PSYA3EATING BEHAVIOUR 5

OBESITY

                                                                                                                                    

DEFINITION OF OBESITY

• Obesity is defined by body mass index (BMI)

• BMI = Weight in Kg• (Height)² in metres

18.5 – 25 = normal 25 – 30 = overweight 30 + = obese

PROBLEMS WITH BM INDEX

• There is no account taken of fat to muscle ratio, so body builders can be classed as overweight

• Waist size and thickness of fatty tissue using callipers are other ways of measuring obesity

ENERGY EXPENDITURE• Taking in more calories Obesity than you burn1. Basal metabolic rate: All cells in the body are

active, so are burning calories even when we are resting. This is our BMR and accounts for 60% of energy expenditure (EE)

2. Dietary thermogenesis: energy spent in digesting food. Accounts for 10%

3. Physical activity: accounts for 30% of EE

Hunger and Satiety

These are influenced by a number of factors, including:• Sensory

• Food taste, texture, smell, sight, temperature (eat less when warm)

• Cognitive• Beliefs about properties of food (need for comfort, ‘good for

you’)• Post-ingestive

• Distension of the stomach tells brain you are full. • rate of gastric (stomach) emptying – if fast to empty, feel less full.

• Post-absorptive • Metabolic processes e.g. action of glucose amino acids

• Individuals have an innate preference for ‘sweet’ foods:

1) e.g. fetuses will increase swallowing in the womb in response to sweet tastes

2) e.g. newborns will turn toward sweet smells and tastes and away from bitter ones.

• Taste preferences can be alterede.g. Sullivan and Birch (1990) They took 39 children aged 4-5. 1 group was exposed to

salty food only, 1 group to sweet only and the other to ‘plain’ tofu. At the end of the experiment, the children now showed a preference for the ‘taste’ they had been exposed to.

CULTURAL VARIATIONS AND OBESITY

• There is more obesity in children of low income families

• Afro-caribbean groups also have high levels of obesity. This may be genetic or may be lifestyle difference

EVOLUTIONARY EXPLANATIONS OF OBESITY

• Wells made the following suggestions:1. For our ancestors, more fat on the body meant a

better chance of survival during shortages2. So they could survive seasonal changes3. The progress from hunter gatherer society to

agriculture left early humans vulnerable to famine (crop failure), so large fat reserves would increase survival

EVOLUTIONARY EXPLANATIONS OF OBESITY

4. The higher proportion of fat in females is essential for the reproductive system, as it provides energy for the foetus to grow. (Menstruation stops when body weight decreases)

5. The developing brain uses large amounts of energy, and the main food source would be a mother’s milk

EVOLUTIONARY EXPLANATIONS OF OBESITY

6. Our feeding behaviour evolved when the food supply was unpredictable. Finding and eating food involves taste and smell which are complex. Systems for stopping and starting eating are not as sensitive and it is easy to overeat

EVOLUTIONARY EXPLANATIONS OF OBESITY

• We live in times of plenty, but our evolutionary tendency is to store more food than we need

EVALUATION OF WELL’S EVOLUTIONARY THEORY

1. The theory is speculative2. Cultural groups used to harsh conditions,

e.g. Pima Indians of Mexico, develop high obesity when exposed to the Western diet

3. It does not satisfactorily explain the sudden rise of obesity in the last 20 years

GENETICS AND OBESITY

• Parents’ and children’s BMI’s show a strong positive correlation. This infers that it is inherited, but parents also provide (environmental)feeding habits

• TWIN STUDIES: show a higher concordance rate for BMI and BMR than DZ twins

LEPTIN AND THE OB MOUSE

• The discovery that leptin levels affect obesity points to a biological explanation.

• Leptin is a satiety hormone released from fat cells and it travels to the hypothalamus to inhibit feeding

• A person with leptin deficiency, like the ob mouse, becomes obese

LEPTIN LEVELS IN THE OBESE

• Obese people have higher than normal leptin, so possibly the feeding system has become insensitive to the satiey effect of leptin

• This may be genetic

Child with leptin deficiencies response to being given leptin.

Child will now experience satiety and reduce food intake.

Leptin deficiency/insensitivity is very rare

FTO ‘obesity’ gene• Mice that have extra copies of the FTO gene ate more and were

more obese than those without.• Point mutations (one ‘letter’ change) in the gene are also linked

to obesity• Humans who carry two copies of the ‘at risk’ form of one of

the variations, on average weigh 3kg more than people who carry two copies of the ‘low risk’ variation

• It is suggested that this form of the gene is more active, which may cause the weight gain

• Individuals are more ‘at risk’ but will not necessarily become obese – it is linked to environmental factors also.

Other genetics

• Bardet-Biedl syndrome - a genetic disorder that affects many body systems and classically causes obesity (as well as mental retardation, blindness etc)

• Prader-Willi syndrome – a genetic disorder caused by mutations in 7 genes of chromosome 15. characterised by extreme and insatiable appetite causing morbid obesity.