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(HealthDay News) &emdash; Drinking alcohol while you are pregnant can cause your baby to be born with a series of physical and mental birth defects called fetal alcohol syndrome (FAS). It's a leading cause of mental retardation.

No one knows exactly how much alcohol a woman has to drink to cause FAS in her baby (and that level may be different among women). So experts agree that the best thing to do is not to drink alcohol at all while you are pregnant &emdash; that includes beer, wine, wine coolers and liquor.

The March of Dimes Birth Defects Foundation offers these tips to help you quit:

* Avoid situations where you usually drink, like parties or bars.

* Ask your health care provider about alcohol treatment programs.

* Ask your partner, family and friends to help you stay away from alcohol.

* Join an Alcoholics Anonymous support group.

Alati, R.; Al Mamun, A.; Williams, G. M.; O'Callaghan, M.; Najman, J. M.; Bor, W.; "In utero alcohol exposure and prediction of alcohol disorders in early adulthood: a birth cohort study", ARCHIVES OF GENERAL PSYCHIATRY (2006); 63 (9): 1009-16. The results of this study show support for a biological origin of adult alcohol disorders and suggest that the association is not explained solely by maternal drinking or smoking during childhood and adolescence or other intervening factors.

Baer, John S.; Sampson, Paul D.; Barr, Helen M.; Connor, Paul D.; Streissguth, Ann P.; "A 21-year longitudinal analysis of the effects of prenatal alcohol exposure on young adult drinking." ARCHIVES OF GENERAL PSYCHIATRY (2003), 60: 377-385. Prenatal alcohol exposure may be a risk factor for the development of alcohol problems in humans. We used data beginning with interviews of women in prenatal care at mid pregnancy to predict alcohol use and alcohol related problems in their offspring now aged 21 years. Maternal drinking during pregnancy was assessed from November 4, 1974, through October 2, 1975, along with measures of maternal smoking, use of caffeine and other drugs, and demographic factors. Family history of alcohol problems was assessed from interviews with parents when offspring were 14 years of age and updated when offspring were 21 years of age. Measures of prenatal use of alcohol and other drugs and many aspects of the family environment were assessed at 7 different ages, prenatally through 21 years. Young adult offspring (age, 21 years [N=4331] provide self-reports of drinking quantity and frequency and completed the Alcohol Dependence Scale as a measure of alcohol-related problems and dependence. Results: Univariate, partial least squares, and regression analyses indicate that prenatal alcohol exposure is significantly associated with alcohol problems at 21 years of age. The relationship persists independent of the effects of family history of alcohol problems, nicotine exposure, other prenatal exposures, and postnatal environmental factors including prenatal use of other drugs. Prenatal nicotine exposure was not associated with alcohol problems by offspring at 21 years of age. The analyses reported herein provide evidence of the relationship, across more than 21 years, between prenatal alcohol exposure and the degree of negative consequences that result from heavy drinking in young adulthood. However, those with persistent alcohol problems in mid life typically began drinking in adolescence and young adulthood.

Burden, Matthew J., Jacobson, Sandra W.; Jacobson, Joseph L.; "Relation of prenatal alcohol exposure to cognitive processing speed and efficiency in childhood", ALCOHOLISM : CLINICAL AND EXPERIMENTAL RESEARCH (2005), 29 (8): 1473-1483. Prenatal alcohol exposure has been linked to deficits in processing speed in both infancy and later in childhood. This study was designed to examine prenatal alcohol-related deficits in both processing speed and processing efficiency in four domains of cognitive function. (Black children n = 337, age, 7.5 years) Prenatal alcohol exposure was associated with slower processing speed on several of the Sternberg tasks, and the number comparison task showed a specific deficit in processing efficiency. These effects on tasks involving effortful processing contrasted with the lack of performance differences on the more automatic R. T measures. The relation of prenatal alcohol exposure to working memory was mediated, in part, by an associated reduction in processing speed. These data confirm reports by other investigators linking prenatal alcohol exposure to slower processing speed and show that this R. T deficit is found within the context of complex cognition but not were automatic processing is involved. The reduction in R. T accounts in part, for the previously reported alcohol-related effects on working memory. The number comparison slope was the only specific component of information processing affected, confirming previous reports of a distinctive prenatal alcohol effect on number processing.

Chang, Grace; McNamara, Tay K.; Orav, E. John; Wilkins-Haug, Louise; "Alcohol use by pregnant women: partners, knowledge, and other predictors", JOURNAL OF STUDIES ON ALCOHOL (2006), 67 : 245-251. Because previous alcohol consumption sue by the pregnant woman was the strongest predictor of prenatal alcohol use, the importance of its accurate identification is emphasized. Although pending further investigation, knowledge about healthy pregnancy behaviors may exert greater impact if it is shared by the pregnant woman and her partner.

Day, N. L.; Leech, S. L.; Richardson, G. A.; Cornelius, M. D.; Robles, N.; Larkby, C.; " Prenatal alcohol exposure predicts continued deficits in offspring size at 14 years of age", ALCOHOLISM: CLINICAL AND EXPERIMENTAL RESEARCH (2002), 26 (10): 1584-1591, October 2002. "Growth deficits are among the cardinal features for the diagnosis of fetal alcohol syndrome. Growth deficits have also been noted among those who were exposed to alcohol prenatally but who do not have fetal alcohol syndrome. Few studies have observed subjects past early and middle childhood, however, to evaluate the longer-term effects of prenatal alcohol exposure on growth in adolescence. This is a report of the effects of alcohol exposure during gestation on the size of the offspring at 14 years of age.

"Women were recruited in their fourth prenatal month. These women were interviewed in the fourth and seventh months of pregnancy and at delivery. The women and their children were seen when the offspring were 14 years of age.

Gans, Steven, "What is Fetal Alcohol Syndrome or FAS?", Describes FAS - Fetal Alcohol Syndrome--primary and secondary characteristics of FAS, Fetal Alcohol Spectrum Disorders, and the fact that FAS is totally preventable.

"Growth deficits associated with prenatal alcohol exposure were identified among the offspring at 14 years of age. Weight, height, head circumference, and skinfold thickness continued to be significantly affected by prenatal alcohol exposure after controlling for other significant predictors of size. These effects exhibited a dose-response pattern, and significant effects were found at levels below one drink per day. For example, first trimester alcohol exposure predicted weights of 152 lbs for the offspring of abstainers, 149 lbs for the offspring of light drinkers (>0 and <0.2 drinks per day), 143 lbs for the offspring of moderate drinkers (>0.2 and <0.89 drinks per day), and 136 lbs for the offspring of heavy drinkers (>0.89 drinks per day).

"Prenatal alcohol exposure continues to affect size at age 14 years in this cohort of children followed since their fourth month of gestation."

Kable, Julie A.; Coles, Claire D.; "The impact of prenatal alcohol exposure on neurophysiological encoding of environmental events at six months;" ALCOHOLISM: CLINICAL AND EXPERIMENTAL RESEARCH (2004), 28(3):498-496. Using methodologies from developmental studies on infant information-processing skills, early manifestations of later long-term neurocognative effects of prenatal alcohol exposure can be explored by assessing primary cognitive processes, including attentional regulation and processing speed. 118 6-month-old infants of moderate prenatal alcohol exposure were studied. The outcomes suggest that prenatal alcohol exposure results in specific impairments in early attentional regulation, which may influence subsequent cognitive development and behavioral outcomes dependent on primary cognitive processes.

O'Leary, C. M,; Nassar, N.; Zubrick, S. R,; Kuriczuk,, J. J., Stanley, F.; Bower, C.' "Evidence of a complex association between dose, pattern and timing of prenatal alcohol exposure and child behaviour problems". ADDICTION, 105 (1): 74-86. 2224 mothers were interviewed three months after delivering their baby and then had follow-up interviews when their child was 2, 5, and 8 years old. Some of the findings of the (survey) study include: children of mothers who drank heavily during the first trimester of pregnancy were three times more likely to suffer anxiety or depression; children of mothers who drank moderately in the first trimester were only twice as likely to suffer anxiety; and children of mothers who drank heavily or moderately during the third trimester were more likely to develop aggressive types of behaviours. The study's author, Colleen O'Leary, stated that. . . "it is important that women have this information about increased risk so that they can make informed decisions to give their child the best start in life."

Ostrea, E. M., Jr.; Hernandez , J. D.; Bielawski, D. M.; Kan, J. M.; Leonardo, G. M.; Abela, M. B.; Church, M. W.; Hannigan, J. H.; Janisse, J. J.; Ager, J. W. ; Sokol, R. J.;"Fatty acid ethyl esters in meconium: are they biomarkers of fetal alcohol exposure and effect?", ALCOHOLISM: CLINICAL AND EXPERIMENTAL RESEARCH (2006), 30(7): 1152-9. The aim of this study was to analyze long-chain fatty acid ethyl esters (FAEEs) in meconium as potential biomarkers of fetal alcohol exposure and effect. The meconium of 124 single infants was studied, 93 of the mothers had consumed alcohol during pregnancy and 31 had not. FAEEs were analyzed in the infants' meconium. The aim of this study was to analyze long-chain fatty acid ethyl esters (FAEEs) in meconium as potential biomarkers of fetal alcohol exposure and effect. The incidence of ethyl linoleate in meconium was found to be significantly higher in the alcohol-exposed group when compared to the control group. There was also a significant association between alcohol exposure and group concentrations of ethyl linoleate. Furthermore, the highest ethyl linoleate concentration was only found in the alcohol exposed infants.

Shankar, Kartik, Ronis, Martin J. J.; Badger, Thomas M,; "Effects of pregnancy and nutrition status on alcohol metabolism," ALCOHOL HEALTH AND RESEARCH WORLD (2007), 30 (1): 55-63. "Metabolism of alcohol (i.e., ethanol) is regulated by genetic and environmental factors as well as physiologic state. For a given alcohol intake, the rate of alcohol clearance, which ultimately determines tissue ethanol concentrations, may be the most significant risk factor for many of the detrimental effects of alcohol. Faster ethanol clearance would help minimize target tissue concentrations, and in pregnant women, mitigate fetal alcohol exposure. Much remains to be known about the effects of the altered endocrine milieu of pregnancy on alcohol metabolism and clearance in the mother. Research has shown that among pregnant rats allowed unrestricted access to alcohol and those fed alcohol containing liquid diets under experimental conditions via a feeding tube (total enteral nutrition [TEN]), urine ethanol concentrations (and thus blood and tissue ethanol concentrations) are lower in pregnant rats compared with non-pregnant females given the same dose of ethanol. Maternal nutritional status also is an important determinant of fetal alcohol toxicity. Research using the TEN system has demonstrated that alcohol-induced fetal growth retardation is potentiated by under nutrition in part via impaired alcohol metabolism and clearance."

Sokol, Robert J.; Janisse, James J.; Ager, Joel; Louis, Judette M.; Bailey, Beth Nordstrom; Jacobson, Sandra W.; Jacobson, Joseph L.; "Extreme prematurity: an alcohol related-birth effect", ALCOHOLISM: CLINICAL & EXPERIMENTAL RESEARCH (2007), May. Sokol and colleague collected data on exposure to alcohol, cocaine, and cigarettes, as well as corresponding outcomes, from 3,130 pregnant women and their infants. The researchers used ultrasound to provide specific pregnancy dating. Of the newborns, 66 were extremely preterm, 462 were mildly preterm, and 2,602 were term deliveries. 92 percent of those studied were African American. Findings indicated that alcohol and cocaine, but not cigarette, use were associated with an increased risk of extreme preterm delivery; alcohol accounted for the lion's share of the risk. Furthermore, the effects were greater in pregnancies among women older than 30 years of age. Sokol and other researchers have seen what appears to be a greater susceptibility to neurobehavioral effects and anatomic congenital anomalies in pregnancies among older women. Sokol stated: "It would be best for women to just not drink during pregnancy."

Willford J ; Leech S ; Day N: "Moderate prenatal alcohol exposure and cognitive status of children at age 10", ALCOHOLISM: CLINICAL AND EXPERIMENTAL RESEARCH (2006), 30(6): 1051-9. "A significant relation was found between alcohol exposure during the first and second trimesters and the composite score of the Stanford-Binet for African American children at age 10. Significant relations were also found for the verbal, abstract/visual, and quantitative subscales. Additional predictors of IQ at age 10 included mother's IQ, home environment, and child's report of depression. There is a significant association between PAE and cognitive ability at age 10 among African American offspring. There was no relation between PAE and scores on the Stanford-Binet scales among the Caucasian offspring."

Willford, Jennifer A.; Richardson, Gale A.; Leech, Sharon L.; Day, Nancy L.; "Verbal and visiospatial learning and memory function in children with moderate prenatal alcohol exposure". ALCOHOLISM : CLINICAL AND EXPERIMENTAL RESEARCH (2004), 28(3): 497-507. This study investigated the effects of moderate prenatal alcohol exposure on learning and memory in 14-year-old adolescents. The Children's Memory Scale was used to assess learning and memory function in the verbal/auditory and visual/spatial domains. In addition, both short-term and long-term memory function were assessed. The project included 580 children and their mothers. Results demonstrated that prenatal alcohol exposure lead to deficits in encoding process as indicated by deficits in verbal learning. Initial deficits in acquisition were responsible for deficits in immediate and delayed recall of verbal information in children who were exposed to alcohol during pregnancy but did not have fetal alcohol syndrome.

updated 12/21/16