Alcohol dependence is not prerequisite to blackouts (either en bloc or fragmentary). Students in one study who reported blackouts were demographically similar to other drinking students. Importantly, however, students reporting blackouts drank more, and had other symptoms of alcoholic drinking, even though they did not fall into the alcoholic range on the Michigan Alcoholism Screening Test (MAST). Half of the students reported having had a blackout during their drinking careers, which closely followed other research findings.

In another study 25% of healthy college students reported being familiar with alcoholic blackouts. 51% of the students reported that they had had at least one blackout. Blackouts were reported during activities such as spending money (27%), sexual conduct (24%), fighting (16%), vandalism (16%), unprotected intercourse (6%), and driving a car (3%). So a significant number of students were engaged in a range of possibly hazardous activities during blackouts.

Of 545 individuals in another study, 161 (29.5%) reported driving drunk, 139 (25.5%) reported a regretted sexual situation, 67 (12.3%) reported unprotected sex, 60 (11%) reported having damaged property, 55 (10.1%) reported getting into a physical fight, and 29 (5.3%) reported injuring someone while under the influence of alcohol in the past 6 months.

Research indicates that some users of alcohol, particularly those with a history of blackouts, are predisposed to experience blackouts more frequently than others. One such study indicated a link between prenatal exposure to alcohol and vulnerability towards blackouts, in addition to the oft-cited link between this type of exposure and alcoholism. Alternatively, another study has indicated that there appears to be a genetic predisposition towards blacking out, suggesting that some individuals are made to be susceptible to alcohol-related amnesia.

From a neurobiological perspective, central serotonin (5-hydroxytryptamine, 5-HT) neurotransmission has been shown to modulate both alcohol consumption and impulsivity. Some variations in 5-HT neurotransmission may thus contribute to a risk of AD (alcohol dependence), especially the forms of AD associated with a high level of impulsivity 2.

As the extracellular concentration of 5-HT is regulated by the activity of the 5-HT transporter (5-HTT), the gene SLC6A4 encoding this protein represents an important potential candidate gene for AD risk. Using a meta-analysis approach, Feinn et al. found evidence for an association of the short allele of the 5-HTTLPR (SLC6A4) with AD, but the overall effect size estimated by odd ratios was found weak. As expected in a complex condition like alcohol dependence, the disagreement in the association between AD and 5-HTTLPR likely reflects the impossibility for a single genetic determinant to explain the whole of the risk.

Aside from chemical components which may cause a predisposition to alcohol dependence and blackouts, expectations of alcohol use may predispose drinkers toward alcoholism and blackouts. In a study of 123 college students significant correlations were found between students’ alcohol expectancies, level of alcohol abuse, and blackout history. The students who experienced blackouts (38.6%) had much higher positive alcohol expectancies than those without blackouts. Positive and negative expectancies were positively correlated among the no-blackout group, but negatively correlated among the blackout group.

The impact of alcohol on weight-gain is contentious: some studies find no effect, others find decreased or increased effect on weight gain.

Alcohol use increases the risk of chronic gastritis (stomach inflammation); it is one cause of cirrhosis, hepatitis, and pancreatitis in both its chronic and acute forms.

A study concluded, "Mild to moderate alcohol consumption is associated with a lower prevalence of the metabolic syndrome, with a favorable influence on lipids, waist circumference, and fasting insulin. This association was strongest among whites and among beer and wine drinkers." This is also true for Asians. A J-curve association between alcohol intake and metabolic syndrome was found: "The results of the present study suggest that the metabolic syndrome is negatively associated with light alcohol consumption (1–15 g alcohol/d) in Korean adults". However, "odds ratios for the metabolic syndrome and its components tended to increase with increasing alcohol consumption."

Alcohol abuse is said to be most common in people aged between 15 and 24 years, according to Moreira 2009. However, this particular study of 7275 college students in England collected no comparative data from other age groups or countries.

Causes of alcohol abuse are complex and are likely the combination of many factors, from coping with stress to childhood development. The US Department of Health & Human Services identifies several factors influencing adolescent alcohol use, such as risk-taking, expectancies, sensitivity and tolerance, personality and psychiatric comorbidity, hereditary factors, and environmental aspects. Studies show that child maltreatment such as neglect, physical, and/or sexual abuse, as well as having parents with alcohol abuse problems, increases the likelihood of that child developing alcohol use disorders later in life. According to Shin, Edwards, Heeren, & Amodeo (2009), underage drinking is more prevalent among teens that experienced multiple types of childhood maltreatment regardless of parental alcohol abuse, putting them at a greater risk for alcohol use disorders. Genetic and environmental factors play a role in the development of alcohol use disorders, depending on age. The influence of genetic risk factors in developing alcohol use disorders increase with age ranging from 28% in adolescence and 58% in adults.

The cause of alcohol abuse is complex. Alcohol abuse is related to economic and biological origins and is associated with adverse health consequences. Peer pressure influences individuals to abuse alcohol; however, most of the influence of peers is due to inaccurate perceptions of the risks of alcohol abuse. According to Gelder, Mayou and Geddes (2005) easy accessibility of alcohol is one of the reasons people engage in alcohol abuse as this substance is easily obtained in shops. Another influencing factor among adolescents and college students are the perceptions of social norms for drinking; people will often drink more to keep up with their peers, as they believe their peers drink more than they actually do. They might also expect to drink more given the context (e.g. sporting event, fraternity party, etc.). This perception of norms results in higher alcohol consumption than is normal.

Alcohol abuse is also associated with acculturation, because social and cultural factors such as an ethnic group’s norms and attitudes can influence alcohol abuse.

Acute intoxication, such as binge drinking and alcoholism, are known potent risk factors for suicide. Binge drinking is also associated with an increased risk of unplanned sex, unprotected sex, unplanned pregnancies, and an increased risk of HIV infection. 10 percent of women and 19 percent of men have reported being assaulted as a result of alcohol. Males who drink more than 35 units of alcohol per week report being physically hurt as a result of alcohol, and 15 percent report physically hurting others as a result of their drinking. Almost 16 percent of binge drinkers report being taken advantage of sexually, and 8 percent report taking advantage of another person sexually as a result of alcohol within a 1-year period. Heavy drinkers cause approximately 183,000 rapes and sexual assaults, 197,000 robberies, 661,000 aggravated assaults, and 1.7 million simple assaults each year. Binge drinking has been associated with high odds of divorce, spousal abuse, and poor job performance. Binge drinking can cause adverse effects on the body including effects on blood homeostasis and its circadian variation, cardiac rhythm, ischaemic heart disease, blood pressure, white blood cell activity, female reproductive hormone levels as well as adverse effects on the fetus. There is also evidence from animal studies that binge drinking causes brain damage. Binge drinking has been associated with lower abdominal pain in women. Ketoacidosis can occur in individuals who chronically abuse alcohol and have a recent history of binge drinking. Alcohol affects brain development quite significantly especially during adolescence when the brain is still developing. The main lobes that are involved in decision making and complex thought processes are undergoing their final development phase during adolescence and binge drinking can negatively stunt the growth of these frontal lobes.

Ethanol is the type of alcohol found in alcoholic beverages. It is a volatile, flammable, colorless liquid that acts as a central nervous system depressant. Ethanol can impair different types of memory.

The high levels of binge drinking among young people and the adverse consequences that include increased risk of alcoholism as an adult and liver disease make binge drinking a major public health issue. Recent research has found that young college binge drinkers who drink 4/5+ drinks on more than 3 occasions in the past 2 weeks are statistically 19 times more likely to develop alcoholism than non-binge drinkers, though the direction of causality remains unclear. This is particularly interesting as drinking for the sole purpose of getting drunk, remains a major health and social problem on college campuses across the United States. Heavy and regular binge drinking during adolescence is associated with an increased risk of alcoholism. Approximately 40 percent of alcoholics report heavy drinking during adolescence. Repeated episodes of excessive drinking, especially at an early age, are thought to cause a profound increase in the risk of developing an alcohol-related disorder (ICD-10, harmful use/dependence syndrome). Heavy drinking is also closely associated with depression. Those with severe depression have higher rates of alcohol abuse than those with low depression. College students who are depressed are more susceptible to use alcohol than college students who are not depressed. In a study conducted by Harvard University it was found that about 32% of students surveyed were diagnosable for alcohol abuse and about 6% were diagnosed as alcohol dependent. Binge drinking is also becoming an increasing problem in Australian adolescents, the Australian School Students Alcohol and Drug survey conducted by the National Cancer Council discovered that around 33 percent of students between Years 7 and 11 consumed alcohol in the week leading up to the survey, they also found that 10 percent of the students participated in binge drinking at a consumption level which is considered dangerous to adults. When the survey results were separated into age groups the findings were that 13 percent of 15-year-old's and 22 percent of 17-year-old's had alcohol consumption levels above the daily maximum suggested to adults and that 20 percent of 17-year-old's had a consumption level of alcohol considered risky to adults.

Other risk factors that influence the development of alcohol abuse or alcoholism include social and genetic factors. Several researchers have found that starting drinking before the age of 15 is associated with a fourfold increased risk for developing alcoholism compared to people that delay drinking until age 20 or later. It has been estimated by some that if the age at which people started drinking could be delayed to age 20, there would be a 50 percent reduction in the number of cases of alcohol use disorder. However, it is unclear whether this is a causal relationship, or a function of confounding familial (and other) factors associated with both age at first drink and propensity for alcoholism.

The main cause of death among adolescents as a result of binge drinking is road traffic accidents; a third of all fatal road traffic accidents among 15- to 20-year-olds are associated with drinking alcohol. Cyclists and pedestrians are likely to have less spatial awareness and concentration while travelling after binge drinking and, also, it is more common that adolescents that binge-drink drive drunk or are the passenger of a drunk driver. It has been found that 50 percent of all head injuries in adolescents in the US are associated with alcohol consumption. Violence and suicide combine to become the third-most-common cause of death associated with binge drinking among adolescents. The suicide risk in adolescents is more than 4 times higher among binge drinkers than non-binge drinking adolescents.

Earlier sexual activity, increased changing of sexual partners, higher rate of unwanted (teenage) pregnancy, higher rate of sexually transmitted diseases, infertility, and alcohol-related damage to the fetus during pregnancy is associated with binge drinking. Female binge drinkers are three times more likely to be victims of sexual assault; 50 percent of adolescent girls reporting sexual assault were under the influence of alcohol or another psychotropic substance at the time.

Adolescents who regularly participated in binge drinking for several years show a smaller hippocampus brain region, in particular those who began drinking in early adolescence. Heavy binge drinking is associated with neurocognitive deficits of frontal lobe processing and impaired working memory as well as delayed auditory and verbal memory deficits. Animal studies suggest that the neurodegenerative effects of alcohol abuse during adolescence can be permanent. Research in humans, which utilised sophisticated brain scanning technology suggests that in adolescent teenagers, drinking more than 4 or 5 drinks once or twice a month results in subtle damage to the teenagers developing brain tissue, in particular the white matter. However, this research is primarily cross-sectional and done with fairly small sample sizes, making causality less certain.

Several studies have been conducted to discover if there is a link between binge drinking in adolescent years and becoming a chronic alcohol consumer when they transition into adulthood. A particular study conducted by the National Longitudinal Survey of Youth found that harmful drinking during adolescent years was significantly associated with the continuance of dangerous levels of alcohol consumption into adulthood years.

A normal liver detoxifies the blood of alcohol over a period of time that depends on the initial level and the patient's overall physical condition. An abnormal liver will take longer but still succeeds, provided the alcohol does not cause liver failure.

People having drunk heavily for several days or weeks may have withdrawal symptoms after the acute intoxication has subsided.

A person consuming a dangerous amount of alcohol persistently can develop memory blackouts and idiosyncratic intoxication or pathological drunkenness symptoms.

Long-term persistent consumption of excessive amounts of alcohol can cause liver damage and have other deleterious health effects.

Alcohol intoxication, also known as drunkenness among other names, is a physiological condition that may result in psychological alterations of consciousness. Drunkenness is induced by the ingestion or consumption of alcohol in a living body. Alcohol intoxication is the result of alcohol entering the bloodstream faster than it can be metabolized by the body. Metabolism results in breaking down the ethanol into non-intoxicating byproducts.

Some effects of alcohol intoxication, such as euphoria and lowered social inhibition, are central to alcohol's desirability as a beverage and its history as one of the world's most widespread recreational drugs. Despite this widespread use and alcohol's legality in most countries, many medical sources tend to describe any level of alcohol intoxication as a form of poisoning due to ethanol's damaging effects on the body in large doses. Some religions consider alcohol intoxication to be a sin.

Symptoms of alcohol intoxication include euphoria, flushed skin, and decreased social inhibition at lower doses, with larger doses producing progressively severe impairments of balance, and decision-making ability as well as nausea or vomiting from alcohol's disruptive effect on the semicircular canals of the inner ear and chemical irritation of the gastric mucosa.

Sufficiently extreme levels of blood-borne alcohol may result in coma or death.

"Prospective memory" involves remembering to carry out an intended action in the future without an explicit reminder. Alcohol has been found to impair this ability. Chronic heavy alcohol users report significantly more prospective forgetting compared to low-dose and alcohol-free controls. The Prospective Memory Questionnaire assesses short-term habitual prospective memory, long-term episodic prospective memory, and internally cued prospective memory. Chronic heavy alcohol users reported significantly greater deficits for all three aspects of prospective memory. Individuals that report heavy alcohol use report 24% more difficulties with prospective memory than those who report that they are light drinkers and 30% more difficulties than those who report that they never drink. The effects of alcohol on prospective memory can also be assessed in the laboratory by simulating prospective memory tasks that individuals face in everyday life. Individuals who are given 0.6 g/kg alcohol prior to performing prospective memory tasks do significantly poorer than a placebo group. Alcohol can damage the prefrontal and frontal areas of the brain, and this may be responsible for prospective memory impairments since prospective memory performance is highly correlated with frontal executive functions.

The cause of sleepwalking is not known. A number of, as yet unproven, hypotheses are suggested for why it might occur. These include a delay in the maturity of the central nervous system, increased slow wave sleep, sleep deprivation, fever, and excessive tiredness.

There may be a genetic component to sleepwalking. One study found that sleepwalking occurred in 45% of children who have one parent who sleepwalked, and in 60% of children if both parents sleepwalked. Thus, heritable factors may predispose an individual to sleepwalking, but expression of the behavior may also be influenced by environmental factors. Genetic studies using common fruit flies as experimental models reveal a link between night sleep and brain development mediated by evolutionary conserved transcription factors such as AP-2

Sleepwalking may be inherited as an autosomal dominant disorder with reduced penetrance. Genome-wide multipoint parametric linkage analysis for sleepwalking revealed a maximum logarithm of the odds score of 3.14 at chromosome 20q12-q13.12 between 55.6 and 61.4 cM.

Medications, primarily in four classes—benzodiazepine receptor agonists and other GABA modulators, antidepressants and other serotonergic agents, antipsychotics, and β-blockers— have been associated with sleepwalking. The best evidence of medications causing sleepwalking is for Zolpidem and sodium oxybate—all other reports are based on associations noted in case reports.

A number of conditions, such as Parkinson's Disease, are thought to trigger sleepwalking in people without a previous history of sleepwalking.

The lifetime prevalence of sleepwalking is estimated to be 4.6%–10.3%. A meta-analysis of 51 studies, that included more than 100,000 children and adults, found that sleepwalking is more common in children with an estimated 5%, compared with 1.5% of adults, sleepwalking at least once in the previous 12 months. The rate of sleepwalking does not vary across ages during childhood.

Anterograde amnesia can also be caused by alcohol intoxication, a phenomenon commonly known as a blackout. Studies show rapid rises in blood alcohol concentration over a short period of time severely impair or in some cases completely block the brain's ability to transfer short-term memories created during the period of intoxication to long-term memory for storage and later retrieval. Such rapid rises are caused by drinking large amounts of alcohol in short periods of time, especially on an empty stomach, as the dilution of alcohol by food slows the absorption of alcohol. Alcohol-related anterograde amnesia is directly related to the rate of consumption of alcohol (and is often associated with binge drinking), and not just the total amount of alcohol consumed in a drinking episode. Test subjects have been found not to experience amnesia when drinking slowly, despite being heavily intoxicated by the end of the experiment. When alcohol is consumed at a rapid rate, the point at which most healthy people's long-term memory creation starts to fail usually occurs at approximately 0.20% BAC, but can be reached as low as 0.14% BAC for inexperienced drinkers. The exact duration of these blackout periods is hard to determine, because most people fall asleep before they end. Upon reaching sobriety, usually after waking, long-term memory creation is completely restored.

Chronic alcoholism often leads to a thiamine (vitamin B) deficiency in the brain, causing Korsakoff's syndrome, a neurological disorder which is generally preceded by an acute neurological condition known as Wernicke's encephalopathy (WE).

The memory impairment that is pathognomonic to Korsakoff's syndrome predominantly affects the declarative memory, leaving non-declarative memory that is often procedural in nature relatively intact. The disproportionate severity in anterograde episodic memory processes in contrast to other cognitive processes is what differentiates Korsakoff syndrome from other conditions such as alcohol-related dementia. Evidence for the preservation of certain memory processes in the presence of severe anterograde episodic memory serve as experimental paradigm to investigate the components of human memory.

Anterograde amnesia is a loss of the ability to create new memories after the event that caused the amnesia, leading to a partial or complete inability to recall the recent past, while long-term memories from before the event remain intact. This is in contrast to retrograde amnesia, where memories created prior to the event are lost while new memories can still be created. Both can occur together in the same patient. To a large degree, anterograde amnesia remains a mysterious ailment because the precise mechanism of storing memories is not yet well understood, although it is known that the regions involved are certain sites in the temporal cortex, especially in the hippocampus and nearby subcortical regions.

Populations groups at risk:

- In the US:

- Children and young adults: Drowning rates are highest for children under 5 years of age and persons 15–24 years of age.

- Males: Nearly 80% of people who die from drowning are male.

- Minorities: The fatal unintentional drowning rate for African Americans between 2005 and 2009 was significantly higher than that of whites across all ages. The fatal drowning rate of African American children of ages from 5 to 14 is almost three times that of white children in the same age range, and 5.5 times higher in swimming pools. These disparities might be associated with lack of basic swimming skills in some minority populations.

Behavioral and physical factors:

- In the US:

- Use of alcohol increases the risk of drowning. Among adolescents and adults, alcohol use is involved in almost a quarter of emergency department visits for drowning.

- Inability to swim: Participation in formal swimming lessons can reduce the risk of drowning among children aged 1 to 4 years.

- Free access to water: Effective barriers prevent young children from gaining access to the water

- Ineffective supervision: Drowning can occur anywhere there is water, and even in the presence of lifeguards.

- Risk can vary with location depending on age. Children between 1 and 4 usually drown in home swimming pools. Drownings in natural water settings increase with age. More than half of drownings among those 15 years and older occurred in natural water environments.

- Failure to wear life jackets or personal flotation devices was implicated in 88% of the boating related drownings in the US during 2010.

- For persons with seizure disorders, drowning is the most common cause of death by unintentional injury, largely in the bathtub.

Most drowning is preventable. It has been estimated that more than 85% of drownings could have been prevented by supervision, training in water skills, technology, regulation and public education.

6,530 patients were admitted to hospitals with poisoning, and 459 deaths reported. Cases reached a peak of hundreds per day in January, and had largely subsided by the beginning of March. The last admittance was on 27 March; admissions represented every age and gender stratum, although those under the age of ten represented a third of admitted cases. This number is "certainly an underestimate", because of the availability of hospital treatment, hospital overcrowding and lack of faith in treatment. In the most severely affected areas, prevalence was 28% and mortality was 21% of the cases. Some Iraqi doctors believe both the number of cases and fatalities are at least ten times too low, with perhaps 100,000 cases of brain damage. One suggested reason for the vast discrepancy between reported and estimated numbers of deaths is the Iraqi custom, common to large parts of the Middle East, for a person to die at home when possible. Home deaths would not have been recorded.

A large number of patients with minor symptoms recovered completely; those with more serious symptoms improved. This was in contrast to expected outcomes, largely based on analysis of Minamata disease in Japan. In boys with mercury levels below clinical poisoning, a reduction in school performance was noted, although this correlation could not be confirmed. In infants, the mercury poisoning caused central nervous system damage. Relatively low doses caused slower development in children, and abnormal reflexes. Different treatments for mercury poisoning have since been developed, and "quiet baby syndrome", characterised by a baby who never cries, is now a recognised symptom of methylmercury-induced brain damage. Ongoing recommendations of the food regulation authorities have focused on consumption by pregnant women and infant children, noting the particular susceptibility of fetuses and infants to methylmercury poisoning. Data from Iraq have confirmed that methylmercury can pass to a child "in utero", and mercury levels were equal to or higher in the newborn child than in the mother.

In 1974, a joint Food and Agriculture Organization (FAO) and World Health Organisation (WHO) meeting made several recommendations to prevent a similar outbreak. These included stressing the importance of labelling bags in the local language and with locally understood warning symbols. The possibility of an additive creating a strong bitter taste was studied. The meeting urged governments to strictly regulate methyl- and ethylmercury use in their respective countries, including limiting use to where no other reasonable alternative was available. It also recommended the involvement of the FAO and WHO in assisting national governments in regulation and enforcement, and the setting up of national poison control centres. Over 9–13 November, a Conference on Intoxication due to Alkylmercury-Treated Seed was held in Baghdad. It supported the recommendations of the FAO/WHO report and further suggested that local and national media should publicise outbreaks, including size and symptoms; it considered the distribution of this information crucial. It also laid out a general plan as to the collection of relevant information from the field and potential analysis for further investigation. It called on national governments to make use of WHO involvement whenever feasible, and absolved world governments in clear terms, saying that "No country should ever feel that any blame will attach to it for allowing an outbreak to occur".

Iraq now has the highest incidence of Parkinson's in the world. Parkinson's symptoms are very similar to mercury poisoning symptoms. Mercury that enters the brain has a half-life of 27.5 years and chelators are not able to remove it.

The effect of mercury took some time – the latent period between ingestion and the first symptoms (typically paresthesia – numbness in the extremities) was between 16 and 38 days. Paresthesia was the predominant symptom in less serious cases. Worse cases included ataxia (typically loss of balance), blindness or reduced vision, and death resulting from central nervous system failure. Anywhere between 20 and 40 mg of mercury has been suggested as sufficient for paresthesia (between 0.5 and 0.8 mg/kg of body weight). On average, individuals affected consumed 20 kg or so of bread; the 73,000 tonnes provided would have been sufficient for over 3 million cases.

The hospital in Kirkuk received large numbers of patients with symptoms that doctors recognised from the 1960 outbreak. The first case of alkylmercury poisoning was admitted to hospital on 21 December. By 26 December, the hospital had issued a specific warning to the government. By January 1972, the government had started to strongly warn the populace about eating the grain, although dispatches did not mention the large numbers already ill. The Iraqi Army soon ordered disposal of the grain and eventually declared the death penalty for anyone found selling it. Farmers dumped their supplies wherever possible, and it soon got into the water supply (particularly the River Tigris), causing further problems. The government issued a news blackout and released little information about the outbreak.

The World Health Organization assisted the Iraqi government through the supply of drugs, analytical equipment and expertise. Many new treatments were tried, since existing methods for heavy metal poisoning were not particularly effective. Dimercaprol was administered to several patients, but caused rapid deterioration of their condition. It was ruled out as a treatment for this sort of poisoning following the outbreak. Polythiol resins, penicillamine and dimercaprol sulfonate all helped, but are believed to have been largely insignificant in overall recovery and outcomes. Dialysis was tested on a few patients late in the treatment period, but they showed no clinical improvement. The result of all treatments was varied, with some patients' blood mercury level being dramatically reduced, but a negligible effect in others. All patients received periods of treatment interspersed with lay periods; continuous treatment was suggested in future cases. Later treatment was less effective in reducing blood toxicity.

Perinatal asphyxia is the medical condition resulting from deprivation of oxygen (hypoxia) to a newborn infant long enough to cause apparent harm. It results most commonly from a drop in maternal blood pressure or interference during delivery with blood flow to the infant's brain. This can occur as a result of inadequate circulation or perfusion, impaired respiratory effort, or inadequate ventilation. There has long been a scientific debate over whether newborn infants with asphyxia should be resuscitated with 100% oxygen or normal air. It has been demonstrated that high concentrations of oxygen lead to generation of oxygen free radicals, which have a role in reperfusion injury after asphyxia. Research by Ola Didrik Saugstad and others led to new international guidelines on newborn resuscitation in 2010, recommending the use of normal air instead of 100% oxygen.