Despite the effort on DSM-5 and ICD-11, few appear satisfied with these classification systems. We suggest that the core reason for dissatisfaction is expecting too much from them; they do not provide discrete categories that map to specific causes of disease, they describe clinical syndromes intended to guide treatment choices. Here we review work on anxiety and anxiety disorders to argue that while clinicians draw a pragmatic distinction between normal and abnormal emotions based on considerations such as severity and duration, (...) understanding the evolutionary origins and utility of the emotions, including the adaptive value of adverse emotions, is key for formulating comprehensive assessments of an individual patient’s symptoms and for providing a conceptual foundation for pharmacotherapy, psychotherapy, and public health. (shrink)

Public health law has focused primarily on combatting stigma through laws targeting discrimination based on attributes, when the reach of stigma extends far beyond mere appearances. By exploring the lived experience of stigmatized individuals, policy makers might more deeply understand public health problems, more appropriately create health policies, and more effectively promote positive health behaviors. Efforts to address stigma must focus on all aspects of stigma to be effective.

ZusammenfassungDer Krankheitsbegriff soll aus der Perspektive der klinischen Medizin am Beispiel der Radioonkologie dargestellt werden. Als theoretisches Modell zum ganzheitlichen Verständnis wird zunächst der interaktive Dualismus eingeführt. Danach wird die Interaktion zwischen Geist und Körper als wesentlich angesehen, um den Patienten mit Würde und Mitgefühl zu behandeln. Auch die Strahlentherapie erfordert nach ihrem Selbstverständnis einen ganzheitlichen Zugang zum Patienten. Demgegenüber zeigt die Analyse der aktuellen radioonkologischen Literatur einen reduktionistischen Krankheitsbegriff, der in erster Linie objektive Kriterien aus ärztlicher Sicht zur Definition (...) von Krankheit heranzieht. Im Dialog könnten stattdessen Arzt und Patient einen gemeinsamen Krankheitsbegriff entwickeln; hierbei finden im Sinne des interaktiven Dualismus gleichermaßen objektive ärztliche wie subjektive patientenbezogene Kriterien Berücksichtigung. Grenzen dieses neuen Konzepts erfordern eine besondere Beachtung und werden zuletzt erläutert. (shrink)

Although natural selection might be expected to reduce the incidence and severity of disease, disease persists. Natural selection leads to increases in the mean fitness of populations and so will reduce the frequency of disease-associated alleles, but other evolutionary processes, such as mutation and gene flow, may introduce or increase the frequency of these deleterious alleles. The pleiotropic actions of genes and the epistatic interactions between them complicate the relationship between genotype and phenotype, and may result in the preservation of (...) disease-associated alleles. Deleterious alleles may also be maintained because of linkage to beneficial alleles. The inability of natural selection to eliminate diseases of aging is a reminder that fitness – success in producing progeny, or in contributing genes to the population gene pool – is not equivalent to the absence of disease. Nutritional or psychosocial cues may lead to life history strategies that maximize survival to reproductive maturity at the expense of disease later in life. Natural selection acts on genes, cells, and groups, as well as on organisms; the outcome of evolution reflects selection at different levels of biological organization. Finally, the human environment is constantly changing, largely because of the evolution of our parasites and because of changes in cultural beliefs and practices; genetic evolution is comparatively slow and lags behind environmental change. An evolutionary nosology complements traditional medical nosologies and enhances our understanding of the persistence of disease and the meaning of human variation. (shrink)

In this article, I argue that distinguishing ‘evolutionary’ from ‘Darwinian’ medicine will help us assess the variety of roles that evolutionary explanations can play in a number of medical contexts. Because the boundaries of evolutionary and Darwinian medicine overlap to some extent, however, they are best described as distinct ‘research traditions’ rather than as competing paradigms. But while evolu- tionary medicine does not stand out as a new scientific field of its own, Darwinian medicine is united by a number of (...) distinctive theoretical and methodological claims. For example, evolutionary medicine and Darwinian medicine can be distinguished with respect to the styles of evolutionary explanations they employ. While the former primarily involves ‘forward looking’ explanations, the latter depends mostly on ‘backward looking’ explanations. A forward looking explanation tries to predict the effects of ongoing evolutionary processes on human health and disease in contem- porary environments (e.g., hospitals). In contrast, a backward looking explanation typically applies evolutionary principles from the vantage point of humans’ distant biological past in order to assess present states of health and disease. Both approaches, however, are concerned with the prevention and control of human diseases. In con- clusion, I raise some concerns about the claim that ‘nothing in medicine makes sense except in the light of evolution’. (shrink)

Conceptual analysis of health and disease is portrayed as consisting in the confrontation of a set of criteria—a “definition”—with a set of cases, called instances of either “health” or “ disease.” Apart from logical counter-arguments, there is no other way to refute an opponent’s definition than by providing counter-cases. As resorting to intensional stipulation is not forbidden, several contenders can therefore be deemed to have succeeded. This implies that conceptual analysis alone is not likely to decide between naturalism and normativism. (...) An alternative to this approach would be to examine whether the concept of disease can be naturalized. (shrink)

In their paper “Is psychopathy a mental disease?”, Thomas Nadelhoffer and Walter Sinnott-Armstrong argue that according to any plausible account of mental disorder, neural and psychological abnormalities correlated with psychopathy should be regarded as signs of a mental disorder. I oppose this conclusion by arguing that at least on a naturalistically grounded account, such as Wakefield’s ‘Harmful Dysfunction’ view, currently available empirical data and evolutionary considerations indicate that psychopathy is not a mental disorder.

Some ‘naturalist’ accounts of disease employ a biostatistical account of dysfunction, whilst others use a ‘selected effect’ account. Several recent authors have argued that the biostatistical account offers the best hope for a naturalist account of disease. We show that the selected effect account survives the criticisms levelled by these authors relatively unscathed, and has significant advantages over the BST. Moreover, unlike the BST, it has a strong theoretical rationale and can provide substantive reasons to decide difficult cases. This is (...) illustrated by showing how life-history theory clarifies the status of so-called diseases of old age. The selected effect account of function deserves a more prominent place in the philosophy of medicine than it currently occupies. _1_ Introduction _2_ Biostatistical and Selected Effect Accounts of Function _3_ Objections to the Selected Effect Account _3.1_ Boorse _3.2_ Kingma _3.3_ Hausman _3.4_ Murphy and Woolfolk _4_ Problems for the Biostatistical Account _4.1_ Schwartz _5_ Analysis versus Explication _6_ Explicating Dysfunction: Life History Theory and Senescence _7_ Conclusion. (shrink)

In a recent article in this journal, Zachary Ardern criticizes our view that the most promising candidate for a naturalized criterion of disease is the "selected effects" account of biological function and dysfunction. Here we reply to Ardern’s criticisms and, more generally, clarify the relationship between adaptation and dysfunction in the evolution of health and disease.

Mental disorders are often thought to be harmful dysfunctions. Jerome Wakefield has argued that such dysfunctions should be understood as failures of naturally selected functions. This suggests, implicitly, that evolutionary biology and other Darwinian disciplines hold important information for anyone working on answering the philosophical question, ‘what is a mental disorder?’. In this article, the author argues that Darwinian theory is not only relevant to the understanding of the disrupted functions, but it also sheds light on the disruption itself, as (...) well as on the harm that attends the disruption. The arguments advanced here are partially based on the view that a core feature of Darwinism is that it stresses the environmental relativity of functions and dysfunctions. These arguments show a very close empirical connection between social judgments and dysfunctions , which is of interest for psychiatric theory. Philosophically, they lead to the conclusion that the concept of mental disorder is identical to the concept of mental dysfunction. Consequently, it is both misleading and redundant to conceptualize mental disorders as ‘harmful dysfunctions’, and not simply as ‘mental dysfunctions’. (shrink)

Mental disorders are often thought to be harmful dysfunctions. Jerome Wakefield has argued that such dysfunctions should be understood as failures of naturally selected functions. This suggests, implicitly, that evolutionary biology and other Darwinian disciplines hold important information for anyone working on answering the philosophical question, 'what is a mental disorder?'. In this article, the author argues that Darwinian theory is not only relevant to the understanding of the disrupted functions, but it also sheds light on the disruption itself, as (...) well as on the harm that attends the disruption. The arguments advanced here are partially based on the view that a core feature of Darwinism is that it stresses the environmental relativity of functions and dysfunctions. These arguments show a very close empirical connection between social judgments and dysfunctions, which is of interest for psychiatric theory. Philosophically, they lead to the conclusion that the concept of mental disorder is identical to the concept of mental dysfunction. Consequently, it is both misleading and redundant to conceptualize mental disorders as 'harmful dysfunctions', and not simply as 'mental dysfunctions'. (shrink)

The Darwinian theory of evolution is itself evolving and this book presents the details of the core of modern Darwinism and its latest developmental directions. The authors present current scientific work addressing theoretical problems and challenges in four sections, beginning with the concepts of evolution theory, its processes of variation, heredity, selection, adaptation and function, and its patterns of character, species, descent and life. The second part of this book scrutinizes Darwinism in the philosophy of science and its usefulness in (...) understanding ecosystems, whilst the third section deals with its application in disciplines beyond the biological sciences, including evolutionary psychology and evolutionary economics, Darwinian morality and phylolinguistics. The final section addresses anti-Darwinism, the creationist view and issues around teaching evolution in secondary schools. The reader learns how current experimental biology is opening important perspectives on the sources of variation, and thus of the very power of natural selection. This work examines numerous examples of the extension of the principle of natural selection and provides the opportunity to critically reflect on a rich theory, on the methodological rigour that presides in its extensions and exportations, and on the necessity to measure its advantages and also its limits. Scholars interested in modern Darwinism and scientific research, its concepts, research programs and controversies will find this book an excellent read, and those considering how Darwinism might evolve, how it can apply to the human sciences and other disciplines beyond its origins will find it particularly valuable. Originally produced in French (Les Mondes Darwiniens), the scope and usefulness of the book have led to the production of this English text, to reach a wider audience. This book is a milestone in the impressive penetration by Francophone scholars into the world of Darwinian science, its historiography and philosophy over the last two decades. Alex Rosenberg, R. Taylor Cole Professor of Philosophy, Duke University Until now this useful and comprehensive handbook has only been available to francophones. Thanks to this invaluable new translation, this collection of insightful and original essays can reach the global audience it deserves. Tim Lewens, University of Cambridge. (shrink)

Randolph Nesse argues that evolutionary theory is the key element in elaborating a valid criterion demarcating the normal from the pathological in psychiatry. By focusing on the application of Nesse’s criterion on the demarcation of normal low mood from pathological depression, I argue – contrary to Nesse’s claims – that evolutionary theory cannot generate a valid criterion from the differentiation of normal low mood states from pathological depression. Indeed, expression in conformity to evolved functions cannot constitute a sufficient condition for (...) normality, as Nesse’s project should imply. Moreover, grounding normality in evolved functions presupposes a kind of fixity of our emotional states, which seems unwarranted in the light of a constantly changing environment. As a result of these limitations, I suggest that the relevant distinction in psychiatry should not be “normality” versus “abnormality”, but, rather, “that which requires intervention” versus “that which does not”. (shrink)

The DSM-III, DSM-IV, DSM-IV-TR and ICD-10 have judiciously minimized discussion of etiologies to distance clinical psychiatry from Freudian psychoanalysis. With this goal mostly achieved, discussion of etiological factors should be reintroduced into the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition. A research agenda for the DSM-V advocated the "development of a pathophysiologically based classification system". The author critically reviews the neuroevolutionary literature on stress-induced and fear circuitry disorders and related amygdala-driven, species-atypical fear behaviors of clinical severity in adult (...) humans. Over 30 empirically testable/falsifiable predictions are presented. It is noted that in DSM-IV-TR and ICD-10, the classification of stress and fear circuitry disorders is neither mode-of-acquisition-based nor brain-evolution-based. For example, snake phobia and dog phobia are clustered together. Similarly, research on blood-injection-injury-type-specific phobia clusters two fears different in their innateness: 1) an arguably ontogenetic memory-trace-overconsolidation-based fear and 2) a hardwired fear of the sight of one's blood or a sharp object penetrating one's skin. Genetic architecture-charting of fear-circuitry-related traits has been challenging. Various, non-phenotype-based architectures can serve as targets for research. In this article, the author will propose one such alternative genetic architecture. This article was inspired by the following: A) Nesse's "Smoke-Detector Principle", B) the increasing suspicion that the "smooth" rather than "lumpy" distribution of complex psychiatric phenotypes may in some cases be accounted for by oligogenic transmission, and C) insights from the initial sequence of the chimpanzee genome and comparison with the human genome by the Chimpanzee Sequencing and Analysis Consortium published in late 2005. Neuroevolutionary insights relevant to fear circuitry symptoms that primarily emerge overconsolidationally are presented. Also introduced is a human-evolution-based principle for clustering innate fear traits. The "Neuroevolutionary Time-depth Principle" of innate fears proposed in this article may be useful in the development of a neuroevolution-based taxonomic re-clustering of stress-triggered and fear-circuitry disorders in DSM-V. Four broad clusters of evolved fear circuits are proposed based on their time-depths: 1) Mesozoic circuits hardwired by wild-type alleles driven to fixation by Mesozoic selective sweeps; 2) Cenozoic circuits relevant to many specific phobias; 3) mid Paleolithic and upper Paleolithic circuits ; 4) Neolithic circuits. More importantly, the author presents evolutionary perspectives on warzone-related PTSD, Combat-Stress Reaction, Combat-related Stress, Operational-Stress, and other deployment-stress-induced symptoms. The Neuroevolutionary Time-depth Principle presented in this article may help explain the dissimilar stress-resilience levels following different types of acute threat to survival of oneself or one's progency. PTSD rates following exposure to lethal inter-group violence are usually 5-10 times higher than rates following large-scale natural disasters such as forest fires, floods, hurricanes, volcanic eruptions, and earthquakes. The author predicts that both intentionally-caused large-scale bioevent-disasters, as well as natural bioevents such as SARS and avian flu pandemics will be an exception and are likely to be followed by PTSD rates approaching those that follow warzone exposure. During bioevents, Amygdala-driven and locus-coeruleus-driven epidemic pseudosomatic symptoms may be an order of magnitude more common than infection-caused cytokine-driven symptoms. Implications for the red cross and FEMA are discussed. It is also argued that hospital phobia as well as dog phobia, bird phobia and bat phobia require re-taxonomization in DSM-V in a new "overconsolidational disorders" category anchored around PTSD. The overconsolidational spectrum category may be conceptualized as straddling the fear circuitry spectrum disorders and the affective spectrum disorders categories, and may be a category for which Pitman's secondary prevention propranolol regimen may be specifically indicated as a "morning after pill" intervention. Predictions are presented regarding obsessive-compulsive disorder and "culture-bound" acute anxiety symptoms. Also discussed are insights relevant to pseudoneurological symptoms and to the forthcoming Dissociative-Conversive disorders category in DSM-V, including what the author terms fright-triggered acute pseudo-localized symptoms. Speculations based on studies of the human abnormal-spindle-like, microcephaly-associated gene, the microcephaly primary autosomal recessive gene, and the forkhead box p2 gene are made and incorporated into what is termed "The pre-FOXP2 Hypothesis of Blood-Injection-Injury Phobia." Finally, the author argues for a non-reductionistic fusion of "distal neurobiology" with clinical "proximal neurobiology," utilizing neurological heuristics. It is noted that the value of re-clustering fear traits based on behavioral ethology, human-phylogenomics-derived endophenotypes and on ontogenomics can be confirmed or disconfirmed using epidemiological or twin studies and psychiatric genomics. (shrink)