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Over 95% of cases of human obesity are due to the impact of an obesogenic lifestyle (overconsumption of energy and/or insufficient energy expenditure) on a variable background of genetic susceptibility Causes of secondary obesity include certain drugs, endocrine disorders and monogenic syndromes The rapid spread of obesity within two generations indicates that environmental factors are mainly responsible for the global obesity epidemic However, individual susceptibility to obesity is predominantly inherited, with family studies suggesting that 50 70% of total variance in BMI is genetically determined Obesity also spreads through social networks Susceptibility to common, lifestyle-related obesity is polygenic, determined by the cumulative effect of many minor genes Putative obesity susceptibility genes include F TO ( fused toe ), INSIG-2 (insulin-induced gene 2) and GAD2 (an isoform of glutamic acid decarboxylase) Their roles in energy balance regulation are yet to be determined.

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Radio in MCE is straightforward. If you have an antenna hooked up to your TV tuner card, MCE tunes in local radio stations for you (see Figure 17-6). Simply enter the frequency with your remote, for example, type in 1005, and it will tune to 100.5. Then sit back and listen! MCE can also pause radio and let you return to it where you left off just as with live TV.

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Certain aspects of energy intake are partly genetically determined, including the total energy consumed at a meal and restraint (the ability to stop eating) Candidate genes include those encoding CNS neurotransmitters that regulate appetite A relatively low energy expenditure may predispose to obesity and this may be partly genetically determined Candidate genes include the 3 adrenoceptor receptor involved in thermogenesis, although its overall importance remains uncertain The persistence of obesity genes has been attributed to the survival value of thrifty genes (promoting food intake and energy storage) during human evolution An alternative suggestion is that body weight has been subject to random genetic drift for 2 million years, since overweight individuals would have been released from predation risk Population-wide increases in obesity can be largely explained by overconsumption of food and sweetened drinks.

Factors shown to favour overconsumption include high energy density of food, larger portions, greater dietary variety, snacking, eating outside the home, and social facilitation , that is, increased consumption when eating with company Reduced energy expenditure may also contribute to the spread of obesity, consistent with increases in the use of labour-saving devices, car ownership and sedentary pursuits; however, direct evidence is lacking The obesogenic effect of watching television is explained by the associated overeating Numerous drugs increase adiposity, by stimulating appetite (eg glucocorticoids, antipsychotic and anti-epileptic drugs), decreasing energy expenditure ( adrenoceptor blockers), or promoting lipogenesis (insulin, sulphonylureas) or adipocyte differentiation (thiazolidinediones) Weight can increase by several kilograms with glucocorticoids, insulin, atypical antipsychotics and anti-epileptic agents Hypothyroidism decreases energy expenditure and causes weight gain, but overt obesity is rare Central and visceral obesity, due mainly to hyperphagia, are characteristic of Cushing syndrome and hypothalamic damage.

Polycystic ovarian syndrome is commonly associated with obesity Over 30 Mendelian syndromes include obesity; the most common is Prader-Willi syndrome, with early-onset hyperphagia and morbid obesity, short stature and mental retardation Other monogenic causes of human obesity, mostly extremely rare, include mutations affecting leptin, the leptin receptor and the melanocortin-4 receptor (MC4-R); the latter may account for 5% of morbid obesity that begins in early childhood..

Choose the Create Separate Hatches option to create separate hatch objects when you are hatching several separate closed areas. Otherwise, you create one hatch object that hatches these separated areas.

where T is the kinetic energy of the particle and the focusing force has been expressed in terms of the gradient B of the external magnetic field.

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