Anemia and testosterone

Testosterone is a hormone that has a fundamental role for the development and well-being of men: it defines its appearance, affects its state of mind and its sexual capacity. But as age advances, production gradually decreases.
Erythropoiesis, ie the formation of red blood cells, whose life is approximately 120 days and indispensable, to carry the oxygen that all our cells need is a hormonally regulated process. At least two hormones have the properties of inducing the production of erythrocytes, erythropoietin (Epo) and testosterone.
-Testosterone and erythropoiesis
Testosterone regulates erythropoiesis in several mammalian species, including humans of both sexes. The increase in hematocrit, that is, the count of red blood cells in the blood is the main problem associated with the administration of testosterone in older men.
Testosterone seems to act directly and indirectly to stimulate erythropoiesis, it also increases the levels of hemoglobin and hematocrit being dose dependent without an associated increase in erythropoietin levels.
While a testosterone effect has been demonstrated on erythrocytic stem cells, testosterone also has the ability to regulate the availability of iron in the body. Iron is an important component of hemoglobin, and its deficiency leads to anemia.
Hepcidin, a polypeptide produced in the liver, is the main iron-regulating hormone that mediates the homeostasis of extracellular iron concentrations. Hepcidin acts by regulating the entry of iron into plasma from tissues: duodenal cells that absorb iron from the diet, hepatocytes that store iron, and macrophages that recycle iron from aged erythrocytes.
More recent discoveries have shown that hepcidin interacts directly with transferrin, a protein that transports iron to the cells that store it (erythrocytes). This is another confirmation that hepcidin is directly involved in iron homeostasis.
Ferroportin is a biological iron pump located in the intestinal epithelium and in the membrane of macrophages, its function is to transport iron from the intestinal cell to the plasma and from the macrophage to the erythroblast.
In hemochromatosis, a physical or functional deficit of hepcidin occurs leading to an increase in ferroportin and, with this, to an excessive iron absorption. In situations of inflammation the opposite occurs, the synthesis of hepcidin is stimulated and the entry of iron in the organism and the synthesis of hemoglobin is blocked.
Anoxia, in conjunction with erythropoietin and factors produced by the erythropoietic tissue itself, under conditions that increase the production of red blood cells, inhibit the transcription of the gene and the production of hepcidin, with which ferroportin provides iron to the cell .
It has recently been shown that testosterone in humans inhibits hepcidin levels, thereby increasing intestinal iron absorption. On the other hand, testosterone produces an active metabolite by the aromatase enzyme called estradiol (E2), which can also regulate the transcription of hepcidin. Iron is an essential nutrient and at the same time a potentially toxic element, it is the most abundant trace element.
A particularity of iron is that unlike other nutrients the body’s ability to excrete it is very limited and is not subject to any regulation, so the excess iron can not be eliminated. For this reason, iron homeostasis depends exclusively on absorbed iron that increases or decreases depending on the iron’s needs.
Erythrocytosis is the most frequent adverse effect of testosterone administration, so it is assumed that the suppression of hepcidin by testosterone could play an important role in this disease. The majority of men who respond to testosterone by increasing hematocrit and hemoglobin levels and with stable levels of erythropoietin would be associated with a decrease in hepcidin levels.
-Function of erythropoietin:
The production of erythropoietin is stimulated by the reduction of oxygen in the tissues (tissue hypoxia) that is detected by the peritubular interstitial cells of the kidney. The existence of an extrarenal sensor is assumed. Noradrenaline, adrenaline and several prostaglandins stimulate the production of EPO. One of the problems of renal insufficiency is the anemia produced by the decrease in erythropoietin.
The erythropoietin produced in the kidney stimulates the stem cells of the bone marrow to increase the production of erythrocytes (red blood cells). In the human body, EPO is formed by 85-90% in the kidney and between 10 and 15% could be produced by the brain, uterus, testes and spleen.
The absorbed iron is transported by the transferrin. Iron always has to be linked to proteins because otherwise it would cause free radicals. The transferrin takes it to the bone marrow to form the red blood cells and after 120 days they go to the spleen to be degraded and the iron is used again.
Transferrin carries the iron to all the cells of the organism so all the cells are going to have receptors for the transferrin to take the iron. The liver is where iron is stored and since it is very oxidizing it has to be linked to an intracellular protein that is ferritin. In the spleen the erythrocytes are destroyed by macrophages and the iron is reused by sending it to the liver.
More recently it has been shown that high levels of testosterone in men with excessive erythrocytosis are due to a rapid metabolism of dehydroepiandrosterone sulfate (DHEAS) to androstenedione and from this to testosterone due to increased activity of the enzyme 17 beta hydroxysteroid dehydrogenase. This also seems to occur in women, where the highest levels of hematocrit is associated with high levels of testosterone associated with low DHEAS values, which reveals a rapid transformation of DHEAS to androstenedione and then to testosterone.
Testosterone, a hormone produced in the testes in men, defines typically masculine characteristics, such as the severity of the voice, facial hair, musculature and sexual capacity.
All men need to have testosterone in order to have a healthy life physically and psychologically. But the level of this hormone decreases naturally with age, it is estimated that 2% per year from 30-40 years.
In the long term, hypogonadism can increase the risk of osteoporosis, a condition that weakens the bones and makes them more fragile and prone to fractures. Hypogonadism is a specific medical condition that is not part of the normal aging process. Its late onset is related to obesity and type 2 diabetes.
The level of testosterone decreases naturally with age, an estimated 2% per year from 30-40 years. The level of testosterone decreases naturally with age, an estimated 2% per year from 30-40 years.
Your diagnosis can be made with a series of blood tests to measure the evolution of the testosterone level, which can vary greatly over the same day. If a deficiency is confirmed, the patient is usually referred to an endocrine specialist.
Testosterone is a hormone produced in the testes whose regulation is in charge of the pituitary gland and the hypothalamus. So any disease that affects the pituitary gland or the hypothalamus can cause hypogonadism.
The reduction of muscle mass and the ability to exercise is a common symptom among men aged 40-50 years, which may or may not have to do with the decrease of testosterone. This condition can also be due to a direct problem with the testicles, such as surgery, injury, Klinefelter syndrome, which is a genetic disorder, or inflammation, known as orchitis.
Infections and liver and kidney diseases, as well as the abuse of alcohol, or treatments such as chemotherapy or radiation therapy can also result in a decrease in testosterone levels.
Among these symptoms is depression, loss of sexual desire, impotence and other physical and emotional symptoms, such as mood swings and irritability, weakening, breast enlargement and reduction of muscle mass and ability to exercise.
Although these common symptoms are very similar to those caused by a low level of testosterone, in many cases they have nothing to do with the production of hormones, but with psychological problems or factors related to lifestyle, such as diet, stress or lack of sleep.
Even so, these symptoms can interfere with the daily life of men and affect their well-being, so it is important to consult them with a doctor to determine what is their cause.
Once the diagnosis is confirmed, the endocrine can offer treatments with hormonal supplements that seek to correct the deficiency, and that can be administered in the form of pills, skin patches, gels or intramuscular injections, depending on which is the underlying cause. All these available options have advantages and disadvantages, as well as certain side effects, therefore it must be done under medical supervision.

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