We Are Our Brains (14 page)

FIGURE 13.
Another example of correspondence I received after publishing the first findings of the difference between the brains of homosexual and heterosexual men. The text reads, “Bet you regret not having been able to work under Mengele in Auschwitz!”

FIGURE 14.
Cartoon by Peter van Straaten after the publication of the first findings of the difference between the brains of homosexual and heterosexual men (1989). The caption read, “Wim's got a big hypothalamus too, eh, Wim?” Original in possession of the author, a present from the Netherlands Institute for Brain Research, NIH.

Five years after that first brouhaha, the publication of our discovery
of a sex-reversed pattern in the brains of transsexuals (Zhou et al.,
Nature
378 [1995]: 68–70; see
fig. 11
in this book) met with an entirely positive response. Transsexuals immediately seized on the article in order to get sex changes registered in birth certificates or passports in countries where that had not previously been possible. It was used to the same end at the European Court of Justice and played a role in the drafting of legislation on the issue in Britain.

Nowadays, articles on the differences between male and female or heterosexual and homosexual brains barely cause a ripple (see for instance Swaab, D. F.,
Proc. Natl. Acad. Sci. USA
105 [2008]: 10273–74), and there's a great interest in the topic in popular science publications.

At the stage when our bodies and brains differentiate along male or female lines, hybrid forms sometimes develop. This can have far-reaching consequences. A controversial example of hybrid sexuality dates back to the Middle Ages, when a woman allegedly became pope, subverting the strict male hierarchy of the Roman Catholic Church. Measures are said to have been taken to prevent such a “disaster” from occurring again.

The story of Pope Joan was chronicled by the Dominican monk Jean de Mailly around 1250, and a film was made of it in 1972. Was it a myth or a cover-up? No one knows for sure. The gist of the legend is as follows. Though born in the German town of Mainz in 833, Joan was of English extraction. Having traversed Europe dressed as a monk, she gained so much respect and authority for her great learning that she succeeded Leo IV as pope in 854, taking the name of Johannes Anglicus (John the Englishman) or John VIII. Three years later, however, she became pregnant, suddenly giving birth during the Easter procession, near the Basilica of San Clemente in Rome. This gave the game away, of course, and she was lynched on
the spot. Her successor, Benedict III, is said to have eradicated all trace of her memory. There's no record of Joan in the Vatican's pontifical yearbook.

Although the Catholic Church systematically denies the story, there are indications that there may be some truth in it. In 1276, Pope John XX was said to have changed his name to John XXI in order to account for the female Pope John. What's more, records indicate that the sculpted head of John VIII, “Femina de Anglica,” stood alongside the busts of all the other popes in the Cathedral of Siena. In 1600, however, her bust was removed by order of Pope Clement VIII.

And then there's the chair with the hole, referred to in Italian as
La Sedia Gestatoria
—meaning “litter” or “sedan chair.” But why would a sedan chair have a hole in the seat? The story goes that, to prevent another female pope from being elected, candidates for the papacy were required to sit on the chair. The youngest cleric present had to stick his hand through the hole, feel the papal candidate's genitals, and then call out loudly, “
Testiculos habet et bene pendentes
” (“He has testicles and they hang well”). The cardinals present would then respond, “
Habe ova nostra Papa
” (“Our father has balls”—as if they were any use to him). The need for such testing suggests that the story of Pope Joan may very well be true. Maria New, a New York pediatric endocrinologist, has put forward the theory that Pope Joan had a form of intersex called congenital adrenal hyperplasia, or CAH (see earlier in this chapter). But this diagnosis is pure speculation.

In her article (1993), New referred to a red marble chair that apparently stood in the Vatican Museum. When I met Dr. New in 2007 at a conference in Rome, however, I asked where exactly the chair was, because I'd been invited to the Vatican the following morning. She told me that she had never gotten to see it. The one depicted in her article had been an identical chair looted by Napoleon, now in the Louvre, to which she had only gained access after negotiating a great deal of red tape.

At the Vatican the next day, on a private tour organized by one of
the pope's doctors, a collaborator of mine immediately said to the head of security that I was especially interested in seeing the chair. No problem, our security man responded, though he immediately added that Maria New's theory was nonsense. According to him, the chair was simply an ancient commode. At the time I wondered how he knew about her article. It was highly technical and published in an academic journal intended for specialists—not the kind of reading you associate with security guards.

He gave us a tour through the hushed corridors of the Vatican. We saw the room where the cardinals elect the pope, the “crying room” to which newly appointed popes are ushered to shed a few tears, the containers of white and black smoke, the chamber with the famous balcony where the pope appears (and from which Pope John Paul II called out in something faintly resembling Dutch, “Thanks for the flowers!”), the terrible murals everywhere, and the Swiss guards flanking each important doorway. We were shown the papal gardens, the secret escape route to the stronghold, and so on. Our guide even got out all the pope's gorgeously embroidered mantles for special occasions so that we could admire and feel them. One was pink. “Is that for Saturday evenings?” I asked the cleric, who was lovingly displaying each garment. “No,” he answered seriously, “that's for prison visits.” The pope's miters were unpacked for us, along with a crucifix that he takes with him on his travels—there was no end to it all.

It was all most impressive and yet not quite what we'd come for, and I reminded our guide of the chair. Yes, yes, it was a bit farther on, he said soothingly. When we had emerged from the silence of the private rooms, had passed the Sistine Chapel with its hordes of tourists, and had gone once again through a series of doors opened and locked behind us by Swiss guards, I mentioned the chair once more.

“Oh, what a pity,” said the head of security. “We passed it about fifteen minutes ago. I'm so sorry, I completely forgot about it.”

“No problem,” I said airily, “we can just go back.”

Alas, this was impossible, “for security reasons,” the security officer
said, as he told us exactly which country had donated each of the many trees and shrubs in the Vatican garden. A complex network of cables hung over our heads, and large antennas betrayed an advanced communications system. The way back to the Middle Ages had been cut off. So that ended my chance to establish the truth of the chair and Pope Joan, but the matter continued to preoccupy me. If the chair didn't exist, why didn't the security officer just say so? Why did he keep stringing us along? Was the chair still being used, or might Pope Benedict XVI have been toying with the idea of reinstating this old custom?

In puberty, the pituitary gland starts to produce sex hormones. These affect the adolescent brain, causing marked and often incredibly annoying behavioral changes. The evolutionary advantage of puberty is clear: Youngsters are being prepared for reproduction. And their annoying behavior, leading to frequent clashes with their families, makes it less likely that reproduction will take place in their own surroundings, thus reducing the risk of inherited defects. The craving for new experiences, the readiness to take great risks, and the impulsive behavior are all part of preparations to leave the nest. Because their prefrontal cortex hasn't yet matured, adolescents can think only in the short term and are unable to take in the negative consequences of risky choices. As a result, they are also more likely to try addictive substances that can permanently damage the developing brain.

A great many chemical changes are needed to initiate puberty. Its onset is triggered by the gene KISS1, which produces the protein kisspeptins in the hypothalamus. The gene is so central to this process that it has been said that “puberty starts with a kiss.” The gene was discovered by American researchers in Hershey, Pennsylvania, and named after the most famous local product, the Hershey Chocolate Kiss. People with a mutation in the KISS1 system never enter puberty.

However, puberty is dependent on other systems, too. For instance, women must have sufficient fat reserves to be able to nourish a fetus at times of scarcity. Before puberty, the brain registers whether there's sufficient fatty tissue by monitoring the amount of leptin, a hormone that's produced by fat cells. If the fat reserves are insufficient—because of an eating disorder, for instance, or intense athletic training—leptin levels decline and puberty is delayed, sometimes for good. Similarly, mutations in the leptin gene can impede puberty and also cause extreme obesity. In such cases, the brain registers the absence of leptin—and therefore of fat. The brain then blocks the onset of puberty because pregnancy would be too risky while also sending out a signal to eat copiously to make up fat reserves—unaware that it's merely leptin, not fat, that's lacking.

Melatonin, a hormone produced by the pineal gland, is one of the substances that prevent the onset of puberty in children. Melatonin's inhibiting effect has been known since 1898, when Otto Heubner described a boy of four and a half who had already entered puberty. He turned out to have a brain tumor that had destroyed his pineal gland, which resulted in a lack of melatonin, in turn spurring the onset of puberty. A Dutch girl who started puberty at the age of three and a half was more fortunate. She didn't have a brain tumor and was given inhibitory hormones up to the age of twelve. Then she entered puberty again and is now flourishing at secondary school. Conversely, some people's melatonin level is too high and has to be normalized before puberty can start.

Puberty can also be disrupted by a condition known as Kallmann syndrome. Normally, the brain cells that stimulate the sex hormones
develop at the place where a fetus's nose develops. The cells then migrate along the olfactory nerve to the hypothalamus. This process is disrupted in patients with Kallmann syndrome, so that not only do they not enter puberty, they also lack a sense of smell.

So we should stop dismissing the embryonic and adolescent brains as organs in which not much is going on yet. On the contrary, they are both undergoing the most complex and delicate modifications.

According to adolescents, it's not their immature brains that are the problem, it's their parents. In fact, they are more or less the same thing: A youngster's parents function as his or her temporary prefrontal cortex (PFC,
fig. 15
). While the adolescent PFC is still immature, parents have to be responsible for a child's planning, organization, moral framework, and limits. These functions are gradually taken over by the slowly maturing PFC. The problem is that today's youngsters have discovered that their parents aren't in a position to enforce their role as human PFC substitutes.