As everyone keeps pointing out, Caster is referring to herself as a women with a genetic condition that causes extra testosterone. I think it’s incredibly unlikely she would risk highlighting the fact that she has male working testicals by undergoing a medical procedure to father children. And we have no evidence she even has functioning testicals! I have tried searching literature for examples /studies of people who have fathered children with her condition but found nothing. Just literature explaining why sperm viability would be extremely unlikely.
Slightly off the main topic, but I just wanted to correct this. Caster Semenya has 5-ARD or 5-alpha reductase deficiency. Her condition is that she is genetically XY (male) and has testes that make testosterone, but lacks the enzyme that converts testosterone into dihydrotestosterone. That is known and is explained in the CAS document linked earlier in the thread.
Pre-birth development of male genitalia is mostly driven by DHT, so people with 5-ARD have ambiguous or female-presenting genitalia at birth. However, puberty is mostly driven by testosterone, so people with 5-ARD go through a regular male puberty, with associated changes to body composition, shape etc.
Regarding ability to have children, people with 5-ARD have varying abilities to produce viable sperm and therefore to father children. They may have a lower sperm count and the sperm may have reduced motility; but fertility can be possible either through intra-uterine fertilization or IVF:
www.ncbi.nlm.nih.gov/pmc/articles/PMC4031759/
Reports of paternity through natural conception and intrauterine insemination reveal the degree of variability in spermatogenesis of affected males (47). Males found to have normal or near normal sperm concentrations and reasonable motility should first attempt intrauterine insemination (IUI). Most often, the semen analysis of affected males reveals severe oligoasthenoteratospermia, low semen volume, and failure of the semen to liquefy, precluding paternity through insemination. IVF/ICSI is the appropriate treatment for these patients (48). The first reported case of paternity through IUI involved a 36-year-old Dominican male homozygous for a thymidine-to-cytosine substitution in exon 5 of the 5α-reductase-2 gene. At birth he was noted to have ambiguous genitalia and bilaterally descended testicles. During puberty, he underwent deepening of the voice and penile enlargement to a stretched length of 3.5cm. Testicular volume, 25mL on the right and 20mL on the left, was normal and the prostate gland was not palpable. At age 34 he was treated with 25mg of topical DHT cream for 7 months, achieving a final penile length of 7.5cm. His wife was an unrelated healthy female with normal menstrual cycles and sequencing of her 5α-reductase-2 gene revealed no abnormalities. Semen analysis revealed low semen volumes but normal concentrations and motility. All specimens were noted to be extremely viscous with initial semen volumes ranging from 0.2–0.5mL, with concentrations ranging from 65 to 350 × 106mL, and motility ranges of 33–61%. Each semen sample was prepared in the standard fashion using a Percoll gradient and final pellet resuspension in 0.5mL of fresh medium.
After appropriate genetic counseling, the subject’s wife was monitored in a natural cycle and an intrauterine insemination was performed 25 hours following the LH surge. Conception occurred on the third attempt to achieve the first pregnancy and on the second attempt to achieve the second pregnancy. The initial pregnancy resulted in premature rupture of the membranes at 33 weeks followed by a cesarean section resulting in a healthy male with normal external genitalia. The second pregnancy resulted in healthy male and female dizygotic twins delivered via repeat cesarean section.
Paternity through IVF has also been reported in a 33-year-old Dominican male with the identical thymidine-to-cytosine substitution known to be common in the Dominican kindred. This patient’s testes did not descend until puberty. His stretched penile length was 5cm. He was noted to have testicular volumes of 14mL and 16mL of right testicle and left testicle, respectively. Initial sperm counts were unquantifiable owing to the high degree of semen viscosity and failure to liquefy. Semen volumes were 0.1mL, sperm density of 8.4×106 mL, and motility of less than 1%. His wife was an unrelated normally menstruating female without 5α-reductase-2 gene abnormalities. Following appropriate genetic counseling, she underwent luteal suppression and stimulation with 200 IU/d of recombinant FSH. Ovulation was triggered on the twelfth day with 5,000 IU hCG when two lead 17mm follicles were present. Four of nine mature oocytes were fertilized with intracytoplasmic sperm injection. Two eight-cell embryos were transferred on day 3, resulting in a twin gestation. Premature rupture of the membranes occurred at 36 weeks of gestation and a healthy male and female were delivered via cesarean section. These examples highlight both the variability in semen parameters in men with 5α-reductase-2 gene mutation as well as the need for individualization in choosing the appropriate treatment regimens.