American Journal of Epidemiology Vol. 149, No.

6
Copyright © 1999 by The Johns Hopkins University School of Hygiene and Public Hearth Printed In U.S.A.
All rights reserved

Caffeine Consumption and Menstrual Function

Laura Fenster,1 Chris Quale,1 Kirsten Waller,1 Gayle C. Windham,1 Eric P. Elkin,1 Neal Benowitz,2 and Shanna
H. Swan1

The relation between caffeine intake and menstrual function was examined in 403 healthy premenopausal
women who belonged to Kaiser Permanente Medical Care Program in 1990-1991. A telephone interview

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collected information about caffeinated beverage intake as well as other lifestyle, demographic, occupational,
and environmental factors. Subjects collected daily urine samples and completed a daily diary for an average of
five menstrual cycles. Metabolites of estrogen and progesterone were measured in the urine, each cycle was
characterized as anovulatory or ovulatory, and a probable day of ovulation was selected when appropriate.
Logistic regression and repeated measures analyses were performed on menstrual parameters. Women whose
caffeine consumption was heavy (>300 mg of caffeine per day) had less than a third of the risk for long menses
(£8 days) compared with women who did not consume caffeine (adjusted odds ratio = 0.30, 95% confidence
interval 0.14-0.66). Those whose caffeine consumption was heavy also had a doubled risk for short cycle length
(£24 days) (adjusted odds ratio = 2.00, 95% confidence interval 0.98-4.06); this association was also evident in
those whose caffeine consumption was heavy who did not smoke (adjusted odds ratio = 2.11, 95% confidence
interval 1.03-4.33). Caffeine intake was not strongly related to an increased risk for anovulation, short luteal
phase (£10 days), long follicular phase (£24 days), long cycle (£36 days), or measures of within-woman cycle
variability. Am J Epidemiol 1999; 149:550-7.

caffeine; estrone; follicular phase; luteal phase; menstrual cycle; menstruation disorders; ovulation; pregnanediol

Caffeine is one of the most commonly ingested,
pharmacologically active substances. It is present in cof-
fee, tea, soda, cocoa, solid milk chocolate, and many
medications (1). Caffeine is rapidly absorbed from the
digestive tract and distributes throughout all tissues (2).
The mechanisms of action of caffeine include inhibition
of hydrolysis of cyclic 3',5'-adenosine monophosphate
and 3',5'-guanosine monophosphate (3) and antagonism
of adenosine (4), making it plausible that caffeine might
alter hormonal profiles and thereby affect menstrual
function. Menstrual function, in turn, may be related to
other health outcomes, such as fertility, osteoporosis, and
breast cancer (5).
The results of studies of coffee and caffeinated bev-
erage consumption in relation to fecundity are incon-
sistent. Several studies in humans have reported an
association between caffeine intake and delayed time
to conception (6-12); in contrast, others have shown
either no association (13, 14) or a relation only at very
high levels of intake (15, 16). Examination of the rela-
tion between caffeine intake and menstrual function
may help to elucidate possible biologic mechanisms by
which caffeine might alter fecundability.
The current study describes the relation between
caffeine intake and menstrual function in the Women's
Reproductive Health Study, which was conducted by
the California Department of Health Services in col-
laboration with the Division of Research of the Kaiser
Permanente Medical Care Program of Northern
California. This study used urinary metabolites of sex
steroids to explore the associations between menstrual
function and several environmental and lifestyle expo-
sures in healthy, premenopausal women.

Received for publication January 28,1998, and accepted for pub- MATERIALS AND METHODS
lication July 9, 1998.
Abbreviations: PdG, pregnanediol-3-glucuronide; SE, standard Subject recruitment
error.
1
Reproductive Epidemiology Section, Department of Hearth The study population, materials, and methods have
Services, Emeryville, CA. been described previously in detail (17). Married
2
Division of Clinical Pharmacology and Experimental
Therapeutics, Department of Medicine, University of California, San women aged 18—39 years who belonged to Kaiser
Francisco, CA. Permanente Medical Care Program and who lived in
550

zip code areas located near the study's field office
were screened by telephone for eligibility. Eligibility
criteria were primarily intended to identify women at
some risk of pregnancy because another goal of the
study was to examine fetal loss and time to conception.
Women were not eligible if they did not speak English;
had not had a menstrual period in 6 weeks; were cur-
rently pregnant; had been surgically sterilized; were
using oral contraceptives, intrauterine devices, or hor-
monal medications; had been having unprotected
intercourse for more than 3 months without becoming
pregnant; or were anticipating travel that would sepa-
rate them from their husbands. Of 6,481 women
screened for eligibility, 1,092 were eligible for recruit-
ment. Of these, 553 agreed to begin the study, 89
dropped out during urine collection, and 61 became
ineligible (e.g., due to beginning oral contraceptives or
separation from their husbands), leaving a total of 403
women who completed the study.
Interviewing
All eligible women were interviewed by telephone
on the following topics: demographics; reproductive
and medical history; lifestyle factors, such as con-
sumption of alcohol, tobacco, and caffeinated bever-
ages, life event stress, and exercise; and occupation,
industry, and job-related exposures. Subjects were
asked to quantify in cups or cans per day their usual
daily consumption of caffeinated coffee, tea, and soda.
Total caffeine consumption was estimated by summing
the usual total per day, assuming a caffeine content of
107 mg/cup of coffee, 34 mg/cup of tea, and 47
mg/can of soda (18). The occurrence of stressful life
events over the 3-month period preceding the inter-
view was assessed using 11 life event items compiled
from two standardized questionnaires (19, 20).
Definition of menstrual endpoints
Each subject collected a sample of first morning
urine daily and recorded vaginal bleeding and other
information in a daily diary. Creatinine and metabolites
of the sex steroid hormones estrone (estrone conju-
gates) and progesterone (pregnanediol-3-glucuronide
(PdG)) were measured in urine by enzyme-linked
immunoassay (21) and were corrected for urine dilu-
tion using the creatinine level. Urinary measures of
estrone conjugates and PdG vary due to individual dif-
ferences in metabolism, but are reliable enough to
enable assignment of the day of ovulation (22).
We determined whether cycles were ovulatory or
nonovulatory based on the rise in PdG levels (17). In
ovulatory cycles, we estimated the day of ovulation by
using a modification of an algorithm designed by
Am J Epidemiol Vol. 149, No. 6, 1999
Caffeine Consumption and Menstrual Function 551
Baird et al (23); the modification is described in the
paper by Waller et al. (17). We discovered that the PdG
analyte occasionally precipitated prior to assay result-
ing in spurious cycle "abnormalities." Since costs pro-
hibited duplicate analyses of all cycles, we reassayed
all nonovulatory cycles and all cycles with an "abnor-
mal" day of ovulation. Abnormal patterns were con-
firmed in 243 (45.6 percent) of the 533 potentially
abnormal cycles that were reanalyzed. We used the
more "normal" assay for reassayed cycles with discor-
dant results (17).
We examined outcomes at the woman level and the
cycle level. Menstrual cycle-level endpoints were
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defined as follows: 1) length of menses = number of
consecutive days a woman reported as bleed days in
her diary; 2) cycle length = number of days from the
date of the start of the cycle to the day before the next
cycle start date; 3) follicular phase length = number
of days from the date of the start of the cycle up to
and including the day of ovulation; 4) luteal phase
length = difference between the cycle length and fol-
licular phase length. We used the fifth and 95th per-
centiles of cycle length to define short and long
cycles. Similarly, we used the 95th percentile to
define long follicular phase length and long menses
and the fifth percentile to define short luteal phase
length. We restricted analysis of each outcome to
cycles with adequate data (17).
Woman-level endpoints included anovulation and
measures of within-woman cycle variability.
Anovulation was defined as 36 or more days without
ovulation (17). Anovulation was analyzed at the
woman level rather than at the cycle level because a
single anovulatory episode could contain several or no
nonovulatory "cycles" depending on whether or not
the woman had breakthrough bleeding. We calculated
within-woman ranges for length of menses, cycle
length, follicular phase length, and luteal phase length
by subtracting each woman's minimum value from her
maximum value for each of these variables; we
dichotomized these ranges at the 75th percentile to
define women with greater variability of these end-
points.
Statistical analyses
Cycle-level endpoints were analyzed using repeated
measures techniques to account for the correlation of
within-woman measurements (24). We also analyzed
cycle-level endpoints as binary variables (25) as fol-
lows: long menses length (>7 vs. <7 days); short cycle
length (<25 vs. 25-35 days); long cycle length (>35
vs. 25-35 days); long follicular phase length (>24 vs.
<24 days); and short luteal phase length (<10 vs. >10
days).
552 Fenster et al.

TABLE 1. Distribution of potential confounders among vromen by caffeine consumption, California Women's Reproductive
Health Study, 1990-1991
Dalty caffeine Intake (mg/day)*

Variable None 1-150 151-300 >300 n

r
No.t %t No. % No. % No. %
(27%) (37%) (22%) (n = 5 1) (13%) valued
(n=109) (n=153) (n-90)
Age (years)
<30 34 (3D 61 (40) 25 (28) 18 (35)
30-34 47 (43) 61 (40) 34 (38) 17 (33)
235 28 (26) 31 (20) 31 (34) 16 (31) 0.19
Age (years)
Mean (SD)§ 32(4.1) 31 (4.3) 33 (4.0) 32 (3.9) 0.04H
Education

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No college 19 (17) 36 (24) 19 (21) 16 (31)
Some college 37 (34) 63 (41) 31 (34) 20 (39)
College graduate 53 (49) 54 (35) 40 (44) 15 (29) 0.17

Race
White 77 (71) 104 (68) 66 (73) 39 (76)
Asian 22 (20) 19 (12) 9 (10) 3 (6)
Other 10 (9) 30 (20) 15 (17) 9 (18) 0.06

Income/year (dollars)
<$35,000 16 (15) 27 (18) 12 (13) 5 (11)
>$35,000-$55,000 50 (46) 56 (38) 30 (34) 21 (45)
>$55,000-$75,000 27 (25) 39 (26) 26 (29) 12 (26)
>$75,000 15 (14) 27 (18) 21 (24) 9 (19) 0.64

Body mass index (kg/m2)

<19.1 13 (12) 9 (6) 5 (6) 3 (6)
19.1-27.3 76 (70) 114 (75) 70 (78) 32 (63)
>27.3 20 (18) 30 (20) 15 (17) 16 (31) 0.16

Gravidity
None 13 (12) 17 (11) 12 (13) 6 (12)
1-2 55 (50) 80 (52) 47 (52) 26 (51)
23 41 (38) 56 (37) 31 (34) 19 (37) 1.00

Parity
None 15 (14) 35 (23) 22 (24) 12 (24)
1-2 73 (67) 103 (67) 59 (66) 33 (65)
23 21 (19) 15 (10) 9 (10) 6 (12) 0.17
Table continues

We used logistic regression to model risk for the fol-
lowing woman-level endpoints: anovulation; large
range for menses length (>3 days); large range for
cycle length (>7 days); large range for follicular phase
length (>7 days); and large range for luteal phase
length >3 days). We restricted the analyses of within-
woman ranges to women with two or more cycles.
We analyzed caffeine consumption primarily as a
categorical variable (no caffeine and 1-150, 151-300,
and >300 mg/day). Covariates that were related to caf-
feine consumption in univariate analyses at p < 0.2
were included in initial models as potential con-
founders. We then used the change-in-estimate method
(26) to examine confounding. We retained all covari-
ates that (upon removal from any model) altered the
effect estimates by more than 10 percent. The follow-
ing covariates were used in all final models: age, edu-
cation, race, body mass index, cigarettes smoked per
day, weekly alcohol consumption, and parity. When
modeling risk of anovulation, we controlled for smok-
ing as a yes/no variable rather than by cigarettes per
day because of small numbers. We also ran models that
excluded anovulatory episodes so that we could ensure
that any effect seen with cycle length or variability was
not due to an increase in anovulation.
RESULTS
Table 1 compares the characteristics of women who
consumed different levels of caffeine. Compared with
Am J Epidemiol Vol. 149, No. 6, 1999
 Caffeine Consumption and Menstrual Function 553

TABLE 1. Continued

Dally caffeine Intake (mg/day)

Variable None 1-150 151-300 >300

n
No. % No. % No. % No. % H
(n=109) (27%) (n> 153) (37%) (n = 90) (22%) (n = 51) (13%) value

History of spontaneous
abortion
None 84 (77) 117 (76) 68 (76) 38 (75)
1 17 (16) 27 (18) 19 (21) 12 (24)
22 8 (7) 9 (6) 3 (3) 1 (2) 0.63

Previous elective abortion

None 87 (80) 97 (63) 59 (66) 29 (57)

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1 17 (16) 36 (24) 17 (19) 16 (31)
22 5 (5) 20 (13) 14 (16) 6 (12) 0.02
MET§ score/week
Mean (SD) 15.4 (21.7) 19.7 (24.9) 19.3 ( 24.4) 16.2 (21 •5) 0.44H
Smoking (cigarettes/day)
0 108 (99) 142 (93) 82 (91) 37 (73)
1-10 1 (1) 4 (3) 5 (6) 6 (12)
>10 0 (0) 7 (4) 3 (3) 8 (16) 0.001

Alcohol (drinks/week)
0 48 (44) 43 (28) 17 (19) 7 (14)
1-3 59 (54) 100 (65) 58 (64) 32 (63)
£4 2 (2) 10 (7) 15 (17) 12 (24) 0.001

Life events
None 41 (38) 71 (46) 46 (51) 18 (35)
1-2 47 (43) 67 (44) 30 (33) 24 (47)
;>3 21 (19) 15 (10) 14 (16) 9 (18) 0.14

Employed
Yes 67 (61) 99 (65) 70 (78) 41 (80)
No 42 (39) 54 (35) 20 (22) 10 (20) 0.02
* Conversion to milligrams of caffeine based on 107 mg/cup of coffee, 34 mg/cup of tea, and 47 mg/can of soda (Bunker and McWilliams,
J Am Diet Assoc 1979;74:28-32).
t Numbers for some variables may not total due to missing values. Percentages for some variables may not total 100 because of round-
ing errors.
t p value is for chi-square test of independence unless noted otherwise.
§ SD, standard deviation; MET, metabolic equivalent.
H p value is for test of Ho: all caffeine categories have the same mean.

nonconsumers, women with heavy caffeine consump-
tion were somewhat older; less likely to have gone to
college; less likely to be Asian; and more likely to have
a higher body mass index, to be nulliparous, to have
had an elective abortion, to have higher levels of alco-
hol and cigarette consumption, and to be employed.
The number of urine samples collected and the number
of cycles available for analyses did not differ appre-
ciably by level of caffeine intake.
Women with heavy caffeine consumption were
somewhat less likely to have an anovulatory episode
(table 2), but the numbers were very small, and the
confidence interval included unity. Caffeine consump-
tion was not appreciably associated with risk for short
luteal phase length, long follicular phase length, or
long cycle length (table 3). However, those with heavy
caffeine consumption were twice as likely to experi-
ence short cycles compared with nonconsumers (table
3). This relation was also seen when cycle length was
examined as a continuous variable; heavy caffeine
intake was associated with a decrease in mean cycle
length of over one third of a day (adjusted coefficient =
-0.38 day, standard error (SE) = 0.44, p value = 0.39).
For those with heavy caffeine intake, the reduction in
cycle length was primarily related to a decrease in fol-
licular phase length (adjusted coefficient = -0.44 day,
SE = 0.46, p value = 0.34). Caffeine consumption was
related in a dose-response manner to a decreased risk
for long menses (table 4). A strong dose-response rela-
tion was also demonstrated between caffeine con-

Am J Epidemiol Vol. 149, No. 6, 1999

554 Fenster et al.

TABLE 2. Risk of anovulation* according to caffeine Intake, tle less than half of a day (adjusted coefficient = -0.39
California Women's Reproductive Health Study, 1990-1991 day, SE = 0.24, p value = 0.10). Caffeine intake was
%of
Caffeine
No.
women
not strongly associated with variability of the menstrual
of Adjusted
Intaket
women
wfthan
OR*
95%CI§ endpoints as measured by within-woman range (table
(mg/day)
(n«365) 5). There was a suggestion of an increased risk for
large luteal phase range related to increasing caffeine
0 99 6.1 Referent
consumption, but the confidence intervals were wide
1-150 139 5.0 0.71 0.22-2.31
151-300 85 6.0 0.97 0.26-3.63 and included unity (table 5).
>300 44 2.3 0.36 0.04-3.36 To determine whether the associations found
• Anovulation episode £36 days.
between caffeine intake and menstrual function might
t Conversion to milligrams of caffeine based on 107 mg/cup of be due to possible residual confounding by smoking or
coffee, 34 mg/cup of tea, and 47 mg/can of soda (Bunker and alcohol, we examined the relation between caffeine
McWilliams, J Am Diet Assoc 1979;74:28-32).
intake and menstrual function in women who did not

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t Adjusted odds ratios (OR) were calculated using multiple logis-
tic regression adjusting for the following variables: maternal age, report smoking and in those who did not report either
race, body mass index, smoking status, weekly alcohol consump- smoking or drinking alcohol. Restricting our analyses
tion, and parity.
§ Cl, confidence interval.
to nonsmokers did not appreciably alter the findings.
For example, in nonsmokers, the adjusted odds ratio
for short cycle for heavy caffeine consumption was
TABLE 3. Risk for binary cycle endpolnts according to 2.11 (95 percent confidence interval 1.03-4.33) and
caffeine Intake, California Women's Reproductive Hearth
Study, 1990-1991
for long menses, it was 0.30 (95 percent confidence
interval 0.13-0.69). Results were similar for the subset
%of
Caffeine No.
cycles Adjusted of women who neither smoked nor drank alcohol, but
Intake* of 95% C l t
(mg/day) cycles
with ORt were based on smaller numbers. In addition, removing
end point
anovulatory episodes did not appreciably affect any of
Short luteal phase length (£10 days) vs. not short (n = 1,436)
our results.
0 403 6.5 Referent
1-150 541 4.8 0.54 0.25-1.18
151-300 317 5.4 0.70 0.29-1.71 DISCUSSION
>300 175 5.1 0.42 0.12-1.46
We found that women who consume caffeine are
Long follicular phase length (>24 days) vs. not long (n = 1,526) less likely to have long menses. This finding is biolog-
0 425 5.9 Referent ically plausible because caffeine is a known vasocon-
1-150 576 4.5 0.68 0.36-1.27 strictor (27). Constriction of uterine blood vessels
151-300 338 4.7 0.92 0.42-2.02
would be expected to reduce uterine blood flow, which
>300 187 5.9 1.10 0.38-3.14
could reduce menstrual bleeding and shorten the dura-
Short cycle (£24 days) vs. normal length (25-35 days) (h = 1,539) tion of menses. Research in pregnant animals (28) and
0 415 9.9 Referent humans (29) indicates that caffeine increases uterine
1-150 584 6.9 0.78 0.42-1.44 vascular resistance and reduces uterine blood flow.
151-300 356 9.3 0.91 0.46-1.81 Our data also indicate that those whose caffeine con-
>300 184 15.8 2.00 0.98-^.06
sumption is heavy are twice as Likely to have a short
Long cycle (236 days) vs. normal length (25-35 days) (h = 1,493) menstrual cycle compared with nonconsumers. The
0 408 8.3 Referent mechanism by which caffeine may alter the duration of
1-150 576 5.6 0.69 0.37-1.29 the menstrual cycle is not clear, but such an effect
151-300 341 5.3 0.84 0.39-1.85 could occur via the effect of caffeine on sex hormones
>300 168 7.7 1.24 0.46-3.39 or the hormone receptors. Kitts (30) found evidence to
• Conversion to milligrams of caffeine based on 107 mg/cup of suggest that constituents of coffee are weakly estro-
coffee, 34 mg/cup of tea, and 47 mg/can of soda (Bunker and genic. Caffeine inhibits the action of adenosine, which
McWilliams, J Am Diet Assoc 1979;74:28-32).
t Adjusted odds ratios (OR) were calculated using generalized
in laboratory studies affects luteinizing hormone and
estimating equation analyses adjusting for the following variables: follicle-stimulating hormone (31, 32), which could in
maternal age, race, body mass index, cigarettes smoked per day, turn affect menstrual cycle length. Gilbert and Rice
weekly alcohol consumption, and parity.
t Cl, confidence interval.
(33) found depressed estrogen levels in female mon-
keys at a dose level of caffeine associated with mis-
carriages, stillbirths, and decreased maternal weight
sumption and a decreased risk for long menses gain. Associations between caffeine intake and estradi-
(adjusted p value = 0.01). Heavy caffeine intake was ol and/or estrone levels have been found in three stud-
associated with a shortening of menses length of a lit- ies of humans (34-36) but not in two others (37, 38).

Am J Epidemiol Vol. 149, No. 6, 1999

 Caffeine Consumption and Menstrual Function 555

TABLE 4. Risk of long menses* according to caffeine Intake, study of menstrual and reproductive health found that
California Women's Reproductive Health Study, 1990-1991 women with short cycle lengths (<26 days) reached
%of
Caffeine
No.
cycles
menopause 1.4 years earlier than did women with nor-
of Adjusted
Intaket
cycles wltha
OR*
95%CI§ mal length cycles and about 2.2 years earlier than did
(mg/day) long
(n= 1,726)
menses
women with long cycle lengths (39). An increased risk
for low bone density has been related to earlier age at
0 477 13.4 Referent
1-150 652 7.4 0.51 0.27-0.96
menopause (40). Women with shorter menstrual cycle
151-300 385 5.2 0.34 0.15-0.76 lengths may also be at increased risk for breast cancer
>300 212 4.7 0.30 0.14-O.66 if, as has been hypothesized, risk increases with more
* 28 days. total lifetime ovulatory menstrual cycles (41-43).
t Conversion to milligrams of caffeine based on 107 mg/cup of However, most epidemiologic studies have not shown
coffee, 34 mg/cup of tea, and 47 mg/can of soda (Bunker and a relation between caffeine intake and an increased
McWilliams, J Am Diet Assoc 1979;74:28-32).
risk for breast cancer (44—46).

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$ Adjusted odds ratios (OR) were calculated using repeated
measures analyses adjusting for the following variables: maternal The potential contribution of caffeine to alterations
age, race, body mass index, cigarettes smoked per day, weekly
alcohol consumption, and parity. in menstrual function has scarcely been examined and
§ Cl, confidence interval. is deserving of further investigation. Cooper et al. (47)
did not observe any notable relation between caffeine
TABLE 5. Risk for large range* of binary cycle endpolnts intake and cycle length, variability, and menses
according to caffeine Intake, California Women's Health length. For this study, menstrual data on 766 women
Study, 1990-1991 aged 29-31 years were collected prospectively; how-
%of ever, the mean age of the women at the time they were
Caffeine No.
intaket of
women Adjusted
95% Cl§ asked to recall their caffeine intake was 73 years. We
with a OR*
(mg/day) women
large range prospectively collected all data and examined poten-
Range of luteal phase length >3 days (n == 330) tial confounders, such as alcohol, cigarette consump-
tion, and stress. We also obtained detailed menstrual
0 91 14.8 Referent
1-150 123 24.3 1.63 0.75-3.55
function data using daily urine metabolites of sex
151-300 75 24.4 1.76 0.74-4.18 steroid hormones, whereas Cooper et al. (47) assessed
>300 41 30.6 1.97 0.71-5.49 menstrual function using questionnaire data, a method
Range of folllcular phase length >3 days (n = 350)
that may be inaccurate (48).
0 98 20.4 Referent
Wilcox et al. (6) prospectively investigated the rela-
1-150 131 16.0 0.71 0.35-1.45 tion between caffeinated beverage consumption and
151-300 77 19.5 1.13 0.51-2.50 time to conception in 100 women who had been trying
>300 44 18.2 0.97 0.36-2.62 to conceive for up to 3 months. Women who drank the
Range of menses length >7 days (n = 366) equivalent of about one cup of caffeinated coffee per
day were half as likely to become pregnant per cycle
0 98 14.3 Referent
1-150 141 13.5 1.00 0.46-2.19 as were women who drank less. In addition, the esti-
151-300 83 8.4 0.55 0.20-1.50 mated relative risk of infertility among women who
>300 44 18.2 1.44 0.51-4.06 drank one cup per day was almost five times that of
Range of cycle length >7 days (n = 354)
those who drank less. Wilcox et al. (6) attempted to
examine an effect of caffeine on ovulation to explain
0 96 22.9 Referent
1-150 134 14.9 0.62 0.31-1.26
the association they found between caffeine consump-
151-300 80 17.5 0.86 0.39-1.90 tion and decreased fertility. They examined daily lev-
>300 44 20.5 0.95 0.36-2.49 els of the urinary metabolite of progesterone for 206
• Longest minus shortest. cycles in approximately 50 women, but found too
t Conversion to milligrams of caffeine based on 107 mg/cup of small a proportion of anovulatory cycles (4 percent) to
coffee, 34 mg/cup of tea, and 47 mg/can of soda (Bunker and explain the caffeine-related decreased fecundability.
McWilliams, J Am Diet Assoc 1979;74:28-32).
t Adjusted odds ratios (OR) were calculated using repeated We also had limited power to investigate rare end-
measures analyses adjusting for the following variables: maternal points such as anovulation, but our findings were in
age, race, body mass index, cigarettes smoked per day, weekly the direction of those reported by Wilcox et al.; that is,
alcohol consumption, and parity.
§ Cl, confidence interval. there was no indication that caffeine intake was relat-
ed to an increased risk for anovulation.
Short cycle length may reflect underlying endocrine Potential exposure misclassification may have
patterns and thereby have potential implications for affected our estimates of total caffeine intake. We esti-
other health endpoints. One long-term prospective mated caffeine dose by interview, and there can be
Am J Epidemiol Vol. 149, No. 6, 1999
556 Fenster et al.
substantial variation in caffeine content according to
differences in serving size, brand, ingredients, method
of beverage preparation, and brewing time (18, 49).
Such random imprecision would tend to bias the effect
estimate toward the null (50). While we did not collect
information on all foods or medications containing
caffeine, their relative contribution to total caffeine
intake has been shown to be minimal (49). Coffee, tea,
and soda are the main sources of caffeine for adults in
the United States (51).
In summary, our data revealed that caffeine con-
sumption was related to a decreased risk for long
menses and that heavy caffeine consumption was asso-
ciated with an increased risk for short cycle length.
These findings could have implications for women's
long-term health. Further studies should be performed
to confirm these findings and to examine subsequent
health outcomes in women.
ACKNOWLEDGMENTS
This research was primarily supported by National
Institute of Child Health and Development grant HD29682.
Support was also received from National Institutes of Health
grant DA01696. The hormone laboratory work was partial-
ly supported by National Institutes of Health grant ESO-
6198.
The authors thank Dr. Bill Lasley for supervising the lab-
oratory analyses and Ceciley Wilder for assistance in manu-
script preparation.
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