Everyone experiences aging—a natural process in itself, but one we can slow down through scientific means. Anti-aging supplements are one such tool: they are not "miracle drugs" that "reverse youth," nor are they useless "intelligence taxes." Their core value lies in targeting key pathways of cellular aging and using specific ingredients to help the body "address weaknesses". For example, if mitochondrial energy supply is insufficient, certain ingredients can promote mitochondrial repair; if there are excessive inflammatory factors, some components can regulate inflammatory pathways; if DNA repair slows down, there are also ingredients that can help activate repair proteins.
To this end, we clarify the mechanism of action and applicable scenarios of 3 anti-aging supplements—without overstating their effects or avoiding precautions. This helps you determine which ingredients are truly suitable for you and how to use supplements more scientifically to assist your body in combating aging.
The core goal of this category is to simulate the "calorie restriction" effect—by activating the AMPK and SIRT1 pathways and inhibiting mTOR signaling, cells are tricked into thinking they are in an "energy-deficient state." This prompts cells to prioritize initiating damage repair, autophagic clearance, and mitochondrial revitalization processes, rather than continuing with substance synthesis.
1. Metformin
As the most widely used drug for treating type 2 diabetes globally, metformin’s anti-aging potential was first discovered in animal experiments. It works by:
- Activating the AMPK pathway (enhancing cellular energy sensing);
- Inhibiting mTOR signaling (reducing excessive anabolic metabolism);
- Boosting the Nrf2 antioxidant system (strengthening free radical scavenging capacity).
These actions put cells into a "resource redistribution" state—energy originally used for cell proliferation is redirected to clearing damaged proteins and repairing mitochondrial function.
A 2013 study in Cell Metabolism confirmed that metformin can extend the lifespan of mice by 5%-10%, while improving insulin sensitivity (reducing cell damage caused by blood glucose fluctuations) and mitochondrial respiratory efficiency (enhancing energy conversion capacity) (DOI: 10.1016/j.cmet.2013.01.016). Currently, the TAME clinical program (Targeting Aging with Metformin), led by the Barzilai team at Albert Einstein College of Medicine in the US, is attempting to develop metformin into the first prescription drug targeting "delaying human aging," and has entered the mid-to-late stages of trials.
2. Rapamycin
Rapamycin was originally used for immunosuppression after organ transplantation (to prevent rejection), but its anti-aging mechanism is closely related to the "mTOR pathway." mTOR acts as a cellular "growth switch": in youth, it regulates the balance between cell proliferation and repair; with age, its overactivation causes cells to continuously synthesize substances, increasing metabolic load and ultimately accelerating aging. Rapamycin can specifically inhibit the mTORC1 complex, switching cells from "growth mode" to "repair mode."
A 2009 study in Nature was the first to confirm that low-dose rapamycin extends the lifespan of male mice by 14% and female mice by 9%, while improving the immune function (e.g., enhancing T cell activity) and cognitive ability of aged mice (DOI: 10.1038/nature08221). In human studies, its derivative RTB101 has shown potential in improving vaccine responses in the elderly (strengthening immune protection) and reducing chronic inflammatory factors, and is currently undergoing clinical trials for "prevention of aging-related diseases."
3. NMN / NR
NMN (nicotinamide mononucleotide) and NR (nicotinamide riboside) are derivatives of vitamin B3. Their core role is to serve as precursor molecules for the synthesis of NAD⁺ (nicotinamide adenine dinucleotide) in the body. NAD⁺ is the "core currency" of cellular energy metabolism—it participates in mitochondrial ATP synthesis (energy conversion) and acts as a "coenzyme" for longevity proteins such as SIRT1 and PARP1 (activating DNA repair and cellular stress responses). However, with age, the body’s NAD⁺ levels drop by more than 50%, directly leading to reduced energy metabolism efficiency and declining repair capacity.
In 2013, a landmark study by David Sinclair’s team at Harvard Medical School, published in Cell, showed that supplementing aged mice with NMN reversed mitochondrial dysfunction (muscle energy supply was restored to youthful levels) and extended healthy lifespan (DOI: 10.1016/j.cell.2013.02.057). A 2022 human trial by Kyoto University further confirmed that daily oral administration of 300mg NMN significantly increased plasma NAD⁺ levels in healthy middle-aged and elderly individuals, while improving walking speed (a physical fitness indicator) and insulin sensitivity (a metabolic indicator) (DOI: 10.1007/s12272-022-01348-4).