What I find interesting is that its the synthetic astaxanthin that is being used in the National Institutes on Aging ITP study that in preliminary results is showing a 12% median lifespan increase in the male mice.
I don’t find Mercola info very trustworthy… in the Wikipedia entry (and many other places I’ve read about him) he seems to not follow the science very closely, or contradicts the best science… in Wikipedia they note:
The site promotes disproven health ideas, including the notions that homeopathy can treat autism and that vaccinations have hidden detriments to human health.[2] An article in BusinessWeek criticized his website as using aggressive direct-marketing tactics:
Mercola gives the lie to the notion that holistic practitioners tend to be so absorbed in treating patients that they aren’t effective businesspeople. While Mercola on his site seeks to identify with this image by distinguishing himself from “all the greed-motivated hype out there in health-care land”, he is a master promoter, using every trick of traditional and Internet direct marketing to grow his business … He is selling health-care products and services, and is calling upon an unfortunate tradition made famous by the old-time snake oil salesmen of the 1800s.[6]
It looks like this is the article where Mercola got his information:
The article says it makes a bio identical molecule to the natural one and they think they can compete with the synthetic for price. Made with GE yeast.
This antioxidant does so by decreasing lactic acid.
the 6-minute walking test demonstrated that the participants from the astaxanthin group increased their walking distance. At the same time, astaxanthin supplementation did not improve muscle strength as shown by hand grip and knee extension tests.
In addition, the researchers measured the change in the participants’ lactic acid levels after the 6-minute walking test pre- and post-supplementation. Astaxanthin supplementation was shown to decrease lactic acid production in these participants.
Astaxanthin has shown a variety of clinical benefits with good tolerability and safety. In double-blind, randomized controlled trials, it reduced oxidative stress by 5 mg or 20 mg/day in obese and overweight subjects and 5 mg, 20 mg or 40 mg/day in smokers [11, 12]. The results showed that oxidative DNA damage was inhibited, C-reactive protein and other inflammatory biomarkers were decreased, and tuberculin skin test immunity was enhanced [13, 14]. In another trial, daily astaxanthin doses of 6, 12, or 18 mg decreased triglycerides and increased HDL cholesterol and improved blood flow in microcirculation models
Placebo lost a little weight, astaxanthin lost more.
Placebo lost muscle mass % and gained body fat %, astaxanthin gained muscle mass% and gained body fat %. Not sure how they could do that without gaining weight. What do we have besides muscle and fat? Bone?
Anyway it is a very expensive supp. and simple and cheap things like glynac should be studied more closely. Everybody is still looking at the one study where they took 9 grams of NAC/day.
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.
Astaxanthin Supplemented with High-Intensity Functional Training Decreases Adipokines Levels and Cardiovascular Risk Factors in Men with Obesity
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.
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.
