About this Research Topic
Over the past three decades, adult obesity rates have more than doubled, while rates among adolescents have quadrupled. Of the 2.5 billion adults classified as overweight, 890 million are living with obesity. The interplay between obesity and diet stands as a significant determinant in this epidemic.
Obesity is a multifaceted condition characterized by an excess accumulation of body fat, posing a medical concern due to its association with various diseases and health complications. These include but are not limited to heart disease, diabetes, high blood pressure, and certain types of cancers, underscoring the broader health risks associated with this condition. Obesity arises from a myriad of contributing factors. Foremost among these factors is the obesogenic environment, coupled with unhealthy eating behaviors, which are widely acknowledged as key drivers of obesity. Saturated fats and trans fats are often labeled as unhealthy due to their ability to elevate LDL cholesterol levels. Saturated fats are primarily found in animal sources such as fatty beef, pork, butter, lard, cream, and poultry with skin. Additionally, plant-based oils like coconut oil and palm oil contain saturated fats, albeit without cholesterol. High intake of saturated fats is associated with weight gain and abdominal obesity, further exacerbating the risk of obesity-related health complications. Moderating intake of these fats is crucial for maintaining health.
Obesity is also associated with 13 different types of cancer such as breast cancer, colorectal cancer, uterine cancer, pancreatic cancer, meningioma, and multiple myeloma, to name a few. Metabolic disorders such as glucose intolerance, hypertension, dyslipidemia, and insulin resistance collectively form metabolic syndrome, exacerbating cancer risk. Obesity-induced alterations in sex hormone metabolism further compound this risk.
There are various mechanisms by which obesity results in cancer risk. Obesity-mediated low-grade inflammation, for instance, can promote cancer development through DNA damage, and suppressing immune response to cancer cells. Obesity also leads to hormonal imbalance, particularly displaying elevated estrogen levels in the post-menopausal phase, contributing to breast and endometrial cancer risk. Additionally, obesity-mediated dysregulation in adipokine secretion, with heightened pro-inflammatory adipokines and diminished anti-inflammatory counterparts, creates an environment conducive to tumor initiation and progression. Insulin resistance, another hallmark of obesity, promotes cancer initiation and progression by elevating insulin and insulin-like growth factor-1 (IGF-1) levels, stimulating cell proliferation and inhibiting apoptosis.
Recent research has underscored the role of the gut microbiota in obesity-mediated cancer risk. Obesity is intricately linked with perturbations in the composition and functionality of the gut microbiota, a phenomenon referred to as dysbiosis. This dysregulation can instigate heightened intestinal permeability, facilitating the translocation of bacterial byproducts into the systemic circulation, thereby inciting systemic inflammation. Additionally, dysbiosis has the potential to modulate the metabolism of dietary constituents, thereby influencing the generation of carcinogenic metabolites, thereby exacerbating the risk of cancer development, notably within the gastrointestinal milieu.
The mechanism of obesity mediates cancer development varies between each cancer type. For instance, breast cancer risk is influenced by estrogen levels, while colorectal cancer risk may be more closely associated with insulin resistance and chronic inflammation.
The intricate interplay between diet and obesity underscores the importance of elucidating the role of diet in the etiology of obesity and its subsequent impact on cancer risk and progression. A comprehensive understanding of these mechanisms is significant in advancing therapeutic strategies and enhancing patient outcomes.
This Research Topic aims to encompass, but is not restricted to, the following major topics:
1. Nutrigenomics and personalized approaches to cancer prevention in obesity.
2. Effect of diet and obesity on the tumor microenvironment.
3. Role of diet and gut microbiota in mediating obesity-cancer link.
4. Role of diet and obesity-associated hormonal imbalance in cancer risk and progression.
5. Influence of diet on epigenetic modifications in obesity-related cancer.
Obesity is a multifaceted condition characterized by an excess accumulation of body fat, posing a medical concern due to its association with various diseases and health complications. These include but are not limited to heart disease, diabetes, high blood pressure, and certain types of cancers, underscoring the broader health risks associated with this condition. Obesity arises from a myriad of contributing factors. Foremost among these factors is the obesogenic environment, coupled with unhealthy eating behaviors, which are widely acknowledged as key drivers of obesity. Saturated fats and trans fats are often labeled as unhealthy due to their ability to elevate LDL cholesterol levels. Saturated fats are primarily found in animal sources such as fatty beef, pork, butter, lard, cream, and poultry with skin. Additionally, plant-based oils like coconut oil and palm oil contain saturated fats, albeit without cholesterol. High intake of saturated fats is associated with weight gain and abdominal obesity, further exacerbating the risk of obesity-related health complications. Moderating intake of these fats is crucial for maintaining health.
Obesity is also associated with 13 different types of cancer such as breast cancer, colorectal cancer, uterine cancer, pancreatic cancer, meningioma, and multiple myeloma, to name a few. Metabolic disorders such as glucose intolerance, hypertension, dyslipidemia, and insulin resistance collectively form metabolic syndrome, exacerbating cancer risk. Obesity-induced alterations in sex hormone metabolism further compound this risk.
There are various mechanisms by which obesity results in cancer risk. Obesity-mediated low-grade inflammation, for instance, can promote cancer development through DNA damage, and suppressing immune response to cancer cells. Obesity also leads to hormonal imbalance, particularly displaying elevated estrogen levels in the post-menopausal phase, contributing to breast and endometrial cancer risk. Additionally, obesity-mediated dysregulation in adipokine secretion, with heightened pro-inflammatory adipokines and diminished anti-inflammatory counterparts, creates an environment conducive to tumor initiation and progression. Insulin resistance, another hallmark of obesity, promotes cancer initiation and progression by elevating insulin and insulin-like growth factor-1 (IGF-1) levels, stimulating cell proliferation and inhibiting apoptosis.
Recent research has underscored the role of the gut microbiota in obesity-mediated cancer risk. Obesity is intricately linked with perturbations in the composition and functionality of the gut microbiota, a phenomenon referred to as dysbiosis. This dysregulation can instigate heightened intestinal permeability, facilitating the translocation of bacterial byproducts into the systemic circulation, thereby inciting systemic inflammation. Additionally, dysbiosis has the potential to modulate the metabolism of dietary constituents, thereby influencing the generation of carcinogenic metabolites, thereby exacerbating the risk of cancer development, notably within the gastrointestinal milieu.
The mechanism of obesity mediates cancer development varies between each cancer type. For instance, breast cancer risk is influenced by estrogen levels, while colorectal cancer risk may be more closely associated with insulin resistance and chronic inflammation.
The intricate interplay between diet and obesity underscores the importance of elucidating the role of diet in the etiology of obesity and its subsequent impact on cancer risk and progression. A comprehensive understanding of these mechanisms is significant in advancing therapeutic strategies and enhancing patient outcomes.
This Research Topic aims to encompass, but is not restricted to, the following major topics:
1. Nutrigenomics and personalized approaches to cancer prevention in obesity.
2. Effect of diet and obesity on the tumor microenvironment.
3. Role of diet and gut microbiota in mediating obesity-cancer link.
4. Role of diet and obesity-associated hormonal imbalance in cancer risk and progression.
5. Influence of diet on epigenetic modifications in obesity-related cancer.
Keywords: Cancer, Obesity, Metabolism, Personalized Nutrition, Nutrigenomic, Epigenetic Modifications, Tumor Microenvironment, Cancer Risk, Cancer Progression
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