Contributed by Ziad Jowhar, Elie Nwefo, Yasmine Alkhalid, Sai Greeshma Magam, Rasika Tangutoori, & Shray Ambe

Imagine waking up everyday with fatigue and joint pain. You constantly fear having a stroke or heart attack that could cause your premature death. Unfortunately, this is a reality for patients dealing with severe forms of sickle cell disease (SCD).

SCD is caused by a recessive mutation on chromosome eleven and primarily affects the cardiovascular system. Red blood cells are essential for transporting oxygen to the rest of your body. These cells are normally round, allowing them to fit through small blood vessels. Individuals with SCD, who are homozygous for the sickle cell allele, have red blood cells that are crest-shaped instead. This deformity can cause blood clots, ultimately leading to tissues in the body to become oxygen deprived. If this blockage occurs in a major vessel, it can cause a stroke, heart attack, or even death. However, there is hope for individuals with the disease, as recent research has found that SCD can be cured through bone marrow transplant. Sadly though, there are limitations — it has been more successful in younger patients who receive transplants from a full sibling or matched donor.

But how can such a harmful disease manage to survive? One misconception is that the fittest organisms in a population are the healthiest. Shouldn’t the sickle cell trait have been erased from the human population long ago since it lowers life expectancy?

Before we dive into why the sickle cell trait still exists, let’s take a step back and learn a little more about SCD’s effects and treatment options from Dr. Kirshma Khemani, a specialist in pediatric hematology and oncology:

1. Could you give a brief background on yourself and your current research?
2. What are the symptoms of sickle cell disease?
3. What are the current treatment options for sickle cell disease?
4. What are the risks of each treatment option for sickle cell disease?
5. Recently stem cell therapy has been identified as a potential cure for sickle cell disease, what are your views on these findings?

   Now, let’s get back to the big question: how could this trait continue to prevail? The sickle cell trait has been found in regions of the world where malaria occurs: 10-40% of the population carries the sickle cell mutation. But wait a second. What is malaria and how is it related to SCD?

   Malaria is a life threatening disease that is caused by a parasite and is transmitted through mosquito bites. There is a correlation between malaria and SCD: individuals who carry the sickle cell trait, who are heterozygous for the sickle cell allele, have a protective advantage against malaria. This occurs because the parasite that causes malaria cannot mature in the oxygen-deprived sickled red blood cells and dies.

   Although SCD does have several disadvantages, the sickle cell trait has been able to survive in the population due to its protective role against malaria.

   For additional information, see the following references:

   Gemmell NJ, Slate J. 2006. Heterozygote advantage for fecundity. PLoS ONE 1(1).

   Kwiatkowski, D. P. 2005. How malaria has affected the human genome and what human genetics can teach us about malaria. The American Journal of Human Genetics, 77(2), 171-192.

   Larremore, D. B. et al. 2015. Ape parasite origins of human malaria virulence genes. Nature Communications Nat Comms, 6.

   Saraf, S. L. et al. 2015. Nonmyeloablative stem cell transplantation with alemtuzumab/low-dose irradiation to cure and improve the quality of life of adults with sickle cell disease. Biology of Blood and Marrow Transplantation.

   Sellis, D., Callahan, B. J., Petrov, D. A., & Messer, P. W. 2011. Heterozygote advantage as a natural consequence of adaptation in diploids. Proceedings of the National Academy of Sciences, 108(51), 20666-20671.

   Williams, T. N. et al. 2005. An immune basis for malaria protection by the sickle cell trait. PLoS Med PLoS Medicine 2: 441-445.

    

    

Contributed by Esther Lee, Rina Lee, Jasmine Labarca, Heather Wang, Phoenix Phung, Enakshi Das

Did you ever wonder what our ancestors ate? I do! The Paleo diet, also known as the caveman diet, Stone Age diet, and hunter-gatherer diet, consists of foods that are assumed to have been available to our ancestors before the Agricultural Revolution began around 333 generations ago. Our ancestors mainly ate meat, fruits, and vegetables before agriculture was developed, but now the Western diet has expanded to include a high number of cereal-grains, milk products, sugar, sweeteners, separated fats and alcohols, which now make up around 70% of our diet (Cordain et al., 2005). These new food sources were made available by the Agricultural and Industrial Revolutions.

During prehistoric times, our ancestors ate raw, unprocessed foods, which require much more energy to digest. Nowadays, cooking, through the process of heating and pounding, breaks down the food, so food is not only easier, but also more efficient to digest (Gibbons 2015). This transition underlies the expensive tissue hypothesis (Suburu 2013), which links changes in diet to evolution of the human brain. The hypothesis is that the brain and gut tissue both require lots of energy, so as our brains became larger, the gut size became smaller. Cooking also allowed us to absorb more energy from food, further shrinking our gut, and allowing us to expand our brain. 

Some people think that the Paleo diet is healthier because it is what sustained our ancestors and it is what we are thus adapted to eat. Instead of getting calories from processed foods, “Paleo dieters” get their nutrients through meat and raw, unprocessed foods. Many critics argue that the Paleo diet lacks food variety and believe that humans are adapted to consuming a varieties of foods, including those available in our modern diet.

This presentation explores the pros and cons of the two diets:

However, neither diet may be optimal for all individuals because of variation in the human population. Each individual reacts differently to the foods offered in each diet (Wan). For example, based on your genes, you can have a sweeter tooth than your friends (Gibbons 2015). There will always be environmental and cultural factors that will determine which diet is the best for you!

For more information see:

Ameur, Adam et al. “Genetic Adaptation of Fatty-Acid Metabolism: A Human-Specific Haplotype Increasing the Biosynthesis of Long-Chain Omega-3 and Omega-6 Fatty Acids.” American Journal of Human Genetics 90.5 (2012):809-820

Boers, Inge, Frits AJ Muskiet, Evert Berkelaar, Erik Schut, Ria Penders, Karine Hoenderdos, Harry J. Wichers, and Miek C. Jong. 2014. Favourable Effects of Consuming Palaeolithic-type Diet on Characteristics of the Metabolic Syndrome: A Randomized Controlled Pilot-study. Lipids in Health and Disease 13:160.

Burger, J., M. Kirchner, B. Bramanti, W. Haak, and M.G. Thomas. “Absence of the Lactase-persistence-associated Allele in Early Neolithic Europeans.” Absence of the Lactase-persistence-associated Allele in Early Neolithic Europeans. N.p., 27 Dec. 2006. Web. 30 Nov. 2015.

Cordain, L., Eaton S.B., Sebastian A., Mann N., Lindeberg S., Watkins B., O’Keefe J., Brand-Miller J. 2005. “Origins and Evolution of the Western diet: health implications for the 21st century. The American Journal of Clinical Nutrition 81: 341-354.

Eaton, S.B., Cordain, L. 1997. Evolutionary Aspects of Diet: Old Genes, New Fuels: Nutritional Changes Since Agriculture. World Rev Nutr Diet 81: 26-37.

Eaton, Stanley Boyd, and Stanley Boyd Eaton Iii. “Paleolithic vs. Modern Diets – Selected Pathophysiological Implications.” European Journal of Nutrition 39.2 (2000): 67-70.

Frassetto, L. A., M. Schloetter, M. Mietus-Synder, R. C. Morris, and A. Sebastian. 2009. Metabolic and Physiologic Improvements from Consuming a Paleolithic, Hunter-gatherer Type Diet. European Journal of Clinical Nutrition Eur J Clin Nutr 63: 947-55.

Gibbons, Ann. “The Evolution of Diet.” National Geographic. N.p., n.d. Web. 30 Nov. 2015.

Jew, Stephanie, Suhad S. AbuMweis, and Peter J.H. Jones. 2009. Evolution of the Human Diet: Linking Our Ancestral Diet to Modern Functional Foods as a Means of Chronic Disease Prevention. Journal of Medicinal Food.

Klonoff, David. “The Beneficial Effects of a Paleolithic Diet on Type 2 Diabetes and Other Risk Factors for Cardiovascular Disease.” Journal of Diabetes Science and Technology 3.6 (2009): 1229-232. Web.

Kowalski, L. M., and J. Bujko. “Evaluation of Biological and Clinical Potential of Paleolithic     Diet.” Rocz Panstw Zakl Hig 63.1 (2012): 9-15. Pub Med. Web. 30 Nov. 2015.

Leonard, William R. “Food for Thought. Dietary Change Was a Driving Force in Human Evolution.” Scientific American (2003): n. pag. ResearchGate. Web. 30 Nov. 2015.

Martens, E., Lowe, E., Chiang, H., Pudlo, N., Wu M., McNulty N., Abbott, D., Henrissat, B., Gilbert, H., Bolam, D., Gordon, J. 2011. Recognition and Degradation of Plant Cell Wall Polysaccharides by Two Human Gut Symbionts. PLOS Biology 9.12.

Milton, Katharine. “The Critical Role Played by Animal Source Foods in Human (Homo) Evolution.” Journal of Nutrition 133:3893S-3897S.

O’dea, K. “Marked Improvement in Carbohydrate and Lipid Metabolism in Diabetic Australian Aborigines after Temporary Reversion to Traditional Lifestyle.” Diabetes 33.6 (1984): 596-603. PubMed. Web. 30 Nov. 2015.

Schaeffer, Juliann. “Evolutionary Eating — What We Can Learn From Our Primitive Past.” Today’s Dietitian 11.4 (2009): 36. Today’s Dietitian. Web. 30 Nov. 2015.

Simmons, A. L., J. J. Schlezinger, and B. E. Corkey. “What Are We Putting in Our Food That Is Making Us Fat? Food Additives, Contaminants, and Other Putative Contributors to Obesity.” Curr Obes Rep 3.2 (2014): 273-85. Print.

Suburu, Janel, Zhennan Gu, Haiqin Chen, Wei Chen, Wei Chen, Hao Zhang, and Young Q.Chen. Fatty Acid Metabolism: Implications For Diet, Genetic Variation, and Disease. Food Biosci (2013) 4: 1-12. .

Tarantino, G., Citro, V., Finelli, C. 2015.Hype or Reality: Should Patients with Metabolic Syndrome-related NAFLD Be on the Hunter-Gatherer (Paleo) Diet to Decrease Morbidity?. Journal of Gastrointestinal and Liver Diseases J Gastrointestin Liver Disease 24: 359-368.

Wan, Samantha. Evolution in the Processed Foods Industry: Exploring the Impact of the Health Foods Movement. N.p.: U of Southern California, n.d. Print.

Contributed by: Maria Berce, Danny Kang, Travise Kinney, Fariah Majid, & Alex Zachowski

Have you ever wondered why certain diseases are maintained in the human population if they are a threat to human health? It turns out that in some situations, a particular trait, potentially even a disease, may help an individual survive and thus can be maintained in a population over time.

Most laypeople believe that mental health illnesses occur when an individual carries a trait that is detrimental to humans. However, in reality, a trait can become a disorder when something that allows an individual to thrive in one environment becomes an obstacle in a different environment. For example, think about our ancestors who were hunters and gatherers. In their environment, being hyper-aware of their surroundings was beneficial because it protected them from attacks by predators. But what if this hyper-awareness was passed down to their offspring and was maintained generation after generation? Now, in our modern environment, being hyper-aware while sitting at a desk for hours on end each day would not lead to “productive” behavior. Thus, the trait of being hyper-aware may now perceived as an illness, specifically Attention-Deficit Hyperactivity Disorder (ADHD).

This animation illustrates the misconception that unfavorable traits are always selected against. 

Just because a trait is maintained in a population does not mean it is favored by natural selection. Take a look below and see if you can now understand the incidence and progression of mental health illnesses through an evolutionary lens.

Attention-Deficit Hyperactivity Disorder (ADHD). There have been a lot of articles in the media lately about the sharp rise in the number of children in the U.S. and other western nations who are being diagnosed with ADHD.  The U.S. government’s Center for Disease Control, or CDC, found that over 11% of children between the ages of four and 17 were diagnosed with ADHD in 2011, and that the rates of diagnosis have been growing by an average of three percent each year from 1997 to 2006. There is some disagreement over whether some of this increase is due to an over-diagnosis of the condition; however, the fact remains that ADHD is widespread and increasing. According to the CDC, children must have six or more symptoms of inattention and six or more symptoms of hyperactivity and impulsivity in order to be classified as ADHD. It is easy to see how these symptoms could make any child’s life a lot more difficult.

But another way of looking at ADHD has recently gained a following in the scientific community. Rather than looking at ADHD as a disorder, researchers have begun to look at it from the perspective of human evolution. In an article published in Journal of the American Academy of Child and Adolescent Psychiatry in 1997, Jensen and others hypothesized  that ADHD is “an adaptation that reflects the optimization of brain function to some environments at the cost of poorer response to the demands of other environments.” In plain English, these scientists hypothesize that some children are genetically programmed to behave in a manner that may be disruptive in an academic or social setting.

Thomas Hartmann, a popular author and radio talk show host, wrote an entire book on this subject, titled “The Edison Gene: ADHD and the Gift of the Hunter Child.” In this book, Hartmann points out that Thomas Edison was expelled from school in the third grade for behavior that today would be labeled as symptomatic of ADHD. In his book, Hartmann argues that individuals with ADHD possess traits that were useful to humans during hunter-gatherer times and now individuals with these same traits are hardwired to be successful innovators, entrepreneurs, explorers, and inventors. Hartmann insists that these people shouldn’t be seen as “disordered” but as vital to our society and its progress, and calls for new alternative education methods for children with ADHD.

Interestingly, what was at once useful in protecting oneself from predators may now be valuable in a crime-infested neighborhood, for example. These scientists see hyper vigilance of one’s surroundings, hyperactivity that leads to an in-depth exploration of those surroundings, and fast response to stimuli – what others might label impulsivity – as “benefits” given the right environment.

Post-Traumatic Stress Disorder (PTSD). Post-traumatic stress disorder is a complex mental health condition that severely impacts the lives of those affected. Occurring after some sort of trauma, symptoms of PTSD include flashbacks, nightmares, and anxiety. According to PTSD United, a charity that provides support to sufferers, over 70% of adults in the United States will experience a trauma over the course of their lifetime, but only 1 in 5 of those people will go on to experience symptoms of PTSD. So why do some people get PTSD and not others?

In a 2004 article published in Clinical Psychology Review, psychologist and sociologist Michael Christopher argues that behaviors associated with PTSD, such as hyper-awareness, replaying the event in one’s head, and maintaining emotional distance from others, are hallmark “adaptive behaviors” to extreme threats.  In other words, people who go through a traumatic situation such as war or robbery at gunpoint are psychologically and biologically transformed by the experience, resulting in the behaviors that we refer to as PTSD. These behaviors, Christopher argues, would all be beneficial to avoiding a similar future danger if they did not become pathological. Thus, in a sense, debilitating PTSD is essentially an “over-adaptation” by the human organism to the need to avoid severe dangers that may re-occur.

Anxiety Disorders. According to the National Institute of Mental Health, about 40 million adults are affected by an anxiety-related disorder, and rates have increased for the past 50 to 70 years. Why are mental disorders such as anxiety persisting in our population? Evolutionary biologists believe that anxiety, also referred to as the fight-or-flight response, was beneficial to our early ancestors when avoiding predators. This response increases heart rate and blood flow to muscles, and prompts us to respond faster in the face of danger. Today, many of us live in relatively peaceful environments, where our mean of survival is typing on a computer for eight hours a day. Although a certain amount of anxiety is beneficial in this environment as well, genetic predisposition to an anxiety disorder, which was selected for as a result of the environment of our ancestors, accounts for the fight-or-flight response even when we are not faced with grave danger. 

We see that the behaviors that characterize these health conditions can be beneficial in some environments but not in others. An environment can determine the extent to which behaviors are harmful to the individual, based on the set of traits expressed by that individual. Although traits that characterize ADHD, PTSD, or anxiety disorders may have been beneficial in other environments, like previous societies, natural selection cannot remove these traits just because the modern environment may not value them. Since there is often no direct fitness consequence to having these mental illnesses , individuals who are diagnosed still pass on their genes, allowing for the illnesses to persist in a population.

When asking members of the Emory University community about their perceptions of mental health disorders, the responses we get are very interesting, some of which acknowledge the ways in which traits that characterize mental illnesses can be beneficial in today’s environment.

https://www.youtube.com/watch?v=Qvl_sBI_6FY

For further information, please refer to the following publications:

Avishai-Eliner, S., Brunson, K.L., Sandman, C.A., & T.Z. Baram. 2002. Stressed-out, or in (utero)? Trends Neurosci. 10: 518-24.

Byars, S.G. 2010. Natural Selection in a Contemporary Human Population. Proceedings of the National Academy of Sciences of the United States of America 107: 1787-792.

Christopher, M. A Broader View of Trauma: A biopsychosocial- evolutionary view of the role of traumatic stress response in the emergence of pathology and or growth. Clinical Psychology Review 24.1: 75-98.

Draganski, B., Gaser, C., Busch, V., Schuierer, G., Bogdahn, U., & A. May. 2004. Neuroplasticity: Changes in Grey Matter Induced by Training. Nature.

Hartmann, T. The Edison Gene. Vermont: Park Street Press, 2003. Print.

Gonçalves, V., Andreazza, A., & J. Kennedy. 2014. Mitochondrial Dysfunction in Schizophrenia: An Evolutionary Perspective. Springer-Verlag Berlin Heidelberg.

Jensen, P., Mrazek, D., Knapp, P., Steinberg, L., Pfeffer, C., Schowalter, J., Shapiro, T. 1997. Evolution and Revolution in Child Psychiatry: ADHD as a Disorder of Adaptation. Journal of the American Academy of Child and Adolescent Psychiatry 36.12: 1672-1681.

Lee, Y., Yamaguchi, Y., & Y. Goto. Neurodevelopmental Plasticity in Pre- and Postnatal Environmental Interactions: Implications for Psychiatric Disorders from an Evolutionary Perspective. Neural Plasticity.

Platter, B.E. 2009. Evidence of Contemporary Modern Human Evolution Contained Within the Human Genome. Lethbridge Undergraduate Research Journal.

Twenge, J. 2000. The Age of Anxiety? Birth Cohort Change in Anxiety and Neuroticism, 1952-1993. Journal of Personality and Social Psychology.

Twenge, J. 2008. Generational differences in psychological traits and their impact on the workplace. Journal of Managerial Psychology.

Twenge, J. 2012. Generational Differences in Young Adults’ Life Goals, Concern for Others, and Civic Orientation, 1966–2009. Journal of Personality and Social Psychology.

Weinstock, M. 2008. The long-term behavioural consequences of prenatal stress. Neuroscience and Biobehavioral Reviews 32: 1073–1086.

Non-Journal Resources:

Centers for Disease Control and Prevention, 2015. Attention-Deficit/Hyperactivity Disorder (ADHD) Data and Statistics. Accessed December 1, 2015 (http://www.cdc.gov/ncbddd/adhd/data.html).

The Decline of Play and Rise in Children’s Mental Disorders. (n.d.). Retrieved from https://www.psychologytoday.com/blog/freedom-learn/201001/the-decline-play-and-rise-in-childrens-mental-disorders

Facts & Statistics | Anxiety and Depression Association of America, ADAA. (n.d.). Retrieved from http://www.adaa.org/about-adaa/press-room/facts-statistics

PTSD United, 2013. PTSD Statistics. Accessed December 1, 2015 (http://www.ptsdunited.org/ptsd-statistics-2/).

Contributed by Jonathan Nelson and Dina Michael

When Charles Darwin and Alfred Wallace presented their argument for speciation through natural selection, they established the foundations of evolutionary biology. Evolution is the process of change that lead from ape like ancestors to modern humans.

For data, scientist often turn to the fossil remains left by early hominids. Their remains exhibit a variety of species that likely evolved from Homo ergaster. Homo ergaster was a hominid species that possessed the capacity to disperse from Africa and colonize multiple areas of Europe and East Asia (Scarre 2005). These separated groups eventually underwent natural selection, and were likely influenced by genetic drift (certain alleles being randomly expressed and prevailing in the absence of natural selection). These developments lead to the evolution of the Homo sapien and Homo neanderthalensis species.  

While many believe that modern humans emerged from these different hominid groups that were present throughout the world, modern evidence collected from mitochondrial DNA proves otherwise. Using this mitochondrial DNA, which is passed solely from mother to child, scientist postulate that all humans likely all came from one mother, who existed any where from 290,000 to 140,000 years ago (Cann 1987).

So why do we care? Well, it turns out that human evolution has plenty of modern implications as well. Modern research into human evolution and pathogens has shown that pathogens have played a large role in the shaping of human evolution. Researchers have found that certain pathogens in an area also drove the presence of certain alleles in a population, with the expression of genes such as those responsible for disorders like celiac disease and type 1 diabetes correlating with presence of certain pathogens in that area. They further hypothesized that traits evolved  to survive in a pathogen rich environment may be the source of many autoimmune disorders, particularly in industrialized societies (Fumagalli 2011).

Mutation is one of the major driving forces of evolution,as it is the ultimate driving force behind variation. understanding the sources of these mutation is one major focuses of modern day research. In one study, scientist showed how the structure of DNA makes it very reactive with electromagnetic fields ( Blank and Goodman 2011) These researchers postulate that this may play a role in recent rises of cancer in our population. The malleability of our DNA only serves to show how we are continuously affected by the evolutionary process.

[jwplayer mediaid=”1296″]

For more information, please refer to the following sources:

 Blank, M., & Goodman, R. 2011. DNA is a fractal antenna in electromagnetic fields. Int J Radiat Biol International Journal of Radiation Biology, 87(4), 409-415.

 Cann, R. L., Stoneking, M., & Wilson, A. C.1987. Mitochondrial DNA and human evolution. Nature, 325(6099), 31-36.

 Fumagalli, M., Sironi, M., Pozzoli, U., Ferrer-Admettla, A., Pattini, L., & Nielsen, R. 2011. Signatures of environmental genetic adaptation pinpoint pathogens as the main selective pressure through human evolution. PLoS Genet, 7(11), e1002355.

 Harding, R. M., Healy, E., Ray, A. J., Ellis, N. S., Flanagan, N., Todd, C., … Rees, J. L. (2000). Evidence for Variable Selective Pressures at MC1R. American Journal of Human Genetics, 66(4), 1351–1361.

 Scarre, C.2005. The human past: World prehistory & the development of human societies . New York, NY: Thames & Hudson.pp. 85-99

 Olson, M. V., & Varki, A. (2003). Sequencing the chimpanzee genome: insights into human evolution and disease. Nature Reviews Genetics, 4(1), 20-28.

Contributed by Jessie Barra, Reem Al-Atassi, and Najdat Zohbi

How can a single celled organism beat something so complex as a human being? It seems like an impossible task, but with the short life span of a single celled bacterium, changes in the genetic code can happen so fast that the human immune system can’t keep up. The bacteria, Streptococcus pneumoniae, better known as pneumococcus, has the ability to cause pneumonia and meningitis once it colonizes the upper respiratory tract, which includes the nose, mouth, and throat (Cobey, 2012). These two infections can be life threatening especially in children, young adults, and the elderly (CDC). There are over 90 different subtypes (known as serotypes) of this bacterial species that differ in their coating that surrounds their DNA (Cobey, 2012). As a response to the threat this bacterial species posed to the human population, a vaccine was created in 2000 called PCV7 that protects against seven serotypes of pneumococcal bacteria (later replaced by PCV13 in 2010 which protected against thirteen) and reduced the rates of disease. The problem with the vaccine is that it only offers protection from a portion of the many natural serotypes. The vaccine has therefore altered the likelihood for certain subtypes of the bacteria to survive inside its human host (Croucher, 2015). As the human population became protected against the seven serotypes represented by the vaccine, other versions of the bacteria replaced them as the cause of most cases of invasive disease (Flasche, 2011).

So, new serotypes decrease the effectiveness of these particular vaccines (Kyaw, 2006). More resistant serotypes have been shown to have tougher outer coatings that don’t cost much energy to make, marking a strategy of pneumococcus to linger in the nasopharynx (Weinberger, 2009). Serotypes that carry on undetected by the immune system have a clear advantage over those that the immune system notices. As a result, natural selection favors serotypes that bypass our immune defenses. We are left, then, with a biological arms race that is characteristic of co-evolution; as we fight pneumococcus through vaccines, the bacteria counters with stealth. Nevertheless, our immune system has an ace in the hole: special white blood cells (referred to as CD4+ TH17 cells) can fight pneumococcus even if it’s not detected normally. Essentially, these cells can decrease the colonization of even the stealthy bacteria (Li, 2012), offering insight into alternative vaccine design. In this instance of co-evolution, our ability to drastically affect the evolutionary response of pneumococcus reminds us that evolution can occur quickly. A common misconception is that evolution spans long stretches of time, but here, we see that this is not the case–evolution is not necessarily so gradual that we can’t directly influence it.

If you’re interested in perusing some pneumococcus primary literature, here are some great places to start:

Cobey, S., Lipstitch, M. 2012. Niche and neutral effects of acquired immunity permit coexistence of pneumococcal serotypes. Science 335: 1376-89.

Croucher, NJ. et al. 2015. Population genomic datasets describing the post-vaccine evolutionary epidemiology of Streptococcus pneumoniae. Sci Data 2:150058.

Flasche, S. et al. 2011. Effect of pneumococcal conjugate vaccination on serotype-specific carriage and invasive disease in England: a cross-sectional study. PLoS Med 8(4): e1001017.

Kyaw, Moe H., et. al. 2006. Effect of Introduction of Pneumococcal Conjugate Vaccine on Drug-Resistant Streptococcus pneumonia. New England Journal of Medicine 354: 1455-1463.

Li, Y et al. 2012. Distinct Effects on Diversifying Selection by Two Mechanisms of Immunity against Streptococcus pneumonia. PLoS Pathogens 8(11): e1002989.

Weinberger, DM., et al. 2009. Pneumococcal capsular polysaccharide structure predicts serotype prevalence. PLoS Pathogens 5(6): e1000476.

Contributed by Adrian Rabin and Asim Lal

“Now, here, you see, it takes all the running you can do, to keep in the same place.”

– Lewis Carroll, Through the Looking-Glass

In this quote from Through the Looking-Glass by Lewis Carroll, The Red Queen gives Alice this explanation for the peculiarities of the land she has just entered. Scientists have used this interpretation, where Alice must “run” in order to stay alive, in order to represent certain scenarios found in nature. In the wild, situations occur where the fates of two species are intertwined. The Red Queen Hypothesis is an instance of coevolution, when two species evolve over time in response to one another.

It is a common misconception that life evolves randomly or by chance. While it is true that randomness is a factor, evolution is also impacted by non-random events. In a situation where the fates of predator and prey are closely linked, the two species become engaged in a deadly arms race, and this is one of the factors that can impact evolution. Prey are constantly evolving novel mechanisms to avoid their predators. In response to this, predators will need to evolve their own mechanisms to identify prey. Many times, this cycle repeats itself, causing both predator and prey to evolve together.

Red Queen and Fruit Flies. A good model of the Red Queen Hypothesis can be seen in the way the fruit fly Drosophila melanogaster evolves when it is infected by a parasite. Recently, researchers found that a phenomenon occurred in the first generation of infected flies where the parents’ genes became shuffled in their offspring: a process known as recombination. Genetic changes like this make it more likely that the mother’s offspring will not be recognizable by the same type of pathogen that attacked her.

Generation 1

Generation 2

The relationship between Drosophila and parasites is a classic example of the Red Queen Hypothesis, where two species evolve together in order to reach some sort of balance. In this case, the host is trying to outpace the parasite by altering the genes of its offspring so that the parasite can’t detect it. Soon enough, the parasite in turn develops new mechanisms to detect the novel prey. These species are engaged in a constant arms race that will never find a perfect balance, and just like Alice in Through the Looking-Glass, must keep running in order to stay alive.

For more information, check out these papers:

Campos, J. L., Halligan, D. L., Haddrill, P. R., and B. Charlesworth. 2014. The relation between recombination rate and patterns of molecular evolution and variation in Drosophila melanogaster. Molecular Biology and Evolution. 31: 1010-1028.

Hunter, C. M., and N. D. Singh. 2014. Do Males Matter? Testing the effects of male genetic background on female meiotic crossover rates in Drosophila melanogaster. Evolution. 68: 2718-2726.

Meselson, M. S., and C. M. Radding. 1975. A General Model for Genetic Recombination. Proceedings of the National Academy of Sciences. 72: 358-61.

O’Shea, K. L., and N. D. Singh. 2015. Tetracycline-exposed Drosophila melanogaster males produce fewer offspring but a relative excess of sons. Ecology and Evolution. 5: 3130-3139.

Shinn, C., Blanchet, S., Loot, G., Lek, S., and G. Grenouillet. 2015. Phenotypic variation as an indicator of pesticide stress in gudgeon: Accounting for confounding factors in the wild. Science of the Total Environment. 538: 733-742

Singh, N. D., Criscoe, D. R., Skolfield, S., Kohl, K. P., Keebaugh, E. S., T. A. Schlenke. 2015. Fruit flies diversify their offspring in response to parasite infection. Evolution. 349: 747-750.