27 replies to this topic

[Turnbuckle]

Background:

Methylation patterns determine how genes are expressed and distinguish one cell type from another. Epigenetic drift is a stochastic process that occurs when genes lose or gain methylation inappropriately, thus detuning cells for their particular function. The methylation pattern of selected genes can be used as a genetic clock that correlates well with chronological age — Horvath’s clock, for instance. How to reverse the clock is an open question.

 

Telomeres can be used as a separate clock, and as cells age and divide their telomeres shorten and eventually the cells become senescent. Telomerase is an enzyme that restores telomeres to a more youthful age, thus that clock can be reversed. Supplements are sold that purport to protect and lengthen telomeres. From LEF.

 

Paradox:

Oddly, gene variants associated with longer telomeres are associated with faster epigenetic aging. It seems that turning back one clock advances the other.

 

Hypothesis:

Most somatic cells typically have undetectable levels of telomerase and thus their ability to divide is finite. If you took supplements that allowed those cells to live longer and divide more times, the expanded numbers of epigenetically old cells would increase the average epigenetic age of the body and advance Horvath’s clock. Conversely, somatic cells derived from stem cells (with their zero age epigenetics) bring down the average epigenetic age. Thus, by using stem cell activators along with telomerase activators that don’t affect somatic cells, the average epigenetic and telomeric age of the body can be decreased. Old somatic cells with damaged epigenetics die and are replaced with stem-cell-derived daughter cells with zero epigenetic age and full length telomeres. Both clocks are reversed.

 

 

Notes:

 

1. The paradox: Long telomeres and epigenetic aging are inversely correlated—

 

The paradoxical finding that TERT alleles associated with longer telomeres are associated with higher IEAA [intrinsic epigenetic age acceleration] ... While the paradoxical finding cannot be disputed on scientific grounds, its biological interpretation remains to be elucidated.

https://www.nature.c...467-017-02697-5

 

 

2. Where stem cells get their epigenetic patterns for differentiation is not yet understood. But clearly part of the pattern must be created de novo and thus starts off with zero age.

 

In contrast to maintenance methylation, the mechanism(s) that determine the specificity of de novo methylation are not completely elucidated.

https://www.ncbi.nlm...les/PMC5027477/

 

 

3. Transplantation of blood stem cells reduces the epigenetic age, at least temporarily—

 

Dynamics of epigenetic age following hematopoietic stem cell transplantation

 

we observed a strong decrease in DNAm age (termed “rejuvenation”) within the first six months of transplantation… We measured a decrease in mean DNAm age to a minimum until day +178 … after transplantation. Afterwards, significant accelerated epigenetic aging was observed.

https://www.ncbi.nlm...les/PMC5541887/

 

[motorcitykid]

It would be interesting to look at the Horvath clocks of super centarians and children with Progeria Syndrome. It's already been shown that these two groups have telomere lengths to the extreme, in opposite directions, long and short respectively. Looking at their Horvath clocks might help us better understand the relationship between methylation and telomere length.

[QuestforLife]

Progeria patients have very short telomeres but a normal epigenetic age, which supports the above hypothesis.

https://www.ncbi.nlm...les/PMC4015143/

Longer telomeres in somatic cells clearly permits a slower replacement from the stem cell pool. That doesnt mean those cells are any less functional. In this way people with longer telomeres and older people appear similar according to the Horvath clock. I've posted about this extensively over on Josh Mitteldorf's site, as I believe he has missed this essential point in his judgement of the merits of telomere therapy.

https://joshmitteldo...#comment-392192

[motorcitykid]

Progeria patients have very short telomeres but a normal epigenetic age, which supports the above hypothesis.

https://www.ncbi.nlm...les/PMC4015143/

Longer telomeres in somatic cells clearly permits a slower replacement from the stem cell pool. That doesnt mean those cells are any less functional. In this way people with longer telomeres and older people appear similar according to the Horvath clock. I've posted about this extensively over on Josh Mitteldorf's site, as I believe he has missed this essential point in his judgement of the merits of telomere therapy.

https://joshmitteldo...#comment-392192

 

DNA methylation levels of semi-supercentarians:   https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4712339/

 

[Graviton]

 

 

Thus, by using stem cell activators along with telomerase activators that don’t affect somatic cells, the average epigenetic and telomeric age of the body can be decreased.

If C60oo can act as a powerful antioxidant while it may induce stem cells differentiation/proliferation, would c60oo action cause increase of epigenetic age or the other way around?

The points are (1) Antioxidants may delay the senescence, which may lead to increase of epigenetical age.

(2) Stem cell differentiation/proliferation may decrease the average epigenetical age.

 

If it can act as a mitochondria antioxidant, it would slow down the senescence of cells, and then the epigenetic age may increase because it might delay either autophagy or apoptosis, which can lead to build up of epigentically older cells.

Edited by Graviton, 29 May 2018 - 05:59 AM.

[Turnbuckle]

If C60oo can act as a powerful antioxidant while it may induce stem cells differentiation/proliferation, would c60oo action cause increase of epigenetic age or the other way around?

The points are (1) Antioxidants may delay the senescence, which may lead to increase of epigenetical age.

(2) Stem cell differentiation/proliferation may decrease the average epigenetical age.

 

If it can act as a mitochondria antioxidant, it would slow down the senescence of cells, and then the epigenetic age may increase because it might delay either autophagy or apoptosis, which can lead to build up of epigentically older cells.

 

 

The same argument could be made for many antioxidants. In fact, in the protocol I suggested in Stem cell self-renewal with C60, I included ascorbic acid, which has been shown to reduce telomere shortening. But this is all in the timing. I'm trying to stimulate the symmetric proliferation of stem cells and protect (if not lengthen) their telomeres simultaneously. There will be no effect on somatic cell telomeres unless they are dividing at the same time.  Separately I proposed a method of getting rid of senescent cells by stimulating mtio fission and P53.

Edited by Turnbuckle, 29 May 2018 - 10:59 AM.

[Turnbuckle]

Results of my 2 epigenetic age tests

 

Summary: Epigenetic age went down by 11 years after 3 months of stem cell treatments.

 

According to 2 epigenetic age results from Osiris Green, I experienced an epigenetic age reversal of 11.2 years in 5 months, the latter 3 months which included my evolving stem cell protocol found in this thread. There were 34 SC treatments in this period, and two days of a treatment to remove senescent cells. The 11-year reversal is a calculated result based on three genes. The detailed results are more complicated. One gene went up 2 years, one went up 10 years, and the third (which supposedly has the lowest deviation) went down 27 years (which is in line with the way I feel). More tests will be needed, for sure.

 

Test 2: (Actual age 66.83)

Estimated age: 55.7 years old, plus or minus 1.8 years (median absolute deviation).

ASPA Gene -- 68.9 plus or minus 8.6 years (median absolute deviation).

EDARADD Gene -- 34.2 plus or minus 2.7 years (median absolute deviation).

ITGA2B Gene -- 86.1 plus or minus 7.2 years (median absolute deviation).

 

Test 1: (Actual age 66.42)

Estimated age: 66.9 years old, plus or minus 1.8 years (median absolute deviation).

ASPA Gene -- 70.8 plus or minus 8.6 years (median absolute deviation).

EDARADD Gene -- 60.9 plus or minus 2.7 years (median absolute deviation).

ITGA2B Gene -- 76.3 plus or minus 7.2 years (median absolute deviation).

 

Caveats: The first test collected saliva, the second gum cells. According to Dr. Neil Copes, CEO of Osiris Green, the second test presented some difficulties. Normally 10-15% of their samples fail QC initially and have to be rerun. Mine failed twice before passing. That is, I assume it passed, as I finally got the results. The discussion can be found here, beginning with post #17.

 

 

 

 

 

Edited by Turnbuckle, 28 July 2018 - 02:41 AM.

[Graviton]

It's kind of surprising that epigenetic age can be highly variable for a short period. Methylation/demethylation between two tests has a kind of big difference.

 

Osiris green has recently updated their method(s).

 

Do you notice any kind of physical sign, other than psychological feeling?

Edited by Graviton, 28 July 2018 - 03:06 AM.

[Turnbuckle]

 

Do you notice any kind of physical sign, other than psychological feeling?

 

See my stem cell thread, posts #201 and #214.

[ryukenden]

Results of my 2 epigenetic age tests

Summary: Epigenetic age went down by 11 years after 3 months of stem cell treatments.

According to 2 epigenetic age results from Osiris Green, I experienced an epigenetic age reversal of 11.2 years in 5 months, the latter 3 months which included my evolving stem cell protocol found in this thread. There were 34 SC treatments in this period, and two days of a treatment to remove senescent cells. The 11-year reversal is a calculated result based on three genes. The detailed results are more complicated. One gene went up 2 years, one went up 10 years, and the third (which supposedly has the lowest deviation) went down 27 years (which is in line with the way I feel). More tests will be needed, for sure.

Test 2: (Actual age 66.83)
Estimated age: 55.7 years old, plus or minus 1.8 years (median absolute deviation).
ASPA Gene -- 68.9 plus or minus 8.6 years (median absolute deviation).
EDARADD Gene -- 34.2 plus or minus 2.7 years (median absolute deviation).
ITGA2B Gene -- 86.1 plus or minus 7.2 years (median absolute deviation).

Test 1: (Actual age 66.42)
Estimated age: 66.9 years old, plus or minus 1.8 years (median absolute deviation).
ASPA Gene -- 70.8 plus or minus 8.6 years (median absolute deviation).
EDARADD Gene -- 60.9 plus or minus 2.7 years (median absolute deviation).
ITGA2B Gene -- 76.3 plus or minus 7.2 years (median absolute deviation).

Caveats: The first test collected saliva, the second gum cells. According to Dr. Neil Copes, CEO of Osiris Green, the second test presented some difficulties. Normally 10-15% of their samples fail QC initially and have to be rerun. Mine failed twice before passing. That is, I assume it passed, as I finally got the results. The discussion can be found here, beginning with post #17.

Apart from EDARADD Gene, other genes were more than your age. Other genes were up over 86. May be your stem cell therapy is not working.

Edited by ryukenden, 01 August 2018 - 05:37 AM.

[Turnbuckle]

Apart from EDARADD Gene, other genes were more than your age. Other genes were up over 86. May be your stem cell therapy is not working.

 

 

 

I believe the age increase in those two genes was due first to the fact that adult stem cells are not entirely methylated de novo during differentiation and thus the age of all genes cannot be reversed this way (with zero age methylation), and second to my overuse of telomerase stimulants in my first experiment, which can rescue senescent cells thus increasing the average epigenetic age. I'd included these stimulants to insure that the stem cells themselves would not undergo shortening of their telomeres in spite of their higher expression of telomerase, but using them every time was excessive as I see now. I have discontinued them for the time being and have increased the use of a senescent cell clearance protocol, which I'd done only once in my first 3 month experiment. See this post.

 

The initial idea was based on the epigenetic theory of ageing: Cells are detuned for their purpose by the accumulation of epimutations, which occur at a far higher rate than mutations to the DNA itself.  So by replacing epigenetically old DNA of senescent cells with zero epigenetic age DNA of differentiated stem cells, the average age of a population of cells can be brought down. With adult stem cells, however, this is only possible for a subset of genes. While the epigenetic age for all genes is close to zero for embryonic cells, the age reversal potential of stem cells falls as the stem cell becomes more specialized. Totipotent stem cells have more age reversal potential than pluripotent SCs, for example, which have more than multipotent SCs. So this protocol produces only an average age reduction where not all genes show dramatic age reversal. 

Edited by Turnbuckle, 01 August 2018 - 09:57 AM.

[QuestforLife]

Test 2: (Actual age 66.83)

Estimated age: 55.7 years old, plus or minus 1.8 years (median absolute deviation).

ASPA Gene -- 68.9 plus or minus 8.6 years (median absolute deviation).

EDARADD Gene -- 34.2 plus or minus 2.7 years (median absolute deviation).

ITGA2B Gene -- 86.1 plus or minus 7.2 years (median absolute deviation).

 

Test 1: (Actual age 66.42)

Estimated age: 66.9 years old, plus or minus 1.8 years (median absolute deviation).

ASPA Gene -- 70.8 plus or minus 8.6 years (median absolute deviation).

EDARADD Gene -- 60.9 plus or minus 2.7 years (median absolute deviation).

ITGA2B Gene -- 76.3 plus or minus 7.2 years (median absolute deviation).

 

Well the change in the three genes from test 1 to test 2 is:

ASPA: -1.9 years (not significant based on the error bound of +/-8.6 years)

EDARADD: -26.7 years (highly significant based on the error bound of +/- 2.7 years)

ITGA2B: +9.2 years (only just significant based on the error bound of +/-7.2 years)

 

The overall result (I'm unclear how they do the weighting?) of a change of -11.2 years is highly significant based on the error bound of +/-1.8 years.

 

So overall I'd say the result is highly encouraging, but more tests are required. 

Edited by QuestforLife, 01 August 2018 - 10:19 AM.

[Turnbuckle]

Well the change in the three genes from test 1 to test 2 is:

ASPA: -1.9 years (not significant based on the error bound of +/-8.6 years)

EDARADD: -26.7 years (highly significant based on the error bound of +/- 2.7 years)

ITGA2B: +9.2 years (only just significant based on the error bound of +/-7.2 years)

 

The overall result (I'm unclear how they do the weighting?) of a change of -11.2 years is highly significant based on the error bound of +/-1.8 years.

 

So overall I'd say the result is highly encouraging, but more tests are required. 

 

 

You are correct, of course, and thanks for pointing that out. OG spreads the results out on 4 pages instead of one and on first glance I got the idea that 2 genes had gone up when in fact 2 genes had gone down, one insignificantly, and one ten times the median deviation. 

Edited by Turnbuckle, 01 August 2018 - 11:13 AM.

[ryukenden]

I believe the age increase in those two genes was due first to the fact that adult stem cells are not entirely methylated de novo during differentiation and thus the age of all genes cannot be reversed this way (with zero age methylation), and second to my overuse of telomerase stimulants in my first experiment, which can rescue senescent cells thus increasing the average epigenetic age. I'd included these stimulants to insure that the stem cells themselves would not undergo shortening of their telomeres in spite of their higher expression of telomerase, but using them every time was excessive as I see now. I have discontinued them for the time being and have increased the use of a senescent cell clearance protocol, which I'd done only once in my first 3 month experiment. See this post.

The initial idea was based on the epigenetic theory of ageing: Cells are detuned for their purpose by the accumulation of epimutations, which occur at a far higher rate than mutations to the DNA itself. So by replacing epigenetically old DNA of senescent cells with zero epigenetic age DNA of differentiated stem cells, the average age of a population of cells can be brought down. With adult stem cells, however, this is only possible for a subset of genes. While the epigenetic age for all genes is close to zero for embryonic cells, the age reversal potential of stem cells falls as the stem cell becomes more specialized. Totipotent stem cells have more age reversal potential than pluripotent SCs, for example, which have more than multipotent SCs. So this protocol produces only an average age reduction where not all genes show dramatic age reversal.

Thank you. Did you do any baseline epigenetic testing to compare with before you started the stem cell renewal?

[Turnbuckle]

Thank you. Did you do any baseline epigenetic testing to compare with before you started the stem cell renewal?

 

See post #7 above--

 

I experienced an epigenetic age reversal of 11.2 years in 5 months, the latter 3 months which included my evolving stem cell protocol found in this thread. There were 34 SC treatments in this period, and two days of a treatment to remove senescent cells.

 

 

Three months treatment (5 months overall as I didn't begin the treatment until 2 months after getting the baseline) produced an 11 year decline in epigenetic age.

 

BTW, I said previously that 2 genes went up in age and one went down, but that was incorrect. It was the opposite--two went down and one went up.

Edited by Turnbuckle, 02 August 2018 - 12:28 PM.

[DareDevil]

Hi Turnbuckle,

 

Thanks for explaining these processes. I have taken quite a few vials of Epitalon in the past few years and note that this might not be ideal if one wishes to rejuvenate one's body and appearance. If I understood correctly, by lengthening telomeres and salvaging senescent cells it makes your body contain a higher proportion of aging cells, preserving you as older rather than renewing cells and making you younger?

 

How would you recommend combining Stem Cell increase with Telomere lengthening? I assume their actions are not entirely incompatible even if they have a somewhat different incidence on the two currently known age clocks. I do seasonal clearance of senescent cells with senolytics, have bone marrow stem cell infusions twice a year, and routinely take Epitalon. Thanks for your advice about what I might be doing wrong according to time clock theories.

 

DareDevil

[Turnbuckle]

 

 

How would you recommend combining Stem Cell increase with Telomere lengthening? I assume their actions are not entirely incompatible even if they have a somewhat different incidence on the two currently known age clocks. I do seasonal clearance of senescent cells with senolytics, have bone marrow stem cell infusions twice a year, and routinely take Epitalon. Thanks for your advice about what I might be doing wrong according to time clock theories.

 

DareDevil

 

I had originally included telomerase supplements with my stem cell protocol, thinking it wouldn't be a problem as it would mostly affect stem cells that were being forced into proliferation by C60. But then I began to wonder how skin could age epigenetically if it was being resupplied by zero age stem cells at the basal level, with differentiated cells moving up and then dying and sloughing off. The sloughed off cells should always be the same age and companies like Osiris Green shouldn't be able to measure epigenetic age with any reliability from buccal cells. But turns out most of the division is done by cells that lie just above the stem cell layer. These "transit amplifying cells" (TACs) are not stem cells but produce telomerase and appear to have more methylation than stem cells. Thus they can age epigenetically, and the more telomerase they produce, the older they can get, while the underlying stem cells are held in reserve. And TACs are not just found in the epidermis. They have been found in the cornea, prostate, hair follicles, mammary gland, intestines, and likely exist in other tissues as well. Given that the aging of TACs would then be a major source of aging in the tissues they supply, I began to think that any telomerase supplement might be bad if you are interested in reversing the epigenetic clock.

 

Transit-Amplifying Cells in the Fast Lane from Stem Cells towards Differentiation

[dlewis1453]

See post #7 above--

 

 

Three months treatment (5 months overall as I didn't begin the treatment until 2 months after getting the baseline) produced an 11 year decline in epigenetic age.

 

BTW, I said previously that 2 genes went up in age and one went down, but that was incorrect. It was the opposite--two went down and one went up.

 

 

Hi Turnbuckle, 

 

You had already supplemented with C60 for several years before your first epigenetic test. Interestingly, your estimated age on this first baseline test matched very closely to your actual age. You did not experience epigenetic age reversal until you began your stem cell renewal protocol. 

 

Were you surprised that C60 alone had no effect on your epigenetic age?  You experienced some apparent rejuvenation from C60 alone, so I would have expected this to be reflected in your first test. 

Edited by dlewis1453, 09 October 2019 - 10:16 PM.

[Turnbuckle]

Hi Turnbuckle, 

 

You had already supplemented with C60 for several years before your first epigenetic test. Interestingly, your estimated age on this first baseline test matched very closely to your actual age. You did not experience epigenetic age reversal until you began your stem cell renewal protocol. 

 

Were you surprised that C60 alone had no effect on your epigenetic age?  You experienced some apparent rejuvenation from C60 alone, so I would have expected this to be reflected in your first test. 

 

I first used C60 in early 2012, and epigenetic tests were not available, so I can only speculate that my epigenetic age first regressed, then moved up again due to depleted stem cell pools. The apparent stem cell effects also reverted back to baseline, though that's hard to say precisely. So I'd say it was probably a combination of things: that my e-age didn't fall back that much to begin with, then began creeping back due to SC depletion, and finally, coincidence. 

[dlewis1453]

I first used C60 in early 2012, and epigenetic tests were not available, so I can only speculate that my epigenetic age first regressed, then moved up again due to depleted stem cell pools. The apparent stem cell effects also reverted back to baseline, though that's hard to say precisely. So I'd say it was probably a combination of things: that my e-age didn't fall back that much to begin with, then began creeping back due to SC depletion, and finally, coincidence. 

 

Interesting, thanks Turnbuckle. 

 

By the way, I was reading the comments on an article at Josh Mitteldorf's blog, and I found the following comment. Looks like there is someone else out there who is thinking similarly to you.

 

_____________________________________________________________________________________

Fast dividing cells will also accumulate such methylation errors through cell division, when methylation has to be removed and then re-added, but so long as they are replaced by more quiescent stem cells (which have less such errors) DNAm age is kept under control and advances only as quickly as it does in the stem cell compartment.

So there are two things going on regarding methylation ‘aging’, 1) aging of somatic tissues that are not replaced, and 2) aging of the stem cell compartment that is replacing proliferating tissues.

A consequence of this is that extending telomeres in proliferating tissues will obviously increase DNAm age because these cells then require replacement by (less metabolically active) stem cells less often. This is why people with longer telomeres have an older DNAm age. But this is a different situation to old people who have a high DNAm age because of the aging of their stem cell compartment, which slows the rate of replacement of somatic cells and therefore leads to the advance of DNAm age in somatic cells as well.

Almost no one, including Horvath, seems to grasp this. But the data is all there in pubmed, for anyone to discover.

But if we could maintain stem cells indefinitely, we would solve both the telomere ‘aging program’ and the methylation error ‘aging program’. This is why I am so interested in ex vivo pluripotent stem cells infusions and also very small embryonic like stem cells (VSELs) that still exist in even old tissues.

[ryukenden]

Do you have plans to repeat the tests? Last test was done in July 2018. About one and half year since. Is it not worth repeating to get compared?

[Turnbuckle]

Do you have plans to repeat the tests? Last test was done in July 2018. About one and half year since. Is it not worth repeating to get compared?

 

I posted the latest results on a couple of threads at the end of December--2 weeks ago--but neglected to post it here. That post is copied below--

 

My latest epigenetic age result from a new company called TruMe is 13.0 years below my chronological age.  TruMe uses white blood cells harvested from spit. This is compared to my pre-protocol baseline result from Osiris Green in February 2018, which was 0.4 years above my chronological age. Like Osiris Green, TruMe uses a reduced set of markers, but different ones. I have another test ordered from myDNAge, which uses a much larger set that in my experience wasn't significantly different from Osiris Green. Osiris Green is now defunct.

 

Edited by Turnbuckle, 13 January 2020 - 01:41 PM.

[ryukenden]

I posted the latest results on a couple of threads at the end of December--2 weeks ago--but neglected to post it here. That post is copied below--

Thank you for the update and it is encouraging. Keep the good work.

[ClarkSims]

In Baati's C60 olive oil experiment, he fasted his rats for 24 hours before giving them large amounts of C60 olive oil.

I have found numerous papers saying that fasting increases mitochondrial fusion, such as: https://www.ncbi.nlm...pubmed/25271058

So maybe this is the secret second ingredient for Baati's surprising results?

 

Thanks for your great thoughts.

Clark

[ClarkSims]

Test 2: (Actual age 66.83)

Estimated age: 55.7 years old, plus or minus 1.8 years (median absolute deviation).

ASPA Gene -- 68.9 plus or minus 8.6 years (median absolute deviation).

EDARADD Gene -- 34.2 plus or minus 2.7 years (median absolute deviation).

ITGA2B Gene -- 86.1 plus or minus 7.2 years (median absolute deviation).

 

Test 1: (Actual age 66.42)

Estimated age: 66.9 years old, plus or minus 1.8 years (median absolute deviation).

ASPA Gene -- 70.8 plus or minus 8.6 years (median absolute deviation).

EDARADD Gene -- 60.9 plus or minus 2.7 years (median absolute deviation).

ITGA2B Gene -- 76.3 plus or minus 7.2 years (median absolute deviation).

e discussion can be found here, beginning with post #17.

 

 

 

 

Is this 4 separate subtest, within a test set, or are these three numbers combined to yield the net number?
If the latter, how do they calculate the final change in age?

Thanks,

Clark
 

[Turnbuckle]

In Baati's C60 olive oil experiment, he fasted his rats for 24 hours before giving them large amounts of C60 olive oil.

I have found numerous papers saying that fasting increases mitochondrial fusion, such as: https://www.ncbi.nlm...pubmed/25271058

So maybe this is the secret second ingredient for Baati's surprising results?

 

Thanks for your great thoughts.

Clark

 

 

They were fasted overnight, actually. 

 

Before C60 administration, the rats were fasted overnight but with access to water. -- https://sci-hub.se/1...als.2012.03.036

 

 

 

And that was for the short term pharmacokinetics and biodistribution studies. It's not clear what they did for the chronic study. I expect the great results come more from the short rat lifespans and the short treatment period of 6 months. I only noticed substantial fading over a much longer period.

[ClarkSims]

 

They were fasted overnight, actually. 

 

 

 

And that was for the short term pharmacokinetics and biodistribution studies. It's not clear what they did for the chronic study. I expect the great results come more from the short rat lifespans and the short treatment period of 6 months. I only noticed substantial fading over a much longer period.

 

Good catch. 12  to 18 hours, not 24 hours.

But this is supposed to be a long fast for a rat.

I have never watched a rat, but I understand they feed constantly.

[nadaepeu]

Is anyone aware of any epigenetic age-testing companies located in Europe?