What’s wrong with rainbow families?

A woman went to a fertility clinic for artificial insemination, and discovered a surprising stipulation. She’s white, so they’ll only allow her access to sperm from white men.

Dr. Calvin Greene, the clinic’s administrative director, confirmed the private facility will not treat couples or singles who insist on using donors of a different ethnicity. The policy has been in place since the clinic opened in the 1980s.

“I’m not sure that we should be creating rainbow families just because some single woman decides that that’s what she wants,” he said. “That’s her prerogative, but that’s not her prerogative in our clinic.”

A statement on the clinic’s website reads: “it is the practice of the Regional Fertility Program not to permit the use of a sperm donor that would result in a future child appearing racially different than the recipient or the recipient’s partner.”

“Rainbow families”? Does Canada have miscegenation laws, because this is the same thing.

Maybe there was a typo in the doctor’s statement. Perhaps these rules were formulated in the 1880s.

I’m feeling really filthy now

Mississippi has horrific rates of teen pregnancy and sexually transmitted diseases, so they’re slowly waking up and realizing that they have to have better sex education in the schools … and they’ve actually adopted a sex-ed curriculum in some of their school districts. Unfortunately, it’s not what most of us would consider good education.

Marie Barnard was delighted when, after decades of silence on the topic, Mississippi passed a law requiring school districts to teach sex education. But the lesson involving the Peppermint Pattie wasn’t what she had in mind for her sons.

The curricula adopted by the school district in Oxford called on students to unwrap a piece of chocolate, pass it around class and observe how dirty it became.

"They’re using the Peppermint Pattie to show that a girl is no longer clean or valuable after she’s had sex — that she’s been used," said Barnard, who works in public health. "That shouldn’t be the lesson we send kids about sex."

Oh, no! I’ve been having sex for about 40 years now, so I pictured a piece of candy — in my case, a Tootsie Roll — getting passed around and stuffed into various damp places and given a hot shower every day, for forty years, and I’m sorry, it didn’t even make it a week before it had melted away and gone down the drain. Now I’m having castration anxiety.

Wait! It only applies to girls? What a relief, for me, at least — my wife is going to be dismayed, though. Maybe we can change the message a bit: lady bits are just like a piece of sweet chocolate candy that never ever disappears, no matter how much you nibble on it.

Unfortunately, the dirty scary chocolate trick still doesn’t work. The outcomes they want to prevent are actually being worsened by their evasive silly little abstinence-only games. So they have a new threat that they make:

Johnson thought he had made a good case for contraception education when he shared disturbing statistics: The local birthrate was 73 out of 1,000 females between 15 and 19; the national rate is 29.4 per 1,000.

He encountered the usual gasps of shock when he revealed that the rate of chlamydia, at 1,346.8 per 100,000 people, was nearly double the rest of Mississippi, and approaching triple the U.S. rate.

But later Johnson got a call from someone who had attended the board meeting — telling him that people who have sex before marriage don’t go to heaven. The board voted for abstinence-only.

Apparently, most of the state of Mississippi is damned to hell, so why is anyone paying attention to those sinners?

Pathways to sex

I was talking about sex and nothing but sex all last week in genetics, which is far less titillating than it sounds. My focus was entirely on operational genetics, that is, how autosomal inheritance vs inheritance of factors on sex chromosomes differ, and I only hinted at how sex is not inherited as a simple mendelian trait, as we’re always tempted to assume, but is actually the product of a whole elaborate chain of epistatic interactions. I’m always tempted in this class to go full-blown rabid developmental geneticist on them and do nothing but talk about interactions between genes, but I manage to restrain myself every time — we have a curriculum and a focus for this course, and it’s basic transmission genetics, and I struggle to get general concepts across before indulgence in my specific interests. Stick to the lesson plan! Try not to break everyone’s brain yet!

But a fellow can dream, right?

Anyway, before paring everything down to the reasonable content I can give in a third year course, I brush up on the literature and take notes and track down background and details that I won’t actually dump on the students (fellow professors know this phenomenon: you have to work to keep well ahead of the students, because they really don’t need to start thinking they’re smarter than you are). But I can dump my notes on you. You don’t have to take a test on it and get a good grade, and you won’t pester me about whether this will actually be on the test, and you won’t start crying if I overwhelm you with really cool stuff. (If any of my students run across this, no, the content of this article will not be on any test. Don’t panic. Go to grad school where this will all be much more relevant.)

Onward. Here’s my abbreviated summary of the epistatic interactions in making boys and girls.

The earliest step in gonad development is the formation of the urogenital ridge from intermediate mesoderm, a thickening on the outside of the mesonephros (early kidney), under the influence of transcription factors Emx2, Wt1 (Wilms tumor 1), Lhx9, and Sf1 (steroidogenic factor 1). Even in the earliest stages, multiple genes interact to generate the tissue! The urogenital ridge is going to form only the somatic tissue of the gonad; the actual germ cells (the cells that will form the gametes, sperm and ova) arise much, much earlier, in the epiblast of the embryo at a primitive streak stage, and then migrate through the mesenteries of the gut to populate the urogenital ridge independently, shortly after it forms.

At this point, this organ is called the bipotential gonad — it is identical in males and females. Two genes, Fgf9 and Wnt4, teeter in a balanced antagonistic relationship — Wnt4 suppresses Fgf9, and Fgf9 suppresses Wnt4 — in the bipotential gonad, and anything that might tip the balance between them will trigger development of one sex or the other. A mutation that breaks Fgf9, for instance, gives Wnt4 an edge, and the gonad will develop into an ovary; a mutation that breaks Wnt4 will let Fgf9 dominate the relationship, and the gonad will develop into a testis (with a note of caution: the changes will initiate differentiation into one gonad or the other, but there are other steps downstream that can also vary). These two molecules may be the universal regulators of the sex of the gonad in animals: fruit flies also use Fgf and Wnt genes to regulate development of their gonads.

But the key to the genetic symmetry-breaking of selecting Fgf9 and Wnt4 varies greatly in animals. Some use incubation temperature to bias expression one way or the other; birds have a poorly understood set of factors that may require heterodimerization between two different proteins produced on the Z and W chromosomes to induce ovaries; mammals have a unique gene, Sry, not found in other vertebrates, that is located on the Y chromosome and tilts the balance towards testis differentiation.

Sry may be unique to mammals, but it didn’t come out of nowhere. Sry contains a motif called the HMG (high mobility group) box, which is a conserved DNA binding domain. There are approximately 20 proteins related to Sry in humans, all given the name SOX, for SRY-related HMG box (I know, molecular biologists seem to be really reaching for acronyms nowadays). SOX genes are found in all eukaryotes, and seem to play important roles in cell and organ differentiation in insects, nematodes, and vertebrates. Sry is simply the member of the family that has been tagged to regulate gonad development in mammals.

If a copy of Sry is present in the organism, which is usually only the case in XY or male mammals, expression of the gene produces a DNA binding protein that has one primary target: a gene called SOX9 (they’re cousins!). In mice, Sry is switched on only transiently, long enough to activate SOX9, which then acts as a transcription factor for itself, maintaining expression of SOX9 for the life of the gonad. Humans keep Sry turned on permanently as well, but there’s no evidence yet that it actually does anything important after activating SOX9; it may be that human males neglect to hit the off switch.

SOX9 binds to a number of genes, among them, Fgf9. Remember Fgf9? The masculinizing factor in antagonism to the feminizing factor Wnt4? This tips the teeter-totter to favor expression of Fgf9 over Wnt4, leading to the differentiation of a testis from the bipotential gonad.

So far, then, we’ve got a nice little Rube Goldberg machine and an epistatic pathway. Sf1/Wt1 and other early genes induce the formation of a urogenital ridge and an ambiguous gonad; Sry upregulates Sox9 which upregulates Fgf9 which suppresses Wnt4, turning off the ovarian pathway and turning on the testis pathway.

But wait, we’re not done! Sry/SOX9 are expressed specifically in a subset of cells of the male gonad, the prospective Sertoli cells. If you recall your reproductive physiology, Sertoli cells are a kind of ‘nurse’ cell of the testis; they’re responsible for nourishing developing sperm cells. They also have signaling functions. The Sertoli cells produce AMH, or anti-Müllerian Hormone, which is responsible for causing the female ducts of the reproductive system to degenerate in males (if you don’t remember the difference between Müllerian and Wolffian and that array of tubes that get selected for survival in the different sexes, here’s a refresher). Defects in the AMH system lead to persistent female ducts: you get males with partial ovaries and undescended testicles. So just having the Sry chain is not enough, there are downstream genes that have to dismantle incipient female structures and promote mature properties of the gonad.

As the gonad differentiates, it also induces another set of cells, the embryonic Leydig cells. We have to distinguish embryonic Leydig cells, because they represent another transient population that will do their job in the embryo, then gradually die off to be replaced by a new population of adult Leydig cells at puberty. The primary function of Leydig cells is the production of testosterone and other androgens. The embryo gets a brief dose of testosterone early that initiates masculinization of various tissues, which then fades (fortunately; no beards and pubic hair for baby boys) to resurge in adolescence, triggering development of secondary sexual characteristics. Embryonic testosterone is the signal that maintains the Wolffian duct system. No testosterone, and the Wolffian ducts degenerate.

Just to complicate matters, while testosterone is the signal that regulates the male ducts, testosterone must be converted to dihydrotestosterone (DHT), the signal that regulates development of the external genitalia. Defects in the enzyme responsible for this conversion can lead to individuals with male internal plumbing, including testes, but female external genitalia. Sex isn’t all or nothing, but a whole series of switches!

By now, if you’re paying attention, you may have noticed a decidedly male bias in this description. I’ve been talking about a bipotential gonad that is flipped into a male mode by the presence of a single switch, and sometimes, especially in the older literature, you’ll find that development of the female gonad is treated as the default: ovaries are what you get if you lack the special magical trigger of the Y chromosome. This is not correct. The ovaries are also the product of an elaborate series of molecular decisions; I think it’s just that they Y chromosome and the Sry gene just provided a convenient genetic handle to break into the system, and really, scientists usually favor the easy tool to get in.

One key difference between the testis and ovary is the inclusion of germ cells. The testis simply doesn’t care; if the germ line, the precursors to sperm, is not present, the male gonad goes ahead and builds cords of Sertoli cells with Leydig cells differentiating in the interstitial space, makes the whole dang structure of the testicle, pumping out testosterone as if all is well, but contains no cells to make sperm — so it’s reproductively useless, but hormonally and physiologically active. The ovary is different. If no germ line populates it, the ovarian follicle cells (the homolog to the Sertoli cells) do not differentiate. If germ cells are lost from the tissue only later, the follicles degenerate.

Ovaries require a signal from the germ line to develop normally. One element of that signal seems to be factors associated with cells in meiosis. The female germ line cells are on a very strict meiotic clock, beginning the divisions to produce haploid egg cells in the embryo, even as they populate the gonad. These oocytes produce a signal, Figα (factor in germ line a) that recruits ovarian cells to produce follicles. The male gonad has to actively repress meiosis in the embryonic germ line to inhibit this signaling; male germ cells are restricted to only mitotic divisions until puberty.

Even before Figα signaling becomes important, there are other factors uniquely expressed in the prospective ovary that shape its development. In particular, Wnt4 induces the expression of another gene, Foxl2, that is critical for formation of the ovarian follicle. The pathways involved in ovarian development are not as well understood as those in testis development, but it’s quite clear that there is a chain of specific genetic/molecular interactions involved in the generation of both organs.

Wait, you say, you need a diagram! You can’t grasp all this without an illustration! Here’s a nice one: I particularly like that cauliflower-shaped explosion of looping arrows early in the testis pathway.

The molecular and genetic events in mammalian sex determination. The bipotential genital ridge is established by genes including Sf1 and Wt1, the early expression of which might also initiate that of Sox9 in both sexes. b-catenin can begin to accumulate as a response to Rspo1–Wnt4 signaling at this stage. In XX supporting cell precursors, b-catenin levels could accumulate sufficiently to repress SOX9 activity, either through direct protein interactions leading to mutual destruction, as seen during cartilage development, or by a direct effect on Sox9 transcription. However, in XY supporting cell precursors, increasing levels of SF1 activate Sry expression and then SRY, together with SF1, boosts Sox9 expression. Once SOX9 levels reach a critical threshold, several positive regulatory loops are initiated, including autoregulation of its own expression and formation of feed-forward loops via FGF9 or PGD2 signaling. If SRY activity is weak, low or late, it fails to boost Sox9 expression before b-catenin levels accumulate sufficiently to shut it down. At later stages, FOXL2 increases, which might help, perhaps in concert with ERs, to maintain granulosa (follicle) cell differentiation by repressing Sox9 expression. In the testis, SOX9 promotes the testis pathway, including Amh activation, and it also probably represses ovarian genes, including Wnt4 and Foxl2. However, any mechanism that increases Sox9 expression sufficiently will trigger Sertoli cell development, even in the absence of SRY.

The molecular and genetic events in mammalian sex determination. The bipotential genital ridge is established by genes including Sf1 and Wt1, the early expression of which might also initiate that of Sox9 in both sexes. b-catenin can begin to accumulate as a response to Rspo1–Wnt4 signaling at this stage. In XX supporting cell precursors, b-catenin levels could accumulate sufficiently to repress SOX9 activity, either through direct protein interactions leading to mutual destruction, as seen during cartilage development, or by a direct effect on Sox9 transcription. However, in XY supporting cell precursors, increasing levels of SF1 activate Sry expression and then SRY, together with SF1, boosts Sox9 expression. Once SOX9 levels reach a critical threshold, several positive regulatory loops are initiated, including autoregulation of its own expression and formation of feed-forward loops via FGF9 or PGD2 signaling. If SRY activity is weak, low or late, it fails to boost Sox9 expression before b-catenin levels accumulate sufficiently to shut it down. At later stages, FOXL2 increases, which might help, perhaps in concert with ERs, to maintain granulosa (follicle) cell differentiation by repressing Sox9 expression. In the testis, SOX9 promotes the testis pathway, including Amh activation, and it also probably represses ovarian genes, including Wnt4 and Foxl2. However, any mechanism that increases Sox9 expression sufficiently will trigger Sertoli cell development, even in the absence of SRY.

So that’s what I didn’t tell my genetics students this time around. Maybe I’ll work it into my developmental biology course, instead.

Kim Y, Kobayashi A, Sekido R, DiNapoli L, Brennan J, Chaboissier MC, Poulat F, Behringer RR, Lovell-Badge R, Capel B. (2006) Fgf9 and Wnt4 act as antagonistic signals to regulate mammalian sex determination. PLoS Biol 4(6):e187

Ross AJ, Capel B. (2005) Signaling at the crossroads of gonad development. Trends Endocrinol Metab. 16(1):19-25.

Sekido R, Lovell-Badge R (2009) Sex determination and SRY: down to a wink and a nudge? Trends Genet. 25(1):19-29.

Sim H, Argentaro A, Harley VR (2008) Boys, girls and shuttling of SRY and SOX9. Trends Endocrinol Metab. 19(6):213-22.

Yao H H-C (2005) The pathway to femaleness: current knowledge on embryonic
development of the ovary. Molecular and Cellular Endocrinology 230:87–93.

Crazy, obsessed, weird, perverse


Sometimes those are good descriptors. I read a happy story for a change this morning: it’s about Arunachalam Muruganantham, an Indian man who embarked on a long crusade to make…sanitary napkins. Perhaps you laugh. Perhaps you get a little cranky at a guy who rushes in to meddle in women’s concerns. And there’s some good reason to feel that way: he starts out with embarrassing levels of ignorance.

He fashioned a sanitary pad out of cotton and gave it to Shanthi [his wife], demanding immediate feedback. She said he’d have to wait for some time – only then did he realise that periods were monthly. “I can’t wait a month for each feedback, it’ll take two decades!” He needed more volunteers.

And then a man who didn’t realize until then that menstrual periods were monthly dedicated himself to years of tinkering and testing to build a machine to manufacture sanitary napkins, which just sounds perversely fanatical and obsessive. But it turns out to be a serious problem for poor women.

Women who do use cloths are often too embarrassed to dry them in the sun, which means they don’t get disinfected. Approximately 70% of all reproductive diseases in India are caused by poor menstrual hygiene – it can also affect maternal mortality.

So Muruganantham set out to teach himself everything about making napkins, and examining and testing used menstrual pads. His wife left him. He was regarded as a sick pariah in his town — the disgusting guy who plays with menstrual blood. He was going up against traditional taboos and public squeamishness.

But he succeeded! He designed and built simple machines that take cotton and cellulose at one end and churn out disposable sanitary napkins — and it was relatively cheap, easy to maintain, and could be distributed to rural India where the women themselves could make the necessaries. And then we learn about his philosophy…

Muruganantham seemed set for fame and fortune, but he was not interested in profit. “Imagine, I got patent rights to the only machine in the world to make low-cost sanitary napkins – a hot-cake product,” he says. “Anyone with an MBA would immediately accumulate the maximum money. But I did not want to. Why? Because from childhood I know no human being died because of poverty – everything happens because of ignorance.”

He believes that big business is parasitic, like a mosquito, whereas he prefers the lighter touch, like that of a butterfly. “A butterfly can suck honey from the flower without damaging it,” he says.

Oh my god, an idealist. I thought they were all extinct! And such a fine beautiful specimen, too! I’m going to steal that metaphor, as well, just because it is so lovely.

Most of Muruganantham’s clients are NGOs and women’s self-help groups. A manual machine costs around 75,000 Indian rupees (£723) – a semi-automated machine costs more. Each machine converts 3,000 women to pads, and provides employment for 10 women. They can produce 200-250 pads a day which sell for an average of about 2.5 rupees (£0.025) each.

Women choose their own brand-name for their range of sanitary pads, so there is no over-arching brand – it is “by the women, for the women, and to the women”.

And my heart grew two sizes that day.

Strident Catholics hurt my brain

I can call them ‘strident,’ can’t I? They apply it to atheists all the time, and this is clearly a case where the adjective is perfectly appropriate. It’s an opinion piece by a militant (I can use that, too!) Catholic who traces the fall of America to a court decision in 1972.

This year, the Supreme Court will render judgment on the institution of marriage. Though most of us don’t realize it, the Court first did so forty-one years ago in Eisenstadt v. Baird, a decision that gravely wounded marriage and set the nation on a course of gradual debilitation by ruling that states could not restrict the sale of contraceptives to unmarried people.

Oooh, marriage was ‘gravely wounded’ by that decision. It was a fairly straightforward issue in civil liberties: could the law decide that contraception could only be sold to married couples? The court decided no, it could not: even unmarried people have a right to regulate their reproduction by means other than abstinence.

Chaos then swept across the country as suddenly men and women were able to fornicate without spawning children! Yes, chaos! His word, not mine.

Having set chaos in motion in Eisenstadt, the Supreme Court quickly built the garbage bin for dumping sexual debris in Roe v. Wade, which gave a green light to the killing of 55 million unborn children, the overwhelming majority of whom were conceived by those unmarried singles with new access to contraceptives.

Having lived through that period (I started high school in 1972, so I was in prime temporal position to witness precisely all the horrible consequences), I’ve got to tell you: some kids were screwing before 1972, most were not. After 1972, some kids were screwing, most were not. There were single mothers, plenty of them, before 1972, and plenty afterwards — conveniently, during this period I worked part time as an assistant custodian in a school for single mothers*, so again I was in exactly the right place to witness the aftermath of sexual chaos.

It didn’t happen.

Also, I’ve got to wonder if the author thought his thesis through. New access to contraception led to a surge in unwanted pregnancies? Only if they weren’t doing it right. Maybe we should have coupled contraception access to better sex education.

Or just maybe the chaos was all in the author’s head.


A lot of things are obviously only playing out in this guy’s head. This is the extreme Catholic position: it’s not just that child-raising must be carried out within a marriage, but sex is supposed to be channeled towards only supporting procreation. Which is scary, speaking as an old (but not dead) guy who has put all his baby-making days behind him.

Thus, in a well-ordered society sex and marriage go together exclusively, because the union of male and female sexual expression must be undertaken in a union that binds them in advance of the coordinated labors needed to raise the children they may bring into the world. To achieve this, a functioning society demands that each citizen channels his sexual capacities in ways appropriate to these two tasks (procreation and child-raising). That is, it demands marriage.

How about if sex has other roles? What if it’s a general social binder that brings people together in close affection? Wouldn’t that be a good thing, too?

And what if marriage isn’t such a great matrix for raising children when the two adults involved have lost that affection? Surely no one can believe that marriage is sufficient to create a healthy family environment, and knowing more than a few stable, happy couples who are not bound by formal marriage, it’s not even necessary.

So how can Catholics justify sacrificing the richness and complexity of human relationships on the altar of their narrow definition of how people must cohabit?

*Predictably, the community felt the need to isolate unwed mothers from other women their age; they might contaminate them. Also predictably, colloquial references to that school called it the ‘school for bad girls’. Further predictability: I did not tell anyone that I was scrubbing floors and cleaning bathrooms there after school and during the summer because every idiot would have lurid fantasies about what I was doing, when actually I spent little time interacting with the women there (I was working outside of school hours), and what little I did see were women in isolated and difficult circumstances.


An organization called the Susan B. Anthony List — it’s an adamantly anti-choice group that has neatly named itself after an icon of women’s liberation — has a wonderful president, Marjorie Dannenfelser, who not only opposes abortion, but is dead set against contraception. She argues here that increasing availability of contraception leads to increasing rates of abortion (what?), apparently because all those frisky couples losing their fear of pregnancy will fornicate more, leading to more unwanted pregnancies.

But…but…abortion rates have been going down as pregnancy rates decline. We can’t therefore account for reduced pregnancy rates by claiming they’ve been terminated by abortion, and it seems kind of unlikely that people are having sex less often, so isn’t the correlation the reverse of what Dannenfelser claims?


Also, I am greatly concerned by the implications of the statement that “to lose the connection between sex and having children leads to problems”. There were precisely 3 periods in my life in which I intentionally had procreative sex, and they were both relatively brief because I married a fertile minx who got knocked up as soon as we both put our minds to it. So, maybe three months where I’ve had sex with reproductive intent, while the other 393 months of my married life I was entirely in frivolous sex-for-fun mode. Furthermore, we have not been the slightest bit interested in having more children for 23 years. Is Dannenfelser trying to suggest that having a monogamous and healthy sex life during those decades should be causing problems because we’ve lost the connection between sex and having children?

Science doesn’t say that!

Have you ever noticed how the religious regard ‘scientism’ and ‘reductionism’ and demands for concrete evidence as barely a notch above obscenities? That is, until they need to reduce complex issues to simplistic claims and don the mantle of Science to support their beliefs. Then they become Holy Writ.

You can really see this behavior in the abortion debate, where suddenly anti-choicers decide that humanity is defined by a particular arrangement of alleles in the genome. Case closed, they say, Science has spoken! Unfortunately, they get the science wrong, and we know their commitment to the authority of sacred science will be discarded the instant a scientist says something they disagree with…like, say, there is no soul and the mind is a product of the brain, or you are an evolved variant of an ape, or maybe, just maybe, genes aren’t the magic ju-ju beans you think they are.

A classic example was published in the Independent. Look how Declan Ganley bows and scrapes to the authority of science, multiple times!

Of course, the only way to guarantee that the law protects all individual members of the human species equally, is that at a minimum, from the moment that a member can be identified as such, the law insures immunity from deliberate bodily destruction.

This moment of identity is unequivocally known today as conception (as indeed the word itself suggests), when the DNA of a new member of the human species arises. It is scientifically indisputable that the DNA discovered here by science is that of a unique individual distinct from their biological mother, and that this DNA is the unique and irreplicable identifier of a unique member of our species.

So the question is not whether we know when the human individual is first created (this is unequivocally proven by science), but rather whether an individual’s right to life can be made subject to another and one individual human can be fully owned by another to the point where their very life is subject only to the whims of another.

None of us are created in the fullness of our potential, but science has shown us that human life is a journey, not a static moment. Our potential is gifted us at our conception – our appearance, talents and very fingerprints are hardcoded, and the rest is up to us. We are all conceived with the destiny to be born, grow, mature, slowly fade and die. The deliberate and targeted interruption of this process at any point is the ending of a single, unique, never-to-be-replaced human existence, and is the most base form of discrimination. That is why we make killing another human the most serious of all the crimes.

I’ve got news for you, Ganley. Science does not have such unambiguous answers as you claim; human-ness is an emergent property of a gradual process of development, and no one is going to ever be able to say, “Here, right here, is the magic instant in which an embryo becomes fully human.” That’s because “human” as used in law and sociology and philosophy and even theology is something complex and very, very hard to define, so looking for a mathematically precise and sharp boundary in the vagueness of complexity is a contradiction in terms.

You can try to do it by putting on blinders and pretending that the genetic sequence of an individual is sole criterion, and that it is well-defined and unambiguous, but it isn’t. It just creates more problems.

Genetically, we’re nearly identical to chimpanzees. They have the same genes in roughly the same organization on their chromosomes; they have some novel variants, or alleles, but every newborn chimp also has a “unique and irreplicable” arrangement of alleles. Why aren’t you declaring their lives precious and demanding protection? Why not say the same for cows and ears of corn? They are also genetically special.

But, you will say, they are uniquely human. And I will ask what that means. If I have a mutant gene (and I do! On average, I’ll carry a few hundred novel mutations relative to my parents) that isn’t shared between me and all other humans, am I still human? If I have a cytologically detectable chromosomal rearrangement, am I still human? How many differences are allowed between two genomes before you can say one is not of the same species as the other? Is an embryo with a unique deletion in one chromosome still human? If an embryo has a unique mutation that makes it infertile as an adult when interbreeding with other members of the species, is it still human?

That magic line in development should be getting a bit smearier in your head about now. Conception isn’t necessarily associated with the generation of a unique person.

I’m glad that he noticed that science sees development as a journey, but a little disappointed that he couldn’t see that that actually contradicts his claims about conception as a singularity. Just the genetic complement is not enough. A blastocyst, a hollow ball of cells with an inner mass that will become the embryo proper, has exactly the same genes as a five year old person or an octagenerian. But it doesn’t have limbs or eyes or brain, it doesn’t think or feel, it doesn’t dance or learn. It is…a hollow ball of cells. It’s got cilia and might spin in place. That’s about it. It’s human only the most trivial, reductionist sense.

That should tell you something. There has to be something more. There has to be a complex history of epigenetic interactions that set up tissue domains and generate morphology and trigger physiologically functional activity in different cells. That isn’t there yet. That history is a significant part of what makes you what you are right now, and it’s absurd to pretend that that doesn’t matter and that everything is plainly established at the moment of conception.

And of course, he’s factually wrong. To claim that “appearance, talents and very fingerprints are hardcoded” is not true, and all you have to do is look at identical twins to see that it is false. There is a good similarity in appearance, but if you know any identical twins at all well, you know that you can tell them apart…and that their differences increase with age. I’ve known a few elderly identical twins, and you wouldn’t know that they were identical unless you’d been told so, because variation accumulates. “Talent” is also meaningless; there is evidence that some broad characteristics (musical ability, for instance) are heritable, but so much of what we call “talent” is not intrinsic, but the product of hard work and discipline.

Also, fingerprints are not hardcoded. Identical twins have general similarities in the arrangements of whorls and loops, but are readily distinguishable in the details.

Science would not belittle the significance of all the essential changes that go on after conception, so I think Mr Ganley was a bit premature in claiming its authority for his dogma. How about if we recognize instead that science actually tells us that the process, that journey he regards as so vital, is the interesting part, and that imposing arbitrary dividing lines on a continuum is a silly exercise that he’s trying to use to put boundaries where there are none?