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Query: UMLS:C0028754 (obesity)
 124,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

An increasing number of people report concerns about the amount of stress in their life. At the same time obesity is an escalating health problem worldwide. Evidence is accumulating rapidly that stress related chronic stimulation of the hypothalamic-pituitary-adrenal (HPA) axis and resulting excess glucocorticoid exposure may play a potential role in the development of visceral obesity. Since adequate regulation of energy and food intake under stress is important for survival, it is not surprising that the HPA axis is not only the 'conductor' of an appropriate stress response, but is also tightly intertwined with the endocrine regulation of appetite. Here we attempt to link animal and human literatures to tease apart how different types of psychological stress affect eating. We propose a theoretical model of Reward Based Stress Eating. This model emphasizes the role of cortisol and reward circuitry on motivating calorically dense food intake, and elucidating potential neuroendocrine mediators in the relationship between stress and eating. The addiction literature suggests that the brain reward circuitry may be a key player in stress-induced food intake. Stress as well as palatable food can stimulate endogenous opioid release. In turn, opioid release appears to be part of an organisms' powerful defense mechanism protecting from the detrimental effects of stress by decreasing activity of the HPA axis and thus attenuating the stress response. Repeated stimulation of the reward pathways through either stress induced HPA stimulation, intake of highly palatable food or both, may lead to neurobiological adaptations that promote the compulsive nature of overeating. Cortisol may influence the reward value of food via neuroendocrine/peptide mediators such as leptin, insulin and neuropeptide Y (NPY). Whereas glucocorticoids are antagonized by insulin and leptin acutely, under chronic stress, that finely balanced system is dysregulated, possibly contributing to increased food intake and visceral fat accumulation. While these mechanisms are only starting to be elucidated in humans, it appears the obesity epidemic may be exacerbated by the preponderance of chronic stress, unsuccessful attempts at food restriction, and their independent and possibly synergistic effects on increasing the reward value of highly palatable food.
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PMID:Stress, eating and the reward system. 1754 57

[Avena, N.M., Rada, P., Hoebel B.G., 2007. Evidence for sugar addiction: Behavioral and neurochemical effects of intermittent, excessive sugar intake. Neuroscience and Biobehavioral Reviews XX(X), XXX-XXX]. The experimental question is whether or not sugar can be a substance of abuse and lead to a natural form of addiction. "Food addiction" seems plausible because brain pathways that evolved to respond to natural rewards are also activated by addictive drugs. Sugar is noteworthy as a substance that releases opioids and dopamine and thus might be expected to have addictive potential. This review summarizes evidence of sugar dependence in an animal model. Four components of addiction are analyzed. "Bingeing," "withdrawal," "craving" and "cross-sensitization" are each given operational definitions and demonstrated behaviorally with sugar bingeing as the reinforcer. These behaviors are then related to neurochemical changes in the brain that also occur with addictive drugs. Neural adaptations include changes in dopamine and opioid receptor binding, enkephalin mRNA expression and dopamine and acetylcholine release in the nucleus accumbens. The evidence supports the hypothesis that under certain circumstances rats can become sugar dependent. This may translate to some human conditions as suggested by the literature on eating disorders and obesity.
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PMID:Evidence for sugar addiction: behavioral and neurochemical effects of intermittent, excessive sugar intake. 1761 61

A concise review of the literature on the influence of electronic media on children's health is given. The exposure to different media is estimated with special reference to the situation in Germany. The impact on violence and aggressive behavior, on sexuality, on physical activity, obesity and nutrition, on substance use and abuse and addiction, on anxiety, depression, irregular sleep, and attention deficits, on cognition, language and reading, creativity is discussed. Although some of the results reported are still in question, there is no doubt that television and other electronic media negatively influence children's mental and somatic well-being. They have fundamentally changed the life of children and expose them to a powerful experiment with unpredictable and possibly irreversible outcome.
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PMID:The impact of electronic media on mental and somatic children's health. 1786 77

The endocannabinoid system (EC) plays a significant role in appetite drive and associated behaviours. Therefore attenuation of the activity of the EC system would have therapeutic benefit in treating disorders that might have a component of excess appetite drive or over-activity of the endocannabinoid system, such as obesity, ethanol and other drug abuse, and a variety of central nervous system and other disorders. Antagonists of cannabinoid receptors have been designed through rational drug discovery essential to exploit these novel targets for potential in obesity, metabolism, addiction, pain and neurologic disorders. Rimonabant is the only compound in this group which along this pathway is now approved as a selective CB (1) (cannabinoid receptor subtype 1) antagonist, or inverse agonist, in the European Union and India and under regulatory review in the United States for the treatment of obesity and associated cardiometabolic risk.
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PMID:Endocannabinoid system--a novel target for cardiometabolic risk. 1787

The rise in obesity is associated with a decline in the amount of physical activity in which people engage. The energy expended through everyday non-exercise activity, called non-exercise activity thermogenesis (NEAT), has a considerable potential impact on energy balance and weight gain. Comparatively little attention has been paid to the central mechanisms of energy expenditure and how decreases in NEAT might contribute to obesity. In this review, we first examine the sensory and endocrine mechanisms through which energy availability and energy balance are detected that may influence NEAT. Second, we describe the neural pathways that integrate these signals. Lastly, we consider the effector mechanisms that modulate NEAT through the alteration of activity levels as well as through changes in the energy efficiency of movement. Systems that regulate NEAT according to energy balance may be linked to neural circuits that modulate sleep, addiction and the stress response. The neural and endocrine systems that control NEAT are potential targets for the treatment of obesity.
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PMID:Central neural and endocrine mechanisms of non-exercise activity thermogenesis and their potential impact on obesity. 1800 22

It is imperative that the management of complex outpatient medical problems be taught using an apprentice system of education. The implementation of highly experienced and outcome successful "master physicians" to train outpatient practicing clinicians will provide a powerful frame of reference and a highly imitatable model on which clinicians can base their presentations of information and medications to patients with complex medical problems such as type 2 diabetes, cardiovascular disease, chronic pain, obesity, or tobacco addiction. Because doctors have always learned by observation, we must ensure that those who they observe will be "worth watching" and that those watched can provide skills of patient management currently not taught in the Flexnor-styled medical educational system, which effectively ended the apprentice system of training. The reintroduction of a carefully crafted apprentice system will foreseeably improve patient care and reduce morbidity, mortality, medical errors, and medical expenses.
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PMID:Proposal for a medical master class system of medical education for common complex medical entities. 1822 60

Cannabis sativa L. preparations have been used in medicine for millenia. However, concern over the dangers of abuse led to the banning of the medicinal use of marijuana in most countries in the 1930s. Only recently, marijuana and individual natural and synthetic cannabinoid receptor agonists and antagonists, as well as chemically related compounds, whose mechanism of action is still obscure, have come back to being considered of therapeutic value. However, their use is highly restricted. Despite the mild addiction to cannabis and the possible enhancement of addiction to other substances of abuse, when combined with cannabis, the therapeutic value of cannabinoids is too high to be put aside. Numerous diseases, such as anorexia, emesis, pain, inflammation, multiple sclerosis, neurodegenerative disorders (Parkinson's disease, Huntington's disease, Tourette's syndrome, Alzheimer's disease), epilepsy, glaucoma, osteoporosis, schizophrenia, cardiovascular disorders, cancer, obesity, and metabolic syndrome-related disorders, to name just a few, are being treated or have the potential to be treated by cannabinoid agonists/antagonists/cannabinoid-related compounds. In view of the very low toxicity and the generally benign side effects of this group of compounds, neglecting or denying their clinical potential is unacceptable--instead, we need to work on the development of more selective cannabinoid receptor agonists/antagonists and related compounds, as well as on novel drugs of this family with better selectivity, distribution patterns, and pharmacokinetics, and--in cases where it is impossible to separate the desired clinical action and the psychoactivity--just to monitor these side effects carefully.
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PMID:Cannabinoids in health and disease. 1828 1

Rates of pediatric obesity have increased dramatically over the past decade. This trend is especially alarming because obesity is associated with significant medical and psychosocial consequences. It may contribute to cardiovascular, metabolic, and hepatic complications, as well as to psychiatric difficulties. The development of obesity appears to be influenced by a complex array of genetic, metabolic, and neural frameworks, along with behavior, eating habits, and physical activity. Numerous parallels exist between obesity and addictive behaviors, including genetic predisposition, personality, environmental risk factors, and common neurobiological pathways in the brain. Typical treatments for pediatric obesity include behavioral interventions targeting diet or exercise. These treatments have yielded mixed results and typically have been examined in specialty clinic populations, limiting their generalizability. There are limited medication options for overweight children and adolescents, and no approved medical intervention in children younger than 16 years old. Bariatric surgery may be an option for some adolescents, but due to the risks of surgery, it is often seen as a last resort. The parallels between addiction and obesity aid in developing novel interventions for pediatric obesity. Motivational enhancement and cognitive-behavioral strategies used in addiction treatment may prove to be beneficial.
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PMID:Pediatric obesity: parallels with addiction and treatment recommendations. 1841 81

Drugs and food exert their reinforcing effects in part by increasing dopamine (DA) in limbic regions, which has generated interest in understanding how drug abuse/addiction relates to obesity. Here, we integrate findings from positron emission tomography imaging studies on DA's role in drug abuse/addiction and in obesity and propose a common model for these two conditions. Both in abuse/addiction and in obesity, there is an enhanced value of one type of reinforcer (drugs and food, respectively) at the expense of other reinforcers, which is a consequence of conditioned learning and resetting of reward thresholds secondary to repeated stimulation by drugs (abuse/addiction) and by large quantities of palatable food (obesity) in vulnerable individuals (i.e. genetic factors). In this model, during exposure to the reinforcer or to conditioned cues, the expected reward (processed by memory circuits) overactivates the reward and motivation circuits while inhibiting the cognitive control circuit, resulting in an inability to inhibit the drive to consume the drug or food despite attempts to do so. These neuronal circuits, which are modulated by DA, interact with one another so that disruption in one circuit can be buffered by another, which highlights the need of multiprong approaches in the treatment of addiction and obesity.
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PMID:Overlapping neuronal circuits in addiction and obesity: evidence of systems pathology. 1864 Sep 12

Smoking and obesity are widely recognized cardiovascular risk factors for significant morbidity and mortality in women. Although women still smoke less than men do, smoking among women is on the increase, especially in younger women and teenagers. Reduction of cardiovascular risk through smoking cessation while maintaining weight is a major goal of intervention. The purpose of this article is to discuss best care practices for women with tobacco addiction using a 3-point integration of clinical expertise, the best available evidence gained from systematic research, and an analysis of satisfaction with care data. A model for a smoking cessation intervention with weight management content is presented using a conceptual framework of social learning theory, self-efficacy judgments, and the 4 principal sources of self-efficacy information. The specific aims of this pilot study are to (1) test the feasibility of the study methods and procedures, including subject accrual, attrition, and reliability of the instruments and protocol; (2) explore utilization of and satisfaction with the intervention; and (3) describe the impact of the intervention on primary (smoking biomarker) and secondary (weight/body mass index, depression, partner support, and smoking cessation self-efficacy temptations) outcomes. Results show that the study is feasible, but modifications are needed to improve utilization and satisfaction with care. The primary outcome showed a reduction in the smoking biomarker while maintaining weight at the 2-month follow-up. There was also improvement in skills to manage temptation situations that supported the conceptual framework. Hypotheses are presented for a future experimental study.
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PMID:Evidence-based practice to assist women in hospital settings to quit smoking and reduce cardiovascular disease risk. 1872 12


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