“It is a common belief that we breathe with our lungs alone, but in point of fact, the work of breathing is done by the whole body…. That is why breathing is the dominant factor in the practice of Yoga.”
― Alexander Lowen, The Voice of the Body.
In some yogic practices and Ayurvedic medicine, the word for breath, prana, implies so much more than the physiologic impulse of breathing, as its Sanskrit definition can also be interpreted as “life force” or “vital principle.” To live is to breathe, and as an unconscious drive, it is often taken for granted. But for the roughly six percent of the US population – about 15.5 million adults – suffering from chronic obstructive pulmonary disease[1] (COPD) it can become a devastatingly difficult daily challenge. It is also big business, which is apparent from the number of pharmaceutical ads you will see whenever you turn on the television. The global market is estimated to be more than $25 billion by 2030.[2] But what if you could improve your lung function by simply changing what you eat?
Most cases of COPD are associated with cigarette smoking. In addition to the gut microbiome, which is a frequent topic of conversation in this column, many other microbiomes exist wherever we interface with our environment. Each of us has a unique skin microflora and a unique lung microbiome that exists at that thin line where the air we breathe in becomes the vital force that sustains our lives. It is no surprise that cigarette smoking directly impacts lung microbiota.
What may be surprising to some is that the gastrointestinal microbiome, the largest and most diverse microbiome in the human body, also appears to be involved in lung function via the gut-lung axis. A recent study from the British Medical Journal, utilizing both a mouse model and a small pilot study of humans, sought to explore the mechanisms behind this correlation.
- The study utilized both a mouse model and a small (16-patient) human pilot study.
- The mouse model sought to replicate the conditions of lung damage associated with COPD through the introduction of cigarette smoke (CS).
- The mouse model also utilized the technique of fecal microbial transfer (FMT) in examining the effects of gut microbiome associated with cigarette smoke versus a healthy native gut microbiome.
- Finally, the effects of diet were examined in the mouse model using a high-resistant starch diet and in humans using inulin versus placebo.
The Take-Away:
- Utilizing FMT from a healthy mouse into a mouse suffering from CS-induced COPD attenuated the characteristics of COPD, such as lung inflammation, alveolar destruction, and impaired lung function.
- Likewise, the transfer of a healthy gut microbiome ameliorated both the gastrointestinal pathology associated with COPD and the negative systemic inflammatory changes that accompany its development.
- Conversely, the transfer of the gut microbiome from mice who developed CS-induced COPD into otherwise healthy mice (who had their native and healthy gut microbiome depleted through the administration of antibiotics) caused lung inflammation and depressed native colonic immunity.
- When the diets of both mice suffering from CS-induced COPD and human patients were supplemented with prebiotic complex carbohydrates, disease outcomes improved, and these dietary effects were in addition to the benefits of smoking cessation.
The Caveat:
Modern Western medicine often treats disease as dysfunction within the confines of distinct and separate organ systems. However, as this study reminds us, we are an extremely complex biological system with a lot of moving parts that are all internally connected. Furthermore, those connections extend to our external environment through such daily and mundane activities as eating, drinking, and breathing.
In people suffering from COPD, which most commonly occurs as a result of cigarette smoking, the effects extend beyond direct injury to the lungs and are associated with reproducible changes to the gut microbiome. In this study utilizing a mouse model, the researchers were able to show through FMT that, when replaced with a healthy gut microbiome, the altered gut microbiome associated with COPD “reproducibly alleviated inflammation, emphysema, impaired lung function, and gastrointestinal pathology” associated with COPD.
A causal effect of the role of the gut microbiota in the development of the pathologies associated with COPD was strengthened by using FMT from CS-induced COPD mice into otherwise healthy mice after the healthy mice were treated with antibiotics to deplete their native bacteria. After the FMT from the CS-induced COPD mice, the previously healthy mice showed “increased lung inflammation” as well as a suppression of native colonic immunity. FMT from mice that were not exposed to cigarette smoke into healthy mice treated with antibiotics induced no such changes, suggesting that the critical difference is the composition of the gut microbiota. As always, extrapolation from mice to humans comes with a caveat.
Mice that developed CS-induced COPD were also subjected to dietary intervention. They were fed either a control diet (control group) or a diet in which all carbohydrates were delivered as resistant starch. Resistant starch carbohydrates are not digested by mice but, instead, they are digested and fermented by their microbiomes. These types of carbohydrates are known as microbiome-accessible carbohydrates or MACs. The affected mice who received the MACs demonstrated reduced airway inflammation.
The human dietary intervention study was a small pilot study, and as such, any extrapolations, inferences, and conclusions should not be widely implemented until larger and more extensive studies have been undertaken. In the 16-patient pilot trial, nine patients received inulin (a complex starch that functions as a MAC in humans), and seven patients served as controls. Inulin is found in a wide variety of fruits, vegetables, and herbs, including wheat, onions, bananas, leeks, artichokes, and asparagus.
The trial was double-blind and placebo-controlled. Those in the intervention arm reported significantly fewer COPD exacerbations, such as worsening respiratory symptoms or a requirement for pharmacological intervention. Additionally, those in the intervention arm reported improved health-related quality of life as measured by both the COPD Assessment Test and the St. George’s Respiratory Questionnaire.
What we eat and how we eat impacts us in a myriad of ways. How we draw our breath, as the sages knew, is an equally impactful exercise. When disassembling the parts, it is important not to lose sight of the fact that the “baked-in” interconnections are what make the whole greater than the sum of its individual components—just like a good chocolate cake!
[1] (Liu, 2023)
[2] (Howard, 2022)
