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National guidelines on alcohol use during pregnancy: a dissenting opinion

John S Whitehall
Med J Aust 2007; 186 (1): 35-37.
Abstract
  • New national guidelines recommend that women who choose to drink alcohol during pregnancy “should have less than seven standard drinks” in any week and “no more than two standard drinks” on any one day, and that they should never become intoxicated.

  • Exposure to alcohol at these recommended levels has been shown to affect brain development and certain behaviours in animals.

  • Some longitudinal studies in human children have detected detrimental affects from exposure to low levels of alcohol.

  • Normal public health standards for exposure to environmental toxins should be applied for the unborn baby. We do not know what level of alcohol exposure is safe and pregnant women can only be advised to abstain.

In March 2006, National clinical guidelines for the management of drug use during pregnancy, birth and the early development years of the newborn were published with the support of the Australian federal, state and territory governments and the New Zealand Government under the guidance of a Steering Committee and “two expert workshops”.1 These guidelines claim to represent a set of nationally agreed, evidence-based guidelines for use by “all health care practitioners working with pregnant women experiencing a drug or alcohol use problem”, but risk being more controversial than helpful, particularly with regard to the consumption of alcohol for which “an abstinence-based approach is not recommended”.

The guidelines advise that a mother should be informed of the risks, and suggest she “may consider not drinking at all” but, if she chooses to do so, “should have less than seven standard drinks” in any week and “no more than two standard drinks” on any one day, and that, “most importantly, [she] should never become intoxicated”. A standard drink is defined as containing 10 g of alcohol.

Consensus guidelines?

The guidelines are the same as those of the National Health and Medical Research Council (NHMRC) for all pregnant women,2 which have generated some controversy within the profession. For example, the Australian Medical Association has urged revision on the basis of “compelling international evidence that mothers who drink even small amounts of alcohol during pregnancy could unwittingly harm their unborn children”.3

There is no international consensus in support of the Australian and New Zealand guidelines. To the contrary, the United States Surgeon General states: “A pregnant woman should not drink alcohol during pregnancy” and, if she has already done so, “should stop in order to minimize further risk”.4 The American College of Obstetricians and Gynecologists advises its members: “Women should be dissuaded from alcohol consumption during pregnancy because there is no known safe amount”.5 Other US authorities urging abstinence include the Centers for Disease Control and Prevention,6 the American Academy of Pediatrics,7 the National Institute on Alcohol Abuse and Alcoholism,8 the March of Dimes,6 and the National Organization on Fetal Alcohol Syndrome.6

How much alcohol during pregnancy?

The contentious issue is how much alcohol can be consumed on a regular basis without damaging the unborn baby. No one appears to doubt that binge drinking is harmful, and the reality of fetal alcohol syndrome has been accepted since its description.9

Implying that one drink a day (but never on Sundays) is safe rejects abundant literature. North American studies show that one drink may produce a level of alcohol in a woman of 0.02%–0.05%, depending particularly on her weight.10,11 As alcohol distributes in body water, the approximate 20% increase in that compartment during pregnancy12 might dilute the concentration of alcohol, particularly from the second trimester. However, the time of exposure of the fetus might be increased. Elimination of alcohol has been prolonged in guinea pigs,13 and amniotic fluid may act as a reservoir.14,15 Because the amniotic fluid contains less fat than plasma, the concentration of alcohol will be higher in amniotic fluid than in blood.

If Australian mothers restricted their alcohol intake to 10 g per day they might have lower alcohol concentrations than suggested by the American studies. However, in practice, our serving size is usually generous, with such small quantities of wine being only rarely served in either private or public settings.16 Serving size of alcoholic drinks has been found to regularly exceed the standard by 70% in urban hotels.17

Regular exposure to the levels of alcohol attainable by one drink has led to disorganisation of neurones in various regions of the brains of laboratory animals. The function of brain cells,18,19 their structure,20 viability,21 development22 and ability to migrate,19 and the behaviour of animals23 and their response to stress24 have all been shown to be disrupted.

The effects on cognition, learning, behaviour and executive function of human brains exposed to these levels of alcohol have been difficult to quantify because of various confounders, and because of the imprecision of psychological measurement. Nevertheless, a number of longitudinal studies have been concluded in North America. One in Detroit suggested a threshold for fetal toxicity of 0.014% blood alcohol.25 One in Ottawa found no deficits in language comprehension or attentional problems at doses less than 8.8 g of alcohol a day.26 One detected no effects on intelligence in 4-year-olds,27 but another found exposure to as little as one drink a week caused children to be three times more likely to have “delinquent behaviour scores in the clinical range compared with non-exposed children”.28 A long-running study in Seattle has reported adverse neurobehavioural effects at various ages after moderate prenatal exposure to alcohol,29,30 while a review of literature by another centre found the results inconsistent.31

If the effects of one drink a day are at the threshold for detection, it does not mean one drink is “safe”. Conclusions are based on statistical averages, and some babies will be more sensitive than others. In any case, how could it be proved that an individual’s potential had been reduced from high to normal?

The best advice?

Because thresholds for toxicity to environmental toxins and food additives are based on group averages, it is normal practice to incorporate a margin of safety when setting a public health standard for an acceptable level of exposure to a particular toxicant. The quantum applied depends on the quality of data and whether they are derived from human or animal sources. A safety factor of 10 is commonly applied to doses of exposure at which no adverse effects can be found within a species. When public health standards are established on the basis of animal studies, another factor of 10 is commonly applied to account for interspecies variation (G Neville, Senior Medical Officer, Environmental Health Unit, Queensland Health, personal communication). According to Australian Government guidelines on acceptable daily intakes of agricultural and veterinary toxins for humans: “The most common safety factor is 100 which takes into account that humans may be 10 times more sensitive to the chemical than experimental animals and that a proportion of the population may be 10 times more sensitive than the average person”. If, however, the toxicity database is incomplete or when the “nature of the potential hazards indicate the need for additional caution, a further safety factor of 10 to 20 may be incorporated”.32

Why does this advice not apply to fetal exposure to alcohol? If the threshold for detection of clinical damage in humans is one drink a day, the amount producing “no obvious adverse effects” would be less than that and, whatever that volume proved to be, normal public health standards would suggest a mother be warned to drink at most one tenth of it per day, more likely less than a thousandth!

Ann Streissguth, a foundational researcher on the fetal alcohol syndrome at the University of Washington School of Medicine, Seattle, is quoted in a report as warning that there is no statistical evidence of any “risk-free” level of drinking or any “threshold” level of prenatal alcohol exposure in the context of dose-response analysis.33

The Australian guidelines state: “An abstinence-based approach is not recommended, in part because it could result in disproportionate anxiety” and “precipitous decisions to terminate a pregnancy”.1 Affected mothers should be persuaded from such decisions with information that many babies show no evidence of damage despite heavy exposure.30 They may be reassured with new knowledge of ways the brain can defend itself, and should be advised to refrain from further risk and permit healing.34 Many mothers of children with fetal alcohol syndrome now complain that no one ever told them about the dangers (E Russell, National Organisation for Foetal Alcohol Syndrome and Related Disorders, personal communication).

The medical profession has a particular responsibility to such mothers, but also a general responsibility to the public. The real answer must lie in better education about the prenatal effects of alcohol. This education should be based on laboratory and clinical evidence, and on accepted public health practice. It should be expressed scientifically. The term “one drink” and the warning that a mother “should never become intoxicated” are as imprecise as the condition itself.

The guidelines devote six pages to appropriate discussion of the effects of cigarettes on the unborn, but only two to alcohol, the most preventable cause of brain damage in the fetus. They discuss many of the perinatal effects of smoking, but refrain from mentioning similar effects from alcohol, which, for example, is associated with an increased rate of stillbirth, low birthweight and premature delivery.35 The guidelines also do not mention that fetuses of mothers over 30 years of age may have increased vulnerability to alcohol.36

To emphasise that risk is highest in the earlier stages of pregnancy might distract attention from evidence that damage may occur from later exposure. Organogenesis occurs in the first weeks, and disruption may lead to the classic abnormalities of fetal alcohol syndrome, but brain development continues and remains vulnerable to low levels of alcohol exposure.22

I do not believe that the national guidelines represent national “grassroots” agreement. They appear to be based more on wishful thinking than on evidence. The guiding principle (that up to seven drinks a week will not harm the baby) has no margin for safety. Established public health standards should apply for the newborn baby and its exposure to the environmental toxin, alcohol. We simply do not know what level of exposure is safe. Abstinence is the only advice we can give to pregnant women.

John S Whitehall, FRACP, MRCP, DCH, Director of Neonatology
The Townsville Hospital, Townsville, QLD.
Competing interests: 

None identified.

Reference Text: 
National clinical guidelines for the management of drug use during pregnancy, birth and the early development years of the newborn. Ministerial Council on Drug Strategy. Sydney: NSW Health, 2006. http://www.health.nsw.gov.au/pubs/2006/ncg_druguse.html (accessed Sep 2006).
Reference Order: 
1
PubMed ID: 
Reference Text: 
Australian alcohol guidelines: health risks and benefits. Canberra: NHMRC, 2001: 16. http://www.nhmrc.gov.au/publications/synopses/ds9syn.htm (accessed Sep 2006).
Reference Order: 
2
PubMed ID: 
Reference Text: 
Australian Medical Association. Media release. AMA calls on NHMRC to revise its guidelines on alcohol consumption during pregnancy. Canberra: AMA, 23 December 2004. http://www.ama.com.au/web.nsf/doc/WEEN-67X2RK (accessed Sep 2006).
Reference Order: 
3
PubMed ID: 
Reference Text: 
United States Department of Health and Human Services. News release. US Surgeon General releases advisory on alcohol use in pregnancy. Washington, DC: US Department of Health and Human Services, 21 February 2005. http://www.surgeongeneral.gov/pressreleases/sg02222005.html (accessed Sep 2006).
Reference Order: 
4
PubMed ID: 
Reference Text: 
American College of Obstetricians and Gynecologists and the American Academy of Pediatrics. Guidelines for perinatal care. 5th ed. Washington, DC: ACOG, 2002: 85.
Reference Order: 
5
PubMed ID: 
Reference Text: 
National Center on Birth Defects and Developmental Disabilities, Centers for Disease Control and Prevention, Department of Health and Human Services in coordination with National Task Force on Fetal Alcohol Syndrome and Fetal Alcohol Effect, American Academy of Pediatrics, American College of Obstetricians and Gynecologists, March of Dimes and National Organization on Fetal Alcohol Syndrome. Fetal alcohol syndrome: guidelines for referral and diagnosis. July 2004. http://www.cdc.gov/ncbddd/fas/documents/FAS_guidelines_accessible.pdf (accessed Sep 2006).
Reference Order: 
6
PubMed ID: 
Reference Text: 
American Academy of Pediatrics Committee on Substance Abuse and Committee on Children with Disabilities. Fetal alcohol syndrome and alcohol-related neurodevelopmental disorders. Pediatrics 2000; 106: 358-361.
Reference Order: 
7
PubMed ID: 
10920168
Reference Text: 
National Institute on Alcohol Abuse and Alcoholism. Fetal alcohol exposure and the brain. Alcohol Alert No. 50, 2000. http://pubs.niaaa.nih.gov/publications/aa50.htm (accessed Sep 2006).
Reference Order: 
8
PubMed ID: 
Reference Text: 
Jones KL, Smith DW. Recognition of the fetal alcohol syndrome in early infancy. Lancet 1973; 2: 999-1001.
Reference Order: 
9
PubMed ID: 
4127281
Reference Text: 
Greater Dallas Council on Alcohol and Drug Abuse. Alcohol impairment charts. http://www.gdcada.org/statistics/alcohol.htm#bac (accessed Sep 2006).
Reference Order: 
10
PubMed ID: 
Reference Text: 
Fisher HR, Simpson RI, Kapur BM. Calculation of blood alcohol concentration (BAC) by sex, weight, number of drinks and time. Can J Public Health 1987; 78: 300-304.
Reference Order: 
11
PubMed ID: 
3690446
Reference Text: 
Butte NF, Ellis KJ, Wong WW, et al. Composition of gestational weight gain impacts maternal fat retention and infant birth weight. Am J Obstet Gynecol 2003; 189: 1423-1432.
Reference Order: 
12
PubMed ID: 
14634581
Reference Text: 
Litvin J, Switzer BR. Pharmacokinetics of ethanol in the guinea pig. Alcohol Clin Exp Res 1988; 12: 71-76.
Reference Order: 
13
PubMed ID: 
3279863
Reference Text: 
Brien JF, Loomis CS, Tranmer J, et al. Disposition of ethanol in human maternal venous blood and amniotic fluid. Am J Obstet Gynecol 1983; 146: 181-186.
Reference Order: 
14
PubMed ID: 
6846436
Reference Text: 
Clarke DW, Steenaart NA, Slack CJ, et al. Pharmocokinetics of ethanol and its metabolite, acetaldehyde, and fetolethality in the third-trimester pregnant guinea pig for oral administration of acute, multiple-dose ethanol. Can J Physiol Pharmacol 1986; 64: 1060-1067.
Reference Order: 
15
PubMed ID: 
3791045
Reference Text: 
Banwell C. How many standard drinks are there in a glass of wine? Drug Alcohol Rev 1999; 18: 99-101.
Reference Order: 
16
PubMed ID: 
Reference Text: 
Stockwell TR. Information provided in Australia about the size of standard drinks [letter]. Med J Aust 1992; 156: 295.
Reference Order: 
17
PubMed ID: 
1738347
Reference Text: 
Farr KL, Montano CY, Paxton LL, et al. Prenatal ethanol exposure decreases hippocampal 3H-glutamate binding in 45 day old rats. Alcohol 1988; 5: 125-133.
Reference Order: 
18
PubMed ID: 
2840094
Reference Text: 
Charness ME, Safran RM, Perides G. Ethanol inhibits neural cell–cell adhesion. J Biol Chem 1994; 269: 9304-9309.
Reference Order: 
19
PubMed ID: 
8132668
Reference Text: 
Zhou FC, Sari Y, Powrozek T, et al. Moderate alcohol exposure compromises neural tube midline development in prenatal brain. Brain Res Dev Brain Res 2003; 144: 43-55.
Reference Order: 
20
PubMed ID: 
12888216
Reference Text: 
Miller MW. Effects of alcohol on the generation and migration of cerebral cortical neurons. Science 1986; 233: 1308-1311.
Reference Order: 
21
PubMed ID: 
3749878
Reference Text: 
Qiang M, Wang MW, Elberger AJ. Second trimester prenatal alcohol exposure alters development of rat corpus callosum. Neurotoxicol Teratol 2002; 24: 719-732.
Reference Order: 
22
PubMed ID: 
12460654
Reference Text: 
Savage DD, Becher M, de la Torre AJ, Sutherland RJ. Dose dependent effects of prenatal ethanol exposure on synaptic plasticity and learning in mature offspring. Alcohol Clin Exp Res 2002; 26: 1752-1758.
Reference Order: 
23
PubMed ID: 
12436066
Reference Text: 
Schneider ML, Moore CF, Kraemer GW. Moderate level alcohol during pregnancy, prenatal stress, or both and limbic-hypothalamic–pituitary–adrenocortical axis response to stress in rhesus monkeys. Child Dev 2004; 75: 96-109.
Reference Order: 
24
PubMed ID: 
15015677
Reference Text: 
Jacobson SW, Jacobson JL, Sokol RJ. Effects of fetal alcohol exposure on infant reaction time. Alcohol Clin Exp Res 1994; 18: 1125-1132.
Reference Order: 
25
PubMed ID: 
7847594
Reference Text: 
Fried PA, Watkinson B, Gray R. A follow up study of attentional behaviour in 6 year old children exposed prenatally to marijuana, cigarettes, and alcohol. Neurotoxicol Teratol 1992; 14: 299-311.
Reference Order: 
26
PubMed ID: 
1454038
Reference Text: 
Greene T, Ernhart CB, Ager J, et al. Prenatal alcohol exposure and cognitive development in the preschool years. Neurotoxicol Teratol 1991; 13: 57-68.
Reference Order: 
27
PubMed ID: 
2046628
Reference Text: 
Sood B, Delaney-Black V, Covington C, et al. Prenatal alcohol exposure and childhood behaviour at age 6 to 7 years. I: Dose-response effect. Pediatrics 2001; 108: e34.
Reference Order: 
28
PubMed ID: 
11483844
Reference Text: 
Streissguth AP, Bookstein FL, Barr HM, et al. Risk factors for adverse life outcomes in fetal alcohol syndrome and fetal alcohol effects. J Dev Behav Pediatr 2004; 25: 228-238.
Reference Order: 
29
PubMed ID: 
15308923
Reference Text: 
Olson H, Streissguth AP, Sampson PD, et al. Association of prenatal alcohol exposure with behavioral and learning problems in early adolescence. J Am Acad Child Adolesc Psychiatry 1997; 36: 1187-1194.
Reference Order: 
30
PubMed ID: 
9291719
Reference Text: 
Linnet KM, Dalsgaard S, Obel C, et al. Maternal life style factors in pregnancy. Risk of attention deficit hyperactivity disorder and associated behaviours: review of the current evidence. Am J Psychiatry 2003; 160: 1028-1040.
Reference Order: 
31
PubMed ID: 
12777257
Reference Text: 
Australian Government Department of Health and Ageing. ADI list. Acceptable daily intakes for agricultural and veterinary chemicals. Canberra: Department of Health and Ageing, June 2006: 5-6. http://www.tga.gov.au/docs/pdf/adi.pdf (accessed Sep 2006).
Reference Order: 
32
PubMed ID: 
Reference Text: 
Eckardt MJ, File SE, Gessa GL, et al. Effects of moderate alcohol consumption on the central nervous system. Alcohol Clin Exp Res 1998; 22: 998-1040.
Reference Order: 
33
PubMed ID: 
Reference Text: 
Wilkemeyer MF, Chen S, Menkari CE, et al. Differential effects of ethanol antagonism and neuroprotection in peptide fragment NAPVSIPQ prevention of ethanol-induced developmental toxicity. Proc Natl Acad Sci USA 2003; 100: 8543-8548.
Reference Order: 
34
PubMed ID: 
12808140
Reference Text: 
Royal College of Obstetricians and Gynaecologists. Alcohol consumption and the outcomes of pregnancy. Statement No 5. London: RCOG, March 2006. http://www.rcog.org.uk/index.asp?PageID=1477 (accessed Sep 2006).
Reference Order: 
35
PubMed ID: 
Reference Text: 
Jacobson JL, Jacobson SW, Sokol RJ. Increased vulnerability to alcohol-related birth defects in the offspring of mothers over 30. Alcohol Clin Exp Res 1996; 20: 359-363.
Reference Order: 
36
PubMed ID: 
8730230