Is Alcohol a Depressant? The Biphasic Effects of Alcohol
Kenneth Anderson, M.A.
First, it is important to define our terms. A stimulant is a drug which raises levels of physiological or nervous activity. A depressant is the opposite of a stimulant, i.e., a depressant is a drug which lowers levels of physiological or nervous activity. A depressant is not a drug which causes depressed mood; the correct term for a drug which causes depressed mood is a depressogen. A depressogen is the opposite of an antidepressant, just as a depressant is the opposite of a stimulant. Although alcohol can act as a depressogen and cause depression in some people, alcohol also acts as a euphoriant, and some people drink to feel less depressed. However, this is beyond the scope of our article, and we shall focus on the stimulant and depressant effects of alcohol.
Looking Back
Throughout most of the 19th century, alcohol was regarded as a stimulant, although in the latter part of the 19th century the question was raised as to whether alcohol should be classed as a stimulant or a depressant. The Dispensatory of the United States of America was the standard drug reference for US doctors of the era, much as the PDR (Physician’s Desk Reference) is today. The 14th edition of the Dispensatory, published in 1879, refers to alcohol as solely a stimulant. It was not until the 15th edition, published in 1883, that alcohol was referred to as a stimulant in small doses, but a depressant in large doses. Emil Kraepelin’s 1883 study found mixed results as to whether alcohol was a stimulant or a depressant.
Oswald Schmiedeberg, known as the father of modern pharmacology, in his 1883 book Grundriss der Arzneimittellehre (translated into English as Elements of Pharmacology in 1887), denied that alcohol had any intrinsic stimulant effects and classed it in the same group as chloroform, ether, paraldehyde, etc. Schmiedeberg claimed that apparent stimulant effects were a secondary byproduct of alcohol’s depressant effects. Gustav von Bunge expressed a similar opinion in his 1887 monograph Die Alkoholfrage [The Alcohol Question]. A 1915 study by Dodge and Benedict showed that alcohol had depressant effects on reaction times and motor coordination. Further experiments were published by Walter R. Miles in 1924. By the time of the publication of the 20th edition of the Dispensatory in 1918, the 21st edition in 1926, and the 23rd edition in 1943, the depressant qualities of alcohol were emphasized.
What Recent Research Shows
However, more recent research has shown that alcohol has both stimulant and depressant effects: this phenomenon is known as the biphasic effect of alcohol.
A 1977 study by Larissa A. Pohorecky showed that small doses of alcohol led to increased physical activity in animals and humans (a stimulant effect), whereas larger doses led to decreased physical activity (a depressant effect).
A 1983 study by Patricia B. Sutker et al. pointed out that people showed elevated positive mood states while blood alcohol content (BAC) was rising, but showed negative mood states while BAC was falling. In other words, there are two phases after alcohol is consumed: During the first phase, alcohol is being absorbed from the digestive tract into the blood stream more quickly than it is being metabolized by the liver and BAC rises. During the second phase, all the alcohol has already been absorbed into the blood stream, and BAC falls as the alcohol is metabolized by the liver. During the first phase, mood is positive, and during the second phase, mood is negative. Since there are two phases, this is called a biphasic effect.
In 1993, Christopher S. Martin et al published the Biphasic Alcohol Effects Scale, which measures the stimulant and sedative (i.e., depressant) effects of alcohol.
A 1998 study by Louis Holdstock and Harriet de Wit found that half of people tested experienced only the sedative (i.e., depressant) effects of alcohol regardless of whether their BAC was rising or falling; the other half experienced stimulant effects while BAC was rising and depressant effects while BAC was falling.
Interestingly, a 2002 study by Andrea C. King et al. found that heavy drinkers reported more stimulant effects of the same dose of alcohol than did light drinkers, who reported more sedative effects. This suggests that it is the stimulant effects of alcohol which give positive reinforcement, and which lead people to become heavy drinkers.
The Most Thorough Study To-Date
The most thorough study of the biphasic effects of alcohol is a 2007 study by Merideth A. Addicott et al. The Addicott group performed an experimental study with 30 subjects, 15 male and 15 female. The Addicott group studied the effects over time of three different doses of alcohol: 0.4, 0.6, or 0.8 g/kg. This is the equivalent of 3, 4.5, and 6 US standard drinks for a person weighing 230 pounds. Alcohol doses were reduced somewhat for female subjects as it is well known that the same dose of alcohol produces higher BACs in women than in men of the same weight.
The experiments were conducted over a period of four days, from 8:00 AM to 4:30 PM. This allowed each subject to get all three different doses of alcohol as well as the placebo dose with no alcohol on different days. Subjects were given either a dose of alcohol concealed in tonic or a placebo consisting of plain tonic with 2 ml of alcohol applied to the rim of the glass to give the smell of alcohol. This was a randomized double-blind controlled trial, neither the researchers nor the subjects knew who got the alcohol and who got the placebo.
In order to measure physical activity, the researchers had each subject wear an Actiwatch on the wrist of their dominant hand. The Actiwatch is a device similar to a Fitbit, which measures physical activity. Subjects were given their dose of alcohol or placebo at 9:00 AM and tracked until 12:30 PM. BAC peaked at 10:15 AM, i.e., prior to 10:15 AM, BAC was rising, after 10:15 AM, BAC was falling. There were no significant differences between the groups in terms of physical activity before the alcohol or placebo was administered at 9:00 AM.
During the period from 9:00 AM to 9:30 AM, the group which received the 0.8 g/kg dose of alcohol was significantly more physically active than the group receiving the placebo. During the period from 9:30 AM to 10:00 AM, all three groups which received alcohol were significantly more physically active than the group receiving the placebo. During the period from 10:00 AM to 10:30 AM, the 0.8 g/kg group and the 0.6 g/kg group were significantly more physically active than the group receiving the placebo. During the period from 10:30 AM to 11:00 AM, the 0.8 g/kg group was significantly more physically active than the group receiving the placebo. During the period from 11:00 AM to 11:30 AM, no group was significantly more physically active than the group receiving the placebo. During the period from 11:30 AM to 12:00 noon, the 0.8 g/kg group and the 0.6 g/kg group were significantly more physically active than the group receiving the placebo. During the period from 12:00 noon to 12:30 PM, no group was significantly more physically active than the group receiving the placebo.
Subjects were also given the Biphasic Alcohol Effects Scale three times on each day of the experiment. They first took the test at 8:15 AM before the alcohol or placebo was administered. There were no significant differences between the groups on either the stimulation subscale or the sedation subscale at this time. They were next given the test at 10:00 AM, when BAC was rising. At this time, the 0.6 g/kg group scored significantly higher on the stimulation subscale than the placebo group, and both the 0.8 g/kg group and the 0.6 g/kg group scored significantly higher than the placebo group on the sedation subscale. In other words, the 0.6 g/kg group was simultaneously both more stimulated and more sedated than the placebo group. The subjects were tested for a third time at 12:30 PM, when BAC was falling. At this time, no group scored significantly higher than the placebo group on the stimulation subscale; however, both the 0.8 g/kg group and the 0.6 g/kg group scored significantly higher than the placebo group on the sedation subscale. Moreover, the sedation scores of these two groups were much higher at 12:30 PM than they had been at 10:00 AM.
After the testing was completed at 12:30 PM, the subjects were given a meal at 1:00 PM, and allowed to sober up until 4:30 PM, when they were sent home.
The neurobiological basis for the sedative (i.e., depressant) effects of alcohol is quite well understood. Alcohol increases the activity of the GABA (gamma aminobutyric acid) system in the brain. GABA is the primary inhibitory neurotransmitter in the brain. The more the GABA system is activated, the more everything in the brain slows down. Barbiturates and benzodiazepines have the same effect on the GABA system that alcohol has. Interestingly, neither barbiturates nor benzodiazepines are reported to have biphasic effects, even though they are cross-tolerant with alcohol.
Likewise, alcohol decreases the activity of the glutamate system in the brain. Glutamate is the primary excitatory neurotransmitter in the brain. The more the glutamate system is suppressed, the more everything in the brain slows down. Ketamine and dextromethorphan are also drugs which inhibit the glutamate system in the brain.
The Answer? Still Up for Debate
It is not entirely clear what the neurobiological basis of the stimulant effects of alcohol is; this is a topic currently under debate by scholars and will be discussed in a future blog post.
Liked this article? You might also be interested in: 12 Myths of Alcohol and Drug Addiction.