IGF-I or IGFBP-3 was affected by menstrual cycle phase. Serum was collected from 31 individuals who were randomly assigned to consume either 0 or 30 g (two drinks) of alcohol daily for three menstrual cycles and who then crossed over to the other alcohol level for three cycles. All calories were provided and weight was maintained during the study. For both alcohol levels, serum was collected during the final cycle at early follicular, periovulatory, and luteal phases. Relative to the follicular phase, IGF-I levels increased by 3.3% and 7.6% in the periovulatory and luteal phases, respectively (P for trend = 0.004). Although alcohol ingestion did not affect this increase, it significantly reduced IGF-I concentrations at all phases (9.5%; P < 0.001), whereas IGFBP-3 was unaffected by either menstrual phase or alcohol. This is the first controlled diet study to show that alcohol decreases serum IGF-I in premenopausal women and that IGF-I significantly increases over the course of the menstrual cycle whether or not alcohol is present.

The effects of moderate alcohol supplementation on estrone sulfate and DHEAS in postmenopausal women in a controlled feeding study.

BACKGROUND: We have demonstrated that moderate alcohol consumption (15 g/d, 30 g/d) for 8 weeks resulted in significantly increased levels of serum estrone sulfate and DHEAS in 51 postmenopausal women in a randomized, placebo-controlled trial. We now report on the relationships between serum estrone sulfate and dehydroepiandrosterone sulfate (DHEAS) levels after 4 weeks of moderate alcohol supplementation, and compare the results to the 8 weeks data to elucidate time-to-effect differences. METHODS: Postmenopausal women (n = 51) consumed 0 (placebo), 15 (1 drink), and 30 (2 drinks) g alcohol (ethanol)/ day for 8 weeks as part of a controlled diet in a randomized crossover design. Blood samples were drawn at baseline, at 4 weeks and at 8 weeks. Changes in estrone sulfate and DHEAS levels from placebo to 15 g and 30 g alcohol per day were estimated using linear mixed models. RESULTS AND DISCUSSION: At week 4, compared to the placebo, estrone sulfate increased an average 6.9% (P = 0.24) when the women consumed 15 g of alcohol per day, and 22.2% (P = 0.0006) when they consumed 30 g alcohol per day. DHEAS concentrations also increased significantly by an average of 8.0% (P < 0.0001) on 15 g of alcohol per day and 9.2% (P < 0.0001) when 30 g alcohol was consumed per day. Trend tests across doses for both estrone sulfate (P = 0.0006) and DHEAS (P < 0.0001) were significant. We found no significant differences between the absolute levels of serum estrone sulfate at week 4 versus week 8 (P = 0.32) across all doses. However, absolute DHEAS levels increased from week 4 to week 8 (P < 0.0001) at all three dose levels. CONCLUSIONS: These data indicate that the hormonal effects due to moderate alcohol consumption are seen early, within 4 weeks of initiation of ingestion.

Dietary fatty acids affect plasma markers of inflammation in healthy men fed controlled diets: a randomized crossover study.

BACKGROUND: The effect of individual dietary fatty acids on emerging risk factors for cardiovascular disease that are associated with subclinical inflammation is unknown. OBJECTIVE: The goal was to evaluate the role of dietary fat and specific fatty acids, especially trans fatty acids, in altering concentrations of markers of inflammation in humans fed controlled diets. DESIGN: In a randomized crossover design, 50 men consumed controlled diets for 5 wk that provided 15% of energy from protein, 39% of energy from fat, and 46% of energy from carbohydrate. Eight percent of fat or fatty acids was replaced across diets with the following: cholesterol, oleic acid, trans fatty acids (TFAs), stearic acid (STE), TFA+STE (4% of energy each), and 12:0-16:0 saturated fatty acids (LMP). RESULTS: Fibrinogen concentrations were higher after consumption of the diet enriched in stearic acid than after consumption of the carbohydrate diet. C-reactive protein concentrations were higher after consumption of the TFA diet than after consumption of the carbohydrate diet, but were not significantly different after consumption of the TFA and TFA+STE diets than after consumption of the LMP diet. Interleukin 6 concentrations were lower after consumption of the oleic acid diet than after consumption of the LMP, TFA, and STE diets. E-selectin concentrations were higher after consumption of the TFA diet than after consumption of the carbohydrate diet. Consumption of the TFA but not the TFA+STE diet resulted in higher E-selectin concentrations than did the LMP diet. CONCLUSIONS: These data provide evidence that dietary fatty acids can modulate markers of inflammation. Although stearic acid minimally affects LDL cholesterol, it does appear to increase fibrinogen concentrations.

Stearic acid absorption and its metabolizable energy value are minimally lower than those of other fatty acids in healthy men fed mixed diets.

Compared with other saturated fatty acids, stearic acid appears to have different metabolic effects with respect to its impact on risk for cardiovascular disease. These differences may in part reflect biologically important differences in absorption. This study was designed to compare the absorption and the metabolizable energy value of stearic acid with other fatty acids from mixed diets fed to healthy humans. Healthy men (n = 11) were fed four diets with multiple fat sources that contained approximately 15% of energy (en%) from protein, 46 en% from carbohydrate and 39 en% from fat with 8 en% substitution across diets of the following: trans monoenes, oleic acid, saturated fatty acids (lauric + myristic + palmitic) or stearic acid fed as triacylglycerides. Fats were incorporated into mixed diets comprised of foods typically consumed in the United States. After a 14-d adaptation period, volunteers collected all feces for 7 d. Across diets, absorption of stearic acid (94.1 +/- 0.2%) was lower (P < 0.0002) than that of palmitic acid (97.3 +/- 0.2%) and higher than generally reported. Absorption of lauric, myristic, oleic, linoleic and trans 18:1 monoenes did not differ from each other (>99%) but was higher than that of stearic and palmitic acids (P < 0.001). Metabolizable energy values were similar for all fatty acids. Although absorption of palmitic and stearic acids was affected by diet treatment, the magnitudes of the differences were small and do not appear to be biologically important, at least in terms of lipoprotein metabolism. On the basis of these results, reduced stearic acid absorption does not appear to be responsible for the differences in plasma lipoprotein responses to stearic acid relative to other saturated or unsaturated fatty acids.

Relationship between serum leptin levels and alcohol consumption in a controlled feeding and alcohol ingestion study.

We examined serum leptin levels in a controlled feeding and alcohol ingestion study to elucidate potential mechanisms by which alcohol may affect cancer and immunologically related health risks. A total of 53 healthy, nonsmoking postmenopausal women completed a random-order, three-period crossover design study in which each woman received zero (0 g of alcohol), one (15 g of alcohol), or two (30 g alcohol) drinks per day. After accounting for differences in body mass index, women who consumed 15 or 30 g of alcohol per day had 7.3% (95% confidence interval [CI] = 3.0% to 15.1%) and 8.9% (95% CI = 1.6% to 16.7%) higher serum leptin levels, respectively (P(trend) =.018), than women who consumed 0 g of alcohol per day. Younger women (i.e., 49-54 years) demonstrated a statistically significantly larger association of alcohol consumption level with the increase in serum leptin levels than older women (i.e., 55-79 years) (24.4%, 95% CI = 9.3% to 42.0% versus 3.7%, 95% CI = -4.1% to 12.1% increase in serum leptin levels for 30 g of alcohol per day relative to 0 g of alcohol per day for the lowest age quartile compared with the three highest age quartiles combined; P =.022). These results indicate that moderate alcohol consumption (15-30 g of alcohol per day) increases serum leptin levels in postmenopausal women and may predispose moderate drinkers to the morbidities associated with chronic elevations of this hormone including cancer.

Black tea consumption reduces total and LDL cholesterol in mildly hypercholesterolemic adults.

Despite epidemiological evidence that tea consumption is associated with the reduced risk of coronary heart disease, experimental studies designed to show that tea affects oxidative stress or blood cholesterol concentration have been unsuccessful. We assessed the effects of black tea consumption on lipid and lipoprotein concentrations in mildly hypercholesterolemic adults. Tea and other beverages were included in a carefully controlled weight-maintaining diet. Five servings/d of tea were compared with a placebo beverage in a blinded randomized crossover study (7 men and 8 women, consuming a controlled diet for 3 wk/treatment). The caffeine-free placebo was prepared to match the tea in color and taste. In a third period, caffeine was added to the placebo in an amount equal to that in the tea. Five servings/d of tea reduced total cholesterol 6.5%, LDL cholesterol 11.1%, apolipoprotein B 5% and lipoprotein(a) 16.4% compared with the placebo with added caffeine. Compared with the placebo without added caffeine, total cholesterol was reduced 3.8% and LDL cholesterol was reduced 7.5% whereas apolipoprotein B, Lp(a), HDL cholesterol, apolipoprotein A-I and triglycerides were unchanged. Plasma oxidized LDL, F2-isoprostanes, urinary 8-hydroxy-2'-deoxyguanosine, ex vivo ferric ion reducing capacity and thiobarbituric acid reactive substances in LDL were not affected by tea consumption compared with either placebo. Thus, inclusion of tea in a diet moderately low in fat reduces total and LDL cholesterol by significant amounts and may, therefore, reduce the risk of coronary heart disease. Tea consumption did not affect antioxidant status in this study.

Personality characteristics as predictors of underreporting of energy intake on 24-hour dietary recall interviews.

OBJECTIVE: To identify characteristics associated with misreporting of energy intake during 24-hour dietary recalls (24 HR). DESIGN: Ninety-eight subjects were administered two 24 HRs. Energy expenditure was determined by doubly labeled water (44 subjects) or intake balance (54 subjects). Data on subjects' physical, lifestyle, and psychosocial characteristics were also collected. Subjects/setting At the Beltsville Human Nutrition Research Center 52 women and 46 men were administered 24HR and completed lifestyle and personality questionnaires and a memory test. Physical characteristics such as weight, percent body fat, and total energy expenditure were measured. Statistical analysis The influences of subject parameters on energy misreporting were assessed by linear regression and Pearson product-moment correlation analysis for continuous variables and by ANOVA for discrete variables. Stepwise regression was used to identify key factors in underreporting. RESULTS: Factors particularly important in predicting underreporting of energy intake include factors indicating dissatisfaction with body image; for example, a 398 kcal/day underreport in subjects attempting weight loss during the past year with a nearly 500 kcal/day underreport in women. Overall, women underreported by 393 kcal/day relative to men and women evinced a social desirability bias amounting to a 26 kcal underreport for each point on the social desirability scale. Gender differences also were evident in the effect of percent body fat (with men underreporting about 16 kcal/day/percent body fat) and in departure from self-reported ideal body weight (with women underreporting about 21 kcal/day/kg). APPLICATIONS/CONCLUSIONS: Body image and fatness are key factors on which health professionals should focus when seeking predictors of underreporting of dietary intake. Dietary interviews must be conducted to minimize bias related to subjects' tendencies to win approval and avoid censure by the interviewer. In addition, dissatisfaction with body image may lead to underestimation of food intake, therefore reducing likelihood of success in weight loss. Thus, health care professionals involved in weight loss counseling may achieve better success if treatment includes generating a more positive body image.

The effect of daily alcohol intake on breath alcohol concentrations of postmenopausal women after a bolus dose.

OBJECTIVE: This study was designed to test whether daily alcohol intake can influence parameters related to rate of alcohol clearance and systemic alcohol exposure. METHOD: Postmenopausal women (N = 14) completed a study in which they consumed an alcohol treatment daily for 8 weeks. In a three-period crossover design, women consumed 0, 15 or 30 g/day ethanol, with each subject completing each treatment level. Following the 8-week adaptation period, the subjects consumed a single dose of 15 g ethanol, and breath samples collected to assess breath alcohol concentration (BrAC) every 5 minutes until the BrAC declined to zero. RESULTS: Adaptation to daily alcohol intake of 30 g/day resulted in reduced breath alcohol response compared to adaptation to 0 g/day. Specifically, area under the BrAC time curve was lower after women had consumed 30 g ethanol per day compared to that after daily consumption of 0 grams per day. Also, the time required for BrAC to decline to 0.01% after the bolus dose was reduced when subjects were adapted to 30g/day compared to 0 g/day. CONCLUSIONS: Daily intake of alcohol at a level of 30 g/day appears to be sufficient to alter the parameters related to systemic alcohol exposure.

Effects of moderate alcohol intake on fasting insulin and glucose concentrations and insulin sensitivity in postmenopausal women: a randomized controlled trial.

CONTEXT: Epidemiologic data demonstrate that moderate alcohol intake is associated with improved insulin sensitivity in nondiabetic individuals. No controlled-diet studies have addressed the effects of daily moderate alcohol consumption on fasting insulin and glucose concentrations and insulin sensitivity. OBJECTIVE: To determine whether daily consumption of low to moderate amounts of alcohol influences fasting insulin and glucose concentrations and insulin sensitivity in nondiabetic postmenopausal women. DESIGN, SETTING, AND PARTICIPANTS: Randomized controlled crossover trial of 63 healthy postmenopausal women, conducted at a clinical research center in Maryland between 1998 and 1999. INTERVENTIONS: Participants were randomly assigned to consume 0, 15, or 30 g/d of alcohol for 8 weeks each as part of a controlled diet. All foods and beverages were provided during the intervention. An isocaloric beverage was provided in the 0-g/d arm. Energy intake was adjusted to maintain constant body weight. MAIN OUTCOME MEASURES: Fasting insulin, triglyceride, and glucose concentrations, measured at the end of each dietary period; insulin sensitivity, estimated with a published index of glucose disposal rate corrected for fat-free mass based on fasting insulin and fasting triglyceride concentrations, compared among treatments with a mixed-model analysis of variance. RESULTS: A complete set of plasma samples was collected and analyzed for 51 women who completed all diet treatments. Consumption of 30 g/d of alcohol compared with 0 g/d reduced fasting insulin concentration by 19.2% (P =.004) and triglyceride concentration by 10.3% (P =.001), and increased insulin sensitivity by 7.2% (P =.002). Normal-weight, overweight, and obese individuals responded similarly. Only fasting triglyceride concentration was significantly reduced when comparing 0 and 15 g/d of alcohol (7.8%; P =.03), and no difference was found between consumption of 15 and 30 g/d of alcohol; however, there was a significant linear trend (P =.001). Fasting glucose concentrations were not different across treatments. CONCLUSIONS: Consumption of 30 g/d of alcohol (2 drinks per day) has beneficial effects on insulin and triglyceride concentrations and insulin sensitivity in nondiabetic postmenopausal women.

Dietary cis and trans monounsaturated and saturated FA and plasma lipids and lipoproteins in men.

Trans monounsaturated fatty acids (TFA) are hypercholesterolemic compared to oleic acid to a degree approaching or equivalent to saturated FA. However, it is unknown to what extent these effects may be due to cholesterol lowering by oleic acid rather than elevation by saturated FA and TFA. In order to better understand the impact of replacing TFA in foods, it is first necessary to know the relative lipid-modifying effects of the major FA that change as TFA are lowered or removed. For 5 wk, 50 normocholesterolemic men were fed controlled diets providing approximately 15% of energy from protein, 39% from fat, and 46% from carbohydrate in a randomized, 6 x 6, crossover design. Eight percent of energy was replaced across diets with the following: carbohydrate (CHO) (1:1 simple to complex); oleic acid (OL); TFA; stearic acid (STE); TFA/STE (4% of energy from each); carbon 12:0-16:0 saturated FA (LMP). LDL cholesterol concentrations (mmol/L) were as follows (different superscripts indicate significance at P < or = 0.01): OL 2.95a; CHO 3.05a,b; STE 3.10b,c; LMP 3.21c,d; TFA + STE 3.32d,e; and TFA 3.36e. HDL cholesterol concentrations (mmol/L) were as allows: STE 1.16a; TFA 1.16a,b; TFA/STE 1.17a,b; CHO 1.19b; OL 1.24c; and LMP 1.30d. Triacylglycerides were highest after STE (1.13) and lowest after OL (0.88) (P < 0.001). Thus, compared to the carbohydrate control diet, TFA raised LDL cholesterol at least equivalent to LMP but had no effect on HDL cholesterol; STE had no effect on LDL cholesterol but lowered HDL cholesterol; LMP raised both LDL cholesterol and HDL cholesterol; and oleic acid raised HDL cholesterol but had no effect on LDL cholesterol.

Plant sterol esters lower plasma lipids and most carotenoids in mildly hypercholesterolemic adults.

The ability of plant sterol esters (PSE) in salad dressing to modify plasma lipids and carotenoids was determined in 26 men and 27 women fed controlled, weight-maintaining, isocaloric diets. Diets contained typical American foods that provided 32% of energy from fat. Dressings contained 8 g (ranch) or 4 g (Italian) of fat per serving. PSE (3.6 g/d) were provided in two servings/d of one of the dressings. Diets with ranch or Italian dressing without and with PSE were fed for 3 wk/diet and crossed over randomly within dressings. Diets were adjusted to similar fat and fatty acid concentrations. Type of salad dressing did not affect plasma lipids, lipoproteins, carotenoids, or fat-soluble vitamins (P > 0.05). Switching from a self-selected baseline diet to the control diet resulted in reduction in low density lipoprotein (LDL) cholesterol of 7.9%, a decrease in high density lipoprotein (HDL) cholesterol of 3.1%, and a decrease in triglycerides (TG) of 9.3%. Consumption of 3.6 g of PSE resulted in further decreases in LDL cholesterol (9.7%) and TG (7.3%) but no additional change in HDL cholesterol. Total plasma carotenoids decreased 9.6% with PSE. An automated stepwise procedure was developed to produce candidate mixed models relating plasma carotenoid response to PSE. These models adjusted for preintervention plasma carotenoid levels and effects of diets on blood lipids. There were significant decreases in beta-carotene, alpha-carotene, and beta-cryptoxanthin (females only) not associated with changes in plasma lipids. Plasma carotenoids on all diets remained within normal ranges. We conclude that low-fat foods, such as salad dressings, are effective carriers for PSE.

Moderate alcohol consumption lowers risk factors for cardiovascular disease in postmenopausal women fed a controlled diet.

BACKGROUND: Moderate alcohol consumption (1-2 drinks/d) may decrease cardiovascular disease risk in postmenopausal women by improving lipid profiles. OBJECTIVE: We measured the effect of moderate alcohol consumption on lipids and lipoproteins in postmenopausal women. DESIGN: Postmenopausal women (n = 51) consumed 0 (control), 15 (1 drink), and 30 (2 drinks) g alcohol (ethanol)/d for 8 wk each as part of a controlled diet in a randomized crossover design. The control diet provided approximately 15%, 53%, and 32% of energy from protein, carbohydrate, and fat, respectively. The energy provided from alcohol in the 15- and 30-g alcohol diets was replaced with energy from carbohydrate. RESULTS: Compared with concentrations after the control diet, plasma LDL cholesterol decreased from 3.45 to 3.34 mmol/L (P = 0.04) and triacylglycerol from 1.43 to 1.34 mmol/L (P = 0.05) after 15 g alcohol/d. There were no additional significant decreases in either lipid after an increase in alcohol intake from 15 to 30 g/d. Compared with concentrations after the control diet, plasma HDL cholesterol increased nonsignificantly from 1.40 to 1.43 mmol/L after 15 g alcohol/d but increased to 1.48 mmol/L after 30 g alcohol/d (P = 0.02). Apolipoprotein A-I increased significantly and apolipoprotein B decreased significantly after 30 g alcohol/d relative to the concentration after the control diet. CONCLUSIONS: Consumption of 15-30 g alcohol/d by postmenopausal women apparently decreases cardiovascular disease risk by improving lipid profiles. Plasma LDL-cholesterol and triacylglycerol concentrations improve after 15 g alcohol/d; plasma HDL cholesterol improves only after 30 g alcohol/d.