Blog Assignment 4 (30/09/2012) ‘Outline and evaluate evolutionary explanations of food preference.’

1. The Environment of Evolutionary Adaptation- it is the environment to which a species is adapted. Animals that lived in different environments or made their livings in different ways faced different reproductive problems, and that’s why all animals aren’t the same.
2. The EEA is involved with our eating behaviours in the way that we have had to adapt from hunter gatherer times. For example, cooking. The hunter gatherers didn’t cook as they didn’t know to; they didn’t know to make fires to cook food so their bodies were prepared to eat raw ingredients, even meat. They would know the good foods from the bad foods purely through trial and error, as there was no way of knowing of foods that could kill. However, modern day we cook our foods. This is because our bodies have adapted to not be able to handle raw meats, and it could kill us so we cook to survive. Now it is completely normal and expected to cook foods, and would be out of the ordinary if we didn’t.
3. Humans have a preference for sweet foods because in the hunter gatherer times, they knew foods such as berries and fruits were ripe, and more importantly, safe to eat if they were sweet. Also, because it is the sweet foods where energy is gained from- carbohydrates. However, nowadays our sweet tooth doesn’t make us crave fruits or berries, but sweets and cakes etc.
4. We eat meat because this is where we gain a lot of protein and calories, and hunter gatherers would have used this energy from calories to hunt. Also, it would have been a lot quicker to hunt an animal, than to forage for hours looking for safe fruits. Humans developed intelligence, which is how they learned to hunt; they would make tools and work as a group, which then lead to social skills, and therefore language. Hunter gatherers would eat the meat for the protein as this contributed to the growth of the brain in humans. The men who hunted the most meat were deemed the most attractive to women as they were intelligent, and would be able to provide for a family.
5. A study to support these ideas is………………………..
6. A study to challenge these ideas is………………………..
7. Deterministic the philosophical principle that every state of affairs, including every human event, act, and decision is the inevitable consequence of antecedent states of affairs. (http://www.thefreedictionary.com/deterministic) This then means that our eating behaviours are pre-disposed, and free will has nothing to do with it. Reductionist is an attempt or tendency to explain a complex set of facts, entities, phenomena, or structures by another, simpler set (http://www.thefreedictionary.com/reductionist)
8. Evolutionary theories can be thought of as deterministic in the sense that eating behaviours have been inherited from our ancestors. They learned to cook food, so now humans don’t even think about cooking foods, the just do it. Some foods they have no choice but to cook because if not they will not survive. So in this sense, eating behaviours are deterministic due to evolution.
9. Evolutionary theories can be thought of as reductionist in the sense that………
10. Non-falsifiable means that a theory can not be proved wrong. It is impossible to disprove it, so therefore it is ‘non-falsifiable’.
11. Evolution is non-falsifiable because there is no way anybody can get evidence to prove its wrong. There are theories that may argue against it, but it is impossible to collect evidence which would prove it 100% wrong.

Neural mechanisms involved in controlling eating behaviour.

The ‘dual control mechanism’ as part of the glucostatic theory.

Eating behaviour is regulated by:

–fat stores (lipostatic hypothesis) and

–glucose levels (glucostatic hypothesis)

The ‘Dual-Centre Theory’ is made up of 2 parts: the ventromedial hypothalamus (VMH) and the lateral hypothalamus (LH). The VMH is like the ‘satiety centre‘ which means this is where fullness is detected and therefore tells the body to stop eating. When the glucose levels are increased, i.e. after eating, then the VMH is activated, achieving satiation (the feeling of being full.) When the eating has been stopped for too long, and the blood glucose levels have dropped, the LH (the ‘hunger centre‘) detects this change and is activated. This makes the body feel hungry, and ghrelin is produced. This is a hormone, and is the familiar rumbling sound stomachs make when an individual is hungry, and is basically the body wanting glucose levels to be increased, and this is achieved by eating.

Every individual has a set point, and their weight is regulated by the set point which is determined by the hypothalamus. The body will maintain this weight as it is practiacally ‘programmed’ into the body.

Karl Lashley was one of the first psychologists to suggest eating behaviour is linked to the brain and isn’t just a reflex.

He used rats to support his growing belief that neural mechanisms are involved in decision making. He cut out different areas of the brain to see the effect on their ability to negotiate a maze successfully and reach the food placed at the exit as a reward. Rats who VMH has been lesioned developed overeating and obesity.

He discovered how vital the role of the hypothalamus is in playing a part in the regulating of food intake. In particular, the LH was identified as the main hunger centre and the VMH as the main satiety centre.

Evidence for the Dual Process 

Research from the 1940’s onwards has been done on animals. It has shown that lesioning areas of the LH in rats, dogs and other animals led to a loss of interest in food and eating, and the animals seemed to be unaware of the fact they were denying their bodies food, therefore starving themselves.

However, Gold (1973) found that lesions restricted to the VMH alone did not result in hyperphagia (overeating) and only produced overeating when they included other areas such as the parvoventricular nucleus.

Evaluation

– These studies are dated, and therefore may not be relevant or contain useful up to date information.

– We can’t generalise for rats to humans. Having different brain structure may mean different things would happen to rats and other mammals than would to human beings.

+ They contain good empirical evidence, therefore isn’t based on just theory.

+ They are still influential and still relate to and support other studies.

The role of leptin (lipostatic theory) in eating behaviour.

Leptin is a hormone, and acts upon various hypothalamic areas and seems to inhibit the release of another neurochemical called neuropeptide Y (NPY) This is the neurotransmitter stimulating hunger and eating behaviour.

Leptin is secreted -> hypothalamus is signalled: calories are high enough -> body ceases to release fat cells -> hypothalamus detects this drop therefore equalling the feeling of hunger.

Ravussin et al (1997) conducted a longitudinal study and investigated the Pima Indians, a population prone to obesity.

Two weight-matched groups were studied over 3 years and it was found that mean plasma leptin concentrations were lower in the group that gained weight than in the group that did not