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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

3.4.1. Normal conditions: the acid barrier

In a truly healthy subject*, fermentation in the stomach is almost absent because it is a highly acidic environment due to hydrochloric acid.

Hostile environment:

The stomach secretes hydrochloric acid, maintaining a very low pH (about 1.5–3.0). This high level of acidity acts as a real safety filter, neutralizing most bacteria and yeasts ingested with food.

Transit speed:

Under normal conditions, simple sugars pass rapidly into the duodenum (about 15–30 minutes), without giving the few surviving microorganisms enough time to initiate fermentation processes.

The stomach, however, is not completely sterile. Some microorganisms may, under certain circumstances, be present and play a limited role:

Yeasts (such as Candida albicans):

They are naturally present in the digestive tract. If sugars remain in the stomach for too long, for example due to a previous meal that is slow to digest, yeasts may metabolize them producing gas (carbon dioxide) and small amounts of ethanol.

Acid-tolerant bacteria:

Some strains of lactobacilli or bacteria coming from the duodenum (especially when gastric acidity is temporarily buffered by food) may contribute to limited fermentative processes.

3.4.2. Altered conditions: when the stomach “ferments”

Fermentation becomes possible when the acid barrier is reduced or when food stagnates in the stomach. The main causes may include:

Chronic stress (brain–gut axis):
Prolonged stress may act on two fronts:

  • Reduced acid secretion: through activation of the sympathetic nervous system, stress may reduce the production of HCl, increasing gastric pH and making the environment more favorable for microbial survival.

  • Altered motility: stress may modify gastric contractions, slowing gastric emptying.

Very complex or high-fat meals:

Fats stimulate hormonal signals that slow gastric emptying and the opening of the pylorus. If simple sugars are introduced on top of this slowdown, gastric contents may remain in the stomach for longer.

Use of medications:

Proton pump inhibitors (PPIs) artificially increase gastric pH, reducing the natural bactericidal effect of hydrochloric acid.

Excess presence of yeasts (SIFO):

In conditions of dysbiosis, yeasts such as Saccharomyces or Candida may more heavily colonize the upper digestive tract and contribute to the fermentation of sugars.

3.4.3. The consequences: what gastric fermentation causes

Although quantitatively lower than intestinal fermentation, fermentation in the stomach is very uncomfortable because it occurs in an organ located high in the torso:

Gas production ($CO_2$):
Gas accumulates rapidly, causing distension of the gastric walls (a balloon-like sensation under the sternum).

Belching and reflux:

Gas pressure pushes against the cardia (the upper valve). This may cause the upward movement of air mixed with acidic vapors or food (reflux).

Organic acidity:

Bacteria and yeasts produce organic acids (such as lactic acid) that irritate the mucosa, creating a burning sensation different from that caused by pure hydrochloric acid.

Postprandial drowsiness:

The production of small amounts of fermentation by-products (such as ethanol or acetaldehyde) may contribute to “brain fog” or extreme tiredness after eating sweets.

In summary

Gastric fermentation does not represent a normal physiological process, but may indicate an alteration of the digestive environment caused by reduced gastric acidity or by delayed gastric emptying. These conditions allow microorganisms to metabolize sugars before complete digestion occurs.

[4] Additives and intestinal health

The impact of food additives on health does not depend only on their intrinsic toxicity (regulated by health authorities), but also on their synergistic effect on the intestinal barrier. In particular, research highlights two critical mechanisms:

4.1. Alteration of the protective mucus layer (Emulsifiers):

Additives such as carboxymethylcellulose (E466) or polysorbate-80 (E433), commonly found in industrial sauces and desserts, may act as surfactants. They tend to “dissolve” the mucus layer that lines the intestine, allowing bacteria to come into direct contact with the mucosal cells, thereby triggering a chronic inflammatory response.

4.2. Dysbiosis and permeability (Sweeteners and preservatives):

The constant intake of mixtures of additives may alter the composition of the microbiota (dysbiosis). A bacterial imbalance, combined with the action of certain preservatives, may weaken the tight junctions between intestinal cells. This increase in permeability (leaky gut) facilitates the passage of bacterial fragments and undigested molecules into the bloodstream, promoting systemic low-grade inflammation.

[5] Undigested gluten

In healthy individuals, according to current knowledge, there is no solid and conclusive clinical evidence demonstrating a significant systemic impact of gluten on intestinal permeability or on the inflammatory balance of the organism.

Nevertheless, in individuals who present genetic predispositions, immune vulnerabilities, or existing clinical conditions—even when not yet clearly manifested clinically—adopting a principle of nutritional caution does not represent excessive prudence but rather an attitude of preventive responsibility. This approach does not necessarily imply the indiscriminate elimination of gluten from the diet, but rather a careful and personalized evaluation of the person’s clinical, metabolic, and nutritional context.

In these cases, diet may contribute—either positively or negatively—to the modulation of the inflammatory and immune balance of the organism, within a systemic view of health.

The quality of daily nutrition does not exert effects exclusively on the intestine. It influences overall immune tone, the level of chronic low-grade inflammation, and indirectly also brain health through the complex mechanisms of the gut–brain axis. Taking care of the intestine therefore largely means taking care of the entire organism.

[5.1] Gluten and intestinal permeability

Gluten is a complex protein rich in prolamins (gliadins) that our enzymatic system is not able to completely digest.

Gliadins are composed of long chains of amino acids—the “building blocks” of proteins—linked together in a way that makes the action of digestive enzymes difficult, preventing the complete separation of these amino acids before absorption by the intestinal wall.

In predisposed individuals, some of these incompletely digested protein fragments may stimulate the release of zonulin, a protein that acts as a regulator of intestinal junctions.

While in a healthy individual these “gates” close rapidly without consequences, in vulnerable subjects they may remain open longer, facilitating intestinal permeability and the appearance of low-grade inflammatory processes, as described in the previous points.

Main scientific references

Below are some high-profile scientific studies that support the concepts described in this guide, particularly regarding intestinal permeability and the possible impact of food additives and emulsifiers on intestinal balance.

1. On intestinal permeability and zonulin (Points [1] and [5])

This research is fundamental because it identified the biological mechanism through which gluten and intestinal health interact, introducing the concept of the “opening” of tight junctions.

Author: Alessio Fasano
Title: Zonulin, regulation of tight junctions, and autoimmune diseases
Year: 2011 (with continuous updates until 2020)
DOI: 10.1146/annurev-med-051809-150355

Extended abstract:

The research describes the discovery of zonulin, one of the main physiological modulators of intestinal tight junctions. The study shows how undigested fragments of gluten (gliadin) stimulate the release of zonulin not only in individuals with celiac disease but also in genetically predisposed individuals. This release increases intestinal permeability, allowing antigens to pass from the intestinal lumen into the bloodstream. The work highlights how this process may underlie chronic low-grade inflammation and trigger systemic immune responses, contributing to the scientific understanding of intestinal permeability.

2. On the effect of emulsifiers and intestinal mucus (Point [4])

This study is a milestone regarding industrially processed foods and explains why the cumulative effect of additives is a concern for the microbiota.

Author: Benoit Chassaing et al.
Title: Dietary emulsifiers impact the mouse gut microbiota promoting colitis and metabolic syndrome
Year: 2015 (published in Nature)
DOI: 10.1038/nature14232

Extended abstract:

The authors analyzed the impact of two common industrial emulsifiers: carboxymethylcellulose and polysorbate-80. The study demonstrates that these substances are not inert but directly alter the composition of the microbiota and the interaction between bacteria and the host. In particular, emulsifiers reduce the thickness of the protective intestinal mucus layer, allowing bacteria to come excessively close to epithelial cells. This leads to chronic intestinal inflammation that is reflected systemically through metabolic alterations (increased blood glucose and adiposity). The research suggests that the widespread use of these additives may have contributed to the global rise in chronic inflammatory diseases.

Why cite these studies in the guide?

  1. Validation of “leaky gut”:
    The research of Alessio Fasano brings the concept of intestinal permeability out of the realm of alternative medicine and into academic medicine.

  2. Risks of ultra-processed foods:
    The study by Benoit Chassaing published in Nature provides biochemical evidence that the problem with industrial foods is not only sugar but also their chemical structure (such as emulsifiers).

  3. Systemic approach:
    Both studies confirm that what happens in the intestine has immediate effects on metabolism and on the overall immune system (low-grade inflammation).

Conclusion

Taking care of the intestine means adopting an attitude of conscious prevention. Absolute rigidity is not necessary, but rather a simple, balanced, and high-quality dietary approach capable of protecting not only the intestine but the entire organism—including brain health.

Low-Grade Chronic Inflammation in Italian Science Communication (2025–2026)

Introduction to Journalistic Sources

Selection of authoritative Italian articles from 2025–2026 that address low-grade chronic inflammation directly or substantially, especially in relation to longevity, diet, physical activity, stress, and metabolism. Among the most relevant are: “Silent Chronic Inflammation: What It Is, Symptoms, and How to Treat It” from Style/Corriere della Sera (April 10, 2026); “Is It True That Sport Does Not Help You Lose Weight?…” from Corriere della Sera (March 21, 2026); “The Three ‘F’s That Keep the Intestine (and the Brain) Healthy” from Cook/Corriere (March 14, 2026); “Yes, Diet Can Slow Aging” from la Repubblica Salute (August 11, 2025); “The Secret of Longevity for 2026? Breathe, Rest, Smile, and Learn to Forgive” from la Repubblica Salute (December 23, 2025); and “Tell Me How You Eat and I’ll Tell You How You Age” from la Repubblica Salute (December 30, 2025).

Below is an extended abstract constructed from these articles.

Extended Abstract

In Italian scientific and health journalism of 2025–2026, low-grade chronic inflammation emerges as a cross-cutting interpretative key for understanding biological aging and many chronic degenerative diseases. The selected articles describe it not as an acute and visible episode, but as a persistent, “silent” state of low-intensity immune activation, often lacking specific symptoms but capable, over time, of promoting insulin resistance, increased abdominal fat, chronic fatigue, and a greater cardiovascular and neurodegenerative risk. Style/Corriere indeed defines it as a “silent enemy” and a “common ground” for numerous clinical conditions, emphasizing how it is often normalized in everyday life.

A first very strong narrative line concerns the relationship between inflammation and aging. la Repubblica Salute explicitly connects low-grade chronic inflammation with “inflammaging,” that is, the process through which the organism ages in the presence of persistent immune activation and oxidative stress. In the article about telomeres, the central idea is that the inflammatory potential of the diet may accelerate or slow telomeric erosion: pro-inflammatory foods are associated with shorter telomeres, while dietary patterns richer in fiber, polyphenols, and unsaturated fats are presented as plausibly protective. The same newspaper, at the end of 2025, reiterates that preventing inflammation is essential for longevity, because it accelerates biological age and increases the risk of the main diseases of older age.

A second thematic area concerns diet as a modulation factor. The articles do not propose miraculous solutions, but converge on some recurring elements: reducing ultra-processed foods or those with a high inflammatory load, stabilizing blood glucose, favoring minimally processed foods, quality fats, fiber, and foods that support the intestinal microbiota. Style/Corriere lists among the most favorable foods fish rich in omega-3, leafy green vegetables, berries, extra-virgin olive oil, oil seeds, turmeric, ginger, and fermented foods, insisting however that the benefit depends on the overall dietary pattern and not on the single “superfood.” la Repubblica reinforces this approach by citing the Dietary Inflammatory Index (DII), used to estimate how pro- or anti-inflammatory a diet is.

A third direction concerns the role of physical movement. In Corriere della Sera of March 21, 2026, physical activity is presented as a “multi-target drug” that does not serve only to burn calories, but acts on insulin sensitivity, liver fat, blood pressure, glycemia, sleep, and mood. In this framework, movement and a healthy diet are described as powerful modulators of low-grade chronic inflammation, also thanks to the production of myokines by contracting muscle, that is, molecules with anti-inflammatory and metabolic effects. The Cook/Corriere article on the microbiota completes the picture by suggesting that regular sport and the health of intestinal mucosae are closely connected, with possible combined benefits on autophagy, immune function, and reduction of systemic inflammation.

A fourth strand concerns stress, sleep, and neuroendocrine regulation. Style/Corriere insists that chronic stress and poor sleep quality directly fuel inflammatory processes; the increase in cortisol, the worsening of insulin sensitivity, and the increase in hunger are recalled as mechanisms that keep the organism in a prolonged state of alert. Wired Italia, although not focused exclusively on low-grade chronic inflammation, reinforces the idea that chronic dysregulation of cortisol and circadian rhythms may contribute to visceral obesity, metabolic alterations, and persistent stress, all elements consistent with the pro-inflammatory framework discussed in the other articles. la Repubblica, in the interview on longevity, extends the reasoning to oral health and psychological well-being, suggesting that periodontal diseases and chronic emotional stress may also increase systemic inflammation.

Overall, these articles present low-grade chronic inflammation as a systemic condition in which nutrition, body composition, stress, sleep, microbiota, physical exercise, and cellular aging converge. The prevailing journalistic message is that it is not a single disease, but rather a “biological substrate” that may precede or accompany many diseases. From this derives a strongly preventive vision: not extinguishing a symptom, but reducing the daily inflammatory load through repeated and realistic interventions on lifestyle.

From a critical point of view, however, it should be observed that these texts are journalistic dissemination articles, not systematic reviews or guidelines. Some report studies or interviews with specialists correctly but in a synthetic way; others use a more lifestyle-oriented tone and simplify a complex biological framework. The convergence among different newspapers, however, is remarkable: all recognize low-grade chronic inflammation as a central node between metabolism and aging, and all indicate lifestyle habits as the main area of intervention. This convergence does not replace clinical evidence, but signals that the topic has now firmly entered the Italian public discourse on prevention and longevity.

Journalistic Sources

Style – Corriere della Sera, April 10, 2026, “Silent Chronic Inflammation: What It Is, Symptoms, and How to Treat It.”
Corriere della Sera, March 21, 2026, “Is It True That Sport Does Not Help You Lose Weight? Here Is Why Exercise Does Not Count Only for the Calories Burned.”
Cook – Corriere della Sera, March 14, 2026, “The Three ‘F’s That Keep the Intestine (and the Brain) Healthy.”
la Repubblica – Salute, August 11, 2025, “Yes, Diet Can Slow Aging.”
la Repubblica – Salute, December 23, 2025, “The Secret of Longevity for 2026? Breathe, Rest, Smile, and Learn to Forgive.”
la Repubblica – Salute, December 30, 2025, “Tell Me How You Eat and I’ll Tell You How You Age.”

In-Depth Analysis of Some Significant Articles

1. Corriere della Sera – Style

Corriere della Sera
Title: Silent Chronic Inflammation: What It Is and How to Counter It with Diet and Lifestyle
Section: Style – Wellness
Date: April 10, 2026

Short quote from the article

“Low-grade chronic inflammation is a silent process that may, over time, promote metabolic, cardiovascular, and neurodegenerative diseases.”

Extended Abstract

The article describes low-grade chronic inflammation as a persistent biological condition characterized by a mild but continuous activation of the immune system. Unlike acute inflammation, it does not present evident symptoms but may develop slowly over time, contributing to the development of various chronic diseases. Among these are obesity, type 2 diabetes, cardiovascular diseases, and processes of accelerated aging.

The text highlights the central role of lifestyle in modulating inflammatory processes. A diet rich in ultra-processed foods, refined sugars, and saturated fats would favor a pro-inflammatory state, while a balanced diet rich in fiber, vegetables, fish, and unsaturated fats would have anti-inflammatory effects. The contribution of the intestinal microbiota in regulating the systemic immune response is also emphasized.

Another relevant dimension concerns the relationship between chronic inflammation and biological aging. The article refers to the concept of inflammaging, that is, accelerated aging associated with a persistent inflammatory state. According to the experts cited, reducing the inflammatory load through balanced nutrition, regular physical activity, adequate sleep, and stress management represents a fundamental preventive strategy.

2. la Repubblica – Salute

la Repubblica
Title: Yes, Diet Can Slow Aging: The Role of Inflammation and Telomeres
Section: Health
Date: August 11, 2025

Short quote

“A diet with a high inflammatory index is associated with shorter telomeres and faster biological aging.”

Extended Abstract

The article analyzes the link between diet, systemic inflammation, and cellular aging. It presents the concept of the Dietary Inflammatory Index (DII), used in epidemiological studies to evaluate the pro- or anti-inflammatory potential of diet. According to the research cited, dietary patterns rich in simple sugars, saturated fats, and highly processed foods are associated with an increase in inflammatory markers and with a greater probability of shorter telomeres. Telomeres, structures that protect the ends of chromosomes, represent a biological indicator of cellular aging. Conversely, a diet rich in fruit, vegetables, fiber, whole grains, legumes, and fish appears correlated with a lower level of systemic inflammation. The article suggests that the Mediterranean dietary pattern may represent an effective strategy for modulating chronic inflammatory processes and promoting greater longevity.

3. Corriere della Sera – Salute

Corriere della Sera
Title: Is It True That Sport Does Not Help You Lose Weight? Why Exercise Matters Beyond Calories
Date: March 21, 2026

Short quote

“Regular physical activity reduces systemic inflammation and improves insulin sensitivity, blood pressure, and metabolism.”

Extended Abstract

The article discusses the role of physical activity in metabolic health and in the prevention of chronic diseases. The text clarifies that physical exercise does not act only through caloric expenditure but produces a series of complex physiological effects that include regulation of blood glucose levels, improvement of insulin sensitivity, and reduction of systemic inflammation levels.

Part of the analysis concerns the production of myokines, molecules released by muscle during contraction that exert anti-inflammatory and metabolic effects. Through these mechanisms, physical activity contributes to the reduction of low-grade chronic inflammation and to the improvement of cardiovascular and metabolic health.

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