For that matter you can sample various tissues (on autopsy) for asta levels. Some tissues accumulate asta preferentially. In people who have had long term high exposure, you can get skin color effects.
All this takes money of course, but given all the hard work and investment in running these trials, it would be nice to extract as much data as possible, it’s a pretty unique resource.
While this would cost a lot of money, the good thing is that to do this wouldn’t require another lifespan study. It would be enough to feed a small group of mice astaxanthin for a few weeks and then measure tissue and fecal levels.
If they weren’t given astaxanthin with fats, then that makes the result even less noteworthy. Everyone knows Astaxanthin needs to be taken with fats in humans. That is just such basic info.
Side rant, I always facepalm when someone tells me that a multivitamin makes them nauseous. I immediately tell them that it’s because they didnt take at the same time as food and then they look perplexed since apparently no one told them that was absolutely mandatory.
Yes, but even though mouse chow is relatively low in fat, it does contain quite significant amounts of it, and typically you need only a little bit of fat along with fat soluble vitamins and carotenoids to absorb them pretty well, so I don’t think the low fat content of their diet is sufficient to explain this. But it’s definitely a factor.
IIRC, Rich Miller says that people can apply to the ITP to obtain samples.
So if any of us here has a lab that could measure it, we could actually get access to the samples.
Another factor, I think, is the formulation, and the stability of the molecule in the food. If you look in the supplemental table, lots of the compounds end up being under-dosed even at the food level.
There was an experiment done years ago by Robert Alan Franklyn (The Lancet, June 12, 1976, p.1296), in which he gave 10 grams a day of BHT to his 18 Scottish Deerhounds (large dogs), starting at an early age. The incidence of cancer occurring in such dogs, at that time anyway, was high, above 30%. None of Franklyn’s dogs died of cancer. They mostly died of heart or kidney failure, and most lived a normal lifespan. The probability of this happening by chance is like .7 to the 18th power. Eighteen control dogs mostly died of cancer.
It could be useful if something similar to this could be used in mice to investigate potential life-extending supplements.
I can’t find the reference/link/discussion, but I seem to recall that a micronized form of astazanthin (similar to the article below) was used in the orginal trials. Maybe the makers of the micronized astazanthin proposed it, idk, but I recall perhaps a youtube discussion where the ITP people weren’t aware of the different forms and aborption rates, so when they dosed with the micronized form the blood levels were higher than what the ITP people had calculated as needed for benefit. They (ITP) never made an addendum or correction on that issue. It would not supprise me if the latest results were based on the simpler more prevalent and cheaper form of astazanthin.
I personally switched to the form of astaxanthin that the previous ITP results used because I wanted to make sure I was taking the good stuff. Are you sure they didn’t use the same formula this time around? That would be really important information.
Haven’t read anything regarding formulation this time. Most people take the simpler version, so it would make sense to test the simpler type. But that would be confusing. But using the micro version the first time and not “announcing” it or even being fully aware of it themselves was confusing. And mis-naming simple E3 was confusing. So they have “confusing” things about 2 of their promising chemicals (20 maybe) so they are batting 900 which is great in baseball, but for 3 premiere scientific universities publishing in peer reviewed journals a 10% failure rate is not so great. Essentially all of the authors have financial interests in longevity start-ups. Does that make them lose their objectivity? Do you “trust” Attia, Sinclair? Well ITP was good while it lasted, but money talks.
I would still guess that they use the exact same formula of astaxanthin as they did the first time, but hopefully we will find out for sure
The contact email for the paper is ron.korstanje@jax.org so someone could just email and ask.
Let us keep in mind, that even if a given med does not prolong lifespan, it may still be vital to take it… So we may want to take these “failed life extension in the ITP” drugs anyway preventatively even without diagnosed disease, us not being mice and all. Though we may gamble on the ITP successes
I think there’s a tendency to outright dismiss anything that failed in the ITP. It goes without saying, but we are not mice. In addition, the human specific diseases like CVD where catastrophic failure in a single organ system results in premature mortality will shorten median lifespan at the population level, but eradicating them won’t move the needle on maximal lifespan much.
Some of our organ systems age quite differently in lab mice. One example is the hematopoietic system, responsible for supplying every other tissue with oxygen, in addition to protecting us from pathogens and cancer. Ours only has to produce approximately 300 billion cells a day to maintain itself. 
While mice and humans share some aspects of hematopoietic aging, such as myeloid skewing, mice display a drastically increased prevalence of lymphoma, whereas humans are far more vulnerable to clonal hematopoiesis. In extremely old humans this phenomenon becomes so extreme (oligoclonality) that you can count the number of distinct remaining clones on one hand.
In one case study, a 115 year old woman had just one clone producing the vast majority of her WBCs (technically two closely related but distinct clones, but still). These HSCs also display extremely short telomeres, suggesting that replicative senescence in the HSC compartment limits maximal human lifespan.
The upshot of this is that drugs which increase clonal diversity might have little effect on mice, whereas in extreme old age they might give the human hematopoietic, and in particular, immune systems more resilience and capacity for adaptation. Similarly, drugs which reduce telomere attrition in HSCs might increase the hematopoietic system’s capacity for long-term renewal in elderly humans, whereas they might just make mice die from lymphoma faster.
I think this is linked to the expression of telomerase which is linked to acetylation levels.