Did God make Adam ‘half-female’?
T.L. from the United States writes:
I was in a debate with a friend of mine about the creation of gender. She stated that Adam could not have been created first because women have two X chromosomes. She goes on to address the X deactivation in women, saying that this only occurs because both X chromosomes are the same making it a “female” chromosome in both men and women (she also said that the master “switch” in males is them “switching” from the “default”). She goes on to say that men are “half female” and women are “fully female”, making them superior in that they bare life. She also said males are pretty much useless and that we can see this in other life (bees, the infrequency of male lions, “all female” lizards, etc). So my questions are, is the first X chromosome a “female” chromosome, even in men? And does this mean that God made Adam “half female”(as my friend puts it)?
CMI’s Shaun Doyle responds:
Thanks for writing in.
No, the X chromosome isn’t a ‘female’ chromosome. Everyone needs it. And no, males (including Adam) are not ‘half female’.
First, your friend is wrong on the science. The idea that female is the ‘default’ embryological condition is now known to be false.1 This idea was based on a few studies in the mid-20th century, and it was thought to be reinforced in the early 1990s by the discovery of the SRY gene, a gene on the Y chromosome which plays a crucial role in testis development. Because of this, female sexual development was thought to proceed as a ‘default’ in the absence of SRY.
However, subsequent research overturned this idea. For instance, the absence of SRY isn’t enough to build a functioning ovary; two X chromosomes are needed. Women with only one X chromosome almost always have ovary dysfunction, and the vast majority are infertile. And those (very) few that can conceive and carry a pregnancy to term are at much higher risk of complications both during and after pregnancy.2
Moreover, some genes, if their products are present in high enough concentrations, can stop male development even when SRY is present. For instance, the NROB1 gene on the short arm of the X chromosome codes for a protein named DAX1. This protein plays an important role in the development of the adrenals, hypothalamus, pituitary, and gonads. The protein is also involved in maintaining hormone production in these glands after they are formed.3 People who have XY chromosomes, but have a duplication of the NROB1 gene, produce enough DAX1 to inhibit the products of SRY. This stops male development completely and the person develops female characteristics.4 This is not merely the taking over of a default; this is an abnormality that overrides the normal development of an XY person.
Furthermore, ovaries and testes require ongoing maintenance throughout life. Researchers found that the gene FOXL2 (on the long arm of chromosome 3) suppresses SOX9 (a gene crucial for male development that is found on the long arm of chromosome 17), which prevents certain cells in the ovary from differentiating differently into ‘testis-like’ cells.5 Similarly, the DMRT1 gene (found on the end of chromosome 9) suppresses certain genes involved in ovarian development. 6 If both require ongoing maintenance, then there is no ‘default’ gonad, whether the testis or the ovary. Many of the tools used for building and maintaining both ovaries and testes are found in the genome outside the “sex” chromosomes.
Together, this shows that proper female development is an active process, and it isn’t simply the ‘default’ path an embryo takes. Instead, during development, a set of cells migrates to the outside of the embryo and hangs out on the allantois. At the appropriate time, they chain up and do a conga line, enter the embryo, find the developing gonads, enter them, and get to work. Before these cells arrive, there is no sexual differentiation. As Kim and Capel explain:
“Unlike most developing organs in the embryo that follow a single developmental track, the gonad forms with the potential to develop as one of two alternative organs, an ovary or a testis. For this reason, the gonad primordium is called ‘the bipotential gonad’.”7
Second, your friend is wrong on theology. Think about it: the all-powerful God couldn’t have created Adam first because of sex chromosomes? Since when is God limited by sex chromosomes in the gender he makes first?
At any rate, from a genetic standpoint, it seems much simpler to make Eve from Adam (as per Genesis 2). Why? All God would have to do to make Eve from Adam’s side is to erase the Y chromosomes in the cells taken from Adam’s body and duplicate the one X chromosome already present (Eve, the rib, and modern genetics). On the other hand, if God created Eve first, he would’ve had to form a Y chromosome de novo to make Adam from Eve. (This is like what God probably did in miraculously creating Jesus’ zygote—i.e. He took one of Mary’s eggs (and the haploid genome in it) and created a second haploid genome within the egg with a brand new Y chromosome.) Of course, neither of these ‘methods’ of creating one gender from the other is a problem for God, since he’s all-powerful.
Third, a woman’s two X chromosomes are not identical (with the possible exception of Eve), since one is inherited from each parent. And one of the pair is deactivated early in embryological development, because only one is needed for gene expression. Having both active would create an excess of many gene products and would lead to all sorts of problems. Nevertheless, as mentioned above and in the linked article, since single-X females are mostly infertile, the presence of a second X chromosome is important for normal female sexual development.
Fourth, comparing us to the rest of the animal kingdom is irrelevant, since sexual differentiation varies across animals. Some can even change their sex in response to environmental conditions (and of course be completely reproductively viable). For example, while some reptiles and fish can perform parthenogenesis (where the females produce young without fertilization from a male), it is generally uncommon and just a ‘fallback’ option in the absence or dearth of males (see ‘Asexual’ lizards and pioneer plants and The weird, wonderfully-designed sawfish). Nor can humans naturally perform parthenogenesis (Was the Virgin Birth non-miraculous?; and should Christians bother with atheists?). Birds’ sexual chromosomes are the opposite of humans (male birds are ZZ, females are ZW), and platypuses have a system that is unlike anything else.
So, men can’t be written off as ‘defective females’ either scientifically or theologically (Are women genetically superior to men?). Nor can women, obviously. We are both made in the image of God (Genesis 1:27) and are thus able to be co-heirs of the grace of life (1 Peter 3:7). Both sexes are equally valuable to God.
Creation Ministries International
References and notes
- The Genetics of sex determination: Rethinking concepts and theories, genderedinnovations.stanford.edu, accessed 26 March 2020. The following few paragraphs basically summarize the scientific material here. Return to text.
- Bondy, C., Turner Syndrome; in: Carrell, D. and Peterson, C. (eds.), Reproductive Endocrinology and Infertility: Integrating Modern Clinical and Laboratory Practice, Springer, New York, pp. 307–324, 2010. Return to text.
- NR0B1 gene, ghr.nlm.nih.gov/gene/NR0B1, March 2015. Return to text.
- Sekido, R. and Lovell-Badge, R., Sex determination and SRY: Down to a wink and a nudge? Trends in Genetics 25(1):19–29, 2009. Return to text.
- Uhlenhaut, N., Jakob, S., Anlag, K., Eisenberger, T., Sekido, R., Kress, J., Treier, A., Klugmann, C., Klasen, C., Holter, N., Riethmacher, D., Schütz, G., Cooney, A., Lovell-Badge, R., and Treier, M., Somatic sex reprogramming of adult ovaries to testes by FOXL2 ablation, Cell 139(6):1130–1142, 2009. Return to text.
- Herpin, A. and Schartl, M., Sex determination: switch and suppress, Current Biology 21(17):R656–R659, 2011. Return to text.
- Kim, Y. and Capel, B., Balancing the bipotential gonad between alternative organ fates: A new perspective on an old problem, Developmental Dynamics 235(9):2292–2300, 2006; p. 2292. Return to text.