Hypomethylation

Drareg

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This where things get complex,hypomethylation is also a factor in aging and disease as much as hypermethylation. If this is correct it means you need a balancing act to get things right,certain drugs to target different areas.
I curious if the interpretation is right,I don't currently have this level of comprehension to decipher it,I'm keen on getting Peats view on hypomethylation and aging,it's starting to smell like the reservatrol scenario.

Distinctive patterns of age-dependent hypomethylation in interspersed repetitive sequences
Pornrutsami Jintaridth, Apiwat Mutirangura
Physiological Genomics Published 1 April 2010 Vol. 41 no. 2, 194-200 DOI: 10.1152/physiolgenomics.00146.2009

Abstract
Interspersed repetitive sequences (IRSs) are a major contributor to genome size and may contribute to cellular functions. IRSs are subdivided according to size and functionally related structures into short interspersed elements, long interspersed elements (LINEs), DNA transposons, and LTR-retrotransposons. Many IRSs may produce RNA and regulate genes by a variety of mechanisms. The majority of DNA methylation occurs in IRSs and is believed to suppress IRS activities. Global hypomethylation, or the loss of genome-wide methylation, is a common epigenetic event not only in senescent cells but also in cancer cells. Loss of LINE-1 methylation has been characterized in many cancers. Here, we evaluated the methylation levels of peripheral blood mononuclear cells of LINE-1, Alu, and human endogenous retrovirus K (HERV-K) in 177 samples obtained from volunteers between 20 and 88 yr of age. Age was negatively associated with methylation levels of Alu (r = −0.452, P < 10−3) and HERV-K (r = −0.326, P < 10−3) but not LINE-1 (r = 0.145, P = 0.055). Loss of methylation of Alu occurred during ages 34–68 yr, and loss of methylation of HERV-K occurred during ages 40–63 yr and again during ages 64–83 yr. Interestingly, methylation of Alu and LINE-1 are directly associated, particularly at ages 49 yr and older (r = 0.49, P < 10−3). Therefore, only some types of IRSs lose methylation at certain ages. Moreover, Alu and HERV-K become hypomethylated differently. Finally, there may be several mechanisms of global methylation. However, not all of these mechanisms are age-dependent. This finding may lead to a better understanding of not only the biological causes and consequences of genome-wide hypomethylation but also the role of IRSs in the aging process.

ARTICLES | Physiological Genomics
 

Drareg

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Interesting the ages where loss of methylation occurs,around 34 is the first drop of youth protective hormones.
 

Dante

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This where things get complex,hypomethylation is also a factor in aging and disease as much as hypermethylation. If this is correct it means you need a balancing act to get things right,certain drugs to target different areas.
I curious if the interpretation is right,I don't currently have this level of comprehension to decipher it,I'm keen on getting Peats view on hypomethylation and aging,it's starting to smell like the reservatrol scenario.

Distinctive patterns of age-dependent hypomethylation in interspersed repetitive sequences
Pornrutsami Jintaridth, Apiwat Mutirangura
Physiological Genomics Published 1 April 2010 Vol. 41 no. 2, 194-200 DOI: 10.1152/physiolgenomics.00146.2009

Abstract
Interspersed repetitive sequences (IRSs) are a major contributor to genome size and may contribute to cellular functions. IRSs are subdivided according to size and functionally related structures into short interspersed elements, long interspersed elements (LINEs), DNA transposons, and LTR-retrotransposons. Many IRSs may produce RNA and regulate genes by a variety of mechanisms. The majority of DNA methylation occurs in IRSs and is believed to suppress IRS activities. Global hypomethylation, or the loss of genome-wide methylation, is a common epigenetic event not only in senescent cells but also in cancer cells. Loss of LINE-1 methylation has been characterized in many cancers. Here, we evaluated the methylation levels of peripheral blood mononuclear cells of LINE-1, Alu, and human endogenous retrovirus K (HERV-K) in 177 samples obtained from volunteers between 20 and 88 yr of age. Age was negatively associated with methylation levels of Alu (r = −0.452, P < 10−3) and HERV-K (r = −0.326, P < 10−3) but not LINE-1 (r = 0.145, P = 0.055). Loss of methylation of Alu occurred during ages 34–68 yr, and loss of methylation of HERV-K occurred during ages 40–63 yr and again during ages 64–83 yr. Interestingly, methylation of Alu and LINE-1 are directly associated, particularly at ages 49 yr and older (r = 0.49, P < 10−3). Therefore, only some types of IRSs lose methylation at certain ages. Moreover, Alu and HERV-K become hypomethylated differently. Finally, there may be several mechanisms of global methylation. However, not all of these mechanisms are age-dependent. This finding may lead to a better understanding of not only the biological causes and consequences of genome-wide hypomethylation but also the role of IRSs in the aging process.

ARTICLES | Physiological Genomics
Peat has said that methylation protects and stabilizes cells when C02 and regeneration are not possible. There is a global loss of methylation during aging however certain genes become hypermethylated like genes for estrogen receptor , insulin like growth factor etc. In oncology, hyper methylation can cause silencing of tumor suppressor genes like p53 (it is selenium based if i remember correctly) , hence the proliferation. However, is that a consequence of hypoxia/ warburg effect( if you assume warburg effect as a cause of cancer) or a cause that i don't know.
 

Drareg

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Peat has said that methylation protects and stabilizes cells when C02 and regeneration are not possible. There is a global loss of methylation during aging however certain genes become hypermethylated like genes for estrogen receptor , insulin like growth factor etc. In oncology, hyper methylation can cause silencing of tumor suppressor genes like p53 (it is selenium based if i remember correctly) , hence the proliferation. However, is that a consequence of hypoxia/ warburg effect( if you assume warburg effect as a cause of cancer) or a cause that i don't know.

It's plausible then that energy is just lowered with aging to the point were you can't even methylate anymore,to protect yourself from your already poor metabolism.
The mainstream are interpreting this as a need to increase methylation as you age?

It makes sense since methylation will protect when metabolic energy is lowered,expressing certain genes for enzymes/proteins require more energy,if you are not providing the energy they will not express themselves because they are methylated.

For me it says humans will need another way of increasing energy for our next advancement without having to eat all day,either we selectively breed things for more nutrition in smaller amounts or we takes cleaner supplements,possibly both. It's interesting we are already on this path.
Eating smaller amounts food with more nutrition has the potential to reduce endotoxin also,probably why some people speculate outer bowels will grow smaller with evolution.
Selectively breeding the food is using epigentic principles on the food.
 

Dante

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It's plausible then that energy is just lowered with aging to the point were you can't even methylate anymore,to protect yourself from your already poor metabolism.
The mainstream are interpreting this as a need to increase methylation as you age?

It makes sense since methylation will protect when metabolic energy is lowered,expressing certain genes for enzymes/proteins require more energy,if you are not providing the energy they will not express themselves because they are methylated.

For me it says humans will need another way of increasing energy for our next advancement without having to eat all day,either we selectively breed things for more nutrition in smaller amounts or we takes cleaner supplements,possibly both. It's interesting we are already on this path.
Eating smaller amounts food with more nutrition has the potential to reduce endotoxin also,probably why some people speculate outer bowels will grow smaller with evolution.
Selectively breeding the food is using epigentic principles on the food.
I don't think that the mainstream is drawing any conclusion whether there is a need for methylation as age increases. These are just observations. I think the selective breeding of food happens . Wheat is one example. There was a golden rice variant for providing vitamin A to poor and undernourished people.
 
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