Addictions arise when substance use becomes disordered, when substances are used more and more in situations where they do harm, and when the user loses control over the use. But how and why does substance use become disordered? Is there individual variability in our vulnerability to develop addictions?
Recent research on addiction has added to our understanding of factors that contribute to the development of addictions, including genetic risk factors (Goldman, Oroszi and Ducci, 2005
). How can addiction be genetically determined? According to the Internet encyclopaedia, Wikipedia (2006)
Genes are regions of nucleic acid that parents pass to offspring during reproduction as chromosomes in nuclei of gametes. These entities encode information essential for the construction and regulation of proteins (such as enzymes) and other molecules that determine the growth and functioning of the organism.
But consumption of drugs is neither protein, nor enzyme. It is not a physiological process that can be determined by the presence or absence of a protein or an enzyme. It is not a psychological process that can be assumed to be determined by the presence or absence of a protein or an enzyme. It is a behaviour that relates to a substance outside of the organism.
The process from gene to addiction is mediated by physiological, psychological, and social processes. In order for genes to increase the risk of addiction, genes must enhance physiological processes that in turn increase the likelihood of psychological processes that in turn increase the likelihood that once drugs are encountered, they will also be consumed, and/or that once drugs are consumed, the person will continue to consume them. Therefore, in addiction as in psychiatry in general, there are no “genes for X disease”.
Addiction has moderate to high heritability, higher than most psychiatric disorders, and this heritability is determined by multiple genes that both interact and work independently of each other. There is also evidence that the use of drugs is partly determined by genetic factors, although the heritability of drug use is weaker than the heritability of drug addiction. In terms of drug use, the genetically predisposed is more likely to use intoxicants in general, rather than specific substances.
Drugs that tend to produce addiction easily, such as cocaine, opiates and tobacco smoking, also show the greatest heritability. Drugs that are less likely to cause addiction, such as cannabis, have the weakest heritability coefficients. This pattern of results is as expected, since the mechanisms that underlie addiction are themselves inheritable.
The impact of multiple independent genes means that humans are born with a degree of risk, rather than with absence or presence of disposition for the disorder.
Addiction liability is not inherited in the same way as, for instance, cystic fibrosis is. In the case of cystic fibrosis, one is either born without any risk, or with risk of the disease, depending on the presence or absence of a single gene. Inheritance is much in the same way that height or intelligence is inherited: people are not born with either a gene variant that predisposes them to become 140 centimeters, or with a gene variant that predisposes them to become 190 centimeters. Rather, they are born with a combination of multiple genes that predispose them to grow to some degree of height, given sufficient nutrition is available.
A different consequence of the fact that multiple genes determine addiction risk is that genetic risk for addiction may both be a risk factor for developing a specific addiction (for example, alcohol), and be a risk factor for addiction to two or more substances. Let's take an instance. Alcoholism and nicotine addiction, for example, are both comorbid and cross-transmitted. Approximately 85% of people with severe alcohol addiction smoke. Around 50% of the genetic liability to nicotine dependence is shared with alcoholism, and 15% of the genetic liability to alcoholism is shared with nicotine dependence (Swan, Carmelli and Cardon, 1997
). Thus, the increased genetic risk for alcohol addiction is small, although it exists, given the liability for tobacco addiction. But the increased genetic risk for tobacco dependence is large given a liability for alcohol addiction.
Multiple independent genes also means multiple pathways, which probably lead from drug genetic disposition to drug addiction. For instance, genetic disposition for stress sensitivity, impulsivity and externalizing behaviour, sensation seeking, and proneness to anxiety and dysphoria may all contribute to the development of drug addiction.
Therefore, it is not surprising that alcohol dependence is associated with familial aggregation of a range of psychiatric conditions, including depression, antisocial personality disorder, dysthymia, general anxiety, obsessive-compulsive disorder, post-traumatic stress disorder, and addiction to several other substances (Nurnberger et al, 2004
2. Environmental Risk Factors
There is little doubt that there also are environmental risk factors for the development of addictions. Obviously, substances must be accessible for addiction to develop. Reducing access to alcohol reduces alcohol-related problems. Similar observations have been made for heroin. When drugs are available, people must use them in order to develop addiction. There is evidence that early exposure leads to increased risk of developing addiction. A widely believed model states that some drugs function as gateway-drugs
, and that there is a general, or even natural, progression from one type of drugs to another. Some drugs (e.g., alcohol) act as gateways, and youth who do not start drinking alcohol rarely progress to marijuana; similarly, almost no cocaine users have not used marijuana previously. This model does not predict that the majority of users must necessarily proceed to the next drug in the sequence, but only that use of drugs later in the sequence is unlikely in the absence of use of drugs earlier in the sequence (Kandel and Yamaguchi, 1993
Whether use of gateway drugs
is an environmental risk factor or an indicator of addiction liability is an important question. There are arguments for both: any addictive drug can alter brain functioning in ways that increase vulnerability to addiction, which makes it probable that substance use is an environmental factor that increases risk of future addictions (Robinson and Berridge, 2000
). But the common heritability of addiction to various drugs suggests that common genetic factors can underlie tobacco, alcohol, marijuana and heroin use (Goldman et al, 2005
). The empirical question is how much actual causation from use of gateway drugs to use of the next drugs is possible, after genetic vulnerability is accounted for.
The evidence for the stress-substance use link in rats suggests that the relationship is very complex, and depends on a number of factors. The effect of stress on behaviour in rat models is stressor-specific, and to some degree, procedure- and drug-class-specific (Lu, Shepard, Scott Hall and Shaham, 2003
). Psychosocial risk factors also seem to influence cocaine use in non-clinical samples, although it is subjective stress more than objective stressors that are associated with use (Karlsgodt, Lukas and Elman, 2003
It is well established that in some socio-economic strata, substance use disorders are more common than in others. Socio-economic factors are related to substance use in a complex way. For instance, American college undergraduates in the 70ties and 80ties who used drugs differed little from non-users on academic performance, and were as active as non-users in extra-curricular activity at their university. In 1999, drug users were fewer than in earlier years, and they differed much more from non-users, both by performing more poorly academically and by not being involved in college activities (both studies reported in Pope, Ionescu-Pioggia and Pope, 2001
). Thus, within the same socio-economic strata, it appears that in different time-periods, different factors are associated with substance use.
3. Learning And The Environment
The complexity of environmental influences on drug and alcohol use suggests that cultural and psychological mechanisms must be taken into account. Cultural and psychological mechanisms have been suggested by symbolic interactionism and social learning theory. In a classical article, Becoming a marijuana user, Howard Becker (1953) presented a model for learning the ‘correct’ way to interpret the effects of cannabis through social interaction with other users. His point of view was that cannabis did not give euphoria until the user learns to recognize the effects and connect them with drug use; and learns to enjoy the sensations he perceives.
Several developments have been made in this area of theory, and Becker's radical view is now generally considered obsolete. Social learning theory has suggested several potentially important mechanisms (Marlatt and Gordon, 1984
). For instance, expectations about drug effects can have an impact on both the effects of drug use and consumptive behaviour (Donovan and Marlatt, 1980
). The environmental factors that influence substance use in humans are in summary more cultural than socio-economic. The right to drink alcohol has in Western societies been a symbol of independence and power that has been associated with the Caucasian adult male (Valverde, 1998
). It is the symbolic meaning of substance use and its variations across cultures, times and groups that defines the environmental influences on substance use in humans (Valverde, 1998