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its all down to genetics
Further information on the FOX gene:

so the question is: 

Does the introduction of Fox gene laden bovine ovary pills , trigger the Changes that some see on Bovine ovary pills? 
does the harvesting of the bovine ovaries at certain times , rely on the amount of Fox at time of harvest? does this indicate why it works for some, and not for others? 


FOXL2, a winged-helix/forkhead domain transcription factor, is a key gene involved in the differentiation and biological functions of the ovary. In a recent transcriptomic analysis, we found that [i]FOXL2[/i] expression in bovine caruncular endometrium was different from that in intercaruncular endometrium. In order to gain new insights into FOXL2 in this tissue, we determined the expression of this transcription factor during the estrous cycle and the establishment of pregnancy in cattle. The endometrial expression of [i]FOXL2[/i] did not vary during maternal recognition of pregnancy (Days 16–20). Using an in vivo bovine model and primary cell cultures, we showed that [i]FOXL2[/i] was not an interferon-tau target gene. Both [i]FOXL2[/i] transcript and protein were expressed from Day 5 to Day 20 of the estrous cycle, and their levels showed a significant increase during the luteolytic phase. A 2-day progesterone supplementation in heifers led to a clear down-regulation of FOXL2 protein levels, suggesting the negative impact of progesterone on [i]FOXL2[/i] expression. Immunohistochemistry data revealed the localization of FOXL2 in endometrial stromal and glandular cells. FOXL2 subcellular distribution was shown to be nuclear in endometrial samples collected during the luteolytic period, while it was not detected in nuclei during the luteal phase and at implantation. Collectively, our findings provide the first evidence that FOXL2 is involved in the regulation of endometrial tissue physiology.
FOXL2 activates P450 aromatase gene transcription: towards a better characterization of the early steps of mammalian ovarian development


Is this the reason that bovine ovaries aromatize the androgens into estrogen?
so, to link up some theorhetical info: ( this was all highlighted and listed in my "interesting article"thread: 
Breast Nexum- Interesting Article Link

ovaries to testes article:

"Slightly more formally, this research shows that the ovary has to maintain constant suppression of the key testis development gene Sox9 by Foxl2; if not ovarian granulosa and theca cells change to become testicular Sertoli and Leydig cells, respectively."

"Uhlenhaut developed a strain of genetically engineered mice, whose copies of FOXL2 could be deleted with the drug tamoxifen. When she did this, she found that the females’ ovaries turned into testes within just three weeks. The change was a thorough one; the altered organs were testes right down to the structure of their cells and their portfolio of active genes. They developed testosterone-secreting Leydig cells, which pumped out as much of the hormone as their counterparts in XY mice. They only fell short of actually producing sperm. ..

FOXL2 also has a partner-in-repression – the oestrogen receptor, a docking molecule for the hormone oestrogen. The two proteins interact with one another and they cooperate to block Sox9.

There have been hints from many species that FOXL2 plays an important role in determining sex.

Also, I have found that the bovine ovaries do contain the FoxL2 gene, dependent on cycle of estrous, there gene expression is greater at certain times.
My thoughts on it all:

So, the question is: "if" it truly does aromatize the testosterone into estrogen via the introduction of FOXL2 at a dose-dependent range. Should one decrease the Testosterone initially to near female range, in order for the FoxL2 gene to "storm the castle" and take hold to work? Or, does actual levels of T not really matter?  I would think that if you can lower the range of testosterone, you might have a better chance of the FoxL2 gene found in the bovine ovary to work. Perhaps if your body gets used to the FoxL2/aromatization, you can eventually cut back on anti androgens and let whatever T would be left to produce, to aromatize into the E, that would be necessary. There may be a chance that the adrenal glands that contain the FoxL2, would also kick in.  I think, if the levels of T are left normal, there is too much of a chance for the male-level T to overpower the introduction of the FoxL2 gene, and it be just a waste of time to consume the FoxL2 laden bovine ovary supplement. The other question is : does the FoxL2 gene survive the dessication into the powder form, even though it is freeze-dried and ground?

Essentially in theory, if you continue to introduce the FoxL2, it should convert the testes into ovaries, since the deletion of FoxL2 turned ovaries into testes.Perhaps this is why there is a "permanent" change for those whom claim after 6 months of Transfemme. even though there is lack of evidence other than anecdotal. There is a possible science behind it, it one thinks about it. I am sure, if you could find and extract the FoxL2 gene specifically, turn it into a pharma-grade pill.. you could turn your own testes into ovaries, then it would just be needed to be stitched up inside where ovaries are supposed to go. 

The other thought that occurred to me , is that most who are on Bovine ovaries, state that their testes have shrunk, which also leads me to believe that they are turned into ovaries, since ovaries are considerably smaller than testes

Mind you, these are all speculations. Real-time laboratory scientific study would need to be performed. I am neither scientist, nor have the sufficient lab to perform  proofs on theory. 

Want to know more? The following comes from ISNA’s Medical Advisory Board member Dr. Charmian Quigley:
SRY, discovered in 1989, is a small gene located at the tip of the short arm of the Y chromosome. So what does it do? Actually, like all genes, it does nothing except to act as a blueprint for a protein. In this case, the protein of the same name does funky things to DNA, like bending it and unwinding the 2 strands, so that other proteins can get in and attach themselves to other genes that are then turned on. So how did this gene get its reputation (and its name) as the “sex determining” gene?
As is pretty common in the world of genetics, this was because of some errant mice. Researchers in England took a laboratory-made copy of this gene and inserted it artificially into a female (XX) mouse embryo at a very early stage of development. The mouse was “converted” from female to male, so the gene must have been responsible – right? Well, maybe not. A few years later, a similar gene was found on human chromosome 17. When the important part of this gene was inserted into a female mouse embryo, the same thing happened. Voila! A male.
So now we have 2 genes that can turn a female into a male, and one of them is not located on the Y chromosome! How can that be? It turns out that SRY is probably just a facilitator that allows a more critical gene (or genes) to function, by blocking the action of another opposing factor. Can the magic of genetics do the opposite – turn a male into a female? Indeed it can. A gene on the X chromosome (the chromosome one typically associates with “femaleness”) called DAX1 when present in double copy in a male (XY) mouse, turns it into a female.
So now we have genes on the Y that can turn females with XX chromosomes into males and genes on the X that can turn males with XY chromosomes into females… wow! Maleness and femaleness are NOT determined by having an X or a Y, since switching a couple of genes around can turn things upside down.

In fact, there’s a whole lot more to maleness and femaleness than X or Y chromosomes. About 1 in 20,000 men has no Y chromosome, instead having 2 Xs. This means that in the United States there are about 7,500 men without a Y chromosome. The equivalent situation - females who have XY instead of XX chromosomes - can occur for a variety of reasons and overall is similar in frequency.

Have to find a way to turn on the DAX1 gene...

The NR0B1 gene provides instructions for making a protein called DAX1. This protein plays an important role in the development and function of several hormone-producing (endocrine) tissues in the body. These tissues include the small glands located on top of each kidney (the adrenal glands), two hormone-secreting glands in the brain (the hypothalamus and pituitary), and the gonads (ovaries in females and testes in males). Before birth, the DAX1 protein helps regulate genes that direct the formation of these tissues. DAX1 also helps regulate hormone production in endocrine tissues after they have been formed.

Since it (DAX1), is found both in ovaries AND testes, I do not think it is specifically DAX1 that would be the "switch" to flipping the genes from male to female. It is also found on the adrenal glands.. so that furthers my thoughts  the FOXL2 gene is more in control than what I thought the DAX1 would do. 

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