Saturday, July 20, 2019
Intravenous Vitamin C with Decitabine Results in Double the Complete Remissions of AML Compared to Decitabine Alone.
The synergy of Vitamin C with decitabine activates TET2 in leukemic cells and significantly improves overall survival in elderly patients with acute myeloid leukemia.
Vitamin C is an immunotherapy via TET2.
Vitamin C is an immunotherapy via TET2.
Tuesday, July 16, 2019
"Anastasis," The Mythical Normal Cellular Invulnerability to Death.
Yes. When this occurs in relation to nuking cancer stem cells, all it takes is one immuno-evasive malignant out of control cell to come back to life and situate a microenvironment where it can divide. Then, metastatic cancer comes roaring back after the declaration of "cancer free."
The thing to remember is that all healthy people are picking off their potentially cancerous cells via their own immune systems, everyday, 24-7, until one of these marauders escape the immune system. The uncomfortable fact is that all people have a tiny bit of cancer everyday, but usually this tiny bit of abnormal cells is destroyed by the immune system. When the appearance of abnormal cells overwhelms the immune system OR, the appearance of "stealth" cancer cells appear, this is when the terrible disease overwhelms a human being.
Until then, "Anastasis" only serves to fuel cancer, not regenerative properties. For the 100 cells that cannot return from apoptosis, the 1 that survives by anastasis may fuel metastastic cancer, but it won't return an Alzheimer's patient back to their 20 year old self. It has never happened. So therefore, anastasis offers a glimpse of what is possible at EARLY INTERVENTION. Inducing anastasis at far advanced Alzheimer's Disease will do nothing.
Anastasis is the target of cancer therapy, so you find a paradox of desirable anastasis in neurodegeneration and undesirable anastasis in neoplastic cancer disorders.
The contradicting forces make "anastasis" a null drug target except in the face of mortality. In this last case scenario, where you do not necessarily care about whether you will return to life from death free of cancer, you would risk certain cancer disease in trade for resurrection from physical death. There are most certainly factors that remain completely misunderstood by the state of the art and science today that would pertain to the concept of "miraculous," that if understood would fit neatly into physically possible phenomena.
The thing to remember is that all healthy people are picking off their potentially cancerous cells via their own immune systems, everyday, 24-7, until one of these marauders escape the immune system. The uncomfortable fact is that all people have a tiny bit of cancer everyday, but usually this tiny bit of abnormal cells is destroyed by the immune system. When the appearance of abnormal cells overwhelms the immune system OR, the appearance of "stealth" cancer cells appear, this is when the terrible disease overwhelms a human being.
Until then, "Anastasis" only serves to fuel cancer, not regenerative properties. For the 100 cells that cannot return from apoptosis, the 1 that survives by anastasis may fuel metastastic cancer, but it won't return an Alzheimer's patient back to their 20 year old self. It has never happened. So therefore, anastasis offers a glimpse of what is possible at EARLY INTERVENTION. Inducing anastasis at far advanced Alzheimer's Disease will do nothing.
Anastasis is the target of cancer therapy, so you find a paradox of desirable anastasis in neurodegeneration and undesirable anastasis in neoplastic cancer disorders.
The contradicting forces make "anastasis" a null drug target except in the face of mortality. In this last case scenario, where you do not necessarily care about whether you will return to life from death free of cancer, you would risk certain cancer disease in trade for resurrection from physical death. There are most certainly factors that remain completely misunderstood by the state of the art and science today that would pertain to the concept of "miraculous," that if understood would fit neatly into physically possible phenomena.
Anastasis: recovery from the brink of cell death
What the scientific community is looking for is an innate mechanism to explain an extrinsic intervention by a purely benevolent faction who clearly do not support their evil ways.The Heart Is A Muscle (Too)
Vitamin C deficiency causes muscle atrophy and a deterioration in physical performance
SMP30-/- is not GULO-/- but results in the same stall in the vitamin C synthesis pathway. You could in fact cross SMP30-/- with Lp(a)+ and it in fact would not be the same thing as GULO-/- ; Lp(a)+.Monday, July 8, 2019
Not so subtle side effects of unnoticed copper deficiency:
Copper deficiency may be a leading cause of ischaemic heart disease
-from the British Medical Journal, 2018.
25% of US citizens do not consume enough dietary copper.
Sunday, July 7, 2019
Not just any collagen. Collagen I is what subtype provides suppleness to arteries.
"Collagen type-I degradation is related to arterial stiffness in hypertensive and normotensive subjects"
There is this huge body of work that contradicts itself if you don't read the above Nature article. Yes, Linus Pauling was right, but greedy usurpers did not help but to obfuscate everything for the worse. It's almost as if they are paid agents of disinformation or saboteurs. As publicly noted by The Los Angeles Times global mainstream associated press and media, Matthias Rath himself would go on to sue Linus Pauling for the same things he initially claimed to Linus Pauling were unimportant to him ($$$money$$$ aka IPR aka patents) in order to gain a foothold at the Palo Alto laboratory.
It's not just any collagen, but Collagen I which is important to the peculiar supple, yielding, resilient, rebounding, hydraulic strain resistant type of strength of arteries. Modern material science could not come up with this blended material because arteries are self repairing and no non-living hydraulic tube could last very long under the same kind of stresses. Arteries need ample vitamin C to repair and make more Collagen I. The wrong overabundance of other subtypes, say ColIII or IV or V cause pathological stiffness and/or fibrosis, which contributes to a more brittle artery structure that instead of giving way and stretching and recoiling, stays motionless and snaps apart beyond a certain systolic blood pressure.
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