Biological Explanations of Eating behaviourNeural Mechanisms in controlling appetite and satiation

Key words you really need to learn: You have a vocab. list in your books and one sent by email.GhrelinHomeostasisHypothalamus both Lateral Hypothalamus (LH) and Ventromedial Hypothalamus (VMH)InsulinGlucoseSet pointLeptinDuel centre model of feedingAsphagia (under eating)Hyperphagia (over eating)Satiation

Basically this unit is about what affects our appetite, i.e. what makes us hungry and what makes us satiated/full. In short it is about our feeding behaviour. As it is biological, this approach will presume that our appetite is not really affected by culture/family/media/ etc but purely our biology. It is therefore, reductionist and deterministic.

Homeostasis; if this did not occur then we would starve to death or eat to death. Knowing if we are full (our set point) is individual however. Each individual has a set point and their weight is regulated around that set point.

It would be tempting to presume that obese and overweight people have a set point that is nearer to hunger and that slim people have one set nearer to satiety. However, some overweight people eat very little and some underweight people eat loads. There are individual differences in set points therefore. Set points are probably influenced by: genetics, family, culture and society. Moreover, some people may be on certain medications which affect weight gain and loss (see the power point on neural mechanisms I sent you for more details) or simply have different metabolic rates, constitutions, exercise levels etc. They may even suffer from medical conditions that can affect weight gain and loss such as low or high Thyroid. Nevertheless, biological explanations do offer insight into our feeding and appetite behaviour.

A01The stomach’s role in appetiteSee your book here very bottom of page 153 for the 1912 study by Cannon. This is a very primitive study on balloon inflation/deflation and feelings of hunger. Seemed to be supportive of the idea that we stop eating/our appetite is quenched when we feel full.

The Hypothalamus’ role in appetiteThe hypothalamus is a portion of the brain that contains a number of small nuclei with a variety of functions. The hypothalamus is located below the thalamus, just above the brain stem. All vertebrate brains contain a hypothalamus. In humans, it is roughly the size of an almond. The hypothalamus controls body temperature, hunger, thirst, fatigue, and circadian cycles.

A01 studies/research on the Hypothalamus The first study on the role of the Hypothalamus is by Hetherington and Ranson,

1942 (This is on page 154 your books).Their study involved lesioning rat’s Hypothalamuses. Lesion is cutting away areas of the brain. In this case, it was either the lateral hypothalamus (LH) or the Venromedial Hypothalamus (VMH). If you forget the part of the hypothalamus you can say when parts of the Hypothalamus are removed. The results from this study show that the Hypothalamus has an ‘on’ and ‘off’ command for eating. The LH functions as the hunger centre. If this area is lesioned in rats, they starve themselves. If however, the VMH is lesioned then they over eat until death. It is suggested that if these areas are dysfunctional they can lead to eating disorders such as Obesity and Anorexia.

Damage to this area has long been known to promote excessive eating (hyperphagia) and weight gain, termed "hypothalamic obesity." This form of

weight gain is not responsive to diet and exercise. Victims of this form of obesity continue to gain weight despite their best efforts, and suffer greatly from this unrelenting scourge.

Tumours in the VMH have lead to excessive binge eating in humans. Hypothalamic obesity is an unfortunate complication in some survivors of brain tumors, especially those diagnosed in childhood. Robert H. Lustig, 2003 ‘The Journal of Clinical Endocrinology & Metabolism’

De Araujo et al, 2006. Implanting electrodes into the brains (hypothalamus) of rats so they can record electrical activity of the feeding cycle. So when a rat is hungry do certain regions of the brain activate and vice versa for when is rat is full up. Yes, they do.

Electrical stimulation of the hypothalamus. When electrodes are implanted into the brain and used to stimulate neurons artificially. Then activity is recorded. Findings are the same as above, e.g. VMH inhibits feeding and the LH stimulation encourages it.

Prader-Willi syndrome is frequently associated with an extreme and insatiable appetite, often resulting in morbid obesity. There is currently no consensus as to the cause for this particular symptom, although genetic abnormalities in chromosome 15 disrupt the normal functioning of the hypothalamus. Given that the hypothalamus regulates many basic processes, including appetite, there may

well be a link. However, no organic defect of the hypothalamus has been discovered on post mortem investigation.

Theory of hormones affecting appetiteThe Glucostatic hypothesisIn short, Insulin controls blood Glucose levels by allowing Glucose in the blood stream to enter the cells of the body. Usually, food intake makes blood Glucose higher and reduces appetite. Insulin converts the blood Glucose into Glycogen. Glycogen is an energy reserve which is stored in the liver and muscles. Low levels of blood sugar should increase appetite.

Insulin and Glucose A01 studies/research In studies where animal’s Insulin levels are low they eat less then usual. When

you give these animals moderate injections of Insulin, their appetite is increased. Rosenzweig et al did the insulin study on a variety of animals in 2002.

It is also known that blood Glucose levels affect hunger. When Glucose levels in rats or Humans are lowered, appetite increases. When Glucose levels are raised, appetite fades.

The Role of LeptinLeptin (A hormone released from fatty Adipose cells/tissue. It acts as an indicator of body weight, controlling long term food intake). Adipose cells: The fat storage cells of the body. After digestion Insulin enables fat in the bloodstream to be stored in Adipose cells. Therefore the idea is, if a lot of Leptin is released from Adipose Cells, the people will have small appetites. If little or no Leptin is released then the theory is that their appetite will be insatiable.

Before and after |Leptin Supplements

The Leptin Link A01 studies/research

Licinio, 2004, researched three adults from a Turkish family who had a genetic deficiency in Leptin; they didn’t produce Leptin at all. Consequently, they were obese with huge appetites. After they were given Leptin supplements their weight and eating behaviour became normal.

London, 2007, based further research on the three members of the Turkish family. He wanted to investigate their neural network for Leptin actions. He found that Leptin does change eating behaviour. London did a FMRI of the three Turkish family members before Leptin treatment and after Leptin treatment. During each FMRI the participants were shown a picture of food. The results of this study showed that before the Leptin treatment, there was a lot of neural activity in the Temporal and Parietal Lobes and that after treatment, the activity changed and became more active in the pre-frontal cortex. This means that the Temporal and Parietal Lobes are probably involved in initiating hunger and eating behaviour and the pre frontal cortex is more involved in feeling satisfied.

Matochik, 2005 also showed that people with Leptin deficiencies have sustained structural changes in their cortex’s (brains) with Leptin supplements

Carlson, 2007, Obese mice (Ob mice) that genetically do not produce Leptin have also backed up the Leptin link as they overeat continuously. Moreover, if injected with Leptin they stop over eating and lose weight.

The role of Ghrelin Ghrelin is a hormone secreted by the stomach when it is empty. The amount is directly proportional to how empty the stomach is. See page 155, 2nd bullet point for more details. Basically, as the time from our last meal increases, we feel hungrier because there is Ghrelin secretion.

Ghrelin A01 studies/research

Cummings, 2006 found injecting animals and humans with Ghrelin increased their appetite. Cummings et al (2004) also studied humans and monitored participant’s (PPs’) Ghrelin levels every 5 minutes PPs had to assess their level of hunger every 30 mins. In 5 of the 6 participants there was a significant correlation between Ghrelin levels, emptiness of the stomach and hunger. The results support the theory of the role of Ghrelin in eating behaviour. See page 155 for more details of the study. This is a good study to A02 as it has sampling issues.

Gastric bands can be fitted on obese people as a way of controlling weight. It has been found that they reduce Ghrelin secretion.

Prader-Willi syndrome patients have high Ghrelin levels, which are thought to directly contribute to the increased appetite, hyperphagia (over eating), and obesity seen in this syndrome.

Table summing up The A01Insulin High (so Blood Glucose low) OvereatBlood Glucose Low (So Insulin High) Overeat

Blood Glucose High (So Insulin Low)Under eat

Insulin Low (So Blood Glucose High)Under eat

Leptin High Under eat

Leptin Low OvereatGhrelin High (when stomach empty) Overeat

Ghrelin Low (When stomach full)Under eat

VMH stops eating behaviour (if damaged or lesioned causes overeating) Overeat

LH initiates eating behaviour (If damaged or lesioned causes starving)Under eat

Rounding it all up/ConclusionsDual Centre Model of feeding

Now you understand the role of the: LH, VMH, Glucose, Insulin, Leptin and Ghrelin I can now tell you about the Dual Centre Model of feeding. I could by the way, tell you so much more about this topic, there are many things we have not even discussed but if you know the Dual Centre model and two other theories well that should be enough.

Dual Centre Model of Feeding (DCMF)

Explanation of DCMFWhen blood glucose levels fall this is sensed by the hypothalamus and the LH is activated and Ghrelin is secreted by the stomach and we feel hungry and eat. As food intake is likely to increase blood glucose, this in turn is sensed by the VMH which then activates us into feeling full and not eating any more, Ghrelin secretion is decreased.

A02 Research and theory applicable to all the above theories

1) Cannot extrapolate/generalise animal findings to humans:Firstly, many animals, such as rats, have different eating behaviour and eating patterns to humans. Some dogs for instance have evolved to gorge themselves because food may have been scarce. Also, it is unclear whether the influences are completely the same for humans though as our eating is not just geared (like many mammals) as an automatic stimulus –response drive. In humans, Cognition/mood/culture may also play a part in our eating habits. Food and over/under eating also has a social significance to us, in how we look, how we are perceived as greedy etc.

2) ReductionismWe can see that biological theories see appetite as being caused by only one factor then. They exclude other approaches yet there are individual differences in set points. Set

points are probably influenced by a whole range of factors: genetics, family, culture and society. Therefore we can say biological reductionism is not a good way to understand set points and appetite, i.e. appetite cannot just be boiled down to a biological concept; it probably can be better understood within a few approaches. Moreover, there is substantial and convincing evidence that social, cultural and psychological factors affect our eating behaviours as is evident from psychological explanations of eating disorders

3) Ecological ValidityHighly controlled lab experiments may lack ecological validity4) Against Animal ethics. All the above are invasive brain techniques. Is it unnecessarily cruel to lesion animals, they probably die or starve overeat to death. Plus there are caging and anaesthesia issues.5) For animal ethicsAre there any psychological/medical advances, especially in understanding the causes of obesity (Heart attacks, diabetes, strokes, and shorter life spans by 9 years) is a very current problem (There are currently 1.6 billion overweight adults in the world, according to the World Health Organization- WHO). That number is projected to grow by 40% over the next 10 years).Anorexia and Bulimia Nervosa are also areas where the end may justify the means. 7) This theory (biological) is deterministic because is says you have no free will over your appetite set point. Set point is determined by biology. This can not be absolutely true as people do have some success at dieting. Surely dieting is an indication of free will, (though it has to be said that most people fail at dieting)? Can physiological drives can be overridden (e.g. desire to loose weight; dislike of certain foods; fear of losing control; social cues to continue eating; food availability)?8) Provides explanation of some differences in eating behaviour9) Such studies provide sound scientific evidence but there is the issue of extrapolating finding from rats to humans10) There is substantial and convincing evidence that social, cultural and psychological factors affect our eating behaviours as is evident from psychological explanations of eating disorders11) Physiological drives can be overridden (e.g. desire to loose weight; dislike of certain foods; fear of losing control; social cues to continue eating; food availability12) Approaches. Compare and contrast biological (NURTURE) explanations to Cognitive, biological, Learning and sociological approaches.

A02 Stomach only1) Less credible when stomach cancer suffers were still able to gauge/regulate their appetite despite having lost parts of their stomach through surgery. So it can’t be all about your tummy being full or empty then! 2) Plus a rubbish study anyway, not scientific at all! There was one participant etc.

A02 Hypothalamus only1) Linking site of damage to behaviourLesions are when areas of the brain are cut away. In the past little was known about the brain so researchers tended to chop away lots, not realising the affect they were having (think Lobotomy). Even a small lesion destroys not just neurons at that site but possibly

pathways travelling through. Even the destroyed neurons have connections to many other neurons and these in turn will be affected by the damage. Neurons in other areas (whose axons or dendrites run through the lesioned area may have their functions altered. A good example of this is when you recognise someone. When I see Leonardo De-Caprio, My occipital lobe is activated (sight); this visual information then travels to my temporal lobe where face recognition takes place. Finally if I am to become consciously aware of this it needs to travel to my frontal lobe (probably the left side where speech is). If somebody were to lesion my brain somewhere in the middle of this pathway I may not be able to recognise Leonardo anymore! How sad would that be for Rianne who suggested him?

One Neuron

Millions of neurons

2) Supporting Evidence Studies such as those involving lesions to the LH and VMH in rats have supported the role of the hypothalamus in regulating eating behaviour although, Gold (1973) found that lesions restricted to the VMH alone did NOT result in hyperphagia and only produced overeating when they included other areas such as the parvoventricular nucleus! However, subsequent research has failed to replicate Gold’s findings...

3) Supporting Evidence Studies involving electrical stimulation of these centres have confirmed their role in feeding and satiety.

A02 Glucose and Insulin only8) Most diabetics have long term high blood Glucose levels yet normal appetites.

See page 156, 4th bullet point for more details.9) Blood Glucose levels do not vary much in most people.

A02 Leptin only

1) The Leptin link has not been shown in all overweight people though. Most overweight people have normal or high levels of Leptin so other mechanisms must be involved, unless many overweight people are Leptin insensitive. See your book, bottom of page 156 and first two paragraphs of page 157 for more details.2) Low calories diets often lead to low Leptin levels; this in turn produces hunger and might one of the reasons why diets fail.

A02 Ghrelin only1)The study used a small sample limiting how far the findings can be generalised and it is likely that the participant’s subjective judgements of hunger were influenced by expectations of food based on meal times (cultural factors rather than biological factors)2) Ghrelin injections result in increased food intake in animals 3) Gastric bands used in treating obesity reduce Ghrelin secretion.

Outline and evaluate the role of neural mechanisms involved in controlling eating and satiation (25 marks) orDiscuss the role of neural Mechanisms involved in controlling eating and satiation (25 marks)

Remember you have ½ an hour only

• AO1: = 9 marks• AO2: =12 marks• AO3: = 4 marks

– Lack of ecological validity (2) – Lack of generalisability (2) – Sampling issues (e.g. Cummings et al, 2004) (2)

Bibliography:AQA Psychology A by James Bailey Et al (your textbook)A2 level psychology by Michael W. EysenckPower point I sent you on neural mechanisms.

Further reading: All other A2 textbooks for AQA A psychology

– Lastly, it should be noted that I have only covered a fraction of the theories on the biological mechanisms of eating behaviour. If you cover the ones listed above that will be enough to gain an ‘A’ grade answer.

–– If however, you would like to look at other theories, the role of

Cholecystokinin (CCK) which is a hormone released when food is detected in the duodenum, it is covered in your textbooks. And I have outlined the role of how drugs can increase or decrease appetite in the power point I sent you.

–– There are still other factors you may wish to look at: the Limbic system,

the role of neurotransmitters, see below:

• 3 main neurotransmitters are found to influence appetite:Neurotransmitters and modulators that decrease food intake

– Catecholamines (dopamine, norepinephrine, and epinephrine): sympathomimetic "fight-or-flight" hormones that are released by the adrenal glands in response to stress

– Serotonin: found extensively in the gastrointestinal tract, it activates the muscles used for feeding. Is also associated to aggression and “happiness”

– Peptides: short polymers formed from the linking, in a defined order, of α-amino acids

Neurotransmitters that increase food intake• Norepinephrine (NE) – injections of NE in hypothalamus

– can stimulate feeding if injected into the paraventricular nucleus – Can reduce feeding if injected into the perfornical area

• Neuropeptide Y (33 amino acid peptide) – high concentrations in the paraventricular hypothalamus and perfornical hypothalamus.

– Rats injected with neuropeptide Y continue eating large amounts of food even when full

– It also seems to cause a preference for carbohydrates• Galanin (29 amino acid peptide) - particularly found in the paraventricular

hypothalamus.– Injections of galanin into rats cause an increase of food intake and a

preference for fats rather than carbohydrates