By Christopher G. Fairburn
This targeted instruction manual offers and integrates almost all that's presently recognized approximately consuming problems and weight problems in a single authoritative, obtainable, and eminently sensible quantity. From prime overseas professionals, 112 concise chapters encapsulate the newest info on all pertinent themes, from organic, mental, and social strategies linked to threat, to scientific equipment for overview and intervention. feedback for additional examining on the finish of every bankruptcy substitute prolonged references and increase the sensible worth and clarity of the amount.
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Additional info for Eating Disorders and Obesity, Second Edition: A Comprehensive Handbook
The fact that all of these knockout animals respond to 28 I. , NPY) molecules, indicates that the response processes are not simple daisy chains of neurons or molecules. The extreme biological importance of these pathways—integrating somatic energy stores with food seeking, neuroendocrine (reproduction, growth), and immune physiology—accounts for the redundancy of the components. Animals lacking functional Lep or Lepr genes still respond to food deprivation with compensatory hyperphagia and declines in energy expenditure, indicating that the leptin axis is not the sole mediator of body weight regulation.
161–174). Baton Rouge: Louisiana State University Press. Copyright 1996 by Louisiana State University Press. Reprinted by permission. work that controls eating and negative feedback inhibits it. Eating continues as long as the potency of the positive feedback to the central network exceeds the potency of the negative feedback. Eating stops when the potency of negative feedback equals or exceeds the potency of the positive feedback. Both feedbacks are initiated by the direct contact of the mechanical and chemical stimuli of ingested food on preabsorptive receptors in the mouth, stomach, and small intestine.
The first paper to suggest that assortative mating contributes to the increase in the prevalence of obesity. Katzmarzyk, P. , Rao, D. , & Bouchard, C. (1999). Familial risk of obesity and central adipose tissue distribution in the general Canadian population. —The first paper to provide evidence that the familial risk for obesity is likely to be caused by both genetic and nongenetic factors. Lee, J. , Reed, D. , & Price, R. A. (1997). Familial risk ratios for extreme obesity: Implications for mapping human obesity genes.