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.

Medical organizations strongly discourage drinking alcohol during pregnancy. Alcohol passes easily from the mother's bloodstream through the placenta and into the bloodstream of the fetus, which interferes with brain and organ development. Alcohol can affect the fetus at any stage during pregnancy, but the level of risk depends on the amount and frequency of alcohol consumed. Regular heavy drinking and binge drinking (four or more drinks on any one occasion) pose the greatest risk for harm, but lesser amounts can cause problems as well. There is no known safe amount or safe time to drink during pregnancy.

Prenatal alcohol exposure can lead to fetal alcohol spectrum disorders (FASDs). The most severe form of FASD is fetal alcohol syndrome (FAS). Problems associated with FASD include facial anomalies, low birth weight, stunted growth, small head size, delayed or uncoordinated motor skills, hearing or vision problems, learning disabilities, behavior problems, and inappropriate social skills compared to same-age peers. Those affected are more likely to have trouble in school, legal problems, participate in high-risk behaviors, and develop substance use disorders themselves.

A study published in the British Medical Journal on 10 July 2014 investigated the correlation between human variants of the ADH1B gene, which codes for the ADH1B enzyme (Alcohol dehydrogenase 1B), and cardiovascular health. The study concluded that carriers of one specific variant of this gene (A-allele of ADH1B rs1229984), which is associated with lower alcohol consumption, '...had a more favourable cardiovascular profile and a reduced risk of coronary heart disease than those without the genetic variant.' The study's authors extrapolated from this finding to suggest that '...reduction of alcohol consumption, even for light to moderate drinkers, is beneficial to health.'

This study contradicts previous findings on the causal relationship between light alcohol consumption and cardiovascular health, and has been criticized on its methodology by members of the International Scientific Forum on Alcohol Research, which stated in its analysis that '...[there are] questions about making generalized statements about the effects of alcohol on disease based on results from the analysis of a single nucleotide polymorphism of a gene.'

Moreover, the study fails to explain or discount previous findings that show a causal link between alcohol intake and cardiovascular health that can not be accounted for by genetic predisposition alone.

Dark cell degeneration as well as inhibition of brain neural stem cell proliferation and neurogenesis are among the causes of alcohol related brain damage. Increases in microglia density also occurs in alcohol abusers which is evidence of neurodegeneration. These increases in microglia persist after abstinence from alcohol according to animal research. People with an alcohol use disorder also show an increased expression of proinflammatory cytokine and microglia protein expression.

Adolescents are naturally at increased risk of alcohol abuse due to increased impulsivity and sensation seeking which results in larger intake of alcohol and more frequent binge drinking episodes. Additionally the developing brain of adolescents is significantly more vulnerable to the neurotoxic and neurodegenerative effects of alcohol abuse. It also appears that there is a genetic risk for proinflammatory cytokine mediated alcohol-related brain damage. There is evidence that variants of these genes are involved not only in contributing to brain damage but also to impulsivity and alcohol abuse and all three of these genetic traits contribute heavily to an alcohol use disorder.

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.

Binge drinkers and alcoholics with multiple detoxifications have impairments in executive control tasks sensitive to dysfunction of prefrontal cortex. Animal studies show that repeated withdrawals are associated with an inability to learn new information. The mechanism of neurotoxicity and kindling of neurotransmission systems is due to alcohol's acute effects on GABAergic enhancement and NMDA suppression, leading to CNS depression leading to a partial acute tolerance to these effects, followed by a rebound effect, during acute withdrawal due to the partial tolerance that developed. The acute withdrawal/rebound causes the neurotransmission systems to go into a hyper-excitability state; if this hyper-excitability state occurs multiple times, kindling and possible neurotoxicity can occur. There is evidence that excitotoxicity may also occur as a result of repeated withdrawals. Similar to people who have been detoxified multiple times from alcohol, binge drinkers show a higher rate of emotional disturbance.

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.

In order to maintain high-quality performance, some musicians take chemical substances. Some musicians take drugs or alcohol to deal with the stress of performing. As a group they have a higher rate of substance abuse. The most common chemical substance which is abused by pop musicians is cocaine, because of its neurological effects. Stimulants like cocaine increase alertness and cause feelings of euphoria, and can therefore make the performer feel as though they in some ways ‘own the stage’. One way in which substance abuse is harmful for a performer (musicians especially) is if the substance being abused is aspirated. The lungs are an important organ used by singers, and addiction to cigarettes may seriously harm the quality of their performance. Smoking causes harm to alveoli, which are responsible for absorbing oxygen.

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.

Based on combined data from SAMHSA's 2004–2005 National Surveys on Drug Use & Health, the rate of past-year alcohol dependence or abuse among persons aged 12 or older varied by level of alcohol use: 44.7% of past month heavy drinkers, 18.5% binge drinkers, 3.8% past month non-binge drinkers, and 1.3% of those who did not drink alcohol in the past month met the criteria for alcohol dependence or abuse in the past year. Males had higher rates than females for all measures of drinking in the past month: any alcohol use (57.5% vs. 45%), binge drinking (30.8% vs. 15.1%), and heavy alcohol use (10.5% vs. 3.3%), and males were twice as likely as females to have met the criteria for alcohol dependence or abuse in the past year (10.5% vs. 5.1%).

Street children in many developing countries are a high risk group for substance misuse, in particular solvent abuse. Drawing on research in Kenya, Cottrell-Boyce argues that "drug use amongst street children is primarily functional – dulling the senses against the hardships of life on the street – but can also provide a link to the support structure of the ‘street family’ peer group as a potent symbol of shared experience."

A complex mixture of genetic and environmental factors influences the risk of the development of alcoholism. Genes that influence the metabolism of alcohol also influence the risk of alcoholism, and may be indicated by a family history of alcoholism. One paper has found that alcohol use at an early age may influence the expression of genes which increase the risk of alcohol dependence. Individuals who have a genetic disposition to alcoholism are also more likely to begin drinking at an earlier age than average. Also, a younger age of onset of drinking is associated with an increased risk of the development of alcoholism, and about 40 percent of alcoholics will drink excessively by their late adolescence. It is not entirely clear whether this association is causal, and some researchers have been known to disagree with this view.

Severe childhood trauma is also associated with a general increase in the risk of drug dependency. Lack of peer and family support is associated with an increased risk of alcoholism developing. Genetics and adolescence are associated with an increased sensitivity to the neurotoxic effects of chronic alcohol abuse. Cortical degeneration due to the neurotoxic effects increases impulsive behaviour, which may contribute to the development, persistence and severity of alcohol use disorders. There is evidence that with abstinence, there is a reversal of at least some of the alcohol induced central nervous system damage. The use of cannabis was associated with later problems with alcohol use. Alcohol use was associated with an increased probability of later use of tobacco, cannabis, and other illegal drugs.

Blackouts are commonly associated with the consumption of large amounts of alcohol; however, surveys of drinkers experiencing blackouts have indicated that they are not directly related to the amount of alcohol consumed. Respondents reported they frequently recalled having "drunk as much or more without memory loss," compared to instances of blacking out. Subsequent research has indicated that blackouts are most likely caused by a rapid increase in a person's blood-alcohol concentration. One study, in particular, resulted in subjects being stratified easily into two groups, those who consumed alcohol very quickly, and blacked out, and those who did not black out by drinking alcohol slowly, despite being extremely intoxicated by the end of the study.

In another study hospital file data showed, that of 67 participants, 39 had reported a blackout. The presence or absence of blackouts was cross-tabulated against various measures of alcohol problem severity. The presence of blackouts was associated to some degree with some indications of severity such as withdrawal and loss of control, but not with duration of problem drinking, physical complications or abnormal liver function.

The presence of blackouts was related to some measures of severity of the problem – withdrawal symptoms and loss of control. The hypotheses that blackouts either reflect a general vulnerability to the cerebral consequences of alcohol abuse or are associated with other forms of more enduring cognitive impairment did not receive any support.

In another study which looked at subjective responses to alcohol as a prime for 21st birthday alcohol consumption, subjective responses to the initial drink were viewed as a prime for more alcohol consumption during 21st birthday celebrations. Current findings show that subjective responses to alcohol have direct effects on both the final BAC achieved and on the experiences of blackouts and hangover that are not explained by level of intoxication. Where a variety of social factors, such as peer pressure and 21st birthday traditions such as 21 shots may influence the amount of alcohol people consume, their subjective experiences with alcohol have clear influences on both consumption and the physiological consequences of drinking. These physiological responses to alcohol may have a biological vulnerability that extends beyond the dose-dependent effects of alcohol.

Self reports from another study showed that 63% of patients in the study gulped their drinks rather than sipped. Five patients recollected vomiting during the drinking episode while 32 drank on an empty stomach and 41 drank more than originally planned. During the drinking episode 31% subjects described blackouts, 20% described brownouts, and 49% reported no amnesic episode.

Marquis states how "Adolescent alcohol

use is not an acceptable rite of passage but a serious threat to adolescent

development and health, as the statistics related to adolescent impairment,

injury, and death attest." Research shows how an adolescent

makes the decision to consume alcohol because they are influenced by various

factors. "These factors include normal maturational changes that all

adolescents experience; genetic, psychological and social factors specific to

each adolescent and the various social and cultural environments that surround

adolescent, including their families, schools and communities". It is also

shown that early onset of alcohol intake can lead to high levels of alcohol use

in adulthood.

Alcoholism throughout adolescents is increasing yearly for a number of different reasons. These reasons include:

- Availability of alcohol

- Peer pressure

- Role model

- Television

- Anxiety or stress

The combination of self-starvation and alcohol abuse can lead to an array of physical and psychological consequences. For example, drinking in a state of malnutrition can predispose individuals to a higher rate of blackouts, alcohol poisoning, alcohol-related injury, violence, or illness. Drinking on an empty stomach allows ethanol to reach the blood system at a swifter pace and raises one's blood alcohol content with an often dangerous speed. This can render the drinker more vulnerable to alcohol-related brain damage. In addition, alcohol abuse can have a detrimental impact on hydration and the body's retention of minerals and nutrients, further exacerbating the consequences of malnutrition and denigrating an individual's cognitive faculties. This can ultimately have a negative impact on academic performance.

These harmful consequences can be more easily induced in women, as women are oftentimes less capable of metabolizing alcohol than men. On CBS News, Carrie Wilkins, PhD, of the Center for Motivation and Change (a private practice group based in New York City) describes how women are more vulnerable to particular toxic side effects of alcohol consumption.

Drunkorexia can lead to short term and long term cognitive problems including difficulty concentrating and difficulty making decisions. It also increases the risk of developing more serious eating disorders or alcohol abuse problems. As binge drinking is involved there is a greater risk for violence, risky sexual behavior, alcohol poisoning, substance abuse and chronic disease later in life.

Drunkorexia is not a medically diagnosed disorder therefore there is no specific treatment. However, as drunkorexia is a combination of two different disorders, binge drinking and eating disorders such as anorexia and bulimia the treatment will need to address both.

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.

A legal minimum age for the buying or consuming of alcohol is in place in many of the world's countries, typically with the intent to protect the young from alcohol-related harm. This age varies between countries; for example, the minimum legal drinking age for Australia is 18, whereas the MLDA in the United States is 21.

Conditions of fatigue correlate positively with increased alcohol consumption.

Low doses of alcohol (one beer) appear to increase total sleep time and reduce awakening during the night. The sleep-promoting benefits of alcohol dissipate at moderate and higher doses of alcohol. Previous experience with alcohol also influences the extent to which alcohol positively or negatively affects sleep. Under free-choice conditions, in which subjects chose between drinking alcohol or water, inexperienced drinkers were sedated while experienced drinkers were stimulated following alcohol consumption. In insomniacs, moderate doses of alcohol improve sleep maintenance.

The onset of alcohol dementia can occur as early as age thirty, although it is far more common that the dementia will reveal itself anywhere from age fifty to age seventy. The onset and the severity of this type of dementia is directly correlated to the amount of alcohol that a person consumes over his or her lifetime.

Epidemiological studies show an association between long-term alcohol intoxication and dementia. Alcohol can damage the brain directly as a neurotoxin, or it can damage it indirectly by causing malnutrition, primarily a loss of thiamine (vitamin B1). Alcohol abuse is common in older persons, and alcohol-related dementia is under-diagnosed. A discredited French study claimed that moderate alcohol consumption (up to four glasses of wine per week) protected against dementia, whereas higher rates of consumption have conclusively been shown to increase the chances of getting it.

While researchers have found that moderate alcohol consumption in older adults is associated with better cognition and well-being than abstinence, excessive alcohol consumption is associated with widespread and significant brain lesions. The effects can manifest much later—mid-life Alcohol Use Disorder has been found to correlate with increased risk of severe cognitive and memory deficits in later life. Alcohol related brain damage is not only due to the direct toxic effects of alcohol; alcohol withdrawal, nutritional deficiency, electrolyte disturbances, and liver damage are also believed to contribute to alcohol-related brain damage.

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.