Sleep all comes down to the mitochondria

Original Article ↗ Hacker News Discussion ↗

Proposed mitochondrial mechanism for sleep

  • Thread centers on a fly study where mitochondrial “electron leak” in specific sleep‑inducing neurons appears to signal the need for sleep; mild uncoupling in those neurons delays sleepiness.
  • Commenters connect this to known adenosine build‑up: inefficient mitochondria → faster ATP use → more adenosine → more sleep pressure.
  • The article’s broader claim: aerobic respiration (using oxygen) inherently requires periodic “mitochondrial downtime,” especially in the nervous system.

Skepticism and limitations

  • Multiple commenters stress this is a theory, not “the answer” to why we sleep.
  • Concerns:
    • Results are in Drosophila; unclear if the mechanism generalizes to mammals or humans.
    • Distinction between regulating sleepiness vs explaining the deeper function of sleep.
    • One domain expert calls the paper “awful,” arguing it overhypes results, conflates control with function, and that the sleep phenotype is weak; expects strong rebuttals in the field.
  • Others doubt a mitochondria‑only story because mitochondria are ubiquitous while sleep is heavily brain‑specific and very costly evolutionarily.

Sleep’s functions and evolution

  • Many argue sleep likely has multiple functions: memory consolidation, synaptic “rebalancing,” glymphatic waste clearance, neuronal maintenance, etc.
  • Debate on whether sleep evolved as a response to the day–night cycle (energy conservation and housekeeping during “off‑hours”) versus being required by fundamental “brain algorithms” needing offline phases.
  • Discussions of animals with unusual sleep patterns (unihemispheric sleep, jellyfish, sponges) challenge brain‑centric accounts and raise questions about what counts as sleep.

Drug, supplement, and “sleep in a pill” ideas

  • Speculation about:
    • Mitochondrial uncouplers that cross the blood–brain barrier as wakefulness promoters.
    • “Healthy” wakefulness vs long‑term harm; comparisons to appetite‑modifying drugs like Ozempic.
    • Restorative‑sleep enhancers (e.g., slow‑wave enhancement) rather than sleep‑eliminating pills.
  • Creatine, keto diets, CoQ10, PQQ, red‑light therapy, and other “mitochondria‑supporting” interventions are discussed anecdotally; evidence is described as fragmentary or unclear.

Mitochondria, disease, and broader physiology

  • Links drawn between mitochondrial dysfunction and conditions like ME/CFS, long COVID, and chronic fatigue, though commenters note inconsistent or inconclusive data.
  • Questions raised about how this theory fits with:
    • The heart’s continuous activity.
    • Sleep apnea and low‑oxygen states.
    • Plants and non‑animal life that use oxygen but (probably) don’t “sleep” in the animal sense.

Meta: analogies and hype

  • Some use neural‑network analogies (training, pruning, garbage collection) to think about sleep; others object that LLM talk is being overextended.
  • Several comments criticize hype cycles in biology (mitochondria now, microbiome earlier) and caution against pop‑science claims that a single paper has “solved” an ancient mystery.