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Rainer H Straub - One of the best experts on this subject based on the ideXlab platform.
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Chapter IV – Evolutionary Medicine
The Origin of Chronic Inflammatory Systemic Diseases and their Sequelae, 2020Co-Authors: Rainer H StraubAbstract:Many arguments discussed in Chapters I–III Chapter I Chapter II Chapter III relate to acute inflammatory episodes such as infection, wound healing, and foreign body removal. At this point, the question appears whether and why these mechanisms are also used in chronic inflammatory systemic diseases. It is discussed that disease-related genes, whether advantageous (by attenuating the disease) or disadvantageous (by boosting the disease), can only be transferred to the progeny if the transfer is not blocked, that is, when reproduction is not blocked. It is demonstrated that in chronic inflammatory systemic diseases, gene transfer can happen in the asymptomatic phase or before but not in the symptomatic phase because reproduction is severely disturbed (negative selection pressure). Genes transferred to offspring in the asymptomatic phase of the disease or before can have adverse gene actions at older ages arising from purely deleterious genes that escaped the force of natural selection or from pleiotropic genes that trade benefit at an early age against harm during the course of chronic inflammatory systemic diseases in later ages. It is discussed that genes and their programs used in symptomatic chronic inflammatory systemic diseases were derived either from acute, highly energy-consuming situations, which are terminated within 3-8 weeks (acute inflammatory episodes and immune effector functions), or from programs that protect energy stores (memory functions such as immune memory or immunoregulation). Sometimes, microbes imitate immunoregulatory functions so that chronic smoldering inflammation is a consequence. With this information, we understand that mechanisms positively selected for acute inflammation are similarly used in chronic inflammatory systemic diseases.
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The brain and immune system prompt energy shortage in chronic inflammation and ageing
Nature Reviews Rheumatology, 2017Co-Authors: Rainer H StraubAbstract:Symptoms associated with chronic inflammatory diseases such as fatigue, depression and muscle loss are often overlooked during treatment. This Perspectives article provides a framework for understanding many of these symptoms that is based on the concepts of Evolutionary Medicine, energy regulation and neuroendocrine–immune crosstalk.
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Evolutionary Medicine and bone loss in chronic inflammatory diseases a theory of inflammation related osteopenia
Seminars in Arthritis and Rheumatism, 2015Co-Authors: Rainer H Straub, Maurizio Cutolo, Roberto PacificiAbstract:Abstract Objective Bone loss is typical in chronic inflammatory diseases such as rheumatoid arthritis, psoriasis, ankylosing spondylitis, systemic lupus erythematosus, multiple sclerosis, inflammatory bowel diseases, pemphigus vulgaris, and others. It is also typical in transplantation-related inflammation and during the process of aging. While we recognized that bone loss is tightly linked to immune system activation or inflamm-aging in the form of acute, chronic active, or chronic smoldering inflammation, bone loss is typically discussed to be an “accident of inflammation.” Methods Extensive literature search in PubMed central. Results Using elements of Evolutionary Medicine, energy regulation, and neuroendocrine regulation of homeostasis and immune function, we work out that bone waste is an adaptive, evolutionarily positively selected program that is absolutely necessary during acute inflammation. However, when acute inflammation enters a chronic state due to the inability to terminate inflammation (e.g., in autoimmunity or in continuous immunity against microbes), the acute program of bone loss is a misguided adaptive program. Conclusions The article highlights the complexity of interwoven pathways of osteopenia.
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Evolutionary Medicine and bone loss in chronic inflammatory diseases—A theory of inflammation-related osteopenia ☆
Seminars in Arthritis and Rheumatism, 2015Co-Authors: Rainer H Straub, Maurizio Cutolo, Roberto PacificiAbstract:Abstract Objective Bone loss is typical in chronic inflammatory diseases such as rheumatoid arthritis, psoriasis, ankylosing spondylitis, systemic lupus erythematosus, multiple sclerosis, inflammatory bowel diseases, pemphigus vulgaris, and others. It is also typical in transplantation-related inflammation and during the process of aging. While we recognized that bone loss is tightly linked to immune system activation or inflamm-aging in the form of acute, chronic active, or chronic smoldering inflammation, bone loss is typically discussed to be an “accident of inflammation.” Methods Extensive literature search in PubMed central. Results Using elements of Evolutionary Medicine, energy regulation, and neuroendocrine regulation of homeostasis and immune function, we work out that bone waste is an adaptive, evolutionarily positively selected program that is absolutely necessary during acute inflammation. However, when acute inflammation enters a chronic state due to the inability to terminate inflammation (e.g., in autoimmunity or in continuous immunity against microbes), the acute program of bone loss is a misguided adaptive program. Conclusions The article highlights the complexity of interwoven pathways of osteopenia.
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concepts of Evolutionary Medicine and energy regulation contribute to the etiology of systemic chronic inflammatory diseases
Brain Behavior and Immunity, 2011Co-Authors: Rainer H StraubAbstract:The etiology of chronic inflammatory diseases (CIDs) is usually based on four criteria: (1) genetic susceptibility, (2) complex environmental priming, (3) exaggerated and continuous immune response against harmless self or foreign antigen, and (4) tissue destruction with a continuous wound response without proper healing but with a fibrotic scarring response. These elements do not include the systemic components of CIDs. Due to improved health care with excellent therapies in CIDs, it becomes more and more clear that many systemic responses need to be future targets of therapies. It is suggested that "the systemic response" should be added to the four etiologic criteria that constitute the full picture of CIDs. As shown in the present review, the systemic response becomes comprehensible in the context of Evolutionary Medicine and energy regulation. Next to the brain and muscles, the immune system is the third major energy consumer in the body. In the context of long-term activation of the immune system during CIDs, the subsequent stimulation of systemic neuroendocrine pathways is necessary to re-allocate energy-rich fuels to the activated immune system. However, re-allocation of energy-rich fuels is the basis of systemic disease sequelae of CIDs, one of which is the metabolic syndrome. It is suggested that Selye's alarm reaction of the 1930s, which is necessary to re-allocate energy-rich fuels to the body, should be called "energy appeal reaction". In CIDs, a continuous energy appeal reaction triggers systemic detrimental consequences for the rest of the body.
Randolph M. Nesse - One of the best experts on this subject based on the ideXlab platform.
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EvMedEd: A Teaching Resource for Integrating Medical Examples into Evolution Education
American Biology Teacher, 2020Co-Authors: Daniel Z. Grunspan, Randolph M. Nesse, Sara E. BrownellAbstract:Teaching evolution using medical examples can be a particularly effective strategy for motivating students to learn Evolutionary principles, especially students interested in pursuing medical and allied health careers. Research in the area of Evolutionary Medicine has expanded the number of ways in which evolution informs health and disease, providing many new and less widely known contexts that can be adopted for classroom use. However, many instructors do not have time to locate or create classroom materials about Evolutionary Medicine. To address this need, we have created EvMedEd, a resource repository to help instructors who want to integrate more medical examples into their evolution instruction or instructors who are teaching a course on Evolutionary Medicine. Some resources are designed to be more appropriate for a high school or introductory biology audience, whereas others are more advanced. We encourage instructors to access this curated website and to share their own teaching materials with this community.
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an Evolutionary Medicine perspective on pain and its disorders
Philosophical Transactions of the Royal Society B, 2019Co-Authors: Randolph M. Nesse, Jay SchulkinAbstract: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 ...
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Evolutionary Medicine a great way to teach biology
American Biology Teacher, 2019Co-Authors: Randolph M. Nesse, Barbara NattersonhorowitzAbstract:Great teaching is often all about the questions posed to students. When learners get their teeth into an interesting question, they grow as they chew on it. As physicians, we have discovered that disease makes more sense if you ask Evolutionary questions, and these questions make a great starting point for science education. One of Darwin's two main questions was how species are related to each other. His answer was that all organisms have common ancestors. This is the foundation for studies of phylogeny. To teach phylogenetic trees, you can use canids or birds, but students are particularly interested if they are tracing the origins of HIV or tuberculosis, or the history of human traits, such as the appendix. Darwin's other question was about why bodies work so well. His answer was natural selection. The characteristics of individuals who have more offspring than others become more common over the generations. This explains why kidneys, hearts, eyes, and brains are so astoundingly well suited to their purposes. As physicians, we constantly confront a very different question. If natural selection is so …
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Evolutionary Medicine – A Great Way to Teach Biology
American Biology Teacher, 2019Co-Authors: Randolph M. Nesse, Barbara Natterson-horowitzAbstract:Great teaching is often all about the questions posed to students. When learners get their teeth into an interesting question, they grow as they chew on it. As physicians, we have discovered that disease makes more sense if you ask Evolutionary questions, and these questions make a great starting point for science education. One of Darwin's two main questions was how species are related to each other. His answer was that all organisms have common ancestors. This is the foundation for studies of phylogeny. To teach phylogenetic trees, you can use canids or birds, but students are particularly interested if they are tracing the origins of HIV or tuberculosis, or the history of human traits, such as the appendix. Darwin's other question was about why bodies work so well. His answer was natural selection. The characteristics of individuals who have more offspring than others become more common over the generations. This explains why kidneys, hearts, eyes, and brains are so astoundingly well suited to their purposes. As physicians, we constantly confront a very different question. If natural selection is so …
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Core principles for Evolutionary Medicine
Oxford Handbook of Evolutionary Medicine, 2019Co-Authors: Randolph M. NesseAbstract:New interest in evolution and Medicine arose late in the twentieth century from the recognition that there are several possible kinds of Evolutionary explanation for aspects of the body that leave it vulnerable to disease, in addition to the inevitability of mutations. Investigations of related hypotheses have led to rapid growth of Evolutionary Medicine, and its expansion to integrate demographic, phylogenetic, and population genetic methods. Evolutionary approaches to understanding disease are part of a major transition in biology, from viewing the body as a designed machine to a fully biological view of the body’s organic complexity as fundamentally different from that of designed machines.
Roberto Pacifici - One of the best experts on this subject based on the ideXlab platform.
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Evolutionary Medicine and bone loss in chronic inflammatory diseases a theory of inflammation related osteopenia
Seminars in Arthritis and Rheumatism, 2015Co-Authors: Rainer H Straub, Maurizio Cutolo, Roberto PacificiAbstract:Abstract Objective Bone loss is typical in chronic inflammatory diseases such as rheumatoid arthritis, psoriasis, ankylosing spondylitis, systemic lupus erythematosus, multiple sclerosis, inflammatory bowel diseases, pemphigus vulgaris, and others. It is also typical in transplantation-related inflammation and during the process of aging. While we recognized that bone loss is tightly linked to immune system activation or inflamm-aging in the form of acute, chronic active, or chronic smoldering inflammation, bone loss is typically discussed to be an “accident of inflammation.” Methods Extensive literature search in PubMed central. Results Using elements of Evolutionary Medicine, energy regulation, and neuroendocrine regulation of homeostasis and immune function, we work out that bone waste is an adaptive, evolutionarily positively selected program that is absolutely necessary during acute inflammation. However, when acute inflammation enters a chronic state due to the inability to terminate inflammation (e.g., in autoimmunity or in continuous immunity against microbes), the acute program of bone loss is a misguided adaptive program. Conclusions The article highlights the complexity of interwoven pathways of osteopenia.
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Evolutionary Medicine and bone loss in chronic inflammatory diseases—A theory of inflammation-related osteopenia ☆
Seminars in Arthritis and Rheumatism, 2015Co-Authors: Rainer H Straub, Maurizio Cutolo, Roberto PacificiAbstract:Abstract Objective Bone loss is typical in chronic inflammatory diseases such as rheumatoid arthritis, psoriasis, ankylosing spondylitis, systemic lupus erythematosus, multiple sclerosis, inflammatory bowel diseases, pemphigus vulgaris, and others. It is also typical in transplantation-related inflammation and during the process of aging. While we recognized that bone loss is tightly linked to immune system activation or inflamm-aging in the form of acute, chronic active, or chronic smoldering inflammation, bone loss is typically discussed to be an “accident of inflammation.” Methods Extensive literature search in PubMed central. Results Using elements of Evolutionary Medicine, energy regulation, and neuroendocrine regulation of homeostasis and immune function, we work out that bone waste is an adaptive, evolutionarily positively selected program that is absolutely necessary during acute inflammation. However, when acute inflammation enters a chronic state due to the inability to terminate inflammation (e.g., in autoimmunity or in continuous immunity against microbes), the acute program of bone loss is a misguided adaptive program. Conclusions The article highlights the complexity of interwoven pathways of osteopenia.
Bjorn Grinde - One of the best experts on this subject based on the ideXlab platform.
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Theoretical Paper An approach to the prevention of anxiety-related disorders based on Evolutionary Medicine
2020Co-Authors: Bjorn GrindeAbstract:AbstractAnxiety-related disorders are among the more common ailments of modern societies. Presumably, their prevalence is partly due toenvironmental factors, which suggests that anxiety may be one of the health problems that are aggravated by discords (adverse mismatches)between the present way of life and what our genes are adapted to. Consequently, it may be possible to find preventive measures by using theperspectiveofEvolutionaryMedicine.Ishallarguethattheprevalenceofanxiety-relatedproblemsreflectsthatthenervecircuitryandendocrineactivity associated with the fear function have developed beyond normal. Moreover, that this expansion is due to excessive or abnormaltriggering, particularly at an early age. Possible discords that may be responsible, such as present child care practices, will be discussed.D 2004 Elsevier Inc. All rights reserved. Keywords: Anxiety; Stress; Mood disorders; Evolutionary Medicine; Discords; Panic; Phobias; Disease prevention IntroductionFear is an innate mammalian function with an obviousadaptive value [1–3]. Compared to other complex functionsinvolving the brain, fear has a reasonably well-understoodneurology, endocrinology, and genetics [4–7].Fearisaneffective stimulator of the dfight-or-flightT response, alsoreferred to as the acute stress response, which impliesactivationofthehypothalamic–pituitary–adrenal(HPA)axis.The rational for this response is presumably to prompt theanimal to either flee (if escape is likely) or freeze/hide (ifescape is not an option).The term anxiety may be considered synonymous withfear, but is typically used for the debilitating state caused byinappropriate or excessive triggering of the fear function,such as in phobias and generalized anxiety disorder. Long-term excessive or inappropriate triggering of the fearfunction may be defined as anxiety disorders according todiagnostic manuals (ICD/WHO or DSM/APA). In additionto reducing the quality of life of the sufferer [8], thecondition may lead to various secondary ailments, such asstress-related diseases [9,10] and depression [11]. Moreover,in both animals and humans, a high level of anxietycorrelates with a shortened life span [9,12,13].According to the National Institute of Mental Health,some 10% of adult Americans suffer from anxiety disorders[14]. Considering the secondary consequences of excessiveanxiety and stress, and that even milder versions of anxiety,not considered pathological, may reduce quality of life [8],anxiety appears to be among the more taxing healthproblems in modern societies [15].The Evolutionary perspective has proven valuable insuggesting causative factors where the prevalence of adisease or a condition is in excess of what one mightreasonably expect would be the case for humans living in anenvironment to which they were genetically adapted [16–19]. The high proportion of people suffering from debilitat-ing problems related to anxiety indicates that this is such acondition; in a natural setting, one would not expect such afunction to become incapacitating except in extreme cases. Ishall combine current understanding of the fear functionwith the Evolutionary perspective in order to proposepossible causes for the prevalence of anxiety-relatedproblems, and thereby point towards preventive measures.A central assumption of Evolutionary Medicine is that, asa rule of thumb, both animals and humans are designed tothrive under the conditions to which their genes are adapted.
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an approach to the prevention of anxiety related disorders based on Evolutionary Medicine
Preventive Medicine, 2005Co-Authors: Bjorn GrindeAbstract:Abstract Anxiety-related disorders are among the more common ailments of modern societies. Presumably, their prevalence is partly due to environmental factors, which suggests that anxiety may be one of the health problems that are aggravated by discords (adverse mismatches) between the present way of life and what our genes are adapted to. Consequently, it may be possible to find preventive measures by using the perspective of Evolutionary Medicine. I shall argue that the prevalence of anxiety-related problems reflects that the nerve circuitry and endocrine activity associated with the fear function have developed beyond normal. Moreover, that this expansion is due to excessive or abnormal triggering, particularly at an early age. Possible discords that may be responsible, such as present child care practices, will be discussed.
George H Perry - One of the best experts on this subject based on the ideXlab platform.
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an Evolutionary Medicine perspective on neandertal extinction
Journal of Human Evolution, 2017Co-Authors: Alexis P Sullivan, Marc De Manuel, Tomas Marquesbonet, George H PerryAbstract:Abstract The Eurasian sympatry of Neandertals and anatomically modern humans – beginning at least 45,000 years ago and possibly lasting for more than 5000 years – has sparked immense anthropological interest into the factors that potentially contributed to Neandertal extinction. Among many different hypotheses, the “differential pathogen resistance” extinction model posits that Neandertals were disproportionately affected by exposure to novel infectious diseases that were transmitted during the period of spatiotemporal sympatry with modern humans. Comparisons of new archaic hominin paleogenome sequences with modern human genomes have confirmed a history of genetic admixture – and thus direct contact – between humans and Neandertals. Analyses of these data have also shown that Neandertal nuclear genome genetic diversity was likely considerably lower than that of the Eurasian anatomically modern humans with whom they came into contact, perhaps leaving Neandertal innate immune systems relatively more susceptible to novel pathogens. In this study, we compared levels of genetic diversity in genes for which genetic variation is hypothesized to benefit pathogen defense among Neandertals and African, European, and Asian modern humans, using available exome sequencing data (three individuals, or six chromosomes, per population). We observed that Neandertals had only 31–39% as many nonsynonymous (amino acid changing) polymorphisms across 73 innate immune system genes compared to modern human populations. We also found that Neandertal genetic diversity was relatively low in an unbiased set of balancing selection candidate genes for primates, those genes with the highest 1% genetic diversity genome-wide in non-human hominoids (apes). In contrast, Neandertals had similar or higher levels of genetic diversity than humans in 12 major histocompatibility complex (MHC) genes. Thus, while Neandertals may have been relatively more susceptible to some novel pathogens and differential pathogen resistance could be considered as one potential contributing factor in their extinction, the expectations of this model are not universally met.
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an Evolutionary Medicine perspective on neandertal extinction
bioRxiv, 2016Co-Authors: Alexis P Sullivan, Marc De Manuel, Tomas Marquesbonet, George H PerryAbstract:The Eurasian sympatry of Neandertals and anatomically modern humans - beginning at least 45,000 years ago and lasting for more than 5,000 years - has long sparked anthropological interest into the factors that potentially contributed to Neandertal extinction. Among many different hypotheses, the "differential pathogen resistance" extinction model posits that Neandertals were disproportionately affected by exposure to novel infectious diseases that were transmitted during the period of spatiotemporal sympatry with modern humans. Comparisons of new archaic hominin paleogenome sequences with modern human genomes have confirmed a history of genetic admixture - and thus direct contact - between humans and Neandertals. Analyses of these data have also shown that Neandertal nuclear genome genetic diversity was likely considerably lower than that of the Eurasian anatomically modern humans with whom they came into contact, perhaps leaving Neandertal innate immune systems relatively more susceptible to novel pathogens. In this study, we compared levels of genetic diversity in genes for which genetic variation is hypothesized to benefit pathogen defense among Neandertals and African, European, and Asian modern humans, using available exome sequencing data (six chromosomes per population). We observed that Neandertals had only 31-39% as many nonsynonymous (amino acid changing) polymorphisms across 73 innate immune system genes compared to modern human populations. We also found that Neandertal genetic diversity was relatively low in an unbiased set of balancing selection candidate genes for primates - genes with the highest 1% genetic diversity genome-wide in non-human apes. In contrast, Neandertals had similar to higher levels of genetic diversity than humans in 13 major histocompatibility complex (MHC) genes. Thus, while Neandertals may have been relatively more susceptible to some novel pathogens and differential pathogen resistance could be considered as one potential contributing factor in their extinction, this model does have limitations.
