Addiction vulnerability

Addiction vulnerability is the genetic, physiological, or psychological predisposition to engage in addictive behaviors. A vulnerability to addiction may lead to an increased risk for a substance dependence. Addictions can arise in both a chemical and a behavioral manner. A chemical addiction refers to a physical substance dependence[1] where a behavioral addiction involves a psychological dependence. Genetics has been shown to account for 40-60% of a person’s likelihood to develop an addiction. Current research is now working toward establishing a comprehensive picture of the neurobiology of addiction vulnerability, including all factors at work in propensity for addiction.

Substance Addiction

A physical, chemical addiction refers to the repeated and uncontrollable abuse of drugs or alcohol. To be physically addicted to a substance means that the normal release of neurotransmitter has been obstructed by the presence of a chemical of abuse. The reward center of the brain gets overstimulated with the pleasurable response of drug or alcohol use and adapts to accommodate these increase levels of chemical input. This creates a neural environment for addiction development. Natural neural reuptake receptors become desensitized to the drug due to repeated exposure and have to adapt to function properly only in the presence of compounding amounts of the substance.[2]

In discussing the potential for drug abuse, it is useful to review the criteria used to diagnosis a substance use disorder. According to the American Psychiatric Association, substance use disorder is a complex behavioral disorder characterized by compulsive drug use, the development of tolerance and withdrawal, and overall functional impairment. In the Diagnostic and Statistical Manual of Mental Disorders IV-TR (DSM-IV-TR) substance use disorder was split into two categories: abuse and dependence. To meet criteria for a substance abuse diagnosis, one or more of the following criteria had to be met: (a) recurrent failure to fulfill major role obligations; (b) recurrent use of the substance in situations in which it might be hazardous; (c) recurrent substance-related legal problems; and (d) continued substance use despite having persistent or recurrent social or interpersonal problems. A substance dependence diagnosis was met if three or more of the following criteria were fulfilled: (a) tolerance; (b) withdrawal; (c) using larger amounts or over a longer period of time than intended; (d) a persistent desire or unsuccessful efforts to cut down or control use; (e) spending a great deal of time obtaining, (f) using or recovering from the effects of the substance; (g) reducing or giving up important activities due to substance use; and (h) persistent physical or psychological problem that are likely due to or exacerbated by the substance.

With the revised edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-5) there has been a shift from the traditional categorization of addiction as substance abuse and/or dependence to a more dimensional model that combines the diagnostic criteria from both “abuse” and “dependence” into a singular disorder. The criteria for diagnosis remains relatively the same in the DSM-5 with a few changes such as the removal of “recurrent legal problems” criteria, the addition of “craving or a strong desire to use the substance,” and the threshold for diagnosis has been revised to include positive identification with two or more criteria. The shift from a categorical to a more dimensional approach exemplifies the evolving conceptualization of addiction in the field.

Three Factor Model

Accepted research now shows that some people have vulnerabilities to addiction and has established a three factor standard for vulnerability to drug addiction: genetic factors, environmental factors and repeated exposure to drugs of abuse.[3] Being vulnerable to addiction means that there exists some factor which makes one individual more likely to develop an addiction than another individual. Additionally, many in the science community agree that addiction is not simply just a result of desensitized neural receptors but also a corollary of long-term associated memories (or cues) of substance use and self-administration.[4] Vulnerability to addiction has both physiological and psychological components.

Genetic Factors

Contemporary research in the neurobiology of addiction points to genetics as a major contributing factor to addiction vulnerability. It has been estimated that 40-60% of the vulnerability to developing an addiction is due to genetics.[5][6] One gene in particular, the D2 subtype of dopamine receptor has been studied at length in association to substance addiction. The D2 receptor responds to the chemical dopamine which produces rewarding and pleasurable feelings in the brain. Through mice studies, agreeing contemporary research has shown that individuals with a deficiency in this dopamine receptor exhibit not only a preference for and increased consumption of alcohol over their genetically normal peers,[7] but also compensated levels of the cannabinoid receptor type CB1.[7] This suggests that both of these genetic factors work together in the regulation of alcohol and cocaine in the brain and in the normal regulation of dopamine. Individuals with this genetic deficiency in the D2 dopamine receptor may be more likely to seek out these recreational pleasure/reward producing substances as they are less receptive to the natural “feel good’’ effects of dopamine.[7] This naturally occurring deficiency is one of the most studied genetic vulnerabilities to substance abuse across the field.

Additionally, genetics play a role on individual traits, which may put one at increased risk for experimentation with drugs, continued use of drugs, addictions, and potential for relapse. Some of these individual personality traits, such as impulsivity, reward-seeking, and response to stress, may lead to increased vulnerability to addiction.[8]

Environmental Factors

A major environmental factor that increases vulnerability to developing addiction is availability of drug. Additionally, other environmental factors come into play, such as socioeconomic status and poor familial relationships, and have been shown to be contributing factors in the initiation (and continued use) of drugs of abuse.[9] Neurobiology again plays a role in addiction vulnerability when in combination with environmental factors. The main risk of chronic stressors contributing to vulnerability is that they can put the brain in a compromised state. External stressors (such as financial concerns and family problems) can, after repeated exposure, affect the physiology of the brain. Chronic stress or trauma has been shown to have neuroadaptive effects such that the brain can essentially physically “rewire” itself to accommodate for the increase in cortisol produced by the stressors. Additionally, when the brain is put under severe stress due to repeated drug use, it has been shown to be physiologically altered.[4][10] This compromised neural state plays a large role in perpetuating addiction and in making recovery more difficult.

Adolescence

Previous research has examined the increased risk of substance use initiation during adolescence. Many factors have been identified as being associated with increased risk of substance use during this period of development including individual differences (e.g., negative affect, decreased harm avoidance, low motivation for achievement, etc.), biological (e.g., genetic predisposition, neurological development, etc.), and environmental factors (e.g., high levels of stress, peer influences, availability of substances, etc.) [11][12][13] Rat studies provide behavioral evidence that adolescence is a period of increased vulnerability to drug seeking behavior and onset addiction[14] The mesolimbic dopamine system of the brain is undergoing reorganization and functional changes during adolescence. As a result, it is more susceptible to become addicted in the wake of drug use during this developmental period.[14] Overall, social, behavioral and developmental factors in adolescence make individuals more liable to drug seeking behavior, and as a result, addiction.

Repeated Exposure

Although it seems obvious that repeated use or exposure to drugs of abuse increases vulnerability to addiction, it is often overlooked as an important factor. Repeated exposure to drugs of abuse is thought to be the third component of the 3-factor model of addiction vulnerability. Repeated exposure to a drug is one of the determining factors in distinguishing recreational substance use from chronic abuse. Many neurobiological theories of addiction place repeated or continued use of the drug in the path of addiction development. For example, researchers have theorized that addiction is the result of the shift from goal-directed actions to habits and ultimately, to compulsive drug-seeking and taking.[15][16] In other words, repeated, deliberate use of the drug plays a role in the eventual compulsory drug-taking and/or habitual drug-taking associated with addiction. Another theory suggests that through repeated use of the drug, individuals become sensitized to drug-associated stimuli which may result in compulsive motivation and desire for the drug.[17] Additionally, a third neurobiological theory highlights the changes in brain reward circuitry following repeated drug use that contributes to the development of addiction such that addiction is conceptualized as being a progression of allostatic changes in which the addicted individual is able to maintain stability but at a pathological set point.[18] Experience-dependent neural plasticity is a hallmark of repeated drug exposure and refers to the adaptation of the brain due to increased levels of the drug in the body.[19] In this sense, repeated exposure falls under the both physiological vulnerability and behavioral/psychological vulnerability to addiction.

Although many variables individually contribute to an increased risk of developing a substance use disorder, no single vulnerability guarantees the development of addiction. It is the combination of many factors (i.e. genetics, environmental stressors, initiation and continued use of the drug) that culminate is the development of this disorder.

References

  1. ↑ "Substance abuse/ chemical dependency". Retrieved 16 March 2013.
  2. ↑ Ambroggi, Frédéric; Turiault, Marc; Milet, Aude; Deroche-Gamonet, Véronique; Parnaudeau, Sébastien; Balado, Eric; Barik, Jacques; van der Veen, Rixt; Maroteaux, Grégoire; Lemberger, Thomas; Schütz, Günther; Lazar, Monique; Marinelli, Michela; Piazza, Pier Vincenzo; Tronche, François (22 February 2009). "Stress and addiction: glucocorticoid receptor in dopaminoceptive neurons facilitates cocaine seeking". Nature Neuroscience. 12 (3): 247–249. doi:10.1038/nn.2282. PMID 19234455.
  3. ↑ Kreek, Mary Jeanne; Nielsen, David A.; LaForge, K. Steven (1 January 2004). "Genes Associated With Addiction: Alcoholism, Opiate, and Cocaine Addiction". NeuroMolecular Medicine. 5 (1): 085–108. doi:10.1385/NMM:5:1:085.
  4. 1 2 Hyman, SE; Malenka, RC; Nestler, EJ (2006). "Neural mechanisms of addiction: the role of reward-related learning and memory". Annual Review of Neuroscience. 29: 565–98. doi:10.1146/annurev.neuro.29.051605.113009. PMID 16776597.
  5. ↑ Goldman, Orozsi; Ducci (2005). "The genetics of addictions: uncovering the genes". Nat Rev Genet. 6 (7): 521–532. doi:10.1038/nrg1635. PMID 15995696.
  6. ↑ Hiroi, Agatsuma (2005). "Genetic susceptibility to substance dependence". Mol Psychiatry. 10 (4): 336–44. doi:10.1038/sj.mp.4001622. PMID 15583701.
  7. 1 2 3 Thanos, Panayotis K.; Gopez, Vanessa; Delis, Foteini; Michaelides, Michael; Grandy, David K.; Wang, Gene-Jack; Kunos, George; Volkow, Nora D. (1 January 2011). "Upregulation of Cannabinoid Type 1 Receptors in Dopamine D2 Receptor Knockout Mice Is Reversed by Chronic Forced Ethanol Consumption". Alcoholism: Clinical and Experimental Research. 35 (1): 19–27. doi:10.1111/j.1530-0277.2010.01318.x.
  8. ↑ Kreek, M. J.; Nielsen, D. A.; Butelman, E. R.; Laforge, K. S. (2005). "Genetic influences on impulsivity, risk taking, stress responsivity and vulnerability to drug abuse and addiction". Nature Neuroscience. 8 (11): 1450–1457. doi:10.1038/nn1583.
  9. ↑ Volkow, N.; Li, T. K. (2005). "The neuroscience of addiction". Nature Neuroscience. 8 (11): 1429–1430. doi:10.1038/nn1105-1429.
  10. ↑ Sinha, Rajita (1 October 2008). "Chronic Stress, Drug Use, and Vulnerability to Addiction". Annals of the New York Academy of Sciences. 1141 (1): 105–130. doi:10.1196/annals.1441.030.
  11. ↑ Fergusson, D. M.; Boden, J. M.; Horwood, L. J. (2008). "The developmental antecedents of illicit drug use: Evidence from a 25-year longitudinal study". Drug and Alcohol Dependence. 96: 165–177. doi:10.1016/j.drugalcdep.2008.03.003.
  12. ↑ Nation, M.; Heflinger, C. A. (2006). "Risk Factors for Serious Alcohol and Drug Use: The Role of Psychosocial Variables in Predicting the Frequency of Substance Use Among Adolescents". The American Journal of Drug and Alcohol Abuse. 32 (3): 415–433. doi:10.1080/00952990600753867.
  13. ↑ Bates, M. E.; Labouvie, E. W. (1997). "Adolescent Risk Factors and the Prediction of Persistent Alcohol and Drug Use into Adulthood". Alcoholism: Clinical and Experimental Research. 21 (5): 944–950. doi:10.1111/j.1530-0277.1997.tb03863.x.
  14. 1 2 Wong, WC; Ford, KA; Pagels, NE; McCutcheon, JE; Marinelli, M (Mar 13, 2013). "Adolescents are more vulnerable to cocaine addiction: behavioral and electrophysiological evidence". The Journal of neuroscience : the official journal of the Society for Neuroscience. 33 (11): 4913–22. doi:10.1523/JNEUROSCI.1371-12.2013. PMID 23486962.
  15. ↑ Everitt, B. J.; Robbins, T. W. (2005). "Neural systems of reinforcement for drug addiction: from actions to habits to compulsion". Nature Neuroscience. 8 (11): 1481–1489. doi:10.1038/nn1579. PMID 16251991.
  16. ↑ Goldstein, R. Z. (2002). "Drug Addiction and Its Underlying Neurobiological Basis: Neuroimaging Evidence for the Involvement of the Frontal Cortex". American Journal of Psychiatry. 159 (10): 1642–1652. doi:10.1176/appi.ajp.159.10.1642.
  17. ↑ Robinson, T. E.; Berridge, K. C. (2008). "The incentive sensitization theory of addiction: Some current issues". Philosophical Transactions of the Royal Society B: Biological Sciences. 363 (1507): 3137–3146. doi:10.1098/rstb.2008.0093.
  18. ↑ Koob, G. F. (2003). "Alcoholism: Allostasis and Beyond". Alcoholism: Clinical and Experimental Research. 27 (2): 232–243. doi:10.1097/01.ALC.0000057122.36127.C2.
  19. ↑ Thomas, Mark J.; Beurrier, Corinne; Bonci, Antonello; Malenka, Robert C. (5 November 2001). "Long-term depression in the nucleus accumbens: A neural correlate of behavioral sensitization to cocaine". Nature Neuroscience. 4 (12): 1217–1223. doi:10.1038/nn757. PMID 11694884.
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