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Circulation. 1997;96:37-43

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(Circulation. 1997;96:37-43.)
© 1997 American Heart Association, Inc.


Articles

Total, LDL, and HDL Cholesterol Decrease With Age in Older Men and Women

The Rancho Bernardo Study 1984–1994

Assiamira Ferrara, MD; Elizabeth Barrett-Connor, MD; ; Jun Shan, PhD

From the Department of Family and Preventive Medicine, University of California, San Diego, School of Medicine (La Jolla).


*    Abstract
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*Abstract
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Background The purpose of the present study was to study the effects of age, weight change, and covariates on lipid and lipoprotein levels cross-sectionally and prospectively in an elderly population.

Methods and Results A community-based sample of 1041 men and 1303 women aged 50 to 93 years was studied cross-sectionally in 1984 to 1987, with follow-up of 372 men and 545 women 8 years later. In the cross-sectional study, levels of total cholesterol (TC) and LDL cholesterol (LDL-C) decreased and levels of HDL cholesterol (HDLC) increased with age in men (all P<.001) but not in women. In the prospective study, TC, LDL-C, and HDL-C levels all decreased in both men and women, in all age groups (50 to 64 years, 65 to 74 years, and >=75 years) and in all weight change groups (>2.5-kg loss, change within 2.5 kg, and >2.5-kg gain) and in all waist girth change groups, for an overall decrement of {approx}1% per year. In multiple linear regression models, change in weight was the most important independent and consistent predictor of changes in TC, LDL-C, and HDL-C. Similar results were obtained in analyses excluding subjects taking lipid-lowering drugs or estrogen and in analyses adjusted for changes in cigarette smoking, alcohol intake, physical activity, medication use, and incident myocardial infarction, cancer, or diabetes.

Conclusions Cross-sectional decrements in TC and LDL-C with age in men are not explained by survivor bias because they are also observed prospectively. Although weight change was the most important explanatory variable, TC, LDL-C, and HDL-C levels also decreased in those who lost or gained weight. Age was not an independent predictor of change. Other prospective studies are recommended to better define the causes and consequences of cholesterol and lipoprotein changes in old age.


Key Words: aging • population studies • lipids • weight change


*    Introduction
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*Introduction
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Total and LDL cholesterol levels tend to increase with age in young or middle-aged adults studied cross-sectionally1 2 3 4 or prospectively.5 6 7 8 9 10 11 12 However, cross-sectional13 14 15 16 17 18 19 20 and prospective12 20 21 22 studies of participants >=65 years of age have reported that total and LDL cholesterol levels decrease with age. Although HDL cholesterol levels do not vary with age in most cross-sectional studies,1 3 14 15 16 17 18 22 levels decreased with age in both men and women in the majority of the prospective studies (of largely middle-aged subjects).5 6 8 9 10 12 22

Few studies have examined lipid and lipoprotein levels prospectively in elderly subjects,12 21 22 23 and none have examined both behavior and medical causes for the observed changes. The purpose of this report was to examine the association of total cholesterol and lipoproteins with age, both cross-sectionally and longitudinally over 8 years of follow-up, and to determine the relative contribution of age, weight change, behavior change, medication use, disease, and mortality to these changes in older community-dwelling adults.


*    Methods
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*Methods
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Between 1984 and 1987, surviving members of the Rancho Bernardo Heart and Chronic Disease Study, a middle to upper-middle class community in southern California, were invited to a baseline clinic visit; 1045 men and 1315 women aged 50 to 93 years (80%) participated.24 All members of this cohort were followed for vital status to 1994. At {approx}8 years after the baseline visit, between May 1992 and December 1994, all surviving participants were invited to a follow-up clinic visit; 372 men (35.6%) and 545 women (41.8%) were reexamined, 343 men (32.8%) and 553 women (42.0%) are awaiting reexamination, and 330 men (31.6%) and 213 women (16.2%) have died.

At both clinic visits, venous samples were drawn in the morning from seated subjects after a requested 12-hour fast. Lipids and lipoproteins at baseline and follow-up visits were measured in the same Centers for Disease Control and Prevention–certified La Jolla Lipid Research Clinic Laboratory. Total plasma cholesterol was measured by enzymatic techniques using an ABA-200 biochromatic analyzer (Abbott Laboratories). HDL cholesterol was measured by precipitating the other lipoproteins with heparin and manganese chloride according to the standardized procedures of the Lipid Research Clinics protocol.25 LDL cholesterol was estimated according to the Friedewald formula.26

Height and weight were measured with subjects wearing light clothing and without shoes; body mass index (BMI) was calculated as weight (kg)/height (m2) and used as a measure of overall obesity. Waist circumference was measured at the bending point, and hip circumference was measured at the iliac crest; the waist-to-hip ratio (WHR) was calculated and used as a measure of central obesity. (These ratios were highly correlated [r=.97] with ratios based on measurements of smallest waist and largest hip circumferences.)

At both clinic visits, demographic data, personal history of current cigarette smoking (yes/no), alcohol consumption (two or more drinks per week), physical activity (three or more times per week), and medication use were determined with a standardized questionnaire. Medications were validated by examination of prescriptions or pills brought to the clinic for that purpose. Participants were asked about physician-diagnosed myocardial infarction, diabetes mellitus, and cancer with onset during the follow-up interval.

After excluding 17 subjects who had fasted for <12 hours, there were 1041 men and 1303 women who were seen at the 1984-to-1987 baseline visit and who form the basis of the cross-sectional analysis. From this cohort, 372 men and 545 women who were examined again between 1992 and 1994 (mean follow-up, 8 years) form the basis of the longitudinal analysis.

Statistical Analysis
Change variables were defined as follow-up values minus baseline values. Sex-specific mean differences between follow-up and baseline visits were tested by paired t test before and after stratifying for age or by ANCOVA when mean differences were adjusted for age in analyses stratified for weight change (>2.5-kg loss, change within 2.5 kg, and >2.5-kg gain) or waist girth change groups. Waist girth change groups were defined by 1 SD of the sex-specific mean change in waist girth. A change of >±1 SD from the mean change was considered to be increased or decreased. The percent lipid and lipoprotein changes per year were calculated. Regression to the mean for repeated measurements was calculated according to the method of Mee and Chua.27

Multiple linear regression of lipid change and lipoprotein change on age and BMI at baseline and changes in age, weight, behaviors (smoking, alcohol consumption, physical activity), medication use (lipid-lowering drugs, thiazides, thyroid hormones, estrogens), and morbidity (myocardial infarction, diabetes mellitus, cancer) were computed separately for men and women. Analyses were repeated after separately excluding all subjects who died within 1 year of the follow-up visit, all those taking lipid-lowering drugs, and all women using estrogen replacement therapy.

The Statistical Analysis System28 was used for all analyses. All probabilities are for two-tailed tests, with statistical significance defined as P<.05.


*    Results
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Cross-sectional Analysis
There were 1041 men and 1303 women aged 50 to 93 years who were examined at the baseline visit between 1984 and 1987. The mean age was 71±10 years in men and 70±9 years in women.

Table 1Down shows sex- and age-specific cross-sectional mean levels of total cholesterol and lipoproteins. Among men, total and LDL cholesterol decreased significantly with increasing age, and HDL cholesterol increased significantly with age. Among women, total cholesterol and lipoprotein levels were not associated with age before (Table 1Down) or after stratification for estrogen replacement therapy (data not shown).


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Table 1. Sex- and Age-Specific Total Cholesterol and Lipoprotein Levels at Baseline: Rancho Bernardo 1984-1987

Longitudinal Analysis
The 372 men and 545 women aged 58 to 96 years who were seen at the follow-up visit had a mean age of 75±8 and 76±9 years, respectively. Participation rates for survivors who were 50 to 69 years at baseline were 60% for men and 58% for women; for those 70 years and older at baseline, rates were 44% in men and 42% in women. Participants were on average 10 years younger than those who died during the 8 years of follow-up. Men who came to the follow-up visit did not differ from those who had appointments pending (n=343) or who had died (n=330) with regard to baseline total, LDL, or HDL cholesterol levels. Women who came to the follow-up visit did not differ significantly from those who were pending or dead with regard to LDL cholesterol levels, but they did have significantly higher total and HDL cholesterol levels than women whose appointments were pending (n=553) or who had died (n=213). Similar results were obtained after adjustment for estrogen replacement therapy (data not shown).

Table 2Down shows the sex-specific mean total and lipoprotein cholesterol levels, mean changes, and percent change per year. In both men and women, total, LDL, and HDL cholesterol levels decreased {approx}1% per year (all P<.001). Fig 1Down shows that the decrease in total, LDL, and HDL cholesterol levels was similar and statistically significant in men and women in all age groups.


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Table 2. Total Cholesterol and Lipoprotein Levels at Baseline and Follow-up Visit With Sex-Specific Change Between Visits and Percent Change per Year: Rancho Bernardo 1984-1994



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Figure 1. Sex-specific mean total cholesterol and lipoprotein change levels and 95% confidence interval by age at baseline.

Fig 2Down shows that weight loss began around age 65 to 74 in both men and women and was characteristic of men and women aged >=75. Significant weight gain was observed only in women aged 50 to 65. Increasing weight loss with increasing age was significant in both men and women (all P linear regression <.001). Weight loss only partially explained the cholesterol changes with age, however. As shown in Fig 3Down, mean total, LDL, and HDL cholesterol levels decreased in men and women who lost, gained or did not change weight; all decrements were statistically significant except decreases in total and LDL cholesterol in women who gained weight.



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Figure 2. Sex-specific mean body weight change and 95% confidence interval by age at baseline.



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Figure 3. Sex-specific age-adjusted mean total cholesterol and lipoprotein change and 95% confidence interval by weight change.

Similar results were obtained in analyses in which change in waist girth was used instead of weight change. During the 8-year follow-up, waist girth significantly increased in both men and women (mean change, 1.8 cm in men and 2.5 cm in women; all P<.001); the degree of increase in waist girth decreased with increasing age (P linear regression, .02 in men and <.001 in women). Waist girth change was also concordant with weight change, increasing in those who maintained or gained weight and decreasing in those who lost weight (standardized ß=.772 and .684 in men and women, respectively). In age-adjusted analyses in which men and women were stratified by sex-specific changes in waist girth, total, LDL, and HDL cholesterol decreased in all waist girth change groups (data not shown). In age-adjusted linear regression models, change in waist girth was a significant independent predictor of change in total and LDL cholesterol in men (ß=.110 and .115, respectively; P<.001) and women (ß=.162 and .152, respectively; P<.001). In men, change in waist girth was not associated with change in HDL cholesterol (ß=-.066; P=.2) but was weakly associated in women (ß=-.087; P=.05).

None of the above results were changed in analyses that excluded the 36 men and 56 women who were using lipid-lowering drugs or the 253 women who were using estrogen at either visit (data not shown).

Among participants in the 8-year follow-up evaluation, 29% of men and 33% of women reported a myocardial infarction, 19% of men and 13% of women reported cancer, and 5% of men and 3% of women reported newly diagnosed diabetes. Except for a decrease in physical activity, there were relatively few changes in behaviors or medications that could affect lipid levels during the 8-year interval, as shown in Table 3Down.


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Table 3. Sex-Specific Proportion With Changes in Behaviors and Medication Use Between Baseline and Follow-up: Rancho Bernardo 1984-1994

Table 4Down shows the results of multiple linear regression used to determine the independent contribution of age, change in weight, behaviors, medication (lipid-lowering drug, thiazide, thyroid hormone, or estrogen), and diseases to changes in total cholesterol and lipoproteins over 8 years. In both sexes, change in body weight was the most consistent and significant predictor of change in total cholesterol and lipoproteins. This effect was independent of age and BMI at baseline and of changes in behaviors, medication use, and morbidity. During the 8-year follow-up, total and LDL cholesterol levels decreased more and HDL cholesterol levels decreased less in persons with weight loss. Change in waist girth was less important than change in weight, based on a comparison of standardized ß coefficients. (We did not use weight change and waist girth change in the same model because they were highly correlated; r=.66 for men and r=.59 for women.)


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Table 4. Standardized ß-Coefficients for 8-Year Change in Total Cholesterol and Lipoproteins: Rancho Bernardo 1984-1994

Cessation of cigarette smoking or alcohol ingestion were each significantly and independently associated with changes in HDL cholesterol levels (Table 4Up). HDL cholesterol levels decreased less in the 15 men and 36 women who quit smoking; HDL cholesterol levels also decreased in the 25 men and 54 women who quit drinking alcohol (P=.05 for men and P=.06 for women). Table 4Up shows that medication changes also were significant and independent predictors of changes in total cholesterol and lipoproteins. Total and LDL cholesterol levels decreased more and HDL cholesterol levels decreased less in 34 men and 51 women who started receiving lipid-lowering drugs. Total and LDL cholesterol levels also decreased more in the 15 men and 47 women who started receiving thyroid hormones. Women who started estrogen replacement therapy (n=57) showed a significant decrease in total and LDL cholesterol levels, and their HDL cholesterol levels decreased less with age (Table 4Up). Incident diseases such as myocardial infarction, diabetes, and cancer were not associated with changes in total cholesterol and lipoproteins. None of the results of multiple linear regression were changed in analyses that excluded those who were using lipid-lowering drugs or estrogen at either visit (data not shown). Similar decreases in total cholesterol and lipoprotein levels were observed after exclusion of the 42 follow-up visit participants who died within the first year of follow-up (possible evidence of occult disease at reexamination) (data not shown).

In additional calculations according to the method of Mee and Chua,27 regression to the mean accounted for <8% of any of the observed changes in total, LDL, or HDL cholesterol (data not shown).


*    Discussion
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up arrowAbstract
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*Discussion
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In the cross-sectional analyses from this community-based study, total and LDL cholesterol levels decreased and HDL cholesterol levels increased with age in men but not women. When studied prospectively, however, men and women showed significant and similar reductions in total, LDL, and HDL cholesterol.

These cross-sectional results are concordant with other cross-sectional studies reporting that total and LDL cholesterol levels in adults increased progressively to age {approx}65 in men and {approx}75 in women, after which concentrations appeared to fall.1 2 3 4 13 14 15 16 17 18 19 20 Most cross-sectional studies have not found HDL cholesterol levels to vary with age,1 3 14 15 16 17 21 but a recent cross-sectional report from the Cardiovascular Health Study18 found that HDL cholesterol levels appeared to increase with age in men but not in women, which is similar to the results reported here.

Longitudinal studies are necessary to show true age-related changes. In this cohort, neither selective mortality nor selective participation accounted for the prospectively observed changes in cholesterol and lipoprotein levels in men. Among women, participation bias was suggested only for changes in HDL cholesterol levels, because women who died or had appointments pending had significantly lower HDL cholesterol levels than did women who were examined at follow-up.

A cohort effect is unlikely to explain the observed changes in total, LDL, and HDL cholesterol levels because changes were similar in all age groups. Laboratory drift in the total cholesterol measurements is an unlikely explanation because the total cholesterol levels reported here (measured in the Lipid Research Clinic laboratory) were also measured as part of a routine diagnostic chemistry panel by an independent clinical laboratory with highly concordant results (r=.957 and r=.983 for baseline and follow-up total cholesterol measurements), and the direction of change and statistical significance were unchanged. Finally, regression to the mean account for <8% of changes in total, LDL, and HDL cholesterol in both men and women.

The decrease in total, LDL, and HDL cholesterol levels with age in the Rancho Bernardo cohort is similar to results in two12 22 but partially discordant with two other21 23 prospective studies of the elderly. In a recent study of elderly Dutch men,23 total cholesterol decreased by 0.04 mmol/L per year with age, which is similar to the decrement in cholesterol observed among Rancho Bernardo men and women, but HDL cholesterol did not change with age. Women were not studied in the Dutch cohort.

In the present study, weight loss was the most important factor associated with lipid change, which is consistent with results from clinical trials,29 30 31 32 but it did not completely explain the observed decrements. Total and LDL cholesterol levels also decreased with age in men and women who gained weight, whereas HDL cholesterol also decreased in men and women who lost weight. These results are concordant with results from a prospective study of older women and men from the Framingham study.12 Decline in HDL cholesterol levels in men and women who lose or maintain weight may be accounted for by a concomitant decline in lean body mass, increase in body fat, or change in fat distribution with age.33 34

Rancho Bernardo men and women who lost weight showed a decrease in waist girth, and change in waist girth was only marginally associated with change in HDL cholesterol and only in women. Change in waist girth, although predictive of change in total and LDL cholesterol, was less important than change in weight. These results are concordant with results from clinical trials in which the degree of weight loss was more important in predicting change in cholesterol and lipoproteins than was weight loss–induced changes in WHR or waist girth.31 32

Few studies have examined behavior change among the elderly.35 36 To our knowledge, this is the first study to determine whether changes in behaviors, medications, or morbidity predict changes in lipids and lipoproteins in community-dwelling elders. The majority of this relatively healthy cohort did not change behaviors or medications known to affect the lipid profile. One exception was cigarette smoking, which, although uncommon, was stopped by approximately half of those who were smokers at baseline (15 of 34 men and 36 of 70 women). Despite the small numbers (and the association between quitting smoking and weight gain), there was a significant independent and favorable effect of smoking cessation on HDL cholesterol levels, similar to that previously reported in younger subjects.8 9 10 37 38 Consistent with previous studies conducted in middle-aged or young adults7 8 9 37 starting alcohol use during the 8-year interval was associated with a marginally significant increase in HDL cholesterol levels. Changes in physical activity were not related to changes in HDL cholesterol levels. These results are concordant with an absent effect of exercise on lipoproteins reported in middle-aged and elderly men32 but inconsistent with the beneficial effects of exercise on lipoprotein levels reported in younger adults.9 39 40 Differences may reflect the difficulty in assessing physical activity by self-report or the infrequency of strenuous activity in the elderly.

Change in dietary habits, an important determinant of lipid and lipoprotein levels,41 could not be directly examined because not all subjects had the same diet assessment at both visits. However, younger individuals (aged 50 to 69 years) from this population were much more likely to report having decreased their dietary fat intake than were persons >=70 years old,36 whereas cholesterol and lipoprotein changes were greatest in oldest subjects, making it less likely that the observed decreases in total and LDL cholesterol levels reflect reduction in fat intake.

Lower cholesterol levels are frequently observed in association with clinical and subclinical diseases.42 43 44 In the present study, decreases in total and lipoprotein cholesterol levels were independent of chronic diseases and use of medications known to affect lipid levels in both multivariate and stratified analyses. Subclinical illness was unlikely to account for the decline in cholesterol levels in Rancho Bernardo because similar changes were observed after excluding participants who died within 1 year of the follow-up visit.

The observed decline in cholesterol levels might reflect inflammatory responses to infections, which increase with age,42 or age-related reduced cholesterol absorption from the intestine.45 Other prospective studies are needed to investigate these and other possible explanatory factors. Regardless of the mechanism, the late life decrease in total cholesterol could explain why high plasma cholesterol levels are less predictive of heart disease in the elderly than in younger persons.46 47 48 49 50 The reduced association between cholesterol levels and ischemic heart disease in old age may also be a consequence of an illness associated with a decline in cholesterol levels, in which ischemic heart disease is the cause of death.48 51 52 On the other hand, the observation that HDL cholesterol levels worsen with age may explain why low HDL cholesterol levels represent an independent risk factor for coronary heart disease in elderly men and women.48 49

Because cholesterol levels decrease in old age and do not reflect lifetime levels, it does not necessarily follow that lowering cholesterol levels is without value in the elderly. Recent primary and secondary prevention trials53 54 have shown that medications that lower LDL and raise HDL levels can significantly reduce the risk of cardiovascular disease and total mortality in older men and women. The results of the present study also indicate that in addition to starting lipid-lowering drugs, weight reduction, quitting smoking, and starting estrogen replacement therapy predicted a favorable change in total, LDL, and HDL cholesterol levels in elderly men and women.


*    Acknowledgments
 
This research was supported by National Institute of Diabetes and Digestive and Kidney Diseases grant DK-31801. Dr Ferrara was a recipient of a fellowship from the Italian Exchange Program of Dottorato di Ricerca on "Pathophysiology and Clinical Aspects of Vascular Disease," Universita' degli Studi di Napoli Federico II, Italy, when this study was conducted.


*    Footnotes
 
Reprint requests to Elizabeth Barrett-Connor, MD, Department of Family and Preventive Medicine, 0607, 9500 Gilman Dr, University of California, San Diego, La Jolla, CA 92093-0607.

Dr Ferrara is currently at the Division of Research, Kaiser Permanente, Oakland, Calif.

Received October 9, 1996; revision received January 16, 1997; accepted January 23, 1997.


*    References
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up arrowAbstract
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*References
 
1. Heiss G, Tamir I, Davis CE, Tyroler HA, Rifkind BM, Schonfeld G, Jacobs D, Frantz ID. Lipoprotein-cholesterol distributions in selected North America populations: the Lipid Research Clinics Program Prevalence Study. Circulation.. 1980;61:302-315.[Free Full Text]

2. Moulopoulos SD, Andamopoulos PN, Diamantopoulos EI, Nanas SN, Anthopoulos LN, Iliadi-Alexandrou M. Coronary heart disease risk factors in a random sample of Athenian adults: the Athens Study. Am J Epidemiol.. 1987;126:882-892.[Abstract/Free Full Text]

3. Heitmann BL. The effects of gender and age on associations between blood lipid levels and obesity in Danish men and women aged 35-65 years. J Clin Epidemiol.. 1992;45:693-702.[Medline] [Order article via Infotrieve]

4. Schaefer EJ, Lamon-Fava S, Cohn SD, Schaefer MM, Ordovas JM, Castelli WP, Wilson PWF. Effects of age, gender, and menopausal status on plasma low density lipoprotein cholesterol and apolipoprotein B levels in the Framingham Offspring Study. J Lipid Res.. 1994;35:779-792.[Abstract]

5. Clark D, Allen MF, Wilson FH. Longitudinal study of serum lipids. Am J Clin Nutr. 1967;20;743-752.

6. Hershcopf RJ, Elahi D, Andres R, Baldwin HL, Raizes GS, Schocken DD, Tobin JD. Longitudinal changes in serum cholesterol in men: an epidemiological search for an etiology. J Chron Dis.. 1982;35:101-114.[Medline] [Order article via Infotrieve]

7. Criqui MH, Frankville DD, Barrett-Connor E, Klauber MR, Holdbrook MJ, Turner JD. Change and correlates of change in high and low density lipoprotein cholesterol after six years: a prospective study. Am J Epidemiol.. 1983;118:52-59.[Abstract/Free Full Text]

8. Anderson KM, Wilson PWF, Garrison RJ, Castelli WP. Longitudinal and secular trends in lipoprotein cholesterol measurements in a general population sample: the Framingham offspring study. Atherosclerosis.. 1987;68:59-66.[Medline] [Order article via Infotrieve]

9. Hubert HB, Eaker ED, Garrison RJ, Castelli WP. Life-style correlates of risk factor change in young adults: an eight-year study of coronary heart disease risk factors in the Framingham offspring. Am J Epidemiol.. 1987;125:812-831.[Abstract/Free Full Text]

10. Berns MA, De Vries JHM, Katan MB. Increase in body fatness as a major determinant of change in serum total cholesterol and high density lipoprotein cholesterol in young men over a 10-year period. Am J Epidemiol.. 1989;130:1109-1122.[Abstract/Free Full Text]

11. Eberle E, Doering A, Keil U. Weight change and change in total cholesterol and high-density-lipoprotein cholesterol: results of the MONICA Augsburg Cohort Study. Ann Epidemiol.. 1991;1:487-492.[Medline] [Order article via Infotrieve]

12. Wilson PWF, Anderson KM, Harris T, Kannel WB, Castelli WP. Determinants of change in total cholesterol and HDLC with age: the Framingham study. J Gerontol.. 1994;49:M252-M257.

13. The Lipid Research Clinics Program Epidemiology Committee. Plasma lipid distributions in selected North America populations: the Lipid Research Clinics Program Prevalence Study. Circulation.. 1979;60:427-439.[Abstract/Free Full Text]

14. Abbott RD, Garrison RJ, Wilson PW, Epstein FH, Castelli WP, Feinleib M, LaRue C. Joint distribution of lipoprotein cholesterol classes: the Framingham Study. Arteriosclerosis.. 1983;3:260-272.[Abstract/Free Full Text]

15. Laurenzi M, Mancini M. Plasma lipids in elderly men and women. Eur Heart J. 1988;9(suppl D):69-74.

16. Kromhout D, Nissinen A, Menotti A, Bloemberg B, Pekkanen J, Giampaoli S. Total and HDL cholesterol and their correlates in elderly men in Finland, Italy, and Netherlands. Am J Epidemiol.. 1990;131:855-863.[Abstract/Free Full Text]

17. Wallance RB, Colsher PL: Blood lipids distributions in older persons: prevalence and correlates of hyperlipidemia. Ann Epidemiol.. 1992;2:15-21.[Medline] [Order article via Infotrieve]

18. Ettinger WH, Wahl PW, Kuller LH, Bush TL, Trucy RP, Manolio TA, Borhami NO, Wong ND, O'Leary DH, for the CHS Collaborative Research Group. Lipoprotein lipids in older people: results from the Cardiovascular Health Study. Circulation.. 1992;86:858-869.[Abstract/Free Full Text]

19. Curb DJ, Reed DM, Yano K, Kautz JA, Albers JJ. Plasma lipids and lipoproteins in elderly Japanese-American men. J Am Geriatr Soc.. 1986;34:773-780.[Medline] [Order article via Infotrieve]

20. Newschaffer CJ, Bush TL, Hale W: Aging and total cholesterol levels: cohort, period, and survivorship effects. Am J Epidemiol.. 1992;136:23-34.[Abstract/Free Full Text]

21. Frishman WH, Ooi WL, Derman MP, Eder HE, Gidez LI, Ben-Zeev D, Zimetbaun P, Heiman M, Aronson M. Serum lipids and lipoprotein in advanced age: intraindividual changes. Ann Epidemiol.. 1992;2:43-50.[Medline] [Order article via Infotrieve]

22. Garry PJ, Hunt WC, Koehler KM, VanderJagt DJ, Vellas BJ. Longitudinal study of dietary intakes and plasma lipids in healthy elderly men and women. Am J Clin Nutr.. 1992;55:682-688.[Abstract/Free Full Text]

23. Weijenberg MP, Feskens EJ, Kromhout D. Age-related changes in total and high-density-lipoprotein cholesterol in elderly Dutch men. Am J Public Health.. 1996;86:798-803.[Abstract/Free Full Text]

24. Wingard DL, Sinsheimer P, Barrett-Connor EL, McPhillips JB. Community-based study of prevalence of NIDDM in older adults. Diabetes Care. 1990;13(suppl 2):3-8.

25. National Heart and Lung Institute, Lipid Research Clinics Program Laboratory Methods Committee. Manual of Laboratory Operations: Lipid and Lipoprotein Analysis, ed 2. Washington, DC: US Government Printing Office; 1974, DHEW publication No. 75-628.

26. Friedewald WJ, Levy RI, Fredrickson DS. Estimation of the concentration of low-density lipoprotein cholesterol in plasma without use of the preparative ultracentrifuge. Clin Chem.. 1972;18:459-502.[Abstract]

27. Mee RW, Chua TC. Regression toward the mean and the paired sample t test. Am Stat.. 1991;45:39-42.

28. SAS Institute Inc. SAS/STAT User' s Guide, Version 6, ed 4. Cary, NC: SAS Institute; 1989.

29. Brownell KD, Stunkard J. Differential changes in plasma high-density lipoprotein-cholesterol levels in obese men and women during weight reduction. Arch Intern Med.. 1981;141:1142-1146.[Abstract/Free Full Text]

30. Zimmerman J, Kaufmann NA, Fainaru M, Eisenberg S, Oschry Y, Friedlander Y, Stein Y. Effect of weight loss in moderate obesity on plasma lipoprotein and apolipoprotein levels and on high density lipoprotein composition. Arteriosclerosis.. 1984;4:115-123.[Abstract/Free Full Text]

31. Wing RR, Jeffery RW, Burton LR, Thorson C, Kuller LH, Folsom AR. Change in waist-hip ratio with weight loss and its association with change in cardiovascular risk factors. Am J Clin Nutr.. 1992;55:1086-1092.[Abstract/Free Full Text]

32. Katzel LI, Bleecker ER, Colman EG, Rogous EM, Sorkin JD, Goldeberg AP. Effect of weight loss vs aerobic exercise training on risk factors for coronary disease in healthy, obese middle-aged and older men: a randomized controlled trial. JAMA.. 1995;274:1915-1921.[Abstract/Free Full Text]

33. Borkan GA, Hults DE, Gerzof SG, Robbins AH, Silbert CK. Age changes in body composition revealed by computer tomography. J Gerontol.. 1983;38:673-677.

34. Flynn MA, Nolph GB, Baker AS, Krause G. Aging in humans: a continuous 20-year study of physiologic and dietary parameters. J Am Coll Nutr.. 1992;11:660-672.[Abstract]

35. Hallfrish J, Muller D, Drinkwater D, Tobin J, Andres R. Continuing diet trends in men: the Baltimore Longitudinal Study of Aging (1961-1978). J Gerontol.. 1990;45:M186-M191.

36. Ferrini RL, Edelstein SL, Barrett-Connor E. Factors associated with health behavior change among residents 50 to 96 years of age in Rancho Bernardo, California. Am J Prev Med.. 1994;10:26-30.

37. Kuller LH, Hulley SB, La Porte RE, Neaton J, Dai WS. Environmental determinants, liver function, and high density lipoprotein cholesterol levels. Am J Epidemiol.. 1983;117:406-418.[Abstract/Free Full Text]

38. Shennan NM, Seed M, Wynn V. Variation in serum lipid and lipoprotein levels associated with changes in smoking behavior in non-obese Caucasian males. Arteriosclerosis. 1985;58;17-25.

39. Williams PT, Wood PD, Krauss RM, Haskell WL, Vranizam KL, Blair SN, Terry R, Farquhar JW. Does weight loss cause the exercise-induced increase in plasma high density lipoproteins? Atherosclerosis.. 1983;47:173-185.[Medline] [Order article via Infotrieve]

40. Williams PT, Wood PD, Haskell WL, Vranizan K. The effects of running mileage and duration on plasma lipoprotein levels. JAMA.. 1982;247:2674-2679.[Abstract/Free Full Text]

41. Grundy SM, Denke MA. Dietary influences on serum lipids and lipoproteins. J Lipid Res.. 1990;31:1149-1172.[Abstract]

42. Ettinger WH, Harris T. Causes of hypocholesterolemia. Coron Artery Dis.. 1993;4:854-859.[Medline] [Order article via Infotrieve]

43. Iribarren C, Reed DM, Chen R, Yano K, Dwyer JH. Low serum cholesterol and mortality: which is the cause and which is the effect? Circulation.. 1995;92:2396-2403.[Abstract/Free Full Text]

44. Pekkanen J, Nissenen A, Vartiainen E, Salonen JT, Punsar S, Karvonen MJ. Changes in serum cholesterol level and mortality: a 30 year follow-up: the Finnish cohort of the Seven Countries Study. Am J Epidemiol.. 1994;139:155-165.[Abstract/Free Full Text]

45. Gylling H, Standemberg T, Tilvis R, Miettimen TA. Regulation of serum cholesterol level in middle-aged and elderly men: relation of cholesterol absorption and synthesis to lipoprotein metabolism. Arterioscler Thromb. 1994:694-700.

46. Manolio TA, Pearson TA, Wenger NK, Barrett-Connor E, Payne GH, Harlan WR. Cholesterol in older persons and women: review of an NHLBI workshop. Ann Epidemiol.. 1992;2:161-176.[Medline] [Order article via Infotrieve]

47. Krumholz HM, Seeman TE, Merrill SS, Mendes de Leon CF, Vaccarino V, Silverman DI, Tsukahara R, Ostefeld A, Berkman LF. Lack of association between cholesterol and coronary heart disease mortality and morbidity and all-cause of mortality in persons older than 70 years. JAMA.. 1994;272:1335-1340.[Abstract/Free Full Text]

48. Denke MA, Winker MA. Cholesterol and coronary heart disease in older adults: no easy answers. JAMA.. 1995;274:575-577.[Abstract/Free Full Text]

49. Corti M-C, Guralnik JM, Salive ME, Harris T, Field TS, Wallace RB, Berkman LF, Seeman TE, Glynn RJ, Hennekens CH, Havlik RJ. HDL cholesterol predicts coronary heart disease mortality in older persons. JAMA.. 1995;274:539-544.[Abstract/Free Full Text]

50. Weijenberg MP, Feskens EJ, Bowles CH, Kromhout D. Serum total cholesterol and systolic blood pressure as risk factor for mortality from ischemic heart disease among elderly men and women. J Clin Epidemiol.. 1994;47:197-205.[Medline] [Order article via Infotrieve]

51. Jacobs D, Blackburn H, Higgins M, Reed D, Iso H, McMillan G, Neaton J, Nelson J, Potter J, Rifkind B, Rossouw J, Shekelle R, Yusuf S, for participants in the Conference on Low Cholesterol: Mortality association: report of the Conference on Low Blood Cholesterol: Mortality Associations. Circulation.. 1992;86:1046-1060.[Abstract/Free Full Text]

52. Iribarren C, Reed DM, Burchfiel CM, Dwyer JH. Serum total cholesterol and mortality: confounding factor and risk modification in Japanese-American men. JAMA.. 1995;273:1926-1932.[Abstract/Free Full Text]

53. Scandinavian Sinvastatin Survival Study Group. Randomized trial of cholesterol lowering in 4444 patients with coronary heart disease: the Scandinavian Sinvastatin Survival Study (4S). Lancet.. 1994;344:1383-1389.[Medline] [Order article via Infotrieve]

54. Shepherd J, Cobbe SM, Ford I, Isles CG, Lorimer AR, Macfarlane PW, McKillop JH, Packard CJ, for the West of Scotland Coronary Prevention Study Group. Prevention of coronary heart disease with pravastatin in men with hypercholesterolemia. N Engl J Med.. 1995;333:1301-1307.[Abstract/Free Full Text]




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