Depressants
You will now shift your study from performance-enhancing drugs to the class of medications that are collectively known as depressants. As classified, these medications collectively bring one “down” and create symptoms in individuals that are the antithesis of the stimulant class of medications (e.g., amphetamines, cocaine, caffeine) that you have previously covered in this course. Keep in mind that these drugs are manufactured in the laboratory and don’t naturally occur in the environment as many classes of drugs that you have previously studied in this course.
What are the major distinctions between barbiturates and benzodiazepines?
One of the original and major classes of depressants is that of barbiturates. They are tasteless and odorless and historically were prescribed as a sleep aid. Compared to benzodiazepines, which will be discussed shortly, barbiturates pose a greater health risk because of their broader, systemic effect upon the body. Depending on the dose taken, the effects of the barbiturates can range from mild relaxation to coma and death. As such, the threat of a lethal overdose is a significant concern.
In and of itself, the effects of barbiturates are positively reinforcing; animal studies have shown how consistency they will respond in an operant learning environment to receive a continuous infusion of barbiturates into their system. Barbiturates are also known to have a synergistic, or additive, affect when taken with alcohol; one can take a non-lethal dose of both but, when taken together, they can be a lethal combination to the unsuspecting user.
Individuals who take barbiturates at relatively low dose report feeling a sense of relaxation and euphoria. As the dose level of barbiturates increase, more primitive areas of the brain are subsequently affected, including those that control autonomic functions like consciousness and respiration. At these higher doses, people report feeling heavily sedated and drowsy. While initially used as a sleep aid, researchers demonstrated that this class of drugs is typically not well suited for that purpose. Specifically, it has been noted that Rapid Eye Movement (REM) sleep is inhibited during the periods when barbiturates have been taken. REM sleep is generally thought of as being one of the deepest stages of sleep and highly restorative to bodily functions. As such, individuals taking barbiturates often report feeling tired upon wakening and describe their sleep as not very restful. Further, upon discontinuation of barbiturates, many individuals experience a sleep “rebound” effect in terms of REM sleep in that they experience inordinately longer cycles of REM sleep than typical and these periods of sleep are characterized by highly vivid and often disturbing dreams.
Using barbiturates as a primary treatment for sleep problems can certainly lead to symptoms of dependence. Physiologically, the body builds up dependence to the drug with regards to effects on sleep, requiring progressively larger amounts of the drug to achieve sleep-inducing effects. Compared to other classes of drugs, the withdrawal from barbiturates can be very dangerous if attempted without medical supervision. Symptoms of withdrawal include tremors, vomiting, perspiration, nausea, convulsions, confusion and high fever. Individuals are negatively reinforced to continue taking the drug in an attempt to avoid these undesirable symptoms. As a result, the use of barbiturates as a sleep aid has largely been discontinued in the United States because of these risks.
Another important and more modern class of depressant is benzodiazepines. Compared to barbiturates, these are the next generations of depressants – they focus more selectively on the concerning symptoms of anxiety without causing global sedation across all bodily systems as its predecessor, barbiturates, do. This is preferred because the risk of a lethal overdose by shutting down the respiratory center in the brain is greatly reduced. In addition, benzodiazepines are absorbed more slowly into the bloodstream, avoiding any reinforcing “rush” effect where the resultant symptoms of relaxation more slowly with a longer duration of effect. As a result, this drug is a poor reinforcer of drug-using behavior. Benzodiazepines work by increasing the activity of the neurotransmitter GABA, which produces an inhibitory effect upon the central nervous system.
It is interesting to note that one of the primary uses for depressants in our society over the years has been to aid and sleep and to lesson symptoms of anxiety. While these drugs have been used with varying degrees of success in treating these ailments, it should be noted that there are a wide variety of cognitive-behavioral interventions that have been supported in research studies to address these problems without the use of drugs. For example, there is a whole body of research on sleep hygiene and the appropriate behavioral habits, routines, and nighttime rituals which can help promote and sustain healthy, natural sleeping patterns in individuals. Similarly, the available psychological literature on cognitive-behavioral treatments to address symptoms of anxiety has been well documented.
For a quick overview of anxiety disorders and how they can disrupt aspects of daily functioning like sleep, check out this 11-minute CrashCourse.com video:
https://www.youtube.com/watch?v=aX7jnVXXG5o
Unfortunately, many individuals in our society as well as healthcare professionals espousing the medical model often look to pharmaceutical interventions as a first-line solution for many problems in living. While it certainly takes fewer appointments and less effort on the part of the individual and care provider to simply prescribe a medication to an individual, as you have learned in reviewing the reading materials and this lesson for the week, it is not without its own risks in terms of health and symptoms of dependence. Other avenues of non-pharmaceutical intervention should be actively explored; often, those strategies can be generalized broadly and have longer-lasting effects for individuals without the risks associated with overreliance on drugs to ameliorate their symptoms.