Been studying folks with only one working CYP21A2 due to the resulting atypical adrenal function and I noticed that their dna also contains all the genetic variants associated with Alzheimer's (some are beneficial in this case). Inquiring about the family tree of the single CYP21A2 I have yet to have someone tell me of an ancestor that died of Alzheimer's. But the family members with two good CYP21A2 (and all of the other typical Alzheimer's genetics) are the ones that end up with Alzheimer's. And for good measure, when someone has 3 CYP21A2 nearly always they will get Alzheimer's. (they also end up with Hypercortisolism).
Subclinical Hypercortisolism has a long association with Alzheimer's. A deficient CYP21A2 and the decreased incidences of Alzheimer's is not talked about other than the fact that it isn't associated with Subclinical Hypercortisolism, but Subclinical Hypocortisolism instead.
All of the known indirect early preventative measures for Alzheimer's result in shifting from Subclinical Hypercortisolism towards Subclinical Hypocortisolism.
This was not my intended area of study, but the pattern is interesting and curious for your thoughts.
Been studying folks with only one working CYP21A2 due to the resulting atypical adrenal function and I noticed that their dna also contains all the genetic variants associated with Alzheimer's (some are beneficial in this case). Inquiring about the family tree of the single CYP21A2 I have yet to have someone tell me of an ancestor that died of Alzheimer's. But the family members with two good CYP21A2 (and all of the other typical Alzheimer's genetics) are the ones that end up with Alzheimer's. And for good measure, when someone has 3 CYP21A2 nearly always they will get Alzheimer's. (they also end up with Hypercortisolism).
Subclinical Hypercortisolism has a long association with Alzheimer's. A deficient CYP21A2 and the decreased incidences of Alzheimer's is not talked about other than the fact that it isn't associated with Subclinical Hypercortisolism, but Subclinical Hypocortisolism instead.
All of the known indirect early preventative measures for Alzheimer's result in shifting from Subclinical Hypercortisolism towards Subclinical Hypocortisolism.
This was not my intended area of study, but the pattern is interesting and curious for your thoughts.