Socioeconomic status and health: Pathways of diseases
Socioeconomic status (SES) affects health: the lower the position in a hierarchy, the poorer the health. The evidence for this relationship is clear. What is less well understood is why SES has such a major impact on health. The effect of the SES cannot be explained by the material conditions only, it appears to depend to a large extent on the psychological impact of one’s position in his socioeconomic hierarchy. The psychological impact of a low SES, whether expressed by shame or hostility, leads to chronic stress.
Stress and socioeconomic status
Stress is the response of an organism to a perturbation of its inner or outer environment. Different areas in the brain are responsible for the response to an acute aggression: some areas detect social threats, other areas detect physiological threats. These areas are responsible for activating pathways in the brain, among them, the hypothalamus and the periaqueductal gray which then trigger a series of change in different parameters such as heart rate, blood pressure, inflammation, glucose levels, and fight, flight, or freeze response. These modified parameters then allow the organism to cope with the acute threat, ultimately allowing the survival of the organism. Once the threat is extinguished, the stress response stops. This, at least, is how the stress response functions normally.
Problems arise when an organism is exposed to chronic threats, chronic sources of stress. In humans, especially in modern industrial nations, the most common source of stress is social: the judgment of others. The repeated or chronic activation of a response designed for acute threats leads to modifications of parameters such as blood pressure, heart rate, sugar level in the blood, and fat deposit around the abdominal viscera. And these modifications then lead to high blood pressure, arrhythmias, diabetes, and abdominal obesity. This overuse of the stress response is one way in which chronic stress can lead to pathological conditions which will shorten life.
Effect of stress on the nervous system
Another way by which chronic stress leads to diseases has to do with inflammation. It has become clear in the last twenty five years that inflammation plays a key role in most modern diseases. Cardiovascular diseases would be due to inflammation of the arterial wall, cancers would be the consequence of long term inflammation of different tissues, and degenerative diseases of the central nervous system (such as Alzheimer’s disease) would be a consequence of inflammation of the brain. A paradox arises however when trying to relate stress and inflammation: stress is anti-inflammatory! Stress activates the hypotahalamo-pituitary-adrenal axis leading to a rise in cortisol which is a potent anti-inflammatory hormone: the effect of cortisol on its receptor is to reduce inflammation. When cortisol is chronically elevated however, the cortisol receptors react by becoming "down regulated", i.e. less numerous and less sensitive. This down regulation compensates for the increase in cortisol levels. When the cortisol level (stress level) falls, even temporarily and relatively, the cortisol receptors remain down regulated for a period of time. This is when a problem arises. A relatively lower cortisol level in presence of down regulated cortisol receptors results in a reduced anti-inflammatory effect of the stress system and therefore to a pro-inflammatory situation. This pro-inflammatory state triggers the onset of inflammation which leads to inflammatory diseases.
SES is a source of chronic stress. The chronic activation of systems designed for acute threats modifies their basal activity. This modification especially the one involving cortisol and its receptors can lead to a pro-inflammatory state responsible for most of diseases of modern industrial nations. This hypothesis allows us to postulate a causal chain from SES to stress, from stress to inflammation, and from inflammation to diseases.
|Author :||Jean-Pierre Roy, MD
Montreal Neurological Hospital
Quan, N., R. Avitsur, J. L. Stark, L. He, W. Lai, F. Dhabbar et J. F. Sheridan (2003), "Molecular mechanisms of glucocorticoid resistance in splenocytes of socially stressed mice", Journal of Neuroimmunology, vol. 137, p. 51-58.
Yudkin, J. S. (2003), "Adipose tissue, insulin action and vascular disease: inflammatory signals", International Journal of Obesity and Related Metabolic Disorders , vol. 27, Suppl 3, p. S25-S28.