Hypoxia Causes Hypermethylation And Cancer Progression; Can Be Reversed

haidut

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The dangers of hypermethylation have been discussed by Peat in many of his articles and interviews. Some of the supplements and foods he has recommended in the past are known methyl group acceptors/depletors and this probably explains a good deal of their beneficial effects. Niacinamide, glycine and CO2 are some of the most effective de-methylators in Peat world.
This study confirmed another point Peat has been writing about for a long time - i.e. that cancer is a disease of suppressed oxygen consumption and the more intense the local tumor hypoxia the faster the tumor progresses. Reversing this local hypoxia stops cancer progression and can often lead to complete tumor regression. I posted another study a few months ago that discovered the same key role hypoxia plays in cancer progression.
Caffeine As A Potential Treatment For Cancer

The new study discovered that hypoxia drive cancer progression by enhancing hypermethylation. Reversing tumor hypoxia or suppressing/reversing hypermethylation stopped the cancer progression.

http://healthmedicinet.com/i/mainta...-be-key-factor-to-stop-progression-of-cancer/

"...The lack of oxygen in tumor cells changes the cells’ gene expression, thereby contributing to the growth of cancer. This is the main conclusion of a research project led by professor Diether Lambrechts and Dr. Bernard Thienpont (VIB-KU Leuven), which was published in the renowned scientific journal Nature. The findings are far-reaching, as the study also proved that maintaining a proper oxygen supply in tumors inhibits these so-called ‘epigenetic aberrations’. The paper’s insights could eventually lead to new anti-cancer drugs that target blood vessels or the epigenetic aberrations."

"...Although epigenetic changes don’t affect the genetic code, they can strongly disturb gene function in a similar way, to the benefit of cancer cells. But until now, the origins of these epigenetic changes mostly remained a mystery. Scientists from the lab of professor Lambrechts investigated one frequent epigenetic alteration: hypermethylation, or the excessive addition of methyl groups to DNA. Hypermethylation silences the expression of tumor suppressing genes, thereby enabling the aberrant behavior of cells and the excessive growth of tumors.

"...Diether Lambrechts (VIB-KU Leuven): “Our study shows that these epigenetic alterations are caused by the environment of the tumor, and more specifically by oxygen shortage – which we call ‘hypoxia’. Oxygen is required by the enzymes that normally remove the methyl groups from the DNA. When there is oxygen shortage, too much methylation is retained, causing hypermethylation. Even more, hypoxia explains up to half of the hypermethylation in tumors. While we dedicated much of our efforts to breast tumors, we also demonstrated that this mechanism has a similarly broad impact in bladder, colorectal, head and neck, kidney, lung and uterine tumors.”

"...Uncovering the link between oxygen shortage and tumor growth was the result of the analysis of over 3,000 patient tumors. As a next step, the researchers verified another assumption: would interfering with tumor oxygen supply strike a blow against the progression of cancer? They were pleased to see this hypothesis confirmed: using mice, they proved that normalizing the blood supply is sufficient to stop the epigenetic alterations from occurring."
 

Drareg

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Is glycine a specific demethylating agent or indirectly assists.
Niacinamide I thought was a hdac inbitor rather than directly demethylating.
 

tyw

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IMO, the "Hypoxia" stimulus is far more important / damaging. The "hypermethylation" response is just a response to the lack of energy.

Methylation is just one of those very normal processes that should happen in cells, and both under and over methylation are problematic -- DNA methylation in cancer: too much, but also too little

Quote from the section, 'DNA modification in cancer: hypo- or hypermethylated relative to what?':

However, there are considerable differences in the amounts and distribution of DNA methylation among different vertebrate tissues because DNA methylation is not only species-specific but also tissue-specific (Ehrlich et al., 1982; Gama-Sosa et al., 1983a).

See also the sections onwards from 'Hypomethylation of highly repeated, interspersed DNA sequences in cancer'​

Therefore, an intervention that directly affects methylation needs to be tuned to the specific tissue, at the specific stage in that tissues lifecycle .... very difficult.

----

Some people will claim that "Undermethylation is more common". If you only look at genetics, then yes, there are more "genetically predisposed undermethylators". It is not known exactly how the environmental component works its way into this, but from the patient population, genetic undermethylators tend to suffer much more acute symptoms.

But in any case, what we are seeing is lack of control over methylation, and not specifically under or over methylation.

Intelligent cells likely know how and when to methylate DNA, and when to actually call for more gene transcription. Ensuring appropriate levels of metabolism to support intelligence is probably a more worthy focus -- http://www.basic.northwestern.edu/g-buehler/cellint0.htm

....
 
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tara

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One of the many reasons to attend to CO2 levels, for instance by undoing hyperventilation habits, bag breathing, CO2 baths etc. As well as the tactics to improve CO2 generation.
 

ejalrp

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IMO, the "Hypoxia" stimulus is far more important / damaging. The "hypermethylation" response is just a response to the lack of energy.

Methylation is just one of those very normal processes that should happen in cells, and both under and over methylation are problematic -- DNA methylation in cancer: too much, but also too little

Quote from the section, 'DNA modification in cancer: hypo- or hypermethylated relative to what?':

However, there are considerable differences in the amounts and distribution of DNA methylation among different vertebrate tissues because DNA methylation is not only species-specific but also tissue-specific (Ehrlich et al., 1982; Gama-Sosa et al., 1983a).

See also the sections onwards from 'Hypomethylation of highly repeated, interspersed DNA sequences in cancer'​

Therefore, an intervention that directly affects methylation needs to be tuned to the specific tissue, at the specific stage in that tissues lifecycle .... very difficult.

----

Some people will claim that "Undermethylation is more common". If you only look at genetics, then yes, there are more "genetically predisposed undermethylators". It is not known exactly how the environmental component works its way into this, but from the patient population, genetic undermethylators tend to suffer much more acute symptoms.

But in any case, what we are seeing is lack of control over methylation, and not specifically under or over methylation.

Intelligent cells likely know how and when to methylate DNA, and when to actually call for more gene transcription. Ensuring appropriate levels of metabolism to support intelligence is probably a more worthy focus -- http://www.basic.northwestern.edu/g-buehler/cellint0.htm

....
Interesting link to Buehler. Thanks. Has he taken his theories any further into the functional medicine area for instance?
 

Peatress

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Conclusions

We showed that PKC stimulation increased the HIF-1α transcriptional activity through PKC-δ by controlling the protein expression and translocation of HIF-1α to the nucleus. VK2 was shown to inhibit both NF-κB activation and PKC activity and revealed the inhibitory effects on HIF-1α transactivation. Since both HIF-1 and NF-κB, as well as PKCs, may be promising targets in cancer therapy, VK2 might be useful for the prevention and treatment of cancer, including HCC.
 

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