#1

I have been taking Astragalus Root for years because of the enormous antiaging and health benefits.

My question is, I stopped it while taking Rapa out of caution as to its possible interaction with immune-suppressing drugs, has anyone else utilized it while on Rapa and willing to share their experiences?

#2

I have been taking Fucoidan which has similar polysaccharides. I haven’t been taking it for long but was taking it while taking rapamycin. If it had any effect I haven’t noticed.

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#3

@desertshores thanks, that’s very helpful

#4

I’m also interesting on this matter. I drink Astragalus decoction. And I wonder - a lot of articles saying that “Astragalus increases and activates your immune system”. It seems like it can reduce Rapamycin effect. Any thoughts?
Should I stop drink it for good? Or is it possible that Astra helps to reduce side effects probabilities, like skin problems et cetera, but Rapa will continue to inhibits mTOR?

#5

interesting study. Especially this

“Therefore, p53 might be also involved in the doxorubicin-induced cardiotoxicity. Zhu et al (34) showed that acute doxorubicin cardiotoxicity is associated with p53-induced inhibition of mTOR. Thus, APS may not only inhibit AMPK activation but also regulate other upstream regulators to regulate mTOR and protect cardiomyocyte.”

I’ve read a lot that inhibition of mTOR and activation of AMPK is beneficial.

Could it lead to cardiotoxicity instead???

#6

Whats AI said…

does astragalus reduce anti-age rapamycin effects?

Yes, based on current understanding of their mechanisms,

it is highly likely that astragalus could reduce the anti-aging effects of rapamycin, as they largely act on the same core pathway but with opposing goals in specific contexts.

Here’s a breakdown of how they interact in the context of aging:

Opposing Mechanisms on the mTOR Pathway

Rapamycin’s primary mechanism for potentially extending lifespan in animal models is through the inhibition of the mTOR complex 1 (mTORC1) signaling pathway, which promotes autophagy (the body’s cellular cleanup process).

In contrast, studies on the anti-aging effects of astragalus polysaccharide (APS) in aged cells often show that it works by activating the AMPK pathway, which subsequently inhibits mTOR (downregulating it) to induce autophagy in pathological/stressed conditions (e.g., in senescent hepatocytes).

While both agents aim to induce autophagy in different scenarios (rapamycin as a direct pharmacological inhibitor, astragalus as an indirect regulator in specific disease states), they might compete or interfere when used simultaneously. In one study, the protective effect of APS on cell senescence was weakened by the presence of chloroquine (an autophagy inhibitor), confirming that autophagy induction is key to its effect. The overall interaction suggests an antagonistic relationship when the goal is a sustained, systemic inhibition of mTOR for longevity purposes.

Effects on Telomere Length

The anti-aging benefits of astragalus are also linked to its ability to activate telomerase and lengthen telomeres, the protective caps on the ends of chromosomes. Rapamycin does not appear to have this same mechanism, focusing instead on cellular metabolism and autophagy.

Immune System Interaction

  • Rapamycin is an immunosuppressant used clinically to prevent organ transplant rejection.
  • Astragalus generally functions as an immune enhancer (immunomodulator).

Combining a substance that boosts immune function with one that suppresses it creates a direct conflict that could reduce the efficacy of the immunosuppression and potentially disrupt the balance needed for optimal anti-aging effects.

#7

I asked Google Gemini what the half-life for Astralagus was, to identify how long its in your system and likely to interact with other drugs you may be taking.

It seems if you don’t consume the Astralagus for 2 or 3 days prior, then the effect would be minimal.

Pharmacokinetics of Astragalus Actives

There is no singular half-life for Astragalus membranaceus because it is a complex botanical matrix. The half-life depends on the specific bioactive compound measured in the plasma. For the compounds relevant to longevity (telomerase activation and anti-inflammatory pathways), the half-life is short, necessitating frequent dosing strategies.

1. Astragaloside IV (The Primary Saponin)

Half-Life (t1/2): Approximately 2 to 5 hours.

2. Cycloastragenol (The Telomerase Activator)

Half-Life (t1/2): Estimated 4 to 6 hours.

  • Metabolic Origin: Cycloastragenol is the deglycosylated aglycone of Astragaloside IV. It is formed via hydrolysis by intestinal bacteria.
  • Kinetics: It has better intestinal permeability than Astragaloside IV but is rapidly cleared by the liver.
  • Clinical Note: Most specific human pharmacokinetic data for Cycloastragenol comes from proprietary industry studies (e.g., TA-65), which generally align with a rapid clearance model requiring twice-daily dosing to maintain therapeutic thresholds.
  • Reference: Cycloastragenol: An exciting novel candidate for age-associated diseases (2018)

3. Flavonoids (Calycosin and Formononetin)

Half-Life (t1/2): Approximately 1 to 3 hours.

Practical Implications for Longevity Regimens

Dosing Frequency
Because the terminal half-life of the primary actives is consistently under 6 hours, a “one-a-day” protocol leaves the body without active compound for 18+ hours.

  • Action: Split daily intake into 2 or 3 doses spaced 6 to 8 hours apart.

Formulation Selection
Raw root powder is inefficient for systemic longevity goals. The conversion of Astragaloside IV to the active Cycloastragenol relies heavily on the gut microbiome, which introduces high inter-individual variability.

  • Action: Prioritize standardized extracts or encapsulated Cycloastragenol to bypass the rate-limiting step of bacterial hydrolysis in the gut.

Metabolic Inhibition
The rapid clearance of these compounds is driven by hepatic enzymes (CYP450 and UGTs).

  • Action: Co-administration with bio-enhancers (like Piperine) may inhibit these enzymes and extend the effective half-life, though precise human data on this specific combination remains sparse.

Would you like me to analyze the bioavailability differences between generic Astragalus root extracts and proprietary formulations like TA-65?

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#8

Thanks
But it means that if you take Rapa once a week, than…3 days before and 3 days after (not to cut the peak) - and there is no time to use it. Sad. Nice herb. Telomerase activator.

#9

I don’t believe that it would have any effect “after” you’ve taken rapamycin… but double check this with Gemini or ChatGPT. Peak Blood levels with rapamycin happens about 2 hours after dosing. Once its in your blood stream I don’t think that Astragalus root extracts are going to have any effect because rapamycin is already in your system doing its mTOR inhibition.