Biological human males do not have the anatomy needed for natural embryonic and fetal development.

Hypoxia, a state of reduced oxygen, may hinder embryonic and fetal development as well as decrease oxygen consumption in adults.

Further, several retrospective studies have noted an increased incidence of spina bifida occurring after low maternal intake of iron during embryonic and fetal development.

Remember, this is not normal embryonic and fetal development; not only is it a graft onto an adult body, it's being pushed to develop faster, in a less natural environment."

Hemoglobin variants are a part of the normal embryonic and fetal development, but may also be pathologic mutant forms of hemoglobin in a population, caused by variations in genetics.

Although most studies have interpreted hypoxia as causing some form of neuronal dysfunction or even subtle damage, it has been suggested that the physiological hypoxia that prevails in normal embryonic and fetal development, or pathological hypoxia or ischemia, may exert an effect by regulating or dysregulating genes involved in neurodevelopment.