Overview

Fetal Alcohol Spectrum Disorders (FASD) is a non-diagnostic umbrella term describing the range of effects that can occur in an individual whose mother consumed alcohol during pregnancy. These effects may include physical, mental, behavioral, and/or learning disabilities with possible lifelong implications. As is discussed in greater detail later in this TIP, these disorders often co-occur with substance abuse and mental health issues, and generally require treatment modifications for successful outcomes. They are 100 percent preventable, however, if those at risk of consuming alcohol during pregnancy are identified and effective prevention strategies are used.

Possible diagnoses within the spectrum include Fetal Alcohol Syndrome (FAS), Partial Fetal Alcohol Syndrome (pFAS), Alcohol-Related Neurodevelopmental Disorder (ARND), Static Encephalopathy/Alcohol-Exposed (SE/AE), and Neurobehavioral Disorder/Alcohol Exposed (ND/AE). (See box, FASD: Key Terms, for a fuller description of the disorders within the spectrum and related terminology.)

Prevalence

The prevalence of FAS in the United States has been estimated at 1–3 per 1,000 live births among the general population (Stratton et al., 1996) and 10–15 per 1,000 in some higher-risk populations, such as children residing in foster care (Astley, Stachowiak, Clarren, & Clausen, 2002; Astley, 2004a). The prevalence of the full spectrum of FASD in the general population is estimated at 9.1 per 1,000 live births, though a review of in-school screening and diagnosis studies suggest that the national rate could potentially be closer to 50 per 1,000 (May et al., 2009). In addition, recent retrospective analyses of hospital admissions data indicate that under-reporting of alcohol misuse by women may further disguise true prevalence (Morleo et al., 2011).

Although prenatal alcohol exposure has been clearly established as a causal factor for FASD in animal models, the amount of alcohol required to cause damage to the fetus remains in question, and may differ based on the individual. Factors such as dose of alcohol, pattern and timing of exposure, genetics, whether the mother also smoked and/or used other drugs, general health and nutrition of the mother, her level of stress and/or trauma, and her age all may play a role in the impact that alcohol has on the developing fetus (Guerri, Bazinet, & Riley, 2009). Animal studies do suggest that binge drinking (four or more drinks on one occasion) is associated with more severe effects (Bonthius & West, 1988; Clarren, Astley, Gunderson, & Spellman, 1992), and it is generally asserted that there is no known ‘safe’ level of alcohol consumption during pregnancy (Office of the Surgeon General, 2005; Hicks & Tough, 2009; Feldman et al., 2012).

Due to the range of deficits—and variability in degree of severity of each deficit—within the diffusely damaged brain, FASD can present as functionally different in each individual that is affected. However, certain cognitive, behavioral, and adaptive functioning problems are common across the spectrum, including lower IQ, impaired learning ability, and difficulty processing information (such as not being able to remember or follow instructions, or poor verbal receptive skills) (Streissguth, Barr, & Bookstein, 1996; Bertrand et al., 2004; Streissguth et al., 2004; Astley et al., 2009a; Astley, 2010). Physical abnormalities and facial dysmorphology (i.e., congenital malformation) are only common with FAS. Other functional issues regularly observed include attention deficit (Nanson & Hiscock, 1990; Lee, Mattson, & Riley, 2004), decreased proficiency in cognitive planning (Kodituwakku, Handmaker, Cutler, Weathersby, & Handmaker, 1995; Kodituwakku, Kalberg, & May, 2001; Rasmussen, 2005), reduced working memory (Burden, Jacobson, Sokol, & Jacobson, 2005; Astley et al., 2009b; Green et al., 2009), reduced response inhibition (Noland et al., 2003; Mattson, Crocker, & Nguyen, 2011), socially inappropriate behaviors (Bishop, Gahagan, & Lord, 2007; Jirikowic, Kartin, & Olson, 2008; Mattson, Crocker, & Nguyen, 2011), and deficits in fine motor (Kalberg et al., 2006; Jirikowic et al., 2008) and visual-spatial functions (Chiodo, Janisse, Delaney-Black, Sokol, & Hannigan, 2009; Mattson et al., 2010).

Cost Factors

Estimates of the cost to raise a child with an FASD vary depending on the source and the factors included in the analysis, and detailed cost estimates are generally only available in relation to the specific condition of FAS. Nonetheless, these costs are significant. In an analysis of medical expenditures for pediatric Medicaid enrollees, Amendah, Grosse, and Bertrand (2010) found that, for a child with identified FAS, incurred health costs were nine times higher than for children without an FASD. Astley, Bailey, Talbot, and Clarren (2000a) further isolated cost factors in a demonstration of primary FAS prevention in an FASD diagnostic clinic that targeted high-risk women; using this approach, the cost of raising a child with FAS was found to be roughly 30 times higher than the cost of preventing FAS in the child.

The most widely acknowledged estimate of the lifetime cost of care for an individual with an FAS is that of Lupton, Burd, and Harwood (2004), who adjusted figures originating with Harwood and Napolitano (1985) for 2002 dollars to suggest that the figure was roughly $2 million (including medical treatment, special education, residential care for persons with mental retardation, and productivity losses; in 2012 dollars, this would be over $2.5 million). The overall annual cost of FAS to the U.S. healthcare system (based on an assumption of 2 cases per 1,000 live births) is estimated at $5 billion (Lupton et al., 2004).

Part 3 of this TIP, the online Literature Review, contains additional information on FASD surveillance and cost factors, as well as the impact of alcohol on the brain and behavior.

Historical Background

FASD is often described as a ‘new’ or ‘recent’ discovery. In fact, references to the harmful effects of maternal drinking on infant outcome date back to biblical times: “Behold, thou shalt conceive, and bear a son; and now drink no wine or strong drink” (Judges 13:7, as noted in Clarren & Smith, 1978). In addition, several comprehensive descriptions were compiled by physician groups in the 18th and 19th centuries (Royal College, 1726; Sullivan, 1899; Goodacre & Mercer, 1965). The more recent history commonly referred to begins in 1968, when Lemoine, Harousseau, Borteyni, and Menuet from France published an article describing children with distinctive facial features and other symptoms related to prenatal alcohol exposure. In 1970, unaware of the Lemoine publication, Ulleland and colleagues published similar observations describing a small group of alcohol-exposed infants admitted to several high-risk maternal-child health clinics at the University of Washington (Ulleland, Wennberg, Igo, & Smith, 1970; Ulleland, 1972). This work would eventually lead to a seminal, collaborative article describing the pattern of outcomes associated with prenatal alcohol exposure (Jones, Smith, Ulleland, & Streissguth, 1973), as well as the publication that coined the term FAS (Jones & Smith, 1973).

In the roughly 40 years that have followed, extensive study has been conducted on alcohol's teratogenic effects, as well as on interventions for women of childbearing age who consume alcohol, leading to several significant federal milestones in addressing FASD. In 1996, the Institute of Medicine (IOM) published Fetal Alcohol Syndrome: Diagnosis, Epidemiology, Prevention, and Treatment (Stratton et al., 1996), leading the National Institute on Alcohol Abuse and Alcoholism (NIAAA) to establish the Interagency Coordinating Committee on FASD (originally Interagency Coordinating Committee on FAS) to address that publication's recommendations. Then, in 2000, Congress set forth mandates related to children's health, including FASD, leading the Centers for Disease Control and Prevention (CDC) to establish the National Task Force on FAS and FAE (completed in 2007), and SAMHSA to establish the FASD Center for Excellence in 2001.

In the decade since the Congressional mandates, the research and knowledge base around FASD has expanded greatly. According to Goodlett (2010), a PubMed search of FAS-, FASD-, or fetal alcohol-specific terminology at the end of 2010 returned nearly 3,900 articles published since 1973, of which more than 38 percent had been published since 2000. This growth is translating to practice: Since 2001, the FASD Center for Excellence alone has funded more than 70 subcontractors across the United States to carry out pilot efforts to implement FASD-related services into existing programs, including substance abuse and mental health treatment settings.

This body of work has revealed an unfortunate paradox: Individuals with an FASD require more intensive and personalized services, and early diagnosis and intervention have been identified as critical to improved outcomes and minimized secondary disabilities (Streissguth et al., 2004; Astley, 2010). Yet, individuals with an FASD often go undiagnosed or are misdiagnosed (Greenbaum, Stevens, Nash, Koren, & Rovet, 2009), are difficult to identify early and may not receive appropriate early intervention (Olson, Jirikowic, Kartin, & Astley, 2007), and often receive services that do not account for their disabilities and thus may result in poor outcomes.

Lack of Success With Typical Treatment Approaches

Prenatal exposure to alcohol has many teratogenic effects, among them that it can alter brain structure and function, meaning that people with an FASD do not process information in the same ways that those without an FASD do. These effects are permanent; an FASD cannot be ‘cured.’ Processing differences that may affect treatment can take many forms, including:

• Poor receptive language skills (difficulty with complex language and multiple instructions);
• Difficulty with social cognition and accurately understanding social cues;
• Difficulty taking in new information, and in generalizing learning to new settings; and
• Not always connecting cause and effect (particularly if the effect is delayed).

Expert consensus suggests that treatment approaches that rely on an assumption of ‘normal’ functioning of these cognitive processes are likely to be less effective with individuals with an FASD. This appears to be true for both mental health and substance abuse treatment settings.

Cognitive–Behavioral Therapy (CBT) models, for instance, are verbally based insight therapies designed to reduce target symptoms, and are based on the idea that inaccurate thoughts are linked to maladaptive feelings and behaviors. However, CBT approaches do not fit well given that individuals with an FASD have biologically based cognitive deficits (O'Connor et al., 2002). Behaviors of individuals with an FASD may result from errors in thinking that are difficult to change because of underlying diffuse brain damage. Modification to CBT, and adding other approaches, will be needed to maximize treatment efficiency and success.

The disease model of substance abuse treatment, which advocates lifelong abstinence from alcohol, also relies on the assumption that a client has normative function. Behavioral health professionals assume that the client can comprehend that he or she has a ‘disease’ and also that he or she can plan ahead to recognize why it is important to achieve abstinence. For an individual with an FASD, this link may be difficult to make, and so his or her substance abuse or mental health target symptoms may be harder to change (and change harder to maintain) because of the underlying diffuse brain damage.

Rapid Developments in the Field

The tremendous growth in FASD-related research and the establishment of the SAMHSA FASD Center for Excellence have practical implications for behavioral health professionals, in that the field of FASD-related practices is growing dynamically. Much of the practical guidance in this TIP has emerged only over the last 5 to 10 years. Even professionals who have had some form of FASD training in the past are likely to discover new and useful strategies in this TIP that can be effectively applied in their programs.

Treatment Barriers

Despite their unique treatment needs, clients with an FASD or pregnant women at risk of an AEP still share with any other client a significant, common barrier to treatment success: The impact of negative self-perception. An individual with an FASD or a woman who has consumed alcohol during pregnancy may perceive themselves negatively, either because of internal feelings of shame, a sense of not belonging, or due to experiencing external shaming or judgment. These internal feelings and external experiences can each become a barrier to treatment (Astley, Bailey, Talbot, & Clarren, 2000b; Salmon, 2008).

When implementing the practices recommended in this TIP, behavioral health professionals are urged to keep sight of the importance of addressing the client's feelings and experiences, as well as the need for sensitivity to issues such as gender, ethnicity, cultural background, and sexuality, as these factors impact treatment success among individuals with an FASD and women of childbearing age as significantly as any other treatment population.