Nature Gives Choice
By Sophia Siedlberg
Salmacis Software, Sussex
Two keywords spring to mind; "Relativism" and "Reductionism" - they seem to be bandied around like insults between the scientific community and its critics. So where am I going to stand when I present this paper, a fundamental heresy embodied within a perfectly rational question. My difficult question is not based on some "hunch" or "subjective big idea" nor is it based on hours and hours of grinding work in a laboratory. It's based on the fact that my own work, independently writing freeware for analysing the sequences published by the Human Genome Project, suddenly started to reveal the questions I always wanted to ask.
There is no hypothesis, no grand theory. Just hours and hours of writing software, comparing it with the output of other packages that work in the same field and being drawn into some anomalous world where the As, Ts, Cs, and Gs, that flash across my computer screen start saying things about themselves that seem to have been missed. Possibly by some form of dogma, or possibly by the need on the part of the Human Genome Project to finish the task of sequencing before actually looking at the sequences in a context more detailed than restriction mapping or locating ORFS.
I will admit to the fact that this paper does represent some of my own vested interests, but it also represents a broader question about determinism and how data is actually read. This is the interesting part of the heretical question, how is data actually interpreted?
I have never really looked at statistical analysis without having a degree of scepticism, I suspect that's because of the many misuses of the methodology in the media and politics. But then again even in the most simplistic model, two opposing researchers will have a subtle bias to their respective opinions. It's not a question of subjective and objective interpretation. It's a question of the inevitable fact that human science is still read by human eyes and subject to human nature. I have introduced my heresy with this line of reasoning simply because I am trying to be objective with myself, to question myself, and hopefully to present my paper with some degree of confidence about the awkward questions it will be asking.
I suspect that the recent debates I have got into about chromosomes X and Y have brought me to realise that those people who claim that X and Y exclusively define sex in the human being are plainly wrong! X and X does not always mean "female" and X and Y does not always mean "male". It's down to two basic mechanisms, the expression of genes such as SRY or their equivalent sequences and the genes that control cell differentiation, metabolism and so on. SRY-like sequences appear on the X chromosome and are sometimes missing or not present in Y chromosomes. This is due to processes such as Translocation and Deletion. And that is just the tip of the iceberg. I mention this not because I am subjectively suspicious of the whole XY diktat, but genuinely because the evidence does not stack up with the simplistic claim that the external morphology of any chromosome will always result in the same outcome. It's the arrangement of the bases and the shapes of individual proteins that seem to be more important.
The bottom line of my argumentative hypothesis is simple. The evidence of X and Y does not support exclusive sex determination, just approximation to one of two basic forms. Gender identity, complete anatomical sex, sexual orientation, are plainly not the sole preserve of these two chromosomes. What about mitochondrial DNA? The theoretical genesis of two sexes lies within that somewhere. How much of the un-translated or "Junk" DNA (introns) in Y carries bits of mtDNA like sequences? I bet there are a few sites with suspect non nuclear DNA lurking neatly between the currently defined exons.
I will be honest, I will be making what appear to be rather intolerant remarks about some in the scientific community who make an issue of re-enforcing the paradigm, mainly because they are in a position to bring about policies in medical practice. Also because they seem to have a "transphobic" agenda. so bear with me if you think there are those who I appear to sneer at and those who I appear to praise.
The Abuse of Genetic Theory
It isn't a "goodies versus baddies" situation. It's a fundamental question about the way data is used or abused and the consequences of it. Here's one example of the stupidity of "Political Geneticists" (They tend not to work in labs or analyse the fundamental nuts and bolts data when not in the lab, rather they look up a chromosome map, find a few regions that may support some populist hypothesis, do some statistical "study" of various patient groups and then boldly scream in the media about some photogenic cause celebre, or not so photogenic supremacist dogma (Anyone read the Bell Curve?)
One example takes the form of one Dr. Emily Hancock who threw her authoritative weight into the debate about someone called "John" who was wrongly feminised as a young boy, and brought up as a girl. The whole boring Nature versus Nurture debate took its predictably nauseating twists and turns, resulting in the disgruntled John being cited as an example of the "Power of the XY chromosome" (Basically he was justifiably angry about being forced to be the wrong sex, as he self-identifies as male) Dr. Emily Hancock came out with her rubbish in the Guardian:(1)
And then it gets even funnier
I don't subscribe to either Nature or Nurture theories. I subscribe to a more scientific approach. Let us look at the great authority vested in Dr Emily Hancock. According to her, there is a new chromosome, the combined XY chromosome, What miracle of translocation is this? We have a pair of chromosomes, I know bits of genetic material often fly around and then reform during crossover and linkage, but I have yet to see this huge blot like single chromosome called XY appear. And this gene which the XY chromosome decides to turn into, must mean that it reduces itself to a few thousand bases in length. Well while I suggest she goes back to school and reads Strickbergers 2nd Edition Genetics (O level biology) I must also point out that her ignorance shows itself further when she claims that genes or "The gene" (I assume SRY) somehow makes little boys into macho men.
As for altering Genetic identity viruses do that with great ease, turning cells into virus factories. Does she really mean "Gender identity" I am sorry but when the ignorant rant about social issues and bring genetics into it, I worry! OK I am guilty of that - writing for a minority publication that has a lot of social comment to be making.
But my real annoyance is aimed at the misuse of science to further a political cause. Especially when that political cause is designed to introduce yet more gender/sex repression.
To give a more disturbing example, what follows is the twittering of someone who had some involvement in the case where Lancashire Health Authority were operating blanket bans on gender reassignment. .Now my problem with some academics is the fact that they honestly don't know their subject. Face it I have spent most of my academic life either studying, or working as a lowly lab technician. I think it's this issue that makes me furious with high ranking academics like Dr Hancock. Here's the other example, where a "Professor of medical ethics" makes the following remark in a letter to a newspaper when Lancashire H.A. were told not to operate blanket bans on gender reassignment.
This ignorant rubbish was provided courtesy of Dr J Stuart Horner, Professor in Medical Ethics, University of Central Lancashire. The fact is that Gender is not determined at conception. But I may not say this because he is a Professor, and I a lowly ex lab technician, who studied maths, and who now writes bio informatics software. I can spend all my life writing critiques of these eugenically challenged people, but it will change little. What needs to be challenged is the way such academics make a point of stating things without empirical evidence.
So what is my argument about questioning all these ideas that p23 XX =girl and XY=boy. It's really very simple, there is a whole wealth of complexity on the molecular level, this certainly means that variability occurs, you don't always get living barbie dolls and action men on the whim of an expressed gene. What about Androgen Insensitivity syndrome (The "XY" female) and then what about the "XX" male? And then what about male to female GID? (As the debate centres around the Y chromosome) and the female to male GID when there is no SRY!
I am bothered about the abuse of data. I will have to admit that at times I do it myself. I read a sequence file, and then before I sit back and think, I am looking for bits and pieces in the page of As, Ts, Gs and Cs for patterns, Orfs (Open reading frames), restriction sites, "nonets" (Nonomer sequences for tripeptides) and inserted plasmids to support some pet theory. But I have to sit back and say to myself that I must be objective and find what IS there rather than what I want to see. This is why I invest large amounts of time obtaining or writing sequence analysis software.
The Real World.
I am not a great authority and I am certainly not recognised as such, but I feel that I have a right to speak when those who claim to have authority talk pure bullshit! That is why the XY-XX debate so deeply upsets me. I cannot support or even agree with any misuse of scientific data. I have heard so much abuse of it every time I look up from my sequences and see people saying "You are......" and "It's in the genes that you must........" when I am sitting there with the actual text in my hands and the means to read it. Here is an example of how the paradigm seems to work with those in the real world.
Lets take a recent Gendys meeting, when Diana Aitchison said "these people find it difficult to justify their female identity when they have X and Y chromosomes" (Referring to male to female transsexuals) It's someone like her, who sees the consequences of these paradigms and dogmas each and every day that makes me unhappy. Her life and the lives of all the people she deals with are only made more difficult by the dogma. Lets face it I would find it next to impossible to run a helpline for partners of transsexuals with all that rubbish about biological and nurtured determinism flying around. She has to plough through all the pseudoscience she has been fed by those in "authority", those like Dr. Emily Hancock. before she can even begin to deal with the issues that matter to her and her clients in the real world.
And what do I tell someone like Diana about SRY? Well that isn't easy, all I can say is that SRY is implicated in the formation of masculinised gonads. A protein called TDF is I believe coded from it. Then I would have to start explaining how in many species SRY takes many different forms - some forms have only 300 or so base pairs. I cannot simplify it. Well when SRY type sequences are expressed as genes, on either X or Y chromosomes, they have a masculinising effect on the forming reproductive tract, they do not control behaviour, They do not determine anything other than some parts of outward anatomical sex and that is that.
I tend to be very argumentative about it all. For example, when I recently tried to develop a mysterious concept called the "In Context Polygenic Array" I was practically made into a smirking target. I dutifully post my ideas onto the bio-informatics billboards, people show an interest, one look at the scripting language and modified terminology and then silence, deadly silence. A few were so quick to dismiss the whole thing as "unscientific" in their own minds, even when the documents were submitted, I had the feeling that they were getting picky about the terminology or methods I have employed. Well fine - but they seem to miss the fact that I am at great pains to point out that the whole idea was a little blue sky, and that a lot of work needs to be done before I can publicly release any software. Was it the unorthodoxy of the approach, or was it the fact that they really didn't like the idea - that somewhere between the lines I was challenging single gene dogma. Take a term, "Alignment". In this case I was referring to the alignment of bases in looped RNA. They obviously felt I had misunderstood the common use of this term. I hadn't - I could only use that term to describe my perceived picture. So I simply continue distributing freeware until someone wakes up, grows up and listens. It's like that with X and Y. To deny the effect of Chromosome Y is heresy, but in the case of Androgen insensitivity syndrome, Y has little or no effect. SRY is not expressed, Why?
So what would the ICPA (In Context Polygenic Array element of some of my software) be saying to anyone who eventually finds it embedded in a sequence analysis package. Well, as far as sex determination goes, there are possibly a large number of genes that, if expressed in a certain way, would make SRY meaningless, or even cause it not to express at all. Bad news for the scientific politic. For one this would legitimise transsexuals on a genetic level because they are genetically their adopted sex, (In the contextualised sense) and the XY, XX complement is the error, not the many non X and Y based genes that would be involved. Face it you can have a "Genetic female" with X and Y for the 23rd pair, and you may also have a "Genetic male" with an X and X configuration.
The Complexity of Sex Determining Genetics.
So where do I go from here, in describing the true complexity of sex determining genetics. It is so great on a molecular level that you can't even apply the most rational sets of terms and labels to define a given phenotype. It's like touring the genome, giving a number of examples where genes work in context with each other. I am not going to discuss in any great depth the "Classic" examples such as C.A.H. simply because the information is often easy to find. I want to discuss those "grey area" situations where gender identity contradicts so called "Genetic sex".
So here is the real picture, the one that says "No XX and XY are not the final word". I want this presentation to be open for a change. I will be arguing for example why the famous "H-Y chromosomal protein" debunking seems so stupid. Or why is it that when people talk about "SRY" they fail to mention autosomal sequences like "SOX9"? Sadly the lay-reader will say "?" So I want to try primarily to introduce each known "gene" I am curious about involved in sex "determination" as it is. As best I can and as simply as possible.
So what is SRY?
SRY is the gene that encodes for gonad differentiation, by producing a protein called TDF. When expressed the genesis of masculinisation occurs. As we all know every fetus is physically asexual, but would, without sex determining processes being active, would be born essentially female. SRY is the gene that "imposes" the masculine over the feminine if you like. This is why in popular imagination it has been seen as the holy grail of sexual dimorphism. However I hope to show that while this tends to be true to a greater extent it is not the whole story.
The Hot and Cold threat to XX or XY
I always think about the irony of the one great threat to the XX or XY model. It comes in the form of a gene that sits at one end of chromosome 9 in humans. I call it the "Damart gene" to remember its designation (DMRT1). If you want to control the temperature of your private parts invest in Damart, if you want to control the formation of your private parts, using heat, invest in DMRT1. Now what makes this gene interesting is the fact that it is mildly AT rich. Which is a paradox because GC rich genes tend to be stable at higher temperatures, and as such are more heat sensitive. (But consider that enzymes are involved which work best in specific temperature ranges) More on this later. The issue here is how DMRT and its equivalents seem to work.
Let's get back to basics - DMRT is basically the chicken version of SRY, except that it needs two copies to be active in normal conditions. This is why. Female chickens have a W and a Z chromosome, while males have two Z chromosomes. Now this raises a fascinating question in my mind. DMRT appears in chromosome 9, in the same relative position as SRY on chromosome Y. Its expression, unlike SRY is also heat sensitive (Baseline stability of DNA and interacting enzyme within the lower temperature ranges actually involved). Mammals incubate their young inside their bodies. Why do mammals do that ? To ensure an exact temperature during fetal development! Why is that so important? Perhaps our friend on top of chromosome 9 can provide an answer, does it need to be expressed for SRY to be active? If so then SRY is not the king of the roost. It is just made to look that way because mammalian incubation is so well controlled.
There is an underlying argument here, pitting two biological models against each other. Thermal Sex Determination (TSD) and Genetic sex Determination (GSD). As GSD is a process evolved from TSD we would need to find XY females with deletions or mutations in the region of chromosome 9 to see if there is a phenotype that expresses as this model predicts. (This would of course require a study).
It's strange willow-the-wisp situations like this that constantly challenge the concrete image of the sex linked chromosomes, via polygenic entities lurking in the autosomes.
A Metabolic Path to enlightenment
There are numerous examples of autosomal genes that produce a protein or enzyme necessary for SRY to make a boy. You have probably all heard of an enzyme called 5 alpha reductase that makes men go bald. Missense mutations are reported to lie at the root of Five alpha reductase deficiencies. Briefly Five alpha reductase converts one mild form of androgenic steroid (Testosterone) into a more potent form (Dihydrotestosterone). This is essential for masculine sex differentiation. When deficient the resulting birth is often that of either a genital intersex or an apparent girl. Now a number of genes that produce enzymes or proteins that are involved in sex differentiation via metabolic pathways and so on are known to mutate in this way. I will for the sake of simplicity concentrate on "5 alpha reductase deficient A.I.S." Missense mutations occur when a single base in a codon (3 base triplet) does not code for the correct amino acid in a polypeptide chain. I can give an example where single bases in codons were missense mutations in a given an exon (active sequence). What would otherwise be categorised as a "male" was in fact categorised as an intersex. A transition at the second nucleotide of codon 85 in exon 1 (GGC --> GAC), substituting glycine for aspartic acid (G85D). had occurred. (Vilchis F, Mendez JP, Canto P, Lieberman E, Chavez B. 2000). Now this is just one amino acid's difference from the "Norm". One base on the nucleotide and one resulting amino acid in the enzyme rendering it non expressive. There are tens of thousands of bases in some genes, the alteration of one results in such a drastic variation. It certainly puts the Y chromosome on shaky ground as a reference point for "maleness" More interesting is the fact that the gene that was involved (SRD5A2) occurs on chromosome (pair) 2, an autosome, not a sex linked chromosome.
Now most clinicians would take a very confused view of this. As Dr Milton Diamond loves to tell us, feminising surgeries are carried out on such infants and in some cases they self identify as male. Meaning that the XY pairing identifies a male gender identity. What he seldom points out is that it is not always so, a few cases who were surgically masculinised as infants hated being defined as male - with a rabid ferocity I hasten to add. Moreover, when, after masculinising surgery as infants, they sought surgery to be female, they were told "You can't be female you have a "Y" chromosome.
The argument of course falls flat when you consider that the self same clinicians tell those they feminised as infants that they are female because they were brought up as females. It seems that the Nature-Nurture debate is cynically used and re-defined to impose an unwanted identity on someone when it suits the clinicians.
It seems that when a male identifying "5 alpha patient" objects to being feminised as a child, that is considered to be a valid complaint according to Dr Milton Diamond. If the same type of patient says they objected to being masculinised as a child and identifies as female then they are considered as essentially (Genetically) male and thus "male (to female) transsexual" (In the pejorative sense).
I have my personal view on this. On a molecular level I see these missense codons as interesting entities, and in many cases they are reported as being GC rich. Considering that the sex reversing elements in DMRT1 are also GC rich, it does cause me to ask the question: Were these codons being "thermally mutated" somewhere in the dim and distant past? I also wonder why there seems to be this idea that gender identity is often identified with the Y chromosome, when the only certain and well documented sex determining gene codes for the differentiation of gonads, via T.D.F. being coded from SRY. There is no evidence of a heterosexual six pack macho gene anywhere.
It's time to bring in another interesting example of a gene people don't like. Who here remembers that stuff about "HY chromosomal protein" being found present in female to male transsexuals, and men, and lacking in male to females and women. Very often you will see "Ah but it was debunked" and "Ah but it's been disproved now" Well I have yet to hear why this was so. I know why some of the protagonists in that particular debate are present and I want answers. Essentially there are two known forms, on the Y chromosome. A gene called DFRY has been sequenced, yet still requires assembly in the next stage of the human genome project. A number of exons have been sequenced and evidence suggests that the masculinising variant contains codons that result in cystiene based disulfide bonds altering the shape of the peptide chains.
The female variant (On X) encodes for another amino acid in the chains. (Pierce RA, Field ED, den Haan JM, Caldwell JA, White FM, Marto JA, Wang W, Frost LM, Blokland E, Reinhardus C, Shabanowitz J, Hunt DF, Goulmy E, Engelhard VH. 1999) So someone has been sequencing DFRY and come up with something I have often thought about.
It has always interested me. I have been working on a piece of software designed to find cystiene based folding in certain types of peptide sequences. And when it comes to cell differentiation and and so on, this sparks my personal interest. It's a pet problem with me, to do with Cystiene (Disulfide bonds) And something I dare not mention to palmists. HY antigens fascinate me, they are encoded on both X and Y and for a time there was the idea going round that female to male transsexuals had these antigens and male to female transsexuals did not.
I don't know why this was debunked, and information is very hard to obtain about either the original studies or the "Stony Brook" debunking. (Conducted it would seem by Dr John Money and Professor Richard Greene, two people I love to disagree with!). My interest lies with the polypeptides themselves here, and the presence of Cystiene bonded with disulfides. My own theoretical model that would need testing, is that cell differentiation is partly regulated by peptides folded with disulphide bonds into specific patterns, the emerging evidence from the HGP suggests HY forms these patterns. I will discuss more on that in a future article, as my own model does involve HY antigens. And to perfectly frank, the debunking of now emerging genetic data which may support the original theory (Bourgeois M, Benezech M 1981) And through a mechanism I myself can identify in my own computer modelling. It makes me a little resentful when all I am given (as an intersex patient) in its place is palmistry, left handedness and the pathological psychosexual theorising, while this is a "Y chromosome based sequence". It poses the question all too horrible for the Six pack Y brigade, that being the possibility of a "Gender identity gene" while existing (Good news for the six packers) It can and does fail to express. (So horrendous for the six packers because it means that the sacred Y can be questioned even then.)
The Gay Gene
This is perhaps a little diversion from the core argument but worth mentioning. It demonstrates something profound about the use of "Single gene" definitions to describe "Atypical" sexual behaviour. Now the "Gene" Xq28 is defined by a locus rather than its gene I.D. (Unless the number sarcastically refers to a certain clause). I suspect that this is because it has not been sequenced and assembled. The "Gay" gene (that people seem so desperate to find in order to eradicate Gays I suppose) is often presented as being on the X chromosome. (Hence the "Xq") Now here we can see that there are the seeds of identifying another roost ruling gene of popular imagination. The claim that is sex linked seems to be that the Mendelian Astrologists love to point out that "Inheritance" of "Gayness" in "Males" is passed down maternally. Notice how the terms work here "Gayness and Males" with that distinct pathologising tone. Why? Well the implication is, as with psychotherapy, that the mother's influence is to blame, the gay gene is a "toxic woman gene affecting the manhood of these boys". Now we don't see a "lesbian" gene oddly enough, yet alone a few hundred bases of a contig that just may be a gene.
So we hear "Where there appears to be a family history of male homosexuality, there is a region, (Xq28 I assume) a 'something' (A visible fragment on the track) that shows a band (electrophoretic gel trace shows a few possible correlations) and is passed on by the mother. It's a classic (Irrefutable!) example of sex linked inheritance" Instead of "This component of human behaviour may be partly linked to the sex linked chromosomes" So why is this evidence so compelling? So there's a fragment that sometimes correlates with male homosexuality. Well - is there a fragment that appears with female lesbianism? Like for example, did the Victorian Laws only pathologise male homosexuals, and is not the differing ages of consent between Gays and Lesbians dictated by anatomical sex? Lesbians are given the same age as heterosexual women, gay men are not. It smacks of male pathologisation I am afraid.(2)
The rich mosaic
We all read of mosaicism, ever cited ever quoted Klinefelters being the big one here, where there is an extra X chromosome. Again this puzzles me. Why do they always say "Klinefelters men"? as if desperate to define such as exclusively male because good old SRY and its parent chromosome holds the key to the universe.(3) Now I am not saying that all these intersex conditions are wrongly defined as male, they are arbitrarily defined as male. Look at it this way. An XXX mosaic is a "Metafemale" and XYY is a "Dangerous psychopath" This lurks in the same arena as the gay gene. Then there is Turners syndrome. Called a mosaic but in fact a "ringed chromosome" situation (XO) where cell lines tend to differentiate as if SRY is there and then as if it isn't. I remember a study (Skuse 1997) that defined these women as men simply because they didn't have a "sensitivity gene".
But then what does "O" describe? Sometimes Y? Sometimes a bit of X? Surely a nice little sensitivity gene can sneak in! Well there were no sequences here, no loci, no not even an exon or a codon. In fact not even a single base of biochemical evidence. Just a questionnaire handed out to parents asking about the "boyish behaviour of their Turners syndrome daughters". Behold they were men! And all men are bad because they have no sensitivity gene either. (X linked reverse socio pathologisation I sarcastically call it). On the subject of mosaics, there is a region on the SRY gene that acts as its Achilles' heel. Known as the "5' non-high mobility group box region" when this region is mutated, there are a wide variety of phenotypes - and in many mosaic cases, this area appears to be implicated.
So where do we go from here?
Having given numerous examples of situations where the "XY Chromosome" is not quite all it appears to be, I have to look at its real meaning.
Admittedly it does seem to have the main say in who becomes male and who does not in a physical sense, but very often it is dependent on its context with other genes. in some cases this could involve thousands of genes, in other cases it could be as a result of one single "letter" (Base) spelling one "word" (Codon) wrongly. Strictly speaking there is no such thing as a genetic female or genetic male.
Identity and biology.
This is, an often a contentious, area that has a lot of theory flying around, but very little of it is lab based. There is one exception that often crops up in the form of Professor D F Swaab, who seems to produce an ever increasing volume of lab based material that suggests a more realistic model of a dynamic process. His work interests me because he uses a language and terminology I understand. I don't understand talk of "single genes and behaviour traits" nor do I really understand behavioural models when they are presented in a way as to define all human behaviour in terms of social conditioning.
Some who have read some of my more "poetic" works, specifically a poem called "The Litany of Apoptosis" will realise just how interesting Professor Swaab's latest findings on the Bed nuclei of the Stria Terminalis would be to me. The process by which the differentiation of size of this structure (Implicated in gender identity in 1995) was often brought into question (Swaab 1995). Well it is consistent with being "inborn" and not as an artefact of medication given to transsexuals. Selective cell death (Apoptosis) seems to occur, during development of a specific region of the BST, the rate being higher in a "Female" BST than in a "Male" BST. Gonadal androgens appear to suppress the process during early development (Chung WC, Swaab DF, De Vries GJ 2000). I suspect that a curious approach to these findings would be to see how many people who are 5 Alpha deficient, for example, would identify as female rather than male. Given that a developing fetus and a baby in the first few weeks of life who was unable to metabolise the more potent androgens would have the process of apoptosis in this region result in a smaller BST. Now this particular bit of data was deduced from studying rat brains. (I know that would distressing to some) but it does quite often apply to humans. I do have a slight problem with the use of rats. Basically because there are differences between rats and humans, but such a differentiation mechanism is often quite universal.
The simplistic image of this whole debate puts Professor D.F. Swaab in the role of the goodie. The interesting thing is, Swaab has released a whole goldmine on lab based data, covering many areas within this debate, yet only the BST study managed to capture the attention of the media.
The evidence that XY, XX paradigms don't add up constantly seems to stack up. What seems to emerge is a picture that tells us all that "Biological sex" is a fluid thing. While certain shopping chains make great pains to point out that they serve real women, standing in fields shouting "I Am Normal" as if perfection lies in "pure womanhood", you can turn the whole argument upside down. I could spend about ten or eleven hours, listing polygenic autosomal expressions that undermine both XY and XX, simply because they evolved from such fluidity. Sex linked chromosomes are basically meaningless if, say, the individual with an XX complement defines themselves as male. Incidentally some species of fish for example change sex, from female to male. The whole issue of polarity goes out of the window when you consider hermaphroditic life forms. It would take me hours to explain and classify all the genetic elements involved.
The only thing that can be said, realistically, is to point out the fallacy when someone paints a picture of DNA as being some form of puppet master, dictating who and what you are. The DNA in reality is doing nothing of the sort, it is too chaotic and fluid in many respects. Here we have the dictatorship coming from someone else's imagination. Yes while there are many biological causes for sex differentiation and gender identity, it would seem both crass and arrogant to say that the totally dimorphic expression of two or three genes, that are unchanging and immutable is complete nonsense. There is no such thing as a real woman and no such thing as a real man. Biologically speaking there is a rainbow of physical expressions that is just as varied and individual as the social and psychological components of gender. People who claim that there are only men and only women and nothing in between show a complete lack of understanding - perhaps a feeble minded arrogance that is dictated by a feeble minded society hell bent on sterilising the true nature of what it is to be human from the equation. It is no use fighting for recognition as a man, a woman or an androgyne if you cannot confront the educated but ignorant with the reality of how nature works. And while in the abstract and the talk I may have not made my point clearly enough for many to understand, I am perfectly happy to teach people who feel the need to use the full range of biological arguments to undermine the lies of pre-determinism.
I want to finish this with a curious debate that sprung up recently, about cloning endangered species. One suggestion was to take the DNA of a surviving individual, of either sex and to create a "Male" and a "Female" version of this individual. Then to mate them and hopefully re-introduce that species. The obvious problem would be the fact that such a limited pool, consisting of one individual genome, would be very unlikely to produce viable offspring. The other problem, (Not mentioned) would be how the autosomes would take to all this tampering.
I assume that the basic idea would be to use an X chromosome in place of a Y to produce a female,. (or vice versa) but here is the problem - would it work out that way? Would something counter to the engineered sex be lurking in the autosomes? If so, what does this mean for the paradigm that arrogantly tells us all that you can simply swap an entire chromosome for another and get the desired result. I am sceptical. Given that simplistic example from the media and from scientists themselves, I am left wondering how ingrained this lie about XX and XY really is. I think in all honesty it's about time that someone was given the chance to question that paradigm, because if we continue down the path of genetic manipulation and start assuming that XX and XY are empirical, there will be a few surprises to challenge that. Worse however, there will be a few people who were born as a result of such technology arguing with the same anger and discontent at the lot they were given as the anger shown within the community today.
Thermal Sex Determination.
In some species incubation temperatures determine sex. The root of this often seems to involve SRY like genes that seem to have different Tm Values (Melting points). These temperature ranges are considerably higher than incubation temperatures, but the additional effects of various enzymes involved, and their optimal working temperatures are significant. There seems to be a relationship between the two. As in many cases, the codons in the DNA code for the same peptides, but the codons differ in the bases that make them up.
Swaab & Vilain (Apoptisis regulators etc)
I have looked at the research of both Professors Eric Vilain and Dick Swaab, who both, independently of each other seemed to have hinted at a process of apoptosis (Controlled Cell death) Swaab cites the underlying mechanisms, discussing the effects of 3-oxy steroids on the regulation of cell death involving neurones in the BSTc. Vilain suggests that p53 (A gene that regulates the cell cycle and thus apoptosis) in implicated in a "Female brain sex" While he does not mention Neural Apoptosis Inhibitory Peptides in the case of a "male brain" his set of genes that determine brain sex are very interesting from an oncological standpoint. Basically the process of brain sex differentiation is significant in terms of studying cancers, mainly brain tumours and steroid dependant "Sex specific" cancers. Which makes the study of Brain sex, quite valid as this impacts on other areas of medicine.
Other articles by Sophia Siedlberg:
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