The DOI matches its Crossref record; 180 of the 181 references it cites were found in a registry or an index; 14 of the 239 sources its claims cite were checked for support.
Chronic inflammation in the etiology of disease across the life span
Open accessAbstract
Although intermittent increases in inflammation are critical for survival during physical injury and infection, recent research has revealed that certain social, environmental and lifestyle factors can promote systemic chronic inflammation (SCI) that can, in turn, lead to several diseases that collectively represent the leading causes of disability and mortality worldwide, such as cardiovascular disease, cancer, diabetes mellitus, chronic kidney disease, non-alcoholic fatty liver disease and autoimmune and neurodegenerative disorders. In the present Perspective we describe the multi-level mechanisms underlying SCI and several risk factors that promote this health-damaging phenotype, including infections, physical inactivity, poor diet, environmental and industrial toxicants and psychological stress. Furthermore, we suggest potential strategies for advancing the early diagnosis, prevention and treatment of SCI.
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Claims the paper makes
101 Not checked yet · 9 Own interpretation · 7 Partly supported · 1 Supported · 1 No basis given · accuracy not yet measured
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In the paper
“a meta-analysis of ten studies and 23,345 older adults (70 to 80 years old) who were followed for 3.9–31 years found that individuals meeting the minimum international physical activity recommendations had a 40% lower risk of Alzheimer’s disease as compared to their physically inactive counterparts103.”
§ Chronic inflammation in the etiology of disease across the life span > Sources of systemic chronic inflammation > Physical activity.
What the sources say
- Partly supportedcites [103] Santos-Lozano, A. et al. Physical activity and Alzheimer disease: a protective association. Mayo. Clin. Proc. 91, 999–1020 (2016). sourceExperimental — accuracy not yet measured
Split into 2 atoms — 1 confirmed, 1 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Partly supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“Childhood obesity, for instance, is strongly associated with major changes in adipose tissue and metabolic dysfunction that cause metabolism-related-SCI, or so-called metainflammation26”
§ Chronic inflammation in the etiology of disease across the life span > Developmental origins of systemic chronic inflammation
What the sources say
- Supportedcites [26] Singer, K. & Lumeng, C. N. The initiation of metabolic inflammation in childhood obesity. J. Clin. Invest. 127, 65–73 (2017). source
The Introduction defines metabolic inflammation as metainflammation and says it is initiated in childhood. “Childhood/adolescence” states that evidence is strong that childhood obesity triggers it, while “When does metainflammation begin?” describes adipose-tissue inflammation and metabolic stress in obese children and adolescents, alongside decreased insulin sensitivity. (LLM, conf=0.89)
boosteddirect- Asserted: passes — The authors put it forward as true.
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- Based: passes — The paper gives a reason why it holds.
- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“greater microbial exposure in infancy is associated with reduced risk of chronic inflammation in adulthood8,168, as predicted by the hygiene, or ‘old friends’, hypothesis82”
§ Chronic inflammation in the etiology of disease across the life span > Developmental origins of systemic chronic inflammation
What the sources say
- Partly supportedcites [8] Renz, H. et al. An exposome perspective: early-life events and immune development in a changing world. J. Allergy Clin. Immunol. 140, 24–40 (2017). sourceExperimental — accuracy not yet measured
The “External microbes, perinatal factors, and immune development” section says altered microbial exposure, particularly in early life, predisposes to chronic inflammatory disease and links this idea to the hygiene and old-friends hypotheses. It does not specify inflammation in adulthood or establish that greater exposure to microbes generally is protective. (LLM, conf=0.84)
- Supportedcites [168] McDade, T. W., Rutherford, J., Adair, L. & Kuzawa, C. W. Early origins of inflammation: microbial exposures in infancy predict lower levels of C-reactive protein in adulthood. Proc. Biol. Sci. 277, 1129–1137 (2010). source
The Discussion reports negative associations between three measures of microbial exposure in infancy and CRP, a marker of inflammation, in young adulthood. It also says these findings are broadly consistent with the hygiene or ‘old friends’ hypothesis. (LLM, conf=0.92)
- Not checked yetcites [82] Rook, G., Bäckhed, F., Levin, B. R., McFall-Ngai, M. J. & McLean, A. R. Evolution, human-microbe interactions, and life history plasticity. Lancet 390, 521–530 (2017). source
plaincorrelational- Asserted: passes — The authors put it forward as true.
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- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Partly supported
In the paper
“These behavioral changes can be critical for survival during times of physical injury and microbial threat14.”
§ Chronic inflammation in the etiology of disease across the life span > Inflammation
What the sources say
- Not checked yetcites [14] Slavich, G. M. Psychoneuroimmunology of stress and mental health. in The Oxford Handbook of Stress and Mental Health (eds K. Harkness & E. P. Hayden) (Oxford University Press, in the press).
plainconditional- Asserted: passes — The authors put it forward as true.
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- Based: passes — The paper gives a reason why it holds.
None of the sources cited for this claim have been checked yet.
In the paper
“Depending on the degree and extent of the inflammatory response, including whether it is systemic or local, metabolic and neuroendocrine changes can occur to conserve metabolic energy and allocate more nutrients to the activated immune system9–12.”
§ Chronic inflammation in the etiology of disease across the life span > Inflammation
What the sources say
- Not checked yetcites [9] Kotas, M. E. & Medzhitov, R. Homeostasis, inflammation, and disease susceptibility. Cell 160, 816–827 (2015). source
- Not checked yetcites [10] Straub, R. H., Cutolo, M., Buttgereit, F. & Pongratz, G. Energy regulation and neuroendocrine-immune control in chronic inflammatory diseases. J. Intern. Med. 267, 543–560 (2010). source
- Not checked yetcites [11] Straub, R. H., Cutolo, M. & Pacifici, R. Evolutionary medicine and bone loss in chronic inflammatory diseases—a theory of inflammation-related osteopenia. Semin. Arthritis Rheum. 45, 220–228 (2015). source
- Not checked yetcites [12] Straub, R. H. & Schradin, C. Chronic inflammatory systemic diseases: an evolutionary trade-off between acutely beneficial but chronically harmful programs. Evol. Med. Public Health 2016, 37–51 (2016).
plainconditional- Asserted: passes — The authors put it forward as true.
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None of the sources cited for this claim have been checked yet.
In the paper
“A normal inflammatory response is characterized by the temporally restricted upregulation of inflammatory activity that occurs when a threat is present and that resolves once the threat has passed9,13,15.”
§ Chronic inflammation in the etiology of disease across the life span > Inflammation
What the sources say
- Not checked yetcites [9] Kotas, M. E. & Medzhitov, R. Homeostasis, inflammation, and disease susceptibility. Cell 160, 816–827 (2015). source
- Not checked yetcites [13] Straub, R. H. The brain and immune system prompt energy shortage in chronic inflammation and ageing. Nat. Rev. Rheumatol. 13, 743–751 (2017). source
- Not checked yetcites [15] Fullerton, J. N. & Gilroy, D. W. Resolution of inflammation: a new therapeutic frontier. Nat. Rev. Drug Discov. 15, 551–567 (2016). source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
None of the sources cited for this claim have been checked yet.
In the paper
“SCI during pregnancy and childhood can have serious developmental consequences that include elevating the risk of non-communicable diseases over the life span7,8,26,27.”
§ Chronic inflammation in the etiology of disease across the life span > Inflammation
What the sources say
- Not checked yetcites [7] Fleming, T. P. et al. Origins of lifetime health around the time of conception: causes and consequences. Lancet 391, 1842–1852 (2018). source
- Not checked yetcites [8] Renz, H. et al. An exposome perspective: early-life events and immune development in a changing world. J. Allergy Clin. Immunol. 140, 24–40 (2017). source
- Not checked yetcites [26] Singer, K. & Lumeng, C. N. The initiation of metabolic inflammation in childhood obesity. J. Clin. Invest. 127, 65–73 (2017). source
- Not checked yetcites [27] Olvera Alvarez, H. A., Kubzansky, L. D., Campen, M. J. & Slavich, G. M. Early life stress, air pollution, inflammation, and disease: an integrative review and immunologic model of social-environmental adversity and lifespan health. Neurosci. Biobehav. Rev. 92, 226–242 (2018). source
plainconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
None of the sources cited for this claim have been checked yet.
In the paper
“In contrast, SCI is typically triggered by DAMPs in the absence of an acute infectious insult or activation of PAMPs30–32.”
§ Chronic inflammation in the etiology of disease across the life span > Systemic chronic inflammation and non-communicable disease risk
What the sources say
- Not checked yetcites [30] Franceschi, C., Garagnani, P., Vitale, G., Capri, M. & Salvioli, S. Inflammaging and ‘garb-aging’. Trends Endocrinol. Metab. 28, 199–212 (2017). source
- Not checked yetcites [31] Liston, A. & Masters, S. L. Homeostasis-altering molecular processes as mechanisms of inflammasome activation. Nat. Rev. Immunol. 17, 208–214 (2017). source
- Not checked yetcites [32] Frank, D. & Vince, J. E. Pyroptosis versus necroptosis: similarities, differences, and crosstalk. Cell Death Differ. 26, 99–114 (2019). source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
None of the sources cited for this claim have been checked yet.
In the paper
“SCI often increases with age30, as indicated by studies showing that older individuals have higher circulating levels of cytokines, chemokines and acute phase proteins, as well as greater expression of genes involved in inflammation1,19,30.”
§ Chronic inflammation in the etiology of disease across the life span > Systemic chronic inflammation and non-communicable disease risk
What the sources say
- Not checked yetcites [1] Furman, D. et al. Expression of specific inflammasome gene modules stratifies older individuals into two extreme clinical and immunological states. Nat. Med. 23, 174–184 (2017). source
- Not checked yetcites [19] Ferrucci, L. & Fabbri, E. Inflammageing: chronic inflammation in ageing, cardiovascular disease, and frailty. Nat. Rev. Cardiol. 15, 505–522 (2018). source
- Not checked yetcites [30] Franceschi, C., Garagnani, P., Vitale, G., Capri, M. & Salvioli, S. Inflammaging and ‘garb-aging’. Trends Endocrinol. Metab. 28, 199–212 (2017). source
hedgeddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Empirical evidence that inflammation plays a role in disease onset or progression is strongest for metabolic syndrome, type 2 diabetes and CVD.”
§ Chronic inflammation in the etiology of disease across the life span > Systemic chronic inflammation and non-communicable disease risk
boostedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- It may state two separate claims as one. 65
- Probably not a substantial claim. 8
- The quote only partly states this claim. 2
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“populations of hunter-gatherers and other existing non-industrialized societies such as the Shuar hunter-gatherers of the Ecuadorian Amazon83,84, Tsimané forager-horticulturalists of Bolivia68, Hadza hunter-gatherers from Tanzania67, subsistence agriculturalists from rural Ghana85 and traditional horticulturalists of Kitava (Papua New Guinea)86—all of whom are minimally exposed to industrialized”
§ Chronic inflammation in the etiology of disease across the life span > Sources of systemic chronic inflammation > Chronic infections.
What the sources say
- Not checked yetcites [65] McDade, T. W. Early environments and the ecology of inflammation. Proc. Natl Acad. Sci. USA 109, 17281–17288 (2012). source
- Not checked yetcites [67] Raichlen, D. A. et al. Physical activity patterns and biomarkers of cardiovascular disease risk in hunter-gatherers. Am. J. Hum. Biol. 29, e22919 (2017). source
- Partly supportedcites [68] Kaplan, H. et al. Coronary atherosclerosis in indigenous South American Tsimane: a cross-sectional cohort study. Lancet 389, 1730–1739 (2017). sourceExperimental — accuracy not yet measured
Split into 2 atoms — 0 confirmed, 2 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.
- Not checked yetcites [83] McDade, T. W. et al. Analysis of variability of high sensitivity C-reactive protein in lowland Ecuador reveals no evidence of chronic low-grade inflammation. Am. J. Hum. Biol. 24, 675–681 (2012). source
- Not checked yetcites [86] Agmon-Levin, N. et al. Antitreponemal antibodies leading to autoantibody production and protection from atherosclerosis in Kitavans from Papua New Guinea. Ann. N. Y. Acad. Sci. 1173, 675–682 (2009). source
plain- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“a recent systematic analysis of dietary data from 195 different countries identified poor diet as the main risk factor for death in 2017, with excessive sodium intake being responsible for more than half of diet-related deaths146”
§ Chronic inflammation in the etiology of disease across the life span > Sources of systemic chronic inflammation > Diet.
What the sources say
- Partly supportedcites [146] GBD 2017 Diet Collaborators. Health effects of dietary risks in 195 countries, 1990-2017: a systematic analysis for the Global Burden of Disease Study 2017. Lancet 393, 1958–1972 (2019). sourceExperimental — accuracy not yet measured
The Discussion (page not available in our copy) says suboptimal diet was responsible for more deaths than any other risk globally. The Results report 11 million diet-related deaths in 2017, of which 3 million were attributable to high sodium intake. More than half were attributable to sodium, low whole grains, and low fruit combined—not sodium alone. (LLM, conf=0.94)
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“The main contributors to the growing worldwide incidence of low omega-3 status are a low intake of fish and high intake of vegetable oils that are high in linoleic acid, which displaces omega-3 fatty acids in cell membrane phospholipids140,141”
§ Chronic inflammation in the etiology of disease across the life span > Sources of systemic chronic inflammation > Diet.
What the sources say
- Not checked yetcites [140] Blasbalg, T. L., Hibbeln, J. R., Ramsden, C. E., Majchrzak, S. F. & Rawlings, R. R. Changes in consumption of omega-3 and omega-6 fatty acids in the United States during the 20th century. Am. J. Clin. Nutr. 93, 950–962 (2011). source
- Partly supportedcites [141] Calder, P. C. Very long-chain n-3 fatty acids and human health: fact, fiction and the future. Proc. Nutr. Soc. 77, 52–72 (2018). sourceExperimental — accuracy not yet measured
In “Omega-3 fatty acids—structure, metabolic interrelationships, dietary sources and intakes” (page unavailable), the paper links low fish consumption to low long-chain omega-3 intake in Western populations. It also says high linoleic-acid intake relative to ALA may reduce ALA conversion to EPA. It does not establish a rising worldwide prevalence of low omega-3 status or say that linoleic-acid-rich vegetable oils displace omega-3 fatty acids from cell membrane phospholipids. (LLM, conf=0.87)
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“the industrial revolution and modern era have ushered in changes in social interactions and sleep quality59,91 that can promote SCI149,150 and insulin resistance151, in turn increasing risk for obesity, type 2 diabetes, CVD and all-cause mortality150–154”
§ Chronic inflammation in the etiology of disease across the life span > Sources of systemic chronic inflammation > Social and cultural changes.
What the sources say
- Not checked yetcites [59] Franceschi, C., Garagnani, P., Parini, P., Giuliani, C. & Santoro, A. Inflammaging: a new immune-metabolic viewpoint for age-related diseases. Nat. Rev. Endocrinol. 159, 1–15 (2018).
- Partly supportedcites [91] Slavich, G. M. & Cole, S. W. The emerging field of human social genomics. Clin. Psychol. Sci. 1, 331–348 (2013). sourceExperimental — accuracy not yet measured
Split into 2 atoms — 1 confirmed, 1 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.
- Partly supportedcites [149] Slavich, G. M. & Irwin, M. R. From stress to inflammation and major depressive disorder: a social signal transduction theory of depression. Psychol. Bull. 140, 774–815 (2014). sourceExperimental — accuracy not yet measured
Split into 2 atoms — 0 confirmed, 2 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.
- Not checked yetcites [150] Tobaldini, E. et al. Short sleep duration and cardiometabolic risk: from pathophysiology to clinical evidence. Nat. Rev. Cardiol. 16, 213–224 (2019). source
- Not checked yetcites [151] Reutrakul, S. & Van Cauter, E. Sleep influences on obesity, insulin resistance, and risk of type 2 diabetes. Metab. Clin. Exp. 84, 56–66 (2018). source
- Partly supportedcites [152] Valtorta, N. K., Kanaan, M., Gilbody, S., Ronzi, S. & Hanratty, B. Loneliness and social isolation as risk factors for coronary heart disease and stroke: systematic review and meta-analysis of longitudinal observational studies. Heart 102, 1009–1016 (2016). sourceExperimental — accuracy not yet measured
Split into 2 atoms — 0 confirmed, 2 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.
- Partly supportedcites [153] Steptoe, A., Shankar, A., Demakakos, P. & Wardle, J. Social isolation, loneliness, and all-cause mortality in older men and women. Proc. Natl Acad. Sci. USA 110, 5797–5801 (2013). sourceExperimental — accuracy not yet measured
Split into 2 atoms — 1 confirmed, 1 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.
- Partly supportedcites [154] Kivimaki, M. & Steptoe, A. Effects of stress on the development and progression of cardiovascular disease. Nat. Rev. Cardiol. 15, 215–229 (2018). sourceExperimental — accuracy not yet measured
Split into 2 atoms — 0 confirmed, 2 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
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It may state two separate claims as one.
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“The concomitant increase in the estimated contribution of environmental chemicals to human disease burden162 has prompted a shift toward data generation using high-throughput screening to investigate the effect of industrial toxicants on cellular pathways, which has been supported by initiatives like the US Federal Tox21 Program, and toward the adoption of translational systems-toxicology”
§ Chronic inflammation in the etiology of disease across the life span > Sources of systemic chronic inflammation > Environmental and industrial toxicants.
What the sources say
- Partly supportedcites [162] Sly, P. D. et al. Health consequences of environmental exposures: causal thinking in global environmental epidemiology. Ann. Glob. Health 82, 3–9 (2016). sourceExperimental — accuracy not yet measured
The Abstract says current disease-burden estimates omit many environmental risk factors, including chemical exposures, and the Conclusions say environmental contributions are underestimated. The paper does not show that the estimated share attributable to chemicals has grown. Citation 162 is attached to that burden-estimate claim, not to the subsequent discussion of screening approaches. (LLM, conf=0.77)
- Could not verifycites [163] Collins, F. S., Gray, G. M. & Bucher, J. R. Toxicology. Transforming environmental health protection. Science 319, 906–907 (2008). sourceExperimental — accuracy not yet measured
The citation is attached to the claim that the estimated contribution of environmental chemicals to human disease burden has increased. The EPA, NCGC, and NTP Joint Activities passage describes a shift toward high-throughput, mechanism-based toxicity testing, but neither it nor the other passages found reports a rising estimate of disease burden attributable to chemicals (searched: estimated contribution, disease burden, environmental chemical exposures). (LLM, conf=0.74)
hedgeddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
- Partly supported
None of the sources cited for this claim have been checked yet.
In the paper
“Evidence is emerging that the risk of developing chronic inflammation can be traced back to early development, and its effects are now known to persist throughout the life span to affect adulthood health and risk of mortality6–8.”
§ Chronic inflammation in the etiology of disease across the life span > Abstract
What the sources say
- Not checked yetcites [6] Miller, G. E., Chen, E. & Parker, K. J. Psychological stress in childhood and susceptibility to the chronic diseases of aging: moving toward a model of behavioral and biological mechanisms. Psychol. Bull. 137, 959–997 (2011). source
- Not checked yetcites [7] Fleming, T. P. et al. Origins of lifetime health around the time of conception: causes and consequences. Lancet 391, 1842–1852 (2018). source
- Not checked yetcites [8] Renz, H. et al. An exposome perspective: early-life events and immune development in a changing world. J. Allergy Clin. Immunol. 140, 24–40 (2017). source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“certain social, environmental and lifestyle factors can promote systemic chronic inflammation (SCI) that can, in turn, lead to several diseases that collectively represent the leading causes of disability and mortality worldwide”
§ Chronic inflammation in the etiology of disease across the life span > Abstract
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Inflammation is an evolutionarily conserved process characterized by the activation of immune and non-immune cells that protect the host from bacteria, viruses, toxins and infections by eliminating pathogens and promoting tissue repair and recovery2,9.”
§ Chronic inflammation in the etiology of disease across the life span > Inflammation
What the sources say
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
In the paper
“chronic inflammatory diseases have been recognized as the most significant cause of death in the world today, with more than 50% of all deaths being attributable to inflammation-related diseases”
§ Chronic inflammation in the etiology of disease across the life span > Abstract
What the sources say
- Not checked yetcites [5] GBD 2017 Causes of Death Collaborators. Global, regional, and national age-sex-specific mortality for 282 causes of death in 195 countries and territories, 1980-2017: a systematic analysis for the Global Burden of Disease Study 2017. Lancet 392, 1736–1788 (2018). source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Specific biobehavioral effects of inflammation thus include a constellation of energy-saving behaviors commonly known as “sickness behaviors,” such as sadness, anhedonia, fatigue, reduced libido and food intake, altered sleep and social-behavioral withdrawal, as well as increased blood pressure, insulin resistance and dyslipidemia10,13.”
§ Chronic inflammation in the etiology of disease across the life span > Inflammation
What the sources say
- Not checked yetcites [10] Straub, R. H., Cutolo, M., Buttgereit, F. & Pongratz, G. Energy regulation and neuroendocrine-immune control in chronic inflammatory diseases. J. Intern. Med. 267, 543–560 (2010). source
- Not checked yetcites [13] Straub, R. H. The brain and immune system prompt energy shortage in chronic inflammation and ageing. Nat. Rev. Rheumatol. 13, 743–751 (2017). source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Shifts in the inflammatory response from short- to long-lived can cause a breakdown of immune tolerance9,15 and lead to major alterations in all tissues and organs, as well as normal cellular physiology, which can increase the risk for various non-communicable diseases in both young and older individuals1,9–11,15,17–21.”
§ Chronic inflammation in the etiology of disease across the life span > Inflammation
What the sources say
- Not checked yetcites [1] Furman, D. et al. Expression of specific inflammasome gene modules stratifies older individuals into two extreme clinical and immunological states. Nat. Med. 23, 174–184 (2017). source
- Not checked yetcites [9] Kotas, M. E. & Medzhitov, R. Homeostasis, inflammation, and disease susceptibility. Cell 160, 816–827 (2015). source
- Not checked yetcites [10] Straub, R. H., Cutolo, M., Buttgereit, F. & Pongratz, G. Energy regulation and neuroendocrine-immune control in chronic inflammatory diseases. J. Intern. Med. 267, 543–560 (2010). source
- Not checked yetcites [11] Straub, R. H., Cutolo, M. & Pacifici, R. Evolutionary medicine and bone loss in chronic inflammatory diseases—a theory of inflammation-related osteopenia. Semin. Arthritis Rheum. 45, 220–228 (2015). source
- Not checked yetcites [15] Fullerton, J. N. & Gilroy, D. W. Resolution of inflammation: a new therapeutic frontier. Nat. Rev. Drug Discov. 15, 551–567 (2016). source
- Not checked yetcites [17] Taniguchi, K. & Karin, M. NF-κB, inflammation, immunity and cancer: coming of age. Nat. Rev. Immunol. 18, 309–324 (2018). source
- Not checked yetcites [18] Gisterå, A. & Hansson, G. K. The immunology of atherosclerosis. Nat Rev. Nephrol. 13, 368–380 (2017). source
- Not checked yetcites [19] Ferrucci, L. & Fabbri, E. Inflammageing: chronic inflammation in ageing, cardiovascular disease, and frailty. Nat. Rev. Cardiol. 15, 505–522 (2018). source
- Not checked yetcites [20] Heneka, M. T., Kummer, M. P. & Latz, E. Innate immune activation in neurodegenerative disease. Nat. Rev. Immunol. 14, 463–477 (2014). source
- Not checked yetcites [21] Miller, A. H. & Raison, C. L. The role of inflammation in depression: from evolutionary imperative to modern treatment target. Nat. Rev. Immunol. 16, 22–34 (2016). source
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“the presence of certain social, psychological, environmental and biological factors has been linked to the prevention of resolution of acute inflammation and, in turn, the promotion of a state of low-grade, non-infective (that is, ‘sterile’) systemic chronic inflammation (SCI)”
§ Chronic inflammation in the etiology of disease across the life span > Inflammation
What the sources say
- Not checked yetcites [13] Straub, R. H. The brain and immune system prompt energy shortage in chronic inflammation and ageing. Nat. Rev. Rheumatol. 13, 743–751 (2017). source
- Not checked yetcites [16] Calder, P. C. et al. A consideration of biomarkers to be used for evaluation of inflammation in human nutritional studies. Br. J. Nutr. 109, S1–S34 (2013). source
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“SCI can also impair normal immune function, leading to increased susceptibility to infections and tumors and a poor response to vaccines22–25.”
§ Chronic inflammation in the etiology of disease across the life span > Inflammation
What the sources say
- Not checked yetcites [22] Shen-Orr, S. S. et al. Defective signaling in the JAK-STAT pathway tracks with chronic inflammation and cardiovascular risk in aging humans. Cell Syst. 3, 374–384.e4 (2016). source
- Not checked yetcites [23] Verschoor, C. P. et al. Serum C-reactive protein and congestive heart failure as significant predictors of herpes zoster vaccine response in elderly nursing home residents. J. Infect. Dis. 216, 191–197 (2017). source
- Not checked yetcites [24] Fourati, S. et al. Pre-vaccination inflammation and B-cell signalling predict age-related hyporesponse to hepatitis B vaccination. Nat. Commun. 7, 10369 (2016). source
- Not checked yetcites [25] McDade, T. W., Adair, L., Feranil, A. B. & Kuzawa, C. Positive antibody response to vaccination in adolescence predicts lower C-reactive protein concentration in young adulthood in the Philippines. Am. J. Hum. Biol. 23, 313–318 (2011). source
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In the paper
“SCI is low-grade and persistent (as the name suggests) and ultimately causes collateral damage to tissues and organs over time, such as by inducing oxidative stress1,4,9,19.”
§ Chronic inflammation in the etiology of disease across the life span > Systemic chronic inflammation and non-communicable disease risk
What the sources say
- Not checked yetcites [1] Furman, D. et al. Expression of specific inflammasome gene modules stratifies older individuals into two extreme clinical and immunological states. Nat. Med. 23, 174–184 (2017). source
- Not checked yetcites [4] Bennett, J. M., Reeves, G., Billman, G. E. & Sturmberg, J. P. Inflammation–nature’s way to efficiently respond to all types of challenges: implications for understanding and managing “the epidemic” of chronic diseases. Front. Med. 5, 316 (2018). source
- Not checked yetcites [9] Kotas, M. E. & Medzhitov, R. Homeostasis, inflammation, and disease susceptibility. Cell 160, 816–827 (2015). source
- Not checked yetcites [19] Ferrucci, L. & Fabbri, E. Inflammageing: chronic inflammation in ageing, cardiovascular disease, and frailty. Nat. Rev. Cardiol. 15, 505–522 (2018). source
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“patients with autoimmune diseases such as rheumatoid arthritis that are characterized by systemic inflammation have insulin resistance, dyslipidemia and hypertension, and that they have higher rates of metabolic syndrome, type 2 diabetes and CVD”
§ Chronic inflammation in the etiology of disease across the life span > Systemic chronic inflammation and non-communicable disease risk
What the sources say
- Not checked yetcites [10] Straub, R. H., Cutolo, M., Buttgereit, F. & Pongratz, G. Energy regulation and neuroendocrine-immune control in chronic inflammatory diseases. J. Intern. Med. 267, 543–560 (2010). source
- Not checked yetcites [12] Straub, R. H. & Schradin, C. Chronic inflammatory systemic diseases: an evolutionary trade-off between acutely beneficial but chronically harmful programs. Evol. Med. Public Health 2016, 37–51 (2016).
- Not checked yetcites [37] Zhang, J. et al. The risk of metabolic syndrome in patients with rheumatoid arthritis: a meta-analysis of observational studies. PLoS One 8, e78151 (2013). source
- Not checked yetcites [38] Armstrong, A. W., Harskamp, C. T. & Armstrong, E. J. Psoriasis and the risk of diabetes mellitus: a systematic review and meta-analysis. JAMA Dermatol. 149, 84–91 (2013). source
- Not checked yetcites [39] Dregan, A., Charlton, J., Chowienczyk, P. & Gulliford, M. C. Chronic inflammatory disorders and risk of type 2 diabetes mellitus, coronary heart disease, and stroke: a population-based cohort study. Circulation 130, 837–844 (2014). source
boostedcorrelational- Asserted: passes — The authors put it forward as true.
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In the paper
“a recent double-blind RCT of the IL-1β inhibitor canakinumab that assessed more than 10,000 adults with a history of myocardial infarction and elevated circulating CRP levels showed that patients treated with canakinumab subcutaneously every 3 months had lower rates of nonfatal myocardial infarction, nonfatal stroke and CVD death compared with those treated with a placebo, despite having no change”
§ Chronic inflammation in the etiology of disease across the life span > Systemic chronic inflammation and non-communicable disease risk
What the sources say
- Not checked yetcites [44] Ridker, P. M. et al. Antiinflammatory therapy with canakinumab for atherosclerotic disease. N. Engl. J. Med. 377, 1119–1131 (2017). source
plaindirectn = 10,000- Asserted: passes — The authors put it forward as true.
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In the paper
“a recent study examined levels of 18 endogenous and ex vivo-stimulated inflammatory markers in 41 healthy volunteers of different ages across the life span. Results revealed that unstimulated levels of IL-12p70 in women and CRP in men were associated with older age, whereas no effects were found for IL-1β, IFN-α or TNF-α50.”
§ Chronic inflammation in the etiology of disease across the life span > Biomarkers for systemic chronic inflammation
What the sources say
- Not checked yetcites [50] Elisia, I. et al. Effect of age on chronic inflammation and responsiveness to bacterial and viral challenges. PLoS One 12, e0188881 (2017). source
plaincorrelationaln = 41- Asserted: passes — The authors put it forward as true.
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In the paper
“a recent study of more than 160,000 people from North Glasgow found that a combination of the inflammatory markers CRP (>10 mg/L; HR 2.71, P < 0.001), albumin (>35 mg/L; HR 3.68, P < 0.001) and neutrophil count (HR 2.18, P < 0.001) predicted all-cause mortality over 8 years, in addition to mortality due to cancer, cardiovascular and cerebrovascular disease45.”
§ Chronic inflammation in the etiology of disease across the life span > Systemic chronic inflammation and non-communicable disease risk
What the sources say
- Not checked yetcites [45] Proctor, M. J. et al. Systemic inflammation predicts all-cause mortality: a Glasgow inflammation outcome study. PLoS One 10, e0116206 (2015). source
plaincorrelational- Asserted: passes — The authors put it forward as true.
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In the paper
“In a recent meta-analysis of eight RCTs that included a total of 260 participants, anti-TNF-α inhibitor therapy was found to significantly reduce insulin resistance in patients with rheumatoid arthritis and to improve their insulin sensitivity42.”
§ Chronic inflammation in the etiology of disease across the life span > Systemic chronic inflammation and non-communicable disease risk
What the sources say
- Not checked yetcites [42] Burska, A. N., Sakthiswary, R. & Sattar, N. Effects of tumour necrosis factor antagonists on insulin sensitivity/resistance in rheumatoid arthritis: a systematic review and meta-analysis. PLoS One 10, e0128889 (2015). source
plaindirectn = 260- Asserted: passes — The authors put it forward as true.
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In the paper
“evidence exists that greater inflammatory activity is associated with older age, but this is not true of all inflammatory markers, and it is possible that these associations are due at least in part to increases in chronic ailments and frailty that are frequently associated with age rather than to biological aging itself.”
§ Chronic inflammation in the etiology of disease across the life span > Biomarkers for systemic chronic inflammation
What the sources say
- Not checked yetcites [50] Elisia, I. et al. Effect of age on chronic inflammation and responsiveness to bacterial and viral challenges. PLoS One 12, e0188881 (2017). source
hedgedcorrelationaln = 41- Asserted: passes — The authors put it forward as true.
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In the paper
“Studies have shown that canonical biomarkers of acute inflammation predict morbidity and mortality in both cross-sectional and longitudinal studies and may thus be used to index age-related SCI46.”
§ Chronic inflammation in the etiology of disease across the life span > Biomarkers for systemic chronic inflammation
What the sources say
- Not checked yetcites [46] Arai, Y. et al. Inflammation, but not telomere length, predicts successful ageing at extreme old age: a longitudinal study of semi-supercentenarians. EBioMedicine 2, 1549–1558 (2015). source
hedgedcorrelational- Asserted: passes — The authors put it forward as true.
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- Rests on an assumption: There are currently no standard biomarkers for indicating the presence of health-damaging chronic inflammation.
None of the sources cited for this claim have been checked yet.
In the paper
“SCI-related disease rates have increased dramatically for both older and younger individuals living in industrialized countries who follow a Western lifestyle but are relatively rare among individuals in non-Westernized populations who adhere to diets, lifestyles and ecological niches that more closely resemble those present during most of human evolution65–71.”
§ Chronic inflammation in the etiology of disease across the life span > Sources of systemic chronic inflammation
What the sources say
- Not checked yetcites [65] McDade, T. W. Early environments and the ecology of inflammation. Proc. Natl Acad. Sci. USA 109, 17281–17288 (2012). source
- Not checked yetcites [66] Carrera-Bastos, P., Fontes-Villalba, M., O’Keefe, J. H., Lindeberg, S. & Cordain, L. The western diet and lifestyle and diseases of civilization. Res. Rep. Clin. Cardiol. 2, 15–35 (2011).
- Not checked yetcites [67] Raichlen, D. A. et al. Physical activity patterns and biomarkers of cardiovascular disease risk in hunter-gatherers. Am. J. Hum. Biol. 29, e22919 (2017). source
- Not checked yetcites [68] Kaplan, H. et al. Coronary atherosclerosis in indigenous South American Tsimane: a cross-sectional cohort study. Lancet 389, 1730–1739 (2017). source
- Not checked yetcites [69] Lindeberg, S. & Lundh, B. Apparent absence of stroke and ischaemic heart disease in a traditional Melanesian island: a clinical study in Kitava. J. Intern. Med. 233, 269–275 (1993). source
- Not checked yetcites [70] Lindeberg, S., Berntorp, E., Nilsson-Ehle, P., Terént, A. & Vessby, B. Age relations of cardiovascular risk factors in a traditional Melanesian society: the Kitava Study. Am. J. Clin. Nutr. 66, 845–852 (1997). source
- Not checked yetcites [71] Lindeberg, S., Eliasson, M., Lindahl, B. & Ahrén, B. Low serum insulin in traditional Pacific Islanders—the Kitava Study. Metabolism 48, 1216–1219 (1999). source
plaincorrelational- Asserted: passes — The authors put it forward as true.
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None of the sources cited for this claim have been checked yet.
In the paper
“The fact that differences exist in the extent to which older adults exhibit SCI52,64 is thought to be indicative of inter-individual differences in exposure to these and other related pro-inflammatory factors, although studies documenting within-person associations between these risk factors and SCI are limited.”
§ Chronic inflammation in the etiology of disease across the life span > Sources of systemic chronic inflammation
What the sources say
- Not checked yetcites [52] Alpert, A. et al. A clinically meaningful metric of immune age derived from high-dimensional longitudinal monitoring. Nat. Med. 25, 487–495 (2019). source
- Not checked yetcites [64] Shen-Orr, S. S. & Furman, D. Variability in the immune system: of vaccine responses and immune states. Curr. Opin. Immunol. 25, 542–547 (2013). source
hedgedcorrelational- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
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In the paper
“The non-endogenous contributors are thought to include chronic infections57, lifestyle-induced obesity58, microbiome dysbiosis59, diet60, social and cultural changes61,62 and environmental and industrial toxicants63.”
§ Chronic inflammation in the etiology of disease across the life span > Sources of systemic chronic inflammation
What the sources say
- Not checked yetcites [57] Effros, R. B. The silent war of CMV in aging and HIV infection. Mech. Ageing Dev. 158, 46–52 (2016). source
- Not checked yetcites [58] Stout, M. B., Justice, J. N., Nicklas, B. J. & Kirkland, J. L. Physiological aging: links among adipose tissue dysfunction, diabetes, and frailty. Physiology (Bethesda) 32, 9–19 (2017).
- Not checked yetcites [59] Franceschi, C., Garagnani, P., Parini, P., Giuliani, C. & Santoro, A. Inflammaging: a new immune-metabolic viewpoint for age-related diseases. Nat. Rev. Endocrinol. 159, 1–15 (2018).
hedgedconditional- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“How senescent cells acquire the SASP is not fully understood, but existing research points to a combination of both endogenous and non-endogenous social, environmental and lifestyle risk factors.”
§ Chronic inflammation in the etiology of disease across the life span > Sources of systemic chronic inflammation
hedgedconditional- Asserted: passes — The authors put it forward as true.
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In the paper
“This enabled the researchers to construct a high-dimensional trajectory of immune aging (IMM-AGE) that described individuals’ immune functioning better than their chronological age. This new metric in turn accurately predicted all-cause mortality”
§ Chronic inflammation in the etiology of disease across the life span > Biomarkers for systemic chronic inflammation
What the sources say
- Not checked yetcites [52] Alpert, A. et al. A clinically meaningful metric of immune age derived from high-dimensional longitudinal monitoring. Nat. Med. 25, 487–495 (2019). source
plaincorrelationaln = 135- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“dietary and lifestyle habits, as well as exposure to a variety of different pollutants, can increase oxidative stress, upregulate mitogenic signaling pathways and cause genomic and epigenomic perturbations8,60,62,63 that can induce the SASP.”
§ Chronic inflammation in the etiology of disease across the life span > Sources of systemic chronic inflammation
What the sources say
- Not checked yetcites [8] Renz, H. et al. An exposome perspective: early-life events and immune development in a changing world. J. Allergy Clin. Immunol. 140, 24–40 (2017). source
- Not checked yetcites [60] Zitvogel, L., Pietrocola, F. & Kroemer, G. Nutrition, inflammation and cancer. Nat. Immunol. 18, 843–850 (2017). source
- Not checked yetcites [62] Carroll, J. E. et al. Partial sleep deprivation activates the DNA damage response (DDR) and the senescence-associated secretory phenotype (SASP) in aged adult humans. Brain Behav. Immun. 51, 223–229 (2016). source
- Not checked yetcites [63] Yuan, J. et al. Long-term persistent organic pollutants exposure induced telomere dysfunction and senescence-associated secretary phenotype. J. Gerontol. A Biol. Sci. Med. Sci. 73, 1027–1035 (2018). source
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“a study of 210 healthy twins between 8 and 82 years old, which found that non-heritable factors are the strongest contributors to differences in chronic inflammation across individuals72 and that exposure to environmental factors, which have been collectively called the exposome, are the main drivers of SCI.”
§ Chronic inflammation in the etiology of disease across the life span > Sources of systemic chronic inflammation
What the sources say
- Not checked yetcites [72] Brodin, P. et al. Variation in the human immune system is largely driven by non-heritable influences. Cell 160, 37–47 (2015). source
plaindirectn = 210- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“chronic infection with HIV causes premature aging of the immune system and is associated with early cardiovascular and skeletal changes57, with such effects being attributed in large part to the accumulation of senescent CD8+ T cells that produce increased levels of pro-inflammatory mediators80.”
§ Chronic inflammation in the etiology of disease across the life span > Sources of systemic chronic inflammation > Chronic infections.
What the sources say
- Not checked yetcites [57] Effros, R. B. The silent war of CMV in aging and HIV infection. Mech. Ageing Dev. 158, 46–52 (2016). source
- Not checked yetcites [80] Chou, J. P., Ramirez, C. M., Wu, J. E. & Effros, R. B. Accelerated aging in HIV/AIDS: novel biomarkers of senescent human CD8+ T cells. PLoS One 8, e64702 (2013). source
plaindirect- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
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In the paper
“Their lifestyles, for example, are characterized by higher levels of physical activity67,71,87, diets composed mainly of fresh or minimally processed food sources66,88,89, and less exposure to environmental pollutants66. In addition, individuals living in these environments generally have circadian rhythms that are more closely synchronized with diurnal fluctuations in sunlight exposure90 and the”
§ Chronic inflammation in the etiology of disease across the life span > Sources of systemic chronic inflammation > Lifestyle, social and physical environment.
What the sources say
- Not checked yetcites [67] Raichlen, D. A. et al. Physical activity patterns and biomarkers of cardiovascular disease risk in hunter-gatherers. Am. J. Hum. Biol. 29, e22919 (2017). source
- Not checked yetcites [71] Lindeberg, S., Eliasson, M., Lindahl, B. & Ahrén, B. Low serum insulin in traditional Pacific Islanders—the Kitava Study. Metabolism 48, 1216–1219 (1999). source
- Not checked yetcites [87] Gurven, M., Jaeggi, A. V., Kaplan, H. & Cummings, D. Physical activity and modernization among Bolivian Amerindians. PLoS One 8, e55679 (2013). source
- Not checked yetcites [66] Carrera-Bastos, P., Fontes-Villalba, M., O’Keefe, J. H., Lindeberg, S. & Cordain, L. The western diet and lifestyle and diseases of civilization. Res. Rep. Clin. Cardiol. 2, 15–35 (2011).
- Not checked yetcites [88] Cordain, L. et al. Plant-animal subsistence ratios and macronutrient energy estimations in worldwide hunter-gatherer diets. Am. J. Clin. Nutr. 71, 682–692 (2000). source
- Not checked yetcites [89] Kuipers, R. S., Joordens, J. C. A. & Muskiet, F. A. J. A multidisciplinary reconstruction of Palaeolithic nutrition that holds promise for the prevention and treatment of diseases of civilisation. Nutr. Res. Rev. 25, 96–129 (2012). source
- Not checked yetcites [90] De la Iglesia, H. O. et al. Ancestral sleep. Curr. Biol. 26, R271–R272 (2016). source
plain- Asserted: passes — The authors put it forward as true.
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A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“while chronic infections appear to contribute to SCI, they are not likely the primary driver.”
§ Chronic inflammation in the etiology of disease across the life span > Sources of systemic chronic inflammation > Chronic infections.
hedgedconditional- Asserted: passes — The authors put it forward as true.
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In the paper
“One study showed that, worldwide, 31% of individuals are considered physically inactive—defined as not meeting the minimum international recommendations for regular physical activity—with levels of inactivity being higher in high-income countries than in low-to-middle-income countries93.”
§ Chronic inflammation in the etiology of disease across the life span > Sources of systemic chronic inflammation > Physical activity.
What the sources say
- Not checked yetcites [93] Hallal, P. C. et al. Global physical activity levels: surveillance progress, pitfalls, and prospects. Lancet 380, 247–257 (2012). source
plaincorrelational- Asserted: passes — The authors put it forward as true.
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Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
In the paper
“In the United States, these numbers are even higher, with approximately 50% of American adults being considered physically inactive94.”
§ Chronic inflammation in the etiology of disease across the life span > Sources of systemic chronic inflammation > Physical activity.
What the sources say
- Not checked yetcites [94] Katzmarzyk, P. T., Lee, I.-M., Martin, C. K. & Blair, S. N. Epidemiology of physical activity and exercise training in the United States. Prog. Cardiovasc. Dis. 60, 3–10 (2017). source
plain- Asserted: passes — The authors put it forward as true.
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Probably not a substantial claim. The paper’s conclusions may not depend on it.
None of the sources cited for this claim have been checked yet.
In the paper
“These effects can, in turn, promote several inflammation-related pathophysiologic alterations, including insulin resistance, dyslipidemia, endothelial dysfunction, high blood pressure and loss of muscle mass (sarcopenia)100, that have been found to increase risk for a variety of conditions, including CVD, type 2 diabetes, NAFLD, osteoporosis, various types of cancer, depression, dementia and”
§ Chronic inflammation in the etiology of disease across the life span > Sources of systemic chronic inflammation > Physical activity.
What the sources say
- Not checked yetcites [95] Fiuza-Luces, C. et al. Exercise benefits in cardiovascular disease: beyond attenuation of traditional risk factors. Nat. Rev. Cardiol. 15, 731–743 (2018). source
- Not checked yetcites [100] Booth, F. W., Roberts, C. K. & Laye, M. J. Lack of exercise is a major cause of chronic diseases. Compr. Physiol. 2, 1143–1211 (2012). source
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“Industrialization conferred many benefits, including social stability; reduced physical trauma; access to modern medical technology; and improved public health measures, such as sanitation, quarantine policies and vaccination, all of which significantly decrease infant mortality rates and increase average life expectancy66.”
§ Chronic inflammation in the etiology of disease across the life span > Sources of systemic chronic inflammation > Lifestyle, social and physical environment.
What the sources say
- Not checked yetcites [66] Carrera-Bastos, P., Fontes-Villalba, M., O’Keefe, J. H., Lindeberg, S. & Cordain, L. The western diet and lifestyle and diseases of civilization. Res. Rep. Clin. Cardiol. 2, 15–35 (2011).
boosteddirect- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
In the paper
“Skeletal muscle is an endocrine organ that produces and releases cytokines and other small proteins, called myokines, into the bloodstream. This occurs particularly during muscle contraction and can have the effect of systemically reducing inflammation95.”
§ Chronic inflammation in the etiology of disease across the life span > Sources of systemic chronic inflammation > Physical activity.
What the sources say
- Not checked yetcites [95] Fiuza-Luces, C. et al. Exercise benefits in cardiovascular disease: beyond attenuation of traditional risk factors. Nat. Rev. Cardiol. 15, 731–743 (2018). source
plaindirect- Asserted: passes — The authors put it forward as true.
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None of the sources cited for this claim have been checked yet.
In the paper
“VAT is an active endocrine, immunological and metabolic organ composed of various cells (including immune cells, such as resident macrophages) that expands mostly through adipocyte hypertrophy, which can lead to areas of hypoxia and even cell death, resulting in activation of hypoxia-inducible factor-1α, increased production of reactive oxygen species, and release of DAMPs”
§ Chronic inflammation in the etiology of disease across the life span > Sources of systemic chronic inflammation > Physical activity.
What the sources say
- Not checked yetcites [105] Schipper, H. S., Prakken, B., Kalkhoven, E. & Boes, M. Adipose tissue-resident immune cells: key players in immunometabolism. Trends Endocrinol. Metabol. 23, 407–415 (2012). source
- Not checked yetcites [106] Tchernof, A. & Després, J.-P. Pathophysiology of human visceral obesity: an update. Physiol. Rev. 93, 359–404 (2013). source
- Not checked yetcites [107] Pellegrinelli, V., Carobbio, S. & Vidal-Puig, A. Adipose tissue plasticity: how fat depots respond differently to pathophysiological cues. Diabetologia 59, 1075–1088 (2016). source
- Not checked yetcites [108] Frasca, D., Blomberg, B. B. & Paganelli, R. Aging, obesity, and inflammatory age-related diseases. Front. Immunol. 8, 1745 (2017). source
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“A recent meta-analysis of studies with cohorts from Europe, the United States and the rest of the world that included 1,683,693 participants found that going from physically inactive to achieving the recommended 150 minutes of moderate-intensity aerobic activity per week was associated with lower risk of CVD mortality by 23%, CVD incidence by 17%, and type 2 diabetes incidence by 26% during an”
§ Chronic inflammation in the etiology of disease across the life span > Sources of systemic chronic inflammation > Physical activity.
What the sources say
- Not checked yetcites [101] Wahid, A. et al. Quantifying the association between physical activity and cardiovascular disease and diabetes: a systematic review and meta-analysis. J. Am. Heart Assoc. 5, e002495 (2016). source
plaincorrelational- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“physical inactivity can increase individuals’ risk for various non-communicable diseases because it is linked to obesity100 and, in particular, excessive visceral adipose tissue (VAT), which is a significant trigger of inflammation104–106.”
§ Chronic inflammation in the etiology of disease across the life span > Sources of systemic chronic inflammation > Physical activity.
What the sources say
- Not checked yetcites [100] Booth, F. W., Roberts, C. K. & Laye, M. J. Lack of exercise is a major cause of chronic diseases. Compr. Physiol. 2, 1143–1211 (2012). source
- Not checked yetcites [104] Pérez, L. M. et al. ‘Adipaging’: ageing and obesity share biological hallmarks related to a dysfunctional adipose tissue. J. Physiol. 594, 3187–3207 (2016). source
- Not checked yetcites [105] Schipper, H. S., Prakken, B., Kalkhoven, E. & Boes, M. Adipose tissue-resident immune cells: key players in immunometabolism. Trends Endocrinol. Metabol. 23, 407–415 (2012). source
- Not checked yetcites [106] Tchernof, A. & Després, J.-P. Pathophysiology of human visceral obesity: an update. Physiol. Rev. 93, 359–404 (2013). source
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“data from 1.44 million participants across several prospective cohort studies revealed that, as compared to individuals exhibiting high levels of leisure-time physical activity (≥90th percentile), those who were physically inactive (≤10th percentile) had a greater risk (>20%) of developing several cancers, including esophageal adenocarcinoma; liver, lung, kidney, gastric cardia and endometrial”
§ Chronic inflammation in the etiology of disease across the life span > Sources of systemic chronic inflammation > Physical activity.
What the sources say
- Not checked yetcites [102] Moore, S. C. et al. Association of leisure-time physical activity with risk of 26 types of cancer in 1.44 million adults. JAMA Intern. Med. 176, 816–825 (2016). source
plaincorrelational- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one. The quote only partly states this claim.
In the paper
“TNF-α and other molecules can cause adipocyte insulin resistance, which increases lipolysis, with the resulting spillover of lipids into other organs, such as the pancreas and liver, where they can contribute to beta-cell dysfunction, hepatic insulin resistance and fatty liver106.”
§ Chronic inflammation in the etiology of disease across the life span > Sources of systemic chronic inflammation > Physical activity.
What the sources say
- Not checked yetcites [106] Tchernof, A. & Després, J.-P. Pathophysiology of human visceral obesity: an update. Physiol. Rev. 93, 359–404 (2013). source
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“These dynamics are known to occur in adults and can promote age-related disease risk, but they first emerge during childhood26.”
§ Chronic inflammation in the etiology of disease across the life span > Sources of systemic chronic inflammation > Physical activity.
What the sources say
- Not checked yetcites [26] Singer, K. & Lumeng, C. N. The initiation of metabolic inflammation in childhood obesity. J. Clin. Invest. 127, 65–73 (2017). source
boosteddirect- Asserted: passes — The authors put it forward as true.
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None of the sources cited for this claim have been checked yet.
In the paper
“visceral obesity accelerates aging and increases risk for cardiometabolic, neurodegenerative and autoimmune diseases, as well as several types of cancer19,104,106,110–112.”
§ Chronic inflammation in the etiology of disease across the life span > Sources of systemic chronic inflammation > Physical activity.
What the sources say
- Not checked yetcites [19] Ferrucci, L. & Fabbri, E. Inflammageing: chronic inflammation in ageing, cardiovascular disease, and frailty. Nat. Rev. Cardiol. 15, 505–522 (2018). source
- Not checked yetcites [104] Pérez, L. M. et al. ‘Adipaging’: ageing and obesity share biological hallmarks related to a dysfunctional adipose tissue. J. Physiol. 594, 3187–3207 (2016). source
- Not checked yetcites [106] Tchernof, A. & Després, J.-P. Pathophysiology of human visceral obesity: an update. Physiol. Rev. 93, 359–404 (2013). source
- Not checked yetcites [110] Versini, M., Jeandel, P.-Y., Rosenthal, E. & Shoenfeld, Y. Obesity in autoimmune diseases: not a passive bystander. Autoimm. Rev. 13, 981–1000 (2014). source
- Not checked yetcites [111] Himbert, C. et al. Signals from the adipose microenvironment and the obesity-cancer link–a systematic review. Cancer Prev. Res. (Phila.) 10, 494–506 (2017). source
- Not checked yetcites [112] van Dijk, G. et al. Integrative neurobiology of metabolic diseases, neuroinflammation, and neurodegeneration. Front. Neurosci. 9, 173 (2015). source
plaindirect- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“These events can induce the secretion of numerous pro-inflammatory molecules, including adipokines, cytokines (for example, IL-1β, IL-6, TNF-α), and chemokines (especially monocyte chemoattractant protein-1) by adipocytes, endothelial cells and resident adipose tissue immune cells (for example, macrophages)105–108. This in turn leads to the infiltration of various immune cells in the VAT,”
§ Chronic inflammation in the etiology of disease across the life span > Sources of systemic chronic inflammation > Physical activity.
What the sources say
- Not checked yetcites [106] Tchernof, A. & Després, J.-P. Pathophysiology of human visceral obesity: an update. Physiol. Rev. 93, 359–404 (2013). source
- Not checked yetcites [107] Pellegrinelli, V., Carobbio, S. & Vidal-Puig, A. Adipose tissue plasticity: how fat depots respond differently to pathophysiological cues. Diabetologia 59, 1075–1088 (2016). source
- Not checked yetcites [108] Frasca, D., Blomberg, B. B. & Paganelli, R. Aging, obesity, and inflammatory age-related diseases. Front. Immunol. 8, 1745 (2017). source
- Not checked yetcites [109] Grant, R. W. & Dixit, V. D. Adipose tissue as an immunological organ. Obesity (Silver Spring) 23, 512–518 (2015). source
plaindirect- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one. The quote only partly states this claim.
In the paper
“the latter is a suspected cause of inflammation through activation of pattern recognition receptors, such as Toll-like receptors, in immune cells and of inflammation-mediated metabolic conditions such as insulin resistance118.”
§ Chronic inflammation in the etiology of disease across the life span > Sources of systemic chronic inflammation > Microbiome dysbiosis.
What the sources say
- Not checked yetcites [118] Jayashree, B. et al. Increased circulatory levels of lipopolysaccharide (LPS) and zonulin signify novel biomarkers of proinflammation in patients with type 2 diabetes. Mol. Cell. Biochem. 388, 203–210 (2014). source
hedgedconditional- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“The typical diet that has become widely adopted in many countries over the past 40 years is relatively low in fruits, vegetables and other fiber- and prebiotic-rich foods66,123–125 and high in refined grains124, alcohol126 and ultra-processed foods125, particularly those containing emulsifiers127.”
§ Chronic inflammation in the etiology of disease across the life span > Sources of systemic chronic inflammation > Diet.
What the sources say
- Not checked yetcites [66] Carrera-Bastos, P., Fontes-Villalba, M., O’Keefe, J. H., Lindeberg, S. & Cordain, L. The western diet and lifestyle and diseases of civilization. Res. Rep. Clin. Cardiol. 2, 15–35 (2011).
- Not checked yetcites [123] Sonnenburg, E. D. & Sonnenburg, J. L. The ancestral and industrialized gut microbiota and implications for human health. Nat. Rev. Microbiol. 17, 383–390 (2019). source
- Not checked yetcites [124] Bentley, J. U.S. trends in food availability and a dietary assessment of loss-adjusted food availability, 1970-2014. EIB-166, U.S. Department of Agriculture, Economic Research Service (2017).
- Not checked yetcites [125] Martínez Steele, E. et al. Ultra-processed foods and added sugars in the US diet: evidence from a nationally representative cross-sectional study. BMJ Open 6, e009892 (2016). source
plain- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
In the paper
“it has been hypothesized that a complex balance exists in the intestinal ecosystem that, if disrupted, can compromise its function and integrity and in turn cause low-grade SCI59.”
§ Chronic inflammation in the etiology of disease across the life span > Sources of systemic chronic inflammation > Microbiome dysbiosis.
What the sources say
- Not checked yetcites [59] Franceschi, C., Garagnani, P., Parini, P., Giuliani, C. & Santoro, A. Inflammaging: a new immune-metabolic viewpoint for age-related diseases. Nat. Rev. Endocrinol. 159, 1–15 (2018).
hedgeddirect- Asserted: fails — The authors may not put it forward as true.
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Probably not a substantial claim. The authors may not put it forward as true.
None of the sources cited for this claim have been checked yet.
In the paper
“serum concentrations of zonulin, a protein that increases intestinal permeability, appear to be elevated in obese children and adults117,119, and in persons with type 2 diabetes118, NAFLD, coronary heart disease, polycystic ovary syndrome, autoimmune diseases and cancer117.”
§ Chronic inflammation in the etiology of disease across the life span > Sources of systemic chronic inflammation > Microbiome dysbiosis.
What the sources say
- Not checked yetcites [117] Sturgeon, C. & Fasano, A. Zonulin, a regulator of epithelial and endothelial barrier functions, and its involvement in chronic inflammatory diseases. Tissue Barriers 4, e1251384 (2016). source
- Not checked yetcites [119] Küme, T. et al. The relationship between serum zonulin level and clinical and laboratory parameters of childhood obesity. J. Clin. Res. Pediatr. Endocrinol. 9, 31–38 (2017). source
- Not checked yetcites [118] Jayashree, B. et al. Increased circulatory levels of lipopolysaccharide (LPS) and zonulin signify novel biomarkers of proinflammation in patients with type 2 diabetes. Mol. Cell. Biochem. 388, 203–210 (2014). source
hedgedcorrelational- Asserted: passes — The authors put it forward as true.
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- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
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It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Obesity, which is strongly linked to changes in the gut microbiome, has also been associated with increased intestinal paracellular permeability and endotoxemia114,117.”
§ Chronic inflammation in the etiology of disease across the life span > Sources of systemic chronic inflammation > Microbiome dysbiosis.
What the sources say
- Not checked yetcites [114] Cani, P. D. & Jordan, B. F. Gut microbiota-mediated inflammation in obesity: a link with gastrointestinal cancer. Nat. Rev. Gastroenterol. Hepatol. 15, 671–682 (2018). source
- Not checked yetcites [117] Sturgeon, C. & Fasano, A. Zonulin, a regulator of epithelial and endothelial barrier functions, and its involvement in chronic inflammatory diseases. Tissue Barriers 4, e1251384 (2016). source
boostedcorrelational- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
In the paper
“salt has been shown to skew macrophages toward a pro-inflammatory phenotype characterized by the increased differentiation of naive CD4+ T cells into T helper (TH)-17 cells, which are highly inflammatory, and decreased expression and anti-inflammatory activity of T regulatory cells135”
§ Chronic inflammation in the etiology of disease across the life span > Sources of systemic chronic inflammation > Diet.
What the sources say
- Not checked yetcites [135] Muller, D. N., Wilck, N., Haase, S., Kleinewietfeld, M. & Linker, R. A. Sodium in the microenvironment regulates immune responses and tissue homeostasis. Nat. Rev. Immunol. 19, 243–254 (2019). source
boosteddirect- Asserted: passes — The authors put it forward as true.
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- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
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It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“These dietary factors can alter the gut microbiota composition and function123,127–130 and are linked to increased intestinal permeability129–131 and epigenetic changes in the immune system129 that ultimately cause low-grade endotoxemia and SCI129–131.”
§ Chronic inflammation in the etiology of disease across the life span > Sources of systemic chronic inflammation > Diet.
What the sources say
- Not checked yetcites [123] Sonnenburg, E. D. & Sonnenburg, J. L. The ancestral and industrialized gut microbiota and implications for human health. Nat. Rev. Microbiol. 17, 383–390 (2019). source
- Not checked yetcites [127] Chassaing, B., Van de Wiele, T., De Bodt, J., Marzorati, M. & Gewirtz, A. T. Dietary emulsifiers directly alter human microbiota composition and gene expression ex vivo potentiating intestinal inflammation. Gut 66, 1414–1427 (2017). source
- Not checked yetcites [128] Zmora, N., Bashiardes, S., Levy, M. & Elinav, E. The role of the immune system in metabolic health and disease. Cell Metab. 25, 506–521 (2017). source
- Not checked yetcites [129] Richards, J. L., Yap, Y. A., McLeod, K. H., Mackay, C. R. & Mariño, E. Dietary metabolites and the gut microbiota: an alternative approach to control inflammatory and autoimmune diseases. Clin. Trans. Immunol. 5, e82 (2016). source
- Not checked yetcites [130] Bishehsari, F. et al. Alcohol and gut-derived inflammation. Alcohol Res. 38, 163–171 (2017).
- Not checked yetcites [131] Lerner, A. & Matthias, T. Changes in intestinal tight junction permeability associated with industrial food additives explain the rising incidence of autoimmune disease. Autoimm. Rev. 14, 479–489 (2015). source
plaindirect- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
In the paper
“orally absorbed advanced glycation and lipoxidation end-products that are formed during the processing of foods or when foods are cooked at high temperatures and in low-humidity conditions are appetite increasing and are linked to overnutrition and hence obesity and inflammation132.”
§ Chronic inflammation in the etiology of disease across the life span > Sources of systemic chronic inflammation > Diet.
What the sources say
- Not checked yetcites [132] Vlassara, H. & Striker, G. E. AGE restriction in diabetes mellitus: a paradigm shift. Nat. Rev. Endocrinol. 7, 526–539 (2011). source
plaincorrelational- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“when combined with low physical activity, consuming hyperpalatable processed foods that are high in fat, sugar, salt and flavor additives147 can cause major changes in cell metabolism and lead to the increased production (and defective disposal) of dysfunctional organelles such as mitochondria, as well as to misplaced, misfolded and oxidized endogenous molecules30,60,148”
§ Chronic inflammation in the etiology of disease across the life span > Sources of systemic chronic inflammation > Diet.
What the sources say
- Not checked yetcites [30] Franceschi, C., Garagnani, P., Vitale, G., Capri, M. & Salvioli, S. Inflammaging and ‘garb-aging’. Trends Endocrinol. Metab. 28, 199–212 (2017). source
- Not checked yetcites [60] Zitvogel, L., Pietrocola, F. & Kroemer, G. Nutrition, inflammation and cancer. Nat. Immunol. 18, 843–850 (2017). source
- Not checked yetcites [148] van Niekerk, G., Toit, du, A., Loos, B. & Engelbrecht, A.-M. Nutrient excess and autophagic deficiency: explaining metabolic diseases in obesity. Metab. Clin. Exp. 82, 14–21 (2018). source
plaindirect- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“they are precursors to molecules such as resolvins, maresins and protectins that are involved in the resolution of inflammation28,29”
§ Chronic inflammation in the etiology of disease across the life span > Sources of systemic chronic inflammation > Diet.
What the sources say
- Not checked yetcites [28] Serhan, C. N. Pro-resolving lipid mediators are leads for resolution physiology. Nature 510, 92–101 (2014). source
- Not checked yetcites [29] Serhan, C. N. & Levy, B. D. Resolvins in inflammation: emergence of the pro-resolving superfamily of mediators. J. Clin. Invest. 128, 2657–2669 (2018). source
plaindirect- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
In the paper
“This specific population is critical for health as it regulates TH17 cells and enhances the integrity of the intestinal epithelial barrier, thus reducing systemic inflammation135”
§ Chronic inflammation in the etiology of disease across the life span > Sources of systemic chronic inflammation > Diet.
What the sources say
- Not checked yetcites [135] Muller, D. N., Wilck, N., Haase, S., Kleinewietfeld, M. & Linker, R. A. Sodium in the microenvironment regulates immune responses and tissue homeostasis. Nat. Rev. Immunol. 19, 243–254 (2019). source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“These factors include deficiencies in micronutrients, including zinc137 and magnesium138, which are caused by eating processed or refined foods that are low in vitamins and minerals”
§ Chronic inflammation in the etiology of disease across the life span > Sources of systemic chronic inflammation > Diet.
What the sources say
- Not checked yetcites [137] Bonaventura, P., Benedetti, G., Albarède, F. & Miossec, P. Zinc and its role in immunity and inflammation. Autoimm. Rev. 14, 277–285 (2015). source
- Not checked yetcites [138] Nielsen, F. H. Effects of magnesium depletion on inflammation in chronic disease. Curr. Opin. Clin. Nutr. Metab. Care 17, 525–530 (2014). source
plainconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“various RCTs have shown that omega-3 fatty acid supplementation reduces inflammation142–144 and may thus have health-promoting effects141–144”
§ Chronic inflammation in the etiology of disease across the life span > Sources of systemic chronic inflammation > Diet.
What the sources say
- Not checked yetcites [142] Kiecolt-Glaser, J. K. et al. Omega-3 supplementation lowers inflammation and anxiety in medical students: a randomized controlled trial. Brain Behav. Immun. 25, 1725–1734 (2011). source
- Not checked yetcites [143] Kiecolt-Glaser, J. K. et al. Omega-3 supplementation lowers inflammation in healthy middle-aged and older adults: a randomized controlled trial. Brain Behav. Immun. 26, 988–995 (2012). source
- Not checked yetcites [144] AbuMweis, S., Jew, S., Tayyem, R. & Agraib, L. Eicosapentaenoic acid and docosahexaenoic acid containing supplements modulate risk factors for cardiovascular disease: a meta-analysis of randomised placebo-control human clinical trials. J. Hum. Nutr. Diet. 31, 67–84 (2017). source
hedgeddirect- Asserted: passes — The authors put it forward as true.
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- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“These altered molecules, which increase with age19,30, can be recognized as DAMPs by innate immune cells, which in turn activate the inflammasome machinery, amplify the inflammatory response1,30,60 and contribute to a biological state that has been called “inflammaging,””
§ Chronic inflammation in the etiology of disease across the life span > Sources of systemic chronic inflammation > Diet.
What the sources say
- Not checked yetcites [1] Furman, D. et al. Expression of specific inflammasome gene modules stratifies older individuals into two extreme clinical and immunological states. Nat. Med. 23, 174–184 (2017). source
- Not checked yetcites [30] Franceschi, C., Garagnani, P., Vitale, G., Capri, M. & Salvioli, S. Inflammaging and ‘garb-aging’. Trends Endocrinol. Metab. 28, 199–212 (2017). source
- Not checked yetcites [60] Zitvogel, L., Pietrocola, F. & Kroemer, G. Nutrition, inflammation and cancer. Nat. Immunol. 18, 843–850 (2017). source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“increased exposure to artificial light, especially the blue spectrum, at atypical biologic times157–159. Exposure to blue light, especially after sundown, increases arousal and alertness at night and thus causes circadian rhythm disruption158,159”
§ Chronic inflammation in the etiology of disease across the life span > Sources of systemic chronic inflammation > Social and cultural changes.
What the sources say
- Not checked yetcites [157] Lunn, R. M. et al. Health consequences of electric lighting practices in the modern world: a report on the National Toxicology Program’s workshop on shift work at night, artificial light at night, and circadian disruption. Sci. Total Environ. 607–608, 1073–1084 (2017). source
- Not checked yetcites [158] Hatori, M. et al. Global rise of potential health hazards caused by blue light-induced circadian disruption in modern aging societies. NPJ Aging Mech. Dis. 3, 9 (2017). source
- Not checked yetcites [159] Touitou, Y., Reinberg, A. & Touitou, D. Association between light at night, melatonin secretion, sleep deprivation, and the internal clock: health impacts and mechanisms of circadian disruption. Life Sci. 173, 94–106 (2017). source
plaindirect- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“psychological stressors that are persistently present in some contemporary work environments, such as those characterized by high job demand and low control, can cause physiologic changes155 that disrupt the ability for glucocorticoids to effectively down-regulate inflammatory activity due to decreased sensitivity caused by chronic elevation in cortisol, leading in turn to SCI and poor health156”
§ Chronic inflammation in the etiology of disease across the life span > Sources of systemic chronic inflammation > Social and cultural changes.
What the sources say
- Not checked yetcites [155] Chandola, T., Brunner, E. & Marmot, M. Chronic stress at work and the metabolic syndrome: prospective study. BMJ 332, 521–525 (2006). source
- Not checked yetcites [156] Cohen, S. et al. Chronic stress, glucocorticoid receptor resistance, inflammation, and disease risk. Proc. Natl Acad. Sci. USA 109, 5995–5999 (2012). source
plaindirect- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“which in turn promotes inflammation160, and is a risk for multiple inflammation-related diseases157,159”
§ Chronic inflammation in the etiology of disease across the life span > Sources of systemic chronic inflammation > Social and cultural changes.
What the sources say
- Not checked yetcites [160] Leproult, R., Holmbäck, U. & Van Cauter, E. Circadian misalignment augments markers of insulin resistance and inflammation, independently of sleep loss. Diabetes 63, 1860–1869 (2014). source
- Not checked yetcites [157] Lunn, R. M. et al. Health consequences of electric lighting practices in the modern world: a report on the National Toxicology Program’s workshop on shift work at night, artificial light at night, and circadian disruption. Sci. Total Environ. 607–608, 1073–1084 (2017). source
- Not checked yetcites [159] Touitou, Y., Reinberg, A. & Touitou, D. Association between light at night, melatonin secretion, sleep deprivation, and the internal clock: health impacts and mechanisms of circadian disruption. Life Sci. 173, 94–106 (2017). source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“These compounds and others promote inflammatory activity via multiple mechanisms. For example, they can be cytotoxic8,162, cause oxidative stress or act as endocrine disruptors, starting in utero8”
§ Chronic inflammation in the etiology of disease across the life span > Sources of systemic chronic inflammation > Environmental and industrial toxicants.
What the sources say
- Not checked yetcites [8] Renz, H. et al. An exposome perspective: early-life events and immune development in a changing world. J. Allergy Clin. Immunol. 140, 24–40 (2017). source
- Not checked yetcites [162] Sly, P. D. et al. Health consequences of environmental exposures: causal thinking in global environmental epidemiology. Ann. Glob. Health 82, 3–9 (2016). source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
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It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“These chemicals are thus suspected of playing a causal role in hormone-dependent cancers, metabolic syndrome, type 2 diabetes, hypertension, CVD, allergy and asthma, and autoimmune and neurodegenerative diseases8,162,166”
§ Chronic inflammation in the etiology of disease across the life span > Sources of systemic chronic inflammation > Environmental and industrial toxicants.
What the sources say
- Not checked yetcites [8] Renz, H. et al. An exposome perspective: early-life events and immune development in a changing world. J. Allergy Clin. Immunol. 140, 24–40 (2017). source
- Not checked yetcites [162] Sly, P. D. et al. Health consequences of environmental exposures: causal thinking in global environmental epidemiology. Ann. Glob. Health 82, 3–9 (2016). source
- Not checked yetcites [166] Floreani, A., Leung, P. S. C. & Gershwin, M. E. Environmental basis of autoimmunity. Clin. Rev. Allergy Immunol. 50, 287–300 (2016). source
hedgedconditional- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
In the paper
“night-shift work has been found to increase risk for the metabolic syndrome and is suspected of being a causal factor in obesity, type 2 diabetes and CVD, as well as in breast, ovarian, prostate, colorectal and pancreatic cancer157”
§ Chronic inflammation in the etiology of disease across the life span > Sources of systemic chronic inflammation > Social and cultural changes.
What the sources say
- Not checked yetcites [157] Lunn, R. M. et al. Health consequences of electric lighting practices in the modern world: a report on the National Toxicology Program’s workshop on shift work at night, artificial light at night, and circadian disruption. Sci. Total Environ. 607–608, 1073–1084 (2017). source
hedgedconditional- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Each year, an estimated 2,000 new chemicals are introduced into items that individuals use or ingest daily, including foods, personal care products, prescription drugs, household cleaners and lawn care products”
§ Chronic inflammation in the etiology of disease across the life span > Sources of systemic chronic inflammation > Environmental and industrial toxicants.
hedged- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
In the paper
“The Tox21 Program has tested more than 9,000 chemicals using more than 1,600 assays and has demonstrated that numerous chemicals to which people are commonly exposed greatly alter molecular signaling pathways that underlie inflammation and inflammation-related disease risk164”
§ Chronic inflammation in the etiology of disease across the life span > Sources of systemic chronic inflammation > Environmental and industrial toxicants.
What the sources say
- Not checked yetcites [164] Kleinstreuer, N. C. et al. Phenotypic screening of the ToxCast chemical library to classify toxic and therapeutic mechanisms. Nat. Biotechnol. 32, 583–591 (2014). source
boosteddirect- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“the immune system is programmed during the prenatal period171 and is affected by epigenetic changes induced by maternal environmental exposures (for example, infectious agents, diet, psychological stress and xenobiotics) during intrauterine life and even before conception, when paternal factors may also have an epigenetic effect26,128,171”
§ Chronic inflammation in the etiology of disease across the life span > Developmental origins of systemic chronic inflammation
What the sources say
- Not checked yetcites [26] Singer, K. & Lumeng, C. N. The initiation of metabolic inflammation in childhood obesity. J. Clin. Invest. 127, 65–73 (2017). source
- Not checked yetcites [128] Zmora, N., Bashiardes, S., Levy, M. & Elinav, E. The role of the immune system in metabolic health and disease. Cell Metab. 25, 506–521 (2017). source
- Not checked yetcites [171] Macpherson, A. J., de Agüero, M. G. & Ganal-Vonarburg, S. C. How nutrition and the maternal microbiota shape the neonatal immune system. Nat. Rev. Immunol. 17, 508–517 (2017). source
hedgeddirect- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“exposure to psychological stress early in life—for example, in the form of abuse, neglect, maltreatment, bullying or living in a low socioeconomic environment—can heighten neural responses to threat that can upregulate inflammatory activity170, alter immuno-competence and lead to SCI throughout the lifecycle27,169”
§ Chronic inflammation in the etiology of disease across the life span > Developmental origins of systemic chronic inflammation
What the sources say
- Not checked yetcites [170] Slavich, G. M., Way, B. M., Eisenberger, N. I. & Taylor, S. E. Neural sensitivity to social rejection is associated with inflammatory responses to social stress. Proc. Natl Acad. Sci. USA 107, 14817–14822 (2010). source
- Not checked yetcites [27] Olvera Alvarez, H. A., Kubzansky, L. D., Campen, M. J. & Slavich, G. M. Early life stress, air pollution, inflammation, and disease: an integrative review and immunologic model of social-environmental adversity and lifespan health. Neurosci. Biobehav. Rev. 92, 226–242 (2018). source
- Not checked yetcites [169] Fagundes, C. P., Glaser, R. & Kiecolt-Glaser, J. K. Stressful early life experiences and immune dysregulation across the lifespan. Brain Behav. Immun. 27, 8–12 (2013). source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“Because obese children often become obese adolescents and adults26, the risk of developing a pro-inflammatory phenotype also frequently persists into adulthood among individuals who were obese as children”
§ Chronic inflammation in the etiology of disease across the life span > Developmental origins of systemic chronic inflammation
What the sources say
- Not checked yetcites [26] Singer, K. & Lumeng, C. N. The initiation of metabolic inflammation in childhood obesity. J. Clin. Invest. 127, 65–73 (2017). source
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
The paper relies on this without support.
There are currently no standard biomarkers for indicating the presence of health-damaging chronic inflammation.
“there are presently no standard biomarkers for indicating the presence of health-damaging chronic inflammation.”
The authors state this as an assumption.
An evolutionary mismatch between human physiology and industrialized lifestyles is a major cause of systemic chronic inflammation.
“This is believed to have created an evolutionary mismatch in humans—characterized by an increasing separation from their ecological niche—and this mismatch, in turn, has been hypothesized to be a major cause of SCI65,66,82,89,92.”
The authors state this as an assumption.
Maternal inflammation during pregnancy passes an inflammatory code through epigenetic modifications to offspring, leading to elevated SCI risk in childhood and adulthood and intergenerational transmission of risk.
“In this model (Fig. 2), SCI and disease risk are hypothesized to be perpetuated transgenerationally.”
“maternal inflammation during pregnancy172,173 is believed to pass an inflammatory ‘code’ through epigenetic modifications to the offspring”
The paper relies on this without support.
A majority of older adults experience down-regulation of immune response components, leading to increased susceptibility to viral infections and weakened vaccine responses.
“Despite the observation that SCI generally increases with age, a majority of older adults experience a down-regulation of components of the immune response that leads to an increased susceptibility to viral infections and weakened responses to vaccines.”
The paper relies on this without support.
No study to date has assessed the entire human exposome over the entire developmental trajectory.
“no study to date has assessed the entire human exposome over the entire developmental trajectory”
The paper relies on this without support.
Only a few studies have investigated how modifying SCI-related processes may benefit human health or longevity.
“only a few studies have investigated how modifying SCI-related processes may benefit human health or longevity”
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 source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“Reductions in CRP levels can be instead achieved by lifestyle interventions that promote better overall health (Furman et al., 2019).”
From Treatment of periodontitis and C ‐reactive protein: A systematic review and meta‐analysis of randomized clinical trials (2023) · cites this paper as Furman et al., 2019
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“Systemic inflammation as assessed by high CRP levels raises the future risk of chronic diseases and their complications like diabetes, renal and CVDs (Libby et al., 2018; Furman et al., 2019).”
From Treatment of periodontitis and C ‐reactive protein: A systematic review and meta‐analysis of randomized clinical trials (2023) · cites this paper as Furman et al., 2019
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“At the same time, inflammation promotes oxidation through inflammatory mediators.205,206”
From Inflammation and aging: signaling pathways and intervention therapies (2023) · cites this paper as [206]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“Periodontitis is a local inflammation and a source of low-grade chronic inflammation, which results from haematogenous dissemination of periodontal bacteria or spillover of inflammatory mediators from periodontal tissues to the bloodstream [4, 9], thus contributing to the systemic inflammatory burden, increasing the risk of several chronic diseases like CVD, type II diabetes mellitus (T2DM), renal”
From Effect of non-surgical periodontal therapy on risk markers of cardiovascular disease: a systematic review and meta-analysis (2024) · cites this paper as [10]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“Chronic inflammation has been shown to greatly increase the risk for LOAD (Furman et al., 2019).”
From Plcg2M28L Interacts With High Fat/High Sugar Diet to Accelerate Alzheimer’s Disease-Relevant Phenotypes in Mice (2022) · cites this paper as Furman et al., 2019
Experimental — accuracy not yet measured
The cited source says what the claim attributes to it.
In the citing paper
“Low‐grade inflammation has been however linked to several chronic diseases like cardiovascular diseases (CVDs), type II diabetes mellitus (T2DM), renal diseases (CKD), cancer and neurodegenerative disorders (Furman et al., 2019).”
From Treatment of periodontitis and C ‐reactive protein: A systematic review and meta‐analysis of randomized clinical trials (2023) · cites this paper as Furman et al., 2019
In the citing paper
“The immune system undergoes numerous and profound changes with aging, which are extensively reviewed elsewhere (3–5).”
From Connecting aging biology and inflammation in the omics era (2022) · cites this paper as [5]
In the citing paper
“Efforts to characterize inflammation in humans have relied on one or a few inflammatory proteins, with IL-6, TNF-α, and CRP being the most widely used (5).”
From Connecting aging biology and inflammation in the omics era (2022) · cites this paper as [5]
In the citing paper
“It is generally accepted that inflammageing occurs in response to an accumulation of exogeneous and endogenous physiological stresses over time and is primarily mediated by immune cells and senescent cells (Figure 1)14,15.”
From SARS-CoV-2, COVID-19 and the aging immune system (2021) · cites this paper as [15]
In the citing paper
“Inflammageing is now being recognized as a hallmark of ageing and a key driver of disease (FIG. 3Aa), including ageing-associated diseases, and has been described as a prominent risk factor for morbidity and death95–97.”
From NAD+ metabolism and its roles in cellular processes during ageing (2021) · cites this paper as [97]
In the citing paper
“Endogenous cytoDNA is a contributor to so-called sterile inflammation, inflammation in the absence of pathogenic infection, which is associated with many chronic age-associated conditions, including cancer, cardiovascular disease, and neurodegenerative disorders (Ferrucci and Fabbri, 2018; Franceschi et al., 2007; Furman et al., 2019).”
From Cytoplasmic DNA: sources, sensing, and role in aging and disease (2021) · cites this paper as Furman et al., 2019
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Metadata
- Authors
- Furman, D., Campisi, J., Verdin, E., Carrera-Bastos, P., Targ, S., Franceschi, C., Ferrucci, L., Gilroy, D. W., Fasano, A., Miller, G. W., Miller, A. H., Mantovani, A., Weyand, C. M., Barzilai, N., Goronzy, J. J., Rando, T. A., Effros, R. B., Lucia, A., Kleinstreuer, N., & Slavich, G. M.
- Affiliations
- Buck Institute for Research on Aging (US)
- University of California, San Francisco (US)
- N. I. Lobachevsky State University of Nizhny Novgorod (RU)
- National Institute on Aging (US)
- University College London (GB)
- Harvard University (US)
- Columbia University Irving Medical Center (US)
- Emory University (US)
- Humanitas University (IT)
- Stanford Medicine (US)
- Albert Einstein College of Medicine (US)
- VA Palo Alto Health Care System (US)
- University of California, Los Angeles (US)
- National Institutes of Health (US)
- Corresponding author
- Furman, David
- ORCID
- Venue
- Nature Medicine
- Published
- 2019-12
- Volume
- 25
- Issue
- 12
- Pages
- 1822-1832
- ISSN
- 1078-8956 (ISSN-L)
- 1546-170X
- PMC
- PMC7147972
- OpenAlex
- W2993908729
- Cited by
- 4,915
- References
- 181
- Citations by year
- 2026: 783 · 2025: 953 · 2024: 969 · 2023: 839 · 2022: 691 · 2021: 465 · 2020: 210 · 2019: 2
- FWCI
- 49.98
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Nature Medicine (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- ABACUS. Repositorio de Producción Científica (Universidad Europea) (submittedVersion)
- UCL Discovery (University College London) (submittedVersion)
- Lund University Publications (Lund University) (submittedVersion)
- Funders
- U.S. Department of Health & Human Services | National Institutes of Health
- Stanford Center on Longevity
- Buck Institute for Research on Aging
- Topics
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Adipokines, Inflammation, and Metabolic Diseases
- Health Sciences › Medicine › Physiology (medical) › Exercise and Physiological Responses
- Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
- Keywords
- chronic systemic inflammation, lifespan, cardiovascular disease, cancer, diabetes mellitus, chronic kidney disease, non-alcoholic fatty liver disease, autoimmune disease, neurodegenerative diseases, infection, physical inactivity, unhealthy diet, environmental toxins, industrial toxicants, psychological stress, early diagnosis, prevention, treatment
- MeSH terms
- Autoimmune Diseases, Cardiovascular Diseases, Chronic Disease, Diabetes Mellitus, Humans, Inflammation, Life Style, Longevity, Neoplasms, Risk Factors, Neurodegenerative Diseases, Renal Insufficiency, Chronic, Non-alcoholic Fatty Liver Disease
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.
A language model drew the claims from the paper on 2026-10-05, under version 3 of the claim definition (model deepseek-v4.1-flash, prompt extract-v3).
A second model labelled each claim on 2026-10-05 (model jev-1.13-20260917, definition revision gold-guideline-v0.2).
Cited sources are checked with a language model’s help (gpt-6-sol).
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.
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