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As the American Psychiatric Association committees begin formal work on DSM-V, we welcomebrief editorials on issues that should be considered in its formulation. Issues for DSM-V: Should Obesity Be Included Obesity (body mass index >30), has increased significantly over the past 30 years (approximately 50% per decade) (1), afflicting 32.2% of adults in the United States (2).
Obesity increases risk for cardiovascular disease, diabetes, cancer, and other diseases,resulting in annual health care costs conservatively estimated for the United States at$70 to $100 billion a year (3) as well as reductions in life expectancy by 5 to 20 years (4).
These facts highlight the urgent need to develop strategies to prevent and treat thoseafflicted.
Although there have been major scientific advances in the treatment of the medical complications of obesity (i.e., diabetes, hypertension hypercholesterolemia), the mor- bidity from this disorder is hampered by the fail-ure of interventions to sustain weight loss. Stan- dard interventions based on promoting lifestylechanges to decrease excessive food consumption (dieting) and increased physical activity (exer- cise) are effective and can normalize weight if fol- target in the treatment of lowed rigorously, but unfortunately they are in- credibly difficult to sustain. The discrepancy between the successes of the metabolic treat- ments of consequences of obesity and the fail- ures of behavioral treatments to prevent or re-verse obesity highlight the fact that this conditionis not only a metabolic disorder but also a brain disorder. Consideration of the mental component of obesity should be a key target in thetreatment of obesity to facilitate compliance and minimize relapse. Here, we proposethat some forms of obesity are driven by an excessive motivational drive for food andshould be included as a mental disorder in DSM-V.
DSM-IV recognizes eating disorders such as anorexia and bulimia as mental disorders with severe impairments and serious adverse outcomes but does not recognize obesitydespite its devastating medical and psychological consequences. Obesity is character-ized by compulsive consumption of food and the inability to restrain from eating de-spite the desire to do so. These symptoms are remarkably parallel to those described inDSM-IV for substance abuse and drug dependence (Table 1), which has led some tosuggest that obesity may be considered a “food addiction” (5).
There are multiple mechanisms contributing to the vulnerability to obesity, including genetic, developmental, and environmental factors that are likely to interact in diverseways among individuals to produce the behavioral phenotype of overeating (6). The“thrifty genotype” hypothesis suggests that evolution shaped the circuits involved inhow our bodies store food as well as the circuits involved in the procurement of food inour ancestors when food was scarce. In current environments, where for the most partfood is widely available and diverse, these circuits can lead to food overconsumption.
The “developmental origin hypothesis” suggests that calorie content as well as exposureto certain nutrients during pregnancy modify how the body and brain develop in anti-cipation of future environments with similar nutrient characteristics.
What brain circuits are associated with obesity? The hypothalamus is recognized as the main brain region that controls the regulatory signals for food consumption. The genetic TABLE 1. DSM-IV Substance Dependence Criteria With Suggested Corresponding Behaviors for Tolerance: increasing amounts of drug to reach Tolerance: increasing amounts of food to maintain Withdrawal symptoms upon drug discontinuation Larger amounts of drug taken than were intended Larger amounts of food eaten than were intended Persistent desire and unsuccessful attempts to cut drug Persistent desire for food and unsuccessful attempts to Great deal of time spent on getting the drug, using the Important social, occupational, or recreational activi- Activities are given up from fear of rejection because ties are given up or reduced because of substance Substance use is continued despite knowledge of hav- Overeating is maintained despite knowledge of ing a persistent or recurrent physical or psychological adverse physical and psychological consequences problem caused or exacerbated by the drug TABLE 2. Disrupted Brain Functions Implicated in the Behavioral Phenotypes of Addiction and Obesity and the Brain Regions Believed to Underlie the DisruptionDisrupted Function Impaired inhibitory control (to drug intake in addic- Prefrontal cortex; anterior cingulate gyrus Enhanced reward (to drugs in addiction; to food in Nucleus accumbens; ventral pallidum; hypothalamus Conditioning/habits (to drugs and drug cues in addiction; to food and food cues in obesity) Enhanced motivation/drive (to consume drugs in Orbitofrontal cortex; mesencephalic dopamine nuclei products that modulate hypothalamic activity (i.e., leptin, ghrelin, insulin) are also ex-pressed in limbic brain regions involved with reward, motivation, learning, emotion, andstress responses that are likely to modulate food consumption (7). In vulnerable individ-uals (because of genetic or developmental factors), how do these brain circuits becomedisrupted to produce compulsive food consumption? As shown in Table 2, we postulatethat the underlying brain mechanisms are similar to those that ultimately result in thecompulsive drug consumption in addiction (8). Both food consumption and drug useare driven by their rewarding properties, which have been linked to increases in dopa-minergic activity in brain reward circuits, but they do this in different ways (9). Food ac-tivates brain reward circuitry via palatability (mediated in part by endogenous opioidsand cannabinoids) and via increases in peptides that modulate dopamine activity (i.e.,insulin, leptin) (10), whereas drugs activate this same circuitry directly through theirpharmacological effects (mediated by their direct effects on dopamine cells or by theireffects on neurotransmitters that modulate dopamine cells such as opioids, nicotine,GABA, and cannabinoids) (11). Repeated supraphysiological dopamine stimulationfrom chronic drug use is believed to induce plastic changes in brain (i.e., glutamatergiccortico-striatal pathways) that result in poor inhibitory control over drug consumptionand compulsive drug intake (12). In parallel, dopaminergic stimulation facilitates condi-tioning to drugs and drug-associated stimuli as well as learned habits that then drive thebehavior to take drugs when exposed to stimuli associated with drugs. Similarly, re-peated exposure to certain foods (particularly those with a high fat and sugar content) invulnerable individuals can also result in compulsive food consumption, poor food intakecontrol, conditioning to food stimuli, and, over time, massive weight gain. It is not sur-prising that there is significant overlap in the medications that have been shown to inter-fere with drug and food consumption in animal models of drug abuse and obesity re-spectively (i.e., cannabinoid antagonists, baclofen, GABA agonists, and CRF antagonists)and in the behavioral interventions that are frequently used in the treatment of bothconditions (incentive motivation, cognitive behavior therapy, and 12-step programs).
Stimulants such as cocaine and methamphetamine can suppress appetite perhaps bysatiating the reward system, but they often lead to abuse and to return of overeating when tolerance develops or they are stopped. In contrast, partial blockade of the rewardsystem by antipsychotics (dopamine D2 receptor antagonists) can result in overeatingand can increase the risk for obesity.
The increasing prevalence and impact of obesity in our society and the urgent need to develop better therapeutic interventions that help mitigate the pathologically intensedrive for food consumption are clear. We have an opportunity in DSM-V to recognize acomponent of obesity as a mental disorder. Because of the complex ideologies of obe-sity it will be important to consider guidelines of which of these deserve to be classifiedas a mental disorder and which do not. This would facilitate the treatment of obesity notjust as a metabolic disorder but also, when appropriate, as a mental disorder.
1. Flegal KM, Carroll MD, Ogden CL, Johnson CL: Prevalence and trends in obesity among US adults, 1999–2000.
2. Ogden CL, Carroll MD, Curtin LR, McDowell MA, Tabak CJ, Flegal KM: Prevalence of overweight and obesity in the United States, 1999–2004. JAMA 2006; 295:1549–1555 3. Allison DB, Zannolli R, Narayan KM: The direct health care costs of obesity in the United States. Am J Public 4. Fontaine KR, Redden DT, Wang C, Westfall AO, Allison DB: Years of life lost due to obesity. JAMA 2003; 289: 5. Cota D, Tschop MH, Horvath TL, Levine AS: Cannabinoids, opioids and eating behavior: the molecular face of hedonism? Brain Res Brain Res Rev 2006; 51:85–107 6. Friedman JM: Modern science versus the stigma of obesity. Nat Med 2004; 10:563–5697. Morton GJ, Cummings DE, Baskin DG, Barsh GS, Schwartz MW: Central nervous system control of food intake and body weight. Nature 2006; 443:289–295 8. Volkow ND, Wise RA: How can drug addiction help us understand obesity? Nature Neuroscience 2005; 8: 9. Wise RA, Rompre PP: Brain dopamine and reward. Ann Rev Psychol 1989; 40:191–225 10. Abizaid A, Gao Q, Horvath TL: Thoughts for food: brain mechanisms and peripheral energy balance. Neuron 11. Hyman SE, Malenka RC, Nestler EJ: Neural mechanisms of addiction: the role of reward-related learning and memory. Annu Rev Neurosci 2006; 29:565–598 12. Kalivas PW, Volkow ND: The neural basis of addiction: a pathology of motivation and choice. Am J Psychiatry Address correspondence and reprint requests to Dr. Volkow, Director, National Institute on Drug Abuse, 6001Executive Blvd., Room 5274, Bethesda, MD 20892; (e-mail). Dr. Volkow reports no competing interests. Dr. O’Brien is a member of the DSM-V Task Force and is a consult-ant to Alkermes and Forest Laboratories. Dr. Freedman has reviewed this editorial and found no evidence ofinfluence from these relationships. Editorials discussing other DSM-V issues can be submitted to the Journal at Submissions should not exceed 500 words.



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