<img loading="lazy" decoding="async" class="alignright size-full wp-image-4436" title="Acute_leukemia-ALL" src="https://blog-api.23andme.com/wp-content/uploads/2009/08/Acute_leukemia-ALL.jpg" alt="Acute_leukemia-ALL" width="330" height="375" srcset="https://blogcms.23andme.com/wp-content/uploads/2009/08/Acute_leukemia-ALL.jpg 347w, https://blogcms.23andme.com/wp-content/uploads/2009/08/Acute_leukemia-ALL-264x300.jpg 264w" sizes="auto, (max-width: 330px) 100vw, 330px" />
Acute lymphoblastic leukemia (ALL) is the most common childhood cancer in developed nations, affecting between 30 and 45 out of every one million kids.   But not much is known about the genetics of the disease.
Two research groups set out to learn more by looking for common genetic variations associated with the disease.   Their results, published online this week in Nature Genetics, provide new insight into the development of ALL.
British researchers led by <a href="https://dx.doi.org/10.1038/ng.430" target="_blank" rel="noopener noreferrer">Elli Papaemmanuil</a> studied a total of 907 ALL cases and 2,398 controls with European ancestry.   They identified three genetic variants associated with increased risk for the disease.
The strongest of these, , is near the IKZF1 gene, which encodes a protein involved in the development of white blood cells.   Deletions of the region of DNA containing this gene are common in forms of ALL that have a poor prognosis.   Each copy of a G at increases the odds of ALL by 1.69 times.
The second most strongly associated SNP was in ARID5B, a gene previously linked to a different form of blood cancer called acute promyelocytic leukemia.   Each copy of a G at was associated with 1.65 times increased odds of ALL.
Finally, Papaemmanuil et al. found that each copy of a G at was associated with 1.34 times increased odds of ALL.
All three SNPs were even more strongly associated with ALL when the researchers restricted their analysis to a subtype of the disease called B-cell ALL.   Within this form of the disease, in ARID5B seems to be highly associated with a further subtype called hyperdiploid ALL.   This form of the disease has a better response to methotrexate chemotherapy than other subtypes of ALL.
The authors conclude that the variations they identified underlie approximately 64% of all cases of ALL.
&#8220;Our findings provide the first unambiguous evidence that common genetic variation influences the risk of developing pediatric ALL and strong rationale for searching for additional risk variants through further GWA [genomewide association] scans,&#8221; the authors write.
In a separate study of 441 ALL cases and 16,912 controls, <a href="https://dx.doi.org/10.1038/ng.432" target="_blank" rel="noopener noreferrer">Lisa Trevino</a> and colleagues from the United States also found evidence for the involvement of variants in and around the ARID5B gene in B-hyperdiploid ALL.   The riskier versions of SNPs closely related to were not only correlated with disease risk, but also with a response to methotrexate that at least partially underlies its greater efficacy in B-hyperdiploid ALL.
&#8220;The data…suggest that the same genetic variation that predisposes to B-hyperdiploid ALL may underlie the superior response of this subtype to chemotherapy.   Thus, genomic variation may affect not only disease risk but treatment outcome as well,&#8221; they write.
Photo: <a href="https://en.wikipedia.org/wiki/File:Acute_leukemia-ALL.jpg" target="_blank" rel="noopener noreferrer">VashiDonsk</a>

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Genetic Variants Associated With Risk Of Childhood Acute Lymphoblastic Leukemia Identified

<img loading="lazy" decoding="async" class="alignright wp-image-1965 size-medium" src="http://35.88.189.111/wp-content/uploads/2008/11/hivvirus-300x223.jpg" alt="" width="300" height="223" srcset="https://blogcms.23andme.com/wp-content/uploads/2008/11/hivvirus-300x223.jpg 300w, https://blogcms.23andme.com/wp-content/uploads/2008/11/hivvirus.jpg 350w" sizes="auto, (max-width: 300px) 100vw, 300px" />
AIDS used to be considered a male-specific health problem – &nbsp;but now, the majority of its victims are female.
Those numbers aside, <a href="http://aje.oxfordjournals.org/cgi/content/abstract/168/5/532" target="_blank" rel="noopener">some studies</a> have shown that certain females take much longer than males to progress to AIDS after being infected with HIV. Now, researchers have now found a mechanism that might explain this difference.
A two-stage study by Siddiqui et al. identified a genetic variant on the X chromosome that may slow progression from HIV-1 to AIDS in women. The study analyzed both primates and humans, demonstrating that genetic association findings can successfully translate across species, even over an evolutionary distance of 25 million years.

The researchers first analyzed 136 rhesus monkeys infected with SIV (simian immunodeficiency virus). They found a common genetic marker on the X chromosome among those monkeys that progressed slowly to AIDS-related disease. Researchers then studied 303 HIV-infected humans and found an analogous marker on the X chromosome –the SNP &nbsp; – &nbsp;that may affect progression to AIDS in human females.
The results, published in the online version of <a href="http://www.cell.com/AJHG/abstract/S0002-9297(09)00304-8" target="_blank" rel="noopener">The American Journal of Human Genetics</a>, indicate that in humans, females with one copy of the C version of progressed to AIDS more slowly than either females with TT or males with a C or T. (Note that females have two X chromosomes, while males only have one.)
Females with one copy of the C version of the SNP took an average of eight years to progress from HIV infection to AIDS, nearly four times less than females with no copies or males. Women with two copies of C are so rare that none were found in the study.
Previous research has linked some degree of HIV resistance to a mutation in SNP i3003626, which is in a gene that encodes the CCR5 receptor.
The CT genotype of is more frequent among Asians than Europeans or Africans, suggesting that future research may find that HIV-1 positive Asian females have a slower progression to AIDS. Future studies may also be able to use this X chromosomal variant as a clue toward new drug development for both genders.

Genetic Variation in X Chromosome May Slow Progression of AIDS

<img loading="lazy" decoding="async" class="alignright size-full wp-image-4361" title="Two young girls bullying other young girl outdoors" src="https://blog-api.23andme.com/wp-content/uploads/2009/08/iStock_000008979485XSmall.jpg" alt="Two young girls bullying other young girl outdoors" width="346" height="229" srcset="https://blogcms.23andme.com/wp-content/uploads/2009/08/iStock_000008979485XSmall.jpg 425w, https://blogcms.23andme.com/wp-content/uploads/2009/08/iStock_000008979485XSmall-300x199.jpg 300w" sizes="auto, (max-width: 346px) 100vw, 346px" />
It&#8217;s no accident that we often refer to rejection or insult as a slap in the face – research shows the same brain signaling pathways are involved in both physical and emotional pain.
And morphine, a drug well known for its ability to dull physical pain, also reduces separation-induced emotional distress in monkeys, dogs, guinea pigs, rats and chickens.   This is thought to depend on changes in signaling through a morphine receptor called MOR (mu-opioid receptor) that is also implicated in emotional pain in humans. Studies have shown that signaling through MOR is reduced when women recall upsetting events like the death of a loved one or the breakup of a romantic relationship.
Given that MOR seems to be at the center of the overlap between physical and emotional pain, researchers from the UCLA Department of Psychology wondered whether a genetic variation in the gene that encodes MOR that is already known to impact sensitivity to physical pain might also affect how thick-skinned a person is.
Baldwin M. Way and colleagues surveyed 122 healthy young adults about their sensitivity to social rejection.   The assessment measured the tendency of study subjects to be fearful that social interactions will result in hurt feelings, criticism and being a burden to others.   The results, published online this week in the <a href="https://dx.doi.org/10.1073/pnas.0812612106" target="_blank" rel="noopener">Proceedings of the National Academy of Sciences</a>, show that people with one or two of the variants had significantly higher levels of self-reported sensitivity to social rejection. The variants are also associated with needing more morphine for pain relief after surgery.
A subset of the study participants also had their brains scanned in an fMRI machine while playing an online ball-tossing game.   The subjects thought they were playing with two people, but in reality they were interacting with a pre-set computer program.   The game simulated social rejection by having the subjects&#8217; virtual playmates leave them out of the fun.
Just as in the survey, the variant was associated with heightened responses to social rejection.   Higher brain activity was recorded in the anterior cingulate cortex and the anterior insula brain regions associated with the processing of both physical and emotional pain, in people with one or two of the variants.
As is usually the case, the results of this study should be considered preliminary until other researchers replicate them. But based on their results, along with previous research, the authors conclude that, &#8220;… at multiple biological levels, including the neurochemical, neuroanatomical, and now genetic, feeling hurt physically shares more than just linguistic commonality with feeling hurt socially.&#8221;

Genetic Variation In Morphine Receptor May Play A Part In Coping With Social Rejection

<img loading="lazy" decoding="async" class="alignright size-medium wp-image-4345" src="https://blog-api.23andme.com/wp-content/uploads/2009/08/african-dog-300x242.jpg" alt="african dog" width="300" height="242" srcset="https://blogcms.23andme.com/wp-content/uploads/2009/08/african-dog-300x242.jpg 300w, https://blogcms.23andme.com/wp-content/uploads/2009/08/african-dog.jpg 400w" sizes="auto, (max-width: 300px) 100vw, 300px" />
The Rexes and Spots of the world have been man&#8217;s best friend for 15,000 years. But when and where did humans begin domesticating these furry companions?
Previous theories suggested that the domesticated dog originated in East Asia and then spread to Africa, Oceania and the Americas. But a recent study by Cornell University researchers has found Mr. Chompers may not have originated in East Asia after all.
Boyko et al. analyzed more than 300 SNPs throughout the genome, as well as a chunk of the maternally inherited mitochondrial DNA and an assortment of other genetic markers in hundreds of village dogs from seven different regions of Egypt, Uganda and Namibia, along with African dog breeds, Puerto Rican street dogs, and mixed-breeds from the United States.

The results, published online ahead of print this month in the <a href="https://www.pnas.org/content/early/2009/07/31/0902129106" target="_blank" rel="noopener">Proceedings of the National Academy of Sciences</a>, showed that African village dogs were the most genetically diverse of all the dogs screened. This diversity was comparable to that in East Asian village dog populations.
Mixed-breed dogs and even African breeds, such as Pharaoh hounds and Salukis, lack such genetic diversity since they have been artificially selected and bred.
African village dogs consistently showed this diverse, indigenous ancestry, with the exception of dogs from central Namibia and Giza who showed genetic signs of some mixing with other non-native dogs. This mixing could be due to earlier mating with human-bred dogs or the relative proximity of Giza to Eurasia, which is home to most known breeds.
<a href="https://blog.23andme.com/2009/04/30/scientists-publish-largest-ever-study-on-the-genetics-of-modern-africans/" target="_blank" rel="noopener">&#8220;Like ancient human populations, these ancient dog populations developed genetic signatures characteristic of their geographic locale,&#8221;</a> the authors wrote.
Africa has the highest amount of <a href="http://www.sciencemag.org/cgi/content/abstract/1172257" target="_blank" rel="noopener">genetic diversity in humans</a> because humans originated and have been living there longer than on any other continent. Similarly, the high genetic diversity of African village dogs suggests that our canine friends may have also originated in Africa. But the similar level of diversity among East Asian village dogs means that region can&#8217;t be ruled out as the birthplace of Canis lupus familiaris. So, more research will be needed to determine exactly when and where canines diverted from baring fangs to chasing boomerangs.
Photo credit: Corin Boyko

Genetic Study Suggests Dogs Domesticated in Africa

<img loading="lazy" decoding="async" class="alignright size-full wp-image-4325" title="RedHairDentalPain" src="https://blog-api.23andme.com/wp-content/uploads/2009/08/RedHairDentalPain.jpg" alt="RedHairDentalPain" width="350" height="233" srcset="https://blogcms.23andme.com/wp-content/uploads/2009/08/RedHairDentalPain.jpg 350w, https://blogcms.23andme.com/wp-content/uploads/2009/08/RedHairDentalPain-300x200.jpg 300w" sizes="auto, (max-width: 350px) 100vw, 350px" />
Redheads might have a better excuse than the rest of us for avoiding the dentist.
For several years now scientists have known that the same genetic variations that give redheads their fiery manes can increase the amount of general or local anesthetic a person needs in order to be properly put out or numbed up.
<h2>Dental Pain</h2>
New research suggests that the effect of these variations is strong enough, and hasn&#8217;t been addressed by dentists well enough, that the people who carry them are more than twice as likely as those who don&#8217;t to avoid going to the dentist altogether.Researchers at the University of Kentucky surveyed 67 redheads and 77 dark haired people about their general anxiety levels, their dental treatment-related anxiety and their fear of dental pain.
The results, published in the July issue of the Journal of the American Dental Association, reveal that while hair color has no effect on general anxiety, redheads are more likely to be apprehensive about sliding into the dentist&#8217;s chair.
A closer look at the data showed that increased dental-treatment anxiety and fear of dental pain is found in all people with the variants in the MC1R gene associated with red hair, even those people who carry these variations despite having dark hair.
<h2>The MC1R Gene</h2>
The protein encoded by the MC1R gene is found in melanocytes, the cells that give hair and skin their color.
The variants associated with <a href="https://www.23andme.com/topics/traits/red-hair">red hair</a> alter the protein&#8217;s function, tipping the balance of pigment production in melanocytes from black-brown eumelanin to red-yellow pheomelanin. Researchers don&#8217;t yet understand how this same protein impacts pain sensitivity and anesthetic needs.
People carrying one or two of the MC1R variants had 2.46 times greater odds of avoiding routine dental care compared to those who carry none. The authors speculate that this might be because prior dental experiences have left them in pain.
The researchers recommend that dentists evaluate all patients, especially those with natural red hair, for dental procedure-related anxiety and take whatever steps are necessary to help them manage their feelings and make it to their regular check-ups, because as the saying goes, &#8220;Ignore your teeth and they&#8217;ll go away.&#8221;

Link Between Red Hair and Avoiding The Dentist

<img loading="lazy" decoding="async" class="alignright size-full wp-image-4273" title="blooddonation" src="https://blog-api.23andme.com/wp-content/uploads/2009/08/blooddonation.jpg" alt="blooddonation" width="350" height="232" srcset="https://blogcms.23andme.com/wp-content/uploads/2009/08/blooddonation.jpg 350w, https://blogcms.23andme.com/wp-content/uploads/2009/08/blooddonation-300x199.jpg 300w" sizes="auto, (max-width: 350px) 100vw, 350px" />
Editor&#8217;s note: This post has been edited to reflect the current product. 
When it comes to blood transfusions, what&#8217;s good for one person might be deadly for another.
This might seem obvious today, but until 1900 the idea of &#8220;blood types&#8221; wasn’t understood. A person in need of a transfusion could find himself getting a donation from just about anyone, and sometimes even an animal!
But in 1900 Austrian scientist <a href="http://nobelprize.org/nobel_prizes/medicine/laureates/1930/" target="_blank" rel="noopener noreferrer">Karl Landsteiner</a> noticed that when the blood of different people was mixed together the cells would often clump up, a process he correctly attributed to an immune reaction between the two blood samples. By the next year he had used this clumping reaction to define three main types of blood, which he named A, B and O. (The fourth blood type, AB, was identified in 1902 by two other scientists, Decastello and Struli.)

After hundreds of years of performing blood transfusions unguided, scientists finally had what they needed to safely transfer blood between people. In 1907, the first blood transfusion utilizing the new typing techniques was successfully carried out, and by World War I transfusions were being performed safely on a large scale.
But knowing what blood to give someone and having it on hand are two different things.
Blood banks are faced with the daunting task of making sure there is enough blood of the right type for everyone who needs it at all times. Blood type O, the &#8220;universal donor,&#8221; tends to be overused. This presents a problem for the approximately 40% of Americans are type O and thus can receive only this type in a transfusion. If supplies run low, their lives could be in danger. At the same time, donated blood with the rare B and AB types can sit unused for so long that it becomes outdated and must be discarded.
One solution to managing the blood supply would be to transform all blood into type O, thus making it suitable for everyone. In the early 1980&#8217;s scientists found a way to do this using an enzyme from coffee beans that could strip certain sugars off of type B blood cells. Clinical trials showed that this method was safe and effective, but the method itself was too time consuming and costly to ever be of clinical use. <a href="http://www.bioedonline.org/news/news.cfm?art=3239" target="_blank" rel="noopener noreferrer">New research, however, has identified bacterial enzymes</a> that can carry out this same process more efficiently. Research with this new method is still in progress.

More on ABO Blood Type: The Key to Compatibility

<img loading="lazy" decoding="async" class="alignright size-full wp-image-4244" title="gray1100" src="https://blog-api.23andme.com/wp-content/uploads/2009/07/gray1100.png" alt="gray1100" width="314" height="223" srcset="https://blogcms.23andme.com/wp-content/uploads/2009/07/gray1100.png 600w, https://blogcms.23andme.com/wp-content/uploads/2009/07/gray1100-300x214.png 300w" sizes="auto, (max-width: 314px) 100vw, 314px" />
A new genetic study has added more evidence to a decades-old association between blood type and the risk for pancreatic cancer.
Close to <a href="http://seer.cancer.gov/statfacts/html/pancreas.html" target="_blank" rel="noopener noreferrer">42,500 men and women</a> are expected to be diagnosed with pancreatic cancer in the United States this year.   Because there is no effective screening test for the disease and it is often not detected until it has spread, the five-year survival rate for people with pancreatic cancer is only about 5%. The new results, published online this week in the journal <a href="https://dx.doi.org/10.1038/ng.429" target="_blank" rel="noopener noreferrer">Nature Genetics</a>, represent one of the first associations of a common genetic variant with this deadly disease.
Researchers from Harvard and the National Cancer Institute studied more than 4,300 people with pancreatic cancer and 4,500 controls.   They found that each copy of the C version of is associated with 1.2 times increased odds of pancreatic cancer compared to two Ts at this SNP.   The study subjects were mainly of European descent, but this association was essentially the same when the small number of people from other ethnic groups (mainly Asian and African American) was also included in the analysis.
The non-risk T version of this SNP is linked to the variation in the ABO gene that results in type O blood.   People with two Ts are type O.   The riskier C version of the SNP is found in people with type A, B and AB blood.
Epidemiological studies from the 1950s and 1960s, as well as more <a href="https://www.ncbi.nlm.nih.gov/pubmed/19276450" target="_blank" rel="noopener noreferrer">recent reports</a>, have suggested that people with type O blood are at lower risk for pancreatic cancer compared to those with type A or type B blood.   Finding the association of with the disease in a genetic study adds more credence to these previous results. What&#8217;s still not understood, however, is why people with type O blood are less likely to get pancreatic cancer.
In their concluding remarks, the authors of the study stressed the need for further research into the genetic risk factors for cancer of the pancreas.
&#8220;As there are few known risk factors, improved diagnostics and a finer understanding of the molecular pathogenesis are urgently needed…. The discovery of additional genetic risk variants for this highly lethal cancer could contribute to improvements in … prevention, early detection and therapeutic approaches to pancreatic cancer,&#8221; the authors write.

Genomewide Study Supports Blood Type As A Risk Factor For Pancreatic Cancer

&#8220;But we always go there!&#8221;
And so begins another Friday night. When it comes to choosing where to go to dinner, my husband likes to stick with the tried and true. I like trying out new places.
A new study suggests that the roots of this conflict could spring partly from our genes. It suggests that a DNA variation affecting the neurotransmitter dopamine influence a person&#8217;s willingness to explore new options instead of sticking with the status quo.
<h6>Trying Something New</h6>
The finding comes from a study by Michael Frank and colleagues from Brown University and the University of Arizona. The researchers focused on how people learn from positive and negative feedback. Subjects were confronted with a clock face that counted down five seconds.   Before time was up they had to push a button to receive points.   In some trials, the experiment was set up so that the faster they pushed the button, the more points they got. In other trials, waiting longer got more points.
To the researchers&#8217; surprise, people showed wide swings in response speed within each type of trial as they adjusted their timing in an attempt to maximize their scores. Computer models showed that a likely reason for these swings is that people change their strategy (pressing the button faster or slower) in proportion to how uncertain they are that a new strategy (speeding up or slowing down from what they&#8217;ve been doing) will yield better results.
It makes sense: If you think a new restaurant might be only marginally better than the one you usually go to (and could be worse), you&#8217;re probably not that likely to vary from the usual routine. Why risk it?
But if you really have no idea how good a place might be — who knows, it could blow your mind – you&#8217;d probably be more inclined to give it a whirl.
<h6>Adventurousness</h6>
Further analysis of the data, which will appear in the August issue of <a href="https://dx.doi.org/10.1038/nn.2342" target="_blank" rel="noopener noreferrer">Nature Neuroscience</a>, showed that the extent to which a person tried out new strategies correlated with variations in the COMT gene. People who carried the &#8220;Met&#8221; version of the gene were more exploratory in the face of uncertainty about what strategy to try next than people with two copies of the &#8220;Val&#8221; version (&#8220;Met&#8221; and &#8220;Val&#8221; refer to particular amino acids encoded by different versions of the gene).
People with two copies of the Met version were the most adventurous, but even those with only one copy were statistically different in their exploration of new strategies from the people with two copies of the Val version.
The protein encoded by the COMT gene is involved in dopamine signaling in the prefrontal cortex, an area of the brain involved in planning and decision-making.   The Met version of the gene leads to increased dopamine activity in this region and has been linked to more efficient information processing.
So does this explain my date-night drama?   Well, there&#8217;s undoubtedly more to it than genes alone, but I do have one copy of the more exploratory Met version of the COMT gene.   And my husband?   Two copies of the stuck-in-a-rut Val version.
<h6>Dopamine and Learning</h6>
In a region of the brain called the basal ganglia, dopamine helps us internalize positive and negative feedback in order to develop those &#8220;gut&#8221; feelings of what strategy will work and what won&#8217;t.
The effects of dopamine in the basal ganglia have been shown in experiments that use drugs to raise or lower levels of the neurotransmitter in the brain.   Higher dopamine levels help people learn to repeat rewarding behaviors, while lower dopamine leads to better learning from bad experiences.   In a game where &#8220;A&#8221; usually yields more points than &#8220;B,&#8221; people with boosted dopamine levels learn to choose A.   People with decreased dopamine levels learn to avoid B.
In non-medicated test subjects, genetic variations that influence dopamine signaling in the basal ganglia also impact so-called &#8220;Go&#8221; (choose A) and &#8220;NoGo&#8221; learning (avoid B). People with two copies of the A version of a variant in the DARPP-32 gene, which increases dopamine signaling, tend to be better at Go learning than their G-version-carrying friends.   
The clock-and-button experiments Frank et al. conducted further tested the association of these two variants with Go and NoGo learning.   Trials that rewarded faster responses measured Go learning.   Trials that rewarded holding off on the action of button pushing measured NoGo learning. 
<h6>Parkinson&#8217;s Disease Connection</h6>
Understanding the role of dopamine in learning from experience may have important implications for treating people with Parkinson&#8217;s disease, which is characterized by a loss of dopamine producing neurons in the brain.   Studies have shown that people with Parkinson&#8217;s have trouble with Go learning.   It&#8217;s thought that the lack of dopamine in their brains prevents the dopamine spikes needed to learn from positive feedback.
This fits with evidence that drugs that increase dopamine help people with Parkinson&#8217;s improve their performance on tasks that require Go learning.   But there is a downside:   because they flood the brain with dopamine, the normal dips in signaling that are needed to learn from negative feedback are blocked by these drugs.   This might explain why some people with Parkinson&#8217;s disease who take dopamine-increasing medications develop gambling problems — they&#8217;re overly attuned to winning, but incapable of learning from their losses.

DNA Variation May Help Us Break Free From Our Routines

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Ten millennia ago, there were about six million people on Earth. Today, there are six billion.
This thousandfold increase in the global population is often thought to be linked to the invention of farming and the domestication of animals about 13,000 years ago in the Near East. Growing crops and raising live animals requires a larger work force than hunting or gathering, so as agriculture took hold, families grew in size. These families grew into villages, villages grew into towns and cities, which eventually consolidated into the vast civilizations in ancient Mesopotamia, Egypt, and elsewhere.
Was this surge during the early days of agriculture the ONLY time in the history of our species that the worldwide population size of humans experienced a substantial boost? The traditional answer was yes. Early human hunter-gatherer populations were relatively stable, their overall size not changing much from generation to generation. Stone-age humans had a limited number of gazelles to hunt, berries to pick and eggs to snatch. Those ecological limitations suggest that pre-agricultural communities would have grown only modestly, even when the hunting was good.
But a new DNA analysis published in the July 29 issue of <a id="a:sf" title="PLoS One" href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0006366" target="_blank" rel="noopener">PLoS One</a> suggests that the world&#8217;s human population grew dramatically even long before the development of farming.

Earlier analyses of mitochondrial DNA (mtDNA) have suggested that there were bursts of population growth much further back in time, but those studies have been unable to pinpoint a specific time span.
Geneticist Michael Hammer and his colleagues looked at nuclear DNA from four African populations: the San hunter-gatherers of the Kalahari Desert, the Biaka Pygmies of the Central African Republic, the Mandenka of Senegal and the Yorubans of Nigeria. Nuclear DNA is useful here because it is more sensitive to population size changes than mtDNA.
The authors found genetic evidence for a surge in human population size about 40,000 to 50,000 years ago. This period, just after humans first set foot outside Africa, is of great interest to archaeologists because it coincides with a dramatic increase in the sophistication of human behavior. People began crafting tools from bone, burying their dead and fashioning clothing to keep themselves warm in cool climates. They developed complex hunting techniques, and created great works of art in the form of cave paintings and jewelery.
The archaeological record also shows that during this time, humans began hunting more dangerous prey and more easily exploiting small game like rabbits and birds. They traveled farther than they had before, perhaps due to the growth of long-distance trade routes &#8211; the first of their kind. Jared Diamond, author of The Third Chimpanzee, calls this period &#8220;The Great Leap Forward,&#8221; when humans burst forth culturally &#8211; finally separating themselves from their evolutionary cousins.
The exact cause for these changes in human behavior may never be known. Some believe a simple genetic mutation or that the evolution of language could have sparked such a dramatic change. But what we do know now, thanks to this new genetic research, is that like the invention of agriculture this explosion of innovation was accompanied by population growth.

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