{"id":{"repo_id":"uiuc","oai_identifier":"oai:www.ideals.illinois.edu:2142/85375"},"canonical_url":"https://search.dev.ndltd.org/etd/uiuc/oai:www.ideals.illinois.edu:2142/85375","repository":{"repo_id":"uiuc","name":"University of Illinois - Urbana-Champaign","base_url":"https://www.ideals.illinois.edu/oai-pmh"},"display":{"title":"Evolutionary, Demographic, Physiological and Behavioral Contributors to Mortality Plateaus","abstract":"\"Common experience and biological theory suggest that mortality rates for a group of same-aged individuals (a cohort) should increase with age, i.e. the older you get, the greater your chances of death. However, in 1992 two studies independently reported experiments in insects showing that mortality rates in late life can stop increasing (plateau), or even decrease at very late ages. Since then, empirical tests have revealed that many organisms show this pattern of mortality in diverse taxa, including yeast, nematodes, beetles, and humans. Although there is now robust evidence for the existence of mortality plateaus, their underlying causes have been the center of heated debate for nearly fifteen years. First, mortality plateaus represent a challenge for evolutionary biologists concerned with the evolution of aging, since traditional forms of aging theory predict that mortality rates should increase without bound after the age at last reproduction, producing a \"\"wall of death\"\". A slightly modified version of the Mutation Accumulation (MA) theory on the evolution of aging, incorporating moderate age-specificity of alleles that affect fitness, predicts mortality plateaus. I present here a brief description, and compelling empirical evidence in support of the modified MA theory. Second, plateaus have been interpreted as a slowing of the aging process in late life. I present evidence that although mortality plateaus are ubiquitous regardless of experimental treatment, both demographic and physiological changes contribute to the timing and severity of mortality plateau. I conclude that mortality plateaus have an evolutionary-genetic basis, and are the product of both demographic selection, and of the transition of individuals to late life physiology.\"","abstract_html":"&quot;Common experience and biological theory suggest that mortality rates for a group of same-aged individuals (a cohort) should increase with age, i.e. the older you get, the greater your chances of death. However, in 1992 two studies independently reported experiments in insects showing that mortality rates in late life can stop increasing (plateau), or even decrease at very late ages. Since then, empirical tests have revealed that many organisms show this pattern of mortality in diverse taxa, including yeast, nematodes, beetles, and humans. Although there is now robust evidence for the existence of mortality plateaus, their underlying causes have been the center of heated debate for nearly fifteen years. First, mortality plateaus represent a challenge for evolutionary biologists concerned with the evolution of aging, since traditional forms of aging theory predict that mortality rates should increase without bound after the age at last reproduction, producing a &quot;&quot;wall of death&quot;&quot;. A slightly modified version of the Mutation Accumulation (MA) theory on the evolution of aging, incorporating moderate age-specificity of alleles that affect fitness, predicts mortality plateaus. I present here a brief description, and compelling empirical evidence in support of the modified MA theory. Second, plateaus have been interpreted as a slowing of the aging process in late life. I present evidence that although mortality plateaus are ubiquitous regardless of experimental treatment, both demographic and physiological changes contribute to the timing and severity of mortality plateau. I conclude that mortality plateaus have an evolutionary-genetic basis, and are the product of both demographic selection, and of the transition of individuals to late life physiology.&quot;","abstract_has_math":false,"creators":["Reynolds, Rose M."],"institution":"University of Illinois at Urbana-Champaign","degree_name":"Ph.D.","degree_level":"Dissertation","degree_discipline":"Biology","degree_department":null,"school":null,"contributors":["Kimberly A. Hughes"],"advisors":[],"committee_chairs":[],"committee_members":[],"year":2015,"date_issued":"2015-09-25T22:42:34Z","date_published":"2015-09-25T22:42:34Z","updated_at":"2026-07-22T22:26:25Z","subjects":["Biology, Genetics"],"languages":["eng"],"rights":[],"rights_urls":[],"identifier_entries":[{"key":"dc:identifier","label":"Identifier","values":["(MiAaPQ)AAI3301217"],"render_values":[{"text":"(MiAaPQ)AAI3301217","href":null,"code":true}]}]},"links":{"outbound_url":"http://hdl.handle.net/2142/85375","outbound_label":"Handle","outbound_source":"dc:identifier"},"metadata_groups":[{"id":"people","label":"People","entries":[{"key":"dc:contributor","label":"Contributor","values":["Kimberly A. Hughes"]},{"key":"dc:creator","label":"Author","values":["Reynolds, Rose M."]}]},{"id":"academic_context","label":"Academic Context","entries":[{"key":"dc:date","label":"Dc Date","values":["2015-09-25T22:42:34Z","10000-01-01","2007"]},{"key":"dc:type","label":"Dc Type","values":["text"]},{"key":"thesis:degree_discipline","label":"Discipline","values":["Biology"]},{"key":"thesis:degree_level","label":"Degree Level","values":["Dissertation"]},{"key":"thesis:degree_name","label":"Degree Name","values":["Ph.D."]},{"key":"thesis:institution_name","label":"Thesis Institution Name","values":["University of Illinois at Urbana-Champaign"]}]},{"id":"subjects_keywords","label":"Subjects and Keywords","entries":[{"key":"dc:subject","label":"Dc Subject","values":["Biology, Genetics"]}]},{"id":"language_rights","label":"Language and Rights","entries":[{"key":"dc:language","label":"Dc Language","values":["eng"]}]},{"id":"identifiers","label":"Identifiers","entries":[{"key":"dc:identifier","label":"Identifier","values":["http://hdl.handle.net/2142/85375","(MiAaPQ)AAI3301217"]}]},{"id":"additional","label":"Additional Metadata","entries":[{"key":"dc:description","label":"Description","values":["\"Common experience and biological theory suggest that mortality rates for a group of same-aged individuals (a cohort) should increase with age, i.e. the older you get, the greater your chances of death. However, in 1992 two studies independently reported experiments in insects showing that mortality rates in late life can stop increasing (plateau), or even decrease at very late ages. Since then, empirical tests have revealed that many organisms show this pattern of mortality in diverse taxa, including yeast, nematodes, beetles, and humans. Although there is now robust evidence for the existence of mortality plateaus, their underlying causes have been the center of heated debate for nearly fifteen years. First, mortality plateaus represent a challenge for evolutionary biologists concerned with the evolution of aging, since traditional forms of aging theory predict that mortality rates should increase without bound after the age at last reproduction, producing a \"\"wall of death\"\". A slightly modified version of the Mutation Accumulation (MA) theory on the evolution of aging, incorporating moderate age-specificity of alleles that affect fitness, predicts mortality plateaus. I present here a brief description, and compelling empirical evidence in support of the modified MA theory. Second, plateaus have been interpreted as a slowing of the aging process in late life. I present evidence that although mortality plateaus are ubiquitous regardless of experimental treatment, both demographic and physiological changes contribute to the timing and severity of mortality plateau. I conclude that mortality plateaus have an evolutionary-genetic basis, and are the product of both demographic selection, and of the transition of individuals to late life physiology.\"","Made available in DSpace on 2015-09-25T22:42:34Z (GMT). No. of bitstreams: 2 license.txt: 4848 bytes, checksum: 96035ab3f5e1c23cc7138a224ce498bd (MD5) 3301217.pdf: 3476200 bytes, checksum: e679be0361c7bb938aaaf71c5ddd2b15 (MD5) Previous issue date: 2007","Embargo set by: Seth Robbins for item 86656 Lift date: Forever Reason: Restricted to the U of I community idenfinitely during batch ingest of legacy ETDs","Restricted to the U of I community idenfinitely during batch ingest of legacy ETDs","U of I Only","156 p.","Thesis (Ph.D.)--University of Illinois at Urbana-Champaign, 2007."]},{"key":"dc:title","label":"Title","values":["Evolutionary, Demographic, Physiological and Behavioral Contributors to Mortality Plateaus"]}]}],"canonical_facts":{"dc:contributor":["Kimberly A. Hughes"],"dc:creator":["Reynolds, Rose M."],"dc:date":["2015-09-25T22:42:34Z","10000-01-01","2007"],"dc:description":["\"Common experience and biological theory suggest that mortality rates for a group of same-aged individuals (a cohort) should increase with age, i.e. the older you get, the greater your chances of death. However, in 1992 two studies independently reported experiments in insects showing that mortality rates in late life can stop increasing (plateau), or even decrease at very late ages. Since then, empirical tests have revealed that many organisms show this pattern of mortality in diverse taxa, including yeast, nematodes, beetles, and humans. Although there is now robust evidence for the existence of mortality plateaus, their underlying causes have been the center of heated debate for nearly fifteen years. First, mortality plateaus represent a challenge for evolutionary biologists concerned with the evolution of aging, since traditional forms of aging theory predict that mortality rates should increase without bound after the age at last reproduction, producing a \"\"wall of death\"\". A slightly modified version of the Mutation Accumulation (MA) theory on the evolution of aging, incorporating moderate age-specificity of alleles that affect fitness, predicts mortality plateaus. I present here a brief description, and compelling empirical evidence in support of the modified MA theory. Second, plateaus have been interpreted as a slowing of the aging process in late life. I present evidence that although mortality plateaus are ubiquitous regardless of experimental treatment, both demographic and physiological changes contribute to the timing and severity of mortality plateau. I conclude that mortality plateaus have an evolutionary-genetic basis, and are the product of both demographic selection, and of the transition of individuals to late life physiology.\"","Made available in DSpace on 2015-09-25T22:42:34Z (GMT). No. of bitstreams: 2 license.txt: 4848 bytes, checksum: 96035ab3f5e1c23cc7138a224ce498bd (MD5) 3301217.pdf: 3476200 bytes, checksum: e679be0361c7bb938aaaf71c5ddd2b15 (MD5) Previous issue date: 2007","Embargo set by: Seth Robbins for item 86656 Lift date: Forever Reason: Restricted to the U of I community idenfinitely during batch ingest of legacy ETDs","Restricted to the U of I community idenfinitely during batch ingest of legacy ETDs","U of I Only","156 p.","Thesis (Ph.D.)--University of Illinois at Urbana-Champaign, 2007."],"dc:identifier":["http://hdl.handle.net/2142/85375","(MiAaPQ)AAI3301217"],"dc:language":["eng"],"dc:subject":["Biology, Genetics"],"dc:title":["Evolutionary, Demographic, Physiological and Behavioral Contributors to Mortality Plateaus"],"dc:type":["text"],"thesis:degree_discipline":["Biology"],"thesis:degree_level":["Dissertation"],"thesis:degree_name":["Ph.D."],"thesis:institution_name":["University of Illinois at Urbana-Champaign"]},"updated_at":"2026-07-22T22:26:25Z"}