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.

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 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.

About 12% of American adults have had an alcohol dependence problem at some time in their life. In the UK the NHS estimates that around 9% of men and 4% of UK women show signs of alcohol dependence.

Another theory is that there may be shared risk factors that can lead to both substance abuse and mental illness. Mueser hypothesizes that these may include factors such as social isolation, poverty, lack of structured daily activity, lack of adult role responsibility, living in areas with high drug availability, and association with people who already misuse drugs.

Other evidence suggests that traumatic life events, such as sexual abuse, are associated with the development of psychiatric problems and substance abuse.

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."

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."

Comorbidity of addictive disorders and other psychiatric disorders, i.e., dual disorders, is very common and a large body of literature has accumulated demonstrating that mental disorders are strongly associated with substance use disorders. The 2011 USA National Survey on Drug Use and Health found that 17.5% of adults with a mental illness had a co-occurring substance use disorder; this works out to 7.98 million people. Estimates of co-occurring disorders in Canada are even higher, with an estimated 40-60% of adults with a severe and persistent mental illness experiencing a substance use disorder in their lifetime.

A study by Kessler et al. in the United States attempting to assess the prevalence of dual diagnosis found that 47% of clients with schizophrenia had a substance misuse disorder at some time in their life, and the chances of developing a substance misuse disorder was significantly higher among patients suffering from a psychotic illness than in those without a psychotic illness.

Another study looked at the extent of substance misuse in a group of 187 chronically mentally ill patients living in the community. According to the clinician's ratings, around a third of the sample used alcohol, street drugs, or both during the six months before evaluation.

Further UK studies have shown slightly more moderate rates of substance misuse among mentally ill individuals. One study found that individuals suffering from schizophrenia showed just a 7% prevalence of problematic drug use in the year prior to being interviewed and 21% reported problematic use some time before that.

Wright and colleagues identified individuals with psychotic illnesses who had been in contact with services in the London borough of Croydon over the previous 6 months. Cases of alcohol or substance misuse and dependence were identified through standardized interviews with clients and keyworkers. Results showed that prevalence rates of dual diagnosis were 33% for the use of any substance, 20% for alcohol misuse only and 5% for drug misuse only. A lifetime history of any illicit drug use was observed in 35% of the sample.

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.

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.

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%).

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.

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.

Treatments for alcohol dependence can be separated into two groups, those directed towards severely alcohol-dependent people, and those focused for those at risk of becoming dependent on alcohol. Treatment for alcohol dependence often involves utilizing relapse prevention, support groups, psychotherapy, and setting short-term goals. The Twelve-Step Program is also a popular process used by those wishing to recover from alcohol dependence.

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.

Amount, frequency, and timing of prenatal alcohol use can dramatically impact the other three key features of FASD. While consensus exists that alcohol is a teratogen, there is no clear consensus as to what level of exposure is toxic. The CDC guidelines are silent on these elements diagnostically. The IOM and Canadian guidelines explore this further, acknowledging the importance of significant alcohol exposure from regular or heavy episodic alcohol consumption in determining, but offer no standard for diagnosis. Canadian guidelines discuss this lack of clarity and parenthetically point out that "heavy alcohol use" is defined by the National Institute on Alcohol Abuse and Alcoholism as five or more drinks per episode on five or more days during a 30-day period.

"The 4-Digit Diagnostic Code" ranking system distinguishes between levels of prenatal alcohol exposure as "high risk" and "some risk". It operationalizes high risk exposure as a blood alcohol concentration (BAC) greater than 100 mg/dL delivered at least weekly in early pregnancy. This BAC level is typically reached by a 55 kg female drinking six to eight beers in one sitting.

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.

For many adopted or adults and children in foster care, records or other reliable sources may not be available for review. Reporting alcohol use during pregnancy can also be stigmatizing to birth mothers, especially if alcohol use is ongoing. In these cases, all diagnostic systems use an unknown prenatal alcohol exposure designation. A diagnosis of FAS is still possible with an unknown exposure level if other key features of FASD are present at clinical levels.

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.

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.

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.

As demonstrated by the chart below, numerous studies have examined factors which mediate substance abuse or dependence. In these examples, the predictor variables lead to the mediator which in turn leads to the outcome, which is always substance abuse or dependence. For example, research has found that being raised in a single-parent home can lead to increased exposure to stress and that increased exposure to stress, not being raised in a single-parent home, leads to substance abuse or dependence. The following are some, but by no means all, of the possible mediators of substance abuse.

As demonstrated by the chart below, numerous studies have examined factors which moderate substance abuse or dependence. In these examples, the moderator variable impacts the level to which the strength of the relationship varies between a given predictor variable and the outcome of substance abuse or dependence. For example, there is a significant relationship between psychobehavioral risk factors, such as tolerance of deviance, rebelliousness, achievement, perceived drug risk, familism, family church attendance and other factors, and substance abuse and dependence. That relationship is moderated by familism which means that the strength of the relationship is increased or decreased based on the level of familism present in a given individual.

Examples of mediators and moderators can be found in several empirical studies. For example, Pilgrim et al.’s hypothesized mediation model posited that school success and time spent with friends mediated the relationship between parental involvement and risk-taking behavior with substance use (2006). More specifically, the relationship between parental involvement and risk-taking behavior is explained via the interaction with third variables, school success and time spent with friends. In this example, increased parental involvement led to increased school success and decreased time with friends, both of which were associated with decreased drug use. Another example of mediation involved risk-taking behaviors. As risk-taking behaviors increased, school success decreased and time with friends increased, both of which were associated with increased drug use.

A second example of a mediating variable is depression. In a study by Lo and Cheng (2007), depression was found to mediate the relationship between childhood maltreatment and subsequent substance abuse in adulthood. In other words, childhood physical abuse is associated with increased depression, which in turn, in associated with increased drug and alcohol use in young adulthood. More specifically, depression helps to explain how childhood abuse is related to subsequent substance abuse in young adulthood.

A third example of a mediating variable is an increase of externalizing symptoms. King and Chassin (2008) conducted research examining the relationship between stressful life events and drug dependence in young adulthood. Their findings identified problematic externalizing behavior on subsequent substance dependency. In other words, stressful life events are associated with externalizing symptoms, such as aggression or hostility, which can lead to peer alienation or acceptance by socially deviant peers, which could lead to increased drug use. The relationship between stressful life events and subsequent drug dependence however exists via the presence of the mediation effects of externalizing behaviors.

An example of a moderating variable is level of cognitive distortion. An individual with high levels of cognitive distortion might react adversely to potentially innocuous events, and may have increased difficulty reacting to them in an adaptive manner (Shoal & Giancola, 2005). In their study, Shoal and Giancola investigated the moderating effects of cognitive distortion on adolescent substance use. Individuals with low levels of cognitive distortion may be more apt to choose more adaptive methods of coping with social problems, thereby potentially reducing the risk of drug use. Individuals with high levels of cognitive distortions, because of their increased misperceptions and misattributions, are at increased risk for social difficulties. Individuals may be more likely to react aggressively or inappropriately, potentially alienating themselves from their peers, thereby putting them at greater risk for delinquent behaviors, including substance use and abuse. In this study, social problems are a significant risk factor for drug use when moderated by high levels of cognitive distortions.

Substance abuse, also known as drug abuse, is a patterned use of a substance (drug) in which the user consumes the substance in amounts or with methods which are harmful to themselves or others.

The drugs used are often associated with levels of intoxication that alter judgment, perception, attention and physical control, not related with medical or therapeutic effects. It is often thought that the main abused substances are illegal drugs and alcohol; however it is becoming more common that prescription drugs and tobacco are a prevalent problem.

Substance-related disorders, including both substance dependence and substance abuse, can lead to large societal problems. It is found to be greatest in individuals ages 18–25, with a higher likelihood occurring in men compared to women, and urban residents compared to rural residents. On average, general medical facilities hold 20% of patients with substance-related disorders, possibly leading to psychiatric disorders later on. Over 50% of individuals with substance-related disorders will often have a "dual diagnosis," where they are diagnosed with the substance abuse, as well as a psychiatric diagnosis, the most common being major depression, personality disorder, anxiety disorders, and dysthymia.

Substance-related disorders were originally subcategorized into "substance use disorders" (SUD) and "substance-induced disorders" (SID). Though DSM-IV makes a firm distinction between the two, SIDs often occur in the context of SUDs.

Risk factors for mental illness include genetic inheritance, such as parents having depression, or a propensity for high neuroticism or "emotional instability".

In depression, parenting risk factors include parental unequal treatment, and there is association with high cannabis use.

In schizophrenia and psychosis, risk factors include migration and discrimination, childhood trauma, bereavement or separation in families, and abuse of drugs, including cannabis, and urbanicity.

In anxiety, risk factors may include family history (e.g. of anxiety), temperament and attitudes (e.g. pessimism), and parenting factors including parental rejection, lack of parental warmth, high hostility, harsh discipline, high maternal negative affect, anxious childrearing, modelling of dysfunctional and drug-abusing behaviour, and child abuse (emotional, physical and sexual).

Environmental events surrounding pregnancy and birth have also been implicated. Traumatic brain injury may increase the risk of developing certain mental disorders. There have been some tentative inconsistent links found to certain viral infections, to substance misuse, and to general physical health.

Social influences have been found to be important, including abuse, neglect, bullying, social stress, traumatic events and other negative or overwhelming life experiences. For bipolar disorder, stress (such as childhood adversity) is not a specific cause, but does place genetically and biologically vulnerable individuals at risk for a more severe course of illness. The specific risks and pathways to particular disorders are less clear, however. Aspects of the wider community have also been implicated, including employment problems, socioeconomic inequality, lack of social cohesion, problems linked to migration, and features of particular societies and cultures.