I got to read this article for my nursing continuing education hours. I don't know whether I agree with the disease model of addiction or not-all those wordy arguments came to be meaningless to me because the only thing
I needed to understand is that
I needed to quit, whether I was diseased, whether my grandpa Hatch passed the bad genetics down to me, whether I was abused without knowing it in my childhood. None of it would change the final verdict.
But this article does explain to me, why it is so hard to quit. Why we can't just put it down. Why we fail at quitting so many times.
It's not all our fault.
Neurobiologic Advances from the Brain Disease Model of Addiction.
Author(s): Volkow N D, et al.
Journal: N Engl J Med. 2016; 374: 363-371. 58 references.Faculty Disclosure: Nora D. Volkow, MD, National Institute on Drug Abuse, 6001 Executive Bld., Rm. 5274, Bethesda, MD 20892. Email: nvolkow@nida.nih.gov
Objective: Review and evaluate the latest advances and newest information in the area of Addiction
"Editor’s Note: This is essentially a plea for more basic research in addiction.
Class: Basic science of addiction
Research guided by the brain disease model of addiction has led to the development of more effective methods of prevention and treatment and to more informed public health policies. Notable examples include the Mental Health Parity and Addiction Equity Act (MHPAEA) of 2008, which requires medical insurance plans to provide the same coverage for substance-use disorders and other mental illnesses that is provided for other illnesses and the proposed legislation that would reduce prison sentences for some nonviolent drug offenders because people who need treatment for drug and alcohol problems or mental health issues will be more likely to improve and reintegrate into society if they receive consistent care.
Advances in neurobiology have begun to clarify the mechanisms underlying the profound disruptions in decision-making ability and emotional balance displayed by persons with drug addiction. Addiction has been divided into three recurring stages: binge and intoxication, withdrawal and negative affect, and preoccupation and anticipation (or craving). Each stage is associated with activation of specific neurobiologic circuits and the consequential clinical and behavioral characteristics.
Binge and intoxication involves the same molecular mechanisms that strengthen synaptic connections during learning and memory formation. Environmental stimuli repeatedly paired with drug use may all come to elicit conditioned, fast surges of dopamine release that trigger craving for the drug, motivate drug-seeking behaviors and lead to heavy "binge" use of the drug. Whereas dopamine cells stop firing after repeated consumption of a "natural reward" (e.g., food or sex) satiating the drive to further pursue it, addictive drugs circumvent natural satiation and continue to directly increase dopamine levels.
Withdrawal and negative affect results because persons with addiction no longer experience the same degree of euphoria from a drug as they did when they first started using it. There are adaptations in the circuitry of the amygdala in the basal forebrain resulting in increases in a person's reactivity to stress and lead to the emergence of negative emotions. In addition to the direct and conditioned pull toward the "rewards" of drug use, there is a correspondingly intense motivational push to escape the discomfort associated with the after effect of use. Many state they continue to take the drug to escape the distress they feel when they are not intoxicated.
In preoccupation and anticipation, there are changes in the function for the prefrontal cortical regions, which involve the executive processes. The impaired signaling of dopamine and glutamate in the prefrontal regions weakens the ability to resist strong urges or to follow through on decisions to stop taking the drug.
Factors that increase vulnerability to addiction include family history (presumably through heritability and child-rearing practices), early exposure to drug use (adolescence is among the periods of greatest vulnerability to addiction), exposure to high-risk environments, and certain mental illnesses (e.g., mood disorders, attention deficit-hyperactivity disorder, psychoses, and anxiety disorders). Susceptibility to addiction differs because people differ in their vulnerability to various genetic, environment and developmental factors.
Awareness of individual and social risk factors and the identification of early substance-use problems make it possible to tailor prevention strategies to the patient. When prevention has failed and there is a need for treatment, research based on the brain disease model of addiction has shown that medical treatment can help to restore health function in affected brain circuitry and lead to improvements in behavior.
Although it is too soon to evaluate the effect of the MHPAEA and the Affordable Care Act, there appears to be increased enrollment and care delivery among patients with substance-use disorders and an overall reduction in spending on emergency departments visits and hospital stays in three states that were initially reviewed.
Important Points: Despite reports of benefits to the public from practices and policies generated by research based on the brain disease model of addiction, mobilizing support for further research will require the public to become better educated about the genetic, age-related, and environmental susceptibilities to addiction as they relate to structural and functional changes in the brain. If early voluntary drug use goes undetected and unchecked, the resulting changes in the brain can ultimately erode a person's ability to control the impulse to take addictive drugs."
