Common monogenic genetic diseases, ones that have unexpectedly high frequencies in certain populations, have attracted a great number of conflicting evolutionary explanations. This paper will attempt to explain the mystery of why two particularly extensively studied common genetic diseases, Tay Sachs disease and cystic fibrosis, remain evolutionary mysteries despite decades of research. I review the most commonly cited evolutionary processes used to explain common genetic diseases: reproductive compensation, random genetic drift (in the context of founder effect), and especially heterozygote advantage. (...) The latter process has drawn a particularly large amount of attention, having so successfully explained the elevated frequency of sickle cell anemia in malaria-endemic areas. However, the empirical evidence for heterozygote advantage in other common genetic diseases is quite weak. I introduce and illustrate the significance of a hierarchy of genetic disease phenomena found within the genetic disease explanations, which include the phenomena: single mutation variants of a common genetic disease, single genetic diseases, and classes of diseases with related phenotypic effects. I demonstrate that some of the confusion over the explanations of common genetic diseases can be traced back to confusions over which phenomena are being explained. I proceed to briefly evaluate the existing evidence for two common human genetic diseases: Tay Sachs disease and cystic fibrosis. The above considerations will ultimately shed light on why these diseases’ evolutionary explanations remain so deeply unresolved after so such a great volume of research. (shrink)

Most attempts to craft a definition of disease seem to have tackled two tasks simultaneously: 1) trying to create a series of inclusion and exclusion criteria that correspond to medical usage of the word disease and 2) using this definition to understand the essence of what disease is. The first task has been somewhat accomplished, but cannot reach closure because the concept of “disease” is based on a prototype, not a logical category. The second task cannot be accomplished by deduction, (...) but only by understanding how the body works and what each component is for, in evolutionary detail. An evolutionary view of the origins of the body and its vulnerabilities that result in disease provides an objective foundation for recognizing pathology. Our social definition of disease will remain contentious, however, because values vary, and because the label “disease” changes judgments about the moral status of people with various conditions, and their rights to medical and social resources. (shrink)

An evolutionary view of the origins of the body and its vulnerabilities that result in disease provides an objective foundation for recognizing pathology. Our social definition of disease will remain contentious, however, because values vary, and because the label "disease" changes judgments about the moral status of people with various conditions, and their rights to medical and social resources.

Godfrey-Smith ( 2001 ) has distinguished three types of adaptationism. This article builds on his analysis, and revises it in places, by distinguishing seven varieties of adaptationism. This taxonomy allows us to clarify what is at stake in debates over adaptationism, and it also helps to cement the importance of Gould and Lewontin’s ‘Spandrels’ essay. Some adaptationists have suggested that their essay does not offer any coherent alternative to the adaptationist programme: it consists only in an exhortation to test adaptationist (...) hypotheses more thoroughly than was usual in the 1970s. Here it is argued that the ‘Spandrels’ paper points towards a genuinely non-adaptationist methodology implicit in much evolutionary developmental biology. This conclusion helps to expose the links between older debates over adaptationism and more recent questions about the property of evolvability. (shrink)

Christopher Boorse's Bio Statistical Theory (BST) defines health as the absence of disease, and disease as the adverse departure from normal species functioning. This paper presents a two-pronged problem for this account. First I demonstrate that, in order to accurately account for dynamic physiological functions, Boorse's account of normal function needs to be modified to index functions against situations. I then demonstrate that if functions are indexed against situations, the BST can no longer account for diseases that result from specific (...) environmental factors. The BST is impaled on either horn of this dilemma and therefore must be dismissed. (shrink)

Phylogenetic information is often necessary to distinguish between evolutionary scenarios. Recently, some prominent proponents of evolutionary psychology have acknowledged this, and have claimed that such evidence has in fact been brought to bear on adaptive hypotheses involving complex human psychological traits. Were this possible, it would be a valuable source of evidence regarding hypothesized adaptive traits in humans. However, the structure of the Hominidae family makes this difficult or impossible. For many traits of interest, the closest extant relatives to the (...) human species are too phenotypically different from humans for such methods to provide meaningful data. While phylogenetic information can be useful for testing adaptive hypotheses in humans, these generally involve traits that are (a) not widely shared in the species or (b) fairly widely shared in the Hominidae family, and hence likely of a lower order of complexity than the sorts of traits evolutionary psychology has so far been interested in. (shrink)

Phylogenetic information is often necessary to distinguish between evolutionary scenarios. Recently, some prominent proponents of evolutionary psychology have acknowledged this, and have claimed that such evidence has in fact been brought to bear on adaptive hypotheses involving complex human psychological traits. Were this possible, it would be a valuable source of evidence regarding hypothesized adaptive traits in humans. However, the structure of the Hominidae family makes this difficult or impossible. For many traits of interest, the closest extant relatives to the (...) human species are too phenotypically different from humans for such methods to provide meaningful data. While phylogenetic information can be useful for testing adaptive hypotheses in humans, these generally involve traits that are not widely shared in the species or fairly widely shared in the Hominidae family, and hence likely of a lower order of complexity than the sorts of traits evolutionary psychology has so far been interested in. (shrink)

The two authors of this paper have diametrically opposed views of the prevalence and strength of adaptation in nature. Hendry believes that adaptation can be seen almost everywhere and that evidence for it is overwhelming and ubiquitous. Gonzalez believes that adaptation is uncommon and that evidence for it is ambiguous at best. Neither author is certifiable to the knowledge of the other, leaving each to wonder where the other has his head buried. Extensive argument has revealed that each author thinks (...) his own view is amply supported by both theory and empirical evidence. Further reflection has revealed that the differences in opinion may start with the different disciplines in which we work: evolutionary ecology for Hendry and community ecology for Gonzalez. In the present paper, we each present devastating evidence supporting our own position and thus refuting that of the other. We then identify the critical differences that led to such opposing views. We close by combining our two perspectives into a common framework based on the adaptive landscape, and thereby suggest means by which to assess the prevalence and strength of adaptation. (shrink)

The effects of mental disorder are apparent and pervasive, in suffering, loss of freedom and life opportunities, negative impacts on education, work satisfaction and productivity, complications in law, institutions of healthcare, and more. With a new edition of the 'bible' of psychiatric diagnosis - the DSM - under developmental, it is timely to take a step back and re-evalutate exactly how we diagnose and define mental disorder. This new book by Derek Bolton tackles the problems involved in the definition and (...) boundaries of mental disorder. It addresses two main questions regarding mental illness. Firstly, what is the basis of the standards or norms by which we judge that a person has a mental disorder - that the person's mind is not working as it should, that their mental functioning is abnormal? Controversies about these questions have been dominated by the contrast between norms that are medical, scientific or natural, on the one hand, and social norms on the other. The norms that define mental disorder seem to belong to psychiatry, to be medical and scientific, but are they really social norms, hijacked and disguised by the medical profession? Secondly, what is the validity of the distinction between mental disorder and order, between abnormal and normal mental functioning? To what extent, notwithstanding appearances, does mental disorder involve meaningful reactions and problem-solving? These responses may be to normal problems of living, or to not so normal problems - to severe psycho-social challenges. Is there after all order in mental disorder? With the closing of asylums and the appearance of care in the community, mental disorder is now in our midst. While attempts have been made to define clearly a concept of mental disorder that is truly medical as opposed to social, there is increasing evidence that such a distinction is unviable - there is no clear line between what is normal in the population and what is abnormal. 'What is Mental Disorder?' reviews these various crucial developments and their profound impact for the concept and its boundaries in a provocative and timely book. (shrink)

The next time you get sick, consider this before picking up the aspirin: your body may be doing exactly what it's supposed to. In this ground-breaking book, two pioneers of the science of Darwinian medicine argue that illness as well as the factors that predispose us toward it are subject to the same laws of natural selection that otherwise make our bodies such miracles of design. Among the concerns they raise: When may a fever be beneficial? Why do pregnant women (...) get morning sickness? How do certain viruses "manipulate" their hosts into infecting others? What evolutionary factors may be responsible for depression and panic disorder? Deftly summarizing research on disorders ranging from allergies to Alzheimer's, and form cancer to Huntington's chorea, Why We Get Sick, answers these questions and more. The result is a book that will revolutionize our attitudes toward illness and will intrigue and instruct lay person and medical practitioners alike. (shrink)

Evolution is the single most important idea in modern biology, shedding light on virtually every biological question, from the shape of orchid blossoms to the distribution of species across the planet. Until recently, however, the theory has had little impact on medical research or practice. Evolutionary Medicine shows how this is beginning to change. Collecting work from leaders in the field, this volume describes an array of new and innovative approaches to human health that are based on an appreciation of (...) our long evolutionary history. For example, it shows how evolution helps to explain the complex relationship between our immune systems and the virulence and transmission of human viruses. It also shows how comparisons between how we live today and how our hunter-gatherer ancestors lived thousands of years ago illuminate a variety of contemporary ills, including obesity, lower-back pain, and insomnia. (shrink)