Heidi Norton
Obesity is a global epidemic and a risk factor for colorectal cancer. Colorectal cancer is the third most common cancer in the United States and the second leading cause of cancer-related deaths worldwide. Obesity is associated with a 1.3 times higher likelihood of developing colorectal cancer.
Obesity is defined as the abnormal or excessive accumulation of fat that may impair health. Excess weight can put people at risk of adverse conditions like diabetes, hypertension, and cardiovascular disease. Obesity has also been linked to the development of certain cancers, including colorectal cancer.
There are several possible reasons why obesity may increase the risk of colorectal cancer. Firstly, excess fat can create a low-oxygen environment, leading to inflammation, which can increase the risk of cancer. Obesity-related inflammation has been linked to colorectal carcinogenesis, where normal cells become cancer cells. Secondly, obesity can cause insulin resistance, leading to higher levels of insulin and insulin-like growth factor 1, which may promote the growth of colon cancer and certain other cancers. Thirdly, obesity is associated with increased levels of leptin, a hormone mainly produced by fat cells, which has been shown to contribute to the growth of colonic epithelial cells and may play a role in the development of colorectal cancer tumours. Finally, obesity during childhood and infancy has been linked to a gut microbiome imbalance and inflammation, which may lead to early-onset colorectal cancer.
The link between obesity and colorectal cancer is clear, but the exact mechanisms are still being explored. Maintaining a healthy weight is essential for reducing the risk of colorectal cancer.
| Characteristics | Values |
|---|---|
| Obesity | A global epidemic |
| Colorectal cancer | The third most diagnosed cancer among men and women in the United States |
| Obesity and colorectal cancer | Obesity is a risk factor for colorectal cancer |
| Insulin | People with obesity are at risk of developing insulin resistance |
| Leptin | People affected by obesity have increased levels of leptin |
What You'll Learn
Insulin resistance and hyperinsulinemia
Insulin resistance is defined as "the inability of a known quantity of exogenous or endogenous insulin to increase glucose uptake and utilization in an individual as much as it does in a normal population". Insulin resistance is a risk factor for cancer.
Insulin is a hormone that regulates blood sugar. Insulin resistance can lead to hyperinsulinemia, which is associated with an increased risk of colon cancer.
Insulin can promote the growth of colon cancer cells by activating the phosphoinositide 3-kinase (PI3K)/Akt signalling pathway. Insulin can also stimulate the growth of colon cancer cell lines.
Insulin resistance is associated with circulating levels of interleukin-6 (IL-6), which has been found in the tumour microenvironment of both murine and human colon cancer. IL-6 may act as a colon cancer-promoting cytokine due to its inflammatory properties.
Obesity is associated with increased levels of leptin, a hormone mainly produced by fat cells. Leptin has been shown to contribute to the growth of colonic epithelial cells and may play a role in the development of colorectal cancer tumours.
Obesity is also associated with increased levels of adiponectin, a protein hormone encoded by the ADIPOQ gene in humans. Adiponectin inhibits colon cancer cell growth through the AMP-activated protein kinase (AMPK)/mammalian target of rapamycin (mTOR) signalling pathway.
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Chronic inflammation
Obesity is associated with increased levels of inflammatory cytokines such as IL-6, TNF-α, CCL2, and PAI-1. These inflammatory markers have been found to be associated with colorectal cancer. For example, elevated levels of circulating CRP or IL-6 in CRC patients were associated with cancer progression, relapse, and worse survival.
Obesity-induced abnormal lipid metabolism may also play a role in colorectal carcinogenesis. Adipocytes surrounding tumours may provide energy or nutrients for the anabolic growth of cancer cells.
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Leptin
Obesity is associated with increased levels of leptin in the blood. This is due to leptin resistance, where the body becomes resistant to the effects of leptin, leading to higher levels of the hormone being produced. Leptin resistance can also be caused by decreased expression of the leptin receptor (LEPR).
The G19A polymorphism in the LEP gene has been studied for its potential association with cancer risk, tumour size, and metastasis. However, the results have been inconsistent, with some studies finding no association and others finding a link to lower colon cancer risk.
The gut microbiome may also play a role in the link between obesity and colorectal cancer. Obesity can lead to an imbalance in the gut microbiome, resulting in increased levels of pro-inflammatory bacteria and decreased levels of beneficial bacteria. This dysbiosis may contribute to the development of colorectal cancer.
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Gut microbiome imbalance
Obesity is a significant risk factor for colon cancer, and this relationship is influenced by factors such as gender, age, and menopausal status. Obesity-related insulin resistance and type II diabetes are strongly implicated in the development of colon cancer. Increased levels of insulin and insulin-like growth factor 1 (IGF-1) are linked to the progression and metastatic potential of colon cancer.
The gut microbiome, comprising approximately 103 different microbial species, plays a crucial role in maintaining gastrointestinal health and nutrient absorption. An imbalance in the gut microbiome, known as dysbiosis, has been a subject of interest in understanding the link between obesity and colon cancer.
The human gut is home to a diverse array of microorganisms, with the colon harbouring approximately 1014 bacteria, accounting for 70% of the body's total microorganisms. The gut microbiome is essential for various bodily functions, including nutrient absorption. An imbalance in this delicate ecosystem, known as dysbiosis, has been implicated in the development of colorectal cancer.
Several studies have explored the link between gut microbiome imbalance and colon cancer. The first observation, dating back to 1975, revealed that germ-free rats developed fewer chemically induced colorectal tumours than conventional rats, indicating the potential role of gut microbiota in colorectal carcinogenesis. This finding has been further supported by experiments with CRC-predisposed mice.
Two primary hypotheses have emerged to explain the connection between gut microbiome imbalance and colon cancer:
- The driver-passenger" theory proposes that specific intestinal bacteria, known as "bacteria drivers," initiate colorectal carcinogenesis by inducing epithelial DNA damage and tumour development. This process promotes the proliferation of "passenger bacteria" that thrive in the tumoral microenvironment.
- The second hypothesis suggests that a dysbiotic microbial community with pro-carcinogenic characteristics can remodel the entire microbiome, triggering pro-inflammatory responses and epithelial cell transformation, ultimately leading to cancer.
Additionally, obesity during childhood and infancy has been associated with gut microbiome imbalance and inflammation, which may increase the risk of early-onset colorectal cancer.
In conclusion, gut microbiome imbalance, or dysbiosis, is a critical piece in the puzzle of understanding the link between obesity and colon cancer. Further research in this area may lead to advancements in cancer prevention and treatment strategies.
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Bile acids
In addition, bile acids stimulate the proliferation of CRC cells and induce cell death through two basic pathways involving either death receptors or mitochondria.
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Frequently asked questions
Obesity is a risk factor for many diseases, including colon cancer. Obese people have a higher risk of developing colon cancer, which is the third most diagnosed cancer among men and women in the United States. Obesity increases the risk of colon cancer by creating a low-oxygen environment, leading to inflammation, which can increase a person's risk of cancer. Obesity also affects how the body manages hormones like insulin and estrogen, which can lead to an increased cancer risk by affecting how and when cells divide and die.
Obesity increases the risk of colon cancer by creating a low-oxygen environment, leading to inflammation. This inflammation can damage the body and increase the risk of cancer. Obesity also affects how the body manages hormones like insulin and estrogen, which can lead to an increased cancer risk by affecting how and when cells divide and die.
People can lower their risk of developing colon cancer by maintaining a healthy weight through a healthy diet and regular exercise. A healthy diet includes limiting red and processed meat, sugar-sweetened drinks, and alcohol intake, while increasing the consumption of whole grains, fruits, and vegetables.
