Idiopathic pulmonary fibrosis is a chronic
and progressive lung
disease with a poor
prognosis. Idiopathic basically means that the cause is not known.
Pulmonary fibrosis is characterized by lung inflammation and abnormal tissue repair, resulting in the replacement of normal functional tissue with an abnormal accumulation of fibroblasts and deposition of collagen in the lung. This process involves cellular interactions via a complex cytokine-signaling mechanism and heightened collagen gene expression, ultimately resulting in its abnormal collagen deposition in the lung. Our current understanding of the pathogenesis of pulmonary fibrosis suggests that in addition to inflammatory cells, the fibroblast and signaling events that mediate fibroblast proliferation and myofibroblasts, play important roles in the diverse processes that constitute fibrosis. Increasing knowledge of cytokine biology, cytokine-signaling and cell matrix interactions have shed some light on the genesis of pulmonary fibrosis; however, the importance of inflammation in pulmonary fibrosis remains controversial. This remains true because the inflammatory component is variable at the time of diagnosis, and the most potent anti-inflammatory drugs that have been widely used in the treatment of pulmonary fibrosis do not seem to interfere with the fibrotic disease progression. Consider signing up to a free natural medicine newsletter sent by email once or twice a month. I will discuss new pulmonary fibrosis studies as they become available.
Pulmonary fibrosis treatment
At present there is no good medical treatment for pulmonary fibrosis. Lung transplantation is a last resort. acetylcysteine is a promising nutrient that may slow the progression of the disease.
Biomed Research International. 2015. Pharmacological Treatment of
Idiopathic Pulmonary Fibrosis: Current Approaches, Unsolved Issues, and Future
Perspectives. Idiopathic pulmonary fibrosis (IPF) is a devastating condition
with a 5-year survival of approximately 20%. The disease primarily occurs in
elderly patients. IPF is a highly heterogeneous disorder with a clinical course
that varies from prolonged periods of stability to episodes of rapid
deterioration. In the last decade, improved understanding of disease mechanisms
along with a more precise disease definition has allowed the design and
completion of a number of high-quality clinical trials. Yet, until recently, IPF
was essentially an untreatable disease. Finally, pirfenidone and nintedanib, two
compounds with antifibrotic properties, have consistently proven effective in
reducing functional decline and disease progression in IPF. This is a major
breakthrough for patients and physicians alike, but there is still a long way to
go. In fact, neither pirfenidone nor nintedanib is a cure for IPF, and most
patients continue to progress despite treatment.
Natural treatment for pulmonary fibrosis
Acetylcysteine - A double-blind, randomized, placebo-controlled multicenter study was conducted that assessed the effectiveness over one year of a high oral dose of acetylcysteine (600 mg three times daily) added to standard therapy with prednisone plus azathioprine. The primary end points were changes between baseline and month 12 in vital capacity and in single-breath carbon monoxide diffusing capacity (DLCO). Conclusions: Therapy with acetylcysteine at a dose of 600 mg three times daily, added to prednisone and azathioprine, preserves vital capacity and DLCO in patients with idiopathic pulmonary fibrosis better than does standard therapy alone.
J Cell Mol Med. 2015. Astaxanthin prevents pulmonary fibrosis by promoting myofibroblast apoptosis dependent on Drp1-mediated mitochondrial fission. Promotion of myofibroblast apoptosis is a potential therapeutic strategy for pulmonary fibrosis. This study investigated the antifibrotic effect of astaxanthin on the promotion of myofibroblast apoptosis based on dynamin-related protein-1 (Drp1)-mediated mitochondrial fission in vivo and in vitro. Results showed that astaxanthin can inhibit lung parenchymal distortion and collagen deposition, as well as promote myofibroblast apoptosis. Astaxanthin provides a potential therapeutic value in pulmonary fibrosis treatment.
Food Chem Toxicol. 2013. Astaxanthin ameliorates lung fibrosis in vivo and in vitro by preventing transdifferentiation, inhibiting proliferation, and promoting apoptosis of activated cells.
Proathocyanidins may be of benefit. Inflammation. 2012. The Efficiency of Proanthocyanidin in an Experimental Pulmonary Fibrosis Model: Comparison with Taurine.
Pulmonary fibrosis symptom
These include shortness of breath, coughing and diminished exercise tolerance.
End stage pulmonary fibrosis is characterized by failure of alveolar re-epithelization, persistence of fibroblasts, deposition of extracellular matrix, and distortion of lung architecture which ultimately results in respiratory failure. Pulmonary fibrosis is a highly lethal disorder, which continues to pose major clinical challenges because an effective therapeutic regimen is yet to be determined.
Pulmonary fibrosis can be caused by many conditions including chronic inflammatory processes (sarcoidosis, Wegener’s granulomatosis ), infections, environmental agents (asbestos, silica, exposure to certain gases), exposure to radiation, chronic conditions (lupus, rheumatoid arthritis), and certain prescription medications. Silicosis is also a cause.
Clin Epidemiol. 2013. Epidemiology of idiopathic pulmonary fibrosis. Idiopathic pulmonary fibrosis is a chronic fibrotic lung disease of unknown cause that occurs in adults and has a poor prognosis. Its epidemiology has been difficult to study because of its rarity and evolution in diagnostic and coding practices. Though uncommon, it is likely underappreciated both in terms of its occurrence (ie, incidence, prevalence) and public health impact (ie, health care costs and resource utilization). Incidence and mortality appear to be on the rise, and prevalence is expected to increase with the aging population. Potential risk factors include occupational and environmental exposures, tobacco smoking, gastroesophageal reflux, and genetic factors. An accurate understanding of its epidemiology is important, especially as novel therapies are emerging.
Q. Does alpha lipoic acid help with pulmonary fibrosis?
A. I have not seen such research regarding the role of alpha lipoic acid in this condition.
My father is 77 yrs old and has pulmonary fibrosis he was diagnosed 4 yrs ago and we have done Chinese medicine on him which has helped but we are interested in anything you can suggest or if you know of any good practitioners in Melbourne, Australia that we can see? His biggest problem is sleep as he suffers from extreme insomnia and coughing which he does all day long. He is on no medication eats lots of greens and has never smoked or drank alcohol, the only supplements he takes are Nac cysteine, magnesium, cq10, vit c and vitamin d.