The effects of depressants are in many ways similar to the effects of alcohol.
Small amounts can produce calmness and very relaxed muscles, but larger doses
can cause slurred speech, staggering gait, and altered perception. Very large
doses can cause respiratory depression, coma, and death. The combination of
depressants and alcohol can multiply the effects of the drugs, increasing
Regular use of depressants over time can result in physical and psychological
addiction. People who suddenly stop taking large doses can experience withdrawal
symptoms, including anxiety, insomnia, tremors, delirium, convulsions, and
death. Babies born to mothers who abuse depressants may also be physically
dependent on the drugs and show withdrawal symptoms shortly after they are
born. Birth defects and behavioral problems also may result.
Historically, people of almost every culture have used chemical agents to
induce sleep, relieve stress, and allay anxiety. While alcohol is one of the
oldest and most universal agents used for these purposes, hundreds of substances
have been developed that produce central nervous system (CNS) depression.
These drugs have been referred to as "downers," sedatives, hypnotics, minor
tranquilizers, anxiolytics, and antianxiety medications. Unlike most other
classes of drugs of abuse, depressants, except for methaqualone, are rarely
produced in clandestine laboratories. Generally, legitimate pharmaceutical
products are diverted to the illicit market.
Although a number of depressants (i.e., chloral hydrate, glutethimide, meprobamate
and methaqualone) have been important players in the milieu of depressant
use and abuse, two major groups of depressants have dominated the licit and
illicit market for nearly a century, first barbiturates and now benzodiazepines.
Barbiturates were very popular in the first half of this century. In moderate
amounts, these drugs produce a state of intoxication that is remarkable similar
to alcohol intoxication. Symptoms include slurred speech, loss of motor coordination
and impaired judgement. Depending on the dose, frequency, and duration of
use, one can rapidly develop tolerance, physical dependence and psychological
dependence on barbiturates. With the development of tolerance, the margin
of safety between the effective dose and the lethal dose becomes very narrow.
That is, in order to obtain the same level of intoxication, the tolerant abuser
may raise his or her dose to a level that can produce coma and death. Although
many individuals have taken barbiturates therapeutically without harm, concern
about the addiction potential or barbiturates and the ever-increasing numbers
of fatalities associated with them led to the development of alternative medications.
Today, only about 20% of all depressant prescriptions in the U.S. are for
Benzodiazepines were first marketed in the 1960s. Touted as much safer depressants
with far less addiction potential than barbiturates, these drugs today account
for about 30% of all prescriptions for controlled substances. It has only
been recently that an awareness has developed that benzodiazepines share many
of the undesirable side effects of the barbiturates. A number of toxic CNS
effects are seen with chronic high dose benzodiazepine therapy. These include
headache, irritability, confusion, memory impairment, depression, insomnia
and tremor. The risk of developing over-sedation, dizziness and confusion
increases substantially wit higher doses of benzodiazepines. Prolonged use
can lead to physical dependence even at recommended dosages. Unlike barbiturates,
large doses of benzodiazepines are rarely fatal unless combined with other
drugs or alcohol. Although primary abuse of benzodiazepines is well documented,
abuse of these drugs usually occurs as part of a pattern of multiple drug
abuse. For example, heroin or cocaine abusers will use benzodiazepines and
other depressants to augment their "high" or alter the side effects associated
with over-stimulation or narcotic withdrawal.