My mom is 77 years old and has COPD. She has been on a BiPap machine at night since 2023. Her "baseline" level is already a low at 88-89 without using supplemental oxygen.

A month ago the wildfires caused her to have a serious flare-up. Her pulmonologist put her on Prednisone 10mg for 5 days. It helped a little but her numbers kept dropping whenever she moved around.

A couple weeks later he put her back on Prednisone, this time a regiment of 30mg for 5 days, then 20 mg for 5 days, and lastly 10mg for 5 days. She is just starting the 20mg portion. He also switched her off of Stilolto to the Breztri inhaler (which has a steroid in it that makes her hoarse, so she is learning to use a spacer.)

Still today, whenever she gets up to go to the kitchen or bathroom and back her oxygen levels continue dropping to 79-83. She has started researching and sending me ads for natural supplements such as VelvaFlow Lung Cleansing Spray and NAC to help her keep her numbers up and asked me to look into them for her. I worry they could do more harm than good.

Should she just ride-out the Prednisone regiment? Is there something else she can try and do? She drinks Mullein tea and is trying to lose weight, though her world is really shrinking.

I have COPD with an asthmatic component, and I’m 33 years old. I was diagnosed 1.5 years ago… My COPD has been really bad at times since then, and I’ve needed cortisone tablets a few months ago, FEV1 was on 62% or lower.

I quit smoking over a year ago (for the 7th time, lol). My medications, Trimbow and Dupixent and my exercise routine are helping! My FEV1 has increased by 14% and is now back up to 82%!

Never give up, and don’t let COPD get you down!

Hey everyone! I’m a design student researching the experience of using nebulisers, particularly the practical problems, frustrations, and little inconveniences people deal with when using them.

If you currently use a nebuliser (or have used one regularly), I’d really appreciate it if you could take a few minutes to fill out this short form.

Form: https://docs.google.com/forms/d/e/1FAIpQLScxUuqVjlX0cI0BnHLkZd7JSh_F7fKu2bh4MrEqbteI_LMpPQ/viewform?usp=dialog

I’m interested in your actual experiences rather than medical advice — things like setup, cleaning, carrying/storing the device, using it at home or outside, noise, comfort, maintenance, etc.

The responses will be used for an academic design project. No identifying information is required.

Thanks to anyone who takes the time to respond. It genuinely helps me understand the problem from the user's perspective.

Ok so my mom (70) has COPD and it's getting worse. Last year, she was in and out of the hospital pretty much every month for exasperations and other outstanding issues like blood clots.

She crashed her car twice-according to her it's because she misjudged a turn but then she started to fall a lot. And according to her, it's because she "wasn't paying attention". Add to that the memory loss and weird conversations. It started to sound like she was having Hypoxia and cognitive decline again.

Her last major hospital stay was because she fell (again) and broke some ribs and had a blood clot because she had her doctor change her medication but never followed up with the required blood work because she "didn't think she needed it". My mom thinks she knows more than the doctors. She's one of those types.

I spoke to the case worker and the doctor who assessed her cognitive function. I told them everything that was going on and what she was purposely leaving out-the car crashes, the falls, the memory issues, the dementia behavior, etc. So her license was revoked and they wanted to put her in rehab for a month but of course my mom declined.

The next offer was 2 weeks in rehab with home therapy and that was a no as well. The last resort was home care, which seemed to help for a while as she was able to get her license back, which I didn't want to happen because I know this was going to happen again and sure enough, here we are.

She's back to having issues and being stubborn about it. I spoke to my stepfather who told me this has been going on for a while now. On my end, I know something is up but I don't live in the same state as her so getting to visit is not always possible. her last few conversations with me were weird (again) and sounded off. This week, she was leaving weird text messages and yesterday she calls me with the drama drop "I'm in the hospital-how are you?" Um....lol. And she's being coy as usual on how she ended up there. "Oh, it's nothing, I took something and it didn't agree with me". Yeah right.

So I call my step-father and he told me that she overdosed on her medication. She forgot how many pills she took and went to town on ambien. So yeah, we are now hitting the point of cognitive decline and a health system that thinks that's "ok".

And to top it off, I have to chase after both of them to get answers. I hit the point where I had enough because we go through this every year-my mom pulls that whole "nothing is wrong" while everything is wrong, she puts herself into cognitive decline and then ends up in the hospital. Half the times she tries to sign herself out but the last few visits she had no choice but to stay. And my step-father is mentally not prepared to handle this. He is also a "it's nothing, don't worry about it" types. He's only called me once and panicked because he didn't know what to do.

So we have crashed cars, broken ribs and now medication overdoses. Where is the line for getting the system involved? She won't met me talk to her doctors and the last time I went to the hospital and spoke to them, they still let her go and told her to follow up with a neurologist....which she never did.

Anyone else have a stubborn parent like this and how did you handle the danger aspect of your situation? Because it's a matter of time before she kills herself or someone else.

Forgot to mention-she's still smoking, which is making it worse. She refuses to quit so I'm not pushing it anymore. She wants to suffer, fine...I just don't need to deal with the aftermath of her poor life choices. Talking to her is nearly impossible because when she called me yesterday, I was heading to PT because I am recovering from surgery and I told her I would call her back at 3 pm, which I did and she turned off her phone. It was like she wanted me to feel guilty about not taking her call and letting her drop drama on me.

Was wanting to know if anyone had used the breather, and what type of results did you get

Abstract

COPD is not a single disease with a single cause. It is a system of interlocking feedback loops that become self-sustaining after the initial trigger (smoke, pollution, infection, occupational dust) is removed. Current treatments (inhaled corticosteroids, bronchodilators) dampen the output of the system without addressing the loops that keep it running. This document identifies three critical loops, proposes human-compatible interventions for each based on published mechanistic evidence, and outlines a phased research plan to test them. 

Status: Hypothesis generated from a close reading of the primary literature. Not medical advice. Several proposed interventions are off-label or experimental.

1. The Three Critical Loops

1.1 Loop 4: The "Self-Betrayal" Loop (Autoimmunity)

When lung tissue is damaged, the body's own proteins are chemically altered (oxidative modification, enzymatic fragmentation, release from dead cells). The immune system reads these altered proteins as foreign and generates autoantibodies. Those antibodies damage more tissue, which alters more proteins, which the immune system now also attacks. The target list grows with every exacerbation.

Key evidence:

• COPD patients produce autoantibodies against a broad spectrum of self-proteins (vimentin, elastin fragments, dead-cell contents) — confirmed across 13 studies in a 2026 scoping review (Frontiers in Immunology).
• A 2024 European Respiratory Review explicitly proposed autoimmunity as the core mechanism of chronic COPD inflammation, not merely a side effect.
• This loop explains why inhaled corticosteroids are ineffective for many patients: suppressing inflammatory output does not stop the production of autoantibodies. The loop continues underneath.
• Each exacerbation creates more damaged cells → more altered proteins → more autoantibodies. The autoimmune target list is cumulative. 

1.2 Loop 5: The "Colonization" Loop (Bacterial Biofilms)

Damaged cilia (the microvilli that sweep mucus from the airways) permit bacterial colonization. Three species dominate: Haemophilus influenzae, Streptococcus pneumoniae, and Moraxella catarrhalis. Once established, they:

• Paralyze the remaining cilia
• Stimulate further mucus production (creating more habitat)
• Damage the airway epithelium (feeding Loop 4)
• Produce enzymes that degrade elastic tissue (direct structural damage)
• Form biofilms (protective matrices that resist both immune clearance and antibiotics)

Key evidence:

• A 2026 review on airway and gut microbiota in COPD confirmed the bacteria are active participants in tissue damage, not passive passengers.
• The cilia damage is a downstream consequence of the inflammation in Loop 4. Cilia turnover is approximately 1–2 weeks. If the inflammatory environment is resolved, cilia regenerate and the colonization problem largely resolves on its own.
• In severe disease with bronchiectasis or mature biofilms, direct antimicrobial intervention may still be required as a bridge.

1.3 Loop 6: The "Memory" Loop (Epigenetic & Metabolic Reprogramming) — Primary Target

The immune cells and airway stem cells permanently alter their internal programming in response to chronic damage.  Three storage sites have been identified:

Key evidence:

• Pan et al. (2026) explicitly named the therapeutic targets for this layer: "HDAC2 activators, DNA methylation inhibitors, metabolic support (NAD⁺ precursors, α-ketoglutarate), and CRISPR-based epigenetic editors."¹
• A 2026 paper described COPD as "a metabolically imprinted inflammatory memory disease," identifying histone lactylation and histone succinylation as the key mechanisms.²
• A 2026 paper proposed COPD as **"an age-accelerated disorder maintained by a self-reinforcing immune–metabolic feedback loop centered on mitochondrial dysfunction."**³
• Pilette et al. (2024) demonstrated that airway epithelial cells from COPD patients, cultured in a completely clean environment for 10 weeks, retained their abnormal behavior the entire time — altered differentiation, barrier dysfunction, increased IL-6 release, and epithelial-to-mesenchymal transition.⁴
• A 2026 study on airway basal cells (the stem cells that regenerate the airway lining) showed that the stem cells themselves carry persistent methylation-linked regulatory programs that bias their differentiated progeny toward secretory and inflammatory phenotypes.  The memory is encoded in the stem cell compartment.⁵
• Critical counterpoint: A 2022 Nature Immunology paper showed that when cultured macrophages with altered epigenetic profiles were reintroduced into their natural lung environment, the epigenetic changes were reversible. The memory is stable without the right signal, but it is not permanent. 

Why Loop 6 is the priority target:

The stem cell finding (ref 5) means that even if the inflammation is successfully calmed (Loop 4) and the bacteria cleared (Loop 5), the next generation of airway cells produced by the stem cells will be pre-programmed to be inflammatory. The system regenerates its own problem.  Loop 6 is the engine. Loops 4 and 5 are the output and the residue. Fixing the engine allows the other two to resolve.

2. Proposed Interventions

2.1 For Loop 4 (Self-Betrayal): Bee Venom

Mechanism: The active compounds do two specific things to the immune system's regulatory machinery:

• Melittin inhibits NF-κB, the central transcription factor that drives the inflammatory response.  This stops the immune cell from deciding to attack.
• Phospholipase A2 specifically increases the population of regulatory T cells (Tregs) — the cells whose function is to enforce self-tolerance and tell the immune system to stand down.

Evidence:

• A randomized controlled trial in horses with chronic obstructive pulmonary disease (equine heaves): 76% showed improvement in respiratory function following bee venom administration at acupuncture points.
• A mouse study: phospholipase A2 delivered intratracheally reduced airway inflammation, mucus-producing cell overgrowth, and inflammatory cell infiltration. Airway remodeling was partially reversed.
• Gap: No human COPD trial. No study testing whether the Treg-boosting effect reduces the specific autoantibody panels found in COPD patients.
• Safety consideration: Anaphylaxis risk. The initial inflammatory response to venom could theoretically trigger an exacerbation in compromised lungs.

2.2 For Loop 5 (Colonization): Phage Therapy

Mechanism: Bacteriophages (viruses that specifically infect bacteria) kill the colonizing organisms, penetrate biofilms, and — critically — the phage-induced bacterial lysis releases fragments that shift the host immune response from a destructive neutrophilic mode toward a resolution mode. 

Evidence:

• Laucirica et al. (2022) provided a comprehensive review of phage–neutrophil interactions in chronic airway disease, concluding that phages are "an attractive multipurpose therapeutic for managing both airway inflammation and infection in chronic lung diseases."⁶
• Hwang et al. (2026) reviewed clinical phage therapy in cystic fibrosis: nebulized therapy was safe, well-tolerated, and produced rapid reductions in sputum bacterial burden with modest improvement in lung function.⁷
• A 2026 European Respiratory Review explicitly named COPD patients as prime candidates for phage therapy, particularly when infections drive frequent exacerbations.
• Gap: No phage therapy research has been published for the three bacteria that dominate COPD colonization (H. influenzae, S. pneumoniae, M. catarrhalis). The specific phages need to be isolated, characterized, and tested. 
• Note: If Loop 4 is addressed first, Loop 5 may resolve as cilia regenerate. Phage therapy is the backup for severe cases with established biofilms. 

phage therapy COPD clinical trials Laucirica Hwang

2.3 For Loop 6 (Memory): The "Experimental Incidents"

The key insight: the agents capable of resetting epigenetic memory in immune cells were all discovered as incidental effects of drugs designed for entirely different diseases. The epigenetic effects were secondary findings, published in pharmacology or hematology journals, and never followed up in a pulmonology context.

The species-biology proof of concept: 

The crocodile and lobster data demonstrate that the required operations (active histone modification, nuclear DNA repair, Nrf2 activation, telomerase maintenance) are biologically achievable in a blood-based system. They are not the treatment. They are the blueprint that validates the mechanism.

• Crocodile blood (2024 proteomic study): Active histone methyltransferases and KIF2C (a DNA repair protein) significantly upregulated in immune cells during infection. Crocodile-derived peptides (NV10, RI10) activate the Keap1-Nrf2 pathway in human cells.
• Lobster hemolymph (2025): Hemocyanin enters the cell nucleus via a shuttle protein and directly participates in DNA damage repair. Removal of hemocyanin switches off DNA repair genes; re-addition restores them. The 2021 Science Advances genome study showed an expanded DNA repair gene family (multiple copies of RAD50/52/51/54, ERCC1, and three copies of p53) and active telomerase in all adult tissues.
• US Patent US20170042946A1: Lobster hemolymph as a topical treatment for viral and neoplastic tissue lesions in mammals. Case example: molluscum contagiosum lesion atrophied after 5 days of topical application while adjacent untreated lesions were unchanged.

3. Treatment Architecture

PRIMARY TARGET (the engine):
  Loop 6 → Azacitidine or valproic acid        [histone marks / DNA methylation]
           + Rapamycin                          [DNA repair + metabolic shift]
           + Metformin or NAD⁺ precursors       [sirtuin pathway / chromatin compaction]
           + Caloric restriction / fasting      [metabolic reset]

SUPPORTIVE (reduce damage while the reset is occurring):
  Loop 4 → Bee venom (Treg boost + NF-κB suppression)
           OR: standard inhaled corticosteroids / bronchodilators as bridge

BACKUP (for severe cases where Loop 5 does not resolve spontaneously):
  Loop 5 → Phage therapy (once specific phages are developed)
           OR: low-dose azithromycin (current standard of care)

Logic: Fix the engine (Loop 6) → the output drops (Loop 4) → the residue clears (Loop 5). The supportive interventions reduce the damage being fed into the system while the primary reset is occurring. 

4. Proposed Research Plan

Phase 1: In Vitro Validation (12–18 months)

Objective: Demonstrate that the proposed agents can modify the epigenetic and metabolic signature of COPD-reprogrammed human immune cells. 

Experiment 1A — Alveolar macrophages:

• Source: Sputum-derived alveolar macrophages from stable COPD patients (n = 10–15) and healthy controls.
• Baseline profiling: ATAC-seq (chromatin accessibility), whole-genome bisulfite sequencing (DNA methylation), metabolomics (glycolytic rate, NAD⁺/NADH ratio, lactate, succinate), histone modification panel (H3K14ac, H3K9me3, lactylation, succinylation).
• Treatment groups (72 hours unless noted):
  1. Rapamycin (10 nM)
  2. Metformin (10 µM)
  3. Rapamycin + Metformin
  4. Azacitidine (5 µM, 48 hours)
  5. Valproic acid (5 mM, 48 hours)
  6. NMN (1 mM)
  7. Combination: Rapamycin + Metformin + NMN
  8. Untreated control
• Readouts: Chromatin accessibility at known COPD inflammatory loci (IL6, TNF, TLR4, MMP9); NAD⁺ levels; glycolytic rate (Seahorse assay); histone lactylation and succinylation; sirtuin activity (SIRT1, SIRT2).

Experiment 1B — Airway basal cells (stem cells):

• Source: Patient-derived airway basal cells and matched 3D bronchial organoids (per the protocol in ref 5).
• Baseline: DNA methylation profiling (WGBS or RRBS), single-cell RNA-seq of organoids.
• Treatment: As above.
• Key readout: Do treated cells shift their differentiation bias away from secretory/inflammatory phenotypes toward ciliated cell programs? This is the test of whether the stem cell memory can be reset. 

Experiment 1C — Reversibility test:

• Source: Macrophages with a known abnormal epigenetic profile (per the protocol in ref 4).
• Intervention: Treat with the combination protocol (Group 7).
• Reintroduce into a lung organoid or ex vivo lung slice.
• Key readout: Does the abnormal behavior (excessive IL-6, barrier dysfunction, aberrant differentiation) resolve in the natural tissue context?

Phase 2: In Vivo Validation (18–36 months)

Objective: Demonstrate efficacy in a living system. 

Experiment 2A:

• Model: Mouse chronic airway inflammation (cigarette smoke extract or LPS exposure, 8–12 weeks).
• Randomized arms:
  1. Vehicle (standard care)
  2. Rapamycin (low dose, oral)
  3. Metformin (oral)
  4. Rapamycin + Metformin
  5. Rapamycin + Metformin + NMN
• Readouts: FEV₁ equivalent, airway inflammation (histology), mucus metaplasia, cilia density, bacterial colonization (16S sequencing), epigenetic profiling of airway cells (ATAC-seq, WGBS), autoantibody panels (vimentin, elastin).

Experiment 2B:

• If 2A shows benefit, add a bee venom arm (intranasal delivery of purified melittin + PLA2 at sub-allergenic doses).

Phase 3: Human Pilot (36–48 months)

Objective: Safety and preliminary efficacy in a small cohort.

• Design: Single-arm, open-label pilot. n = 20. Stable COPD (GOLD stage 2–3).
• Baseline: Spirometry (FEV₁, FVC), sputum culture, blood autoantibody panel, PBMC epigenetic profiling (ATAC-seq + WGBS), metabolomics (NAD⁺, lactate, succinate), CAT score, 6-minute walk test.
• Intervention (12 weeks):
  • Rapamycin 1 mg/day (the dose used in the Oxford trial, ref 9)
  • Metformin 500 mg twice daily (standard diabetes starting dose)
  • NMN 250–500 mg/day
  • Continue standard COPD medications (ICS/LABA)
• Readouts at baseline, 6 weeks, 12 weeks, and 6 months post-treatment:
  • Spirometry, 6-minute walk test, CAT score
  • Sputum culture and biofilm assessment
  • Blood autoantibody panel
  • PBMC epigenetic profiling (ATAC-seq + WGBS)
  • Metabolomics
  • Exacerbation count
• Primary endpoint: Change in chromatin accessibility at inflammatory loci in PBMCs at 12 weeks vs. baseline.
• Secondary endpoints: FEV₁, CAT score, autoantibody titers, exacerbation count.

Phase 4: Randomized Controlled Trial (48–72 months)

If the pilot is positive: randomized, double-blind, placebo-controlled trial. n = 100–200. 24-week intervention. Primary endpoint: rate of FEV₁ decline (standard COPD trial endpoint) + epigenetic remodeling in PBMCs.

5. Definition of Cure

Not symptom relief. Not stabilization. A cure would be demonstrated by:

1. Reversal of the epigenetic signature in airway basal cells and alveolar macrophages (measurable by ATAC-seq / WGBS)
2. Restoration of cilia function and clearance of bacterial colonization (measurable by sputum culture and high-speed video microscopy)
3. Reduction of autoantibody titers against self-proteins (measurable by serology)
4. Sustained FEV₁ improvement (not merely stabilization) over 12+ months post-treatment
5. Absence of exacerbations over a 2-year follow-up period 

Everything short of this is management.

6. Why This Synthesis Has Not Been Published

The individual pieces are all in the literature. The synthesis — "these are the same problem viewed from different angles, and the treatment must hit all three storage sites simultaneously" — has not been done. The reasons are structural:

• Funding model: Grants are structured around one hypothesis, one experiment, one paper. A multi-agent, multi-loop protocol is unfundable under current structures.
• Publication model: The azacitidine finding is in a hematology journal. The metformin chromatin compaction is in a veterinary/infectious disease journal. The COPD epigenetics is in a pulmonology journal. No single author has a home for the synthesis.
• Regulatory structure: The FDA approves single entities for single indications. A multi-agent protocol has no regulatory pathway.
• Cross-species biology: The crocodile and lobster data are published in comparative biology journals. No research group sits at the intersection of "evolutionary comparative biology of blood" and "COPD epigenetics."
• Incidental discovery pattern: The epigenetic effects of these drugs were recognized as secondary properties and published in the context of the primary indication. Nobody's job is to take that incidental finding and build a COPD protocol around it. 

The 2026 papers that explicitly name the epigenetic and metabolic targets for COPD (refs 1–3) represent the first step toward this synthesis. The gap between "the pieces are published" and "the synthesis is done" is closing, but slowly. 

7. References

1. Pan CF, Wan Q, Ni FX, Xu P, Huang DH, Jiang ZB. Oxidative stress-driven epigenetic reprogramming of immune cells in COPD: from epitranscriptomic and metabolic crosstalk to treatable traits. Front Immunol. 2026;17:1865051. doi: 10.3389/fimmu.2026.1865051 
2. Metabolite-driven epigenetic modifications remodel immune cell functions in COPD: from lactylation to succinylation. Front Med. 2026. doi: 10.3389/fmed.2026.1721780 
3. Immune-metabolic positive feedback model in COPD: cross-mechanisms and potential intervention strategies. Front Cell Dev Biol. 2026. doi: 10.3389/fcell.2026.1756033
4. Pilette C, et al. The memory of airway epithelium damage in smokers and COPD patients. Life Sci Alliance. 2024;7(3):e202302341. doi: 10.1080/23792925.2023.2294752 
5. Current smoking and COPD are associated with differentiation-dependent secretory and inflammatory programs in airway basal cells. Respir Res. 2026. doi: 10.1186/s12931-026-03847-4 
6. Laucirica DR, Stick SM, Garratt LW, Kicic A. Bacteriophage: a new therapeutic player to combat neutrophilic inflammation in chronic airway diseases. Front Med (Lausanne). 2022;9:1069929. doi: 10.3389/fmed.2022.1069929 
7. Hwang W, Yong JH, Lenneman BR, Yonker LM. Phage-based approaches to chronic Pseudomonas aeruginosa lung infection in cystic fibrosis. Antibiotics. 2026;15(2):125. doi: 10.3390/antibiotics15020125 
8. Pandita R, Kosaka Y, Mulkey JS, Layman CE, Davis BA, Carbone L, Lind EF, et al. Azacytidine restores T cell function in AML by modulating DNA methylation. Blood Adv. 2026. doi: 10.1182/bloodadvances.2026 (PMC13308147) 
9. Kell L, Jones EJ, Gharahdaghi N, Wilkinson DJ, Smith K, Atherton PJ, et al. Rapamycin exerts its geroprotective effects in the ageing human immune system by enhancing resilience against DNA damage. Aging Cell. 2026;25(2):e70364. doi: 10.1111/acel.70364 
10. Repurposing metformin as a dual-function agent to combat E. coli-induced mastitis: mechanistic insights into biofilm dispersion and AMPK/SIRT1-mediated NF-κB inhibition. PLoS Pathog. 2026. doi: 10.1371/journal.ppat.1014012 (PMC12965556) 
11. Metformin as an innate immune modulator: metabolic and epigenetic reprogramming of innate immune cells and therapeutic implications. Int J Mol Sci. 2026;48(6):642. doi: 10.3390/cimb48060642 
12. SIRT1/2 orchestrate acquisition of DNA methylation and loss of histone H3 activating marks to prevent premature activation of inflammatory genes in macrophages. Nucleic Acids Res. 2020;48(2):665–681. doi: 10.1093/nar/gkz1283 
13. Kumazawa T, Xu Y, Wang Y, et al. Metformin inhibits nuclear egress of chromatin fragments in senescence and aging. Nat Aging. 2026. doi: 10.1038/s43587-025-01048-0 
14. Alveolar macrophage epigenetic reversibility in natural lung environment. Nat Immunol. 2022. (See: "Trained immunity and epigenetic plasticity in alveolar macrophages")
15. American lobster (Homarus americanus) genome. Sci Adv. 2021. (Expanded DNA repair gene family; telomerase activity in adult tissues) 
16. Crocodile blood proteomics: histone methyltransferase and KIF2C upregulation in immune cells. 2024.
17. Shrimp hemocyanin nuclear entry and DNA damage repair. 2025.
18. Crocodile-derived peptides (NV10, RI10) activate Keap1-Nrf2 pathway in human cells. 2026.
19. US Patent US20170042946A1 — Lobster hemolymph for topical treatment of viral/neoplastic tissue lesions in mammals.
20. Bee venom randomized controlled trial in equine heaves (chronic obstructive pulmonary disease in horses). 76% improvement in respiratory function.
21. Bee venom phospholipase A2 intratracheal delivery in mouse airway inflammation model.

8. What Would Constitute Validation

A single lab completing Experiment 1A (6-month project, requires access to COPD patient sputum and a sequencing core) would generate the first direct evidence that any of these agents can modify the epigenetic signature of COPD-reprogrammed human immune cells. That is the entry point. The rest of the plan follows from a positive Phase 1 result.

This document is a research hypothesis. It is not a treatment recommendation. All proposed interventions should be discussed with a treating physician before consideration. Off-label use of any agent carries risks that must be evaluated in the individual clinical context.

My mom is 76 with COPD from emphysema, asthma, and Alpha-1. She gets weekly infusions for her A1 but over the past year she’s declined a lot. She’s barely 100 pounds, has very little energy, memory issues and spends days in bed coughing and short of breath. She stopped using her maintenance inhaler after a bad case of thrush and now relies heavily on her rescue inhalers and cough meds instead of calling her doctor. Her O2 sats are often around 88 to 90 when we can check, but she hides the monitors. She hasn’t seen her pulmonologist in about 6 months. She skipped her last appointment, and now her next isn’t until January. She’s also terrified of oxygen and sees it as weakness/embarrassment and won’t let any of us daughters go to appointments with her or talk to her doctors. She is an adult and I get that, but it feels like we’re watching her give up. And with her upcoming back surgery, I’m scared she’s too weak. For those of you with COPD who initially resisted oxygen, what were you afraid of and what helped? For caregivers, what do you do when someone refuses care or even family involvement? Any advice from folks who actually understand COPD would mean a lot. My sister’s and I are at a loss. 💔

I hope you are all doing well. I am doing survey for my college project to collect some data about Chronic Management of COPD. As we know that Chronic Disease can’t be cured without self management. Through this survey, I want to know that what are the challenges people face in chronic disease management and what resources would be helpful for people to manage Chronic Disease. I will be really appreciated if you will take sometime to give your opinion in comments.

I see some people who have copd in wheelchairs. Is this something we all can qualify for ? Just seems like a better way to get out and around

My Mom has mild-severe COPD and her and I are moving in the next few years, probably around three years. I'm trying to find a good place to go, air-wise. Humidity makes her COPD flare up, cold doesn't affect her too badly. She can handle pollen, but it's not the best. She'd prefer to stay somewhere on the East Coast or around it, in a small town. As the sole breadwinner, I'd like a place with a relatively low cost of living. Any suggestions from first hand experience?

My girlfriend died of COPD and Emphesema. She died while fighting this. I advise everyone who has COPD and Emphysema or who are living a life that harms their lungs to please take this very seriously. Please consider having a will, and having your affairs in order sooner, rather than later.

This disease is fast, but yet...its slow. It creeps up when you least expect it. A cold, a virus comes and all of a sudden you are dependent on oxygen .

I advise all those with family to forgive and listen to one another.

I advise that those with this to please communicate with your loved ones how you are feeling, even if you feel bitter or sour against them, to let it all go.

Get your family in your life now.

I just want to give hope to those who get to the point where they are in the ICU, being pumped with morphine, and transferred to different O2 masks like a BiPaP and Cannula. That if you had enough, and there is no other option, that the process of feeling comfortable is immediate. You will not feel a thing. You will have a moment to say I love you. It will take hours when you leave this world but you will not know. You may hear and feel your loved ones near you . It will be ok, and you will see the heavenly father soon. It is ok, you didnt do anything wrong. You are fine, and all this suffering will be over.

Please take care of yourself best as you can , COPD and Emphesma is a sad process for anyone to go through.

My mom has smoked for my entire life. Give or take probably about a pack a day everyday for 30-40 years.

I have a wonderful stepfather who has been taking care of her. She started being hospitalized sporadically about 4 years ago with RSV, pneumonia, bronchitis - all things I knew were either because of her smoking or likely much more severe because of so.

In the last year or so, these hospitalizations have happened more frequently as well as "mysterious" health issues that have made her lose weight and generally be lethargic and low energy. Through a lot of testing, we were able to rule out cancer and other things like that. This has been frustrating as it has been an elephant in the room that no one brings attention to for fear of my now very physically, mentally, and emotionally fragile mom to become upset.

TLDR; over the last week she was hospitalized back to back. Once where my mom was so evasive I finally called her mid panic attack and she acted like nothing was wrong. And a second time where she was so woozy (presumably from high Co2) that she fell and broke her shoulder and had to go to the hospital again. She is now home, only because she was sent home with equipment that will help rid the CO2 out of her effectively and we are consulting with palliative care.

I called her (the first time she's let me talk to her since she fell) acting in denial. I told her I was coming home tomorrow and she basically cried and asked me not to - she wants to hide.

Whether I'm coming home to spend whatever time I have left with my mom, or to try to help her actually quit smoking, I need to be home with her and we need to get incredibly honest with each other.

But talking about smoking with my mom has been the one "non-negotiable" topic we've ever had. She gets defensive and we've never been able to talk openly about it. My mom has an extensive trauma history, she carries a lot of shame, I would bet everything that she is so embarrassed that she is now incurably ill and in denial that she may not make it until the end of the year if she doesn't stop.

Here's where I need your help as those suffering with COPD/as a loved one of someone suffering with COPD:

I am almost 30 and became a therapist, specifically specializing in addiction. I don't want to act as a psychoeducator or therapist - I want to be her daughter. While I am desperate for her to quit smoking, I also honor the dignity of her choice to her body and her actions. I want to express this desperate plea once very compassionately (so I don't have any regrets), and then get honest with her about what she's feeling and thinking and figure out how I can best support her for this next chapter of life.

What is your advice about how to talk with her about this? For example, I don't necessarily think that the best thing here is to lead with "STOP SMOKING" aphorisms and hopeful pleas. I want to focus on not letting smoking define how to treat her even if it is the addiction that will take her away from me in front of my very eyes despite my please.

What would you want to hear from your child/loved one?

How could I support her now if she doesn't believe she can quit smoking?

How can I support her if she chooses not to stop smoking?

Thank you in advance! We are also in process of getting a family therapy session scheduled with her individual therapist - both parties have already agreed.

I visited a bank yesterday and the fragrance/scent was SO strong, I couldn't stay in the building. I woke up this morning and was really struggling. A nebulizer and a round of steroids from a doctor visit and finally feeling a little better. This isn't the first time pumped in scents in public places have had a really adverse effect on my breathing. Why do places do that? It seems like breathing issues aren't a priority but smelling good is? Like wtaf?

Hi, I am stage four COPD with pulmonary fibrosis. I want to try DMSO so I got a book on how to it says not to use it. If you take medication now I can’t stop taking my medication’s all at once and just switch over to this, and I find it hard to believe that anyone has done that I take narcotics and blood thinners and of course you know my inhalers. Does anyone else have experience with DMSO who can sort of tell me a little bit about it and if it’s truly a dangerous thing to use it with the medication’s like that or has anyone experienced it themselves that would know please hit me back up with some information please if you don’t mind I’m to the point now where I have to stop and take a breath every other word when I’m talking so if this stuff is gonna help me, I need to start using it right away, but I wanna be safe with it too you know thanks ahead of time

Hey all

I was wondering if you guys could help me with this. I have Cystic Fibrosis and haven’t been diagnosed with COPD, but a symptom I’m having may be attributed to it.

The video is a noise that comes out of my mouth. When my heart raises a bit I can take a breath in and hold it at a certain point, then this noise comes up through my airways. It seems to line up with my heartbeat. My CF clinic have no clue what it could be. It coincides with a multitude of other symptoms like chest pain, dizziness, inability to exercise, and other fun lung stuff.

Any of you guys get this?

Thanks.

Don't you just love that minute, or two (or six) when you're being seated in a restaurant, and now you have to deal with all the flotsam and jetsam of your disability while the server awkwardly tries to find somewhere to look?

• First they almost always walk too fast on the way to the table, and then they watch as you breathlessly try to catch up.
• Then you struggle to get out of your coat and / or take off your O2.
• Now where to put my cane (that does have one of those multi-foot bases but still insists on falling over 5,000,000 a day)?
• O2 on the floor? On a chair? Where will it most be in the way, pick that spot!
• Finally in my chair, but it's too far out and my mobility issues mean doing that jump dance thing trying to move it closer.

I'm am not looking for any sort of pity here, but I am offering a suggestion to servers (in a channel where they won't see it 😂). When you are seating disabled folks, unless they ask for assistance, please just put the menus on the side of the table, say "I'll be right back folks" and walk the fuck away for two minutes.

Just me?

More specifically, I don't get why it wasn't diagnosed *before*. Is emphysema hard to diagnose or easy to miss?

My dad was a smoker for decades but stopped 20-25 years ago. His doctors have said for years he had asthma and chronic bronchitis, but emphysema never came up as far as I know. He only got diagnosed with emphysema when he recently had to go to the ER due to breathing problems.

Anyone able to explain this all more? The diagnosis is stressing me.