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Manipulating mitochondrial dynamics

nad nad+ c60 mito fission fusion stearic acid mtdna methylene blue

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#721 Andey

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Posted 15 January 2018 - 06:14 PM

I got a lipid profile back, and this protocol seems to lower cholesterol. My total cholesterol went from 211 to 178, and LDL was reduced from 145 to 114 mg/dL (LDL calculated). HDL was unchanged at around 40.

 

That would seem to provide a bit of anecdotal evidence that niacinamide  + riboside is more effective than niacinamide by itself. I was taking 1.5 g nicotinamide and about twice that in riboside.

 

  Don't know where to start )   It actually doesn't mean something good happened. Before, you were in a  sweet spot for all-cause mortality, now you are a bit too low

http://vernerwheeloc...ause-mortality/

High cholesterol is a bad sign if you have high inflammatory markers, otherwise, I would better have it higher than lower. It's also highly dependent(inversely correlated) on fatty food intake in previous 3 days, this could explain new values.


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#722 Turnbuckle

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Posted 15 January 2018 - 06:42 PM

I got a lipid profile back, and this protocol seems to lower cholesterol. My total cholesterol went from 211 to 178, and LDL was reduced from 145 to 114 mg/dL (LDL calculated). HDL was unchanged at around 40.

 

That would seem to provide a bit of anecdotal evidence that niacinamide  + riboside is more effective than niacinamide by itself. I was taking 1.5 g nicotinamide and about twice that in riboside.

 

Not surprising. In high cholesterol mice given exogenous mitochondria, LDL cholesterol dropped dramatically with the number of injections. See Fig. 3E of this paper--

 

Mitotherapy for Fatty Liver by Intravenous Administration of Exogenous Mitochondria in Male Mice

 

Here we suggest that mitochondria isolated from hepatoma cells are used as a mitotherapy agent to treat mouse fatty liver induced by high-fat diets. When the mitochondria were intravenously injected into the mice, serum aminotransferase activity and cholesterol level decreased in a dose-dependent manner. Also, the mitotherapy reduced lipid accumulation and oxidation injury of the fatty liver mice, improved energy production, and consequently restored hepatocyte function. 

https://www.ncbi.nlm...les/PMC5422541/

 

 

 

And unless your mitochondria are in truly bad shape, it should not make any difference if you get an injection of new mitochondria, or clean up your own.



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#723 brosci

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Posted 16 January 2018 - 01:00 AM

I got a lipid profile back, and this protocol seems to lower cholesterol. My total cholesterol went from 211 to 178, and LDL was reduced from 145 to 114 mg/dL (LDL calculated). HDL was unchanged at around 40.

 

That would seem to provide a bit of anecdotal evidence that niacinamide  + riboside is more effective than niacinamide by itself. I was taking 1.5 g nicotinamide and about twice that in riboside.

 

I've read that B3 tends to raise glucose over the long haul and can decrease insulin sensitivity, is this not an issue with B3-Riboside?  If so, why not?


Edited by brosci, 16 January 2018 - 01:01 AM.

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#724 Turnbuckle

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Posted 16 January 2018 - 03:00 AM

 

I got a lipid profile back, and this protocol seems to lower cholesterol. My total cholesterol went from 211 to 178, and LDL was reduced from 145 to 114 mg/dL (LDL calculated). HDL was unchanged at around 40.

 

That would seem to provide a bit of anecdotal evidence that niacinamide  + riboside is more effective than niacinamide by itself. I was taking 1.5 g nicotinamide and about twice that in riboside.

 

I've read that B3 tends to raise glucose over the long haul and can decrease insulin sensitivity, is this not an issue with B3-Riboside?  If so, why not?

 

 

 

Dysfunctional mitochondria are associated with insulin resistance, thus improving mitochondria with this protocol is going in the right direction. See-- 

 

Skeletal Muscle Nucleo-Mitochondrial Crosstalk in Obesity and Type 2 Diabetes

Skeletal muscle mitochondrial dysfunction, evidenced by incomplete beta oxidation and accumulation of fatty acid intermediates in the form of long and medium chain acylcarnitines, may contribute to ectopic lipid deposition and insulin resistance during high fat diet (HFD)-induced obesity.

https://www.ncbi.nlm...les/PMC5412415/

 

 

 

In rodents, nicotinamide has been found to improve insulin resistance, and does this more than nicotinic acid--

 

 

Nicotinamide improves glucose metabolism and affects the hepatic NAD-sirtuin pathway in a rodent model of obesity and type 2 diabetes.

 

NAM 100 treatment affected glucose control significantly, as shown by lower levels of accumulative area under the curve during oral glucose tolerance test, serum fasting glucose, serum fasting insulin, and homeostasis model assessment of insulin resistance, and higher levels of serum adiponectin.

https://www.ncbi.nlm...pubmed/24314867

 


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#725 Moumou

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Posted 18 January 2018 - 06:54 AM

Turnbuckle, would you use Taurine in your setup? and more hypothetical question, trying a reduction of beta-Alanine blood concentration by overdosing Carnosine to improve mitochondrial metabolism?


Edited by Moumou, 18 January 2018 - 06:56 AM.


#726 Turnbuckle

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Posted 18 January 2018 - 09:40 AM

Turnbuckle, would you use Taurine in your setup? and more hypothetical question, trying a reduction of beta-Alanine blood concentration by overdosing Carnosine to improve mitochondrial metabolism?

 

 

No, I'm not using anything that improves mitochondrial metabolism in this protocol. The idea is to force mitochondria to perform on their own without outside help, and to kill those that don't measure up. Survival of the fittest. It's what your cells have been doing for decades without help, but now their quality control has gone awry, and you're going to have to help them out.


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#727 Nate-2004

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Posted 18 January 2018 - 01:51 PM

 

Turnbuckle, would you use Taurine in your setup? and more hypothetical question, trying a reduction of beta-Alanine blood concentration by overdosing Carnosine to improve mitochondrial metabolism?

 

 

No, I'm not using anything that improves mitochondrial metabolism in this protocol. The idea is to force mitochondria to perform on their own without outside help, and to kill those that don't measure up. Survival of the fittest. It's what your cells have been doing for decades without help, but now their quality control has gone awry, and you're going to have to help them out.

 

 

What if I have A/G alleles on the rs4880 SNP that results in naturally low levels of SOD2? Will that help or hurt?



#728 Turnbuckle

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Posted 18 January 2018 - 02:41 PM

 

 

Turnbuckle, would you use Taurine in your setup? and more hypothetical question, trying a reduction of beta-Alanine blood concentration by overdosing Carnosine to improve mitochondrial metabolism?

 

 

No, I'm not using anything that improves mitochondrial metabolism in this protocol. The idea is to force mitochondria to perform on their own without outside help, and to kill those that don't measure up. Survival of the fittest. It's what your cells have been doing for decades without help, but now their quality control has gone awry, and you're going to have to help them out.

 

 

What if I have A/G alleles on the rs4880 SNP that results in naturally low levels of SOD2? Will that help or hurt?

 

 

As that is a gene in the nuclear DNA, you can't eliminate it using this protocol, nor can you eliminate any mito deficiency that you were born with (short of a mito transplant). The best you can hope for is to restore your mtDNA to a more youthful state, and thus I'm suggesting that you avoid supplements that mitochondria could use as a crutch to avoid being detected as defective in the fissioned state. For instance, supplementing any of the intermediates or enzymes of the citric acid cycle could allow mitochondria with a deficiency in making that intermediate to escape recycling. And I suspect the long term supplementation of NAD precursors could produce such a dependency. 



#729 Nate-2004

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Posted 18 January 2018 - 03:21 PM

 

 

 

Turnbuckle, would you use Taurine in your setup? and more hypothetical question, trying a reduction of beta-Alanine blood concentration by overdosing Carnosine to improve mitochondrial metabolism?

 

 

No, I'm not using anything that improves mitochondrial metabolism in this protocol. The idea is to force mitochondria to perform on their own without outside help, and to kill those that don't measure up. Survival of the fittest. It's what your cells have been doing for decades without help, but now their quality control has gone awry, and you're going to have to help them out.

 

 

What if I have A/G alleles on the rs4880 SNP that results in naturally low levels of SOD2? Will that help or hurt?

 

 

As that is a gene in the nuclear DNA, you can't eliminate it using this protocol, nor can you eliminate any mito deficiency that you were born with (short of a mito transplant). The best you can hope for is to restore your mtDNA to a more youthful state, and thus I'm suggesting that you avoid supplements that mitochondria could use as a crutch to avoid being detected as defective in the fissioned state. For instance, supplementing any of the intermediates or enzymes of the citric acid cycle could allow mitochondria with a deficiency in making that intermediate to escape recycling. And I suspect the long term supplementation of NAD precursors could produce such a dependency. 

 

 

That makes sense, not sure if PQQ is one of those? It helps with SOD2 scavenging.

 

As for NAD precursors, I've my doubts there's any dependency since most of what NAD+ depends on comes exogenously from niacin and tryptophan. Supplying it with closer upstream precursors shouldn't make it anymore dependent since the process in the cycle where B3 and Tryp finally make it to becoming NAM (or NAM directly), it's all coming from diet anyway. Isn't it by nature, dependent? 



#730 Turnbuckle

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Posted 18 January 2018 - 03:39 PM

 

 

 

That makes sense, not sure if PQQ is one of those? It helps with SOD2 scavenging.

 

As for NAD precursors, I've my doubts there's any dependency since most of what NAD+ depends on comes exogenously from niacin and tryptophan. Supplying it with closer upstream precursors shouldn't make it anymore dependent since the process in the cycle where B3 and Tryp finally make it to becoming NAM (or NAM directly), it's all coming from diet anyway. Isn't it by nature, dependent? 

 

 

I've previously included PQQ during fusion. During fusion you can take all sorts of things as long as it doesn't promote fission. As for your doubts about dependency, you've noted yourself that HPN recommends taking a 3 day break between bottles of NR. You might ask them why.


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#731 Nate-2004

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Posted 18 January 2018 - 04:42 PM

 

 

 

 

That makes sense, not sure if PQQ is one of those? It helps with SOD2 scavenging.

 

As for NAD precursors, I've my doubts there's any dependency since most of what NAD+ depends on comes exogenously from niacin and tryptophan. Supplying it with closer upstream precursors shouldn't make it anymore dependent since the process in the cycle where B3 and Tryp finally make it to becoming NAM (or NAM directly), it's all coming from diet anyway. Isn't it by nature, dependent? 

 

 

I've previously included PQQ during fusion. During fusion you can take all sorts of things as long as it doesn't promote fission. As for your doubts about dependency, you've noted yourself that HPN recommends taking a 3 day break between bottles of NR. You might ask them why.

 

 

Interesting, they do. I don't take NR or NAM+R every day, just on "fission days".



#732 Moumou

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Posted 18 January 2018 - 08:55 PM

When you say survival of the fittest, you mean you choose marathonian style, efficency over efficacity - same energy with less ressources, mimicking old age mito respiration to train them.

 

Activities like freediving could improve it (i do it myself - 3min 15s is my best underwater). Or high altitudes runs. Improving deoxygenated myoglobin delay & rieske protein overall potency.

 

And "Maybe" we can train mitochondrias when asleep, because our Brain is consuming less "energy", then it would improve day to day training of Braincells mitos.

 

Also, using metabolism enhancers with pre-Selected mitochondiras would be a good crutch for the old age, adding life quality to longer life span, No?

 

 

Talking of Mito Natrual Selection : http://jeb.biologist...3719.full.pdf  

                                              https://www.ncbi.nlm...les/PMC4490732/

 

Would interest you : https://www.ncbi.nlm...les/PMC3783979/


Edited by Moumou, 18 January 2018 - 09:04 PM.


#733 Turnbuckle

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Posted 18 January 2018 - 09:51 PM

When you say survival of the fittest, you mean you choose marathonian style, efficency over efficacity - same energy with less ressources, mimicking old age mito respiration to train them.

 

 

 

I mean killing mitochondria that exhibit no membrane potential when fissioned to one loop of DNA. This is the way the body does it, which this protocol takes to the extreme. See my post #218.


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#734 Nate-2004

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Posted 18 January 2018 - 10:30 PM

Back to apigenin, I found another source that says parsley has 45mg per gram, this has to be wrong. That's an enormous amount for so little parsley. Worth just adding these to a smoothie, way cheaper and more certain than Swanson's bad rep for label inaccuracy and food sources may have better absorption.


Edited by Nate-2004, 18 January 2018 - 10:31 PM.


#735 Turnbuckle

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Posted 18 January 2018 - 10:48 PM

Back to apigenin, I found another source that says parsley has 45mg per gram, this has to be wrong. That's an enormous amount for so little parsley. Worth just adding these to a smoothie, way cheaper and more certain than Swanson's bad rep for label inaccuracy and food sources may have better absorption.

 

 

Very unlikely--

 

Bioavailability of Apigenin from Apiin-Rich Parsley in Humans 
The apigenin content in parsley was 11.89 mg/100 g edible portion. 
PMID: 16407641

 

 



#736 Nate-2004

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Posted Yesterday, 12:05 AM

What if I ate it with some fats? Avocado? Nuts? Flax? That study doesn't mention it.



#737 Turnbuckle

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Posted Yesterday, 03:36 AM

Why don't you buy apigenin in caps? It isn't expensive.



#738 Moumou

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Posted Yesterday, 06:04 AM

So, its two stage protocol. First pruning then regrowth of mitos. How long and how many times for a first stage do you think it should goes on?


Edited by Moumou, Yesterday, 06:05 AM.


#739 Nate-2004

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Posted Yesterday, 01:18 PM

Why don't you buy apigenin in caps? It isn't expensive.

 

Because it's only available from a single company I don't trust. In caps it also may be even less bioavailable than what you posted above for just parsley. I trust it's in parsley and parsley is cheap. It has a low lipid and low water solubility which explains why it's so difficult to absorb.


Edited by Nate-2004, Yesterday, 01:27 PM.


#740 Turnbuckle

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Posted Yesterday, 01:37 PM

So, its two stage protocol. First pruning then regrowth of mitos. How long and how many times for a first stage do you think it should goes on?

 

Judging by your profile picture, a year. ;)

 

I did various versions of the protocol for more than six months, but I'm approaching 70 and had a lot of defective mitochondria. At first I had rather dramatic effects, but these gradually tapered off as (presumably) defective mitochondria were recycled and replaced. If you are older or otherwise suspect you have a problem, start off slow. Some cells may have only a few good mtDNA loops, and tendons don't have many mitochondria to begin with.



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#741 Moumou

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Posted Today, 12:02 AM

I am on my 30's and btw not really looking like Professor Farnsworth xD - in fact i am in real good shape for my age, many people think i am on my early 20's...

 

I am looking to improve my own protocol, some sort of hypoxia training, which involve fasting/diving phases and rest/rejuvenation phases, really close to your own protocol. Except, I am searching to train my mitos to pursue their cycles on harsh environements, not willing to kill them directly, but instead hoping to reactivate for most of them their epigenetical inheritage... I think it might kill most of those who can't survive the harsh phases.

 

I do it twice a year, march for phase 1 / april phase 2 - september p1/ october p2. Adding that p2 is also an attempt to clean lysosomal residues from cells mostly chelation and mito metabolics enhancements with NR, spermine, pqq, etc...

 







Also tagged with one or more of these keywords: nad, nad+, c60, mito, fission, fusion, stearic acid, mtdna, methylene blue

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