Here are some interesting scientific studies that might shed some light on why we see so many incidents of unusual, abnormal, or inappropriate sexual behaviors in children and adults with FAS or FAE.
Social play in juvenile rats prenatally exposed to alcohol.
Teratology 1986 Aug;34(1):1-7 (ISSN: 0040-3709)
Meyer LS; Riley EP
Offspring of rat dams that consumed isocaloric liquid diets containing either 35% or 0% ethanol-derived calories (EDC) from gestation days 6-20 were tested for play-fighting behavior as juveniles. Offspring from a group of dams maintained on standard lab chow and water throughout gestation were also included. Animals were tested in pairs, with offspring from each of the three prenatal treatment conditions (35% EDC, 0% EDC, and lab chow) being paired with another same-sex animal from one of these three prenatal treatment groups. Although play-fighting in juveniles is normally sexually dimorphic, this normal pattern was absent in juveniles prenatally exposed to alcohol. Male alcohol-exposed offspring displayed feminized behavior while female alcohol-exposed offspring showed masculinized behavior. This reversal of the normal sexually dimorphic aspects of play suggests that some of the behavioral disturbances associated with prenatal alcohol exposure may result, in part, from an alcohol-induced disruption of the hormonal environment in which the fetus develops.
Alcohol's possible covert role: brain dysfunction, paraphilias, and sexually aggressive behaviors.
Sex Abuse 1999 Apr;11(2):147-58 (ISSN: 1079-0632)
Ontario Institute for Studies in Education, University of Toronto, Canada.
A number of studies have suggested a relationship between sexually anomalous behavior and brain dysfunction. However, in most cases, the etiology of this dysfunction remains elusive. In this paper, alcohol exposure in utero (fetal alcohol syndrome) is offered as one possible explanation for the neurophysiological abnormalities that appear to characterize a notable proportion of individuals within the paraphilic and sexually aggressive populations. It is noteworthy that the teratogenic effects of alcohol upon humans and animals often leads to a number of the behavioral and physiological abnormalities exhibited by some of these individuals.
Fetal alcohol exposure blocks full masculinization of the dorsolateral nucleus in rat spinal cord.
Physiol Behav 1999 Jun;66(4):571-5 (ISSN: 0031-9384)
Ward IL; Romeo RD; Denning JH; Ward OB
Department of Psychology, Villanova University, PA 19085-1699, USA. IWARD@EMAIL.VILL.EDU.
Male rats prenatally exposed to a combination of stress and ethanol show severely impaired ejaculatory patterns. This study examined two sexually dimorphic nuclei in the lumbar spinal cord implicated in the control of male copulatory reflexes in rats whose mothers were exposed to alcohol, to stress, or to both treatments during pregnancy. Alcohol exposure led to a marked decrease (22%) in the number of motor neurons in the dorsolateral nucleus (DLN) of the adult male offspring, but no significant change in cell count was detectable in the sexually dimorphic nucleus of the bulbocavernosus (SNB). The combination of alcohol and stress did not enhance the effect on the DLN above that produced by alcohol alone. Somal sizes in the DLN and SNB were not altered by any of the treatment conditions. Alcohol exposure probably leads to incomplete masculinization of the DLN in male rats by decreasing testicular steroidogenesis during the fetal stage(s) when sexual differentiation is ongoing in that CNS structure.
Executive functioning in children with heavy prenatal alcohol exposure.
Alcohol Clin Exp Res 1999 Nov;23(11):1808-15 (ISSN: 0145-6008)
Mattson SN; Goodman AM; Caine C; Delis DC; Riley EP
Center for Behavioral Teratology, San Diego State University, California, USA. firstname.lastname@example.org.
BACKGROUND: Children with heavy prenatal alcohol exposure have well documented deficits in overall cognitive ability. Recently, attention has turned to the executive function (EF) domain in this population. Until recently, comprehensive measures of EF have not been available within one test battery. This study used a battery of tests to assess four domains of EF in alcohol-exposed children. METHODS: The Delis-Kaplan Executive Function Scale was used to evaluate EF in 18 children with heavy prenatal alcohol exposure, with and without a diagnosis of fetal alcohol syndrome (FAS), and 10 nonexposed controls. Children ranged in age from 8 to 15 years. Measures from four domains of executive functioning were analyzed: planning ability, cognitive flexibility, selective inhibition, and concept formation and reasoning. Tasks consisted of primary EF measures as well as measures of secondary component skills. RESULTS: Alcohol-exposed children were deficient on EF measures compared with nonexposed controls. Furthermore, in most cases, children with and without the FAS diagnosis did not differ from one another. These deficits were not entirely explainable by concomitant deficits on component skills. Specific impairments were identified within the domains of planning and response inhibition, with additional deficits in abstract thinking and flexibility. CONCLUSIONS: Deficits in executive functioning were observed in alcohol-exposed children with or without the diagnosis of FAS and in the absence of mental retardation. Performance on these EF tasks provides insight into the cognitive processes driving overall performance and has implications for adaptive and daily functions. These results are consistent with anecdotal and empirical reports of deficits in behavioral control and with neuroanatomical evidence of volumetric reductions in structures within the frontal-subcortical system in children with heavy prenatal alcohol exposure.
Behavioral and psychosocial profiles of alcohol-exposed children.
Alcohol Clin Exp Res 1999 Jun;23(6):1070-6 (ISSN: 0145-6008)
Roebuck TM; Mattson SN; Riley EP SDU/UCSD Joint Doctoral Program in Clinical Psychology, Center for Behavioral Teratology, Department of Psychology, San Diego State University, California 92120, USA.
BACKGROUND: It is widely known that prenatal alcohol exposure is related to cognitive and behavioral deficits throughout childhood and adolescence. Much research has focused on understanding and quantifying the cognitive profile of children with fetal alcohol syndrome (FAS) with relatively less empirical research on behavioral or psychosocial adjustment. The primary purpose of this study was to examine the behavioral and psychosocial profile of children exposed to heavy amounts of alcohol prenatally. METHOD: Two groups of subjects were evaluated: an alcohol-exposed group (ALC) and a nonexposed control group (NC) each made up of 32 subjects matched for age, gender, and ethnicity. The alcohol-exposed group consisted of children heavily exposed to alcohol in utero, including 19 children diagnosed with FAS. The Personality Inventory for Children (PIC) was completed by the caretaker of each child. Four validity/screening scales and 12 clinical scales were scored for all subjects. RESULTS: Analyses revealed significant group differences on four validity/screening scales and 12 substantive scales. Within the ALC group, the profile of children without FAS was similar to that of children with FAS, with the exception that their profiles were consistent with less cognitive impairment. CONCLUSIONS: These findings indicate that in addition to previously reported cognitive impairments, heavy prenatal alcohol exposure is related to significant impairments in psychosocial functioning. Even children without alcohol-related physical anomalies suffer from impaired psychosocial functioning. Because impairments of this nature can interfere with functioning across multiple domains, effective early intervention programs should be considered for families of alcohol-exposed children. Furthermore, given the similarities of alcohol-exposed children with and without FAS, it is imperative to obtain prenatal alcohol exposure histories on all children experiencing cognitive or psychosocial deficits
Direct and indirect effects of prenatal alcohol damage on executive function.
Dev Neuropsychol 2000;18(3):331-54 (ISSN: 8756-5641)
Connor PD; Sampson PD; Bookstein FL; Barr HM; Streissguth AP
Department of Psychiatry and Behavioral Sciences, University of Washington, Fetal Alcohol and Drug Unit, 180 Nickerson Street, Suite 309, Seattle, WA 98109, USA. email@example.com.
Patients with Fetal Alcohol Syndrome (FAS) and Fetal Alcohol Effects (FAE) often have difficulty functioning appropriately in everyday life and seem to employ poor problem-solving strategies. Tests of executive function are relevant for quantifying the functional deficits and underlying real-life problems associated with prenatal alcohol exposure. This study considers two pathways for the effects of prenatal alcohol on executive function: a direct effect and an indirect effect through prenatal alcohol's effect on IQ. We compared 30 men who had been diagnosed with FAS or FAE with young adults participating in a longitudinal prospective study (n = 419) and 15 control participants that comprised a comparison group. This study is unique in its analysis of the same battery of assessments of executive function in both a large low dose longitudinal study sample and a clinically diagnosed group. Participants were evaluated on 9 tests (including 58 scores) of executive function. For some but not all of the tests in this executive function battery, the decrement in the alcohol exposure group is greater than would be predicted from their IQ scores. We found that 3 of 6 Stroop scores, 2 of 4 Trails scores, 9 of 16 Wisconsin Card Sorting scores, 1 of 2 Ruff's Figural Fluency scores, and 2 of 4 Consonant Trigrams scores appear to be particularly sensitive to the direct effects of prenatal alcohol damage for patients with FAS and FAE. The findings suggest that these executive function tests would be particularly useful in clinical evaluations of persons suspected of fetal alcohol damage because they would not simply reflect deficits in IQ or facial stigmata.
The effects of prenatal stress, and of prenatal alcohol and nicotine exposure, on human sexual orientation.
Physiol Behav 2001 Sep 1-15;74(1-2):213-26 (ISSN: 0031-9384)
Ellis L; Cole-Harding S Minot State University, 58707, Minot, ND, USA. firstname.lastname@example.org.
BACKGROUND: Studies of rats have shown that mothers who are subjected to stress during pregnancy are more likely than mothers who are not stressed during pregnancy to have male offspring who exhibit female-typical sexual receptivity postures (lordosis) in the presence of other males following the onset of puberty. More recent animal experiments have indicated that prenatal exposure to alcohol affects the sexual preferences of male offspring in ways that are similar to the effects of prenatal stress. Research with human subjects have thus far yielded inconsistent findings regarding the effects of prenatal stress on male sexual orientation, and no research has yet addressed the possible involvement of prenatal exposure to alcohol or other widely used recreational drugs, such as nicotine. PURPOSE: The present study was undertaken to determine if prenatal stress could be one of the causes of variations in sexual orientation in humans, both singularly and in conjunction with prenatal exposure to alcohol and nicotine. METHODS: Over 7500 offspring and their mothers provided information regarding the offspring's sexual orientation and the mother's stressful experiences and use of alcohol and nicotine during pregnancy. RESULTS: Findings indicate that prenatal stress has a modest but significant effect on the sexual orientation of male offspring, particularly when the stress occurred during the first trimester of pregnancy. Regarding prenatal exposure to alcohol, no evidence was found to suggest that it impacted offspring sexual orientation of either males or females. Prenatal nicotine exposure, however, appears to significantly increase the probability of lesbianism among female offspring, especially if the exposure occurred in the first trimester along with prenatal stress in the second trimester. CONCLUSION: The present study is consistent with animal models suggesting that prenatal stress disrupts the typical sex hormonal milieu within which male fetal brains are sexed, thereby feminizing/demasculinizing the male's sexual orientation. However, little support was found for similar effects of prenatal alcohol exposure. In the case of prenatal nicotine, this study is the first to suggest that this drug has masculinizing/defeminizing effects on the sexual orientation of female offspring.
Some implications of prenatal alcohol exposure for the treatment of adolescents with sexual offending behaviors.
Sex Abuse 2002 Oct;14(4):313-27 (ISSN: 1079-0632)
Prenatal alcohol exposure can seriously harm the fetus, resulting in a wide range of physical and central nervous system abnormalities. A follow-up study of persons prenatally exposed to alcohol found that 49% of adolescents and adults had repeatedly displayed inappropriate sexual behavior. While these persons are likely to present to sexual offender treatment programs, they are unlikely to be recognized as neurologically impaired because the sequelae of prenatal alcohol exposure are seldom accurately identified by clinicians. Persistent impairments in response inhibition, memory, and executive functions are common, requiring adaptations to standard sexual offender assessment and treatment.
Postparturitional testosterone surge in male offspring of rats stressed and/or fed ethanol during late pregnancy.
Horm Behav 2002 Mar;41(2):229-35 (ISSN: 0018-506X)
Ward OB; Ward IL; Denning JH; French JA; Hendricks SE Department of Psychology, Villanova University, Villanova, Pennsylvania 19085, USA.
Male offspring of rats exposed to restraint stress and/or alcohol during late pregnancy show aberrant patterns of sexual behavior masculinization and defeminization that vary as a function of treatment. The impact of these treatments on the postparturitional testosterone (T) surge that contributes to sexual behavior differentiation was investigated. Plasma T was measured using radioimmunoassay in individual males sampled on day 21 of gestation within 10 min of cesarean delivery or 1, 2, or 4 h thereafter. Neonatal T in the group exposed only to stress did not differ from that in the control group. T was lower than control levels at birth in both alcohol groups. The magnitude of the T surge that occurred during the first hour of birth in the control group was diminished by 50% in both alcohol groups, whose T pattern was very similar. There was no common alteration in postparturitional T associated with the increased lordotic behavior potential that males in all three treatment groups typically share, nor were there idiosyncratic endocrine abnormalities linked to the very different male copulatory pattern each exhibits. Exposure to an abnormal T milieu during fetal as well as neonatal ontogeny may underlie the etiology of the different sexual behavior patterns exhibited by males exposed to stress and/or alcohol. Possible unique effects each treatment exerts on perinatal plasma T and it's aromatization to estradiol in hypothalamic targets are discussed. [Copyright 2002 Elsevier Science (USA).].
Compiled by Teresa Kellerman