The serious damage to male reproductive health caused by the toxicity of raw cottonseed oil, disease factors, and environmental chemicals.

137. Male Infertility Caused by Raw Cottonseed Oil: Years of research have confirmed that long-term consumption of unprocessed raw cottonseed oil by both men and women can lead to infertility. This is because cottonseed oil contains gossypol, an oxidative phosphorylation uncoupling agent. In large doses, it is toxic to various cells; in small doses, it has a specific inhibitory effect on male reproductive epithelial cells, preventing sperm production. Prolonged consumption can cause the disappearance of spermatogenic cells at all levels, resulting in azoospermia and irreversible infertility. In women, gossypol primarily inhibits the endometrium (and possibly the ovaries), potentially inducing amenorrhea. Consuming raw cottonseed oil not only causes male and female infertility but can also cause a condition called "fever disease." Those afflicted with this disease experience intense heat throughout their body and feel only relief when naked and lying on cool ground. Patients gradually become emaciated, weak, and lose their ability to work. Therefore, people are strongly advised against consuming unprocessed raw cottonseed oil, as it may lead to the risk of infertility.

Mumps can lead to male infertility. Doctors at male infertility clinics often ask patients if they have had mumps. This is because mumps and infertility are indeed closely related. One characteristic of mumps is that the virus not only affects glands but also nerve tissue, the pancreas, and especially has a significant affinity for the testes. One-fifth to one-quarter of mumps patients also have orchitis. Two-thirds of these cases are unilateral, and one-third are bilateral. The illness lasts 3-5 days, but in severe cases, it can last up to two weeks. Orchitis occurring during puberty can cause irreparable damage to the epithelial cells and interstitial cells of the seminiferous tubules of the testes, potentially leading to testicular atrophy. Furthermore, bilateral mumps-orchitis in adult men can cause hypogonadism, sometimes resulting in azoospermia or a severely reduced sperm count, below 4 million per milliliter. Recent studies have also shown that adult men who have mumps-orchitis may experience feminization. This is because the interstitial cells' ability to secrete testosterone is significantly impaired, while their ability to produce estrogen remains unaffected. Due to the reduced androgen production, the aromatization of androstenedione at sites outside the gonads increases, coupled with the increased estrogen production, causing an alteration in the androgen/estrogen ratio and exacerbating gynecomastia in men. Due to varying incidence rates, treatment for pre-pubertal mumps patients focuses primarily on the mumps itself; for post-pubertal mumps-orchitis patients, treatment focuses primarily on the orchitis. Supportive therapy includes strict bed rest, early treatment, meticulous nursing care, placing cold compresses on the testes to relieve pain, and using a T-bandage to support the scrotum to alleviate symptoms (pain and swelling), thereby preventing and reducing the occurrence of sequelae. Timely use of sufficient anti-inflammatory and analgesic drugs is crucial, especially in cases of severe testicular pain. In summary, mumps-orchitis can affect male fertility and even sexual function, and early treatment is essential. Medication use should be strictly followed according to medical advice; negligence should be avoided to prevent serious sequelae.

Epididymal tuberculosis can cause infertility because sperm produced in the testes must mature further in the epididymis before being expelled through the vas deferens during ejaculation. Epididymal tuberculosis can also spread to the prostate and vas deferens through bloodstream and urinary tract infection, causing the vas deferens to become enlarged and uneven, sometimes appearing as beaded nodular cords. Therefore, when the lesion affects both epididymis, it not only affects sperm development but can also obstruct sperm expulsion, leading to obstructive azoospermia and infertility. If detected early and treated promptly to prevent bilateral epididymal involvement, fertility can be preserved. Otherwise, even long-term medication or surgery cannot restore the damaged tissue to normal; only the progression of the disease can be controlled, and fertility is unlikely to be restored.

A new study suggests that prolonged exposure to car exhaust fumes can decrease sperm quality, thus affecting male fertility. Researchers at the University of Naples in Italy studied 85 men working at highway tollbooths. They found that while their sperm count was similar to other young and middle-aged men in the same area, their sperm motility was lower, resulting in decreased fertility. The tollbooth workers underwent comprehensive medical examinations, and 83% of the men were married. Of the 71 married men, 7 had not had children. The study showed that these men worked long hours in environments with high concentrations of nitrogen monoxide, sulfur monoxide, carbon monoxide, and lead from car exhaust fumes. Nitrogen monoxide and lead are particularly damaging to sperm quality. Researchers are calling for further research on this topic, and for healthcare professionals to pay attention to the negative impacts of environmental pollution on human health.

Perfume and soap may harm sperm. A study by American scientists has found that a chemical found in perfumes can damage the DNA of adult male sperm. This chemical is called diethyl phthalate, and it is commonly found in soaps, perfumes, and other fragrance-containing cosmetics. A research team at Harvard University conducted the study on 168 adult men. The results showed a correlation between damage to sperm DNA and the level of diethyl phthalate in the participants' bodies. Environmentalists have long condemned the use of chemicals, arguing that they cause health problems, but manufacturers and chemical industry experts insist that they are "safe."

Drugs that can become "sperm killers" In recent years, medical research has found that 10% to 30% of infertility is caused by drugs. These drugs are: (1) Cimetidine, tamethasone and other anti-ulcer drugs can suppress male and female libido, which can lead to male and female frigidity and male impotence. (2) Erythromycin, spiramycin, midecamycin and other macrolide antibiotics can reduce the organic division frequency of testicular cells, kill sperm, and significantly weaken the vitality of surviving sperm. (3) Neomycin, furan drugs and other drugs have toxic effects on the gonads. (4) Sleeping pills can suppress libido, or even cause loss of libido, and can reduce testosterone production in men, cause erectile dysfunction, anejaculation and menstrual disorders or amenorrhea in women. (5) Compound antihypertensive tablets, reserpine, methyldopa, antihypertensive drugs and other antihypertensive drugs can affect erectile function, causing decreased libido, impotence, anejaculation and menstrual disorders in women. (6) Antidepressants such as amitriptyline hydrochloride and fluphenoxypropylamine hydrochloride can impair libido in both men and women. (7) Cyclophosphamide, methotrexate, colchicine, etc., can lead to reduced or absent semen, decreased sperm motility, testicular atrophy, etc., and can cause menstrual disorders, anovulation, amenorrhea, etc. in women. (8) Spironolactone, thyroid preparations, etc., can lead to decreased libido, menstrual disorders, ovulation disorders, and endocrine abnormalities. (9) Tylenol, chlorpyrifos, atropine, etc., can commonly cause impotence. (10) Alcohol can lower the level of testosterone in the blood and can damage, deform, reduce, and impair the development and motility of eggs and sperm. Long-term drinking can also lead to impotence and anejaculation. Therefore, frequent use of medicinal wine can lead to infertility.