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Articles

Changes in Women's Plasma Lipid and Lipoprotein Concentrations Due to Moderate Consumption of Alcohol Are Affected by Dietary Fat Level

Diet and Human Performance Laboratory, Beltsville Human Nutrition Research Center, ARS, USDA, Beltsville, MD, and the Lipid Research Clinic Laboratory, George Washington University, Washington D.C.

¹To whom correspondence should be addressed at Diet and Human Performance Laboratory, BHNRC, Building 308, Room 206, BARC-east, Beltsville, MD 20705. E-mail: rumpler{at}bhnrc.arsusda.gov

	ABSTRACT

TOP ABSTRACT INTRODUCTION MATERIALS AND METHODS RESULTS DISCUSSION REFERENCES

 
We studied the impact of substituting ethanol for dietary carbohydrate, in high- and low-fat diets, on plasma lipids and lipoprotein concentrations. During a 12-wk, weight maintaining, controlled feeding study, women consumed only food and beverage provided by the Human Studies Facility of the USDA Beltsville Human Nutrition Research Center. Twenty-six women (age 41–59 y) consumed either a high-fat diet (38% of energy from fat) or a low-fat diet (18% of energy from fat) for 12 wk. The 12-wk feeding period was divided into two 6-wk periods in a cross-over design during which either ethanol or carbohydrate was added to the diet (5% of total daily energy intake). When the women consuming the high-fat diet had ethanol added to their diet, they had 6% lower plasma cholesterol (P = 0.003), 11% lower LDL cholesterol (P = 0.001) and 3% higher HDL cholesterol (P = 0.06) than when they had an equal amount (% energy) of carbohydrate added to their diet. The greater HDL cholesterol concentration was due to a 21% greater the HDL₂ subfraction (P = 0.001). The ratio of LDL to HDL cholesterol was 14% lower. No significant differences existed in plasma lipids in women consuming the low-fat diet between the periods in which they had ethanol or carbohydrate added to their diet. This study suggests that the decreases in cardiovascular disease risk factors typically seen with moderate alcohol consumption may not be evident in individuals consuming a diet low in fat. Therefore changes in the risk factors associated with a low-fat diet and moderate alcohol consumption do not appear to be additive.

KEY WORDS: • blood lipids • plasma cholesterol • ethanol consumption • dietary fat • humans

	INTRODUCTION

TOP ABSTRACT INTRODUCTION MATERIALS AND METHODS RESULTS DISCUSSION REFERENCES

 
Elevated levels of LDL cholesterol and decreased levels of HDL cholesterol were consistently shown to be risk factors for cardiovascular disease (CVD)² (Gordon et al. 1977 , Lipid Research Clinics Program. 1988 , Manninen et al. 1988 ). HDL cholesterol levels were also shown to be a strong predictor of CVD in women (Bush et al. 1988 , Crouse 1989 ). Over the last two decades numerous studies utilizing a variety of methodologies showed that a reduction in the risk of CVD can be achieved by the consumption of a diet lower in fat than currently consumed by the American population (NRC 1989 ). This reduction in risk of CVD is generally accepted to be a consequence of a decrease in circulating levels of LDL cholesterol. Low-fat diets, however, reduce both LDL and HDL cholesterol concentrations, and in our studies do not an improve the ratio of LDL cholesterol to HDL cholesterol (Clevidence et al. 1992 ).

Numerous population-based studies reported a significant relationship between alcohol consumption and changes in blood lipids and lipoproteins. In one of the first reports to examine the relationship between alcohol consumption and blood lipid levels Ostrander et al. (1974) reported significantly higher triglyceride levels in men who drank alcohol regularly. They also reported elevated cholesterol levels in men under 50 y of age who consumed alcohol but no difference in men over 50 y. Their observation of higher circulating triglycerides was a consistent finding in subsequent studies in individuals with high alcohol consumption but was less so in subjects with ethanol intakes below 60–80 g/d (Srivastava et al. 1994 ). The effect on circulating cholesterol levels was less consistent with some studies reporting higher levels in drinkers (Barboriak 1984 , Cushman et al. 1986 ) and other studies reporting no effect (Avagaro and Cazzolato 1975 , Burr et al. 1986 ). Srivastava et al. (1994) in a review, suggested that some of the inconsistency seen in the response of cholesterol to ethanol consumption might be related to the fat level in the diet. They observed that individuals consuming a high-fat diet might be more sensitive to the effects of alcohol on blood lipids. Additionally, gender differences may have contributed to the variation in the responsiveness of blood lipids to alcohol consumption. Taylor et al. (1981) observed, in males but not females, higher triglyceride levels in drinkers than in nondrinkers.

Circulating levels of VLDL, LDL, and HDL were found to be powerful risk factors for CVD (Campos et al. 1991 , Gordon et al. 1989 , Stampfer et al. 1988 ). At least half of the reduced risk in CVD associated with alcohol consumption was attributed to changes in circulating levels of HDL and HDL subfractions (Langer et al. 1992 ). Observational studies of large populations showed that regular consumers of alcohol have higher circulating levels of HDL cholesterol than do those who abstain from alcohol (Hein et al. 1996 , Jackson et al. 1991 , Paunio et al. 1996 ), and these higher HDL levels are associated with lower CVD risk. Clinical trials confirmed the effect of alcohol consumption on circulating HDL levels in premenopausal women (Clevidence et al. 1995 ) and in men (Belfrage et al. 1977 , Valimaki et al. 1988 ). However, there does seem to be some gender difference in the response to alcohol consumption (Taylor et al. 1981 , Weidner et al. 1991 ).

Concentrations of some subfractions of HDL were correlated with the risk of CVD. Initially it was believed that HDL₂ was more protective than HDL₃ (Miller et al. 1981 ). However in more recent studies by Stampfer et al. (1991) , both HDL₂ and HDL₃ were inversely related to CVD risk, and HDL₃ was the stronger predictor. The effect of alcohol on these subfractions is not entirely clear. In a study of premenopausal women, Clevidence et al. (1995) reported that both HDL₂ and HDL₃ concentrations were increased by alcohol consumption. However, Valimiki et al. (1988) reported a dose-dependent response. They found that HDL₂ increased when men consumed ca. two drinks (12/g/ethanol) per day, and both HDL₂ and HDL₃ increased when alcohol consumption was increased to five drinks per day. Women may be more sensitive to the effect of alcohol on HDL. At an ethanol intake of one drink per day or less, a more pronounced effect on HDL cholesterol can be expected in women than in men (Taskinen et al. 1987 , Taylor et al. 1981 ). In this study we examined the possibility that a low-fat diet combined with the regular moderate consumption of alcohol would have an additive effect on the improvement of both plasma lipid levels and lipoprotein profiles.

	MATERIALS AND METHODS

TOP ABSTRACT INTRODUCTION MATERIALS AND METHODS RESULTS DISCUSSION REFERENCES

 
Healthy adult females (32), ages 40–65 y, were selected from the general population. During the initial screening, height, weight and percent body fat by bioelectric impedance analysis were measured. In addition, alcohol consumption and physical activity questionnaires were completed. All subjects were normotensive, nondiabetic and had normal blood chemistry values. Exclusion criteria included smoking, abstinence from alcohol, a history of alcohol abuse, body mass index (BMI) greater than 32 kg/m² or plasma cholesterol concentration greater than 7 mmol/L. Six of the women were considered pre- or perimenopausal with the remaining women postmenopausal. Ten of the postmenopausal women were receiving hormone replacement therapy; type and dosage did not change throughout the study. Menstrual cycle or hormone replacement therapy schedule was not considered in the scheduling of blood sampling. Diet treatments were balanced for hormonal status of the women (peri- or postmenopausal) as well as hormone replacement therapy. A cooperating physician conducted physical evaluations of all subjects prior to selection and reviewed and monitored all procedures for possible medical implications and health hazards. All subjects were informed of the general purpose of the study and had all procedures explained to them. Expectations of the researchers for subjects were explained in detail in special written information and/or in consent forms. Informed consent was obtained and documented. The Institutional Review Board of Georgetown University approved all procedures. Subjects agreed, in writing, not to drive or operate machinery after consuming the alcoholic beverages. As a stipulation for participating in the study, subjects agreed to consume the alcoholic beverages or their nonalcoholic counterparts just prior to bedtime.

Subjects were fed at the Human Studies Facility of the Beltsville Human Nutrition Research Center throughout the 12-wk study. Diets were formulated to meet or exceed the Recommended Dietary Allowances for known nutrients. Foods utilized consisted of those normally found in human diets; no test chemicals or test food additives were added other than those consistent with the objective of the study as outlined below.

Diets.

Two diets, which differed in their fat content, were consumed in this study. The menus were formulated at various energy levels in increments of ca. 1 MJ/d. These diets were formulated using values from the USDA Nutrient Database for Standard Reference (Release 11) to provide ca. 14% of dietary energy from protein and either 18% (low-fat) or 38% (high-fat) of dietary energy from fat. (Saturated, monounsaturated and polyunsaturated fat constituted ca. 31, 37, 26% of total fat in the high-fat and 32, 33, 24% in the low-fat diet, respectively. Cholesterol content of the diets was 37 mg cholesterol/MJ diet and 23 mg cholesterol/MJ diet in the high- and low-fat diets, respectively.) The higher fat level was chosen to approximate the average fat content of the American diet (NRC 1989 ). The lower fat level was arbitrarily chosen to provide a substantially lower fat content, yet maintain palatability of the overall menu. High- and low-fat designations were intended to be relative to the current recommendation that Americans consume an average of 30% of total energy or less from fat (NRC 1989 ). The energy intake for each individual was set as the nearest formulated energy level. However, all reported values in this paper are based on the actual metabolizable energy intake and available fat, protein and carbohydrate determined as previously reported (Rumpler et al. 1996 ).

The subjects consumed breakfast and dinner in the dining room of the Human Studies Facility under the supervision of a registered dietitian or a dietary technician. Lunches, snacks and weekend meals were packed for consumption away from the Human Studies Facility. Beverage and medication records were maintained throughout the diet study. Foods and energy-containing beverages were limited to those provided by the study. Initial energy intakes were estimated for each subject before the beginning of the study, utilizing a resting energy expenditure measurement and adjusting the energy intake level by a lifestyle factor as described by the World Health Organization. Energy intakes were adjusted to maintain body weight throughout the study.

Subjects consumed an alcoholic beverage during half of the study. The amount of ethanol consumed was scaled to provide 5% of daily energy intake, a level considered to be within the range of moderate drinking. A standard drink was defined as 12 g of ethanol. Using a standard food value of 28.8 kJ/g (6.9 kcal/g) of ethanol, an individual consuming 8372 kJ/d (2000 kcal/d) of food received 14.3 g of ethanol/d (1.2 drinks/d). An individual consuming 12558 kJ/d (3000 kcal/d) of food received 21.45 g/d (1.8 drinks/d). These values represent the extremes of ethanol consumption during the study.

Subjects were given the beverage for consumption at home with a small amount of food saved from the evening meal. Ethanol for consumption was provided as grain alcohol, mixed into either a grape-colored, nonfruit juice, beverage (Gatorade Co., Chicago, IL) or or a nonalcoholic red wine (Cabernet Sauvignon, Ariel Vineyards, Napa, CA). During the nonethanol period, each subject consumed the same drink plus an amount of a highly soluble carbohydrate powder (Polycose®, Ross Laboratory, Columbus, OH) that was equal in total energy to the amount of ethanol added during the ethanol period. The beverage was weighed daily, and the supplements (ethanol or soluble carbohydrate powder) were mixed into the beverage before distribution to the subjects. Data from the two carrier beverages were pooled since there was no significant differences in any variable measured in this study due to carrier beverage.

Plasma lipid and lipoprotein analysis.

Blood samples were drawn after an overnight fast (12 h) immediately before breakfast, with replicates taken on Monday and Wednesday, or Tuesday and Thursday. Baseline samples were collected during the week before initiation of the controlled feeding. Subsequently, blood was collected during the sixth week of each of the controlled feeding periods. Blood was drawn from antecubital veins of subjects after an overnight fast, mixed with 1.5 g of disodium EDTA/L and cooled on ice. Plasma samples were analyzed at the George Washington University Lipid Research Clinic Laboratory (Hainline et al. 1982 ), where standardization with the Centers for Disease Control was maintained throughout the study for analysis of total cholesterol and triglycerides and HDL cholesterol. Cholesterol and triglycerides were analyzed enzymatically using Abbott ABA-100 analyzers with reagents supplied by Abbot Diagnostics (North Chicago, IL). On the day of plasma sample collection, HDL and HDL₃ fractions were obtained by sequential precipitation techniques as described by Gidez et al. (1982) . These fractions were frozen at -80°C and analyzed for cholesterol at the end of the study. All of a given subject's samples were analyzed in a single analytical run. HDL₂ cholesterol was determined as the difference between HDL cholesterol and HDL₃ cholesterol values. LDL cholesterol was derived by the method of Friedewald et al. (1972) . Apolipoprotein A-I and apolipoprotein B were determined by rate immunonephelometry with a Beckman ICS Analyzer II (Beckman Instruments, Inc., Brea, CA). Boehringer Mannheim (Indianapolis, IN) antiserum was diluted in Beckman nephelometric buffer; lipoproteins were disrupted using 1% Tween-20 in 0.15 mol/L of NaCl.

Experimental design and statistical analysis.

The overall design of the study was a split plot on diet (high-fat or low-fat) with a crossover within each subplot on supplement (ethanol or carbohydrate). Subjects were randomly assigned to one of the two experimental diets for the duration of the study (split plot). During the first 6-wk period, subjects were randomly assigned to either the carbohydrate or ethanol supplement. The supplement treatment was then switched for the second 6-wk period (subplot crossover) while the diet consumed by the subject remained the same as in the first period. Two main effects of diet and supplement were examined in this study. Values for analysis were averages of replicate samplings taken on 2 d at the end of each dietary period. Data for the perimenopausal women, postmenopausal women receiving hormone replacement therapy and for those women not receiving hormone replacement therapy were pooled since no effect on heterogeneity of variance or significant interaction terms were detected. Thus, the experiment was analyzed using a mixed model analysis of variance where diet and supplement each had two levels. Comparisons of ethanol vs. carbohydrate within diet had the greatest statistical power since each subject received both ethanol and carbohydrate in a crossover design and within subject variation can be accounted for in the statistical analysis. Comparisons between diets have a weaker statistical power due to the inability of this type of design to account for individual variation. This design selection was intentional since the primary treatment of interest was the comparison of ethanol with carbohydrate followed by the interaction of diet and ethanol and finally the effect of diet. Data are presented as the least square means with the standard error. Where appropriate, the probability (P ||T||) values for specific contrasts are presented. Baseline values (Table 1 )were used as covariates in lipid/lipoprotein analysis; age was used as a covariate for apoprotein analysis.

	RESULTS

TOP ABSTRACT INTRODUCTION MATERIALS AND METHODS RESULTS DISCUSSION REFERENCES

The six premenopausal women were equally distributed between the high- and low-fat diet treatments and none withdrew from the study. Six of the subjects, two in the low-fat and four in the high-fat treatment, failed to complete both periods of the study, and their data were excluded from the analysis in accordance with the study plan. This resulted in the five of seven remaining women receiving hormone replacement therapy having been assigned to the low-fat treatment and two to the high-fat treatment.

Baseline characteristics of the 26 subjects completing the study are presented in Table 1 . The women ranged in ages from 41 to 59 y (mean of 51.5 y), had a BMI that ranged from 18 to 31 kg/m² and had total body weights that ranged from 49 to 92 kg. Subjects consuming the high-fat diet had a 6% higher average body weight and BMI than those consuming the low-fat diet. Energy intake averaged 8.4 MJ/d in subjects that consumed the high-fat and 8.2 MJ/d in those that consumed the low-fat diet. However, there were no significant differences in plasma lipid concentrations (Table 1) at baseline, between the high- and low-fat groups.

Changes in plasma lipids and lipoproteins.

Plasma lipid and lipoprotein values are presented in Table 2 as least square means, adjusted for baseline values, after 6 wk of treatment. The main effects of the statistical model (ethanol vs. carbohydrate, high-fat vs. low-fat diets) were significant for a number of variables measured. Women who consumed the low-fat diet had a 5% lower concentration of plasma cholesterol (P 0.06), 7 % lower concentration of LDL cholesterol (P 0.05) and 9% lower concentration of HDL-cholesterol (P 0.09) than did those consuming the high-fat diet. The ratio of LDL-cholesterol/HDL-cholesterol was unaffected by diet. Apo A-I concentration was 18% lower (P 0.02) in women consuming the low-fat diet. HDL cholesterol concentration was greater by 3% (P 0.03), and the ratio of LDL cholesterol to HDL cholesterol was lower by 9% (P 0.05) when women consumed ethanol.

	DISCUSSION

TOP ABSTRACT INTRODUCTION MATERIALS AND METHODS RESULTS DISCUSSION REFERENCES

 
Fat intake and the pattern of alcohol consumption are lifestyle choices that modulate risk factors for CVD (Hegsted and Ausman 1988 , NRC 1989 ). Diets high in fat, particularly saturated fat, increase the incidence of CVD, while regular, moderate consumption of alcohol decreases the incidence. The impact on CVD of alcohol consumption and the amount of dietary fat, in large part, were related to their effects on blood lipid and lipoprotein profiles. Individuals consuming a diet lower in fat were shown repeatedly to have lower plasma cholesterol and LDL cholesterol concentrations (Clevidence et al. 1992 , Hegsted et al. 1993 ). Responses of other lipoproteins to changes in dietary fat levels were not as dramatic (Criqui et al. 1987 ). However, it was shown (Avogaro and Cazzolato 1975 ) that the regular consumption of moderate levels of alcohol can have a positive impact on lipoprotein profiles by both decreasing LDL cholesterol and increasing HDL cholesterol. In this study we investigated the possibility that an additive effect might be produced when subjects consumed a low-fat diet in conjunction with moderate amounts of alcohol.

The effects of the two fat treatments on plasma lipids were as expected. Women consuming a low-fat diet had lower levels of plasma cholesterol as well as LDL and HDL cholesterol. This resulted in no change in the LDL to HDL cholesterol ratio. The plasma lipid response to consumption of ethanol was also as expected. LDL cholesterol levels were decreased, and HDL cholesterol levels were increased by alcohol consumption. Such changes have been reported from a number of studies (Avogaro and Cazzolato 1975 , Belfrage et al. 1977 , Clevidence et al. 1995 , Ostrander et al. 1974 , Valimaki et al. 1988 ) where higher levels of alcohol were administered. In this study, the increase in HDL₂ cholesterol accounted for the increase in HDL cholesterol. This differs from a previous study of ethanol consumption in premenopausal women in which there was a proportional increase in HDL₂ and HDL₃ fractions (Clevidence et al. 1995 ). This inconsistency could represent a difference in metabolic response between premenopausal women and the predominantly postmenopausal women in the current study. Consistent with other studies of postmenopausal women (Grandjean et al. 1998 , Li et al. 1996 ), HDL₃ cholesterol represented a large proportion of the total HDL cholesterol. However, the ratio of HDL₂ to HDL₃ was low, regardless of treatment. It is noteworthy that recent epidemiological data showed that both HDL₂ and HDL₃ are related to decreased risk of CVD (Stampfer et al. 1988 ).

When we separated the data by dietary fat treatment, clearly there was little or no effect of ethanol consumption on the blood lipid variables measured in those subjects consuming a low-fat diet. The significant effects of ethanol treatments occurred in subjects that consumed the high-fat diet. In subjects consuming the high-fat diet, consumption of ethanol decreased plasma cholesterol by 6% and LDL cholesterol by 11%, and these lower levels were similar to those produced by the low-fat diet with or without ethanol consumption. HDL cholesterol, in particular HDL₂, increased in response to ethanol consumption when subjects consumed the high-fat diet.

The responses to ethanol seen in the women consuming the high-fat diet are similar in direction and magnitude to those differences reported between drinkers and nondrinkers in population-based studies (Hegsted and Ausman 1988 , Ostrander et al. 1974 ). This was expected since the high-fat diet used in this study is similar in fat level to the "typical diet" consumed by free-living individuals in the United States. The lack of response to ethanol consumption in individuals consuming a low-fat diet complicates further the interpretation of studies on alcohol consumption in which diet composition is not controlled. For example, in the Health Professionals Follow Up Study (Ascherio et al. 1996 ), those individuals who consumed the highest levels of total fats and saturated fats also consumed the lowest levels of alcohol, fruits, vegetables and dietary fiber. The clustering of dietary habits, as observed in the Health Professionals Follow Up Study study, would indicate that the assessment of alcohol-induced changes in population studies is difficult due to changes in a number of other dietary variables. This suggests that the controlled feeding study is a particularly appropriate approach to the study of dietary components that modulate alcohol-induced changes in plasma lipoproteins.

From a public health standpoint, this study suggests that even low levels of alcohol consumption can improve the lipoprotein profile of women consuming the high-fat diet typical in the U.S. However, most of the beneficial effects of alcohol consumption on blood lipids can be achieved by a low-fat diet alone and little if any additional benefit is garnered by the inclusion of alcohol in the diet. This observation could simplify the choice to drink or not by individuals at high risk for diseases, such as breast cancer and hypertension, for which alcohol consumption may be a risk factor.

	FOOTNOTES

 
² Abbreviations used: BMI, body mass index; CVD, cardiovascular disease.

Manuscript received March 5, 1999. Initial review completed March 26, 1999. Revision accepted May 24, 1999.

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