Kolmogorov complexity of the human brain at one instant:
synapses (compare to neurons)10 to 1000 bits per synapse for weights
Total:
to bitsProbably not significantly compressible, considering that e.g. Claude Opus is significantly smarter than Claude Haiku
Kolmogorov complexity of “100 years of subjective experience that thinks he is [puffymist], a particular human who lived on Earth at ”?
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Temporal resolution of perception (“frame rate”): 10 to 30 frames per second
excludes audio, which has high sample rate but low bitrate
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Uncompressed information per subjective-moment “frame”:
to bits per frameEmpirically: conscious processing
40 bits/second, or about 1 bit per “frame”Let’s say there are
to bits of felt-sense “richness” per bit of conscious processing
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Compression: call it a factor of
(99.9% compression) to (90% compression)Low-level redundancy: video compression-like between-frame redundancy
High-level redundancy: routines, mental “well-worn grooves”, repetitive daily / yearly patterns
Semantic description: think of image / video generation from prompts of 10 to 100 words
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Putting it all together:
Low end:
High end:
This is the consciously accessed data stream only, which is why it is much smaller than the full human brain.
“But the full latent input-output capabilities of human brain can be obtained by training the brain on its experience!” Yes, and that training makes use of data not consciously accessed, which I believe is much bigger than the consciously-accessed data stream.
Kolmogorov complexity of a human baby’s brain
A baby hasn’t begun learning, so I’ll assume that the human genome is a sufficient description of a baby’s brain.
Kolmogorov complexity
Kolmogorov complexity of any generic human-level observer
I really have no idea. The space of mind designs is huge; there are likely some very compact designs.
As-treated analysis measures the biological effect only if the experiment design absolutely fixes the treatment actually received. For example: hospitalised patients, treatment / control given under supervision, 100% adherence, there were no other attempted-trials discarded because adherence < 100%. Otherwise, “as-treated analysis” is confounded via patient adherence.
Intention-to-treat analysis is important for being unconfounded.
A recap from Judea Pearl’s Causality:
( = randomised assignment, = treatment received, = outcome)
( = common causes, = mediators, e.g. lifestyle, baseline health)
Intention-to-treat analysis measures . You’re not conditioning on , so the potential confounder path is blocked by (collider). measures exactly the effect . It is unconfounded.
( is randomised, so there are no nodes affecting ).
As-treated analysis measures . There is which is what we want, but there is also which confounds our measurement of .
A classic example is the 1980 Coronary Drug Project, where treatment (clofibrate) vs placebo made no difference, but good adherence (to either treatment or placebo) was correlated with halving the 5-year mortality.
If, like Viliam below, you want to figure out “the causal effect if I intervene to do X with absolute 100% adherence”, you want complier average causal effect analysis.