The etiology of ED is intricate and complex, usually the result of multiple factors. The erection of the penis is a complex vascular activity under neuroendocrine regulation, and this activity requires close synergy of neurological, endocrine, vascular, penile corpus cavernosum and psychological factors, and is affected by systemic diseases, nutrition and drugs and other factors, any abnormality of which may lead to ED. I. Psychosomatic etiology Many domestic and foreign literature reports that psychosomatic disorders can lead to ED. psychological stress is closely related to ED is closely related to, such as daily husband-wife relationship incompatibility, lack of sexual knowledge, bad sexual experience, work or economic pressure, incorrect understanding of media propaganda, fear of disease and prescription drug side effects caused by anxiety and depression psychological disorders and environmental factors. Likewise, erectile dysfunction as a psychological factor can cause depression, anxiety and somatic symptoms. Experimental studies in rats have shown that sympathetic nervous system hyperexcitability during anxiety is an important cause of psychogenic ED. It has been reported that psychogenic ED may be more than a purely functional disorder, and that the hypothalamus may be involved in the pathophysiological processes of psychogenic ED, and that there may be unrecognized underlying etiological and pathophysiological mechanisms of psychogenic ED. Psychiatric diseases are also one of the common causes of ED, such as schizophrenia patients, the incidence of ED can be as high as 16%-78%, and its causes are complex and diverse, the severity of the patient’s psychiatric symptoms and sexual dysfunction are positively correlated. The incidence of endocrine ED in patients with erectile dysfunction with abnormal serum sex hormones is reported to be 16.1%. (1) Hypogonadism: testosterone secreted by the male gonads (testes) is an important factor for normal and smooth erection of the penis, and any disorder that leads to lower blood testosterone levels almost inevitably impairs erectile function. Patients with primary hypogonadism have lower serum testosterone with elevated serum LH or/and FSH in the testes, hence the name hypergonadotrophic hypogonadism. Most of these patients have severe irreversible impairment of testicular function. Congenital factors include Crohn’s syndrome and bilateral anencephaly; acquired factors include gonadal injury and systemic diseases. In secondary hypogonadism, the lesion is located in the hypothalamus or pituitary gland, and LH, FSH and serum testosterone are reduced, which is also called hypogonadotropic hypogonadism. Congenital factors include selective GnRH deficiency, selective LH deficiency, congenital gonadotropin syndrome; acquired factors include injury (trauma, infarct disease, tumor, surgery, radiotherapy, etc.), excess exogenous or endogenous hormones (androgens, estrogens, glucocorticoids, growth hormone, thyroxine), hyperprolactinemia (idiopathic, pharmacologic, tumor), etc. Reduced synthesis or incomplete action of androgens: several rare genetic disorders reduce testosterone synthesis due to enzyme deficiencies, resulting in genital malformation or inadequate masculinization at birth. 5α-reductase abnormalities or lack of androgen receptors cause androgen tolerance. The clinical manifestations of androgen tolerance syndrome can range from mere sterility to hermaphroditism. Those with androgen activity disorders may show complete or incomplete loss of testicular function, resulting in ED. (2) Thyroid disease: Abnormal thyroxine can alter the hypothalamic-pituitary-gonadal axis and cause ED. increased secretion of estradiol and reduced clearance of its metabolites in hyperthyroid patients increases serum estradiol levels and diminishes the response of testosterone to HCG. Hypoactive sexual desire in hyperthyroid patients may be related to the hypermetabolic effect of thyroxine and the inhibition of interstitial cell function due to elevated circulating estradiol. In addition, sexual dysfunction can also occur in hypothyroid patients, who have reduced serum testosterone levels and metabolism of testosterone to phenytoinolone. Erectile dysfunction can also occur in patients with primary hypothyroidism who have increased blood prolactin due to feedback regulation of thyrotropin-releasing hormone (TRH) or enhanced response to endogenous TRH. (3) Other endocrine disorders: serum growth hormone levels are elevated in acromegaly, libido and sexual performance are reduced in 50% of patients, their blood LH is reduced, and the response of LH to GnRH is diminished, suggesting hypothalamic-pituitary insufficiency. Elevated serum prolactin in patients with acromegaly may partially explain their gonadal dysfunction. Elevated serum cortisol levels in patients with Cushing’s syndrome inhibit LH secretion and cause a decrease in serum testosterone levels, which can also cause secondary hypogonadism. Third, metabolic causes metabolic diseases resulting in ED, diabetes is the most common, the incidence of up to 30%-70%, 2 to 5 times higher than non-diabetic patients. With the age of diabetic patients and the prolongation of the disease, the incidence of ED will increase significantly. Because of the complex pathophysiological changes caused by diabetes, including neurovascular and other multifaceted factors, but in essence, the initiating factor may still be endocrine factors. In patients with diabetes, varying degrees of functional, organic or neurotransmitter alterations of the autonomic and somatic nerves as well as peripheral nerves can occur. Diabetes can also cause abnormalities in the white membrane of the penile corpus cavernosum, mainly manifested by increased thickness of the envelope, loss of the wave-like structure of collagen, and a large number of proliferating collagen fibers between the corpus cavernosum and smooth muscle resulting in decreased compliance of the corpus cavernosum, i.e., impaired cavernous diastolic function. Abnormal lipid metabolism is also an important risk factor for ED, and the mechanism is inconclusive. It may involve changes in vascular structure and function, endothelial cells, smooth muscle and nerves, etc. Hyperlipidemia is more closely associated with ED in men over 40 years of age. Most studies have concluded that dyslipidemia affects penile arterial blood flow in two main ways: first, it leads to atherosclerosis of large blood vessels such as the internal iliac artery, internal pubic artery and penile artery, which reduces the blood flow in penile arteries; second, it damages the endothelial cells of blood vessels and affects the relaxation of vascular smooth muscle during penile erection. Fourth, vascular etiology Normal vascular function is the basis for physiological erection of the penis. Vascular lesions are the main cause of ED, accounting for nearly 50% of ED patients, and with the increase in male age incidence has a significant trend of increasing. Arterial ED is one of the common causes of ED in men over the age of 40. Arterial causes of ED include any disease that may lead to reduced blood flow in the cavernous arteries of the penis, such as: atherosclerosis, arterial injury, arterial stenosis, pubic artery shunts, and abnormal cardiac function. Hypertension and the development of erectile dysfunction share common risk factors, and almost all risk factors that can lead to hypertension, such as smoking, hyperlipidemia, and obesity, can increase the incidence of ED. The incidence of venous ED is also high, accounting for approximately 25-78% of ED patients, including venous leakage due to reduced smooth muscle in the penile white membranes and cavernous sinuses. Common causes of venous lesions include congenital venous dysplasia, impaired valve function from various causes (venous degeneration in the elderly, smoking, trauma, and diabetes may cause occlusive dysfunction after venous damage), thinning of the cavernous white membrane, abnormal venous traffic branches, and abnormal shunts caused by surgical treatment of abnormal penile erections. Clinical and morphological data suggest that venous leakage increases with age. V. Neurological etiology Lesions of the brain, spinal cord, cavernous nerve, pubic nerve and nerve endings, small arteries and receptors on the corpus cavernosum can cause ED, and the pathophysiological mechanisms are different due to different sites of injury. 1, central nervous system diseases: brain diseases such as cerebrovascular accidents, Parkinson’s disease, tumors, epilepsy, senile dementia and organic psychosis may cause hypothalamic central dysfunction, or excessive inhibition of the spinal cord center and cause ED. spinal cord and many diseases of the central nervous system often complicate ED, ED is only one of a wide range of lesions in the central nervous system due to a variety of dysfunctions, these functional abnormalities through a variety of Diseases at the spinal cord level such as spina bifida, disc herniation, spinal cavitation, tumors and multiple sclerosis can affect afferent and efferent nerve pathways, resulting in dysfunction. 2, spinal cord injury: ED caused by spinal cord injury depends on the degree of injury and injury site. After complete injury to the upper spinal cord, 95% of patients have the ability to erect (reflex erection); while the lower spinal cord is completely injured, only 25% of patients can retain erectile function (psychological erection); however, if the incomplete injury, more than 90% of patients in both groups preserve the ability to erect. It is now believed that the sympathetic pathway in the thoracolumbar segment may transmit the impulse for psychogenic erection, and since only 25% of patients with complete injury to the lower spinal cord obtain erection through the sympathetic pathway, it is clear that the parasympathetic neurons in the sacral segment are the most important erection center. 3, peripheral neuropathy: pelvic fractures, rectal, bladder, prostate surgery may damage the cavernous nerve or pubic nerve, destroying the nerve pathway, all of which can lead to erectile dysfunction. Peripheral neuropathy such as diabetes, chronic alcoholism, vitamin deficiency, etc. can also cause neuropathy, which may affect the cavernous nerve endings and cause a lack of neurotransmitters. Sensory erectile dysfunction caused by somatosensory nerve damage can have normal nocturnal erections that start with a normal response to sexual stimulation but do not maintain a firm erection. In contrast, autonomic erectile dysfunction caused by damage to parasympathetic pathways is impaired in all types of erections. Sixth, drug etiology In recent years, the awareness of drugs leading to ED has gradually improved, the discovery of drugs that may cause ED. The primary varicocele is likely to be a risk factor for erectile dysfunction, and its secondary psychological factors can also be the cause of erectile dysfunction. The psychological factors that can also be a psychological cause of erectile dysfunction. Obstructive sleep apnea hypoventilation syndrome (obstrucfivesleepapnea/hypopneasyndrome, OSAHS) further causes intermittent hypoxemia and sleep fragmentation, which can lead to long-term damage to several target organs of the body, such as hypertension, ischemic heart disease, and stroke. These are also the primary risk factors for ED, suggesting that there may be a link between the two in terms of pathogenesis. Domestic reports of 121 cases of penile erectile dysfunction after vasectomy, that most of them are psychological ED. Eight, mixed etiology ED is mostly a manifestation of different pathological processes of multiple diseases, that is, ED can be caused by one or more diseases and other factors. Commonly, such as diabetes, hypertension, cardiovascular disease, trauma, surgical injury and other primary diseases, as well as drugs, lifestyle habits, social and environmental factors. Various diseases and causative factors lead to the occurrence of ED through their different or common pathways. Nine, ED risk factors ED and male ageing is closely related to the United States epidemiological survey shows that the prevalence of less than 40 years old is only 1%-9%, while the prevalence of 60-69 years old increased to 20%-40%, when the age increases to 79-80 years old, the prevalence of up to 50%-75%. The lifestyle of smoking, alcoholism, exercise, regular sexual activity, as well as obesity, atherosclerosis, diabetes, hypertension and dyslipidemic metabolic diseases, depression, lower urinary tract symptoms (LUTS), and benign prostatic hyperplasia (BPH) are important factors that influence the early and severe occurrence of the disease. Many medications used to treat hypertension and psychiatric disorders are also capable of causing ED.