The Surprising Link Between Intermittent Fasting, Diabetes, and Cancer. Dr. Jason Fung Explains PT 1
Target Cancer・2 minutes read
Hyperinsulinemia is linked to breast cancer growth, especially in diseases like obesity and type two diabetes, as discussed by Dr. Sanjay Juneja and Dr. Jason Fung. Cancer development involves shifting from a growth-focused perspective to targeting genetic mutations for treatment, challenging the somatic mutation theory with studies showing millions of mutations in cancer genomes.
Insights
- Hyperinsulinemia is a significant factor in fueling the growth of breast cancer cells, especially when compared to normal cells, linking diseases like obesity and type two diabetes to increased breast cancer risk.
- Contrary to the traditional somatic mutation theory, research suggests that cancer development involves more than random genetic mutations, with factors like insulin levels playing a crucial role in impacting cancer risk and cell growth, necessitating a shift towards targeting specific genetic mutations for effective treatment.
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Recent questions
How does hyperinsulinemia relate to breast cancer?
Hyperinsulinemia can fuel the growth of breast cancer cells more than normal cells. Diseases like obesity and type two diabetes are linked to breast cancer due to hyperinsulinemia. Breast cancer cells have a high number of insulin receptors, indicating their dependence on insulin for glucose intake. Understanding cancer development involves shifting from viewing it as a growth disease to recognizing genetic mutations and targeting them for treatment. Modifying factors like insulin levels can impact cancer risk, with high insulin levels promoting cell growth.
What is discussed in the Target Cancer podcast?
The Target Cancer podcast features Dr. Sanjay Juneja, a hematologist and medical oncologist. Dr. Jason Fung, a nephrologist and metabolic expert, discusses glucose regulation and intermittent fasting. Different durations of intermittent fasting can be effective for reducing cancer risk and weight loss. Fasting impacts cancer risk in complex ways beyond simple metabolic effects. Fasting affects insulin, AMPK, and mTOR, all of which are growth factors and nutrient sensors.
How does obesity affect cancer risk?
Obesity is a significant risk factor for various cancers, including breast, colorectal, and pancreatic cancer. Diseases like obesity and type two diabetes, associated with hyperinsulinemia, are linked to increased breast cancer risk. Lowering insulin levels, not increasing them, is crucial for reversing type two diabetes and addressing hyperinsulinemia. Insulin resistance and hyperinsulinemia are distinct issues, with the latter being a primary problem. Growth and nutrition are closely linked, with the body using the same molecule for growth and nutrient sensing.
What is the role of insulin in cancer development?
Insulin serves as a key molecule in signaling nutrient intake and growth, indicating the availability of food. Insulin and insulin-like growth factor are interconnected, playing roles in both nutrition and growth. Cancer is viewed as a disease of growth, with cancer cells being autonomous but still responsive to growth factors. Cancer cells rely heavily on insulin for glucose, with insulin sensitivity crucial for their survival. Modifying factors like insulin levels can impact cancer risk, with high insulin levels promoting cell growth.
How has the understanding of cancer development evolved?
Traditional understanding of cancer development was based on the somatic mutation theory, which suggested that cancers arise from random genetic mutations. However, it was found that patients with colorectal cancer had an average of 70 mutations, making treatment challenging due to the vast number of mutations present. Contrary to the belief in random mutations, research showed that cancers from different individuals, even across different nationalities and time periods, displayed similar characteristics despite having distinct genetic mutations. The somatic mutation theory was further debunked as studies revealed that there were around 6 million mutations in cancer genomes, making it difficult to target specific mutations for effective treatment. The theory of a few targeted mutations causing cancer was proven inaccurate, leading to a shift in understanding cancer development.
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