Fiber and Inflammation: How a High-Fiber Diet Reduces Chronic Inflammation
By Cole Stubblefield | Last Updated: March 2026 | 13 min read
Chronic low-grade inflammation is the common thread connecting cardiovascular disease, type 2 diabetes, cancer, Alzheimer's disease, and accelerated aging. Dietary fiber addresses it through four distinct biological mechanisms. Here is the complete picture.
Affiliate Disclosure: This article contains affiliate links. If you purchase through our links, we may earn a commission at no additional cost to you. See our full Affiliate Disclosure.
Medical Disclaimer: This content is for educational purposes only and does not constitute medical advice. Always consult a qualified healthcare provider before changing your diet or supplement protocol. See our Medical Disclaimer.
Table of Contents
- What Chronic Inflammation Actually Is
- Inflammaging: The Slow Burn That Ages You
- How Fiber Reduces Inflammation: Four Mechanisms
- What the Clinical Trials Show: CRP, IL-6, and TNF-alpha
- The Harvard Cohort Finding: Why Results Vary Between Individuals
- Fiber vs. Other Anti-Inflammatory Interventions
- Fiber and Specific Inflammatory Conditions
- The Best Fiber Sources for Reducing Inflammation
- Practical Protocol: How to Use Fiber to Lower Inflammation
- Frequently Asked Questions
What Chronic Inflammation Actually Is
Acute inflammation is the immune system working correctly. When you cut your finger or catch a cold, the redness, swelling, and heat you feel are the result of immune cells rushing to the site of damage or infection to neutralize the threat and begin repair. This is a tightly regulated, purposeful process that resolves when the threat is eliminated.
Chronic low-grade inflammation is something entirely different. It is a persistent, low-level activation of the immune system with no clear trigger and no resolution. Inflammatory cytokines including C-reactive protein, interleukin-6, and tumor necrosis factor-alpha remain chronically elevated. The immune system is not responding to an acute threat. It is stuck in a state of background activation that quietly damages tissues, impairs cellular function, and accelerates biological aging.
The downstream consequences of this chronic inflammatory state are significant. Chronic low-grade inflammation is now recognized as a shared pathological mechanism underlying virtually every major non-communicable disease. Atherosclerosis is driven by inflammatory processes in arterial walls. Insulin resistance is perpetuated by inflammatory cytokine signaling in adipose tissue and skeletal muscle. Alzheimer's disease involves chronic neuroinflammation driven by activated microglia. Colorectal cancer development is promoted by the inflammatory microenvironment of a dysbiotic gut. Even depression has an inflammatory component, with elevated IL-6 and CRP consistently associated with depressive symptoms in population studies.
The primary drivers of chronic low-grade inflammation in modern populations are well characterized: obesity, physical inactivity, sleep deprivation, psychological stress, smoking, and diet. Among dietary drivers, ultra-processed food consumption, excess refined carbohydrate intake, inadequate antioxidant intake, and critically, chronically low dietary fiber intake are the most consistently implicated.
Inflammaging: The Slow Burn That Ages You
Inflammaging is a term coined by immunologist Claudio Franceschi to describe the chronic, sterile, low-grade inflammatory state that accumulates with aging and is associated with accelerated disease and mortality.
As the gut microbiome becomes less diverse with age, driven partly by declining dietary variety and fiber intake, butyrate-producing bacterial populations decline. Gut barrier integrity degrades. Bacterial lipopolysaccharide enters systemic circulation in increasing concentrations. Pattern recognition receptors on innate immune cells are chronically activated. The result is a self-reinforcing cycle of microbiome degradation, gut barrier failure, systemic immune activation, and tissue inflammation that compounds over decades.
A February 2025 review published in the International Journal of Molecular Sciences examining the impact of dietary fiber on inflammation confirmed that insoluble cereal fiber intake shows the strongest and most consistent protective associations with long-term health outcomes related to inflammaging, noting that cohort studies consistently link high intake of cereal fiber and whole grain products with decreased risk of type 2 diabetes, cancer, cardiovascular disease, and chronic inflammatory disorders, all conditions that are at least partially driven by inflammaging.
The fibermaxxing framework is, in part, a direct anti-inflammaging protocol. Maintaining high, diverse fiber intake throughout adulthood sustains the butyrate-producing bacterial populations that protect gut barrier integrity, which prevents the LPS-driven immune activation cascade that drives inflammaging at its source.
How Fiber Reduces Inflammation: Four Mechanisms
Dietary fiber does not reduce inflammation through a single pathway. Four distinct and reinforcing mechanisms operate simultaneously.
Mechanism 1: Gut Barrier Protection and LPS Reduction
The most fundamental mechanism connects fiber to inflammation through the gut barrier. When butyrate production is adequate, colonocytes are well-fueled and the tight junction proteins sealing the gaps between them are robustly expressed. The mucus layer over the epithelium is thick and intact. Bacterial lipopolysaccharide, a pro-inflammatory component of gram-negative bacterial cell walls, is confined to the gut lumen where it belongs.
When fiber intake drops and butyrate production falls, the gut barrier degrades. LPS enters systemic circulation through the portal vein and activates toll-like receptor 4 on macrophages, dendritic cells, and endothelial cells throughout the body. This activation triggers NF-kB signaling and the subsequent production of inflammatory cytokines including TNF-alpha, IL-1-beta, IL-6, and CRP. This is the primary mechanism connecting low fiber intake to systemic chronic inflammation. Repairing the gut barrier through consistent high fiber intake is the most upstream intervention available for reducing this source of chronic immune activation.
Mechanism 2: SCFA-Mediated NF-kB Inhibition
Short-chain fatty acids produced through fiber fermentation directly inhibit the NF-kB inflammatory signaling pathway through multiple mechanisms. Butyrate inhibits histone deacetylase activity, which reduces the transcriptional activity of NF-kB target genes including those encoding TNF-alpha, IL-6, and cyclooxygenase-2. Propionate and acetate bind to GPR41 and GPR43 receptors on immune cells and activate intracellular signaling cascades that suppress NF-kB independently of the HDAC mechanism.
This direct anti-inflammatory SCFA activity operates systemically. SCFAs produced in the colon enter portal circulation, distribute to the liver and peripheral tissues, and suppress inflammatory gene expression in macrophages, adipocytes, and vascular endothelial cells throughout the body. The anti-inflammatory effect of dietary fiber is not confined to the gut. It operates wherever circulating SCFAs reach, which is essentially everywhere.
Mechanism 3: Regulatory T Cell Induction
As detailed in the fiber and immune system article, butyrate promotes the differentiation of naive T cells into regulatory T cells through HDAC inhibition and Foxp3 upregulation. Regulatory T cells are the immune system's anti-inflammatory moderators. They suppress excessive cytokine production, prevent autoimmune tissue attack, and maintain immune homeostasis.
Populations with higher butyrate-producing bacterial loads consistently show higher Treg counts and lower baseline inflammatory cytokine levels. This mechanism represents a long-term immune recalibration rather than an acute anti-inflammatory effect. It develops over weeks and months of consistent high-fiber intake as butyrate levels rise and Treg populations expand.
Mechanism 4: Microbiome Diversity and Competitive Displacement of Pro-Inflammatory Species
A well-fed, diverse gut microbiome physically and chemically outcompetes pro-inflammatory bacterial species for colonization space and nutrients. High-fiber diets consistently shift the microbiome toward higher Faecalibacterium prausnitzii, Akkermansia muciniphila, Bifidobacterium, and Roseburia populations. These species are associated with anti-inflammatory metabolite production and gut barrier support.
Conversely, low-fiber diets enrich pro-inflammatory species including Enterobacteriaceae and certain Proteobacteria, which produce LPS and other pro-inflammatory compounds in larger quantities. Maintaining a high-fiber diet is an ongoing competitive intervention that continuously selects against pro-inflammatory species and for anti-inflammatory ones.
What the Clinical Trials Show: CRP, IL-6, and TNF-alpha
CRP Reduction in Overweight and Obese Adults
A meta-analysis of 14 randomized controlled trials examining the effect of dietary fiber on circulating CRP levels in overweight and obese adults found that fiber intervention produced a significant reduction of 0.37 mg/L in circulating CRP compared to control groups. The effect was significant only when the fiber intake difference between intervention and control groups exceeded 8 grams per day, confirming the dose-dependent nature of fiber's anti-inflammatory effect. Small increases in fiber intake produce minimal CRP reduction. Reaching the clinical fibermaxxing threshold produces a meaningful one.
CRP Reduction in Children and Adolescents
A 2025 systematic review and meta-analysis published in Current Developments in Nutrition examined 25 randomized controlled trials studying the effect of dietary fiber on chronic low-grade inflammation markers in children and adolescents. The meta-analysis for CRP concentrations across 10 studies revealed a significant decrease of 0.640 mg/L following fiber interventions compared to controls. The review noted that fiber supplementation produced significantly greater CRP reductions than dietary change advice alone, supporting the use of targeted fiber supplementation when dietary change is insufficient.
Anti-Inflammatory Dietary Patterns
A 2025 umbrella review of dietary patterns and inflammatory markers published in Nutrition Reviews examined 30 systematic reviews covering 225 primary studies. The findings confirmed that plant-based foods including green leafy vegetables, legumes, and whole grains, which are rich in fiber, magnesium, and antioxidants, are consistently associated with lower CRP and IL-6 concentrations. The Mediterranean diet, which is characterized by high fiber intake from legumes, whole grains, fruits, and vegetables, showed the strongest and most consistent evidence for CRP reduction across all dietary patterns reviewed.
A complementary meta-analysis published in Frontiers in Nutrition in 2025 found that anti-inflammatory dietary patterns produced significant reductions in systolic blood pressure, LDL cholesterol, total cholesterol, and high-sensitivity CRP compared to omnivorous control diets. The fiber content of these dietary patterns was identified as a primary contributor to their anti-inflammatory effects, alongside polyphenols and omega-3 fatty acids.
Fiber Supplementation vs. Whole Food Sources
The 2025 pediatric meta-analysis found that fiber supplementation produced significantly greater CRP reductions than dietary advice to increase fiber-rich food consumption. This finding has practical implications. While whole food fiber sources are preferable for their nutritional breadth, targeted fiber supplementation, particularly with fermentable prebiotic fibers that drive SCFA production, may produce faster and more reliable inflammatory marker reductions in people who cannot achieve adequate intake through diet alone.
The Harvard Cohort Finding: Why Results Vary Between Individuals
One of the most clinically important findings in recent fiber and inflammation research comes from a 2021 Harvard cohort study published in Genome Medicine, involving 307 healthy men with detailed microbiome profiling and inflammatory marker tracking over six months.
The headline finding confirmed the expected: higher dietary fiber intake was associated with shifts in gut microbiome composition toward Clostridiales species capable of carbohydrate utilization, and these shifts corresponded with lower circulating CRP levels. Fruit fiber, particularly pectin, produced the strongest microbiome and CRP effects.
The more striking finding was the individual variability. Fiber intake was associated with significantly greater CRP reduction in individuals without substantial Prevotella copri carriage in the gut, whereas those with P. copri carriage maintained stable CRP levels regardless of fiber intake.
Prevotella copri is a common gut bacterium found at high abundance in some individuals but not others. In the context of this study, its presence appeared to blunt the CRP-lowering effect of increased fiber intake entirely. The mechanism is not fully understood but likely involves Prevotella copri competing with the Clostridiales species that produce the anti-inflammatory SCFAs responsible for fiber's CRP-lowering effect.
The practical implication is important. If you have increased your fiber intake and found minimal inflammatory marker improvement, your individual microbiome composition may be a factor. This is one of the strongest arguments for microbiome testing before designing a fiber protocol. Knowing your specific bacterial composition allows for more targeted intervention than simply increasing total fiber intake and hoping for the expected average result.
Viome Gut Intelligence uses metatranscriptomic sequencing to profile not just which bacteria are present but which ones are metabolically active. For people whose inflammatory markers are not responding as expected to dietary change, this level of individual microbiome characterization can identify the specific bacterial patterns driving the resistance. See our Shop page for details on the Viome test.
Fiber vs. Other Anti-Inflammatory Interventions
Anti-inflammatory interventions are not all equivalent. Framing fiber's place in the landscape honestly requires comparing it to the alternatives.
Fiber vs. Anti-Inflammatory Supplements
Omega-3 fatty acids, curcumin, and resveratrol are the most commonly used anti-inflammatory supplements. The evidence for omega-3 supplementation for CRP reduction is modest and inconsistent across trials. Curcumin has demonstrated anti-inflammatory activity in clinical trials but has poor bioavailability in standard formulations, limiting real-world effectiveness without specialized delivery systems. Resveratrol's clinical evidence is less robust than its preclinical profile.
Dietary fiber's CRP-reducing effect, while modest in individual trials, is mechanistically upstream of the pathways these supplements target. Fiber reduces gut barrier permeability and LPS translocation, which is the source of the inflammatory signal that these supplements attempt to suppress downstream. Addressing the source rather than the downstream signal is the more fundamental approach.
Fiber vs. Exercise
Regular physical activity reduces CRP and systemic inflammatory markers through mechanisms including adipose tissue reduction, skeletal muscle anti-inflammatory myokine production, and improved insulin sensitivity. The CRP reductions from regular aerobic exercise are comparable in magnitude to those from dietary fiber increase. The two interventions work through different mechanisms and are complementary rather than competing. A high-fiber diet combined with regular exercise produces greater inflammatory marker reductions than either alone.
Fiber vs. Caloric Restriction
Caloric restriction reduces inflammation through body fat reduction, which decreases adipose tissue-derived inflammatory cytokine production. The 2025 Nature Communications finding that high-fiber diets mimic caloric restriction's anti-aging transcriptomic signatures without requiring food intake reduction is relevant here. Fiber may produce some of the same anti-inflammatory benefits as caloric restriction without the adherence challenge that caloric restriction imposes.
Fiber vs. Pharmaceutical Anti-Inflammatory Agents
NSAIDs and corticosteroids produce acute, potent suppression of inflammatory pathways. They are appropriate for acute inflammatory conditions but are not suitable as long-term chronic inflammation management strategies due to significant side effect profiles. Dietary fiber produces smaller magnitude effects but operates through upstream, physiological mechanisms with a strong safety profile and no adverse long-term effects at recommended intakes. For chronic low-grade inflammation prevention and management in otherwise healthy individuals, dietary fiber is the more appropriate long-term intervention.
Fiber and Specific Inflammatory Conditions
Cardiovascular Disease
Chronic vascular inflammation drives atherosclerotic plaque formation and progression. CRP is both a marker and a mediator of this process. Fiber's consistent CRP-lowering effect, combined with its LDL-reducing and blood pressure-supporting activities, makes it one of the most comprehensive dietary cardiovascular protective interventions available. The anti-inflammatory dietary pattern meta-analysis published in Frontiers in Nutrition in 2025 confirmed significant reductions in both inflammatory markers and cardiovascular risk factors from high-fiber dietary patterns.
COPD and Respiratory Inflammation
A 2026 case-control study examining the gut-lung axis in COPD patients found that COPD patients had significantly lower dietary fiber intake compared to healthy controls and significantly elevated CRP and IL-6 levels. Dietary fiber intake was inversely correlated with CRP and positively correlated with lung function parameters. Low dietary fiber intake below 20 grams per day was associated with a 3.2-fold increased odds of COPD after adjusting for confounders. The gut-lung axis mechanism, through which SCFA-mediated immune modulation reduces respiratory inflammatory tone, connects these findings to a plausible biological pathway.
Metabolic Syndrome
Metabolic syndrome is characterized by a cluster of conditions including central obesity, elevated triglycerides, low HDL cholesterol, elevated blood pressure, and elevated fasting glucose, all of which are driven in part by chronic low-grade inflammation. High-fiber dietary patterns address multiple components of metabolic syndrome simultaneously through anti-inflammatory, lipid-modulating, and glycemic-stabilizing mechanisms. The comprehensive anti-inflammatory dietary pattern review consistently found the greatest inflammatory marker improvements in populations with metabolic syndrome components.
Inflammatory Bowel Disease
The relationship between fiber and IBD is more nuanced than with other inflammatory conditions. During active flares of Crohn's disease or ulcerative colitis, high-fiber intake can exacerbate symptoms due to increased fermentative activity in an already inflamed intestinal environment. During remission, carefully selected fiber types, particularly soluble and prebiotic fibers that feed anti-inflammatory Faecalibacterium prausnitzii populations, may support maintenance of remission by restoring the butyrate production and gut barrier integrity that IBD disrupts. Anyone with IBD should work with a gastroenterologist before adjusting fiber intake.
The Best Fiber Sources for Reducing Inflammation
Resistant Starch
Resistant starch is the most potent driver of butyrate production and therefore the most direct dietary driver of the gut barrier protection and NF-kB inhibition mechanisms described above. Cooked and cooled legumes, potatoes, and grains maximize resistant starch through retrogradation. Regular resistant starch intake consistently increases Faecalibacterium prausnitzii populations, the butyrate producer most strongly associated with anti-inflammatory gut function.
Oat and Barley Beta-Glucan
Beta-glucan has direct anti-inflammatory activity through Dectin-1 receptor binding on innate immune cells alongside its fermentation-driven SCFA benefits. Clinical trials have specifically demonstrated CRP reductions from beta-glucan supplementation in populations with elevated baseline inflammation. Three grams of beta-glucan per day from oats or barley is the threshold most consistently associated with inflammatory marker improvement in clinical studies.
Pectin-Rich Fruits
The Harvard cohort study found that fruit fiber, particularly pectin, produced the strongest associations with beneficial microbiome shifts and CRP reduction among all fiber subclasses. Apples, pears, citrus fruits, and berries are the most accessible pectin sources. Eating these fruits with the skin intact maximizes pectin delivery. The polyphenol content of these fruits, particularly quercetin and anthocyanins, provides independent anti-inflammatory activity that compounds with the fiber's effect.
Legumes
Legumes provide the broadest fermentation substrate of any food category, simultaneously fueling butyrate-producing Firmicutes, Bifidobacterium, and Akkermansia populations. Their resistant starch, soluble fiber, and galactooligosaccharide fractions drive the competitive displacement of pro-inflammatory bacterial species through multiple parallel pathways. A cup of lentils or black beans at one meal per day delivers a sustained anti-inflammatory fiber dose across all four relevant fiber type categories.
Cruciferous Vegetables
Broccoli, Brussels sprouts, kale, and cabbage deliver insoluble fiber alongside sulforaphane and indole-3-carbinol, compounds with direct NF-kB inhibitory activity independent of fiber fermentation. The combination of fiber-mediated SCFA production and direct phytochemical anti-inflammatory activity makes cruciferous vegetables one of the most multi-mechanistic anti-inflammatory food categories available.
Prebiotic Alliums
Garlic and onion deliver inulin and fructooligosaccharides that specifically feed Bifidobacterium and Akkermansia populations associated with gut barrier maintenance and anti-inflammatory SCFA output. Garlic also contains allicin, which has direct antimicrobial activity against pro-inflammatory bacterial species. Using garlic and onion as the flavor base for cooked meals is the lowest-friction way to ensure daily prebiotic anti-inflammatory fiber intake.
Practical Protocol: How to Use Fiber to Lower Inflammation
Reducing chronic low-grade inflammation through dietary fiber is a 12-week minimum commitment. The inflammatory marker changes that fiber drives through microbiome remodeling and gut barrier repair operate on a timeline of weeks to months, not days.
The protocol runs as follows.
Establish your baseline. Before changing anything, get a fasting CRP test. High-sensitivity CRP is available through most primary care physicians and many direct-to-consumer lab services. A baseline measurement gives you a reference point to evaluate your progress at 8 and 12 weeks. A CRP above 3 mg/L indicates elevated cardiovascular inflammatory risk. A CRP between 1 and 3 mg/L indicates moderate risk. Below 1 mg/L is the target range for low chronic inflammatory burden.
Calculate your fiber target. Use our Precision Fiber Target Calculator to find your personalized daily goal. The anti-inflammatory benefits of fiber are dose-dependent and most reliably achieved at or above the clinical threshold of 14 grams per 1,000 calories consumed.
Build toward your target gradually. Increase fiber by 5 grams per week from your baseline to avoid the GI discomfort that derails most protocol attempts in the first two weeks. Focus the first two weeks on soluble and prebiotic fibers, which drive the most rapid microbiome shifts. Add resistant starch sources in weeks three and four. By week six, incorporate the full range of fiber types across your daily meals.
Prioritize fiber diversity over fiber quantity. Eating 40 grams of fiber from a single source feeds a single bacterial population. Eating 38 grams across six different fiber types feeds a diverse community that drives broader anti-inflammatory microbiome shifts. Rotate your fiber sources throughout the week to maximize microbial diversity.
Track inflammatory markers at 8 and 12 weeks. CRP is the most accessible and widely studied marker. Requesting a full inflammatory panel including IL-6 and fibrinogen alongside CRP provides a more complete picture of the protocol's effect. Results at 8 weeks will show early microbiome-mediated changes. Results at 12 weeks reflect the more stable microbiome remodeling and gut barrier improvements.
For a structured meal plan built around anti-inflammatory fiber diversity, see our Clinical Meal Protocol. For vetted synbiotic supplements that accelerate the Bifidobacterium and Akkermansia population growth driving the anti-inflammatory microbiome shift, see our Shop page.
Frequently Asked Questions
How long does it take for fiber to reduce CRP? The clinical trial data shows CRP reductions emerging at 4 to 8 weeks of consistent high-fiber intake, with the strongest effects at 12 weeks or more. The timeline reflects the gradual microbiome remodeling and gut barrier repair that drive the anti-inflammatory mechanism rather than an acute pharmacological effect.
Is a high-fiber diet anti-inflammatory overall? Yes. High-fiber dietary patterns are among the most consistently evidence-backed anti-inflammatory dietary approaches available. The 2025 umbrella review in Nutrition Reviews examining 30 systematic reviews confirmed that plant-based, high-fiber dietary patterns consistently reduce CRP and IL-6 concentrations. The Mediterranean diet, which is characterized primarily by its high fiber content from legumes, whole grains, and vegetables, showed the strongest evidence base of all dietary patterns reviewed.
Does fiber help with joint inflammation? The evidence here is less specific than for cardiovascular and metabolic inflammation. Rheumatoid arthritis is associated with gut microbiome dysbiosis in multiple studies, and high-fiber dietary patterns that restore microbiome diversity and reduce systemic LPS-driven inflammation may reduce the inflammatory burden that drives joint symptoms. However, joint-specific inflammatory mechanisms involve additional pathways beyond those addressed by fiber alone. Anyone managing inflammatory joint disease should work with a rheumatologist before relying on dietary change as a primary intervention.
What is the most anti-inflammatory fiber? No single fiber type is universally most anti-inflammatory. Resistant starch is the most potent driver of butyrate production and gut barrier protection. Beta-glucan has the most direct anti-inflammatory activity at the immune cell receptor level. Prebiotic inulin-type fibers drive the most selective Bifidobacterium and Akkermansia growth. Pectin from fruits showed the strongest microbiome-CRP relationship in the Harvard cohort study. The most anti-inflammatory dietary approach uses all four categories rather than maximizing any single one.
Why did my CRP not improve after increasing fiber intake? Individual microbiome composition is the most likely explanation for variable CRP responses to fiber. The Harvard cohort study demonstrated that Prevotella copri carriage specifically blunted fiber's CRP-lowering effect in affected individuals regardless of intake level. Other factors including concurrent ultra-processed food consumption, inadequate hydration impairing gel formation, insufficient intake magnitude, and fiber type monotony can all reduce the expected anti-inflammatory response. Microbiome testing can identify specific bacterial patterns that may be limiting your response to dietary change.
Does fiber help with neuroinflammation? The gut-brain axis connects gut microbiome health to neuroinflammatory processes through SCFA-mediated modulation of microglial activation and blood-brain barrier integrity. Short-chain fatty acids produced by fiber fermentation cross the blood-brain barrier and interact with receptors that modulate neuroinflammatory signaling. Population studies link higher dietary fiber intake to lower risk of cognitive decline and neurodegenerative disease, though the causal relationship between fiber intake, neuroinflammation, and cognitive outcomes is still being characterized in prospective clinical research.
Start Your Anti-Inflammatory Protocol
Step 1: Calculate your personalized daily fiber target
Step 2: Generate a diverse, anti-inflammatory clinical meal plan
Step 4: Read the complete fibermaxxing protocol guide
Step 5: Understand how butyrate drives the anti-inflammatory mechanisms described in this article
This article is for educational purposes only and does not constitute medical advice. Consult your physician before making significant changes to your diet or supplement protocol, particularly if you are managing a diagnosed inflammatory condition. See our full Medical Disclaimer.
Sources: Benedicto-Toboso MI et al. Effect of Dietary Fiber Intake on Chronic Low-Grade Inflammation in Children and Adolescents: A Systematic Review and Meta-Analysis. Current Developments in Nutrition, July 2025; Wastyk HC, Sonnenburg JL et al. Gut-Microbiota-Targeted Diets Modulate Human Immune Status. Cell, 2021; Dahl WJ et al. Impact of Dietary Fiber on Inflammation in Humans. International Journal of Molecular Sciences, February 2025; Jiang R et al. Impact of Anti-Inflammatory Diets on Cardiovascular Disease Risk Factors: A Systematic Review and Meta-Analysis. Frontiers in Nutrition, March 2025; Nguyen NK et al. Dietary Patterns Associated With Anti-Inflammatory Effects: An Umbrella Review. Nutrition Reviews, July 2025; Dahl WJ, Zeng Y. Nutrition and the Gut Microbiome: A Symbiotic Dialogue. Frontiers in Nutrition, 2026; Yao Y et al. Dietary Fiber Intake, the Gut Microbiome, and Chronic Systemic Inflammation in a Cohort of Adult Men. Genome Medicine, 2021; Lu L et al. Gut-Lung Axis in COPD: Investigating the Impact of Dietary Fiber Intake. COPD: Journal of Chronic Obstructive Pulmonary Disease, March 2026; Ma Y et al. Effect of Dietary Fiber on Circulating C-Reactive Protein in Overweight and Obese Adults: A Meta-Analysis of Randomized Controlled Trials. PubMed, 2014; Franceschi C, Campisi J. Chronic Inflammation and Its Potential Contribution to Age-Associated Diseases. Journals of Gerontology, 2014.