35 replies to this topic

[Ukko]

I would rather call out broader themes. Not fully sure on how to act on them ideally:

 

1) The NAD+/NADH Ratio: everything around NR, Niacin, NAMPT, the CLOCK gene, CD38 etc.

 

2) Ergothioneine: amazing that there is a transport system in our bodies for this mushroom super anti oxidant, which neither animals nor plants even produce.

 

3) The importance of the gut microbiome: prebiotics, short chain fatty acid synthesis, vagus nerve, the gut as a source of neurotransmitters etc.

 

4) Autophagy, senolytics, (intermittent) fasting

 

And, yes, I find those things around glucosamine and lithium to be pretty amazing as well.

 

Ukko

 

Edited by Ukko, 17 January 2019 - 06:48 PM.

[Guest]

I get your experiment. The studies are promising but far from RCT (I glanced at them). I'm surprised if there's nothing else out there that's shown similar correlations in similar types of studies


the results seem too good to be true. basically they found some people who claimed to take glucosamine then followed up years later. what are the odds that those people kept taking glucosamine that whole time? Isn't it likely that they were just more active and it's a spurious correlation? Just thinking out loud - I didn't read in detail

why would tumor suppressor genes be naturally downregulated?

 

 

to not clutter this thread I made a considerably more extended write up and analysus about the current evidence about glucosamine as a separate thread:

 

https://www.longecit...vention-thread/

 

 

I still find it a fascinating evidence, considering that in prospective cohort studies in healthy humans it basically behaves like metformin/rapamacyn (and supposedly resveratrol) are theorized to deliver results (and activating much of the same genes)

[smithx]

This is interesting to me, because I've been taking at least 12g of n-acetyl glucosamine a day since 2010 (because it suppresses an auto-immune condition).

 

I wonder if there's any data on whether this plus rapamycin (+ metformin, + NMN, etc.) is synergistic or antagonistic.

 

to not clutter this thread I made a considerably more extended write up and analysus about the current evidence about glucosamine as a separate thread:

 

https://www.longecit...vention-thread/

 

 

I still find it a fascinating evidence, considering that in prospective cohort studies in healthy humans it basically behaves like metformin/rapamacyn (and supposedly resveratrol) are theorized to deliver results (and activating much of the same genes)

 

[smithx]

Actually I think that n-acetyl glucosamine is one of the biggest revelations (although it's a bit more than 5 years) since it treats auto-immune conditions ranging from multiple sclerosis to rheumatoid arthritis to crohn's disease.

 

 

[Francesco Calderone]

I stopped taking MitoQ after seeing this study:

 

The targeted anti‐oxidant MitoQ causes mitochondrial swelling and depolarization in kidney tissue

https://www.ncbi.nlm...les/PMC5880956/

 

What are your thoughts about it?

 

I sent the report ncbi.nhi to Mitoq to have their rating and this is their response mail: from Customer Service (mitoQ):

 

"Hi Francesco

Thanks for your concern regarding the recent kidney paper.

We can confidently assure you that this paper is not relevant for those taking MitoQ. This research was done in a test tube and at concentrations much higher than would ever occur in the body. MitoQ has been extensively evaluated for safety and is currently being evaluated in a clinical trial to assist with kidney health at Delaware University

Please find below a list of studies which show that MitoQ is protective in kidneys:

1. Mitochondria-targeted antioxidant MitoQ reduced renal damage caused by ischemia-reperfusion injury in rodent kidneys: Longitudinal observations of T2 -weighted imaging and dynamic contrast-enhanced MRI. Liu X et al. Magn Reson Med. 2018 Mar;79(3):1559-1567. DOI: 10.1002/mrm.26772

2. Reactive oxygen species promote tubular injury in diabetic nephropathy: The role of the mitochondrial ROS-TXNIP-NLRP3 biological axis. Han Y et al. Redox Biol. 2018 Feb 15;16: 32-46. DOI: 10.1016/j.redox.2018.02.013

3. Mitochondrial abnormality facilitates cyst formation in autosomal dominant polycystic kidney disease. Ishimoto Y et al. Mol. Cell. Biol. 2017 Dec. 37: 24 e00337-17. DOI: 10.1128/MCB.00337-1

4. The mitochondria-targeted antioxidant MitoQ ameliorated tubular injury mediated by mitophagy in diabetic kidney disease via Nrf2/PINK1. Xiao L et al. Redox Biol. 2017 Apr; 11: 297–311. DOI: 10.1016/j.redox.2016.12.022

5. Targeted mitochondrial therapy using MitoQ shows equivalent renoprotection to angiotensin converting enzyme inhibition but no combined synergy in diabetes. Ward MS et al. Scientific Reports 2017. 7: 15190. DOI: 10.1038/s41598-017-15589-x

6. The swan-neck lesion: proximal tubular adaptation to oxidative stress in nephropathic cystinosis. Galaretta CI et al. Am J Physiol Renal Physiol. 2015 May 15;308(10): F1155-66. DOI: 10.1152/ajprenal.00591.2014

7. Protection against renal ischemia–reperfusion injury in vivo by the mitochondria targeted antioxidant MitoQ. Dare AJ et al. Redox Biol. 2015 Aug; 5: 163–168. DOI: 10.1016/j.redox.2015.04.008

8. Contribution of mitochondrial function to exercise-induced attenuation of renal dysfunction in spontaneously hypertensive rats. Gu Q et al. Mol Cell Biochem. 2015 Aug;406(1-2):217-25. DOI: 10.1007/s11010-015-2439-6

9. Peroxynitrite induced mitochondrial biogenesis following MnSOD knockdown in normal rat kidney (NRK) cells. Marine A et al. Redox Biol. 2014; 2: 348–357. DOI: 10.1016/j.redox.2014.01.014

10. Preclinical evaluation of the mitochondria-targeted antioxidant mitoquinone to treat sepsis-induced acute kidney injury. Patil NK et al. FASEB J. 2013 27:1_supplement, 889.8-889.8 (LINK)

11. Prevention of diabetic nephropathy in Ins2+/−AkitaJ mice by the mitochondria-targeted therapy MitoQ. Chacko BK et al. Biochem J. 2010 Nov 15; 432(Pt 1): 9–19. DOI: 10.1042/BJ20100308

I hope this clarifies things for you and if there is anything further I can help with, please be sure to let me know.

Wishing you all good things

Ella"

[smithx]

Actually I think that n-acetyl glucosamine is one of the biggest revelations (although it's a bit more than 5 years) since it treats auto-immune conditions ranging from multiple sclerosis to rheumatoid arthritis to crohn's disease.

 

Someone marked this as "needs references". The references are not hard to find, but here are a few anyway:

 

Initial study about NAG and Crohn's disease:

https://www.ncbi.nlm...pubmed/11121904

 

UC Irvine news release that got me interested:

https://news.uci.edu...ype-1-diabetes/

 

Summary of the research:

https://www.faculty....faculty_id=5788

 

Study which indicated that my diagnosed Guillain-Barré syndrome is associated with NAG issues:

https://www.ncbi.nlm...cles/PMC186479/

My symptoms are kept in check (completely gone) with about 14G of NAG per day and start to return if I decrease the dosage

 

Current clinical trial:

http://www.ucihealth...etylglucosamine