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Foetal Alcohol Spectrum Disorder (FASD) is a devastating life-long

disability involving physical, psychological, social and

behavioural impairments (Alcohol Healthwatch, 2006). Within this

spectrum is Foetal Alcohol Syndrome (FAS), considered the most

severe form and involving characteristic facial dysmorphia, pre

and/or postnatal growth retardation and central nervous system

impairments such as learning and behavioural problems (Carpenter,

Blackburn and Egerton, 2014). Although FASD is a global issue, New

Zealand babies are particularly vulnerable given our high rates of

alcohol consumption among woman, limited awareness of the risks

associated with drinking in pregnancy and high proportion of

unplanned pregnancies (Sellman & Connor, 2009). Consequently

researchers estimate 1200-3000 affected babies are born in New

Zealand each year – twice the number of babies born with Down

Syndrome (Hayward, 2012, Summer). Sadly prenatal alcohol exposure

is highly prevalent, with 29% of New Zealand woman continuing to

drink after pregnancy recognition (Ministry of Health, 2007; Watson

& McDonald, 1999). FASD is a major public health issue with each

case estimated to cost $NZ3.5 million with the impacts felt

throughout the health, educational, social welfare and justice

sectors (Alcohol Healthwatch, 2007). The burden placed on effected

individuals and their families can not be overstated. Implementing

evidenced-based prevention strategies could dramatically reduce

this burden. In addition to prevention, a more systematic

comprehensive approach to screening, diagnosis and early

intervention is much needed in New Zealand to achieve better long-

term outcomes and prevent secondary conditions such as criminal

activity, school failure and unemployment (Alcohol Healthwatch,

2007).

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Of those exposed to prenatal alcohol, some suffer devastating

impairments while others do not appear to be effected at all, and

within the subset that are affected the severity and types of

impairments vary widely (Riley, Clarren, Weinberg & Jonsson, 2011).

Despite the long-association between alcohol use in pregnancy and

poor foetal outcomes it remains impossible to accurately predict

the effects of alcohol exposure in each case; due to the numerous

biological and environmental factors that influence the effects of

alcohol (Hayward, 2012, Summer). For instance increased maternal

age, high parity, maternal ill-health, malnutrition and co-use of

other drugs all increase the risk of adverse foetal effects from

alcohol exposure (Carpenter et al., 2014). This may explain why

low-income woman are more likely to have a baby with FASD, despite

drinking less than their high-socio-economic peers (Mcleod, Pullon,

Cookson & Cornford, 2002; Riley et al., 2011). A dose-response

relationship is seen with heavy use considered most dangerous and

heavy episodic use generally causes more severe neuropathology than

regularly heavy use (Kotrla & Martin, 2009; Olson,

Jirikowic, Kartin & Astley, 2007). Although it is important to note

that even low-level drinking is associated with social, cognitive

and behavioural problems, prematurity and growth retardation

(Jaddoe et al., 2007; Swedish National Institute of Public Health,

2009). Notably Haycock’s (2009) research demonstrates that maternal

alcohol use preconception may induce epigenetic changes that could

effect future generations. However, currently, gestational exposure

is considered the most concerning. Drinking in different stages of

pregnancy causes different effects as different organ system

develop at different rates and times (Riley et al., 2011). The

first six weeks of pregnancy is a particularly critical period as

the cerebral cortex, face, eyes and heart are forming hence the

risk of severe brain damage, vision abnormalities and cardiac

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defects are at their peak. It is alcohol use during this period

that causes the dysmorphic facial features of a smooth philtrum,

short palpebral fissures and thin upper lip, which are required for

a FAS diagnosis (O’Neil, 2013). Second trimester use is mainly

associated with miscarriage and musculoskeletal defects, while

third trimester use can result in learning difficulties, growth

retardation and susceptibility to Sudden Unexpected Death in

Infancy (SUDI) (Twin Cities Health Professionals Education

Consortium, 2010). The genetic makeup of the mother is an important

variable; various genes enhance alcohol metabolism, thus lessening

foetal exposure (Haycock, 2009; Riley et al., 2011). Similarly twin

studies where there has been discordance, with one twin displaying

FASD and the other unaffected, suggest an element of foetal genetic

vulnerability (Streissguth & Dehaene, 1993). Given these

complexities complete abstinence for all women pregnant or at-risk

of pregnancy must be promoted.

Alcohol alters foetal development in various ways. Alcohol readily

crosses the placenta entering foetal circulation (Olson et al.,

2007). The foetus is exposed to the alcohol for much longer than

their mother as their immature liver is inefficient in metabolising

alcohol and the amniotic fluid acts as a reservoir, resulting in

extended exposure for the vulnerable developing brain (Hayward,

2012, Summer; Heller & Burd, 2014). Alcohol causes cell death of

neurons, disrupts cellular proliferation, differentiation and

growth (Lebel et al., 2012). Thus resulting in a brain that is

potentially smaller, less dense and unsymmetrical; hence alcohol is

the leading cause of intellectual disability (Haycock, 2009;

Hayward, 2012, Summer; Niccols, 2000). Alcohol inhibits both the

mother’s ability to absorb nutrients and the transfer of nutrients

and oxygen across the placenta – resulting in a nutrient-deprived

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environment and therefore growth retardation (Kotrla & Martin,

2009). There is evidence that the foetal environment can prime for

mental health conditions, for instance; alcohol inhibits serotonin

production and alters the hypothalamic-pituitary-adrenal axis

impairing resiliency and increasing the risk of attention deficit

hyperactivity disorder (ADHD), anxiety disorders and depression

(Fast & Conry, 2009; Ornoy & Ergaz, 2010). Aside from the neuro-

developmental effects, alcohol is associated with multiple physical

abnormalities. These include; cleft lip, cardiac anomalies, neuro-

tube defects, renal hypoplasia, atoptic dermatitis, conductive

hearing loss, microencephaly, vision impairments, epilepsy and

musculoskeletal defects (Ornoy & Ergaz, 2010). Grotmol, Weiderpass

and Tretli (2006) even suggest a vulnerability to cancer in later

life. Like all babies born with a low birth weight, the risk of

metabolic syndrome in adulthood is elevated (Phillips, 2004).

Philips (2004) suggests babies born with a low birth weight,

whether due to their mother’s use of alcohol or tobacco, poor

nutritional intake or other causes, are effectively primed to

thrive in a nutrient deprived environment. Hence when given

sufficient nutrition following birth they readily develop obesity,

hypertension and diabetes. These physical health problems provide

further reason to actively identify FASD cases as diagnosis enables

these physical health problems to be identified and treated.

The impact of FASD is felt throughout the lifespan. New-borns are

often born premature and underweight (Stratton, Howe & Battaglia,

1996). They may experience difficulty feeding and consequently

their growth is slow. They are frequently described as irritable

with an exaggerated startle response and hyper-sensitivity to light

and sounds; excessive crying and difficulties sleeping are common

parental concerns (Olson et al., 2007). Consequently maternal-child

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bonding is often impacted (Kotrla & Martin, 2009). During the

preschool years developmental delays may become apparent as speech,

cognition, fine and gross motor skills develop more slowly.

Behavioural difficulties often cause concern; hyperactivity,

impulsivity, inattention and frequent temper tantrums are commonly

reported (Martin, 2008). Herman’s (2008) research found 68% of boys

with FASD also meet the criteria for ADHD. Interestingly children

are often perceived as having advanced social skills as they are

generally very friendly and willing to engage with strangers

(Fagerlund, Autti-Rämö, Hoyme, Mattson & Korkman, 2011). However on

closer inspection difficulties with socialisation usually become

obvious, especially around turn-taking, sharing and following rules

(Martin, 2008). As these children enter school, academic

difficulties become problem-some, particularly with organisation,

memory, judgement and abstract thought. Often the most frustrating

aspect for caregivers and teachers is their difficulty in learning

from experience or predicting outcome (Martin, 2008). Sadly

O’Connor and Kasari’s (2000) study found worryingly high rates of

depression among 5 year old children who had been exposed to

alcohol in utero with a 19% prevalence compared to the 1%

prevalence rate commonly reported among this group. Girls and those

who had a mother with depression were at particularly high risk.

Adolescence can be especially challenging. A lack of motivation,

self-esteem and resiliency are commonly reported. Supports are

usually needed to prevent academic failure and inappropriate

behaviour (Kotrla and Martin, 2009). Streissguth, Bookstein, Barr,

Sampson, O’Malley and Young (2004) found most have an intellectual

impairment with an average IQ of 86 with the more dysmorphic

tending to have more significant cognitive impairments (Ervalahti,

Korkman, Fagerlund, Autti-Rämö, Loimu & Hoyme, 2007). However

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adaptive functioning is usually considerably lower hence their

abilities are often less than their IQ would suggest (Carpenter et

al., 2014). Disengagement from school is a serious risk, with

around half suspended at some point (Streissguth et al., 2004).

Sadly without the structure of school-life risky behaviours, such

as substance abuse, criminal activity and sexualised behaviour tend

to become increasingly problematic (Kotrla & Martin, 2009). Brown,

Gudjonsson and Connor (2011) describe people with FASD as eager to

be liked, gullible and impulsive with limited judgement and risk

perception, which makes them vulnerable to negative peer group

influences as others can easily take advantage of them. The

overwhelming majority suffer poor mental health with depression,

anxiety disorders, personality disorders and psychosis prevalent

(Famy, Streissguth & Unis, 1998; Hellemans, Sliwowska, Verma &

Weinberg, 2010). Unsurprisingly occupational options are often

limited leading to unemployment and poverty (Martin, 2008). Around

two thirds are the victim of a physical or sexual assault at some

point in their lives and a similar percentage engage as an offender

in crime (Hayward, 2012, Summer; Streissguth, et al., 2004). Around

half need support with daily living such as with budgeting, keeping

appointments and cooking (Carpenter et al., 2014). Interestingly

Faas, Spontón, Moya and Molina (2000) suggest alcohol exposure in-

utero primes an infant to have a preference for the taste and smell

of alcohol, potentially predisposing for an alcohol abuse problem

later in life (Yates, Cadoret, Troughton, Stewart & Giunta, 1998).

Hence FASD can sadly become an intergenerational issue.

Unfortunately New Zealand lacks a systematic approach to

identifying and supporting people with FASD, with the majority of

cases believed to be undiagnosed (Alcohol Healthwatch, 2010).

However extensive evidence suggests early diagnosis enables early

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intervention, prevents secondary conditions such as school failure,

conduct problems and mental illness, and improves long-term

outcomes (Olson et al., 2007). The lack of biological markers to

detect gestational alcohol exposure, means that diagnosis is

subjective, complex and challenging (Martin, 2008). The difficulty

in distinguishing FASD from other developmental conditions, such as

ADHD, forms a major challenge to diagnosis (Burns, 2013).

Furthermore many children with suspected FASD also experience other

adverse factors in utero and early life; such as maternal drug

abuse, poor parent-child attachment, maternal mental illness or

additions, domestic violence, poverty, child abuse and transience –

which could all account for the learning and behavioural

difficulties experienced by the child (Martin, 2008).

Unsurprisingly children with the facial characteristics of FAS are

considerably more likely to be diagnosed and supported with early

intervention services. Interestingly despite having more

significant neuropathology they achieve better long-term outcomes

compared to children without the characteristic facial features –

indicating the enormous benefits early intervention services can

have (Streissguth et al., 2004). Many health and educational

professionals are reluctant to refer or diagnose due to a

perception that diagnosis is stigmatising and pointless (Alcohol

Healthwatch, 2010; Wouldes, 2009). Interestingly this perception

among professionals is not supported in the literature which shows

that families and individuals value a formal diagnosis as it

enables them to access much-needed services, promotes empathy and

understanding of the difficulties and may even allow the prevention

of FASD in subsequent siblings (Salmon, 2008). A lack of clarity

around whether alcohol was used during pregnancy is often an issue.

Many children presenting with suspected FASD are brought for

medical assessment by their foster or adoptive parents or child

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protection services who may not know whether alcohol was consumed

during pregnancy (Olson et al., 2007). And even when the birth

mother is engaged with the health service, determining the extent

of alcohol use is dependent of self-reports which are notoriously

unreliable (Bakhireva & Savage 2011; Ernhart, Morrow-Tlucak, Sokol

and Martier, 1988; Martin, 2008). Lastly Wouldes (2009) reveals a

significant knowledge deficit among health professionals in New

Zealand with only one in four aware of the key diagnostic features

of FASD. It is important we actively address these barriers given

the overwhelming benefits of diagnosis (Alcohol Healthwatch, 2007).

The earlier diagnosis occurs the better the long-terms outcomes are

(Alcohol Healthwatch, 2007). Thus numerous experts have advocated

for routine new-born screening (Pass & Mizejewski, 2009). Certainly

early infancy is a critical period to implement various

interventions which have potential to dramatically improve life

outcomes (Olson et al., 2007). For instance; there is strong

evidence that nutritional supplements of fish oils, choline, zinc,

folate acid and vitamin E given in infancy, enhance cognitive

development (Ballard, Sun & Ko, 2002). Importantly a diagnosis

prompts professionals and services to give information and support

to families; this can include respite care, financial supports,

parenting courses and support groups (Alcohol Healthwatch, 2007).

Lowe (2006) encourages health professionals to teach mothers how to

recognize their infant’s stress cues and encourage parents to be

more responsive through play, thus fostering positive mother–infant

interactions, promoting stronger attachment and enhanced self-

regulation. Parents can be informed of their child’s increased risk

of SUDI and strategies they can implement to reduce this risk

(Friend, Goodwin & Lipsitt, 2004). Environmental enrichment, early

childhood education, speech-language therapy, social-skills

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training and teacher-aide support can all foster the child to reach

their potential (Olson et al., 2007). However the symptoms of FASD

can be subtle and difficult to detect in early infancy, hence the

need for additional screening programs to complement. Poitra et al.

(2003) demonstrates the effectiveness of school-based screening,

while Burns (2013) advocates for infants known to be exposed to

alcohol in utero to be routinely re-called for pediatric

assessments even if they appear well at birth, to allow FASD to be

detected as early as possible.

There is overwhelming evidence showing the damaging effects of

growing-up in a deprived or dysfunctional family environment

(Streissguth et al., 2004). Parental mental illnesses, addictions,

domestic violence, poverty, transience, abuse and neglect all

significantly impact child health and development. Children with

FASD are more likely to be born into a deprived or dysfunctional

home environment as well as being more vulnerable to the harms

associated with such an environment (Fagerlund et al., 2011).

Importantly Streissguth et al. (2004) revealed that a stable

nurturing home was the most influential factor on positive long-

term outcomes for people with FASD. Hence a FASD diagnosis must

prompt an assessment of family functioning. The family may require

intensive support, and if this is not possible or unsuccessful

being uplifted early and placed into a stable, nurturing and safe

care environment is of upmost importance. As individuals with FASD

reach adulthood they are likely to require intensive support around

vocational training, sustaining employment and daily living skills,

such as budgeting, cooking and parenting (Streissguth et al.,

1992). Many will develop secondary conditions, such as school

truancy, mental illness, addictions and criminality; thus an

increased understanding of FASD across all sectors of society will

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also enable their needs to be better meet (Streissguth et al.,

1992).

Although diagnosis and support services for those with FASD are

crucial, it must be remembered that FASD need not occur – it is a

completely preventable condition (Clarren & Salmon, 2010). Hence

prevention strategies must be forefront. The widely-held perception

that FASD is purely caused by a woman’s choices is a major barrier

to prevention (International Charter on Prevention of FASD, 2009).

The social, political, economic and cultural context which promotes

alcohol abuse among New Zealand woman and thus impacts maternal and

child health must be addressed (Sellman & Connor, 2009). We must

all accept responsibility for preventing FASD. Firstly men have an

important role to play. Importantly paternal alcohol use is

associated with growth retardation and cognitive delays even in the

absence of gestational exposure hence the fallacy in directing all

culpability towards mothers (Abel, 2004). Secondly men who abuse

alcohol, are unsupportive of their partner’s pregnancy, become

violent or demand their partner drink with them, must take some

responsibility for the outcome (International Charter on Prevention

of FASD, 2009). A society which encourages woman to drink and all-

too-often fails to effectively support woman to cope with the

hopelessness of poverty, violence, mental illness and ill-health in

ways other than through alcohol use must share the burden. Alcohol

producers and retailers that market and advertise to woman of

child-bearing age without mentioning the risks also contribute.

Lastly health professionals must be proactive in informing woman of

the risks of an alcohol-exposed pregnancy, support access to

effective affordable contraception and provide meaningful alcohol

abstinence support to woman who are actively trying to conceive,

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at-risk of pregnancy or currently pregnant (Floyd, 2009; Ismail,

Buckley, Budacki, Jabbar & Gallicano, 2010).

The serious risks associated with alcohol exposure during the first

few weeks of pregnancy, a period when most are unaware they are

pregnant, complicated by the high rates of unintended pregnancy

provides ample support for a universal prevention approach,

reaching woman pre-conception (Clarren & Salmon, 2010; Floyd,

2009). The New Zealand Law Commission (2010) describes the

extensive harm caused by our “pervasive culture of drinking to excess” (p.9)

and provides comprehensive evidenced-based guidelines detailing

changes that would be conducive to less risky alcohol use. This

report argues that alcohol is currently viewed as an ordinary

commodity by New Zealanders and not as the psychoactive addictive

and dangerous drug that it is. Reducing the availability and

affordability of alcohol is arguably is the most effective

intervention policy-makers can take (World Health Organisation,

2010). This could include increasing the purchasing age,

restrictions on the trading hours, placement and density of retail

outlets, increasing excise taxation and imposing minimum prices

(New Zealand Law Commission, 2010). Efforts to increase the

public’s knowledge of the risk alcohol poses to a foetus and to

discourage risky consumption have shown mixed results suggesting

that knowledge alone is not enough to result in actual behaviour

changes (Hankin, 2002). For instance while mandatory warning labels

on alcoholic beverages initially reduce drinking among pregnant

woman with low-risk drinking habits, pregnant woman engaging in

high-risk drinking are largely unaffected, and over time drinkers

become habituated to the message (Hankin, 2002). Likewise whilst

school-based education programs increase knowledge levels, they do

not seem to alter behaviour at all (Anderson, Chisholm & Fuhr,

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2009). Finally the impact of alcohol advertising and marketing

cannot be underestimated and must be addressed by policy-makers

(Riley et al., 2011; Sellman & Connor, 2009).

Another important component of primary prevention involves the

promotion of family planning. Given that 44% of New Zealand

pregnancies are unplanned and the dangers of alcohol during the

first few weeks when woman are usually unaware of their pregnancy,

many woman are unintentionally placing their baby at risk (Mallard

& Houghton, 2013). Furthermore pregnancy recognition and initiation

of antenatal care generally occur later than in planned pregnancies

(Mallard & Houghton, 2013). Promoting access to reliable

contraception and encouraging woman to plan their pregnancies

enables woman to ensure they are alcohol-free before conception

(Mallard & Houghton, 2013). Pregnancy planning also enables woman

to make other health-promoting changes, such as; smoking cessation,

commencing folate supplementation and ensuring good nutrition,

creating an optimal utero environment. Sadly woman in poverty who

are most at risk of unintended pregnancy are also the population

most likely have high-risk drinking patterns (Naimi, Lipsomb,

Brewer & Gilbert, 2003). Hence improving availability,

affordability and awareness of family planning is an important

component of FASD prevention.

Routinely screening woman of childbearing age for alcohol use is

arguably the most evidence-based secondary prevention strategy

(Floyd 2009; Hankin, 2002). Health services that work with at-risk

woman, such as woman accessing emergency contraception,

terminations, mental health services or support for substance-abuse

problems must be particularly vigilant around screening. Given that

around 80% of NZ woman of child-bearing age regularly drink

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alcohol, 39% continue to drink when actively trying to conceive and

28% drink after pregnancy-recognition, positive screening rates

will be high (Ho & Jacquemard, 2009; Matthew, Kitson, & Watson,

2001; Mcleod, Pullon, Cookson & Cornford, 2002; MOH, 2007).

Although the stigma and shame attached to drinking in pregnancy may

contribute to under-reporting, hence the need for an empathetic

non-judgmental approach (Burns, 2013). Screening should be followed

by information provision around contraception, the risks alcohol

poses to a developing foetus and referrals for alcohol treatment

services or contraception if indicated (Floyd, O'Connor, Sokol,

Bertrand & Cordero, 2005). Likewise assessing for alcohol

consumption and providing abstinence advice should be a core focus

of all antenatal health encounters as sadly 50% of Kiwi woman

believe it safe to drink some alcohol in pregnancy (Alcohol

Healthwatch, 2007; MOH, 2007; Parackal, Parackal, Ferguson &

Harraway, 2006). Clarke and Gibbard (2003) argues that during this

assessment it is crucial to consider the risk factors for alcohol

consumption in pregnancy, these include; having a partner who is a

heavy drinker, a past-history of physical or sexual abuse, a

history of mental illness or drug abuse and being socially

isolated. Interestingly Clarren and Salmon (2010) found around half

of mother’s with a FASD-effected child also meet the diagnostic

criteria for FASD themselves. Hence the alcohol use may be viewed,

in some situations, as a self-administered treatment for difficult

life circumstance; any interventions must address these root causes

as well as the alcohol use itself.

Encouragingly Clarke and Gibbard (2003) suggest indicated

prevention such as supportive counselling and case management for

alcohol-using pregnant woman can result in a 35-50% reduction in

heavy alcohol consumption. Burns (2013) explains the need to give

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pregnant woman priority placements at alcohol rehabilitation units

and to address the barriers to accessing such services – lack of

childcare and transport, stigma and fear of notifications to child

protection agencies. While supporting a woman to cease her alcohol

use, a range of interventions can be employed to reduce the risk of

alcohol affecting the foetus. Nutritional supplements, such as

Vitamin C, Vitamin E, folic acid, beta-carotene and flavonoids

should be given to counteract the nutritional deficits caused by

alcohol use (Ballard et al., 2002; Krangle, 2002). Likewise

cessation of tobacco and other drugs must be encouraged, as these

can have a synergistic effect with alcohol dramatically increasing

the risk of prematurity, low birth weight and SUDI (Riley et al.,

2011).

It is important to recognise that a woman who has already had a

baby with FASD is at very high risk of having another effected

child, with some researchers suggesting a risk of up to 75% (Burns,

2013). Hence the importance of tertiary prevention strategies

involving intensive case management to address the medical and

social needs of the family to prevent further exposed pregnancies

(Hankin, 2002). Several successful models have been used

internationally, for example in Canada all birth mothers are

contacted and engaged into a service when their child is diagnosed

with FASD, even if the child is no longer in their custody. The

mothers are provided a comprehensive wrap-around mentoring service

involving addiction services, mental health support, advocacy,

contraception, budgeting and domestic violence intervention

(Clarren & Salmon, 2010). Possibly New Zealand could benefit from

such a program.

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To conclude; alcohol is a potent drug which causes significant

wide-ranging harms throughout society, however its effects are

particularly devastating when consumed in pregnancy. Irreversible

intellectual impairments, a range of medical conditions and mental

health problems all place a heavy and preventable burden on the

individual, family and wider society. The trajectories for effected

individuals are often very poor (Streissguth et al., 2004). However

an early diagnosis and assess to support services are both

substantial protective factors (Streissguth et al., 2004). There is

major scope for improvement within New Zealand around promoting

early assessment, diagnosis and effective support services (Foetal

Alcohol Network New Zealand, 2014). The harms associated with

gestation exposure have been recognised for centuries with

references made in early Greek and Roman mythology; however alcohol

consumption in pregnancy remains highly prevalent (Ho & Jacquemard,

2009). Thus the risks of drinking in pregnancy are significantly

underappreciated. Prevention must start pre-conception to protect

woman from unknowingly harming their baby. Addressing the cultural

context which normalises and encourages alcohol use is of utmost

importance (Sellman & Connor, 2009). Similarly health professionals

must actively screen for alcohol use and inform all female patients

who are pregnant or at-risk of pregnancy of the risks alcohol poses

to a foetus (Floyd et al., 2005). Promoting family planning, access

to effective addiction services and intensive case management for

high-risk mothers, will also help (Floyd et al., 2005). With a co-

ordinated comprehensive approach significant improvements are

possible.

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References:

Abel, E. (2004). Paternal contribution to fetal alcohol

syndrome. Addiction Biology

9(2), 127- 133.

Alcohol Healthwatch (2006). Fetal Alcohol Spectrum Disorder: The Effect of

Alcohol on

Early Development. Wellington: Alcohol Healthwatch.

Alcohol Healthwatch (2007). Fetal Alcohol Spectrum Disorder in New

Zealand: Activating

the Awareness and Intervention Continuum. Wellington: Alcohol

Healthwatch.

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Alcohol Healthwatch (2010). Towards Multidisciplinary Diagnostic Services

for Fetal

Alcohol Spectrum Disorder. Wellington: Alcohol Healthwatch.

Anderson, P., Chisholm, D., & Fuhr, D. (2009). Alcohol and

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Bakhireva, L & Savage, D. (2011). Focus on: Biomarkers of

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Ballard, M., Sun, M. & Ko, J. (2002). Vitamin A, folate, and

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Brown, N., Gudjonsson, G. & Connor, P. (2011). Suggestibility

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Alcohol Research Centre

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Ernhart, C., Morrow-Tlucak, M., Sokol, R. & Martier, S.

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Ervalahti, N., Korkman, M., Fagerlund, A., Autti-Rämö, I.,

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Relationship between dysmorphic features and

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Fagerlund, Å.,Autti-Rämö, I., Hoyme, H., Mattson, E. & Korkman,

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Famy, C., Streissguth, A. & Unis, A. (1998). Mental illness in

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(2005). Recognition and

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prevention of foetal alcohol syndrome. Obstetrics

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Friend, K., Goodwin, M. & Lipsitt, L. (2004). Alcohol use and

sudden infant death syndrome.

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