Whether you’re new to weed, or you’ve been smoking it for years, you may be wondering if it can cause lung cancer. Here’s what you need to know.
Long-Term Marijuana Users Have More Cancers
Several epidemiological studies have found an association between marijuana and lung cancer. However, most of these studies have been limited by small numbers of heavy long-term users. The results may be masked by poor exposure assessment or inadequate follow-up.
Two systematic reviews have examined the association between marijuana and lung cancer. The first reviewed fourteen studies and found evidence of biological plausibility. The second reviewed two cohort studies and found mixed evidence.
The largest study included 49,321 male participants. The smallest study included 33 lung cancer cases. The study also included a population-based control group. The results were presented at the annual meeting of the American Thoracic Society.
The largest study was performed in the United States. The results were presented in a press conference at the conference. The study compared the risk of lung cancer in marijuana users and non-users. The odds of lung cancer was 2.4 in marijuana users and 1.7 in non-users. The most notable finding was that long-term marijuana users had more lung cancers than their non-using counterparts.
The study also found a positive relationship between marijuana and cigarette smoking. Smoking marijuana produces four times as much tar in the lung. The odds of lung cancer increased 7% for each pack-year of cigarette smoking. The study also showed that long-term marijuana users were more likely to smoke tobacco.
Several studies have also found an association between marijuana and head and neck cancer. The risk of cancer in marijuana users was estimated to be 2.4 times higher than in non-users.
The second most notable study, conducted by the Swedish military conscripts, was published in the Journal of Thoracic Oncology. The study included a number of cancers including lung, squamous cell carcinoma, non-small cell lung cancer and lung adenocarcinoma.
Inflammation And Cell Damage
During inflammation, white blood cells initiate an immune response that helps the body fight off infections. In addition, the inflammatory process removes harmful stimuli and helps heal tissue. However, inflammation can also be damaging and may lead to the development of cancer.
Researchers are interested in understanding how inflammation and cell damage contribute to the development of cancer. In fact, one in five cancers are believed to be caused by inflammation. While the exact cause of cancer remains elusive, researchers have identified a few factors that trigger an inflammatory response. These factors include smoking, obesity, and certain cancer-initiating mutations.
Understanding the inflammatory process is important for treating patients with lung inflammation. There are two main types of mathematical models used to study this topic. Continuous-time models represent the process in a continuous manner over time, while discrete-time models describe changes in the system at certain points.
Continuous-time models usually manifest as differential equations. Some models use a combination of ordinary and partial differential equations (ODEs) and PDEs. These models may be useful for modeling the distribution of inflammatory mediators. However, models that use ODEs may be better suited for modeling inflammation over a longer period of time.
The inflammatory process may generate free radicals that can damage DNA. It can also stimulate fibroblast proliferation, which can lead to emphysema. It also causes cellular proliferation at the site of injury. In addition, cytokines are released, which bring oxygen and nutrients to the tumor.
One multiscale model has shown that chronic inflammation may occur due to increased chemotactic attractants. These attractants include TGF-b, which stimulates fibroblast proliferation. It may also include increased levels of inflammatory cytokines. These cytokines are important for lung homeostasis.
Smoking Cannabis Causes Injury To The Airways
Several studies have shown that smoking cannabis may have harmful effects on the respiratory system. Several case studies have shown that cannabis use can cause pneumothorax, pulmonary infection, and other respiratory complications. While the risk of developing lung cancer is uncertain, the risk of developing asthma and other respiratory disorders is higher among cannabis users.
The most common form of cannabis administration is through inhalation. The smoke contains many carcinogens, a number of which are found in tobacco smoke. Smoking cannabis causes injury to the airways and may result in chronic bronchitis, COPD, and lung cancer.
In addition to respiratory effects, marijuana smokers have been shown to have increased secretions, a change in bronchial epithelial cells, and an increase in alveolar macrophages. Chronic marijuana smokers have been found to have more shortness of breath, an increase in the number of acute bronchitic episodes, and a higher prevalence of wheezing.
Cannabis smoke also contains many carcinogens and mutagenic compounds. It is difficult to ascertain the actual risks associated with cannabis use because of the co-administration of nicotine.
Earlier observational studies have shown an association between cannabis use and respiratory complications. However, most studies try to minimize confounding by controlling for factors such as smoking tobacco and social factors.
While tobacco smoking is associated with emphysema, COPD, and lung cancer, the association between cannabis and lung cancer is less clear. There are no large population-based case-control studies on this topic.
Studies have been conducted in the US, North Africa, and Europe. The studies have included male and female smokers. The results have been mixed. Some studies have shown a positive association, while others have not.
The smoking of cannabis has also been linked to precancerous changes in the bronchial tree. The term “bong lung” is used to describe the histological change in chronic cannabis smokers.
Cannabis Oil Is A Potent Bronchodilator
Various studies have shown that cannabis oil is a potent bronchodilator. However, its role in the pathophysiology of chronic obstructive pulmonary disease (COPD) has not been fully explored. In this study, we evaluated the effect of cannabis oil on a human primary lung epithelial cell (HSAEpC) model.
We used pathway-focused polymerase chain reaction (PCR) array technology to test the effects of cannabis oil on 84 respiratory immune response genes in HSAEpC. The array consisted of a combination of transcription factors, genes encoding Th2 cytokines and chemokines, and related proteins. The results indicate that cannabis oil has the potential to reduce inflammation and modulate Th1 and Th2 immune response gene expression in HSAEpC.
In addition to reducing inflammation, cannabis oil extract may also affect the expression of genes involved in mucin production. It has been hypothesized that inhibiting mucin production genes could be effective in COPD.
The array included a number of genes related to the KEGG pathway, including PPARG (peroxisome proliferator-activated receptor gamma), MAF (V-maf musculoaponeurotic fibrosarcoma oncogene homolog), CLCA1 (chloride channel accessory 1), EPX (eosinophil peroxidase), and TSLP (thymic stromal lymphopoietin). In addition to promoting the expression of Th2 cytokines, cannabis oil extract modulated 11 genes in the KEGG pathway.
IL1RL1 (IL-1 receptor-like protein 1) is a protein that is important in the Th2 immune response. It is also important in the repair of injured tissue and is associated with downstream production of Th2 cytokines. This protein was up-regulated by all three dilutions of cannabis oil extract. The IL1RL1 up-regulation is a potential biomarker for further studies.
Cannabis oil also modulated genes in the KEGG pathway affecting JAK-STAT signaling. Activation of JAK-STAT is thought to promote lung epithelial cell migration and repair.
Cannabis Is An Immunosuppressant
Phytocannabinoids are compounds found in cannabis. They interact with the endogenous cannabinoid system (ECS) and may influence cellular immunity. They may modulate cell growth, cell death, inflammation and autophagy, and suppress tumor growth. They may also inhibit the proliferation of T cells.
Cannabinoids inhibit inflammatory responses by suppressing migration of neutrophils, macrophages, and NK cells. They also suppress growth of tumor cells, increase tumor immunogenicity, and increase T cells’ ability to lyse tumor cells. They may also stimulate apoptosis.
The THC in cannabis is a known immunosuppressive agent. Some of its effects include inhibition of BAD activation and RAS-MAPK cascade. It has also been shown to suppress the therapeutic effect of PD-1 blockade in mice with depleted B cells. The THC-mediated suppression of T cell immunity against cancer is important in cancer immunotherapy.
Despite the potential of cannabis for cancer immunotherapy, there is limited data on the combined effects of cannabis and immunotherapy. More research is needed to determine whether cannabinoids and immunotherapy are associated with adverse effects and to identify possible interactions between these agents. There are some promising findings.
A study has shown that full botanical extracts, which are typically made from cannabis flowers rich in CBD, have anti-neoplastic activity. These agents may be more effective than isolated compounds. They may also act synergistically with CBD. They may also affect innate and adaptive immune responses.
There are also indication-specific therapies. In the future, cannabinoid-based therapies will be patient-oriented and will become a part of the cancer treatment landscape. However, more studies are needed to understand the potential of cannabis in cancer immunotherapy. Until then, medical personnel will prescribe cannabinoid-based therapies.
Cancer immunotherapy has shown promise as an effective treatment for many types of cancer. Despite the benefits of immunotherapy, patients often face challenges, including resistance to immunotherapy drugs and poor response to immunotherapy. Using full botanical extracts, which can influence the PI3kg pathway and macrophage polarization, can improve the response to ICIs.
