I haven’t measured or tracked this, but I’m going to try another round of high Astaxanthin testing starting in a week or so. I’m thinking of testing 200mg to 400mg / day Astaxanthin levels. Previously have done as high as 240mg/day testing with no issues.
Will do pre-test bloodwork and post-test bloodwork. Will report when I get the final results.
That is a fair amount astaxanthine capsules or do you have access to astaxanthine in powder form?
That’s really a huge amount, can we know which brand did you use and why did you chose it? we are exited to see your result later.
A new Astaxanthin study:
The aim of this study was to investigate the effects of 12 weeks of high-intensity training with astaxanthin supplementation on adipokine levels, insulin resistance and lipid profiles in males with obesity. Sixty-eight males with obesity were randomly stratified into four groups of seventeen subjects each: control group (CG), supplement group (SG), training group (TG), and training plus supplement group (TSG). Participants underwent 12 weeks of treatment with astaxanthin or placebo (20 mg/d capsule daily). The training protocol consisted of 36 sessions of high-intensity functional training (HIFT), 60 min/sessions, and three sessions/week. Metabolic profiles, body composition, anthropometrical measurements, cardio-respiratory indices and adipokine [Cq1/TNF-related protein 9 and 2 (CTRP9 and CTRP2) levels, and growth differentiation factors 8 and 15 (GDF8 and GDF15)] were measured. There were significant differences for all indicators between the groups (p < 0.05). Post-hoc analysis indicated that the levels of CTRP9, CTRP2, and GDF8 were different from CG (p < 0.05), although levels of GDF15 were similar to CG (p > 0.05). Levels of GDF8 were similar in the SG and TG groups (p > 0.05), with reductions of GDF15 levels in both training groups (p < 0.05). A total of 12 weeks of astaxanthin supplementation and exercise training decreased adipokines levels, body composition (weight, %fat), anthropometrical factors (BMI), and improved lipid and metabolic profiles. These benefits were greater for men with obesity in the TSG group.
I’ve been using BioAstin product as mentioned earlier. I may change if I find something that seems good at a lower price.
Huang C, Wen C, Yang M, Li A, Fan C, Gan D, Li Q, Zhao J, Zhu L, Lu D. Astaxanthin Improved the Cognitive Deficits in APP/PS1 Transgenic Mice Via Selective Activation of mTOR. J Neuroimmune Pharmacol. 2021 Sep;16(3):609-619. doi: 10.1007/s11481-020-09953-4. Epub 2020 Sep 18. PMID: 32944864.
In this abstract, it reported that the activation of mTOR enhanced by Astaxanthin was reversed when rapamycin was injected into the mice.
Wondering how this would work for those of us taking Rapamycin?
Good find! Sounds like something we want to read up on. Full paper below:
Astaxanthin (Ast) is an effective neuroprotective and antioxidant compound used to treat Alzheimer’s disease (AD); however, the underlying in vivo molecular mechanisms remain unknown. In this study, we report that Ast can activate the mammalian target of rapamycin (mTOR) pathway in the 8-month-old APP/PS1 transgenic mouse model of AD. Our results suggest that Ast could ameliorate the cognitive defects in APP/PS1 mice by activating the mTOR pathway. Moreover, mTOR activation perturbed the mitochondrial dynamics, increased the synaptic plasticity after 21 days of treatment with Ast (10 mg/kg/day), and increased the expression of Aβ-degrading enzymes, mitochondrial fusion, and synapse-associated proteins and decreased the expression of mitochondrial fission proteins. Intraperitoneal injection of the mTOR inhibitor, rapamycin, abolished the effects of Ast. In conclusion, Ast activates the mTOR pathway, which is necessary for mitochondrial dynamics and synaptic plasticity, leading to improved learning and memory. Our results support the use of Ast for the treatment of cognitive deficits. Graphical abstract In summary, Ast ameliorates cognitive deficits via facilitating the mTOR-dependent mitochondrial dynamics and synaptic damage, and reducing Aβ accumulation. This model supports the use of Ast for the treatment of cognitive deficits.
s11481-020-09953-4.pdf (4.3 MB)
Ast = Astaxanthin
In AD animal models, mTOR regulates a series of physiological processes involved in learning and memory (Bhattacharya et al.* 2012*). To elucidate the effect of Ast on learning and memory in APP/PS1 mouse, the MWM test and PAT were performed. In theMWMtest, APP/PS1 mice showed a longer escape latency in the spatial navigation test as compared to the WT group. Ast treatment significantly reduced the escape latency in APP/PS1 mice (* p < 0.05, Fig. 1A*). Representative tracks of each mice group on day 7 of the navigation test and day 8 of the spatial probe test are shown in Fig.* 1B*. In the exploratory experiment, compared with the WT group, APP/PS1 mice stayed in the target quadrant for a significantly shorter duration and crossed the target quadrant fewer times (* p < 0.05, Fig. 1C and D*).
Spatial learning was improved in the Ast-treated APP/PS1 mice (* p < 0.05). After 24 h of training, we performed the PAT to assess the conditional fear and memory in mice, and observed that memory retention was significantly improved after Ast treatment (p < 0.05, Fig. 1E and F). These findings suggest that Ast treatment significantly alleviates the cognitive impairments in APP/PS1 transgenic mice. Moreover, the observed effects of Ast treatment were significantly attenuated by intraperitoneal injection of the mTOR inhibitor rapamycin (* p < 0.05, Fig. 1A and F*) suggesting that Ast improves learning and memory via mTOR activation in APP/PS1 transgenic mice.
Ast treatment significantly enhanced both working memory and memory recall in APP/PS1 mice as determined by Morris water maze; these effects of Ast were attenuated by coadministration of rapamycin. Next, we investigated whether the neuroprotective properties of Ast are mediated via the activation of themTOR pathway in APP/PS1 transgenic mice.
Ast treatment markedly increased the levels of phosphorylated (activated) mTOR and phosphorylated S6 in the cerebral cortex of APP/PS1 transgenic mice (* p < 0.05; Fig. 2A and D*). This increase in the levels of p-mTOR and p-S6 in the cerebral cortex was attenuated by intraperitoneal injection of the mTOR inhibitor rapamycin (* p < 0.05, Fig. 2A and D*). These findings suggest that Ast could effectively activate the mTOR pathway in APP/PS1 transgenic mice.
Its hard to tell how this applies exactly. I assume that the mTOR pathway is the same in this AD model mouse is going to function the same as any other mTOR pathway. The Alzheimers Disease aspects of the model may or may not be relevant to our experiences.
It does seem likely that the issue of mTOR activation is something we need to factor in. It would seem like you don’t want to simultaneously inhibit mTOR via Rapamycin at the same time adding Astaxanthin which activates mTOR. From the sounds of this paper - Rapamycin is the stronger inhibitor of mTOR than Astaxanthin as a promoter (because the rapamycin cancelled out the Astaxanthin effects). So - I would guess, from my limited knowledge, that you’d want to dose Astaxanthin a few days after the rapamycin (e.g. days 3,4,5,6,7). Anyone else have thoughts on how you might best combine the two?
we report that Ast can activate the mammalian target of rapamycin (mTOR) pathway in the 8-month-old APP/PS1 transgenic mouse model of AD
Thats kinda what I was thinking, however, biology being so unpredictable, who really knows? But being a novice biohacker I’m thinking; why not try? I have also chosen to work out on rapamycin days, mostly because it feels good, even though that is speculated that this may counteract the mTOR suppression.
Hi RapAdmin,
Great work as always!
I’m a bit skeptical of the quoted amounts of astaxanthin in the capsules from the “Cost per 4mg astaxanthin” graphic.
Astaxanthin is a keto-carotenoid within a group of chemical compounds known as terpenes. Algae (Haematococcus pluvialis) are the primary natural source of astaxanthin in the aquatic food chain. The microalgae accumulate the highest levels of astaxanthin in nature other than potentially, engineered cyanobacteria.
It’s very difficult to extract and purify the algae to high % of astaxanthin. There are usually other safe and efficacious carotenoids in the compound ie beta carotene. Do we know the purity of astaxanthin in these products?
The paper below outlines composition amounts for a couple of the products and seems to indicate astaxanthin at much lower levels, perhaps 10% or less? Do we know the source and purity of the astaxanthin in the ITP Lab?
My view on astaxanthin is simply eat some salmon. Good bang for your buck and you don’t have be particularly concerned about whether the astaxanthin is actually there or not - heard of red food coloring found instead of astaxanthin in supplements.
If you prefer synthetic astaxanthin - farmed salmon has it at low cost. If you prefer algae derived “natural” astaxanthin - wild caught sockeye salmon (not particularly cost effective).
Alrhough these are good suggestions the problem arises when you wish to constrain overall food intake and dont have tha spare dietary capacity for enough salmon.
Depends how much you are constraining. I think it’s quite practical in most cases. A typical person can do “mild” 10% or even moderate CR with 100 g of salmon. ~200 calories isn’t really all that much to get ~4mg astaxanthin. (I’m not saying that anyone should be on CR - but CR diets are a way to illustrate low total calorie without malnutrition).
Here’s an example of a ~1200-calorie CR diet with 99% complete nutrition. One can choose to switch some of the cheese and eggs for whole grains, beans, and berries. (This is not my diet, I just grabbed the first one I could find)
Really hard to do significantly less than 1,200 cal without a lot of supplements for any extended period of time. But considering roughly ~2,000 calories a day for women and ~2,500 for men is typically right around the “official recommendation” - I think it’s pretty reasonable to say most people can pull it off through diet rather than unnecessarily go to a lot of extra supplements.
But then again, I have a lot of room to maneuver my diet due to above-average amounts of total lean mass and exercise with what would be considered “mild CR” an overwhelming majority of the time (only a very occassional heavy restaurant meal on a rest day will put me over and that’s alright with me). Muscles are a pretty large glucose sink. This can vary by individual.
I love salmon and eat it regularly, but the numbers I’m seeing suggest it would take a lot of salmon to get 1 gram of astaxanthin per day.
Given the 12% median lifespan increase achieved by the ITP recently with astaxanthin, I’m thinking of in the near future doing my bloodwork (a pre-test), and then ramping up my astaxanthin uptake to a relatively high number for a few months (say 1 gram / day) and retest to see any impact on blood biomarkers. I’ve taken up to 240mg daily for weeks at a time in the past as a test, with no ill effects - so it seems like a pretty safe effort to move up to 1 gm/day for a few months.
@tongMD I’d appreciate your input - thoughts pro and con to this idea and test approach. Any input greatly appreciated.
Trying to do this with salmon seems like a challenge given the numbers below.
Here is what I’m seeing from this site:
Source: Natural Astaxanthin Foods: 20 Best High Potency Food Sources – Superfoodly
Ah 240 mg to 1 g a day would be difficult to get with salmon.
I was merely assuming 4 mg, which is typically the dose in supplements. You can tell roughly how much is in it by the color of the flesh and whether it is “natural” or “synthetic” depending on what it typically feeds on and wild vs farmed.
As for my views on megadosing it to match ITP extrapolated levels - I thought about it - I have no idea for or against whether it would work or not - as you know, there isn’t enough human data.
My diet already consists of other carotenoids - beta-carotene, zeaxanthin, lutein, etc which has related and similar biological activities. While none of these are tested in ITP - I don’t feel comfortable taking any individual “antioxidant” type of intervention as megadose supplementation for a long period of time without more data on humans.
“Antioxidant” supplementation has shown to lead to potentially slightly increased mortality in several cases - we saw that with megadose beta carotene supplementation in smokers that was supposedly expected to be long-term safe and a promising treatment has significantly much higher mortality - the opposite of what was expected.
On the other hand, we could potentially mitigate any individual “antioxidant” agent’s potential toxicity by combining different ones at lower levels ie what Protandim does as seen in the ITP. It would be interesting to see if Protandim + astaxanthin would interfere with each other or not.
Ultimately, I’m not sure how much extra potential benefit I would derive from these megadosed amounts over what has been consumed if I have a mix of most of these antioxidants tested in the ITP but at lower than extrapolated doses from food on top of a diet that already has a good amount of dietary “antioxidants” and a sizable amount of dietary NRF2 activators that go on the higher level of endogenous antioxidant regulatory factors.
The only study I’m aware of that suggests long-term safety is roughly 8-12 mg. I suspect one might even push it a bit more to 20 mg or so but much beyond that I would be far less comfortable based on the issues so far until more human trials are done at least for a longer term. Now some people will have much higher risk tolerance. That’s just not me.
When i spoke with Richard Miller about 6 months ago about the astxanthin study he mentioned that he would like to do a lower dose follow-up study with astxanthin to see what sort of response they could get with less extreme doses, so I think we may see that in the future.
How were you able to take 240 mg? I have only found 12 mg capsules, so that’d be 20 a day. Were you able to find another source of Astaxanthin?
A lower dose study would be excellent.
Yes, i was taking 20 X 12 mg capsules a day.
