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

Neonatology ◽  
2021 ◽  
pp. 1-7
Author(s):  
Michael Obladen
Keyword(s):  
Fetal Alcohol Syndrome ◽  
High Rate ◽  
Fetal Alcohol ◽  
Parental Alcoholism ◽  
Maternal Alcohol Consumption ◽  
Citation Practice ◽  
History Of ◽  
Maternal Alcoholism ◽  
The 19Th Century ◽  
Severe Growth

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.

ADRENAL CARCINOMA IN CHILD WITH HISTORY OF FETAL ALCOHOL SYNDROME

The Lancet ◽  
1977 ◽  
Vol 310 (8051) ◽  
pp. 1292-1293 ◽  
Author(s):  
Lusia Hornstein ◽  
Carol Crowe ◽  
Ralph Gruppo
Keyword(s):  
Fetal Alcohol Syndrome ◽  
Adrenal Carcinoma ◽  
Fetal Alcohol ◽  
History Of

Fetal Alcohol Syndrome

1986 ◽  
Vol 8 (4) ◽  
pp. 122-126
Author(s):  
Kenneth L. Jones
Keyword(s):  
Mental Retardation ◽  
Fetal Alcohol Syndrome ◽  
The United States ◽  
Prenatally Exposed ◽  
Fetal Alcohol ◽  
The Third ◽  
Two Factors ◽  
Maternal Alcoholism ◽  
Unborn Baby ◽  
Alcohol Alcohol

The fetal alcohol syndrome is the third most common recognizable cause of mental retardation in the United States. Many of the features of the fetal alcohol syndrome are secondary to the effect of alcohol on brain development. These include microcephaly, short palpebral fissures, the long smooth philtrum and thin vermilion of the upper lip, joint anomalies, altered palmar crease pattern, and mental retardation. Approximately 40% of babies born to alcoholic women and 11% of babies born to nonalcoholic moderately drinking women have evidence of the prenatal effect of alcohol. Alcohol, like other teratogens, causes a spectrum of defects. Thus, affected children may show great variability from the fullblown fetal alcohol syndrome to much milder effects of alcohol, some of which may not be obvious until school age. A "safe" amount of alcohol probably does not exist for the pregnant woman. Depending on unknown factors, what may be a "safe" amount for some women, may be devastating to the unborn baby of another. Two factors, the severity of the maternal alcoholism and the extent and severity of the pattern of malformation, seem to be most predictive of the ultimate prognosis for children with the fetal alcohol syndrome. Any decision to file child abuse changes against a mother whose baby was prenatally exposed to alcohol should be based on the parents ability to provide a stable home environment and not on whether the baby has features of the fetal alcohol syndrome. The fetal alcohol syndrome, the third most common recognizable cause of mental retardation, is completely preventable. All attempts must be made to educate people regarding the deleterious effect of alcohol.

Toluene Embryopathy: Delineation of the Phenotype and Comparison With Fetal Alcohol Syndrome

PEDIATRICS ◽  
1994 ◽  
Vol 93 (2) ◽  
pp. 211-215
Author(s):  
Margaret A. Pearson ◽  
Mary E. Rimsza ◽  
H. Eugene Hoyme ◽  
Laurie H. Seaver
Keyword(s):  
Fetal Alcohol Syndrome ◽  
Perinatal Period ◽  
Postnatal Growth ◽  
Clinical Findings ◽  
Embryonic Cell ◽  
Common Mechanism ◽  
Fetal Alcohol ◽  
Growth Deficiency ◽  
History Of ◽  
Craniofacial Features

Objective. To determine if maternal toluene abuse produces any structural or developmental disabilities in the developing fetus, a cohort of toluene-exposed infants was ascertained and examined. Methodology. Eighteen infants with a history of in utero toluene exposure were examined at birth. Nine of these infants were reexamined 3 to 36 months after their initial evaluations. The clinical findings in these patients were compared with those of similarly exposed children from the literature and with patients who had the fetal alcohol syndrome. Results. Thirty-nine percent of all toluene-exposed infants described in this and other studies were born prematurely, and 9% died during the perinatal period. Fifty-four percent were small for gestational age, and 52% exhibited continued postnatal growth deficiency. A 33% incidence of prenatal microcephaly, a 67% incidence of postnatal microcephaly, and an 80% incidence of developmental delay were observed. Eighty-three percent of the patients had craniofacial features similar to the fetal alcohol syndrome, and 89% of these children had other minor anomalies. Conclusions. Data from the patients herein described and the available scientific literature suggest that the mechanism of alcohol craniofacial teratogenesis may be nonspecific, with a variety of teratogens, including toluene, giving rise to phenotypic facial abnormalities similar to those of the fetal alcohol syndrome. We propose a common mechanism of craniofacial teratogenesis for toluene and alcohol, namely a deficiency of craniofacial neuroepithelium and mesodermal components due to increased embryonic cell death.

Developmental Language Disability As a Consequence of Prenatal Exposure to Ethanol

PEDIATRICS ◽  
1981 ◽  
Vol 68 (6) ◽  
pp. 850-855 ◽  
Author(s):  
Sally E. Shaywitz ◽  
Barbara K. Caparulo ◽  
Elizabeth Susan Hodgson
Keyword(s):  
Developmental Delay ◽  
Fetal Alcohol Syndrome ◽  
Prenatal Exposure ◽  
Head Circumference ◽  
Language Disability ◽  
Growth Failure ◽  
Facial Features ◽  
Fetal Alcohol ◽  
Aged Patients ◽  
History Of

Two pre-school-aged patients with a history of prenatal exposure to ethanol had abnormal head size and developmental delay. Both children were strikingly similar in physical appearance, behavior, and cognitive dysfunction. Facial features were typical of fetal alcohol syndrome. Head circumference >97th percentile without hydrocephalus and no evidence of prenatal or postnatal growth failure were unusual for ethanol teratogenicity. Each child had a similar pattern of verbal and behavioral dysfunctions characterized by (1) marked hypervigilence, (2) distractability, and (3) cognitive confusion manifested as anxiety and behavioral disorganization. It is suggested that a history of prenatal exposure to ethanol associated with (1) large head circumference, (2) facial features of fetal alcohol syndrome, and (3) early developmental delay, particularly in language acquisition, and impaired modulation of attention and arousal may represent a possible new effect of alcohol teratogenicity.

Fetal Alcohol Spectrum Disorders

2010 ◽  
Author(s):  
John C. Thorne ◽  
Tracy Jirikowic
Keyword(s):  
Fetal Alcohol Syndrome ◽  
Fetal Alcohol Spectrum Disorders ◽  
Alcohol Exposure ◽  
Fetal Alcohol ◽  
Growth Deficiency ◽  
Facial Phenotype ◽  
History Of ◽  
Similar Range ◽  
Spectrum Disorders ◽  
Fetal Alcohol Spectrum

Fetal alcohol spectrum disorders (FASD) is an umbrella term used to refer to the range of negative outcomes associated with prenatal ethyl-alcohol exposure (PAE). Although the impact of maternal drinking on the pre and postnatal development of children was examined as early as the late 19th century (Sullivan 1899), the teratogenic effects of PAE were not widely recognized until 1973, when Jones and Smith discussed PAE. The fetal alcohol syndrome (FAS) they described is now recognized internationally as a permanent birth defect syndrome resulting from PAE. Fetal alcohol syndrome is characterized by growth deficiency, a unique cluster of three minor facial anomalies, and evidence of central nervous system (CNS) abnormalities. At an estimated prevalence of one to three cases per 1,000 live births, FAS is the leading known preventable cause of developmental and intellectual disabilities (Bailey and Sokol 2008). Because the distinctive FAS facial phenotype provides a specific diagnostic marker of PAE (Astley 2006), FAS is the most readily recognized of the FASD. Fetal alcohol spectrum disorders that lack the tell-tale facial phenotype of FAS are more difficult to diagnose, but share a similar range and severity of CNS impairments and social costs. Other FASDs are many times more prevalent than FAS (Bailey and Sokol 2008) and may occur in as many as 1% of all children. Along with CNS, craniofacial, and growth impairments, FASD may also include ophthalmologic, cardiac, renal, and orthopedic abnormalities. Although heavier PAE, particularly binge drinking, leads to increased risk of FASD, no safe exposure level has been established. It is apparent that risk is substantially increased if the mother is older, has a history of alcoholism, has a family history of FASD, or is living in poverty. However, no clear set of risk or protective factors has been determined for any FASD that would allow for evidence-based advice to a particular mother on the relative risk that a particular level of drinking might have on her child’s development (Bailey and Sokol 2008; Jacobson et al. 2004; Maier and West 2001; Nulman et al. 2004; see also Disney et al. 2008).

NATURAL HISTORY OF THE FETAL ALCOHOL SYNDROME: A 10-YEAR FOLLOW-UP OF ELEVEN PATIENTS

The Lancet ◽  
1985 ◽  
Vol 326 (8446) ◽  
pp. 85-91 ◽  
Author(s):  
AnnPytkowicz Streissguth ◽  
SterlingKeith Clarren ◽  
KennethLyons Jones
Keyword(s):  
Natural History ◽  
Fetal Alcohol Syndrome ◽  
Fetal Alcohol ◽  
History Of
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