Can Diet Change the Gut Microbiome in Pulmonary Fibrosis?

Can What We Eat Influence the Gut–Lung Axis?

Yes.

Among all environmental factors that influence the intestinal microbiome, diet is one of the most powerful and modifiable.

What we eat determines which substrates reach intestinal microorganisms.

Those microbes then convert dietary components into hundreds of metabolites capable of interacting with:

• intestinal epithelial cells

• immune cells

• metabolism

• distant organs

The lung is one of those organs.

This has created interest in whether dietary modification might influence pulmonary fibrosis through the gut–lung axis.

The scientifically accurate answer is:

Diet can clearly change aspects of the gut microbiome.

What has not been demonstrated is that a microbiome-directed diet can stop or reverse human pulmonary fibrosis.

What Does the Human Diet–Microbiome Evidence Show?

A 2026 systematic review evaluated 80 controlled clinical trials examining dietary interventions and gut microbiota.

The review included Mediterranean, plant-based, high-fiber, ketogenic, gluten-free, Western, Japanese, Korean, low-FODMAP and other dietary patterns.

Dietary interventions altered microbial taxa and metabolic markers, although changes in overall alpha and beta diversity were inconsistent.

Mediterranean, high-fiber, plant-based, high-polyphenol and several traditional dietary patterns tended to increase SCFA- or lactic-acid-producing bacteria or reduce opportunistic organisms.

In contrast, Western, animal-based, ketogenic, gluten-free and low-FODMAP dietary patterns were associated in some studies with reductions in SCFA-producing organisms. (PubMed⁠)

This confirms an important principle:

food changes microbial function.

But Has Diet Been Proven to Change IPF Outcomes Through the Microbiome?

No.

There are currently no large randomized clinical trials demonstrating that a microbiome-targeted diet:

• improves FVC

• improves DLCO

• reverses HRCT fibrosis

• prevents progression

• improves survival in IPF

Therefore, a distinction is necessary between:

diet modifies the microbiome

and

diet treats pulmonary fibrosis by modifying the microbiome.

The first is supported.

The second remains unproven.

Why Might Diet Matter in Pulmonary Fibrosis?

Diet could influence pulmonary biology indirectly through:

• SCFAs

• tryptophan metabolites

• bile acids

• metabolic health

• systemic inflammation

• intestinal-barrier integrity

Recent pulmonary fibrosis reviews identify all of these as potential gut–lung pathways. (PubMed⁠)

Dietary Fiber

Fiber is one of the best-studied microbiome substrates.

Different fibers can be fermented by intestinal microorganisms.

This generates:

• acetate

• propionate

• butyrate

A 2025 review specifically examined dietary fiber, microbial metabolites and lung immunity, concluding that SCFAs can influence pulmonary immune responses through GPCR signaling, HDAC inhibition and immune-cell programming. (PubMed⁠)

Why Butyrate Is Interesting

Butyrate can:

• support colonocyte metabolism

• strengthen intestinal barrier function

• influence Treg activity

• inhibit histone deacetylases

• modify inflammatory signaling

These effects make butyrate particularly interesting for diseases involving immune and fibrotic pathways.

But increasing dietary fiber does not guarantee clinically meaningful pulmonary butyrate exposure.

Nor has a high-butyrate diet been shown to treat IPF.

Resistant Starch

Resistant starch reaches the colon without being fully digested in the small intestine.

Gut organisms can ferment it and generate SCFAs.

Sources may include selected:

• legumes

• grains

• potatoes

• rice

• green bananas

depending on preparation and individual tolerance.

But patients with substantial bloating, SIBO or dysmotility may not tolerate high amounts.

Mediterranean-Style Diet

A Mediterranean-style pattern commonly includes:

• vegetables

• fruits

• legumes

• nuts

• seeds

• olive oil

• fish

• minimally processed foods

The 2026 systematic review found Mediterranean dietary interventions associated with microbiome and biomarker changes, including enrichment of some metabolically favorable organisms. (PubMed⁠)

This makes the Mediterranean pattern a reasonable general model for metabolic and microbiome health when tolerated.

But it has not been validated as an antifibrotic IPF diet.

Polyphenols

Polyphenols are found in foods such as:

• berries

• herbs

• vegetables

• cocoa

• tea

• olive products

Gut microbes metabolize many polyphenols into bioactive compounds.

Polyphenols may also influence microbial composition.

This represents another diet–microbiome pathway that may be relevant to systemic inflammation.

Direct pulmonary fibrosis trials remain lacking.

Protein and Pulmonary Fibrosis

A microbiome-focused diet must not ignore protein.

People with ILD can experience:

• weight loss

• sarcopenia

• frailty

• reduced exercise capacity

Maintaining muscle is clinically important.

A diet excessively focused on plants or fiber at the expense of adequate protein may be harmful in a patient already losing lean body mass.

Muscle Is Part of Lung Health

Dyspnea can reduce physical activity.

Reduced activity promotes muscle loss.

Loss of skeletal muscle further reduces exercise capacity.

Therefore, the nutrition strategy for pulmonary fibrosis should prioritize:

lung + muscle + metabolism + gut

rather than the microbiome alone.

Western Dietary Patterns

Western dietary patterns are often characterized by:

• highly processed foods

• refined carbohydrates

• low fiber

• low plant diversity

• high saturated fat

Controlled diet studies suggest Western-style dietary patterns can alter microbial ecology and may reduce some beneficial metabolic functions. (PubMed⁠)

This provides another reason to emphasize whole-food dietary patterns.

High-Fat Diet and Endotoxemia

Certain high-fat dietary patterns can influence:

• bile acid metabolism

• intestinal microbial composition

• intestinal permeability

This may increase systemic exposure to LPS in some contexts.

Whether this contributes meaningfully to human pulmonary fibrosis is unknown.

Tryptophan and Diet

Tryptophan is an essential amino acid found in many protein-containing foods.

It can follow several pathways:

• serotonin

• kynurenine

• microbial indoles

Different tryptophan metabolites can have very different immune effects.

Some microbial indoles activate AhR and support mucosal immune regulation.

Other pathways may participate in profibrotic signaling.

This means simply increasing or eliminating dietary tryptophan would be biologically simplistic.

The relevant biology depends on how tryptophan is metabolized.

Bile Acids

Diet influences bile-acid production and microbial transformation.

Gut organisms convert primary bile acids into secondary bile-acid metabolites.

These interact with receptors such as:

• FXR

• TGR5

which influence metabolic and immune signaling.

Bile-acid pathways are emerging as possible mediators of gut–lung communication in fibrosis. (PubMed⁠)

TMAO

Trimethylamine N-oxide is generated through interactions involving diet, intestinal microbes and hepatic metabolism.

Foods containing precursor compounds can influence TMAO production.

TMAO has received substantial cardiovascular attention and is also being investigated in pulmonary fibrosis biology.

Its exact clinical role remains uncertain. (PubMed⁠)

Should Patients With IPF Eat More Fiber?

Not automatically.

For many patients, increasing dietary diversity and fiber gradually may support metabolic and gut health.

But a blanket recommendation can be problematic.

Some ILD patients have:

• severe bloating

• SIBO

• constipation

• diarrhea

• dysmotility

• systemic sclerosis

• reflux

For these individuals, fiber needs to be individualized.

Systemic Sclerosis Is a Special Case

Systemic sclerosis may involve:

• esophageal dysmotility

• gastroparesis

• slow intestinal transit

• SIBO

Simply prescribing a high-fermentation diet may worsen symptoms.

Correcting motility, nutritional deficits and gastrointestinal complications may be more important than maximizing fiber intake.

Low-FODMAP Diet

A low-FODMAP diet can reduce fermentation-related symptoms in selected gastrointestinal conditions.

But the 2026 controlled-trial review found that low-FODMAP patterns can also reduce some SCFA-producing microbial populations. (PubMed⁠)

Therefore, long-term unnecessary restriction may not be ideal.

It should be used strategically when clinically indicated.

Gluten-Free Diet

There is no evidence that all patients with pulmonary fibrosis need to avoid gluten.

A gluten-free diet is clearly indicated in celiac disease.

Outside appropriate indications, unnecessarily restrictive diets may reduce dietary diversity and alter microbiome composition.

Ketogenic Diet

Ketogenic diets significantly alter metabolism and the gut microbiome.

However, there is no evidence that a ketogenic diet treats IPF.

The 2026 systematic review also found ketogenic dietary interventions associated with reductions in some SCFA-producing organisms. (PubMed⁠)

That does not mean ketogenic diets are inherently harmful, but it argues against presenting them as an evidence-based pulmonary fibrosis microbiome strategy.

Intermittent Fasting

Animal work has explored fasting in bleomycin-induced fibrosis.

Some studies suggest altered immune-cell responses and reduced experimental fibrosis. (PubMed⁠)

But this remains preclinical.

Fasting may be inappropriate for patients with:

• low body weight

• sarcopenia

• advanced disease

• inadequate caloric intake

Anti-Inflammatory Diets

“Anti-inflammatory diet” is not one precisely defined medical diet.

In practical terms, it often means a whole-food pattern emphasizing:

• vegetables

• fruits

• quality protein

• healthy fats

• minimally processed foods

This may support general metabolic health.

There is no evidence that such a diet reverses established fibrosis.

Can Diet Change the Lung Microbiome?

Potentially indirectly.

Diet strongly influences the gut microbiome.

Gut-derived immune signals may then affect pulmonary immunity.

Whether dietary modification produces clinically meaningful changes in the lung microbiome of IPF patients remains largely unexplored.

Food Diversity and Microbial Diversity

Greater plant variety provides a broader range of microbial substrates.

This may help support microbial functional diversity.

But there is no magic number of plant foods that has been proven to improve IPF.

Nutrition During Nintedanib

Nintedanib commonly causes gastrointestinal side effects, particularly diarrhea.

Dietary priorities may therefore include:

• maintaining hydration

• maintaining adequate intake

• adjusting foods according to tolerance

A high-fiber microbiome strategy may not be appropriate during significant diarrhea.

Nutrition During Pirfenidone

Pirfenidone can cause:

• nausea

• reduced appetite

• gastrointestinal discomfort

Maintaining adequate calories and protein may take priority over aggressive dietary experimentation.

Functional and Integrative Medicine Perspective

Diet is one of the most reasonable ways to influence the gut microbiome because it:

• acts continuously

• affects microbial substrates

• affects metabolism

• contributes essential nutrients

But an integrative approach should avoid turning food into an unproven antifibrotic prescription.

The clinically appropriate goals include:

• adequate nutrition

• muscle preservation

• metabolic health

• bowel function

• individualized microbial support

What We Know

We know that:

• diet modifies the human gut microbiome

• controlled dietary interventions can alter microbial taxa and metabolites

• fiber influences SCFA production

• SCFAs influence pulmonary immune pathways

• pulmonary fibrosis is associated with altered gut microbiota

(PubMed⁠)

What We Do Not Know

We do not know:

• the ideal IPF microbiome diet

• whether increasing SCFAs changes IPF progression

• whether Mediterranean diets improve fibrosis

• whether microbiome-guided diets improve survival

• which patients might benefit most

What Should a Future Dietary Trial Measure?

Future trials should evaluate:

• diet

• stool metagenomics

• metabolomics

• SCFAs

• inflammatory biomarkers

• FVC

• DLCO

• HRCT progression

• muscle mass

• quality of life

The outcome should be pulmonary benefit—not simply microbiome change.

Frequently Asked Questions

What is the best diet for the gut microbiome in pulmonary fibrosis?

No specific diet has been validated. A diverse, nutrient-dense, minimally processed diet is a reasonable starting framework when tolerated.

Should people with IPF eat more fiber?

Often fiber can support microbial metabolism, but intake should be individualized.

Can a Mediterranean diet reverse fibrosis?

No evidence shows that it reverses lung fibrosis.

Should patients avoid gluten?

Not routinely unless there is a specific indication.

Does diet replace antifibrotic treatment?

No.

Conclusion

Diet unquestionably influences the gut microbiome.

That makes nutrition one of the most interesting potential ways to modify the gut–lung axis.

Current human evidence shows that Mediterranean, plant-rich, high-fiber and high-polyphenol dietary patterns can modify microbial composition and metabolic function. (PubMed⁠)

SCFAs generated by microbial fermentation can influence pulmonary immune responses. (PubMed⁠)

Meanwhile, human IPF research demonstrates that gut microbial features are associated with pulmonary disease severity. (PubMed⁠)

These observations create a coherent biological hypothesis:

diet → microbiome → microbial metabolites → immune regulation → lung

But the final step remains unproven clinically.

There is currently no diet proven to stop or reverse pulmonary fibrosis by changing the microbiome.

For now, the most defensible strategy is to use diet to support:

• nutritional adequacy

• muscle mass

• metabolic health

• gastrointestinal function

• microbial diversity when tolerated

while continuing evidence-based pulmonary treatment.

About Dr. Samar Shadly

Dr. Samar Shadly is a Consultant Pulmonologist and Certified Functional Medicine Practitioner, with advanced subspecialty training in interstitial lung disease, pulmonary fibrosis, pulmonary hypertension, and lung transplantation, together with expertise in functional and integrative medicine.

Her approach combines evidence-based pulmonary medicine with a broader assessment of factors that may influence a patient’s overall health, including nutrition, gastrointestinal health, the gut microbiome, metabolic health, lifestyle, and relevant environmental exposures.

A particular focus of her work is the emerging field of Integrative and Functional Pulmonology, especially in pulmonary fibrosis and autoimmune-associated interstitial lung disease. Her goal is to bridge conventional respiratory medicine with scientifically grounded integrative strategies, while clearly distinguishing established clinical evidence from promising but still experimental research.

Living with Pulmonary Fibrosis or Interstitial Lung Disease?

If you are looking for a more comprehensive assessment that combines specialist pulmonary expertise with a functional and integrative perspective, you can explore whether this approach may be appropriate for your individual condition.

To learn more about consultation options or request an assessment, contact us through the consultation page or WhatsApp.

Integrative care is intended to complement—not replace—evidence-based pulmonary treatment and should always be individualized according to the diagnosis and clinical situation.