National Drug Strategy
National Drug Strategy

Intergovernmental committee on Drugs working party on Fetal Alcohol Spectrum Disorders

Monograph

Fetal Alcohol Spectrum Disorders in Australia: An Update

June 2012

6.1 Risk factors for FAS and FASD

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Prevention initiatives should be driven by information that describes the correlates of FAS and FASD. Data from the Australian Paediatric Surveillance Unit (APSU) indicate some of these correlates. Many of the mothers of children with FAS used a range of substances in addition to alcohol in pregnancy (including heroin, solvents and cocaine) and few progressed beyond secondary education. As few as one-third of children reported with FAS were currently living with a biological parent, many having been placed in foster care and about half the mothers had more than one child with FAS (Elliott and Bower 2004). Women who were aged more than 30 years have been found to be more likely to have babies with Alcohol-Related Birth Defects, possibly because maternal body fat-to-water ratio increases with age, leading to higher and longer peak alcohol levels (Jacobson et al. 1996). Women over 30 years are also less likely to reduce alcohol use after learning they are pregnant, indicating greater alcohol dependence and difficulty in reducing or eliminating alcohol use during pregnancy Centers for Disease and Control 2002).

Low socioeconomic status has been associated with FAS (Jones et al. 1973). An interaction between FAS and poor nutrition, genetic and social factors, and the cumulative effect of intergenerational maternal alcoholism has also been noted (O'Leary 2004). Other factors associated with low socioeconomic status (SES) including exposure to environmental pollutants such as lead, which can directly affect the CNS, psychological stress, physical abuse and smoking, are thought in combination to increase susceptibility to the teratogenic effects of alcohol. There are also contributory issues specific to the Indigenous population, such as the effects of colonisation, marginalisation, and loss of traditional culture (Elliott and Bower 2004).

The finding that concordance for alcohol-related birth defects is higher among monozygotic twins than among dizygotic twins born to women who drink during pregnancy suggests the importance of genetic factors in determining susceptibility to FAS (Streissguth and Dehaene 1993). A number of potential genetic markers have been identified, including the presence or absence of particular gene polymorphisms involved in alcohol metabolism, which may impact on ethanol clearance rates (McCarver 2001; Chambers and Jones 2002; Gemma et al.
2007). Genetic differences in serotonergic function have also been identified (Kraemer et al. 2008). Serotonin has an influence on the formation of neural circuits during development, particularly those involved in emotional behaviour (Ansorge et al. 2008). In this way, prenatal alcohol exposure may alter the development of neurobiological systems underpinning responses to stress and affect regulation in the fetus (Kraemer et al. 2008).

The place of alcohol in Australian society and the changing way that women drink in risky patterns is described by Roche, later in this publication. There is a strong association between overall consumption levels, rates of risky drinking and levels of long and short-term harm experienced by that population (Chikritzhs et al. 2003), and it would be helpful to know if there is also an association between rates of consumption and the incidence of FASD in a population. It may be reasonable, however, to assume that if decreases in risky drinking across the population are associated with a reduction in harms, then reductions in FASD across that population may also be possible.

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