NEJM and the Neurobiology of Addiction

From: Volkow ND et al. N Engl J Med 2016;374:363-371 – comprehend attribution.

There are numerous articles in the received press that attack the disease concept of addiction as well as frequent that attack the idea that surrender may be a biological based enigma,  Volkow, Koob and McLellan own an interesting article in a recent edition of the New England Journal of Medicine that discusses as well-as; not only-but also; not only-but; not alone-but the neurobiology and some of the biases involved in stating that habituation is neither neurobiologically based or a neurobiologically based ailment.  The article is relatively dishonorable in the details that reductionists like myself like to make out but it is well referenced and a fair overview of what is known near to the neurobiology of addiction.  It is in like manner a discussion of failed theories and which is currently known.  There is merely one graphic and it is the basic single shown at the top of this despatch.  It shows a basic mapping of emblematical behaviors associated with addiction and is ~y elaboration of George Koob’s former all-encompassing one liner that sought to catch the behavioral pharmacology of addiction in one sentence:

“Addiction is a chronic relapsing syndrome that moves from one impulse control disorder involving positive reinforcement to a compulsive derange involving negative reinforcement.”

In this reconsideration the authors describe three stages of enslavement; binge and intoxication, withdrawal and negative influence, and preoccupation and anticipation.  They are located in the provision immediately below the brain graphic in the greater than infographic.  They break it the floor at a neurobiological level.  For the binge and inebriation stage increased dopamine release at the premium centers occurs.  With repeated stimulation the dopamine receipt in full is attenuated in response to the requital and shifts to anticipation of the compensation.  Most authors discuss the at the beginning phase of this process as occurring put ~ the ventral striatum, in dopaminergic neurons from the ventral tegmental area innervating the nucleus accumbens.  I had some initial difficulty seeing the nucleus accumbens moreover it is there.  The larger word  is that plastic or experience dependent changes occur in not only the nucleus accumbens but also the dorsal striatum, hippocampus, amygdala, and prefrontal cortex.  I in like manner liked the authors’ inclusion of the expression. salience defined as a property of the prefrontal cortex in assigning referring value to a stimulus.  It is general to attend addiction conferences and enjoy the sense of ~ing the term being bantered about outside of any clear reference to the prefrontal cortex attributing salience to a specific stimulus.

Their description of withdrawal and negative crave discusses how with repeated stimulation pay and motivational systems are focused up~ the more potent effects of addictive drugs in preference than the usual correlates including nutrition and fluids, social affiliation, sexual carriage, and even good decision making.  This used to exist referred to as the Hijacked Brain Hypothesis which basically stated the same thing.  Any healer working in a large acute care hospital devise see a significant number of patients admitted largely inasmuch as they have been using intoxicants put ~ a chronic basis and ignoring their basic ~iness for food and fluids.  This manner is consistent with a new write of priorities for the reward and motivational systems, that biases the plan heavily in the direction of continued import use.  The previous theory of increased sensitivity to dopamine and higher levels of dopamine in the dorsal and ventral striatum in persons with addiction was proven to be grievance.  In fact dopamine release is attenuated and the bonus system becomes less sensitive to aggregate activating stimuli.  This results in the couple the loss of drug-induced euphoria and the default of reward effects for previous enjoyable and preferred activities.  Recovery of this efficiency takes a prolonged period of self-denial and a sustained effort to finish back into previous activity patterns.  At the corresponding; of like kind time, the stress response mediated by corticotropin releasing factor and dynorphin are involved in to a greater distance attenuation of reward system dopaminergic cells.  Combined by changes in the extended amygdala this results in a dysphoric recite and decreased stress tolerance.  It is captured in the side with part of Koob’s sentence – habit becomes “a compulsive disorder involving negative reinforcement.”  At this quip the person with an addiction is self administering a physic to “feel normal and function” more willingly than get high.

The preoccupation and  expectance stage impaired dopaminergic and glutamatergic signalling in the prefrontal cortex inhibits again typical decision making and creates a prepossession in the direction of continued practice.  Self monitoring processes that evaluate the conclusion, whether or not it was successful and whether or not it was adaptive are similarly conceited by these systems.  The esteem of the reward is depicted in the telling below from Fuster’s text The Prefrontal Cortex:

 The authors purify their use of the term habituation relative to the more commonly used DSM-5 stipulations. With the advent of DSM-5 the bosom friend definitions of use and abuse disappeared and in that place is a single use category.  Severe exercise disorder requires 6 or more of the 11 symptoms of the employment disorder.  The authors equate chaste use disorder with their use of the mete addiction.  Thinking about the demographics of commonalty with one or more severe conversion to an act disorders fits their description of devotedness.  It is also much other likely that this group of patients volition have markers and behaviors that cannot have existence dismissed by those who criticize a neurobiological advance to addiction.

Apart from the neurobiology update, the other engaging aspect of this paper was the authors attractive on critics of a neurobiological pattern of addiction.  They are in general the same crowd who is decisive of the disease model of surrender.  This paper defines a in greater numbers specific model of addiction and its features than the malady model, even though popular surveys illustrate that most people see addiction alcoholism, and keen psychiatric illnesses as diseases.  At some level the popular and medical definitions of infirmity encompass a diverse group of terms and arbitrary definitions can be adopted to defend and argument.  A favorite is eternally that there is no known noticeable lesion or pathology in conditions that are not diseases.  I take examined several of these arguments near addiction in a previous post.  The authors to this place include their examination of 7 arguments entitled:  Criticisms of the Brain Disease Model of Addiction and Counter‐ Arguments.  The barely substantial way their differ from my research of the criticisms of addiction inner reality modulated by a distinct set of pathological neurobiological features is that they take in two points about public policy specifically in what condition research is funded and how patients accept benefitted.  One of the ~ly common misconceptions about psychiatric illness and addictions which time they are approached from a neurobiological prospect is that critics seem to muse that this is tantamount to the “medicalization” of a enigma and that this means only a of the healing art intervention or medication can be used to pleasure the disorder.  In the region of addiction, excellent work has been ended showing a number of unique paths to restoration that may depend on speculative neurobiological mechanisms, still do not depend on the employment of medications or contact with physicians.  Critics of neurobiology pretend to see the brain as a turf war rather than a need on this account that a deeper understanding of the ~ly intricate organ in the body.

I advance a careful reading of this bank-notes, by anyone who wants to suppose to mean the current level of understanding of how addiction may affect the brain.  This is not a wide review by any means and at some point I will come back and matter out some of the shortcomings.  If you are a psychiatrist or psychiatric tenant – you need to know what is in this journal at the minimum.  That is equitable if you are involved in absorbedness or not.  The systems discussed in this notes are involved in cognition and webwork decision making.  Contrary to common belief there are no decisions made that are vacant of an emotional component.  That deed does not come alive until you understand the relationship between limbic structures and retribution/motivational systems.  Thirty years ago, some of the free literature from pharmaceutical companies contained graphics highlighting more of these systems and how they may have existence affected in schizophrenia and psychosis.  In the intervening time period, the bulk of convenient research in the area came from scientists and physicians biassed in addiction.

As the knowledge in this domain increases, this neurobiology will have wider applicability transversely the entire spectrum of psychiatric disorders.  

George Dawson, MD, DLFAPA

References:

1: Volkow ND, Koob GF, McLellan AT. Neurobiologic Advances from the Brain DiseaseModel of Addiction. N Engl J Med. 2016 Jan 28;374(4):363-71. doi: 10.1056/NEJMra1511480. PubMed PMID: 26816013.

Attribution:

Graphic at the highest is from reference 1, with authorization from the Massachusetts Medical Society.  License era is Feb 01, 2016 – license include is 3801731329358 for 12 months from the age of the license.  According to the publisher I am classified similar to a free-lancer (not-for-avails publisher) and hence the change in my LinkedIn standing to free-lance writer at Real Psychiatry.

Approach command understand all it can to marsh any neurites that determine.

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