Special nutrition causes cancer cells to starve – healing practice

Dietary changes can improve cancer therapy

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

researchers of Rogel Cancer Center the University of Michigan (USA) have shown in a current research project that a Switching to a low-protein diet the standard treatment of colon cancer can improve. The study results were recently published in the journal “Gastroenterology” presented.

No growth without nutrients

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

mTORC1 is the main regulator of cell growth

mTORC1 is therefore often referred to as Main regulator of cell growth designated. The molecule enables cells to recognize different nutrients, thereby making 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 hyperactive

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

starve cancer cells

“In colon cancer, if you reduce the nutrients available in the tumors, the cells don’t know what to do”explains the first author of the study professor dr Yatrik M Shah.

According to him, without the nutrients needed for growth, cancer cells experience a kind of crisis that ultimately leads to cell death leads. The tumor cells are literally starved.

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

So far, mTORC1 cannot be inhibited with medication

It is already known from standard colorectal cancer treatment that mTORC1 has different mutations forms, which can lead to the cancer cells resisting treatment resistant will. According to the study, this process could be slowed down by 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”highlights study author dr Sumeet Solanki out. The diet must combined with other measures. Because giving up protein is not entirely risk-free. Cancer sufferers often suffer anyway muscle weakness and weight loss. A low-protein diet could make these symptoms worse.

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

In further research work, the team now wants to refine this concept in order to be able to integrate it into therapy. (vb)

Author and source information

This text corresponds to the requirements of medical specialist literature, medical guidelines and current studies and has been checked by medical professionals.


Graduate editor (FH) Volker Blasek


  • Sumeet Solanki, Katherine Sanchez, Varun Ponnusamy, et al.: Dysregulated amino acid sensing drives colorectal cancer growth and metabolic reprogramming leading to chemoresistance; in: Gastroenterology (2022), gastrojournal.org
  • University of Michigan: Dietary change starves cancer cells, overcoming treatment resistance (published: 11/18/2022), labblog.uofmhealth.org

Important NOTE:
This article contains general advice only and should not be used for self-diagnosis or treatment. He can not substitute a visit at the doctor.

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