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Nutritional Epidemiology

The Combination of High Fruit and Vegetable and Low Saturated Fat Intakes Is More Protective against Mortality in Aging Men than Is Either Alone: The Baltimore Longitudinal Study of Aging¹

Jean Mayer U.S. Department of Agriculture Human Nutrition Research Center on Aging at Tufts University, Boston, MA and ^* National Institute on Aging Intramural Program, National Institutes of Health, Bethesda, MD

²To whom correspondence should be addressed. E-mail: katherine.tucker{at}tufts.edu.

	ABSTRACT

TOP ABSTRACT SUBJECTS AND METHODS RESULTS DISCUSSION LITERATURE CITED

 
Saturated fat (SF) intake contributes to the risk of coronary heart disease (CHD) mortality. Recently, the protective effects of fruit and vegetable (FV) intake on both CHD and all-cause mortality were documented. However, individuals consuming more FV may be displacing higher-fat foods. Therefore, we investigated the individual and combined effects of FV and SF consumption on total and CHD mortality among 501 initially healthy men in the Baltimore Longitudinal Study of Aging (BLSA). Over a mean 18 y of follow-up, 7-d diet records were taken at 1–7 visits. Cause of death was ascertained from death certificates, hospital records, and autopsy data. After adjustment for age, total energy intake, BMI, smoking, alcohol use, dietary supplements, and physical activity score, FV and SF intakes were individually associated with lower all-cause and CHD mortality (P < 0.05). When both FV and SF were included in the same model, associations of each were attenuated with CHD mortality, and no longer significant for all-cause mortality. Men consuming the combination of 5 servings of FV/d and 12% energy from SF were 31% less likely to die of any cause (P < 0.05), and 76% less likely to die from CHD (P < 0.001), relative to those consuming <5 FV and >12% SF. Men consuming either low SF or high FV, but not both, did not have a significantly lower risk of total mortality; but did have 64–67% lower risk of CHD mortality (P < 0.05) relative to those doing neither. These results confirm the protective effects of low SF and high FV intake against CHD mortality. In addition, they extend these findings by demonstrating that the combination of both behaviors is more protective than either alone, suggesting that their beneficial effects are mediated by different mechanisms.

KEY WORDS: • fruit and vegetables • saturated fat • coronary heart disease • mortality • men

Coronary heart disease (CHD)³ is the leading cause of death in the United States, accounting for 31% of deaths in 1998 (1). The identification of preventable risk factors for CHD is, therefore, of tremendous importance. Until recently, the discussion of diet and heart disease has focused almost exclusively on dietary fat and cholesterol. A 1983 review on CHD and diet did not consider fruit and vegetables (FV) (2). A recent review on FV intake and cardiovascular disease (CVD) supported the importance of high FV intake, but noted that the biologic mechanisms for observed protective effects are not clear and may be multiple (3). The Dietary Approaches to Stop Hypertension (DASH) Trial highlighted the role of higher FV intake in blood pressure control (4). Based in large part on this trial, the recently released AHA Dietary Guidelines issued, for the first time, recommendations to choose 5 FV servings/d (5).

Despite a growing awareness of the benefits of FV, their consumption remains inadequate. Data from the 1989–1991 USDA Continuing Survey of Food Intakes by Individuals revealed that only 12% of the U.S. adult population consumed the recommended 2 servings of fruit and 3 of vegetables per day (6).

Because both SF and FV consumption are modifiable lifestyle variables, it is important to quantify their effects on CHD mortality. However, it is often difficult to separate the effects of each because FV intake tends to correlate inversely with intake of SF, the most widely accepted dietary risk factor for CHD (7). In this study, we examine associations between habitual FV and SF intake, separately and in combination, and subsequent CHD and total mortality among men in the Baltimore Longitudinal Study of Aging (BLSA). We also examine mortality associations with specific components of FV intake, adjusted for SF intake.

	SUBJECTS AND METHODS

TOP ABSTRACT SUBJECTS AND METHODS RESULTS DISCUSSION LITERATURE CITED

 
The BLSA, begun in 1958, was designed to study normal human aging (8) and precursors to disease and death. The current analysis includes 501 BLSA men who met the following criteria: 1) at least 4 completed days of 7-d diet record for 1 biennial visit; 2) born before 1929 and age 80 y at first dietary record; and 3) no history of angina pectoris or myocardial infarction (MI) at baseline. These men completed dietary records for 4–49 d (mean = 19 d) at 1–7 visits over a mean follow-up of 18 y. Because diet may be affected by major illness, we excluded dietary records obtained 2 y before death or subsequent to the development of clinical CHD. All subjects gave informed consent for participation in this study, and the protocol was approved by institutional review boards at the National Institutes of Health and Tufts New England Medical Center.

    Dietary intake. Dietary data were collected by 7-d diet record during 4 time periods: 1961–1965; 1968–1975; 1984–1991; and 1993 to the present time. Earlier reports of dietary intake in the BLSA participants were published (9,10). BLSA participants were trained to record their food intake by dietitians during their examination visit. Ambiguous or incomplete records were clarified by telephone interview.

Dietary data from 1961 to 1965 were sent to the Heart Disease Control Branch of the NIH for nutrient analysis. From 1968 to 1975, diet was analyzed at Washington University. From 1984 to 1991, records were coded into a nutrient database maintained by the BLSA. Since 1993, data have been entered into the Minnesota Nutrient Data System (NDS) at Tufts University (11). For this analysis, all dietary data were recoded into the NDS to make data comparable over time. Earlier nutrient intakes were back-adjusted to correct for food supply changes, using data from the USDA for appropriate time intervals for the composition of pork, beef, breakfast cereals, and other fortified foods (12,13).

The NDS system codes data at the ingredient level, and FV servings include portions of recipes. Daily servings were determined by comparing the weight of reported intake with the food guide pyramid serving size for each type of FV, averaging for the 4–7 d for each time point. Reported supplements were also entered into the NDS system.

    Control variables. Because dietary patterns may covary with other lifestyle and demographic characteristics, we adjusted for potentially confounding variables, including age at first visit, BMI, energy intake, physical activity score, smoking status, alcohol use, and vitamin supplement use.

Self-reported physical activity since the prior biennial visit was determined with a questionnaire covering specific activities at home, work, and recreation. Times spent in each activity were multiplied by respective estimated energy costs standardized by body weight, and summed to create energy expenditure scores (10). Smoking was categorized at each time point as either past, current 1 pack of cigarettes/d, or current <1 pack/d, with those who never smoked as the comparison group. Self-reported alcohol intake was classified following American Heart Association recommendations (5): nondrinkers, light (<1 drink, 13.2 g alcohol/d), moderate (1–2 drinks, 13.2–26.4 g/d), or heavy drinkers (>2 drinks/d).

    CHD diagnosis and mortality. All participants in the BLSA were followed for vital status. Cause of death was determined by consensus of 3 physicians using death certificates, hospital and physician records, and autopsy data, as available. For this analysis, all-cause mortality included those who died from any cause, and CHD mortality included those deaths due to acute MI or sudden coronary death. In addition, we noted time of CHD diagnosis by including the earliest time point of either confirmation of heart disease by Q-wave, occurrence of nonfatal MI, or CHD death, whichever came first.

    Statistical analysis. We used Cox proportional hazards analysis to estimate risk of total and CHD mortality associated with number of servings of FV and associated nutrients (dietary fiber, magnesium, ß-carotene, folate, and vitamin C), and with SF as independent variables. With the exception of age, all variables were included as time-dependent covariates. This allowed the use of all of the multiple measures taken for each variable before each point of comparison at incident events. Due to their skewed distribution, micronutrient variables were log-transformed. Unpaired t tests and ² analyses compared characteristics in survivors with men who died of any cause and with those who died of CHD.

Associations between dietary variable and mortality were adjusted for age, energy intake, BMI, physical activity score, smoking, alcohol use, and supplement use. A second set of models added the complementary dietary measure, i.e., SF for the FV model and vice versa. A third set of models added an indicator for this secular trend (first visit before vs. after 1980), based on slight changes in dietary entry methodology before and after this date, as well as an observed increase in FV intake in the more recent vs. earlier dietary records. To further control for other fat intake variables, we repeated all models adding, one at a time, intake of the following: trans fat, (n-3) fatty acids, polyunsaturated fat, total nonsaturated fat, and servings of whole grains. We also tested for interactions between SF and FV intake in relation to each outcome.

To examine the combined effects of FV and SF intake on all-cause and CHD mortality, we created a categorical variable. Intake of 5 servings of FV/d plus >12% energy from SF (although <10% is recommended, fewer than 12% of the men in this sample achieved that) served as the reference group. This group was then compared with groups of men with 5 servings of FV, but >12% energy from SF, those with 12% energy from SF, but <5 servings of FV, and those with both low SF and high FV intake. We adjusted for covariates, as above, and repeated this analysis, with adjustment for the secular trends in FV and SF intake observed after vs. before 1980. To investigate the effect on CHD diagnosis, we repeated these analyses replacing the mortality variable with diagnosis. Finally, we repeated these models including each of the fat intake and whole-grain variables.

	RESULTS

TOP ABSTRACT SUBJECTS AND METHODS RESULTS DISCUSSION LITERATURE CITED

 
Among these 501 men, there were 71 deaths from CHD over a mean 18 y of follow-up. Mean numbers of diet records available were 2.2, 2.4, and 2.5 (18, 18, and 20 diet days) for those who died of CHD, of other causes, and survivors, respectively. The age range at baseline, 34–80 y, was similar for all 3 groups.

As expected, survivors were younger (P < 0.05) at first visit (Table 1). There were no significant differences for BMI, energy intake, or alcohol intake between survivors and decedents. Survivors were less likely to smoke during the time of follow-up relative to those who died of CHD (P < 0.05). Supplement use did not vary significantly across groups. Survivors had significantly greater intakes of FV, dietary fiber, magnesium, and vitamin C, and lower intakes of saturated fat than those who died from CHD or other causes, and higher intake of folate than those who died from CHD.

    Micronutrient intake on risk of mortality. None of the individual nutrients were significantly associated with total mortality after adjusting for confounders and SF intake. Therefore, we present results only for CHD mortality. Because nutrient intakes were skewed, log transformations provided improved model fit (Table 3). For interpretation, we present them both in original scale and log-transformed. There was a 50% reduction in CHD mortality per 100 mg of magnesium intake, adjusted for covariates and SF (P < 0.001), and this remained significant after adjusting for secular trend. In fully adjusted models, ß-carotene showed a 10% reduction in risk/mg (P < 0.05), and dietary fiber a 6% reduction/g (P < 0.05).

	DISCUSSION

TOP ABSTRACT SUBJECTS AND METHODS RESULTS DISCUSSION LITERATURE CITED

Because low SF intake is usually associated with higher FV intake, few studies examined the independent effects of these dietary components. Our results confirm the importance of FV and SF consumption individually against CHD mortality. Each serving of FV was associated with a 6% reduction in all-cause mortality and a 21% reduction in CHD mortality, and each additional gram of SF was associated with an increased risk of 7% for CHD mortality. However, these individual results were attenuated (although still significant for CHD mortality), when adjusted for the other. By categorizing the men into groups based on the combination of dietary behaviors, we were able to demonstrate that total mortality was 31%, and CHD mortality up to 76% lower among men with both low SF and high FV intake, relative to those with low FV and high SF intake, and that this combination was considerably more protective than either behavior alone. Further, these results remained significant after adjusting for potential confounding variables, including other dietary components and secular trend. Interaction terms for SF and FV were not significant, suggesting that the effects are additive rather than interactive.

Many studies have evaluated the intake of nutrients associated with FV, rather than FV themselves. Antioxidant vitamins are thought to protect against CHD by inhibiting oxidation of LDL, and significant inverse associations with heart disease were seen for ß-carotene (17,18) and vitamin C (19). Magnesium (20–22) and the soluble fiber in FV (23) were also associated with a reduced risk of heart disease. Recently, through its ability to lower homocysteine, there has been considerable interest in folate as a cardioprotective nutrient (24,25). Each of these nutrients could be contributing to the effects seen with FV intake. We found significant protection against CHD mortality with magnesium, ß-carotene, and dietary fiber, but not with vitamin C or folate.

Major strengths of the current study lie in the length of follow-up and the dietary detail obtained. Most previous studies of diet and mortality used FFQ. Although these instruments measure usual dietary intake that ranks individuals well for many nutrients and foods, the use of grouped food categories and assumed portion sizes may lead to error. We collected detailed dietary data for a mean of 19 d/person, a number sufficient to substantially reduce misclassification due to intraindividual intake variability. The database used has detail to capture precise individual intakes (11). The ability to detect significance despite a modest sample size is most likely due to this precision in individual intake classification.

This study also has some limitations. As in any such long-term study, there have been changes in methodology. We recoded the early dietary data to standardize values over time and to utilize recent food composition values. Although some detail may have been lost, this recoding should have little effect on FV classification. We also corrected for changes in the food supply that could affect assessment of earlier diet, particularly the fat composition of meats. Because men entered the study over a 34-y period, the effects of secular trend in dietary habits were difficult to separate from those of diet per se. During these 3 decades, there was a decline in CHD mortality accompanied by dietary changes. The Minnesota Heart Survey demonstrated that the annual decline in CHD death among men was greater during 1979–1988 (4.8%) than in 1970–1978 (3.9%) (26). We noted an increase in FV intake and a decrease in SF intake that was most pronounced after 1980. This trend is supported by USDA data showing increases of 19% in fruit, 69% in citrus juice, and 24% in vegetable consumption; and a 22% decrease in animal fat consumption from 1965 to 1987 (27). To the extent that these dietary changes reduced CHD mortality, secular trend adjustment will dilute their observed effect; on the other hand, residual confounding from improvements in heart disease care during this time period cannot be excluded.

Participants in the BLSA are not a random population sample, but are predominantly white men of relatively high socioeconomic status. They may have better quality diets, and be more responsive to messages on health behavior change than the general population. To the extent that these characteristics limit the range of dietary variation, however, associations seen here may be weaker than those in larger, more diverse populations. Finally, the current analysis was limited to men because women were not recruited into the BLSA until 1978.

The findings that dietary combinations offer greater health benefits than do individual nutrients support a growing body of literature on dietary patterns. Only recently, with the success of the DASH diet intervention (4) and observed benefits of the Mediterranean diet, has interest in total dietary pattern emerged. In one study, Italian survivors of MI with the highest vs. lowest quartile of Mediterranean diet scores were 49% less likely to die during a 6.5 y follow-up (28). In Sweden, women consuming >15 "healthy foods" were 53% less likely to die from CHD than women consuming <9 such foods (29). Lower CHD mortality was also seen among men in the Health Professionals Follow-up Study in the highest vs. lowest quintile of a "prudent" combination of foods, including FV. Conversely, there was 64% greater mortality in the highest vs. lowest quintile of a "Western" combination, including red meat, a major source of SF (30). Our results that high FV and low SF together provide greater protection against CHD mortality than do either alone, contribute to the growing evidence that dietary patterns, rather than single foods or nutrients, are important and that multiple dietary components may be cardioprotective.

In conclusion, the results of this study support earlier observations that dietary intakes low in SF or high in FV each offer protection against CHD mortality. In addition, however, our data suggest that the combination of both high FV with relatively low SF intake offers greater protection against both total and CHD mortality than either practice alone.

	FOOTNOTES

 
¹ Supported in part by the U.S. Department of Agriculture Agricultural Research Service contract 53–3K06–01 and the National Institutes of Health National Institute on Aging Intramural Program.

³ Abbreviations used: BLSA, Baltimore Longitudinal Study of Aging; CHD, coronary heart disease; DASH, Dietary Approaches to Stop Hypertension; FV, fruit and vegetables; HR, hazard ratio; High FV, intake of 5 servings/d of fruit and vegetables; High SF, dietary intake of saturated fat > 12% energy; Low FV, intake of <5 servings/d of fruit and vegetables; Low SF, dietary intake of saturated fat 12% energy; MI, myocardial infarction; NDS, Nutrient Data System; SF, saturated fat.

Manuscript received 3 September 2004. Initial review completed 6 October 2004. Revision accepted 30 November 2004.

	LITERATURE CITED

TOP ABSTRACT SUBJECTS AND METHODS RESULTS DISCUSSION LITERATURE CITED

 

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This Article Abstract Full Text (PDF) Purchase Article View Shopping Cart Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Tucker, K. L. Articles by Fleg, J. L. Search for Related Content PubMed PubMed Citation Articles by Tucker, K. L. Articles by Fleg, J. L.