ReviewArthritis research & therapy2014
Insulin resistance, selfish brain, and selfish immune system: an evolutionarily positively selected program used in chronic inflammatory diseases.
Review in Arthritis research & therapy, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
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Who cites it
44 citing papers in PubMed, 99 citations in OpenAlex.
- Cerebrospinal fluid glucose levels and their association with disability, depression, and cognitive function in multiple sclerosis.Metabolic brain disease · 2026Article
- Interplay between obesity-associated insulin resistance and immune system through the lens of evolutionary medicine.Molecular metabolism · 2026Review
- Uncovering non-linear dietary predictors of cardiovascular disease risk in older adults with periodontitis: a cross-sectional analysis.Frontiers in nutrition · 2026Article
- Association between triglyceride-glucose index and depression in middle-aged and older adults with hypertension: insights from the CHARLS study.Scientific reports · 2025Article
- Article
- Recognizing the Role of Insulin Resistance in Polycystic Ovary Syndrome: A Paradigm Shift from a Glucose-Centric Approach to an Insulin-Centric Model.Journal of clinical medicine · 2025Review
- Anti-Inflammatory Actions of Plant-Derived Compounds and Prevention of Chronic Diseases: From Molecular Mechanisms to Applications.International journal of molecular sciences · 2025Review
- Article
- Urbanization Shifts Immunometabolism in a Common Bumblebee.Ecology and evolution · 2024Article
- Rheumatic diseases and metabolism: where centre and periphery meet.Nature reviews. Rheumatology · 2024Review
- JAK/STAT mediated insulin resistance in muscles is essential for effective immune response.Cell communication and signaling : CCS · 2024Article
- Association between triglyceride glucose index and depression in hypertensive population.Journal of clinical hypertension (Greenwich, Conn.) · 2024Article
- Energy Regulation in Inflammatory Sarcopenia by the Purinergic System.International journal of molecular sciences · 2023Review
- Metabolic Effects of Anti-TNF-α Treatment in Rheumatoid Arthritis.Diseases (Basel, Switzerland) · 2023Article
- Pleiotropy promotes the evolution of inducible immune responses in a model of host-pathogen coevolution.PLoS computational biology · 2023Article
- Immunometabolic regulation during the presence of microorganisms and parasitoids in insects.Frontiers in immunology · 2023Review
- Metabolic strategy of macrophages under homeostasis or immune stress inMarine life science & technology · 2022Review
- The transition between acute and chronic infections in light of energy control: a mathematical model of energy flow in response to infection.Journal of the Royal Society, Interface · 2022Article
- Association of higher plasma leptin levels with HOMA-IR index, high sensitivity C-reactive protein and glycolipid metabolism in patients with chronic schizophrenia: A multi-center cross-sectional study.Frontiers in psychiatry · 2022Article
- The possible role of Interleukin-6 as a regulator of insulin sensitivity in patients with neuromyelitis optica spectrum disorder.BMC neurology · 2021Article
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Insulin resistance (IR) is a general phenomenon of many physiological states, disease states, and diseases. IR has been described in diabetes mellitus, obesity, infection, sepsis, trauma, painful states such as postoperative pain and migraine, schizophrenia, major depression, chronic mental stress, and others. In arthritis, abnormalities of glucose homeostasis were described in 1920; and in 1950 combined glucose and insulin tests unmistakably demonstrated IR. The phenomenon is now described in rheumatoid arthritis, systemic lupus erythematosus, ankylosing spondylitis, polymyalgia rheumatica, and others. In chronic inflammatory diseases, cytokine-neutralizing strategies normalize insulin sensitivity. This paper delineates that IR is either based on inflammatory factors (activation of the immune/ repair system) or on the brain (mental activation via stress axes). Due to the selfishness of the immune system and the selfishness of the brain, both can induce IR independent of each other. Consequently, the immune system can block the brain (for example, by sickness behavior) and the brain can block the immune system (for example, stress-induced immune system alterations). Based on considerations of evolutionary medicine, it is discussed that obesity per se is not a disease. Obesity-related IR depends on provoking factors from either the immune system or the brain. Chronic inflammation and/or stress axis activation are thus needed for obesity-related IR. Due to redundant pathways in stimulating IR, a simple one factor-neutralizing strategy might help in chronic inflammatory diseases (inflammation is the key), but not in obesity-related IR. The new considerations towards IR are interrelated to the published theories of IR (thrifty genotype, thrifty phenotype, and others).
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