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Cocaine Addiction
Links Between Genetics & Social Status

By Terence T. Gorski
January 24, 2002

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Posted On: January 26, 2002          Updated On: January 26, 2002
© Terence T. Gorski, 2001

Cocaine Addiction
Links Between Genetics & Social Status

By Terence T. Gorski
January 24, 2002

1.    Genes and environments are locked together in complex loops that affect each other.  Certain environmental conditions stimulate the activity of certain genetic traits.  Other environmental conditions inhibit the activity of certain genetic traits.  This means that genetics provide dispositions or tendencies that require certain environmental conditions in order to be activated.  Hence, genetics influence but do not control or determine behavior.

2.    Michael Nader and his colleagues at Wake Forest University, in Winston-Salem, North Carolina, examined whether there was any relationship between an animal's social status and its tendency to get addicted. 

3.    They found that there was indeed a difference between the addictive propensities of individuals. The difference seemed to be linked to a cluster of factors including social status, personality style, and the activities of a specific gene. 

4.     This difference in addictive propensities was note exclusively caused by genetics. 

5.     It was caused by an interaction between genetics and psychosocial factors.  Three seem to interact in a predictable but complex way to raise or lower the risk of addiction.  These three factors are:  social status/dominance, personality style, and genetic predisposition.  

6.    Social status affects personality style by providing limitations within a social context for action and reaction.  A person born and raised in the lowest classes of totalitarian kingdom in the middle ages would have far more constraints upon access to knowledge, power, and influence than a person born into a wealthy family of modern industrial nation whose family has a successful history in business and politics.

7.     Personality style is in turn is affected by genetic predispositions that affect brain chemistry and behavior.  People with genetic tendencies that create aptitudes for social cooperation, assertiveness, and intelligence will influence personality tendencies different than a person born with genetic tendencies that create an aptitude for good hand-eye coordination, the ability to notice cause effective relationships among physical object, and the tendency to be shy and isolated.

8.    These genetic predispositions create propensities and impose limits on the ability of the individual to adapt and respond to certain social expectations.  

9.     The social and personality factors in turn influence the activation of genes that regulate the base-line levels of dopamine and other neurotransmitters.  

10.   These differences in in neurotransmitter levels influence emotional and motor responses and the ability tolerate and manage stress.  

11.   Different base-line levels of dopamine and other neurotransmitters, in turn, cause differences in the subjective feelings experienced when cocaine and other drugs are used.

12.    An individual's position in a group's dominance hierarchy determines the activity of a dopamine receptor protein called D2.  Socially dominant monkeys produce higher base-line levels of D2 than monkeys who are not dominant. 

13.    Because D2 is a dopamine reuptake inhibiter, high levels of D2 result in base-line levels of dopamine.  Low levels of D2 result in low base-line levels of dopamine.

14.   Different levels of social dominance result in different base-line levels of D2, which in turn causes different base-line levels of dopamine.  

15.  Engaging in the behaviors needed to maintain high levels of social dominance creates a tendency to produce high levels of D2 and dopamine.  

16.   People who don't engage in the behaviors associated with social dominance produce lower levels of D2 and Dopamine.  

16.   Individuals at the lowest end of the social dominance scale may have such low levels of D2 that they could be described as having a dopamine deficiency.  

17.  Cocaine can compensate for this deficiency because it is a dopamine reuptake inhibiter that can raise the level of dopamine and normalize neurochemical functions.  

18.   So individuals with low levels of D2 and dopamine who take cocaine have a normalization phase before the intoxication phase.  When the Cocaine is stopped, the dopamine levels return to their previous deficient levels.  This causes a return of the symptoms of dopamine deficiency which creates a strong incentive to use more cocaine.  

19.  Since high dominance individuals have more D2 and hence higher base-line levels of dopamine, they don't experience the symptoms associated with low dopamine levels.  When they use cocaine they feel a drug effect, but it is less dramatic than the person with a D2 deficiency.  This is because they have higher levels of baseline D2 and dopamine and usually do not experience the dysphoric symptoms of dopamine deficiency.  When the individual with high base-line levels of D2 stops cocaine, the level of D2 and dopamine return to the previous higher base-line level rather than to lower deficient level.  Hence there are no symptoms of dopamine deficiency and no strong urges or cravings to use more cocaine to raise dopamine levels to relieve those symptoms.  

20.   This study would suggest that people with low social dominance and social status will have lower levels of D2 and lower levels of dopamine.  Those at the lowest baseline levels will tend to experience dysphoric symptoms associated with a dopamine deficiency.  When they use cocaine they experience a normalization effect first and need to take more cocaine to experience an intense high.  When they stop they will experience strong dysphoric effects as the dopamine levels crash back down to their original deficient levels.  This will create powerful conditioned cravings that motivates continued use and can lead to addiction.

21.   In contrast, people with high social dominance and social status will not be likely to experience symptoms of dopamine deficiency and would be less likely to seek cocaine or other drugs to normalize relieve the dysphoria.  Upon using cocaine they tend to experience a less dramatic mood change because of a low relative change in Dopamine levels.  When they stop their dopamine levels will tend to return to normal, rather than deficient levels.  Hence they will be less like to experience cravings to keep using and be less likely to become addicted.

22.   This does not mean that people with high social dominance and high social status can't become addicted to cocaine.  Clinical experience shows that many do.  It means that more cocaine will need to be used for longer periods of time before craving, loss of control and addiction occurs.  The principles of tolerance dictates the frequent and heavy use will alter preexisting brain chemistry processes.  In essence, if a person is taking cocaine which is producing a surplus of Dopamine, the natural system for producing D2 will state to become lazy and slow down the production of D2 lowering the natural level of dopamine and creating need for the use of more cocaine to get the desired effect.  Then when cocaine is stopped, the level of D2 will be low and the person will experience the symptoms of dopamine deficiency and be more likely to experience craving and to keep using and become addicted.

The following article from The Economist summarizes Michael Nader's research.  

Cocaine addiction

Having it all

From The Economist print edition Jan 24th 2002
Experiments on monkeys suggest drug use is linked to social status
<Read this story on The Economist Website>

BIOLOGISTS are often accused of taking a rigidly deterministic approach to behavior. Often this is in the context of reports of a “gene for this” or a “gene for that”. One example is the idea of an addictive personality, which some people have tried to link to versions of particular genes whose products are found in the brain. But genes do not act in isolation from the environment. Rather, genes and environments are locked together in complex loops that feed back on each other.

A report in Nature Neuroscience illustrates this. Michael Nader and his colleagues at Wake Forest University, in Winston-Salem, North Carolina, have been investigating cocaine addiction in macaque monkeys, with a view to testing out ideas about the drug's effects on people. They wanted to examine whether there was any relationship between an animal's social status and its tendency to get hooked. Is addiction the prerogative of the monkey equivalent of the executive washroom, the ghetto crack den, or both?

As the addictive-personality model would predict, there was indeed a difference between the addictive propensities of individuals. It seemed to be linked to the activity of a specific protein derived from a specific gene. However, the cause of the difference was not, as the naive determinist might have supposed, genetic. It was, rather, environmental.

Cocaine belongs to a class of drugs known as dopamine re-uptake inhibitors. Dopamine is one of the chemical messengers, known as neurotransmitters, that allow signals to jump the gaps between nerve cells. The electrical impulses that conduct signals along nerve filaments stimulate the release of neurotransmitter molecules when they reach the end of a filament. Those molecules are picked up by specialised receptor proteins on the surface of a cell on the other side of the gap, and the binding between neurotransmitter and receptor triggers a sequence of events that sets off an electrical impulse in the second nerve cell. The receptor then lets go of the neurotransmitter.

In some cases, when the neurotransmitter has done its job, it is sucked back into the cell whence it came, by a process known as re-uptake. Dopamine is one of these cases. So a molecule that blocks the protein channels through which re-uptake happens means that dopamine hangs around in the gap, and can re-stimulate the cell on the other side. Since the parts of the brain that control mood often rely on dopamine-mediated nerve cells, dopamine re-uptake inhibitors can have a profound effect on mood, which is why some people are willing to spend large amounts of money buying cocaine.

Monkeys like cocaine too, and for much the same reasons. But, unlike people, they can be experimented on. Dr Nader and his colleagues were particularly interested in the relation between a monkey's position in a group's dominance hierarchy, how addicted it was to cocaine, and the activity of a dopamine receptor protein called D2.

The experiment began with 20 male monkeys, which were housed individually for 18 months. During this time, their D2 activity was measured using a brain-scanning technique called positron-emission tomography (PET). Positrons are the antimatter equivalent of electrons, and are produced in a rare type of radioactive decay. PET works by introducing biologically active molecules containing positron-emitting atoms into the tissue to be studied, and seeing where the chemical concentrates by watching the effects of the positrons. Dr Nader's group used a substance that has an affinity for D2 receptors and thus accumulates in tissues where they are found.

Once their time in individual cages was over, the monkeys were housed in groups of four. Animals in such groups quickly establish who is in and who is out. Based on earlier work, Dr Nader suspected that such dominance and subordination would reflect D2 activity, and it did—but not in the way that genetic determinists might have predicted. Dominant animals had more D2 activity than subordinates, but that was a consequence of their dominance, and not its cause. Regardless of their D2 activity when kept individually, monkeys that became subordinate showed little change in their PET responses after they had been put into company. In the animals that became dominant, by contrast, D2 activity increased significantly.

The other thing that Dr Nader did with his experimental subjects was to introduce them to cocaine. They were able to obtain the drug by pressing a lever. They could thus control their own intake.

Like D2 activity, cocaine use was related to social status. Dominant animals found a preferred level, then stuck to it. Subordinates, though, seemed to need bigger and bigger fixes as time went on. That is a classic symptom of addiction—and it may well be linked directly to D2 activity.

This is because the overstimulation that cocaine causes makes the body behave as though too much of the neurotransmitter is being churned out. Production of dopamine drops in response, so that when the cocaine goes away, too little stimulation takes place. The quickest way to restore the situation is to take more cocaine—in other words, to be addicted.

Individuals with a higher baseline of D2 activity might be expected to be less susceptible to this process, since the relative overstimulation caused by a given dose of the drug will be smaller. So dominants, which have more D2 activity as a result of their status, are less likely to become addicts. Propensity to addiction, in other words, is not a predisposition of the individual, but the result of social context.

If these results translate to human experience, they will be a sad example of the biblical adage that unto everyone that hath shall be given; but from him that hath not, shall be taken away even that which he hath. Not only are those at the bottom of the heap more likely to be convicted and locked up for using drugs than those at the top (which they are), they are more likely to have to carry on using them, once they have started.


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