Rapamycin Reigns Supreme: New Data from the Cricket Model of Aging

I don’t care too much about results in crickets in terms of indicating translation of results to humans (we don’t have much data to suggest that crickets are a specifically good model for successful translation of a small molecule to effectiveness in humans), but its good to see yet another model organism that rapamycin has proven successful in. Rapamycin has proven successful in extending lifespan in every organism its been tested in, from yeast, to fungi, to rotifers, to nematodes (worms), to fruit flies, to fish, to crustaceans, to mice and monkeys… and now crickets! The mTOR pathway has been conserved well over a billion years of evolution.

In a new study attempting to establish the house cricket (Acheta domesticus) as a scalable longevity model, researchers from the University of Washington tested intermittent “pulse” dosing of three top-tier geroprotective candidates: Rapamycin, Acarbose, and Phenylbutyrate. The results provide a stark warning against assuming “safe” diabetes drugs are universally beneficial across sexes.

While Rapamycin solidified its status as the “gold standard,” extending survival by nearly 60% in males and preserving juvenile-like cognitive and locomotor function, Acarbose—a drug widely considered benign in the biohacker community—dramatically reduced the lifespan of female crickets (Hazard Ratio ~3.0), effectively tripling their risk of death despite inducing weight gain. This contradicts established mouse data where Acarbose is sex-neutral or weakly beneficial in females, highlighting a potential metabolic “mismatch” or toxicity that could be relevant to specific human phenotypes.

Phenylbutyrate, often touted for its HDAC inhibition and ammonia scavenging, failed to extend lifespan significantly in the overall cohort but did show sex-specific survival benefits in females, albeit with reduced locomotor performance. This study reinforces the “Rapamycin or bust” trend in recent longevity literature while casting a shadow of uncertainty over Acarbose for females.

Source:

Novelty

  • Durability of “Pulse” Dosing: Most longevity studies use continuous dosing. This proves that a short, 2-week “vacation” on Rapamycin in mid-life can permanently alter the survival trajectory in an invertebrate model.
  • Invertebrate Validation: Establishes the cricket as a fast, cheap screening tool that (mostly) aligns with mouse data—except for the specific Acarbose/Female divergence.

Critical Limitations

  • Translational Gap (Phylogeny): Crickets are insects. They lack a closed circulatory system, a liver, and a mammalian immune system. The Acarbose toxicity could be due to insect-specific carbohydrate biology that does not apply to humans.
  • Small Sample Size: N=20 is statistically fragile. A few accidental deaths could skew the Hazard Ratios significantly.
  • Preprint Status: The data has not been stress-tested by peer review. The “weight gain” in Acarbose females needs histological verification to ensure it wasn’t edema or egg retention/impaction rather than “healthy fat.”

So we have:

    1. Yeast
    1. C Elegans
    1. Fruit flies
    1. Hydra
    1. Killifish
    1. freshwater cnidarian Hydra
    1. Daphnia Magna
    1. Mice (1. Het3, 2. B6)
    1. rotifers
    1. crickets

In progress:

    1. Marmosets monkeys
    1. Dogs
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I used Google Gemini Pro Deep Search on this issue. I would include marmosets as being successful because its been reported by Adam Salmon already, though publication is still to be done.

The Phylogeny of Longevity: An Exhaustive Analysis of Rapamycin-Induced Lifespan Extension Across the Tree of Life

1. Introduction: The Pharmacological conquest of Time

The quest to decouple biological aging from the passage of time has long been the purview of mythology, but in the last three decades, it has transitioned into a rigorous scientific discipline. Central to this paradigm shift is a compound isolated from the soil of Easter Island (Rapa Nui): rapamycin (sirolimus). Originally identified for its potent antifungal properties and subsequently developed as an immunosuppressant for organ transplantation, rapamycin has emerged as the premier “geroprotector”—a pharmacological agent capable of slowing the fundamental biological processes of aging.

The universality of rapamycin’s effects is underpinned by the evolutionary conservation of its target, the mechanistic Target of Rapamycin (mTOR). This serine/threonine kinase functions as a master nutrient sensor, integrating signals regarding amino acid availability, energy status (ATP/AMP ratio), and growth factors to dictate the cellular decision between anabolism (growth and reproduction) and catabolism (maintenance and repair). The “Hyperfunction Theory” of aging posits that aging is not merely the accumulation of damage, but the purposeless continuation of developmental growth programs into adulthood—a state of cellular over-activation driven by mTOR. By inhibiting this pathway, rapamycin effectively mimics a state of nutrient scarcity, forcing the organism into a protected mode of somatic maintenance, thereby extending lifespan.

This report provides an exhaustive, phylogenetic review of every model organism in which rapamycin has been proven to extend lifespan. Drawing from a comprehensive dataset of preclinical studies, we analyze the efficacy, mechanisms, dosing nuances, and sex-specific responses ranging from unicellular fungi to complex mammals. We also scrutinize the emerging data from pre-clinical primate and canine models, where the translational potential of this compound is currently being adjudicated.

Full report here: https://gemini.google.com/share/fb87f4e825fc

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