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Erectile dysfunction due to metabolic and endocrine disorders

An erectile dysfunction of endocrine origin is actually a rare variant, up to 5% of all cases of erectile dysfunction. It must be distinguished from psychogenic, organic, and also from that arising as a result of the loss of a vital state, which manifests itself during a long somatic illness. An erectile dysfunction of endocrine origin can be divided into four main categories:

  • Erectile dysfunction in conditions of hypogonadism, i.e. conditions characterized by a decrease in testosterone secretion;
  • Erectile dysfunction in conditions of hyperestrogenism;
  • Erectile dysfunction in hyperprolactinemia;
  • Erectile dysfunction in common endocrinopathies.

Five common endocrinopathies can lead to sexual dysfunction: acromegaly, hypothyroidism, hyperthyroidism, hypercorticism, and hypercorticism.

Erectile dysfunction in conditions of hypogonadism

Testosterone has been shown to be essential for shaping and maintaining male sexual behavior. On the other hand, when the sexual behavior is already established, testosterone plays only a partial role in maintaining it. Testosterone deficiency:

  • reduces libido;
  • dilutes automatic erection;
  • however, it does not significantly alter the mental erection;
  • causes delayed ejaculation;
  • leads to a decrease in the volume of ejaculation.

The effect of testosterone on sexuality is proportional to its level in the circulating blood. Normally, in different people, it ranges from 2 to 4.5 ng / ml. Sexual activity increases the secretion of testosterone. Testosterone circulates in the blood primarily bound to various proteins, the most specific of which is the sex-binding protein. Only the remaining unbound (free) part is capable of exerting a biological effect.

There is no physiological andropause. With age, there is a progressive and relatively parallel decline in free and total testosterone levels. However, there is a slight increase in sex-binding protein with age, which to a certain extent determines the anticipatory decrease in free testosterone, which is also biologically active compared to the global one.

From these data we can conclude:

  • A decrease in plasma testosterone levels below 2 ng/ml is always associated with a violation of sexuality;
  • However, a moderate decrease in plasma testosterone levels between 2 and 4 ng/ml leads to persistent sexual dysfunction and can potentiate other factors;
  • This type of mild decrease in testosterone can be both a consequence and a cause of erectile dysfunction. Decreased sexual activity and resulting psychological disorders can cause erectile dysfunction, which is accompanied by a moderate decrease in plasma testosterone levels.


Erectile dysfunction is common in diabetics – from 30 to 60%. It has been proven that the main mechanism of erectile dysfunction in diabetics is neurological: at the stage of early involvement, demyelinated nerve fibers are histologically proven, which causes autonomic neuropathy. In turn, this leads to circulatory disorders, digestive disorders, as well as genitourinary disorders.

Relaxation of the internal sphincter sometimes causes infertility due to retrograde ejaculation in diabetics. This is a manifestation of sympathetic denervation. However, in all cases, the mechanism of erectile dysfunction in diabetics is heterogeneous and not caused by a single cause. First of all, it is necessary to take into account the vascular mechanism, especially since diabetic neuro- and angiopathy are often combined. In addition, the endocrine factor can also be considered as a cause in the context of various hormonal disorders found in diabetics. We should not lose sight of the importance of the psychological factor, the role of which is indisputable, but which, unfortunately, cannot be quantified.


Although alcohol can stimulate libido, chronic alcohol intoxication is often accompanied by sexual dysfunction. Sometimes it turns out to be definitive and remains persistent despite the cessation of alcohol intake. As in diabetics, damage to the structures of the autonomic nervous system and, of course, especially to peripheral nerves is most likely in the context of ethyl polyneuritis. However, cerebro-medullary involvement is not excluded, as it is known that alcohol can cause significant damage at all levels of the nervous system. As with diabetics, other factors overlap, in particular the causes and consequences of the psychosocial component of alcoholism.

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