Chapter 14, Page 168: The Scars of Evolution by Elaine Morgan
Brains and Baboons

"The surest and best characteristic of a well-founded and extensive deduction is when verification of it springs up, as it were spontaneously, into notice from quarters whence they might be least expected." J. F. W. Herschel

At one time it was assumed that the crucial change in man's cerebral evolution began with Homo Habilis - that is , much later than the fossil gap. However, Robert Martin in 1982 re-examined the evidence from fossils and comparative anatomy. With the use of scaling analysis he demonstrated that hominid brain growth relative to that of other anthropoids began at least five 5mya. It was no a sudden event but a progressive phenomenon, though it apparently accelerated about the time of H. habilis.

Robert Martin's approach was an original one. Instead of asking why brain growth might have been adaptive or desirable, he asked what made it more attainable in one particular primate than in others. In energy terms brain tissue, as compared with other body tissues, is uniquely expensive to produce and maintain, making heavy demands on the mother during pregnancy and lactation. That may be one reason why there is in many species a correlation between relative brain size and different diets. For example, fruit bats' brains are twice the size of the brains of insect-eating bats. Similarly, leaf-eating monkeys have relatively smaller brains than fruit-eating ones of closely related species. A move from a forest diet to a savannah one does not seem to facilitate brain growth.

Among Cercopithecine monkey species, for example - the family that includes baboons, mandrills and patas and rhesus monkeys - there is no distinction in brain size between forest-dwelling and savannah-dwelling species. Martin concluded: "Homo sapiens must have evolved in response to a rather unusual combination of environmental factors which made available a relatively steady, predictable supply of food lacking in significant toxic levels." Michael Crawford in 1989 speculated that a seashore diet could have had special advantages in relation to brain growth in addition to those abundance, variety and year-round availability. He pointed out that the building of brain tissue needs a consistent one-to-one balance between Omega-6 and Omega-3 fatty acids. These two types of polyunsaturated fatty acids are both essential for health, and the body cannot use one in place of the other. The latter type (Omega-3) is relatively scarce in the land food chain, but predominates in the marine food chain.

The most popular attitude to the question of brain size has always been the idea that having more room inside the skull enabled Man to become intelligent. This may be described as the Red Riding Hood approach: "Oh, Homo sapiens, what a big head you've got." "All the better to think with, my child." This is a questionable assumption. Within our own species intelligence bears no relation to the size of skull - either its absolute size or its relative size. Even in today's complex civilization we only utilize a small fraction of the brain's potential, and brain scans have shown that people with up to half of the brain destroyed can lead a normal life. As between species, there is no correlation between skull size and intelligence. Recent researches into the intelligence of parrots have led some people to re-class them as "honorary primates." In the bird's small brain there is an ability to categorise objects and grasp abstract concepts like similarity of colour, shape and texture, which rivals a chimpanzee's. People have sometimes speculated that the dolphin's large brain is necessary to house the intricate mental processes necessary for interpreting its surroundings by sonar. But a bat with a brain no larger than that of a mouse has a miniaturised sonar processor which works at least as well as a dolphin's. Even within the evolutionary history of our own species the correlation between brain size and intelligence does not hold good. Most of us are happy to believe that as man evolved and his skull expanded he grew ever more and more intelligent. But most of us would be reluctant to believe that Neanderthal man was more intelligent than modern man simply because there were more cubic centimetres inside his skull. We might also find difficulty in accepting that the increase in human intelligence stopped dead when the increase in human skull size came to a halt.

So the Red Riding Hood approach is now less in evidence. It is the neoteny model which remains most influential - the concept that we are juvenilised versions of a more ape-like ancestor. The tempo of our growth rates has in some respects slowed down; we spend longer in various stages of development between birth and death, and that includes spending longer in the infantile stage during which the brain is expanding very rapidly. The extended period of rapid brain growth means that we end up with relatively large skulls - a head/body ratio more typical of juvenile anthropoids than adult ones. (The neoteny factor and the ecological one are not, of course, mutually exclusive. Neoteny is a mechanism of evolutionary charge; environmental conditions, such as changes in the food supply, could either facilitate the working of the mechanism or inhibit it.) In 1989 C.P. Groves published a book entitled A Theory of Human and Primate Evolution, a detailed and meticulously documented account ranging from the earliest primate fossils to modern man. Near the end of it he declares himself ready to "...defend the following proposition: brain enlargement is an epiphenomenon of neoteny." This is the reverse of the more usual neoteny scenario, which suggests that the large brain somehow became so desirable and adaptive that other (disadvantageous) features such as hairlessness had to be tolerated as part of the package. Groves is suggesting that brain growth was "...not selected for as such," but happened fortuitously as a result of the changing tempo of our patterns of growth. He then asks two very good questions. Most accounts of neoteny are content to compare modern H. Sapiens with modern or primitive hominids. Groves raises the question of exactly when the neotenous trend began. He is inclined to regard it rather as Martin regards brain expansion - as a progressive phenomenon. A few neotenous features ©¤ such as the shortened face - appear very early; they are detectable, for example, in Lucy.

The second question he asks is why it happened. The probability is that a species does not become neotenous for no reason. The star example is that famous amphibian, the axolotl. It turns into a salamander when climatic conditions around its pond are sufficiently damp and shady to keep its skin moist. But if the surrounding land becomes too dry it retains its neotenous form, remains a tadpole all its life, and is capable of reproducing without becoming in other respects 'mature.' Why, then, apparently at some time during the fossil gap, did man's ancestors take the first steps along the neotenous path? Groves does not attempt to answer the question. He merely points out that it exists, and he indicates the extreme complexity of the issues involved. But in the course of his discussion he makes some interesting points, such as: "The most advanced example of neoteny among mammals appears to be the order Cetacea" (That is, whales and dolphins). He cites a long list of resemblances between the general body form of an adult whale or dolphin and the form of the embryo of a land mammal such as a cow, pig or deer at the stage when the limb buds are forming. Like such an embryo, the dolphin has a hairless skin, a torpedo-shaped body with no neck, no external appendages such as ears, poorly formed ribs with no breast bone, hardly any hind-limb skeleton, and compared to most adult land mammals a very large brain in relation to body size - a characteristic of most mammal foetuses. Groves speculated that the dolphin's large brain was neither adaptive nor maladaptive but "exaptive" -a side-effect of the prolongation of foetal growth rates; it happened because in any mammal foetus at that stage the organ that is growing fastest happens to be the brain. He adds parenthetically: "Doubtless all marine mammals are neotenous to some degree."

It is not known why in mammals a move to an aquatic environment seems to be one of the triggers which sets in a train a trend to neoteny. It is tempting to envisage it as an instance of reculer pour mieux sauter. (Take a step back so you can take a big jump forward)
Conceivably, a species finding itself in a radically new environment (such as water) begins to shed the more advanced features which fitted it for its old environment. It back-tracks to a more unspecified foetus-like form, before re-adapting to the new habitat. If that were the case, then our own ancestors, having moved from land to the water and subsequently from water to land, would have been subjected to an impetus towards neoteny on two successive occasions. It would explain why in our case the trend was unusually powerful.

All the hypotheses in this field are highly speculative; the problem is intensely complex and remains unsolved. The two possible connections between AAT (Aquatic Ape Theory) and brain growth are those already indicated: (a) that a coastal environment, unlike a savannah one, would have provided the food resources without which brain growth could not have been afforded, and (b) that brain growth appears to be related to neoteny, and a trend towards neoteny is common among aquatic mammals but not among savannah ones.

Derek Ellis of the University of Victoria, Canada, has therefore analysed the ecology of all the various types of marine ecosystems found in tropical latitudes in relation to the observed behaviour of extant primates, with the object of assessing the viability of an aquatic ape. He examined the resources available in such environments as mangrove forests, slat-marsh lagoons, archipelagos, estuaries, reefs and rock shores, and collected data about swimming and other water activities in 26 primate species. His starting point was a succinct encapsulation of minimal AAT premise: "We need a habitat other than a forest-savannah boundary ecotone for the separation of ape and human stocks." His conclusion was that "...the tropical coastal environment provides productive ecosystems exploitable by a range of extant monkeys. There is no evident reason to believe that an ape could not converge to successful adaptation there." Yet this is precisely what many people find hard to accept. Most of the attempts to refute AAT consist of alleged reasons why an aquatic ape could never have survived. It would, they imply, have been doomed to perish. It was not stream-lined; it was quite the wrong shape for a swimmer. It was warm blooded; once its fur was wet, the water would have drained it of its body heat. Its movements would be slow and inefficient; it could never move fast enough under water to catch a fish, and it would have starved. In the meantime its helpless young would have been greedily devoured by crocodiles and sharks, and it would have left no descendents.

These are all the reasons why it would have been impossible for any land mammal to survive in water. They apply with equal force to the dog-like animal which went into the water and in the course of millions of years turned into a seal. Yet that primitive dog survived. Probably only some kind of duress would have driven it to resort to such a desperate measure, and doubtless many of the pioneers did perish. But enough of them survived, and today their descendents are found in oceans all over the world. It happened again and again - to the bear-like creature that turned into a walrus, and the mole-like creature that turned into a platypus, and the elephant's cousin that turned into a manatee, and the flying sea bird that turned into a penguin, and the ancient unknown quadrupeds that turned into whales and dolphins.

If the sea of Afar had not been cut off from the Indian Ocean we might have been able to add a primate to the list; some of the aquatic apes might have ventured into the open sea and stayed there while our own ancestors returned to the African continent. It would have been fascinating to find cousins in the sea as genetically close to us as our cousins in the forest. But when the evaporating inland sea became untenably briny, any aquatic apes would perforce have gravitated to the inland shore where the water was fresher, and southward along the waterways, until ultimately the dependence on water as a food source was weakened and became dispensable. Alistair Hardy lived and died in the hope that some kind of proof might be dug up by the fossil hunters which would settle the matter. But it is hard to conceive of any fossil evidence that would be regarded as conclusive one way or the other. To take a parallel situation, if fossil hunters in five million years' time unearthed the fossilized skeletons of an otter and a stoat, they would be able to deduce that two closely related mustelids co-existed in Scotland in 20th century. They would find it very difficult to establish whether one of them was aquatic. For a long time it appeared impossible to prove or disprove either the savannah theory or AAT. It seemed that belief in one or the other must always hinge on the balance of probability rather than anything more definite. And when, finally, a new and quite unambiguous piece of evidence came to light it was widely ignored. When the molecular biologists entered the field of evolutionary research, their first claim was that they could supply evidence about the timing of certain evolutionary events - the dates at which one species split off from another. During the 1970s their techniques were refined and developed, and they began to make statements about place as well as time. As G. J. Todaro declared: "There is in fact a record of our history, however tenuous, that is recorded in all of us in our genes, and we are beginning to read that history."

The best known example of a genetic marker giving evidence about our geographical origins is that of the haemoglobin S gene, which is of medical importance because it can sometimes cause sickle cell anaemia. This property is obviously maladaptive, and the normal expectation would be that it would have been bred out by natural selection. But it was discovered that it had another property which meant that in parts of Africa it increased the chances of survival: it provides 'a degree of resistance' to malarial infection. Since the gene is not found in all human beings, it has obviously been acquired since the races of mankind dispersed and became differentiated. It is now fully accepted that the presence of the sickle cell gene is a marker which proves that its possessor must have had at least one African ancestor, though the family may have lived outside Africa for hundreds of years. Far less familiar is the most challenging of all these markers. It is known as the "baboon marker." Its existence was first revealed in 1976 by a team of researchers from the National Cancer Institute in Bethesda, Maryland. Their paper was entitled: "Baboons and their close relatives are unusual among primates in their ability to release non-defective endogenous type C viruses," and the authors were G. J. Todaro, C. J. Sherr and R. E. Benveniste. A subsequent article in Nature by Benveniste and Todaro had a more arresting title: "Evolution of type C viral genes; evidence for an Asian origin of man." The infectious type C virus identified in the first paper belongs, like the AIDS virus, to the class known as retro-viruses. When such a virus infects an animal, the RNA of the virus is converted into DNA inside the cells. This means that it becomes part of the genetic make-up of the infected animal and can be genetically transmitted from parent to offspring. Retroviruses can also be passed on and re-integrated into the DNA of other animals of the same species (as with AIDS), and even on rare occasions into the genetic information of distantly related species. The type C virus is endogenous only in baboons - that is, it is a normal part of their make-up and has no harmful effect on them. But when it crosses the species barrier it has the potential to cause disease in other primates. The Bethesda team was able to establish that the baboon virus must at one time have constituted a threat to all the primates of Africa except the baboons themselves, because every African monkey and ape species they examined contained, in their chromosomes, viral gene sequences closely related to RNA genomes of the baboon virus; these sequences evolved to act as a kind of antibody, a protection against the baboon virus.
One thing we can deduce is that when the baboon virus first manifested itself it was able to cause - in all primates except themselves - a serious and probably life-threatening disease.

Every extant African monkey or ape species carries the protective gene sequence in its chromosomes. If any such species failed to develop this resistance, it failed to survive. The second thing we can deduce is that the virus was highly infectious. Unlike the AIDS virus, it was certainly not spread mainly by sexual contact. It was almost certainly airborne, because baboons are diurnal ground-dwellers, yet the species affected by the virus include not only other ground-dwellers like chimpanzee and gorilla, but also arboreal species like the colobus monkey and even small prosimians living high in the forest, like the bush baby and the galago. Baboons still carry the virus, but it appears to have lost its virulence in the course of time. By now it constitutes no particular threat to other primate species, even those not carrying the protective marker. These are, of course, the South American and Asian primates whose ancestors were never in the vicinity of the baboons when the plague was at its height. Among primates, then, the gene sequence (the "baboon marker") is a reliable indication of African origin, just as the sickle-cell gene is in humans. Of the ape and monkey species tested, 23 showed the presence of the "baboon marker" - and none of them were African. The most remarkable aspect of Todaro's discovery emerged when he examined Homo sapiens for the "baboon marker." It was not there. All races of Homo sapiens - including the African races - lack the baboon marker. Todaro drew one firm conclusion: "The ancestors of man did not develop in a geographical area where they would have been in contact with the baboon. I would argue that the data we are presenting imply a non-African origin of man millions of years ago."

His own choice of a non-African site was Asia. His paper implies that, following the split from apes, some populations of hominids spread into Asia; that they were therefore absent when the baboon plague erupted; that any hominid population remaining in Africa at that time ultimately died out; and that all extant humans are descended from the Asian emigres, some of whom returned westward and crossed the Suez isthmus back into Africa. There is no evidence which actually rules out the hypothesis of an Asian origin. (The theory of descent from an "African Eve' is irrelevant in this context; it refers to a population bottle-neck on the continent of Africa millions of years later, around 200kya.) Todaro's scenario, involving dispersal to the East followed later by a trek back to the West, was felt by some to be inherently improbable, but no one suggested any other way of accounting for the absence of the "baboon marker" in man. A non-African site does not necessarily imply Java or Peking. If the baboon plague broke out during the fossil gap when Afar was flooded, man's ancestors could have been living on Danakil - then an off-shore island miles away - or somewhere on the opposite shore of the proto-Red Sea. In either case, not even an airborne virus could have reached them, and by the time their descendants found themselves on the mainland, the baboon plague would have lost its virulence and they would never have needed to acquire the protective gene sequence.

The Bethesda findings made one thing perfectly clear. The idea that man's ancestors left the trees and subsequently spent all their time on the baboon-haunted African savannah has to be discarded. As Sarich said about molecular dating: "One no longer has the option" of clinging to that version of events. Todaro knew that his findings would not be welcomed, but he wrote: "As I see it , one of our major functions in the area of research is to act as historians - to report what actually happened rather than what we would have liked to happen." He was certainly not reporting what savannah theorists like to think happened. Their reaction to the "baboon marker" discovery was more or less the same as to Alister Hardy - the response was nil. Discussion of human evolution continued along the old familiar lines as if nothing had happened.
But there is a fundamental difference between trying to ignore a new hypothesis and trying to close the mind to new data. "I don't wish to know that" was a favourite line of patter among cross-talk comedians, but no scientist can resort to it and hope to retain credibility. In recent years the climate of opinion has begun to change. In 1987 an international conference was held at Valkenburg in the Netherlands, where the pros and cons of AAT were publicly debated, and that event represented some kind of watershed. By now a number of scientists are prepared to endorse the theory as a tenable hypothesis. Others, while remaining neutral, have been willing to offer constructive criticism, provide a platform, or suggest additional lines of enquiry. To all of these I owe a permanent debt of gratitude. As Michael Ruse observed in a different connection: "You can always find some way of propping up a crumbling theory but, if you are prepared to stay with science, then there really does come a time when the facts start to bite:" For the crumbling savannah theory, that time has arrived.