Does metformin help your lungs? Exploring the Evidence on Respiratory Benefits

October 11, 2025 •

5 min read

Metformin, a first-line medication for type 2 diabetes, is currently used by an estimated 20 million people in the U.S. alone, but its potential benefits beyond blood sugar control are increasingly under investigation. Amidst this expanding research, one key question has emerged from the medical community: Does metformin help your lungs?

Quick Summary

This article examines the evidence supporting metformin's potential respiratory benefits, including its anti-inflammatory effects in COPD and asthma, its ability to reverse pulmonary fibrosis in models, and its potential anti-cancer properties.

Key Points

Anti-inflammatory Action: Metformin can reduce lung inflammation in conditions like COPD, asthma, and ARDS through mechanisms that often involve the activation of the AMPK pathway and reduction of pro-inflammatory cytokines.
Anti-fibrotic Properties: Preclinical studies show metformin can reverse established lung fibrosis by inhibiting fibrotic activity, influencing cell metabolism, and potentially stimulating the repair of alveolar stem cells.
Potential for COPD Treatment: In diabetic patients with COPD, some studies suggest that metformin is associated with lower rates of exacerbation, fewer hospitalizations, and a slower decline in lung function.
Asthma Benefits: Observational data indicate a link between metformin use and a reduced risk of asthma attacks, with research exploring its anti-remodeling effects on airways.
Lung Cancer Prevention and Efficacy: Metformin has shown a dose-dependent chemopreventive effect against lung cancer, particularly in overweight/obese diabetic patients, and can potentially boost the effectiveness of immunotherapy.
Metabolic Pathway Regulation: The lung benefits are thought to stem from metformin's metabolic effects, specifically modulating energy sensors like AMPK and combating oxidative stress, rather than solely its glucose-lowering function.

Understanding Metformin's Role in Lung Health

Metformin is primarily known for its ability to lower blood glucose levels by decreasing liver glucose production and increasing insulin sensitivity. However, its mechanism of action is far-reaching, influencing cellular metabolism, inflammation, and oxidative stress through the activation of AMP-activated protein kinase (AMPK). As chronic lung diseases like Chronic Obstructive Pulmonary Disease (COPD) and asthma are characterized by inflammation and metabolic dysfunction, researchers are exploring whether metformin's systemic effects could translate into pulmonary benefits.

Metformin and Chronic Obstructive Pulmonary Disease (COPD)

Research on metformin's effect on COPD, a leading cause of death globally, has yielded mixed but promising results. Several observational studies have found potential benefits, particularly in patients with coexisting type 2 diabetes.

Potential Benefits in COPD

Lower Exacerbation and Hospitalization Rates: A 2024 study reviewed medical records of diabetic patients with COPD and found that metformin users experienced lower rates of exacerbation and hospitalization compared to non-users.
Slower Lung Function Decline: The same study also reported that metformin use was associated with a significant improvement in the rate of Forced Expiratory Volume in 1 second (FEV1) decline, suggesting it could slow disease progression.
Anti-inflammatory and Anti-aging Effects: Preclinical studies have shown that metformin can protect against cigarette smoke-induced lung inflammation, oxidative stress, and premature aging, potentially slowing damage that leads to emphysema. This is linked to its ability to activate the AMPK pathway.

Conflicting Findings in COPD

Despite the positive observations, other large cohort studies have presented conflicting data. A 2020 retrospective study of Taiwanese patients with COPD and T2DM found that metformin users had a higher risk of pneumonia, hospitalization for COPD, and invasive mechanical ventilation. The researchers suggest this could be due to unmeasured confounding factors, such as disease severity or medication bias, and that further investigation is needed. The potential risk of lactic acidosis in hypoxic patients with severe COPD also remains a concern, making careful monitoring essential.

The Anti-fibrotic Effect of Metformin

Pulmonary fibrosis, particularly Idiopathic Pulmonary Fibrosis (IPF), involves the progressive scarring of lung tissue and currently has limited treatment options. Metformin has shown significant anti-fibrotic potential in preclinical studies.

Evidence from Preclinical and Human Studies

Reversing Fibrosis in Mice: A 2018 study from the University of Alabama at Birmingham demonstrated that metformin could reverse established lung fibrosis in a mouse model. The drug targeted and re-sensitized abnormal myofibroblasts to programmed cell death (apoptosis), helping to resolve the fibrotic tissue.
Modulating Fibroblast Fate: A 2019 study published in Nature Communications detailed how metformin accelerated the resolution of lung fibrosis by altering the fate of myofibroblasts, converting them into non-fibrotic lipofibroblasts.
Activating Alveolar Stem Cells: More recent research from 2025 further illuminates metformin's mechanism, showing it promotes fibrosis resolution by activating alveolar epithelial stem cells via AMPK and FGFR2b signaling, leading to better alveolar repair.
Improved Clinical Outcomes in Real-World Studies: A 2022 observational study of IPF patients with diabetes found that metformin use was associated with reduced all-cause mortality and hospitalizations. However, researchers cautioned that randomized clinical trials are still needed to confirm these findings.

Metformin's Impact on Other Lung Conditions

Asthma

Reduced Attacks: A 2024 study suggests that metformin was associated with a lowered risk of asthma attacks in patients with co-occurring diabetes, potentially due to its anti-inflammatory effects.
Anti-inflammatory and Anti-remodeling Effects: Preclinical studies in mice have shown that metformin can mitigate airway inflammation and remodeling, including goblet cell hyperplasia and collagen deposition. This protective role is linked to restoring AMPK activity in lung tissues.

Lung Cancer

Chemoprevention and Improved Outcomes: Research from 2024 and 2025 suggests metformin may have a dose-dependent chemopreventive effect against lung cancer in diabetic patients. A study also showed metformin could improve outcomes and boost immunotherapy efficacy in overweight or obese lung cancer patients.

Comparing Metformin's Primary and Emerging Lung Applications


Feature	Primary Use (Diabetes)	Emerging Lung Applications
Mechanism	Inhibits liver glucose production; increases insulin sensitivity.	Activates AMPK pathway; reduces inflammation and oxidative stress; regulates cell metabolism and fate.
Targeted Area	Liver and muscles for glucose uptake and metabolism.	Lung cells, including alveolar epithelial stem cells, fibroblasts, and immune cells.
Regulatory Status	FDA-approved for the treatment of type 2 diabetes since 1995.	Largely off-label and investigational; further clinical trials are required.
Main Goal	Blood glucose management.	Reducing inflammation, preventing or reversing fibrosis, and slowing disease progression.
Patient Population	Individuals with type 2 diabetes.	Potentially, patients with COPD, pulmonary fibrosis, asthma, and lung cancer, with or without diabetes.

Conclusion

Metformin's potential to benefit lung health, as revealed by a growing body of research, is a compelling and active area of study. Preclinical and observational human data suggest it may act as a potent anti-inflammatory, anti-fibrotic, and anti-cancer agent within the lungs, primarily through its metabolic effects and activation of the AMPK pathway. For patients with coexisting diabetes and lung conditions like COPD, asthma, or lung cancer, evidence points toward favorable outcomes, such as reduced exacerbations and possibly disease progression. However, the evidence is not entirely consistent, especially regarding respiratory infections. It is crucial to remember that metformin is not yet approved for the treatment of lung diseases, and further large-scale, randomized controlled clinical trials are necessary to confirm its efficacy and safety for this purpose, particularly in non-diabetic individuals. The prospect of repurposing this well-established, affordable medication to treat severe lung conditions is revolutionary, but patients should consult their healthcare provider before considering any off-label use.

Ongoing Research and the Road Ahead

Researchers are now focused on several key areas to advance our understanding of metformin's role in lung health. This includes conducting larger, longer-term randomized controlled trials to address the conflicting results observed in some retrospective studies, especially for COPD. Additionally, studies are investigating optimal dosing and duration, as well as identifying specific patient subpopulations (e.g., those with obesity or particular metabolic profiles) who may respond best to metformin treatment. By mapping the full extent of metformin's mechanisms in lung cells, scientists hope to move toward clinical trials that could change the treatment landscape for chronic lung diseases. You can find more information about relevant research projects on the American Lung Association website: https://www.lung.org/research/about-our-research/advancing-research/advancing-research-2024-2025.

Frequently Asked Questions

Metformin is not currently an approved treatment for lung conditions in non-diabetic individuals. While research is ongoing into its off-label uses for respiratory health, you should only take this medication under the strict supervision of a healthcare provider and for a condition it is prescribed to treat.

Metformin primarily activates an enzyme called AMP-activated protein kinase (AMPK), which acts as a cellular energy sensor. Through this and other pathways, it exerts anti-inflammatory, anti-oxidative, and metabolism-regulating effects that can protect and repair lung tissue.

Yes, metformin is being studied for its effects on COPD. Observational studies suggest it may reduce exacerbation and hospitalization rates in diabetic COPD patients, and ongoing trials are investigating its potential to slow disease progression.

Metformin is generally safe, but there is a very rare risk of lactic acidosis, especially in patients with poor kidney function or conditions causing hypoxia. Some retrospective studies have also shown increased risk of pneumonia in metformin users with COPD, highlighting the need for more research.

In mouse models, metformin was shown to accelerate the resolution of lung fibrosis by converting scar-producing myofibroblasts into non-fibrotic lipofibroblasts and reactivating alveolar stem cells to aid repair.

Research suggests metformin may have a chemopreventive effect against lung cancer in diabetic patients and may enhance the effectiveness of immunotherapy in overweight or obese patients.

Many studies are preclinical (animal models) or observational, meaning they can only show associations, not causation. There are also conflicting results in some areas, particularly concerning COPD outcomes. More large-scale, randomized controlled trials are needed for definitive conclusions.

Preclinical studies in mouse models of allergic asthma have shown that metformin can reduce markers of airway inflammation and remodeling, supporting its potential anti-inflammatory effects in asthma.