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Telomer activator equivalent to ???  This thread currently has 1,165 views. Print Print Thread
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Amazone I.
Thursday, June 14, 2012, 9:38pm Report to Moderator Report to Moderator

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Kyosha Nim
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I just saw this commercial and asked myselve in what might be the quivalent to AT 1 65 Perhaps Trehalose'?)

http://www.t-e-l-o-m-e-r-e.com

and if I understood it well here, the message of antiaging products aren't only to be found in giving hormonal treatments... so far I always was right to recommend aminoacids and other orthomolecular stuffs .....
and something else is important as an antiaging effect.... 1.) sleep and tens-technic .....


MIfHI K-174
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Lloyd
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From the website and no surprise to GTD students:

Quoted Text
Vitamins and Minerals

■Folate – This B vitamin is important for DNA and RNA structure and function.
■Vitamin B12 – In conjunction with folate, this B vitamin is important for the methylation, or detoxification, of homocysteine. Higher levels of homocysteine are associated with increased oxidative stress.
■Niacin (nicotinamide) – Can influence telomere length through its multiple regulatory and coenzymatic activities.
■Vitamin A and beta-carotene – These antioxidants reduce concentrations of harmful signaling molecules and increase beneficial ones to help reduce oxidative stress.
■Vitamin D – Higher levels of vitamin D lower levels of c-reactive protein (CRP), a protein with harmful effects and associated with shortened telomere length. Vitamin D appears to inhibit some of CRP’s harmful effects.
■Vitamins C and E – These antioxidant vitamins are widely acknowledged for limiting oxidative stress and its damage on DNA and telomeres.
■Magnesium – The mineral required for the activity of a number of enzymes involved in DNA replication and repair. Low amounts of this mineral are also associated with higher concentrations of CRP.
■Zinc – This mineral is necessary for a variety of enzymes including DNA polymerases, which are important for DNA and telomere maintenance.
■Iron – In contrast to the other nutrients, iron supplementation is associated with shorter telomeres. This is likely because of iron’s pro-oxidant ability to stimulate free radical generation. While iron supplements may increase oxidative stress, iron from diet or multivitamins (containing less iron) is not negatively associated with telomere length. Other Bioactives

■Curcumin and turmeric – Turmeric, and its primary component curcumin, are common dietary spices that stimulate synthesis of antioxidants, thereby protecting against oxidative stress. Mice fed diets containing curcumin had a trend for longer telomeres compared with controls.
■Long-chain omega-3 fatty acids (fish oil) – Higher plasma levels of long-chain omega-3 fatty acids docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA) may protect against oxidative stress by enhancing activity of the antioxidant enzymes superoxide dismutase, catalase, and glutathione peroxidase.
■Polyphenols – Polyphenols from grape seed and green tea provide additional protection for DNA and telomeres from oxidative stress. Those who drink tea regularly have longer telomeres while mice fed grape seed polyphenols had longer telomeres compared to controls.
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Lola
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Conor
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I previously read a research paper about a telomerase-related study performed by a biopharmaceutical company called Geron (as well as another study by them which was done in conjunction with the University of Texas). I recall that Geron developed a concentrated form of astragalus which contains high amounts of a molecule called TA-65. This molecule in astragalus is apparently able to activate the gene that makes the enzyme telomerase. In the course of their research, they were able to observe TA-65 activate telomerase and restore telomeres to more youthful cellular lengths.

One of the things I found interesting in reading about telomere research is that when our cells divide, i.e., reproduce, while the resultant daughter cell may be genetically identical to the parent cell, it is really not truly identical because it doesn't have an absolute complete copy of the parent cell's DNA ... a minute portion of the telomere at the end of the chromosome is missing. However, telomerase, when present, allows each dividing cell to replace the lost bit of DNA (at least, that's my layperson understanding of it).

I also recall that an individual with high levels of the non-protein amino acid homocysteine can have daughter cells that lose as much as three times more of the telomere length during cell division as compared to a person with lower levels of homocysteine. It seems to me that this would, in effect, cause one to age three times more quickly.

Anyhow, there's some very interesting research being done with telomerase, especially as it applies to the "Hayflick Limit."



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yaeli
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Is it true that the shortening of telomeres is very important to health, because it induces apoptosis in good time?  


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Conor
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Quoted from yaeli
Is it true that the shortening of telomeres is very important to health, because it induces apoptosis in good time?

Hi yaeli, my understanding is, yes, that's true, i.e., cell death is telomere-length dependent. I've seen the Hayflick Limit noted as being anywhere from 40 to 80.

Quoted from The University of Utah
In human blood cells, the length of telomeres ranges from 8,000 base pairs at birth to 3,000 base pairs as people age and as low as 1,500 in elderly people. (An entire chromosome has about 150 million base pairs.) Each time a cell divides, an average person loses 30 to 200 base pairs from the ends of that cell's telomeres.

Cells normally can divide only about 50 to 70 times, with telomeres getting progressively shorter until the cells become senescent, die or sustain genetic damage that can cause cancer.

Telomeres do not shorten with age in tissues such as heart muscle in which cells do not continually divide.

In another document I read that with each mitosis, as the telomeres shorten, they cause the chromosome to fold differently ... exposing a different portion of the genome. This would seem significant. (By the way, I enjoyed the following very straightforward demonstration of cellular replication on NOVA: How Cells Divide.)

Bottom line, it seems the research is saying that by optimally maintaining telomeres at a greater length, i.e., a more youthful length, it goes a long way toward helping one avoid genomic instability.



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Amazone I.
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Kyosha Nim
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thanx all for your beautiful statements....

and Conor you are right about the mentioned thema but you forgot that in replications cells might go wrong and even then replica will perfomr normally ... but if there are too much of those erroning steps... diseases are appearing.... ....and due to high amounts of homocystein cells age quicker coz of an overlap of toxins...


MIfHI K-174

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Amazone I.  -  Sunday, June 17, 2012, 2:33pm
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yaeli
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Thank you Conor for elaborating on this.




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yaeli  -  Saturday, June 16, 2012, 3:06pm
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Spring
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Quoted from yaeli
Thank you Conor for elaborating on this. In other words, maybe I get it right, (1) on one hand, the telomeres secure genomic stability, (2) on the other hand, the too-short-lengths of the telomeres indicate to MTOR   to order the cell to proceed killing itself ???????? Nobody said that.  


Dr. D.:
Autophagy that is MTOR dependant (inhibited that way) may make cancer cells a little more likely to survive.

The concern is that there is some conflicting results showing that when autophagy is MTOR dependant, there is the possibility that cancer cells in the autophagic process are less susceptible to apoptosis from chemotherapy.  There is also evidence that activating tumor suppressor cells increases autophagy.

Since Trehalose stimulates autophagy independantly from MTOR, it no longer is affected by growth factors, etc. that are in the normal autophagy control loop.  This is really important to get you out of the questionable area of "Am I doing good if I have a cancer patient?" kind of thing...


Does this help?


"We are all born ignorant, but one must work hard to remain stupid." -- Benjamin Franklin
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yaeli
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Thanks Spring!     I haven't seen these particular paragraphs before!

I should have read Dr. D's lesson on telomeres first, it makes my question unnecessary (therefore I erased it).  



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yaeli
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Quoted from Lola
Quoted from text
However, it has been hypothesized that there is a tradeoff between cancerous tumor supression and tissue repair capacity, and that by lengthening telomeres we might slow aging and in exchange increase vulnerability to cancer (Weinstein and Ciszek, 2002).
Is there or isn't there, that is the question.  The wikipedia entry says that there exist counter-hypotheses.


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Spring
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Notice the date on the article, yaeli. The latest info is from Dr. D.'s comment recently.


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yaeli
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Quoted from Spring
Notice the date on the article, yaeli. The latest info is from Dr. D.'s comment recently.
Please Spring which recent comment do you mean?



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Spring
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The one I copied and pasted first. The other info is ten years old and only an  "hypothesis."


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yaeli
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I'm sorry, there was a mix-up of 2 separate subjects which may create issues for cancer patients:

1) Extending telomeres

2) Stimulation of autophagy by Trehalose



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Conor
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Quoted from University of Texas Southwestern

UT Southwestern research reveals how cancer-driving enzyme works

DALLAS – May 6, 2011 – Cancer researchers at UT Southwestern Medical Center are helping unlock the cellular-level function of the telomerase enzyme, which is linked to the disease’s growth.

Their latest findings, published today in Molecular Cell, demonstrate that telomerase repairs chromosomes in one of two ways – depending on whether a cell is dividing normally or if the cell is under stress from enzyme inhibition – and could lead to new or improved cancer-fighting therapies that promote inhibition of this enzyme.

“It’s a significant advance in our understanding of how telomerase works,” said Dr. Woodring Wright, professor of cell biology and senior author of the study. “Our goal is to identify new targets for inhibiting telomerase.”

The number of times a cell divides is determined by telomeres, protective caps on the ends of chromosomes that indicate cell age. Every time a cell divides, the telomeres shorten. When telomeres shrink to a certain length, the cell either dies or stops dividing.  In cancer cells, the enzyme telomerase keeps rebuilding the telomeres, so the cell never receives the cue to stop dividing.

Although telomerase was discovered in 1985, exactly how this enzyme repairs telomeres to enable cancer cells to divide and grow was largely unknown. Until now, researchers didn’t know how many telomerase molecules went into action at the telomeres and under what conditions.

“It’s a single molecule under normal cancer growth conditions, but if you shorten telomeres artificially by inhibiting telomerase, now it’s more than one molecule acting on the ends of the telomeres,” Dr. Wright said of the study’s findings.

When acting as a single molecule at the telomeres, telomerase adds about 60 nucleotide molecules “in one fell swoop to the end of the chromosome,” Dr. Wright said.

Researchers also discovered that structures in cells called Cajal bodies help process telomerase during chromosome-repair activity. Cajal bodies assemble ribonucleic acid (RNA) within proteins.

“Telomerase uses this RNA in order to add the sequences onto the end, and this complex is assembled or modified in some way in these Cajal bodies,” Dr. Wright said.

UT Southwestern scientists next will work to pinpoint the precise molecules that bring telomerase to telomeres for potential development of inhibitors that would be new cancer drugs.

“We now need to find the molecules that are doing that as targets for additional inhibitors,” Dr. Wright said. “We have identified the step, but we haven’t yet identified the molecules involved.”

One drug that blocks telomerase, Imetelstat or GRN163L, was developed by the biotechnology company Geron with help from Drs. Wright and Jerry Shay, professor of cell biology. That drug, tested at UT Southwestern, is currently in clinical trials for treatment of several types of cancer.

Other UT Southwestern researchers involved in this study were lead author and assistant instructor Dr. Yong Zhao; Dr. Jinyong Kim and Dr. Guido Stadler, both postdoctoral fellows in cell biology; Ugur Eskiocak, a student research assistant in cell biology; and Dr. Shay. Biochemistry and molecular biology and genetics researchers at the University of Georgia also participated.



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Dr. Jerry Shay Gives Keynote Address on Telomeres at A4M, Las Vegas, December 2011 (33:00)



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yaeli
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Quoted from yaeli
Is it true that the shortening of telomeres is very important to health, because it induces apoptosis in good time?  
This question is truly very much beside, even far away from the point, which is to fortify the regular, healthy cells, and to enable a regulated expression of tolamerase in order to heal and to stay young and healthy.



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Conor
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Quoted from yaeli
Is it true that the shortening of telomeres is very important to health, because it induces apoptosis in good time? ... This question is truly very much beside, even far away from the point, which is to fortify the regular, healthy cells, and to enable a regulated expression of tolamerase in order to heal and to stay young and healthy.

I guess another way to look at it is not so much in "good time," but, rather, bad time, i.e., apoptosis occurs before their time.

And, I agree with your latter point. (:



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Spring
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For my part, I am a lot more interested in feeling well for as long as possible rather that worrying about living to be ninety or above! I want to enjoy my children  and grandchildren now instead of worrying about not seeing them graduate from high school! So all these wonderful foods and supplements that are helping me do that are worth every penny and every effort!

However, I do understand that people with, or who have had, severe health problems are another story altogether. They need all the help they can get from anyone who can help them attain better health and keep it.

It is amazing how much has been learned in the last ten years that was unheard of  before!! I don't know how Dr. D.'s brain ever "goes to sleep" at night with all the different angles of this huge mountain of information and how it will affect the other mountain that he has already learned and put into use. Boggles my mind.


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Conor
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Quoted from Spring
It is amazing how much has been learned in the last ten years that was unheard of  before!! I don't know how Dr. D.'s brain ever "goes to sleep" at night with all the different angles of this huge mountain of information and how it will affect the other mountain that he has already learned and put into use. Boggles my mind.

Agreed ... and another thing that amazes me is, despite all the information we've gained up to this point, we realize that we're just scratching the surface in a number of respects. Pretty humbling.



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yaeli
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Quoted from Conor

I guess another way to look at it is not so much in "good time," but, rather, bad time, i.e., apoptosis occurs before their time.

And, I agree with your latter point. (:
Blessed be Thou God our Lord the maker of apoptosis! As long as apoptosis occurs, be it in a relatively young age, it is good times - wonderful times - myriadfold better than the horrible times when cancerous cells start to proliferate God forbid!  






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Quoted from Conor
Pretty humbling.
Amen.



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No wonder Dr. D. is such a humble man..... I like this remark, "You, your genes, and your life experience come together to create a unique melody that no one else will ever quite duplicate. I invite you to take a moment to share my wonder at that fact."

I've been sharing a great deal more in that wonder with this latest experience with Trehalose Complex. I'm more than glad  Dr. D. took the baton on that one!! Everyone I've been around since I started taking it want to try it. Not so much by what I have said, but what they see.


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Amazone I.
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there are some good therapists who think that cancer is a product of cell-fermentation..... I think the Dr. Coy's recommendations are based upon that....
and if I've understood it well... so really what is oxidative stress to the cells...how and what is created whithin this process... yup I think the idea of cell-fermentation isn't that far away at all.....so apoptosis must be induced instantly instead of continioug ongoing of cell-fermentations ......

Inhibiting of..... this is heared everywhere... but how and why not using *prevention* instead ....

btw. there are a lot of approaches and understanding what cancer is about and how it is created... but ther's a reply to be seen here :www.orthokennis.org   all about salvestroles.... ....


MIfHI K-174

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