We have touched briefly on the subject of fasting autophagy in “What is Intermittent Fasting About” and in other articles on this site. Recall that autophagy is the consumption of an organism’s own tissue for metabolic purposes. The fear is that if fasting is taken to the extreme, autophagy becomes destructive to the health of the organism.
At which point is fasting autophagy harmful? Where is the line between fasting and starvation? Read to find out.
Autophagy and Fasting
Like every nutrient and medicine we take, excessive fasting can be harmful. The evolutionary hack we are after is to trick our bodies into preparing for starvation to get all the ancillary benefits of the physiological changes that take place. The objective is not to actually starve our bodies of essential nutrients.
In fact, many fasting regimens permit intake of low carbohydrate foods during the fasting period to allow for essential nutrient intake. It is not necessary to undergo a water fasting cycle to get the benefits of fasting.
Starvation vs Intermittent Fasting
To be clear, starvation is a chronic nutritional and caloric insufficiency. It can be said that extreme forms of fasting can result in starvation and degeneration. If taken to the extreme, starvation will result in death.
Fasting intermittently can be seen as a frequency adjustment to the caloric intake of an organism. The overall calorie count does not need to change to induce weight loss and other health benefits. We know that weight loss happens because fasting triggers ketosis.
Intermittent Fasting and Autophagy
When we speak about intermittent fasting, all nutrients necessary to keep the organism fit and healthy are available. In the absence of dietary sources of energy, ketones and glucose are synthesized in the liver. Ketones, which feed the nervous system, are synthesized from fatty acids. Glucose is synthesized by breaking down glycogen and proteins.
Almost everyone is ok with the body synthesizing essential nutrients from fat stores, but not many people would agree that breaking down protein to synthesize glucose is a good thing, especially when the source of this protein is the body’s own tissue.
With the body’s amino acid requirements for cellular reproduction and regeneration, how is it that the body can keep healthy levels of amino acids available during an intermittent fasting cycle?
Here is that beautiful concept we read about when trying to understand why a lower caloric intake slows down metabolic rate. Simply stated, homeostasis is the organism’s ability to adjust its internal environment – metabolic pathways, epigenetic modifications, metabolic rate, etc. – to maintain system stability and equilibrium. In the case of lower caloric intake, the equilibrium is achieved by the body’s adaptation to lower total energy expenditure.
In the case of lower dietary intake of amino acids, the equilibrium is achieved by the inhibition of the mTORC1 pathway and breakdown of damaged tissue in the process of autophagy. Without getting too technical, mTORC1 is a protein synthesis signaling mechanism that regulates cell growth and proliferation through anabolic processes. Fasting autophagy triggers catabolic processes that break down cells as opposed to anabolic processes that build cells.
To further reduce amino acid demand, the metabolic rate adjusts to minimize oxidation of amino acids. The system tightly regulates amino acid levels in the blood, and there is no shortage of plasma amino acids.
As all intermittent fasting regimens do, the recommendation is to eat to satiety during the refeeding period. What is interesting is that insufficient protein is a trigger for hunger, and protein happens to be the most satiating macronutrient per calorie.
When the refeeding period begins and protein intake is resumed, an increase in amino acid levels stimulates insulin, IGF-1, and mTORC1 is activated to promote protein synthesis for the rebuilding of cells. The replenishment of protein and activation of the mTORC1 work to suppress appetite.
Protein is prioritized during the refeeding period to allow the body to rebuild cells. Therefore, there is no malnutrition from this temporary lack of proteins in the diet. Every other nutrient is either permitted during the fast or can be synthesized by the body in sufficient quantities.
Is autophagy good?
If autophagy is intermittent and does not persist for a prolonged period, it provides benefits for health and longevity by promoting cellular regeneration. Aside from its protective benefit from non-volitional starvation, autophagy helps to:
- break down damaged and aged cells,
- eliminate pathogens and break them down,
- suppress cancer,
- regulate cell death,
- clear proteins within cells,
- boost the immune system,
- lowers inflammation, and
- regenerate cellular tissue throughout the body.
The last one is most visible to the naked eye in skin cells and muscle tissue. As many of us who have tried intermittent fasting can attest to, this dietary pattern of eating leaves you with young looking skin and lean muscle.
Intermittent fasting is not starvation and it does not cause malnutrition. Exploiting an evolutionary quirk that allowed homo sapiens to survive long periods of famine can be done without the reduction in the overall calorie count. It is simply the composition and frequency that needs to be changed.
The composition of calories must be increased to favor healthy fats over refined carbohydrates. This eliminates hunger and makes ketogenesis easier. Protein intake should not change, but it will be limited to the intermittent refeeding periods.
Intermittent autophagy can be achieved by:
- intermittent fasting,
- intermittent caloric restriction,
- the Fasting Mimicking Diet,
- physical exercise, and
- pharmacological induction of autophagy.
Moro, Tatiana et al. “Effects of Eight Weeks of Time-Restricted Feeding (16/8) on Basal Metabolism, Maximal Strength, Body Composition, Inflammation, and Cardiovascular Risk Factors in Resistance-Trained Males.” Journal of Translational Medicine 14 (2016): 290. PMC. Web. 27 Dec. 2017.
Morrison, Christopher D., Scott D. Reed, and Tara M. Henagan. “Homeostatic Regulation of Protein Intake: In Search of a Mechanism.” American Journal of Physiology – Regulatory, Integrative and Comparative Physiology 302.8 (2012): R917–R928. PMC. Web. 27 Dec. 2017.