Diverse explanations
Several explanations (or "models") have been presented to explain oxycontin addiction
:
* The moral model states that oxycontin addiction
are the result of human weakness, and are defects of character. Those who advance this model do not accept that there is any biological basis for oxycontin addiction
. They often have scant sympathy for people with serious addictions, believing either that a person with greater moral strength could have the force of will to break an oxycontin addiction
, or that the addict demonstrated a great moral failure in the first place by starting the oxycontin addiction
. The moral model is widely applied to dependency on illegal substances, perhaps purely for social or political reasons, but is no longer widely considered to have any therapeutic value. Elements of the moral model, especially a focus on individual choices, have found enduring roles in other approaches to the treatment of oxycontin addiction
.
* The opponent-process model generated by Richard Soloman states that for every psychological event A will be followed by its opposite psychological event B. For example the pleasure one experiences from heroin is followed by an opponent process of withdrawal. This model is related to the opponent process color theory. If you look at the color red then quickly look at a gray area you will see green. There are many examples of opponent processes in the nervous system including taste, motor movement, touch, vision, and hearing.
* The disease model holds that oxycontin addiction
is an illness, and comes about as a result of the impairment of healthy neurochemical or behavioral processes. While there is some dispute among clinicians as to the reliability of this model, it is widely employed in therapeutic settings. Most treatment approaches involve recognition that dependencies are behavioral dysfunctions, and thus involve some element of physical or mental disease.
* The genetic model posits a genetic predisposition to certain behaviors. It is frequently noted that certain oxycontin addiction
"run in the family," and while researchers continue to explore the extent of genetic influence, there is strong evidence that genetic predisposition is often a factor in dependency. Researchers have had difficulty assessing differences, however, between social causes of dependency learned in family settings and genetic factors related to heredity.
* The cultural model recognizes that the influence of culture is a strong determinant of whether or not individuals fall prey to certain oxycontin addiction
. For example, alcoholism is rare among Saudi Arabians, where obtaining alcohol is difficult and using alcohol is prohibited. In North America, on the other hand, the incidence of gambling addictions soared in the last two decades of the 20th century, mirroring the growth of the gaming industry. Half of all patients diagnosed as alcoholic are born into families where alcohol is used heavily, suggesting that familiar influence, genetic factors, or more likely both, play a role in the development of oxycontin addiction
.
* The blended model attempts to consider elements of all other models in developing a therapeutic approach to dependency. It holds that the mechanism of dependency is different for different individuals, and that each case must be considered on its own merits.
Physiological basis
Although the term oxycontin addiction
is sometimes often used loosely rather than as a medical classification, there are some physiological conditions related to everyday behaviors that are also related to the more commonly recognized mechanisms associated with addiction. Pleasurable activities cause the release of endorphins, and this endorphin-rush can conceivably become 'addictive'. Evolutionary biologists have suggested this process of attentuating pleasure pathways is part of the brain's natural system for ensuring that humans develop abiding interests. Since human societies depend on enduring attachments, many theorists suggest such addictions are not necessarily a problem. Other views, such as the those summarized in Buddhist concept of tanha, suggest trivial attachments are at the root of much human suffering.
The pathways oriented to endorphins, sometimes called pleasure centers originated in small organisms such as insects, which rely on the neurological system to help them find familiar sources of food.
Endorphins stimulate activity of the neurotransmitter dopamine after initially activating opioid receptors earlier in the nervous circuit. Increased dopamine activity is often met by a decrease in the number of receptors sensitive to dopamine. This process is called downregulation. The decreased number of receptors tends to result in reduced electrical activity along post-synaptic nerve pathways, unless some behavior or substance causes a continued high level of dopaminergic stimulation. The absence of a pleasurable sensation in conditions that were formally sufficient can cause a mild feeling of let-down after receptors have been downregulated. The increased requirement for dopamine to maintain the same electrical activity is the basis of both physiological tolerance and withdrawal associated with oxycontin addiction
.
The middle striatal reward pathway has been most strongly linked with addictive and reward behavior. This pathway utilizes dopamine as a neurotransmitter and receives presynaptic input (from earlier in the circuit--it gets signals from these earlier in the circuit cells) from cells that respond to cannibinoids, nicotine (receptor subtype is nicotinic), and from cells that respond to endogenous opioid substances such as endorphins or enkephalins. Cells that are said to respond to a particular neurotransmitter (or agonists) contain, at the postsynaptic end (receiving area of the cell) receptors for that neurotransmitter. Many believe that there are more neurotransmitters involved with addiction than just dopamine including seratonin, norpenephrine, and the endocannibinoid anandinine.
In cases of physical dependency on depressants of the central nervous system such as opioids, barbiturates, or alcohol, the absence of the substance sometimes leads to symptoms of severe physical discomfort and withdrawal can even result in death from alcohol and barbiturates (but is generally only very uncomfortable in the case of opioids despite media disinformation to the contrary). In these cases, a body has become so dependent on a chemical that it has stopped producing the necessary neurotransmitters required to maintain a comfortable status.
Opioids present extreme risks of dependency because they are chemically similar to endorphins, causing an upregulation of dopaminergic receptors without stimulation of the endorphin systems. Cocaine and amphetamines also pose risks associated with physical attenuation, in both cases because they cause increasees in the levels of the neurotransmitters dopamine and norepinephrine which acts indirectly to stimulate dopaminergic pathways in the brain.
