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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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Chronic low-grade inflammation: what it is and how to reduce it through diet and lifestyle

by luciano

This guide gathers practical dietary and behavioral recommendations useful for reducing the factors that may promote a state of chronic low-grade inflammation.

Chronic low-grade inflammation refers to a mild but persistent inflammatory condition of the body, often not very evident or scarcely perceived. Unlike acute inflammation — which is intense, visible, and temporary (as in the case of an infection, injury, or illness) — this form is more silent and may persist over time. In recent years, numerous studies have highlighted how this inflammatory state may contribute to the development or worsening of several metabolic and immune conditions.

Introduction

The proposed diet consists of a set of dietary guidelines and practices aimed at maintaining the intestinal microbiota in balance and promoting the best possible functioning of the immune system.

To achieve this goal, it is useful to reduce or eliminate factors that may alter the balance of the intestinal microbiota and interfere with the efficiency of the immune system.

The microbiota is naturally dynamic: a certain variability is physiological and may depend, for example, on changes in diet, lifestyle, or environment. In response to these variations, the microbiota may adapt physiologically or develop less favorable responses.

Not all variations in the microbiota are therefore negative. However, when these changes lead to persistent imbalances in the intestinal ecosystem, they may promote conditions of microbiota alteration and contribute to the onset of chronic low-grade inflammation.

Reducing this condition is therefore one of the main objectives of the pathway.

Even in the presence of ongoing diseases, adopting dietary and behavioral recommendations that help reduce chronic low-grade inflammation may contribute to preventing further worsening of the clinical condition and to promoting a better overall balance of the organism.

The diet should also be accompanied by some lifestyle guidelines, particularly regarding:
stress and anxiety management

1. regular physical activity

2. balanced lifestyle habits

This aspect is far from marginal. Numerous studies on the gut–brain axis have in fact highlighted a close bidirectional relationship between the nervous system, the intestine, and the microbiota.

Consequently, prolonged stress conditions may negatively influence intestinal balance and may partially or completely compromise the positive effects of a correct and effective diet.

Finally, but no less important, it should be remembered that the great variability of individual psychophysical conditions and the heterogeneity of responses to therapies, treatments, and dietary regimens often require careful personalization of the diet, possibly supported by one’s physician or a specialist.

It should be emphasized from the outset that:

In a truly healthy subject*, the immune system and the organs responsible for regulating homeostasis are physiologically able to maintain the state of health and defend the organism from external agents, including those of dietary origin. This balance depends on the body’s ability to appropriately modulate inflammatory responses, preserve the integrity of the intestinal barrier, and maintain effective communication between the intestine, the immune system, and the nervous system.

The method: what to avoid and why

  1. Consuming too much food: the stomach should be able to work (digest) as efficiently as possible. It is better to eat several times rather than having one large meal. The most recent scientific literature suggests that the presence of food that is not completely digested in the intestinal lumen may contribute, in specific contexts [1], to processes of chronic low-grade inflammation and to increased intestinal permeability.
    By “specific contexts” we mean the coexistence of an inefficient gastric barrier (hypochlorhydria), slowed intestinal transit (stasis), and altered intestinal permeability (leaky gut), conditions that can transform undigested food residues into pro-inflammatory stimuli for the immune system.

  2. Meals composed of many different dishes [2]: the simpler the composition of a meal, the easier gastric digestion will be. A significant presence of fats [2.1] may slow the passage of food to the intestine, prolonging digestion and potentially causing sensations of heaviness and bloating. Simple sugars are digested very quickly, usually in the small intestine. However, if they are eaten after a complete meal (perhaps rich in proteins and fiber), they remain “trapped” in the stomach [2.3] while waiting for the rest of the food to be processed and may ferment [3].

  3. Industrial food products [4]: as little as possible; they contain additives which, if consumed individually only occasionally, do not usually cause problems but, when accumulated together, may have a more or less marked pro-inflammatory action depending on the individual’s health status. In summary, it is not necessary to rigidly eliminate every food containing additives, but favoring a diet based on minimally processed foods reduces overall exposure to mixtures of additives and represents a simple, safe, and potentially beneficial strategy for intestinal and systemic health.

  4. Industrial beverages: as little as possible; they generally contain large amounts of sugar, sweeteners, and additives.

  5. Foods for people with celiac disease: as little as possible when there is no real medical necessity. Many industrial gluten-free products may contain high amounts of sugars, fats, and additives, and often have a lower fiber content than traditional products. For this reason, it is preferable to limit their consumption when not strictly necessary. It should also be remembered that the additives contained in these products, when combined, may have a pro-inflammatory effect depending on the individual’s health condition.

  6. Wine/beer: with great moderation, because alcohol may interfere with liver metabolism, increase caloric intake, and, if consumed frequently, promote inflammatory processes and alterations of intestinal balance.

  7. Spirits: avoid except in occasional situations.

  8. Coffee: yes, in amounts compatible with individual tolerance to caffeine, but with attention to the overall sugar content that may accompany it.

  9. Spices: yes, favoring those with digestive and antioxidant properties (turmeric, ginger, cinnamon, cumin) and using more irritating ones (black pepper, chili pepper) more moderately.

  10. Fried foods: in moderation because frying increases the caloric content of foods and may produce oxidized compounds and irritating substances that, if consumed frequently, may promote inflammatory processes and make digestion more difficult.

  11. Fiber: essential. Preferably 3–4 times per day. Fiber represents the main and most important source of nourishment for the microbiota: through it the microbiota produces short-chain fatty acids (butyrate, acetate, propionate) that are beneficial for intestinal health.

  12. Processed meats: sparingly, because they generally contain high amounts of salt, preservatives (nitrites and nitrates), and fats—elements which, if consumed frequently, may promote inflammatory processes and metabolic imbalances.

  13. Cheese: yes, in amounts compatible with the individual (limited if intolerant to lactose or casein). They should not be completely eliminated when well tolerated, because they represent a good source of proteins, calcium, and other micronutrients useful for the body. It is nevertheless preferable to favor simple, good-quality cheeses consumed in moderation.

  14. Sweets: in amounts compatible with the individual. If there are problems with sugars (for weight or blood glucose), they should be consumed in appropriate quantities to avoid imbalances. However, it should not be forgotten that they can also represent a compensatory source of pleasure in many situations of stress or anxiety: moderation yes, but without eliminating them completely.

  15. Gluten [5][5.1]: if possible, choose whole or semi-whole wheat pasta; bread: preferably semi-whole or whole made from durum wheat or einkorn/emmer varieties. Soft wheat contains a component of gluten that is very difficult to digest (33mer). Whenever possible, include products made with grains whose gluten is less strong and more tolerable (many ancient grains have these characteristics).

  16. Non-celiac gluten sensitivity (NCGS). This type of intolerance is “dose-dependent.” Once it has been established that a person is intolerant but not celiac, it is necessary to identify the quantity that can be tolerated without causing problems. In these cases, products made with grains whose gluten is less tenacious and more tolerable (many ancient grains have these characteristics) may help manage the issue better. It should also be emphasized that many products for people with celiac disease contain several additives: regarding this aspect, see what was stated in point 3 and note [4].

  17. Water: drink regularly during the day in adequate quantities. Water is essential for the proper functioning of metabolism, digestion, and waste elimination processes. (Doctors keep reminding us… 1.5–2 liters…)

  18. Green tea: because it contains polyphenols and antioxidant substances that may contribute to cellular protection and metabolic balance.

  19. Medications: only when truly necessary and under medical prescription.

  20. Supplements: to be used after consulting a specialist in order to define a “personalized” intake based on the existing disorder or condition. In addition, many supplements have not been sufficiently tested on large and well-characterized populations.

Specific behaviors:

  1. Engage in physical activity, even at a moderate level.

  2. If working, try to avoid situations where work leads to excessive stress.

  3. If in the post-working phase of life, engage in activities that require concentration and, if possible, creativity. Developing projects is highly beneficial for keeping cognitive functions active.

  4. Do not smoke.

  5. With your physician, define the routine general check-ups necessary for proper monitoring of your health, in addition to specific examinations for already diagnosed medical conditions.

*It is also important to clarify that the concept of a “healthy subject” does not simply coincide with the absence of clinically diagnosed diseases. In a more rigorous physiological sense, a person can be defined as truly healthy when they do not present ongoing diseases and are not in a state of chronic low-grade inflammation. This distinction is far from marginal, since in clinical practice the term “healthy” is often used in a reductive sense, coinciding only with the absence of formal diagnoses.

Notes:

[1] Undigested food

Low-grade inflammation is not caused by food itself, but by the disruption of the balance between digestion, microbiota, and the intestinal barrier. In particular:

1. Enzymatic and acid failure: If the stomach (due to stress or medications) does not break proteins down into small amino acids, long peptide chains remain that the body may mistake for threats.

2. Biochemical transformation: Undigested residues, when stagnating, undergo processes of putrefaction (proteins) or excessive fermentation (sugars), producing toxic metabolites (ammonia, phenols, gases) that irritate the intestinal mucosa.

3. The immune breach: In the presence of a “permeable” intestinal mucosa, these macromolecules and toxins cross the cellular wall and come into direct contact with the immune system, keeping it in a constant state of alert (release of inflammatory cytokines).

[2] Simplicity and enzymatic “load”

Each macronutrient (carbohydrates, proteins, fats) requires different enzymes and breakdown times. When we mix too many different foods:

  • The stomach must manage a complex chemical mixture.

  • The body struggles to optimize gastric pH for each food.

Result: A faster and “cleaner” digestion occurs when meals consist of a few well-combined ingredients.

[2.1] The role of fats

Fats are the slowest nutrients to digest. Their presence sends hormonal signals (such as cholecystokinin) that tell the stomach to slow the emptying toward the duodenum.

The positive side: They provide a prolonged sense of satiety.

The negative side: If the meal is excessively fatty, food stagnates in the stomach. This process of stagnation or fermentation is what causes the sensation of a “brick in the stomach” and abdominal bloating.

[2.3] Tips for a balanced but light meal

To avoid heaviness without giving up taste, you could follow these small precautions:

  • Prefer simple cooking methods: steaming, grilling, or baking rather than frying or prolonged sautéing.

  • Limit different protein sources: avoid mixing eggs, cheese, and meat in the same meal.

  • Add fats raw: use extra virgin olive oil at the end of cooking to preserve its properties and facilitate digestion.

In summary

The fewer “obstacles” we give our digestive system in the form of complex combinations and heavy fats, the more energy we will have available after a meal instead of feeling sleepy and bloated.

[3] Sugars

While fats slow digestion for reasons of “biochemical management” (the stomach closes the valve to take more time), simple sugars consumed at the end of a meal (here quantity plays an important role) create a sort of digestive “queue” in the stomach.

3.1. The “plug” effect and fermentation

Simple sugars are digested very quickly, usually in the small intestine. If they are consumed after a complete meal (perhaps rich in proteins and fiber), they remain “trapped” in the stomach while waiting for the rest of the food to be processed.

Consequence: In that warm and humid environment, sugars begin to ferment.

Result: Gas production, immediate abdominal bloating, and a sensation of acidity.

3.2. Fluid attraction (Osmosis)

Sugars are “osmotic” substances, meaning they attract water into the stomach and intestines in order to be diluted.

This influx of fluids can cause a sensation of abdominal distension and, in some cases, cramps or accelerated intestinal transit (not necessarily in a beneficial sense).

3.3. The impact on insulin

Unlike fats, which do not significantly stimulate insulin, a dessert at the end of a meal (again, quantity plays an important role) may cause a significant glycemic spike.

If the preceding meal was already rich in carbohydrates (pasta or bread), the dessert becomes the “last drop that makes the cup overflow.”

This spike is often followed by a crash (reactive hypoglycemia) that makes you feel tired and lacking energy shortly after eating.

Characteristic

High Fat

Sugars (Sweets)

Main action

Slow gastric emptying.

Ferment while waiting to be digested.

Sensation

Heaviness, “stone in the stomach”.

Bloating, gas in the abdomen, drowsiness.

Hormonal effect

Prolonged feeling of satiety.

Insulin spike followed by fatigue.

3.4. Fermentation in the stomach

Related topics with “Chronic low-grade inflammation (or chronic silent inflammation)”

by luciano

1 – Paradigmatic cases (In depth of Chronic low-grade inflammation (or chronic silent inflammation)

Obesity

Obesity—especially visceral obesity—is accompanied by a state of chronic low-grade inflammation. Excess adipose tissue secretes pro-inflammatory cytokines (such as TNF-α and IL-6) that contribute to the development of insulin resistance. It is therefore not surprising that obese patients often show elevated levels of C-reactive protein (CRP) (a marker of systemic inflammation) and a higher risk of type 2 diabetes. Lifestyle interventions aimed at weight reduction (a balanced diet and exercise) help to “cool down” this metabolic inflammation, also improving clinical parameters.

Metabolic syndrome

Metabolic syndrome is closely associated with a state of chronic low-grade (or “silent”) inflammation, in which excess visceral fat acts as an endocrine organ by secreting pro-inflammatory cytokines (such as IL-6 and TNF-α). This persistent process—often referred to as “meta-inflammation”—promotes insulin resistance, vascular dysfunction, and increases the risk of diabetes and cardiovascular disease.

Rheumatoid arthritis (autoimmune disease)

References
Wellen & Hotamisligil, J Clin Invest, 2003
Shoelson et al., J Clin Invest, 2006

Rheumatoid arthritis

Rheumatoid arthritis (RA) is a chronic autoimmune inflammatory disease that primarily affects the joints, causing pain, swelling, and symmetrical stiffness, with onset often between 40 and 60 years of age. The immune system mistakenly attacks healthy tissues, creating chronic low-grade inflammation which, if left untreated, leads to progressive deformities and joint damage.

Biomarkers

The most commonly used markers of low-grade inflammation include C-reactive protein (CRP), interleukin-6 (IL-6), fibrinogen, and reactive oxygen species (ROS). These markers can be measured through blood tests and indicate a chronic inflammatory state that may be associated with various health conditions.

References
McInnes & Schett, NEJM, 2011
Smolen et al., Lancet, 2016

2 – Appendix A

Generalized inflammation, also known as systemic inflammation, is a condition in which the inflammatory process simultaneously involves multiple body districts rather than remaining confined to a specific site. This means that inflammatory mechanisms—normally activated as a protective response to infections, injuries, or tissue damage—remain diffusely and persistently active.

Systemic inflammation can develop in two main ways, characterized by different mechanisms, onset times, and clinical significance. On the one hand, it may result from the generalization of an initially localized acute inflammation; on the other, it may arise from the progressive extension of a low-grade chronic inflammatory state, which over time becomes systemic.

In the first case, inflammation begins at a specific site—such as pneumonia, appendicitis, or an infected wound—and rapidly spreads throughout the body. This occurs due to the massive release of inflammatory mediators, including cytokines (such as TNF-α, IL-1, IL-6), prostaglandins, and other pro-inflammatory molecules that enter the circulation, producing a generalized response. Typical examples include sepsis, septic shock, extensive burns, and major trauma. This form—known as acute systemic inflammation or SIRS (Systemic Inflammatory Response Syndrome)—is characterized by rapid onset, high intensity, and marked symptoms such as high fever, tachycardia, hypotension, and major metabolic alterations.

In the second case, inflammation is slow, persistent, and low-intensity. It initially affects one or more specific tissues—such as adipose tissue, the gut, or the joints—and later tends to spread systemically. The underlying mechanism is the continuous production of small amounts of inflammatory mediators that do not trigger an evident acute response but progressively accumulate over time. This condition is termed chronic low-grade systemic inflammation and is frequently associated with obesity, type 2 diabetes, metabolic syndrome, cardiovascular disease, and autoimmune disorders.

Among the main sites of origin of low-grade chronic inflammation, the gut plays a central role due to its large surface area, intense immune activity, and close interaction with the microbiota. Alterations in the intestinal barrier and microbial composition can promote the translocation of pro-inflammatory molecules into the bloodstream, contributing to the systemic spread of the process.

The causes of systemic inflammation—especially in its chronic form—are multiple and include chronic or recurrent infections, obesity, chronic inflammatory diseases such as rheumatoid arthritis and ulcerative colitis, chronic stress, an unbalanced diet rich in saturated fats, sugars, and ultra-processed foods, deficiencies of vitamins, minerals, and antioxidants, as well as smoking and excessive alcohol consumption.

Symptoms of generalized inflammation may vary depending on the cause and severity, but frequently include chronic fatigue, widespread muscle and joint pain, difficulties with concentration and memory, mood swings with irritability, anxiety or depression, digestive disturbances such as constipation or diarrhea, and in some cases a mild, persistent fever.

Over the long term, systemic inflammation represents an important risk factor for numerous chronic diseases, including cardiovascular disease (hypertension, atherosclerosis, myocardial infarction), type 2 diabetes, certain cancers (especially colon and breast), kidney disease, and worsening of autoimmune conditions.

In summary, systemic inflammation can reflect either an acute response that becomes generalized or the outcome of a low-grade chronic process that progressively extends. Although these are different conditions, both involve the simultaneous involvement of multiple organs and systems and have a relevant impact on overall health.

3 – Appendix B

Undigested food

Undigested food can trigger chronic low-grade inflammation, a biological process known as metabolic endotoxemia.

Here are the main mechanisms linking impaired digestion to inflammation:

1. “Leaky gut” (intestinal permeability)

When food macromolecules are not properly broken down (due to enzyme deficiency or insufficient chewing), they can damage the intestinal tight junctions.

Mechanism: Fragments of undigested proteins and bacterial toxins (LPS) pass directly into the bloodstream.
Response: The immune system recognizes these particles as “intruders,” activating a persistent but mild systemic inflammatory response.

2. Dysbiosis and fermentation

Undigested food reaching the colon becomes a substrate for fermentation by pathogenic bacteria.
Protein putrefaction: If proteins are not digested in the stomach/small intestine, their breakdown in the colon produces toxic metabolites such as ammonia and hydrogen sulfide, which irritate the intestinal mucosa and increase pro-inflammatory cytokine levels.
Excess LPS: Overgrowth of Gram-negative bacteria increases lipopolysaccharides (LPS), among the most powerful activators of low-grade inflammation detectable via hs-CRP.

3. Non–IgE-mediated food intolerances

Unlike acute allergies, constant exposure to foods the body cannot properly process (e.g., lactose or fructose malabsorption) keeps the immune system in a state of chronic alert.

Signs to monitor

If you suspect your inflammation is linked to digestion, look for:

  • Immediate or post-prandial abdominal bloating

  • Visible food fragments in the stool

  • Brain fog after meals

4 – A special case: the role of gluten

“The role of gluten: Gluten exerts multiple harmful effects that compromise human health, not only in gluten-dependent diseases but also in chronic inflammatory conditions unrelated to gluten. After consumption, indigestible gluten peptides are modified by luminal microbial transglutaminase or transported across the intestinal epithelium to interact with the densely populated immune cells of the mucosa. As disruptors of intestinal permeability, undigested gluten peptides compromise the integrity of tight junctions, allowing foreign immunogenic molecules to reach internal compartments. Gliadin peptides are systemically distributed to remote organs, where they encounter endogenous tissue transglutaminase. Following post-translational deamidation or transamidation, the peptides become immunogenic and pro-inflammatory, inducing organ dysfunction and pathology. Cross-reactivity and sequence homology between gluten/gliadin peptides and human epitopes may contribute to molecular mimicry in the induction of autoimmunity. As proof of concept, gluten withdrawal alleviates disease activity in chronic inflammatory, metabolic, and autoimmune conditions, and even in neurodegeneration. We recommend combining a gluten-free diet with the Mediterranean diet to leverage the advantages of both. Before recommending gluten withdrawal for non–gluten-dependent conditions, patients should be asked about intestinal symptoms and screened for celiac-associated antibodies. The current list of gluten-induced diseases includes celiac disease, dermatitis herpetiformis, gluten ataxia, wheat allergy, and non-celiac gluten sensitivity. Given that gluten is a universal pro-inflammatory molecule, other non-celiac autoinflammatory and neurodegenerative conditions should be investigated for potential gluten elimination.” Gluten is a Proinflammatory Inducer of Autoimmunity. Aaron Lerner et al. Journal of Translational Gastroenterology 2024; 2(2):109–124. DOI: 10.14218/JTG.2023.00060.

Bibliographic references

  1. Furman D, et al. Chronic inflammation in the etiology of disease across the life span. Nature Medicine. 2019.
    A landmark review describing systemic chronic inflammation as a central trait in the major causes of global morbidity (cancer, cardiovascular disease, diabetes, chronic kidney disease, and others) and discussing social, environmental, and biological drivers.

  2. Franceschi C, et al. Inflamm-aging and immune-metabolic changes with aging. Cell. 2018.
    This article introduces the concept of inflammaging—age-associated low-grade chronic inflammation—and highlights the role of persistent inflammatory mediators.

  3. Khanna D, Khanna S, et al. Obesity: A chronic low-grade inflammation and its markers. Journal of Inflammation Research. 2020.
    A review analyzing obesity as a paradigmatic model of low-grade systemic inflammation, with extensive discussion of key inflammatory markers produced by adipose tissue.

  4. Chen L, et al. Inflammatory responses and inflammation-associated diseases in organs. Journal of Biomedical Research. 2017.
    A comprehensive review of the molecular mechanisms of acute and chronic inflammatory responses and their implications in multiple systemic diseases (cardiovascular, metabolic, autoimmune, and neoplastic).

Chronic low-grade inflammation (or chronic silent inflammation)

by luciano

Highlight – Why this is a central topic
Although intermittent increases in inflammation are essential for survival during physical injury and infection, recent research has revealed that certain social, environmental, and lifestyle-related factors can promote systemic chronic inflammation (SCI), which in turn may lead to a variety of 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 diseases.

References
Furman et al., Science, 2019
Calder et al., Nutrients, 2017

What is inflammation
Inflammation is a central component of innate (nonspecific) immunity. In general terms, inflammation is a local response to cellular damage characterized by increased blood flow, capillary dilation, leukocyte infiltration, and localized production of a series of chemical mediators that contribute to the elimination of toxic agents and the repair of damaged tissues.

It is now clear that the termination (also known as resolution) of inflammation is an active process involving cytokines and other anti-inflammatory mediators, particularly lipid mediators, rather than a simple shutdown of pro-inflammatory pathways.

Inflammation acts both as a “friend and a foe”: it is an essential component of immune surveillance and host defense; however, a persistent inflammatory state over time is a pathological feature of a wide range of chronic conditions.

References
Medzhitov, Nature, 2008
Serhan et al., Nature, 2007

Acute inflammation
Acute inflammation is the body’s rapid, short-term response to injury or infection, characterized by redness, swelling, heat, and pain. It is a beneficial process that helps protect against pathogens and initiates tissue repair. Although it may last from a few hours to a few days, it differs from chronic inflammation, which persists for longer periods and can be harmful.

(Personal note: The classic signs of acute inflammation—heat, redness, swelling, pain—indicate that the body is fighting and healing.)

References
Abbas et al., Cellular and Molecular Immunology
Serhan et al., Nature, 2007

Chronic low-grade inflammation
Low-grade, or “silent,” inflammation is a chronic, non-infectious, low-intensity immune response that persists for months or years. It is often triggered by obesity, metabolic stress, and poor nutrition, which includes not only unhealthy food choices but also incomplete digestive processes and microbiota imbalances.

This condition is characterized by slightly elevated blood markers that are often technically within normal ranges (such as CRP), making clinical diagnosis extremely challenging. It acts as a “silent killer,” serving as a precursor to serious conditions such as diabetes, heart disease, and chronic pain.

Key aspects of low-grade inflammation include:
Multifactorial causes:

In addition to physical inactivity and environmental factors, metabolic disturbances and alterations of the intestinal barrier play a crucial role. When food is not properly digested, it can trigger a persistent immune reaction that fuels the inflammatory state.

Systemic impact:
This chronic state causes mild but continuous tissue damage, directly linked to diseases such as Alzheimer’s disease, type 2 diabetes, cardiovascular disorders, and certain cancers.
How to diagnose it:
A. First phase:
Because standard tests do not detect acute abnormalities, diagnosis must rely on analysis of persistent symptoms such as unexplained fatigue, chronic pain, and cognitive changes (brain fog).
B. Second phase:
High-sensitivity C-reactive protein (hs-CRP) blood test. Unlike standard CRP, hs-CRP can measure values below 0.3 mg/dL, allowing detection of minimal fluctuations that would otherwise remain invisible.
C. Third phase

Interlukin-6 (IL-6). This is a specialized test. In most laboratories, IL-6 is considered “normal” up to about 5–10 pg/mL. In acute infection, IL-6 can rise to 100 or 1000 pg/mL.
In low-grade inflammation, IL-6 may increase from 1 to 3 pg/mL.
Although tripled (and therefore abnormal), the laboratory result will still read “Below limit: NORMAL.” This is why it is an “elusive” marker for general practitioners, but an “advanced biomarker” for specialists who can interpret subtle variations. Specialists often evaluate IL-6 together with the Neutrophil-to-Lymphocyte Ratio (NLR), a simple calculation from the complete blood count that confirms whether the immune system is in a state of chronic alert.

References
Minihane et al., British Journal of Nutrition, 2015
Hotamisligil, Nature, 2006
Pearson et al., Circulation, 2003
Lucius, Integrative and Complementary Therapies, 2023

Low-grade chronic inflammation and systemic inflammation
When the inflammatory state simultaneously involves multiple body districts, it is referred to as systemic inflammation. This condition may arise either from the generalization of an acute inflammatory process or from the progressive extension of an initially localized low-grade chronic inflammatory state.

The intestine represents one of the main sites of origin due to its extensive surface area, intense immune activity, and interaction with the microbiota. However, the process affects numerous organs and tissues.

References
Furman et al., Science, 2019
Franceschi et al., Cell, 2018

Global prevalence
Chronic inflammatory diseases are the leading cause of death worldwide. It is estimated that about 3 out of 5 people globally die from diseases linked to chronic inflammatory processes.
“Chronic inflammatory diseases are the most significant cause of death in the world. The World Health Organization (WHO) ranks chronic diseases as the greatest threat to human health. The prevalence of diseases associated with chronic inflammation is anticipated to increase persistently for the next 30 years in the United States. in 2000, nearly 125 million Americans were living with chronic conditions and 61 million (21%) had more than one. In recent estimates by Rand Corporation, in 2014 nearly 60% of Americans had at least one chronic condition, 42% had more than one and 12% of adults had 5 or more chronic conditions. Worldwide, 3 of 5 people die due to chronic inflammatory diseases like stroke, chronic respiratory diseases, heart disorders, cancer, obesity, and diabetes. 2022”.

References
Furman et al., Science, 2019

Main causes and triggering factors
Gut dysbiosis: Alteration of the intestinal bacterial flora, which may be caused by an unbalanced diet, excessive use of antibiotics, or other toxic substances.

Unhealthy diet: Excessive consumption of processed foods rich in refined sugars and saturated fats, which can promote inflammation.
Stress: Chronic stress can negatively affect the immune system and increase susceptibility to inflammation.
Environmental pollution and toxins: Exposure to chemicals present in the environment or in food may contribute to oxidative stress and inflammation.
Smoking and alcohol: These factors can worsen oxidative stress and damage cells, thereby promoting inflammation.

References
Cani et al., Diabetes, 2007
Tilg & Moschen, Gut, 2014
Egger & Dixon, AJPM, 2014
Slavich & Irwin, Psychological Bulletin, 2014
Common symptoms
Digestive disorders: Bloating, abdominal cramps, diarrhea or constipation, which may vary in intensity and frequency.
Persistent fatigue: Chronic tiredness, lack of energy, and difficulty concentrating.
Joint pain: Widespread muscle and joint pain.
Skin alterations: Rashes, eczema, or other skin manifestations.
Sleep problems: Difficulty falling asleep or maintaining deep sleep.
Skin manifestations

References
Dantzer et al., Brain Behav Immun, 2008
Miller et al., Biol Psychiatry, 2009
Long-term consequences
If left untreated, low-grade intestinal inflammation may contribute to the development of chronic diseases such as:
Cardiovascular diseases: Increased risk of heart attack, stroke, and other cardiovascular conditions.
Type 2 diabetes: Higher likelihood of developing insulin resistance and diabetes.

Autoimmune diseases: Increased susceptibility to conditions such as rheumatoid arthritis, lupus, etc.
Neurodegenerative disorders: Increased risk of developing diseases such as Alzheimer’s or Parkinson’s.
Certain types of cancer: Increased risk of developing some cancers.
General measures that may help reduce inflammation
Follow a balanced diet: Rich in fiber, fruits, vegetables, and whole foods, with a low glycemic index.
Reduce intake of processed foods, refined sugars, and saturated fats.
Manage stress: Through relaxation techniques, meditation, yoga, or other stress-reducing activities.
Maintain a healthy weight: Obesity and overweight can increase inflammation.
Limit alcohol consumption and quit smoking.
Supplement with probiotics: They may help restore the balance of the intestinal bacterial flora.
References
Estruch et al., NEJM, 2018
Calder et al., Br J Nutr, 2011

Note
Low-grade chronic inflammation (or “silent” inflammation) is a key factor in the development and progression of cardiovascular diseases, including atherosclerosis, hypertension, and myocardial infarction. This often asymptomatic process causes endothelial dysfunction, stimulates the formation and rupture of atherosclerotic plaques, and may lead to acute coronary syndromes.

References
Ridker et al., NEJM, 2017
Libby, Nature, 2002

Topics covered in the in-depth study
1 – Paradigmatic cases (Obesity, Metabolic syndrome, Rheumatoid arthritis (autoimmune disease), Biomarkers.
2 – Appendix A: Generalized inflammation
3 – Appendix B: Undigested food
4 – A special case: the role of gluten