Concepts of evolutionary medicine and energy regulation contribute to the etiology of systemic chronic inflammatory diseases
Abstract
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.
Integrity signals
Registry
Cites
Statistics
Claims the paper makes
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
The "systemic response" can be added to the list of classical etiologic factors of chronic inflammatory diseases and can be disease perpetuating.
“Thus, one can add the “systemic response” to the list of classical etiologic factors of chronic inflammatory diseases (Table 5) [10]. The “systemic response” in itself can be disease perpetuating.”
From Evolutionary medicine and chronic inflammatory state—known and new concepts in pathophysiology (2012) · cites this paper as [10]
Typical disease-related sequelae that are very common in chronic inflammatory diseases have been linked to transient inflammatory episodes, where they support the transiently activated immune system and tissue inflammation.
“On the basis of these considerations, typical disease-related sequelae that are very common in chronic inflammatory diseases have been linked to transient inflammatory episodes [9, 10]. Here, these sequelae have an important function in supporting the transiently activated immune system and tissue inflammation (Table 4).”
From Evolutionary medicine and chronic inflammatory state—known and new concepts in pathophysiology (2012) · cites this paper as [10]
Genes responsible for energy regulation have been positively selected under conditions without chronic inflammation.
“It has been hypothesized that genes responsible for energy regulation have been positively selected under conditions without chronic inflammation [8, 10].”
From Evolutionary medicine and chronic inflammatory state—known and new concepts in pathophysiology (2012) · cites this paper as [10]
Cites
Cellular energy utilization and molecular origin of standard metabolic rate in mammals
Rolfe, D. F., & Brown, G. C. (1997) · Physiological Reviews · doi:10.1152/physrev.1997.77.3.731 · Cited by 2,021 · see citing works
Positional cloning of the APECED gene
Nagamine, K., Peterson, P., Scott, H. S., Kudoh, J., Minoshima, S., Heino, M., Krohn, K. J. E., Lalioti, M. D., Mullis, P. E., Antonarakis, S. E., et al. (1997) · Nature Genetics · doi:10.1038/ng1297-393 · Cited by 1,439 · see citing works
Aaltonen, J., Björses, P., Perheentupa, J., Horelli‐Kuitunen, N., Palotie, A. V., Peltonen, L., Lee, Y. S., Francis, F., Henning, S., Thiel, C. S., et al. (1997) · Nature Genetics · doi:10.1038/ng1297-399 · Cited by 1,214 · see citing works
Energy metabolism in animals and man
(1990) · Choice Reviews Online · doi:10.5860/choice.27-5756 · Cited by 782 · see citing works
(1922) · PubMed · Cited by 753 · see citing works
MacIver, N. J., Jacobs, S. R., Wieman, H. L., Wofford, J. A., Coloff, J. L., & Rathmell, J. C. (2008) · Journal of Leukocyte Biology · doi:10.1189/jlb.0108024 · Cited by 501 · see citing works
Drappa, J., Vaishnaw, A. K., Sullivan, K. E., Chu, J., & Elkon, K. B. (1996) · New England Journal of Medicine · doi:10.1056/nejm199611283352204 · Cited by 473 · see citing works
Dicke, W. K., Weijers, H. A., & Kamer, J. H. V. D. (1953) · Acta Paediatrica · doi:10.1111/j.1651-2227.1953.tb05563.x · Cited by 461 · see citing works
Energy regulation and neuroendocrine–immune control in chronic inflammatory diseases
Straub, R. H., Cutolo, M., Buttgereit, F., & Pongratz, G. (2010) · Journal of Internal Medicine · doi:10.1111/j.1365-2796.2010.02218.x · Cited by 382 · see citing works
Self-citationRegulation of T Lymphocyte Metabolism
Frauwirth, K. A., & Thompson, C. B. (2004) · The Journal of Immunology · doi:10.4049/jimmunol.172.8.4661 · Cited by 371 · see citing works
Association between Psoriasis and the Metabolic Syndrome
Cohen, A. D., Sherf, M., Vidavsky, L., et al. (2008) · Dermatology · doi:10.1159/000111512 · Cited by 271 · see citing works
Straub, R. H., & Cutolo, M. (2007) · Arthritis & Rheumatism · doi:10.1002/art.22368 · Cited by 262 · see citing works
Self-citationChung, C. P., Avalos, I., Oeser, A. M., Gebretsadik, T. S., Shintani, A., Raggi, P., & Stein, C. M. (2006) · Annals of the Rheumatic Diseases · doi:10.1136/ard.2006.054973 · Cited by 258 · see citing works
(1990) · PubMed · Cited by 237 · see citing works
Dessein, P. H., Stanwix, A. E., & Joffe, B. I. (2002) · Arthritis Research & Therapy · doi:10.1186/ar428 · Cited by 183 · see citing works
Karvounaris, S. A., Sidiropoulos, P. I., Papadakis, J. A., Spanakis, E. K., Bertsias, G. K., Kritikos, H. D., Ganotakis, E. S., & Boumpas, D. T. (2006) · Annals of the Rheumatic Diseases · doi:10.1136/ard.2006.053488 · Cited by 155 · see citing works
Straub, R. H., Herfarth, H., Falk, W., Andus, T., & Schölmerich, J. (2002) · Journal of Neuroimmunology · doi:10.1016/s0165-5728(02)00047-4 · Cited by 115 · see citing works
Self-citationHärle, P., Straub, R. H., Wiest, R., Mayer, A., Schölmerich, J., Atzeni, F., Carrabba, M., Cutolo, M., & Sarzi-Puttini, P. (2006) · Annals of the Rheumatic Diseases · doi:10.1136/ard.2005.038059 · Cited by 114 · see citing works
Self-citationFuel utilization by cells of the immune system
Calder, P. C. (1995) · Proceedings of The Nutrition Society · doi:10.1079/pns19950038 · Cited by 106 · see citing works
Kamer, J. H. V. D., & Weijers, H. A. (1955) · Acta Paediatrica · doi:10.1111/j.1651-2227.1955.tb04269.x · Cited by 102 · see citing works
Straub, R. H., & Besedovsky, H. O. (2003) · The FASEB Journal · doi:10.1096/fj.03-0433hyp · Cited by 85 · see citing works
Self-citationStraub, R. H., GÜNZLER, C., Miller, L. E., Cutolo, M., Schölmerich, J., & Schill, S. (2002) · The FASEB Journal · doi:10.1096/fj.02-0085com · Cited by 81 · see citing works
Self-citationSelye, H., & Fortier, C. (1949) · PubMed · Cited by 63 · see citing works
Comparison of cardiovascular risk in ankylosing spondylitis and rheumatoid arthritis.
McCarey, D. W., & Sturrock, R. D. (2010) · PubMed · Cited by 35 · see citing works
Whole-body energy mapping under physical exercise using positron emission tomography
Iemitsu, M., Itoh, M., Fujimoto, T., et al. (2000) · Medicine & Science in Sports & Exercise · doi:10.1097/00005768-200012000-00016 · Cited by 23 · see citing works
STRAUB, R. H., DEL REY, A., & BESEDOVSKY, H. O. (2007) · Psychoneuroimmunology · doi:10.1016/b978-012088576-3/50014-9 · Cited by 14 · see citing works
Self-citation
Flagged first, then by citations
Cited by
Sorted by citations
Adverse childhood experiences, allostasis, allostatic load and age-related disease
Danese, A., & McEwen, B. S. (2012) · Physiology & Behavior · doi:10.1016/j.physbeh.2011.08.019 · Cited by 2,140 · see citing works
Ruiz-Núñez, B., Pruimboom, L., Dijck-Brouwer, D. A. J., & Muskiet, F. A. J. (2013) · The Journal of Nutritional Biochemistry · doi:10.1016/j.jnutbio.2013.02.009 · Cited by 246 · see citing works
Evolutionary medicine and chronic inflammatory state—known and new concepts in pathophysiology
Straub, R. H. (2012) · Journal of Molecular Medicine · doi:10.1007/s00109-012-0861-8 · Cited by 105 · see citing works
Self-citationEnergy metabolism and rheumatic diseases: from cell to organism
Spies, C. M., Straub, R. H., & Buttgereit, F. (2012) · Arthritis Research & Therapy · doi:10.1186/ar3885 · Cited by 47 · see citing works
Self-citation
- Authors
- Straub, R. H.
- Affiliations
- University Hospital Regensburg (DE)
- Corresponding author
- Straub, Rainer H.
- ORCID
- Straub, Rainer H.
- Venue
- Brain, Behavior, and Immunity
- Publisher
- Elsevier BV
- Published
- 2011-01
- Volume
- 25
- Issue
- 1
- Pages
- 1-5
- ISSN
- 0889-1591 (ISSN-L)
- OpenAlex
- W2055407923
- Cited by
- 69
- References
- 26
- Citations by year
- 2026: 3 · 2025: 1 · 2024: 2 · 2023: 3 · 2022: 4 · 2021: 3 · 2020: 5 · 2019: 4 · 2018: 3 · 2017: 2 · 2016: 8 · 2015: 8 · 2014: 4 · 2013: 6 · 2012: 8
- FWCI
- 2.61
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Brain Behavior and Immunity (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Deutsche Forschungsgemeinschaft
- Topics
- Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
- Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
- Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
- Keywords
- chronic inflammatory diseases, evolutionary medicine, energy regulation, systemic response, neuroendocrine pathways, energy reallocation, metabolic syndrome, etiology, fibrosis, wound healing
- MeSH terms
- Animals, Chronic Disease, Competitive Behavior, Energy Metabolism, Biological Evolution, Humans, Immune System, Inflammation, Reproduction
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review