title: Does rheumatoid arthritis represent an adaptive, thrifty condition?
abstract: The present article presents epidemiological, and comparative evidence supporting the hypothesis that rheumatoid arthritis (RA) may represent a thrifty adaptation selected to compel animals to minimize voluntary energy expenditure. The autoimmune, pathophysiological manifestations underlying RA are framed here as constituting an evolved, protective mechanism that would have influenced animals to avoid exertion and maintain a sedentary lifestyle in order to minimize metabolic output and ultimately escape starvation. Arthritic pain is characterized here as a defensive, innate signal much like fatigue, fever, nausea and reflexive pain, and like these, is seen on a continuum varying between imperceptible encumbrance and debilitating disability. The epigenetic relationship between acute psychological stress and flare-up of arthritic symptoms is examined and taken to suggest that arthritis may be a predictive, adaptive response to severe stress allowing reductions in metabolism to follow adverse conditions or nutritional scarcity. The close associations between rheumatoid arthritis and the metabolic syndrome are also explored along with potential ties to the "thrifty genotype" and "thrifty phenotype" phenomena. This hypothesis is examined in the contexts of evolutionary medicine, phenotypic plasticity, the stress response and the bioenergetics of thrift. A brief and exploratory review of pertinent evidence suggests that RA, its subclinical manifestations, and even other forms of arthropathy may possibly represent adaptations that promoted metabolic thrift during our evolutionary past.
authors.affiliation: University of Southern California, 16380 Meadow Ridge Road, Encino CA 91436, USA. jared@jaredreser.com
authors.forename: Jared E
authors.initials: JE
authors.lastname: Reser
authors.forename: William W
authors.initials: WW
authors.lastname: Reser
mesh_terms: D000818:Animals; D001172:Arthritis, Rheumatoid / Q000175:diagnosis / Q000503:physiopathology*; D015551:Autoimmunity / Q000502:physiology; D018450:Disease Progression; D005838:Genotype; D006801:Humans; D008954:Models, Biological; D008962:Models, Theoretical; D009068:Movement; D010641:Phenotype; D013315:Stress, Psychological / Q000150:complications / Q000175:diagnosis*