Guns, Germs And Steel Part 8

A subtler expression of this geographically varying ease of spread is the phenomenon termed preemptive domestication. Most of the wild plant species from which our crops were derived vary genetically from area to area, because alternative mutations had become established among the wild ancestral populations of different areas. Similarly, the changes required to transform wild plants into crops can in principle be brought about by alternative new mutations or alternative courses of selection to yield equivalent results. In this light, one can examine a crop widespread in prehistoric times and ask whether all of its varieties show the same wild mutation or same transforming mutation. The purpose of this examination is to try to figure out whether the crop was developed in just one area or else independently in several areas.

If one carries out such a genetic a.n.a.lysis for major ancient New World crops, many of them prove to include two or more of those alternative wild variants, or two or more of those alternative transforming mutations. This suggests that the crop was domesticated independently in at least two different areas, and that some varieties of the crop inherited the particular mutation of one area while other varieties of the same crop inherited the mutation of another area. On this basis, botanists conclude that lima beans (Phaseolus lunatus), common beans (Phaseolus vulgaris), and chili peppers of the Capsic.u.m annuum / chinense Capsic.u.m annuum / chinense group were all domesticated on at least two separate occasions, once in Mesoamerica and once in South America; and that the squash group were all domesticated on at least two separate occasions, once in Mesoamerica and once in South America; and that the squash Cucurbita pepo Cucurbita pepo and the seed plant goosefoot were also domesticated independently at least twice, once in Mesoamerica and once in the eastern United States. In contrast, most ancient Southwest Asian crops exhibit just one of the alternative wild variants or alternative transforming mutations, suggesting that all modern varieties of that particular crop stem from only a single domestication. and the seed plant goosefoot were also domesticated independently at least twice, once in Mesoamerica and once in the eastern United States. In contrast, most ancient Southwest Asian crops exhibit just one of the alternative wild variants or alternative transforming mutations, suggesting that all modern varieties of that particular crop stem from only a single domestication.

What does it imply if the same crop has been repeatedly and independently domesticated in several different parts of its wild range, and not just once and in a single area? We have already seen that plant domestication involves the modification of wild plants so that they become more useful to humans by virtue of larger seeds, a less bitter taste, or other qualities. Hence if a productive crop is already available, incipient farmers will surely proceed to grow it rather than start all over again by gathering its not yet so useful wild relative and redomesticating it. Evidence for just a single domestication thus suggests that, once a wild plant had been domesticated, the crop spread quickly to other areas throughout the wild plant's range, preempting the need for other independent domestications of the same plant. However, when we find evidence that the same wild ancestor was domesticated independently in different areas, we infer that the crop spread too slowly to preempt its domestication elsewhere. The evidence for predominantly single domestications in Southwest Asia, but frequent multiple domestications in the Americas, might thus provide more subtle evidence that crops spread more easily out of Southwest Asia than in the Americas.

Rapid spread of a crop may preempt domestication not only of the same wild ancestral species somewhere else but also of related wild species. If you're already growing good peas, it's of course pointless to start from scratch to domesticate the same wild ancestral pea again, but it's also pointless to domesticate closely related wild pea species that for farmers are virtually equivalent to the already domesticated pea species. All of Southwest Asia's founder crops preempted domestication of any of their close relatives throughout the whole expanse of western Eurasia. In contrast, the New World presents many cases of equivalent and closely related, but nevertheless distinct, species having been domesticated in Mesoamerica and South America. For instance, 95 percent of the cotton grown in the world today belongs to the cotton species Gossypium hirsutum Gossypium hirsutum, which was domesticated in prehistoric times in Mesoamerica. However, prehistoric South American farmers instead grew the related cotton Gossypium barbadense Gossypium barbadense. Evidently, Mesoamerican cotton had such difficulty reaching South America that it failed in the prehistoric era to preempt the domestication of a different cotton species there (and vice versa). Chili peppers, squashes, amaranths, and chenopods are other crops of which different but related species were domesticated in Mesoamerica and South America, since no species was able to spread fast enough to preempt the others.

We thus have many different phenomena converging on the same conclusion: that food production spread more readily out of Southwest Asia than in the Americas, and possibly also than in sub-Saharan Africa. Those phenomena include food production's complete failure to reach some ecologically suitable areas; the differences in its rate and selectivity of spread; and the differences in whether the earliest domesticated crops preempted redomestications of the same species or domestications of close relatives. What was it about the Americas and Africa that made the spread of food production more difficult there than in Eurasia?

TO ANSWER THIS question, let's begin by examining the rapid spread of food production out of Southwest Asia (the Fertile Crescent). Soon after food production arose there, somewhat before 8000 question, let's begin by examining the rapid spread of food production out of Southwest Asia (the Fertile Crescent). Soon after food production arose there, somewhat before 8000 B.C. B.C., a centrifugal wave of it appeared in other parts of western Eurasia and North Africa farther and farther removed from the Fertile Crescent, to the west and east. On this page I have redrawn the striking map (Figure 10.2) a.s.sembled by the geneticist Daniel Zohary and botanist Maria Hopf, in which they ill.u.s.trate how the wave had reached Greece and Cyprus and the Indian subcontinent by 6500 B.C. B.C., Egypt soon after 6000 B.C. B.C., central Europe by 5400 B.C. B.C., southern Spain by 5200 B.C. B.C., and Britain around 3500 B.C. B.C. In each of those areas, food production was initiated by some of the same suite of domestic plants and animals that launched it in the Fertile Crescent. In addition, the Fertile Crescent package penetrated Africa southward to Ethiopia at some still-uncertain date. However, Ethiopia also developed many indigenous crops, and we do not yet know whether it was these crops or the arriving Fertile Crescent crops that launched Ethiopian food production. In each of those areas, food production was initiated by some of the same suite of domestic plants and animals that launched it in the Fertile Crescent. In addition, the Fertile Crescent package penetrated Africa southward to Ethiopia at some still-uncertain date. However, Ethiopia also developed many indigenous crops, and we do not yet know whether it was these crops or the arriving Fertile Crescent crops that launched Ethiopian food production.

Of course, not all pieces of the package spread to all those outlying areas: for example, Egypt was too warm for einkorn wheat to become established. In some outlying areas, elements of the package arrived at different times: for instance, sheep preceded cereals in southwestern Europe. Some outlying areas went on to domesticate a few local crops of their own, such as poppies in western Europe and watermelons possibly in Egypt. But most food production in outlying areas depended initially on Fertile Crescent domesticates. Their spread was soon followed by that of other innovations originating in or near the Fertile Crescent, including the wheel, writing, metalworking techniques, milking, fruit trees, and beer and wine production.

Why did the same plant package launch food production throughout western Eurasia? Was it because the same set of plants occurred in the wild in many areas, were found useful there just as in the Fertile Crescent, and were independently domesticated? No, that's not the reason. First, many of the Fertile Crescent's founder crops don't even occur in the wild outside Southwest Asia. For instance, none of the eight main founder crops except barley grows wild in Egypt. Egypt's Nile Valley provides an environment similar to the Fertile Crescent's Tigris and Euphrates Valleys. Hence the package that worked well in the latter valleys also worked well enough in the Nile Valley to trigger the spectacular rise of indigenous Egyptian civilization. But the foods to fuel that spectacular rise were originally absent in Egypt. The sphinx and pyramids were built by people fed on crops originally native to the Fertile Crescent, not to Egypt.

Second, even for those crops whose wild ancestor does occur outside of Southwest Asia, we can be confident that the crops of Europe and India were mostly obtained from Southwest Asia and were not local domesticates. For example, wild flax occurs west to Britain and Algeria and east to the Caspian Sea, while wild barley occurs east even to Tibet. However, for most of the Fertile Crescent's founding crops, all cultivated varieties in the world today share only one arrangement of chromosomes out of the multiple arrangements found in the wild ancestor; or else they share only a single mutation (out of many possible mutations) by which the cultivated varieties differ from the wild ancestor in characteristics desirable to humans. For instance, all cultivated peas share the same recessive gene that prevents ripe pods of cultivated peas from spontaneously popping open and spilling their peas, as wild pea pods do.

Evidently, most of the Fertile Crescent's founder crops were never domesticated again elsewhere after their initial domestication in the Fertile Crescent. Had they been repeatedly domesticated independently, they would exhibit legacies of those multiple origins in the form of varied chromosomal arrangements or varied mutations. Hence these are typical examples of the phenomenon of preemptive domestication that we discussed above. The quick spread of the Fertile Crescent package preempted any possible other attempts, within the Fertile Crescent or elsewhere, to domesticate the same wild ancestors. Once the crop had become available, there was no further need to gather it from the wild and thereby set it on the path to domestication again.

The ancestors of most of the founder crops have wild relatives, in the Fertile Crescent and elsewhere, that would also have been suitable for domestication. For example, peas belong to the genus Pisum Pisum, which consists of two wild species: Pisum sativum Pisum sativum, the one that became domesticated to yield our garden peas, and Pisum fulvum Pisum fulvum, which was never domesticated. Yet wild peas of Pisum fulvum Pisum fulvum taste good, either fresh or dried, and are common in the wild. Similarly, wheats, barley, lentil, chickpea, beans, and flax all have numerous wild relatives besides the ones that became domesticated. Some of those related beans and barleys were indeed domesticated independently in the Americas or China, far from the early site of domestication in the Fertile Crescent. But in western Eurasia only one of several potentially useful wild species was domesticated-probably because that one spread so quickly that people soon stopped gathering the other wild relatives and ate only the crop. Again as we discussed above, the crop's rapid spread preempted any possible further attempts to domesticate its relatives, as well as to redomesticate its ancestor. taste good, either fresh or dried, and are common in the wild. Similarly, wheats, barley, lentil, chickpea, beans, and flax all have numerous wild relatives besides the ones that became domesticated. Some of those related beans and barleys were indeed domesticated independently in the Americas or China, far from the early site of domestication in the Fertile Crescent. But in western Eurasia only one of several potentially useful wild species was domesticated-probably because that one spread so quickly that people soon stopped gathering the other wild relatives and ate only the crop. Again as we discussed above, the crop's rapid spread preempted any possible further attempts to domesticate its relatives, as well as to redomesticate its ancestor.

WHY WAS THE spread of crops from the Fertile Crescent so rapid? The answer depends partly on that east-west axis of Eurasia with which I opened this chapter. Localities distributed east and west of each other at the same lat.i.tude share exactly the same day length and its seasonal variations. To a lesser degree, they also tend to share similar diseases, regimes of temperature and rainfall, and habitats or biomes (types of vegetation). For example, Portugal, northern Iran, and j.a.pan, all located at about the same lat.i.tude but lying successively 4,000 miles east or west of each other, are more similar to each other in climate than each is to a location lying even a mere 1,000 miles due south. On all the continents the habitat type known as tropical rain forest is confined to within about 10 degrees lat.i.tude of the equator, while Mediterranean scrub habitats (such as California's chaparral and Europe's maquis) lie between about 30 and 40 degrees of lat.i.tude. spread of crops from the Fertile Crescent so rapid? The answer depends partly on that east-west axis of Eurasia with which I opened this chapter. Localities distributed east and west of each other at the same lat.i.tude share exactly the same day length and its seasonal variations. To a lesser degree, they also tend to share similar diseases, regimes of temperature and rainfall, and habitats or biomes (types of vegetation). For example, Portugal, northern Iran, and j.a.pan, all located at about the same lat.i.tude but lying successively 4,000 miles east or west of each other, are more similar to each other in climate than each is to a location lying even a mere 1,000 miles due south. On all the continents the habitat type known as tropical rain forest is confined to within about 10 degrees lat.i.tude of the equator, while Mediterranean scrub habitats (such as California's chaparral and Europe's maquis) lie between about 30 and 40 degrees of lat.i.tude.

But the germination, growth, and disease resistance of plants are adapted to precisely those features of climate. Seasonal changes of day length, temperature, and rainfall const.i.tute signals that stimulate seeds to germinate, seedlings to grow, and mature plants to develop flowers, seeds, and fruit. Each plant population becomes genetically programmed, through natural selection, to respond appropriately to signals of the seasonal regime under which it has evolved. Those regimes vary greatly with lat.i.tude. For example, day length is constant throughout the year at the equator, but at temperate lat.i.tudes it increases as the months advance from the winter solstice to the summer solstice, and it then declines again through the next half of the year. The growing season-that is, the months with temperatures and day lengths suitable for plant growth-is shortest at high lat.i.tudes and longest toward the equator. Plants are also adapted to the diseases prevalent at their lat.i.tude.

Woe betide the plant whose genetic program is mismatched to the lat.i.tude of the field in which it is planted! Imagine a Canadian farmer foolish enough to plant a race of corn adapted to growing farther south, in Mexico. The unfortunate corn plant, following its Mexico-adapted genetic program, would prepare to thrust up its shoots in March, only to find itself still buried under 10 feet of snow. Should the plant become genetically reprogrammed so as to germinate at a time more appropriate to Canada-say, late June-the plant would still be in trouble for other reasons. Its genes would be telling it to grow at a leisurely rate, sufficient only to bring it to maturity in five months. That's a perfectly safe strategy in Mexico's mild climate, but in Canada a disastrous one that would guarantee the plant's being killed by autumn frosts before it had produced any mature corn cobs. The plant would also lack genes for resistance to diseases of northern climates, while uselessly carrying genes for resistance to diseases of southern climates. All those features make low-lat.i.tude plants poorly adapted to high-lat.i.tude conditions, and vice versa. As a consequence, most Fertile Crescent crops grow well in France and j.a.pan but poorly at the equator.

Animals too are adapted to lat.i.tude-related features of climate. In that respect we are typical animals, as we know by introspection. Some of us can't stand cold northern winters with their short days and characteristic germs, while others of us can't stand hot tropical climates with their own characteristic diseases. In recent centuries overseas colonists from cool northern Europe have preferred to emigrate to the similarly cool climates of North America, Australia, and South Africa, and to settle in the cool highlands within equatorial Kenya and New Guinea. Northern Europeans who were sent out to hot tropical lowland areas used to die in droves of diseases such as malaria, to which tropical peoples had evolved some genetic resistance.

That's part of the reason why Fertile Crescent domesticates spread west and east so rapidly: they were already well adapted to the climates of the regions to which they were spreading. For instance, once farming crossed from the plains of Hungary into central Europe around 5400 B.C. B.C., it spread so quickly that the sites of the first farmers in the vast area from Poland west to Holland (marked by their characteristic pottery with linear decorations) were nearly contemporaneous. By the time of Christ, cereals of Fertile Crescent origin were growing over the 8,000-mile expanse from the Atlantic coast of Ireland to the Pacific coast of j.a.pan. That west-east expanse of Eurasia is the largest land distance on Earth.

Thus, Eurasia's west-east axis allowed Fertile Crescent crops quickly to launch agriculture over the band of temperate lat.i.tudes from Ireland to the Indus Valley, and to enrich the agriculture that arose independently in eastern Asia. Conversely, Eurasian crops that were first domesticated far from the Fertile Crescent but at the same lat.i.tudes were able to diffuse back to the Fertile Crescent. Today, when seeds are transported over the whole globe by ship and plane, we take it for granted that our meals are a geographic mishmash. A typical American fast-food restaurant meal would include chicken (first domesticated in China) and potatoes (from the Andes) or corn (from Mexico), seasoned with black pepper (from India) and washed down with a cup of coffee (of Ethiopian origin). Already, though, by 2,000 years ago, Romans were also nourishing themselves with their own hodgepodge of foods that mostly originated elsewhere. Of Roman crops, only oats and poppies were native to Italy. Roman staples were the Fertile Crescent founder package, supplemented by quince (originating in the Caucasus); millet and c.u.min (domesticated in Central Asia); cuc.u.mber, sesame, and citrus fruit (from India); and chicken, rice, apricots, peaches, and foxtail millet (originally from China). Even though Rome's apples were at least native to western Eurasia, they were grown by means of grafting techniques that had developed in China and spread westward from there.

While Eurasia provides the world's widest band of land at the same lat.i.tude, and hence the most dramatic example of rapid spread of domesticates, there are other examples as well. Rivaling in speed the spread of the Fertile Crescent package was the eastward spread of a subtropical package that was initially a.s.sembled in South China and that received additions on reaching tropical Southeast Asia, the Philippines, Indonesia, and New Guinea. Within 1,600 years that resulting package of crops (including bananas, taro, and yams) and domestic animals (chickens, pigs, and dogs) had spread more than 5,000 miles eastward into the tropical Pacific to reach the islands of Polynesia. A further likely example is the east-west spread of crops within Africa's wide Sahel zone, but paleobotanists have yet to work out the details.

CONTRAST THE EASE of east-west diffusion in Eurasia with the difficulties of diffusion along Africa's north-south axis. Most of the Fertile Crescent founder crops reached Egypt very quickly and then spread as far south as the cool highlands of Ethiopia, beyond which they didn't spread. South Africa's Mediterranean climate would have been ideal for them, but the 2,000 miles of tropical conditions between Ethiopia and South Africa posed an insuperable barrier. Instead, African agriculture south of the Sahara was launched by the domestication of wild plants (such as sorghum and African yams) indigenous to the Sahel zone and to tropical West Africa, and adapted to the warm temperatures, summer rains, and relatively constant day lengths of those low lat.i.tudes. of east-west diffusion in Eurasia with the difficulties of diffusion along Africa's north-south axis. Most of the Fertile Crescent founder crops reached Egypt very quickly and then spread as far south as the cool highlands of Ethiopia, beyond which they didn't spread. South Africa's Mediterranean climate would have been ideal for them, but the 2,000 miles of tropical conditions between Ethiopia and South Africa posed an insuperable barrier. Instead, African agriculture south of the Sahara was launched by the domestication of wild plants (such as sorghum and African yams) indigenous to the Sahel zone and to tropical West Africa, and adapted to the warm temperatures, summer rains, and relatively constant day lengths of those low lat.i.tudes.

Similarly, the spread southward of Fertile Crescent domestic animals through Africa was stopped or slowed by climate and disease, especially by trypanosome diseases carried by tsetse flies. The horse never became established farther south than West Africa's kingdoms north of the equator. The advance of cattle, sheep, and goats halted for 2,000 years at the northern edge of the Serengeti Plains, while new types of human economies and livestock breeds were being developed. Not until the period A.D. A.D. 1200, some 8,000 years after livestock were domesticated in the Fertile Crescent, did cattle, sheep, and goats finally reach South Africa. Tropical African crops had their own difficulties spreading south in Africa, arriving in South Africa with black African farmers (the Bantu) just after those Fertile Crescent livestock did. However, those tropical African crops could never be transmitted across South Africa's Fish River, beyond which they were stopped by Mediterranean conditions to which they were not adapted. 1200, some 8,000 years after livestock were domesticated in the Fertile Crescent, did cattle, sheep, and goats finally reach South Africa. Tropical African crops had their own difficulties spreading south in Africa, arriving in South Africa with black African farmers (the Bantu) just after those Fertile Crescent livestock did. However, those tropical African crops could never be transmitted across South Africa's Fish River, beyond which they were stopped by Mediterranean conditions to which they were not adapted.

The result was the all-too-familiar course of the last two millennia of South African history. Some of South Africa's indigenous Khoisan peoples (otherwise known as Hottentots and Bushmen) acquired livestock but remained without agriculture. They became outnumbered and were replaced northeast of the Fish River by black African farmers, whose southward spread halted at that river. Only when European settlers arrived by sea in 1652, bringing with them their Fertile Crescent crop package, could agriculture thrive in South Africa's Mediterranean zone. The collisions of all those peoples produced the tragedies of modern South Africa: the quick decimation of the Khoisan by European germs and guns; a century of wars between Europeans and blacks; another century of racial oppression; and now, efforts by Europeans and blacks to seek a new mode of coexistence in the former Khoisan lands.

CONTRAST ALSO THE ease of diffusion in Eurasia with its difficulties along the Americas' north-south axis. The distance between Mesoamerica and South America-say, between Mexico's highlands and Ecuador's-is only 1,200 miles, approximately the same as the distance in Eurasia separating the Balkans from Mesopotamia. The Balkans provided ideal growing conditions for most Mesopotamian crops and livestock, and received those domesticates as a package within 2,000 years of its a.s.sembly in the Fertile Crescent. That rapid spread preempted opportunities for domesticating those and related species in the Balkans. Highland Mexico and the Andes would similarly have been suitable for many of each other's crops and domestic animals. A few crops, notably Mexican corn, did indeed spread to the other region in the pre-Columbian era. ease of diffusion in Eurasia with its difficulties along the Americas' north-south axis. The distance between Mesoamerica and South America-say, between Mexico's highlands and Ecuador's-is only 1,200 miles, approximately the same as the distance in Eurasia separating the Balkans from Mesopotamia. The Balkans provided ideal growing conditions for most Mesopotamian crops and livestock, and received those domesticates as a package within 2,000 years of its a.s.sembly in the Fertile Crescent. That rapid spread preempted opportunities for domesticating those and related species in the Balkans. Highland Mexico and the Andes would similarly have been suitable for many of each other's crops and domestic animals. A few crops, notably Mexican corn, did indeed spread to the other region in the pre-Columbian era.

But other crops and domestic animals failed to spread between Mesoamerica and South America. The cool highlands of Mexico would have provided ideal conditions for raising llamas, guinea pigs, and potatoes, all domesticated in the cool highlands of the South American Andes. Yet the northward spread of those Andean specialties was stopped completely by the hot intervening lowlands of Central America. Five thousand years after llamas had been domesticated in the Andes, the Olmecs, Maya, Aztecs, and all other native societies of Mexico remained without pack animals and without any edible domestic mammals except for dogs.

Conversely, domestic turkeys of Mexico and domestic sunflowers of the eastern United States might have thrived in the Andes, but their southward spread was stopped by the intervening tropical climates. The mere 700 miles of north-south distance prevented Mexican corn, squash, and beans from reaching the U.S. Southwest for several thousand years after their domestication in Mexico, and Mexican chili peppers and chenopods never did reach it in prehistoric times. For thousands of years after corn was domesticated in Mexico, it failed to spread northward into eastern North America, because of the cooler climates and shorter growing season prevailing there. At some time between A.D. A.D. 1 and 1 and A.D. A.D. 200, corn finally appeared in the eastern United States but only as a very minor crop. Not until around 200, corn finally appeared in the eastern United States but only as a very minor crop. Not until around A.D. A.D. 900, after hardy varieties of corn adapted to northern climates had been developed, could corn-based agriculture contribute to the flowering of the most complex Native American society of North America, the Mississippian culture-a brief flowering ended by European-introduced germs arriving with and after Columbus. 900, after hardy varieties of corn adapted to northern climates had been developed, could corn-based agriculture contribute to the flowering of the most complex Native American society of North America, the Mississippian culture-a brief flowering ended by European-introduced germs arriving with and after Columbus.

Recall that most Fertile Crescent crops prove, upon genetic study, to derive from only a single domestication process, whose resulting crop spread so quickly that it preempted any other incipient domestications of the same or related species. In contrast, many apparently widespread Native American crops prove to consist of related species or even of genetically distinct varieties of the same species, independently domesticated in Mesoamerica, South America, and the eastern United States. Closely related species replace each other geographically among the amaranths, beans, chenopods, chili peppers, cottons, squashes, and tobaccos. Different varieties of the same species replace each other among the kidney beans, lima beans, the chili pepper Capsic.u.m annuum / chinense Capsic.u.m annuum / chinense, and the squash Cucurbita pepo Cucurbita pepo. Those legacies of multiple independent domestications may provide further testimony to the slow diffusion of crops along the Americas' north-south axis.

Africa and the Americas are thus the two largest landma.s.ses with a predominantly north-south axis and resulting slow diffusion. In certain other parts of the world, slow north-south diffusion was important on a smaller scale. These other examples include the snail's pace of crop exchange between Pakistan's Indus Valley and South India, the slow spread of South Chinese food production into Peninsular Malaysia, and the failure of tropical Indonesian and New Guinean food production to arrive in prehistoric times in the modern farmlands of southwestern and southeastern Australia, respectively. Those two corners of Australia are now the continent's breadbaskets, but they lie more than 2,000 miles south of the equator. Farming there had to await the arrival from faraway Europe, on European ships, of crops adapted to Europe's cool climate and short growing season.

I HAVE BEEN HAVE BEEN dwelling on lat.i.tude, readily a.s.sessed by a glance at a map, because it is a major determinant of climate, growing conditions, and ease of spread of food production. However, lat.i.tude is of course not the only such determinant, and it is not always true that adjacent places at the same lat.i.tude have the same climate (though they do necessarily have the same day length). Topographic and ecological barriers, much more p.r.o.nounced on some continents than on others, were locally important obstacles to diffusion. dwelling on lat.i.tude, readily a.s.sessed by a glance at a map, because it is a major determinant of climate, growing conditions, and ease of spread of food production. However, lat.i.tude is of course not the only such determinant, and it is not always true that adjacent places at the same lat.i.tude have the same climate (though they do necessarily have the same day length). Topographic and ecological barriers, much more p.r.o.nounced on some continents than on others, were locally important obstacles to diffusion.

For instance, crop diffusion between the U.S. Southeast and Southwest was very slow and selective although these two regions are at the same lat.i.tude. That's because much of the intervening area of Texas and the southern Great Plains was dry and unsuitable for agriculture. A corresponding example within Eurasia involved the eastern limit of Fertile Crescent crops, which spread rapidly westward to the Atlantic Ocean and eastward to the Indus Valley without encountering a major barrier. However, farther eastward in India the shift from predominantly winter rainfall to predominantly summer rainfall contributed to a much more delayed extension of agriculture, involving different crops and farming techniques, into the Ganges plain of northeastern India. Still farther east, temperate areas of China were isolated from western Eurasian areas with similar climates by the combination of the Central Asian desert, Tibetan plateau, and Himalayas. The initial development of food production in China was therefore independent of that at the same lat.i.tude in the Fertile Crescent, and gave rise to entirely different crops. However, even those barriers between China and western Eurasia were at least partly overcome during the second millennium B.C. B.C., when West Asian wheat, barley, and horses reached China.

By the same token, the potency of a 2,000-mile north-south shift as a barrier also varies with local conditions. Fertile Crescent food production spread southward over that distance to Ethiopia, and Bantu food production spread quickly from Africa's Great Lakes region south to Natal, because in both cases the intervening areas had similar rainfall regimes and were suitable for agriculture. In contrast, crop diffusion from Indonesia south to southwestern Australia was completely impossible, and diffusion over the much shorter distance from Mexico to the U.S. Southwest and Southeast was slow, because the intervening areas were deserts hostile to agriculture. The lack of a high-elevation plateau in Mesoamerica south of Guatemala, and Mesoamerica's extreme narrowness south of Mexico and especially in Panama, were at least as important as the lat.i.tudinal gradient in throttling crop and livestock exchanges between the highlands of Mexico and the Andes.

Continental differences in axis orientation affected the diffusion not only of food production but also of other technologies and inventions. For example, around 3,000 B.C. B.C. the invention of the wheel in or near Southwest Asia spread rapidly west and east across much of Eurasia within a few centuries, whereas the wheels invented independently in prehistoric Mexico never spread south to the Andes. Similarly, the principle of alphabetic writing, developed in the western part of the Fertile Crescent by 1500 the invention of the wheel in or near Southwest Asia spread rapidly west and east across much of Eurasia within a few centuries, whereas the wheels invented independently in prehistoric Mexico never spread south to the Andes. Similarly, the principle of alphabetic writing, developed in the western part of the Fertile Crescent by 1500 B.C. B.C., spread west to Carthage and east to the Indian subcontinent within about a thousand years, but the Mesoamerican writing systems that flourished in prehistoric times for at least 2,000 years never reached the Andes.

Naturally, wheels and writing aren't directly linked to lat.i.tude and day length in the way crops are. Instead, the links are indirect, especially via food production systems and their consequences. The earliest wheels were parts of ox-drawn carts used to transport agricultural produce. Early writing was restricted to elites supported by food-producing peasants, and it served purposes of economically and socially complex food-producing societies (such as royal propaganda, goods inventories, and bureaucratic record keeping). In general, societies that engaged in intense exchanges of crops, livestock, and technologies related to food production were more likely to become involved in other exchanges as well.

America's patriotic song "America the Beautiful" invokes our s.p.a.cious skies, our amber waves of grain, from sea to shining sea. Actually, that song reverses geographic realities. As in Africa, in the Americas the spread of native crops and domestic animals was slowed by constricted skies and environmental barriers. No waves of native grain ever stretched from the Atlantic to the Pacific coast of North America, from Canada to Patagonia, or from Egypt to South Africa, while amber waves of wheat and barley came to stretch from the Atlantic to the Pacific across the s.p.a.cious skies of Eurasia. That faster spread of Eurasian agriculture, compared with that of Native American and sub-Saharan African agriculture, played a role (as the next part of this book will show) in the more rapid diffusion of Eurasian writing, metallurgy, technology, and empires.

To bring up all those differences isn't to claim that widely distributed crops are admirable, or that they testify to the superior ingenuity of early Eurasian farmers. They reflect, instead, the orientation of Eurasia's axis compared with that of the Americas or Africa. Around those axes turned the fortunes of history.

PART THREE

FROM FOOD TO GUNS, GERMS, AND STEEL

CHAPTER 11

LETHAL G GIFT OF L LIVESTOCK

WE HAVE NOW TRACED HOW FOOD PRODUCTION AROSE in a few centers, and how it spread at unequal rates from there to other areas. Those geographic differences const.i.tute important ultimate answers to Yali's question about why different peoples ended up with disparate degrees of power and affluence. However, food production itself is not a proximate cause. In a one-on-one fight, a naked farmer would have no advantage over a naked hunter-gatherer. in a few centers, and how it spread at unequal rates from there to other areas. Those geographic differences const.i.tute important ultimate answers to Yali's question about why different peoples ended up with disparate degrees of power and affluence. However, food production itself is not a proximate cause. In a one-on-one fight, a naked farmer would have no advantage over a naked hunter-gatherer.

Instead, one part of the explanation for farmer power lies in the much denser populations that food production could support: ten naked farmers certainly would have an advantage over one naked hunter-gatherer in a fight. The other part is that neither farmers nor hunter-gatherers are naked, at least not figuratively. Farmers tend to breathe out nastier germs, to own better weapons and armor, to own more-powerful technology in general, and to live under centralized governments with literate elites better able to wage wars of conquest. Hence the next four chapters will explore how the ultimate cause of food production led to the proximate causes of germs, literacy, technology, and centralized government.

The links connecting livestock and crops to germs were unforgettably ill.u.s.trated for me by a hospital case about which I learned through a physician friend. When my friend was an inexperienced young doctor, he was called into a hospital room to deal with a married couple stressed-out by a mysterious illness. It did not help that the couple was also having difficulty communicating with each other, and with my friend. The husband was a small, timid man, sick with pneumonia caused by an unidentified microbe, and with only limited command of the English language. Acting as translator was his beautiful wife, worried about her husband's condition and frightened by the unfamiliar hospital environment. My friend was also stressed-out from a long week of hospital work, and from trying to figure out what unusual risk factors might have brought on the strange illness. The stress caused my friend to forget everything he had been taught about patient confidentiality: he committed the awful blunder of requesting the woman to ask her husband whether he'd had any s.e.xual experiences that could have caused the infection.

As the doctor watched, the husband turned red, pulled himself together so that he seemed even smaller, tried to disappear under his bedsheets, and stammered out words in a barely audible voice. His wife suddenly screamed in rage and drew herself up to tower over him. Before the doctor could stop her, she grabbed a heavy metal bottle, slammed it with full force onto her husband's head, and stormed out of the room. It took a while for the doctor to revive her husband and even longer to elicit, through the man's broken English, what he'd said that so enraged his wife. The answer slowly emerged: he had confessed to repeated intercourse with sheep on a recent visit to the family farm; perhaps that was how he had contracted the mysterious microbe.

This incident sounds bizarrely one-of-a-kind and of no possible broader significance. In fact, it ill.u.s.trates an enormous subject of great importance: human diseases of animal origins. Very few of us love sheep in the carnal sense that this patient did. But most of us platonically love our pet animals, such as our dogs and cats. As a society, we certainly appear to have an inordinate fondness for sheep and other livestock, to judge from the vast numbers of them that we keep. For example, at the time of a recent census, Australia's 17,085,400 people thought so highly of sheep that they kept 161,600,000 of them.

Some of us adults, and even more of our children, pick up infectious diseases from our pets. Usually they remain no more than a nuisance, but a few have evolved into something far more serious. The major killers of humanity throughout our recent history-smallpox, flu, tuberculosis, malaria, plague, measles, and cholera-are infectious diseases that evolved from diseases of animals, even though most of the microbes responsible for our own epidemic illnesses are paradoxically now almost confined to humans. Because diseases have been the biggest killers of people, they have also been decisive shapers of history. Until World War II, more victims of war died of war-borne microbes than of battle wounds. All those military histories glorifying great generals oversimplify the ego-deflating truth: the winners of past wars were not always the armies with the best generals and weapons, but were often merely those bearing the nastiest germs to transmit to their enemies.

The grimmest examples of germs' role in history come from the European conquest of the Americas that began with Columbus's voyage of 1492. Numerous as were the Native American victims of the murderous Spanish conquistadores, they were far outnumbered by the victims of murderous Spanish microbes. Why was the exchange of nasty germs between the Americas and Europe so unequal? Why didn't Native American diseases instead decimate the Spanish invaders, spread back to Europe, and wipe out 95 percent of Europe's population? Similar questions arise for the decimation of many other native peoples by Eurasian germs, as well as for the decimation of would-be European conquistadores in the tropics of Africa and Asia.

Thus, questions of the animal origins of human disease lie behind the broadest pattern of human history, and behind some of the most important issues in human health today. (Think of AIDS, an explosively spreading human disease that appears to have evolved from a virus resident in wild African monkeys.) This chapter will begin by considering what a "disease" is, and why some microbes have evolved so as to "make us sick," whereas most other species of living things don't make us sick. We'll examine why many of our most familiar infectious diseases run in epidemics, such as our current AIDS epidemic and the Black Death (bubonic plague) epidemics of the Middle Ages. We'll then consider how the ancestors of microbes now confined to us transferred themselves from their original animal hosts. Finally, we'll see how insight into the animal origins of our infectious diseases helps explain the momentous, almost one-way exchange of germs between Europeans and Native Americans.

NATURALLY, WE'RE DISPOSED to think about diseases just from our own point of view: what can we do to save ourselves and to kill the microbes? Let's stamp out the scoundrels, and never mind what to think about diseases just from our own point of view: what can we do to save ourselves and to kill the microbes? Let's stamp out the scoundrels, and never mind what their their motives are! In life in general, though, one has to understand the enemy in order to beat him, and that's especially true in medicine. motives are! In life in general, though, one has to understand the enemy in order to beat him, and that's especially true in medicine.

Hence let's begin by temporarily setting aside our human bias and considering disease from the microbes' point of view. After all, microbes are as much a product of natural selection as we are. What evolutionary benefit does a microbe derive from making us sick in bizarre ways, like giving us genital sores or diarrhea? And why should microbes evolve so as to kill us? That seems especially puzzling and self-defeating, since a microbe that kills its host kills itself.

Basically, microbes evolve like other species. Evolution selects for those individuals most effective at producing babies and at helping them spread to suitable places to live. For a microbe, spread may be defined mathematically as the number of new victims infected per each original patient. That number depends on how long each victim remains capable of infecting new victims, and how efficiently the microbe is transferred from one victim to the next.

Microbes have evolved diverse ways of spreading from one person to another, and from animals to people. The germ that spreads better leaves more babies and ends up favored by natural selection. Many of our "symptoms" of disease actually represent ways in which some d.a.m.ned clever microbe modifies our bodies or our behavior such that we become enlisted to spread microbes.

The most effortless way a germ could spread is by just waiting to be transmitted pa.s.sively to the next victim. That's the strategy practiced by microbes that wait for one host to be eaten by the next host: for instance, salmonella bacteria, which we contract by eating already infected eggs or meat; the worm responsible for trichinosis, which gets from pigs to us by waiting for us to kill the pig and eat it without proper cooking; and the worm causing anisakiasis, with which sushi-loving j.a.panese and Americans occasionally infect themselves by consuming raw fish. Those parasites pa.s.s to a person from an eaten animal, but the virus causing laughing sickness (kuru) in the New Guinea highlands used to pa.s.s to a person from another person who was eaten. It was transmitted by cannibalism, when highland babies made the fatal mistake of licking their fingers after playing with raw brains that their mothers had just cut out of dead kuru victims awaiting cooking.

Some microbes don't wait for the old host to die and get eaten, but instead hitchhike in the saliva of an insect that bites the old host and flies off to find a new host. The free ride may be provided by mosquitoes, fleas, lice, or tsetse flies that spread malaria, plague, typhus, or sleeping sickness, respectively. The dirtiest of all tricks for pa.s.sive carriage is perpetrated by microbes that pa.s.s from a woman to her fetus and thereby infect babies already at birth. By playing that trick, the microbes responsible for syphilis, rubella, and now AIDS pose ethical dilemmas with which believers in a fundamentally just universe have had to struggle desperately.

Other germs take matters into their own hands, figuratively speaking. They modify the anatomy or habits of their host in such a way as to accelerate their transmission. From our perspective, the open genital sores caused by venereal diseases like syphilis are a vile indignity. From the microbes' point of view, however, they're just a useful device to enlist a host's help in inoculating microbes into a body cavity of a new host. The skin lesions caused by smallpox similarly spread microbes by direct or indirect body contact (occasionally very indirect, as when U.S. whites bent on wiping out "belligerent" Native Americans sent them gifts of blankets previously used by smallpox patients).

More vigorous yet is the strategy practiced by the influenza, common cold, and pertussis (whooping cough) microbes, which induce the victim to cough or sneeze, thereby launching a cloud of microbes toward prospective new hosts. Similarly, the cholera bacterium induces in its victim a ma.s.sive diarrhea that delivers bacteria into the water supplies of potential new victims, while the virus responsible for Korean hemorrhagic fever broadcasts itself in the urine of mice. For modification of a host's behavior, nothing matches rabies virus, which not only gets into the saliva of an infected dog but drives the dog into a frenzy of biting and thus infecting many new victims. But for physical effort on the bug's own part, the prize still goes to worms such as hookworms and schistosomes, which actively burrow through a host's skin from the water or soil into which their larvae had been excreted in a previous victim's feces.

Thus, from our point of view, genital sores, diarrhea, and coughing are "symptoms of disease." From a germ's point of view, they're clever evolutionary strategies to broadcast the germ. That's why it's in the germ's interests to "make us sick." But why should a germ evolve the apparently self-defeating strategy of killing its host?

From the germ's perspective, that's just an unintended by-product (fat consolation to us!) of host symptoms promoting efficient transmission of microbes. Yes, an untreated cholera patient may eventually die from producing diarrheal fluid at a rate of several gallons per day. At least for a while, though, as long as the patient is still alive, the cholera bacterium profits from being ma.s.sively broadcast into the water supplies of its next victims. Provided that each victim thereby infects on the average more than one new victim, the bacterium will spread, even though the first host happens to die.

SO MUCH FOR our dispa.s.sionate examination of the germ's interests. Now let's get back to considering our own selfish interests: to stay alive and healthy, best done by killing the d.a.m.ned germs. One common response of ours to infection is to develop a fever. Again, we're used to considering fever as a "symptom of disease," as if it developed inevitably without serving any function. But regulation of body temperature is under our genetic control and doesn't just happen by accident. A few microbes are more sensitive to heat than our own bodies are. By raising our body temperature, we in effect try to bake the germs to death before we get baked ourselves. our dispa.s.sionate examination of the germ's interests. Now let's get back to considering our own selfish interests: to stay alive and healthy, best done by killing the d.a.m.ned germs. One common response of ours to infection is to develop a fever. Again, we're used to considering fever as a "symptom of disease," as if it developed inevitably without serving any function. But regulation of body temperature is under our genetic control and doesn't just happen by accident. A few microbes are more sensitive to heat than our own bodies are. By raising our body temperature, we in effect try to bake the germs to death before we get baked ourselves.

Another common response of ours is to mobilize our immune system. White blood cells and other cells of ours actively seek out and kill foreign microbes. The specific antibodies that we gradually build up against a particular microbe infecting us make us less likely to get reinfected once we become cured. As we all know from experience, there are some illnesses, such as flu and the common cold, to which our resistance is only temporary; we can eventually contract the illness again. Against other illnesses, though-including measles, mumps, rubella, pertussis, and the now defeated smallpox-our antibodies stimulated by one infection confer lifelong immunity. That's the principle of vaccination: to stimulate our antibody production without our having to go through the actual experience of the disease, by inoculating us with a dead or weakened strain of microbe.

Alas, some clever microbes don't just cave in to our immune defenses. Some have learned to trick us by changing those molecular pieces of the microbe (its so-called antigens) that our antibodies recognize. The constant evolution or recycling of new strains of flu, with differing antigens, explains why your having gotten flu two years ago didn't protect you against the different strain that arrived this year. Malaria and sleeping sickness are even more slippery customers in their ability rapidly to change their antigens. Among the slipperiest of all is AIDS, which evolves new antigens even as it sits within an individual patient, thereby eventually overwhelming his or her immune system.

Our slowest defensive response is through natural selection, which changes our gene frequencies from generation to generation. For almost any disease, some people prove to be genetically more resistant than are others. In an epidemic those people with genes for resistance to that particular microbe are more likely to survive than are people lacking such genes. As a result, over the course of history, human populations repeatedly exposed to a particular pathogen have come to consist of a higher proportion of individuals with those genes for resistance-just because unfortunate individuals without the genes were less likely to survive to pa.s.s their genes on to babies.

Fat consolation, you may be thinking again. This evolutionary response is not one that does the genetically susceptible dying individual any good. It does mean, though, that a human population as a whole becomes better protected against the pathogen. Examples of those genetic defenses include the protections (at a price) that the sickle-cell gene, Tay-Sachs gene, and cystic fibrosis gene may confer on African blacks, Ashken.a.z.i Jews, and northern Europeans against malaria, tuberculosis, and bacterial diarrheas, respectively.

In short, our interaction with most species, as exemplified by hummingbirds, doesn't make us or the hummingbird "sick." Neither we nor hummingbirds have had to evolve defenses against each other. That peaceful relationship was able to persist because hummingbirds don't count on us to spread their babies or to offer our bodies for food. Hummingbirds evolved instead to feed on nectar and insects, which they find by using their own wings.

But microbes evolved to feed on the nutrients within our own bodies, and they don't have wings to let them reach a new victim's body once the original victim is dead or resistant. Hence many germs have had to evolve tricks to let them spread between potential victims, and many of those tricks are what we experience as "symptoms of disease." We've evolved countertricks of our own, to which the germs have responded by evolving counter-countertricks. We and our pathogens are now locked in an escalating evolutionary contest, with the death of one contestant the price of defeat, and with natural selection playing the role of umpire. Now let's consider the form of the contest: blitzkrieg or guerrilla war?

SUPPOSE THAT ONE counts the number of cases of some particular infectious disease in some geographic area, and watches how the numbers change with time. The resulting patterns differ greatly among diseases. For certain diseases, like malaria or hookworm, new cases appear any month of any year in an affected area. So-called epidemic diseases, though, produce no cases for a long time, then a whole wave of cases, then no more cases again for a while. counts the number of cases of some particular infectious disease in some geographic area, and watches how the numbers change with time. The resulting patterns differ greatly among diseases. For certain diseases, like malaria or hookworm, new cases appear any month of any year in an affected area. So-called epidemic diseases, though, produce no cases for a long time, then a whole wave of cases, then no more cases again for a while.

Among such epidemic diseases, influenza is one personally familiar to most Americans, certain years being particularly bad years for us (but great years for the influenza virus). Cholera epidemics come at longer intervals, the 1991 Peruvian epidemic being the first one to reach the New World during the 20th century. Although today's influenza and cholera epidemics make front-page stories, epidemics used to be far more terrifying before the rise of modern medicine. The greatest single epidemic in human history was the one of influenza that killed 21 million people at the end of the First World War. The Black Death (bubonic plague) killed one-quarter of Europe's population between 1346 and 1352, with death tolls ranging up to 70 percent in some cities. When the Canadian Pacific Railroad was being built through Saskatchewan in the early 1880s, that province's Native Americans, who had previously had little exposure to whites and their germs, died of tuberculosis at the incredible rate of 9 percent per year.

The infectious diseases that visit us as epidemics, rather than as a steady trickle of cases, share several characteristics. First, they spread quickly and efficiently from an infected person to nearby healthy people, with the result that the whole population gets exposed within a short time. Second, they're "acute" illnesses: within a short time, you either die or recover completely. Third, the fortunate ones of us who do recover develop antibodies that leave us immune against a recurrence of the disease for a long time, possibly for the rest of our life. Finally, these diseases tend to be restricted to humans; the microbes causing them tend not to live in the soil or in other animals. All four of these traits apply to what Americans think of as the familiar acute epidemic diseases of childhood, including measles, rubella, mumps, pertussis, and smallpox.

The reason why the combination of those four traits tends to make a disease run in epidemics is easy to understand. In simplified form, here's what happens. The rapid spread of microbes, and the rapid course of symptoms, mean that everybody in a local human population is quickly infected and soon thereafter is either dead or else recovered and immune. No one is left alive who could still be infected. But since the microbe can't survive except in the bodies of living people, the disease dies out, until a new crop of babies reaches the susceptible age-and until an infectious person arrives from the outside to start a new epidemic.

A cla.s.sic ill.u.s.tration of how such diseases occur as epidemics is the history of measles on the isolated Atlantic islands called the Faeroes. A severe epidemic of measles reached the Faeroes in 1781 and then died out, leaving the islands measles free until an infected carpenter arrived on a ship from Denmark in 1846. Within three months, almost the whole Faeroes population (7,782 people) had gotten measles and then either died or recovered, leaving the measles virus to disappear once again until the next epidemic. Studies show that measles is likely to die out in any human population numbering fewer than half a million people. Only in larger populations can the disease shift from one local area to another, thereby persisting until enough babies have been born in the originally infected area that measles can return there.

What's true for measles in the Faeroes is true of our other familiar acute infectious diseases throughout the world. To sustain themselves, they need a human population that is sufficiently numerous, and sufficiently densely packed, that a numerous new crop of susceptible children is available for infection by the time the disease would otherwise be waning. Hence measles and similar diseases are also known as crowd diseases.

OBVIOUSLY, CROWD DISEASES could not sustain themselves in small bands of hunter-gatherers and slash-and-burn farmers. As tragic modern experience with Amazonian Indians and Pacific Islanders confirms, almost an entire tribelet may be wiped out by an epidemic brought by an outside visitor-because no one in the tribelet had any antibodies against the microbe. For example, in the winter of 1902 a dysentery epidemic brought by a sailor on the whaling ship could not sustain themselves in small bands of hunter-gatherers and slash-and-burn farmers. As tragic modern experience with Amazonian Indians and Pacific Islanders confirms, almost an entire tribelet may be wiped out by an epidemic brought by an outside visitor-because no one in the tribelet had any antibodies against the microbe. For example, in the winter of 1902 a dysentery epidemic brought by a sailor on the whaling ship Active Active killed 51 out of the 56 Sadlermiut Eskimos, a very isolated band of people living on Southampton Island in the Canadian Arctic. In addition, measles and some of our other "childhood" diseases are more likely to kill infected adults than children, and all adults in the tribelet are susceptible. (In contrast, modern Americans rarely contract measles as adults, because most of them get either measles or the vaccine against it as children.) Having killed most of the tribelet, the epidemic then disappears. The small population size of tribelets explains not only why they can't sustain epidemics introduced from the outside, but also why they never could evolve epidemic diseases of their own to give back to visitors. killed 51 out of the 56 Sadlermiut Eskimos, a very isolated band of people living on Southampton Island in the Canadian Arctic. In addition, measles and some of our other "childhood" diseases are more likely to kill infected adults than children, and all adults in the tribelet are susceptible. (In contrast, modern Americans rarely contract measles as adults, because most of them get either measles or the vaccine against it as children.) Having killed most of the tribelet, the epidemic then disappears. The small population size of tribelets explains not only why they can't sustain epidemics introduced from the outside, but also why they never could evolve epidemic diseases of their own to give back to visitors.

That's not to say, though, that small human populations are free from all infectious diseases. They do have infections, but only of certain types. Some are caused by microbes capable of maintaining themselves in animals or in the soil, with the result that the disease doesn't die out but remains constantly available to infect people. For example, the yellow fever virus is carried by African wild monkeys, whence it can always infect rural human populations of Africa, whence it was carried by the transatlantic slave trade to infect New World monkeys and people.

Still other infections of small human populations are chronic diseases such as leprosy and yaws. Since the disease may take a very long time to kill its victim, the victim remains alive as a reservoir of microbes to infect other members of the tribelet. For instance, the Karimui Basim of the New Guinea highlands, where I worked in the 1960s, was occupied by an isolated population of a few thousand people, suffering from the world's highest incidence of leprosy-about 40 percent! Finally, small human populations are also susceptible to nonfatal infections against which we don't develop immunity, with the result that the same person can become reinfected after recovering. That happens with hookworm and many other parasites.

All these types of diseases, characteristic of small isolated populations, must be the oldest diseases of humanity. They were the ones we could evolve and sustain through the early millions of years of our evolutionary history, when the total human population was tiny and fragmented. These diseases are also shared with, or similar to the diseases of, our closest wild relatives, the African great apes. In contrast, the crowd diseases, which we discussed earlier, could have arisen only with the buildup of large, dense human populations. That buildup began with the rise of agriculture starting about 10,000 years ago and then accelerated with the rise of cities starting several thousand years ago. In fact, the first attested dates for many familiar infectious diseases are surprisingly recent: around 1600 B.C. B.C. for smallpox (as deduced from pockmarks on an Egyptian mummy), 400 for smallpox (as deduced from pockmarks on an Egyptian mummy), 400 B.C. B.C. for mumps, 200 for mumps, 200 B.C. B.C. for leprosy, for leprosy, A.D. A.D. 1840 for epidemic polio, and 1959 for AIDS. 1840 for epidemic polio, and 1959 for AIDS.