Intermittent fasting or "intermittent fasting". Can it really be instrumental in the prevention or even treatment of cancer?
Intermittent or intermittent fasting is, in short, the voluntary restriction of the time during which one can eat.
The most popular fasting protocol is the 16-hour window in the day, but there are many others, such as 18:6, 5:2, Eat/Stop/Eat and the Warrior Diet.
I make a short introduction to it by describing its greatest benefit in "How many meals a day should we eat" .
The term "autophagy" is used to describe a physical process of cells. There are many types of autophagy, but the one we refer to in this article is essentially a mechanism for self-cleansing. When a part of the cell is damaged or dead, this mechanism takes place by cleansing that part with the ultimate goal of rebuilding it.
Serious diseases have been linked to a lack of self-eating, such as diabetes and cancer. In humans, autophagy occurs when we are in a period of caloric deficit, since it is interrupted by any other process associated with an effect or result of caloric intake until it is complete.
So when we do intermittent fasting, the body senses that it is in a caloric deficit and autophagy takes place.
Understandably, many blogs, both reputable and not, praise intermittent fasting and give it anti-cancer properties.
Apparently, though. Because the truth is quite different.
THE TARGET OF THALMIC RABABABYCIN (mTOR)
But before we go any further, we need to understand some basic processes.
Our cells have the ability to respond to various external signals.
These external signals activate intracellular information pathways and, depending on the signal, this response can mean the survival of the cell, its division, its differentiation or even its death.
The first such pathway we will look at is the so-called mammalian target of rapamycin, or mTOR.
It is a part of the PI3K/Akt signalling pathway.
The coordination of the growth of our cells, our body and the size and shape of our organs is largely controlled by a serine/threonine kinase (in simple terms, an enzyme that acts on one of these two proteins), mTOR, or the mammalian target of rapamycin.
mTOR has two complexes: mTORC1 and mTORC2.
The mTORC1 complex incorporates signals that detect the availability of amino acids, oxygen, growth factors as well as cellular energy or stress levels.
It promotes cell growth by supporting protein biosynthesis, the cell cycle and cell metabolism as well as inhibiting autophagy.
We still don't know too much about the mTORC2 complex, but we do know that it plays key roles in several biological processes, including cell survival, cell metabolism, new cell formation and cell skeleton organisation.
AMP-activated protein kinase (AMPK)
AMP-activated protein kinase, or AMPK, is also a serine/threonine kinase.
AMPK is responsible for adapting cellular metabolism in response to nutritional and environmental changes.
If you remember from "How Our Body Works I" and "How Our Body Works II", ATP is the main form of energy for cell metabolism.
Adenosine triphosphate (ATP), is broken down into adenosine diphosphate (ADP) and then adenosine monophosphate (AMP). That's where AMP comes from in the name of AMPK. When we have too much AMP, it will mean that there is too little ATP available.
The AMP-activated protein kinase is activated in order to replenish ATP levels. In turn, it activates other pathways for this purpose and as a result processes such as fatty acid oxidation and autophagy occur.
AMPK also blocks the pathways that consume ATP. Thus, it is a regulator that negatively affects processes such as lipid and protein synthesis.
When AMPK is activated, the cell is under stress conditions and therefore mTOR is expected to be inactive. Some examples: low glucose, hypoxia, ischemia, heat shock, etc.
WHAT IT ALL MEANS
Let's recap very quickly and briefly.
mTOR = anabolism: we were given enough stimuli for cell growth, so we signal growth and AMPK to terminate.
AMPK = Catabolism: we need more ATP, so there has to be a breakdown to find energy and shut down the growth mechanism.
However, a recent study has come to overturn what we knew about the interaction of mTOR and AMPK.
Although until now we were convinced that essentially only one of these two intracellular pathways could be activated, research shows that the mTORC2 complex is activated under conditions of high energy stress.
In other words, "too much time spent" on AMPK can accelerate the availability of nutrients to proliferating cells resulting in tumor feeding. Exactly the opposite of what the charlatans promise you with their alternative therapies and trendy fasting models that is.
What we have, then, shows us that intermittent fasting is something terribly dangerous for cancer patients. Not only because it is a dietary restriction, which in itself is just plain bad for the cancer patient, but it is directly harmful.
Update 20 Dec 2020: We now know that AMPK can play a major role in both tumour development and especially in tumour metastasis. More information in the links at the end of the article.
Don't believe the scammers.
-Suprastratum: The authority on health, fitness and nutrition
Sources/bibliography/more reading:
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- Jacinto E. Amplifying mTORC2 signals through AMPK during energetic stress. sci Signal. 2019 Jun 11;12(585):eaax5855. doi: 10.1126/scisignal.aax5855. PMID: 31186374.
- Vara-Ciruelos D, Russell FM, Hardie DG. The strange case of AMPK and cancer: Dr Jekyll or Mr Hyde? †. Open Biol. 2019 Jul 26;9(7):190099. doi: 10.1098/rsob.190099. epub 2019 Jul 10. PMID: 31288625; PMCID: PMC6685927.
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