Garth Nicolson and Henrich Kremer have been preaching this for decades. Nothing was โdiscoveredโ My posts have talked about this.
The question is what is causing the membrane damage/depletion beyond redox buffering capacity?
Other than normal aging:
Intracellular infections.
Researchers discovered that declining levels of phosphatidylcholine may be a major cause of age-related mitochondrial dysfunction and loss of cellular energy. Remarkably, boosting this nutrient restored more youthful mitochondrial performance
https://t.co/v0y5Huvi9n
@ChrisMasterjohn Not just Vitamin D/VDR, a bunch of nuclear receptors form hererodimers with retinoid X receptor alpha.
VDR, PXR, GCR, etc.
Its why in viral infections HDAC2 is upregulated to complex RXRa and drive down global gene transcription in infected cells (through the TLR3-IRF3 axis).
When you think about things they seem obvious.
Also, almost the entirety of the longevity movement is ignorant to the fact that senescence is a primary anti-viral defense strategy.
TLR3->IRF3->HDAC2->RXRa
@ImmunoFever NOS and Oxphos are downregulated in response to mitochondrial membrane damage as a protective adaptation. NO + superoxide ->peroxynitrate -> membrane damage.
ME, LC, GWS etc is downstream of this (which is mostly downstream of intracellular infection).
๐ฅ Vitalik recently shared a new idea for building stablecoins on Ethereum.
Instead of the current way โ where you deposit ETH, borrow dollars against it, and risk getting liquidated if the price drops โ he suggests splitting the ETH into two tokens. One token works like a stable dollar with much lower risk of big losses. The other token takes the upside when ETH goes up. These two tokens always add up to the original ETH, so thereโs no debt and no forced liquidation when prices fall.
This approach could become a new trend in DeFi. It trades a small amount of price drift for a much safer and simpler system that doesnโt rely on constant price monitoring or sudden liquidations.
Ethereum has always moved forward because of people and teams willing to try new ideas early. We need more projects experimenting with concepts like this to help the ecosystem grow stronger.
DTCC has their own collateral appchain built on Hyperledger Besu and the Chainlink runtime environment. All of these other chains like Canton, Stellar and hundreds of others can just connect to it. XRP canโt because Ripple was doing stock buybacks for their shareholders (not you) instead of integrating Chainlink CCIP.
Look to the MMP and elastase genes not the COLA genes.
Much of hEDS is inducible, most often infection related.
The monocytes and mast cells secrete large amounts of gelatinases, elastases, MMPs in response to TLR agonists.
There are cases in the literature of hEDS reversal in humans after putative antibiotic treatment for chronic infection (bartonella henselae for example). Also a mouse study where hypermobility was induced via borrelia infection and reversed with aggressive antibiotics.