What is Drug?

A drug is any animal, vegetable, or mineral substance used in the composition of medicines. It also refers to any stuff used in dyeing or in chemical operations. It is a substance that is used as a medicine or narcotic. A drug is capable of altering natural biological processes, with their manipulating nature used in medicine as a corrective measure against deviances from these normal biological processes. As described in the Webster Dictionary (1992), a drug, is a substance, other than food intended for use in the diagnosis, cure, mitigation, treatment, or prevention of disease in man or other animals.

It is any narcotic; also any substance or chemical agent, exclusive of food, employed for other than medical reasons to obtain a given physiological effect or to satisfy a craving. The drug affects the mind or body. The effect depends on the type of drug, the amount taken, when and how it is used, and the person who takes it (Webster, 1992). Drugs may be classified as uppers, downers, narcotics, mind-affecting (hallucinogens), or volatile chemicals. Uppers are stimulants that affect the nervous system to excite the user.

Downers are depressants that affect the central nervous system to relax the user. Narcotics affect the nervous system, and change many of the normal activities of the body, and often produce an intense state of excitement or distortion of the user’s senses. Volatile chemicals are depressants acting upon the central nervous system. It is important for the first aider to be able to detect possible drug abuse at the overdose level and to relate certain signs to certain types of drugs (Webster, 1992 p. FA-28). There are four levels of drug use.

Abstinence means not taking any drugs or any particular drug. Experimentation means trying a drug for the first time. It could be a doctor prescribing medicine, or a young person sniffing glue. If a user likes the effects of a drug, he or she may move to casual, recreational or regular use. Casual use is taking a drug only when a person feels like it or when a it is offered. Recreational use is a drug use for enjoyment in social situations. Regular use means taking drugs almost everyday. Habitual or problem drug becomes dependent (needs to have some of the drug everyday).

The user may have very little control over his or her problem drug use. The effects of this dependence can be serious, and sometimes fatal. With certain drugs, the user can develop a tolerance, or get used to the drug. He or she has to take very large amounts to feel the same effects. These drugs include alcohol, opiates, LSD, caffeine, amphetamines and tranquilisers. Psychological dependence can develop with any type of drug. The user believes that he or she will not be able to lead a normal life without taking the drug and becomes very upset if it is not available.

Physical dependence, when the body cannot work without a regular supply of the drug may happen with long term use. This is common with depressants and analgesics. Depressants slow the nervous system and relax the body. Alcohol is the most common, but other legal depressants are abused for these effects. These include barbiturates (sleeping pills), tranquilisers and solvents (glue and gases). Analgesics reduce the user’s reaction to pain, discomfort and anxiety. Opium, heroin and codeine are obtained from opium poppies.

Methadone and pethidine are synthetic (chemical rather than natural) analgesics. Many analgesics have medical uses. Withdrawal symptoms, which make the user feel unwell, can happen when a regular user stops taking a drug. When a person has an overdose, he or she takes more of the drug than the body can cope with, becomes very ill and may even die (Brown and King 1990). Mechanisms of Drug Action To describe the mechanism of drug action in the brain, whenever a person uses a drug and the effect it produces is somehow pleasant, this effect gets a rewarding quality for that person.

As experimental research by behavioural psychologists has demonstrated, all behaviours that are reinforced by a reward have a tendency to be repeated and learned. Successive repetitions, besides fixing the reward-producing behaviours, also fix all previously indifferent stimuli, sensations, and situations, eventually associated with those behaviours. Seeing particular places or persons, hearing specific music, etc, for instance, triggers in drug users the craving for their preferred drug. Using Positron Emission Tomography (PET), Dr.

Edythe D. London and her colleagues at the Addiction Research Centre, in Baltimore, obtained images showing that in cocaine-users, cues associated with the use of the drug sparked an increase in the metabolism of glucose in brain areas that are associated with memory and learning (lateral pre-frontal cortex, amygdala, and cerebellum). Up to now, is far from complete our knowledge about the cerebral, chemical and structural changes that underlie reward and act as reinforcers for different behaviours, including that of drug use.

Nevertheless, recent researches point to a chain of reactions, involving several neurotransmitters, leading to the release of the neurotransmitter dopamine in a brain region. Compare and contrast the Physical Dependence and Positive Incentive theories of drug addiction. Drug addiction has two components: physical dependency, and psychological dependency. Physical dependency occurs when a drug has been used habitually and the body has become accustomed to its effects. The person must then continue to use the drug in order to feel normal, or its absence will trigger the symptoms of withdrawal.

Psychological dependency occurs when a drug has been used habitually and the mind has become emotionally reliant of its effects, either to elicit pleasure or relieve pain, and does not feel capable of functioning without it. Its absence produces intense cravings, which are often brought on or magnified by stress. A dependent person may have either aspects of dependency, but often has both. “Chipping” is also a term used to describe a pattern of drug use in which the user is not physically dependent and sustains ‘controlled use’ of a drug.

This is done by avoiding influences that reinforce dependence, such that the drug is used for relaxation and not for escape. Physical Dependency Model After repeated exposure to certain drugs, withdrawal symptoms appear if the drug is discontinued. Withdrawal symptoms are compensatory reactions that oppose the primary effects of the drug. Therefore they are the opposite of the effects of the drug. Withdrawal effects are unpleasant and reduction in these effects would therefore constitute negative reinforcement.

[Negative reinforcement is the reinforcement of behaviour that terminates an aversive stimulus] Negative reinforcement could explain why addicts continue to take the drug. However some addicts will endure withdrawal symptoms (go ‘cold-turkey’) in order to reduce their tolerance so that they can recommence drug intake at a lower dose which costs less to purchase. Concentrating on the role of physical withdrawal effects at the expense of other psychological factors led to the failure to recognize the addictive properties of cocaine.

Cocaine does not produce physical dependency (tolerance and withdrawal symptoms) but it is more addictive than heroin. This diagram (redrawn from Julien, 1995), shows the changing pattern in the major drug used by patients admitted to drug treatment programs in New York City during the 1980s. It is also important to emphasize that reduction in withdrawal symptoms does not explain why people take drugs in the first place. Negative reinforcement may account for initial drug taking in some situations. For example, someone who is suffering from unpleasant emotions may experience a reduction in these feelings (i.

e. negative reinforcement) following drug administration. However the most likely reason for drug taking involves positive reinforcement. Positive Reinforcement Model The reinforcing properties of a drug are thought to be reason why most people become addicted to drugs. Addictive drugs are positive reinforcers (Carlson, 2001). As you know positive reinforcement can lead to learning a new response, and the maintenance of existing behaviours. It follows that the behaviours associated with taking an addictive drug (i. e. injecting or smoking it) will increase in probability.

One way of testing this claim is to examine the reinforcing properties of drugs in animals. We already know that conventional reinforcers support bar-pressing in animals, therefore if a drug maintains a response such as bar-pressing in an animal, it is a reinforcing stimulus. At one time it was believed that animals could not be made addicted to drugs, but that view is now rejected because technical developments have shown that animals will learn new behaviours that cause injection of drugs into their body. Explain how the study of reward circuits has provided a potential explanation of drug addiction.

The study of reward circuits has provided a potential explanation of drug addiction. The reinforcing effects of drugs during intoxication create an environment that, if perpetuated, triggers the neuronal adaptations that result in addiction. Imaging studies in drug abusers as well as non–drug abusers have shown that drugs of abuse increase the extra-cellular concentration of drug addiction in the striatum and that these increases were associated with their reinforcing effects. The subjects who had the greatest increases in drug addiction were the ones who experienced drug effects such as “high,” “rush,” or “euphoria” most intensely.

These studies also showed that the reinforcing effects appeared to be associated not only with the magnitude but also with the abruptness of the drug addiction increase. Thus, for an equivalent increase in drug addiction, the drug was experienced as reinforcing when it was injected intravenously, which leads to fast drug uptake in the brain and presumably very fast changes in drug addiction concentration, but not when it was given orally, which leads to a slow rate of brain uptake and presumably slow increases in drug addiction concentration.

The dependency of the reinforcing effects of drugs on fast and large increases in drug addiction concentration is reminiscent of the changes in drug addiction concentration induced by phasic drug addiction cell firing (fast-burst firing > 30 Hz), which also leads to fast changes in drug addiction concentration and whose function is to highlight the saliency of stimuli. This contrasts with tonic drug addiction cell firing (slow firing at frequencies around 5 Hz), which maintains base-line steady-state drug addiction levels and whose function is to set the overall responsiveness of the drug addiction system.

This led us to speculate that the ability of drugs of abuse to induce changes in drug addiction concentration that mimic but exceed those produced by phasic drug addiction cell firing results in over-activation of the neuronal processes that highlight saliency, and that this is one of the relevant variables underlying their high reinforcing value. However, studies show that increases in drug addiction concentration during intoxication occur in both addicted and non-addicted subjects, so this by itself cannot explain the process of addiction.

Since drug addiction requires chronic drug administration, we suggest that addiction results from the repeated perturbation of reward circuits (marked drug addiction increases followed by drug addiction decreases) and the consequent disruption of the circuits that it regulates (motivation/drive, memory/learning, and control). Indeed, imaging studies in drug-addicted subjects have consistently shown long-lasting decreases in the numbers of drug addiction D2 receptors in drug abusers compared with controls.

In addition, studies have shown that cocaine abusers also have decreased drug addiction cell activity, as evidenced by reduced drug addiction release in response to a pharmacological challenge with a stimulant drug. We postulate that the decrease in the number of drug addiction D2 receptors, coupled with the decrease in drug addiction cell activity, in the drug abusers would result in a decreased sensitivity of reward circuits to stimulation by natural reinforcers.

This decreased sensitivity would lead to decreased interest in ordinary (day-to-day) environmental stimuli, possibly predisposing subjects for seeking drug stimulation as a means to temporarily activate these reward circuits. Imaging studies provide evidence of disrupted sensitivity to natural reinforcers in addiction. For example, in a study by Martin-Solch and colleagues, the meso-striatal and meso-corticolimbic circuits of opiate addicts were not activated in response to natural reinforcers, whereas they were in controls subjects.

Similarly, in a second study by the same group, DA-regulated reward centres in tobacco smokers failed to activate in response to monetary reward. Interestingly, decreased sensitivity of reward circuits to acute alcohol administration has also been documented in cocaine abusers compared with control subjects. These findings suggest an overall reduction in the sensitivity of reward circuits in drug-addicted individuals to natural reinforcers, but also possibly to drugs besides the one to which they are addicted (extracted from the Journal of Clinical Investment May 15, 2003).