We Are Our Brains (54 page)

In recent years, adherents of the Intelligent Design movement—some of them Dutch—have made desperate and completely futile attempts to undermine Darwin's theory of evolution. Of course, denying evolution isn't against the law, but to publicly deny the truth of scientific findings, as this movement does, is evidence of double standards: Blasphemy is still a crime in the Netherlands, but blaspheming Darwin isn't. Some Intelligent Design campaigners have sought to deny the considerable contribution of molecular biology to our understanding of evolution. In Cees Dekker's book on Intelligent Design (2005), the physicist Arie van den Beukel claims, “It's often said that the findings of molecular biology over the past few decades provide conclusive support for Darwin's theory. Nothing could be further from the case.” I shall give a few examples to show just how nonsensical this sweeping assertion is.

It's scarcely credible that in 1859 Darwin was able, without any of the advanced molecular knowledge we have today, to theorize that life originated from a single primeval ancestor. Darwin could not have known that all living tissue is so
chemically
similar. Molecular biologists have fairly recently been able to provide this visionary notion with a firm foundation. Evolution can, for instance, be traced in DNA through gradual molecular changes in the genes that code for proteins, through the doubling of genes and the consequent formation
of new functional genes, through the disappearance of genes and, lastly, through evolutionary mutations in those parts of RNA that don't code for proteins but that importantly regulate cellular functions. Molecular research is constantly generating new knowledge and theories about the course of evolution and its mechanisms. The genes of the nervous system are a case in point. Given the close molecular similarities in their nervous systems, worms, insects, and vertebrates—from fish to humans—must have had a single common ancestor who lived 600 million years ago. Take the tiny ragworm
Platynereis dumerilii
, which is considered to be a living fossil. Its embryonic development has been shown to proceed along the same molecular lines as mammals'.

Darwin would no doubt have greatly appreciated the molecular research done on the mitochondrial DNA of the famous finches that he discovered on the Galapagos Islands during the voyage of the
Beagle.
It showed that the thirteen species indeed had a common ancestor, as he suspected. That ancestor must have migrated from the South American continent to the Galapagos Islands around 2.3 million years ago. Molecular evidence has also been found for Darwin's belief that the ancestors of man originated in Africa: Both the “maternal” mitochondrial DNA and the “paternal” Y chromosomal DNA have been traced back to that continent. Darwin's theory of human migration from Africa through Europe and Asia has also been proved correct. It's now known that there were two waves of human migration out of Africa. The first, of
Homo erectus
, between 2 million and 1.6 million years ago, and the second, of
Homo sapiens
(modern man) around 50,000 to 60,000 years ago. The lack of genetic variation between populations outside Africa shows that only a few dozen
Homo sapiens
individuals originally migrated from Africa. Sexual intercourse between the two species of hominids in various regions of the world caused
Homo erectus
to be assimilated into
Homo sapiens.

A recent field of study focuses on the molecular-genetic mutations that resulted in the emergence of humankind in the three hundred
thousand generations following the split from chimpanzees. It's often said that the human and chimpanzee genomes differ by only 35 million or so DNA building blocks, or a mere 1 percent. (That figure has become something of a popular myth; the difference is more like 6 percent.) However, this considerable similarity is misleading, since only a few genes would have been needed for the tripling of ourbrain weight since we separated from the chimpanzees—as various findings now indicate. One of the characteristic differences between human and chimpanzee brains is that in our case, the genes involved in metabolic activity in the brain are much more strongly expressed—a difference for which only a couple of genes (transcription factors) are responsible. Efforts to identify the instrumental factors in humankind's development are lending weight to the “few genes” argument. These studies involve looking for the genes whose mutation can lead to undersized brains (microcephaly) and mental retardation in humans. The brains of people born with primary microcephaly, an inheritable condition, are just as small as those of the great apes, while their general structure remains intact. Such individuals have a normal appearance and show no neurological deviations. This developmental disorder can be localized in at least six different places in the DNA. All of the genes that have been identified are involved in cell division, making their contribution to increased brain size over the course of evolution plausible. One is the ASPM gene, the mutation of whose DNA building blocks accelerated after the split between humans and chimpanzees, around 5.5 million years ago. The theory has also been put forward that the human brain is still evolving, on the grounds that a genetic variant of ASPM is thought to have originated only 5,800 years ago and then spread rapidly through the population. A genetic variant of the microcephalin gene (D allele of MCPH1), which regulates brain size, is thought to have only entered the DNA of
Homo sapiens
during the last ice age, around 37,000 years ago—yet 70 percent of the current world population carries this variant. A rapid increase of this kind is only possible if a variant confers a clear evolutionary advantage.

Genes whose mutations are associated with human language have also been found. Mutations of the FOXP2 gene cause language and speech disorders that run in families. And ASPM and microcephalin also appear to have a linguistic connection.

In the course of evolution, new functional genes have also come into being. The best example is the gene that allows primates to see three colors. As a result of the doubling of the gene-produced pigment (opsin) that is sensitive to green, followed by mutation and selection, primates developed the red opsin. This conveyed the evolutionary advantage of being able to distinguish ripe fruit from unripe fruit. Humans are still programmed to find red exciting, whereas the dominant color in nature, green, has a calming effect, even in the case of placebos (see
chapter 16
). (That's why operating theaters are painted green.)

Genes have also been lost over time. Mice possess 1,200 olfactory receptor genes, while humans have only 350 left. The loss of a particular gene, MYH16, may have indirectly affected human brain size. This gene was responsible for the massive jaw muscles of our ancestors. Its loss is thought to have allowed skull size to increase in order to accommodate our larger brains.

Another strategy for identifying the genes that have crucially influenced the development of the brain entails the mapping of the entire genomes of various precursors in man's evolution. At the Max Planck Institute for Evolutionary Anthropology in Leipzig, the Swedish biologist Svante Pääbo is currently sequencing all the base pairs in the genome of Neanderthals, who died out 30,000 years ago. He has extracted DNA from three fossil bones of Neanderthal women who lived 38,000 to 44,000 years ago, inventing techniques to distinguish between the greatly fragmented Neanderthal DNA and contaminations caused by bacteria and modern humans. Within a few years he hopes to be able to compare Neanderthal DNA in its entirety to that of modern man and thus to identify the genetic mutations that enabled us to make such rapid strides in our evolution. Now that 60 percent of Neanderthal DNA has been mapped, the
first surprising findings have already emerged. Europeans, Chinese, and Papuans bear traces of sexual contact with Neanderthals that must have taken place in the Middle East between 50,000 and 80,000 years ago. Between 1 and 4 percent of this group's DNA derives from Neanderthals. (Africans, by contrast, share no genetic material with Neanderthals.) This link makes one wonder what characteristics we have inherited from our Neanderthal ancestors. Until now, fifty-one genes that developed very rapidly after the split between
Homo sapiens
and Neanderthals have been found. Many differences have also been found in the parts of DNA that code for RNA and have regulatory functions (see below), and seventy-eight genes that are identical in all modern humans but differ in Neanderthals have been found. The differences affect a relatively large number of genes that relate to the brain and could therefore provide future insights about the emergence of the unique characteristics of modern humans.

As far as the 6 percent difference between human and chimpanzee DNA is concerned, it's important to remember that extremely small changes in genes, known as polymorphisms, can completely alter the structure of a protein and thus its function. A single gene can also produce many different proteins. A member of my research team, Tatjana Ishunina, discovered that our brains contain over forty variants of the estrogen receptor alpha, one of the proteins that receives the estrogen message. The production of these variants is influenced by age, brain area, cell type, and pathology. It has also recently been shown that that there is no need to focus so strongly on the genes that code for proteins when charting the evolution of the brain, because 98 percent of the genome doesn't code for proteins but only for RNA, and micro-RNA is thought to have been especially influential in the expansion of the human brain. Pieces of RNA regulate many cellular processes, and there are often great differences between humans and chimpanzees in this respect. As of now, the main difference has been found in the HAR1 (human accelerated region 1), a segment of a recently discovered RNA gene. The RNA that is expressed in early development (HAR1F) is specific
to the reelin-producing Cajal-Retzius cells in the brain. HAR1F comes to expression together with reelin in the seventeenth to nineteenth weeks of fetal development, a crucial stage in the formation of the six-layered cerebral cortex. The mutations in this human gene are probably over a million years old and could have played a crucial role in the emergence of modern humankind.

Throughout our evolution, an enormous amount of junk and repetition has piled up in our DNA. These scars of our evolutionary history contain important information about our genesis but can hardly be seen as an argument for an Intelligent Designer and even less as evidence for regarding DNA as “God's language.” Nothing has changed since Darwin concluded in 1871 that the key principle of evolution was undeniable, at least if you didn't look at natural phenomena with the eyes of a savage. Over 130 years later, adherents of Intelligent Design occupy a lonely place among the few remaining “savages” who deny evolution.

This book is based on a series of columns on the brain that I was asked to write for the Dutch newspaper
NRC Handelsblad
in response to readers' questions. One of the questions was: Why are societies all over the world structured around the week?

According to the Bible, God created the earth in six days and rested on the seventh. Your first thought might be that it wouldn't have hurt to devote an extra day to the creation of humans. But it also makes you wonder whether we have seven-day weeks because, according to the Bible, the creation took seven days or whether it's the other way around, and the creation story owes its seven-day structure to our having a seven-day biological rhythm.

All living things, from unicellular organisms to humans, have biological rhythms instilled over millions of years of evolution, enabling them to cope with the regular changes that affect our planet. The biological clock in our hypothalamus has a rhythm of approximately twenty-four hours; it warns us that it will soon grow dark and that it's time to return to the safety of the cave. As night ends, this clock prepares our bodies again for the activities that will start a few hours later by increasing the levels of the stress hormone cortisol. The day-night rhythm of our biological clock reflects the revolution of the earth. It also has an annual rhythm based on the Earth's rotation around the sun. The annual rhythm helped us estimate when we needed to sow, harvest, or prepare for winter. We have also internalized the rhythm of the moon, as shown by the female menstrual cycle.

Might we have a biological clock with a weekly rhythm? Weekly rhythms can indeed be seen in concentrations of substances in our blood and urine. Blood pressure, the incidence of heart attacks, brain infarcts, suicides, and births also fluctuate according to a weekly pattern. But these weekly fluctuations might reflect the rhythm of our social activities rather than an internal weekly rhythm. A scientist who measured hormone levels in his own urine for fifteen (!) years has plausibly demonstrated a biological weekly rhythm. Over a three-year period, the fluctuations showed patterns of around a week but weren't synchronous with the working week. A “free-running” rhythm of this kind points to the existence of a biological clock that measures time in roughly weekly installments. An experiment in which people spent one hundred days in a cave without time markers showed that they kept to a seven-day cycle. Studies of an insect,
Folsomia candida
, revealed that it stuck to its weekly egg-laying patterns even when kept in constant darkness. The last two examples seem to undermine the theory that our weekly biological fluctuations are caused by social factors. However, the strongest argument for a biological weekly rhythm is provided by fossils of human precursors discovered in East Africa. Two types of microscopic growth
lines were found on the dental enamel of skull number 1500, “Turkana Boy”: one with a twenty-four-hour periodicity and one with a periodicity of around seven days. In other words, the dental enamel of these hominids developed at a fixed rate for a six-day period and at a different rate on the seventh day. The same has been shown to apply to other primates. It's been suggested that this weekly periodicity might be accounted for by a fluctuation in the sun's radiation, but eminent astronomers oppose this theory. It's much more likely that our weekly rhythm dates back to the evolutionary period in which organisms made the transition from sea to land and started looking for food on beaches. The weekly fluctuations in tides caused by the gravitational pull of the sun and the moon would have had huge consequences for coastal foragers in terms of both food availability and type. Whatever the basis of that rhythm, a biological week existed 3.6 to 3.8 million years before the Bible was written and millions of years before our social week came into being. This biological rhythm may also have given rise to the idea that God completed his task of creation in a week and not, say, eight or nine days, let alone 4.5 billion years.