What Is Inflammaging? Causes, Health Effects, and Ways to Reduce Inflammation

Add News Medical on Googleas a preferred source By Hugo Francisco de SouzaReviewed by Benedette Cuffari, M.Sc. IntroductionWhy does inflammation increase with age?The biological mechanisms behind inflammagingHow inflammaging contributes to age-related diseasesThe role of the gut microbiome in inflammagingCan lifestyle changes reduce inflammaging?Targeting inflammation to promote healthy agingReferencesFurther reading

As the body ages, subtle changes in immune function can fuel persistent inflammation. Scientists are uncovering the cellular processes behind this phenomenon and investigating whether diet, exercise, and emerging therapies could change its course.

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Acute inflammation is a protective immune response to injury or infection that normally resolves after the trigger is cleared and tissue repair proceeds. Chronic inflammation can develop when inflammatory triggers persist, or the mechanisms that regulate and resolve inflammation become impaired.1

Inflammaging is commonly described as a state of persistent, low-grade, and chronic inflammation that develops with advancing age, often without an overt infection.1 It is a research concept without a single, universally accepted diagnostic threshold.1,4 Over time, inflammaging can compromise tissue integrity, disrupt immune function, and contribute to age-related functional decline.1 It is associated with cardiovascular disease (CVD), neurodegeneration, metabolic disorders, and physical frailty, all of which contribute to age-related multimorbidity.4

Immunosenescence, which refers to age-related changes in immune function, contributes to impaired pathogen defense and clearance of damaged or senescent cells. These changes can coexist with persistent inflammatory signaling, linking immunosenescence and inflammaging in a mutually reinforcing relationship.1 Simultaneously, telomere attrition, mitochondrial dysfunction, and oxidative stress promote cellular senescence and damage. Molecules released or exposed by damaged cells can act as damage-associated molecular patterns (DAMPs) to activate inflammatory pathways.1,3

The exposome refers to an individual’s lifetime environmental exposures and includes influences associated with lifestyle factors like physical activity, diet, and stress.4 Physical inactivity, poor diet, and psychological stress are among the factors associated with systemic chronic inflammation.2 Visceral obesity is another recognized contributor.4 As adipose tissue expands, immune cell infiltration and the accumulation of senescent cells can increase inflammatory mediator production, thereby compounding the inflammatory burden associated with aging.1

At the molecular level, inflammaging involves dysregulated inflammatory signaling, including changes in cytokine levels, particularly interleukin-6 (IL-6), IL-1β, and tumor necrosis factor-alpha (TNF-α), and various chemokines.3 The senescence-associated secretory phenotype (SASP), which includes inflammatory cytokines, chemokines, and tissue-remodeling enzymes, is one contributor to this persistent inflammatory state.1

Some aging cells enter a state of stable cell-cycle arrest, meaning they stop dividing, and become resistant to apoptosis, or programmed cell death.1 The SASP produced by these senescent cells can damage surrounding healthy tissues, thereby inducing secondary senescence and degrading the extracellular matrix.1 Temporary senescence and its associated signaling support tumor suppression and wound healing; persistent senescent cells and inadequate clearance can sustain tissue damage.1,10

Persistent immune signaling can also alter transcriptional and epigenetic regulation, changing gene activity and impairing the functions of specialized cells without necessarily killing them.5 Impaired autophagy, the cellular process that breaks down and recycles damaged components, and excessive reactive oxygen species (ROS) can promote activation of the NLRP3 inflammasome.1,3 NLRP3 is the sensor within this multiprotein complex, which activates caspase-1 to process the inflammatory cytokines IL-1β and IL-18. These pathways can sustain a reinforcing cycle of cellular damage and inflammation.1,3

Cell senescence plays a central role in inflammageing. A variety of stressors promote cell senescence, including age-related telomere attrition, DNA damage, oxidative stress, proteostatic stress, and oncogene activation. Senescence of immune cells can lead to immune failure, while age-related decreased immunity results in the poor immunological clearance of senescent cells. Obesity is associated with a pro-inflammatory state that can drive senescence, with senescent cells detected in adipose tissue; it also predisposes sufferers to diabetes, wherein altered blood sugar control may trigger senescence through glycation and metabolic stress. Inflammation is a primary response to infection, but some inflammatory signals (e.g., IL-6) can promote cell senescence. Moreover, certain viral and bacterial infections can also drive senescence. The pro-inflammatory secretome produced by senescent cells is associated with age-related diseases. Hence, senescent cells lie at the heart of a multi-faceted vicious circle leading to increased inflammation, age-related diseases, and ultimately, death. 1

In cardiovascular disease, chronic inflammation contributes to vascular dysfunction and atherosclerosis, with clinical trials supporting a causal role for inflammation in cardiovascular events.4 Inflammatory signaling also interferes with metabolic regulation. For example, experimental studies link obesity-related NLRP3 activation and IL-1β production to impaired insulin signaling.3 In the central nervous system, inflammatory signaling and altered immune cell activity are implicated in Alzheimer’s disease and other neurodegenerative disorders.1,3

Inflammaging may contribute to disease development across multiple organ systems, but the strength of causal evidence varies by condition.4 The inflammatory aging clock, iAge, was developed using deep learning and blood immune profiles from 1,001 individuals aged 8–96 years. The resulting score tracked multimorbidity, immunosenescence, frailty, and cardiovascular aging. CXCL9 was its strongest contributor and was implicated in cardiac and vascular dysfunction.6 These findings support further research, but do not establish iAge as a routine clinical test for individual risk assessment or treatment selection.6

Image Credit: Corona Borealis Studio / Shutterstock.com

Aging can be accompanied by changes in gut microbial composition and diversity, but severe dysbiosis is not universal among older adults.1,7 Reported changes include shifts in short-chain fatty acid (SCFA)-producing bacteria and increases in taxa associated with inflammatory markers. A systematic review identified seven relevant studies, six in animals and one in humans, limiting conclusions about causality in people.7

Age-related dysbiosis may interact with impaired intestinal epithelial barrier function, leading to increased intestinal permeability. Microbial products like lipopolysaccharides can then cross the barrier and stimulate innate immune receptors, potentially sustaining systemic inflammation.1,7

Modulating lifestyle factors offers a non-pharmacological approach to reducing chronic inflammation.1,9 For example, regular physical activity can reduce visceral adiposity and influence inflammatory signaling through muscle-derived myokines.9 Structured exercise, including aerobic, resistance, and combined training, can lower resting C-reactive protein (CRP) and TNF-α levels in older adults. Findings for IL-6 are less consistent, and responses vary across studies and exercise programs. Temporary increases in cytokines during exercise are distinct from persistent resting inflammation.9

Diets rich in fiber and plant-based foods, such as the Mediterranean diet, can influence gut microbial composition and the production of SCFAs, which participate in intestinal barrier and immune regulation.1,8 In a randomized study of 38 middle-aged female macaques, a Mediterranean-type diet increased Oscillospira abundance and fecal acetate and propionate compared with a Western-type diet. These findings support a diet–microbiome relationship but do not establish that the same intervention reduces inflammaging in humans.8

Geroscience research is investigating pharmacological interventions like senolytics, agents that selectively clear senescent cells, to reduce SASP-associated inflammation. Evidence includes animal studies and early human trials, which have reported changes in senescence and inflammatory markers; benefits for human lifespan or prevention of age-related multimorbidity remain unproven.1 Other approaches focus on metabolic modifiers, such as mechanistic target of rapamycin (mTOR) inhibitors and metformin, which can affect autophagy and inflammatory signaling. Their effects differ by drug and experimental context, and available evidence does not establish them as treatments for inflammaging in otherwise healthy adults.1

Microbiome-directed approaches are also under investigation, but evidence that they reliably reverse inflammaging in humans remains limited.1,7 Any intervention must balance the reduction of persistent inflammation with preservation of the immune responses needed for pathogen clearance and tissue repair.1,10

Further ReadingAll Inflammaging ContentA Guide to Healthy AgingGut Microbiome and Aging: How Gut Bacteria Influence Health and LongevityYour Biological Age vs. Chronological Age: Why It MattersIs Cellular Senescence the Real Cause of Aging?More… 

Hugo Francisco de Souza is a scientific writer based in Bangalore, Karnataka, India. His academic passions lie in biogeography, evolutionary biology, and herpetology. He is currently pursuing his Ph.D. from the Centre for Ecological Sciences, Indian Institute of Science, where he studies the origins, dispersal, and speciation of wetland-associated snakes. Hugo has received, amongst others, the DST-INSPIRE fellowship for his doctoral research and the Gold Medal from Pondicherry University for academic excellence during his Masters. His research has been published in high-impact peer-reviewed journals, including PLOS Neglected Tropical Diseases and Systematic Biology. When not working or writing, Hugo can be found consuming copious amounts of anime and manga, composing and making music with his bass guitar, shredding trails on his MTB, playing video games (he prefers the term ‘gaming’), or tinkering with all things tech.

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Francisco de Souza, Hugo. "What Is Inflammaging? Causes, Health Effects, and Ways to Reduce Inflammation". News-Medical. https://www.news-medical.net/health/What-Is-Inflammaging-Causes-Health-Effects-and-Ways-to-Reduce-Inflammation.aspx. (accessed October 20, 2026).

Francisco de Souza, Hugo. 2026. What Is Inflammaging? Causes, Health Effects, and Ways to Reduce Inflammation. News-Medical, viewed 20 October 2026, https://www.news-medical.net/health/What-Is-Inflammaging-Causes-Health-Effects-and-Ways-to-Reduce-Inflammation.aspx.

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