Atherosclerosis 161 (2002) 409–415
Effects of menopause on intraindividual changes in serum lipids,
blood pressure, and body weight—the Chin-Shan community
cardiovascular cohort study
Pao-Ling Tornga, Ta-Chen Sub, Fung C. Sungc, Kuo-Liong Chienb,
Su-Cheng Huanga, Song-Nan Chowa, Yuan-Teh Leeb,*
aDepartment of Obstetric and Gynecology, National Taiwan Uni?ersity College of Medicine, Taipei 10020, Taiwan, ROC
bDepartment of Internal Medicine, National Taiwan Uni?ersity College of Medicine, No. 7, Chungshan South Road, Taipei, Taiwan, ROC
cInstitute of En?ironmental Health, National Taiwan Uni?ersity College of Public Health, Taipei, Taiwan, ROC
Received 13 March 2001; received in revised form 24 June 2001; accepted 10 July 2001
In Taiwan, the Chin-Shan Community Cardiovascular Cohort (CCCC) was assessed prospectively to determine whether the
changes in cardiovascular risk factors for women age 45–54 years are due to menopause. The average paired percentage changes
that occurred between baseline (1990–1991) and follow-up (4 years later) in fasting serum lipids were compared in three groups
of women including groups of 59 and 224 who were pre- and postmenopausal, respectively, and a group of 118 who had
spontaneously stopped menstruating. Postmenopausal women had the least gain in body mass index (BMI), whereas, mainly
premenopausal women had increased systolic blood pressure (P?0.05). All women had elevated total cholesterol (TC) levels, with
the greatest elevation in women transitioning into menopause (P?0.001). Low-density lipoprotein cholesterol (LDL-C) levels
increased before and during the transition to menopause, but decreased after menopause (P?0.01). Age had significant
association with changes in TC, triglyceride (TG) and LDL-C levels, whereas BMI had significant association with changes in TG,
LDL-C, and high-density lipoprotein cholesterol (HDL-C) levels (P?0.05). After controlling for age and BMI, only differences
in TC remained significant, with the greatest gain in women who stopped menstruating (12.9%) followed by pre- (6.5%) and
postmenopausal women (4.8%). Changes in both systolic and diastolic blood pressures, and TG and HDL-C levels were not
significantly different, but HDL-C levels declined between 11.5 and 14.7% in all groups. This study suggests an unfavorable effect
of menopause on lipid metabolism, especially on the TC level, which was predominantly elevated during the transition to
menopause. The decline of HDL-C is of concern. © 2002 Elsevier Science Ireland Ltd. All rights reserved.
Keywords: Menopause; Transition; Lipids; Lipoproteins; Taiwanese women
Numerous studies consider menopause a risk factor
for coronary heart disease (CHD) [1,2] and suggest that
postmenopausal women have atherogenic risks. Several
cross-sectional studies found higher plasma levels of
total cholesterol (TC), low-density lipoprotein choles-
menopausal women [3–7]. The association between
menopause and changes in these cardiovascular risk
factors is difficult to study because menopausal status
and age are correlated. Aging has been associated with
increased TC, TG and LDL-C levels, and the rises of
these lipids were particularly marked at the onset of
menopause, including Asian women [8,9]. In a recent
age-matched cross-sectional study, menopausal women
(compared with premenopausal women) appear to have
significantly higher TC, LDL-C but not HDL-C levels
* Corresponding author. Tel.: +886-2-23562000; fax: +886-2-
E-mail address: email@example.com (Y.-T. Lee).
0021-9150/02/$ - see front matter © 2002 Elsevier Science Ireland Ltd. All rights reserved.
P.-L. Torng et al. / Atherosclerosis 161 (2002) 409–415410
. Our previous cross-sectional study based on the
baseline data collected from the Chin-Shan Commu-
nity Cardiovascular Cohort (CCCC) in 1990–1991
also showed atherogenic lipids were higher in post-
than in premenopausal women. The postmenopausal
increases were particularly significant in TC and
LDL-C among women age 45–49 years, and in TG
and Apo B among women age 50–54 years .
Several longitudinal studies focusing on the lipid
changes in relation to menopause also have been car-
ried out. An age-matched 2.5-year follow-up study
found that women with natural menopause have in-
creased LDL-C and decreased HDL-C levels, but un-
changed blood pressure and body weight . An
earlier prospective study of Swedish women who stop
menstruating showed intraindividual increases of TC,
TG and body weight but not blood pressure .
They found, on the other hand, a significant increase
of blood pressure in women with no change of
menopausal status during the 6-year follow-up. The
trend for serum cholesterol levels in both natural and
surgically menopausal Japanese women, whereas no
trend existed for systolic blood pressure (SBP) or
body weight . The study of Poehlman et al. ,
however, showed no effect on TC in menopausal
women during a 6-year follow-up, although they did
observe elevated LDL-C and TG but lowered HDL-
C.Koet al. suggested
menopause might further increase CVD risk for Chi-
nese women. The CHD mortality rate has been fairly
static in Taiwan , justifying the conduct of longi-
tudinal studies to clarify the correlation of menopause
to theage-related cardiovascular
Most of the above-mentioned longitudinal studies
compared CVD risk factor changes for individuals
between pre- and postmenopause. Changes associated
with the confounding effect of age were few and were
measured by comparing women whose menopausal
status changed with those whose status was un-
changed during a similar follow-up period. In our
previous cross-sectional study based on CCCC data,
the age-associated changes in lipid levels were as-
sumedtobe constant regardless
status. The CCCC has been followed-up since 1990 to
compare the absolute average intraindividual percent-
age changes between the baseline and succeeding mea-
surements of body weight, blood pressure, lipid and
lipoprotein levels in women who either remained pre-
menopausal, spontaneously stopped menstruation, or
became postmenopausal during the follow-up period.
Less confounded by the effect of aging, this method
of observation is more sensitive and able to demon-
strate changes of lipids at menopause.
2. Patients and methods
2.1. Study population
The CCCC study was established in 1990–1991 as
previously reported [11,18]. In brief, the study cohort
consisted of 3602 adults, age 35 and above, residing in
a suburban community 20 miles north of metro Taipei.
The mortality pattern in Chin-Shan was generally simi-
lar to that of the general Taiwanese population .
Among 1899 female respondents, 428 age 45–54 years
were included in the baseline survey in 1990–1991, and
401 returned and completed the follow-up study 4 years
later in 1994–1995. Women excluded from this report
were those with hormone replacement therapy prior to
or during the follow-up study period. Women with a
history of diabetes, fasting sugar ?140 mg, hysterec-
tomy, oophorectomy, oral contraceptive pill use, or
menopause before the age of 45 years also were not
included in this study. Only subjects with secondary
amenorrhea for at least 1 year were defined as
menopausal. Subjects whose last menstruation was 3–
11 months earlier were excluded because of uncertainty
in their menopausal status.
2.2. Data collection and assays
The study team consisted of several cardiologists,
senior residents, senior medical students, two assistant
nurses and local practitioners. Trained medical students
canvassed door-to-door with the assistance of commu-
nity leaders to extend invitations for the baseline and
biannual follow-up surveys. Written consent was ob-
tained during the face-to-face questionnaire interview,
and physicians later conducted physical examinations
and laboratory tests on participants invited to the clinic
established in the community. Specimens for blood
analyses were also collected at the clinic.
All venous blood samples were taken after a 10-h
overnight fast, immediately refrigerated at 4 °C, and
transported to the National Taiwan University Hospi-
tal within 6 h. Assay of serum TC and TG levels were
normally performed within 24 h. Otherwise, the serum
samples were stored at −70 °C for batch assay of
LDL-C and HDL-C as previously described [11,17,18].
In brief, standard enzymatic methods for serum TC and
TG were used (Merck 14354 and 14366, Germany,
respectively). The HDL-C concentration in the super-
natant was measured after precipitation with magne-
14993). The concentration of LDL-C was calculated as
‘total cholesterol minus cholesterol in the supernatant,’
and LDL-C precipitated by heparin-citrate reagent
Body mass index (BMI), an indicator related to the
amount of visceral fat, was used as a measure of obesity
P.-L. Torng et al. / Atherosclerosis 161 (2002) 409–415 411
and was calculated as body weight in kg divided by
height in m2; these parameters were measured at the
time of blood sampling. Blood pressure measurements
were performed with mercury sphygmomanometer in a
standardized fashion, cuff size adjusted to the circum-
ference of the arm, and the arm placed with the cuff at
the level of heart. Blood pressure was recorded using
the mean of two measurements taken after 5 min of rest
in the supine position. Systolic and diastolic blood
pressures were defined according to Korotkoff sounds I
2.3. Statistical analysis
To distinguish the effect of menopause, data analyses
emphasized comparing paired differences in serum
lipids, body weight and blood pressure between the
baseline and follow-up levels, among the three groups
of study women identified at the time of follow-up
survey. In doing so, average relative percentage changes
in each factor between the two surveys were calculated
for each individual, expressed in mean?S.E.M. These
changes were also analyzed using paired t-test. A multi-
variate regression analysis was further conducted con-
trolling for age and BMI as dependent variables. All
statistical analyses were performed with SAS statistical
software (Version 6.12, SAS Institute, Cary NC, USA).
P values below 0.05 were considered statistically
Of the 401 women from whom both baseline and
follow-up data was collected, 59 women were still pre-
menopausal, 118 had stopped menstruating (designated
as ‘transition’ in the Figure and Tables) and 224 were
postmenopausal during the 4-year follow-up period.
The baseline average ages (S.D.) were 47.2 (1.8) years
for women who remained premenopausal, 48.8 (2.5)
years for those who became menopausal and 51.5 (2.6)
years for those who were postmenopausal (Fig. 1).
Fig. 1. Average baseline measurements of body weight, body mass index, blood pressure and lipids in Chin-Shan women categorized by
menopausal status at the time of follow-up survey. Abbreviations: BP, blood pressure (mmHg); TC, total cholesterol (mg/dl); TG, triglyceride
(mg/dl); LDL-C, low-density lipoprotein cholesterol (mg/dl); Pre, premenopause; Trans, transition from premenopause to postmenopause; post,
postmenopause at follow-up. Data are expressed as the mean?S.D. P=P-value for difference among pre-, peri- and postmenopausal groups
(t-test). * P?0.05, **P?0.01, *** P?0.001 at the baseline.
P.-L. Torng et al. / Atherosclerosis 161 (2002) 409–415412
Average paired percentage changes occurring between baseline and follow-up surveys of pre-, peri- and postmenopausal women in Chin-Shan
Community Cardiovascular Cohort (CCCC)
Transition (n=118) Postmenopause (n=224)
Data are expressed as the mean?S.E. of mean (SEM). P=P-value for differences among pre-, peri- and postmenopausal groups (general linear
Fig. 1 also depicts the average baseline body weights,
BMIs, blood pressures and lipid profiles among these
menopause grew heavier, no significant differences in
average body weight and BMI were found among the
three groups. Levels of TC, TG and LDL-C showed a
progressive elevation among the three groups (P?0.05
to 0.001) with the highest values all in postmenopausal
women. Differences in blood pressure and HDL-C were
minor among three groups.
Based on the average paired percentage changes be-
tween the baseline and the follow-up data, all women
showed elevations in body weight, BMI, SBP and TC
levels in 4 years (Table 1). All these changes were the
smallest in postmenopausal women. Changes in BMI,
SBP and LDL-C were the largest in premenopausal
women (P?0.05), and the change in TC was the
largest in women approaching menopause (P?0.001).
Decline in HDL-C was observed among all groups.
When age and BMI were adjusted in multivariate
analysis, results showed percentage changes of body
weight, BMI, DBP, SBP and HDL-C were independent
of age, however, changes of TC, SBP and DBP were
independent of BMI (Table 2). Changes of TG and
LDL-C were age- and BMI-dependent, and the change
of TC was age-dependent (P?0.05). However, only the
changes of TC were significantly different among the
three groups (P?0.05), with women who were ap-
proaching menopause having the greatest elevation of
TC (12.9%). LDL-C levels remained elevated for pre-
and perimenopausal women, and lowered in post-
menopausal women. TG levels were increased in post-
menopausal women but decreased in premenopausal
menopause in the follow-up period.
Table 2 also shows changes in HDL-C was indepen-
dent of age, and all groups had declines in HDL-C
levels. In both pre and postmenopausal women, HDL-
C declined 14.7, 3.2% greater than the decline in
women approaching menopause.
4.1. Changes of serum lipids with menopause
Our previous analyses  based on cross-sectional
menopausal women had higher serum levels of TC, TG,
LDL-C and Apo B than premenopausal women.
Among the women 45–54 years old, younger post-
menopausal women showed significantly higher TC and
LDL-C levels than premenopausal women, whereas
older postmenopausal women showed significantly
higher levels of TG. These trends are likely age and
BMI-associated. The changes in coronary heart disease
risk factors affecting the CCCC women (followed up
for 4 years) were compared based on their menopausal
status at the end of follow-up, and this study focused
on those changes attributed to menopause, obesity and
Postmenopausal women appeared to have higher TC,
TG and LDL-C levels than premenopausal women and
those women who became menopausal during the fol-
low-up period. All women had elevated TC levels and
the average elevation was the greatest in women ap-
proaching menopause. This pattern persisted after con-
trolling for age and BMI. Though Poehlman et al.
reported in a prospective study that natural menopause
had no effect on TC levels , our data parallels that
of other studies, showing that TC levels increase 2–3
years before [14,19] and may continue to increase 6
years after menopause . The increase in TC may be
slower for postmenopausal women.
In our study, after age and BMI adjustment, the
decreased TG levels in crude data reverted to increased
levels in postmenopausal women in the follow-up pe-
riod, and women approaching menopause showed no
net changes in TG. An earlier study also found that TG
level was unaffected by menopause .
The trend of LDL-C was opposite to the trend of TG
in this study. Ushiroyama, et al.  found elevations of
P.-L. Torng et al. / Atherosclerosis 161 (2002) 409–415413
TG and LDL-C levels at perimenopausal levels, partic-
ularly just before the onset of menopause. Do et al. 
foundthat, during the
menopause, LDL-C and TG levels increased and HDL-
C levels decreased. The consistent rising trend of LDL-
C as menopause approaches is similar to our study, but
contradicts our finding that LDL-C declines post-
menopausally. This trend is age- and BMI-associated
and statistically insignificant after controlling for these
two factors. Therefore, despite the decline of LDL-C in
postmenopausal women, their LDL-C level remained
the highest because their baseline level was higher.
A decline of estrogen levels during menopause has
been suggested to be associated with the rise of TG and
LDL-C levels . However, recent studies did not show
the relation between endogenous sex hormone and lipid
levels in pre , peri , and postmenopausal women
. And the opposite patterns in TG and LDL-C
levels in our study cannot be further explained solely by
the possible decrease in estrogen levels as menopause
approaches. The contrasting decline of LDL-C levels in
postmenopausal groups and decline of TG levels in
premenopausal groups suggests that changes in lipids
and lipoproteins are probably multifactorial in origin.
The continued decline in HDL-C level, regardless of
menopausal status, is the most striking change. With a
14.7% decrease in HDL-C, the 12.9% increase in TC
indicated higher risk for women at menopause. Signifi-
cant association of HDL-C levels with cardiac function
in Chinese patients has been reported in our population
, suggesting that HDL-C is an important indepen-
dent risk factor for CHD in Chinese women as they age
regardless of menopausal status.
Most women in Chin-Shan community have active
daily routines and they seldom use hormone replace-
ment therapy. The few that were using hormone re-
placement were excluded from our study. Herbal
medicines for menopausal complaints were seldom
taken. Consumption of a diet that included lots of soy
beans and their products, which contain phyto-estro-
periodof transition to
gens that possibly improve menopausal syndrome and
women of every age, and so had little effect on the lipid
profile changes that occurred as a result of menopausal
status in this study. However, physician’s visits during
surveys might influence participants’ life styles and
modify their CHD risk factors .
4.2. Blood pressure in premenopausal and
Chow et al.  found both systolic and diastolic
blood pressures are higher in women after menopause
than in men of the same age, suggesting that estrogen
deficiency might influence the age-related increase in
blood pressure. However, in this study, systolic blood
pressure markedly increased in the women who re-
mained premenopausal at follow-up. After age and
BMI were adjusted, this trend remained but was no
longer significant. Postmenopausal women or women
who became menopausal had only minor SBP increase.
Lindquist et al.  also found a similar pattern of SBP
change in their 6-year follow-up study. Several reports
did not find that the change of SBP with menopause
was significant [10,12,14], but the European study
found SBP significantly increased after menopause .
Administration of estrogen after menopause either at-
tenuated the increase of both systolic and diastolic
blood pressures [28–30] or had no detectable effect
[31,32]. After menopause, with the cessation of ovula-
tion, several hormones were diminished other than
estrogen . Therefore, the effect of hormone profiles
on blood pressure before and after menopause was
Menopause was reported to have no effect on DBP
[10,14,15]. But Shelley et al. reported in a longitudinal
study that DBP increases as BMI increases during
menopausal transition . We did not observe any
effect of natural menopause, age and BMI on DBP.
Diastolic blood pressure may thus be a unique value to
evaluate individual risk of CHD.
A baseline and follow-up surveys of pre-, peri- and postmenopausal women in Chin-Shan Community Cardiovascular Cohort (CCCC)
Premenopause (n=59) Transition (n=118) Postmenopause (n=224)
P=P-value for difference among pre-, peri- and postmenopausal groups using age and BMI as dependent variables (ANOVA); B1, r-value for
age; B2, r-value for weight.
P.-L. Torng et al. / Atherosclerosis 161 (2002) 409–415414
4.3. Body weight in premenopausal and postmenopausal
Weight gain over time has been observed pre, peri
and post-menopausally [34,35], and menopause acceler-
ates the inverse distribution in central obesity . Our
study showed that, during the follow-up period, women
who were already postmenopausal had the least gain in
BMI, similar to the finding of Pasquali et al. . But,
Matthews et al.  did not find BMI and weight
changes during the transition to menopause, in contrast
to the changesin women
menopausal. However, they did not investigate the
BMI change of women who were the same age and in
menopause. The body weights and BMIs of our post-
menopausal women changed very little. The results of
Lindquist et al.  were closer to ours. We found the
changes of TG and LDL-C levels were both age- and
BMI-dependent; and the change of TC level was age-
This study followed up changes occurring in three
female subcohorts based on their menopausal status.
Complete lipid profile data from pre, peri, and post-
menopausal women were not yet available for every
subcohort. Some cohort effects may still exist in the
data. However, it can still be concluded that the high
lipid profile in postmenopausal women is due to aging
and weight gain.
Of the changes in lipid profile that occur during the
transition to menopause, the increase in TC levels is the
only significant change resulting from menopause. Ele-
vation of TC, though influenced by age, is an indepen-
dent anthropometric variable, which changes with
menopausal status. Levels of LDL-C were age, BMI
and menstruation-status-dependent. LDL-C does not
increase in postmenstrual women. Age and obesity
cause LDL-C levels to increase further before and
decline after menopause. Decline in HDL-C is of
This work was supported by contract numbers DOH-
79-06, DOH-80-30, DOH-83 and DOH-84 the Depart-
ment of Health, Republic of China.
 Colditz GA, Willett WC, Stampfer MJ, Rosner B, Speizer FE,
Hennekens CH. Menopause and the risk of coronary heart
disease in women. New Engl J Med 1987;316:1105–10.
 Kannel WB, Wilson PWF. Risk factors that attenuate the female
coronary disease advantage. Arch Intern Med 1995;155:57–61.
 Campos H, McNamara JR, Wilson PWF, Ordovas JM, Schaefer
EJ. Differences in low density lipoprotein subfractions and
apolipoproteins in premenopausal and postmenopausal women.
J Clin Endocrinol Metab 1988;67:30–5.
 Brown SA, Hutchinson R, Morrisett J, Boerwinkle E, Davis CE,
Gotto AM Jr, Patsch W. Plasma lipid, lipoprotein cholesterol
and apoprotein distributions in selected US communities. The
atherosclerosis risk in communities (ARIC) study. Arterioscler
 Stevenson JC, Crook D, Godsland IF. Influence of age and
menopause and serum lipid and lipoproteins in healthy women.
 Lyu LC, Shieh MJ, Ordovas JM, Lichtenstein AH, Wilson PW,
Schaefer EJ. Plasma lipoprotein and apolipoprotein level in
Taipei and Framingham. Arterioscler Thromb 1993;13:1429–40.
 Pasquali R, Casimirri F, Pascal G, Tortelli O, Morselli Labate
AM, Bertazzo D, Vicennati V, Gaddi A. Influence of menopause
on blood cholesterol levels in women: the role of body composi-
tion, fat distribution and hormonal milieu. J Intern Med
 Ushiroyama T, Okamoto Y, Sugimoto O. Plasma lipid and
lipoprotein levels in perimenopausal women. Acta Obstet Gy-
necol Scand 1993;72:428–33.
 Ko GT, Chan JC, Lau EM, Yueng VT, Chow CC, Wai HP, Li
JK, So WY, Cockram CS. The effect of age on cardiovascular
risk factors in Chinese women. Int J Cardiol 1997;61:221–7.
 Peters HW, Westendorp IC, Hak AE, Grobbee DE, Stehouwer
CD, Hofman A, Witteman JC. Menopausal status and risk
factors for cardiovascular disease. J Intern Med 1999;246:521–8.
 Torng PL, Su TC, Sung FC, Chien KL, Huang SC, Chow SN,
Lee YT. Effect of menopause and obesity on lipids in middle-
aged Taiwanese women. Atherosclerosis 2000;153:413–21.
 Matthews KA, Meilahn E, Kuller LH, Kelsey SF, Caggiula AW,
Wing RR. Menopause and risk factors for coronary heart dis-
ease. New Engl J Med 1989;321:641–6.
 Lindquist O. Intraindividual changes of blood pressure, serum
lipids, and body weight in relation to menstrual status: results
from a prospective population study of women in Goteborg,
Sweden. Prev Med 1982;11:162–72.
 Akahoshi M, Soda M, Nakashima E, Shimaoka K, Seto S, Yano
K. Effects of menopause on trends of serum cholesterol, blood
pressure, and body mass index. Circulation 1996;94:61–6.
 Poehlman ET, Toth MJ, Ades PA, Rosen CJ. Menopause-asso-
ciated changes in plasma lipids, insulin-like growth factor 1 and
blood pressure: a longitudinal study. Eur J Clin Invest
 Health and Vital Statistics, 1995. Department of Health. Execu-
tive Yuan, Republic of China, Taipei, Taiwan. 1995:134–47.
 Chien KL, Lee YT, Sung FC, Hsu HC, Su TC, Lin RS.
Hyperinsulinemia and related atherosclerotic risk factors in the
population at cardiovascular risk: a community-based study.
Clin Chem 1999;45:938–46.
 Lee YT, Lin RS, Sung FC, Yang CY, Chien KL, Chen WJ, Su
TC, Hsu HC, Huang YC. Chin-Shan community cardiovascular
cohort in Taiwan—baseline data and five-year follow-up mor-
bidity and mortality. J Clin Epidemiol 2000;53:838–46.
 Van Beresteijn EC, Korevaar JC, Huijbregts PC, Schouten EG,
Burema J, Kok FJ. Perimenopausal increase in serum choles-
 Do KA, Green A, Guthrie JR, Dudley EC, Burger HG, Denner-
stein L. Longitudinal study of risk factors for coronary heart
disease across the menopausal transition. Am J Epidemiol
P.-L. Torng et al. / Atherosclerosis 161 (2002) 409–415 415 Download full-text
 Longcope C, Herbert PN, McKinlay SM, Goldfield SR. The
relationship of total and free estrogens and sex hormone-binding
globulin with lipoproteins in women. J Clin Endocrinol Metab
 Shelley JM, Green A, Smith AM, Dudley E, Dennerstein L,
Hopper J, Burger H. Relationship of endogenous sex hormones
to lipids and blood pressure in mid-aged women. Ann Epidemiol
 Cauley JA, Gutai JP, Kuller LH, Powell JG. The relation of
endogenous sex steroid hormone concentrations to serum lipid
and liporpotein levels in postmenopausal women. Am J Epi-
 Wang TD, Lee CM, Wu CC, Lee TM, Chen WJ, Chen MF,
Liau CS, Sung FC, Lee YT. The effects of dyslipidemia on left
ventricular systolic function in patients with stable angina pec-
toris. Atherosclerosis 1999;146:117–24.
 Aldercreutz H, Mazur W. Phyto-oestrogens and Western dis-
eases. Ann Med 1997;29:95–120.
 Wang JS, Carson EC, Lapane KL, Eaton CB, Gans KM,
Lasater TM. The effect of physician office visits on CHD risk
factor modification as part of a worksite cholesterol screening
program. Prev Med 1999;28:221–8.
 Chow SN, Huang CC, Lee YT. Demographic characteristics and
medical aspects of menopausal women in Taiwan. J Formos
Med Assoc 1997;96:801–11.
 Van Ittersum FJ, van Baal WM, Kenemans P, Mijatovic V,
Donker AJ, van der Mooren MJ, Stehouwer CD. Ambulatory—
not office—blood pressure decline during hormone replacement
therapy in healthy postmenopausal women. Am J Hypertens
 Mercuto G, Zoncu S, Pano D, Pilia I, Lao A, Melis GB, Cherchi
A. Estradiol-17 beta reduces blood pressure and restores the
normal amplitude of the circadian blood pressure rhythm in
postmenopausal hypertension. Am J Hypertens 1998;11:909–13.
 De Meersman RE, Zion AS, Giardina EG, Weir JP, Lieberman
JS, Downey JA. Estrogen replacement, vascular distensibility,
and blood pressure in postmenopausal women. Am J Physiol
 Lee M, Giardina EG, Homma S, DiTullio MR, Sciacca RR.
Lack of effect of estrogen on rest and treadmill exercise in
postmenopausal women without known cardiac disease. Am J
 Hunt BE, Davy KP, Jones PP, DeSouza CA, Van Pelt RE,
Tanaka H, Seals DR. Systemic hemodynamic determinants of
blood pressure in women: age, physical activity, and hormone
replacement. Am J Physiol 1997;273:H777–85.
 Burger HG. The endocrinology of menopause. J Steroid
Biochem Mol Biol 1999;69:31–5.
 The VMH Collaborative Group, Pasquali R, Casimirri F, La-
bate AM, Tortelli O, Pascal G, Anconetani B, Flamia R, Capelli
M, Barbbara L. Body weight, fat distribution and menopausal
status in women. Int J Obes Relat Metab Disord 1994;18:614–
 Wing RR, Matthews KA, Kuller LH, Meilahn EN, Plantinga
PL. Weight gain at the time of menopause. Arch Intern Med
 Tohernof A, Poehlman ET. Effects of menopause transition on
body fatness and body fat distribution. Obes Res 1998;6:246–54.