Benign Prostatic Hyperplasia (BPH)

Benign Prostatic Hyperplasia (BPH) is a noncancerous enlargement of the prostate gland that Ray Peat argued is driven primarily by estrogen, not testosterone, in the context of a declining metabolic rate. 2 Peat explained that the conventional view—that testosterone causes prostate growth and estrogen inhibits it—was a logical error derived from an oversimplified model of sex hormones. 11 In aging men, thyroid deficiency weakens the liver's ability to detoxify hormones, causing testosterone to be converted into estrogen. 2 This estrogen then activates inflammatory and cell multiplication processes, directly promoting the growth of the prostate. 1 Peat noted that men with the highest testosterone levels generally have the lowest estrogen and the lowest prostate cancer problems, framing a deficiency of testosterone as a consequence of this estrogenic conversion. 2

The hormonal environment of aging creates a permissive state for BPH. Peat observed that by the age of 50, men often show an excess of both prolactin and estrogen, alongside a deficiency of thyroid and testosterone, which is precisely when prostate enlargement becomes noticeable. 8 The active thyroid hormone T3 declines with age, which necessarily lowers the production of the protective steroids pregnenolone and progesterone. 3 Progesterone, which Peat noted has been used in Europe to shrink enlarged prostates, and pregnenolone both decline, and their absence allows estrogen's effects to go unopposed. 2 Furthermore, estrogen rises in men during old age, as it does in stress, disease, and malnutrition, and is also produced in fat tissue, which tends to increase with age when thyroid and progesterone are deficient. 3

Peat identified several nutritional and hormonal interventions to oppose the estrogenic and inflammatory drivers of BPH. He considered vitamin D a major anti-inflammatory factor, possibly the single most important thing besides thyroid function, and recommended sunlight as the best source. 2 He also stressed keeping calcium intake high relative to phosphate to support metabolic balance. 2 To directly inhibit the aromatase enzyme that converts testosterone to estrogen, Peat pointed to aromatase inhibitors found in foods such as oranges (naringenin) and guavas (apigenin), as well as the drug aspirin, which blocks the production of inflammatory prostaglandins. 2 The supplement pregnenolone was described as indirectly able to increase progesterone and lower estrogen production. 2 Additionally, the raw carrot salad, made with grated carrots, olive oil, vinegar, and salt, was recommended for its mild antibiotic functions to reduce intestinal irritation and systemic endotoxin load, which can contribute to hormonal imbalance. 2

Georgi Dinkov has extended this framework by challenging the causal link between BPH and prostate cancer, stating that it has never been proven that BPH will progress to cancer or that any causal relationship exists. 5 He described the development of 5-alpha-reductase inhibitors like finasteride as a "chemical castration therapy" designed to sell a drug by mimicking a deficiency of the enzyme that converts testosterone to DHT, a condition in which the prostate remains small. 2 Dinkov warned that these drugs lead to depression, suicide, feminization, and ironically, a more aggressive type of prostate cancer. 5 He also highlighted the role of serotonin in directly stimulating the growth of prostate cancer and accelerating the conversion of BPH into high-grade cancer, noting that people on SSRI drugs have a dramatically higher chance of developing that type of cancer. 10 To oppose this, Dinkov recommended anti-prolactin drugs, vitamin B6 (as pyridoxal 5-phosphate) to suppress prolactin and increase dopamine, and serotonin antagonists like cyproheptadine. 10 Danny Roddy has noted that BPH, pattern baldness, and cardiovascular disease are tightly interrelated, reflecting a systemic problem rather than an isolated local condition. 9