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 is 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 is impossible to imagine genetics without modern evolutionary
theory, called the modern synthesis, since it describes the forces that act on our inherited
traits. It is the conceptual framework through which we can understand the historical forces
acting on the gene pool of a population.
I won't exclude human caused 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 7 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
microevolution representing changes that happen within a species, and macroevolution representing
changes between species. Biologists recognize that the process is the same, just over different
scales of time. However, it does represent a break point 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 camoflage requires that an animal closely
resemble 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 coevolution
and the Red Queen when we apply it to human coevolution with our pathogens.
For example, a 2006 review paper in Nature Reviews Microbiology examines the valuable
evidence we are obtaining by looking at coevolutionary markers in HIV-1. Our understanding of how
HIV-1 evolves in response to the patient's histocompatibility markers has allowed us
to develop some very exciting gene therapies and vaccine strategies. We've 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 macroevolution 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 infection. 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 coevolution.
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 combatting 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, SNPs, 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 percent, but Non-Hispanic blacks have
diabetes rates of 14.7 percent. 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 allelic 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 snips or S-N-Ps, 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
appear to have acquired an insulin resistance 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 is 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
butt 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. The technologies for studying genomes
were also developed with population genetics in mind, and later adapted to the fields of
criminal law.
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.