Special Nutrition Starves Cancer Cells: Healing Practice

Diet changes may improve cancer therapy

A conversion to a special nutritionin which the recording of protein is drastically restricted, according to a recent study, it can contribute to cancer cells die and eventually resistors overcome during treatment.

researchers of Rogel Cancer Center the University of Michigan (USA) have shown in a current research project that a Switch to a low protein diet improve the standard of care for colorectal cancer. The results of the study were recently presented in the journal “Gastroenterology.”

There is no growth without nutrients

In order for cancer cells to survive, grow, and multiply, they need certain nutrients. According to the US working group, a molecule called mTORC1 a crucial role in the recognition of nutrients.

mTORC1 is the main regulator of cell growth

Therefore, mTORC1 is often referred to as Main regulator of cell growth designated. The molecule allows cells to recognize different nutrients and therefore produce the appropriate ones. incentives to grow and given to multiply.

However, when certain nutrients are limited or absent, cells turn off mTORC1, which also limits cell growth and proliferation.

In colon cancer cells, mTORC1 is overactive

Previous research has shown that in colorectal cancer cells, mTORC1 hyperactive it is. This led to the thesis that colon tumors abuse signaling pathways for nutrient recognition, and this is so to grow faster.

starve cancer cells

“In colon cancer, if the nutrients available in the tumors are reduced, the cells do not know what to do”explains the first author of the study Professor Dr. Yatrik M. Shah.

According to him, without the necessary nutrients for growth, cancer cells experience a kind of crisis that ultimately leads to cell death Guides. Tumor cells are literally starving.

In mice with colon cancer, the researchers were able to show that a low protein diet it blocks the same nutrient signaling pathway exploited by colon cancer cells.

So far, mTORC1 cannot be inhibited with drugs

It is already known from standard treatment of colorectal cancer that mTORC1 has different mutations forms, which can cause cancer cells to resist treatment resistant Will. According to the study, this process could be slowed down with a low-protein diet.

There have already been attempts to block mTORC1 with an active substance. However, the tested substances caused significant side effects and the effect ended as soon as the drugs were discontinued. A low protein diet seems an alternative and more natural way to turn off mTORC.

Not suitable as sole therapy.

“A low protein diet is not the only treatment”have student car Dr Sumeet Solanki outside. The diet have to combined with other measures. Because giving up protein isn’t entirely risk-free. Cancer patients often suffer anyway muscular weakness Y weightloss. A low protein diet could make these symptoms worse.

“Putting cancer patients on a low-protein diet long-term is not ideal”confirms Shah. The appropriate time window for this measure must be found and, at the same time, supplemented with another treatment method to increase its effectiveness.

In further research, the team now wants to refine this concept so that it can be integrated into therapy. (verb)

Author and source of information

This text meets the requirements of specialized medical literature, medical guidelines, and current studies and has been reviewed by medical professionals.

Author:

Graduate Editor (FH) Volker Blasek

Sources:

  • Sumeet Solanki, Katherine Sanchez, Varun Ponnusamy, et al: Dysregulated Amino Acid Sense Drives Colorectal Cancer Growth and Metabolic Reprogramming Leading to Chemoresistance; In: Gastroenterology (2022), gastrojournal.org
  • University of Michigan: Change in diet starves cancer cells and overcomes resistance to treatment (veröffentlicht: 18.11.2022), labblog.uofmhealth.org

Important note:
This article contains general advice only and should not be used for self-diagnosis or treatment. It cannot replace a visit to the doctor.

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