Strengthen lungs at home with these tips

People often overlook keeping their lungs whole and well. Since the start of the pandemic, more individuals have been trying to take better care of themselves. Boosting the immune system and improving lung capacity have become a priority. Dr. Lisa M. Cannon shares on this post the best ways to keep lungs strong and healthy.

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Avoid smoking. It has long been established that smoking increases a person’s risk of having respiratory problems such as asthma, idiopathic pulmonary fibrosis, COPD, and lung cancer. Exercise is integral in keeping the lungs in tip-top shape. Regular workout ensures that the heart is strong and the lungs are healthy. Having strong lungs helps a person’s body hold out against aging and sickness.

Check your posture in order to give the lungs enough space. Sitting tall and trying to reach above the head ensure the lungs are given room. The lungs have a mucosal lining that should be kept thin for the lungs to perform effectively. Stay hydrated by drinking enough water throughout the day. Laugh more to engage the abdominal muscles and improve lung capacity. According to pulmonologist Dr. Lisa M. Cannon, laughing removes stale air from the body, which permits fresh air to fill the parts of the lungs.

During these times, it is best to stay home to avoid air pollutants and viruses. With more industries reopening, it can be tempting to go out and enjoy a little bit of freedom. However, only go to public areas when it is necessary, and avoid staying out of the house too long to reduce the risk of catching the virus.

Dr. Lisa M. Cannon earned her medical degree from New York College of Medicine and her fellowship in pulmonary disease, critical care, and sleep medicine from Mount Sinai Hospital. Get quick updates from Dr. Lisa M. Cannon by following her on Twitter.

The end stage: What is stage IV COPD?

Talking about “the end” when suffering from a disease may connote both positive and negative vibes. Positive when the end means the disease has been obliterated completely and negative when it means that the condition has reached its peak, and all hope for cure is futile. How the word is perceived in terms of medical implications vary, but what does it mean in cases of COPD?

Chronic Obstructive Pulmonary Disease (COPD) is described as "inflammatory lung disease affecting the airflow from the lungs." It has four stages –mild COPD, moderate COPD, severe COPD, and very severe COPD, which is also known as the end stage.

                                                             
                                                        Image Source: Timeinc.net

Very severe COPD is the fourth stage of the disease. Respiratory failure caused by either low blood oxygen or high carbon dioxide levels and signs of heart failure exist during this stage. This is regarded as the end stage because exacerbations may occur at least three times within the year, leading to the overall health of the patient becoming highly at risk.

Because of the various complications that occur during stage IV COPD, it is said that people die "with" their disease and not from it. Researches show that COPD is not the primary cause of the death, but other medical conditions that a patient also acquires while battling COPD. Lung cancer and heart failure are the usual medical conditions that cause death, and not COPD itself.

                                                         
                                                             Image source: Temple.edu

Studies also show that the condition of COPD may still improve even after reaching the end stage with the help of bronchodilators and corticosteroids. Continuing with proper health care, quitting smoking, and avoiding lung irritants will also greatly help in dealing with the end stage.

 Dr. Lisa Marie Cannon specializes in pulmonary diseases and critical care. For more articles about pulmonary diseases, visit this blog.

REPOST: Enhancing and Inhibiting Autophagy in Lung Disease is Double-Edged

According to this article, understanding the role of this double-edged-sword hypothesis of autophagy in pulmonary diseases will help in the development of personalized therapies to treat pulmonary diseases. 

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Researchers from the Weill Cornell Medical College and New York-Presbyterian Hospital in New York recently discussed the role of autophagy in lung diseases in a study titled “Autophagy in lung disease pathogenesis and therapeutics,” recently published in the journal Redox Biology.

Autophagy is a physiological process that deals with the destruction of cells in the body. It helps maintain homeostasis or normal functioning by protein degradation and turnover of destroyed cell organelles for new cell formation. In the most common form of autophagy, cytosolic materials (the fluid component of cytoplasma) are sequestered into double-membrane compartments called autophagosomes, which subsequently fuse to lysosomes where their contents are enzymatically degraded.

Recently, autophagy gained attention in human pulmonary diseases, both as a modulator of pathogenesis and as a potential therapeutic target. Studies suggest that the autophagic clearance of mitochondria, a potentially protective program, may worsen the chronic obstructive pulmonary disease by activating cell death programs.

In the review, researchers and coauthors Setfan Ryter and Augustine Choi stated that autophagic clearance of cilia components could contribute to airway dysfunction in chronic lung diseases. In certain diseases such as pulmonary hypertension, autophagy may offer protection by modulating proliferation and cell death. In other disorders, such as idiopathic pulmonary fibrosis and cystic fibrosis, impaired autophagy may contribute to pathogenesis.

The authors point out the multiple functions of autophagy and its selective autophagy subtypes may be of significance to the pathogenesis of human disease, with an emphasis on lung disease and therapeutics. In chronic obstructive pulmonary disease (COPD) for example, autophagy modulation can be observed in lung macrophages, bronchial and epithelial cells upon CS exposure and in the lungs of COPD patients, with recent studies suggesting that autophagy promotes lung epithelial cell death, airway dysfunction, and emphysema in response to CS exposure in vivo.

In certain diseases such as sepsis, autophagy may provide a pro-survival advantage by promoting bacterial clearance, and by modulating inflammation. In cigarette smoke exposure models, evidence showed an amplification of disease process when autophagy or mitophagy is activated. Currently, compounds that can modulate autophagy include the mTOR inhibitor rapamycin (an inducer of autophagy) and chloroquine or hydroxychloroquine (inhibitors of autophagy).

As the authors discussed in their review, autophagy has the ability to cause contrasting effects, indicating that a complete understanding of the pathogenic process and the impact of autophagy would be prudent before attempting to modulate autophagy in the context of human disease.

Lastly, a better understanding of the multiple pathways of selective autophagy and their impact on disease pathogenesis may also facilitate the design of more specific therapies for the treatment of pulmonary diseases, and other related diseases where autophagy may contribute to pathogenesis.


Dr. Lisa Marie Cannon focuses on diagnosting and treating patients with sleep disorders. Visit this blog for related articles and news.