sirolimus vehicle

Can I ask, from where did you source the powder? Thank you!

The new protocol:

VITAMIN C 1,000 MG WAS ADDED BY TURNBUCKLE TO INCREASE BIOAVABILITY 

I use AKGG 4 grams instead of AKG 1 gram, but must take 1 hour before other supplements.

 This new procedure is much simplified. It requires only two doses, Mito1 and Mito2, which are alternated on a daily basis.

 Mito1 (fission)

● NAM+R, 1 g of each

● AKG, 1 g=4 g AAKG(1 hour before rest)

● PQQ, 20 mg

 

Mito2 (fusion)

● GMS, 1 g

● AKG, 1 g=4g AAKG(1 hour before rest)

● PQQ, 20 mg

 

NAM+R (nicotinamide plus ribose) is a fission promoter, GMS (glycerol monostearate) is a fusion promoter, AKG (alpha-ketoglutarate) is a demethylase promoter, and PQQ is a biogenesis promoter. All of these are fast acting.

 A two week experiment using reps to failure:

 Warm water was sufficient to dissolve everything, but the PQQ was taken in a capsule to insure that the other ingredients got a slight head start (probably unnecessary).

 Mito1 and Mito2 were taken on alternating days. Each dose was taken in the evening and reps of dumbbell curls to failure counted first thing in the morning — five or six hours after dosing — using the same arm.

 Background:

 Previously I posted methods of cycling mitochondrial morphology to clean up defective mtDNA, which eliminated mutations via the PINK1/Parkin QC process. The normal QC process can detect mutated mtDNA genes during fission as all mito genes are critical and thus the mito membrane potential goes to zero if just one is defective. Greatly magnifying fission and fusion with supplements will aid that process. But there is another source of mitochondrial damage that isn’t so easily eliminated — epigenetic damage. Like nDNA, mtDNA also picks up aberrant methylation with age. This methylation degrades ATP production, but the QC process doesn’t catch it unless the problem is addressed at a critical time, like during biogenesis. If a mitochondrion with one loop of methylated mtDNA runs out of enzymes while involved with replication, then membrane potential may dip to zero and it will get labeled for recycling. Thanks to methylation, it won’t have as much enzyme reserves as other mitochondria, so it will be preferentially targeted. Also, biogenesis is the best time to demethylate mtDNA as methyltransferase can’t operate while there is only one strand.

 Until recently, mtDNA wasn’t even known to have methylation, and researchers are still confused as to why it is there. Some speak of mtDNA hypermethylation like it is bad while normal methylation has some purpose.

 See, for instance: Hypermethylation of mitochondrial DNA in vascular smooth muscle cells impairs cell contractility

 I don’t agree. I say all mtDNA methylation is bad. Methylated mtDNA mooches enzymes off other mtDNA, and because they don’t produce as much ATP they don’t produce as much ROS, and thus have a survival advantage as they are less prone to mutation. Eventually the cell will become full of moochers and result in fatigue and many other problems of aging.

 So I say get rid of them all, mutations and methylation alike.

 The new protocol:

This new procedure is much simplified. It requires only two doses, Mito1 and Mito2, which are alternated on a daily basis.
Mito1 (fission)

● NAM+R, 1 g of each

● AKG, 1 g

● PQQ, 20 mg

 

Mito2 (fusion)

● GMS, 1 g

● AKG, 1 g

● PQQ, 20 mg

 NAM+R (nicotinamide plus ribose) is a fission promoter, GMS (glycerol monostearate) is a fusion promoter, AKG (alpha-ketoglutarate) is a demethylase promoter, and PQQ is a biogenesis promoter. All of these are fast acting.

A two week experiment using reps to failure:

Warm water was sufficient to dissolve everything, but the PQQ was taken in a capsule to insure that the other ingredients got a slight head start (probably unnecessary).

Mito1 and Mito2 were taken on alternating days. Each dose was taken in the evening and reps of dumbbell curls to failure counted first thing in the morning — five or six hours after dosing — using the same arm.

My hypothesis was that the number of reps would reflect mito damage. With mito fusion, enzymes are shared, thus ATP production and reps would be maximum. With fission, methylated (or otherwise damaged) mtDNA produce less ATP and reps would be minimum. The difference would reflect average damage, and if the treatment worked, the difference should decline. If all damage was removed, then the difference should go to zero.

 Which in fact it did. See the plot below. The y-axis shows the reps and % difference, while the x-axis shows days. The curve labeled baseline is without any treatment, and likely reflects the normal intermediate situation with mito morphology in a dynamic state. It is stable at 16 reps. The upper fusion curve is relatively flat and higher than baseline as expected, while the lower fission curve is lower than baseline, but rises to meet the fusion curve after about two weeks, and stays there. Thus the percent difference goes to zero.

Results:

Improvement in running endurance, reduced hunger, and reduced need for hypertension medication.

The old protocol is no longer needed. With the new protocol, mutated mtDNA will be removed first just as in the old one, as their membrane potential will zero out first, before the epimutated. It was my expectation that if epimutations were not eliminated, the experimental curves might never intersect. But they did.

 

Results will vary according to your damage level. If you have a lot of damage, it could take a lot longer. If you have none, you will see no difference between fission and fusion. To know when you're done, keeping track of it numerically will work better than vague subjective feelings.

 As for AKG, I used the simplesa liquid for the greatest bioavailability. You could use powder too, of course, though I suggest dissolving it first. For the experiment I left the PQQ in caps and took everything else in water. Taking a few grams of AAKG an hour before would also be an option. I was looking for a unitary dose, but what's the worst that could happen if you don't get that part right? It just won't work as well, I expect. And if you are monitoring your progress numerically, you will see it.

Anecdotal report. I did the original mitochondrial protocol for 15 cycles. I got to the point where the niacinamide/d-ribose combination had no subjective effect on me.

 I have done one fusion and one fission cycle using the updated protocol. I experienced a strong reaction to the fission day (the same low energy I had at the start of the original protocol), so I guess there is some demethylation needed there.

 The gram of GMS on the fusion day brought my blood pressure up to about 137/80. I can't say that my endurance on a 4 mile run the next day was any better. I'll do some more cycles and continue to monitor.