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Journal of the American College of Nutrition, Vol. 17, No. 3, 263-269 (1998)
Published by the American College of Nutrition

Original Paper

Prospective Assessment of Coronary Heart Disease Risk Factors: The NHANES I Epidemiologic Follow-up Study (NHEFS) 16-Year Follow-up

Peter S. Gartside, PhD, Ping Wang, PhD and Charles J. Glueck, MD, FACN

University of Cincinnati College of Medicine, Biostatistics Division (P.S.G.), Jewish Hospital of Cincinnati, Ohio
Cholesterol Center (P.W., C.J.G.), Jewish Hospital of Cincinnati, Ohio

Address reprint requests to: C.J. Glueck, MD, FACN, Cholesterol Center, Jewish Hospital, 3200 Burnet Ave, Cincinnati, OH 45229


   ABSTRACT
TOP
 ABSTRACT
INTRODUCTION
 METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 
Objective: Our specific aim in the 16 year prospective NHANES I epidemiologic follow-up study (NHEFS) was to assess the important roles of modifiable dietary and behavioral factors in causation and prevention of deaths and hospitalizations for coronary heart disease (CHD).

Methods: Using NHEFS 16 year follow-up data (1971 to 1987), we studied 5811 subjects, 1958 with and 3853 without CHD events, using logistic regression.

Results: In age groups 40 to 49, 50 to 59, 60 to 69, and 70 to 74 years (at study entry in 1971–4), the numbers of men and women were respectively 597 and 1019, 570 and 619, 932 and 1042, and 486 and 546. The following factors were independently positively associated (p<.05) with CHD: age, serum cholesterol, body mass index, cigarette use, and region (Midwest, Northeast). The following factors were independently negatively associated (p<.05) with CHD: gender (female), race (black), fish intake, alcohol, high school education, moderate exercise, and moderate and heavy habitual physical activity. Subjects with serum cholesterol >249 mg/dl benefitted less (p=.04) from fish intake than those with 209 to 249 or <209, and benefitted less (p=.03) from alcohol intake (CHD incidence [%]):


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Conclusions: These associations emphasize the important role of modifiable dietary and behavioral factors in the causation and prevention of CHD.

Key words: coronary heart disease, fish, alcohol, serum cholesterol


   INTRODUCTION
TOP
 ABSTRACT
 INTRODUCTION
METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 
Using NHANES I prospective 10-year follow-up data, we recently studied 8,251 subjects, 492 with cardiovascular events and 7,759 without events during the follow-up period 1971–1975 to 1982–1984 [1]. By logistic regression, the following factors were independently, significantly, and inversely associated with coronary heart and vascular disease hospitalizations: alcohol intake, dietary riboflavin, dietary iron, serum magnesium, leisure time exercise, habitual physical activity, and female gender. Positive significant independent determinants of CHD events included cigarette smoking, sedimentation rate, Quetelet index, maximum body weight, and age [1]. These associations emphasized the important role of modifiable dietary and behavioral characteristics in the causation and prevention of coronary heart disease [1].

Our specific aim in the 16-year longitudinal assessment of 5,811 subjects in the NHANES I epidemiologic follow-up study (NHEFS) [1–5] was to prospectively assess the important roles of modifiable dietary and behavioral characteristics in the causation and prevention of coronary heart disease.


   METHODS
TOP
 ABSTRACT
 INTRODUCTION
 METHODS
RESULTS
 DISCUSSION
 REFERENCES
 
NHANES I
The National Health and Nutrition Examination Survey I (NHANES I) was carried out from 1971 to 1975 [3]. A longitudinal follow-up evaluation of NHANES I subjects, the NHANES I Epidemiologic Follow-up Study (NHEFS), was carried out in 3 waves (1982–1984, 1986, 1987) in 14,407 subjects aged 25 to 74 who participated in NHANES I [4,5]. The NHEFS follow-up predominantly involved questionnaire information; blood pressure and weight were measured in 1982–1984 [4,5]. As summarized by Harris et al [6], for those persons who had died between 1971–1975 and 1987, death certificates were obtained and coded for 97% of the deceased. Hospital records were obtained and coded as well [6]. In our current report, the 16 year follow-up data from the 1987 follow-up were available and were utilized.

Cholesterol Measurement.
All blood samples for measurements of serum total cholesterol were quantitated at a single centralized laboratory [5] to avoid between-laboratory variation. Only total cholesterol was assessed in our current report since HDL cholesterol and triglyceride levels were not measured.

Study Population.
The total sample in NHANES I (1971–1974) included 20,749 persons [3]. In the 1971–1974 initial screening for NHANES I, 14,407 subjects were examined ages 25–74, and at the 16 year follow-up in 1987 of those ages 25 to 74 in 1971–1974, 11,018 (77%) were traced. Of these 11,018 subjects, 8721 had complete data sets for the variables of interest in the current analysis. Of those who were age 40 to 74 at the initial exam in 1971–1974, 5811 (with complete data sets, not using any special diets) were analyzed in 16 year follow-up (now ages 56 to 90 years) for evaluation of coronary heart disease morbidity and mortality, providing a total of 69,158 person years. In age groups 40 to 49, 50 to 59, 60 to 69, and 70 to 74 years (at study entry in 1971–4), the numbers of men and women were respectively 597 and 1019, 570 and 619, 932 and 1042, and 486 and 546. The number of subjects identified as Asians was very small, 9 Chinese and 10 Japanese.

To reduce the possibility of extraneous conclusions due to changes in diet caused by, or as a consequence, of disease discovery [7], we excluded all subjects who, by questionnaire response, had been using any special diet including those designed to reduce CHD risk, providing a cohort of 5,811 subjects. We did not exclude subjects taking antioxidant vitamins or estrogens; estrogen use was not included in the NHEFS data tape. Of these 5,811 individuals with 16 year follow-up, 3,853 (66%) had no hospitalizations or death from coronary heart disease, whereas 1,958 (34%) had CHD hospitalization or death. Cause-specific mortality [6] was determined from death certificates (ICD-9 codes 410–414, 420–441 with ICD 410–414 for coronary heart disease). Hospitalizations were also coded by ICD-9, and codes 410–414 and 420–441 were likewise included as events for cardiovascular and coronary heart disease.

Statistical Methods
The dependent variable of interest was cardiovascular and coronary heart disease mortality and hospitalization.

The explanatory variables [1] included age, sex, race, serum total cholesterol, poverty class (poverty index divided by tertiles), ethnic group (Hispanic, other European, Black, American Indian, Asian, other), geographic region (Northeast, Midwest, West, South), and urban class (urban, suburban, rural). The poverty index consists of income divided by the number of persons in the household. Additional explanatory variables included log body mass index (BMI), cigarette use, education level of the head of household, leisure time exercise (little or none, moderate or much), and habitual physical activity (little, moderate, much). NHEFS did not obtain data on the waist/hip ratio.

Information was collected on specific food items (i.e., fish, milk, fruit, legumes, desserts cheese etc). Legume intake included peas, beans, peanuts, and peanut butter. Desserts included cakes, pies, cookies, puddings, and ice cream. The NHEFS data tape did not uniquely identify vegetarians. We included food groups in our analytical models as explanatory variables. Demographic variables were included in all models along with the other variables. Interactions among the explanatory variables were included in the multiple regression calculation.

Since age is a powerful predictor of hospitalization for CHD and vascular disease [1], it was modeled by grouping within decades.

The relative risks of the various CHD risk factors were adjusted by analysis of covariance for the other explanatory variables. Hence, a statistically significant relative risk is independent of the other explanatory variables’ effect on CHD (Fig. 1a, 1b, 1c).



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  		Fig. 1a, b, c. Adjusted CHD risk odds ratios with 95% confidence intervals.

 
Because the NHANES I design [2–5] involves stratification, several levels of clustering, and special weighting of selected age and race groups, the logistic regression analysis program from Research Triangle Institute accounting for NHANES sampling methods (LOGISTIC) [8] would conventionally be utilized as recommended by the National Center for Health Statistics (NCHS) [9]. However, the tape which we received from NCHS lacked the stratification, clustering, and special weighting markers which would allow use of LOGISTIC. Hence, we carried out the analysis of the data using the general logistic regression analysis program (LOGIST) from the SAS Institute.

Each of the food items, including fish, bread, dessert, cheese, and alcohol, were recorded in one of four frequency categories: none; less than 1/week; 1 to 6 times/week; one or more times/day. For any of these food items, whenever the category increases by one level (e.g., from <1/week to 1 to 6 times/week), with all other variables unchanged, the risk of CHD (denoted by "r") then becomes "r" times as large as before,Fig. 1c.

The regression models allowed interaction terms for all of the above explanatory variables to enter into the models, but multi-way interactions could not be included due to limitations on model size.


   RESULTS
TOP
 ABSTRACT
 INTRODUCTION
 METHODS
 RESULTS
DISCUSSION
 REFERENCES
 
Population Studied
In NHANES I, carried out between 1971 and 1974, there were 14,407 individuals ages 25 to 74. In the follow-up of NHANES I in 1987, 11,018 of these 14,407 (77%) individuals had been traced; the data was analyzed for 5,811 individuals ages 40 to 74 in 1971 to 1974, now 16 years older (ages 56 to 90). In the 1987 follow-up evaluation there were 69,158 person years of follow-up. The CHD event rate over the follow-up period of 16 years was 34%.

Significant Independent Determinants of Coronary Events
As displayed in Fig. 1a, b, and c, significant independent variables in the stepwise logistic regression positively associated with CHD events included, age, geographic region, serum cholesterol, cigarette smoking, body mass index, and bread intake.

Significant independent variables inversely associated with CHD events included race, female sex, education of the head of the household, alcohol intake, habitual exercise, physical activity, fish, cheese, and dessert intake (Fig. 1a, b, c).

There was a fish*serum cholesterol interaction ({chi}2=4.2, p=.04, 1df) (Fig. 2). The lowest percentage of people who developed coronary heart disease over the 16 year follow-up (26%), were those who ingested fish one or more times/week and had serum cholesterol <209 mg/dl (Fig. 2). In contrast, those with no fish intake and serum cholesterol >249 mg/dl had a 45% likelihood of sustaining CHD over the 16 year follow-up period (Fig. 2).



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  		Fig. 2. Interaction between fish intake and serum cholesterol for CHD events.

 
There was an alcohol*cholesterol interaction ({chi}2=4.74, p=.03, 1 df) (Fig. 3). The lowest cardiac event rate (23%) was seen in subjects who took alcohol 1 to 6 times a week and had serum cholesterol <209 mg/dl, with higher event rates (41%) in those who took no alcohol and had serum cholesterol >249, or (42%) in those who took one or more alcoholic beverage/day and had serum cholesterol >249 mg/dl (Fig. 3).



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  		Fig. 3. Interaction between alcohol intake and serum cholesterol for CHD events.

 
There was an alcohol*age interaction ({chi}2=5.1, p=.025, 1 df) (Fig. 4). In the 40 to 49 year old age group, CHD events rose in the 1 to 6/week and >=1/day alcohol intake groups. In the 50 to 59 and 60 to 69 year old age groups, CHD events fell with increasing alcohol through the 1 to 6 beverage/week category (Fig. 4).



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  		Fig. 4. Interaction between alcohol intake and age for CHD events.

 
There was an age*legume interaction such that in age groups 50 to 59 (p=.053) and 60 to 69 (p=.013) years, CHD events fell as legume intake rose (Fig. 5). There was a region*legume interaction for the midwest region such that CHD events fell as legume intake rose (Fig. 6).



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  		Fig. 5. Interaction between legume intake and age for CHD events.

 


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  		Fig. 6. Interaction between legume intake and region for CHD events.

 
There was an ethnic group*butter interaction such that in African-Americans and in American Indians, Hispanics, and Asians, CHD events increased as butter intake rose (p=.026, p=.015).

There was a region*exercise interaction such that in the Northeast or South, CHD fell as exercise levels rose (p=.03, .013).

There was a weight change*work interaction such that in blue collar workers, CHD events rose as weight increased (p=.016).

There were no other consistent, significant interactions for CHD event rates.


   DISCUSSION
TOP
 ABSTRACT
 INTRODUCTION
 METHODS
 RESULTS
 DISCUSSION
REFERENCES
 
Many of the positive correlates of coronary heart disease events, age, race (whites higher), gender (males higher), geographic region (Midwest and Northeast higher than West) are immutable. However, many positive correlates of coronary heart disease can be changed including serum cholesterol [10,11], habitual exercise and physical activity [12–15], smoking [16–18], and ponderosity [19–21]. When these variables are changed, CHD risk falls [10–21]. Habitual diet [22–24] and changes in diet [25–28] have well documented relationships to CHD risk and to change in CHD risk. Within this frame of reference [22–28], significant, independent, associations of specific food classes with CHD events are of considerable interest, since intake of these classes can be relatively easily altered.

The inverse associations of fish intake with CHD events, revealed again in the current study, are not new [29–31]. However, the interactions of fish intake with serum cholesterol revealed in the current study appear to be more unique. Within "low" (<209 mg/dl), "midrange" (209 to 249 mg/dl), and "high" serum cholesterol (>249 mg/dl) categories, as fish intake rose, CHD events fell. There were, however, no "silver bullets", i.e., high fish intake did not negate high serum cholesterol. On the other hand, the lowest CHD event rate (26%) was seen in subjects with fish intake >=1/week and serum cholesterol <209, suggesting that the benefits of low saturated fat, low cholesterol diet (with resultant low serum cholesterol) might be amplified by high fish intake.

The inverse associations of alcohol intake with CHD events, revealed again in the current study, are also not new [32–34]. However, the interactions of alcohol intake with serum cholesterol appear to be more unique. For serum cholesterol categories <209 and 209 to 249 mg/dl, CHD event rates were highest for non-drinkers and lowest for those taking 1 to 6 alcoholic beverages/week. As was the case for fish intake, there were no "silver bullets", i.e., high alcohol intake was not protective when serum cholesterol was >249 mg/dl. Moreover, for all serum cholesterol categories, alcohol had a "U" shaped relationship with CHD events, with CHD events higher for both non-drinkers and for those ingesting >=1 alcoholic beverage/day.

The significant inverse association of cheese intake with CHD events is puzzling, since increased cheese intake suggests increased saturated fat and cholesterol intake which would normally be expected to increase CHD event rates.

Approximately one-third of the saturated fatty acids in American diet come from dairy products [35]. It has been suggested that the type of saturated fats found in dairy foods raises total and LDL cholesterol more so than beef or cocoa butter saturated fats [35]. Despite these properties [35], consumption of cheese was negatively associated with the development of CHD in the NHEFS. It is possible that socioeconomic status is related to increased cheese and dessert consumption, and that affluent, educated subjects, known to have low CHD event rates [36], are eating more cheese and dessert, also inversely associated with CHD events in the current study. Despite covariance adjustment for socioeconomic status, cheese intake might, speculatively, still reflect some socioeconomic status effect. It is interesting to note that Danish volunteers fed a "heart healthy diet" which did not contain high fat cheese had cravings for cheese during the dietary intervention. Once returned to their habitual diet of choice, serum cholesterol increased to pre-intervention levels due to the inclusion of cheese in the diet [37].

It is possible that saturated fat intake might be more atherogenic in certain ethnic groups. In the current study, butter intake was positively associated with CHD event rates in subjects with pigmented skin, African-Americans, American Indians, Hispanics, and Asians, but not in Caucasians.

We speculate that lacto-ovo-vegetarians in the NHEFS population, known to have lower CHD event rates than omnivores [38,39], contributed to the inverse association of cheese with CHD. In longitudinal studies of Seventh Day Adventists, there was no difference in relative risk of heart disease in those with high and low frequency of cheese and dairy product consumption [40–42]. Vegetarian diets that include cheese are able to lower cholesterol levels equally compared to cholesterol lowering diets that include meat [43]. Lifetime studies of cohorts of lacto-ovo vegetarians (Seventh Day Adventists in California) produced significant negative relationships to mortality rates from green salad consumption and a significant positive relationship for meat and egg consumption [42]. Within Seventh Day Adventists [42], as in the current study, there were lower mortality rates for those who consumed cheese 1 to 6 times/week. Based on the NHEFS results of the current study, and those from other studies [38–43], it appears that frequent consumption of cheese may not constitute undue cardiovascular risk.

The inverse associations of legume intake with CHD event rates in the Midwest region, and in age groups 50 to 59 and 60 to 69 probably reflect the cardioprotective effects of diets rich in fruits and vegetables, rich in magnesium and in antioxidant vitamins A, C, E, and beta-carotene [44,45].

The 16 year NHEFS observational epidemiologic follow-up study emphasizes again [1,7] the important role of modifiable dietary and behavioral factors in the causation and prevention of CHD.


   ACKNOWLEDGMENTS
 
Supported in part by the Jewish Hospital Medical Research Council.

Received April 1, 1997. Accepted October 1, 1997.


   REFERENCES
TOP
 ABSTRACT
 INTRODUCTION
 METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 

  1. Gartside PS, Glueck CJ: The important role of modifiable dietary and behavioral characteristics in the causation and prevention of coronary heart disease hospitalization and mortality: the prospective NHANES I follow-up study. J Am Coll Nutr 14: 71–79, 1995.[Abstract]
  2. Stanton MF, Lowenstein FW: Serum magnesium in women during pregnancy, while taking contraceptives, and after menopause. J Am Coll Nutr 6(4): 313–319, 1987.[Abstract]
  3. Miller HW: Plan and operation of the National Health Nutrition Examination Survey, United States, 1971–1973. National Center for Health Statistics. Vital and Health Stat 1(10a), 1977.
  4. Cohen BB, Barbano HE, Cox CS, Feldman JJ, Finucane FF, Kleinman JC, Madans JH: Plan and operation of the NHANES I Epidemiologic Follow-up Study: 1982–1984. Hyattsville, MD: National Center for Health Statistics. Vital and Health Stat 1(22), 1987.
  5. Finucane FF, Freid VM, Madans JH, Cox CS, Kleinman JC, Rothwell ST, Banbano HE, Feldman JJ: Plan and operation of the NHANES I Epidemiologic Follow-up Study: 1986. Hyattsville, MD. National Center for Health Statistics. Vital and Health Stat 1(25), 1990.
  6. Harris T, Feldman J, Kleinman JC, Ettinger WH, Makuc DM, Schatzkin AG: The low cholesterol-mortality association in a national cohort. J Clin Epidemiol 45: 595–601, 1992.[Medline]
  7. Gartside PS, Glueck CJ: Dietary intake: relationship to hospital admission for coronary heart and vascular disease, the NHANES II National Probability Study. J Am Coll Nutr 12: 676–684, 1993.[Abstract]
  8. Holt MM, Revised by Shah BV: SURREGR: Standard Errors of Regression Coefficients from Sample Survey Data. Research Triangle Park, NC: Research Triangle Institute, 1981.
  9. National Center for Health Statistics, Maurer KR: Plan and operation of the Hispanic Health and Nutrition examination survey 1982–1984. Vital and Health Statistics. Series 1, #19, DHS publication # (PHS) 85–1321. Public Health Service. Washington. US Government Printing Office, 1985.
  10. Nestel PJ: Controlling coronary risk through nutrition. Can J Cardiol Suppl G, 11: 9G–14G, 1995.
  11. Truswell AS: Review of dietary intervention studies: effect on coronary events and on total mortality. Aust New Z J Med 98–106, 1994.
  12. Videau BD, Wenger NK: Physical exercise and training in elderly patients with coronary heart disease. Cardiology in the Elderly 1: 654–568, 1993.
  13. Katzel LI, Bleecker ER, Colman EG, Rogus EM, Sorkin JD, Goldberg AP: Effects of weight loss vs aerobic exercise training on risk factors for coronary disease in healthy, obese, middle-aged, and older men: randomized controlled trial. JAMA 274: 1915–1921, 1995.[Abstract/Free Full Text]
  14. Lavie CJ, Milani RV, Littman AB: Benefits of cardiac rehabilitation and exercise training in secondary coronary prevention in the elderly. J Am Coll Cardiol 22: 678–683, 1993.[Abstract]
  15. Haapanen N, Miilunpalo S, Vuori I, Oja P, Pasanen M: Characteristics of leisure time physical activity associated with decreased risk of premature all-cause and cardiovascular disease mortality in middle aged men. Am J Epidemiol 143: 870–880, 1996.[Abstract/Free Full Text]
  16. Haskell WL, Alderman EL, Fair JM, Maron DJ, Mackey SF, Superko HR, Williams PT, Johnstone IM, Champagne MA, Krauss RM, et al. Effects of intensive multiple risk factor reduction on coronary atherosclerosis and clinical events in men and women with coronary artery disease: the Stanford Coronary Risk Intervention Program (SCRIP). Circulation 89: 975–990, 1994.[Abstract/Free Full Text]
  17. Launer LJ, Feskens EJ, Kalmijn S, Kromhout D: Smoking, drinking, and thinking. The Zutphen Elderly Study. Am J Epidemiol 143: 219–227, 1996.[Abstract/Free Full Text]
  18. Paunio M, Virtamo J, Gref CG, Heinonen OP: Serum high density lipoprotein cholesterol, alcohol, and coronary mortality in male smokers. Brit Med J 312: 1200–1203, 1996.[Abstract/Free Full Text]
  19. Balcazar H, Cobas JA: Overweight among Mexican Americans and its relationship to life style behavioral risk factors. J Community Health 18: 55–67, 1993.[Medline]
  20. Fox AA, Thompson JL, Butterfield GE, Gylfadottir U, Moynihan S, Spiller G. Effects of diet and exercise on common cardiovascular disease risk factors in moderately obese older women. Am J Clin Nutr 63: 225–233, 1996.[Abstract/Free Full Text]
  21. Tanaka H, Kakiyama T, Takahara K, Yamauchi M, Tanaka M, Sasaki J, Taniguchi T, Matsuo H, Shindo M. The association among fat distribution, physical fitness, and the risk factors of cardiovascular disease in obese women. Obes Res 3 Suppl 5: 649S–653S, 1995.[Medline]
  22. Keli SO, Feskens EJ, Krohhout D: Fish consumption and risk of stroke. The Zutphen Study. Stroke 25: 328–332, 1994.[Abstract]
  23. Lindeberg S, Lundh B: Apparent absence of stroke and ischaemic heart disease in a traditional Melanesian island: a clinical study in Kitava. J Intern Med 233: 269–275, 1993.[Medline]
  24. Feskens EJ, Kromhout D: Epidemiologic studies on Eskimos and fish intake. Ann NY Acad Sci 683: 9–15, 1993.[Medline]
  25. Kafatos A, Kouromalis I, Valachonikolis I, Theodorou C, Labadarios D: Coronary heart disease risk factor status of the Cretan Urban Population in the 1980s. Am J Clin Nutr 54: 591–598, 1991.[Abstract/Free Full Text]
  26. Artaud-Wild SM, Connor SL, Sexton G, Connor WE: Differences in coronary mortality can be explained by differences in cholesterol and saturated fat intakes in 40 countries but not in France and Finland. A paradox. Circulation 88: 2771–2779, 1993.[Abstract/Free Full Text]
  27. Sperber AD, Galil A, Sarov B, Stahl Z, Shany S: A combined community strategy to reduce cholesterol and other risk factors. Am J Prev Med 12: 123–128, 1996.[Medline]
  28. Schaefer EJ, Lichtenstein AH, Lamon-Fava S, Contois JH, Li Z, Goldin BR, Rasmussen H, McNamara JR, Ordovas JM. Effects of National Cholesterol Education Program Step 2 diets relatively high or relatively low in fish derived fatty acids on plasma lipoproteins in middle aged and elderly subjects. Am J Clin Nutr 63: 234–241, 1996.[Abstract/Free Full Text]
  29. Kromhaut D, Feskens EJ, Bowles CH: The protective effect of a small amount of fish on coronary heart disease mortality in an elderly population. Int J Epidemiol 24: 340–345, 1995.[Abstract/Free Full Text]
  30. Rodriguez BL, Sharp DS, Abbott RD, Burchfiel CM, Masaki K, Chyou PH, Huang B, Yano K, Curb JD. Fish intake may limit the increase in risk of coronary heart disease morbidity and mortality among heavy smokers. The Honolulu Heart Program. Circulation 94: 952–956, 1996.[Abstract/Free Full Text]
  31. Kromhout D, Bleomberg BP, Feskens EJ, Hertog MG, Menotti A, Blackburn H: Alcohol, fish, fibre and antioxidant vitamins intake do not explain population differences in coronary heart disease mortality. Int J Epidemiol 25: 753–759, 1996.[Abstract/Free Full Text]
  32. Rimm EB, Ellison RC: Alcohol in the Mediterranean diet. Am J Clin Nutr 61: 1378S–1382S, 1995.[Abstract]
  33. Kushi LH, Lenart EB, Willett WC: Health implications of Mediterranean diets in light of contemporary knowledge. 2. Meat, wine, fats, and oils. Am J Clin Nutr 61 (Suppl 6): 1416S–1427S, 1995.[Abstract]
  34. Carmelli D, Swan GE, Page WF, Christian JC: World War II veteran male twins who are discordant for alcohol consumption: 24 year mortality. Am J Public Health 85: 99–101, 1995.[Abstract/Free Full Text]
  35. Denke MA, Grundy SM: Effect of fats high in stearic acid on lipid and lipoprotein concentration in men. Am J Clin Nutr 54: 1036–1040, 1993.[Abstract/Free Full Text]
  36. Bucher HC, Ragland DR: Socioeconomic indicators and mortality from coronary heart disease and cancer: a 22 year follow-up of middle aged men. Am J Pub Health 85: 1231–1236, 1995.[Abstract/Free Full Text]
  37. Holm L: Cultural and social acceptability of a healthy diet. Eur J Clin Nutr 47: 592–599, 1993.[Medline]
  38. Dwyer JT: Health aspects of vegetarian diets. Am J Clin Nutr 48: 712–738, 1988.[Abstract/Free Full Text]
  39. Keys A: Mediterranean diet and public health: personal reflections. Am J Clin Nutr 995:61(suppl): 1321S–1323S, 1995.
  40. Fraser GE: diet and coronary heart disease. Beyond dietary fats and low density lipoprotein cholesterol. Am J Clin Nutr 59 (suppl): 1117S–1123S, 1994.[Abstract/Free Full Text]
  41. Snowden DA: Animal product consumption and mortality in seventh day adventists. Am J Clin Nutr 48: 789–798, 1988.
  42. Kahn HA, Phillips RL: Association between reported diet and all-cause mortality. Am J Epidemiol 119: 775–787, 1988.[Abstract/Free Full Text]
  43. Masarei JR, Rouse IL, Lynch WJ, Robertson K, Vandongen R, Beilin LJ. Effects of lacto-ovo-vegetarian diet on serum concentrations of cholesterol, triglyceride, HDL-C, HDL2-C, HDL3-C, apoprotein-B, and Lp(a). Am J Clin Nutr 40: 468–479, 1984.[Abstract/Free Full Text]
  44. Singh RB, Ghosh S, Niaz MA, Singh R, Beegum R, Chibo H, Shoumin Z, Postiglione A. Dietary intake, plasma levels of antioxidant vitamins, and oxidative stress in relation to coronary artery disease in elderly subjects. Am J Cardiol 76: 1233–1238, 1995.[Medline]
  45. Singh RB, Rastogi V, Fastogi SS, Niaz MA, Beegom R: Effect of diet and moderate exercise on central obesity and associated disturbances, myocardial infarction and mortality in patients with and without coronary artery disease. J Am Coll Nutr 15: 592–601, 1996.[Abstract]



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