Stress and appetite

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Introduction to the neural mechanisms of appetite control and the interconnections to the HPA axis

In the paragraph above we were introduced to the HPA axis and what it entails. This section aims to give a general understanding to how the brain is involved in regulating appetite, and how it is connected to the HPA axis to allow for stress to have an impact on appetite, which will be discussed in greater detail further along.

In light of the current obesity epidemic there has been a great deal of research gone into trying to figure out exactly what causes an obese person to over-eat, or store more energy, compared with a normal weight person. And recent years have seen a great deal of light shed on the neural mechanisms of appetite control. A full account of the control of appetite and its areas in the brain are beyond the scope of this article, but this section aims to highlight the key features so that the connection between stress and appetite can be made.

There are several peptides circulating in our bodies which inform the brain of the body’s nutritional status. These include insulin (acts to suppress appetite), leptin (acts to suppress appetite) and ghrelin (acts to induce appetite) which are able to cross the blood-brain barrier and enter the hypothalamus via the Arcuate Nucleus (ARC) where they have their effect (Schwartz et al, 2000). In ARC there are populations of neurons which produce and release substances which have either orexigenic effects (induce feeding) or anorexigeninc effects (suppress feeding). The orexigenic neurons, which signal hunger, or a negative energy state, are Neuropeptide Y (NPY)/Agouti-related Peptide (AgRP). These are inhibited by increased levels of insulin and leptin, which demonstrates that insulin and leptin act as appetite inhibitors. However, increasing levels of insulin and leptin have excitatory effects on another type of neuron, the anorexigenic peptide releasing neuron Pro-opiomelanocortin (POMC) which releases pro-opiomelanocortin, which is cleaved into melanocortins. Key here is alpha-MSH, a potent anorexigenic molecule, which acts on the MC4 receptor. An additional feature of the orexigenic pathway is that AgRP antagonises MC4, thus increasing NPY/AgRP neurons orexigenic power (Schwartz et al., 2000).

Neurons from the ARC extend to other parts of the hypothalamus, such as to the Lateral Hypothalamus (LH), and the Paraventricular hypothalamus (PVN) and it is here the second-order signalling is postulated to take place. PVN stimulation causes inhibition of eating, whilst LH stimulation has the opposite effect. (Schwartsz et al, 2000). It is in the PVN we see the interconnection between feeding control and the HPA (stress) axis and it is here where the main activator of the HPA axis, Corticotropin-releasing factor (CRF), is synthesised. It has been demonstrated that NPY neurons have abundant projections here, and that they are in close proximity to CRF cell bodies (Demitrov et al, 2007). (Demitrov et al, (2007), also showed that NPY had a stimulatory effect on CRF release, indicating that hunger can cause stress, but this will not be discussed here). Studies by Jhanwar-Uniyal et al (1993) showed us two important things, first that PVN is indeed innervated by NPY neurons projecting from the ARC (shown by correlation of NPY levels in the PVN and ARC, this correlation did not exist for other hypothalamic areas) and secondly, they found that direct injection of NPY into the PVN potently affected eating behaviour, leading to an increase of ingestion of carbohydrate dense food (no increase was seen in ingestion of protein and fat). This preference for carbohydrate dense food when stressed; and the biological relevance, will be discussed further along.

So as stated above, the key area of connection between the HPA axis and regulation of feeding is the PVN. Here there are innervating NPY neurons (Orexigenic) and CRF synthesis (Activator of the HPA axis) which seem to act on each other in a classic feedback loop. CRF inhibits NPY thus initially being anorexigenic, however, once it has activated the HPA axis and glucocorticoids (GCs) are produced which then feed back to the brain and inhibit CRF, this inhibition is blocked, and feeding occurs. The more GCs present in the body (ie sustained activation of the HPA axis) the greater the inhibition of the CRF inhibition on NPY, thus, GCs stimulate NPY resulting in an orexigenic drive. However, as said, GCs inhibit CRF release which downstream will stop the release of GCs, thus completing the feedback loop (Cavagnini et al, 2000).

Green indicates anorexigenic pathways/neurons and red indicates orexigenic pathways. This figure represents the basic neural mechanisms of appetite, with emphasis on the PVN and how it relates to the HPA axis

So as stated above, the key area of connection between the HPA axis and regulation of feeding is the PVN. Here there are NPY neurons (Orexigenic) and CRF synthesis (Activator of the HPA axis) which seem to act on each other in a classic feedback loop. CRF inhibits NPY thus initially being anorexigenic, however, once it has activated the HPA axis and glucocorticoids (GCs) are produced which then feed back to the brain and inhibit CRF, this inhibition is blocked, and feeding occurs. The more GCs present in the body (ie sustained activation of the HPA axis) the greater the inhibition of the CRF inhibition on NPY, thus, GCs stimulate NPY resulting in an orexigenic drive. However, as said, GCs inhibit CRF release which downstream will stop the release of GCs, thus completing the feedback loop (Cavagnini et al, 2000). Figure 2.1 summarizes the neural mechanisms of appetite control and how they relate to the HPA axis.

The control of appetite is immensely complex and this section only offers a brief overview (please see references for more detail). As has been described, there are several mechanisms in which appetite and stress are related to each other, and the significance of this will be discussed further along. The aim behind most research done in this field is to offer a solution to the growing morbidity of our generation as a result of obesity. Stress-induced eating has been shown to play a part in the obesity epidemic and it is the main objective of this paper to discuss the impact of stress on eating.

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Why do you reach for that extra double chocolate chip cookie after a stressful day?

Stress is known to affect every body system and contributes to many of the negative health behaviours which impact todays’ society, including cardiovascular disease, diabetes and hypertension. With obesity becoming the world-wide epidemic which underlies many of these life-threatening diseases, many researchers have chosen to study the connection between novel stressors and an individuals eating behaviour, for example amount of food eaten and choice of food.

Both human and rodent studies into this area have illustrated a greater caloric intake after exposure to a novel lab stressor. Quick run-down of mechanisms behind this.

Paragraph on why you choose sweeter / fatty foods after acute stress

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