Pulmonary Hypertension and Gut Health: What Does the Evidence Show?
Can gut health affect pulmonary hypertension? Could changes in the gut microbiome contribute to inflammation in the pulmonary arteries? And can diet, probiotics, or microbiome treatments improve pulmonary arterial hypertension?
These questions are receiving increasing scientific attention. Researchers have found differences in the gut microbiome of some people with pulmonary arterial hypertension and chronic thromboembolic pulmonary hypertension. Studies have also identified possible links between pulmonary hypertension, intestinal permeability, inflammation, and metabolites produced by gut bacteria.
However, this field is still emerging. Gut dysbiosis has not been proven to be a primary cause of pulmonary hypertension, and no probiotic, microbiome test, special diet, antibiotic, or fecal microbiota transplant is currently an established treatment for pulmonary hypertension.
The most important message is this:
Supporting digestive and nutritional health may be valuable as part of comprehensive pulmonary hypertension care, but it must not replace pulmonary hypertension medications, risk assessment, rehabilitation, oxygen when indicated, diuretics, or other evidence-based treatments.
What Is Pulmonary Hypertension?
Pulmonary hypertension is a condition in which the pressure in the blood vessels of the lungs becomes abnormally elevated.
It is not one single disease. Pulmonary hypertension is classified into five major groups:
Pulmonary arterial hypertension.
Pulmonary hypertension caused by left-sided heart disease.
Pulmonary hypertension associated with lung disease or low oxygen levels.
Pulmonary hypertension caused by obstruction of the pulmonary arteries, particularly chronic thromboembolic pulmonary hypertension.
Pulmonary hypertension caused by unclear or multiple mechanisms.
This distinction is critical because the causes and treatments differ substantially between the five groups.
Current definitions describe pulmonary hypertension as a mean pulmonary arterial pressure above 20 mmHg at rest, measured by right-heart catheterization. Right-heart catheterization remains essential for confirming the diagnosis and classifying its hemodynamic pattern in appropriate patients. (academic.oup.com, academic.oup.com, publications.ersnet.org)
Pulmonary arterial hypertension, or PAH, is a specific form of pulmonary hypertension in which the small pulmonary arteries become narrowed and remodeled. This increases resistance to blood flow and places greater strain on the right side of the heart.
Over time, the right ventricle may become enlarged, weakened, and eventually unable to pump blood effectively.
What Is the Gut–Lung Axis?
The gut–lung axis describes the bidirectional communication between the gastrointestinal tract, its microorganisms, the immune system, and the lungs.
Trillions of microorganisms live in the digestive tract. Collectively, their genes, biological functions, and interactions with the body are known as the gut microbiome.
Gut bacteria help:
Process components of food.
Produce biologically active metabolites.
Maintain the intestinal barrier.
Interact with immune cells.
Influence inflammation.
Support the production of certain vitamins.
Regulate aspects of metabolism.
The intestines and lungs do not communicate through a physical tube. Their interaction occurs through the bloodstream, immune signaling, bacterial metabolites, hormones, nerves, and inflammatory mediators.
In pulmonary hypertension, this relationship may be even more complex because the right side of the heart, the liver, the intestines, and the pulmonary circulation can all affect one another.
What Is the Right Heart–Gut Axis?
The right ventricle pumps blood through the pulmonary arteries.
When pulmonary pressure and vascular resistance become severely elevated, the right ventricle may struggle to move blood forward. This can cause blood to back up in the veins, producing systemic venous congestion.
Venous congestion may affect:
The liver.
The kidneys.
The stomach and intestines.
Nutrient absorption.
Appetite.
Fluid balance.
The intestinal barrier.
Congestion of the intestinal wall may cause swelling and reduce effective blood flow to the intestinal lining. This could impair barrier function and allow bacterial components to move from the intestines into the circulation.
Therefore, the relationship may work in both directions:
Gut-derived products might influence inflammation and pulmonary vascular function.
Pulmonary hypertension and right-heart failure might alter the intestinal environment and gut microbiome.
This makes cause and effect difficult to separate. Gut dysbiosis could contribute to disease pathways, result from advanced pulmonary hypertension, or both. (journals.physiology.org, pmc.ncbi.nlm.nih.gov, pubmed.ncbi.nlm.nih.gov, pmc.ncbi.nlm.nih.gov)
Is the Gut Microbiome Different in Pulmonary Arterial Hypertension?
Human studies suggest that the gut microbiome may differ in some people with pulmonary arterial hypertension.
One early metagenomic study compared stool samples from 18 people with PAH with samples from 13 reference participants. Researchers found differences in microbial composition and metabolic pathways.
The PAH group showed an increased abundance of bacterial pathways associated with trimethylamine production and changes in amino-acid and purine metabolism. The reference group had a greater abundance of several bacteria associated with the production of butyrate and propionate.
The study was scientifically important, but it was small. It showed an association and could not prove that the microbiome changes caused PAH. (pmc.ncbi.nlm.nih.gov)
A separate study evaluated 11 patients with chronic thromboembolic pulmonary hypertension and 22 healthy participants. The patients with CTEPH had differences in their gut microbiota, lower bacterial diversity, and higher circulating endotoxin and inflammatory cytokine levels.
Again, this was a small, single-center observational study. It cannot establish whether the microbiome changes contributed to CTEPH or occurred because of the disease, medications, diet, congestion, or other factors. (pmc.ncbi.nlm.nih.gov, link.springer.com, pubmed.ncbi.nlm.nih.gov)
What Is Gut Dysbiosis?
Gut dysbiosis is a broad term describing an alteration in the composition or function of the gut microbial community.
It does not refer to one universally defined microbiome pattern, and there is no single clinical test that can diagnose “dysbiosis” in every patient.
Potential influences on the gut microbiome include:
Diet.
Age.
Geography.
Medications.
Antibiotic exposure.
Gastrointestinal disease.
Constipation or diarrhea.
Physical activity.
Smoking.
Alcohol.
Metabolic health.
Heart failure and venous congestion.
The method used to collect and analyze the sample.
Finding a difference between the microbiomes of patients and healthy participants does not automatically mean that the difference causes disease or that it should be treated.
How Could Gut Health Influence Pulmonary Hypertension?
Several possible mechanisms are being investigated.
1. Increased Intestinal Permeability and Endotoxin
The intestinal lining normally separates the contents of the gut from the bloodstream while allowing controlled absorption of nutrients.
If this barrier becomes impaired, bacterial components such as lipopolysaccharide, also called LPS or endotoxin, may enter the circulation in greater amounts.
LPS can activate immune cells and inflammatory pathways, including signaling through toll-like receptor 4. These pathways may affect vascular endothelial cells, macrophages, platelets, and remodeling of the pulmonary blood vessels.
Higher circulating LPS and markers of immune activation have been reported in some patients with PAH and CTEPH. However, increased intestinal permeability may be caused by right-heart failure and intestinal congestion rather than being the original driver of pulmonary hypertension. (pmc.ncbi.nlm.nih.gov, mdpi.com, journals.physiology.org, pubmed.ncbi.nlm.nih.gov)
2. Short-Chain Fatty Acids
Certain gut bacteria ferment dietary fiber and produce short-chain fatty acids, including:
Butyrate.
Propionate.
Acetate.
These metabolites help support the intestinal lining and interact with immune and metabolic pathways.
Some studies have found lower representation of bacteria associated with butyrate and propionate production in PAH. Animal studies also suggest that changes in these metabolites may be related to intestinal barrier dysfunction and pulmonary vascular inflammation.
This does not prove that taking a short-chain fatty-acid supplement or dramatically increasing fiber will treat PAH. It identifies a potential biological pathway that requires further human research.
3. TMAO
Trimethylamine N-oxide, or TMAO, is a metabolite influenced by interactions between food, gut bacteria, and liver metabolism.
Gut bacteria can metabolize nutrients such as choline and carnitine into trimethylamine. The liver then converts trimethylamine into TMAO.
In observational studies of patients with pulmonary hypertension, higher circulating TMAO levels were associated with more severe disease and poorer outcomes.
One study included 124 people with PAH, while another included 163 patients across several pulmonary hypertension groups. A further cohort evaluated changes in TMAO over time. These studies found associations between higher TMAO levels, indicators of disease severity, and adverse clinical outcomes. (pubmed.ncbi.nlm.nih.gov, pmc.ncbi.nlm.nih.gov, pmc.ncbi.nlm.nih.gov, pmc.ncbi.nlm.nih.gov, pubmed.ncbi.nlm.nih.gov)
These findings do not establish TMAO as a routine clinical test or treatment target.
TMAO levels may be affected by:
Kidney function.
Liver metabolism.
Diet.
Gut microbiome composition.
Medications.
Disease severity.
There is currently no guideline recommendation to measure TMAO routinely in patients with pulmonary hypertension.
4. Bile Acids and Tryptophan Metabolites
Gut bacteria modify bile acids and metabolize dietary tryptophan into several compounds that interact with immune and vascular pathways.
Recent reviews identify bile acids and tryptophan-related metabolites as possible contributors to the relationship between the microbiome and pulmonary hypertension.
Most of this work remains mechanistic or experimental. These metabolites are not currently established targets for routine PAH treatment. (pubmed.ncbi.nlm.nih.gov, sciencedirect.com, sciencedirect.com)
5. Immune-System Regulation
Pulmonary arterial hypertension involves more than vasoconstriction. Inflammation, immune-cell activity, endothelial dysfunction, metabolic abnormalities, and vascular remodeling may all contribute.
The gut microbiome can influence the balance and activity of immune cells. Researchers are therefore studying whether microbiome changes might contribute to inflammatory signaling around the pulmonary vessels.
This is biologically plausible, but it has not yet produced an approved microbiome-directed treatment for patients with pulmonary hypertension.
Can Pulmonary Hypertension Cause Digestive Problems?
Yes. Digestive symptoms in a person with pulmonary hypertension should not automatically be attributed to dysbiosis.
Possible causes include:
Right-heart failure and venous congestion.
Swelling of the intestinal wall.
Liver congestion.
Ascites.
Reduced blood flow to the digestive tract.
Medication adverse effects.
Iron supplements.
Changes in physical activity.
Dietary restrictions.
Another gastrointestinal disease unrelated to pulmonary hypertension.
Symptoms may include:
Reduced appetite.
Early fullness.
Abdominal bloating.
Nausea.
Constipation.
Diarrhea.
Abdominal discomfort.
Unintentional weight loss.
Difficulty eating full meals.
Pulmonary hypertension medications may also cause gastrointestinal effects. Depending on the medication, these may include nausea, diarrhea, vomiting, abdominal discomfort, reduced appetite, or reflux.
Do not stop a pulmonary hypertension medication because of digestive symptoms. The PH team may be able to adjust timing, dosing, supportive treatment, or the medication plan.
Can Poor Gut Health Cause Pulmonary Hypertension?
Current evidence does not prove that common digestive problems, constipation, SIBO, food intolerance, or an abnormal stool microbiome test cause pulmonary hypertension in humans.
The strongest evidence currently shows:
Associations between PH and altered microbial patterns.
Associations between some microbial metabolites and disease severity.
Plausible inflammatory and metabolic mechanisms.
Experimental improvement after microbiome interventions in some animal models.
This is not the same as proving that gut dysfunction causes PAH.
Pulmonary hypertension has several established causes and risk factors, including connective-tissue disease, congenital heart disease, portal hypertension, HIV, certain drugs and toxins, chronic lung disease, left-heart disease, and chronic thromboembolic disease. Some cases are heritable or idiopathic.
A gut-health evaluation must never delay proper pulmonary hypertension testing or referral to a specialist center.
Can Improving Gut Health Treat Pulmonary Hypertension?
There is currently no evidence that a gut-health intervention can replace established pulmonary hypertension treatment.
The 2022 ESC/ERS guidelines and the 2024 Seventh World Symposium treatment algorithm emphasize accurate classification, risk assessment, PAH-targeted medication, early combination therapy for appropriate patients, frequent reassessment, and treatment escalation when required.
Current guideline-based PAH therapies target four major pathways:
Endothelin signaling.
Nitric-oxide signaling.
Prostacyclin signaling.
Activin signaling.
Gut microbiome therapy is not part of the current PAH treatment algorithm. (academic.oup.com, publications.ersnet.org, pmc.ncbi.nlm.nih.gov, publications.ersnet.org)
Supporting gut and nutritional health may still help address symptoms, medication tolerance, nutritional deficiencies, bowel regularity, and overall health. That is supportive care—not a treatment proven to reverse pulmonary vascular disease.
Are Probiotics Helpful for Pulmonary Hypertension?
At present, there are no convincing human clinical trials showing that a probiotic improves pulmonary artery pressure, right-heart function, hospitalization, or survival in adults with PAH.
Some encouraging results come from animal models.
For example, a probiotic reduced pulmonary hypertension and right-ventricular hypertrophy in a rodent model involving postnatal growth restriction. A more recent experiment found that a specific strain of Lacticaseibacillus rhamnosus altered the microbiome and reduced pulmonary vascular remodeling in rats with experimentally induced PH. (pmc.ncbi.nlm.nih.gov, pubmed.ncbi.nlm.nih.gov, pubmed.ncbi.nlm.nih.gov, pmc.ncbi.nlm.nih.gov)
These results cannot be directly translated into a recommendation for patients.
The strain, dose, disease model, age, and biological context matter. A probiotic that affects PH in a rat model may not have the same effect in an adult with idiopathic PAH, systemic-sclerosis-associated PAH, lung-disease-associated PH, or CTEPH.
Probiotics may also cause bloating or other adverse effects and require greater caution in people who are critically ill or severely immunocompromised.
Should Patients Take Antibiotics to Change the Microbiome?
No. Antibiotics should not be used to treat pulmonary hypertension or presumed gut dysbiosis outside a legitimate medical indication or clinical trial.
A 2025 study combined retrospective human observations, microbiome data, and experiments in rats with hypoxia-induced PH. It generated an interesting hypothesis that microbiome modification may influence pulmonary hypertension, but it does not prove that prescribing antibiotics improves outcomes in patients with PH.
Unnecessary antibiotic exposure can:
Disrupt the microbiome.
Cause diarrhea.
Increase antimicrobial resistance.
Produce medication interactions.
Cause serious infections such as Clostridioides difficile.
Trigger allergic or other adverse reactions.
The study should be viewed as a research signal, not a treatment instruction. (pubmed.ncbi.nlm.nih.gov, pmc.ncbi.nlm.nih.gov, link.springer.com)
Can Fecal Microbiota Transplantation Treat Pulmonary Hypertension?
Fecal microbiota transplantation, or FMT, is not an established treatment for pulmonary hypertension.
It should not be offered as a general “microbiome reset.” FMT has specific recognized medical uses, particularly selected cases of recurrent Clostridioides difficile infection, and it carries risks related to infection transmission and other complications.
Research into microbiota transplantation and pulmonary hypertension remains experimental.
Are Commercial Microbiome Tests Useful in Pulmonary Hypertension?
Commercial stool microbiome tests can describe some organisms detected in a stool sample, but they cannot currently:
Diagnose pulmonary hypertension.
Identify the pulmonary hypertension group.
Measure pulmonary artery pressure.
Determine PAH severity.
Select PAH medication.
Predict whether a probiotic will work.
Prove that dysbiosis caused the disease.
Microbiome composition can also vary over time and with food, medication, geography, sample handling, and laboratory methods.
Routine microbiome testing is not included in current pulmonary hypertension guidelines.
Is There a Recommended Pulmonary Hypertension Diet?
There is no single evidence-based “PAH diet” proven to reverse pulmonary hypertension.
Nutrition should be individualized according to:
The type and severity of pulmonary hypertension.
Right-heart function.
Fluid retention.
Kidney and liver function.
Body weight.
Appetite.
Diabetes or insulin resistance.
Iron status.
Medication effects.
Other medical conditions.
Research on dietary intervention in PAH remains limited. Earlier reviews found that beyond individualized attention to sodium and fluid intake, there was insufficient evidence to prescribe one specific diet for all patients with PAH. (pmc.ncbi.nlm.nih.gov, pubmed.ncbi.nlm.nih.gov)
Practical Nutritional Priorities
1. Follow Individual Sodium and Fluid Advice
People with right-heart failure or fluid retention may be advised to reduce sodium and, in some cases, limit fluid intake.
The appropriate limit is not identical for everyone. Excessive restriction may contribute to low blood pressure, dehydration, kidney dysfunction, poor intake, or electrolyte abnormalities.
Follow the plan provided by your pulmonary hypertension team, particularly if you take diuretics.
2. Maintain Adequate Protein and Energy Intake
Reduced appetite, early fullness, fatigue, and intestinal congestion may make eating difficult.
Some patients tolerate:
Smaller, more frequent meals.
Nutrient-dense foods.
Protein distributed across meals.
Earlier meals when energy is better.
Reduced intake of highly processed, sodium-rich foods.
Unintentional weight loss or muscle loss should be addressed early.
3. Include Plant Foods as Tolerated
Vegetables, fruits, legumes, whole grains, nuts, and seeds can provide fiber and micronutrients and support microbial diversity.
However, recommendations must be adapted when a person has:
Severe bloating.
Gastroparesis.
Irritable bowel syndrome.
Fluid or potassium restrictions.
Kidney disease.
Difficulty consuming large meals.
Anticoagulant-related dietary considerations.
Increasing fiber too quickly may worsen gas and bloating. Fiber intake should be increased gradually when appropriate.
4. Correct Constipation
Constipation may be related to reduced activity, low food intake, fluid restriction, iron supplements, or medications.
Treatment must be individualized. A person with fluid restrictions should not simply increase water intake without discussing it with the PH team.
5. Assess Iron Status
Iron deficiency is common in PAH and may contribute to fatigue and reduced exercise capacity.
Current PH guidelines recommend attention to anemia and iron status. Testing and treatment should be directed by the clinical team rather than starting iron without confirming the need. (academic.oup.com)
6. Avoid Unnecessary Restrictive Diets
Eliminating gluten, dairy, grains, legumes, histamine-containing foods, lectins, oxalates, or multiple other food groups is not a standard treatment for pulmonary hypertension.
An elimination diet may occasionally be used for a separate confirmed or suspected gastrointestinal condition, but it should have a clear purpose, defined duration, and reintroduction plan.
What About Exercise and the Gut Microbiome?
Regular physical activity can influence metabolic and microbial health, but its established value in PAH is related primarily to exercise capacity, conditioning, symptoms, and quality of life.
Guidelines recommend supervised exercise training or rehabilitation for appropriate patients who are clinically stable and receiving optimized medical treatment.
Patients with severe hemodynamic impairment, syncope, significant arrhythmia, or advanced symptoms require individualized assessment and closer monitoring. (academic.oup.com, academic.oup.com)
Exercise should not be prescribed solely as a method of changing the microbiome.
What Gut Symptoms Should Be Discussed with a PH Specialist?
Contact your healthcare team if you develop:
Persistent nausea or vomiting.
Severe or prolonged diarrhea.
New or worsening abdominal swelling.
Significant early fullness.
Loss of appetite.
Unintentional weight loss.
Blood in the stool.
Persistent abdominal pain.
Difficulty taking medications.
Symptoms beginning after a new medication or dose change.
Constipation that does not improve.
Rapid weight gain accompanied by swelling or breathlessness.
New abdominal swelling may represent gas, constipation, weight gain, liver enlargement, or fluid accumulation. It should not automatically be treated as “gut dysbiosis.”
What Can Patients Do Now?
If you have pulmonary hypertension and digestive symptoms:
Continue your prescribed pulmonary hypertension treatment.
Discuss persistent gastrointestinal symptoms with your PH team.
Review whether symptoms began after a medication change.
Monitor body weight according to your clinical plan.
Follow individualized sodium and fluid instructions.
Ask whether iron status, anemia, kidney function, liver function, or nutritional status should be assessed.
Avoid unnecessary antibiotics and highly restrictive diets.
Do not use probiotics, DAO supplements, herbal products, or microbiome protocols as substitutes for PAH treatment.
Seek evaluation for a separate gastrointestinal disorder when clinically indicated.
Consider support from a dietitian familiar with heart failure or pulmonary hypertension if eating has become difficult.
Frequently Asked Questions
Is Pulmonary Hypertension Related to Gut Health?
Research has found associations between pulmonary hypertension, altered gut microbiota, intestinal permeability, inflammation, and microbial metabolites. It is not yet clear how much these changes cause disease versus result from pulmonary hypertension, medications, diet, or right-heart failure.
Can Gut Problems Cause Pulmonary Hypertension?
Common digestive symptoms do not prove that gut dysfunction caused pulmonary hypertension. The disease has several established causes and requires formal cardiopulmonary evaluation.
Can Healing the Gut Reverse Pulmonary Hypertension?
There is no clinical evidence that a “gut-healing” protocol reverses pulmonary hypertension. Appropriate medical therapy, risk assessment, and specialist follow-up remain essential.
What Is the Gut–Lung Axis in Pulmonary Hypertension?
The gut–lung axis refers to communication between the gut microbiome, intestinal barrier, immune system, microbial metabolites, and lungs. In PH, right-heart congestion adds another possible connection between the intestines and pulmonary circulation.
Is Leaky Gut Associated with Pulmonary Hypertension?
Some research suggests increased intestinal permeability and circulating bacterial products in PAH and CTEPH. However, intestinal barrier dysfunction may be caused or worsened by right-heart failure and venous congestion.
Can Probiotics Lower Pulmonary Artery Pressure?
This has not been demonstrated in human clinical trials. Positive findings are primarily from animal models and are not sufficient to recommend probiotics as a PAH treatment.
Should I Have a Gut Microbiome Test?
Commercial microbiome testing is not routinely recommended for diagnosing or treating pulmonary hypertension. Results currently cannot guide PAH medication selection or replace established testing.
What Is the Best Diet for Pulmonary Hypertension?
There is no single diet for every patient. A balanced, nutrient-dense diet with adequate protein and individualized sodium and fluid advice is generally more appropriate than an extreme or restrictive diet.
Are Fermented Foods Good for Pulmonary Hypertension?
There is no evidence that fermented foods treat pulmonary hypertension. Some products may also contain large amounts of sodium or worsen gastrointestinal symptoms in certain people.
Can Constipation Affect Pulmonary Hypertension?
Constipation does not usually cause pulmonary hypertension, but straining, discomfort, reduced intake, medications, and fluid restrictions can complicate symptom management. Persistent constipation should be discussed with the healthcare team.
The Bottom Line
The relationship between pulmonary hypertension and gut health is scientifically plausible and increasingly supported by observational and experimental research.
Studies suggest that patients with PAH or CTEPH may have:
Altered gut microbial profiles.
Changes in bacteria that produce short-chain fatty acids.
Higher circulating endotoxin.
Associations between TMAO and disease severity.
Intestinal changes related to right-heart congestion.
But major questions remain.
We do not yet know whether microbiome changes are a cause, consequence, disease modifier, or a combination of all three. No microbiome-directed treatment has been proven to improve clinical outcomes in patients with pulmonary hypertension.
The practical approach is to treat pulmonary hypertension according to current guidelines while also addressing nutrition, medication tolerance, constipation, gastrointestinal disease, iron deficiency, weight loss, and symptoms of right-heart congestion.
Gut health may eventually become a therapeutic target in pulmonary hypertension. Today, it remains an important research frontier—not a replacement for established care.
For a comprehensive evaluation of pulmonary hypertension, respiratory health, digestive symptoms, and associated systemic factors, you can book a consultation with Dr. Samar Shadly.
Dr. Samar Shadly, MD, IFMCP
Consultant Pulmonologist
Consultant Transplant Pulmonologist
Functional Medicine Practitioner
Online consultations are currently available.
Selected References
Humbert M, et al. 2022 ESC/ERS Guidelines for the Diagnosis and Treatment of Pulmonary Hypertension. European Heart Journal. 2022.
Chin KM, et al. Treatment Algorithm for Pulmonary Arterial Hypertension. Proceedings of the Seventh World Symposium on Pulmonary Hypertension. European Respiratory Journal. 2024.
Kim S, et al. Altered Gut Microbiome Profile in Patients with Pulmonary Arterial Hypertension. Hypertension. 2020.
Ikubo Y, et al. Altered Gut Microbiota and Its Association with Inflammation in Patients with Chronic Thromboembolic Pulmonary Hypertension. BMC Pulmonary Medicine. 2022.
Yang J, et al. Gut Microbiota, Metabolites, and Pulmonary Hypertension: Mutual Regulation and Potential Therapies. Microbiological Research. 2025.
Zhou X, et al. Higher Circulating Trimethylamine N-Oxide Levels Are Associated with Worse Severity and Prognosis in Pulmonary Hypertension. Respiratory Research. 2022.
Rischard FP, Hemnes AR. Right Ventricular Function, Inflammation, and the Gut Microbiome in Pulmonary Hypertension: A Translational Frontier. Circulation: Heart Failure. 2025.