Studies indicate that dietary patterns may affect development of BPH, but further research is needed to clarify any important relationship. Studies from China suggest that greater protein intake may be a factor in development of BPH. Men older than 60 in rural areas had very low rates of clinical BPH, while men living in cities and consuming more animal protein had a higher incidence. On the other hand, a study in Japanese-American men in Hawaii found a strong negative association with alcohol intake, but a weak positive association with beef intake. In a large prospective cohort study in the US (the Health Professionals Follow-up Study), investigators reported modest associations between BPH (men with strong symptoms of BPH or surgically confirmed BPH) and total energy and protein, but not fat intake. There is also epidemiological evidence linking BPH with metabolic syndrome (concurrent obesity, impaired glucose metabolism and diabetes, high triglyceride levels, high levels of low-density cholesterol, and hypertension).

Most experts consider androgens (testosterone and related hormones) to play a permissive role in the development of BPH. This means that androgens must be present for BPH to occur, but do not necessarily directly cause the condition. This is supported by evidence suggesting that castrated boys do not develop BPH when they age. In an unusual study of 26 eunuchs from the palace of the Qing dynasty still living in Beijing in 1960, the prostate could not be felt in 81% of the studied eunuchs. The average time since castration was 54 years (range, 41–65 years). On the other hand, some studies suggest that administering exogenous testosterone is not associated with a significant increase in the risk of BPH symptoms, so the role of testosterone in prostate cancer and BPH is still unclear. Further randomized controlled trials with more participants are needed to quantify any risk of giving exogenous testosterone.

Dihydrotestosterone (DHT), a metabolite of testosterone, is a critical mediator of prostatic growth. DHT is synthesized in the prostate from circulating testosterone by the action of the enzyme 5α-reductase, type 2. DHT can act in an autocrine fashion on the stromal cells or in paracrine fashion by diffusing into nearby epithelial cells. In both of these cell types, DHT binds to nuclear androgen receptors and signals the transcription of growth factors that are mitogenic to the epithelial and stromal cells. DHT is ten times more potent than testosterone because it dissociates from the androgen receptor more slowly. The importance of DHT in causing nodular hyperplasia is supported by clinical observations in which an inhibitor of 5α-reductase such as finasteride is given to men with this condition. Therapy with a 5α-reductase inhibitor markedly reduces the DHT content of the prostate and, in turn, reduces prostate volume and BPH symptoms.

Testosterone promotes prostate cell proliferation, but relatively low levels of serum testosterone are found in patients with BPH. One small study has shown that medical castration lowers the serum and prostate hormone levels unevenly, having less effect on testosterone and dihydrotestosterone levels in the prostate.

While there is some evidence that estrogen may play a role in the cause of BPH, this effect appears to be mediated mainly through local conversion of androgens to estrogen in the prostate tissue rather than a direct effect of estrogen itself. In canine "in vivo" studies castration, which significantly reduced androgen levels but left estrogen levels unchanged, caused significant atrophy of the prostate. Studies looking for a correlation between prostatic hyperplasia and serum estrogen levels in humans have generally shown none.

In 2008, Gat et al. published evidence that BPH is caused by failure in the spermatic venous drainage system resulting in increased hydrostatic pressure and local testosterone levels elevated more than 100 fold above serum levels. If confirmed, this mechanism explains why serum androgen levels do not seem to correlate with BPH and why giving exogenous testosterone would not make much difference.

While some dietary factors have been associated with prostate cancer the evidence is still tentative. Evidence supports little role for dietary fruits and vegetables in prostate cancer occurrence. Red meat and processed meat also appear to have little effect in human studies. Higher meat consumption has been associated with a higher risk in some studies.

Lower blood levels of vitamin D may increase the risk of developing prostate cancer.

Folic acid supplements have no effect on the risk of developing prostate cancer.

There are also some links between prostate cancer and medications, medical procedures, and medical conditions. Use of the cholesterol-lowering drugs known as the statins may also decrease prostate cancer risk.

Infection or inflammation of the prostate (prostatitis) may increase the chance for prostate cancer while another study shows infection may help prevent prostate cancer by increasing blood flow to the area. In particular, infection with the sexually transmitted infections chlamydia, gonorrhea, or syphilis seems to increase risk. Finally, obesity and elevated blood levels of testosterone may increase the risk for prostate cancer. There is an association between vasectomy and prostate cancer; however, more research is needed to determine if this is a causative relationship.

Research released in May 2007, found that US war veterans who had been exposed to Agent Orange had a 48% increased risk of prostate cancer recurrence following surgery.

In urologic pathology, high-grade prostatic intraepithelial neoplasia, abbreviated HGPIN, is an abnormality of prostatic glands and believed to precede the development of prostate adenocarcinoma (the most common form of prostate cancer).

It may be referred to simply as prostatic intraepithelial neoplasia (abbreviated as PIN). It is considered to be a pre-malignancy, or carcinoma in situ, of the prostatic glands.

There are several reasons why PIN is the most likely prostate cancer precursor. PIN is more common in men with prostate cancer. High grade PIN can be found in 85 to 100% of radical prostatectomy specimens, nearby or even in connection with prostate cancer. It tends to occur in the peripheral zone of the prostate. With age, it becomes increasingly multifocal, like prostate cancer. Molecular analysis has shown that high grade PIN and prostate cancer share many genetic abnormalities. This has been confirmed in a transgenic mouse model.

The risk for men with high grade PIN of being diagnosed with prostate cancer after repeat biopsy has decreased since the introduction of biopsies at more than six locations (traditional sextant biopsies).

ASAP is considered an indication for re-biopsy; in one survey of urologists 98% of respondents considered it a sufficient reason to re-biopsy.

A case report of male breast cancer subsequent to bicalutamide-induced gynecomastia has been published. According to the authors, "this is the second confirmed case of breast cancer in association with bicalutamide-induced gynaecomastia (correspondence AstraZeneca)." It is notable, however, that gynecomastia does not seem to increase the risk of breast cancer in men. Moreover, the lifetime incidence of breast cancer in men is approximately 0.1%, the average age of diagnosis of prostate cancer and male breast cancer are similar (around 70 years), and millions of men have been treated with bicalutamide for prostate cancer, all of which are potentially in support of the notion of chance co-occurrences. In accordance, the authors concluded that "causality cannot be established" and that it was "probable that the association is entirely coincidental and sporadic."

Bicalutamide may cause sexual dysfunction, including decreased sex drive and erectile dysfunction. However, the rates of these side effects with bicalutamide monotherapy are very low. In the trial, at 7.4 years follow-up, the rates of decreased libido and impotence were only 3.6% and 9.3% in the 150 mg/day bicalutamide monotherapy group relative to 1.2% and 6.5% for placebo, respectively. Most men experience sexual dysfunction only moderately or not at all with bicalutamide monotherapy, and the same is true during monotherapy with other . In clinical trials, about two-thirds of men with advanced prostate cancer (and of almost invariably advanced age) treated with bicalutamide monotherapy maintained sexual interest, while sexual function was slightly reduced by 18%.

Similarly to men, bicalutamide is likely to be associated with minimal or no sexual dysfunction in women. Studies have not found a significant correlation between libido and circulating testosterone levels in premenopausal women, and treatment of premenopausal women with low doses of testosterone has not been found to improve sexual function in most research. However, low-dose testosterone therapy has been found to significantly improve multiple domains of sexual function (frequency, libido, orgasm, satisfaction, others) in postmenopausal women, particularly in those who have undergone ovariectomy. Conversely, women with PCOS, who have higher levels of testosterone, do not show increased sex drive, and treatment with oral contraceptives, which contain estrogen and decrease free testosterone levels, have been found not to decrease sexual function but to increase it in both healthy women and those with PCOS. In addition, women with CAIS show normal or even increased sexual function in spite of complete loss of AR signaling. It has been suggested that increased sex drive and sexual function associated with testosterone may be mediated by aromatization into estradiol rather than necessarily via activation of the AR.

On a subsequent biopsy, given the diagnosis of ASAP, the chance of finding prostate adenocarcinoma is approximately 40%; this is higher than if there is high-grade prostatic intraepithelial neoplasia (HGPIN).

Nipple adenomas most commonly occur in 30- to 40-year-old women, but can also occur in men. They can also occur at any age, including in the elderly, in adolescence, and in infants.

The annual prevalence in the general population of chronic pelvic pain syndrome is 0.5%. 38% of primary care providers, when presented with a vignette of a man with CPPS, indicate that they have never seen such a patient. However, the overall prevalence of symptoms suggestive of CP/CPPS is 6.3%. The role of the prostate was questioned in the cause of CP/CPPS when both men and women in the general population were tested using the (1) National Institutes of Health Chronic Prostatitis Symptom Index (NIH-CPSI) —with the female homolog of each male anatomical term use on questionnaires for female participants— (2) the International Prostate Symptom Score (IPSS), and (3) additional questions on pelvic pain. The prevalence of symptoms suggestive of CPPS in this selected population was 5.7% in women and 2.7% in men, placing in doubt the role of the prostate gland. New evidence suggests that the prevalence of CP/CPPS is much higher in teenage males than once suspected.

Serous cystadenoma may refer to:

- Ovarian serous cystadenoma, a very common benign tumour of the ovary.

- Pancreatic serous cystadenoma, also known as "serous microcystic adenoma".

Prostatic congestion is a medical condition of the prostate gland that happens when the prostate becomes swollen by excess fluid and can be caused by prostatosis. The condition often results in a sufferer feeling the urge to urinate frequently.

In recent years the prognosis for CP/CPPS has improved with the advent of multimodal treatment, phytotherapy, protocols aimed at quieting the pelvic nerves through myofascial trigger point release and anxiety control, and chronic pain therapy.

Parathyroid cancer occurs in midlife at the same rate in men and women.

Conditions that appear to result in an increased risk of parathyroid cancer include multiple endocrine neoplasia type 1, autosomal dominant familial isolated hyperparathyroidism and hyperparathyroidism-jaw tumor syndrome (which also is hereditary). Parathyroid cancer has also been associated with external radiation exposure, but, most reports describe an association between radiation and the more common parathyroid adenoma.

Prostatitis is inflammation of the prostate gland. Prostatitis is classified into acute, chronic, asymptomatic inflammatory prostatitis, and chronic pelvic pain syndrome.

In the United States, prostatitis is diagnosed in 8 percent of all urologist visits and 1 percent of all primary care physician visits.

A nipple adenoma is a type of intraductal papilloma that arises within the lactiferous ducts that are located within the nipple.

Prostatic secretions escape into the stroma and elicit an inflammatory response.

Granulomatous prostatitis is an uncommon disease of the prostate, an exocrine gland of the male reproductive system. It is a form of prostatitis, i.e. inflammation of the prostate, resulting from infection (bacterial, viral, or fungal), the BCG therapy, malacoplakia or systemic granulomatous diseases which involve the prostate.

Asymptomatic inflammatory prostatitis is a painless inflammation of the prostate gland where there is no evidence of infection. It should be distinguished from the other categories of prostatitis characterised by either pelvic pain or evidence of infection, such as chronic bacterial prostatitis, acute bacterial prostatitis and chronic pelvic pain syndrome (CPPS). It is a common finding in men with benign prostatic hyperplasia.

There are two types of prostatic stent: temporary and permanent.

Although a permanent prostatic stent is not a medical treatment, it falls under the classification of a surgical procedure. Placement of a permanent prostatic stent is carried out as an outpatient treatment under local, topical or spinal anesthesia and usually takes about 15–30 minutes.

A temporary prostatic stent can be inserted in a similar manner to a Foley catheter, requiring only topical anesthesia.

Glandular and epithelial neoplasm is a grouping of tumors arising from the glands and epithelium.

An example is adenoma.

Little is known about the total incidence of salivary gland tumours as most benign tumours go unrecorded in national cancer registries. The majority of salivary tumours are benign (65-70%). Within the parotid gland 75 - 80% of tumours are benign. Around 50% of the tumours found in the submandibular glands are benign. Sublingual gland tumours are very rare but if present, they are most likely to be malignant.

In the United States, salivary gland cancers are uncommon with an incidence rate of 1.7 in 100000 between 2009 and 2013.

This is a very rare neoplasm accounting for approximately 0.0003% of all tumors and about 2.5% of all external ear neoplasms. There is a wide age range at initial presentation, although the mean age is about 50 years of age. Females are affected slightly more often (1.5:1).