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Low Oxygen Reverses Mitochondrial Disease in Mice

hypoxia brain damage mitochondrial dysfunction

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#1 alc

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Posted 08 May 2017 - 10:39 PM


"Low Oxygen Reverses Mitochondrial Disease in Mice"

 

http://www.hhmi.org/...al-disease-mice


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#2 Ark

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Posted 09 May 2017 - 05:35 PM

I remember watching a interview with Michael J. Fox and he talked about recovering from his Parkinson's somewhat of a remission when staying in a monastery high up in the mountains for months. I wonder if this process they discovered had anything to do with it?

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#3 alc

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Posted 10 May 2017 - 02:47 AM

I remember watching a interview with Michael J. Fox and he talked about recovering from his Parkinson's somewhat of a remission when staying in a monastery high up in the mountains for months. I wonder if this process they discovered had anything to do with it?

 

I sure hope that would be the case, but we don't know until serious studies are done.

Of course anecdotal reports are encouraging, but we need controlled studies.

On the other hand if that was the case, we do not see monks that live at that altitude reversing some aspects of aging or have organs regenerated.

So there should be a more subtle connection between low oxygen and regeneration (like the case for GDF-11).

For some years I'm keeping an eye on Histogen, as they have proprietary technology that mimics low oxygen environment (3-5%):

 

http://www.histogeni.../technology.htm



#4 tunt01

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Posted 10 May 2017 - 07:30 PM

Probably can get a similar mechanistic pathway via Noopept, which has been shown to induce HIF-1a.

 



#5 xEva

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Posted 10 May 2017 - 07:42 PM

I think this effect is seen in traditional eastern meditation, when one learns to breathe long deep and smoothly. A breathing cycle can slow down to 1-2 breaths a minute even for a novice. After some time of practice, it is usual to see some improvement in all parameters of health. Could be this -? 



#6 Turnbuckle

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Posted 10 May 2017 - 09:24 PM

If this hypoxic effect is driven by mito fission, then the same thing ought to be achieved by dosing with NR (or nicotinamide + ribose, or nicotinamide alone), which also drives mito fission by increasing the NAD+/NADH ratio--

 

Mitochondria need to be fragmented prior to engulfment by phagophores, the precursors to autophagosomes. However, how these 2 processes are finely regulated and integrated is poorly understood. We have shown that the outer mitochondrial membrane protein FUNDC1 is a novel mitochondrial-associated membrane (MAM) protein, enriched at the MAM by interacting with the ER resident protein CANX (calnexin) under hypoxia. As mitophagy proceeds, it dissociates from CANX and preferably recruits DNM1L/DRP1 to drive mitochondrial fission in response to hypoxic stress.

 

https://www.ncbi.nlm...pubmed/27314574

 

 

and

 

we found that exposure of cells to nicotinamide causes a decrease in mitochondrial content and an increase in mitochondrial membrane potential (MMP) by activating autophagy and inducing mitochondrial fragmentation. Here, we present evidence to show that the effect of nicotinamide is mediated through an increase of the [NAD+]/[NADH] ratio 

 

https://www.ncbi.nlm...les/PMC3365962/

 

 


Edited by Turnbuckle, 10 May 2017 - 09:36 PM.

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#7 aconita

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Posted 10 May 2017 - 11:03 PM

The study reports that only at 11% oxygen the results becomes evident (we are talking about rats, of course), 11% equals to what you'll get at slightly above 5000mt altitude, not many humans are inhabiting those altitudes and I suspect the few whom does so aren't living a very healthy life because of the extremes of conditions (climate, food, health care, etc...).

 

La Rinconada, Peru, is a 50,000 inhabitants town just at the perfect altitude for 11% oxygen, the highest permanent human settlement in the world, unfortunately is a gold mine heavily polluted with mercury where everybody works in very miserable conditions therefore not health wise very significant.

 

We don't know if continuous or intermittent exposition to hypoxic conditions are best, some hypoxic athletic training protocols involve intermittent exposure, since it is possible that the athletic performance enhancement achieved by such protocols is at least partially due to mitochondrial rejuvenation (as that seen in the mentioned study) maybe whom undergoes such training protocols are better candidates for further research in this direction.

 

It is actually quite exciting since an hypoxic apparatus comes new at about 2000$ which isn't that much when compared with supplements considering it will last a lifetime.

 

https://www.higherpe...tudechart.html      



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#8 SearchHorizon

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Posted 06 June 2017 - 07:28 AM

SIRT1 and NAD research has already shown that adaptive mechanism behind longevity works through HIF1 (hypoxia inducible factor 1). This tells you that low-oxygen condition is a stress - which also means that constant oxygen deprivation should be very bad for the mice. 

 

 


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