Published on October 31, 2024
Cancer is a complex disorder of cell growth and differentiation, akin to escape prisoners breaking free from their constraints. Cells, which usually have a life cycle of birth, function, and death, sometimes undergo mutations that allow them to persist longer than they should, leading to the potential for subsequent mutations and eventually cancer. Despite the considerable amount of detailing we have on cancer mutations, entirely preventing them remains beyond our grasp.
Cancer stems from a series of mutations. Each mutation marginally increases the survival likelihood of a cell, diminishing its likelihood to die as programmed. Over time, these mutations accumulate, sometimes in the dozens, eventually leading to cancer. Understanding this process has been the lifelong pursuit of many oncologists, including those who study virus-induced cancers.
Viruses have been known to cause cancers, predominantly in animals like mice, but also in humans. The study of viruses such as retroviruses has provided insights into the mechanisms that cause cellular mutations leading to cancer. A landmark realization was that oncogenic viruses often thrive in chronic inflammatory settings.
Chronic inflammatory states provide a fertile environment for cancer cells to survive and multiply. Persistent inflammation hampers the immune system's ability to detect and destroy cancerous cells, thus facilitating the progression of mutations. This connection is evident in many cancers, such as hepatoma, which is linked to hepatitis B and C viruses.
Historically, liver cancer was attributed to alcoholism, but research uncovered its significant link to hepatitis B and C viruses. These viruses lead to chronic hepatitis and liver cirrhosis, a state characterized by high levels of inflammation and angiogenesis, granting mutated cells the environment to thrive and evolve into cancer.
The association between chronic inflammation and cancer is not limited to viral causes. Non-infective chronic inflammations, such as those due to smoking or chronic bronchitis, similarly predispose individuals to cancer. This understanding bridges viral cancer developments with broader cancer genesis models.
Obesity is increasingly recognized as a chronic inflammatory state. The abundance of adipose tissue in obese individuals creates a milieu rich in inflammatory mediators, increasing the likelihood of cancer development across the body. This underscores the public health importance of managing obesity to reduce cancer risks.
Regular physical activity has been conclusively linked to slower tumor growth in experimental models, suggesting its protective role against cancer. Similarly, diets rich in anti-inflammatory foods, coupled with sufficient micronutrients like vitamin D and potentially iodine, are advocated to manage chronic inflammation.
Exposure to radiation, either through medical x-rays or environmental radios, along with pollution from diesel microparticles, are known cancer risk factors. These agents cause direct cellular damage, perpetuating inflammation and mutation risks.
Understanding the multifaceted causes of cancer, particularly the role of chronic inflammation, opens avenues for prevention through lifestyle changes and targeted healthcare interventions. By addressing inflammation through diet, exercise, and recognizing environmental risks, we can mitigate our cancer risk.
# Inflammation
Author
