Oh, well. I guess that settles it. This "bloviationary profundity" is meaningless:
All genetic diseases collectively affect only about 1% of the human population. In contrast, more and more human disease and death is associated with chronic systemic diseases, such as coronary artery disease, stroke, hypertension, and Alzheimer's disease. These diseases emerge from a complex set of interactions between genes and environment. This complexity makes it difficult to study the linkage between genes and systemic disease. Evolutionary principles and approaches have already had a major impact on the study of this linkage (65). For example, some genes, because of their known biochemical or physiological functions, can be identified as "candidate genes" for contributing to a systemic disease. However, there is so much molecular genetic variation at these candidate loci in the general human population that it is finding the specific variants associated with disease risk is akin to the proverbial search for the needle in the haystack. Evolutionary phylogenetic techniques can be used to estimate a gene tree from this genetic variation. Such a gene tree represents the evolutionary history of the genetic variants of the candidate gene. If any mutation has occurred during evolutionary history that has altered risk for a systemic disease, then the entire branch of the gene tree that bears that mutation should show a similar disease association. Gene tree analyses have already been successfully used to discover genetic markers that are predictive of risk for coronary artery disease (23), risk for Alzheimer's disease (58), and the response of cholesterol levels to diet (18).
And this "bloviationary profundity":
Infectious diseases are caused by parasitic organisms such as viruses, bacteria, protists, fungi, and helminths (worms). Control and treatment of infectious disease requires not only medical but also ecological research and actions. Critical questions include: What is the disease-causing organism? Where did it come from? Do other host species act as reservoirs for the organism? How is it spread? If it is spread by a carrier agent such as an insect, how far does the carrier typically disperse, and what other ecological properties of the carrier might be exploited to control the spread? How does the organism cause disease, and how might it be treated with drugs or other therapies? How does it reproduce—sexually or asexually or both? Is it likely to evolve resistance to drugs or the body's natural defenses, and if so, how quickly? Is it likely to evolve greater or lesser virulence in the future, and under what conditions will it do so? To each of these questions, evolutionary biology can and does provide answers. Identifying a disease-causing organism, and its carrier if there is one, is a matter of systematics. If, like HIV, it is a previously unknown organism, phylogenetic systematics can tell us what its closest relatives are, which immediately provides clues to its area of origin, other possible host species, and many of its likely biological characteristics, such as its mode of transmission. If a new species of malaria-causing protozoan (Plasmodium) were found, for example, we could confidently predict that it is carried by Anopheles mosquitoes, like other Plasmodium species. Similarly, identifying disease carriers using the methods of systematics is essential. Progress in controlling malaria in the Mediterranean region was slow until it was discovered that there are six almost identical species of Anopheles mosquitoes, differing in habitat and life history, only two of which ordinarily transmit the malarial organism. [SIDEBAR 5 - Human Immunodeficiency Virus] The methods of population genetics are indispensable for discovering the mode of reproduction of pathogens and their carriers, as well as their population structure—that is, the sizes of and rates of exchange among local populations. For example, by using multiple genetic markers to study Salmonella and Neisseria meningitidis (the cause of meningococcal disease), population geneticists have found that both of these pathogenic bacteria reproduce mostly asexually, but do occasionally transfer genes by recombination, even among distantly related strains. The immunological variations that bacteriologists have traditionally used to classify strains of these bacteria are not well correlated with the genetic lineages revealed by multiple genetic markers, nor with variations in pathogenicity or host specificity. Thus, predicting these traits in public health studies will require the use of multiple genetic markers (3, 7). Similarly, population genetic methods can estimate rates and distances of movement of disease-carrying organisms, which affect both disease transmission and potential for control. Molecular analysis of a gene in a species of mosquito showed that the gene had recently spread among three continents, evidence of this insect's enormous dispersal capability (49). The potential rapidity of evolution in natural populations of microorganisms, many of which have short generation times and huge populations, has exceedingly important implications. One, an evolutionary lesson that should have been learned long before it was, is that pathogens may be expected to adapt to consistent, strong selection, such as that created by widespread, intense use of therapeutic drugs. Resistance to antimicrobial drugs has evolved in HIV, the tuberculosis bacterium, the malarial protozoan, and many other disease-carrying organisms, rendering previously effective therapeutic controls ineffective. Many of these organisms, indeed, are resistant to drugs, partly because antibiotic resistance genes are often transferred between species of bacteria (42). The evolution of drug resistance has greatly increased the cost of therapy, has increased morbidity and mortality, and has raised fears that many infectious diseases will be entirely untreatable in the near future (10). Evolutionary theory suggests that such a grim future may be averted by reducing selection for antibiotic resistance, and the World Health Organization has indeed recommended more judicious, sparing use of antibiotics (67). Further studies of the population genetics of pathogens will be important in future containment efforts. The virulence of pathogens can also evolve rapidly. The theory of parasite/host coevolution predicts that greater virulence may evolve when opportunities for transmission among hosts increase. Some researchers have postulated that major outbreaks of influenza and other pandemics have been caused by such evolutionary changes that transpired in crowded cities and among mass movements of refugees. Likewise, there is suggestive evidence that HIV has evolved higher virulence due to high rates of transmission by sexual contact and sharing of needles by intravenous drug users (17, 64). It is well established that the population of HIV viruses in an infected person evolves during the course of the infection, and some authors attribute the onset of AIDS—the disease itself—to this genetic change.
And this "bloviationary profundity":
Concepts such as heritability, components of genetic variance, and genetic correlation, as well as experimental elucidation of phenomena such as hybrid vigor, inbreeding depression, and the basics of polygenic (quantitative) variation, play equally central roles in agricultural genetics and evolutionary theory. The most recent example of this mutualistic interaction between fields is the development and application of techniques using molecular markers to locate the multiple genes responsible for continuously varying traits, such as fruit size and sugar content, and to identify the metabolic function of these genes (called quantitative trait loci, or QTL). In the past, only a few model organisms, such as Drosophila, were sufficiently well known genetically to provide such information. Now, due to research by crop geneticists, population geneticists, and the Plant Genome Project, it is possible to map genes of interest in virtually any organism, whether it be a domesticated species or a wild species used for evolutionary studies. Genetic variation, the stock in trade of evolutionary biologists, is the sine qua non of successful agriculture.
And, the article contains discussions of quite an array of other practical applications. Come on, fess up. You didn't read the article, did you.
Sorry about the lack of paragraphs in the quoted material. Bad formatting day.
WHITE SPACE
every 7-12 lines or so . . . are a welcome and needed micro-rest for tired eyes--especially older tired eyes used to FREEPING many hours a day.
Paragraphs are friends.
Short paragraphs are better friends.