Vol. 81, No.

1
Journal of Clinml Endocrinology and Metabolism Printed in U.S.A.
Copyright 0 1996 by The Endocrine Society

Ethanol Decreases Nocturnal Plasma Levels of

Thyrotropin and Growth Hormone But Not Those of
Thyroid Hormones or Prolactin in Man*
ANN-CHARLOTTE EKMAN, OLLI VAKKURI, MIKA EKMAN,
JUHANI LEPPiiLUOTO, AIM0 RUOKONEN, AND MIKAEL KNIP
Department of Physiology (A-C.E., O.V., M.E., J.L.), Uniuersity of Oulu, 90220 Oulu, Finland; and

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Departments of Clinical Chemistry (A.R.) and Pediatrics (M.K.), Oulu University Hospital, 90220
Oulu, Finland

ABSTRACT by ethanol. Plasma TSH was 1.4 2 0.2 mu/L at 1800-2200 h and rose
Previous studies on the effects of ethanol on circulating pituitary to 2.3-2.4 mU/L for 0100-0700 h (P < 0.001) in the control subjects.
hormones have been carried out mostly during daytime when the Ethanol 1.0 g/kg suppressed plasma TSH to 1.4 + 0.2 mU/L (P < 0.05
secretion of these hormones is generally at a nadir. Therefore, we at 0100 h and P < 0.01 at 0200 h). According to the area under the
studied the effects of ethanol on the nocturnal secretion of GH, PRL. curve analyses, the suppression in the nocturnal TSH was 32% in the
TSH, and thyroid hormones (protocol I, nine healthy subjects, five 0.5 g/kg group and 45% in the 1.0 g/kg group (P < 0.05 for both cases).
women) and on the TSH and PRL responses to synthetic TRH (pro- Circulating free or total T, and T, did not show any statistically
tocol II, healthy subjects, four women). Ethanol was given in doses of significant changes that could explain the ethanol-induced inhibition
0,0.5, or 1.0 g/kg of BW (protocol I) and 0 or 1.0 g/kg (protocol 111 and in the nocturnal TSH peak. In protocol II, synthetic TRH (1 /&kg BW)
ingested po at 1900-1945 h. In protocol I, plasma GH rose from 0.6 was given intravenously, and blood samples were collected before, at
? 0.2 pg/L (mean 2 SE) at 2200 h to 25.0 2 4.3 pg/L at 0100 h in control 20 and 60 min. TRH significantly stimulated plasma TSH and PRL,
subjects and was almost completely inhibited at 4.5 i- 1.7 pg/L at but ethanol (1.0 g/kg BWl had no effect on these responses.
0100 h in subjects receiving 1.0 g/kg ethanol (P < 0.011. In subjects In conclusion,small amounts of ethanol have unexpectedly great
receiving 0.5 g/kg ethanol, the inhibition was also significant (P < effects on nocturnal surges of TSH. and esneciallv on those of GH, that
0.011, plasma GH being 8.2 2 2.5 pg/L at 0100 h. Plasma GHRH was are apparently mediated by suprapituitary mechanisms. On the other
measured after solid phase separation in RIA, but it did not show any hand, ethanol did not affect the nocturnal PRL surge. These inhibitory
ethanol-related changes. Plasma PRL exhibited a clear diurnal effects of ethanol may have unfavorable effects on growth and me-
rhythm in control subjects and rose from 77 2 16 at 1800 h to 248 2 tabolism in adolescent drinkers. (J Clin Endocrinol Metab 81: 2627-
62 pg/L at 0700 h (P < 0.01). The plasma PRL profile was not affected 2632, 1996)

S ERUM CONCENTRATIONS of pituitary hormones ex-

hibit well-known diurnal rhythms in adult man. The
secretion of GH peaks at night, approximately 1.5-2 h after
falling asleep, and the total amount of GH secreted during
the night is several times greater than the amount released
during the daytime (l-3). PRL shows an initial rise 60-90 min
after falling asleepand reaches maximal levels at 0500-0700
h (4). Circulating TSH also presents a diurnal rhythm with
elevated nighttime levels (5-7); the mean TSH pulse ampli-
tude increasesat night by 82% and 92% in men and women,
respectively (8). It is evident that the rhythmic patterns in the
releaseof pituitary hormones depend on environmental cues
and on endogenous oscillators in the brain where various
transmitters and releasing hormones bring about these phys-
iological rhythms.
Administration of ethanol results in deleterious effects
on physical and mental performance, and these effects are
believed to be mediated by ethanol-induced interference
Received November 20, 1995. Revised February 15, 1996. Accepted
February 23, 1996.
Address correspondence and requests for reprints
M.D., Department of Physiology, University of Oulu,
Finland.
* This study was supported by the Alcohol Research
Finland.
with cell membrane functions and synaptic transmission
in the central nervous system. For example, ethanol is
known to increase y-aminobutyric acid activity and to
decrease the affinity of P-receptors in the brain (9,101. We
have recently shown that the administration of small or
moderate doses of ethanol delayed the nyctohemeral me-
latonin surge but stimulated the secretion of noradrenaline
and P-endorphin during early evening and night (11, 12).
Most previous studies on the effects of ethanol on other
pituitary hormones have been carried out during the day-
time. In these studies, ethanol has been found to suppress
the daytime secretion of GH, but the changes have been
small (13, 141, or no changes have been observed (151.
Instead, a substantial reduction in nocturnal GH levels by
ethanol has been reported in one study in which ethanol
was given in the evening and blood samples taken during
night (16). Data on the effects of ethanol on PRL secretion
are inconsistent and mostly daytime levels have been mea-
sured. It has been demonstrated that ethanol stimulates
PRL secretion (17-191, but contradictory findings have also
been reported (14,20-22). The inhibitory role of ethanol on
to: J. LeppCluoto, PRL secretion was emphasized in studies in which ethanol
90220 Oulu,
decreased the PRL response to TRH when the test was
Foundation of performed 14 h from the beginning of alcohol intake (15)
or to breast stimulation (23).

2627
 EKMAN ET AL. JCE & M . 1996
Vol 81 . No 7

The acute effects of ethanol on TSH secretion are poorly Hoechst, Frankfurt am Main, Germany) was given iv. The following
understood, with two previous studies suggesting no blood samples were taken at 20 and 60 min from the injection of TRH.
All subjects completed the study and no serious adverse effects or
changes in circulating daytime TSH levels or in TSH re- differences in sleep habits between the control and experimental subjects
sponses to TRH after ethanol intake (13,151. In another pre- were observed.
vious study, ethanol was ingested late in the evening and
blood samples were taken every 20 or 30 min during the Biochemical assays
following night (24). No effects of ethanol on plasma TSH
Blood was taken into EDTA tubes for GH, GHRH, PRL, TSH, T,, free
were, however, observed. T4 (ET,), T,, and free T, (ET,) measurements, and into glass tubes for
At the time when we started these series of experiments serum ethanol measurements. The tubes were centrifuged within 30 min
(11,12) there were no detailed data available about the effects and the plasma and sera stored at -70 C. GHRH from the solid-phase
of ethanol on the nyctohemeral secretion of other pituitary plasma extracts was analyzed by RIA (25). Plasma GH was analyzed by
a kit from Pharmacia (Uuusala, Sweden). Plasma PRL and TSH were
hormones than GH (16) and PRL (14). In the case of TSH, this

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analyzed with Gamma-BCT PRL IRMA and TSH IRMA kits (IDS, Tyne
was unexpected because the major part of its secretion occurs & Wear, Boldon, UK), respectively, according to the instructions of the
at night. Also the usual social ingestion of ethanol in the manufacturer. Plasma concentrations of T, and T, (Orion Diagnostica,
evening would imply that studies on the effects of ethanol on Turku, Finland) as well as ET, (Diagnostic Products Corp., Los Angeles,
CA,) were determined by RIA and ET, levels by a chemiluminescence
the secretion of pituitary hormones should be carried out
system (Ciba-Corning ACS:180 Analyzer, Medfield, MA) following the
through the night. Therefore we wanted to study the effects instructions of the manufacturer. Serum ethanol was determined by gas
of ethanol on nighttime levels of circulating TSH, GH, and chromatography. The intra- and interassay variation in GHRH RIAs
PRL. In addition, we measured circulating thyroid hormones were 11% and 18%, respectively, and in the other assays <4% and <9%,
and TSH and PRL responses to synthetic TRH to explore respectively. Detection limits were 0.1 mU/L for TSH, 5 pg/L for PRL,
0.3 kg/L for GH, 3 rig/L for GHRH, 5 nmol/L for T,, 1.3 pmol/L for
mechanisms by which the possible effects of ethanol are
ET,, 0.2 nmol/L for T,, and 0.3 pmol/L for ET,.
mediated.
Statistical analyses
Subjects and Methods Results are expressed as means ? SEM. Series of measurements of each
Subjects hormone formed a complete 3 X 9 in protocol I and 2 X 3 in protocol
II (doses x time points) block with 9 or 6 replicas and were analyzed with
The trial took place at the Department of Physiology. Fifteen healthy one-way repeated measures ANOVA, followed by the Newman-Keuls
medical students who gave written informed consent (five women and test to assess the significance of differences between doses and various
four men in protocol I and four women and two men in protocol II, aged time points. Calculations for area under the curve (AUC) were carried
21-23 yr) were chosen as test subjects. A detailed history was taken, and out using the FigP graphics program (Biosoft, Ferguson, MO1 and an-
a routine medical examination was performed before commencing the alyzed as explained above.
trial. None of the subjects were excessive drinkers, because their con-
sumption (as stated on their informed consent form) was less than 100 g
ethanol per week (see also below). The protocol for the study was Results
approved by the Ethical Review Board of the University of Oulu Medical Protocol I
School and the National Agency for Medicines, Helsinki, Finland. The
subjects were not allowed to use any alcoholic beverages for 1 week The serum ethanol concentrations (data not shown)
before or during the 2-3 test weeks. The consumption of caffeine-con- peaked at 2000 h, 1 h after the start of the ethanol intake, i.e
taining products also was prohibited during the test days, and was 13.1 ? 1.1 mmol/L (mean ? SE, n = 9) and 26.8 2 1.8 mmol/L
limited to a maximum of 200 mg/day during the test weeks. The use of
any medications and smoking was also prohibited during the test weeks. in subjects receiving 0.5 and 1.0 g of ethanol/kg BW, respec-
tively (P < 0.001 between the groups). Thereafter serum
ethanol decreased to undetectable levels (~0.4 mmol/L) in
Study design both groups within 5 h and 11 h, respectively. Subjects from
Protocol I comprised a dose-dependent, double-blind, randomized, the control sessions also had undetectable serum ethanol
cross-over experiment in which the subjects received single oral doses levels.
of 0,0.5, and 1 .O g ethanol/kg BW mixed in a sugar-free carbonated drink In the control group, plasma GH was 8.4 t 1.6 kg/L at
(600 mL) at l-week intervals. The amount of ethanol of the 0.5-g/kgdose
is 35 g in a 70-kg subject and represents approximately the amount of 1800 h and decreased to 0.6 + 0.2 pg/L at 2200 h. These
alcohol present in a half liter bottle of wine with a concentration of 7%. relatively high GH levels at 1800 h most probably present a
The subjects arrived at the site of the trial at 1700 h, at which time a small GH peak in the evening in the wakeful state as reported
cannula was inserted in a dorsal vein of the hand. Heparin 5000 IU/lOO earlier (25). After midnight, plasma GH presented an ex-
mL (Medica, Helsinki, Finland) in physiological sodium solution (200
pected large peak, 25.0 t 4.3 pg/L at 0100 h. Ethanol had no
PL) was used to keep the cannulae open. The drinks were given at 1900 h
and were to be consumed at a constant pace by 1945 h. The blood significant effects on plasma GH at 2000 h or at 2200 h until
sampling was started at 1800 h (before intake of alcohol or vehicle) at 0100 h and 0200 h, when the higher dose (1.0 g/kg) almost
followed by samples at 2000, 2200, 2400, 0100, 0200, 0300, 0400, and completely inhibited the nocturnal GH peak (P < 0.01, Fig.
0700 h. Lights were turned off at 2300 h, at which time the subjects were 1A). The lower dose also decreased nocturnal GH levels at
asked to go to bed. The blood samples were thereafter taken in the dark
(under 2 lux). The subjects had been fasting since 1500 h and received 0100 h and 0200 h, but to a lesser degree (P < 0.01, Fig. 1A).
a standardized snack containing bread, butter, cheese, 0.2 L of orange In the subjects receiving the lower ethanol dose, plasma GH
juice, and a banana at 2100 h. was significantly higher (P < 0.05) than the control value at
Protocol II was an open, randomized experiment carried out after the 0400 h, possibly because of a rebound phenomenon.
information of protocol I was available. Each of the six subjects received
In the control subjects plasma immunoreactive GHRH
po 0 or 1.0 g ethanol/kg BW mixed in a drink as in protocol I. The 0-min
blood sample was taken between 2250 and 2310 h from the subjects, and showed a diurnal variation, so that the levels at 0200, 0400,
immediately thereafter 1 pg of synthetic TRH/kg BW (Relefact TRH, and 0700 h were significantly (P < 0.01, Fig. 1B) lower than
 ETHANOL AND NIGHTTIME TSH, GH, AND PRL 2629

30 3

A 0.5 g/kg Ethanol . 05 g/kg Ethanol

. 10 g/kg Ethanol . 1.0 g/kg Ethanol

= 20
= 2
z .

2
5
CL 10
5
I- 1

0
16 20 22 24 02 04 06 06

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0 I I I / I I I

16 20 22 24 02 04 06 08
B
T 300
E =. 1

2 20.

3
?I!
- 200 -
LiL .5

:
10’8 I I I I I I 1 I
z loo-
16 20 22 24 02 04 06 06 L
FIG. 1. Effect of ethanol ingestion on plasma immunoreactve GH (A)
and GHRH (B) in nine healthy volunteers (mean i- SE) after intake
of 0 (0 and solid line), 0.5 (A and dashed line), and 1.0 g/kg BW (0 and OJ, 1 , I I I

solid line) of ethanol in 600 mL of beverage between 1900 and 1945 h. 16 20 22 24 02 04 06 08

*, P < 0.05; **, P < 0.01; ***, P < 0.001 us. controls. #, P < 0.05 TIME OF DAY
between ethanol groups.
FIG. 2. Effect of ethanol ingestion on plasma TSH (A) and PRL (B) in
nine healthy volunteers. For explanations see legend of Fig. 1.
those at 1800h in the control subjects.No significant changes
were found in plasma GHRH (Fig. 1B) after ethanol
administration.
Plasma TSH (Fig. 2A) showed a significant (P < 0.01)
nyctohemeral rhythm in the control group. It was 1.4 ? 0.2
mU/L at 1800 h, and the nocturnal rise began after 2200 h,
reaching maximal levels of 2.4 ? 0.4 mU/L at 01.00 h and
remaining high until morning (2.1 2 0.3 mU/L at 0700h). We
were able to show that the higher dose of ethanol inhibited
the nocturnal TSH increase. The inhibition was significant at
0100 (P < 0.05) and 0200 h (P < 0.01) with plasma TSH
concentrations of 1.4 +- 0.2 mu/L. Although there were de-
creases after the lower dose, these were not significant.
Plasma PRL levels (Fig. 2B) in the control subjects were at **

the samelevel at 1800-2200 h, 60-80 pg/L, whereafter they I I I

gradually increased to 105 at midnight and to 248 pg/L at 0 0.5 1 .o

0700 h (P < 0.001). Interestingly, ethanol had no significant
effect on plasma PRL in our study.
Figure 3 shows the ethanol-induced
nal PRL, TSH, and GH secretions based on AUC analyses.
When the relative area under the plasma GH curve between
2200and 0300 h was taken as 100% in the control group, the
lower and higher ethanol dose reduced the nocturnal GH
surge to 37% and 20%, respectively (P < 0.01 for both cases).
Correspondingly, when the relative area under TSH curves
between 2200 and 0700 h was taken as 100% in the control
subjects,the inhibition was 32% and 45% in subjectsreceiving
0.5 g/kg and 1.0 g/kg ethanol, respectively (P < 0.05 for both
cases).Ethanol had no effects on PRL secretion as measured
by AUC analyses, confirming our plasma measurements.
Ethanol dose (g/bwkgl
FIG. 3. Effects of graded doses of ethanol on PRL, TSH, and GH
inhibition of noctur- secretion as analyzed by the AUC method in nine healthy volunteers
(mean ? SEM). The level of inhibition (%) is given on the y-axis and
ethanol doses on the x-axis. Asterisks indicate significance as in leg-
end of Fig. 1.
When we observed that ethanol resulted in a significant
inhibition of plasma TSH after midnight, we wanted to know
if this inhibition was preceded by an increase in the plasma
levels of thyroid hormones. Because of the much longer
half-lives, measurements on 2-4 time points in each test
group were carried out. PlasmaT, (Fig. 4A) measured at 1800
and 0700h or ET, (Fig. 4B) measured at 1800,2200,0300, and
 EKhIAN JCE & M . 1996
2630 ET AL. Vol81 l No 7

210 -- A - c

60 -

FIG. 4. Effect of ethanol ingestion on

plasma T, (A), free T, (B), T, (0, and O-
free T, (D) in nine healthy volunteers 07 07

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(mean ? SEM) after the intake of 0 (open Em"
TIME OF DAY TIME OF DAY
column), 0.5 (single-hatched column),
and 1.0 g/kg BW (cross-hatched column) 1B
of ethanol in 600 mL of beverage be-
tween 1900 and 1945 h. *, P < 0.05 VS. 5-
controls.
2 4-
z
E
-e 3

r
!-I- 2-

l-

o- . . ,
03 07 1ef 22 07
ElDH ElOH
TIME OF DAY TIME OF DAY

0700 h were similar and showed no significant changes be- pg/kg BW, totaling 55-88 pg/subject) led to a 5.5-fold in-
tween the test groups. Plasma T, (Fig. 40 at 2200 h did not crease at 20 min and a 4.2-fold increase at 60 min in the
change significantly from the values at 1800 h but exhibited control subjects, and to 5.4- and 4.4-fold increases in the
a statistically significant decrease (P < 0.05) at 0700 h in the ethanol-treated subjects, respectively (P < 0.01 in both cases).
0.5 g ethanol/kg BW group (1.64 ? 0.13 ZIS.1.97 2 0.2 nmol/ There were no significant changes between control and eth-
L), most possibly a random event. It should be noted that anol-treated subjects. Synthetic TRH led to significant in-
plasma IT, (Fig. 4D) measured at 1800,220O and 0700 h were creases in plasma PRL but no significant differences were
similar and showed no changes between the test groups. found between control subjects and ethanol-treated subjects
(Table 1).
Protocol II

After we observed that the changes in plasma thyroid Discussion

hormones most possibly do not explain the reduced plasma Ethanol administration has been shown to result in di-
TSH after ethanol intake, we performed a TRH stimulation minished circulating GH levels in studies carried out in the
test and measured TSH and PRL (Table 1). Synthetic TRH (1 evening or at night. For example, an earlier study from this
laboratory demonstrated that large doses of ethanol (1.5
TABLE 1. Plasma TSH and PRL in six healthy subjects in the g/kg BW) inhibited the small evening surge of GH (13) but
TRH test after ethanol or vehicle intake no nighttime measurements were performed. Later, acute
Time after TRH” and chronic effects of ethanol (0.8 g/kg) on sleep pattern and
Treatment GH secretion were studied and it was found that ethanol
Before 20 min 60 min
decreased nighttime GH secretion by 70% (16). We observed
TSH(mU/JJ
in this study that ethanol caused a significant and dose-
dependent decrease in plasma GH levels during 4 h after
Vehicle 2.2 k 0.6 12.2 2 2.3’ 9.3 2 1.4b
Ethanol (1 g/kg) 15.1 -+ 1.56 12.4 -+ l.l* midnight and, what is more important, the abolition of the
2.8 2 0.5
nocturnal GH surge was almost total (80% after the dose of
PRL (pg/L) ethanol 1.0 g/kg BW). The lower dose also led to a substantial
(63%) inhibition at 0100 h when ethanol had disappeared
Vehicle 102 * 19 1433 2 263’ 601 5 76’ from circulation. Thus, our present results agree with those
Ethanol (1 g/kg) 150 5 18 1422 5 265b 683 -+ 9gb
of Prinz et al. (16) and show, in addition, that a relatively
a TRH was given 1 pg/kg BW at time 0 min, and TSH and PRL small ethanol dose (0.5 g/kg) corresponding to the amount
prolactin were measured 20 and 60 min thereafter.
‘P < 0.01 vs. before values. Note that there were no significant of ethanol present in half a bottle of wine, also effectively
changes in TSH or PRL responses between ethanol- and vehicle- suppresses nocturnal GH secretion. We wish to emphasize
treated subjects. that the suppression was evident although there was no
 ETHANOL AND NIGHTTIME TSH, GH, AND PRL 2631

longer any ethanol detectable in serum, indicating that eth- surements and AUC analyses. There are previous human
anol had caused a long-lasting (up to 8 h) interference with studies that partly describe the effect of ethanol on nocturnal
a cellular mechanism related to the nocturnal GH surge. TSH secretion (13, 15). However, in both studies TSH was
We have previously found that in peripubertal children monitored only until midnight and no changes were ob-
the majority of nocturnal GHRH pulses precedes or coincides served. Therefore the reason for these negative results may
with GH pulses (26). Therefore we also measured plasma be that TSH levels were not followed long enough. In another
GHRH and observed that plasma GHRH levels before the previous report, nighttime levels of plasma TSH were mea-
nocturnal GH surge were stable. Evidently the long sampling sured after ethanol intake, but all the samples were pooled
interval in our present study (l-4 h) did not make it possible and no significant differences were observed between con-
to detect the pulsatile secretion of GHRH. Anyway, plasma trol night and first ethanol night (24). In the aforementioned
GHRH in subjects receiving vehicle only was significantly study ethanol (0.8 g/kg) was ingested late in the evening,
lower at 0400 and 0700 h than between 1800-0100 h, indi- which also explains why it did not have any effects.

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cating the presence of a diurnal rhythm in the secretion of If the regulation principles of TSH secretion are taken into
GHRH. We found no changes in circulating immunoreactive account, the decrease in plasma TSH by ethanol may be
GHRH levels after ethanol administration, suggesting that caused by elevated levels of thyroid hormones or caused by
the GH suppressing effect of ethanol could be mainly me- central mechanisms. Therefore we studied the effects of eth-
diated by factors other than hypothalamic GHRH. However, anol on the serum levels of free and total thyroid hormones
small changes in portal GHRH caused by ethanol could be and found no significant changes before plasma TSH was
lost when peripheral GHRH is monitored as in our present inhibited. We also performed a TRH stimulation test by using
study. According to previous studies carried out in experi- low TRH doses. We reasoned that the usual TRH dose (200
mental animals, ethanol seems to have multiple effects: it pg/subject) may be too high, so that the possible ethanol-
inhibits GH and GHRH gene expression (27, 28) and signal induced inhibition at the pituitary thyrotrope level may not
transduction in the pituitary somatotrophs (29). In man, GH be detected. Therefore we used TRH doses that were 55-88
response to synthetic GHRH was similar in vehicle- and pg (adjusted for BW). These TRH doses led to greater than
ethanol-treated subjects (301, indicating a suprapituitary 5-fold increases in plasma TSH, but the TSH response did not
mechanism for the ethanol-induced inhibition of GH. change after ethanol intake. Thus our present results suggest
The effects of ethanol on the GHRH-GH axis may have that there is a central mechanism behind the ethanol-induced
important clinical implications on growth and development TSH decrease.
in children. It is known that maternal alcohol abuse leads to The adenohypophyseal secretion of TSH and PRL are un-
fetal alcohol syndrome associated with intrauterine growth der the control of hypothalamus, principally of dopamine,
retardation and slow postnatal growth (31). This phenome- but also of TRH. Based on bromocriptine tests, Ida et rzl. (19)
non might be caused by the inhibitory effect of ethanol on GH have proposed that the stimulation of PRL by ethanol may
secretion that we describe in this study, although other fac- be mediated by ethanol-induced inhibition of hypothalamic
tors such as nutrition are also important. The main evidence dopamine. Because we observed no changes in plasma PRL
comes from animal studies: animals fed with ethanol-con- but a decrease in plasma TSH, the role of the dopaminergic
taining diets exhibit decreased growth even when food in- mechanism remains unproven.
take and other nutritional factors are controlled (32). In conclusion, we have demonstrated that ethanol in low
In our control subjects (both females and males) plasma doses inhibits nocturnal TSH and GH secretion, and that the
PRL was low between 1800 and 2200 h, but thereafter it inhibition occurs in a dose-dependent manner, disturbing
gradually increased, reaching its maximum (a 4-fold rise) the the normal diurnal rhythms of TSH and GH. The inhibition
next morning. Our results are in accordance with previous is most probably mediated by a suprapituitary mechanism.
studies on a diurnal rhythm in circulating PRL: the peak It is of interest that the same ethanol doses have no significant
values have been observed at night and especially in early effect on plasma PRL. Thus the nocturnal secretion of TSH
morning (4). In the present study, we observed no effect of and especially that of GH are extremely sensitive to alcohol,
ethanol either on the nocturnal PRL secretion or PRL re- which may have undesired effects on growth and metabo-
sponse to synthetic TRH. These results differ from those lism, especially in adolescents, even if ingested in small
performed during daytime when increased (17-19) or de- amounts.
creased (14, 20-22) PRL levels have been observed after
alcohol intake. In a previous report, the PRL response to TRH
was similar in control and ethanol-exposed healthy subjects References
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