mTOR is a protein complex and a typical rapamycin target protein. In this protein group, there are two different complexes. One is mTORC1 and the other is mTORC2.

mTORC1 is mainly composed of Raptor, GβL, DEPTOR, and mTOR. Its main function is to sense nutrition and environmental fluctuations. When mTORC1 senses that it is immersed in a nutrient-rich environment (this nutrition is mainly amino acids, glucose, and oxygen), its reaction activity will increase significantly. In many studies, some believe that Raptor sends regulatory signals to downstream S6K, while others believe that DEPTOR sends control signals to S6K. In fact, in a conservative functional environment, its overall architecture and components are likely to and can issue influence commands to its substrate. In the meantime, factors including increasing age can also independently promote the activity of mTORC1 to rise.

The high-activity mTORC1 sends a strong and stable signal to the downstream S6K through its structural components. Under the action of stable signals, the cell division rate, of course, also restrains the increase in the rate of telomere depletion. This is a state of being deeply trapped in accelerated aging. As long as the activity of S6K does not attenuate and fluctuate, aging will always be in a long-term accelerated process. The sign during this period is that autophagy decreases sharply and aging-related diseases continue.

After the action of rapamycin, the activity of mTORC1 is inhibited, and the interaction between mTOR-Raptor causes it to lose its phosphorylation ability. The main mTOR architecture and Raptor and DEPTOR send signals to their downstream substrates that inhibit S6K. Inhibiting S6K promotes the rapid slowing of overall inflammation, and age-related diseases also accelerate the development of aging, tend to be orphaned, and finally calm down. Of course, what people are most looking forward to is the unmeasurable extension of life.

By inhibiting S6K, the body's inflammation is suppressed, autophagy is enhanced, immune aging is slowed down, and life span is effectively extended, but excessive inhibition will go to the opposite side, that is, shortening life span. This strongly confirms that the mTOR-S6K channel is the key to life span.

Here, we want to emphasize that although rapamycin inhibits mTORC1 and blocks S6K activity, which is an important bridge for us to extend lifespan, rapamycin is not the only drug that can inhibit mTORC1. Increased mTORC2-Raptor intensity can also inhibit mTORC1, including blocking S6K and extending lifespan. In daily life, if you can pay great attention to reducing the intake of methionine, isoleucine and fructose, you can also reduce mTORC1 activity to a limited extent, inhibit S6K and slow down the intensity of cell aging. The key is the problem of persistence and intensity. It is difficult to fundamentally change the aging process of the body and compensate for lifespan factors by simply adjusting the diet. In our supplement grouping, there are more than 10 substances that can inhibit mTORC1. Their effectiveness may not be as strong as rapamycin, but for time-dependent operational targets, low doses, long periods of time, and multiple targets work synergistically. What we hope for is no risk and no pursuit of extreme intensity. Of course, there is also price. For long-term consumption, price is also a factor worth considering.