 What good is evolution? Do we really need it? Are there any applications for it? Does it have any bearing on human health? Why would a doctor or engineer or teacher or politician need to understand it, beyond the need to satisfy an educational directive? Does it really affect our lives? Let me start by saying that the primary goal of most science is not technology. It's discovery. We attempt to increase our knowledge about the natural world. Products like microwaves and Teflon are byproducts of that attempt. Drugs and diagnostics are built on the research of biological systems, but they are rarely the intent of that research. So when I talk about the benefits of evolution, I will take it as read that the primary benefit is a deeper understanding of the natural forces acting on populations of organisms. Some critics of this video will no doubt point out that I am muddling together topics, especially genetics and evolution, but it's impossible to imagine genetics without modern evolutionary theory, since it describes the forces that act on our inherited traits. It's the conceptual framework through which we can understand the historical forces acting on the gene pool of a population. I won't exclude human cause selection in this list. In today's world, humans are the landscape, the weather, and the ecology. And it's been this way since we made extinct many of the large animals on seven continents over 20,000 years ago, using little more than wood and stone tools. Evolution is often incorrectly broken down by non-scientists into micro and macro, with micro evolution representing changes that happen within a species, and macro evolution representing changes between species. Biologists recognize that the process is the same, just over different scales of time. However, it does represent a breakpoint for what some creationists are willing to accept, so I will break the sections into micro and macro evolutionary applications for convenience. Section 1. Pathogen Evolution and the Red Queen The natural world is locked in constant struggle. Predators and prey, pathogens and hosts, forever striving to overcome the other. Each side must constantly adapt to the competition, just to keep from being wiped out. This has been compared to a scene in Lewis Carroll's Through the Looking Glass. The Red Queen, speaking to Alice, says it takes all the running you can do to keep in the same place. This has come to be known as the Red Queen Principle, which can be restated as, for an evolutionary system, continuing development is needed just in order to maintain its fitness relative to the systems it is co-evolving with. We can apply this concept to phenomenon like mimicry in the animal world. A moth that resembles a wasp is less likely to be eaten by a predator. Good camouflage requires that an animal closely resembles the local flora, and any changes that occur to the plants in an area could be fatal to an animal that was unable to adapt to the new selection pressures. But while this is interesting to biologists, there is also a very practical application to co-evolution and the Red Queen when we apply it to human co-evolution with our pathogens. For example, a 2006 review paper in Nature Reviews Microbiology examines the valuable evidence we are obtaining by looking at co-evolutionary markers in HIV-1. Our understanding of how HIV evolves in response to the patient's histocompatibility markers has allowed us to develop some very exciting gene therapies and vaccine strategies. We've also discovered dozens of genetic changes that have resulted in resistance to HIV infection and also genotypes with a low progression rate to full-blown AIDS such as CCL3L2. This is more of a macro-evolution application, but when we compare HIV to the other viruses in its family, those that infect monkeys, horses, cows, cats, and so forth, we can see what regions have changed the most rapidly in the progression to infecting humans and causing disease. This was a useful shortcut to determining the function of most of the HIV gene products. By comparison to the closely related simian, feline, bovine, and equine lentiviruses. We've also studied the evolutionary responses of viruses during infection where the emergence of a new genotype results in fresh outbreaks of virus in the blood. Millions may benefit from this understanding of our co-evolution with HIV. The same could be said for malaria. The same gene that causes sickle cell disease confers a resistance to malarial infections. So do some other disease genes like G6PD deficiency. Looking at how the human genome has responded to malaria lets us know why the disease is so prevalent in certain areas, but it's also provided information about how malaria enters and infects human cells. Smart scientists in the years before molecular biology was fully developed were able to determine what cellular proteins viruses used to enter cells by looking at polymorphic genotypes. Vaccines and therapies are made possible by understanding this co-evolution. The recent re-emergence of H1N1 influenza has made us all a little more aware of how quickly viruses can evolve and the implications for human health. Our knowledge of evolutionary change in genes is vital to combating deadly disease. We could repeat this for almost any human pathogen. Our understanding of selection pressures in evolution directs much of our strategies for long-term combat against the agents of illness. I've intentionally avoided antibiotic and antiviral resistance because it's such an obvious benefit, but it's worth adding to the list here. Section 2, Human Genetic Disease Snips and Forensics The last section was on infectious disease, but what about non-infectious diseases like diabetes, cancer, obesity, heart disease, all major killers in the developed world? While there is a strong environmental component to those diseases, it's obvious from studies of different human populations that there's also a genetic link. For example, type 2 diabetes rates among non-Hispanic whites in the US are 9.8%, but non-Hispanic blacks have diabetes rates of 14.7%. There are some indigenous American groups in southern Arizona where more than 30% of the population live with diabetes. What accounts for that difference? Researchers are currently looking at the genetic markers associated with type 2 diabetes in hopes of identifying the genetic linkages. We call these genetic association studies, and they're enabled by an understanding of allillic change over time, also known as evolution. The results of association studies could lead to better and earlier diagnostics, as well as therapies for those affected. The genetic markers used are called SNPs, or SNPs, single nucleotide polymorphisms, which is what a point mutation is called when it spreads through a population. Different human populations that diverged from each other a long time ago will have different SNP marker sets. For example, the ancestors of the Pima Indians and San Carlos Apaches appeared to have acquired an insulin-resistant SNP, possibly in response to a long period of starvation and hardship, which may have selected for individuals that were better able to maintain energy stores, sometimes called the thrifty phenotype. This is still a controversial idea, but it's supported by observations of our nearest relatives, the chimps, who also show evidence of genetic diversity based on their specific mating groups' history with starvation. This is a typical example of how evolutionary biologists, uncovering clues about our distant past, can help us here in the present. This kind of effort is what led us to sequence the human genome, and there are projects currently in progress to map human variations, to look at global inheritance patterns, so that our knowledge of genetics is enhanced by a historical perspective. One such project is the International Human Haplotype Map, or HAPMAP project, which seeks to uncover how genetic markers are inherited in human populations and how historical isolation has produced distinctive patterns in different populations. A haplotype is a group of markers that tend to be co-inherited, so we can test for a single marker and know the identities of the others. These markers will someday allow us to diagnose disease, select the best drug and optimal dose for treatment, and discover genetic factors in disease. Another application is in forensics. We've all seen the crime dramas where a single cigarette but dropped at a crime scene can lead to a positive identification and arrest. Each person's genome represents a nearly unique pattern, distinctive to them. When presenting this evidence in a courtroom, we need to know how useful the match is. The math for this calculation comes from population genetics, which was developed by evolutionary biologists studying model organisms like fruit flies and mice. Today, DNA evidence, while still sometimes controversial, has become an accepted fact of jurisprudence. Paternity, criminal law, and even patent or intellectual property cases often hinge on the findings of evolutionary patterns of inheritance. So our understanding of human genetic diversity aids in investigating, detecting, and curing diseases, and it may make our society a more just and safe place to live.