(3) Neural and Hormonal Mechanisms

Homostasis: Involves mechanisms that detect whether the body had enough nutrients, within that it detects hunger levels using 2 separate systems. One turns eating 'on' and the other turns it 'off'. Glucose decreses = hunger increases as the blood activates the lateral hypothalumus. The person then eats = rise in glucose and the ventromedal hypothalamus is activated.

The Lateral Hypothalamus (LH): Research: Damage to the LH in rats caused a condition called aphagia (stops eating) and that the stimulation of the LH elicits feeding behaviour. Suggesting that the LH is the hunger switch. When neuropeptide Y (a neurotransmitter found in the hypothalumus) is injected into the LH of rats it causes them to being eating even when full. Repeated injection caused obesity in a few days, suggesting it also plays a part in turning on eating.

The Ventromedial Hypothalamus (VMH): Research discovered that damage to the VMH caused rats to overeat which led to hyperphagia (overeating) and that stimulation of the VMH inhibits feeding. Concluded that the VMH signals stop eating as a result of the glucose receptors in the area. However, damage to the erve fibres passing through the VMH damages another area of the hypothalamu, the paraventricular nucleus - which is now believed to cause hyperphagia as it detects foods our body needs.

Ghrelin: Increases appetite when hungry. It is released in the stomach and stimulates the hypothalamus to increase appetite. Role was first discovered when ghrelin was injected into the bloodstream of rats it stimulated food intake.

Leptin: Decreases appetite when body has enough energy. Researchers found that leptin would cause mice to lose weight. Produced by fat tissue and secreted into the bloodstream where it travels to the brain and decreases appetite. Circulating leptin levels act a a long-term signal of the amount of fat stored in adipose tissue - short-term fluctuations in leptin levels provide information regarding changed in calorific intake. 

Limitations of a homeostatic explanation: For a hunger mechanism to be adaptive it needs to be able to anticipate and prevent energy deficits - this means the theory that hunger and eating are only triggered when energy resources fall below their desired level doesn't fit with the reality the some systems would have evolved. For it to be adaptive it must promote levels of consumption that maintain bodily resources about the optimal level to save for if food becomes limited in the future.

Problems with the role of the lateral hypothalamus: Damage to the LH caused deficits in other aspects of behaviour (thrist, sex) not just hunger, suggesting it can't be the 'on' switch/brains 'eating' centre. Recent research = Eating behaviour is controlled by neural circuits throughout the brain, not just by the hypothalamus.

Support for the role of the venromedial hypothalamus: Research found that lesions/damage to the VMH resulted in hyperphagia and obesity in different species. Designated the VMH as the 'satiety centre' in eating behaviour - PVN has an important role in this.

Research support for the role of Ghrelin in appetite control: Wren et al - Randomised double-blind study of 9 healthy volunteers. They either recieved intravenous ghrelin or saline infusion and a week later they recieved the other condition. Appetite measured in terms of the amount of food taken and consumed at a buffet under each condition. Result: Significant increase in food consumption in ghrelin condtion compared to salne. SHowed an imporatant role of ghrlin in non-human species.

Leptin resistance: Some people devlop as resistance to leptin so it can't control appetite and weight gain. It is ussually found in overweight/obese people. This can't just be linked to leptin deficiency - a study with obese adults found that doses of leptin 20-30x normal concentrations of the hormone were necessary to produce significant weight reduction.