When is fetus susceptible to alcohol

The amount of alcohol ingested the length of period using alcohol and the developmental stage of the embryo and fetus at exposure mediate the effects of ethanol intake on the developing fetus. Alcohol drinking, even in moderate amounts, is also associated with an increased risk of spontaneous abortions, especially in the first trimester of pregnancy and with infertility in males and females [ 20 ].

It is, however, important to note that a meta-analysis of reports on the incidence of fetal malformations in moderately alcohol abusing women during pregnancy did not show an increase in the rate of congenital anomalies [ 22 ]. Alcohol drinking was associated with increased risk of fetal death.

Hazard ratio was 1. An odds ratio of 1. It has been demonstrated repeatedly that high alcohol consumption during pregnancy may seriously affect the developing embryo. Intra uterine growth retardation as well as postnatal long-term height and weight deficits is well demonstrated among children born to ethanol using women. Further, Covington et al. Recognition of the syndrome was made by Dr. David Smith and Dr. Kenneth Jones in based on the evaluation of eight children born to mothers who were defined as chronic alcoholic [ 29 ].

The principal features of FAS were determined as prenatal and postnatal growth deficiency, short stature, developmental delay, microcephaly, fine-motor dysfunction and facial dysmorphism. In addition there may be cleft palate, joint and cardiac anomalies and, altered palmar creases.

The above described facial dysmorphism tends to improve with the advancement in age of the affected individuals. The criteria are based on growth deficiency, facial phenotype, central nervous system damage and evidence of intrauterine alcohol exposure.

The more commonly used scores are the institute of medicine criteria [ 30 ] and the Washington criteria [ 31 ]. Hoyme et al. Even several of these clinical findings are sufficient for diagnosis if there is a positive history of alcohol exposure. Alcohol is known to affect not only the CNS but also organs that are developmentally related to CNS derivatives, including those developmentally dependent on neural crest cells like the cranio-facial complex and the heart.

A number of reports addressed a potential correlation between alcohol consumption and oral clefts. In a case control surveillance study Meyer et al. Based on the maternal report of alcohol use during the first 4 month of pregnancy, the authors failed to link low levels of alcohol use and oral clefts. Even the highest level of alcohol consumption did not result in a higher number of infants born with a cleft than with the use of less than one drink per week or less than one drink per drinking day.

In addition, folic-acid supplemented multivitamins used by some of the women did not modify the association between oral clefts and ethanol consumption. In contrast, Romitti et al. A moderate link was identified for multiple clefts and for Pierre-Robin syndrome, although based on small numbers.

An increased risk of oro-facial clefts was also observed among infants born to binge-drinking five or more drinks per occasion mothers exposed in the first trimester of pregnancy. Maternal binge-drinking may be particularly harmful since it results in a greater peak of blood ethanol concentrations [ 35 ]. It is accepted that about one third of children with alcohol embryopathy will also have congenital cardiac problems.

A higher risk of VSD [ 37 ], ASD [ 38 ] D-transposition [ 39 ], conotruncal heart defect [ 40 ], coarctation and hypoplastic aortic arch [ 41 ] were associated with maternal alcohol consumption. Krasemann and Klingebiel [ 42 ] retrospectively reviewed data of electrocardiogram ECG and echocardiogram EchoCG of all patients with clinical signs of alcoholic embryopathy between the years and Measurements of ECG and EchoCG often showed shortened QT in about half and shortened left ventricular diameter in about a quarter of the patients with alcoholic embryopathy consequently concluding that alcohol abuse during pregnancy as a primary toxin can lead to minor cardiac abnormalities, even without structural congenital cardiac defects.

Maternal alcohol consumption early in pregnancy was found to be related to increased risk of neural tube defects. Chen found in the literature nine cases of NTD related to prenatal exposure to ethanol, but speculated that this effect may result from the folate deficiency induced by alcohol abuse [ 43 ].

A hazard ratio of 1. Opposed to these findings, periconceptual maternal alcohol use did not reveal increased risk for neural tube defects using a population based case control study between — in California [ 44 ]. Binge drinking during the second month of pregnancy was associated with bilateral renal agenesis or hypoplasia among 75 infants evaluated between — in North Carolina [ 45 ]. Alcohol consumption during pregnancy was associated with increased risk of atopic dermatitis in early infancy that resolved during childhood.

This effect was mainly increased when the two parents had allergic disease. The highest risk was seen in high-risk infants of mothers who consumed four or more drinks per week at 30 weeks of gestation [ 46 ]. Alcohol is considered one of the risk factors for Attention Deficit Hyperactivity Disorder ADHD , independently of prenatal nicotine exposure or other familial risk factor.

A positive correlation between alcohol and ADHD was reported in 26 prenatally alcohol exposed children. Of the 24 children followed up, 10 were diagnosed as having ADHD, 2 were with Asperger syndrome a relatively mild form of autistic spectrum disorder and one with mild mental retardation.

The severity of the disorder correlated in a linear pattern with the amount of alcohol used by the mother during pregnancy. Discontinuation of the alcohol consumption by the 12th week resulted in normally developed children, demonstrating the fact that the cerebral cortex is more vulnerable to these effects of ethanol from the second trimester of pregnancy, post the organogenetic period.

Moreover, consumption of less than one alcoholic drink per day in the last three months of pregnancy, in spite of heavier drinking earlier, did not result in ADHD, learning disabilities or cognitive impairment at the age of 14 years [ 47 ]. Among 10 alcohol dependent adults who had maternal and paternal history of alcoholism, 8 had ADHD; seven of them were at risk of suicide, and all had a history of violence during intoxication.

When compared to a group of matched control alcohol addicts without a family history of alcoholism, none of the controls had ADHD, one had a risk of suicide and two were violent when drunk [ 48 ]. It has been difficult to define and characterize developmental risks associated with binge drinking or moderate drinking in pregnancy [ 49 ] and some studies failed to demonstrate an association between alcohol exposure and sustained attention performance in school age children [ 50 ].

Alcohol in pregnancy may affect intellectual ability that together with attention span and behavior are being considered higher functions of the cerebral cortex. Studies in 7 year-old school children following prenatal exposure to moderate amount of alcohol showed a decrement of 7 points in IQ [ 51 ]. Nine years old participants with FAS were significantly weaker than control children in reading, spelling, addition, subtraction, phonological awareness, and other tests of early literacy.

A deficit in phonological awareness, a key pre-function for reading may be a primary cognitive phenotypic characteristic in children with FAS. Syllable manipulation, letter sound knowledge, written letters, word reading and non-word reading and spelling were improved after nine months manipulation class [ 52 ].

Delayed motor functions, mostly fine motor skills were found in 22—68 months old FAS children [ 53 ]. In addition, alcohol may also affect the cerebellum. In the human cerebellum, Purkinje cell migration is completed and their dendritic outgrowth begins around gestational week 26 extending to the third trimester of pregnancy.

Consequently, a period of enhanced vulnerability of Purkinje cells to binge alcohol exposure in humans would be predicted near the end of the second trimester and may extend over the third trimester [ 54 ]. Cerebellar developmental disorders and disproportionate reduction in the anterior cerebellar vermis have been identified by MRI in children that were exposed prenatally to alcohol during each trimester of pregnancy [ 55 ].

Children with FAS were found to have the frontal lobes smaller with lower choline concentrations in MRS MR spectroscopy as a marker of cell membrane stabilizer and myelinization. The caudate nucleus was found disproportionately smaller in children with neuropsychological impairment. The prevalence to have one or more brain regions 2 or more SD below mean size in controls was proportional to their neurological damage [ 56 ].

Decreased cerebellar growth and decreased cranial to body growth in fetuses of alcohol abusing mothers was also observed on fetal ultrasound performed on the 18 week of gestation [ 57 ]. If the mothers stopped drinking at the beginning of pregnancy, cerebellar growth was normal. Adults exposed to binge drinking while in utero were found to have increased rate of somatoform disorders, substance dependence, paranoid, passive aggressive, anti social and other personality disorders [ 58 ].

Different mechanisms have been offered to explain the teratogenic effects of alcohol on the developing embryo. They include the following: 1 Increased oxidative stress; 2 Disturbed glucose, protein, lipid and DNA metabolism; 3 Impaired neurogenesis and increased cellular apoptosis, especially of neural crest cells [ 26 , 59 — 61 ]; 4 Endocrine effect; 5 Effects on gene expression.

Ethanol can induce oxidative stress directly by formation of free radicals which react with different cellular compounds, or indirectly by reducing intracellular antioxidant capacity, such as decreased glutathione peroxidase levels. Help for your child may include extra support in school, social skills training, job training, and counseling.

Community services may be able to help your family handle the costs of and emotions from raising your child. Finding alcohol effects early, even if they are mild, gives a child the best chance to reach his or her full potential in life.

Finding the problem early may help prevent problems in school and mental health problems, such as substance use disorder , depression , or anxiety. There is no treatment that can reverse the impact of alcohol on your baby's health. And there's no treatment that can make the effects less severe.

Author: Healthwise Staff. This information does not replace the advice of a doctor. Healthwise, Incorporated, disclaims any warranty or liability for your use of this information. Your use of this information means that you agree to the Terms of Use.

Learn how we develop our content. To learn more about Healthwise, visit Healthwise. Healthwise, Healthwise for every health decision, and the Healthwise logo are trademarks of Healthwise, Incorporated. Updated visitor guidelines. You are here Home » Alcohol Effects on a Fetus. Top of the page. Topic Overview What effect does alcohol have on a fetus? The effects of alcohol can include: Distinctive facial features.

A child may have a small head, flat face, and narrow eye openings, for instance. This gets more obvious by age 2 or 3 years. Growth problems. Children who were exposed to alcohol before they were born may be smaller than other children of the same age.

The fetus is not as sensitive to the effects of alcohol as is the embryo, and in the third trimester the fetus begins to self-regulate and redirect resources to cope with environmental damages.

Self- regulation is observed in the pre-natal growth deficiencies that accompany FAS, which fall into two broad categories, symmetric or asymmetric intrauterine growth restrictions. If alcohol impacts cellular proliferation in the first and second trimester , or consistently throughout the entire pregnancy , then the growth deficiencies will be symmetric and observed across all parts of the developing fetus.

Asymmetric growth restrictions, which result in a normal-sized head but smaller than normal abdominal cavity, may result in the third semester. The head is a normal size because in the third trimester the fetus can redistribute cardiac resources to the command centers of the body, like the brain and heart, at the expense of other less vital processes like digestion.

There is no point during development when prenatal alcohol exposure lacks consequences, the occurrence of the more severe birth defects correlates with exposure to alcohol in the embryonic stage rather than the fetal stage.

FAS and related alcohol-induced birth defects are an example of what can happen when a mother heavily imbibes alcohol during the course of the pregnancy. In the United States, the Surgeons General caution women against drinking while pregnant and require warnings be displayed on all alcoholic products.

Keywords: Fetal alcohol syndrome , Human development. Developmental Timeline of Alcohol-Induced Birth Defects Maternal consumption of alcohol ethanol during pregnancy can result in a continuum of embryonic developmental abnormalities that vary depending on the severity, duration, and frequency of exposure of ethanol during gestation. Sources Armstrong, Elizabeth M. Bookstein, Fred L. Sampson, Paul D. Connor, and Ann P. Gilbert, Scott. Developmental Biology , 8 ed.

There are still questions about what factors may influence the risk of fetal alcohol syndrome, Chambers said. Those factors could include diet, body fat levels, genetic differences, or other environmental exposures, said Ed Riley of San Diego State University, who also studies prenatal exposure to alcohol. Other studies have found little or no affect on babies born to mothers who drank only occasionally — having one or two drinks a week — throughout pregnancy. But most previous studies relied on mothers' recall of their drinking after birth, whereas in the new study, researchers interviewed women periodically throughout pregnancy.

Riley said the new study adds weight to the argument against drinking any alcohol during pregnancy, and emphasized that the new study showed that any alcohol consumption led to an increased risk.