neurological causes of addication
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Addiction – Biological and Neurological Causes
An academic paper by
This paper is about the biological and neurological causes of addiction, how it affects many people, and systems of the body that are affected.
The category that addiction best falls into is a behavioral syndrome, noted for compulsive drug use with relapse into more drug use. Addiction can happen without being physically dependent, and physical dependency can happen without being addicted (Spanagel & Heilig, 2005). For the past 20 years scientists have looked at positive drug reinforcement as what lies beneath addictions. According to Spanagel & Heilig (2005), other neuronal systems must aid in addictive behavior, all systems work together. This means that one system affects the other. One of these systems, which detect influencing environmental stimuli, is the mesolimbic dopamine system, which affects the core brain reinforcement system. The hypothesis for the neurobiology of addiction is that there are changes on the molecular and structural levels that are irreversible, caused by the dopaminergic reinforcement system having synaptic plasticity, due to constant drug use. (Spanagel & Heilig, 2005). Scientists seem to think that there is some kind of modular switch that explains the irreversible transition from controlled drug use to compulsive drug use. These scientists say “It has been claimed that transcription factors such as “AFosB” may constitute such a molecular switch” (Spanagel & Heilig, 2005, p. 2). This transition factor builds up in the mesolimbic dopamine system with continuous drug use. However a modulator of transcription factors is Per2 and that does remain in the brain for quite a few weeks after drug treatment. Some change in the mesolimbic dopamine system that is irreversible that has been seen is the micro structural alterations on the dendrites of medium spiny neurons, which are the essential cell population inside the mesolimbic dopamine system. However, that change is not seen past 3 months after drug treatment ends. That contradicts the irreversible switch theory of moving from controlled drug use to compulsive drug use (Spanagel & Heilig, 2005).
Schepis, Adinoff, & Rao, state that adolescents are more persistently and acutely affected by addiction than are adults. These differences possibly have to do with neuroplastic changes that aid entrenchment and accelerated use, which leads to more neurobiological liability and SUD (substance use disorder) being great factors as the outcome (Schepis et al., 2008). This study also shows that adolescents with a family history of substance use are more likely to have neurobiological and neurobehavioral dysfunctions (Schepis et al., 2008). Adolescence is the period when most neurons grow. Neurocognitive functions such as decisions, monitoring oneself, controlling impulses, and gratification delay, are relative to the PFC (prefrontal cortex) and the anterior cingulate activity; these things seem to be affected by changes in pretty much all of the neurotransmitter systems. The most important factors in becoming a SUD are alterations in the dopamine related systems. Dopamine is a key factor in the mesolimbic neural pathways (Schepis et al., 2008). According to Schepis et al., “This circuit originates in the ventral tegmental area (VTA) and projects to the nucleus accumbens (NAc) and various limbic structures” (p. 8). A variety of environmental reinforcers trigger the mesostriatal to release dopamine (DA). In order to assign value to these reinforcing stimuli, there needs to be an increase in striatal concentrations of DA (Schepis et al., 2008).
In an article about SUD by Taylor, he explains Gray’s behavioral inhibition system (BIS) and the behavioral activation system (BAS), which, may be seen in the physiological reactions and shown in the psychopathology. Gray also says that the neural structure of the BIS incorporates information to the prefrontal cortex (PFC), and the neural structure of the BAS could be related to the dopaminergic reward circuit (Taylor, 2005).
Love passion, what some people consider an addiction, has neurobiological links with addiction. In love passion, neurochemicals that play a part in wanting that feeling all the time are dopamine, ocytocin, and vasopressin. Dopamine plays a major role in addictions. Other neurotransmitter systems that are common between addiction and love passion are GABA and glutamate, noradrenaline and serotonin, opioid, and cannabinnoid. These are implicated in the addiction process, as is the corticotrophin system that regulates the oxytocinergic and dopaminergic systems (Reynaud, Karila, Blecha, & Benyamina, 2010). Even though love passion is not considered to have a recognized definition or diagnosis criteria, it is very similar to addiction.
Alcohol affects GABAA receptors and a subtype of glutamate receptors called N-methyl-D-aspartate (NMDA). These neurotransmitters control the excitatory tone and activity of the brain. GABA is the inhibitory neurotransmitter and glutamate is the excitatory neurotransmitter (Devaud, Risinger, & Selvage, 2006). Incoordination, reduced nervousness, anticonvulsant, and relaxation, the symptoms of intoxication, are partly controlled by coming across these neurotransmitter systems. These actions show how the central nervous system (CNS) reacts to more GABAergic activity and less glutmatergic activity (Devaud, et al., 2006). GABAA and NMDA receptors are part of a larger receptor family and each has their own protein make-up. The different neurological responses are due to the combination of the different receptors. Men and women have a different chemical make-up as far as systems go. The difference between men and women when they drink is in the brain- and endocrine-mediated stress reactions. Men take the flight or fight response, whereas women tend to try to nurture the other and avoid aggressiveness (Devaud et al., 2006).
Another test shows that substance use and most psychiatric disorders are common and complex and have multiple genes that play into the phenotype, which show no pattern of Mendelian transmissions. There are two parallel mechanisms that influence this genetic complexity. One is the explanation of polygenicity, which means many genes come together at the same time to ensure vulnerability. In SUD, the genes that might be involved are genes related to drug-specific metabolism, neurobiological processes regulators similar to all abused drugs, and some that comorbidity-related that change environmental vulnerability. The second parallel mechanism that influences genetic complexity is heterogeneity, which shows that it is only one genetic variation that could make up a single specific phenotype that could be needed for the initiation and possibly the upkeep of addictions (Schumann, 2007).
Different people have different chemical make-ups, so everyone, more than likely, will have different effects from addictions. The many different receptors bind with different chemicals; if there is some disruption of that binding, many different affects could happen. Some people simply do not to become addicted to things, where others become addicted very easily. It is all in how chemicals bind together with the receptors, and apparently in the genetics.
Alcoholism is a terrible addiction that has been shown to be passed down from generation to generation. People who have a history of alcohol abuse in their family, have a greater chance of using themselves. According to previous studies Hanson, Medina, Nagel, Spadoni, Gorlick, and Tapert, (2010) hypothesis says that there is a difference in the size of the hippocampus of adolescents with a family history alcohol use problems and those adolescents who do not have a history of alcohol use issues. When the hippocampi of non-drinking youth with a family history of alcohol use was compared with youth who did not have a history of alcohol use in the family, those who had the history had smaller hippocampi or asymmetry that was abnormal (Hanson et al., 2010). The hippocampus is involved in making new memories. There is ongoing myelination in teen years, so if there is a problem with family history of alcohol use, then there will no doubt be a neurodevelopmental lag that hinders the proper growth of the left and right hemispheres of the hippocampus (Hanson et al., 2010). From their own preliminary findings, their hypothesis found not to be correct. Hanson et al. (2010) found that the hippocampal asymmetry was the same for youth with and without a family history of alcohol use.
Slutske et al. (2002) looked at four different studies on alcohol expectancies. Out of those four, three of them were done on twins. All of the participants of these studies were experienced drinkers (Slutske et al., 2002). What people expect of alcohol starts when they are young. Children see adults drink all the time, whether it is on the television, the radio, in a restaurant, or, sadly enough, in their own homes. From these experiences we can see how others are affected by alcohol. They look like they are having a lot of fun. Whether they are laid back and relaxed, laughing hysterically, or not afraid of anything, almost superhero type, so we expect what we see to happen to us. With that in mind we start to drink. Those who have a family history may start sooner than others, because they were exposed to it much younger and on a regular basis. In a recent study Slutske et al. (2002), examined how genetics, parents’ thoughts, and the same peer groups, affected thoughts of alcohol use, compared to thoughts of alcohol use with factors that are unrelated, peer groups that are not the same. What they came up with from this study, was that genetics alone did not make a significant difference, but when added to the family environment, together they made a huge difference on how people thought of alcohol and its use (Slutske et al., 2002). The thought here is that the social learning theory has more to do with alcohol use and dependence than does only genetics.
The ethanol in alcohol effects the predisposition of abuse and dependence. The way neural pathways are activated or deactivated by alcohol. With this in mind, research has turned to pharmacology, where medications affect cellular and physiological levels in the brain (Ray et al., 2010). These endophenotypes affect the subjective responses of alcohol, therefore may work to help treat alcoholism. The medication that is approved by the FDA has shown to lessen the good feelings of the alcohol, bring out more of the fatigue, stress, and confusion felt by alcohol use, therefore lowering the enjoyment (Ray et al., 2010).
Carlson (2010) explains that there are variations of genes that do play a big role in becoming addicted to substances. Environment also has a lot to do with whether you become dependent or not. He also goes on to explain that being prone to becoming an addict could be how your body metabolizes substances or by how the structures and biochemistries in your brain differ (Carlson, 2010).
A cause for alcoholism could be that the person is predisposed to the genetics of an alcoholic. However, just because you may be predisposed to alcoholism does not mean you will automatically become an alcoholic yourself. It may take outside factors to play a role in becoming an alcoholic. Coming from a line of alcoholics and seeing it every day, may have great impact on how you see the disease. Having friends that you spend most of your time with, could also have a great impact on whether or not you drink. A trusted friend, colleague, boss, or family member may offer you a drink to calm down, and it works, you like it, therefore you use it to chase away the blues or your bad day. You repeat these feelings of being alright enough that you now need it to get through your day. You become addicted.
Carlson, N. R. (2010). Physiology of behavior (10th ed.). Boston, MA: Pearson Education.
Devaud, L. L., Risinger, F. O., & Selvage, D. (2006). Impact of the hormonal milieu on the neurobiology of alcohol dependence and withdrawal. Journal of General Psychology, 133(4), 337-356. doi:10.3200/GENP.133.4.337-356
Hanson, K. L., Medina, K., Nagel, B. J., Spadoni, A. D., Gorlick, A., & Tapert, S. F. (2010). Hippocampal volumes in adolescents with and without a family history of alcoholism. American Journal of Drug & Alcohol Abuse, 36(3), 161-167. Retrieved from EBSCOhost.
Ray, L. A., Mackillop, J., & Monti, P. M. (2010). Subjective responses to alcohol consumption as endophenotypes: Advancing behavioral genetics in etiological and treatment models of alcoholism. Substance Use & Misuse, 45(11), 1742-1765. Retrieved from EBSCOhost.
Reynaud, M., Karila, L., Blecha, L., & Benyamina, A. (2010). Is love passion an addictive disorder? The American Journal of Drug and Alcohol Abuse, 36(5), 261-267. doi:10.3109/00952990.2010.495183
Schepis, T. S., Adinoff, B., & Rao, U. (2008). Neurobiological processes in adolescent addictive disorders. The American Journal on Addictions, 17(1), 6-23. doi:10.1080/10550490701756146
Schumann, G. (2007). Okey lecture 2006: Identifying the neurobiological mechanisms of addictive behaviour. Addiction, 102(11), 1689-1695. doi:10.1111/j.1360-0443.2007.01942.x
Slutske, W. S., Cronk, N. J., Sher, K. J., Madden, P. F., Bucholz, K. K., & Heath, A. C. (2002). Genes, environment and individual differences in alcohol expectancies among female adolescents and young adults. Psychology of Addictive Behaviors, 16(4), 308-317. doi:10.1037/0893-164X.16.4.308
Spanagel, R., & Heilig, M. (2005). Addiction and its brain science. Addiction, 100(12), 1813-1822. doi:10.1111/j.1360-0443.2005.01260.x
Taylor, J. (2005). Substance use disorders and cluster B personality disorders: Physiological, cognitive, and environmental correlates in a college sample. American Journal of Drug & Alcohol Abuse, 31(3), 515-535.