In detail

How stress affects our physical health

How stress affects our physical health

People undergoing chronic stress have more health problems in the later stages of their lives than other people of the same age and socioeconomic status who have not gone through chronic stressful circumstances.


  • 1 Effects of stress on cardiovascular and renal functions
  • 2 Chronic stress and cardiovascular diseases
  • 3 Stress and metabolism
  • 4 Stress and digestive system
  • 5 Stress and growth
  • 6 Stress, sex and reproduction
  • 7 Effects of stress on the hippocampus

Effects of stress on cardiovascular and renal functions

In response to stress, an increase in cardiac output and redistribution of blood flow occur in the body, in order to preserve brain and cardiac functions and increase the blood supply to the muscles:

The heart accelerates, increasing the speed and intensity of the beats, by activating the sympathetic nervous system and inactivating the parasympathetic.

Constriction of some major arteries occurs.

The arteries of the mesenteric system - which supply blood to the digestive tract and the blood vessels of the kidneys and skin - narrow, and allow increased blood flow to the muscles and brain.

To keep the blood volume constant, water is needed, but much of this body water has a probable process of elimination through the formation of urine. So, the brain will send information to the kidneys so that they stop the process of urine formation and the water can be reabsorbed by the blood.

Chronic stress and cardiovascular diseases

The stress response causes both the heart and blood vessels to work longer, which generates greater physiological wear. Certainly, with stress there is an increase in the motive force of blood flow, increasing the likelihood of small lesions in the vessels.

Fats, glucose and blood clotting cells (platelets) circulating in the blood adhere to the damaged layer of the inner lining of the blood vessels, and generate a thickening of it. In this way, blood vessels begin to clog, consequently decreasing blood flow. Both adrenaline and glucocorticoids aggravate the formation of these seals, called atherosclerotic plaques.

In a stress situation, the heart consumes more glucose and oxygen and, therefore, needs vasodilation; the presence of atherosclerotic plaques will cause vasoconstriction.

Stress and metabolism

When we eat food, nutrients are stored and mobilized (in case of needing energy) in a differential way:

Proteins are stored as such, but in a stressful situation they are mobilized as amino acids..

Starch, sugars and other carbohydrates are stored as glycogen in the muscles and in the liver, but they are mobilized in the form of glucose in an emergency situation.

Fats are stored as triglycerides, but in response to stress they are mobilized as fatty acids and other compounds.

Most of the body's energy stores are stored as fats (triglycerides) and a small amount will be stored as glycogen or protein.

Keep in mind that one gram of fat is capable of storing twice as much energy as one gram of glycogen.

Mobilization of energy before a stressful agent: in a stressful situation, glucocorticoids (such as cortisol), glucagon and adrenalin stimulate the conversion of triglycerides (TG) into free fatty acids. Cortisol also helps convert inactivated muscle proteins into amino acids. Thus, both amino acids and fatty acids reach the liver, where they will eventually be transformed into glucose, through the gluconeogenesis process. The glucose stored in the liver is also converted to glucose (glycogenolysis). During stress, insulin is inhibited because this hormone stimulates the storage of fatty acids such as triglycerides and amino acids as proteins..

Prolonged stress generates an inhibition of all activities directed towards growth, reproduction and resistance to infection, in favor of the mechanisms that facilitate the immediate mobilization of energy.

Stress and digestive system

As we have seen, during the stress response, the sympathetic nervous system the parasympathetic is activated and inhibited - the latter would be the branch of the autonomic nervous system mediating digestion.

Within the stress response also decreases the blood flow that reaches the stomach, to be able to supply oxygen and glucose to other parts of the body.

The digestion process requires a high energy expenditure and, therefore, is interrupted quickly as a result of stress.

Peptic Ulcer Formation

An ulcer is an injury to the wall of an organ; When this injury occurs in the stomach or adjacent organs we can talk about peptic ulcers.

The stress response affects the overproduction of hydrochloric acid inside the gastrointestinal system and decreases the stomach defenses before the effects of this acid on the cells that constitute its walls. It also facilitates infection by bacteria that can damage the walls of the digestive system.

In 1943, a paper was published that collected Wolf and Wolff's observations about a New Yorker (Tom) who, eating soup, burned his esophagus at the age of 9. This subject was fed by putting food directly in the stomach, using a fistula. This accident served Wolf and Wolff to observe the changes generated in the stomach mucosa while Tom experienced various emotional states. With the study, they showed that emotional reactions can affect the changes in body physiological systems.

It has been found that the electrical stimulation of the amygdala Increases the release of hydrochloric acid and reduces blood flow in the stomach.

Stress and growth

The growth process requires energy. In this sense, various hormones have the function of mobilizing the energy and materials necessary for the expansion of the body.

Growth inhibition during stress response

The hypothalamus releases, through the adenohypophysis, two hormones that regulate the secretion of growth hormone (GH): the GH-releasing hormone (GHRH) and somatostatin, or also called the GH inhibitory hormone. The normal fluctuation of the GH level depends on the integration of the brain stimulation signals by the GHRH with the inhibition signals by the somatostatin.

Different animal studies have shown that the effect of stress on growth could be due to an excess of somatostatin.

A study in a German orphanage revealed the important effects of stress on growth. With the end of World War II, two groups of children were under the supervision of two different nannies. One of them had a lot of emotional contact with the children, while the other reduced contact as much as possible, merely solving the biological needs. The study showed that the children of the first nanny had a growth rate much higher than the children of the second.

Growth hormones also participate in bone tissue repair. GH, somatomedin, parathyroid hormone and vitamin D make it possible for old parts of the bones to disintegrate and constantly renew. Stress hormones alter calcium traffic and make bone turnover impossible.

Glucocorticoids inhibit the growth of new bones, since they interrupt the division of bone precursor cells at the ends of the bone.

GH secretion is stimulated during short-term stress, as this hormone facilitates the breakdown of stored nutrients and contributes to energy mobilization. In the long term, however, GH secretion is inhibited, since its main function is to stimulate growth, a process that requires a lot of energy expenditure.

Stress, sex and reproduction

Under normal conditions, hypothalamic cells release the luteinizing hormone releasing hormone (LHRH) into the portal system. This stimulates secretion into the bloodstream, by the adenohypophysis, luteinizing hormone (LH) and follicle stimulating hormone (FSH). LH and FSH will cause the sex gonads (testicles and ovaries) to secrete sex hormones.

Stress, through the production of endorphins, is able to inhibit the production of LHRH. Also, prolactin is released in the stress response, which decreases adenohypophytic sensitivity for LHRH.

It has been found that glucocorticoids reduce the response of the sexual gonads to LH and that CRF secretion promotes LHRH inhibition.

Stress reduces testosterone levels, in males, and estradiol, in females, affecting different levels of the endocrine beam.

Male sexual response

In the human being, the erection is hemodynamic, that is, it occurs with an increase in the blood flow of the penis and with the blockage of the blood outflow path, so that the penis fills with blood and hardens.

Hemodynamic erection is controlled by the parasympathetic nervous system; in situations of stress, the latter is inhibited, and produces a blockage of such behavior.

Stress affects penile erection, by inhibiting the parasympathetic nervous system.

Female sexual response

The female endocrine system contains a small amount of male hormones, coming from the adrenal glands. In female fat cells there is an enzyme, a -aromatase, which converts these male hormones into estrogens (female hormones).

Stress reduces the number of fat cells and, therefore, decreases the amounts of α -aromatase; with this, some aspects of the female reproductive system are inhibited.

The stress response facilitates the secretion of endorphins and enkephalins, substances that inhibit the secretion of LHRH. Also, the release of prolactin and glucocorticoids during the stress response inhibits the sensitivity of the gonads to LH.

Stress inhibits the levels of progesterora, which interrupts the maturation of the uterine walls.

Because estrogens contribute to recalcify bones and help prevent atherosclerosis, their inhibition during stress can affect the cardiovascular and musculoskeletal systems.

The decrease in circulating estrogen levels during stress inhibits sexual desire in women.

Effects of stress on the hippocampus

During old age, high levels of glucocorticoids are given, due to an error in the inhibitory feedback of blood glucocorticoids on the release of CRF and ACTH.

This feedback deficit is due to the fact that, with old age, there is a degeneration of a structure very rich in glucocorticoid receptors: the hippocampus. This seems to degenerate by exposure to the same glucocorticoids throughout the life of the subject.

Bruce McEwen described that the hippocampus was very sensitive to glucocorticoids, since it had large amounts of receptors for these hormones. In the 1980s, it could be shown that overexposure to glucocorticoids released to the stress response had a neurotoxic effect on hippocampal neurons.

Several studies established by Sapolsky et al. Have shown that long-term exposure to glucocorticoids destroys CA1 neurons in the hippocampus, making them more sensitive to aversive situations, such as decreased blood flow.

Glucocorticoids inhibit glucose supply in hippocampal neurons, and make them more susceptible to degenerative processes.


Bloom, F.E. i Lazerson, A. (1988). Brain, Mind, and Behavior. Nova York: Freeman and Company.

Selye, H. (1960). The tension in life. Buenos Aires, Argentina: Cía. General Fabril

Selye, H. (Ed.). (1980). Selye's guide to stress research. New York: Van Nostrand Reinhold

Tobeña, A. (1997). Harmful stress. Madrid: Aguilar.

Turner, R. J., Wheaton, B. & Lloyd, D. A. (1995). The epidemiology of social stress. American Sociological Review, 60, 104-125.

Valdés, M. & Flores, T. (1990). Psychobiology of stress (2nd ed. Current.). Barcelona: Martínez Roca

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