Eating 2- Obese Flashcards
Intro: Definition of obese?
Overweight and obesity are defined as abnormal or excessive fat accumulation that presents a risk to health. A crude population measure of obesity is the body mass index (BMI), a person’s weight (in kilograms) divided by the square of his or her height (in metres). A person with a BMI of 30 or more is generally considered obese. A person with a BMI equal to or more than 25 is considered overweight.
Overweight and obesity are major risk factors for a number of chronic diseases, including diabetes, cardiovascular diseases and cancer. Once considered a problem only in high income countries, overweight and obesity are now dramatically on the rise in low- and middle-income countries, particularly in urban settings.
Obesity: when body mass index (BMI) is 20% above the ideal weight. BMI is a crude measure of body fat based on just height and weight: BMI: weight in kg / height in meters2 e.g. 90kg/1.802=27.8. Obesity in UK: 2011: 24.8% of adults (aged 16 and over) and 16.3% of children (aged 2 -15 years old) are obese by 2050: ~60% of men, 50% of women and 25% of children are likely to be obese.
Intro: Consequences of obesity:
Medical: Diabetes, Heart diseases, High blood pressure, Arthritis, hypertension, diabties, cardio vascular disease. Indigestion, Gallstones, Some cancers (e.g., breast and prostate cancers), Snoring and sleep apnoea, Infertility; Financial: £6.4bn per year by 2015 to the NHS, Psychosocial, Discrimination and negative attitudes, Mental health, Stress, Anxiety, Depression.
The world health organisation of obesity:
In 2014, 39% of adults aged 18+ were overweight (BMI ≥ 25 kg/m2) (39% men and 40% of women). In 2014, 39% of adults aged 18+ were overweight (BMI ≥ 25 kg/m2) (39% of men and 40% of women) and 13% were obese (BMI ≥30 kg/m2) (11% of men and 15% of women). Thus, nearly 2 billion adults worldwide are overweight and, of these, more than half a billion are obese.
The Global Nutrition Transition: The Pandemic of Obesity in Developing Countries Popkin et al (2012)
Decades ago discussion of an impending global pandemic of obesity was thought of as heresy. Diets in the 1970’s began to shift toward increased reliance upon processed foods, increased away from home intake and greater use of edible oils and sugar-sweetened beverages. Reduced physical activity and increased sedentary time was seen also. These changes began in the early 1990-‘s in the low and middle income world but did not become clearly recognized until diabetes, hypertension and obesity began to dominate the globe. Urban and rural areas from sub-Saharan Africa and South Asia’s poorest countries to the higher income ones are shown to have experienced rapid increases in overweight and obesity status. Concurrent rapid shifts in diet and activity are documented. An array of large-scale programmatic and policy shifts are being explored in a few countries; however despite the major health challenges faced, few countries are serious in addressing prevention of the dietary challenges faced.
At a practical level..
At a practical level, food provides material to enable growth and renewal of body tissues as well as providing energy. Different individuals have different energy requirements but remain in a state of energy balance if their total energy intake equals their total energy expenditure. When energy intake is greater than expenditure, individuals are said to be in a positive energy balance and surplus energy will frequently be stored as fat, leading the individual to weight gain and potential obesity.
At a biological level…
At a biological level, the hormone leptin secreted from adipose (fat) tissue, acts as a long term satiety signal inducing feelings of fullness. Coleman (1979) found that mice who lack leptin eat more, convert calories to fat more efficiently and use their calories more efficiently than control mice; they also have 5 times the fat of normal mice. Obese humans who lack leptin or its receptors because of a genetic mutation, show considerable food intake and develop severe obesity (prader-willi syndrome). However, only 5-10 % of individuals whom are obese have low leptin levels and therefore in most cases, human obesity does not result from a lack of adequate leptin signals, so this alone cannot explain how individuals become obese.
What explains obesity: Set-point theory (Nisbett, 1972)
Nisbett (1972) put forward a biological theory for what controls eating. He suggested individuals engage in eating behaviour to maintain internal homeostasis (a stable, constant internal state). The system aims for a set-point or target; so if energy levels are below that target we eat, and if set-point is reached we will stop eating. Researchers were unclear about what exactly is the system trying to maintain i.e. glucose or body fat levels (gluco- or lipo-static set-point, or combination of being gluco- and fat-deprived)? An idea put forward by Mayer is the glucostatic theory, that people become hungry when blood sugar levels drop significantly below their set-point. This idea was well received as glucose is the brains primary fuel. Kennedy proposed the other complementary lipostapic theory set point theory. This theory postulates that all people have a set point for body fat and deviations from this set point produce compensatory adjustments in their levels of eating that return their levels of body fat to their set point. Obese individuals may have higher lipostatic set-points than non-obese individuals. This would be equivalent to being stuck with a fixed biologically determined set-point!
Settling-point theory (Hill et al 1994):
Core idea: In most humans, weight loss and gain are related to patterns of diet and physical activity that people “settle” into as habits, based on the interaction of their genetic dispositions, learning, and environmental cues to behaviour. Obese people are more sensitive to food-related stimuli in the social and physical environment, which influence their energy intake. The settling-point moves in an upward direction. Once gained, fat cells remain as receptacles ready to store any excess in energy intake. Fat cells can reduce in size, not in number. Once gained they remain as receptacles ready to store any excess in energy intake. Hence, we gain weight easily, but lose it with difficulty.
Criticism of set point theories
However Herman (2002) argue that if we all have eating systems whose primary function is to maintain a set-point then eating disorders should be rare, however, quite the opposite is happening. Another criticism of set point theories comes from Low (1993) who states we eat even when glucose levels are high and therefore not suffering from an energy deficit.
Evidence from this comes from Rozin et al (1998) RH was a patient with bilateral damage to his medial temporal lobe and suffered amnesia as a result. RH was offered a second meal 15 minutes after eating and accepting. The same process was repeated 15 minutes later. Rozin concluded that RH’s hunger clearly wasn’t the result of an energy deficit and therefore refutes set-point theories of how obesity can occur. This led to the proposal of the positive incentive theory; the idea that rather than being drawn to eat because internal energy requirements/deficits people eat because of the anticipated pleasure of eating.
Positive incentive theory
Factors influencing the anticipated pleasure of eating include the time since a person last ate, whether or not others are eating and learned associations with food and pleasure. This theory is superior to set point theories as it does not single out one factor as the major determinant of hunger. As a species, humans have evolved taste preferences for sweet, salty and fatty tastes in order to gain the nutrients needed for survival. In line with positive incentives theory, Epstein (2007) proposed that perhaps obese individuals have a stronger preference for the taste of high calorie foods. Along with differences in food consumption, differences in energy expenditure may contribute to rising obesity.
Booth and Neufer (2005) hunter-gatherers expenditure
Booth and Neufer (2005) compared modern day activity to the activity engaged by our hunter-gatherers ancestors: They state that besides the calorie intake of the hunter gathers being 3000 kcal per day in comparison to our daily intake today of 2400 kcal per day. The difference lies with the hunter gatherer daily energy expenditure of 1000 kcal in physical activity per day in comparison to the average person’s expenditure of todays of 300 kcal in physical activity per day. This has been suggested to be due to modern technological advances e.g. playing tennis 477kcal per 1hr vs. playing a video games 143kcalp per 1hr. People walk 25miles p/week less than in 1950s, therefore increases obesity rates could be due to the increasingly access to modern day advances.
Thrifty Genotype = Obesity (Neel, 1962)
Core idea: In our early evolutionary history, genes (thrifty genes) that promoted efficient fat deposition were advantageous because they allowed their holders to survive at periods of famine, which were common occuences in hunter gatherer societies. Thus he suggested a thrifty genotype that natural section favoured in order to allow our ancestors to store energy.
Howerer, in modern society, such genes are disadvantageous because they promote fat deposition in preparation for a famine that never comes, and the result is widespread obesity and diabetes.
Free-living men eating ad libitum. Thrifty Genotype + Modern Diet=Rising obesity (Stubbs 1995)
This was demonstated by Stubbs et al whom allocated six men to one of three diets over seven days. these diets were matched on palatbility but had different proportions of fat (20%, 40% and 60%). Their results found that although the same amount of food was consumed, there was a gradual weight loss with 20%, Slight fat accumulation with 40% and a greater fat accumulation with 60% thus the excess fat stored and therefore contributes to obesity.
Thrifty Genotype + Modern Diet= Rising obesity: Biologically we are better adapted for a hunter-gatherer diet (high in fibre and low in fat and sugar) than for a modern diet rich in fat and sugar.
THE NEUROCIRUITARY MODEL OF ENERGY
The idea that the ventralmedial hypothalamus (VMH) is exclusively a satiety centre and the lateral hypothalamus (LH) a hunger centre no longer warrants serious consideration, instead a more complex theory of hunger and satiety has been put forward, the neurocircuitary of energy homeostasis. This theory advocates that hunger and satiety are regulated by a number of peptides released in the gastrointestinal tract. In terms of glucoprivation, ghrelin is released from the stomach and neuro peptide Y (NPY) from the ventrolateral medulla, these travel via the arcuate nucleus to the LH. The peptides released hert, orexin and melanin concentrating hormone (MCH) are the two that ultimately motivate eating behaviour.
In conclusion
THE NEUROCIRUITARY OF MODELOF ENERGY consumption is the main scientific theory that explains short term hunger and satiety suffciently. It acknowledges there is a comlex network involved along with a number of peptides. The discovery of these peptides has major effects on the search for neural mechanisms of hunger and satiety. The number of peptides discovered so far indicate the neuroal system reacts to many different signals, not just glucose and fat. Although the hypothalamous has been largely impliacted in short term hunger and satiety
There are many factors that influnece the rising incidences of obesity in most societies today. The set point theory advocated by Nisbett argues perhaps obese individuals have a higher body fat set point than non obese people. The perfered and more complex posotive insentives theory acknowledges there are a number of factors that have contributed to the increase in obesity such as our modern diet and lack of exercise which increases our chances of becoming overweight and suffering ill health. As a western society, we must educate people on eating and how to control eating behaviour to unsure the number of indiviuals who are obese do not rise expotentially.
