After analyzing how the body is balanced both internally and before changes in the external environment and see the consequences of stress, we are now in a position to review the consequences of continued stress, chronic stress, what we have called, Metabolic stress syndrome chronic.

stress consequences

What are the consequences of stress

The first thing we should know is that a situation of long-term stress, chronic stress, triggers a series of changes among which stand out:

Let's look in more detail at each of these aspects.

Metabolic changes due to stress

El stress acts at the metabolic level In many ways, although it has two main pathways, the response of the vegetative system, with mobilization of catecholamines: adrenaline and norepinephrine and the response of the hypothalamic-pituitary hormonal system, with cortisol mobilization.

The increase of catecholamines in chronic stress acts on the adipose cells of the abdomen, metabolize their fatty deposits and pour them into the blood in the form of fatty acids. These high levels are maintained since they are not consumed because there is no greater requirement of energy expenditure (there is no flight behavior), there is no physical effort. The fatty acids in the blood, in part, return to the liver and partly go to other regions of the body. Those that return to the liver are transformed back into triglycerides, accumulating inside and triggering what we know as fatty degeneration of the liver. The rest of the fatty acids that circulate in the blood are directed to other regions of the organism, infiltrating the muscular tissue or depositing themselves again in the adipocytes of the abdominal fat.

Atherosclerosis and thrombus formation

The lack of exercise and the excess of fatty and sweet foods, favors the increase of cholesterol in the blood, especially LDL, which is deposited in the arteries and due to the action of free radicals in the body, penetrates the wall of the vessel, forming atheromas and atherosclerosis. Faced with an extreme situation, due to excessive fatigue or annoyance, a large amount of free radicals are generated that can break the atheroma, inducing blood clotting at that point, ending up obstructing the vessel, a thrombosis, with the consequences that This entails depending on the affected vessel (myocardial infarction in the heart or stroke in the cerebral vessels).

Currently we know that high levels of catecholamines and cortisol, elevated in chronic stress, favor a state of greater coagulability of the blood, which is known as pre-thrombotic state, which still favors the formation of thrombi, adding to what has been said previously.

The generalized inflammation of these patients with metabolic syndrome, also activates the macrophages to phagocytose cholesterol deposits in the blood vessels, they are transformed in the known foam cells, loaded with fat, which still favor more the formation of atheromas and the phenomenon of thrombosis The inflammation, its mediators, the cytokines, also cause the muscular cells to proliferate in the wall of the vessels, thickening them and resulting even more in the thrombotic phenomenon.

Adipogenesis

The activation of the sympathetic system in chronic stress, among the multiple effects that it triggers, produces the increase of the levels of one of the mediators of this system, the neuropeptide Y (NPY), which plays an important role in obesity related to the chronic stress

The neuropeptide Y is released especially in the presence of an excess of fatty and sweet foods, directly on the fat cells and there acts on the Y2 receptors that stimulate the formation of new fat cells from precursors, preadipocytes, and facilitate their fat filling (adipogenesis ) and also stimulates the vascularization of that area, to facilitate the growth of new cells, adipocytes, (angiogenesis).

The final result is the increase in fat mass, especially at the abdominal level, since the adipocytes in this area are those that have more Y2 receptors.

Chronic stress inflammation

This situation causes the transformation of adipose cells, which are full of fat, break down and release adipocytokines, with inflammatory capacity and responsible for generating a local environment of inflammation, which favors fibrosis of tissues at that level (what we know such as cellulite) and on the other hand, they are responsible for the state of generalized inflammation suffered by these subjects, with high production of free radicals and oxidative stress.

We currently know that hyperalimentation enhances the cortisol response and this excess cortisol would also influence the activation of NPY secretion, further promoting its negative effects, greater production of adipocytes and subsequent inflammatory response. It seems that this circuit of activations is highly influenced by epigenetic factors that would activate the expression of the genes that synthesize neuropeptide Y.

Systemic inflammation

We have just seen how the metabolism of adipocytes, stress, overfeeding and lack of physical exercise, trigger a reaction of local and generalized inflammation.

One of the basic elements to explain the systemic inflammation is the proportion of omega-6 and omega-3 fat, which must be 6-5 / 1 or even lower. 4 / 1 in Japan, with a high degree of longevity in its population. An imbalance with an increase in omega-6 will trigger an excess of saturated fats and a high level of free radicals, causing a situation of oxidative stress and generalized systemic inflammation.

It is important to know that omega-3 supplements, their theoretical beneficial effect is under debate since polyunsaturated fat molecules, such as omega-3s, are very susceptible to attack by free radicals that circulate in the body (lipoperoxidation), generating even more free radicals. Omega-3 supplements, in their purification process, lose the protective factor that accompanies natural foods rich in omega-3.

Natural foods with abundant polyunsaturated fats, have protective elements, with a large amount of antioxidants, which prevent the oxidation of their own fats, and protect them from the action of free radicals that circulate through the body. It is therefore better to take omega-3 in natural foods and not in capsules or other types of pharmaceutical supplements.

Blood pressure

Another important effect of the increase in cortisol and norepinephrine, the basis of chronic stress, is the action on the mechanisms that regulate blood pressure. These substances act on the renin-angiotensin axis of the kidney, there is an increase in angiotensin, aldosterone and ACTH and ADH that, retain water in the kidney, reduce the caliber of the arteries and, as a final result, there is an increase in blood pressure. blood pressure, increasing cardiac effort and its subsequent loss of efficiency as well as the risk of hemorrhages in the microcirculation of organs such as the brain, kidney or retina.

Immune system

Chronic stress also affects the immune system, there is a reduction in the defenses and an increase in certain responses that lead to autoimmune diseases. It is characteristic of those who suffer from frequent colds, flu, allergies, asthma, ulcerative colitis, etc. The deterioration of the immune system also constitutes one of the bases in the genesis of cancer.

To determine if the alteration of the immune system has occurred, the number of leukocytes, subpopulations of lymphocytes and NK cells, response of macrophages, levels of immunoglobulins, cytokines and interferon can be analyzed.

Aging due to stress

About aging also has a strong influence. The permanent excess of cortisol and the imbalance in the metabolism of glucose, allows the oxidizing agents to act, free radicals, and to remain a state of generalized systemic inflammation that produces the alteration of the blood vessels, atherosclerosis.

In the same way, the increase of free radicals, attack the telomeres of the DNA, reducing the replicative capacity of the cells and inducing changes in the genetic structure, mutations, that accelerate the aging and the appearance of cancer.

Cancer

The issue of cancer is a point of conflict, although there are many theories to explain its appearance, it seems clear that the action of chronic stress favors conditions of attack to telomeres, increased mutations and depression of the immune system, a key point, since there is a decrease in the action of the "vigilant" cells, which detect abnormal cells and their subsequent destruction, such as tumor cells.

There is increasing evidence of how the brain modulates neuroendocrine and immunological signals that can control tumor growth in tissues.

Behavior and stress profiles

There are two basic behavior profiles, type A profiles and type B profiles.

Dominant behavior due to stress

These subjects have a strong dominant character, are nervous and very active. In this type of individuals there are relatively low levels of cortisol and high levels of testosterone and DHEA, a profile that characterizes them with a high level of aggressiveness. Testosterone does not cause aggressiveness on its own, it only exaggerates a preexisting pattern and enhances the response to environmental triggering aggression. They are characterized by a predominance of the sympathetic system.

The immune response is also different, in type A subjects with respect to type B subjects, there is a predominance of the Th1 response, cell type, more effective to fight against infections, but with a negative aspect, the appearance of a state hyperimmune, potentiated by low levels of cortisol, which favors the appearance of inflammation and autoimmune problems.

Calmed behavior

They are calmer, more reflective and less active subjects. Individuals with this profile have a high reactivity of the pituitary-adrenal axis, with high cortisol values ​​and an increase in serotonin neurotransmission. They have a predominance of the parasympathetic system. They also have a hypocampor very developed that provides them with a great capacity to store and organize useful information in any threatening situation, they keep a memory of what happened.

In type B individuals there is a predominance of the Th2 immune response, humoral, very effective in the fight against parasites but insufficient for the rest of infections, especially viral infections.

Stress reduces the levels of anabolic hormones, such as androgens (testosterone and DHEA), estrogen, growth hormone and the so-called growth factors (IGF-1) and increases the production of catabolizing hormones such as cortisol, glucagon and catecholamines (adrenaline and noradrenaline). This imbalance in the anabolic-catabolic mediators aggravates chronic stress, promoting the tendency to disease and accelerating aging. The main factor in this scenario is the high rate of cortisol.

It is important to remember that cortisol is especially high in individuals with a type B profile, therefore, stress determines even higher levels in these individuals, while in individuals with a type A profile, with lower cortisol levels, the stress will bring cortisol levels back to normal. This is important to take into account when making cortisol determinations to assess the level of stress in patients, the normality values ​​will be different depending on the personality profile.

The increase of cortisol in chronic stress in type A individuals, favors cardiovascular overload, with myocardial fibrosis and hypertension, there is a greater tendency to myocardial infarction, aggravated by the tendency of noradrenaline to the destruction of myocardial muscle cells, elevated in these individuals.

In type B subjects, the increase in cortisol produces abdominal fat accumulation, increased fatty acids and insulin resistance, inducing the onset of obesity and atherosclerosis, with all its consequences.

Cognitive impairment and neurodegenerative disease

Chronic stress also has a fundamental role in brain health. We have already seen how the brain is responsible for detecting alarm situations and how it regulates the response to them, the problem is that the brain also becomes a target organ against this chronic stress response. The main effect of chronic stress is cognitive deterioration, on learning, memory, early aging and the appearance of neurodegenerative diseases such as Alzheimer's.

Sapolsky demonstrated in the 2003 how severe and prolonged stress can alter the capacity of plasticity and learning of hypocampor. We know that light stress can even improve cognitive abilities, attention and calculation systems are stimulated, we adapt to a possible alarm situation but, if the stress is maintained over time and becomes chronic, the levels of stress rise. cortisol and memory functions are blocked, mobilization of cognitive resources and all the intellective functions, by action on the hypocampoy especially about the amygdala, activating the emotional, negative, fear and anxiety response, which blocks the action of the prefrontal lobes, the executive center, to analyze and plan the action responses.

Chronic stress induces a failure in our responses, our actions, less effective in solving problems, which creates a vicious circle that generates even more anxiety and stress, and ends up leading us in most cases to depression. Mental alterations related to stress are the fastest growing occupational disease in the USA.

The neurological deterioration is aggravated by the action of the systemic inflammatory state, which also reaches the brain and peripheral nerves, there is an affectation of the myelin, it disappears and the disorders that we know as demyelinating degenerations begin.

Addiction and drug addiction

In this line of negative actions of chronic stress, the issue of drug addiction stands out. Chronic stress is one of the main culprits for the abuse of alcohol, tobacco, gambling and other addictions. Although it is true that not all people have the same facility to fall into addiction, when chronic stress occurs, mediators are secreted that use the same neural pathways that drugs use to produce their pleasant and addictive effect.

Chronic exposure to stress sensitizes certain neuronal pathways, especially those that use dopamine as a neurotransmitter, producing the same effect as psychostimulants, since both produce the same effect when using the same neuronal receptors, enhancing the effect of drugs and addictions In general, the pleasurable effect caused by drugs is enhanced. In the same way, a person who does not take drugs, this effect of chronic stress, translates into seeking the pleasurable reward for a rise in blood glucose, and that explains the "addiction" to chocolate, sweets in general or overeating, or in another order of things, to seek the pleasure of betting, to practice sex, alcohol and in the end, drugs.

In the habitual consumers of heroin a reduction of the endogenous opiates that produces the organism takes place since in the blood they are circulating great amount of similar substances, the heroin. These high levels of heroin cause the body does not need to synthesize opiates such as endorphins and enkephalins, the receptors that signal blood levels are "cheated" by the presence of drugs, very similar to these substances.

Endorphins and enkephalins are the natural substances that secrete the body to fight against pain, even producing a sense of well-being, so that in the face of possible damage suffered in an attack, the response of flight is not blocked, a process inherited from the It was Paleolithic. When heroin is removed from a drug addict, his body is left without pain protection, there are no natural opiates and the lack of drugs leaves the pain receptors exposed, this is what we know as "the monkey", in which the drug addict suffers strong and unbearable pain, even by the rubbing of clothes.

Fertility and sexual appetite

Chronic stress also acts on the mechanisms of fertility, there is an inhibition in the pituitary gonadotrophin-releasing hormones, LH and FSH, in both women and men.

Gonadal inhibition occurs with reduction of libido, sexual appetite and fertility (erectile dysfunction in man).

Summary
Consequences of stress
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Consequences of stress
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We explain the consequences of stress and how stress affects our body in diseases such as cancer, fertility or aging.
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Name of the editor
Área Oftalmológica Avanzada
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