Afarensis

Bioarchaeologists frequently study the distribution of dental caries in populations in order to try and understand subsistence, diet, and status. Rarely, however, does one hear about the study of dental caries aiding paleoanthropology. A recent study mentioned on Science Daily is an exception. Before going further let's look at what dental caries are.

Your mouth is full of bacteria. Before you freak out and start washing your mouth with the nearest antibacterial soap, I should point out this is a good thing. The bacteria in your mouth help break down the food you have just eaten. A byproduct of this breakdown is a sticky biofilm that forms plaque. Plaque is acidic and eventually starts dissolving the enamel outer layer of a tooth. The picture below should help:

[1] Early stages : acids dissolve the enamel in the crown of the tooth
[2] Moderate tooth decay : here the dentin is attacked by acids and bacteria invade the cavity.
[3] Advanced tooth decay : inflammation of the pulp.
[4] Necrosis (death) of the pulp tissue.
[5] Periapical abcess forms at the apex of the root

One of the bacteria in your mouth is Streptoccocus mutans. Streptoccocus mutans has evolved receptors to help them stick to your teeth and produce lactic acid as a byproduct of sugar digestion. S. mutans is also transmitted from mother to offspring.

Enter Dr. Page Caufield. Dr. Caufield is Professor of Cariology and Comprehensive Care at the New York University College of Dentistry. He is interested in three areas. First:

The first area concerns the delineation of the natural history of oral bacteria responsible for dental caries, including genetic and environmental events that influence the acquisition and transmission of bacteria indigenous to humans. More specifically, our present focus is in three areas: 1) windows of infectivity for acquisition of indigenous bacteria, 2) fidelity of genotypic transmission and 3) clonality of caries-associated strains of Streptococcus mutans. We are looking at what biological rules govern the opening and closing of this window in infants; infants who do not become infected with S. mutans during this window may remain free of these organisms and do not manifest disease, i.e., caries. The recent development of a DNA fingerprinting techniques allows us to study transmission /acquisition as well as describe polymorphic behavior inherent to indigenous bacteria that are vertically transmitted. The conservation of S. mutans within both racial and familial lines suggests a pattern of co-evolution between host and parasite. Because S. mutans is transmitted vertically, i.e., mother to child, clonal types are confined within racial and familial cohorts. If clonality proves to be true for all strains of S. mutans, then virulence factors can be traced based on commonality of certain clones among children with severe caries. It follows that diagnostic tools can then be developed capable of predicting risk before the initiation of caries.

In other words, he is trying to use an understanding of the evolutionary history of S. mutans to develop clinical applications for prevention and treatment of dental carries. Second:

Our second major interest is developing techniques for characterizing diversity of bacteria within plaque biofilms associated with dental caries. To do this, we have developed two systems of DNA profiling - one using gradient gels (DGGE) to separate distinct 16S rDNA moieties representing individual species of bacteria from biofilm and the second subtraction DNA hybridization of genetic fragments. Both approaches are culture-independent, hence we should be able to expand our knowledge of the cariogenic biota to include the non-cultivable, and majority portion of the dental biofilm. These studies give us clues as to why some strains are more virulent than others.

Basically, you carry - in your oral cavity - your very own experiment in natural selection and evolution. As one example, there are a wide variety of bacteria in your mouth and each one competes for the resources present. Natural selection applies and the bacteria evolve various strategies to out reproduce their competitors. As I mentioned above, when S. mutans digests most sugars it produces lactic acid as a byproduct. When it digests sucrose, however, it produces a sticky substance that allows S. mutans to bind together forming plaque.

Dr. Caufield's third area of interest is:

Our third area of research is in the population structure of Streptococcus mutans and its co-evolution with its human host. Comparing phylogenies of different strains with and without plasmids reveal separate evolutionary pathways between plasmid and chromosomal frames. As humans migrated out of Africa, they carried their intraoral commensal biota, including S. mutans. These migrations parallel S. mutans phylogeny.

To that end he has published an interesting paper in the February issue of the Journal of Bacteriology. According to Science Daily (I don't have access to the Journal of Bacteriology) Dr. Caufield gathered over 600 samples of S. mutans covering six continents. From Science Daily:

His final analysis focused on over 60 strains of S. mutans collected from Chinese and Japanese; Africans; African-Americans and Hispanics in the United States; Caucasians in the United States, Sweden, and Australia; and Amazon Indians in Brazil and Guyana.

"By tracing the DNA lineages of these strains," Caufield said, "We have constructed an evolutionary family tree with its roots in Africa and its main branch extending to Asia. A second branch, extending from Asia back to Europe, traces the migration of a small group of Asians who founded at least one group of modern-day Caucasians."

Additional branches, tracing the coevolution of humans and bacteria from Asia into North and South America, will be drawn in the next phase of Caufield's analysis.

The bottom line is that his research on S. mutans provides some support to the Out-of-Africa theory of human origins.

So, let's summarize. Dr Egnor first claimed that:

Doctors don't study evolution. Doctors never study it in medical school, and they never use evolutionary biology in their practice. There are no courses in medical school on evolution. There are no 'professors of evolution' in medical schools. There are no departments of evolutionary biology in medical schools.

When this was shown to be incorrect he changed his story to:

In addition, a common Darwinist argument is that the presence on medical school faculties of scientists who study some aspects of evolutionary biology is evidence that evolutionary biology is indispensable to medicine. That argument is flawed, but it does raise an important issue. I'll address that issue here, and I'll address the other issues, one by one, in ensuing posts.

Many, even most, scientists whose work includes evolutionary biology are fine scientists. They have been my teachers, and many are now my colleagues and friends. They contribute to medical education in major ways. They contribute as anatomists, or as physiologists, or as microbiologists, or as molecular biologists. I hold them in high regard, and I am indebted to them for much of my own education.

These fine scientists do not, however, contribute to medicine by studying or teaching evolutionary biology. They contribute to medicine by their work in anatomy, or physiology, or microbiology, or molecular biology. The central assertion of Darwinism--that all biological complexity arises by random heritable variation and natural selection--is of interest to evolutionary biologists (and to those of us who disagree with it), but the assertion that randomness is the raw material for all biological complexity plays no role in medical education or research.

Yet, as the example above illustrates, the medical community does use evolutionary theory to guide research and to create clinical applications based on the results of that research. Not only that, in the above example we an example of a member of the medical community making an interesting and significant contribution to the study of human origins.

So, my challenge to Dr. Egnor is threefold:

1) If, as you say, evolutionary biologists contribute to medical education in major ways, and if you are indebted to them for much of your own education, then why did you start out saying:

There are no courses in medical school on evolution. There are no 'professors of evolution' in medical schools. There are no departments of evolutionary biology in medical schools.

I ask because it looks like you are not being truthful about the question.

2) Dr. Caufield is studying the co-evolution of various bacteria with each other and their human host and is coming up with clinical applications. How do you reconcile that with your claim that evolutionary theory contributes nothing to medicine? How could "design theory" do better?

3) The practice of medicine, like evolutionary biology and other sciences, is grounded in a materialist, empirical paradigm. Yet the Discovery Institute, which you are affiliated with, is dedicated to overthrowing materialistic based science and, hence, medicine. Do you think this is a good thing for medicine? Do you think medical professionals should be studying non-material causes for disease and non-material cures?

You can find Orac's challenge here.