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Manipulating mitochondrial dynamics

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

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#151 Turnbuckle

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Posted 21 June 2017 - 01:22 PM

 

But mutations are only half the problem, and assuming the trial I did a couple of days ago continues to look good over the next week or so, I may have a protocol that addresses the rest of it. 

 

 

If mutations are only half the problem, what is the other half?

 

 

 

Methylation, an epigenetic process that represses the activity of genes. Few studies have been done so far on mitochondria, but correlations have been found between methylation of mtDNA and CVD--

 

We measured platelet mtDNA methylation in healthy individuals and patients with CVD...Mean MT-CO1 DNA methylation was 4.45% ... in healthy individuals and 22.97% ... in CVD patients.

All ten CVD patients had hypertension ... Patients were selected upon the basis of diagnosis with hypertension and/or atherosclerosis, as these are the most common causes of CVD..

https://www.ncbi.nlm...les/PMC4404685/

 

 

 

Which is the cause and which is the effect is open to question, but note that all the CVD patients had hypertension, and that's what my latest experiment was directed to. While this modified atomic protocol brought my systolic press down to 120 without medication, it could very well be a temporary effect. And I'll be surprised if it isn't, as I wouldn't expect it to work after only one cycle.


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#152 Andey

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Posted 21 June 2017 - 01:41 PM

I tried the Atomic Protocol, as described here and felt nearly nothing. Given the way this protocol has affected others, this lack of response lends support to that large doses of NR for 6 days invokes mitophagy. My 5 rounds of this protocol described here and ending here was very likely effective.

 

 I had same results yesterday actually. Felt a bit strange for few hours but it resolve itself before noon.

I cant say my experience is representative though as

   1. I am quite a coach potato lately, and my excercize routine was pullups, pushups, crunches and running stairs. I am not sure if Ive stressed my body enough.

   2. I ve practiced intermittent NR (250mg QD) and fast mimicking diet

   3. I eat a lot of chocolate (like 2 pounds a week) and it could also influence mitochondria population

It was just a first glimpse day after my niacinamide and ribose have arrived, I will practice it more


Edited by Andey, 21 June 2017 - 01:43 PM.


#153 Fafner55

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Posted 21 June 2017 - 01:46 PM

 

 

But mutations are only half the problem, and assuming the trial I did a couple of days ago continues to look good over the next week or so, I may have a protocol that addresses the rest of it. 

 

 

If mutations are only half the problem, what is the other half?

 

 

 

Methylation, an epigenetic process that represses the activity of genes. Few studies have been done so far on mitochondria, but correlations have been found between methylation of mtDNA and CVD--

 

We measured platelet mtDNA methylation in healthy individuals and patients with CVD...Mean MT-CO1 DNA methylation was 4.45% ... in healthy individuals and 22.97% ... in CVD patients.

All ten CVD patients had hypertension ... Patients were selected upon the basis of diagnosis with hypertension and/or atherosclerosis, as these are the most common causes of CVD..

https://www.ncbi.nlm...les/PMC4404685/

 

 

 

This tread is becoming very interesting. Thanks for the insight.


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#154 StanG

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Posted 21 June 2017 - 05:36 PM

I now take stearic acid once a week and NR twice daily for three nonconsecutive days a week. I took the stearic yesterday when I do my weekly 36 hour semi fast where I only eat 500 calories in that period. When I went to the gym this morning, I didn't realize how fast I was going and round up burning 337 calories in 28 minutes on the  elliptical machine. My third highest total and I didn't overly exert myself doing it. Since I take 80 supplements on supplement days it's hard to tell what does what anymore but I really think the stearic is a contributing factor. 

 

At 74 years of age, it's great to feel I'm helping myself achieve a longer healthspan!

 

Thanks for your help.


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#155 hsibai

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Posted 21 June 2017 - 07:26 PM

Today was my third (and last) day of this procedure. On each of the three days, I took 2g of N and 4.5g of R in the morning followed by 3-4 g of Lysine and 750 mg TMG.

First day workout was easy but I stuck to 50% of my normal weights. I was able to do one hour of weights at the end of which there was a slight onset of dizziness which I took as a sign to stop. During the workout, my heart rate was in the Aerobic range according to Garmin 121-136.

On the second day, I did weights for about 45 minutes and I was struggling to work hard but just could not push my heart rate above 100. Just did not have the energy.

On the third day, I skipped the gym and did some walking. I had a big lunch and a three course dinner and by 10 pm as I was getting ready for bed, I realized that I have a headache (back of my head above my neck). I suspected this could be caused by low blood pressure so I measured it and sure enough it was 105/65 (measured it twice). This is quite strange and hard to explain as I have measured it earlier in the afternoon and it was closer to my normal reading of 140/83.

The evening stack has Glycine, K, D, PQQ, Broccomax, Taurine, Ginko Biloba, Bacopa and 35g of 85% dark chocolate. Hope it is synergistic with this protocol.






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#156 Fafner55

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Posted 21 June 2017 - 07:39 PM

mtDNA methylation is correlated with age.

 

"Quantification of global mitochondrial DNA methylation levels and inverse correlation with age at two CpG sites" (2016) https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4925819/



#157 stephen_b

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Posted 21 June 2017 - 09:54 PM

From https://www.ncbi.nlm...es/PMC4568926/: "Astaxanthin demonstrated pro-apoptotic function in myofibroblasts by contributing to mitochondrial fission..."

Something to consider for fission days?

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#158 Turnbuckle

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Posted 21 June 2017 - 09:57 PM

mtDNA methylation is correlated with age.

 

"Quantification of global mitochondrial DNA methylation levels and inverse correlation with age at two CpG sites" (2016) https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4925819/

 

Yes, I've seen that paper. But there's not nearly enough data to justify their curve fitting. And it's not clear to me that they controlled for haplogroups.

 

On a larger scale, mutations in mtDNA can be used to help group cohorts or ‘haplogroups’. Throughout evolution, mutations in mtDNA may be conserved and passed on through maternal inheritance, thus allowing for the tracing of common ancestral lineage by comparing haplogroups. Numerous studies have identified both contributory and protective effects of different haplogroups in AD. For example, haplogroup K reduces the risk of developing sporadic AD in apolipoprotein ε4 (APOε4) carriers in an Italian population [80] but not in the Polish population [81]. This presents an additional potential caveat in mitochondrial epigenetics, as mitochondrial haplogroups have been found to affect global levels of DNA methylation [60]. As such, extra care should be taken to account for haplogroup variability in AD mitochondrial epigenetic studies.

 

https://www.ncbi.nlm...les/PMC4329914/

 

 


Edited by Turnbuckle, 21 June 2017 - 10:15 PM.

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#159 Turnbuckle

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Posted 21 June 2017 - 11:26 PM

Since exercise is seen as enhancing longevity and health-span, one should ask what is happening to mitochondria due to exercise. Do they gain methylation or lose it? You'd expect they would lose it, and they do, at least with the obese subjects studied in this paper--

 

Changes in DNA Methylation
 
Both resistance and endurance exercise training induced hypomethylation. ... Together these data suggest that endurance and resistant training induce epigenetic changes in different molecular pathways.
 

 

 

Fig. 2 gives a dramatic picture of what happens to mito methylation with exercise.

 

And another paper on healthy but sedentary men--

 

Acute Exercise Remodels Promoter Methylation in Human Skeletal Muscle

 

DNA methylation is a covalent biochemical modification controlling chromatin structure and gene expression. Exercise elicits gene expression changes that trigger structural and metabolic adaptations in skeletal muscle. We determined whether DNA methylation plays a role in exercise-induced gene expression. Whole genome methylation was decreased in skeletal muscle biopsies obtained from healthy sedentary men and women after acute exercise...Collectively, our results provide evidence that acute gene activation is associated with a dynamic change in DNA methylation in skeletal muscle and suggest that DNA hypomethylation is an early event in contraction-induced gene activation.

 

http://www.cell.com/...58?showall=true

 

 


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#160 stephen_b

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Posted 23 June 2017 - 02:20 PM

From PMID 27521081:

 

 

curcumin enhanced mitochondrial fusion activity and reduced fission machinery

 


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#161 zorba990

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Posted 24 June 2017 - 03:45 AM

Since exercise is seen as enhancing longevity and health-span, one should ask what is happening to mitochondria due to exercise. Do they gain methylation or lose it? You'd expect they would lose it, and they do, at least with the obese subjects studied in this paper--

Changes in DNA Methylation

Both resistance and endurance exercise training induced hypomethylation. ... Together these data suggest that endurance and resistant training induce epigenetic changes in different molecular pathways.

https://www.ncbi.nlm...les/PMC4200377/

Fig. 2 gives a dramatic picture of what happens to mito methylation with exercise.

And another paper on healthy but sedentary men--

Acute Exercise Remodels Promoter Methylation in Human Skeletal Muscle

DNA methylation is a covalent biochemical modification controlling chromatin structure and gene expression. Exercise elicits gene expression changes that trigger structural and metabolic adaptations in skeletal muscle. We determined whether DNA methylation plays a role in exercise-induced gene expression. Whole genome methylation was decreased in skeletal muscle biopsies obtained from healthy sedentary men and women after acute exercise...Collectively, our results provide evidence that acute gene activation is associated with a dynamic change in DNA methylation in skeletal muscle and suggest that DNA hypomethylation is an early event in contraction-induced gene activation.

http://www.cell.com/...58?showall=true

Here's an interesting article on epigenetics, methylation, and exercise.

http://www.bodybuild...epigentics.html

One excerpt:
"Your Natural Methylation Brigade

As stated earlier, scientists like Dr. Cooney have discovered that several natural supplements have the ability to enhance the methylation process, keeping you juiced at the cellular, genetic and metabolic level, where anabolic action or drive starts and is maintained. The synopsis that follows will give you a brief overview of some of the dynamic methylating agents that will keep your anabolic processes working overtime. You may also be surprised to find out that these aren’t your household power names like beta-alanine, ribose, nitric oxide, glutamine, whey, HMB or carnitine to name a few. However, based on what we have learned here they are the spark that ignites, maintains, protects and rejuvenates metabolic pathways, atoms, genes and not only virtually all of your body’s internal anabolic activities, but life’s processes. The synopsis that follows outlines some key methylation agents:

1.Dimenthyglycine (DMG) – DMG is a methylated amino acid found in all cells. It serves as a methyl donor and also acts as a powerful antioxidant. While this amino acid enhances immunity, it is best known for its ability to increase energy levels. Studies indicate that DMG has the ability to increase stamina by 40% by its ability to oxygenate cells and reducing the production of lactic acid, which causes muscle fatigue.

2.Inositol – In cases of under methylation researchers utilize this B-vitamin due to the fact it is one of the primary secondary messengers responsible for stabilizing over excitable neurotransmission signals between brain cells. This action will keep you on an even keel and mentally focused reducing anxiety and improving sleep.

3.SAME – SAME is one of the body’s primary methyl donating agents in the body. It is responsible for initiating one of the body’s most dominant methylation cascade of reactions, in which the amino acid methionine is used to methylate proteins and DNA. However, a by-product of methionine breakdown is homocysteine that has been linked to heart disease. SAME is responsible for methylating homocysteine so that it can be converted back to methionine. Methionine assists in the breakdown of fats, acts as an antioxidant and is involved with the proper metabolism of the amino acids L-cysteine, gluthione and taurine. It also helps the body manufacture glucose and glycogen to fuel tired muscles and also assists in the synthesis of creatine, epinephrine and melatonin, all powerful anabolic compounds.

4.Tri_Methyl-Glycine (TMG) – TMG, also known as betaine, is metabolized into DMG during the synthesis of methionine from homocysteine. It is considered to be one of the most effective known methylation agents. It regenerates SAME production, and like SAME has powerful anti-depressant properties. Studies have shown that it can also decrease fat production. Researchers contend that human subjects have experienced a loss of 5 pounds of fat while gaining as much as 12 pounds of muscle at dose ranges of 500-2,000 mg/d. TMG also elevates glutathione one of the body’s most powerful antioxidants and liver detoxifying agents. TMG also improves mood, sleep patterns and increases stamina, as well as being intimately involved in methylation processes that keep homocysteine in balance.

5. Methylated With B-12
Vitamin B-12 is known as the red vitamin and is critical to proper energy production, immune function, the formation of red blood cells and the proper utilization of iron. It is also needed for proper digestion, food absorption, carbohydrate and fat metabolism. Based on the above attributes it appears that vitamin B-12 may be one vitamin that serves as a co-enzyme that jump-starts and regulates many anabolic processes.

Well, for all intents and purposes it is involved in over 100 enzymatic reactions, which also includes protein metabolism and its proper synthesis. As you know, protein metabolism is a term used to denote the bio-chemical processes the body uses to breakdown proteins into amino acids. This is referred to proteolysis. There is also emerging time data that shows that vitamin B-12 when methylated has a direct impact on muscle hypertrophy (the increase in size of muscle cells) via its metabolic amplifying effect on protein and amino acid synthesis."

Edited by zorba990, 24 June 2017 - 04:35 AM.

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#162 hsibai

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Posted 24 June 2017 - 11:03 AM



[quote name="Turnbuckle" post="819421" timestamp="1498087606"]Since exercise is seen as enhancing longevity and health-span, one should ask what is happening to mitochondria due to exercise. Do they gain methylation or lose it? You'd expect they would lose it, and they do, at least with the obese subjects studied in this paper--

[quote]
Changes in DNA Methylation

Both resistance and endurance exercise training induced hypomethylation. ... Together these data suggest that endurance and resistant training induce epigenetic changes in different molecular pathways.
The synopsis that follows outlines some key methylation agents:

1.Dimenthyglycine (DMG)
2.Inositol
3.SAME
4.Tri_Methyl-Glycine (TMG)
5. Methylated With B-12


Any significance to the order of listing such as effictiveness/efficiency?

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#163 Turnbuckle

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Posted 24 June 2017 - 11:15 AM

There's no question that methylation is important in many processes, and in nDNA is essential in keeping cells differentiated. But while methylation of nDNA serves to select between one of 200 cell types, methylation of mtDNA is likely no more than a volume knob. If you have a need for muscles, for example, ATP production is turned up by demethylation, and if you don't, it goes the other way. That way energy is conserved and the food requirement reduced.


Edited by Turnbuckle, 24 June 2017 - 11:41 AM.

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#164 zorba990

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Posted 24 June 2017 - 03:18 PM

There's no question that methylation is important in many processes, and in nDNA is essential in keeping cells differentiated. But while methylation of nDNA serves to select between one of 200 cell types, methylation of mtDNA is likely no more than a volume knob. If you have a need for muscles, for example, ATP production is turned up by demethylation, and if you don't, it goes the other way. That way energy is conserved and the food requirement reduced.


I'm not understanding that. Are you saying we need to enhance demethylation during exercise and enhance repleting it on fusion days only? (This would remove tmg from the atomic protocol but add what?). I'm seeing some articles about HDAC and mitochondrial epigenetics, like this with sodium butyrate, http://onlinelibrary.../bph.13058/full but not sure on the timing of using it - it seems to affect acetylation of lysine by remiving acetyl groups, not sure it has any effect on methylation directly

"Sodium butyrate epigenetically modulates high-fat diet-induced skeletal muscle mitochondrial adaptation, obesity and insulin resistance through nucleosome positioning
NaB prevented HF diet-induced increases in body weight and adiposity without altering food intake or energy expenditure, improved insulin sensitivity as measured by glucose and insulin tolerance tests, and decreased respiratory exchange ratio. In skeletal muscle, NaB increased the percentage of type 1 fibres, improved acylcarnitine profiles as measured by metabolomics and produced a chromatin structure, determined by MNase-seq, similar to that seen in LF. Targeted analysis of representative nuclear-encoded mitochondrial genes showed specific repositioning of the −1 nucleosome in association with altered gene expression."

#165 Turnbuckle

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Posted 24 June 2017 - 03:52 PM

I'm not understanding that. Are you saying we need to enhance demethylation during exercise and enhance repleting it on fusion days only? 

 

 

I'm not saying anything of the sort. 


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#166 Shai Hulud

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Posted 24 June 2017 - 03:58 PM

 

 

But mutations are only half the problem, and assuming the trial I did a couple of days ago continues to look good over the next week or so, I may have a protocol that addresses the rest of it. 

 

 

If mutations are only half the problem, what is the other half?

 

 

 

Methylation, an epigenetic process that represses the activity of genes. Few studies have been done so far on mitochondria, but correlations have been found between methylation of mtDNA and CVD--

 

 

 

 

If regular exercising solves that problem (high/hyper methylation of mtDNA), which I recall you are already doing, where do you see further room for improvement?

Training neglected parts of the body?



#167 Andey

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Posted 24 June 2017 - 06:57 PM

 


I'm not understanding that. 

 

 

  If I understand Turnbuckle correctly he means thats its a known fact that methylation profile of DNA and mtDNA changes with age. I believe its the marker David Sinclair have used to measure the effect from NMN. You could read here about it https://genomebiolog...017-1245-8#CR13, or google 'intrinsic epigenetic age acceleration'. And while cell DNA methylation profile is very complex and we not in a position to influence it effectively, the mtDNA methylation should be quite simple and could be treated as a power knob.



#168 Shai Hulud

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Posted 24 June 2017 - 07:05 PM

Yes, but while you can reverse it partly, is there a way to completely reverse age-related methylation?

#169 Andey

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Posted 24 June 2017 - 07:20 PM

Yes, but while you can reverse it partly, is there a way to completely reverse age-related methylation?

 $1000000 question ) It remains to be seen.

I havent read papers but from a common sense perspective exercise should not be equivalent to returning methylation profile to a younger age. Even more, in this paper http://www.aging-us....cle/101168/text exercise only influence immune system age but not IEAA (cell age). Its kinda mind boggling though.


Edited by Andey, 24 June 2017 - 07:30 PM.

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#170 stephen_b

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Posted 24 June 2017 - 08:05 PM

It appears that fission events sometimes result in mitochondria with high membrane potential (desired) and sometimes with low membrane potential (undesired). Those with higher membrane potential are more likely to undergo subsequent fusion, according to the link.

 

Astaxanthin seems to increase membrane potential, at least in some tissue types.


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#171 Fafner55

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Posted 24 June 2017 - 08:50 PM

Nature has provided an example of aging without sarcopenia. Naked mole rats show little sign of mitochondrial DNA deletions and maintain Complex IV respiration.

 

"Naked mole-rats maintain healthy skeletal muscle and Complex IV mitochondrial enzyme function into old age" (2016) http://www.aging-us....le/101140/text 



#172 Turnbuckle

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Posted 24 June 2017 - 09:40 PM

Nature has provided an example of aging without sarcopenia. Naked mole rats show little sign of mitochondrial DNA deletions and maintain Complex IV respiration.

 

"Naked mole-rats maintain healthy skeletal muscle and Complex IV mitochondrial enzyme function into old age" (2016) http://www.aging-us....le/101140/text 

 

 

You paper also says, "Meanwhile Complex I expression is significantly lower in aged animals, perhaps due to their high levels of oxidative stress."  According to Wikipedia, Complex I is one of the main sites at which premature electron leakage to oxygen occurs, thus being one of the main sites of production of superoxide.


Edited by Turnbuckle, 24 June 2017 - 09:43 PM.

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#173 Fafner55

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Posted 24 June 2017 - 09:52 PM

 

Nature has provided an example of aging without sarcopenia. Naked mole rats show little sign of mitochondrial DNA deletions and maintain Complex IV respiration.

 

"Naked mole-rats maintain healthy skeletal muscle and Complex IV mitochondrial enzyme function into old age" (2016) http://www.aging-us....le/101140/text 

 

 

You paper also says, "Meanwhile Complex I expression is significantly lower in aged animals, perhaps due to their high levels of oxidative stress."  According to Wikipedia, Complex I is one of the main sites at which premature electron leakage to oxygen occurs, thus being one of the main sites of production of superoxide.

 

 

A lower Complex I might also contribute to mitochondria depolarizing more easily, leading to mitophagy and fewer dysfunctional mitochondria.


Edited by Fafner55, 24 June 2017 - 10:00 PM.


#174 lost69

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Posted 25 June 2017 - 10:18 AM

There's no question that methylation is important in many processes, and in nDNA is essential in keeping cells differentiated. But while methylation of nDNA serves to select between one of 200 cell types, methylation of mtDNA is likely no more than a volume knob. If you have a need for muscles, for example, ATP production is turned up by demethylation, and if you don't, it goes the other way. That way energy is conserved and the food requirement reduced.

 

sorry if questions maybe stupid but i am extremely ignorant on epigenetics and mitochondria.

 

on gdf11 they re checking dna methylation by a urine test on this website http://www.zymoresearch.com/ as baseline and then followup

 

can this dna methylation test be useful also on your protocol as baseline and then followup?or mitochrondria dna mehtylation is something else?

 

thank you



#175 Turnbuckle

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Posted 25 June 2017 - 01:08 PM

I’m not yet ready to post a protocol for reducing the methylation of mitochondria, but here is my thinking behind it—

 

Some facts and background:

 

1.      Methylation reduces gene expression, and in mitochondria lowers ATP output.

2.      DNA methylation is transferred from one strand of DNA to another by DNA methyltransferase, which uses S-Adenosylmethionine (SAMe) as the methyl donor.

3.      After mito biogenesis, a population of hemimethylated mtDNA is fully methylated in a process that is likely stochastic, where methylation of individual strands happens quickly, but methylation of the entire population can take a while, depending on the availability of methyltransferase. This time is not known, but is possibly hours or even days.

 

So here is my proposed protocol, without any detail:

 

1.      Mitophagy is promoted to clear room in the cell.

2.      A first burst of biogenesis is stimulated that does not fill up the cell.

3.      A second burst of biogenesis is stimulated before methylation is completed in the first burst, thus producing new mitochondria that are totally unmethylated, thus reducing the overall methylation level of the population.

 

This is possibly the mechanism by which exercise reduces mito methylation. Since exercise promotes biogenesis, repeated exercise within a window of time can accomplish exactly what I’m proposing with this protocol. The difference is, this protocol would work for all mitochondria and not just those in muscles.

 

And finally, one has to ask if this is a good thing or a bad thing. The result is what’s called hypomethylation, and in muscles it seems to be good, but it’s also been associated with stem cell senescence (induced by exposure to hydrogen peroxide)—

 

Mitochondrial DNA Hypomethylation Is a Biomarker Associated with Induced Senescence in Human Fetal Heart Mesenchymal Stem Cells

 

Of course, an association is not a cause, and the NAD+ that would be boosted in step one is known to have the reverse effect on senescence--

 

NAD+ repletion improves mitochondrial and stem cell function and enhances life span in mice

 

Adult stem cells (SCs) are essential for tissue maintenance and regeneration yet are susceptible to senescence during aging. We demonstrate the importance of the amount of the oxidized form of cellular nicotinamide adenine dinucleotide (NAD+) and its impact on mitochondrial activity as a pivotal switch to modulate muscle SC (MuSC) senescence. Treatment with the NAD+ precursor nicotinamide riboside (NR) induced the mitochondrial unfolded protein response (UPRmt) and synthesis of prohibitin proteins, and this rejuvenated MuSCs in aged mice. NR also prevented MuSC senescence in the Mdx mouse model of muscular dystrophy.

 

 

 


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#176 stephen_b

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Posted 25 June 2017 - 06:10 PM

Question: if mitochondria can't be created from scratch, does this mean that every supplement that 'increases mitochondrial biogenesis', like PQQ and rhodiola rosea, does so by increasing fission?



#177 Turnbuckle

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Posted 25 June 2017 - 06:29 PM

Question: if mitochondria can't be created from scratch, does this mean that every supplement that 'increases mitochondrial biogenesis', like PQQ and rhodiola rosea, does so by increasing fission?

 

In biogenesis, new loops of mtDNA are created. Fission and fusion don't change the number of loops, only the number of packages they come in. By forcing single loops into the smallest possible packages with fission, defective loops can be identified and disposed of. Going the other way with fusion, multiple loops with defective genes and can cover for each other so that the mitochondrion that contains them still functions. 

 

So saying a supplement creates new mitochondria is not accurate. It's really increasing the mtDNA copy number, and as a byproduct, the total mitochondrial mass will increase.


Edited by Turnbuckle, 25 June 2017 - 06:34 PM.

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#178 hsibai

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Posted 25 June 2017 - 06:54 PM

I did the Atomic Protocol this morning again and I am now sure it's causing an annoying drop in my BP. My typical uncorrected BP is 135/85 and by evening it was 105/65. The annoying part is that the drop in BP causes a headache in the back of my head. BP should be normal again in the morning like the last time I did the protocol. I recall Turnbuckle mentioned this drop in BP before so it must be a common occurance. I am just curious as to what is causing it and if everyone's experience is similar.

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#179 RWhigham

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Posted 25 June 2017 - 07:46 PM

I did the Atomic Protocol this morning again and I am now sure it's causing an annoying drop in my BP. My typical uncorrected BP is 135/85 and by evening it was 105/65. The annoying part is that the drop in BP causes a headache in the back of my head. BP should be normal again in the morning like the last time I did the protocol. I recall Turnbuckle mentioned this drop in BP before so it must be a common occurance. I am just curious as to what is causing it and if everyone's experience is similar.

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I also did the atomic protocol this morning 8AM-to-10AM.  My BP before the protocol was 104/70. My BP 3-hrs after the protocol was 102/64. In between I felt normal so I didn't check it.  This contrasts sharply with post #114  (11 days ago) when my BP took a nose dive.

 

This time I took:

T=0   2 g NAM + 5 g ribose + 2 caps BroccoMax

T=30 min   1.2 g TMG + 4 g lysine + 3 g citrulline  - dissolved in 1 cup green tea with 2 tbsp heavy cream

T=1 hr  full-on intense 1 hour of exercise -  body by science protocol

T=2hr  finished exercising

T= 3hr  walked to lunch, definitely not feeling very energetic, but otherwise fine.

 

Take Away:  My BP drop was likely a side-effect that no longer occurs after several cycles of the protocol.

 

[Body by Science protocol:  Choose a weight to reach muscle failure at 2 min followed by a 4 min rest. Repeat for squat, overhead press, bench press, curl, and deadlift. Add pushups, situps, pullups, and kettlebell swing (6-min per exercise). Do each exercise in slow-motion 1-to-3 reps. Then you get to relax and be in recovery mode for a whole week.]



#180 Turnbuckle

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Posted 25 June 2017 - 08:06 PM

 

 

This time I took:

T=0   2 g NAM + 5 g ribose + 2 caps BroccoMax

 

 

 

Why would you mix fission promoters with a fusion promoter?


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