Gold has pioneered the hypothesis of hedonic overeating or pathological attachment to food as an addiction and over eating as a substance dependence disorder that causes obesity.
A great deal has been learned in the past decade about the structure of the striatum and nucleus accumbens, the latter in particular being an important neural substrate of the acute reinforcing effects of drugs of abuse and of the motivational aspects of drug dependence. This work has delineated different subsets of neurons within these structures and has begun the arduous process of defining each subtype based on its chemical constituents (e.g., the types of proteins such as dopamine receptors and neuropeptides it expresses) and on its afferent and efferent connections. Given the important role of the nucleus accumbens in drug-related behaviors, continued efforts in this area are needed, and these efforts must be integrated more effectively with ongoing research at the molecular and cellular levels as outlined above. For example, the chemical constituents of selected subtypes of nucleus accumbens neurons represent potential targets for medication development and human genetic analyses.
Gateway Hypothesis: Shortcomings of the Reward Model
the motivational aspects of cocaine and other drug addictions (see above). This work has had an important impact on evolving molecular and systems analyses of drug dependence, and continued efforts are needed. Moreover, very little is known about the long-term effects of other drugs of abuse. For example, whereas considerable information is available concerning chronic opiate action on certain neuronal cell types, virtually no information is available concerning the long-term effects of opiates on neurons in the mesolimbic dopamine system and its connections. Even less is known about the consequences of chronic cannabinoid, nicotine, and psychotomimetic exposure. This type of information is critical to understand molecular phenomena within a functional context and to understand interactions among neurons at the systems level. Translation of molecular events to cellular interactions is essential to link drugs, which are molecular entities, to behavior.
of drug withdrawal in addiction ..
Compared to people without depression, people with depression are about twice as likely to be smokers, and are less likely to succeed in quit attempts. They are also more nicotine dependent, more likely to suffer from negative mood changes after nicotine withdrawal, more likely to relapse, and experience disproportionate morbidity and mortality from smoking-related disease. Depression is also related to psychosocial characteristics that make it more difficult to stop smoking, for example, lower self-esteem and self-efficacy for quitting, and greater likelihood of unemployment, poorer social support networks and poorer physical health. Recent findings from the Four Country (Canada, US, UK, and Australia) International Tobacco Control Study showed that smokers with depressive symptoms or diagnosis make more quit attempts than people without depression, but they were also more likely to relapse in the first month. Despite this, meta-analyses suggest that a lifetime history of major depressive disorder, in itself, does not predict failure to quit smoking. A 2015 review of depression and smoking concluded that: depressed smokers are motivated to quit; smoking cessation does not exacerbate symptoms of depression; depression does not have a negative impact on smoking cessation outcomes; and the self-medication hypothesis does not account for tobacco dependence and depression co-morbidity.89 Indeed, a growing body of evidence supports the beneficial role of quitting in reducing depression.
Theories of addiction | What is the meaning of addiction?
An important consideration in treating nicotine dependence is the impact of smoking on psychiatric treatment. Smoking complicates the treatment and course of psychiatric disorders through its profound effect on the metabolism of pharmacotherapies, and is therefore one of the factors that leads to individual differences in drug responses. For example, smoking can interfere with the medications taken for schizophrenia and depression, therefore the doses of some psychotropic medications may need to be decreased following cessation. Patients with mental illness can be offered the same cessation medications as the general population, but should be monitored closely. The typically higher levels of nicotine dependence among smokers with mental illness mean that larger doses of NRT, combination pharmacotherapy, and a longer duration of therapy may be necessary. Australian research found that cessation support after discharge from an inpatient psychiatric facility was effective in encouraging quit attempts and reducing cigarette consumption up to 6 months post-discharge.