The key of FASD can vary between individuals exposed to alcohol during pregnancy. While consensus exists for the definition and diagnosis of FAS, minor variations among the systems lead to differences in definitions and diagnostic cut-off criteria for other diagnoses across the FASD continuum. The central nervous system damage criteria particularly lack clear consensus. A working knowledge of the key features is helpful in understanding FASD diagnoses and conditions, and each is reviewed with attention to similarities and differences across the four diagnostic systems. More than 400 problems, however, can occur with FASD.

In terms of FASD, growth deficiency is defined as significantly below average height, weight or both due to prenatal alcohol exposure, and can be assessed at any point in the lifespan. Growth measurements must be adjusted for parental height, gestational age (for a premature infant), and other postnatal insults (e.g., poor nutrition), although birth height and weight are the preferred measurements. Deficiencies are documented when height or weight falls at or below the 10th percentile of standardized growth charts appropriate to the population.

Criteria for FASD are least specific in the IOM diagnostic system ("low birth weight..., decelerating weight not due to nutrition..., [or] disproportional low weight to height" p. 4 of executive summary), while the CDC and Canadian guidelines use the 10th percentile as a cut-off to determine growth deficiency. The "4-Digit Diagnostic Code" allows for mid-range gradations in growth deficiency (between the 3rd and 10th percentiles) and severe growth deficiency at or below the 3rd percentile. Growth deficiency (at severe, moderate, or mild levels) contributes to diagnoses of FAS and pFAS, but not ARND or static encephalopathy.

Growth deficiency is ranked as follows by the "4-Digit Diagnostic Code":

- Severe: Height and weight at or below the 3rd percentile.

- Moderate: Either height or weight at or below the 3rd percentile, but not both.

- Mild: Either height or weight or both between the 3rd and 10th percentiles.

- None: Height and weight both above the 10th percentile.

In the initial studies that discovered FAS, growth deficiency was a requirement for inclusion in the studies; thus, all the original people with FAS had growth deficiency as an artifact of sampling characteristics used to establish criteria for the syndrome. That is, growth deficiency is a key feature of FASD because growth deficiency was a criterion for inclusion in the study that defined FAS. This suggests growth deficiency may be less critical for understanding the disabilities of FASD than the neurobehavioral sequelae to the brain damage.

Alcohol in pregnancy is the use of alcohol (also known formally as ethanol) during gestation. This also includes the time period between conception and awareness of the pregnancy. Alcohol use not only can result in Fetal Alcohol Spectrum Disorder (FASD), but it can result in one or many other disorders and conditions. Not all women who consume alcohol during pregnancy will have a baby with all of the features and characteristics of FASP. Alcohol use during pregnancy also can cause spontaneous abortion, stillbirth, low birthweight, and prematurity. Not all infants exposed to alcohol in utero will have defects related to the alcohol consumption. Alcohol use during pregnancy can also result in the inability to care for an infant after the birth if the drinking continues. The use of alcohol during pregnancy is associated with domestic violence and potential harm to the infant.

Different body systems in the infant grow, mature and develop at specific times during gestation. The consumption of alcohol during one or more of these developmental stages may only result in one or few conditions.

From conception and to the third week, the most susceptible systems and organs are the brain, spinal cord, and heart. Though these body systems complete their development later in the pregnancy, the effects of alcohol consumption early in the pregnancy can result in defects to these systems and organs.

During the fourth week of gestation, the limbs are being formed and it is at this point that alcohol can effect the development of arms, legs, fingers and toes. The eyes and ears also form during the fourth week and are more susceptible to the effects of alcohol.

By the sixth week of gestation, the teeth and palate are forming and alcohol consumption at this time will affect these structures.

By the 20th week of gestation the formation of organs and organ systems is well-developed. The infant is still susceptible to the damaging effects of alcohol.

The baby’s brain, body, and organs are developing throughout pregnancy and can be affected by exposure to alcohol at any time. Because every pregnancy is different, drinking alcohol may hurt one baby more than another. A child that has been affected by alcohol before birth may be appear 'normal' at birth. Intellectual disabilities may not appear until the child begins school.

Drug use during pregnancy can have temporary or permanent effects on the fetus. Any drug that acts during embryonic or fetal development to produce a permanent alteration of form or function is known as a teratogen. Drugs may refer to both pharmaceutical drug and recreational drugs.

Prenatal cocaine exposure (PCE), theorized in the 1970s, occurs when a pregnant woman uses cocaine and thereby exposes her fetus to the drug. "Crack baby" was a term coined to describe children who were exposed to crack (freebase cocaine in smokable form) as fetuses; the concept of the crack baby emerged in the US during the 1980s and 1990s in the midst of a crack epidemic. Other terms are "cocaine baby" and "crack kid". Early studies reported that people who had been exposed to crack in utero would be severely emotionally, mentally, and physically disabled; this belief became common in the scientific and lay communities. Fears were widespread that a generation of crack babies were going to put severe strain on society and social services as they grew up. Later studies failed to substantiate the findings of earlier ones that PCE has severe disabling consequences; these earlier studies had been methodologically flawed (e.g. with small sample sizes and confounding factors). Scientists have come to understand that the findings of the early studies were vastly overstated and that most people who were exposed to cocaine "in utero" do not have disabilities.

No specific disorders or conditions have been found to result for people whose mothers used cocaine while pregnant. Studies focusing on children of six years and younger have not shown any direct, long-term effects of PCE on language, growth, or development as measured by test scores. PCE also appears to have little effect on infant growth.

However, PCE is associated with premature birth, birth defects, attention deficit hyperactivity disorder, and other conditions. The effects of cocaine on a fetus are thought to be similar to those of tobacco and less severe than those of alcohol. No scientific evidence has shown a difference in harm to a fetus between crack and powder cocaine.

PCE is very difficult to study because it very rarely occurs in isolation: usually it coexists with a variety of other factors, which may confound a study's results. Thus, studies have failed to clearly show that PCE has negative cognitive effects, partly because such effects may be due to concurrent factors. Pregnant mothers who use cocaine often use other drugs in addition, or they may be malnourished and lacking in medical care. Children in households where cocaine is abused are at risk of violence and neglect, and those in foster care may experience problems due to unstable family situations. Factors such as poverty that are frequently associated with PCE have a much stronger influence on children's intellectual and academic abilities than does exposure to cocaine in isolation. Thus researchers have had difficulty in determining which effects result from PCE and which result from other factors in the children's histories.

Cocaine use during pregnancy can be discovered by asking the mother, but sometimes women will not admit to having used drugs. Mothers may lie for fear of prosecution or having their children taken away, but even when they are willing to tell the truth their memories may not be very accurate. It may also not be possible to be sure of the purity of the drug they have taken. More reliable methods for detecting cocaine exposure involve testing the newborn's hair or meconium (the infant's earliest stool). Hair analysis, however, can give false positives for cocaine exposure, and a newborn may not have enough hair to test. The newborn's urine can be tested for cocaine and metabolites, but it must be collected as soon as possible after birth. It is not known how long after exposure the markers will still show up in a newborn's urine. The mother's urine can also be tested for drugs, but it cannot detect drugs used too far in the past or determine how much or how often the drugs were used. Tests cannot generally detect cocaine use over a week prior to sample collection. Mothers are more honest about cocaine use when their urine is also tested, but many users still deny it. Both maternal and neonatal urine tests can give false negatives.

Developmental toxicity is any structural or functional alteration, reversible or irreversible, which interferes with homeostasis, normal growth, differentiation, development or behavior, and which is caused by environmental insult (including drugs, lifestyle factors such as alcohol, diet, and environmental toxic chemicals or physical factors). It is the study of adverse effects on the development of the organism resulting from exposure to toxic agents before conception (either parent), during prenatal development, or post-natally until puberty. The substance that causes developmental toxicity from embryonic stage to birth is called teratogens. The effect of the developmental toxicants depends on the type of substance, dose and duration and time of exposure.

Certain Pathogens are also included since the toxins they secrete are known to cause adverse effects on the development of the organism when the mother or fetus is infected. Developmental toxicology is a science studying adverse developmental outcomes. This term has widely replaced the early term for the study of primarily structural congenital abnormalities, teratology, to enable inclusion of a more diverse spectrum of congenital disorders. Typical factors causing developmental toxicity are radiation, infections (e.g. rubella), maternal metabolic imbalances (e.g. alcoholism, diabetes, folic acid deficiency), drugs (e.g. anticancer drugs, tetracyclines, many hormones, thalidomide), and environmental chemicals (e.g. mercury, lead, dioxins, PBDEs, HBCD, tobacco smoke). The first-trimester exposure is considered the most potential for developmental toxicity.

Once fertilization has taken place, the toxicants in the environment can pass through the mother to the developing embryo or fetus across the placental barrier. The fetus is at greatest risk during the first 14th to 60th day of the pregnancy when the major organs are being formed. However, depending on the type of toxicant and amount of exposure, a fetus can be exposed toxicant at any time during pregnancy. For example, exposure to a particular toxicant at one time in the pregnancy may result in organ damage and at another time in the pregnancy could cause death of the fetus and miscarriage. There are a number of chemicals, biological agents (such as bacteria and viruses), and physical agents (such as radiation) used in a variety of workplaces that are known to cause developmental disorders. Developmental disorders can include a wide range of physical abnormalities, such as bone or organ deformities, or behavioral and learning problems, such as a mental retardation. Exposures to some chemicals during pregnancy can lead to the development of cancer later in the life of the child and are called transgenerational carcinogens. Exposure to toxicants during the second and the third trimester of a pregnancy can lead to slow fetal grown and result in low birth weight.

Alcohol abuse among pregnant women causes their baby to develop fetal alcohol syndrome. Fetal alcohol syndrome is the pattern of physical abnormalities and the impairment of mental development which is seen with increasing frequency among children with alcoholic mothers. Alcohol exposure in a developing fetus can result in slowed development of the fetal brain, resulting in severe retardation or death. Surviving infants may suffer severe abnormalities such as abnormal eyes, fissures, lips and incomplete cerebella. Some infants may develop lung disease. It is even possible that the baby throughout pregnancy will develop heart defects such as ventricular septal defect or atrial septal defect. Experts suggest that pregnant women take no more than one unit of alcohol per day. However, other organizations advise complete abstinence from alcohol while pregnant.

Alcohol (also known as ethanol) has a number of effects on health. Short-term effects of alcohol consumption include intoxication and dehydration. Long-term effects of alcohol consumption include changes in the metabolism of the liver and brain and alcoholism. Alcohol intoxication affects the brain, causing slurred speech, clumsiness, and delayed reflexes. Alcohol stimulates insulin production, which speeds up glucose metabolism and can result in low blood sugar, causing irritability and possibly death for diabetics. A 2014 World Health Organization report found that harmful alcohol consumption caused about 3.3 million deaths annually worldwide.

However, some effects of alcohol consumption are beneficial. Although even moderate alcohol consumption increased the risk of death in younger people, it has been shown to "decrease" the risk of death for individuals ages 55+ (due to decreased risk of ischemic heart disease).

The median lethal dose of alcohol in test animals is a blood alcohol content of 0.45%. This is about six times the level of ordinary intoxication (0.08%), but vomiting or unconsciousness may occur much sooner in people who have a low tolerance for alcohol. The high tolerance of chronic heavy drinkers may allow some of them to remain conscious at levels above 0.40%, although serious health hazards are incurred at this level.

Alcohol also limits the production of vasopressin (ADH) from the hypothalamus and the secretion of this hormone from the posterior pituitary gland. This is what causes severe dehydration when alcohol is consumed in large amounts. It also causes a high concentration of water in the urine and vomit and the intense thirst that goes along with a hangover.

Stress, hangovers, and the oral contraceptive pill may increase the desire for alcohol because these things will lower the level of testosterone and alcohol will acutely elevate it. Tobacco has the same effect of increasing the craving for alcohol.

Individuals with an alcohol use disorder will often complain of difficulty with interpersonal relationships, problems at work or school, and legal problems. Additionally, people may complain of irritability and insomnia. Alcohol abuse is also an important cause of chronic fatigue.

Signs of alcohol abuse are related to alcohol's effects on organ systems. However, while these findings are often present, they are not necessary to make a diagnosis of alcohol abuse. Signs of alcohol abuse show its drastic effects on the central nervous system, including inebriation and poor judgment; chronic anxiety, irritability, and insomnia. Alcohol's effects on the liver include elevated liver function tests (classically AST is at least twice as high as ALT). Prolonged use leads to cirrhosis and liver failure. With cirrhosis, patients develop an inability to process hormones and toxins. The skin of a patient with alcoholic cirrhosis can feature cherry angiomas, palmar erythema and — in acute liver failure — jaundice and ascites. The derangements of the endocrine system lead to the enlargement of the male breasts. The inability to process toxins leads to liver disease, such as hepatic encephalopathy.

Alcohol abuse can result in brain damage which causes impairments in executive functioning such as impairments to working memory, visuospatial skills, and can cause an abnormal personality as well as affective disorders to develop. Binge drinking is associated with individuals reporting fair to poor health compared to non-binge drinking individuals and which may progressively worsen over time. Alcohol also causes impairment in a person's critical thinking. A person's ability to reason in stressful situations is compromised, and they seem very inattentive to what is going on around them. Social skills are significantly impaired in people suffering from alcoholism due to the neurotoxic effects of alcohol on the brain, especially the prefrontal cortex area of the brain. The social skills that are impaired by alcohol abuse include impairments in perceiving facial emotions, difficulty with perceiving vocal emotions and theory of mind deficits; the ability to understand humour is also impaired in alcohol abusers. Adolescent binge drinkers are most sensitive to damaging neurocognitive functions especially executive functions and memory. People who abuse alcohol are less likely to survive critical illness with a higher risk for having sepsis and were more likely to die during hospitalization.

Alcohol tolerance refers to the bodily responses to the functional effects of ethanol in alcoholic beverages. This includes direct tolerance, speed of recovery from insobriety and resistance to the development of alcoholism.

Signs and symptoms of alcohol withdrawal occur primarily in the central nervous system. The severity of withdrawal can vary from mild symptoms such as sleep disturbances and anxiety to severe and life-threatening symptoms such as delirium, hallucinations, and autonomic instability.

Withdrawal usually begins 6 to 24 hours after the last drink. It can last for up to one week. To be classified as alcohol withdrawal syndrome, patients must exhibit at least two of the following symptoms: increased hand tremor, insomnia, nausea or vomiting, transient hallucinations (auditory, visual or tactile), psychomotor agitation, anxiety, tonic-clonic seizures, and autonomic instability.

The severity of symptoms is dictated by a number of factors, the most important of which are degree of alcohol intake, length of time the individual has been using alcohol, and previous history of alcohol withdrawal. Symptoms are also grouped together and classified:

- Alcohol hallucinosis: patients have transient visual, auditory, or tactile hallucinations, but are otherwise clear.

- Withdrawal seizures: seizures occur within 48 hours of alcohol cessations and occur either as a single generalized tonic-clonic seizure or as a brief episode of multiple seizures.

- Delirium tremens: hyperadrenergic state, disorientation, tremors, diaphoresis, impaired attention/consciousness, and visual and auditory hallucinations. This usually occurs 24 to 72 hours after alcohol cessation. Delirium tremens is the most severe form of withdrawal and occurs in 5 to 20% of patients experiencing detoxification and 1/3 of patients experiencing withdrawal seizures.

Typically the severity of the symptoms experienced will depend on the amount and duration of prior alcohol consumption, as well as the number and severity of previous withdrawals. Even the most severe of these symptoms can occur in as little as 2 hours after cessation; therefore, the overall unpredictability necessitates either pre-planned hospitalization, treatment coordinated with a doctor, or at the very least rapid access to medical care, and a supporting system of friends or family should be introduced prior to addressing detoxification. In many cases, however, symptoms follow a reasonably predictable time frame as exampled below:

Six to 12 hours after the ingestion of the last drink, withdrawal symptoms such as shaking, headache, sweating, anxiety, nausea or vomiting occur. Other comparable symptoms may also exist in this period. Twelve to 24 hours after cessation, the condition may progress to such major symptoms as confusion, hallucinations (with awareness of reality), tremor, agitation, and similar ailments.

At 24 to 48 hours following the last ethanol ingestion, the possibility of seizures should be anticipated. Meanwhile, none of the earlier withdrawal symptoms will have abated. Seizures carry the risk of death for the alcoholic.

Although, most often, the patient's condition begins to improve past the 48-hour mark, it can sometimes continue to increase in severity to delirium tremens, characterized by hallucinations that are indistinguishable from reality, severe confusion, more seizures, high blood pressure and fever which can persist anywhere from 4 to 12 days.

The long-term effects of alcohol (also known formally as ethanol) consumption range from cardioprotective health benefits for low to moderate alcohol consumption in industrialized societies with higher rates of cardiovascular disease to severe detrimental effects in cases of chronic alcohol abuse. Health effects associated with alcohol intake in large amounts include an increased risk of alcoholism, malnutrition, chronic pancreatitis, ], and cancer. In addition, damage to the central nervous system and peripheral nervous system can occur from chronic alcohol abuse. The long-term use of alcohol is capable of damaging nearly every organ and system in the body. The developing adolescent brain is particularly vulnerable to the toxic effects of alcohol. In addition, the developing fetal brain is also vulnerable, and fetal alcohol spectrum disorders (FASDs) may result if pregnant mothers consume alcohol.

The inverse relation in Western cultures between alcohol consumption and cardiovascular disease has been known for over 100 years. Many physicians do not promote alcohol consumption, however, given the many health concerns associated with it, some suggest that alcohol should be regarded as a recreational drug, and promote exercise and good nutrition to combat cardiovascular disease. Others have argued that the benefits of moderate alcohol consumption may be outweighed by other increased risks, including those of injuries, violence, fetal damage, liver disease, and certain forms of cancer. Alcohol liver disease (ALD) accounted for four fifths of all chronic diseases in Ireland in 2013.

Withdrawal effects and dependence are also almost identical. Alcohol at moderate levels has some positive and negative effects on health. The negative effects include increased risk of liver diseases, oropharyngeal cancer, esophageal cancer and pancreatitis. Conversely moderate intake of alcohol may have some beneficial effects on gastritis and cholelithiasis. Of the total number of deaths and diseases caused by alcohol, most happen to the majority of the population who are moderate drinkers, rather than the heavy drinker minority. Chronic alcohol misuse and abuse has serious effects on physical and mental health. Chronic excess alcohol intake, or alcohol dependence, can lead to a wide range of neuropsychiatric or neurological impairment, cardiovascular disease, liver disease, and malignant neoplasms. The psychiatric disorders which are associated with alcoholism include major depression, dysthymia, mania, hypomania, panic disorder, phobias, generalized anxiety disorder, personality disorders, schizophrenia, suicide, neurologic deficits (e.g. impairments of working memory, emotions, executive functions, visuospatial abilities and gait and balance) and brain damage. Alcohol dependence is associated with hypertension, coronary heart disease, and ischemic stroke, cancer of the respiratory system, and also cancers of the digestive system, liver, breast and ovaries. Heavy drinking is associated with liver disease, such as cirrhosis. Excessive alcohol consumption can have a negative impact on aging.

Recent studies have focused on understanding the mechanisms by which moderate alcohol consumption confers cardiovascular benefit.

The short-term effects of alcohol consumption range from a decrease in anxiety and motor skills at lower doses to unconsciousness, anterograde amnesia, and central nervous system depression at higher doses. Cell membranes are highly permeable to alcohol, so once alcohol is in the bloodstream it can diffuse into nearly every cell in the body.

The concentration of alcohol in blood is measured via blood alcohol content (BAC). The amount and circumstances of consumption play a large part in determining the extent of intoxication; for example, eating a heavy meal before alcohol consumption causes alcohol to absorb more slowly. Hydration also plays a role, especially in determining the extent of hangovers. After excessive drinking, unconsciousness can occur and extreme levels of consumption can lead to alcohol poisoning and death (a concentration in the blood stream of 0.40% will kill half of those affected). Alcohol may also cause death indirectly, by asphyxiation from vomit.

Alcohol can greatly exacerbate sleep problems. During abstinence, residual disruptions in sleep regularity and sleep patterns are the greatest predictors of relapse.

About one third of children whose mothers are taking this drug during pregnancy typically have intrauterine growth restriction with a small head and develop minor dysmorphic craniofacial features and limb defects including hypoplastic nails and distal phalanges (birth defects). A smaller population will have growth problems and developmental delay, or intellectual disability. Methemoglobinemia is a rarely seen side effect.

Heart defects and cleft lip may also be featured.

The apprehension is not necessarily data driven and is a cautionary response to the lack of clinical studies in pregnant women. The indication is a trade-off between the adverse effects of the drug, the risks associated with intercurrent diseases and pregnancy complications, and the efficiency of the drug to prevent or ameliorate such risks. In some cases, the use of drugs in pregnancy carries benefits that outweigh the risks. For example, high fever is harmful for the fetus in the early months, thus the use of paracetamol (acetaminophen) is generally associated with lower risk than the fever itself. Similarly, diabetes mellitus during pregnancy may need intensive therapy with insulin to prevent complications to mother and baby. Pain management for the mother is another important area where an evaluation of the benefits and risks is needed. NSAIDs such as Ibuprofen and Naproxen are probably safe for use for a short period of time, 48–72 hours, once the mother has reached the second trimester. If taking aspirin for pain management the mother should never take a dose higher than 100 mg.

Alcoholism, also known as alcohol use disorder (AUD), is a broad term for any drinking of alcohol that results in mental or physical health problems. The disorder was previously divided into two types: alcohol abuse and alcohol dependence. In a medical context, alcoholism is said to exist when two or more of the following conditions is present: a person drinks large amounts over a long time period, has difficulty cutting down, acquiring and drinking alcohol takes up a great deal of time, alcohol is strongly desired, usage results in not fulfilling responsibilities, usage results in social problems, usage results in health problems, usage results in risky situations, withdrawal occurs when stopping, and alcohol tolerance has occurred with use. Risky situations include drinking and driving or having unsafe sex, among other things. Alcohol use can affect all parts of the body, but it particularly affects the brain, heart, liver, pancreas, and immune system. This can result in mental illness, Wernicke–Korsakoff syndrome, an irregular heartbeat, cirrhosis of the liver, and an increase in the risk of cancer, among other diseases. Drinking during pregnancy can cause damage to the baby resulting in fetal alcohol spectrum disorders. Women are generally more sensitive then men to the harmful physical and mental effects of alcohol.

Environmental factors and genetics are two components that are associated with alcoholism, with about half the risk attributed to each . A person with a parent or sibling with alcoholism is three to four times more likely to become an alcoholic themselves. Environmental factors include social, cultural, and behavioral influences. High stress levels, anxiety, as well as inexpensive cost and easy accessibility to alcohol increase the risk. People may continue to drink partly to prevent or improve symptoms of withdrawal. After a person stops drinking alcohol, they may experience a low level of withdrawal lasting for months. Medically, alcoholism is considered both a physical and mental illness. Questionnaires and certain blood tests may both detect people with possible alcoholism. Further information is then collected to confirm the diagnosis.

Prevention of alcoholism may be attempted by regulating and limiting the sale of alcohol, taxing alcohol to increase its cost, and providing inexpensive treatment. Treatment may take several steps. Due to medical problems that can occur during withdrawal, alcohol detoxification should be carefully controlled. One common method involves the use of benzodiazepine medications, such as diazepam. This can be either given while admitted to a health care institution or occasionally while a person remains in the community with close supervision. Mental illness or other addictions may complicate treatment. After detoxification support such as group therapy or support groups are used to help keep a person from returning to drinking. One commonly used form of support is the group Alcoholics Anonymous. The medications acamprosate, disulfiram, or naltrexone may also be used to help prevent further drinking.

The World Health Organization estimates that as of 2010 there were 208 million people with alcoholism worldwide (4.1% of the population over 15 years of age). In the United States about 17 million (7%) of adults and 0.7 million (2.8%) of those age 12 to 17 years of age are affected. It is more common among males and young adults, becoming less common in middle and old age. It is the least common in Africa at 1.1% and has the highest rates in Eastern Europe at 11%. Alcoholism directly resulted in 139,000 deaths in 2013, up from 112,000 deaths in 1990. A total of 3.3 million deaths (5.9% of all deaths) are believed to be due to alcohol. It often reduces a person's life expectancy by around ten years. In the United States it resulted in economic costs of $224 billion USD in 2006. Many terms, some insulting and others informal, have been used to refer to people affected by alcoholism; the expressions include tippler, drunkard, dipsomaniac, and souse. In 1979, the World Health Organization discouraged the use of "alcoholism" due to its inexact meaning, preferring "alcohol dependence syndrome".

Alcohol-related brain damage is the damage that occurs to brain structures or function of the central nervous system as a result of the direct neurotoxic effects of alcohol intoxication or acute withdrawal. The frontal lobes are the most damaged region of the brains of alcohol abusers but other regions of the brain are also affected. The damage that occurs from heavy drinking/high blood alcohol levels causes impairments in judgement and decision making and social skills. These brain changes are linked to poor behavioural control and impulsivity, which tend to worsen the existing addiction problem.

The problems of alcoholism are well known, such as memory disorders, liver disease, high blood pressure, muscle weakness, heart problems, anaemia, low immune function, disorders of the digestive system and pancreatic problems as well as depression, unemployment and family problems including child abuse. Recently attention has been increasingly focused on binge drinking by adolescents and young adults due to neurochemical changes and brain damage which, unlike with alcoholism, can occur after a relatively short period of time; the damage is particularly evident in the corticolimbic region. This brain damage increases the risk of abnormalities in mood and cognitive abilities, increases the risk of dementia and additionally binge drinkers have an increased risk of developing chronic alcoholism.

Individuals who are impulsive are at high risk of addiction due to impaired behavioural control and increased sensation seeking behaviour. Alcohol abuse, especially during adolescence, causes a deterioration of executive functions in the frontal lobe. This brain damage from alcohol actually increases impulsivity and therefore worsens the addictive disorder.

There are five main stages of alcoholism. The first stage,occasional abuse and binge drinking, in this stage one may want to just experiment with alcohol and test their limits. These drinkers may be new to different forms of alcohol. This experimental stage is commonly seen in teens and young adults. These experimental drinkers also frequently engage in binge drinking. While they may not drink regularly, they consume exceptionally enormous amounts of alcohol at one time.

The second stage, increased drinking, in this stage one will leave the experimental stage and start drinking on a regular basis. Instead of just drinking at parties occasionally, one may find themselves drinking every weekend. Increased alcohol consumption can also lead to drinking for these reasons: as an excuse to get together with friends, to alleviate stress, out of boredom, or to combat sadness or loneliness.

The third stage, problem drinking, one will drink to get rid of their problems for them at any moment. As increased drinking continues, one becomes more dependent on alcohol and are at risk of developing alcoholism.

The fourth stage, alcohol dependence, this forms after the problem drinking stage. At this point, one has an attachment to alcohol that has taken over their regular routine. They are aware of the adverse effects, but no longer have control over their alcohol consumption. Alcohol dependence also means that one has developed a tolerance to drinking. As a result, they may have to consume larger quantities to get “buzzed” or drunk.

The fifth stage, addiction and alcoholism, this is the final and most harmful stage. One is addicted and dependent and must have alcohol all the time, if not they have withdrawals. Alcohol withdrawal is the changes the body goes through when a person suddenly stops drinking after prolonged alcohol abuse, or if one does not have alcohol for a period of time. Symptoms include trembling (shakes), insomnia, anxiety, and other physical and mental symptoms. If the alcohol is withdrawn suddenly, the brain is like an accelerated vehicle that has lost its brakes. Not surprisingly, most symptoms of withdrawal are symptoms that occur when the brain is overstimulated (Drugs.com). People with alcohol addiction physically crave the substance and are often inconsolable until they start drinking again. With prolonged abstinence neurogenesis occurs which can potentially reverse the damage from alcohol abuse.

Low birth weight (LBW) is defined by the World Health Organization as a birth weight of a

infant of 2,499 g or less, regardless of gestational age. Subcategories include very low birth weight (VLBW), which is less than 1500 g (3 pounds 5 ounces), and extremely low birth weight (ELBW), which is less than 1000 g (2 pounds 3 ounces). Normal weight at term delivery is 2500–4200 g (5 pounds 8 ounces – 9 pounds 4 ounces).

Warning signs of alcoholism include the consumption of increasing amounts of alcohol and frequent intoxication, preoccupation with drinking to the exclusion of other activities, promises to quit drinking and failure to keep those promises, the inability to remember what was said or done while drinking (colloquially known as "blackouts"), personality changes associated with drinking, denial or the making of excuses for drinking, the refusal to admit excessive drinking, dysfunction or other problems at work or school, the loss of interest in personal appearance or hygiene, marital and economic problems, and the complaint of poor health, with loss of appetite, respiratory infections, or increased anxiety.

Alcohol is a liquid form substance which contains ethyl alcohol (also known formally as ethanol) that can cause harm and even damage to a persons DNA. "Alcohol consumption is recognized worldwide as a leading risk factor for disease, disability, and death." and is rated as the most used and abused substance by adolescences. Adolescence is a transitional stage of physical and psychological changes, usually a time in a person life in which they go through puberty. Combining these transitional stages and the intake of alcohol, can leave a number of consequences for an adolescent.

Fetal hydantoin syndrome, also called fetal dilantin syndrome is a group of defects caused to the developing fetus by exposure to teratogenic effects of phenytoin or carbamazepine. Dilantin is the brand name of the drug phenytoin sodium in the United States, commonly used in the treatment of epilepsy.

It may also be called congenital hydantoin syndrome, Fetal Hydantoin Syndrome, Dilantin Embryopathy, or Phenytoin Embryopathy.

Association with EPHX1 has been suggested.

Developmental toxicity is the alterations of the developmental processes (organogenesis, morphogenesis) rather than functional alterations of already developed organs. The effects of the toxicants depends on the dose, threshold and duration. The effects of toxicity are:

1. Minor structural deformities - e.g. Anticonvulsant drugs, Warfarin, Retinoic Acid derivatives

2. Major structural deformities - e.g. DES (diethylstilbestrol), cigarette smoking

3. Growth Retardation - e.g. Alcohol, Polychlorinated Biphenyls

4. Functional alterations - e.g. Retinoic Acid derivatives, Polychlorinated Biphenyls, Phenobarbitol, Lead

5. Death- e.g. Rubella, ACE inhibitors