BIOLOGICAL EXPLANATIONS OF EATING BEHAVIOUR
To read up on biological explanations of eating behaviour, refer to pages 199–208 of Eysenck’s A2 Level Psychology.
Ask yourself
· How is eating behaviour related to hunger?
· How is eating behaviour not related to hunger? Do we eat when we’re not hungry?
· How might the lifestyle of our evolutionary ancestors have shaped the way we eat?
What you need to know
NEURAL MECHANISMS INVOLVED IN CONTROLLING EATING AND SATIATION / EVOLUTIONARY EXPLANATIONS OF FOOD PREFERENCE· Hunger, satiety, and the brain
· The role of hormones / · Research evidence for and against evolutionary explanations
NEURAL MECHANISMS INVOLVED IN CONTROLLING EATING AND SATIATION
Hunger, Satiety, and the Brain
There are key centres in the brain that control hunger: these are the neural mechanisms involved in the drive to eat (hunger) and the feeling of fullness that switches off the hunger drive (satiety).
RESEARCH EVIDENCE FOR NEURAL MECHANISMS
· Research by de Araujo et al. (2006, see A2 Level Psychology pages 199–200) focuses on the lateral hypothalamus, orbitofrontal cortex, insular cortex, and amygdala. de Araujo et al. planted electrodes in these areas in rat brains so that they could monitor the excitation during periods of feeding and satiety. They found that they could identify individual neurons that were activated during different phases of the feeding cycle (see the diagram at the top of page 200 of A2 Level Psychology).
· Two significant eating control centres are in the hypothalamus. One is in the lateral hypothalamus (or LH), also know as the “start” switch, the other is in the ventro-medial hypothalamus (or VMH), also known as the “stop” switch. The parietal and temporal cortex are also involved with hunger and the prefrontal cortex is involved with satiety.
· Research from the 1940s onwards showed that lesioning (i.e. destroying) tiny areas in the LH in rats, dogs, and other mammals led to a loss of interest in food and eating, the animals seemingly unaware that they were starving themselves. Whereas the opposite happened with lesions to the VMH as this led to the animals concerned eating voraciously, so they became obese. This suggested that the LH initiates eating behaviour (hence the “start” switch) and the VMH stops this behaviour (hence the “stop” switch).
· Another neural mechanism is interconnected with the stomach. The stomach sends nerve impulses to the brain, stretch receptors in the stomach walls send signals via the vagus nerve to the hypothalamus, and these stimulate feelings of satiety. However, there is a time delay between the arrival of the food into the stomach and these messages being sent, and so this is why we are advised to eat slowly, because eating too quickly could mean going past the satiety point without the brain realising it; whereas slower eating allows the gut time to communicate with the brain.
The Role of Hormones
Hormones such as insulin and leptin are also involved in eating behaviour. Leptin acts upon various hypothalamic areas and seems to inhibit the release of another neurochemical, neuropeptide Y, which is the neurotransmitter stimulating hunger and eating behaviour. Thus, low levels of leptin will increase hunger and eating behaviour. Blood glucose imbalances as a result of insulin insensitivity are also linked to either increased or decreased eating behaviour.
RESEARCH EVIDENCE FOR THE ROLE OF HORMONES
· Blood glucose levels affect hunger. When glucose levels were lowered in rats or in humans, appetite increased; when they were raised, appetite faded away (Smith & Campfield, 1993; Lavin et al., 1996, see A2 Level Psychology page 201).
· Animal studies showed that when blood insulin levels were low the animals ate much more than usual, whereas injections of moderate levels of insulin seemed to reduce appetite, probably by reducing hunger (Rosenzweig, Breedlove, & Leiman, 2002, see A2 Level Psychology page 201).
· Licinio et al. (2004, see A2 Level Psychology page 201) researched three adults from the same Turkish family to demonstrate that when they were given leptin supplements body weight and eating behaviour became normal.
· London (2007, see A2 Level Psychology page 201) showed some sustained structural changes in the cortex with the same leptin supplements of those three adults. London continued to research these three family members who had no leptin production of their own. Thus, investigation of the neural circuits for leptin action using fMRI imaging was possible. Neural activity was measured in the absence of leptin and then in the presence of leptin to identify the brain areas leptin acted upon. The results were reduced activity in the insular, parietal, and temporal cortices, and increased brain activity in the prefrontal cortex after the leptin treatment. This fits in with the insular, parietal, and temporal cortex areas being concerned with hunger but the prefrontal areas being concerned with satiety, and so leptin decreases eating behaviour (see diagram in A2 Level Psychology page 202).
· Ravussin et al.’s (1997, see A2 Level Psychology page 202) longitudinal study investigated the Pima Indians, a population prone to obesity. Two weight-matched groups (i.e. participants matched based on their weight) 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 gain weight. This confirms leptin’s influence on appetite and weight gain.
RESEARCH EVIDENCE AGAINST BIOLOGICAL EXPLANATIONS
· Lesions have a wider effect. In criticism of the conclusions from brain-lesioning studies, Logue (2004, see A2 Level Psychology page 200) and others have pointed out that lesions could affect far more neurons and neural activity than that of the cell bodies in the destroyed area because nerve fibres may be damaged in nearby areas.
· The delayed signaling between stomach and brain is challenged by Johnstone et al.’s (2006, see A2 Level Psychology page 202) study on the drive to eat. They used rats on a strict and regular diet where food was presented for 2 hours a day. Brain activity was analysed when fasting, when anticipating feeding, and when actually feeding. The results showed that appetite-stimulating neurons start firing off before feeding starts in anticipation of the food. Also appetite-suppressing neurons started to activate as soon as food was being eaten. Thus, this seems to contradict the research on the time delay between food entering the stomach and the brain receiving this information. However, extrapolation is clearly an issue (see below).
EVALUATION OF NEURAL MECHANISMS AND THE ROLE OF HORMONES
· The role of cognition is ignored. The neurons with cell bodies in the LH or VMH could be affected by sensory input relayed from other areas, in particular the frontal cortex. This is supported by the fact that we all have food preferences, and so cognition also plays a part in eating and stopping eating; these behaviours are not just automatic stimulus–response drives. Thus, hunger, eating, and satiety are not just a result of biological processes, and the LH and VMH control system is far from a set of simple on–off switches.
· Extrapolation. The influence of cognition is true of animals as well as humans, but more so in humans due to the greater role of cognition in human behaviour, and so this leads to the issue of extrapolation from animal research as findings on animals may lack generalisability to humans. It cannot be assumed that what is true of animals is the same for the far more complex human brain.
· Individual differences. There are wide individual differences showing that the biological mechanisms do not work in a uniform way. Horvath (2005, see A2 Level Psychology page 201) suggests that each person has their individual set point (a balance between hunger and satiety) as a result of genetic factors and early nutritional experience. Thus, if the set point is nearer to hunger, then that person might have a tendency to eat more and be overweight, whereas if the balance point is nearer satiety then that person will eat less and will be unlikely to be overweight. This may well be true but it doesn’t account for people who can eat large amounts and not put on weight, nor whether this set point can change, for example with the season (we tend to eat more during the winter) or mood (comfort eating). Also the Prisoners of War released from the German concentration camps were all severely underweight and so everyone can lose weight, it is not a physiological impossibility.
· Cause and effect and direction of effect. The roles of neural mechanisms and hormones in eating behaviour are unclear because it is not clear whether it is their dysfunction that causes abnormal eating behaviour or whether the eating behaviour causes the neural mechanism dysfunction or hormonal imbalance. Furthermore, because the real-life cases of brain damage provide only correlational evidence we cannot establish cause and effect (i.e. that neural damage causes abnormal eating behaviour), conclusions are limited to association.
· Mundane realism. Clearly the lesioning of the VMH and LH shows damage to these areas can cause dysfunctional eating behaviour but this does not mean this is the direction of effect in real life. Thus, the findings may lack generalisability to real life and so have limited external validity.
· Sample bias. The sample sizes of the research, e.g. the three family members in the leptin research, mean the research is unrepresentative of the general population. We cannot generalise from such research and so it lacks population validity as we cannot be sure how true the findings are for other populations.
· Increased understanding and positive applications. Research is beginning to show how the hormones interact with the brain centres, and this increased understanding offers the possibility of positive applications in terms of treatment for obesity. The leptin supplements used by Licinio et al. (2004, see A2 Level Psychology page 201) are one example of how this has already begun. However, if this was joined up with the action of PYY (peptide tyrosine tyrosine) then perhaps even more effective treatments can be developed.
EVOLUTIONARY EXPLANATIONS OF FOOD PREFERENCE
Evolutionary explanations focus on what factors could have been adaptive, i.e. what could have been advantageous and so helped our evolutionary ancestors survive and reproduce in the EEA (evolutionary environment of adaptation). Food preferences may have been adaptive, for example, being omnivorous (eat plants and animals) would be more adaptive than being either herbivorous (plant eating) or carnivorous (meat eating) as eating both animals and plants affords a greater food range and this would increase chances of survival and consequently reproduction. In harsh conditions there would be a fine line between the energy expended in hunting for and gathering food, and the energy and nutrients gained from the food. Foods rich in energy and nutrients would be more likely to have a positive energy balance, i.e. the energy from the food outweighs that used to find it. This may explain the universal human preference for foods rich in protein, fat, oils, and sugar, and this suggests that these preferences are genetic, innate, and hard-wired into us.
RESEARCH EVIDENCE FOR EVOLUTIONARY EXPLANATIONS OF FOOD PREFERENCE
· Fats and oils contain twice as many calories as carbohydrates or proteins. This would suggest that a preference and searching for fatty foods would have been adaptive for our ancestors.
· Protein-rich foods would also have been necessary for health as these are needed to repair and build body tissue, especially in pregnant or lactating (breast-feeding) women.
· Eaton and Konner (1985, see A2 Level Psychology page 204) suggest humans have a genetically controlled preference for fatty, meaty foods and this is evident in the “paleolithic diet” of meat, fish, and fatty/oily foods plus fruits and vegetables, which has been put forward as the only healthy way for humans to eat. Fatty foods have fat-soluble vitamins such as vitamin D and so they are sources of more than just calories. Eaton and Konner suggest carbohydrates give empty calories because they do not contain many other vitamins and link the high-carbohydrate content of the modern diet to serious health issues such as hypertension, coronary heart disease, and obesity.
· Evidence for the types of food eaten by our evolutionary ancestors takes a number of forms: cave drawings and paintings show people out hunting and gathering food; tooth-wear patterns from skulls can be analysed to give insight into the types of food eaten; there is also evidence from buried refuse heaps as radioactive isotope analysis can reveal how long ago the food refuse, such as bone and shell fragments and seed cases, was thrown away.
· The early hominids, or australopithecines, ate wild plant food and occasionally scavenged animal carcasses for meat and bone marrow, etc.
· About 2.4 million years ago the first of our Homo group emerged: Homo habilis, who ate a wide variety of animals including deer, birds, rabbits, fish, and shellfish, as well as wild plants (O’Neill, 2008).
· As Homo sapiens emerged, Africa’s climate was changing and the environment was drying out. This meant searching for food would be harder and take more time and energy. It is estimated that the modern hunter-gatherers travelled up to 8 miles per day for food and that they obtained an average of 40–60% of their dietary energy from animal foods such as meat and milk. The latest techniques for analysing carbon and nitrogen isotopes in hominid bones show that these ancestral types were already obtaining almost all of their dietary protein from animals.
· The australopithecines’ (our earliest evolutionary ancestor) brains averaged 400 cm3, whereas our brains are on average 1,350 cm3. The larger brain is a very energy-expensive structure, though it forms only 2% of our body mass it consumes 20–25% of our energy and nutrient resources. Hence, the evolution of brain size may have driven our preference for energy-dense foods.
RESEARCH EVIDENCE AGAINST EVOLUTIONARY EXPLANATIONS OF FOOD PREFERENCE
· In contradiction to the view that humans need a very specific diet for optimal health is the view that humans have evolved to be flexible eaters (Leonard, 2002, see A2 Level Psychology page 204).