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Alcohol , Drug Use and Pregnancy Outcome

Alcohol , Drug Use and Pregnancy Outcome

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Published by Alan Challoner

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Published by: Alan Challoner on Nov 15, 2012
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Page 1 of 6
Alcohol, Drug Use and Pregnancy Outcome
Alan Challoner MA(Phil) MChSCurrent concerns about the effects of alcohol consumption on the unborn child may beassessed from this summary of some of the research that has been carried out since the1970s.The suggestion that alcohol has an adverse effect on pregnancy and child developmenthas a long history. Modernconcern about the influenceof alcohol on pregnancyoutcome was revived in theearly 1970s when a series ofarticles by researchers waspublished.
. These reportsculminated in thedescription, by Jones andSmith
, of a
fetal alcohol syndrome
(the FAS) amongthe offspring of severely andchronically alcoholicmothers, who continued todrink throughout pregnancy.A study in USA has shown thatthere is a seven point deficitin a child’s IQ where itsmother has taken just oneunit of alcohol daily duringpregnancy.
 The principal characteristicsthat have been associatedwith the FAS are:
pre-natal and post-natalgrowth retardation;
central nervous systemdysfunction includingmental deficiency,neurological problemsand behaviouraldysfunction;
a characteristic pattern of facial anomalies including the nose, mouth, ears and jaw;
and various other malformations mainly of the skeletal, urogenital and cardiac systems.The effects are dose-related and therefore every woman must realise the potential hazardfor her child-to-be.
Research from the late 1990s
indicates that pregnant women maydrink a small amount of alcohol without harming the foetus. The acceptable level that wasconsidered reasonable was one unit per day (i.e. small glass of wine; half a pint of ordinarybeer, or a single measure of spirits. More than this may hinder the growth of the foetus,leading to a smaller baby. Consumption of over 15 units a week may be associated withintellectual impairment.
: A combination of birthdefects, including organ deformities and mental, motor,and/or growth retardation, that results from maternalalcohol abuse as well as some additional, but lessimportant, factors.However where the syndrome is diagnosed, the alcoholabuse is most often accompanied by adverseenvironmental circumstances. Foetuses conceived byheavy drinkers are more likely to miscarry, are smaller atbirth, do not thrive so well initially and are poor suckers,whether from the bottle or breast. It is not uncommon tofind that as the child reaches primary school-age, he willbe less intelligent and be less integrated with his peers.Alcoholic mothers are likely to have infants suffering fromfetal alcohol syndrome, which is characterized bydeformities of the heart and joints, face (short eyelid slitsand abnormal jaw protrusion), and hand (altered palmar crease patterns), lags in motor development and motor dysfunction, and severe mental handicap. Even moderatedrinking
less than one drink per day
has been found tobe related to attentional deficits in children at four years ofage, Streissguth
et al.,
, decreased fetal growth, andincreased risk of miscarriage, Mills
et al.,
. Results of animalstudies by Furey also show serious problems resulting fromsingle episodes of heavy alcohol consumption around thetime of conception.
 In view of these research findings, the USA Surgeon Generalhas warned that all pregnant women should avoid alcoholentirely. Some areas, such as New York City, have passedordinances that require all bars, restaurants, and liquor stores to post notices such as; “
Warning: Drinking alcoholicbeverages during pregnancy can cause birth defects.”
Page 2 of 6The Seattle research group
, examined intellectual development in the children of motherswho were addicted to alcohol and reported a significantly reduced IQ at 7 years of age. Itis not clear whether the investigators who made this assessment knew the alcohol status ofthe mother. Moreover, 32% (6/19) of the alcoholics’ children were apparently lost to follow-up before 7 years of age compared with none of the controls.
However, despite the smallnumbers and the questionable nature of the comparison, the authors recommended that:
“serious consideration should be given to the early termination of pregnancy in severechronically alcoholic women . . . ” [ since] “. . . the offspring of chronic alcoholic women,whose development and function are often permanently damaged by their adverseintrauterine environment, frequently became a problem for society in postnatal life.”
These and other studies reported that the babies of women who drank excessively duringpregnancy were disadvantaged in some way. All reported that the birth-weight of babieswas significantly reduced among women considered to be alcohol abusers. There arehowever some inconsistencies in the findings of some studies. Two, the Cleveland andBuffalo studies, agree that the babies of alcohol abusers tend to be small for dates. TheCleveland and Seattle groups found an overall increase in the rate of congenitalmalformations, but the Buffalo group did not. The Cleveland group found no increase inperinatal mortality whereas the Seattle group did. Moreover, the Seattle studyretrospectively diagnosed 32% (6/19) cases of the FAS, whereas the Cleveland studyretrospectively diagnosed 2.5% (5/204). These discrepancies may reflect the fact thatdifferent definitions of alcoholism were used. Only 0.04% of women were classifiedalcoholic by the Seattle researchers compared with 1.7% by the Cleveland researchers.The outcome of moderate drinking in pregnancy is clear following reports of investigationsthat were set up to look at these effects. A large number of epidemiological studies havebeen reported on and the findings from five are summarized in the Table below.The studies outlined in the Table above show inconsistencies. Some of the reasons for thesemay be that the studies were conducted at different times, in different places, by differentpeople using different methodologies. The inconsistencies are however important. A largenumber of other studies, besides those in the Table, have been published and there isclearly no consensus about the relationship between moderate drinking and adversepregnancy outcome. (Roman,
Pregnancy Variables Paris S. California Boston Denver LondonGestation - + + + NRBirth-weight + + - - +Small for dates + NR - - +Congenital abnormality - NR - - NRStill-birth + NR - - NR
+ = statistically significant negative association between alcohol and the outcome reported- = no statistically significant negative association between alcohol and the outcome reportedNR = not reported
Reported association between various aspects of pregnancy outcome andalcohol consumption in early pregnancy
[after Roman]
Page 3 of 6Several studies of the effect of alcohol have been made using pregnant rats. Of those thatwere fed liquid alcohol diets during pregnancy the following results were found:140 subjects were tested for activity irregularities ten days after birth, passiveavoidance learning, and spontaneous alternation in a T-maze. The subjects showedage-related increased activity; but deficits in passive avoidance learning andresponse perseveration that were not age-related. Abel suggests that the exposureto alcohol brought about a developmental delay in the response inhibitionmechanisms underlying activity. They also were less maternally responsive than non-treated controls.
Poland found that the neuro-toxic effects of the fetal alcoholexposure on neuro-endocrine function may become evident when there is a stresschallenge.
 Alcoholism runs in families, and does so even when the children of alcoholics are separatedfrom their parents and raised by non-alcoholic adoptive parents. Twin studies suggestgenetic factors. Childhood behaviour problems weakly predict future alcoholism.
 Recent concerns should allow for more current research to be considered as there may bea differing view to be obtained. An article in the issue of
dated 11
February 2000reported that a single exposure to high levels of
(the alcohol in beer, wine andspirits) can kill nerve cells in the developing brain. The researchers found that the rat brain issensitive to this toxic effect during a brain development stage that corresponds to the braingrowth spurt in humans. This is known as synaptogenesis because it is the time when braincells form most of their interconnections, the brain growth spurt lasts from about the sixthmonth of pregnancy to a child's second birthday. The investigators believe that thediscovery that cells can die after a single episode of alcohol intoxication means it would beprudent for expectant mothers to avoid alcohol intoxication during pregnancy.The investigators also studied the mechanism of this alcohol-induced brain cell death. It isknown that alcohol can interfere with certain transmitter systems in the brain. The systemsuse chemical molecules, such as glutamate and GABA, to activate nerve cell receptorsand transmit messages from one cell to another. In research reported in 1999, in
 Olney and colleagues found that drugs called NMDA antagonists, which interfere withglutamate transmission in the same way that alcohol does, have a similar cell-killing effectin the infant rat brain when given as a single high dose. In the current study, theinvestigators found that drugs that excessively activate GABA receptors, as alcohol does,also can kill nerve cells in the infant rat brain.This evidence documents that alcohol acts by two mechanisms — blockade of glutamatetransmission and excessive stimulation of GABA transmission. By combining these twomechanisms, it produces a compound pattern of damage that is greater than either mechanism would produce by itself.
 There are other concerns that were highlighted by this research team. Much of thesignificance of these findings comes from the fact that alcohol is so widely used throughoutthe world. Numerous other drugs act either by blocking glutamate receptors or activatingGABA receptors, and many of these drugs are drugs of abuse and/or are used in paediatricmedicine as sedatives, anticonvulsants or anaesthetics. Drugs of abuse that block NMDAglutamate receptors include phencyclidine (PCP or "angel dust"), ketamine (special "K")and nitrous oxide (laughing gas). Both ketamine and nitrous oxide are used frequently inpaediatric anaesthesia. GABA receptor activators that are frequently abused and/or usedin paediatric anaesthesia include benzodiazepines, barbiturates, isoflurane, and propofol.

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