♌Toobusy_Hustlin♌ @DemarcisG - Twitter Profile

about 2 months ago

Penis size is set before birth by maternal health, metabolism, and hormone exposure (including birth control) Penis size is largely determined during fetal development through the maternal–placental endocrine system. Masculinization depends on DHT acting locally in genital tissue. Fetal circulating DHT is often very low, which shows that the androgenic signal is generated inside tissues from precursors rather than delivered directly through blood. A major part of this signal comes from the backdoor pathway. Placental progesterone is converted across fetal tissues into intermediates such as androsterone, which are then converted locally into DHT in target organs. This pathway bypasses testosterone as an obligatory step. The placenta provides a continuous supply of progesterone derived from maternal cholesterol, so androgen production depends on maternal substrate availability and its processing across fetal liver, adrenal glands, and peripheral tissues. The system is distributed and depends on coordinated enzymatic activity rather than a single endocrine source. Conversion efficiency depends on metabolic conditions. Thyroid function, mitochondrial activity, oxygen availability, and stress signaling determine whether progesterone is efficiently converted into androgenic intermediates or diverted toward other pathways. Maternal endocrine state directly modifies these conditions. Hormonal contraceptives suppress endogenous progesterone production, alter estrogen signaling, and modify stress-axis regulation, replacing a cyclical endocrine pattern with a static pharmacological one. This changes substrate dynamics, timing, and pathway organization during fetal development. Synthetic progestins are not equivalent to physiological progesterone. They activate receptors but do not function as interchangeable substrates within steroidogenesis, so downstream androgen and neurosteroid pathways are altered. Puberty mainly amplifies androgen exposure and completes growth. The structural baseline is established earlier through progesterone availability, metabolic capacity, enzyme expression, and local DHT production shaped by the maternal environment.