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Addiction Hypnotherapy Programs - Seattle Healing Hypnosis
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Addiction is a brain disorder characterized by compulsive involvement in useful stimuli despite adverse consequences. Despite the involvement of a number of psychosocial factors, biological processes - caused by repeated exposure to addictive stimuli - are the core pathologies that promote the development and maintenance of addictions. The two traits that characterize all addictive stimuli are that they strengthen (that is, they increase the likelihood that a person will look for repeated exposure to them) and are intrinsically rewarding (ie, they are perceived as positively, desirable, and inherently fun).

Addiction is a disorder of the brain reward system that arises through transcriptional and epigenetic mechanisms and occurs over time from high levels of chronic exposure to addictive stimuli (eg eating food, cocaine use, involvement in sexual intercourse, participation in cultural activities such as gambling, etc.). ). Fosb, the gene transcription factor, is an important component and a common factor in the development of almost all forms of behavioral addiction and drugs. Two decades of research on the role of Fosb in addiction has shown that addiction arises, and related compulsive behaviors intensify or weaken, along with Fosb's overexpression in a D1-type spiny neuron of the nucleus accumbens. Because of the causal relationship between? Fosb expression and addiction, it is used preclinically as an addiction biomarker. This expression phosaph in neurons directly and positively regulates drug self-administration and values ​​sensitization through positive reinforcement, while reducing sensitivity to rejection.

As described by two groups of researchers, addiction demands "tremendous financial and human casualties" to individuals and society as a whole through the direct adverse effects of drugs, related health care costs, long-term complications (eg, lung cancer with tobacco smoking, cirrhosis of the liver by drinking alcohol, or meth mouth of intravenous methamphetamine), functional consequences of changes in neural plasticity, and loss of productivity as a result. The classic signs of addiction include impaired control over substances or behavior, preoccupation with substance or behavior, and continue to use despite consequences. Habits and patterns associated with addiction are usually characterized by immediate gratification (short-term rewards), coupled with a deleterious effect of delay (long-term costs).

Examples of drug addiction and behavior include alcoholism, amphetamine addiction, cocaine addiction, nicotine addiction, opioid addiction, food addiction, gambling addiction, and sexual addiction. The only addictive behavior recognized by DSM-5 and ICD-10 is gambling addiction. The term addiction is often misused to refer to other compulsive behaviors or disorders, especially dependence , in the news media. An important difference between drug dependence and dependence is drug dependence is a disorder in which discontinuation of drug use causes an unpleasant withdrawal state, which may lead to further drug use. Addiction is the compulsive use of a substance or performance of a behavior that does not depend on withdrawal.

Video Addiction



Neuropsychology

Cognitive control and stimulus control, associated with classical operands and conditioning, represent opposing processes (ie, internal vs. external or environment, respectively) that compete above individual behavioral control. Cognitive control, and especially behavioral inhibition control, is impaired in addictive disorder and attention to hyperactive deficits. The stimulus-driven behavioral response (ie, stimulus control) associated with a particular award stimulus tends to dominate one's behavior in addiction.

Stimulus Control behavior

Cognitive behavior control


Maps Addiction



Behavioral addiction

The term behavior addiction correctly refers to the necessity to engage in a natural gift - which is a behavior that is inherently beneficial (ie, desirable or attractive) - despite adverse consequences. Preclinical evidence has shown that marked improvement in expression? FosB through repeated and exaggerated exposure to natural gifts induces the same behavioral effects and neuroplasticity as happens in drug addiction.

Reviews of both human clinical research and preclinical studies involving? FosB has identified compulsive sexual activity - in particular, all forms of intercourse - as an addiction (ie, sexual addiction). In addition, cross-sensitization rewards between amphetamines and sexual activity, which means that exposure to one increases the desire for both, has been shown to occur pre-selectively and clinically as dopamine dysregulated syndrome; FosB expression is required for this cross sensitization effect, which increases with the level of FosB expression.

Preclinical studies have shown that long-term and excessive consumption of fat or sugar can lead to addiction (food addiction).

Gambling is a natural gift associated with compulsive behavior and the clinical diagnostic guide, DSM-5, has identified diagnostic criteria for "addiction". There is evidence of functional neuroimaging that gambling activates reward systems and mesolimbic pathways in particular. Similarly, shopping and playing videogames are associated with compulsive behavior in humans and have also been shown to activate mesolimbic pathways and other parts of the reward system. Based on this evidence, gambling addiction, video game addiction and shopping addiction are classified accordingly.

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Risk factors

There are various genetic and environmental risk factors for developing addictions that vary across the population. About half of a person's risk for developing an addiction comes from genetics, while the other half comes from the environment. However, even in individuals with relatively low genetic loads, high doses of addiction drug additives for long periods (eg, weeks) can cause addiction. In other words, anyone can become an addict in the right situation.

Genetic factors

It has long been established that genetic factors as well as environmental factors (eg, psychosocial) are significant contributors to addictive susceptibility. Epidemiological studies estimate that genetic factors are responsible for 40-60% risk factors for alcoholism. The same level of heritability for other types of drug addiction has been demonstrated by other studies. Knestler hypothesized in 1964 that genes or groups of genes might contribute to the tendency of addiction in some way. For example, changes in normal protein levels due to environmental factors can then alter the structure or function of specific brain neurons during development. These altered brain neurons can alter a person's susceptibility to early drug use experiences. To support this hypothesis, animal studies show that environmental factors such as stress can affect animal genotypes.

Overall, data involving specific genes in drug addiction development are mixed for most genes. One reason for this may be because the case is due to the current research focus on common variants. Many addiction studies focus on common variants with allele frequencies greater than 5% in the general population, but when associated with the disease, this only provides a small number of additional risks with a probability ratio of 1.1-1.3 percent. On the other hand, the rare variant hypothesis states that genes with low frequencies in the population (& lt; 1%) give far more additional risk in disease progression.

Genome association study (GWAS) is a recently developed research method used to examine genetic relationships with addiction, addiction, and drug use. These studies use an unbiased approach to finding genetic associations with specific phenotypes and assigning equal weight to all areas of DNA, including those with no apparent connection to metabolism or drug response. These studies rarely identify genes from proteins previously described through the model of the knockout animals and candidate gene analysis. In contrast, a large percentage of genes involved in processes such as cell adhesion are usually identified. This is not to say that previous findings, or GWAS findings, are wrong. The important effects of endophenotypes are usually unable to be captured by this method. Furthermore, genes identified in GWAS for drug addiction may be involved either in adjusting brain behavior before drug experience, after them, or both.

A study that highlights the important genetic role in addiction is a twin study. Twins have the same genetics and are sometimes identical. Analyzing these genes in relation to genetics has helped genetics understand how much the role of genes in addiction. Studies conducted on twins found that rarely are only one addicted twin. In most cases where at least one twin suffers from addiction, both do so, and often on the same substance.

Environmental factors

An environmental risk factor for addiction is the experience of an individual during their lifetime that interacts with the individual's genetic composition to increase or decrease his susceptibility to addiction. A number of different environmental factors have been implicated as risk factors for addiction, including various psychosocial stresses; However, one's exposure to addictive drugs is the most significant environmental risk factor for addiction. The National Institute for Drug Abuse cites the lack of parental supervision, the prevalence of peer use, the availability of drugs, and poverty as a risk factor for drug use among children and adolescents.

Poor childhood experience (ACE) is a variety of forms of child abuse and dysfunction experienced in childhood. A Study of the Adverse Children's Experience by the Centers for Disease Control and Prevention has shown a strong dose-response relationship between ACE and various health, social, and behavioral issues throughout a person's lifetime, including those associated with substance abuse. The neurological development of children can be permanently disrupted when they are chronically exposed to stressful events such as physical, emotional, or sexual abuse, physical or emotional neglect, witnessing domestic violence, or imprisoned or mentally ill parents. As a result, a child's cognitive function or ability to cope with negative or disturbing emotions can be disrupted. Over time, children may adopt the use of substances as a coping mechanism, especially during adolescence. A study of 900 court cases involving abused children found that large numbers of them continue to suffer from some form of addiction in their adolescence or adult life. The pathway to addiction that opens through stressful experiences during childhood can be avoided by changes in environmental factors throughout the individual's life and the opportunities for professional help.

Age

Adolescence is a period of unique vulnerability to developing addictions. In adolescence, the incentive-reward system in the brain matures well before the cognitive control center. This consequently gives the system incentives a disproportionate amount of power in the behavioral decision-making process. Therefore, teens are increasingly likely to act on their impulse and engage in risky behavior and potentially addictive before considering the consequences. Not only are teenagers more likely to start and maintain drug use, but once their addiction is more resistant to treatment and more recurrent.

Statistics show that those who start drinking alcohol at a younger age are more likely to become dependent later on. About 33% of the population tasted their first alcohol between the ages of 15 and 17, while 18% had experienced it before. As for alcohol abuse or dependence, the numbers start high with those who first drank before they were 12 and then dropped afterwards. For example, 16% of alcoholics start drinking before the age of 12, while only 9% first touch alcohol between 15 and 17. This percentage is even lower, ie 2.6%, for those who first start habit after age 21.

Most people are exposed and use addictive drugs for the first time during their adolescence. In the United States, there are more than 2.8 million new users of illegal drugs by 2013, or about 7,800 new users per day. More than half (54.1 percent) are under the age of 18.

comorbid disorder

Individuals with comorbidity (ie, coincidental) mental health disorders such as depression, anxiety, attention-deficit/hyperactivity disorder (ADHD) or post-traumatic stress disorder are more likely to develop substance use disorders. The National Institute for Drug Abuse cites early aggressive behavior as a risk factor for drug use.

Transgenerative epigenetic inheritance

Epigenetic genes and their products (eg, proteins) are key components that influence the environmental impact on individual genes; they also serve as the mechanisms responsible for transgenerational epigenetic inheritance, a phenomenon in which environmental influences on genes from parents can influence the associated properties and phenotypes of their offspring behavior (eg, behavioral responses to certain environmental stimuli). In addiction, the epigenetic mechanism plays a central role in the pathophysiology of disease; it has been noted that some changes in the epigenome that arise through chronic exposure to addictive stimulation during addiction can be transmitted across generations, in turn affecting the behavior of one's children (eg, children's behavioral responses to addictive drugs and natural rewards). More research is needed to determine the specific epigenetic mechanisms and inherited phenotypes of behavior that arise from addiction to humans. Based on preclinical evidence with laboratory animals, the behavioral phenotype associated with cross-generational interdependence may serve to increase or decrease the risk of children developing addictions.

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Mechanism

The use of chronic addictive drugs causes a change in gene expression in mesocorticolimbic projection. The most important transcription factor that produces this change is? FosB, cAMP element binding protein (CREB), and nuclear factor kappa B (NF-? B). Fosb is the most important biomolecular mechanism in addiction because Fosb's overexpression in middle-spaced neurons of type D1 in the nucleus accumbens is necessary and sufficient for many nerve adaptations and behavioral effects (eg, increased expression dependent on self-administration and reward sensitization drugs) seen in drug addiction. Expression of FosB in nucleus accumbens D1-type medium spiny neurons directly and positively regulates self-administration of drugs and values ​​sensitization through positive reinforcement and reduces sensitivity to aversion. Which drug addiction is where? FosB has been involved in alcohol addiction, amphetamines, cannabinoids, cocaine, methylphenidate, nicotine, phenylcyclidine, propofol, opiates, and substituted amphetamines, among others. ? JunD, transcription factor, and G9a, histone methyltransferase, both opposed to Fosb function and inhibited the increase in expression. Increased expression of nucleus accumbens? JunD (via gene-mediated viral transfer) or G9a expression (by pharmacological means) reduces, or with large increases can even block, many nerve changes and behaviors resulting from chronic high-dose use of addictive drugs (ie, changes mediated by? FosB ).

Fosb also plays an important role in regulating behavioral responses to natural rewards, such as good food, sex, and exercise. Natural rewards, such as drug abuse, induce gene expression? FosB in the nucleus accumbens, and this chronic appreciation can produce the same pathological addictive state through FosB overekspression. Consequently, Fosb is a key transcription factor involved in the addiction of natural rewards (ie, behavioral addiction) as well; in particular, Fosb in the nucleus accumbens is essential for the effect of strengthening sexual rewards. Research on the interaction between natural and drug rewards suggests that dopaminergic psychostimulants (eg, amphetamines) and sexual behavior act on the same biomolecular mechanisms to induce? FOSB in the nucleus accumbens and has a bidirectional cross sensitizing effect mediated through? FosB. This phenomenon is notorious for, in humans, dopamine dysregulated syndrome, characterized by drug induced compulsive involvement in natural rewards (in particular, sexual activity, shopping and gambling), has also been observed in some individuals taking dopaminergic drugs.

Fosob inhibitors (drugs or treatments that oppose their actions) may be an effective treatment for addictions and addictive disorders.

The release of dopamine in the nucleus accumbens plays a role in strengthening the quality of various forms of stimulation, including naturally reinforcing stimuli such as delicious food and sex. Dopamine neurotransmission changes are often observed following the development of addictive states. In laboratory humans and animals that have developed an addiction, changes in the neurotransmission of dopamine or opioids in nucleus accumbens and other parts of the striatum are evident. Research has found that the use of certain drugs (eg cocaine) affects the cholinergic neurons that involve the gift system, which in turn affects dopamine signaling in the region.

A summary of addictive plasticity

Gift system

Mesocorticolimbic Path

Understanding the pathway in which the drug acts and how the drug can alter the pathway is key when examining the biological basis of drug addiction. The prize path, known as the mesolimbic pathway, or its extension, the mesocorticolimbic pathway, is characterized by the interaction of several areas of the brain.

  • Projection of the ventral tegemental area (VTA) is a network of dopaminergic neurons with locally coupled postsynaptic glinkamid receptors (AMPAR and NMDAR). These cells respond when the gift indication stimulus is present. VTA supports learning and developing sensitization and releasing DA to the forebrain. These neurons also project and release DA into the nucleus accumbens, via the mesolimbic pathway. Almost all drugs that cause drug addiction increase the release of dopamine in mesolimbic pathways, in addition to their specific effects.
  • The nucleus accumbens (NAcc) is one of the outputs of the VTA projection. The nucleus accumbens themselves are largely composed of GABAergic medium spiny neurons (MSNs). The NACC is associated with acquiring and performing conditioned behaviors, and is involved in increasing sensitivity to drugs when addiction takes place. Excessive expression from? FosB in the nucleus accumbens is a common factor required in all known forms of addiction; ? FosB is a strong positive modulator of positive reinforced behavior.
  • The prefrontal cortex, including the anterior cingulate and orbitofrontal cortex, is another VTA output in the mesocorticolimbic pathway; important for the integration of information that helps determine whether a behavior will be generated. It is also important to form associations between the precious experiences of drug use and environmental cues. Importantly, these cues are powerful mediators of drug-seeking behavior and can trigger relapse even after months or years of abstinence.

Other brain structures involved in addiction include:

  • The basolateral amygdala project into the NACC and is considered also important for motivation.
  • The hippocampus is involved in drug addiction, because of its role in learning and memory. Much of this evidence comes from investigations that show that manipulating cells in the hippocampus alters the level of dopamine in NACC and the activation rate of dopaminergic VTA cells.

The role of dopamine and glutamate

Dopamine is the main neurotransmitter reward system in the brain. It plays a role in regulating movement, emotion, cognition, motivation, and feelings of pleasure. Natural rewards, such as eating, and the use of recreational drugs lead to the release of dopamine, and are linked to the properties of these stimulating boosters. Almost all addictive drugs, directly or indirectly, act on a brain reward system by increasing dopaminergic activity.

Excessive intake of many types of addictive drugs leads to the release of large amounts of dopamine, which in turn affects the prize path directly through the increased activation of dopamine receptors. High and abnormal dopamine levels in the synaptic cleft may induce downregulation of receptors in the neural pathways. Downregulation of mesolimbic dopamine receptors may cause a decrease in sensitivity to natural reinforcement.

The drug-seeking behavior is induced by glutamatergic projection from the prefrontal cortex to the nucleus accumbens. This idea is supported by data from experiments showing that drug-seeking behavior can be prevented after inhibition of the AMPA glutamate receptor and glutamate release in the nucleus accumbens.

Won sensitization

Gift sensitization is the process that leads to an increase in the number of rewards (in particular, the importance of incentives) provided by the brain to beneficial stimuli (eg, drugs). In simple terms, when sensitization of rewards against specific stimuli (eg, drugs) arises, the "wishes" or desire of one's own stimulus and related cues increase. The prize imagination usually occurs after the level of exposure to chronic stimulus exposure. Expression of FosB (DeltaFosB) on a D1 type medium-spaced neuron in nucleus accumbens has been shown to directly and positively regulate the sensitization of rewards involving natural medicines and rewards.

"Induced desire by senses" or "desire-induced desire", a form of desire that occurs in addiction, is responsible for most of the compulsive behaviors demonstrated by addicts. During the development of addiction, repeated associations of neutral and even unfavorable stimuli with drug consumption trigger an associative learning process that causes this neutral stimulation to act as a conditioned positive reinforcement of the use of addictive drugs (ie, this stimulus begins to function as a drug cue). As a conditioned positive amplifier of drug use, this previously neutral stimulus is given incentive siusence (which manifests as desire) - sometimes at a high pathological level due to reward sensitization - that can be transferred to the main amplifier (eg, drug addiction) originally paired.

Research on the interaction between natural and drug rewards suggests that dopaminergic psychostimulants (eg, amphetamines) and sexual behavior act on the same biomolecular mechanisms to induce? FosB in the nucleus accumbens and has the effect of mediated bidirectional sensitization through? FosB. Different from? The FosB-sensitive effect, CREB transcript activity reduces the user's sensitivity to the beneficial effects of the substance. CREB transcription in nucleus accumbens is involved in psychological dependence and symptoms involving lack of pleasure or motivation during drug withdrawal.

A set of proteins known as "regulator G protein signaling" (RGS), especially RGS4 and RGS9-2, have been involved in modulating some forms of opioid sensitization, including reward sensitization.

Neuroepigenetic mechanism

Changes in epigenetic regulation of gene expression in the brain reward system play a significant and complex role in the development of drug addiction. Addictive drugs are associated with three types of epigenetic modification in neurons. These are (1) histone modification, (2) DNA epigenetic methylation at CpG sites in (or adjacent to) certain genes, and (3) epigenetic downregulation or upregulation of microRNAs that have specific target genes. For example, while hundreds of genes in nucleus accumbens (NAc) cells exhibit histone modification after exposure to drugs - in particular, changes in acetylation and methylation conditions of histone residues - most other genes in NAc cells do not show such changes.

Reframing The Language Of Addiction: Researcher Pushes To Strike ...
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Diagnosis

5th Edition The Diagnostic and Statistical Manual of Mental Disorders (DSM-5) uses the term "Substance Use Disorder" to refer to the spectrum of conditions associated with use. DSM-5 eliminates the terms "misuse" and "dependency" of the diagnostic category, instead of using "light", "moderate" and "heavy" determinants to indicate the degree of disruption of use. The determinant is determined by the number of diagnostic criteria present in a particular case. This manual never really uses the term "addiction" in a clinical way. Currently, only drug addiction and gambling addiction are listed in DSM-5 . Previous editions have used physical dependence and related withdrawal syndromes to identify addictive states. Physical dependence occurs when the body has adjusted by incorporating substances into the "normal" function - that is, achieving homeostasis - and therefore physical withdrawal symptoms occur after discontinuation of use. Tolerance is the process by which the body continues to adapt to the substance and requires an increasing amount to achieve the original effect. Withdrawal refers to the physical and psychological symptoms experienced when reducing or stopping the substance that becomes dependent on the body. Withdrawal symptoms generally include but are not limited to anxiety, irritability, a strong desire for substance, nausea, hallucinations, headache, cold sweat, and tremors.

Medical researchers who are actively studying addiction have criticized the classification of DSM addictions due to disability and involve arbitrary diagnostic criteria. Writing in 2013, director of the US National Institute of Mental Health discusses the invalidity of the classification of mental disorders DSM-5:

Although DSM has been described as "the Bible" for this field, at least, the dictionary, create a set of labels and define each one. The strength of each DSM edition has been "reliability" - each edition has ensured that doctors use the same term in the same way. The disadvantage is the lack of validity. Unlike our definition of ischemic heart disease, lymphoma, or AIDS, the diagnosis of DSM is based on a consensus on cluster clinical symptoms, rather than the size of an objective laboratory. In the remainder of the drug, this would be equivalent to creating a diagnostic system based on the nature of chest pain or quality of fever.

Recently, though, the NIH recognizes progress in identifying biomarkers, noting they outperform traditional phenomenological categories in identifying the types of psychosis. As a diagnostic biomarker, Fos Fosb expression can be used to diagnose addiction in humans, but this will require brain biopsy and is therefore not used in clinical practice.

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Treatment

According to a review, "to be effective, all pharmacological or biological-based treatments for addiction need to be integrated into other established forms of rehabilitation, such as cognitive behavioral therapy, individual and group psychotherapy, behavior modification strategies, twelve- step programs, and care facilities housing. "

Behavioral therapy

A meta-analytic review of the efficacy of various behavioral therapies to treat drug and behavioral addiction found that cognitive behavioral therapy (eg, relapse prevention and contingency management), motivational interviews, and community empowerment approaches were effective interventions with moderate effect sizes. Preclinical studies using exposure therapy exposure (CET) models of mice showed that this type of treatment was more effective in adults than in adolescents, but adolescent outcomes could be increased with acute treatment at time (CET) with dopamine 2 agonist receptors.

Clinical and preclinical evidence suggests that consistent aerobic exercise, particularly endurance exercises (eg, marathon running), actually prevents the development of certain drug addictions and is an effective adjunctive to drug addiction, and for psychostimulant addiction in particular. Consistent aerobic exercise, highly dependent (ie, based on duration and intensity) reduces the risk of drug addiction, which appears to occur through the reversal of drug-related addiction-related neuroplasticity. One review noted that exercise can prevent the development of drug addiction by altering the immunoreactivity of FosB or c-Fos in the striatum or other parts of the reward system. Aerobic exercise decreases self-administration of drugs, reduces the possibility of relapse, and has the opposite effect on dopamine striatal receptors D 2 (DRD2) signaling (increase of DRD2 density) to those induced by addiction to some drug classes (decreased density DRD2). Consequently, consistent aerobic exercise can lead to better treatment outcomes when used as an adjunct to drug addiction.

Medication

Alcohol addiction

Alcohol, such as opioids, can induce a state of severe physical dependence and produce withdrawal symptoms such as delirium tremens. Because of this, treatment for alcohol addiction usually involves a combined approach that relates to addiction and addiction simultaneously.

Pharmacological treatments for alcohol addiction include drugs such as naltrexone (opioid antagonists), disulfiram, acamprosate, and topiramate. Instead of replacing alcohol, these drugs are intended to influence the desire to drink, either by directly reducing cravings such as with acamprosate and topiramate, or by producing unpleasant effects when alcohol is consumed, such as with disulfiram. These medications can be effective if treatment is maintained, but adherence can be a problem because alcohol patients often forget to take their medication, or discontinue use due to excessive side effects. According to a Cochrane Collaboration review, naltrexone opioid antagonists have proven to be an effective treatment for alcoholism, with effects lasting three to twelve months after the end of treatment.

Behavioral addictions

Behavioral addiction is a treatable condition. Treatment options include psychotherapy and psychopharmacotherapy (ie, drugs) or a combination of both. Cognitive behavioral therapy (CBT) is the most common form of psychotherapy used in treating behavioral addiction; focuses on identifying patterns that trigger compulsive behavior and making lifestyle changes to promote healthier behavior. Currently, no drug is approved for the treatment of behavioral addiction in general, but some drugs used for the treatment of drug addiction can also be useful with certain behavioral addictions. Any unrelated psychiatric disorders must remain in control, and be distinguished from contributing factors that cause addiction.

addicted to Cannabinoid

In 2010, there were no effective pharmacological interventions for cannabinoid addiction. A 2013 review of cannabinoid addiction notes that the development of CB1 receptor agonists that have reduced interaction with signaling? -arrestin 2 may be useful therapeutically.

Nicotine addiction

Another area where drug treatment has been widely used is in the treatment of nicotine addiction, which usually involves the use of nicotine replacement therapy, nicotinic receptor antagonists, or partial nicotinic reconstitution agonists. Examples of drugs that act on nicotinic receptors and have been used to treat nicotine addiction include antagonists such as bupropion and partial varenicline agonists.

opioid addiction

Opioids cause physical dependence, and treatment usually overcomes addiction and addiction.

Physical dependence is treated using substitutes such as suboxone or subutex (both containing buprenorphine active ingredients) and methadone. Although these drugs perpetuate physical dependence, the goal of opiate maintenance is to provide a measure of control over pain and cravings. The use of a substitute drug increases the ability of an addicted individual to function normally and eliminates the negative consequences of obtaining an unlawfully controlled substance. Once the prescribed dose is stabilized, treatment enters the maintenance or reduction phase. In the United States, opiate-replacement therapy is strictly regulated in methadone clinics and under DATA 2000 laws. In some countries, other opioid derivatives such as levomethadyl acetate, dihydrocodeine, dihidroetorphine and even heroin are used as substitutes for illegal road opiates, The different ones are given depending on the needs of each patient. Baclofen has succeeded in decreasing cravings for stimulants, alcohol, and opioids, as well as relieving the alcohol withdrawal syndrome. Many patients claim that they "become ignorant of alcohol" or "do not care about cocaine" overnight after starting baclofen therapy.

Psychostimulant addiction

As of May 2014, there is no effective pharmacotherapy for any form of psychostimulant addiction. Reviews from 2015 and 2016 show that TAAR1 selective agonists have significant therapeutic potential as a treatment for psychostimulary addiction; however, in February 2016, the only compound known to function as a TAAR1 selective agonist was an experimental drug.

Research

Research shows that vaccines that use anti-drug monoclonal antibodies can reduce the positive reinforcement triggered by the drug by preventing the drug from moving across the blood-brain barrier; However, current vaccine-based therapies are only effective in a relatively small subset of individuals. In November 2015, vaccine-based therapy is being tested in human clinical trials as a treatment for addiction and precautions against drug overdose involving nicotine, cocaine, and methamphetamine.

Because addiction involves abnormalities in glutamate and GABAergic neurotransmission, the receptors associated with these neurotransmitters (eg AMPA receptors, NMDA receptors, and GABAB receptors) are potential therapeutic targets for addiction. N-acetylcysteine, which affects metabotropic glutamate receptors and NMDA receptors, has shown some benefits in preclinical and clinical studies involving cocaine addiction, heroin, and cannabinoids. It may also be useful as an adjunctive therapy for amphetamine-type stimulant addiction, but more clinical research is needed.

Recent medical reviews of research involving laboratory animals have identified a class of drug-class I histone deacetylase inhibitors - which indirectly inhibit function and a further increase in accumbal expression? FosB by inducing G9a expression in nucleus accumbens after long-term use. This review and subsequent preliminary evidence using oral administration or intraperitoneal administration of sodium salt from other classic butyrat acid or other classical HDAC inhibitors for a long period of time suggests that the drug has efficacy in reducing addictive behavior in laboratory animals that have developed an addiction to ethanol, psychostimulant (ie, amphetamines and cocaine), nicotine, and opiates; However, in August 2015 no clinical trials involving human addicts and any HDAC class I inhibitors have been performed to test the efficacy of treatment in humans or to identify optimal dosing regimens.

Gene therapy for addiction is an active area of ​​research. One line of gene therapy research involves the use of viral vectors to increase the expression of dopamine D2 receptor proteins in the brain.

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Epidemiology

Due to cultural variation, the proportion of individuals developing drug or behavior addictions within a certain period of time (ie, prevalence) varies over time, by the state, and across the demographics of the national population (eg, by age group, socioeconomic status, etc.).

Asia

Australia

The prevalence of substance abuse disorders among Australians was reported at 5.1% in 2009.

Europe

United States

Based on a representative sample of the young US population in 2011, the prevalence of lifelong alcohol and drug addiction is estimated at 8% and 2-3%, respectively. Based on a sample representing the US adult population in 2011, the 12-month prevalence of alcohol and drug addiction is estimated at about 12% and 2-3% respectively. 12 months and the prevalence of lifetime prescription drug dependence is currently unknown.

By 2016, about 22 million Americans need treatment for alcoholism, nicotine, or other drugs. Only about 10%, or slightly over 2 million, receive any form of treatment, and who generally do not receive evidence-based care. One-third of hospital admissions and 20% of all deaths in the US each year are the result of untreated addictions and the use of substances. Regardless of the overall massive economic cost to society, which is greater than the cost of diabetes and all forms of cancer combined, most doctors in the US have no training to effectively deal with drug addiction.

Other reviews recorded lifetime prevalence rates for some behavioral addictions in the United States, including 1-2% for compulsive gambling, 5% for sexual addiction, 2.8% for food addiction, and 5-6% for compulsive shopping. The systematic review shows that the prevariant time-invariant rate for sexual addiction and related compulsive sexual behavior (eg, compulsive masturbation with or without pornography, compulsive cybersex, etc.) in the United States ranges from 3-6% of the population.

According to a 2017 poll conducted by the Pew Research Center, nearly half of US adults know family members or close friends who have struggled with drug addiction at some point in their lives.

South America


Opioid Addiction FAQ: Experts' guide to the hard facts - NY Daily News
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Theories of personality about addiction

The theory of addiction personality is a psychological model that connects personality traits or ways of thinking (ie, affective states) with an individual's inclination to develop an addiction. The model of addiction risk proposed in the psychology literature including the disregulation model influences positive and negative psychological influences, the theory of the sensitivity of impulsive reinforcement and behavioral inhibition, and the impulsive model of reward and impulsive sensitization.

The Financial cost of Addiction - ABC Money
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See also


Opioid Addiction FAQ: Experts' guide to the hard facts - NY Daily News
src: www.nydailynews.com


Note

Image legend

The Financial cost of Addiction - ABC Money
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References


12 Straight Truths About Addictions
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External links

  • "The Science of Addiction: Genetics and Brain". learn.genetics.utah.edu . Learn.Genetics - University of Utah.
  • Why are our brains addicted? - a TEDMED 2014 discussed by Nora Volkow, director of the National Institute on Drug Abuse at NIH.
  • Brain Activation Delay for Addiction Risk Factors

Kyoto Encyclopedia of Genes and Genomes (KEGG) marks the transduction path:

  • KEGG - human alcohol addiction
  • KEGG - human amphetamine addiction
  • KEGG - addicted to human cocaine

Source of the article : Wikipedia

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