Addiction Treatment Regimes
In the past, addiction was treated as a moral or personal flaw, not a physiological condition.
Thus treatment often was nonexistent.
As the need for therapy became clear, early treatment regimes were instituted.
Treatment often consisted of psychological support for the patient, or occasionally, not even that: in some nations, treatment consisted of forcing the individual to undergo "cold turkey" withdrawal in a prison cell.
While psychological support for the patient is a necessary part of any treatment regime, methods based only on such support or m a worst case scenario on simultaneous deprivation of both substance and support were only partially successful.
There have been actual attempts to treat the underlying physical symptoms of the problem.
Two methods involved in these early attempts to treat the physiology of RDS were the application of agonists and the application of antagonists.
Agonists are substances which themselves are received or otherwise stimulate reception of a neurotransmitter in the neurons, resulting in a "substitution" of one substance, the abused substance, with another: its agonist.
The theory is that the craving will be satiated without recourse to the abused substance.
Methadone is an example of a heroin agonist.
While some positive results were achieved, it is uncertain if methadone treatment actually offered a higher rate of success than psychological support.
Numerous "nicotine patches" are offered as a type of substitution therapy for nicotine addiction: while the agonist was in fact the abused substance nicotine, many other dangerous chemicals found in cigarettes, cigars and chewing tobacco are eliminated.
In addition, the patient can control the dosage self administered, offering the opportunity to gradually end the nicotine dependency.
However, most agonist therapies to date have suffered from a common weakness: they attempt to satisfy craving by replacing the desired substance with some other desirable substance, rather than by offering the patient's body the ability to return the patient's neurochemistry to a healthy state.
Obviously, reduction of the craving would be preferable to merely satisfying it.
In addition, certain agonist can themselves become addicting, and the patient's tolerance can increase, resulting in the need for higher dosages of the medication, not lower.
Antagonists, on the other hand, actually reduce the potency of the abused substance, resulting in reduced reward for its administration.
Naltrexone is an example of a substance which blocks the effects of heroin.
In this case, the operative theory is that with reduced reward, the individual will eventually cease to abuse the substance.
However, the craving itself is not reduced, merely left unsatisfied by administration of the abused substance.
Unfortunately, the action of blocking the effects of the abused substance is rather similar to simply denying the patient the substance in the first place: the craving remains, unsatiated.
Worse, the patient's level of well-being spends long periods of time in the "anhedonia" or "dysphoric" (unhappy) phase of the abuse cycle, possibly inflicting as much pain as a "cold turkey" incarceration would have, and demonstrating no overwhelming reduction in the rate of recidivism.
Even worse, the internal blockade of the abused substance may simply lead the sufferer to attempt greater dosages of it, with potentially catastrophic results.
U.
S.
Pat.
No.
5,824,684 issued to Viner on Oct.
20, 1998, may be taken as an example of a medication including an antagonist agent.
There have also been attempts to combine the agonist and antagonist therapies: See U.
S.
Pat.
No.
5,935,975, issued to Rose et al on Aug.
10, 1999, for "Agonist-Antagonist Combination to Reduce the Use of Nicotine and Other Drugs".
In the method, the agonist (or even the substance abused) is administered to the patient.
At the same time or shortly thereafter, the subject is administered the antagonist to the abused substance.
In theory, the approach leaves a lesser number of receptors available to respond to the abused substance, while at the same time minimizing the negative effects of a pure antagonist therapy.
(See col.
4.
lines 38-42.
) Each of these two methods and even combined methods such as the '975 patent do not attempt to return the neurotransmission system to a normal state.
While therapy using an agonist temporarily reduces craving, the reduction is simply due to the administration of the abused substance or another having the same psycho-physiological effects.
In no case is the actual source of the craving itself--the brain's neurotransmitter imbalances--really lessened, nor is the brain's reward system moved towards a normal balance.
Thus, new and promising therapies have concentrated on a different approach: craving reduction.
Thus treatment often was nonexistent.
As the need for therapy became clear, early treatment regimes were instituted.
Treatment often consisted of psychological support for the patient, or occasionally, not even that: in some nations, treatment consisted of forcing the individual to undergo "cold turkey" withdrawal in a prison cell.
While psychological support for the patient is a necessary part of any treatment regime, methods based only on such support or m a worst case scenario on simultaneous deprivation of both substance and support were only partially successful.
There have been actual attempts to treat the underlying physical symptoms of the problem.
Two methods involved in these early attempts to treat the physiology of RDS were the application of agonists and the application of antagonists.
Agonists are substances which themselves are received or otherwise stimulate reception of a neurotransmitter in the neurons, resulting in a "substitution" of one substance, the abused substance, with another: its agonist.
The theory is that the craving will be satiated without recourse to the abused substance.
Methadone is an example of a heroin agonist.
While some positive results were achieved, it is uncertain if methadone treatment actually offered a higher rate of success than psychological support.
Numerous "nicotine patches" are offered as a type of substitution therapy for nicotine addiction: while the agonist was in fact the abused substance nicotine, many other dangerous chemicals found in cigarettes, cigars and chewing tobacco are eliminated.
In addition, the patient can control the dosage self administered, offering the opportunity to gradually end the nicotine dependency.
However, most agonist therapies to date have suffered from a common weakness: they attempt to satisfy craving by replacing the desired substance with some other desirable substance, rather than by offering the patient's body the ability to return the patient's neurochemistry to a healthy state.
Obviously, reduction of the craving would be preferable to merely satisfying it.
In addition, certain agonist can themselves become addicting, and the patient's tolerance can increase, resulting in the need for higher dosages of the medication, not lower.
Antagonists, on the other hand, actually reduce the potency of the abused substance, resulting in reduced reward for its administration.
Naltrexone is an example of a substance which blocks the effects of heroin.
In this case, the operative theory is that with reduced reward, the individual will eventually cease to abuse the substance.
However, the craving itself is not reduced, merely left unsatisfied by administration of the abused substance.
Unfortunately, the action of blocking the effects of the abused substance is rather similar to simply denying the patient the substance in the first place: the craving remains, unsatiated.
Worse, the patient's level of well-being spends long periods of time in the "anhedonia" or "dysphoric" (unhappy) phase of the abuse cycle, possibly inflicting as much pain as a "cold turkey" incarceration would have, and demonstrating no overwhelming reduction in the rate of recidivism.
Even worse, the internal blockade of the abused substance may simply lead the sufferer to attempt greater dosages of it, with potentially catastrophic results.
U.
S.
Pat.
No.
5,824,684 issued to Viner on Oct.
20, 1998, may be taken as an example of a medication including an antagonist agent.
There have also been attempts to combine the agonist and antagonist therapies: See U.
S.
Pat.
No.
5,935,975, issued to Rose et al on Aug.
10, 1999, for "Agonist-Antagonist Combination to Reduce the Use of Nicotine and Other Drugs".
In the method, the agonist (or even the substance abused) is administered to the patient.
At the same time or shortly thereafter, the subject is administered the antagonist to the abused substance.
In theory, the approach leaves a lesser number of receptors available to respond to the abused substance, while at the same time minimizing the negative effects of a pure antagonist therapy.
(See col.
4.
lines 38-42.
) Each of these two methods and even combined methods such as the '975 patent do not attempt to return the neurotransmission system to a normal state.
While therapy using an agonist temporarily reduces craving, the reduction is simply due to the administration of the abused substance or another having the same psycho-physiological effects.
In no case is the actual source of the craving itself--the brain's neurotransmitter imbalances--really lessened, nor is the brain's reward system moved towards a normal balance.
Thus, new and promising therapies have concentrated on a different approach: craving reduction.
Source...