The association between Internet addiction and psychiatric disorder: a review of the literature.
Ko C H,Yen J Y,Yen C F,Chen C S,Chen C C
European psychiatry : the journal of the Association of European Psychiatrists
Internet addiction is a newly emergent disorder. It has been found to be associated with a variety of psychiatric disorders. Information about such coexisting psychiatric disorders is essential to understand the mechanism of Internet addiction. In this review, we have recruited articles mentioning coexisting psychiatric disorders of Internet addiction from the PubMed database as at November 3, 2009. We describe the updated results for such disorders of Internet addiction, which include substance use disorder, attention-deficit hyperactivity disorder, depression, hostility, and social anxiety disorder. We also provide discussion for possible mechanisms accounting for the coexistence of psychiatric disorders and Internet addiction. The review might suggest that combined psychiatric disorders mentioned above should be evaluated and treated to prevent their deteriorating effect on the prognosis of Internet addiction. On the other hand, Internet addiction should be paid more attention to when treating people with these coexisting psychiatric disorders of Internet addiction. Additionally, we also suggest future necessary research directions that could provide further important information for the understanding of this issue.
Addictive genes and the relationship to obesity and inflammation.
Heber David,Carpenter Catherine L
There is increasing evidence that the same brain reward circuits involved in perpetuating drug abuse are involved in the hedonic urges and food cravings observed clinically in overweight and obese subjects. A polymorphism of the D2 dopamine receptor which renders it less sensitive to dopamine stimulation has been proposed to promote self-stimulatory behavior such as consuming alcohol, abusing drugs, or binging on foods. It is important to determine how this polymorphism may interact with other well-known candidate genes for obesity including polymorphisms of the leptin receptor gene and the opiomelanocortin gene. Leptin is a proinflammatory cytokine as well as a long-term signal maintaining body fat. Upper-body obesity stimulates systemic inflammation through the action of multiple cytokines including leptin throughout many organs including the brain. The association of numerous diseases including diabetes mellitus, heart disease, as well as depression with chronic low-grade inflammation due to abdominal obesity has raised the possibility that obesity-associated inflammation affecting the brain may promote addictive behaviors leading to a self-perpetuating cycle that may affect not only foods but addictions to drugs, alcohol, and gambling. This new area of interdisciplinary research holds the promise of developing new approaches to treating drug abuse and obesity.
Hypothalamic Dysfunction in Obesity and Metabolic Disorders.
Carmo-Silva Sara,Cavadas Cláudia
Advances in neurobiology
The hypothalamus is the brain region responsible for the maintenance of energetic homeostasis. The regulation of this process arises from the ability of the hypothalamus to orchestrate complex physiological responses such as food intake and energy expenditure, circadian rhythm, stress response, and fertility. Metabolic alterations such as obesity can compromise these hypothalamic regulatory functions. Alterations in circadian rhythm, stress response, and fertility further contribute to aggravate the metabolic dysfunction of obesity and contribute to the development of chronic disorders such as depression and infertility.At cellular level, obesity caused by overnutrition can damage the hypothalamus promoting inflammation and impairing hypothalamic neurogenesis. Furthermore, hypothalamic neurons suffer apoptosis and impairment in synaptic plasticity that can compromise the proper functioning of the hypothalamus. Several factors contribute to these phenomena such as ER stress, oxidative stress, and impairments in autophagy. All these observations occur at the same time and it is still difficult to discern whether inflammatory processes are the main drivers of these cellular dysfunctions or if the hypothalamic hormone resistance (insulin, leptin, and ghrelin) can be pinpointed as the source of several of these events.Understanding the mechanisms that underlie the pathophysiology of obesity in the hypothalamus is crucial for the development of strategies that can prevent or attenuate the deleterious effects of obesity.
Depression and obesity: evidence of shared biological mechanisms.
Milaneschi Yuri,Simmons W Kyle,van Rossum Elisabeth F C,Penninx Brenda Wjh
Depression and obesity are common conditions with major public health implications that tend to co-occur within individuals. The relationship between these conditions is bidirectional: the presence of one increases the risk for developing the other. It has thus become crucial to gain a better understanding of the mechanisms responsible for the intertwined downward physiological spirals associated with both conditions. The present review focuses specifically on shared biological pathways that may mechanistically explain the depression-obesity link, including genetics, alterations in systems involved in homeostatic adjustments (HPA axis, immuno-inflammatory activation, neuroendocrine regulators of energy metabolism including leptin and insulin, and microbiome) and brain circuitries integrating homeostatic and mood regulatory responses. Furthermore, the review addresses interventional opportunities and questions to be answered by future research that will enable a comprehensive characterization and targeting of the biological links between depression and obesity.