Almost since the 1871 publication of “The Descent of Man,” in which Charles Darwin applied his theory of natural selection to the human species, biologists have argued over whether the dramatic series of evolutionary events that led to the emergence of Homo sapiens continues to this day.

Some have argued that culture and technology have eclipsed the powerful biological forces that shaped our species in its formative years. In their view the species, no longer faced with a daily struggle for survival, is adrift in an evolutionary Sargasso Sea.

“There’s been no biological change in humans in 40,000 or 50,000 years. Everything we call culture and civilization we’ve built with the same body and brain,” the famed evolutionary biologist Stephen J. Gould once said in an interview.

In their new book “The 10,000 Year Explosion,” anthropologists Henry Harpending and Gregory Cochran argue the contrary position. They claim that in fact, far from grinding to a halt, human evolution has accelerated dramatically since the origins of agriculture about 10,000 years ago.

“We intend to make the case that human evolution has accelerated in the past 10,000 years, rather than slowing or stopping, and is now happening about 100 times faster than its long-term average over the 6 million years of our existence,” they write.

In evolutionary terms, 10,000 years is no time at all — about 400 human generations. Rabbits can go through 400 generations in not much more than a century — can you imagine rabbits being substantially different than they were 100 years ago?

Far from ending the chain of dramatic evolutionary changes that led to upright walking, advanced cognitive abilities and spoken language, Cochran and Harpending argue, the adoption of agriculture so dramatically changed the human environment that a new wave of genetic innovations flourished. These new genetic variants thrived because they helped people cope with the challenges an agricultural way of life presented, such as the shift to a low protein, high carbohydrate diet; the creation of an organized, stratified society and the rise of infectious diseases in response to increased population density.

In fact, many of the genetic variations that 23andMe provides information about are relics of those evolutionary changes. The SNP that confers lactose tolerance, for example, appears to have arisen in Europe about 8,000 years ago among the first people to herd cows and other milk-producing animals. The lactose-digesting variant quickly spread throughout the parts of Eurasia that were ecologically suited to pastoralism.

There are also a number of genetic variations covered by 23andMe that cause physiological problems when two mutated copies are present, but provide protection against infectious disease when a person has one of each version of the gene. For example, the genetic variations that cause sickle cell anemia and G6PD deficiency confer resistance to malaria. Geneticists call this situation balancing selection; over the entire population, the reproductive cost to those who end up with the genetic disease is outweighed by the benefit to others who are resistant to the infectious one.

At the end of the book, Cochran and Harpending make the controversial argument that balancing selection is responsible for the increased incidence of a number of genetic diseases among people of Ashkenazi Jewish descent — and for their higher intelligence relative to other groups.

The authors do raise some interesting points about the anomalously high frequency among Ashkenazi of genetic disorders that stimulate the growth of neurons in the brain. And they cite studies that have shown increased intelligence among people with some of these diseases.

But genetic explanations for between-group differences in intelligence are best taken with a whopping dose of skepticism. Even the definition of intelligence is a matter of intense debate, not to mention the degree to which it can be inherited through genetics. in the end, their case is little more than a just-so story.

In telling it Cochran and Harpending blunt the rest of their book’s powerful message: human evolution is not over by a long sight.

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Last week in the Spittoon we reported on a new study that identified an interesting genetic trade-off — a genetic variant known that has one effect on a person’s vulnerability to malaria, and the opposite on susceptibility to HIV infection. The “Duffy negative” version of the gene, which is common among Africans and African Americans, appears to protect a person against malaria but increases vulnerability to infection by HIV.

As it turns out, Duffy is not the only example of a genetic trade-off in humans.  There are many instances of genetic variation throughout the human genome that offer both genetic advantages and disadvantages to their carriers.  Here are some of the most interesting:

1.    Sickle Cell Anemia vs. Malaria

Sickle cell anemia is caused by a genetic mutation that alters the shape of an individual’s red blood cells.  This mutation, called Hb^s, causes red blood cells to take on a sickle-shape, as opposed to the normal round shape.  The sickle-shaped cells then get stuck in the veins and arteries, causing tremendous pain and discomfort.  Sickle cell anemia is recessively inherited, meaning that someone must inherit the Hb^s mutation from both parents in order to have the disease.

Malaria is a disease that kills between 1 and 3 million people worldwide each year, mainly in the tropics.  After scientists noticed similarities between the geographic distribution of sickle cell anemia and malaria, they began to wonder if there was some sort of connection between the two.

Experiments soon confirmed that sickle cell anemia is a sort of genetic Faustian bargain. Recall that individuals with two copies of Hb^s suffer from sickle cell anemia, but people with only one copy of the mutation do not.  They do however, display a resistance to malaria compared with people who have no copies of Hb^s.  Occasionally, a pair of malaria-resistant parents will both pass Hb^s — and thus sickle cell anemia — to their child. But overall, having only one copy improved the survival rate in human history so much that the Hb^s mutation continues to exist in in spite of the disease burden it causes.

2.    Hereditary Hemochromatosis vs. Iron Deficiency

Hereditary hemochromatosis (HH) is a genetic condition in which the body absorbs too much iron from the diet.  This leads to the toxic build-up of iron in the tissues of major organs such as the liver and heart.  Without treatment, HH can lead to organ failure.

Genetic studies have found that HH, like sickle-cell, is a recessive trait. It appears to have evolved about 1,400 years ago, probably in western Europe, at a time when people ate mostly cereal grains — which are very low in iron. Because having some amount of iron in the diet is essential to maintain normal body functions, this was a serious problem.  

During this time period, the ability to store extra iron in the body would have been helpful.  Individuals with HH could take iron from foods when it was available, and then store it in the organ tissues, dipping into those reserves when the supply of iron-rich foods was low.  Today, however, iron is much more abundant. It is an excess of iron, not a lack of it, that threatens the health of people with HH.

3.    The Paleolithic Diet vs. Obesity

Why is it that humans crave the very foods that are unhealthy?  Why do we prefer donuts and candy to celery and spinach?  Like hereditary hemochromatosis, the source of this cruel irony lies in the history of our species.

The human brain is a very expensive organ to maintain.  It requires a lot of energy to keep all the synapses working correctly, and simply feasting on celery would not do the trick.  Hundreds of thousands of years ago, our ancestors began eating meat as a way to get the required energy their brains needed.  Meat is high in the energy that humans needed to survive, and also in long-chain polyunsaturated fats, which are essential to maintenance of brain tissue.  Bone marrow, the fatty substance inside long bones, is also high in fat and calories, and was thus another prized item in our ancestors’ early diet.  

Because foods high in fat and calories were so important to our ancestors, they would have searched them out and evolved a natural preference for them.  Their bodies would have evolved to store any excess fat, in case there were was a long hiatus until the next piece of meat or bone marrow came their way. 

This ‘thrifty’ metabolic approach to fat has persisted to the present day, despite drastic changes in the way we feed ourselves.  Now, instead of searching constantly for food we have seemingly unlimited access to Twinkies, beer and other high-calorie delights.  But our bodies are still storing the excess fat.

The genetics of obesity are complicated, and by no means can they be fully explained by our ancestors’ diet. But the dramatic change in the human diet since the Stone Age does help explain our cravings from an evolutionary perspective.

Variations in the human genome are full of examples such as these: genetic mutations that are beneficial in some ways but harmful in others, or that used to be beneficial, but now result in an increased waistline.  Understanding these genetic ‘trade-offs’ is helpful to understanding the history of the human genome, and could be helpful in tackling conditions such as sickle-cell anemia, hereditary hemochromatosis, obesity and many others.

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