Ignored Papers, Invented Quotations: A History of Fetal Alcohol Syndrome

Given the high rate of alcoholism throughout history, its effects on the fetus may have existed for millennia. But, the claim that Greeks and Romans were aware of fetal alcohol syndrome rests on incorrect citations. From 1725, maternal alcohol consumption was associated with retarded fetal growth and neurological anomalies. From 1809, scientists followed Lamarck’s theory that the disorders parents acquire during their lifetime are passed on to their offspring. Fetal effects were thought to be inherited mainly from the father. During the 19th century, parental alcoholism became associated with malformations. In 1915, Ballantyne distinguished genetic influence via germ cells from toxin’s effect on the embryo. Fetal alcohol syndrome was characterized by Rouquette [Influence de la toxicomanie alcoolique parentale sur le développement physique et psychique des jeunes enfants] in 1957 and Lemoine et al. [Ouest Medical. 1968;21:476–482] in 1968 as consisting of 4 features: (A) facial anomalies (narrow forehead, retracted upper lip, and cupped ears), (B) severe growth retardation (prenatal and postnatal), (C) malformations (limbs, cardiac, and visceral), and (D) central nervous system anomalies (hyperexcitability and mental retardation). But, their studies, written in French, remained disregarded. In 1973, Jones et al. [Lancet. 1973;302:999–1001] reported “the first association between maternal alcoholism and aberrant morphogenesis in the offspring.” The history of fetal alcohol syndrome reveals shortcomings in citation practice. Alleged quotations remained unverified, non-English publications neglected, and short quotations taken out of context. Prejudiced by religious and abstinence groups, reports on alcohol damage to the unborn were fraught with emotions, moralizing, social implications, and presentism, the interpretation of past events with present knowledge.

Antisocial Alcoholism in Parents of Adolescents and Young Adults With Childhood ADHD

Objective: Test the hypothesis that alcoholism, including antisocial alcoholism, is more prevalent among mothers and fathers of children with versus without ADHD. Method: Mothers (312 ADHD group, 235 non-ADHD group) and fathers (291 ADHD group, 227 non-ADHD group) in the Pittsburgh ADHD Longitudinal Study were interviewed along with their adolescent and young adult offspring. Results: Maternal and paternal alcoholism, with and without comorbid antisociality, was more prevalent in the ADHD group. Paternal alcoholism without antisociality was only marginally higher for probands after controlling for paternal ADHD. Offspring conduct disorder comorbidity was associated with parental antisociality but not parental antisocial alcoholism. Conclusion: Our findings that 44% of proband fathers and 25% of proband mothers experienced alcohol problems with or without antisociality are further evidence of increased alcoholism prevalence in families affected by ADHD. Maternal alcoholism and antisociality are prominent contributors to this family-level vulnerability. These findings indicate the need to assess long-term offspring outcomes as a function of parental alcohol and externalizing comorbidities, and perhaps other indicators of parental alcoholism phenotype, as familial vulnerability unfolds across development.

QT prolongation in the newborn and maternal alcoholism

I discuss a newborn whose mother is addicted to alcohol. On the third day of life, the newborn was found to have ventricular tachycardia. After spontaneous termination of the abnormal rhythm, the duration of the corrected QT interval was 0.48 s. During the next days, the duration of the interval normalized, and has now remained stable for 5 years. I conclude that the so-called “alcohol withdrawal syndrome of the newborn” might cause postnatal prolongation of the QT interval.

Childhood parental loss and alcoholism in women: a causal analysis using a twin-family design

SynopsisChildhood parental loss may be an important risk factor for psychiatric illness in adulthood. While this association has been carefully examined for depression, little is known about the role of parental loss in predisposing to alcoholism. We examined an epidemiological sample of female twin pairs with the same history of continuity or disruption in parent–child relationships (N = 1018 pairs; mean age 30 years), using a range of definitions of alcoholism. Childhood parental loss through separation, but not death, substantially increased the risk in adulthood for all definitions of alcoholism. Furthermore, both paternal and maternal alcoholism substantially increased the probability of parental separation from their children. Proposing a structural equation twin-family model that incorporates childhood parental loss as a specified environmental risk factor, we examined how much of the association between childhood parental loss and alcoholism was causal (i.e. mediated by environmental factors) v. non-causal (mediated by genetic factors, with parental loss serving as an index of parental genetic susceptibility to alcoholism). Both the causal and non-causal paths were significant for all definitions of alcoholism. However, the causal–environmental pathway consistently accounted for most of the association. While a significant proportion of the association is due to non-causal genetic mechanisms, childhood parental loss (or the familial discord that precedes or follows it) is probably a direct and significant environmental risk factor for the development of alcoholism in women.