Sleep, 5(4)318-328
© 1982 Raven Press, New York
Increased Severity of Obstructive Sleep
Apnea After Bedtime Alcohol Ingestion:
Diagnostic Potential and Proposed
Mechanism of Action
Lawrence Scrima, Michael Broudy, Kenneth N. Nay, and
Martin A. Cohn
Sleep Disorders Center, Mount Sinai Medical Center, Miami Beach, Florida
Summary: To assess the effect of 3 oz of 80-proof alcohol on the frequency
and severity of obstructive sleep apnea (OSA), we studied six OSA patients
and six healthy subjects on 2 nights. During the 1st night, when no alcohol was
given, five patients demonstrated mild and one severe OSA episodes associated with a decline in arterial oxygen saturation to at least 92% (hypoxic
event). On the 2nd night after ingesting 3 oz of alcohol just prior to bedtime, all
the patients demonstrated a significant increase in the number and/or severity
of hypoxic events compared with the no-alcohol night. Furthermore, the most
severe hypoxic events occurred within 80 to 160 min after sleep onset, a significantly shorter latency after sleep onset than on the no-alcohol night. In contrast, the healthy subjects had no incidents of hypoxic events or breathing
abnormalities during sleep after ingesting 0.8 gm/kg of alcohol. Possible mechanisms for these results are discussed. An OSA provocation test using alcohol
is proposed during a 2nd night of evaluation for patients with mild to moderate
or intermittent OSA conditions, but not for patients demonstrating severe
hypoxic events or with alcohol intolerance. The alcohol provocation test would
serve to determine the influence of alcohol on the frequency and severity of
hypoxic events, providing the patient with a measure of the adverse effects of
social drinking on their condition. Key Words: Obstructive sleep apneaAlcohol-Hypoxia-Carotid body-Provocation test.
The sleep apnea syndromes have only recently been extensively described and
studied (1,2) and are now receiving increasing attention by the medical community. Obstructive sleep apnea (OSA), characterized by recurring upper airway
obstruction during sleep, associated with loud snoring and gasping, causes mild to
severe hypoxia, pulmonary hypertension, and cardiac arrhythmias that are potentially life-threatening. OSA is further characterized by repeated arousals from
Accepted for publication August 1982.
Address correspondence and reprint requests to Lawrence Scrima, Ph.D., Director, Sleep Evaluation and Treatment Center, Department of Neurology, University of Miami School of Medicine (D4-5),
1501 N.W. 9th Avenue, Miami, FL 33136.
318
ALCOHOL EXACERBATES OBSTRUCTIVE SLEEP APNEA
319
sleep prior to resumption of air exchange, resulting in marked reduction of stages
3 and 4 (delta) NREM sleep and fragmentation of stages 1 and 2 NREM and REM
sleep. The fragmentation of sleep and delta deprivation contribute significantly to
the prominent symptom of chronic drowsiness in OSA patients, who experience
fatigue even after a prolonged night of sleep and/or long naps. Since the severity of
symptoms is related to the frequency, duration, and degree of hypoxic events, it is
important to delineate substances or conditions that accentuate hypoxic episodes,
such as sleep deprivation (3,4) and obesity (5). Although alcohol is contraindicated
for OSA patients, as are all central nervous system (eNS) depressants, OSA patients probably succumb to social pressure to drink occasionally. It is therefore
important to assess the effect of alcohol on respiration during sleep in OSA patients.
Alcohol ingested by OSA patients before bed has been reported in brief communications and abstracts to increase the frequency and severity of hypoxic
events caused by OSA 1 (3 - 8), as well as causing earlier occurrences of the most
severe OSA induced dip in arterial oxygen saturation (7). Such reports led to the
proposal of an alcohol provocation and tolerance test for OSA (9). The twowithin-subjects experiments reported here comparatively assess the effects of3 oz
of alcohol on OSA patients and 0.8 gm/kg of alcohol on normal individuals.
EXPERIMENT 1
Methods
Five male OSA patients, ages 28-58, with mild to moderate hypoxic events
associated with arterial oxygen saturation (Sao2) levels of 92-80%, and one 67year-old female OSA patient with severe hypoxic events, having Sao 2 as low as
60%, underwent two overnight polysomnography studies. Each patient signed an
informed consent approved by our institutional review board. The polysomnographic parameters, which were monitored and recorded on both nights, included
respiratory pattern by respiratory inductive plethysmography (Respitrace®, Ambulatory Monitoring, Inc., Ardsley, New York) (10), arterial oxygen saturation by
ear oximetry (Hewlett-Packard, Waltham, Massachusetts), and electrocardiography, as well as the usual EEG, EOG, and chin-EMG montage, which were later
evaluated by an established method to determine sleep stages (11). All OSA patients were referred to the Sleep Disorders Center with symptoms of excessive
daytime sleepiness, loud nocturnal snoring, with frequent sleep arousals, and at
least one all-night polysomnogram demonstrating obstructive sleep apnea
episodes terminated by brief arousals, presumably due to hypoxia-related stimuli
(Table 1). The OSA patients agreed to abstain from alcoholic beverages for 48 h
prior to a 2nd night of recording their sleep and respiration, at which time they
drank 3 oz of their preferred 80-proof alcoholic beverage, starting 30 min before
bedtime (between 2200 and 2400 h). Blood samples were drawn from the first two
subjects before alcohol ingestion and at the end of the night. Since no trace of
1 Scrima L, Broudy M, Cohn M. Effects of 3 ounces of ethyl alcohol on patients with obstructive
sleep apnea: a pilot study. Southern Sleep Soc., Miami Beach, December 5, 1980.
Sleep, Vol. 5, No.4, 1982
L. SCRIMA ET AL.
320
TABLE 1. Polysomnography diagnostic profile of OSA subjects
Subject
Mild OSA
1
2
3
4
5
Mean
SE ±
Severe OSA
6
a
Ht
(cm)
Wt
(kg)
Total
number of
apneas
17
532
64
32
460
221.0
113.1
Age
Sex
38
30
28
58
40
38.8
5.3
M
M
M
M
M
175.3
180.3
172.7
172.7
167.6
173.7
2.0
90
104
88
88
91
92.2
3.0
67
F
154.9
79
410
Lowest
arterial
Longest
duration
(s)
saturation
Total
sleep time
(min)
12 (ll)a
40(20)
30 (15)
50(30)
45 (20)
35.4 (19.2)
6.7(3.2)
95
86
86
80
80
85.4
2.7
303
353
385
235
345
324.2
25.9
65
273
65(20)
O2
Approximate mean in parentheses.
alcohol was found in either the evening or morning samples, and intra-night sampling would have disrupted their sleep, this procedure was not repeated for the
other subjects. The method of assessing OSA for each subject consisted of making
comparisons between the 1st and 2nd night of equal durations of recorded arterial
oxygen saturation after lights out, by means of frequency counts of hypoxic
episodes, starting at or below 92% arterial oxygen saturation. In addition, the
temporal occurrence of the hypoxic episodes from the 1st night recording without
alcohol was compared with the 2nd night with alcohol.
Results
All hypoxic events were due to complete (apnea) and/or partial (hypopnea)
upper airway obstructions. The frequency and/or severity of oxygen saturation
decrements for the six subjects (S) are shown in Table 2. The data from patient 6
were analyzed separately, since this subject had severe OSA, in contrast to the
other subjects with milder conditions. Excluding S 6, the total number of hypoxic
episodes incre.ased significantly (p < .05), from 538 during the nights with no
alcohol (NA) to 863 with alcohol (WA). The total number of episodes associated
with a fall in Sa0 2 to below 89% increased from 197 without alcohol to 571 with
alcohol. Although S 6 had fewer hypoxic episodes after alcohol, the number of
episodes during which the oxygen saturation reached 76% or below increased
significantly, from 3 without alcohol to 25 with alcohol (p < .05) attributable to an
increase in the duration of the episodes and a lack of complete return of oxygen
saturation to baseline after long apneas.
The plot of the temporal occurrences of hypoxic episodes for all six OSA
subjects (Fig. la) illustrates that, without alcohol, the most severe hypoxic
episodes occurred in the last third of the night, usually during REM sleep (R) and
after 5 h of sleep. However, the amount of time from sleep onset to the most severe
hypoxic events decreased significantly (p < .01) after alcohol ingestion. Moreover,
these events occurred within the first 160 min, and hypoxic events of greater than
usual severity recurred throughout the first 4 h of sleep after alcohol ingestion. The
plots of the lowest Sao z within 20-min intervals for each OSA subject (Fig. 1b)
confirm the consistency of the overall results, illustrating that the greatest decre-
Sleep, Vol. 5, No.4, 1982
TABLE 2. Frequency and extent of hypoxic episodes with alcohol (WA) and with no alcohol (NA) matched for recording time (RT)
a
::r:
a
Number of hypoxic episodes within 4% Sao. ranges:
92-88%
S
I
2
3
4
5
WA
38
19
46
77
112
---
Total
292
88-84%
NA WA NA
0
29
4
37
271
I
28
7
13
321
341
370
173
20
0
4
125
23
~
,...
'~""
....
....
~
4
---
149
24
WA
842
210.5 ± 75.3
27
---
31
NA WA
NA WA
175
135
100
127
n:
Mean ± SE:
WA
72-68%
68-64%
NA WA NA WA
64-60%
0
27
34T
85.3 ± 39.3
0
5
---
---
0
5
12
3
0
0
WA
21
9
0
- - ---
3
0
9
---
---
---
0
9
0
0
0
* p < .05, paired t test.
S = Subject number; N = number of hypoxic episodes; SE = standard error.
3
NA
4.2 ± 1.4
O±O
3
0
WA
t"'-<
NA
340
60
4\0
259
376
39
72
53
94
605
0
29
7
42
460
0
*Mean:
± SE:
863
172.6
108.5
538
\07.6
88.4
0
25
5.0 ± 1.4
WA
3
~
~
~
V:l
~
V:l
c:::
(J
NA WA NA
0
~~
(J
;;;j
0
WA
n:
*Mean ± SE:
3
RT
(min)
--- ---
WA
NA WA NA WA NA
8
0
21
n:
Mean ± SE:
NA
NA
457
114.25±37.5
0
--- ---
Total
(N)
<60%
NA WA NA WA NA
0
NA
538
134.5 ± 78.8
WA NA WA
201
NA
76-72%
I
WA
'"
~""
80-76%
WA NA WA
--- --- --- ---
n:
Mean ± SE:
6
0
0
3
4
166
84-80%
~
t"'-<
(J
2
NA
-30.6 ± 0.4
2
RT
WA
NA
300
366
460
:::l
~
V:l
t"'-<
~
"tl
~
"e
~~
.....
tv
......
L. SCRIMA ET AL.
322
-'
z
o
~
!!~
'" 1-
~~
100
I:~
____________--';--
90
80
":Z
~ ~
v
70
~
.§.s 1-6
o
100
200
300
400
FIG. 1. Percent lowest arterial oxygen saturations reached during 20-min intervals of sleep
with alcohol (---) and without alcohol
(- - - -) ingestion are compared. Sleep stages
of NREM (1,2,3,4) and REM (R) associated
with hypoxic events are also given. a (left):
Mean arterial oxygen saturation values for
GSA patients and healthy subjects. Note that
alcohol had no effect on arterial oxygen saturation of the healthy subjects, in contrast to
the GSA patients. b (below): Means for each
subject. For S 2, arterial oxygen saturation
was recorded for only 60 min; therefore, apnea
durations are also depicted for the no-alcohol
(---) and alcohol (---) nights. Note the
earlier occurrences of lower levels of arterial
oxygen saturation on the alcohol night compared with the no-alcohol night in all subjects
(paired t, p < .01).
100
90
80
70
60
I I
100
90
100
80
90
80
70
.§.3
100
100
90
90
80
80
70
70
60
.§.4
100
200
300
.§.6
400
100
200
300
400
TIME IN MIN AFTER LIGHTS OUT
ment of arterial oxygen saturation with alcohol occurred between the first 80-160
min of sleep (mean: 123.3, SE: ± 12.0) as compared with 200- 380 min (mean:
283.3, SE: ± 27.1) without alcohol and always during REM sleep, except for S 1,
in whom it occurred during stage 2 NREM sleep.
For S 2, the arterial oxygen saturation without alcohol was not recorded after
the 1st h of sleep. A line-graph plot of the durations of S 2' s apneic episodes (Fig.
1b), which have a direct semiquantitative relationship to hypoxia, illustrates that
the longest apneas without alcohol occurred in the last half of the sleeping period,
whereas with alcohol the longest apparently occurred between the 180th and 220th
Sleep, Vol. 5, No.4, 1982
ALCOHOL EXACERBATES OBSTRUCTIVE SLEEP APNEA
323
min, associated with an arterial oxygen saturation of 80%. The lowest level of
oxygen saturation (66%) occurred between the 120th and 140th min, which demonstrates the semiquantitative relationship of rapid repetitions of obstruction
aborting full oxygen saturation recovery, resulting in shorter apneas, albeit with
more severe hypoxic effects. Finally, the plot for S 6 illustrates the most dramatic
temporal reversal of the severest hypoxic events with alcohol.
Table 4 shows that there were no significant differences in the standard sleep
parameters between the two sleep nights of the OSA patients (12).
EXPERIMENT 2
Since only 3 oz of alcohol significantly accentuated the number and severity of
hypoxic events in OSA patients during sleep, another experiment was done with
normal subjects, using a larger amount of alcohol to see if they are similarly
affected. This experiment also provides a preliminary test of the potential for an
alcohol provocation test for OSA.
Methods
Six healthy, nonobese, snorkel divers (Ss 7-14), ages 23-32, volunteered to
have 3 nights of polysomnography recording. Each subject signed an informed
consent form approved by our institutional review board. The 1st night was for
adaptation and screening for sleep disorders. Normality was determined by a
sleep disorders evaluation and by a polysomnographic recording. The subjects
denied symptoms of excessive daytime sleepiness, insomnia, snoring, or frequent
arousals from sleep, and had normal polysomnograms. The 2nd and 3rd nights
were counterbalanced, so that half the subjects received alcohol on the 2nd night
and the other half received alcohol on the 3rd night. On the alcohol night the
subjects drank 0.8 gmlkg of alcohol (80-proof vodka) mixed with orange juice,
over a 30-min period, consuming one glass (one-third of the total amount) per
lO-min interval. On the placebo night the subjects drank an equal amount of fluid,
consisting of orange juice and only 1 ml of alcohol, distributed among the three
glasses over a 30-min interval, before bedtime. All other procedures for these
subjects were the same as those for the OSA patients.
TABLE 3. Profile of normal subjects
Subject
Sex
Age
Ht (cm)
Wt (kg)
1
2
3
4
5
6
M
M
F
M
M
F
27
26
23
26
32
28
177.8
185.4
160.0
170.2
167.6
167.6
70
85
55
74
65
55
27.0
1.2
171.4
3.6
67.3
4.7
Mean
SE ±
Sleep, Vol, 5, No, 4, 1982
L. SCRIMA ET AL.
324
TABLE 4. Sleep parameters for the no-alcohol (NA) night and the night with alcohol (WA)
OSA patients
NA
Time in bed a
Sleep period time a
Total sleep time a
Sleep Efficiency Index
Sleep latency (I)a
Sleep latency (2)a
Number of stages
N umber of stage I shifts
Number of awakenings
Average of I-REM duration a
Number of REM periods
Percent
Percent
Percent
Percent
Percent
stage
stage
stage
stage
stage
3 +4
2
I
REM
0
Latency to stage REMa
P
370 ± 26.1
359 ± 22.9
316 ± 22.8
85 ± 4.5
II± 4.0
20 ± 4.6
45 ± 3.7
32 ± 2.8
9± 1.7
18 ± 7.1
4± 1.0
12
32
26
16
14
±
±
±
±
±
<.16
<.17
<.10
3.2
6.3
9.3
2.9
4.8
<.15
166 ± 25.1
<.17
<.10
<.15
Norma! subjects
WA
(3 oz.
80 prooO
NA
p
WA
(.8 g1kg)
416 ± 26.0
410 ± 21.2
395 ± 25.3
94 ±
.9
6± 2.3
9± 2.1
52 ± 3.2
19 ± 2.6
7± 1.1
17 ± 2.6
.8
6±
349 ±
343 ±
329 ±
92±
5±
15 ±
48 ±
35 ±
6±
13 ±
6±
16.2
14.6
14.9
2.2
2.6
3.5
6.2
7.6
1.3
3.2
1.0
409 ± 23.4
407 ± 23.5
384 ± 23.2
93 ±
.7
I ±
.6
5± 1.4
61 ± 6.4
31 ± 3.9
10 ± 1.5
17 ± 2.4
6 ± 1.0
6±
37 ±
29 ±
22±
5±
2.9
8.4
11.5
2.4
1.3
14 ± 1.I
46 ± 2.7
9± 1.8
23 ± 2.3
6±
.7
<.07
21 ± 2.5
46 ± 1.6
.7
4±
23 ± 1.6
.9
S±
111 ± 22.2
59 ± 6.5
<.05
118 ± 16.7
<.05
<.05
Time in minutes.
All values are means ± SEM.
For the OSA patients. there were no significant differences between NA and W A.
Values >.20. paired t-test. are not listed.
a
Results
Collectively, the normal subjects had no hypoxic events during their sleep on
the alcohol night and maintained a mean Sao2 of about 97%_ Only infrequent
minor breathing irregularities were observed, especially during REM sleep. These
were considered within normal limits and none produced Sao 2 ~92%.
There were only three significant differences in the sleep of the subjects between the alcohol and no-alcohol nights (Table 4). On the alcohol night, the
number of stage 1 shifts and the number of awakenings declined significantly (p <
.05), and the latency to stage REM increased (p < .05) in comparison with the
no-alcohol night. The percentage delta sleep (stages 3 and 4) also tended (p < .07)
to be greater on the alcohol night.
GENERAL DISCUSSION
The results indicate that as little as 3 oz of alcohol prior to sleep in OSA patients
markedly exacerbates the frequency and severity of hypoxic events (Table 2) and
significantly shortens the time from sleep onset to the most severe event (Fig. 1).
After alcohol, the latency to REM sleep tended to decrease in OSA patients and
increase in normals (Table 4), perhaps because the OSA patients had a greater
pressure to REM sleep and less alcohol. Moreover, as compared with their noalcohol night, OSA patients had fewer arousals lasting longer than 30 s after
consuming alcohol. Finally, as judged from S 1, ingestion of 3 oz or more of
alcohol may induce partial or complete OSA episodes in patients with a "normal"
Sleep, Vol. 5, No.4, 1982
ALCOHOL EXACERBATES OBSTRUCTIVE SLEEP APNEA
325
first polysomnogram or those with an intermittent OSA condition. S 1 also demonstrated more OSA (60 events) of longer duration (longest: 40 s, mean: 20 s)
associated with lower Sao2 (lowest: 90%) on a 3rd night of recording without
alcohol. In general, OSA patients had more frequent and severe hypoxic events
after alcohol ingestion, due to a combination of increased frequency and duration of apneas, as well as conversions from partial obstructions (prolonged inspirations during snoring with decreased tidal volumes) to complete obstructions
(inspiratory muscle efforts with no tidal volume).
Although counterbalancing to control for a 1st-night effect was not done for the
OSA patients, Table 4 illustrates that the sleep parameters of the two testing
nights were not significantly different. Therefore, the results should be attributable only to the ingested alcohol, and within subject variation. There were also
some trends worth noting. After alcohol ingestion the OSA patients tended to
have shorter latencies to REM sleep (p < .17) and a greater number of REM
periods (p < .10) and percentage of stage REM (p < .10), as well as decreased
latencies to stages 1 (p < .16) and 2 (p < .17) and decreased percentages of stages
3 and 4 (p < .15) and stage 0 (p < .15) compared with the no-alcohol night. Hence,
alcohol appears to have a two-sided effect on the sleep of OSA patients, preventing or shortening awake time (stage 0) while increasing stages 1, 2, and REM
sleep, the very stages that are associated with the greatest number of hypoxic
events due to OSA. The alcohol augmentation of these sleep stages and suppression of arousals in OSApatients, therefore, may be responsible at least in part for
the exacerbation of hypoxic events by increasing the arousal threshold and causing longer apneas (13).
In the normal subjects, for whom an adaptation night, counterbalancing, and
larger amounts of alcohol were used, the typical effects of alcohol on sleep were
clearly observed. There were fewer arousals and stage 1 shifts, an increased
percentage of stages 3 and 4, and a longer latency to the first REM sleep period.
However, percent REM sleep was not reduced, as described when large amounts
of alcohol are consumed (14).
Although the specific mechanism of the exacerbating effect of alcohol cannot be
determined from our data, several possible mechanisms may be responsible. The
central nervous system (eNS) depressant effects of alcohol may affect the respiratory centers that control the tone of pharyngeal muscles, thereby promoting
upper airway obstruction by increasing the likelihood of pharyngeal closure during
sleep. Alcohol may promote OSA by causing irritation and edema of the pharyngeal
tissues (15). Since alcohol is also known to affect primarily the accessory
somatosensory cortex and secondarily the reticular formation (16), inhibition of
activity of these areas by alcohol would result in a diminution of the perception
threshold and an increase in the arousal threshold. Finally, alcohol may depress
impulses from the peripheral hypoxic chemoreceptors (i.e., glomus cells) of the
carotid body by enhancing presynaptic inhibition, as has been demonstrated with
alcohol in the trigeminal cutaneous afferents (17), causing a reduction in the sensitivity of these receptors.
The latter mechanism gains credence from recent reports that the sensitivity of
Sleep, Vol. 5, No.4, 1982
326
L. SCRIMA ET AL.
carotid body chemoreceptors is regulated by both efferent and afferent presynaptic inhibition and disinhibition (18), During bradycardia and hypoxia, there is an
increase in blood flow and volume in the carotid body; the absorption and utilization of oxygen by the carotid body also increases (19). When alcohol is present
in the blood, the responsiveness of the carotid body to hypoxia probably would be
diminished due to the effect of the alcohol being absorbed along with oxygen from
the blood. Recent denervation studies with dogs demonstrated the primary importance of the carotid body for generating impulses that lead to arousal from
hypoxic events due to upper airway obstruction (20- 22). Carotid body responsiveness to hypoxia, depressed by alcohol absorption, would thus result in longer
apneas and more severe hypoxic events. The acute central and peripheral nervous
system depressing effects of alcohol, coupled with the irregular breathing, characteristic of REM sleep, may interact to promote the occurrence of the most severe hypoxic episodes of the night within the first 2 - 3 h of sleep after alcohol
ingestion.
There may be utility in using ethyl alcohol on a 2nd night of evaluation as an
OSA diagnostic provocation test, which would also provide useful information
regarding OSA patients' sleep respiratory tolerance to alcohol, especially since
larger amounts of alcohol had essentially no similar effects on our polysomnographically proven normal and healthy subjects. The rationale for such a test and
its application is reinforced by the realistic probability that OSA patients will
often be tempted to drink alcohol, since it is a prominent part of socializing.
Such a provocation test may make a more efficient 2nd night of diagnostic
testing possible by avoiding the problem of missing the most severe hypoxic
events because of the patient's restlessness or other causes that abort or disrupt
REM sleep or shorten a full night's recording. Therefore, the results of an alcohol
provocation test may yield a more accurate assessment of the pathology of OSA
for patients with an intermittent or mild condition and avoid false negative results
due to an otherwise temporary asymptomatic period for the patient. For example,
on the no-alcohol night, S 1 had arterial oxygen saturation levels that remained
within normal limits; however, with only 3 oz of alcohol, pathologically significant
hypoxic episodes became manifest. Obviously, the alcohol provocation test would
not be recommended for those with severe OSA, as diagnosed from the 1st night
of testing, or intolerant to alcohol.
Our results also raise questions concerning the epidemiology and mechanisms
of OSA. For example, many "normal" individuals are anecdotally described
as loud snorers (reflecting partial or complete obstructions) after an evening of
drinking alcohol. In a recent report by Taason et al. (23), 20 "normal" males exhibited a significant increase in apneas and hypoxic episodes after drinking 2 mllkg
(5-6 oz, 80 proof) of vodka at bedtime. There are major differences between
the normals of Taason et al. and the ones used in this study; namely, our normals
were all near ideal weight, were on the average 21 years younger, and were all
screened by overnight polysomnography to ensure that none of them had a sleep
disorder. Anyone of these differences might explain why some of the 11 subjects
of Taason et al. had an average of 10 apneas after ingesting alcohol and 4 subjects
Sleep, Vol. 5, No.4, 1982
ALCOHOL EXACERBATES OBSTRUCTIVE SLEEP APNEA
327
had an average of 5 apneas when no alcohol was ingested before sleep. Since
Taason et al. did not utilize an initial adaptation night in the sleep laboratory before the two testing nights, their data show greater variability.
Since most OSA patients do not believe they have any sleep problems, the
method of Taason et al. of verbally screening for sleep abnormalities may be
insufficient to determine subject normality. Furthermore, the subject's mean
weight values indicate that some of their "normal" subjects were overweight,
especially in group B, where there were many more hypoxic events during the
no-alcohol night. Except for one subject who had hypoxic events up to 64% Sao 2 ,
the mean values of the group B subjects was 87%, suggesting that most subjects
had only very mild hypoxic events, and therefore the mean value may have been
affected by a few subjects with more frequent and severe OSA and hypoxic
events. On the other hand, since their subjects were, on the average, 20 years
older than the healthy normals of the present study, and the amount of ingested
alcohol was the same, the data may reflect a decreased respiratory tolerance to the
effects of alcohol associated with aging. However, such a generalization is based
on the assumption that their subjects were truly normal, which cannot be verified
from their report.
Collectively, these results raise epidemiological questions. Does age influence
susceptibility to OSA? At what weight above the ideal is OSA induced? Does the
temporal occurrence of the most severe hypoxic events reflect the intensity of
REM sleep, the level of fatigue, pain threshold, arousal threshold and/or CNS or
peripheral nervous system depression? We hope that future research will help to
formulate answers to such questions.
Acknowledgment: This work was supported in part by a grant from the National Heart,
Lung and Blood Institute (grant HL-10622).
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