Adrenal hyperplasia 1 (AH1): The most severe form of adrenal hyperplasia. It is a condition characterized by onset of profound adrenocortical insufficiency shortly after birth, hyperpigmentation reflecting increased production of pro-opiomelanocortin, elevated plasma renin activity as a consequence of reduced aldosterone synthesis, and male pseudohermaphroditism resulting from deficient fetal testicular testosterone synthesis. Affected individuals are phenotypic females irrespective of gonadal sex, and frequently die in infancy if mineralocorticoid and glucocorticoid replacement are not instituted. [MIM:201710]
One study has been conducted in athletes given D-aspartic acid supplementation at a dose of 3g daily for 28 days, and there was a failure to increase testosterone concentrations when measured at 28 days.  This study noted a statistically significant induction of serum D-aspartate oxidase (DAO) which degrades D-aspartate  to a near doubling;  this suggests a possible form of negative feedback, and aromatase (may also be induced by D-aspartic acid  ) was not thought to contribute due to estrogen being unchanged.