Association Between Paternal Alcoholism and Adverse Outcomes Observed in Individuals with Prenatal Alcohol Exposure Receiving a Fetal Alcohol Spectrum Disorder Diagnostic Evaluation at the Washington State Fetal Alcohol Syndrome Diagnostic & Prevention Network Clinic
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University of WashingtonAbstract Association Between Paternal Alcoholism and Adverse Outcomes Observed in Individuals withPrenatal Alcohol Exposure Receiving a Fetal Alcohol Spectrum Disorder Diagnostic Evaluation
at the Washington State Fetal Alcohol Syndrome Diagnostic & Prevention Network Clinic Emma Esteve Manley Chair of Thesis Committee:Susan J (Astley) Hemingway
Department of Epidemiology Background: Prenatal alcohol exposure (PAE) can cause a spectrum of adverse outcomes calledfetal alcohol spectrum disorders (FASD). This spectrum includes a multitude of life-long adverse
outcomes such as behavioral issues, learning challenges, brain structural changes, and physical
abnormalities. Since the 1990s, the Fetal Alcohol Syndrome Diagnostic & Prevention Network
Clinic has used a multitude of neuropsychological tests conducted by an interdisciplinary team to
understand, diagnose, and provide services to individuals living with PAE. At the FASDPN, a 4-
Digit Diagnostic Code is used when evaluating and diagnosing patients. Throughout the decades,
it has been evident that maternal alcohol consumption is a risk factor for developing FASD,
however less is known about the role of paternal alcoholism. This study examined whether
reported paternal alcoholism was associated with an increased severity of a FASD diagnosis and
adverse outcomes among patients with PAE. Methods: A retrospective study using data abstracted from FASDPN patient records wasconducted with patient consent and human subjects approval to assess the association between
paternal alcoholism and severity of FASD diagnosis as well as adverse fetal outcomes. 468 out
of 871 patients were selected by a multitude of inclusion and exclusion criteria. We sampled all
different diagnoses, races, ethnicities, sexes at birth, all ages, and patients whose biological
father was known. Patients were excluded if no information was given on paternal alcoholism
and/or any biological father's health history. Paternal alcoholism was recorded if the section for
paternal alcoholism was check marked by individuals completing the New Patient Information
form. Growth, facial and structural, neurological, and functional brain outcomes were compared
between the two groups. Maternal alcohol exposure was also compared between the two groups.
Chi-squared tests, independent t-tests, and Oneway ANOVA with linear-by-linear association
when appropriate, were used to compare outcomes between the two groups. Statistical
significance set at p < 0.05.
Results: Out of the 468 patients, 184 (39%) did not have reported paternal alcoholism and 284
(61%) did have reported paternal alcoholism. Paternal alcoholism was significantly associated
with increased severity of FASD diagnosis, increased neuropsychological impairment, and more
severe maternal alcohol consumption during pregnancy (all p-values < 0.05). Paternal alcoholism
was not observed to be significantly associated with growth deficiency or the FAS facial features
(all p-values > 0.05).
Conclusion and Discussion: Our findings suggest paternal alcoholism may be an important risk
factor contributing to adverse neurodevelopmental outcomes of patients with PAE. These
findings are consistent with both laboratory and clinical studies published by other investigators
in the last 5 years. These observations warrant further epidemiological studies to examine
paternal alcohol consumption effects on the longitudinal brain, development, and growth
outcomes of individuals with PAE.
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Thesis (Master's)--University of Washington, 2026
