Sounds like it’s not a sustainable hack in the long run 
This is really interesting! Jiu-jitsu might be good for overall health, but it’s a disaster for the joints. I actually have an MRI for my elbow scheduled for tomorrow due to pretty advanced osteoarthritis there–so anything that helps joints, I’m always interested in. Thanks!
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Ask your doctor to check for ulnar neuropathy- a common source of an elbow pain
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Conclusion
Nice!
While studies have long indicated that rapamycin is effective in extending lifespan, researchers are continually discovering how best to augment its longevity benefits. Exhaustive testing from the ITP confirms that, at the present time, acarbose stands out as the single best addition to a rapamycin longevity protocol. The two medications, when taken together, have the strongest data on their potential to increase lifespan. Those using rapamycin to promote cellular health and extend lifespan should not hesitate to discuss with their doctor adding acarbose to their regimen.
I hope I am in the group that is not resistant.
Acarbose is an inhibitor of both human and bacterial α-glucosidases3, limiting the ability of the target organism to metabolize complex carbohydrates. Using biochemical assays, X-ray crystallography and metagenomic analyses, we show that microbiome-derived acarbose kinases are specific for acarbose, provide their harboring organism with a protective advantage against the activity of acarbose, and are widespread in the microbiomes of western and non-western human populations.
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Does Acarbose reduce fasting Glucose level or does it just prevent post meal spikes in glucose? I ask given I want to start Acarbose but my fasting glucose levels in recent labs was 63 (range 70-99). So if it does not reduce fasting glucose levels, I will start it. Thoughts?
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I think they do both… flatten the spikes, and lower the baseline too (same for the SGLT2 inhibitors). I forget the exact paper… here is a discussion related to canagliflozin: Canagliflozin - Another Top Anti-aging Drug - #61 by MAC
But when I’ve been using Acarbose its a little hard to tell… the dosing is you take it at the beginning of every meal (or with the first bite). And it has a very short half life… basically its only operating in your body for about 2 hours, so just enough to process with your meal.
I think I will try both together next month, and use my CGM to monitor for any potential hypoglycemia.
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Thank you RapAdmin for the reply. I think the key for me is to buy a CGM monitor and make sure my glucose readings in morn not going down any further than current levels or not too much lower.
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I get my CGM sensors for free from a friend who has diabetes and has extras. I’m not sure its worth the convenience… not that it isn’t nice to have, I’m just not sure its worth the $100/month for the information. Something like this is fine too:
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Thanks. I will check this system out.
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“Increased Butyrate and other SCFA’s after fiber fermentation in lower intestine, protects against leaky gut etc? The might be the key longevity point of Acarbose? I only speculate, but I have a gut feeling about this.”
Could be.
Acarbose raises serum butyrate in human subjects with impaired glucose tolerance - PubMed.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4693467/
" Butyrate is a four‐carbon fatty acid that is produced in the gut as a product of fermentation. Butyrate is a general HDAC inhibitor and protects against high‐fat diet‐induced metabolic changes (Gao et al ., 2009), has anti‐inflammatory properties (Maslowski et al ., 2009) and extends lifespan in a mouse model of progeria (Krishnan et al ., 2011) and Drosophila (Zhao et al ., 2005)."
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I’m not worried about how much Acarbose lowers blood glucose.
Acarbose works partly by increasing SCFA production, decreasing starch (and ultimately glucose) absorption, and thus increasing ketone production on a ketogentic diet. Increased ketones are known to drive down fasting blood glucose safely, since the body is using ketones (and SCFA) as a fuel source and reduces its glucose usage. Most people start feeling low blood glucose at 70mg/dL, but for me on a keto diet, it is around 60, and I can walk around feeling okay into the 50s.
Any contrary stories out there?
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Perhaps Acarbose works like this:
But ant queens can have it all. In some ant species, queens live more than 30 years while laying the thousands upon thousands of eggs that become all the workers in the nest. In contrast, worker ants, which are females that don’t reproduce, live only months. Yet if circumstances demand it, the workers of some species can step up to become pseudo-queens for the good of the nest — and to reap a significant extension in their life span.
What governs this gigantic range in ant life span is poorly understood, but two recent studies have revealed important details about what makes the life spans of ants so flexible. In Science, researchers at New York University showed that some ant queens produce a protein that suppresses the aging effect of insulin so that they can consume all the additional food needed for their egg-laying without shortening their lives. And in a preprint recently posted on the biorxiv.org server, researchers in Germany described a parasite that greatly lengthens the lives of its ant hosts by secreting a rich cocktail of antioxidants and other compounds. Both studies add to the evidence that the observed life spans of organisms have little to do with limitations imposed by their genes.
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Insects are so strange and amazing. It does seem to prove that extending life by a huge amount is possible, but maybe only in bugs. It seems like science fiction sometimes. Great article thanks.
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The paper is below.
Xinna Li, Xiaofang Shi, Madaline McPherson, Mary Hager, Gonzalo G. Garcia, Richard A. Miller
Cap-independent translation of GPLD1 enhances markers of brain health in long-lived mutant and drug-treated mice
https://onlinelibrary.wiley.com/doi/10.1111/acel.13685
pdf version below.
https://onlinelibrary.wiley.com/doi/epdf/10.1111/acel.13685
Below are all the open view papers by Xinna Li:
https://experts.umich.edu/4566-xinna-li/publications
Included is her 2014 paper entitled:
Rapamycin-mediated lifespan increase in mice is dose and sex
dependent and metabolically distinct from dietary restriction
Gonzalo Garcia’s publications are below.
https://www.researchgate.net/profile/Gonzalo-Garcia-5
Earlier publications from Spain:
https://www.researchgate.net/scientific-contributions/Gonzalo-Garcia-16100608
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I made that comment because there’s a possibility that resistance to acarbose may develop. Unfortunately there’s a dearth of info about this, but I’m expecting it won’t work indefinitely in myself.
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Acarbose, an α-Glucosidase Inhibitor, Maintains Altered Redox Homeostasis During Aging by Targeting Glucose Metabolism in Rat Erythrocytes
Jitendra Kumar Arya, Raushan Kumar, Akanksha Singh, Parisha Srivastava,
Arun Kumar Yadawa, and Syed Ibrahim Rizvi
Published Online: 27 Jan 2023
https://doi.org/10.1089/rej.2022.0032
Abstract
Increasing age is the single largest risk factor for a variety of chronic illnesses. As a result, improving the capability to target the aging process leads to an increased health span. A lack of appropriate glucoregulatory control is a recurring issue associated with aging and chronic illness, even though many longevity therapies result in the preservation of glucoregulatory control. In this study, we suggest that targeting glucose metabolism to improve regulatory control can help slow the aging process. Male Wistar rats, both young (age 4 months) and old (age 24 months), were given acarbose (ACA) (30 mg/kg b.w.) for 6 weeks. An array of oxidative stress indicators was assessed after the treatment period, including plasma antioxidant capacity as determined by the ferric reducing ability of plasma (FRAP), reactive oxygen species (ROS), lipid peroxidation (malondialdehyde [MDA]), reduced glutathione (GSH), total plasma thiol (sulfhydryl [SH]), plasma membrane redox system (PMRS), protein carbonyl (PCO), advanced oxidation protein products (AOPPs), advanced glycation end products (AGEs), and sialic acid (SA) in control and treated groups. When compared with controls, ACA administration increased FRAP, GSH, SH, and PMRS activities in both age groups. The treated groups, on the contrary, showed substantial decreases in ROS, MDA, PCO, AOPP, AGE, and SA levels. The effect of ACA on almost all parameters was more evident in old-age rats. ACA significantly increased PMRS activity in young rats; here the effect was less prominent in old rats. Our data support the restoration of antioxidant levels in older rats after short-term ACA treatment. The findings corroborate the potential role of ACA as a putative calorie restriction mimetic.
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I am no rat… but this type if research makes me more confident about my decision to drop Metformin and go with Acarbose.
For me my gut feels very stable and stools are healthy and plenty.
I have not had diarrhea once in 3 months on Acarbose.
With Metformin… was diarrhea, fatigue and weakness all the time. For my phenotype Acarbose works.
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I personally do the following:
- mix in multiple naturally occurring inhibitors from diet to potentially reduce the risk of “acarbose resistance”
- use slow digesting carbohydrates (examples are lentils/beans)
- maximum dose
Can you elaborate what the maximum dose means ?
Do you suggest that using maximum dose like 300mg(or more) acarbose a day, then it may prevent from developing acarbose resistance? And what’s the reason behind it?
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I took 100mg of Acarbose upon waking yesterday, which is about 30minutes before I eat anything. I believe this is similar to what Bryan Johnson does. Bloat and GI issues were considerably lessened, but then it makes me question whether it’s effective or not
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