Biological explanations for obesity

When fat accumulates to BMI of 30kg/m2. Britain in 2011, 25% obese, estimated cost to NHS of £6.4 billion per year. USA, condition 2nd biggest cause of preventable death -> cardiovascular diseases, diabetes etc. 9% health costs attributed to obesity.

Symptoms inc breathlessness, lethargy, difficulty in performing physical activities, excess fat in breast, abdomen + upper arm regions, varicose veins etc. Influenced by bio + psychological factors.

Inherited genetic basis to obesity, some appear more genetically predisposed. Doesn't seem to be single 'obesity gene', instead those w/ multiple genes towards obesity + more vulnerable to developing condition.

Generally tested by looking at incidence of obesity among related individuals eg twin studies, as well as gene-profiling studies that search for common genes among sufferers.

Obesity may be evolutionary hangover. Survival used to depend on finding food, not always plentiful. Selective pressure favourited individuals able to store excess energy as fat to see themselves through times of famine. Now, food always available, evolution causes bodies to behave as if still living in past, genes once favoured survival now favour obesity.

Fatty foods preferred as energy rich, humans overeat to lay down fat stores in ancient times would see them through regular periods of food scarcity. Evolution sees humans preferring lazy lifestyles as in EEA conserving energy essential to survival. Modern humans behave as if food supplies irregular -> dysfunctional overating, over-eat foods not part of past, don't trigger neural mechanisms that control appetite.

Evolution explains why some more vulnerable to dramatic weight increases, by reference to thrifty gene model, believes in EEA there was selective advantage for people w/ insulin resistance as would've been able to metabolise food more efficiently. Adantageous in times of food scarcity, now food always available -> obesity.

Link between abnormal biochemisty + neural explanations.

Neurological explanations focus on idea faulty functioning hypothalamus associated w/ development of obesity. Attention focused on workings of VMH, which normally functioning person acts as satiety centre, informs individual they're full - allows eating to stop. 

Research also investigated specific mechanisms. Eg action of leptin, hormone produced by fat cells in stomach in proportion to amount of body fat, upon POMC + neuropeptide Y (NPY) neurones seen as especially importance. Amount of leptin influences neurones, which regulate appetite.

Neurological factors investigated by studying animals + faulty functioning brain structures + neurological mechanisms of obese individuals.

Stunkard et al (1990) compared body-mass similarities b/ween twins, 154 MZ pairs reared together, 93 MZ pairs reared apart, 208 DZ pairs reared together, 218 DZ pairs reared apart. Highest concordance rates MZ twins reared together - reared apart only slightly low. Suggests body weight (+ obesity) heavily influenced by genes.

Musani et al (2008) suggest obese people may be more fertile, reproduce more ultimately increase genes favouring obesity in population.

Genes can't explain upsurge in obesity. Genes haven't changed, but environmental factors eg availability of food have, suggests environment plays larger role.

Generally acknowledged genes one number of factors contributing to onset + maintenance of obesity, but research needs to focus on how genes interact w/ other factors to develop better understanding of disorder.

DiMeglio + Mates (2000) found participants given liquid cals, rather than equal amount solid cals, increased weight, implies liquid cals caused huge increase in obesity b/c humans not shaped by evolution to cope w/ them.

Thrifty gene hypothesis explains why identifiable groups of people who don't have gene able to eat lots + not put on weight, eg people of Nile delta historically there were not food shortages.

Idea foodstuff not present in EEA causing obesity open to criticism due to fact obesity levels also risen in countries where HFCS not commonly used.

Yang et al (2012) found increase in signalling in POMC neurons was positively correlated to age-dependent obesity in mice, suggests neural factors may be able to explain why obesity increases w/ age.

Stice et al (2008) found obese people have poorly functioning dorsal striatum -> lessened dopamine signalling in brain, causing overeating. Demonstrates role of neurotransmitter dopamine in determining obesity.

Hopes leptin injections would prove effective treatment for obesity, but only work for few people, doubt on importance of leptin's role.

Although some indication abnormally functioning brain mechanisms can contribute to obesity, research indicates main bio factors are genetic + evolutionary ones.

Much of research into leptin done on mice, results may not be generalisable to humans.