Addiction, Choice, and the I-function

It is widely accepted that addiction is the result of not only environmental and genetic factors, but also chemical imbalances in the brain. Certain activities such as smoking, drug use, alcohol consumption, and gambling can alter the neurobiology of the brain resulting in addiction. Interestingly, some of these activities cause unnatural additions and some cause natural addictions but both types have the same effect on reward pathways in the brain. Reward pathways in many cases determine human behavior. Many of the choices we make are guided by our reward pathways. Reward pathways are, therefore, arguably a component of the I-function which gives humans the ability to make choices and to act freely. This paper will argue that addiction, which has been described as a brain disease (Leshner 1997 and Wise 2000), is also an inhibition of the I-function.

As an adaptive feature of the brain reward pathways are necessary for survival. They give humans a feeling of pleasure when engaging in activities necessary for survival. (Tomkins et al. 2001) However, they can also provide a feeling of pleasure when engaging in activities that are not necessary for our survival. The result can often be an addiction to an activity or substance.

The reward pathway in the human brain occurs between the ventral tegmental area (VTA) and the nucleus accumbens (NAcc). ((Tomkins et al. 2001) Connecting these two regions of the brain is the medial forebrain bundle (MFB) which consists of a group of neurons where many pathways occur. (Tomkins et al. 2001) Within this bundle lies the mesolimbic dopamine pathway. (Tomkins et al. 2001) This pathway begins with the activation of neurons in the VTA and results in the release of the neurotransmitter dopamine into the NAcc. (Tomkins et al. 2001). The dopamine released into NAcc interacts with dopamine receptors on the postsynaptic membranes of neurons resulting in reward. (Tomkins et al. 2001)

Using addictive substances can disrupt the normal reward pathway in several ways. GABA interneurons have an inhibitory effect on the cell bodies of neurons in the VTA. By inhibiting their activation, they limit the amount of dopamine being transmitted released into the NAcc. (Tomkins et al. 2001) Some substances, however, block the control from the GABA interneurons effectively allowing the activation of the cell bodies in the VTA. Thus, higher than normal levels of dopamine are released into the NAcc. (Tomkins et al. 2001) Substances can also have an excitatory effect on the cell bodies in the VTA both directly and indirectly. As one would expect, the result is also an increased level of dopamine release into the NAcc. (Tomkins et al. 2001)

The increased level of dopamine being released into the NAcc is one effect that leads to addiction. Use of addictive substances is not the only cause of addiction-causing increased dopamine levels. Some pleasurable activities, such as sexual intercourse, gambling, and eating have been associated with this effect as well. These pleasurable activities are often referred to as “natural addictions.” (Nestler 2005) When the brain frequently receives these rewards it becomes accustomed to the more frequent high level releases of dopamine into the NAcc. This is true of both “natural” and “unnatural” rewards.

Following chronic substance use or chronic engagement in pleasurable activities the “baseline levels of dopamine are reduced, and normal rewarding stimuli may be less effective at eliciting typical increases in dopaminergic transmission.” (Nestler 2005) The brain then becomes reliant on those external influences to achieve the same level of reward needed for normal functioning. For this reason, individuals usually have a desire to engage in a similar activity or use a similar substance to those that originally provided the increased reward sensation.

This change in the reward pathway begins to help dictate behavior even more strongly than when it is at a normal state. All forms of addiction have similar effects on the brain and addiction is, therefore, considered a brain disease by many scientists. (Leshner 1997 and Wise 2000) Individuals with this disease lose some control over their own actions. Even though many people understand at least that substances they use or activities they engage in can be detrimental to their bodies as well as their emotional and social well-being, their addiction causes them to behave in ways contrary to rational thinking. Therefore, addiction reduces our free will to make our own choices and may even inhibit a human’s I-function. Many people are aware of the dangers of smoking cigarettes as well as the financial cost they often suffer when buying the addictive products. Many of these people willingly admit that they want to or wish they could stop smoking. Despite all of this, their damaged reward pathways in their diseased brains somehow make them perform the actions of going to a store and spending money they do not want to spend to smoke cigarettes that they say they do not want to smoke anymore. Are these addicted people really making autonomous decisions that stem from their I-functions or is something inhibiting the I-function? Of course a person can stop walking on their way to the store. They have not lost the I-function completely and they do still have control of their bodies. However, it is likely that that person will eventually get to the store somehow to buy cigarettes. The reward pathway is important to human survival but when damage is done it can take over the body causing a person to behave in ways that detract from survival and often cause bodily harm. Addiction as a brain disease may also be a disease of the I-function.

References

<http://learn.genetics.utah.edu/units/addiction/>

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Nestler, E.J. (2005). Is there a common molecular pathway for addiction. Nature 8, 1445-1449.

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Tamminga, C.A., and Nestler, E.J. (2006). Pathological gambling: focusing on the addiction, not the activity. The American Journal of Psychiatry 163, 180-181.

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Wise, R.A. (2000). Addiction becomes a brain disease. Neuron 26, 27-33.