Baby Spends One Day Drinkinh and 1 Day Asleep

Alcohol. Author manuscript; available in PMC 2009 Dec 29.

Published in terminal edited class as:

PMCID: PMC2799509

NIHMSID: NIHMS163463

Slumber disturbances after acute exposure to alcohol in mothers' milk

Abstract

The results of previous research in our laboratory revealed that breast-fed infants feel significantly less active sleep later on exposure to booze in their mothers' milk than practise breast-fed infants not exposed to alcohol. The present study tested the hypothesis that infants would compensate for such reductions if their mothers then refrained from drinking alcohol. To this end, 23 breast-fed infants from 3 to 5 months of age and their mothers were tested on 2 days separated past 1 week. A pocket-sized, computerized movement detector, an actigraph, was placed on the infants' left ankles to monitor sleep and action patterning after which they were bottle fed mother's milk alone (command status) on 1 test day and mother'south milk containing 32 mg of ethanol per 100 ml — the average concentration detected in human milk subsequently lactating women drank an acute dose (0.3 m/kg) of alcohol — on the other. The infants' behaviors were monitored for the side by side 24 h; the first 3.5 h of monitoring on each test day took place at the Monell Middle. Consequent with previous findings, infants exhibited significantly less active slumber during the 3.5 h immediately after exposure to booze in mothers' milk compared with the control status; the decrease in agile sleep was observed in all merely iv of the infants tested. Compensatory increases in active sleep were then observed in the side by side 20.5 h, when mothers refrained from drinking booze. Although the mechanisms underlying the reduction in sleep remain to be elucidated, these findings demonstrate that short-term exposure to small amounts of alcohol in mothers' milk produces distinctive changes in the infants' sleep–wake patterning.

Keywords: Alcohol, Lactation, Sleep, Activity, Infant behavior

1. Introduction

Because of the striking paucity of scientific investigations of alcohol and breast feeding, women, and consequently their infants, have had to rely on a rich sociology that has been passed downwards from generations (see Fildes, 1986). This lore relates that alcohol has galactogenic properties that facilitate milk allow down and rectify milk insufficiency and has allaying properties that alleviate and calm the "fussy" infant (Adams & Davidson, 1987; Auerbach et al., 1987; Grossman, 1988; Lawrence, 1989; Mennella, 1999). Such advice is remarkably reminiscent of that given to meaning women about alcohol utilize before the scientific and clinical investigations of prenatal booze exposure (Davidson et al., 1981). That is, there are no dangers and it is salubrious and your baby! Such beliefs continue to be ingrained in current medical practice. Although some women are brash to abstain from drinking during pregnancy, Mulder and colleagues (1998) report that, in Britain, women are oftentimes told that drinking one to ii drinks once or twice a week is unlikely to impact fetal development (Dillner et al., 1996). Similarly, the results of a recent study revealed that 25% of the 410 lactating women surveyed in the Delaware Valley reported that they were encouraged by a wellness professional person to drink alcohol to improve the quality, quantity, and flow of their milk or to assistance their babies become a good dark's slumber (Mennella, 2002).

Research has revealed that acute exposure to alcohol in mothers' milk contradistinct the infants' slumber–wake patterning in ways that are contrary to this medical lore (Mennella & Beauchamp, 1991; Mennella & Gerrish, 1998). Infants, whose mothers drank little during both pregnancy and lactation, slept for significantly shorter periods during the hours immediately after the consumption of alcohol in their mothers' milk compared with their being fed mothers' milk containing no booze (Mennella & Gerrish, 1998). This reduction was due, in role, to a shortening in the amount of time that the infants spent in active sleep, a finding consistent with that observed in the near-term fetus (Mulder et al., 1998), in normal adults (Rundell et al., 1972; Williams et al., 1983), and in other animals (Mendelson & Hill, 1978) after alcohol exposure.

The goals of the present written report were to replicate our previous findings that infants exposed to alcohol in their mothers' milk have altered sleep patterns and to exam the hypothesis that breast-fed infants volition recoup for the disruptions in agile slumber that occur after exposure to alcohol in their mothers' milk if their mothers and so refrain from drinking booze. That they are capable of such compensation is suggested by the observation that newborns whose mothers drank heavily throughout pregnancy spent a greater proportion of time in both tranquillity and active sleep during the immediate postpartum period if they were predominantly formula fed afterwards birth (Chernick et al., 1983; Rosett et al., 1979; Scher et al., 1988). Of boosted interest is the finding that day-old infants who were manually awakened during slumber exhibited a recovery of sleep after such sleep deprivation (Anders & Roffwarg, 1973).

2. Methods

2.one. Subjects

Twenty-three nonsmoking, lactating women who had consumed at to the lowest degree one alcoholic beverage during lactation and who had infants with experience in drinking human milk from a bottle were recruited from ads in local newspapers and from the Women, Infants, and Children (WIC) centers in Philadelphia, PA. The mothers (82.half-dozen% multiparous) were 32.7 ± 1.2 years of age, and their infants (13 girls, 10 boys) ranged in age from 3.1 to five.1 months (mean = 4.0 ± 0.i months). None of the infants or mothers were taking any medication that would have affected slumber. Four boosted female parent–infant pairs began testing only were excluded considering the infants would not accept the bottle. Informed consent was obtained from each woman earlier testing began. All procedures used in this study were canonical by the Committee on Studies Involving Human Beings at the University of Pennsylvania.

At the end of testing, mothers were interviewed and asked to complete a series of questionnaires that elicited such information as the blazon of advice, if any, given to them nigh alcohol use during lactation. They also estimated the number, types, and frequency of alcoholic beverages consumed during pregnancy and lactation past completing a time-line, follow-dorsum questionnaire (Sokol et al., 1981). All but one of the mothers reported drinking very little during pregnancy (range = 0–16 alcoholic beverages per month; hateful = 1.5 ± 0.7 drinks per month) and slightly, but not significantly, increasing booze intake during lactation to, on average, 4.9 ± 2.1 alcoholic beverages per calendar month [range = < i–50 drinks per month; paired t(22df) = −one.75; P = .09]. Approximately one-third (34.8%) of the mothers reported drinking at least one alcoholic beverage in the 2 weeks preceding their participation in the report. In addition, approximately 35% of the mothers reported that they were advised to drink alcohol during lactation past a health professional to facilitate lactation, to help their babies slumber improve, or both, whereas the remaining women were non given whatever advice about drinking. Similar findings were obtained when we assessed the type of advice given past family members and friends (34.8% were encouraged to drink; 17.4% were discouraged, whereas the remaining received no advice).

2.2. Procedures

A within-subjects design was implemented. Each mother–baby pair was tested at the Monell Center on 2 days separated past an interval of approximately 1 week (come across Mennella & Gerrish, 1998, for more details). Mothers were instructed to refrain from drinking whatsoever alcoholic beverages on the 3 days earlier and the two days later on each exam twenty-four hour period. Each mother arrived with her infant at the Monell Middle at approximately 9:30 a.m., having terminal fed her infant at approximately the aforementioned time on each testing twenty-four hour period [paired t(22df) = −ane.06; P = .30]. Testing took identify in a private, carpeted room containing a portable crib for the infants. After acclimatization to the room and personnel, each mother expressed approximately 100 ml of milk, normally from both breasts, by using an electrical breast pump (Medela, Crystal Lake, IL), and an actigraph was placed on each baby's left leg.

After the actigraph had been in place for approximately 15 min, the infants were bottle fed approximately 100 ml of their mothers' milk alone on i examination day and an equal book of their mothers' milk containing 32 mg of ethanol on the other test solar day; this amount of ethanol is the average concentration detected in human being milk approximately 1 h afterwards lactating women drank an astute dose (0.3 yard/kg) of alcohol (Mennella & Beauchamp, 1991, 1993). The infants were fed their mothers' milk from a bottle because previous enquiry revealed that intake is macerated when infants feed at the breast after maternal alcohol consumption (Mennella & Beauchamp, 1991, 1993). Xi of the infants were fed the control milk on the first and the alcohol-containing milk on the second test day; the order was reversed for the remaining infants. There were no significant furnishings of order of testing or of sex of the baby on whatsoever of the variables tested.

The infants were monitored for at least 24 h after they consumed the chest milk from the bottle. The first three.5 h of monitoring on both testing days took identify at the Monell Eye, after which each female parent–infant pair immediately returned dwelling with the actigraph fastened to the infant's leg. Throughout the day, the mothers nursed their infants on demand; milk intake, during the first 3.v h of testing on both days, was assessed by weighing the infants immediately before and after each feed on an Acme Medical Calibration (San Leandro, CA), which was accurate to 5.0 thou. The infants were always placed prone in a crib or on the floor while sleeping because the actigraph-monitored infant activity must be independent of their mothers' activity and because body position influences sleep patterning in infants (Kahn et al., 1993; Sahni et al., 1999). Mothers were contacted by telephone to ensure compliance. The mothers were not informed of the order of testing, and at the end of each examination session they were asked several questions virtually their infants' behavior.

2.three. Dose delivered to the infant

The amount of alcohol ingested by the infants in this report (estimated by multiplying the book of milk ingested past the concentration of alcohol) ranged from 24.3 to 32.0 mg (hateful = 30.5 ± 0.3 mg). With the body weight of each babe taken into business relationship, the estimated dose ranged from 3.5 to 5.9 mg/kg (mean = 4.five ± 0.1 mg/kg); this amount is similar to that ingested at the breast after the consumption of a 0.3-g/kg dose past the female parent (Mennella & Beauchamp, 1991, 1993).

2.4. Method for measuring infant sleep and activity rhythms

The actigraph (AMA-32 Ambulatory Monitoring, Ardsley, NY), a self-contained microcomputer consisting of a piezoelectric accelerometer, generates a voltage in proportion to the mechanical deflection of the gratuitous end equally the actigraph is moved (Sadeh et al., 1989, 1991, 1995). Motion levels were sampled in the zero-crossing mode at a constant rate of 10 Hz. In this mode, an activeness count was scored each time that an baby's leg movement fell higher up the unit'southward sensitivity threshold. The number of nix crossings was stored in the actigraph's memory in 1-min epochs and later analyzed with the use of a computer program (Ambulatory Monitoring Ltd., Ardsley, NY). The automatic scoring algorithm on which this program is based has been validated by a behavioral observational state taxonomy assessment of sleep stages in infants of this age and can reliably distinguish between agile and quiet sleep (Sadeh et al., 1995). From the raw action data, the program adamant the number of minutes spent in agile and tranquillity slumber, the number of sleeping bouts, and the mean activity count (boilerplate number of zero crossings of the piezoelectric beam) during wakefulness that occurred during each iii.five-h (0–iii.five h) exam session for each baby and and then for the 20.5 h (iii.5–24 h) that followed each 3.v-h test session for all but one of the infants, whose cess was compromised by technical difficulties.

2.5. Information analyses

Repeated measures analyses of variance (2 × 2 repeated measures ANOVAs) were conducted to determine whether there were significant differences in these measures as a function of time since exposure (0–iii.5, 3.v–24 h postexposure) and day of the experimental period (control, alcohol). To allow for comparisons between the two time periods (east.one thousand., 0–three.v h versus 3.5–24 h) for the interval data, we adamant the hourly rate for each measure (e.chiliad., minutes per hour, number of bouts per hour), with the exception of hateful activity count during wakefulness, which is expressed as the average number of zippo crossings of the piezoelectric beam in each time period. Significant effects in the ANOVA were probed by paired t tests. All summary statistics reported in this article are expressed every bit means ± South.Due east.M., and all P values stand for two-tailed tests.

3. Results

There was a pregnant interaction between the fourth dimension since exposure (0–3.5 vs. three.5–24 h) and the experimental test day (i.e., command, alcohol) for the corporeality of time that infants spent in active slumber [F(1,21df) = fourteen.ane; P = .001]. Consistent with previous findings (Mennella & Gerrish, 1998), infants spent less time in agile sleep [paired t(22df) = 2.11; P = .05] during the hours immediately subsequently exposure to alcohol in their mothers' milk (Table ane). A decrease in active sleep was observed in 19 of the 23 infants.

Table 1

Short-term effects of exposure to alcohol in female parent's milk on sleep and activity levels

	Time since feeding
	0 to 3.5 h		3.5 to 24 h
	Milk only	Alcohol + milk	Milk only	Alcohol + milk
Total sleep (min)	72.ii ± 7.4	66.6 ± 9.1	675.7 ± 25.3	711.eight ± 21.9
Quiet slumber (min)	thirty.seven ± four.0	33.0 ± v.2	346.3 ± 24.seven	326.4 ± sixteen.1
Active slumber (min)	41.5 ± five.4	33.5 ± 5.three*	329.iv ± 20.0	385.iv ± 22.vi*
Longest sleep bout (min)	55.5 ± 6.ane	51.7 ± 7.5	301.9 ± 27.four	340.five ± 29.seven
Number of sleeping bouts	ii.3 ± 0.ii	2.two ± 0.3	9.9 ± 0.6	x.5 ± 0.8
Mean activity count during wakefulness	218.1 ± four.ane	209.0 ± half-dozen.1	210.7 ± iii.v	212.5 ± 4.vii

As well consistent with previous findings (Mennella & Gerrish, 1998), the furnishings of booze exposure on active sleep were not immediate [F(i,22df) = 8.68; P = .007]. As seen in Fig. i, there was no significant deviation in the amount of fourth dimension spent in active slumber during the offset half of the 3.5-h testing sessions [paired t(22df) = −0.88; P = .39; non significant]. However, infants spent significantly less fourth dimension in active slumber during the second half of the test session (i.e., 1.75–three.5 h), in which they were fed alcohol in mothers' milk, compared with being given mothers' milk containing no alcohol [paired t(22df) = three.68; P = .001]. The data also revealed that infants compensated for such decreases when their mothers then refrained from drinking alcohol [paired t(21df) = −2.73; P = .01]. On boilerplate, infants exhibited a 22.4 ± 7.0% increase in active sleep during the 20.5 h later the exam session in which they were exposed to alcohol compared with when they were exposed to mothers' milk containing no booze (Fig. 2). There were no significant interactions betwixt time since exposure (0–3.five vs. iii.5–24 h) and experimental test mean solar day (i.eastward., control, booze) for whatever of the other variables tested (eastward.g., longest slumber tour, total sleep, quiet slumber, number of bouts, action during wakefulness; all values of P > .10).

Hateful number of minutes that the infants spent in agile sleep during the first and 2d half of the 3.five-h testing session in which they consumed mothers' milk non containing alcohol (open circles) or mothers' milk containing ethanol (airtight circles) [F(1,22df) = 8.68; P = .007]. ROH = booze.

Mean percent difference in the time that infants spent in agile sleep during the first iii.5 h (0–three.5 h) and then the following 20.5 h (3.v–24 h) in which the infants were bottle fed approximately 100 ml of their mothers' milk containing ethanol compared with when they were canteen fed mothers' milk not containing alcohol.

Mothers were plain unaware of the differences in their infants' behaviors after alcohol exposure. That is, they were as probable as not to report that they idea that their infants consumed the booze-containing milk on either test solar day (Fisher exact probability test; P = 1.0; not significant). Moreover, there were no significant differences in the number of times that the infants chest fed [control vs. alcohol: 2.4 ± 0.3 vs. 2.5 ± 0.ii; paired t(22df) = 0.42; P = .68; not significant] or in the boilerplate amount of breast milk consumed during each feed [control vs. alcohol: 69.9 ± 8.0 vs. 70.2 ± v.5 ml; paired t(22df) = 0.03; P = .97; non significant]. Equally a preliminary step in determining whether maternal beliefs affected the infants' responses to booze exposure, an ANOVA was conducted to make up one's mind whether at that place were differences between infants whose mothers were encouraged to drinkable booze during lactation by a health professional person (35%) and those whose mothers received no advice at all (65%). In that location were no significant effects between these two groups on the infants' responses to booze for whatever of the sleep or activeness measures studied [e.g., active sleep: F(i,20df) = 0.27; P = .61)].

4. Discussion

The findings in the present written report further demonstrate that exposure to alcohol in mothers' milk alters the patterning of infant sleep. That is, breast-fed infants spent significantly less time in active sleep and tended to be less active during wakefulness in the hours immediately after exposure to alcohol in their mothers' milk. The effects of alcohol were not immediate, however, and were evidenced during the terminal half of the 3.5-h testing session. Such findings resemble observations made in the near-term fetus. Mulder and colleagues (1998) found that the acute consumption of ii glasses of wine (dose = 0.25 k/kg) by meaning women who drank very picayune or not at all during pregnancy had an effect on the fetal behavioral-country organization. Rapid eye move sleep, in item, was reduced, and breathing activity was suppressed.

Equally shown in Fig. 2, the infants then compensated for this reduction in active sleep during the twenty.5 h later on alcohol exposure. Recall that their mothers refrained from drinking alcohol during this period. Whether similar findings would be observed if mothers continued to drinkable seems unlikely. Of detail interest here is the observation that the fetus tin can compensate, in function, for sleep disturbances induced by booze exposure in utero if they are not additionally exposed to alcohol after birth. That is, infants of mothers who drank heavily throughout pregnancy spent a greater proportion of time in both quiet and active slumber during the firsthand postpartum menstruum if they were predominantly formula fed after birth, compared with infants of mothers who abstained from drinking (Chernick et al., 1983; Rosett et al., 1979; Scher et al., 1988). Compensatory increases in active sleep in the afterward part of the dark later on the acute consumption of alcohol past nonalcoholic mothers also have been reported (Rundell et al., 1972; Williams et al., 1983; Yules et al., 1966), and although tolerance to the sleep-confusing effects of alcohol develops within a few nights, compensatory increases in agile slumber recur when alcohol is discontinued.

Sleep, the about frequent land of consciousness of infants, can exist influenced by a variety of ecology and physiological factors. The present study aimed to experimentally control a diversity of such factors. For example, each of the test sessions was held at the same fourth dimension of twenty-four hours, and testing took identify in a individual, placidity room. The infants were placed decumbent in a crib or on a rug as much as possible, so that the infants' actigraph-monitored sleep and activity measures were independent of their mothers' action (Kahn et al., 1993; Sahni et al., 1999). The mothers were unaware of the order of testing and did non reliably identify which day their infants consumed the alcohol-containing milk. Moreover, there was no difference in the patterning of feeding immediately before or during the two testing days, which were separated by an interval of 1 week. And, finally, there were no significant effects of maternal beliefs, as assessed by the blazon of advice received by the mothers about booze use during lactation, on any of the sleep measures studied. Although possible, it seems unlikely that the alterations in the patterning of slumber were due to changes in the infants' interaction with their mothers. Rather, it appears that exposure to this small amount of alcohol in the mothers' milk had directly, albeit subtle, effects on the infants.

The mechanisms underlying these changes in sleep patterning and the long-term result of chronic exposure on development remain to be elucidated (refer to Little et al., 1989). Because the drug in the nursing infants' blood or urine was not measured, we exercise non know the corporeality that was absorbed from the milk. However, the available information on pediatric pharmacokinetics has demonstrated significant differences in the absorption, distribution, metabolism, and excretion of a variety of drugs from those of older children and adults (Milsap & Jusko, 1994). Some evidence supports the suggestion that infants have limited capacity to oxidize ethanol (Pikkarainen & Raiha, 1967), which, in plow, may render the dose more potent. The results of animal-model studies take revealed that infant rats showroom a lower alcohol-related metabolic chapters, longer half-life of alcohol, and, in plow, higher peak blood alcohol levels (Kelly et al., 1987), and they are more than sensitive to the effects of alcohol on sure cognitive processes (Chen et al., 1992) compared with older-aged conspecifics.

The goal of our research programme is to experimentally investigate the relation between alcohol and breast feeding, so that we can provide mothers and health professionals with some answers to frequently asked questions on this topic (Auerbach et al., 1987; Grossman, 1988). Dissimilar a pregnant woman, a nursing adult female who drinks occasionally can limit her baby's exposure to booze by timing chest feeding in relation to her drinking. That is, booze is non stored in breast milk; rather, its presence parallels that plant in maternal plasma, peaking approximately 1-half hour to an hour later the cessation of drinking and decreasing thereafter (Lawton, 1985; Mennella & Beauchamp, 1991). Contrary to popular conventionalities but consistent with the results of several fauna-model studies (Heil & Subramanian, 2000; Oyama et al., 2000; Subramanian, 1995, 1999; Subramanian & Abel, 1988; Swiatek et al., 1986; Vilaró et al., 1987), infants really ingest less milk at the breast in the hours immediately afterward maternal alcohol consumption (Mennella & Beauchamp, 1991, 1993). This macerated intake is due, in function, to a direct effect of alcohol on milk product by the female parent (Mennella, 1998). If a nursing mother is told to drink to aid her baby sleep better, she and her caretakers tin refer to the research, albeit limited, that calls this lore into serious question. Results of the present study, which expand on previous research findings (Mennella & Gerrish, 1998), demonstrate that infant slumber is disrupted during the 24 h after exposure to alcohol in mothers' milk.

Acknowledgments

We acknowledge the valuable comments and assist of Dr. Carolyn Gerrish. This research was supported by grant no. AA09523 from the National Institute on Alcohol Abuse and Alcoholism and the Office of Research on Women'south Health.

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