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bazı kaynaklarda okuduğuma göre şu şekil bir teori var en basit temel mantığı ile şöyle söylim dnrd atmayın diye
orgasm olduktan sonra artan dopamin seviyeleri bir anda azalır
dopamin prolaktini baskılayan birşey olduğu için
31 sonrası yarım saatden fazla prolaktin artışı gözlemleniyor
prolaktininde dolaylı yollardan jinekomastiye sebep olduğunu kanıtlayan bazı makalelerde bulunuyor
şunu baştan söylim bunlar haftada 1 31 gibi küçük sayılarda pek etki edeceğini sanmıyor sadece bir 31de artan prolaktinin çok bir etkisi olacağını düşünmüyorum
belirli ve kesin birşey söylememekle birlikte günde bir kaç kez veya daha fazla uzun süre 31 işlemini eylemiş ve bu etkilerde kalmış insanlar için geçerli olduğunu düşünüyorum
A longitudinal study by Mieritz et al. in 2014, involving 501 Danish boys, including 31 with gynecomastia, reported elevated prolactin levels preceding the onset of gynecomastia in affected individuals, suggesting a potential contributory role of prolactin in its development [18]. Although prolactin itself is not considered a direct cause of PG, hyperprolactinemia might contribute to the development of gynecomastia by causing secondary hypogonadism. Studies by Trinchieri and Kilic suggested that prolactin inhibits GnRH secretion at the hypothalamic level, leading to secondary hypogonadism [32,41]. Prolactin receptors have also been found in male breast tissue, suggesting that PRL might promote the development of PG. Mieritz’s study found strong PRL receptor positivity in immunohistochemical staining of surgical specimens from 39 PG patients, indicating that prolactin may play a role in gynecomastia [12]. These receptors may be co-expressed with growth hormone and progesterone receptors, with potential cross-regulation. The activation of progesterone receptors is often associated with reduced androgen receptor expression, which may impair the androgen-mediated inhibition of breast tissue growth observed under normal hormonal homeostasis. Sansone et al. suggested that, apart from hypogonadism, hyperprolactinemia may induce male gynecomastia through a different pathway: elevated prolactin might promote breast tissue growth by overactivating progesterone receptors and reducing androgen receptors [36]. However, a 2020 study by Reinehr pointed out that prolactin concentrations were consistently within the normal range in both boys with gynecomastia (median 9.3 [IQR 7.0–16.2] ng/mL) and boys with pseudogynecomastia (median 10.3 [IQR 8.0–14.3] ng/mL), with no significant difference between the two groups [21].
Causes of hyperprolactinemia include pituitary adenomas, other sellar lesions that disrupt the hypothalamic–pituitary dopaminergic pathway (the so-called “stalk effect”), impaired PRL clearance due to kidney disease, and drug-induced hyperprolactinemia from various medications (especially antipsychotics) [2]. Trinchieri et al.’s review found that antipsychotic drugs can block pituitary dopamine D2 receptors, preventing the inhibition of prolactin secretion [32]. Specifically, risperidone and paliperidone, which are commonly used for the treatment of psychiatric disorders in adolescents, have been found to elevate prolactin levels and are associated with male gynecomastia. Han Jingjian et al. suggested that H2 antihistamines might cause excessive prolactin secretion by inhibiting pituitary dopamine receptors [23]. Chronic kidney disease can also lead to elevated prolactin levels due to reduced renal clearance and increased production.
Overall, prolactin (PRL) plays a significant role in pubertal gynecomastia (PG) by disrupting hormonal balance and enhancing breast tissue sensitivity. Elevated PRL levels can induce secondary hypogonadism by suppressing GnRH, LH, and FSH secretion, leading to reduced testosterone and impaired androgenic inhibition of breast growth. The presence of prolactin receptors in male breast tissue further highlights PRL’s direct role, potentially acting through cross-regulation with progesterone and growth hormone pathways. Drug-induced hyperprolactinemia, particularly from antipsychotics, is a significant contributor to PG, emphasizing PRL’s multifaceted impact on disease progression.
Ayrıca bazı makaleler prolaktinin jinoyla bir alakası olmadığınıda söylüyor;
(makaleleri kendim buldum bir yerden kopyala yapıştır yapmadım hatalar olabilir)
yani açıkası kanım dondu kanım buz gibi oldu detaylı konuşabiliriz sizin düşünceleriniz neler?
orgasm olduktan sonra artan dopamin seviyeleri bir anda azalır
dopamin prolaktini baskılayan birşey olduğu için
31 sonrası yarım saatden fazla prolaktin artışı gözlemleniyor
prolaktininde dolaylı yollardan jinekomastiye sebep olduğunu kanıtlayan bazı makalelerde bulunuyor
şunu baştan söylim bunlar haftada 1 31 gibi küçük sayılarda pek etki edeceğini sanmıyor sadece bir 31de artan prolaktinin çok bir etkisi olacağını düşünmüyorum
belirli ve kesin birşey söylememekle birlikte günde bir kaç kez veya daha fazla uzun süre 31 işlemini eylemiş ve bu etkilerde kalmış insanlar için geçerli olduğunu düşünüyorum
Effects of Prolactin (PRL) on Pubertal Gynecomastia
Prolactin (PRL) is a multifunctional hormone secreted by the anterior pituitary gland. While its role in lactation in females is well known, PRL also has significant endocrine effects in males. Prolactin inhibits the activity of Leydig cells in the testes, reducing testosterone secretion. It inhibits the secretion of gonadotropin-releasing hormone (GnRH) from the hypothalamic–pituitary–gonadal (HPG) axis, indirectly downregulating luteinizing hormone (LH) and follicle-stimulating hormone (FSH) production. Reduced LH and FSH levels lead to decreased testosterone and reduced spermatogenesis. Additionally, high PRL levels can directly affect the pituitary through a feedback mechanism, reducing GnRH, LH, and FSH release, thereby impairing male reproductive function. Elevated prolactin levels can lead to reduced libido, erectile dysfunction, mood swings, and depression. Thus, prolactin plays multiple roles in the male endocrine system, and its balance is crucial for maintaining reproductive and psychological health in men.A longitudinal study by Mieritz et al. in 2014, involving 501 Danish boys, including 31 with gynecomastia, reported elevated prolactin levels preceding the onset of gynecomastia in affected individuals, suggesting a potential contributory role of prolactin in its development [18]. Although prolactin itself is not considered a direct cause of PG, hyperprolactinemia might contribute to the development of gynecomastia by causing secondary hypogonadism. Studies by Trinchieri and Kilic suggested that prolactin inhibits GnRH secretion at the hypothalamic level, leading to secondary hypogonadism [32,41]. Prolactin receptors have also been found in male breast tissue, suggesting that PRL might promote the development of PG. Mieritz’s study found strong PRL receptor positivity in immunohistochemical staining of surgical specimens from 39 PG patients, indicating that prolactin may play a role in gynecomastia [12]. These receptors may be co-expressed with growth hormone and progesterone receptors, with potential cross-regulation. The activation of progesterone receptors is often associated with reduced androgen receptor expression, which may impair the androgen-mediated inhibition of breast tissue growth observed under normal hormonal homeostasis. Sansone et al. suggested that, apart from hypogonadism, hyperprolactinemia may induce male gynecomastia through a different pathway: elevated prolactin might promote breast tissue growth by overactivating progesterone receptors and reducing androgen receptors [36]. However, a 2020 study by Reinehr pointed out that prolactin concentrations were consistently within the normal range in both boys with gynecomastia (median 9.3 [IQR 7.0–16.2] ng/mL) and boys with pseudogynecomastia (median 10.3 [IQR 8.0–14.3] ng/mL), with no significant difference between the two groups [21].
Causes of hyperprolactinemia include pituitary adenomas, other sellar lesions that disrupt the hypothalamic–pituitary dopaminergic pathway (the so-called “stalk effect”), impaired PRL clearance due to kidney disease, and drug-induced hyperprolactinemia from various medications (especially antipsychotics) [2]. Trinchieri et al.’s review found that antipsychotic drugs can block pituitary dopamine D2 receptors, preventing the inhibition of prolactin secretion [32]. Specifically, risperidone and paliperidone, which are commonly used for the treatment of psychiatric disorders in adolescents, have been found to elevate prolactin levels and are associated with male gynecomastia. Han Jingjian et al. suggested that H2 antihistamines might cause excessive prolactin secretion by inhibiting pituitary dopamine receptors [23]. Chronic kidney disease can also lead to elevated prolactin levels due to reduced renal clearance and increased production.
Overall, prolactin (PRL) plays a significant role in pubertal gynecomastia (PG) by disrupting hormonal balance and enhancing breast tissue sensitivity. Elevated PRL levels can induce secondary hypogonadism by suppressing GnRH, LH, and FSH secretion, leading to reduced testosterone and impaired androgenic inhibition of breast growth. The presence of prolactin receptors in male breast tissue further highlights PRL’s direct role, potentially acting through cross-regulation with progesterone and growth hormone pathways. Drug-induced hyperprolactinemia, particularly from antipsychotics, is a significant contributor to PG, emphasizing PRL’s multifaceted impact on disease progression.
Ayrıca bazı makaleler prolaktinin jinoyla bir alakası olmadığınıda söylüyor;
(makaleleri kendim buldum bir yerden kopyala yapıştır yapmadım hatalar olabilir)
yani açıkası kanım dondu kanım buz gibi oldu detaylı konuşabiliriz sizin düşünceleriniz neler?
