Why Our Immune Systems Make Us Feel Sick: Pathologies, Adaptations, and Evolutionarily Novel Conditions.

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dc.contributor.advisorSnodgrass, Josh
dc.contributor.authorSchrock, Joshua
dc.date.accessioned2020-09-24T17:43:30Z
dc.date.issued2020-09-24
dc.description.abstractThree decades of research in neuroimmunology has demonstrated that the state of sickness is generated by the host’s immune system when it detects internal indicators of pathology. But why do our own immune systems make us feel sick? Chapter I introduces this research question. Chapter II reviews the evidence that infectious disease has been a selection pressure throughout our evolutionary history. It outlines problems that arise for the host when the immune system is activated to fight infection. It describes how the regulatory changes that occur during sickness can help solve the problems posed by immune activation. For example, fatigue and sadness during infection may help the host prioritize immune function during infection by reducing physical activity, thereby making more metabolic resources available to the immune system. Experimental studies have demonstrated that acute inflammatory immune activity can induce fatigue and low mood, but studies of associations between inflammation and mood in real-world settings have produced mixed findings, raising questions about the dose and chronicity of inflammation needed to induce fatigue and sadness. Chapter III finds that greater inflammation is associated with stronger feelings of sickness but not fatigue or sadness in a sample of Shuar forager-horticulturalists in the northern Amazon, who experience frequent acute, but mild, inflammation. This suggests that inflammation may generate internally perceptible cues, even when the dose and chronicity of inflammation are insufficient to increase fatigue or sadness. Chapter IV finds that greater chronic morbidity is associated with stronger feelings of fatigue in six culturally distinct countries. Chronic disease-induced fatigue may often be a maladaptive response to evolutionarily novel diseases – one that suppresses physical activity in the long term, which is a risk factor for further disease progression and acquisition of additional morbidities. Chapter V finds that, among diurnal primates, greater relative brain size is strongly associated with less resting time and more active time. Intensive reciprocal helping behavior during sickness in humans may have evolved due in part to high levels of pathogen exposure and the limits on resting time imposed by the nutritional requirements of our large brains. This dissertation includes previously published co-authored material.en_US
dc.description.embargo2022-08-17
dc.identifier.urihttps://hdl.handle.net/1794/25710
dc.language.isoen_US
dc.publisherUniversity of Oregon
dc.rightsAll Rights Reserved.
dc.subjectBehavioral Ecologyen_US
dc.subjectComparativeen_US
dc.subjectEmotionen_US
dc.subjectEvolutionary Anthropologyen_US
dc.subjectHealthen_US
dc.subjectSickness Behavioren_US
dc.titleWhy Our Immune Systems Make Us Feel Sick: Pathologies, Adaptations, and Evolutionarily Novel Conditions.
dc.typeElectronic Thesis or Dissertation
thesis.degree.disciplineDepartment of Anthropology
thesis.degree.grantorUniversity of Oregon
thesis.degree.leveldoctoral
thesis.degree.namePh.D.

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