“Alcohol” is the name of a family of closely-related and naturally-occurring chemicals. Each of the chemicals that are called “alcohol” is made up of molecules that contain a single oxygen atom and varying numbers of hydrogen and carbon atoms.
Ingestible alcohol is known as ethyl alcohol or ethanol. It is this type of alcohol that is found in beer, wine, or liquor and that is most often consumed in the form of a standard drink. Regardless of the type of drink that is consumed (e.g., a can of beer, a glass of wine, or a shot of liquor), it contains the same amount of ethanol. It is this type of alcohol that is commonly consumed in combination with driving to result in impaired driving incidents.
Ethanol is a central nervous system depressant, meaning it does not affect a person until it gets into his or her central nervous system (e.g., the brain, brain stem and spinal cord). Ethanol gets to the brain by getting into the blood. In order to get into the blood, it has to get into the body.
Alcohol can be ingested and absorbed in a variety of ways. For example, fumes can be inhaled, it can be injected, or it can be inserted as an enema. However, in most cases alcohol is ingested orally by drinking.
Once alcohol gets into the stomach, it moves into the blood by absorption through the walls of the stomach. However, the alcohol does not have to be digested in order to be absorbed. Drinking on an empty stomach creates an ideal circumstance for rapid absorption.
When alcohol gets into an empty stomach, about 20% of it will make its way directly through the walls of the stomach. The remaining 80% will pass through the base of the stomach and enter the small intestine, where it is readily absorbed into the blood. Due to the fact that the body doesn’t need to digest the alcohol before admitting it to the bloodstream, the small intestine will be open to the alcohol as soon as it hits the stomach.
However, when the brain senses food in the stomach, it commands a small muscle (the pyloric valve) at the base of the stomach to constrict and cut off the passage of alcohol to the small intestine. When the muscle is constricted, the food and any alcohol remain trapped in the stomach. Some of this alcohol will begin to break down chemically before it ever gets into the blood. The pylorus will begin to relax as food is digested but the overall effect will be to slow the absorption of alcohol significantly. So, when food is in the stomach, the alcohol will get into the blood more slowly. At the same time, the body will continue to process and eliminate the alcohol that does manage to get into the blood. For this reason, the drinker’s BAC will not climb as high as it would if he or she had been drinking on an empty stomach.
Alcohol has an affinity for water. Once it moves from the stomach into the blood it will be distributed throughout the body in the various tissues and organs in proportion with their water content. Brain tissue has a fairly high water content so it receives a substantial share of the distributed alcohol.
There are some important differences in the way that alcohol is distributed in men and women. This is because, unlike other drugs, alcohol is not very soluble in fat. The affinity of alcohol for water, and its lack of affinity for fat, helps explain an important difference in the way alcohol affects men and women. A Swedish pioneer in alcohol research, E.M.P. Widmark, determined that the typical male body is about 68% water; the typical female body has only about 55% water. Thus, when a woman drinks, she has less fluid – pound for pound – in which to distribute alcohol.
As a result, when a man and a woman drink exactly the same amount of alcohol under the same circumstances, the woman’s BAC will be higher. In addition, women are generally physically smaller then men, meaning that they have fewer pounds across which to distribute the alcohol. So the effects of alcohol on women are generally compounded: first because of the lower water content and second because of their smaller size.
As soon as alcohol enters the bloodstream the body starts trying to get rid of it. Some alcohol that is expelled by the body is chemically unchanged (e.g., in breath, urine, sweat, and tears). A small portion of the ingested alcohol (about 2-10%) will be directly eliminated in this manner.
However, the majority of alcohol that is consumed is eliminated by the body through the process of metabolism. Metabolism is a process of chemical change in which alcohol reacts with oxygen in the body and changes into carbon dioxide and water, both of which are directly expelled from the body.
Most of the metabolism of alcohol in the body takes place in the liver. An enzyme called alcohol dehydrogenase acts to speed up the reaction of alcohol with oxygen. The speed of this reaction varies somewhat from person to person, and even from time to time for any given person. On average, a male’s BAC will drop by about 0.015 per hour. For example, if a male reaches a maximum BAC of 0.15, it will take about 10 hours for him to eliminate all of the alcohol. In practical terms, this means that a typical male will eliminate about two-thirds of a drink per hour; a typical female will burn up about one-half of a drink in that hour.
Once alcohol has been consumed there is nothing that can be done to speed up the metabolism or the process of elimination. Drinking coffee, exercise, deep breathing, or a cold shower will NOT speed up the elimination process.
BAC stands for blood alcohol concentration. It is the concentration of alcohol in the blood, expressed as the weight of alcohol in a fixed volume of blood and is a measure used to determine an individual’s level of intoxication. BAC is measured by a percentage based on milligrams of alcohol per decilitre of blood. For example, 80mg is 0.08 grams. 0.08 grams of alcohol in 100 mLs is written as 0.08%. In other words, 80 mg% is equal to 0.08% which is equal to 80 mg/dL (deciliter; 100 mLs). This value can also be described as 0.08 BAC (which is the legal limit in most countries).
An individual’s alcohol concentration can depend on a number of factors such as body weight, the quantity and rate of alcohol ingestion, and the rates of alcohol absorption and metabolism. One thing is constant however – the higher the BAC, the greater the degree of physical and mental impairment.
Breath alcohol concentration (BrAC) is comparable to BAC and is easier to measure. Due to the strong correlation between the two measurements, they can be used as proxies for one another. Because of this, a breath alcohol concentration is accepted in court in lieu of a blood alcohol concentration.
Binge drinking can be defined as the consumption of large amounts of alcohol within a short period of time with the primary goal of becoming heavily intoxicated. In other words, binge drinking is a heavy, single occasion of drinking. According to the Canadian Medical Association, a binge drinking episode consists of five or more standard drinks for men and four or more standard drinks for women on a single occasion. Binge drinking can overlap with social drinking and is a growing concern among youth, particularly college/university students.
* A standard drink is considered to be one 355 ml bottle of beer or one 150 ml glass of wine or approximately 40 ml of spirits (e.g., rum, vodka, whisky, etc.).
Binge drinking can lead to many negative consequences that may have serious or life-long effects and possible death. Some of the risks associated with excessive alcohol consumption are:
a) Alcohol poisoning. Alcohol depresses the nervous system which is responsible for controlling involuntary bodily functions such as breathing. The nervous system also controls the gag reflex which prevents a person from choking. Large doses of alcohol can interfere with or prevent these functions. Due to the fact that alcohol is an irritant to the stomach, a person who consumes too many drinks will likely vomit (Canadian Public Health Association 2010). If the gag reflex is not working, there is a high likelihood that they will be unable to breath. Other symptoms of alcohol poisoning include unconsciousness, confusion, seizures, slow and/or irregular breathing, and pale/bluish skin (Centre for Addiction and Mental Health 2010).
b) Impaired judgment. The consumption of large amounts of alcohol has the ability to inhibit an individual from making sound decisions (Canadian Public Health Association 2010). This impaired judgment can lead individuals to take risks that they would not take if they were sober such as having unprotected sex (which carries with it a risk of sexually transmitted diseases), engaging in reckless behaviour that could lead to injury, or driving under the influence (Zeigler et al. 2005).
c) Mental health. Binge drinkers have a harder time focusing on tasks on a daily basis and for this reason they are less likely to succeed in school or maintain employment (Zeigler et al. 2005). Excessive and prolonged drinking can disrupt sleep patterns which affects an individual’s ability to concentrate (NIAAA 1998). It can also produce mood changes/swings, brain damage, and memory loss.
d) Alcoholism. Individuals who engage in binge drinking frequently (three or more episodes in a two week period) may be classified as alcoholics and begin to exhibit some of the symptoms associated with alcoholism (NIAAA 2007). These symptoms include stomach ulcers, sexual problems (impotency and infertility), cirrhosis of the liver, heart disease, nutritional deficiencies, alcoholic dementia, etc.
The long-term consequences of alcohol consumption vary and affect almost every part of the human body. Those who regularly consume large quantities of alcohol are at greater risk of developing heart problems, liver disease, and brain damage. The following is a list of potential ailments that alcohol abuse can cause/exacerbate:
The consumption of alcohol can also result in injuries linked to irresponsible or risky behaviour (e.g., falls, sports injuries, self-inflicted injuries, domestic violence, and other social conflicts). The slowing of reaction times, diminished coordination, increased aggression, and impaired judgment can result in an unintentional injury.
An unborn fetus is placed at risk of brain damage when a mother consumes alcohol during the course of her pregnancy. Fetal Alcohol Spectrum Disorder (FASD) is a term that describes a range of disabilities that may affect people whose mothers drank alcohol while they were pregnant. These disorders include:
The most commonly cited disorder is FAS which is characterized by growth deficiencies, facial anomalies, and damage to the central nervous system (including mental retardation). Babies who suffer from FAS are also more likely to be born prematurely and have lower weights at birth. People who have FAS will have trouble learning and controlling their behaviour. Recent estimates suggest that approximately 1% of the Canadian population (300,000) suffer from FASD (Public Health Agency of Canada, 2010).
There is no safe quantity of alcohol that can be consumed during a pregnancy as studies have not been able to determine if there is a specific amount that causes FASD. For these reasons, all doctors advise against alcohol consumption during pregnancy.
It is obvious that alcohol has an impact on the brain as common side effects of consumption are lapses in memory, slurred speech, slowed reaction times, and impaired motor skills. While most of these side effects will subside once an individual has sobered, continual consumption can lead to permanent brain damage.
Alcohol not only impairs judgment, it also affects memory. Alcohol has the ability to disrupt the processing of recent events and experiences into long-term memories (Westrick et al. 1988; Mintzer and Griffiths 2002). Large quantities of alcohol can produce a blackout, a period of time where the person does not remember what occurred (White 2003). These lapses in memory are especially common during episodes of binge drinking. During these intervals of time, individuals can participate in risky or dangerous behaviour such as drunk driving or having unprotected sex without being aware of their actions. They are unlikely to recall what occurred even when sober. Blackouts may also result from the way alcohol suppresses REM sleep.
Studies done on repeat impaired driving offenders reveal that they suffer from neurocognitive impairments particularly with regard to memory capacity and executive functioning (Ouimet et al. 2007). These offenders are unable to learn and retain information or successfully engage in treatment interventions. They also have few behavioural inhibitions and seek immediate gratification (Brown et al. 2009).
Prolonged and excessive drinking can also affect cognition by physically shrinking the brain, which MRI scans show is especially striking in women, who have less of a stomach enzyme that assists in the digestion of alcohol (Wuethrich 2001).
The National Institute on Alcohol Abuse and Alcoholism (NIAAA) identifies several factors that will determine to what extent alcohol consumption will affect the brain. These factors include:
As previously mentioned, long-term alcohol consumption can lead to strokes, dementia, alcohol-related psychoses, and development issues in unborn children. It can also contribute to depression and exacerbate other mental health disorders such as schizophrenia. A common brain disorder that many alcoholics have is Wernicke-Korsakoff Syndrome. The disorder is a combination of two syndromes (Wernicke’s encephalopathy and Korsakoff’s psychosis) that affect several areas of the brain, particularly the cerebellum. Some of the symptoms associated with the disorder include mental confusion, paralysis of the ocular nerves, loss of muscle coordination, difficulty learning and retaining information, and loss of memory (National Institute of Neurological Disorders and Stroke 2007).
Much of the brain damage linked to alcohol consumption is irreversible and can result in the need for full-time custodial care.
There is evidence that links alcohol consumption to depression (Davidson and Ritson 1993; Gorwood 1999). Alcohol consumption and depression often occur in combination and can have a cyclical relationship where one enhances the other. Research has found that alcohol dependence and major depressive episodes occur together, typically within short periods of time (Kessler et al. 1996; Kessler et al. 1997; Lynskey 1998). The greater the amount of alcohol consumed, the more symptoms of depression are likely to appear (Mehrabian 2001). Depression is found more frequently in patients who are being treated for alcohol abuse than in the general populace (Lynskey 1998). Similarly, a higher frequency of alcohol abuse is seen in patients who are being treated for depression (Alpert et al. 1999). It is difficult to isolate alcohol consumption as a cause of depression, however, excessive alcohol consumption may precede the onset of depression and symptoms tend to decrease during a period of abstinence which seems to suggest that alcohol is a factor in depression (World Health Organization 2004).
Responsible drinking is the opposite of excessive alcohol consumption or binge drinking. In order to drink responsibly, an individual should plan ahead and consume alcohol in moderation. The National Alcohol Strategy Working Group (2007) states that there needs to be a shift in public attitudes and thinking in order to develop a ‘culture of moderation’ which includes “understanding when, when not, and how much to drink, appropriate motivations for drinking, and settings in which responsible drinking should take place” (1). In other words, individuals should drink sensibly so as not to put themselves in situations where they are likely to sustain injuries or experience harm – i.e., impaired driving.
It should be noted that being responsible does not mean abstaining from alcohol. In fact, there are proven health benefits associated with moderation consumption (see next question). The recommended consumption is one drink per day for women (up to 9 drinks per week) and one to two drinks per day for men (up to 14 drinks per week) (Canadian Public Health Association 2010).
While excessive consumption of alcohol can cause and/or contribute to many physical and psychological ailments there are numerous benefits associated with moderate and responsible consumption. These include:
In order to safely drive a vehicle, an individual must be alert and have quick reaction times. The more alcohol a person consumes, the harder it becomes for them to drive in a proper and safe manner. As noted in the Magnitude section, many studies have determined that human performance skills, including driving, begin to decline at BACs above zero (Borkenstein et al. 1964; Blomberg et al. 2009; Peck et al. 2008). The greater the level of impairment becomes, the more likely that individual is to be involved in a collision. This is called relative risk – essentially, as a driver’s BAC increases the risk of collision also increases.
A study conducted in Long Beach, California and Fort Lauderdale, Florida revealed that a notable relationship between risk and BAC begins at .04-.05 and increases exponentially once BACs reach .10 or greater (Blomberg et al., 2009). This means that driving with even a legal amount of alcohol in one’s system greatly increases the risk of collision. Every drink that a person consumes has the ability to slow their reaction time which can also be hindered by the other effects of consumption such as blurred vision and drowsiness. Essentially, a person who is impaired has a greater likelihood of being involved in a crash than someone who is sober.
Drowsiness increases with the length of time a person has been awake. People who get inadequate sleep or experience poor quality sleep may experience acute or chronic sleepiness (Findley et al. 1989; Cohen et al. 1992; Young et al. 1997). Drowsiness or sleepiness normally refers to the urge to fall asleep as the result of a biological needs – it is a physiological state of the body that is irreversible in the absence of sleep (Beirness et al. 2005). It is governed by a circadian sleep-wake cycle that makes most people feel sleepy twice a day – at night and in the afternoon (Dement and Vaughn 1999).
Sleep loss can increase drowsiness and the risk of crash involvement. Alcohol and other medications are known to enhance drowsiness (Horne et al. 2003; Ray et al. 1992; Ceutel 1995). More importantly, the use of alcohol can exacerbate the performance deficits associated with drowsiness creating a level of risk greater than either factor alone.
Low doses of alcohol relax the drinker by slowing the activity of the sympathetic nervous system (Roehrs and Roth 2001). With larger doses, alcohol can further slow reactions and diminish one’s ability to perform tasks such as driving. When paired with inadequate sleep, alcohol can become a very potent sedative and increase an individual’s risk of crashing.
Prolonged alcohol consumption can potentially induce sleep disorders as it disrupts normal sleep patterns and the time that an individual sleeps per night (NIAAA 1998). The consumption of alcohol within an hour of bedtime may help one to fall asleep more quickly but it is likely to result in inadequate sleep during the second half of the sleep period – this is characterized with being awakened by dreams and having difficulty falling back asleep (Landolt et al. 1996). This disruption in sleep can lead to fatigue and drowsiness during the day as well as a lack of alertness.
Therefore, drivers under the influence of alcohol are at risk for involvement in crashes due to fatigued driving because alcohol has sedating effects that, when combined with fatigue or drowsiness, can exacerbate performance deficits (Horne et al. 2003; Lumley et al. 1987).
An extensive body of research has clearly established that alcohol use by drivers can increase the risk of collision (e.g., Mayhew et al. 1986). There have also been multiple studies that have tracked the changes in the magnitude of the problem over the past thirty years and shown that the prevalence of alcohol use by drivers has declined, along with the prevalence of alcohol in serious collisions (Mayhew et al. 2005). By contrast, much less is known about the contribution of drug-impaired driving to serious collisions or about the prevalence of drug use by drivers.
There are many reasons for the disparity between the extent of knowledge about the role of alcohol in crashes and the role of drugs in crashes (see for example, Simpson 1985, 1986; Simpson and Vingilis 1991). Among them are:
Mixing alcohol with drugs (both legal and illegal) can be very dangerous. Alcohol is a depressant that slows down the body’s central nervous system which controls heart rate and breathing. The sedative effects of the alcohol can be enhanced when combined with another drug to the point where the body could completely shut down. This combined effect of alcohol and drugs further impairs an individual’s ability to drive and places them at an increased risk of collision. The combined effect is greater than the impairment of either substance on its own – i.e., the effects are addictive.
For example, there is a substantial body of evidence that shows a high correlation between alcohol use and marijuana use (e.g., Christophersen 2006). In studies that have examined alcohol and drugs among drivers involved in serious crashes, it is not uncommon to find ¾ of those who are positive for cannabis are also positive for alcohol. Based on 2006 survey data, 69% of those who reported driving after using marijuana also reported driving within two hours of drinking. This has important safety implications because it has been established that the combined use of marijuana and alcohol increase the risk of collision (Stewart 2006) – some have suggested that the two substances impair different sets of skills and capacities, so the combined effects are additive.
Self-report surveys have been used to examine the extent to which people consume drugs and drive. The Canadian Road Safety Monitor conducted by the Traffic Injury Research Foundation (TIRF) revealed that 2.4% of respondents to a public opinion poll in 2005 admitted to driving within two hours of taking drugs in the last 12 months, and that the problem is growing given that this percentage has increased from 1.5% in 2002 to 2.1% in 2004 (Simpson et al. 2006). These findings are also comparable to other Canadian research. Indeed, a similar 2004 survey by the Canadian Centre on Substance Abuse (CCSA) now puts the estimate at over 4% (Adlaf et al. 2005).
Research into the drugged driving issue has also taken the form of roadside surveys, including one conducted in British Columbia in 2008. This survey showed that 10.4% of drivers tested positive for drug use with cannabis and cocaine being the most frequently detected drugs (Beirness and Beasley 2009). A 2007 American national roadside survey funded by the National Highway Traffic Safety Administration (NHTSA) revealed that more than 16% of weekend, nighttime drivers tested positive for illegal, prescription, or over-the-counter medication (NHTSA 2007). More than 11% tested positive for illicit drugs.
Studies have also repeatedly demonstrated that drugs are often found among fatally injured drivers. Research has confirmed that although the total prevalence of drugs (licit and illicit) is less than the prevalence of alcohol, the use of drugs is by no means uncommon. For example, in a study in British Columbia 48% of the cases tested positive for alcohol and 20% tested positive for some drug (Jeffery et al. 1995); in a more recent Quebec study, 35% of the cases were positive for alcohol and 30% were positive for some drug (Dussault et al. 2002).
Moreover, all the studies conducted in Canada over the past few decades have found that the most commonly detected illegal substance was cannabis — 11% in the TIRF studies in Ontario (Cimbura 1982, Cimbura et al. 1990); 13% in the B.C. study and 19.5% in the Quebec study, both of which were cited above. Drivers who were positive for cannabis were much more likely to be male and under the age of 25. Such findings are not unique to Canada (see for example Drummer et al. 2004 for examples of Australia). However, one of the factors that make it difficult to determine what role cannabis played in the fatal crashes is the presence of not only the drug, but alcohol as well. For example, in the Ontario study, among those who were positive for cannabis, 84% were also positive for alcohol. Therefore, it becomes difficult to determine which substance caused the impairment (and to what degree) that resulted in the fatal collision.
Young people are vulnerable to alcohol-induced brain damage, which could contribute to memory loss and poor performance in the classroom (and later in the workforce) as well as behavioural problems. Adolescence is the transition period between childhood and adulthood. During this time, significant changes occur in the body including the formation of new networks in the brain. Frontal lobe development and the refinement of neural pathways and connections continue until during teenage years and into the early 20s (Begley 2000). Damage from alcohol at this time can be long-term and irreversible affecting both memory and behaviour control (White 2001; Brown et al. 2001). By exposing the brain to alcohol during this period, key processes of brain development may be interrupted which can cause damage.
Medical findings confirm this danger: the hippocampus, the part of the brain that is the centre for learning and memory, is smaller in adolescents who are alcohol-dependent (Nagel et al. 2005). These youth may never be able to catch up to their peers in adulthood because they will have learning difficulties, memory loss, and trouble maintaining employment and relationships.
The problem of youth drinking is cause for concern. According to the 2004 Canadian Addiction Survey, the majority of Canadian youth aged 15 and older have consumed alcohol, both in the past year (82.9%) and in their lifetime (90.8%). The average age that these youth are initiated into drinking is 15.6 years. Similar numbers exist in the US as the 2008 National Survey on Drug Use and Health found that about 10.1 million Americans between ages 12-20 report current alcohol consumption; this represents nearly 26% of this age group for whom alcohol consumption is illegal (SAMHSA 2008).
Statistics such as these are disturbing given that the earlier the age of onset alcohol consumption, the greater the likelihood that its usage may develop into an addiction later in life. The earlier that youth start drinking, the more likely they are to drink heavily on a frequent basis and experience alcohol-related harm (National Alcohol Strategy Working Group 2007). People who begin drinking before age 15 are four times more likely to develop alcohol dependence at some time in their lives compared to those who have their first drink at 20 or older.
The negative consequences associated with underage drinking are numerous:
Given the serious nature of these consequences, adolescents should be educated about the dangers of alcohol.