Inflammation and aging combine to create “inflammaging.”
Dicken Weatherby, N.D. and Beth Ellen DiLuglio, MS, RDN, LDN
Aging has been associated with a perpetual inflammatory cascade that involves IL-1alpha, IL-6, and NF-kappa B. Inflammaging refers to chronic low-grade systemic inflammation associated with aging but not caused by an infectious agent.
This age-related cytokine dysregulation can contribute to chronic diseases such as Alzheimer’s, atherosclerosis, diabetes, rheumatoid arthritis, cancer, etc. [1]
Sources of inflammaging include:[2]
- Buildup of cellular debris
- Microbial byproducts and toxins, especially translocation from the gut or oral cavity
- Mitochondrial activation of the Nlrp3 inflammasome
- Cellular senescence
- Immunosenescence with decreased adaptive immunity and increased innate immunity
- Increased activation of coagulation
- Impaired regulation of the complement pathway
- Note there is a paradox for individuals over the age of 100 (centenarians) who appear to adapt to higher plasma IL-6 and IL-8, hypercoagulability, and decreased antioxidant status without the development of chronic diseases such as diabetes, cancer, and CVD, possibility because of adequate anti-inflammatory mechanisms.
Biomarkers of inflammation [3] [4] [5] [6]
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Asymmetric dimethylarginine (ADMA) Basophils Ceruloplasmin Cholesterol, total, HDL Eosinophil Erythrocyte sedimentation rate (ESR) Hs-CRP IL-1, IL-6, IL-8, IL-10, IL-17 Iron Ferritin Fibrinogen |
Globulin Haptoglobin Homocysteine IgA, IgE, IgG Insulin LDH Liver enzymes (ALT, AST, GGT, LDH, alkaline phosphatase) Lp-PLA2, Lp-PLA2 activity Neutrophil/lymphocyte ratio Oxidative stress markers (8-OHdG, isoprostanes, malondialdehyde) |
Oxidized LDL Platelets PSA RDW Rheumatoid factor Serum amyloid A (SAA) TNF-alpha Triglycerides Uric acid Vitamin D 25-OH White blood cells (elevated) |
Optimal Takeaways
So, our basic takeaways for an overview of inflammation include:
- Inflammation is a defense mechanism triggered by pathogens, toxins, radiation, injury, etc.
- Short-term inflammation is beneficial, while prolonged, chronic inflammation is detrimental.
- Persistent inflammation is associated with many chronic diseases including cardiovascular disease, diabetes, cancer, neurodegenerative disease, etc.
- The inflammatory cascade is complex and can become perpetual.
- Several biomarkers reflect an inflammatory state in the body and can be monitored and addressed.
- In this blog series, we will focus on cytokines and inflammation, biomarkers and monitoring, and dietary and lifestyle factors that affect inflammation perpetuation and resolution.
References
[1] Rea, Irene Maeve et al. “Age and Age-Related Diseases: Role of Inflammation Triggers and Cytokines.” Frontiers in immunology vol. 9 586. 9 Apr. 2018.
[2] Franceschi, Claudio, and Judith Campisi. “Chronic inflammation (inflammaging) and its potential contribution to age-associated diseases.” The journals of gerontology. Series A, Biological sciences and medical sciences vol. 69 Suppl 1 (2014): S4-9.
[3] Moeller, Mark et al. “Mortality is associated with inflammation, anemia, specific diseases and treatments, and molecular markers.” PloS one vol. 12,4 e0175909. 19 Apr. 2017.
[4] Martínez-Urbistondo D, Beltrán A, Beloqui O, Huerta A. The neutrophil-to-lymphocyte ratio as a marker of systemic endothelial dysfunction in asymptomatic subjects. Nefrologia. 2016 Jul-Aug;36(4):397-403. English, Spanish.
[5] Chen, Linlin et al. “Inflammatory responses and inflammation-associated diseases in organs.” Oncotarget vol. 9,6 7204-7218. 14 Dec. 2017.
[6] Mahan, L. Kathleen; Raymond, Janice L. Krause's Food & the Nutrition Care Process - E-Book (Krause's Food & Nutrition Therapy). Elsevier Health Sciences. Kindle Edition.