A question that needs some certainty is whether mice are euthanised or actually die from cancer. This does not come out in the results, but is an important piece of information.
I am not opposed to having animal welfare standards, but as they vary from place to place there needs to be some indication as to what effects they have on results.
But the mouse plasma concentration is dismal. They ended up with ~20ng/ml, whereas a human taking 12mg per day has a plasma concentration of more like ~200ng/ml. (https://www.researchgate.net/publication/276042544_Kinetics_of_plasma_and_erythrocyte-astaxanthin_in_healthy_subjects_following_a_single_and_maintenance_oral_dose)
The previous (positive) ITP result for Astaxanthin was 4,000ppm which I would guess puts the mice more into the 100ng/ml range.
So you can’t just look at the dose, but you have to consider how much is actually absorbed. The mouse food is dry low-fat pellets, but all the supplements come in oil capsules.
Rodents (rats in this study) seem to also metabolise Asta extremely quickly: Pharmacokinetics and first-pass metabolism of astaxanthin in rats - PubMed After oral administration, 90% doesn’t even reach systemic circulation.
I wouldn’t throw away your Astaxanthin quite yet 
I would suspect it would only make only a couple of days of difference. If the animal is cachexic, not moving etc, it won’t survive long. That’s always been the case in studies that I’ve done (though I never had mice survive until the end of their natural lifespan), where if they have cancer, they don’t spend long circling the drain before dying.
The ITP is using 150 males per treatment, versus male 300 controls, and 150 females vs 300 female controls. Controls are shared with all the other treatments that year. They claim they are 80% powered to detect a lifespan difference of 10%, and based on a lifespan of ~900 days that would be around 90 days. So I don’t think sacrificing animals a few days, or even weeks, ahead of their natural death would move the needle.
IMO it tells us that it is useless and does nothing to extend life in mice let alone humans. In top of that it does not provide a therapeutic benefit for any condition therefore for me it is money down the drain. In studies that show moderate lifespan it basically means one has to spend $1000’s per month when in fact there is substances i.e. captopril (and many others) that showed better results (longer lifespan) yet it can be had for 20 cents per day, and you get therapeutic benefits to boot.
I took Astaxanthin 10-15 years ago (when I was big on supplements) for about two years and felt nothing and have never used it again. To me at best could be harmless but not worth taking especially in doses available, and this study just reinforced what I felt all along.
I don’t think the point is what happens to mice in labs (I for once don’t even care but that is a different story), I think the more important point is why do mice die in the wild, meaning the ones that reach the old age (not the ones that become food for other animals). As we know humans die mostly of heart disease, cancer, infections etc., then question is what do mice in old age die from? And if they do not die of CVD (naturally) testing CVD drugs doesn’t paint the right picture as to the translation in humans IMO (regardless of results in mice) . A better animal to test would be dogs (for such drugs) as an example (assuming dogs die of heart disease, since I have no clue why dogs die either LOL)
In case anyone wants a summary of the human evidence for Astaxanthin, here is Claude’s analysis. It looks like skin probably has the most evidence in humans
Here’s a summary of the current human evidence for astaxanthin, organized by health domain:
Astaxanthin: Human Clinical Evidence
What It Is
Astaxanthin is a natural C40 carotenoid with numerous reported biological functions, most associated with its antioxidant and anti-inflammatory activity. It stands out from other antioxidants, having shown the highest oxygen radical absorbance capacity (ORAC) — 100–500 times higher than α-tocopherol and 10 times higher free radical inhibitory activity than related antioxidants like β-carotene, lutein, and lycopene. 
Antioxidant & Anti-Inflammatory Effects (Strongest Human Evidence)
A 2026 systematic review of 15 human studies found that astaxanthin consistently reduced pro-inflammatory cytokines (IL-6, TNF-α, TGF-β1) and oxidative stress indices, while increasing antioxidant capacity markers (SOD, TAC). 
Skin Health (Reasonably Well-Supported)
A systematic review found 11 clinical studies on astaxanthin and skin health, including six randomized, placebo-controlled, double-blind trials.  The findings include:
** ∙ A 10-week double-blind placebo-controlled study in 23 healthy participants found that astaxanthin supplementation protected against UV-induced skin deterioration, increased the Minimal Erythema Dose, and attenuated UV-induced decreases in skin moisture. **
** ∙ A 6-week RCT in 36 men found that 6 mg/day of astaxanthin improved the appearance of crow’s feet wrinkles, skin elasticity, and transepidermal water loss compared to placebo. **
** ∙ Research suggests long-term supplementation may slow the skin aging process via anti-inflammatory effects. **
Metabolic & Cardiovascular Health (Promising but Needs More Data)
Combined astaxanthin and exercise interventions improved body composition, lipid profiles, insulin sensitivity, and immune recovery in human studies.  Astaxanthin modulates key enzymes associated with lipid regulation (including HMG-CoA reductase) and influences the Nrf2 antioxidant pathway, but more large-scale RCTs are still needed to confirm these effects at moderate-to-high doses (6–24 mg/day). 
Cognitive Function (Early but Encouraging)
A clinical trial in adults found that taking astaxanthin significantly improved cognitive function after eight weeks of supplementation, with benefits to memory and learning.  However, in the sphere of neurodegeneration, a strong majority of human-based research is still cell-based, and larger trials in healthy or disease-specific human populations are needed. 
Reproductive Health
In women with Polycystic Ovary Syndrome (PCOS) or endometriosis, astaxanthin downregulated endoplasmic reticulum stress-related apoptotic pathways and improved oocyte and embryo quality. 
Fatigue & Mood
In separate clinical trials, 12 mg/day of astaxanthin was shown to reduce fatigue, and another trial reported improvements in mood including reductions in depression. 
Overall Verdict
The human evidence is most solid for skin health (multiple RCTs) and antioxidant/anti-inflammatory biomarkers. Evidence for metabolic, cognitive, and cardiovascular benefits is promising but still limited by relatively small trials and short durations. Larger-scale and long-term clinical trials are still needed to validate efficacy and safety across most disease applications. 
Typical doses studied range from 4–12 mg/day, and it is generally considered safe at these levels.
I don’t understand how you can reach that conclusion with any certainty. They can put a huge dose in the food, but if the mice aren’t absorbing it then it’s the same as if they aren’t taking it. And in the past, when they gave a bigger dose, it showed significant increases in lifespan.
Your observation about “you felt nothing” doesn’t mean anything. How are you going to feel a reduced incidence of cancer?
And no, it wouldn’t cost $1000’s per month. I already showed that a 12mg/d dose for a human would give you plasma levels 20x higher than the mice achieved in this study.
Astaxanthin is one of those supplements where, if it was discovered today or synthesised by a biotech company, it would be patented as a drug. It’s a very potent molecule, hitting AMPK, Nrf2, FOXO3, and autophagy. Lots of studies (in animals) show it is acutely protective after injury too - from traumatic brain injury to liver toxicity and myocardial infarction.
I tend to agree with the skin part but didn’t do anything for my inflammation/auto immune issues I had and to some degree still have. As an example, a much better antioxidant effect for me had 2 spoonfuls of ground flax seeds than any (or most, at least the ones I tried) supplements that claim such benefits. Even consuming wild salmon, I could notice significant improvement on inflammation (way beyond the placebo effect) and to be honest there isn’t one single supplement that has given me nearly as much of an effect as certain foods, then to me why spent money since I can manage it pretty well with foods that I already eat (or have to eat).
What you say could very well be true, but I find hard to believe it because if it were such a powerful substance one has to feel something, anything if taken for a relatively long time. I just gave the example of the flaxseeds above and I can absolutely tell the effect in 1/2hour after I consume it. Now, I’m not able to confirm nor deny benefits of Astaxanthin but as a rule of thumb I try something for a period of time (usually 6months to one year) and if I can’t find any effect whatsoever, I discontinue using it. By trying so many of them in last 20 years, I had come to my own conclusion (obviously non-scientific) long time ago, that supplements are harmless (for most part) but are not needed (or add nothing to one’s health and longevity) unless there is a measured deficiency in the body. I’m somewhat relieved that few (not just one) of the doctors in the field are now coming to the same conclusion.
My money is on the drug side of the equation (for longevity).
I didn’t expect such a huge debate over astaxanthin. In my view, it’s just a very ordinary compound. You can take it with lutein to boost the effects, but whether you take it or not won’t make a bit of difference to your lifespan.
Even in skincare, astaxanthin is just a minor player at best.
The way I see it, if what @relaxedmeatball ’s post about absorption issues is correct, then the last Astaxanthin result is more credible than the recent one.
Fair enough. I don’t have this skill apparently. I had a huge smoothie earlier with spinach, celery, kale, almonds, walnuts, actually some flax seeds, some yoghurt, half a banana, blueberries and a few other things - and I felt absolutely nothing (except a bit full). And the only long-term effect I notice is nice smooth poops 
Interesting. I see it as basically a drug which is (un)fortunate enough to be sold as a supplement. It makes it nice and accessible, but also means that it doesn’t really get the proper quality research that we’d love to see. At least based on in vitro assays and animal experiments, I believe it’s pretty potent.
Yes exactly. When I have more time, I’ll go check what plasma concentration they got in the previous ITP result. If the numbers scale proportionally, even the 4000ppm probably works out to be less than a human taking 12mg/d (which is what I take).
Unfortunately this is a pretty recurring issue for the ITP failing to achieve the doses that actually work. I wish they weren’t so resource constrained.
Well, first of all, your 1/2 banana (and maybe spinach) is poisoning otherwise a miracle (for health) drink LOL and your last sentence just proved exactly my point that is to say, if you consume/take the right foods/drugs, you do get an almost instantaneous benefit, in your case a VERY big and an important one I might add. LOL. So yeah, I’m not changing my mind on supplements LOL, as a rule of thumb, if you don’t subjectively get a benefit, it is not worth spending money on.
One wonders what ITP findings – still being on mice, which do not generalize nearly as well to humans as some conversations would support – would look like if the endpoints were specific diseases that kill most of one ultimate target of this research: humans over their mean survival age. From 80 on up, ASCVD is almost 3X more likely than cancer to be a cause of death (more than 3X if you collapse ASCVD to include stroke). One table:
If it turns out that most of the deaths used as a DV in the research are from cancer, ITP and its followers have been shortsighted at the least. Contrasting this position, ITP does not use mice bred to develop cancer.
From Claude AI when asked “Based on these new ITP results, does it look like Astaxanthin may no longer extend life in human males or is it hard to extrapolate this since mice bioavailability of astaxanthin is low?”
This is a really nuanced question worth unpacking carefully. Let me break it down:
What the ITP paper actually found
The ITP tested astaxanthin (among other compounds) in UM-HET3 mice and found no significant lifespan increase in either male or female mice.  Critically, astaxanthin had previously been associated with lifespan extension in the ITP, but showed no benefit when administered at different doses or starting at later ages.  So this appears to be a dose/timing replication attempt rather than a straight repeat of the original positive finding — which is an important nuance.
Does this rule out a human benefit?
Probably not conclusively, and here’s why your bioavailability instinct is well-founded:
Astaxanthin is notoriously poorly bioavailable in rodents. Mice lack the carotenoid-binding proteins that help absorb and transport lipophilic carotenoids efficiently, and the earlier ITP result that did show a lifespan benefit in males may have been at a dose that happened to achieve marginally adequate tissue levels. A different dose or timing could easily fall below a therapeutic threshold in a species already struggling to absorb the compound. Humans, by contrast, absorb astaxanthin considerably better, particularly when taken with fat.
The bigger picture from the ITP data
The paper itself emphasizes that timing and dosage are critical variables in aging intervention studies, and the results reinforce the need for cautious interpretation of single-site or single-cohort findings.  The original positive male-specific signal from astaxanthin in the ITP was always a somewhat fragile result, and this new data doesn’t decisively replicate or refute the original — it tests a different parameter space.
Bottom line
You can’t cleanly extrapolate a null result in mice to “astaxanthin won’t extend life in human males” for several reasons: the null result may reflect dose/timing issues specific to this experiment, mouse bioavailability is genuinely poor for this compound, and the prior positive ITP signal was male-specific and may reflect a biological mechanism (e.g., antioxidant effects on male-pattern oxidative stress) that could still be relevant in humans. That said, the overall ITP track record suggests we should hold longevity claims for any supplement loosely — very few compounds survive rigorous multi-site replication.
Lol, how do you die from hypertension? You already listed ASCVD and stroke, plus kidney, so don’t say those.
Just posting a quick and dirty frequency distribution from the medical community @CronosTempi, focusing on the relationship between heart disease and cancer. No conceptual analysis engaged. Had there been, I would have said the tabulations might have been based on primary Dx. Arguably, the causal nexus of all of those categories are – at minimum – partially conflated
I had free time this morning so I spent a little time digging into ITP protocols. Most will know the following, but to refresh:
ITP’s primary mandate is to identify agents that extend median and maximal lifespan across three independent sites. Resources for deep phenotyping (like echocardiograms or specialized atherosclerosis assays) are often relegated to “Collaborative Interactions.”
ITP performs necropsies on mice that die or are euthanized when moribund. These analyses provide data on Incidence and severity of neoplasia and age-sensitive pathologies including kidney lesions, liver changes, and cardiac fibrosis.
This protocol leaves what I see as a very large gap between its findings and what kills humans. UM-HET3 mice do not naturally develop human-like atherosclerosis. They lack the high LDL-C and the specific vascular architecture necessary for plaque formation. Most UM-HET3 mice die with multiple tumors. If a drug like Rapamycin extends life, it is largely by delaying cancer or general “frailty” rather than preventing a myocardial infarction that would never have occurred in that model.
Therefore, unless an intervention is specifically tested in a sensitized model (which would also be weak in terms of generalization) the ITP protocol cannot directly measure or even infer “ASCVD and related protection” in the way it appears in a human over 80, or even younger for that matter. The reports, especially when you listen to their presentations, create an undocumented inferential leap between dying of a neoplasm and dying of anything else, although marginal evidence is presented on kidney, liver, and cardiac structure which, again, is dissimilar to humans.
To me, this means taking ITP with a 3X grain of salt. Specifically, there is no preponderance of evidence to suggest that any substance that failed to show even marginal significance for mice would not be beneficial to humans,
I’m sticking with asta for the time being for several reasons. The original paper finding benefit noted several well-established positive indicators.
“Asta extended the lifespan in various models. In Caenorhabditis elegans, Asta increased the lifespan 16–30% in wild-type and age-1 worms, but not in daf-16 knock-out worms [30]. Furthermore, Asta extended the lifespan in C. elegans by inducing autophagy through the IIS and TOR signaling pathways [31]. In Saccharomyces cerevisiae yeast, Asta increased the lifespan by decreasing oxidative stress and apoptosis [32]. Asta also extended the lifespan of D. melanogaster flies under oxidative stress [33, 34]. The present ITP study is the first evaluation of Asta in a mammalian lifespan model, so the target dose of 4000 ppm in the diet is based on chronic mammalian studies other than lifespan. Despite the fact that the average diet contained 1840 ppm Asta (only 46% of the target), median lifespans of male UM-HET3 mice were significantly improved.”
Given asta’s safety profile, availability, and low cost, that alone is just about good enough for me. But there is the inflammation benefit, the neat way it spans the cell membrane, and the cool pinkish, blushing white-boy skin tone I get from high doses.
And I seem to recall, when I did a deep dive into asta before starting, that the sourcing, dosing, and form were confused. They used a state-of-the-art micronized form from Hawaii that penetrated the blood better and that I use now (along with cheaper BulkSupplements asta for “bulk”). And the micronized form is supposed to have 3x the absorption. So the mice blood-level estimations were way off for the positive trials. I never saw an official correction on this matter. And I haven’t seen what “brand” of asta they used for this run. It could be that the mouse chow doesn’t fire off whatever primitive bile system mice might have, and so with regular astaxanthin none gets absorbed and no health effect is seen. IDK.
After they almost pulled off the E3 (simple actual name) switcheroo to 16α-hydroxyestriol (complicated fake name), I have not trusted them as much. Big money is involved, and most of the experts own interests in longevity ventures. mtc
I wouldn’t throw it away but for now I don’t see any reason to dose beyond 12-24mg/d. Too expensive for potentially no lifespan extension effects and the 12mg dose already works well for extra UV protection and eye health.