The EvMed Assessment: A test for measuring student understanding of core concepts in evolutionary medicine.

Background and objectives: Universities throughout the USA increasingly offer undergraduate courses in evolutionary medicine (EvMed), which creates a need for pedagogical resources. Several resources offer course content (e.g. textbooks) and a previous study identified EvMed core principles to help instructors set learning goals. However, assessment tools are not yet available. In this study, we address this need by developing an assessment that measures students' ability to apply EvMed core principles to various health-related scenarios. Methodology: The EvMed Assessment (EMA) consists of questions containing a short description of a health-related scenario followed by several likely/unlikely items. We evaluated the assessment's validity and reliability using a variety of qualitative (expert reviews and student interviews) and quantitative (Cronbach's α and classical test theory) methods. We iteratively revised the assessment through several rounds of validation. We then administered the assessment to undergraduates in EvMed and Evolution courses at multiple institutions. Results: We used results from the pilot to create the EMA final draft. After conducting quantitative validation, we deleted items that failed to meet performance criteria and revised items that exhibited borderline performance. The final version of the EMA consists of six core questions containing 25 items, and five supplemental questions containing 20 items. Conclusions and implications: The EMA is a pedagogical tool supported by a wide range of validation evidence. Instructors can use it as a pre/post measure of student learning in an EvMed course to inform curriculum revision, or as a test bank to draw upon when developing in-class assessments, quizzes or exams.

Evolutionary psychiatry: foundations, progress and challenges.

Evolutionary biology provides a crucial foundation for medicine and behavioral science that has been missing from psychiatry. Its absence helps to explain slow progress; its advent promises major advances. Instead of offering a new kind of treatment, evolutionary psychiatry provides a scientific foundation useful for all kinds of treatment. It expands the search for causes from mechanistic explanations for disease in some individuals to evolutionary explanations for traits that make all members of a species vulnerable to disease. For instance, capacities for symptoms such as pain, cough, anxiety and low mood are universal because they are useful in certain situations. Failing to recognize the utility of anxiety and low mood is at the root of many problems in psychiatry. Determining if an emotion is normal and if it is useful requires understanding an individual's life situation. Conducting a review of social systems, parallel to the review of systems in the rest of medicine, can help achieve that understanding. Coping with substance abuse is advanced by acknowledging how substances available in modern environments hijack chemically mediated learning mechanisms. Understanding why eating spirals out of control in modern environments is aided by recognizing the motivations for caloric restriction and how it arouses famine protection mechanisms that induce binge eating. Finally, explaining the persistence of alleles that cause serious mental disorders requires evolutionary explanations of why some systems are intrinsically vulnerable to failure. The thrill of finding functions for apparent diseases is evolutionary psychiatry's greatest strength and weakness. Recognizing bad feelings as evolved adaptations corrects psychiatry's pervasive mistake of viewing all symptoms as if they were disease manifestations. However, viewing diseases such as panic disorder, melancholia and schizophrenia as if they are adaptations is an equally serious mistake in evolutionary psychiatry. Progress will come from framing and testing specific hypotheses about why natural selection left us vulnerable to mental disorders. The efforts of many people over many years will be needed before we will know if evolutionary biology can provide a new paradigm for understanding and treating mental disorders.

How evolutionary psychiatry can advance psychopharmacology
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The prevailing paradigm for psychopharmacology focuses on understanding brain mechanisms as the key to finding new medications and improving clinical outcomes, but frustration with slow progress has inspired many pleas for new approaches. Evolutionary psychiatry brings in an additional basic science that poses new questions about why natural selection left us vulnerable to so many mental disorders, and new insights about how drugs work. The integration of neuroscience with evolutionary psychiatry is synergistic, going beyond reductionism to provide a model like the one used by the rest of medicine. It recognizes negative emotions as symptoms, that are, like pain and cough, useful defenses whose presence should initiate a search for causes. An integrative evolutionary approach explains why agents that block useful aversive responses are usually safe, and how to anticipate when they may cause harm. More generally, an evolutionary framework suggests novel practical strategies for finding and testing new drugs.
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El paradigma común para la psicofarmacología se centra en entender los mecanismos cerebrales como la clave para encontrar nuevos medicamentos y mejorar los resultados clínicos, pero la frustración con el lento progreso ha inspirado muchos motivos para nuevas aproximaciones. La psiquiatría evolutiva conlleva una ciencia básica adicional que plantea nuevas preguntas sobre el por qué la selección natural nos dejó vulnerables a tantos trastornos mentales y aporta nuevas perspectivas sobre cómo funcionan los fármacos. La integración de las neurociencias con la psiquiatría evolutiva es sinérgica, y va más allá del reduccionismo para proporcionar un modelo como el que utiliza el resto de la medicina. Reconoce las emociones negativas como síntomas, que son, como el dolor y la tos, defensas útiles cuya presencia debe iniciar una búsqueda de causas. Un enfoque evolutivo integrador explica por qué los agentes que bloquean las respuestas aversivas útiles suelen ser seguros y cómo anticipar cuándo pueden causar daño. De manera más general, un marco evolutivo sugiere nuevas estrategias prácticas para encontrar y probar nuevos medicamentos.

Le modèle prévalent de la psychopharmacologie se concentre sur la compréhension des mécanismes du cerveau comme la clé pour découvrir de nouveaux médicaments et améliorer les résultats cliniques, mais la frustration ressentie devant les lents progrès de cette méthode a inspiré de nombreux plaidoyers pour d'autres approches. La psychiatrie évolutionniste apporte une connaissance scientifique fondamentale supplémentaire qui pose de nouvelles questions sur la raison pour laquelle la sélection naturelle nous a laissé si vulnérables à tant de troubles mentaux, et des idées nouvelles sur la façon dont fonctionnent les médicaments. L'intégration de la psychiatrie évolutionniste aux neurosciences est source de synergies, allant bien au-delà du réductionnisme en fournissant un modèle semblable à celui utilisé par le reste de la médecine. Il reconnaît les émotions négatives comme des symptômes, exactement comme le sont la douleur et la toux, défenses habituelles qui doivent initier une recherche des causes. Une approche évolutionniste intégrative explique pourquoi des agents qui bloquent des réactions pertinentes d'aversion sont généralement sans danger, et comment anticiper lorsqu'ils pourraient causer un préjudice. Plus généralement, un modèle évolutionniste propose de nouvelles stratégies pratiques pour trouver et tester de nouveaux médicaments.

An evolutionary medicine perspective on pain and its disorders.

Enormous progress in understanding the mechanisms that mediate pain can be augmented by an evolutionary medicine perspective on how the capacity for pain gives selective advantages, the trade-offs that shaped the mechanisms, and evolutionary explanations for the system's vulnerability to excessive and chronic pain. Syndromes of deficient pain document tragically the utility of pain to motivate escape from and avoidance of situations causing tissue damage. Much apparently excessive pain is actually normal because the cost of more pain is often vastly less than the cost of too little pain (the smoke detector principle). Vulnerability to pathological pain may be explained in part because natural selection has shaped mechanisms that respond adaptively to repeated tissue damage by decreasing the pain threshold and increasing pain salience. The other half of an evolutionary approach describes the phylogeny of pain mechanisms; the apparent independence of different kinds of pain is of special interest. Painful mental states such as anxiety, guilt and low mood may have evolved from physical pain precursors. Preliminary evidence for this is found in anatomic and genetic data. Such insights from evolutionary medicine may help in understanding vulnerability to chronic pain. This article is part of the Theo Murphy meeting issue 'Evolution of mechanisms and behaviour important for pain'.

The state of evolutionary medicine in undergraduate education.

BACKGROUND AND OBJECTIVES: Undergraduate courses that include evolutionary medicine (EM) are increasingly available, but quantified data about such courses are lacking. In this article, we describe relevant course offerings by institution and department type, in conjunction with information on the backgrounds and experiences of associated instructors. METHODOLOGY: We searched course catalogs from 196 American universities to find courses that include EM, and sent a survey to 101 EM instructors to ask about their backgrounds and teaching experiences. RESULTS: Research-focused universities (R1) were much more likely to offer at least one course that covers evolutionary applications to health and disease than universities that granted only bachelor's or master's degrees. A survey course on EM was offered in 56% of 116 R1 universities, but only 2% of the 80 non-R1 universities we searched. Most EM instructors have backgrounds in anthropology or biology; each instructor's area of expertise provides clues as to how continued growth of EM may occur differently by discipline. CONCLUSIONS AND IMPLICATIONS: Undergraduates are most likely to learn about EM in research-intensive universities from an anthropological or biological perspective. Responses from anthropology and biology instructors, including whom they share course materials with, highlight that courses may differ depending on the discipline in which they are taught. LAY SUMMARY: Recognition of evolution's relevance to understanding health and disease is growing, but documentation of coverage in undergraduate education is lacking. This study explores where evolutionary medicine (EM) content is taught across 196 undergraduate institutions and how 53 instructors describe their experiences teaching EM.

Core principles of evolutionary medicine: A Delphi study.

BACKGROUND AND OBJECTIVES: Evolutionary medicine is a rapidly growing field that uses the principles of evolutionary biology to better understand, prevent and treat disease, and that uses studies of disease to advance basic knowledge in evolutionary biology. Over-arching principles of evolutionary medicine have been described in publications, but our study is the first to systematically elicit core principles from a diverse panel of experts in evolutionary medicine. These principles should be useful to advance recent recommendations made by The Association of American Medical Colleges and the Howard Hughes Medical Institute to make evolutionary thinking a core competency for pre-medical education. METHODOLOGY: The Delphi method was used to elicit and validate a list of core principles for evolutionary medicine. The study included four surveys administered in sequence to 56 expert panelists. The initial open-ended survey created a list of possible core principles; the three subsequent surveys winnowed the list and assessed the accuracy and importance of each principle. RESULTS: Fourteen core principles elicited at least 80% of the panelists to agree or strongly agree that they were important core principles for evolutionary medicine. These principles over-lapped with concepts discussed in other articles discussing key concepts in evolutionary medicine. CONCLUSIONS AND IMPLICATIONS: This set of core principles will be helpful for researchers and instructors in evolutionary medicine. We recommend that evolutionary medicine instructors use the list of core principles to construct learning goals. Evolutionary medicine is a young field, so this list of core principles will likely change as the field develops further.

Evolutionary public health: introducing the concept.

The emerging discipline of evolutionary medicine is breaking new ground in understanding why people become ill. However, the value of evolutionary analyses of human physiology and behaviour is only beginning to be recognised in the field of public health. Core principles come from life history theory, which analyses the allocation of finite amounts of energy between four competing functions-maintenance, growth, reproduction, and defence. A central tenet of evolutionary theory is that organisms are selected to allocate energy and time to maximise reproductive success, rather than health or longevity. Ecological interactions that influence mortality risk, nutrient availability, and pathogen burden shape energy allocation strategies throughout the life course, thereby affecting diverse health outcomes. Public health interventions could improve their own effectiveness by incorporating an evolutionary perspective. In particular, evolutionary approaches offer new opportunities to address the complex challenges of global health, in which populations are differentially exposed to the metabolic consequences of poverty, high fertility, infectious diseases, and rapid changes in nutrition and lifestyle. The effect of specific interventions is predicted to depend on broader factors shaping life expectancy. Among the important tools in this approach are mathematical models, which can explore probable benefits and limitations of interventions in silico, before their implementation in human populations.

Does selection for short sleep duration explain human vulnerability to Alzheimer's disease?

Compared with other primates, humans sleep less and have a much higher prevalence of Alzheimer 's disease (AD) pathology. This article reviews evidence relevant to the hypothesis that natural selection for shorter sleep time in humans has compromised the efficacy of physiological mechanisms that protect against AD during sleep. In particular, the glymphatic system drains interstitial fluid from the brain, removing extra-cellular amyloid beta (eAß) twice as fast during sleep. In addition, melatonin - a peptide hormone that increases markedly during sleep - is an effective antioxidant that inhibits the polymerization of soluble eAß into insoluble amyloid fibrils that are associated with AD. Sleep deprivation increases plaque formation and AD, which itself disrupts sleep, potentially creating a positive feedback cycle. These and other physiological benefits of sleep may be compromised by short sleep durations. Our hypothesis highlights possible long-term side effects of medications that reduce sleep, and may lead to potential new strategies for preventing and treating AD.

Anorexia: A perverse effect of attempting to control the starvation response.

Starvation arouses evolved protective mechanisms including binge eating and increased metabolic efficiency and fat storage. When aroused by dieting, the experiences of out-of-control eating, increased appetite, and increased fat storage arouse greater fears of obesity, spurring renewed attempts to restrict intake severely. The resulting positive feedback cycle escalates into bulimia for many, and anorexia in a few.

Social selection is a powerful explanation for prosociality.

Cultural group selection helps explain human cooperation, but social selection offers a complementary, more powerful explanation. Just as sexual selection shapes extreme traits that increase matings, social selection shapes extreme traits that make individuals preferred social partners. Self-interested partner choices create strong and possibly runaway selection for prosocial traits, without requiring group selection, kin selection, or reciprocity.

Human compulsivity: A perspective from evolutionary medicine.

Biological explanations address not only proximal mechanisms (for example, the underlying neurobiology of obsessive-compulsive disorder), but also distal mechanisms (that is, a consideration of how particular neurobiological mechanisms evolved). Evolutionary medicine has emphasized a series of explanations for vulnerability to disease, including constraints, mismatch, and tradeoffs. The current paper will consider compulsive symptoms in obsessive-compulsive and related disorders and behavioral addictions from this evolutionary perspective. It will argue that while obsessive-compulsive disorder (OCD) is typically best conceptualized as a dysfunction, it is theoretically and clinically valuable to understand some symptoms of obsessive-compulsive and related disorders in terms of useful defenses. The symptoms of behavioral addictions can also be conceptualized in evolutionary terms (for example, mismatch), which in turn provides a sound foundation for approaching assessment and intervention.

Evolutionary Ecology of Organs: A Missing Link in Cancer Development?

There is striking variation in the incidence of cancer in human organs. Malignant tumors are common in the colon and breast but rare in the heart and small bowel. The uterus frequently develops benign fibroid tumors but uterine cancers are relatively rare. The organ-specific difference in cancer prevalence has been explained primarily by the relative roles of intrinsic and extrinsic risk factors. In this opinion article, we propose also considering organs as distinct but connected ecosystems whose different vulnerabilities to malignant transformation may be partially explained by how essential each organ is for survival through the age of reproduction. We present and discuss some of the basic concepts and assumptions of this perspective on evolutionary medicine.

What are 'good' depression symptoms? Comparing the centrality of DSM and non-DSM symptoms of depression in a network analysis.

BACKGROUND: The symptoms for Major Depression (MD) defined in the DSM-5 differ markedly from symptoms assessed in common rating scales, and the empirical question about core depression symptoms is unresolved. Here we conceptualize depression as a complex dynamic system of interacting symptoms to examine what symptoms are most central to driving depressive processes. METHODS: We constructed a network of 28 depression symptoms assessed via the Inventory of Depressive Symptomatology (IDS-30) in 3,463 depressed outpatients from the Sequenced Treatment Alternatives to Relieve Depression (STAR*D) study. We estimated the centrality of all IDS-30 symptoms, and compared the centrality of DSM and non-DSM symptoms; centrality reflects the connectedness of each symptom with all other symptoms. RESULTS: A network with 28 intertwined symptoms emerged, and symptoms differed substantially in their centrality values. Both DSM symptoms (e.g., sad mood) and non-DSM symptoms (e.g., anxiety) were among the most central symptoms, and DSM criteria were not more central than non-DSM symptoms. LIMITATIONS: Many subjects enrolled in STAR*D reported comorbid medical and psychiatric conditions which may have affected symptom presentation. CONCLUSION: The network perspective neither supports the standard psychometric notion that depression symptoms are equivalent indicators of MD, nor the common assumption that DSM symptoms of depression are of higher clinical relevance than non-DSM depression symptoms. The findings suggest the value of research focusing on especially central symptoms to increase the accuracy of predicting outcomes such as the course of illness, probability of relapse, and treatment response.

The status of evolutionary medicine education in North American medical schools.

BACKGROUND: Medical and public health scientists are using evolution to devise new strategies to solve major health problems. But based on a 2003 survey, medical curricula may not adequately prepare physicians to evaluate and extend these advances. This study assessed the change in coverage of evolution in North American medical schools since 2003 and identified opportunities for enriching medical education. METHODS: In 2013, curriculum deans for all North American medical schools were invited to rate curricular coverage and perceived importance of 12 core principles, the extent of anticipated controversy from adding evolution, and the usefulness of 13 teaching resources. Differences between schools were assessed by Pearson's chi-square test, Student's t-test, and Spearman's correlation. Open-ended questions sought insight into perceived barriers and benefits. RESULTS: Despite repeated follow-up, 60 schools (39%) responded to the survey. There was no evidence of sample bias. The three evolutionary principles rated most important were antibiotic resistance, environmental mismatch, and somatic selection in cancer. While importance and coverage of principles were correlated (r = 0.76, P < 0.01), coverage (at least moderate) lagged behind importance (at least moderate) by an average of 21% (SD = 6%). Compared to 2003, a range of evolutionary principles were covered by 4 to 74% more schools. Nearly half (48%) of responders anticipated igniting controversy at their medical school if they added evolution to their curriculum. The teaching resources ranked most useful were model test questions and answers, case studies, and model curricula for existing courses/rotations. Limited resources (faculty expertise) were cited as the major barrier to adding more evolution, but benefits included a deeper understanding and improved patient care. CONCLUSION: North American medical schools have increased the evolution content in their curricula over the past decade. However, coverage is not commensurate with importance. At a few medical schools, anticipated controversy impedes teaching more evolution. Efforts to improve evolution education in medical schools should be directed toward boosting faculty expertise and crafting resources that can be easily integrated into existing curricula.

Depression sum-scores don't add up: why analyzing specific depression symptoms is essential.

Most measures of depression severity are based on the number of reported symptoms, and threshold scores are often used to classify individuals as healthy or depressed. This method--and research results based on it--are valid if depression is a single condition, and all symptoms are equally good severity indicators. Here, we review a host of studies documenting that specific depressive symptoms like sad mood, insomnia, concentration problems, and suicidal ideation are distinct phenomena that differ from each other in important dimensions such as underlying biology, impact on impairment, and risk factors. Furthermore, specific life events predict increases in particular depression symptoms, and there is evidence for direct causal links among symptoms. We suggest that the pervasive use of sum-scores to estimate depression severity has obfuscated crucial insights and contributed to the lack of progress in key research areas such as identifying biomarkers and more efficacious antidepressants. The analysis of individual symptoms and their causal associations offers a way forward. We offer specific suggestions with practical implications for future research.

Depression is not a consistent syndrome: An investigation of unique symptom patterns in the STAR*D study.

BACKGROUND: The DSM-5 encompasses a wide range of symptoms for Major Depressive Disorder (MDD). Symptoms are commonly added up to sum-scores, and thresholds differentiate between healthy and depressed individuals. The underlying assumption is that all patients diagnosed with MDD have a similar condition, and that sum-scores accurately reflect the severity of this condition. To test this assumption, we examined the number of DSM-5 depression symptom patterns in the "Sequenced Treatment Alternatives to Relieve Depression" (STAR*D) study. METHODS: We investigated the number of unique symptom profiles reported by 3703 depressed outpatients at the beginning of the first treatment stage of STAR*D. RESULTS: Overall, we identified 1030 unique symptom profiles. Of these profiles, 864 profiles (83.9%) were endorsed by five or fewer subjects, and 501 profiles (48.6%) were endorsed by only one individual. The most common symptom profile exhibited a frequency of only 1.8%. Controlling for overall depression severity did not reduce the amount of observed heterogeneity. LIMITATIONS: Symptoms were dichotomized to construct symptom profiles. Many subjects enrolled in STAR*D reported medical conditions for which prescribed medications may have affected symptom presentation. CONCLUSIONS: The substantial symptom variation among individuals who all qualify for one diagnosis calls into question the status of MDD as a specific consistent syndrome and offers a potential explanation for the difficulty in documenting treatment efficacy. We suggest that the analysis of individual symptoms, their patterns, and their causal associations will provide insights that could not be discovered in studies relying on only sum-scores.

The impact of individual depressive symptoms on impairment of psychosocial functioning.

Previous studies have established that scores on Major Depressive Disorder scales are correlated with measures of impairment of psychosocial functioning. It remains unclear, however, whether individual depressive symptoms vary in their effect on impairment, and if so, what the magnitude of these differences might be. We analyzed data from 3,703 depressed outpatients in the first treatment stage of the Sequenced Treatment Alternatives to Relieve Depression (STAR*D) study. Participants reported on the severity of 14 depressive symptoms, and stated to what degree their depression impaired psychosocial functioning (in general, and in the five domains work, home management, social activities, private activities, and close relationships). We tested whether symptoms differed in their associations with impairment, estimated unique shared variances of each symptom with impairment to assess the degree of difference, and examined whether symptoms had variable impacts across impairment domains. Our results show that symptoms varied substantially in their associations with impairment, and contributed to the total explained variance in a range from 0.7% (hypersomnia) to 20.9% (sad mood). Furthermore, symptoms had significantly different impacts on the five impairment domains. Overall, sad mood and concentration problems had the highest unique associations with impairment and were among the most debilitating symptoms in all five domains. Our findings are in line with a growing chorus of voices suggesting that symptom sum-scores obfuscate relevant differences between depressed patients and that substantial rewards will come from close attention to individual depression symptoms.