Caffeine promotes the expression of telomerase reverse transcriptase to regulate cellular senescence and aging

cupofcoffee

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Telomere shortening is one of the main causes of cellular senescence. Caffeine is a natural stimulant most commonly found in coffee and tea. In this study, caffeine was found to promote the expression of telomerase reverse transcriptase (TERT) at both mRNA and protein levels, and consequently extended the telomere length and prevented cellular senescence. Knockdown of TERT eliminated the effect of caffeine on telomere elongation. Moreover, animal studies indicated that caffeine promoted the expression of TERT and extended the telomere length in the thymus and spleen of mice treated with caffeine for a long period of eight months. In addition, caffeine restored the decline of organ index and improved the histological structural change of the thymus, spleen and liver of mice due to aging. These results suggest that caffeine promotes the expression of TERT to delay cellular senescence and aging, which help to understand the mechanism for the beneficial effects of caffeine containing foods on health.
 

Rick K

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This is something Canadians have always inherently understood which is why there is a Tim Horton's on every corner. :canada3
 

Mauritio

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Interesting! Let's see how the peaters will squeeze that into the peat picture , as it's commonly seen as something negative .

I personally think that's great and another reason to drink coffee.
 

SeamusR

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Telomere shorting is a natural protection mechanism designed to nullify any misbehaving genetic mutations that may occur over the 60 to 90 divisions of a normal cell.

If any compound blocks or reverses this protective shortening (like coffee) then it potentially enhance the risk of a rogue mutation turning the cell tumorogenic.

Telomere shortening was evolutionarily adopted by the human cell for a reason.

There is no free lunch unfortunately.
 

Nighteyes

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If any compound blocks or reverses this protective shortening (like coffee) then it potentially enhance the risk of a rogue mutation turning the cell tumorogenic.

Telomere shortening was evolutionarily adopted by the human cell for a reason.

There is no free lunch unfortunately.
Wait what is the free lunch you mean? Isnt coffee associated with lower risk of most cancers or are you saying coffee could potentially lead to tumor growth?
 

SeamusR

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Wait what is the free lunch you mean? Isnt coffee associated with lower risk of most cancers or are you saying coffee could potentially lead to tumor growth?
I’m saying anything that decreases or reverses natural telomere shortening will logically affect the evolutionary benefit of why telomere shortening evolved in the first place, so in this case most likely increase the potential of tumor growth.
 

Mauritio

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I’m saying anything that decreases or reverses natural telomere shortening will logically affect the evolutionary benefit of why telomere shortening evolved in the first place, so in this case most likely increase the potential of tumor growth.
Then why do some telomere studies show lower tumor risks with increased telomere length ?
 

Mauritio

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Can you share some examples ?
The experiment worked: the long telomere mice lived an average of 24 percent longer, were slimmer, and less likely to develop cancer. Various indicators of metabolic ageing turned out to be lower too, the researchers report.

These mice had less 'bad' cholesterol in their bodies, and their DNA wasn't damaged as much as the animals got older. What's more, their mitochondria functioned better as well.

 

Mauritio

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this is just a small study. unlikely for any human transfer effects Id guess
Why do you think studies are carried out in mice ? They are there to be useful to humans . So why exactly do you think there's no human transfer?
 

SeamusR

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Why do you think studies are carried out in mice ? They are there to be useful to humans . So why exactly do you think there's no human transfer?

Here is a link to a detailed study that explains the "no free lunch" concept much better than I could ever hope to.

Long telomeres and cancer risk: the price of cellular immortality


Some Extracts:

"The distribution of telomere length in humans is broad, but it has finite upper and lower boundaries. Growing evidence shows that there are disease processes that are caused by both short and long telomere length extremes."

"Although the role of germline telomerase and shelterin mutations in familial cancer may at first appear limited to small subsets of cancer patients, there is epidemiologic evidence supporting long telomere length itself as being associated with cancer risk."

"Long telomeres promote cancer-related mortality in mice and proposed mechanism for long-telomere melanomagenesis."

Some relevant quick links:
 

meatbag

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Here is a link to a detailed study that explains the "no free lunch" concept much better than I could ever hope to.

Long telomeres and cancer risk: the price of cellular immortality


Some Extracts:

"The distribution of telomere length in humans is broad, but it has finite upper and lower boundaries. Growing evidence shows that there are disease processes that are caused by both short and long telomere length extremes."

"Although the role of germline telomerase and shelterin mutations in familial cancer may at first appear limited to small subsets of cancer patients, there is epidemiologic evidence supporting long telomere length itself as being associated with cancer risk."

"Long telomeres promote cancer-related mortality in mice and proposed mechanism for long-telomere melanomagenesis."

Some relevant quick links:
I think there has been some posts about how the telomere issue isn't really as clear cut as they make it out to be;
Inflammation, Not Telomere Length, Predicts Longevity
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About ten years ago, Geron corporation announced that it was developing products to control aging and cancer, by regulating telomerase, the enzyme that lengthens a piece of DNA at the end of the chromosomes. Their argument was that telomeres get shorter each time a cell divides, and that after about 50 divisions, cells reach the limit identified by Leonard Hayflick, and die, and that this accounts for the aging of the organism. Cancer cells are immortal, they said, because they maintain active telomerase, so the company proposed to cure cancer, by selling molecules to inhibit the enzyme, and to cure aging, by providing new enzymes for old people. However, Hayflick's limit was mainly the effect of bad culture methods, and the theory that the shortening of telomeres causes aging was contradicted by the finding of longer telomeres in some old people than in some young people, and different telomere lengths in different organs of the same person.


But it's true that cancer cells have active telomerase, and that most healthy cells don't. It happens that telomerase is activated by cellular injury, such as radiation, that activates phosphorylases, and that it is inactivated by phosphatases. Estrogen activates telomerase, and progesterone inhibits it."
RU486, cancer, estrogen, and progesterone.
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Other researchers, simply by changing a single factor, caused great increases in the longevity of the cultured cells. Simply using a lower, more natural oxygen concentration, the cells were able to undergo 20 more divisions. Just by adding niacin, 30 more divisions; vitamin E, 70 more divisions. Excess oxygen is a poison requiring constant adaptation.

Hayflick also published the observation that, while the cells kept in dishes at approximately body temperature deteriorated, cells kept frozen in liquid nitrogen didn't deteriorate, and he concluded that "time" wasn't the cause of aging. When I read his comments about the frozen cells, I wondered how anyone of normal intelligence could make such stupid statements. Since then, facts that came out because of the Freedom of Information Act, cause me to believe that a financial motive guided his thoughts about his cultured fibroblasts.

Hayflick and his followers have been attacking the idea of anti-aging medicine as quackery. But he is closely involved with the Geron corporation, which proposes that genetic alterations relating to telomeres may be able to cure cancer and prevent aging. Their claims were reported by CNN as "Scientists discover cellular 'fountain of youth'."

The "wear and tear" doctrine of aging that derived from the ideology of the gene was reinforced and renewed by Hayflick's cell culture observations, and it continued to rule the universities and popular culture.

But detailed investigation of skin cell growth showed that cells in the lower layer of the skin divide at least 10,000 times in a normal lifetime, and similar processes occur in the lining of the intestine. The endometrium and other highly renewable tissues just as obviously violated Hayflick's limit. Transplantation experiments showed that pieces of mammary tissue or skin tissue could survive through ten normal lifetimes of experimental animals without suffering the effects of aging.

Stem cells, cell culture, and culture: Issues in regeneration
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Why You Don't Want Long Telomeres

Study Says Coffee/caffeine Shortens Lifespan By Shortening Telomeres

Fat-free Cultured Cells: No Need For PUFAS; Where Are The Studies ?
 

SeamusR

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But it's true that cancer cells have active telomerase, and that most healthy cells don't. It happens that telomerase is activated by cellular injury, such as radiation, that activates phosphorylases, and that it is inactivated by phosphatases. Estrogen activates telomerase, and progesterone inhibits it."
RU486, cancer, estrogen, and progesterone.

OK, so longer Telomeres & it's impact on cancer probability is aligned with Peat thinking, via Estrogen/Progesterone modulation, quite interesting.

Also, telomerase activation by cellular injury (and hense heightened cancer risk via longer telomeres) is again very interesting, I had not seen this correlation before!
 

SeamusR

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But it's true that cancer cells have active telomerase, and that most healthy cells don't. It happens that telomerase is activated by cellular injury, such as radiation, that activates phosphorylases, and that it is inactivated by phosphatases. Estrogen activates telomerase, and progesterone inhibits it."
RU486, cancer, estrogen, and progesterone.

Actually I dont see an references quoted by Peat to support the "telomerase is activated by cellular injury" statement, anyone got any study links ?.
 

soul_rebel

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I think Peat in his latest interview with Patrick Timpone (March 15), said he does not take too much stock in telemere length. He begins talking about it at 01 : 10 : 45 (an hour ten minutes) in the podcast.
 
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