Alcohol and Pregnancy Don't Mix!
The effects of alcohol use during pregnancy can last for a lifetime. Fetal Alcohol Spectrum Disorder (FASD) is a group of birth defects that are caused when a woman drinks while she is pregnant. The most severe of FASDs is Fetal Alcohol Syndrome (FAS). Children born with FAS often have growth problems, central nervous system problems, and abnormal facial features. There are believed to be at least 3 times as many people affected with FASDs as those with FAS. FASDs can be found in all racial and socio-economic groups.
Below is a collection of information on how alcohol affects the developing child. These effects are lifelong- there is no cure for FASDs but they are 100% preventable.
It is important to note that alcohol can harm a baby at any time during pregnancy - even before the mother knows she is pregnant.
During the first trimester, it can:
- Cause the greatest brain damage
- Impair cell development
- Affect major organs such as the heart, liver and kidneys
- Cause facial malformations
- Cause miscarriage
During the second trimester it can:
- Impair brain development
- Cause miscarriage which may be life threatening for the mother
- Damage muscles, skin, teeth, glands and bones
Third trimester alcohol use may:
- Impair brain and lung development
- Prevent adequate weight gain for the fetus
- Cause premature labor and delivery
There is NO safe time to drink during pregnancy.
There is no known amount of alcohol that is safe during pregnancy.
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Recommended Articles:
How much alcohol is too much during pregnancy?
from March of Dimes
No level of drinking alcohol has been proven safe during pregnancy. According to the U.S. Surgeon General, the patterns of drinking that place a baby at greatest risk for FASDs are binge drinking and drinking seven or more drinks per week (7). However, FASDs can occur in babies of women who drink less.
Researchers are taking a closer look at the more subtle effects of moderate and light drinking during pregnancy.
A 2002 study found that 14-year-old children whose mothers drank as little as one drink a week were significantly shorter and leaner and had a smaller head circumference (a possible indicator of brain size) than children of women who did not drink at all (8).
A 2001 study found that 6- and 7-year-old children of mothers who had as little as one drink a week during pregnancy were more likely than children of non-drinkers to have behavior problems, such as aggressive and delinquent behaviors. These researchers found that children whose mothers drank any alcohol during pregnancy were more than three times as likely as unexposed children to demonstrate delinquent behaviors (9).
A 2007 study suggested that female children of women who drank less than one drink a week were more likely to have behavioral and emotional problems at 4 and 8 years of age. The study also suggested similar effects in boys, but at higher levels of drinking (10).
Other studies report behavioral and learning problems in children exposed to moderate drinking during pregnancy, including attention and memory problems, hyperactivity, impulsivity, poor social and communication skills, psychiatric problems (including mood disorders) and alcohol and drug use (2).
-from March of Dimes
What Kinds of Damage Can Occur
From Alcohol In Utero Exposure?
by Bruce Ritchie - The Triumf Project
In Utero Damage Can Include These Primary Disabilities (Disabilities a child is born with)
- Developmental speech and language disorder
- Developmental coordination disorder
- Central auditory processing disorder
- Loss of intellectual functioning (IQ)
- Severe loss of intellectual potential
- Intellectual Disability
- Rigidity
- Epilepsy
- Deafness
- Cleft palate
- Night terrors
- Sleep disorders
- Tourette's traits
- Asthma
- Precocious puberty
- Sociopathic behavior
- Serious maxilo-facial deformities
- Tremors
- Immune system malfunctioning
- Poor judgment
- Renal (liver) failure
- Cerebral palsy
- Complex seizure disorder
- Developmental delay
- Height and weight deficiencies
- Tight hamstrings
- Cognitive perseveration
- Adaptive esotropia
- Heart failure
- Heart defects
- ADD/ADHD
- Dental abnormalities
- Mild to severe vision problems
- Higher than normal to dangerously high pain tolerance
- Little or no capacity for interpersonal empathy
- Little or no retained memory
- Little or no capacity for moral judgment
- Echolalia
- Autistic traits
- Extreme impulsiveness
- Dyslexia
- Hypersensitivity
And these Secondary Disabilities which develop as a result of failure to properly deal with the primary disabilities
- Learning disabilities
- Early school drop-out
- Juvenile delinquency
- Poverty
- Chronic unemployment
- Sexual acting-out
- Social problems
- Behavioral problems
- Reactive Outbursts
- Homelessness
- Violence
- Crimes against property
- Depression
- Prostitution
- Suicide
- Addiction
- Alcoholism
- Promiscuity
- Sexual assault
- Mental illness
- Early pregnancy
The majority of FASD individuals will display many or even all of these symptoms!
FASD is a lifetime disability. It is not curable. A child does not "grow out of it". However, early diagnosis and intensive, and appropriate, intervention can make an enormous difference in the prognosis for the child. There is a small window of opportunity; up to about age 10 or 12, to achieve the greatest potential for an alcohol affected child. That period is when the greatest development of fixed neural pathways occurs. That is when alternative "coping" pathways are most easily built as "work-arounds" to damaged areas of the brain. Time is of the essence.
While FAE (Fetal Alcohol Effects) individuals may lack the outward physical appearance of alcohol damage, and generally have higher IQ's, the internal damage to the brain and other organs can be just as serious as full FAS. IQ measures convergent fact based thinking. Life skills require divergent adaptive thinking that in FAE individuals will be substantially lower than their IQ. However, because FAE individuals "look normal" they are expected to perform normally. These issues lead to secondary disabilities. Primary disabilities are those the child is born with. Secondary disabilities are those that develop as a result of failure to properly deal with the primary disabilities.
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Brain of baby with Brain of baby with heavy
no exposure to alcohol prenatal exposure to alcoholPhoto courtesy of Sterling Clarren, MD
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Fetal Brains Suffer Badly From Effects of Alcohol
New York Times
November 4, 2003
By LINDA CARROLL
Thirty years ago, scientists linked prenatal alcohol exposure with a perplexing pattern of birth defects including neurological problems, low birth weight, mental retardation and a set of facial malformations. Up to that time, many doctors had assumed that alcohol was so harmless that it was sometimes administered intravenously to women who were thought to be at risk of losing their pregnancies.
But in recent decades, scientists have discovered that alcohol can be remarkably toxic — more than any other abused drug — to developing fetuses. New research with imaging techniques is helping experts uncover which parts of the developing brain are damaged by alcohol exposure. By pinpointing the damaged areas, they are beginning to understand the origins of the problem behaviors and learning disabilities linked to alcohol. Scientists are also homing in on a protein important to the developing brain that is affected by alcohol. It is possible, they say, that a medication can be created to protect the brains of developing fetuses, even if pregnant women cannot quit drinking. It is not surprising that it has taken researchers so long to tease out the link between alcohol exposure and birth defects. For one thing, the effects of alcohol exposure seem to vary widely. Some fetuses seem to escape unscathed, even when their mothers drink heavily, while others are severely damaged. No one knows why.
"It's not like thalidomide, where anyone who took it had an affected child," said Dr. Sandra W. Jacobson, a professor at Wayne State School of Medicine in Detroit, referring to the morning-sickness drug linked to birth defects in the late 1950's and early 1960's. "There's a range with alcohol. You might get the full-blown syndrome in 4 out of 100 heavy drinkers."
There are also many babies who are affected, but not severely enough for the syndrome to be diagnosed. Some with fetal alcohol effects may appear relatively normal but have behavioral problems and learning deficits like those with the syndrome. Further complicating matters is the question of how much alcohol it takes to cause harm. In the past few years, successive studies have shown an effect at increasingly lower levels. One study, published last year, found a small but significant effect on average in children born to women who consumed just a drink and a half a week. "We were surprised by this," said the lead author, Dr. Nancy Day, a professor of psychiatry at the Western Psychiatric Institute and Clinic in Pittsburgh. The women in the study were recruited from a prenatal clinic between May 1983 and July 1985. "The children were in the normal range of growth," Dr. Day said, "but if you compare them to children whose mothers didn't drink at all, they weighed less, were shorter and had smaller head circumferences."
The effect of low levels of alcohol appears to be subtle, said Dr. James R. West, head of the department of anatomy and neurobiology at the Texas A&M medical school. "Perhaps instead of having an I.Q. of 120, you might end up with 115," he said. "You might seem perfectly normal, but not have the motor skills to make the high school football team." Another factor making it difficult to tease out the impact of alcohol is its widespread effects on the developing brain and body. "Alcohol is a dirty drug, " Dr. West added. "It affects a number of different neurotransmitters, and all cells can take it up." Compare this with cocaine, Dr. West said, which is taken up by only one neurotransmitter. It is also difficult to identify the effects of alcohol because a woman's drinking habits seem to make a big difference. Experts say it matters when a pregnant woman drinks, how often she drinks and what her pattern of drinking is: whether she drinks small amounts daily or periodically binges.
Drinking in the first trimester can lead to facial malformations, while in the second it can interrupt nerve formation in the brain, Dr. West said. During the third, it can kill existing neurons and interfere with nervous system development, he added. Researchers have also determined that babies are more likely to be affected if mothers drink in a binge pattern, like five drinks one day rather than a single drink daily, Dr. Jacobson of Wayne State said. Because alcohol affects so many sites in the brain, researchers have come to believe that alcohol is far worse for the developing fetus than any other abused drug. Dr. Jacobson's study included cocaine users who also used varying quantities of alcohol. "We found more serious cognitive impairment in relation to alcohol than cocaine or other drugs, including marijuana and smoking," Dr. Jacobson said. The damage done to fetuses often has been wrongly connected to cocaine, many experts say.
"The consensus, I think, at this point is that most of the adverse effects that had been reported due to cocaine and crack use were from alcohol use," said Dr. Kenneth R. Warren, the director of the office of scientific affairs at the National Institute on Alcohol Abuse and Alcoholism. "It is the leading cause of birth defects due to an ingested environmental substance in this country."
In 1973, researchers coined the phrase fetal alcohol syndrome to describe babies born with a certain pattern of neurologic and physiologic defects related to alcohol exposure in utero. Early on, it was clear that exposed children were wired differently from normal ones and that they exhibited an array of disabilities. Dr. Ann P. Streissguth, the director of the fetal alcohol and drug unit at the University of Washington and a professor at the medical school there, ticked off a list: "These included attention problems, hyperactivity, learning problems — particularly in arithmetic — language problems, memory problems, fine and gross motor problems, poor impulse control, poor judgment, intellectual deficits and difficulty integrating past experience to plan and organize future behavior."
Researchers wondered whether specific areas of the brain were being consistently harmed by alcohol exposure in utero. Poor judgment, for example, might point to damage to the frontal lobes. The lobes, as the control center of the brain, are involved in planning, organizing and inhibiting inappropriate responses, the researchers say. Thirty years ago, the only way researchers could learn about the effects of alcohol on the brain was to study children who died shortly after birth.
"We knew from brain autopsies that in severe cases the brains were terribly disorganized," said Dr. Edward P. Riley, the director of the Center for Behavioral Teratology at San Diego State University. Now, researchers use imaging techniques like M.R.I.'s to look at the damage caused by alcohol. Several recent studies using magnetic resonance imaging have shown damage to the corpus callosum, a band of nerve fibers that connects the left and right sides of the brain. A report published in 2002 compared the brain scans of adults and children who had severe or mild alcohol-related disabilities with the scans of healthy counterparts. The researchers found that the corpus callosa were abnormally shaped in 80 percent of those who had been exposed to alcohol in utero.
Another study found that the corpus callosum was smaller and shifted forward in children and young adults with the syndrome. Using a technique known as diffusion tensor imaging to look closer at the corpus callosum, researchers at Emory University have seen abnormalities in the myelin, the substance that insulates nerve cells.
When the myelin is damaged, signals do not carry as crisply through the cells, said Dr. Claire D. Coles, director of the Fetal Alcohol Center at the Marcus Institute and a professor of psychiatry and behavioral sciences at Emory. Another study published in 2002 found that frontal lobe structures were smaller in teenagers and young adults who had been exposed to alcohol prenatally. By pinpointing which sections of the brain are most likely to be damaged by alcohol, scientists may find a way to block its effects.
Researchers recently recognized that some of alcohol's effects were similar to those experienced by children born with defects in genes that control L1 adhesion cells. Fetal cells that are destined to grow into the brain and nervous system bind to one another with the help of adhesion molecules like L1, said Dr. Michael E. Charness, an associate professor of neurology at Harvard. In laboratory experiments, Dr. Charness and his colleagues showed that alcohol could interfere with L1's stickiness, thus hampering crucial cell-to-cell attachments. In an article published in The Proceedings of the National Academy of Sciences in July, they showed that a protein, NAP, could block alcohol's effect on L1. When NAP was given to mice exposed to alcohol, the protein appeared to stave off neurological effects.
"The idea of giving drugs to pregnant women is controversial," Dr. Charness said. "Drugs may have their own risks." But, he said, there are areas of the world where fetal alcohol syndrome is a huge problem. In parts of South Africa, the incidence of the syndrome in first graders is around 4.5 percent, he said. "The rate of drinking is high," Dr. Charness added. "And the women won't stop drinking despite interventions. It might be reasonable to give them a drug that can prevent the more serious effects of alcohol."
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Alcohol, Chemistry and You
Maternal Drinking and Child Development
Dr. Bill Boggan
Drinking ethanol while pregnant is the same as feeding ethanol to the baby. Since ethanol freely mixes with the body water through diffusion, it is rapidly distributed into the blood. Since the mothers blood circulation is connected to that of the fetus, the alcohol is rapidly transported to the fetus to be distributed in the cells and tissues of the infant and into the fluid surrounding the fetus.
Once distributed, alcohol has the opportunity to directly influence the growth and development of the child. Alterations by ethanol in the function of growth factors and other chemical mediators known to be important in guiding the development of the fetus have in fact been amply demonstrated.
Ethanol can also influence fetal development indirectly by exerting effects on the mother, which in turn influence the fetus. These indirect effects can include altering the nutritional status of the mother so that the fetus gets less nutrition; altering the function of the placenta, so that fewer nutrients and/or oxygen gets to the fetus; producing metabolites of ethanol such as acetaldehyde, which is known to be toxic; and compounding the effects of other drugs (therapeutic and nontherapeutic) that mother might be taking. Each of these possibilities has been the focus of extensive investigation in both animal and human studies (10th Special Report to the U.S. Congress on Alcohol and Health, 2000).
The degree of damage incurred by the fetus is influenced by several factors, including the period of gestation when alcohol exposure occurs, how much the mother drinks during pregnancy, the pattern and timing of her drinking, and the genetic makeup of both mother and child. Because of these factors and others, it is not possible to know what level of drinking is safe for each individual, and so abstinence is recommended to all women who are pregnant, nursing, or who may become pregnant. Recent studies have shown several risk factors for delivering alcohol-affected children. These include alcohol consumption during pregnancy (and specifically, binge drinking, maternal age > 25, low socioeconomic status, unemployment, living in a culture that is tolerant of heavy drinking, social transience, and being separated, divorced or never married (May, 1995).
Manifestations of Prenatal Alcohol Exposure
The detrimental effects of prenatal exposure to ethanol were long suspected (cf Judges 13:3-5), but only first documented by Lemoine et al (1968) in France and later by Jones and Smith (1973) and Jones et al (1973) in the United States. Early diagnoses and descriptions were based on "the highly distinctive appearance of children of alcoholic parents, particularly alcoholic mothers" and amplified to include not only characteristic facial features, but also growth deficiency and central nervous system dysfunction. Thus, the term, Fetal Alcohol Syndrome (FAS) was coined (Jones and Smith, 1973) and defined on the basis of these three criteria. FAS is now recognized as the most common cause of mental retardation in America, surpassing Down syndrome, cerebral palsy, and spina bifida.
While FAS is the disorder that enjoys the most public awareness, other alcohol-related developmental disorders, which are more common than FAS (conservative estimates suggest a 10:1 ratio), go relatively unnoticed. Unfortunately, if a child does not exhibit all three criteria for an FAS diagnosis, the child may go unrecognized and/or untreated, even though (s)he has some of the same cognitive and behavioral problems due to the effects of alcohol on the brain and may often fall "through the cracks". When left untreated, these individuals are at risk to develop secondary disabilities, a term used by Streissguth and colleagues (Streissguth, 1997, Streissguth and Kanter, 1999) to describe the host of problems that often arise when individuals with prenatal alcohol exposure do not receive support or assistance. These include mental health problems, disrupted school experiences, trouble with the law, incarceration, alcohol and drug abuse, and sexual misconduct or victimization.
The manifestations of Prenatal Exposure to Alcohol fall on a continuum from severely affected (including death) to near normalcy. The most severely affected show:
1. particular craniofacial patterns
2. pre-and/or postnatal growth deficiencies
3. central nervous system dysfunctions
4. psychiatric disturbances; and
5. impairments in psychosocial skills.
Within these categories are a multitude of more specific problems as capsulated below. Less severe impact may result in the individual manifesting only subsets of these (10th Special Report to Congress, 2000).
The craniofacial features of children with FAS are fairly readily distinquished from those of normal children and include small eye slits (palpebral fissures), a flat nasal bridge, and absent philtrum.
Growth deficiencies include being small for gestational age and retarded postnatal growth both in body size, weight, and cranial size. Brain insults include:
1. small or even absent corpus callosum;
2. smaller cerebellum, involved in coordination and balance;
3. diminished size of the vermis; and
4. significant reductions in the volume of the basal ganglia.
In addition, the prefrontal cortex important in cognitive functioning, and the hippocampus, involved in learning and memory, also appear to be damaged. Also, there may be alterations in babies’ cry patterns (Zeskind et al, 1996) and brain electrical activity (Kaneko et al, 1996a,b), which also reflect brain damage and CNS dysfunction.
The damage to the brain translates into a host of cognitive and behavioral deficits (Mattson & Riley, 1998) including mental retardation, apparent learning and memory deficits , lack of executive functioning, hyperactivity, attention deficits, loss of motor control, and inability to recognize and utilize visual/spatial relationships.
References:
Famy, C., Streissguth, A.P., and Unis, A.S. (1998) Mental illness in adults with fetal alcohol syndrome or fetal alcohol effects. American Journal of Psychiatry 155(4):522-554.
Gordis, E. (1991) Alcohol Research: Promise for the Decade. Rockville, MD: National Institute on Alcohol Abuse and Alcoholism.
Jones, K.L. and Smith, D.W. (1973). Recognition of the fetal alcohol syndrome in early infancy. Lancet 2:999-1001.
Jones, K.L., Smith, D.W., Ulleland, C.N., and Streissguth, A.P. (1973) Pattern of malformations in offspring of chronic alcoholic mothers. Lancet 1 (815):1267-1271.
Kaneko, W.M., Ehlers, C.L., Philips, E.L., and Riley, E.P. (1996a). Auditory event-related potentials in fetal alcohol syndrome and Down’s syndrome children. Alcohol Clinical and Experimental Research 20(1):35-42.
Kaneko, W.M., Phillips, E.L., Riley, E.P., and Ehlers, C.L. (1996b). EEG findings in fetal alcohol syndrome and Down syndrome children. Electroencephalography and Clinical Neurophysiology 98(1):20-28.
Lemoine, P., Harouseau, H., Borteryu, J.T., Menuet, J.C. (1968). Les enfants des parents alcooliques: Anomalies observees apropos de 127 cas. Ouest Medical 21:476 – 482.
Mattson, S.N., Jernigan, T.L., and Riley, E.P. (1994) MRI and prenatal alcohol exposure: Images provide insight to FAS. Alcohol Health and Research World 18(1):49 – 52.
Mattson, S.N. and Riley, E.P. (1998). A review of the neurobehavioral deficits in children with fetal alcohol syndrome or prenatal exposure to alcohol. Alcoholism: Clinical and Experimental Research 22:279-294.
May, PA (1995). A multiple-level comprehensive approach to the prevention of fetal alcohol syndrome (FAS) and other alcohol-related birth defects (ARBD). International Journal of Addiction 30:1549-1602.
Sampson, P.D., Streissguth, A.P., Bookstein, F.L., and Barr, H.M. (2000). On categorizations in analyses of alcohol teratogenesis, Environmental Health Perspectives, 108 (3):1-15.
Streissguth, A.P. (1997). Fetal Alcohol Syndrome: A Guide for Families and Communities. Paul Brooks Publishing Co: Baltimore, MD.
Streissguth, A.P. and Kanter, J. (1999) The Challenge of Fetal Alcohol Syndrome: Overcoming Secondary Disabilities. University of Washington Press, Seattle.
Tenth Special Report to the US Congress on Alcohol and Health (2000). US Departmentof Health and Human Services (NIH publication number 00-1583). Washington, DC.
Thomas, S.E., Kelly, S.J., Mattson, S.N., Riley, E.P. (1998). Comparison of social abilities of children with fetal alcohol syndrome to those of children with similar IQ scores and normal controls. Alcoholism: Clinical and Experimental Research 22:528-533.
Zeskind, P.S., Platzman, K., Coles, C.D., and Schuetze, P.A. (1996). Cry analysis detects subclinical effects of prenatal alcohol exposure in newborn infants. Infant Behavior and Development 19(4):497-500.
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