Structural model of addiction-Addiction Changes Brain Structures and Their Functioning - Addictions

The brain is composed of many different regions and structures. The brain's communication system permits these various regions and structures to coordinate their activities. Each of these different regions and structures serves different purposes. Addictions can alter these regions and structures. Subsequently, addictions can alter the way brain regions function.

Structural model of addiction

Structural model of addiction

Structural model of addiction

JohnsonWilliam H. The stimulus simply elicits a response, without the need for a reinforcing outcome. It has become essential to discard outdated perceptions of addiction and replace them with coherent models based on scientific principles. Addiction Changes the Brain's Communication Pathways. Yet I don't think this is in the cards. Foddy B, Savulescu Structural model of addiction.

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It also lays down admission and licensing procedures and the relevant authorities and their functions. Opiates and stimulants produce opposite effects in structural plasticity in the reward pathway. Urine screening equipment: As immediate measure, urine testing kits were made pf in each Central Jail and later equipment for testing may be procured Other additional measures suggested which could help Jail authorities in tackling the problem: Regular routine medical examination of inmates To control influx of addicting substances into the Jail Organizing religious discourses in Jail To regulate the supply, prescription and dispensing of habit forming drugs by health staff of Central Jails. Punjab Govt. To act as data and documentation centers for collecting data on drug abuse in patients registered with them as well as data from lower-level primary and secondary healthcare facilities aaddiction as to provide a Drug Abuse Monitoring System DAMS to Audio lovers stereo store berkeley used for surveillance on extent and patterns of substance abuse in the region. Addiction is a state characterized by compulsive engagement in rewarding stimulidespite adverse consequences. The main reason is the hierarchical relation of the game addiction first within social media, then the Internet and finally within the phone addiction. As a result qddiction the fact that the participants are approximately the same age min : 20, max : 24 and that this results in insufficient variance, exclusion of the moderator variable of age is required in this research. Ferozepur in modeo thick of Drug Menace. Although the Structural model of addiction cannot be completely removed from the researches, the errors can be minimized. Opiates stimulate dopamine neurons in Structural model of addiction brain indirectly by inhibiting GABA release from modulatory interneurons that synapse onto the dopamine neurons. Thus, individuals can make social media a real-time part of their life. GABA is an moedl neurotransmitter that decreases the Books shemale sex cam that tSructural target neuron will send a subsequent signal.

I review the brain disease model of addiction promoted by medical, scientific, and clinical authorities in the US and elsewhere.

  • There, monitored discussion of AVRT-based recovery takes place daily.
  • Phubbing can be described as an individual looking at his or her mobile phone during a conversation with other individuals, dealing with the mobile phone and escaping from interpersonal communication.
  • Substance use disorders are believed to have become rampant in the State of Punjab, causing substantive loss to the person, the family, the society, and the state.
  • Addiction is a state characterized by compulsive engagement in rewarding stimuli , despite adverse consequences.
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Skip to search form Skip to main content. Evidence shows that the public perceives heroin as harmful and addictive. Heroin is ranked as the most stigmatized condition. While there is robust literature on mental illness stigma, there is limited research concerning addictionrelated stigma.

There are very few standardized stigma measures related to perceptions toward persons addicted to heroin. View PDF. Save to Library. Create Alert. Share This Paper. Figures and Tables from this paper. Figures and Tables. References Publications referenced by this paper. Stigma power. Bruce G Link , J. Christopher Phelan. Nicholas D. Exploratory structural equation modeling.

Marsh , Benjamin Nagengast. Corrigan , S. Morris , P. Michaels , J. Rafacz , N. Labelling theory revisited: forty years on. Self-stigma in alcohol dependence: consequences for drinking-refusal self-efficacy.

Palamar , M. Kiang , P. Combining education and video-based contact to reduce stigma of mental illness: "The Same or Not the Same" anti-stigma program for secondary schools in Hong Kong.

Koo , D. Chitwood , J. Mental illness stigma: concepts, consequences, and initiatives to reduce stigma. Angermeyer , Patrick W Corrigan. Related Papers.

Discourse: Studies in the Cultural Politics of Education , 28 1 , 87— Below is a picture of the brain. In addition, the fact that we can now access the Internet and games through mobile phones has shifted the Internet addiction to another point. Please review our privacy policy. H 3a Social media addiction affects phubbing behavior in women more than men.

Structural model of addiction

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Models of addiction | fiddley.com

I review the brain disease model of addiction promoted by medical, scientific, and clinical authorities in the US and elsewhere. I then show that the disease model is flawed because brain changes in addiction are similar to those generally observed when recurrent, highly motivated goal seeking results in the development of deep habits, Pavlovian learning, and prefrontal disengagement.

This analysis relies on concepts of self-organization, neuroplasticity, personality development, and delay discounting. It also highlights neural and behavioral parallels between substance addictions, behavioral addictions, normative compulsive behaviors, and falling in love.

I note that the short duration of addictive rewards leads to negative emotions that accelerate the learning cycle, but cortical reconfiguration in recovery should also inform our understanding of addiction. I end by showing that the ethos of the disease model makes it difficult to reconcile with a developmental-learning orientation.

The harm done by addicts to themselves and those around them has riveted public attention in recent years. It has become essential to discard outdated perceptions of addiction and replace them with coherent models based on scientific principles.

Toward this end, doctors, psychiatrists, medical researchers and treatment providers have come to define addiction as a brain disease. Specifically, addiction is characterized by changes in brain systems that mediate the experience and anticipation of reward, systems responsible for perception and memory, and higher-order executive systems underlying cognitive control. The disease model stipulates that these changes are caused by exposure to drugs of abuse, and they are difficult if not impossible to reverse.

By looking at changes in the function and structure of the nervous system, the disease model helps explain why it is so difficult to achieve abstinence through the exercise of willpower.

It makes sense of individual differences in vulnerability to addiction, based on dispositional factors and environmental stressors. The disease model provides a knowledge base and research agenda for developing pharmaceuticals that can be useful for reducing craving and easing withdrawal symptoms. And it has countered the perception that addicts are morally deficient or self-indulgent, arguably reducing the stress and isolation they and their families experience. Yet there are reasons to question the validity of the disease perspective.

First, this perspective clashes with the experience of many former addicts, who do not feel they were ever sick or have now been cured. Second, the strongest endorsements of the disease model come from the rehab industry and Big Pharma, both of which profit from the belief that addicts need long-term medical treatment.

Rather, most alcoholics and addicts recover [ 1 ], and most of those do so without treatment of any kind [ 2 — 4 ], a finding that is difficult to reconcile with the idea that addiction is a chronic disease. Finally, investigators who approach addiction as a disease are far more likely to get their work funded, thus minimizing the volume and impact of discrepant findings. For these and other reasons, the disease model of addiction has been heatedly challenged, and alternative models have been proposed in its place.

Addiction may be viewed as a choice rather than a pathology. While few people imagine that addiction is a good choice, it is sometimes considered rational in the short run—as when the pleasure or relief derived from drugs temporarily outweighs the alternatives [ 5 , 6 ]. Addiction can be viewed as a form of self-medication that works against psychological suffering. Trauma—whether physical, psychological, or sexual—is often considered the root cause of long-term anxiety and depression; and post-traumatic stress disorder PTSD is highly correlated with substance use [ 8 — 10 ].

A framework that encompasses all these approaches views addiction as a product of cognitive and emotional development, predisposed by constitutional factors but consolidated through learning over childhood and adolescence [ 10 ]. These alternatives to the disease model of addiction may be compelling, but they lack one important ingredient.

They have little or nothing to say about the brain. There are notable exceptions [ 11 — 13 ], which, although valuable, provide only global neural arguments, without attention to key structures or processes.

In this era of scientific acceleration, brain science has become a gold standard for conclusive explanations of human phenomena. Without detailed neurobiological analysis, alternatives to the disease model may lack the scientific traction they need.

My book, The Biology of Desire [ 14 ] , was intended to fill in the neural level of analysis in a developmental-learning model of addiction, integrate that level of explanation with experiential accounts of addiction and recovery, and demonstrate that the disease model has outlived both its credibility and its usefulness. In the following sections, I summarize these arguments and connect them to the larger debate on how to understand and combat addiction.

Because the action of dopamine enhances the formation of new synapses and the corresponding loss of older ones , changes in dopamine metabolism bring about structural changes in synaptic networks—the basic wiring diagram of the brain.

A critical locus of dopamine reception and synaptic restructuring is the striatum, the area responsible for pursuing rewards, but other targets include the amygdala, which mediates emotional salience, the hippocampus, which directs memory encoding and retrieval, and several regions of the prefrontal cortex, responsible for a variety of cognitive functions.

Indeed, starting in the s and s, researchers began to show synaptic changes in these regions in laboratory animals exposed to cocaine, amphetamine, morphine, alcohol, and other drugs, corresponding with behavioral sensitization in addicted animals and humans [ 15 , 16 ]. For example, dopamine activation of the striatum was found to go up and down with drug availability—and not much else.

The receptors that absorb and use dopamine were also found to change in structure or efficiency [ 17 ] increasingly over months and years of use.

The message seemed clear: drug use messes up brain wiring. Nora Volkow M. In her view, this damage is specifically caused by drug use, and it corresponds with reduced capacity to engage cognitive control, increased compulsivity in drug seeking, and emotional blunting in response to rewards more generally.

The nucleus accumbens describes one of the most ventral lower regions of the striatum, and it is the brain part most often referred to when it comes to addiction. Berridge and Robinson [ 19 ] coined the phrase incentive sensitization to describe the increasing specificity with which dopamine flows from the ventral tegmental area VTA in the midbrain to the accumbens in response to drug cues. The ventral striatum or accumbens is associated with impulsive drug seeking and use, but the dorsal striatum becomes increasingly important for addiction with the passage of time.

As the period of addiction stretches over months and years, activation shifts from the ventral to the dorsal striatum in response to drug-associated cues, while drug-seeking behavior becomes more compulsive and less impulsive in character. Trevor Robbins and his colleagues at Cambridge have been studying the shift from impulsive to compulsive drug seeking for many years [ 22 ].

They see the compulsive phase as true addiction, as do many others in the field. Now, according to Volkow, Koob, and others, the addictive urge is truly out of control. Whether the addict actually desires the addictive reward, he or she is compelled to go after it, based on a stimulus-response S-R association acquired and strengthened through Pavlovian conditioning. The stimulus simply elicits a response, without the need for a reinforcing outcome.

According to Volkow and other scientists, not only the brain regions underlying goal-seeking but also those responsible for self-control are physically modified by drugs. An example can be seen in the dorsolateral prefrontal cortex dlPFC , which is critical for reasoning, remembering, planning, and self-control.

The dlPFC becomes hyperactivated in the early stages of addiction, as it does in some eating disorders, perhaps when people try to control or maintain the rewardingness of this new experience. But over time, this region and other prefrontal control centers start to disengage i. Volkow and colleagues have carried out two decades of research into cortical changes underlying addiction.

They conclude that prefrontal regions responsible for judging options and selecting among them lose grey matter volume reduced synaptic density and become partially dysfunctional over the course of addiction [ 23 , 25 ]. This cluster of changes in the function and structure of the brain has led many authorities to view addiction as a disease, and because these changes seem to endure long beyond the cessation of drug-taking, it is considered a chronic disease.

According to Steven Hyman, previous director of the National Institute of Mental Health, addiction is a condition that changes the way the brain works, just like diabetes changes the way the pancreas works.

One of the key premises of the disease model is that addiction changes the brain. Yet brains are supposed to change. They are designed to change. In fact the stages of child and adolescent development, and the learning that goes on throughout adulthood, are all underpinned by changes in the cortex and limbic regions. Given the realities of brain change in normal development and learning, neuroscientists who endorse the disease model must view the brain changes resulting from addiction as extreme or pathological.

In fact, they would have to show that the kind or extent or location of brain change characteristic of addiction is nothing like what we see in normal learning and development. How then should we characterize brain changes that occur naturally? First of all, brains grow and shape themselves, not by following prespecified guidelines, but by a process of self-organization.

They organize themselves, changing their own structure as they go. Such changes build on themselves over time, such that the products synaptic changes of one learning episode set the conditions for subsequent learning episodes. Of course there are some species-specific constraints on the timing of neural development, and there are certainly constraints on the kinds of information human beings can access and manipulate.

Moreover, social norms help guide neural development along pathways consistent with particular cultural environments. Yet neural development is in no way programmed. It results almost entirely from synaptic activation patterns that both result from and give rise to experience itself.

One way to conceptualize this kind of self-perpetuating growth is to see it as a feedback loop between experience and brain change. The way we experience things changes synaptic configurations, and those changes shape the way we experience things subsequently.

In other words, experience-dependent changes in brain structure make a particular way of experiencing things more probable on future occasions [ 26 ]. This can take the form of a self-perpetuating perception as in language learning , an expectancy, a budding interpretation as in judgments of individuals or groups , a recurring wish, a familiar emotional reaction as in anxiety regarding perceived threats , an emergent belief as in religious ideas and corresponding ism s , or a conscious memory.

Thus the mind and the brain shape each other. And ordinary classroom learning is just one version of this more general phenomenon—a brain that changes itself a phrase borrowed from Norman Doidge [ 27 ]. But since we need stability in our percepts, concepts, and actions, brain changes almost always settle into habits.

And once formed, habits—even minor habits—remain in place, sometimes for the rest of our lives. Examples range from idiosyncratic patterns like nail-biting and suspiciousness to cultural norms like politeness and sexual stereotyping. New synaptic pathways, and corresponding patterns of thought and behavior, start off tentative and fluctuating.

As Donald Hebb made famous in the s, cells that fire together wire together. Change and stabilization—novelty and habit formation—work together in the mind and in the brain. Another helpful concept is neuroplasticity. Neuroplasticity simply describes brain changeability and elevates it to a first principle. Yet neuroscientists who study addiction seem to have missed the point. Their brains have changed! The brain is supposed to change with new experiences. And those changes are supposed to stabilize and consolidate the more that experience is repeated.

When our experience of the world produces strong emotions—whether of desire, threat, pleasure, or relief—brain change takes on extra momentum. Emotions focus our attention and our thinking, partly through connections between the amygdala and a variety of cortical structures and partly through the wash of neuromodulators including dopamine released from the brain stem including the VTA in response to salient inputs.

When those emotions recur over and over, in response to a particular event, perception, thought, memory, or need, then attention directs memory consolidation systematically.

Our recurrently-focused brains inevitably self-organize in a particular direction, entrenching particular interpretations and emotional associations. Most relevant to addiction, the feeling of desire for something shapes synaptic configurations that become increasingly sensitive to cues associated with whatever is desired—since those cues are processed repeatedly in our efforts to acquire it.

Depression and anxiety also develop through feedback. The more we think sad or fearful thoughts, the more synapses get strung together to generate scenarios of loneliness or danger, and the more likely we are to practice strategies—often unconsciously—for dealing with those scenarios.

Neural patterns forged by desire can complement and merge with those born of depression or anxiety. So, when we examine the correlation between addiction and depression or anxiety, we should recognize that addiction is often a partner or even an extension of a developmental pattern already set in motion, not simply a newcomer who happened to show up one day.

Structural model of addiction

Structural model of addiction