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Low-grade chronic inflammation: the topic in science communication and the international press in 2026

by luciano

Communication analysis document: how the topic is presented, interpreted, and communicated by the international scientific and general press
This article is part of a three-part series:
1. Integrated approach to reducing low-grade chronic inflammation — the operational document: which behaviors and strategies to adopt.
2. Integrated approach to reducing low-grade chronic inflammation in light of 2026 scientific research — the scientific verification document: which elements of the Approach are supported by the most recent literature and with what degree of evidence.
3. Low-grade chronic inflammation: the topic in science communication and the international press in 2026 — the communication analysis document: how the topic is presented, interpreted, and communicated by the international scientific and general press.
Introduction
Interest in low-grade chronic inflammation in 2026 has not remained confined to the specialist literature. The topic has also been covered by major Italian and international publications, from different but converging perspectives: nutrition, microbiota, cardiovascular health, stress, biological aging, and the immune system. This attention in science communication does not constitute additional scientific evidence, but shows how the concept of low-grade chronic inflammation and inflammaging is increasingly entering the debate on prevention, longevity, and lifestyles.

Italian and international press review

1. Corriere Style – April 10, 2026
Infiammazione cronica: come contrastarla con alimentazione e stile di vita
The article presents low-grade chronic inflammation as an often silent condition and points to nutrition and lifestyle as tools for prevention and control. It is particularly close to the general framework of the Integrated Approach, although it is a journalistic science communication article. [1]
2. Corriere della Sera / Salute – July 8, 2026
Longevità: i «segreti» per spegnere l’infiammazione cronica del cuore
The article links chronic inflammation, atherosclerosis, cardiovascular prevention, and longevity. It also discusses the role of inflammation in atherosclerotic disease and the clinical significance of the CANTOS study. It is useful because it shows how the topic of persistent inflammation has now also entered cardiovascular science communication. [2]
3. la Repubblica / Salute – July 17, 2026
Un diffusissimo addensante alimentare può infiammare l’intestino e alterare il microbiota
The article reports on research concerning xanthan gum (E415) and the possible effects of prolonged daily consumption on the colon and microbiota. Its interest, in the context of the Integrated Approach, is mainly methodological: it shows why additives continue to be the subject of research and why it may be reasonable to apply a precautionary principle, without turning a single study into a general condemnation of food additives. [3]
4. The Guardian – April 24, 2026
Food for thought: Is your diet ageing you?
The article addresses the relationship between nutrition and aging through several mechanisms: refined carbohydrates, advanced glycation end products, visceral fat, fiber, omega-3, intestinal integrity, and immunosenescence. It is a good example of international science communication that interprets aging as a systemic phenomenon rather than simply an effect of chronological age. [4]
5. The Washington Post – June 11, 2026
The midlife habits that could make or break your brain health long-term
The article describes the growing focus of dementia-prevention research on midlife and emphasizes that cognitive decline depends not only on changes in the brain, but also on the accumulation over time of metabolic stress, inflammation, and vascular damage throughout the body. The connection with the Integrated Approach is therefore primarily systemic. [5]
6. El País / Salud y Bienestar – April 16, 2026
Relacionarse con personas tóxicas (sobre todo en la familia o el trabajo) acelera el envejecimiento
The article reports the results of a study on negative social relationships, associated with greater inflammation and accelerated biological aging. It is particularly interesting because it broadens the perspective beyond diet and physical activity and provides science-communication support for the role assigned in the Integrated Approach to persistent stress and psychophysical regulation. [6]

International science communication: Nature

7. Nature Reviews Immunology – February 13, 2026
The ageing immune system as a driver of systemic ageing
The review describes how biochemical and functional changes in immune cells with age may contribute to chronic inflammation, reduced response to pathogens, and organ dysfunction. It is a high-level reference for the relationship among immunosenescence, inflammaging, and systemic aging. [7]
8. Nature Reviews Immunology – April 23, 2026
The long-lived immune system of centenarians
The review considers centenarians as a biologically distinctive population in which exceptional longevity, relative preservation of immune function, and resistance to some aspects of immunosenescence and inflammaging may coexist. Among other topics, NLRP3, autophagy, and SASP are discussed. [8]
9. npj Aging / Nature Portfolio – February 26, 2026
From wrist data to lifespan: elucidating inflammation-driven biological aging via activity rhythms captured by wearable devices
The study links inflammaging, biological aging, and activity rhythms measured through wearable devices. It is interesting because it shows the transition from an exclusively molecular interpretation of aging to models that integrate biomarkers, everyday behavior, and longitudinal measurements. [9]
A convergence of perspectives
Overall, this review shows an interesting convergence. The publications do not all tell the same story: The Guardian approaches the topic through nutrition and aging; The Washington Post through brain health and prevention; El País through stress and social relationships; Corriere through cardiovascular prevention and lifestyle; la Repubblica through microbiota and additives; Nature through the immunology of aging and new measurement tools. This plurality of perspectives itself reflects the multidimensional nature of low-grade chronic inflammation also highlighted by the 2026 scientific literature.
Methodological note
The journalistic articles cited above are included as documentation of science communication and media coverage of the topic in 2026. They do not have the same evidentiary value as peer-reviewed scientific studies and are not used as independent proof of the effectiveness of the Integrated Approach. The three publications from the Nature group are instead scientific works and are also cited here because of their particular relevance in international science communication.
Sources and references
[1] Corriere Style. “Infiammazione cronica: come contrastarla con alimentazione e stile di vita”. April 10, 2026.
[2] Corriere della Sera / Salute. “Longevità: i «segreti» per spegnere l’infiammazione cronica del cuore”. July 8, 2026.
[3] la Repubblica / Salute. “Un diffusissimo addensante alimentare può infiammare l’intestino e alterare il microbiota”. July 17, 2026.
[4] The Guardian. “Food for thought: Is your diet ageing you?”. April 24, 2026.
[5] The Washington Post. “The midlife habits that could make or break your brain health long-term”. June 11, 2026.
[6] El País / Salud y Bienestar. “Relacionarse con personas tóxicas (sobre todo en la familia o el trabajo) acelera el envejecimiento”. April 16, 2026.
[7] Jang IH, Niedernhofer LJ, Robbins PD, Camell CD. The ageing immune system as a driver of systemic ageing. Nature Reviews Immunology. 2026;26:489–506. DOI: 10.1038/s41577-026-01269-3.
[8] Plaza-Florido A, et al. The long-lived immune system of centenarians. Nature Reviews Immunology. 2026. DOI: 10.1038/s41577-026-01291-5.
[9] Shim J, Bishehsari F, Mahdavinia M, Zeitzer JM, Fleisch E, Barata F. From wrist data to lifespan: elucidating inflammation-driven biological aging via activity rhythms captured by wearable devices. npj Aging. 2026;12:49. DOI: 10.1038/s41514-026-00349-x.
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Integrated approach to reducing low-grade chronic inflammation in light of 2026 scientific research

by luciano

Scientific verification document: which elements of the Approach are supported by the most recent literature and with what degree of evidence
This article is part of a three-part series:
1. Integrated approach to reducing low-grade chronic inflammation — the operational document: which behaviors and strategies to adopt.
2. Integrated approach to reducing low-grade chronic inflammation in light of 2026 scientific research — the scientific verification document: which elements of the Approach are supported by the most recent literature and with what degree of evidence.
3. Low-grade chronic inflammation: the topic in science communication in the international press in 2026 — the communication analysis document: how the topic is presented, interpreted, and communicated by the international scientific and general press.
Introduction
The Integrated Approach to reducing low-grade chronic inflammation considers this phenomenon not as the result of a single factor, but as the expression of the interaction among nutrition, metabolism, body composition, physical activity, muscle function, gut microbiota, sleep, circadian rhythms, stress, and the biological processes of aging.
Scientific research published in 2026 provides several points of support for this framework. In particular, recent literature on inflammaging describes low-grade chronic inflammation as a systemic and multifactorial process in which cellular senescence, mitochondrial dysfunction, metabolic alterations, changes in immune function, microbiota, nutrition, physical activity, and environmental and behavioral factors converge [1].
Not all elements of the Integrated Approach have the same level of evidence, and it would not be correct to interpret the convergence among different studies as experimental proof of the entire model. What is relevant is that numerous components of the Approach are supported, separately and sometimes jointly, by the most recent scientific literature. This chapter therefore distinguishes among direct support, mechanistic support, and general consistency with the evidence.
1. Low-grade chronic inflammation as a systemic phenomenon
Support for the Integrated Approach
One of the fundamental premises of the Integrated Approach is that low-grade chronic inflammation should not be interpreted exclusively as a local phenomenon or as the consequence of a single disease. Instead, it may represent a systemic biological state arising from the interaction of multiple mechanisms.
2026 Research
Andrea Cossarizza’s review, “Inflammaging: Experimental Insights and Translational Advances,” published in the European Journal of Immunology, defines inflammaging as persistent, sterile, low-grade inflammation associated with aging and analyzes a network of mechanisms including cellular senescence, the senescence-associated secretory phenotype (SASP), mitochondrial dysfunction, immune-cell senescence, hyperactivation of innate immunity, defective resolution of inflammation, and dysregulation of nutrient-sensing systems [1].
Assessment of the evidence
The support is strong. The work directly supports the systemic and multifactorial conception adopted in the Integrated Approach: low-grade chronic inflammation emerges as the result of interconnected biological networks rather than as the linear consequence of a single causal element.
2. Nutrition as a modulator of inflammation
Support for the Integrated Approach
The Integrated Approach assigns nutrition an important but not exclusive role. Diet is considered one of the main modifiable factors capable of influencing chronic inflammation through different metabolic, oxidative, immune, and microbiota-related pathways.
2026 Research
The review “Dietary Bioactive Compounds and Inflammaging: Pro- and Anti-Inflammatory Effects” analyzes both dietary components capable of promoting the activation of inflammatory pathways — including advanced glycation end products, lipid peroxidation products, oxysterols, and trans fats — and bioactive compounds with potentially modulatory effects, including polyphenols, omega-3 fatty acids, carotenoids, vitamins, and certain micronutrients. The authors describe multiple molecular pathways involved, including NF-κB, Nrf2, sirtuins, and inflammation-resolution systems [2].
Assessment of the evidence
The support is strong at the biological level and consistent with an essential point of the Approach: not attributing to a single food the ability to “switch off” inflammation, but interpreting nutrition as a modulator of a complex biological network. The effect must be assessed within the context of the overall dietary pattern and the individual’s other physiological and behavioral conditions.
3. Physical activity and control of inflammatory pathways
Support for the Integrated Approach
In the Integrated Approach, physical activity is not considered simply a tool for increasing energy expenditure. Exercise modifies the functioning of numerous metabolic and immune systems and may contribute to regulation of the inflammatory state.
2026 Research
The review “Exercise-Mediated Modulation of the NLRP3 Inflammasome” analyzes one of the mechanisms through which exercise may influence inflammation: modulation of the NLRP3 inflammasome. The authors report that physical activity can reduce NLRP3 activation through different interconnected biological pathways, within a framework in which mitochondrial dysfunction, oxidative stress, and metabolic alterations contribute to inflammaging [3].
Assessment of the evidence
The support is primarily mechanistic but important. It strengthens the decision to consider movement as an autonomous component of the Approach, closely connected with metabolism, body composition, and muscle function.
4. Skeletal muscle, myokines, and systemic communication
Support for the Integrated Approach
The Approach considers skeletal muscle a metabolically active organ and not merely a structure responsible for movement. During and after exercise, muscle produces signaling molecules capable of interacting with other organs and systems.
2026 Research
The review “The Myokine Adaptome in Health and Disease: Exercise-Induced Cellular Signaling, Muscle–Organ Crosstalk, and Therapeutic Plasticity” proposes the concept of the myokine adaptome, namely a context-dependent signaling network through which skeletal muscle translates contractile, metabolic, mechanical, and inflammatory stimuli into systemic effects. Myokines and exerkines participate in communication with other organs and influence glucose and lipid metabolism, immune regulation, vascular function, neuroplasticity, and tissue regeneration [4].
Assessment of the evidence
The support is strong for the general concept of muscle as an endocrine and metabolic organ. Prudence is nevertheless required regarding the clinical effects attributed to individual myokines, because part of the evidence remains experimental or context-dependent.
5. Metabolism and inflammation
Support for the Integrated Approach
Another central element of the Approach is the bidirectional relationship between metabolic alterations and inflammatory status. Insulin resistance, visceral adiposity, alterations in glucose and lipid metabolism, and mitochondrial dysfunction do not necessarily represent phenomena independent of inflammation, but may interact with it.
2026 Research
Cossarizza’s review includes mitochondrial dysfunction and dysregulation of cellular nutrient-sensing and nutrient-utilization systems among the mechanisms of inflammaging [1]. A further 2026 paper, “Inflammaging: Immune–Metabolic Crosstalk Between the Prostate–Testis and Musculoskeletal System,” describes circuits in which inflammation, oxidative stress, metabolism, mitochondrial function, and the endocrine system can mutually reinforce one another [5].
Assessment of the evidence
The support is strong at the level of pathophysiological integration. It supports the decision not to observe a single metabolic parameter in isolation, but to assess metabolic and inflammatory indicators together and, above all, their evolution over time.
6. Gut microbiota, barrier, and immunity
Support for the Integrated Approach
The Integrated Approach considers the intestine and microbiota as one of the components of systemic immune regulation, while avoiding attribution to the microbiota of an exclusive role in the origin of chronic inflammation.
2026 Research
The review “From Primates to People: Mapping Host-Microbiome-Health Relationships in Aging,” published in Ageing Research Reviews, links age-associated dysbiosis with inflammaging and systemic decline. The microbiome is described as an important modulator of physiology, metabolism, and immune function; however, the authors emphasize that causality and mechanisms are not yet fully clarified and highlight the limitations of human studies and experimental models [6].
Assessment of the evidence
The support is strong for inclusion of the microbiota within the network, but does not justify a monocausal explanation. Diet, age, physical activity, medications, environment, and individual characteristics can modify the microbiota; in parallel, the microbiota can influence metabolism, the intestinal barrier, and the immune response. The relationship is therefore dynamic and bidirectional.
7. Sleep, circadian rhythms, and immunometabolic regulation
Support for the Integrated Approach
In the Integrated Approach, sleep is not considered merely a period of rest, but a component of metabolic, endocrine, circadian, and immune regulation.
2026 Research
The review “Sleep Deterioration as a Systems-Level Readout of Aging Biology: Integrating Metabolic, Inflammatory and Circadian Mechanisms,” published in Ageing Research Reviews, interprets deterioration of sleep during aging as an expression of the progressive alteration of interconnected metabolic, inflammatory, and circadian systems [7].
The review “Circadian–Immune Crosstalk in Insomnia Disorder: Mechanisms and Therapeutic Implications” specifically analyzes the interaction among circadian rhythms, melatonin, endocrine function, and immune-inflammatory activity, highlighting the role of low-grade inflammation in chronic insomnia [8].
Assessment of the evidence
The support is strong for inclusion of sleep and chronobiology in the model. The bidirectional nature of the relationship must nevertheless be maintained: persistent alterations in sleep and circadian rhythms may be accompanied by metabolic and immune changes, while diseases, stress, metabolic dysfunction, and inflammation may in turn impair sleep.
8. Chronic stress and neuroendocrine regulation
Support for the Integrated Approach
The Integrated Approach includes chronic stress among the factors potentially capable of maintaining neuroendocrine and metabolic conditions favorable to inflammation. The central point is not the single episode of stress, which constitutes a normal adaptive response, but the persistent alteration of physiological regulation and recovery systems.
Relationship with 2026 evidence
The 2026 reviews on sleep, circadian rhythms, and inflammaging show the close communication among neuroendocrine, metabolic, and immune systems [1,7,8]. However, among the works selected for this chapter there is no single 2026 study sufficiently general to demonstrate that every form of chronic stress directly causes low-grade chronic inflammation.
Assessment of the evidence
The support is therefore primarily systemic and mechanistic. The inclusion of stress in the Approach is consistent with contemporary physiology, but must avoid the simplistic equation “stress = inflammation.”
9. Inflammaging and biological aging
Support for the Integrated Approach
The Approach assigns particular importance to biological age and considers low-grade chronic inflammation one of the processes that may contribute to the progressive loss of efficiency of physiological systems.
2026 Research
Cossarizza’s review represents the most important general reference among those examined because it places persistent low-grade inflammation within the biological processes of aging and age-related diseases [1]. The work by Bossio and colleagues also interprets inflammaging through a network of immunometabolic, endocrine, and muscular interactions [5].
Assessment of the evidence
The support is strong. Chronological age cannot be modified; numerous factors that interact with the aging process can, at least in part, be modified. The realistic objective of the Approach is therefore not to “eliminate” inflammaging, but to act on modifiable factors that may contribute to its intensity and evolution.
10. Convergence of factors: why an integrated approach
The perhaps most significant aspect of the 2026 scientific research examined is not the support for a single element of the Approach, but the growing representation of chronic inflammation and aging as multidimensional phenomena [1–8].
Nutrition, physical activity, muscle, metabolism, microbiota, sleep, circadian rhythms, stress, and aging do not act as completely independent variables. Physical activity modifies metabolism and inflammatory signaling; muscle participates in endocrine communication through myokines; diet interacts with metabolism and microbiota; the microbiota communicates with the immune system; sleep and circadian rhythms are linked to metabolic, endocrine, and immune regulation; aging acts transversally across all these systems.
The 2026 literature does not demonstrate the existence of a single protocol capable of globally controlling low-grade chronic inflammation. It does, however, provide important conceptual support for a strategy that simultaneously observes multiple modifiable factors and follows their evolution over time.
From this perspective, the Integrated Approach to reducing low-grade chronic inflammation appears consistent with the tendency of recent research to interpret inflammaging and the regulation of inflammation through interconnected biological networks, rather than through a single causal factor or a single intervention.
Conclusion
Comparison with the 2026 scientific literature shows that the general framework of the Integrated Approach finds significant support in contemporary research. The strongest support concerns the systemic and multifactorial nature of inflammaging, the interaction between metabolism and inflammation, the role of physical activity and muscle, the participation of the microbiota, and the integration among sleep, circadian rhythms, and immunometabolic function [1–8].
The convergence of evidence does not, however, amount to clinical validation of a specific therapeutic protocol. Many of the cited works are reviews and integrate results from different studies; some mechanisms are better demonstrated than others, and individual responses to interventions remain variable.
The value of the Integrated Approach therefore currently lies above all in its consistency with an increasingly systemic view of the biology of aging: acting on modifiable factors, avoiding monocausal explanations, and monitoring over time the evolution of clinical, metabolic, and inflammatory parameters.
Bibliographic references
[1] Cossarizza A. Inflammaging: Experimental Insights and Translational Advances. European Journal of Immunology. 2026;56(7):e70239. DOI: 10.1002/eji.70239.
[2] Moskalev A, et al. Dietary Bioactive Compounds and Inflammaging: Pro- and Anti-Inflammatory Effects. 2026. PubMed PMID: 42425421.
[3] Zhang Y, et al. Exercise-Mediated Modulation of the NLRP3 Inflammasome. 2026. PubMed PMID: 42557399.
[4] Mănescu DC, Plastoi CD, Pîrvan A, Dîrnu R, Floroiu EA, Popescu A. The Myokine Adaptome in Health and Disease: Exercise-Induced Cellular Signaling, Muscle–Organ Crosstalk, and Therapeutic Plasticity. Cells. 2026;15(14):1236. DOI: 10.3390/cells15141236.
[5] Bossio S, Russa D, Rago V, Di Dio M, Aversa A, Perri A. Inflammaging: Immune–Metabolic Crosstalk Between the Prostate–Testis and Musculoskeletal System. International Journal of Molecular Sciences. 2026;27(8):3612. DOI: 10.3390/ijms27083612.
[6] Olmo-Fontánez A, Reveles KR, Sharan R, Cheeseman I, Phillips KA, Wolford KL, Ross CN. From Primates to People: Mapping Host-Microbiome-Health Relationships in Aging. Ageing Research Reviews. 2026;121:103278. DOI: 10.1016/j.arr.2026.103278.
[7] Murillo-Cancho AF, Lozano-Paniagua D, Martín-Latorre MDM, Ramírez-Santos J, Nievas-Soriano BJ. Sleep Deterioration as a Systems-Level Readout of Aging Biology: Integrating Metabolic, Inflammatory and Circadian Mechanisms. Ageing Research Reviews. 2026;118:103084. DOI: 10.1016/j.arr.2026.103084.
[8] Huang Y, Wang X, Chen X, Liu Y. Circadian–Immune Crosstalk in Insomnia Disorder: Mechanisms and Therapeutic Implications. Frontiers in Neuroscience. 2026;20:1881195. DOI: 10.3389/fnins.2026.1881195.
Methodological note
The works cited do not all have the same nature or the same evidentiary value. Several are reviews and therefore synthesize knowledge produced by previous studies rather than constituting new clinical experiments. Their value for the purposes of this article lies primarily in showing how different strands of contemporary scientific research converge on the existence of interactions among inflammation, metabolism, muscle function, microbiota, biological rhythms, and aging. This convergence represents scientific support for the general framework of the Integrated Approach, but should not be interpreted as clinical validation of a specific therapeutic protocol.

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Continue → Low-grade chronic inflammation: the topic in science communication and the international press in 2026

 

Integrated Approach to Reducing Low-Grade Chronic Inflammation August 18, 2026 update

by luciano

This article is part of a three-part series:
1. Integrated approach to reducing low-grade chronic inflammation — the operational document: which behaviors and strategies to adopt.
2. Integrated approach to reducing low-grade chronic inflammation in light of 2026 scientific research — the scientific verification document: which elements of the Approach are supported by the most recent literature and with what degree of evidence.
3. Low-grade chronic inflammation: the topic in science communication in the international press in 2026 — the communication analysis document: how the topic is presented, interpreted, and communicated by the international scientific and general press

(Low-grade chronic inflammation is not a disease in the strict sense, but a persistent biological state that promotes the development of numerous chronic diseases. This document proposes an integrated approach aimed at modulating it through lifestyle.)

Furthermore:
In the absence of univocal and definitive solutions, the most rational strategy for reducing low-grade chronic inflammation consists of adopting a lifestyle that minimizes exposure to potentially pro-inflammatory factors* and promotes protective ones.

The importance of low-grade chronic inflammation.
Although intermittent increases in inflammation are essential for survival during physical injury and infection, recent research has revealed that certain social, environmental, and lifestyle factors can promote chronic systemic inflammation, particularly low-grade chronic inflammation (LGCI), which, in turn, can lead to several diseases that, taken together, 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 diseases. (see article: https://glutenlight.eu/2025/08/21/infiammazione-cronica-basso-grado/ [1]

This type of inflammation has multiple triggers:
Gut dysbiosis:
Alteration of the intestinal bacterial flora, which can be caused by an unbalanced diet, excessive use of antibiotics, or other toxic substances.
Poor diet:
Excessive consumption of processed foods, rich in refined sugars and saturated fats, which can promote inflammation. [11]
Stress: Chronic stress can negatively affect the immune system and increase susceptibility to inflammation. [3–5]
Environmental pollution and toxins:
Exposure to chemicals present in the environment or in food can contribute to oxidative stress and inflammation. [12]
Smoking and alcohol:
These factors can aggravate oxidative stress and damage cells, promoting inflammation. (see article: oxidative stress)
Drug use is not included among the triggers because drugs are considered always and in any case to be avoided.

Another consideration concerns the individual’s general state of health. In this document, the term “healthy” does not coincide solely with the absence of diagnosed diseases, trauma, wounds, or other events capable of activating acute inflammation. In a more rigorous physiological sense, an individual is considered truly healthy if they have no active disease and are not persistently in a state of low-grade chronic inflammation. This distinction is important because the absence of a formal diagnosis does not, by itself, demonstrate the absence of a persistent inflammatory state.
It is important to emphasize that, in the presence of acute inflammation, the biological markers used to assess low-grade chronic inflammation are elevated, making it difficult to distinguish the two phenomena and potentially masking any improvements in LGCI.

Having made these clarifications, we can begin the Integrated Approach
1️⃣ Stress management.
This is a very important factor given the emerging scientific evidence concerning the gut–brain axis, a bidirectional communication system through which psychological stress, emotions, and mental states influence intestinal motility, barrier permeability, and microbiota composition, and vice versa. Alterations in this axis can promote inflammation, digestive disorders, and metabolic imbalances. Stress should be managed independently using existing techniques or, if this is not possible, with the help of a psychologist. [3–5]
2️⃣ Environmental pollution (air, water, etc.): it goes without saying that the more we can avoid it, the better. This factor is relevant to oxidative stress. [12]
3️⃣ Nutrition: here we can do a great deal
Important point:
Nutrition must be closely related to age, activity level, eating habits, and general state of health.
Foods to avoid
1. Industrial foods: they may contain numerous additives. At authorized doses, occasional exposure to a single additive is generally considered low risk in the general population; greater caution may be reasonable when exposure is frequent, involves mixtures of several additives, or concerns individuals with specific vulnerabilities. Therefore, without turning every additive into a certain risk, it is advisable to favor minimally processed foods and reduce unnecessary overall exposure [A]. [2,11]
2. Industrial beverages: generally contain large amounts of sugars/sweeteners/additives.
Many gluten-free products, especially industrial ones, are highly processed and may contain numerous additives. This does not imply that such products are inherently pro-inflammatory, but, when there is no medical need to consume them, it may be prudent to limit their consumption and prefer naturally gluten-free or less processed foods, thereby reducing overall exposure to additives and refined ingredients. [11]
3. Foods to consume in moderation
4. Wine/beer: in moderation
5. Alcoholic beverages: occasionally (spirits: NO)
6. Coffee: in moderation
7. Processed meats: very moderately
8. Sweets: in moderation. If there are problems with sugars (because of weight or blood glucose), they should be consumed in appropriate amounts so as not to cause problems.
9. Cheese: very moderately and to the extent compatible with the individual (reduction/elimination if intolerant to lactose/casein protein; possible replacement with lactose-free products)
10. Spices: in moderation
11. Fats: fewer trans (hydrogenated) fats and, to a lesser extent, excess saturated fats; more extra-virgin olive oil (oleic acid)
12. Refined sugars: it is advisable to limit their intake, especially when they contribute to a caloric surplus, frequent glycemic excursions, or occur in a context of overweight, visceral adiposity, or insulin resistance. In these contexts, repeated glucose and insulin spikes may contribute to a metabolic environment more favorable to pro-inflammatory processes. [11]
12. Gluten: in moderation. If possible, whole-grain/semi-whole-grain pasta; bread: if possible, whole-grain durum wheat/spelt. Common wheat contains a component of gluten that is very difficult to digest (33mer). Given the relationship between gluten strength and digestibility, products made with grains that have less tenacious gluten should preferably be chosen. Among “ancient grains” there are several with this characteristic (in fact, even among modern grains there are cultivars with less tenacious gluten: they are used to make cakes but not bread): these should be preferred. Those who are gluten intolerant but not celiac, considering that this intolerance is “dose-dependent,” can, with the help of a physician, determine the threshold (amount) that does not cause problems. Grains with less tenacious gluten make it easier to consume products made from them. Further reading: Difference between ancient and modern grains (Published separately)
Foods to consume abundantly:
1. Fiber (compatibly with any intestinal problems): 3–4 times a day.
2. Fruit (compatibly with any problems involving sugars, blood glucose and/or weight).
3. Green tea: it can be a useful component of a balanced diet. It is rich in catechins, particularly EGCG, and several studies suggest possible favorable effects on oxidative stress, metabolism, and some inflammatory markers; however, the magnitude of the benefit in humans varies according to dose, duration of intake, and individual characteristics [D]. [19]
The essential contribution of water to maintaining proper hydration and normal physiological functions, including kidney function, circulation, and solute transport, should also be remembered. Significant dehydration can alter various metabolic and physiological processes. The lymphatic system performs an important function in draining interstitial fluids and participates in the transport of mediators and cells of the immune system; through these functions it contributes to maintaining tissue homeostasis and to the processes of regulation and resolution of inflammation.
It is therefore advisable to maintain hydration appropriate to individual needs, taking into account age, physical activity, environmental temperature, and any clinical conditions. See: The role of water in reducing low-grade inflammation
It should be emphasized, in summary, that the Mediterranean diet and, more generally, dietary patterns with anti-inflammatory characteristics have shown in numerous studies and meta-analyses a reduction in markers of low-grade chronic inflammation. For the Mediterranean diet, the most recent evidence documents, in particular, significant reductions in hs-CRP and IL-6 [8–10].
4️⃣ Eating behaviors
Nutrition rests on two main pillars: quantity and quality.
The amount of food consumed should be that required for physiological functions plus that needed for the activities performed. This simple principle would greatly help us maintain a correct and healthy weight. This is not an easy goal for two simple reasons: the first is “temptation,” the second is that the “full/satiated” mechanism is delayed relative to actual fullness, meaning that the sensation of satiety does not coincide with the actual filling of the stomach, but comes later. As early as 50 years ago, the family doctor advised getting up from the table with a slight desire for more food. Quality: it goes without saying that the more genuine and “clean” foods are (that is, free of toxic substances), the better.
What follows should also be considered a general framework because, as already stated, it must be “designed around the individual.”
A – Avoid as much as possible consuming too much food in a single meal
The stomach should be put in a position to work (digest) as well as possible. It is often preferable to eat several times rather than have a single very large meal. Ideally: finish eating and “not feel the stomach,” with the result of avoiding postprandial “mental fog.” Further reading: Why smaller, distributed meals work better. (Published separately)
Food that is not completely digested, in healthy people*, is subsequently processed in the intestine and then eliminated. However, if the gastrointestinal system is compromised or altered, the passage of inadequately digested substrates into the intestine can promote bacterial fermentation and be pro-inflammatory. (https://glutenlight.eu/2025/06/12/cibo-non-digerito-e-infiammazione-intestinale/)
Not only the stomach, but also and above all the intestine must be able to work at its best and continue digesting food so as to make it absorbable. [B] [C]
*Here the critical point is: does the truly healthy individual still exist?
B – Avoid mixing foods that are too different
The stomach works in an acidic environment, where pepsin digests proteins (which are further digested in the intestine by trypsin and other enzymes). Sugars begin digestion in the mouth (ptyalin) and are then digested mainly in the intestine (pancreatic amylase). Some clarifications are necessary here: [13–16]
Carbohydrates and proteins in the stomach generally do not create problems. A pasta first course followed by fish, meat, cheese and perhaps vegetables, in quantities suited to one’s digestive capacity, does not create problems.
If the second course is a very fatty food, it should be considered that gastric digestion slows and, depending on the amount, may slow gastric emptying, with the possible passage into the intestine of food that has not been completely digested. [13–16]
The situation is different if we include a portion of dessert in the meal.
Here we are dealing with a significant amount of simple sugars, not complex carbohydrates (pasta, for example, consists mainly of starch, and only part of it is converted into sugars already in the mouth; therefore, mainly starch reaches the stomach).
Sugars are not digested in the stomach except to a negligible extent:
“The stomach has a highly acidic environment that prevents fermentation there; the undigested sugars travel to the small intestine and large intestine, where they are fermented by the gut bacteria.”
Dessert at the end of a meal (meaning a moderate portion) does not cause problems in a healthy person (who is relatively rare today), but makes digestion less easy for many people, not only because of possible subsequent intestinal effects, but also because of the sensation of heaviness that may occur. [17,18]
It should be clarified that this is not a dogma: there are people who digest practically everything without difficulty — we are all different.
Age also plays a fundamental role. Older people tend to feel better the simpler the meal is. Further reading: Sugars and proteins in stomach digestion (Published separately)
Important point
In the case of diet-related diseases, intervention by a specialist (dietitian or nutritionist) is strictly necessary.
5️⃣ Specific behaviors:
Engage in physical activity, even if only moderate. [6,7]
If employed, avoid as far as possible allowing work to cause persistent stress. Chronic stress should in any case be managed because, through neuroendocrine and immune mechanisms and the gut–brain axis, it can contribute to maintaining a state of low-grade inflammation. [3–5]
In the presence of overweight, and especially excess visceral adiposity, it is advisable to agree with one’s physician or a specialist on a realistic pathway for weight reduction and improvement of body composition.
After working life, engage in activities that require concentration and, if possible, creativity. Carrying out projects is highly useful for keeping brain functions active
6️⃣ Assessments:
Together with one’s physician, define the routine general assessments necessary for good monitoring of one’s health, in addition to specific assessments for any diseases.
Final Summary:
We must build a personalized lifestyle model for reducing low-grade chronic inflammation.
In a healthy person, a meal containing proteins and sugars in moderate amounts does not cause problems. The combination becomes potentially problematic when sugars are highly concentrated, especially in liquid form and in large quantities. In people with a sensitive or altered gastrointestinal system, even moderate portions (such as a dessert at the end of a meal) can cause digestive discomfort.
The integrated approach to reducing low-grade chronic inflammation is based on the available scientific evidence, reported in the bibliography section. Since many studies show significant associations without demonstrating an absolute causal relationship, a precautionary principle should be adopted: reduce or eliminate, where possible, potentially harmful factors, favoring choices with low biological risk.
Final notes
Note [A]: Intestinal barrier and additives. In certain experimental or clinical contexts, some components of the Western diet — including excess saturated fat and salt, alcohol, and some additives in ultra-processed foods — have been associated with alterations in the intestinal barrier or microbiota. For gluten, effects on permeability are particularly relevant in celiac disease and in predisposed individuals and should not automatically be generalized to “healthy” people. It is therefore preferable to speak of factors that “may alter” the barrier, in relation to dose, duration of exposure, and individual vulnerability. Stress can also negatively affect the gastrointestinal barrier, including through the CRF–mast cell axis [2–5]
Protective effects on the barrier may instead be exerted by: caloric restriction or fasting, prebiotics, probiotics, butyrate (SCFA), vitamins D and A, flavonoids, omega-3 polyunsaturated fatty acids, zinc, mucoprotective agents (gelatin tannate and tyndallized probiotics)
Note [B]: Fermentation and gastric emptying. Prolonged retention of food in the stomach can generate fermentation, especially if food remains longer than normal because of slow digestion. This phenomenon can cause gas accumulation, bloating, abdominal tension, and belching. Causes may include both slow gastric emptying and the consumption of certain foods. [13–16]
How symptoms present
Bloating and abdominal tension: Fermentation produces gas that can accumulate, causing a sensation of fullness and distension.
Frequent belching: Excess gas can be expelled through belching.
Flatulence: Gas can also be released as flatulence.
Feeling of fullness: Even after eating little, one may feel satiated.
Common causes of slow digestion
Large meals or meals eaten too quickly: Chewing too little and swallowing quickly can slow the digestive process.
Poor diet: A diet rich in sugars and carbohydrates can promote fermentation.
Diseases or disorders: Some medical conditions can slow gastric emptying.
Note [C]: Symptoms of poor digestion. A sandwich gulped down quickly and poorly chewed in the rush of a lunch break that is too short or spent on the phone; one bite too many so as not to leave that excellent baked pasta because “when will I ever find one this good again”; dessert ordered at the end of the meal out of temptation, despite already feeling full; the ice-cold carbonated drink or granita, because “it really is a pleasure in this heat.” The result is always the same: a sensation of stomach heaviness that is difficult to tolerate and is often accompanied by pain, acidity, heartburn, abdominal bloating, belching, and all the other symptoms of poor digestion. Occasional stomach heaviness is not related to particular diseases or significant health problems, but almost always to consuming excessive and/or difficult-to-digest foods, which require the gastric mucosa to secrete, in a short time, an amount of gastric juices greater than its capacity and require the liver, gallbladder, and pancreas to rapidly release enzymes to support the complete digestion and absorption of the fats, proteins, and carbohydrates consumed during the meal. [13–18]
Conversely, if the symptoms of poor digestion tend to recur frequently or even after every meal, including meals that are not particularly large, the underlying cause of the discomfort may be:
functional dyspepsia (also aggravated by anxiety and stress)
irritable bowel syndrome or chronic inflammatory bowel disease
allergies or intolerances to particular foods
alterations in liver function, obstruction of the bile ducts or, more rarely, chronic pancreatitis.
If, on the other hand, in addition to heaviness, abdominal bloating, and mild nausea, there are also (or predominantly) acidity, heartburn, acid reflux, cramps, and stomach pain, the cause may be gastritis, gastric ulcer, hiatal hernia or, in a very small minority of cases, a stomach tumor.
Note [D] Green tea.
1) Rich in anti-inflammatory polyphenols
Green tea contains high amounts of catechins, particularly EGCG (epigallocatechin gallate), one of the most studied natural antioxidants. [19]
These molecules help to:
Inhibit pro-inflammatory enzymes
Reduce the production of inflammatory cytokines
Positively modulate the immune response
Result: less activation of the processes that maintain inflammation over time.
2) Strong antioxidant action
Chronic inflammation is closely linked to oxidative stress (excess free radicals).
Green tea helps to:
Neutralize free radicals
Protect cell membranes
Protect DNA from oxidative damage
This helps interrupt the vicious circle between oxidation and inflammation.
3) Positive influence on metabolic pathways
Regular consumption of green tea is associated with: [19]
Improved insulin sensitivity
Reduction of inflammatory markers in the blood
Support for fat metabolism
Since obesity and inflammation are strongly correlated, this effect is particularly important.
4) Benefits for the gut microbiota
Green tea promotes the growth of “good” intestinal bacteria and limits potentially harmful ones.
A balanced microbiota:
Reduces intestinal permeability
Limits the passage of toxins into the blood
Lowers activation of the immune system
All of this contributes to reducing systemic inflammation.
❤️ 5) Cardiovascular protection
Low-grade chronic inflammation is associated with an increased cardiovascular risk and may contribute to atherosclerotic mechanisms. [1]
Green tea:
Improves endothelial function
Reduces oxidation of LDL cholesterol
Helps maintain arterial elasticity
Contributing to a less inflamed vascular environment.
☕ How much green tea should be consumed?
Studies and nutritional recommendations frequently consider amounts in the range of 2–3 cups per day; however, effects may vary among individuals; preferably without sugar and away from main meals if one has anemia (it can reduce iron absorption). [19]
Note at the end of the article
For some factors, such as food additives, numerous studies suggest an association between intake and possible negative health effects. These findings must nevertheless be interpreted in the context of the research methods used, which often include observational studies, experimental models, or numerically limited samples. A result obtained in an animal model does not automatically demonstrate that the same effect occurs in humans; however, it may represent a biological signal that should not be ignored, especially when reducing exposure entails minimal cost or risk. Long-term clinical studies in humans, particularly for chronic exposure to individual ingredients or mixtures of additives, are often complex, expensive, and difficult to conduct. Moreover, economic incentives to fund large studies are generally greater when there is a product or intervention to develop than for research aimed simply at establishing whether it is advisable to reduce or avoid a substance already on the market. In this approach, such evidence is therefore considered sufficient to adopt a precautionary principle, even in the absence of definitive causal proof. The absence of definitive proof of harm in humans should not, in fact, be confused with proof of absolute harmlessness.
Essential bibliography
Low-grade chronic inflammation (LGCI) and cardio-metabolic risk
[1] Low-grade inflammation as a risk factor for cardiovascular events and all-cause mortality in patients with type 2 diabetes — Sharif S, et al. (2021). Cardiovascular Diabetology. DOI: 10.1186/s12933-021-01409-0. (PubMed)
“Western” diet, intestinal permeability, and dysbiosis
[2] Western diet components that increase intestinal permeability with implications on health — Jaquez-Durán G, Arellano-Ortiz AL. (2024). Int J Vitam Nutr Res. DOI: 10.1024/0300-9831/a000801. (PubMed)
Stress → intestinal permeability (CRF, mast cells) and the gut–brain axis
[3] Psychological stress and corticotropin-releasing hormone increase intestinal permeability in humans by a mast cell-dependent mechanism — Vanuytsel T, et al. (2014). Gut. DOI: 10.1136/gutjnl-2013-305690. (PubMed)
[4] CRF induces intestinal epithelial barrier injury via the release of mast cell proteases and TNF-α — Overman EL, et al. (2012). PLOS ONE. DOI: 10.1371/journal.pone.0039935. (Semantic Scholar)
[5] Role of corticotropin-releasing factor in gastrointestinal permeability (review/overview useful for linking the pieces) — Rodiño-Janeiro BK, et al. (2015). J Neurogastroenterology and Motility. DOI: 10.5056/jnm14084. (jnmjournal.org)
Physical activity and reduction of inflammatory markers
[6] Effect of exercise training on C reactive protein: a systematic review and meta-analysis of randomised and non-randomised controlled trials — Fedewa MV, Hathaway ED, Ward-Ritacco CL. (2017). Br J Sports Med. DOI: 10.1136/bjsports-2016-095999. (PubMed)
[7] Effect of exercise training on chronic inflammation (review) — Beavers KM, Brinkley TE, Nicklas BJ. (2010). Aging and Disease (PMC). (Excellent as a general framework “lifestyle → inflammation”). (PMC)
Mediterranean diet and inflammatory biomarkers
[8] Mediterranean Diet Reduces Inflammation in Adults: A Systematic Review and Meta-analysis of Randomized Controlled Trials — Keshani M, et al. (2025). Nutrition Reviews. DOI: 10.1093/nutrit/nuaf213. (OUP Academic)
[9] Reyneke GL, Lambert K, Beck EJ. Dietary Patterns Associated With Anti-inflammatory Effects: An Umbrella Review of Systematic Reviews and Meta-analyses. Nutrition Reviews. 2026;84(6):1167–1192. DOI: 10.1093/nutrit/nuaf104.
[10] Pourrajab B, Fotros D, Asghari P, Shidfar F. Effect of the Mediterranean diet supplemented with olive oil versus the low-fat diet on serum inflammatory and endothelial indexes among adults: a systematic review and meta-analysis of clinical controlled trials. Nutrition Reviews. 2025;83:e1421–e1440. DOI: 10.1093/nutrit/nuae166.
Ultra-processed foods and inflammation (CRP/hs-CRP, etc.)
[11] Ultra-Processed Food Consumption and Systemic Inflammatory Biomarkers: A Scoping Review — Ciaffi J, et al. (2025). Nutrients. DOI: 10.3390/nu17183012. (PubMed)
Pollution, oxidative stress, and systemic inflammation
[12] Particulate air pollution, systemic oxidative stress, inflammation, and atherosclerosis — Araujo JA, Nel AE. (2010). Air Quality, Atmosphere & Health. DOI: 10.1007/s11869-010-0101-8. (PMC)
“Sugars + proteins,” gut hormones, and gastric emptying
[13] Ghrelin, CCK, GLP-1, and PYY(3–36): Secretory Controls and Physiological Roles in Eating and Glycemia in Health, Obesity, and After RYGB — Steinert RE, Feinle-Bisset C, et al. (2017). Physiological Reviews. DOI: 10.1152/physrev.00031.2014. (Physiology journals)
[14] Effects of a Protein Preload on Gastric Emptying, Glycemia, and Gut Hormones After a Carbohydrate Meal in Diet-Controlled Type 2 Diabetes — Ma J, Stevens JE, et al. (2009). Diabetes Care (PMC). (Experimental study: proteins → ↑CCK/GLP-1 and slowed emptying). (PMC)
[15] Effects of GLP-1 and Its Analogs on Gastric Physiology in Diabetes Mellitus and Obesity — Maselli DB, Camilleri M. (2021). DOI: 10.1007/5584_2020_496. (Semantic Scholar)
[16] Evaluation of interactions between CCK and GLP-1 in their effects on appetite and gut function — Brennan IM, et al. (2005). Am J Physiol Regul Integr Comp Physiol. DOI: 10.1152/ajpregu.00732.2004. (Physiology journals)
“Dessert stomach” and sensory-specific satiety
[17] Sensory specific satiety in man — Rolls BJ, Rolls ET, Rowe EA, Sweeney K. (1981). Physiology & Behavior. DOI: 10.1016/0031-9384(81)90310-3. (PubMed)
[18] Sensory-specific satiety (brief/classic review) — Rolls BJ. (1986). Nutrition Reviews. DOI: 10.1111/j.1753-4887.1986.tb07593.x. (PubMed)
[19] Dehzad MJ, Ghalandari H, Nouri M, Makhtoomi M, Askarpour M. Effects of green tea supplementation on antioxidant status and inflammatory markers in adults: a GRADE-assessed systematic review and dose-response meta-analysis of randomised controlled trials. Journal of Nutritional Science. 2025;14:e25. DOI: 10.1017/jns.2025.13.
Diet, microbiota, and inflammation – analysis of Italian media coverage (2025–2026). (Published separately)
Continued → Integrated approach to reducing low-grade chronic inflammation in light of 2026 scientific research