Drugs are built to interfere with those messages, causing the release of too many neurotransmitters for the wrong behavior—taking drugs. This causes a huge spike in pleasure for a destructive activity that eclipses normally pleasant activities needed for survival. Drug use also prevents normal reuptake of these brain chemicals, throwing off the entire process and your natural balance, altering your mood. Soon, all that matters is to produce that flood of neurotransmitters again—and due to the addiction, there’s just one way to do that: drug use.
Another approach is to use medicines that interfere with the functions of the drugs in the brain. Similarly, one can also substitute the misused substance with a weaker, safer version to slowly taper the patient off of their dependence. Such is the case with Suboxone in the context of opioid dependence. These approaches are aimed at the process of detoxification. Medical professionals weigh the consequences of withdrawal symptoms against the risk of staying dependent on these substances. These withdrawal symptoms can be very difficult and painful times for patients. Most will have steps in place to handle severe withdrawal symptoms, either through behavioral therapy or other medications. Biological intervention should be combined with behavioral therapy approaches and other non-pharmacological techniques. Group therapies including anonymity, teamwork and sharing concerns of daily life among people who also suffer from substance dependence issues can have a great impact on outcomes. However, these programs proved to be more effective and influential on persons who did not reach levels of serious dependence.
Two factors have been identified as playing pivotal roles in psychological dependence: the neuropeptide "corticotropin-releasing factor" (CRF) and the gene transcription factor "cAMP response element binding protein" (CREB). The nucleus accumbens (NAcc) is one brain structure that has been implicated in the psychological component of drug dependence. In the NAcc, CREB is activated by cyclic adenosine monophosphate (cAMP) immediately after a high and triggers changes in gene expression that affect proteins such as dynorphin; dynorphin peptides reduce dopamine release into the NAcc by temporarily inhibiting the reward pathway. A sustained activation of CREB thus forces a larger dose to be taken to reach the same effect. In addition, it leaves the user feeling generally depressed and dissatisfied, and unable to find pleasure in previously enjoyable activities, often leading to a return to the drug for another dose.
Changes in the brain that support physical and psychological dependency on mind-altering substances are the direct cause of addiction, but those changes do not occur at random. Addiction experts believe drug addiction emerges from an interplay of genetic and environmental factors, although one factor or the other may be strong enough to make a person vulnerable to addiction in some instances.
From the comfort of your home you can connect with the greater Aftercare community via our private online social network site. As an alumnus of our alcohol recovery program, you can also participate in our refresher weekend getaways. As part of the Smart Recovery community we run an Aftercare program that hosts virtual meetings all across Canada, England, the USA and Australia.
Drug addiction is defined as a chronic disease characterized by drug seeking and use that is compulsive, or difficult to control, despite harmful consequences.3 It is possible to be physically dependent upon a drug without having an addiction to the substance. However, when addiction is an issue, the negative consequences experienced during drug abuse become overwhelming, which makes it impossible for the patient to function in relationships with others, at work, at school or in the community.
Nalmefene, an opiate antagonist that is similar in its chemical structure to naltrexone, is one of the most recent drugs being investigated for the treatment of alcoholism. Like naltrexone (sold as ReVia, Depade, or Vivitrol), nalmefene deprives the person struggling with substance use of the pleasurable feelings associated with drinking. But nalmefene is less toxic to the liver than naltrexone. As of 2013, nalmefene was still undergoing clinical trials through the U.S. National Institutes of Health before receiving FDA approval. From Rehab to a Body Bag | Dying for Treatment: VICE Reports (Full Length)