How stress affects our physical health

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Basil Manning
How stress affects our physical health

People under chronic stress have more health problems later in life than other people of the same age and socioeconomic status who have not experienced chronic stressful circumstances.

Contents

  • Effects of stress on cardiovascular and kidney functions
  • Chronic stress and cardiovascular disease
  • Stress and metabolism
  • Stress and digestive system
    • Peptic ulcer formation
  • Stress and growth
    • Growth inhibition during stress response
  • Stress, sex and reproduction
    • Male sexual response
    • Female sexual response
  • Effects of stress on the hippocampus
    • References

Effects of stress on cardiovascular and kidney functions

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

The heart accelerates, increasing the speed and intensity of the heartbeat, 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 blood vessels to the kidneys and skin - narrow, allowing increased blood flow to the muscles and brain.

Water is needed to keep the blood volume constant, but much of this body water is likely to be eliminated through the formation of urine. Thus, the brain will send information to the kidneys so that they stop the process of urine formation and the water can be reabsorbed into the blood..

Chronic stress and cardiovascular disease

The stress response causes both the heart and blood vessels to work longer, thereby generating greater physiological wear and tear. Certainly, with stress there is an increase in the driving force of blood flow, increasing the probability of small lesions in the vessels..

Fats, glucose, and blood clotting cells (platelets) that circulate in the blood adhere to the damaged layer of the inner lining of the blood vessels, causing it to thicken. In this way, the blood vessels begin to clog, consequently decreasing the flow of blood. Both adrenaline and glucocorticoids aggravate the formation of these fillings, called atherosclerotic plaques..

In a stressful 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 (if energy is needed) 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 liver, but are mobilized as 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 reserves are stored as fats (triglycerides) and a small amount will be stored as glycogen or protein.

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

Mobilization of energy in the face of a stressor: in a stressful situation, glucocorticoids (such as cortisol), glucagon and adrenaline 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 finally be transformed into glucose, through the process of gluconeogenesis. Glucose stored in the liver is also converted into glucose (Glycogenolysis). During stress, insulin is inhibited because this hormone stimulates the storage of fatty acids 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 is activated and the parasympathetic nervous system is inhibited - the latter would be the branch of the autonomic nervous system that mediates digestion..

Within the stress response, the blood flow to the stomach also decreases, in order to supply oxygen and glucose to other parts of the body..

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

Peptic ulcer formation

An ulcer is a lesion in the wall of an organ; when this injury occurs in the stomach or adjacent organs we can speak of peptic ulcers.

The stress response affects the overproduction of hydrochloric acid inside the gastrointestinal system and reduces the stomach's defenses against the effects of this acid on the cells that make up its walls. It also facilitates infection by bacteria that can damage the walls of the digestive system..

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

It has been shown that 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 anterior pituitary gland, two hormones that regulate the secretion of growth hormone (GH): GH-releasing hormone (GHRH) and somatostatin, or also called GH inhibitory hormone. The normal fluctuation of the GH level depends on the integration of brain signals of stimulation by GHRH with signals of inhibition by somatostatin.

Different studies with animals 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 significant 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 affective contact with the children, while the other minimized contact, limiting itself to solving biological needs. The study showed that the children of the first babysitter had a much higher growth rate than the children of the second.

Growth hormones are also involved in the repair of bone tissue. GH, somatomedin, parathyroid hormone and vitamin D allow the old parts of the bones to be disintegrated and to be constantly renewed. Stress hormones alter calcium traffic and prevent bone renewal.

Glucocorticoids inhibit the growth of new bones by disrupting the division of bone precursor cells at the ends of the bone.

During short-term stress, GH secretion is stimulated, as this hormone facilitates the breakdown of stored nutrients and contributes to the mobilization of energy. 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, the hypothalamic cells release luteinizing hormone-releasing hormone (LHRH) into the portal system. This stimulates the secretion of luteinizing hormone (LH) and follicle-stimulating hormone (FSH) into the bloodstream from the anterior pituitary. LH and FSH will cause the sex gonads (testes and ovaries) to secrete sex hormones.

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

Glucocorticoids have been shown to reduce the response of the sexual gonads to LH and that CRF secretion promotes LHRH inhibition.

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

Male sexual response

In humans, the erection is hemodynamic, that is, it occurs with an increase in the blood supply of the penis and with the blockage of the blood outlet path, with which the penis fills with blood and hardens.

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

Stress affects penile erection by inhibiting the parasympathetic nervous system.

Female sexual response

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

Stress reduces the number of adipose 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 LHRH secretion. Likewise, the release of prolactin and glucocorticoids during the stress response inhibits the sensitivity of the gonads to LH..

Stress inhibits progesterone levels, thereby disrupting the maturation of the uterine walls.

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

Decreased circulating estrogen levels during stress inhibits sexual desire in women.

Effects of stress on the hippocampus

During old age, elevated levels of glucocorticoids occur, due to an error in the inhibitory feedback of glucocorticoids present in the blood on the release of CRF and ACTH.

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

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

Several studies established by Sapolsky and colleagues 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, making them more susceptible to degenerative processes.

References

Bloom, F.E. i Lazerson, A. (1988). Brain, Mind, and Behavior. New 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. Actual.). Barcelona: Martínez Roca


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