(and even MIGHT be in "stardust" i.e. "the pyrroloquinoline quinone (PQQ)-like materials detected in chondrite meteorites and comets 9P/Tempel-1(Krueger et al. 2004) and Hayutake (Henning and Salama 1998)."
Which sorta makes sense...building blocks of "life" are "out there". Isn't "HE" wonderful, amazing? :-)
I'll let you know if, without exercising, I observe any benefits...
Primer...we get our DNA from "mom and dad", but it is different from our mitochondrial DNA which comes solely from "mom".
In many diseases there is mitochondrial damage and as we age, the # of mitochondria go down, not because of a lack of stem cells (we make those all the time!), but those cells look to suffer from "bystander damage" when a lot of inflammatory cytokines are present/released nearby.
Stem Cells Require Healthy Mitochondria.
[ 06-22-2014, 09:43 AM: Message edited by: Marnie ]
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Marnie
Frequent Contributor (5K+ posts)
Member # 773
posted
1. we know Bb uses Mn for all of its enzyme reactions.
2. We know Mg levels plummet at the outset of lyme.
Mn can be bad for our mitochondria in excess:
If an infant or child was fed soy formula there is increased risk of mitochondrial disorder
because of high levels of manganese in the formula.
Infants who have been fed soy-based formula should be checked for mitochondrial disorder before vaccination.
Here are some links for information about soy formula, manganese and mitochondrial disorder:
Mitochondrial dysfunction is at the heart of many diseases...including cancer!
Role of Mitochondrial Dysfunction in Insulin Resistance
Collectively, these observations suggest that mitochondrial dysfunction may be a central cause of insulin resistance and associated complications.
In this review, we discuss mechanisms of mitochondrial dysfunction related to the pathophysiology of insulin resistance in classic insulin-responsive tissue, as well as cardiovascular tissue.
Summary : Most human cells can only replicate a limited number of times in cultures before they
***lose the ability to divide,
a phenomenon known as replicative senescence,***
which seems to play a role in aging at the organismal level.
Recent studies have shown that culture in low magnesium (Mg) accelerates the senescence of human endothelial cells and fibroblasts.
Given the numerous critical roles of Mg, it seems likely that Mg inadequacy would interfere with cellular metabolism, which could affect the senescence process.
Since i) several pieces of evidence link low Mg to aging and age-related diseases and ii) the Occidental diet is relatively deficient in Mg, we propose that broadly correcting nutritional intakes of Mg might contribute to healthier aging and the prevention of age-related diseases.
So...PQQ can help us replicate our powerhouses (mitochondria) to produce a lot more ATP, but ATP binds to Mg...so formulations should also contain some Mg (it would appear).
I believe increased ATP drives Mg back into the cells -> Mg-ATP.
There are also some key nutrients the mitochondria need to be healthy once they are made and they are in several of the formulations.
Some persons went to Italy to try ICHT...to speed up glycolysis (burn fat) to increase ATP levels.
Some persons went to Germany for photon transfer...once again to increase ATP levels.
Some people tried coconut oil (caprylic acid -> liver -> BHB, a ketone -> brain cells -> into citric acid cycle -> more ATP.
That has been the goal...getting ATP levels back up.
Our mitochondria make a LOT of ATP IF we have enough mitochondria and if the mitochondria are healthy.
IMO...sure worth trying PQQ with added nutrients to make and support the stem cells' mitochondria - esp.
PQQ looks to "mimic calorie restriction". When we restrict our calorie intake OR exercise a lot, we burn fat, right?
Have we not been told...to live longer, exercise and lose the excess pounds?
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I'm still following the learning curve for some of this stuff, but my impressions from PQQ is that it is something worth considering.
Posts: 474 | From US | Registered: May 2014
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Marnie
Frequent Contributor (5K+ posts)
Member # 773
posted
I'm a tad concerned about Bb's location in Iceman's hip...
Too friggin close to stem cells which do have TLR9 in them to recognize a pathogens' undermethylated DNA and which do have mitochondria which could be damaged, but...
See under "discussion" re: berberine’s impact on stem cells
If using PQQ, I'd consider taking some form of Mg also (could even apply it topically).
The thought is...trigger the mitochondria to replicate and feed them with the other nutrients that are in the PQQ formulation.
Then the cells may be able to make more ATP which will drive Mg back into the cells where Mg attaches to ATP as Mg-ATP...provided one has sufficient Mg available.
Keep in mind...TLR9 (in stem cells and in other cells) recognizes UNDERMETHYLATED bacterial DNA which is NOT THE KIND WE HAVE:
Toll-like receptor 9 (TLR9) recognizes
specific *unmethylated* CpG motifs prevalent in microbial but not vertebrate genomic DNA leading to innate and acquired immune responses.
Of course there is always genetic differences in each of us...even genetic differences in TLR9 which can be beneficial sometimes and harmful other times.
Mg supplement restored the "health" of our own antibody to Bb's OspB. Ancient research posted here many times. Our own antibody wasn't totally functional.
Read one customer's review - mentions lyme (2nd one):
"These enzymes containing PQQ are called quinoproteins. Glucose dehydrogenase, one of the quinoproteins, is used as a glucose sensor. Subsequently, PQQ was found to stimulate growth in bacteria."
4. "The ability to utilize glycerol AND chitin as energy sources through the glycolytic pathway, which is unique to B. burgdorferi, is consistent with the existence of an arthropod-specific stage in the life cycle of this spirochete." http://www.ncbi.nlm.nih.gov/pmc/articles/PMC97324/
Chitin = a long-chain polymer of a N-acetylglucosamine, a derivative of glucose.
Yes...I know...N-acetylglucosamine (also reduces IL6) for MS and low in HIV also.
Can't help wonder...when Bb is in the tick, it needs/uses the tick's chitin, but when in humans gets glycerol provided via oxidative stress?
Taking this another step (backwards)...the WFL hunts for food at night and is covered in Bb filled ticks. When they are full and fall off, they have no Bb.
The WFL has to be able to SEE its prey (insects) at night and thus has a lot of eye RODS which make rhodopsin.
Remember Bb picks up a protein to inhibit mannose binding lectin at the outset…throwing off our defense system.
If Bb uses the tick's chitin to get "at" N-acetylglucosamine, but the lizard uses it instead to make rhodopsin...isn't Bb thus "starved" of N-acetylglucosamine?
[ 06-23-2014, 06:19 PM: Message edited by: Marnie ]
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