this could be important.
How do you know this exactly?
TruDiagnostic
FWIW I took it using someone else’s kit so it has HIS bio info rather than mine and that has to be filtered out.
Patient report:
page 1: cover
page 2: includes info on intrinsic age, extrinsic age, chronological age, change over time, population. I believe X said unfortunately these are his age not yours, but I will delete them anyways (plan: to delete the age related numbers)
page 3: dunedinPace value, change over time (plan: delete all dunedin pace numbers on the page)
page 4: telomere length numbers (plan: keep)
page 5: mitotic clock number, stem cell divisions per stem cell per year, average estimate for intrinsic rate of stem-cell division, percentiles (plan: keep)
page 6: type 2 diabetes risk, PHOSPH01 epitype value, related DNA methylation score at the ABCG1 locus (plan: keep)
page 7: obesity risk, FGFRL1, NCAPH2, PNKD, SMAD3 DNA methylation score at FGFRL1 locus (plan: keep)
page 8: weight loss response based on DNA methylation scores at the above loci, (plan: keep)
page 9: smoking, disease risk, DNA methylation score at AHRR locus, alcohol consumption and DNA methylation, risk percentile (plan: keep)second part, your epigenetic methylation data:
page 1-4: scientific introduction on theory and methods (plan: keep)
page 5-17: your CpG values in table form, with a list of your beta values for various genes. There are NO age or relative age data, only a long list of beta values. (plan: keep)
he is significantly younger than his chronological age, his telomeres are longer than his age group, and his rate of stem cell division is lower than 99.8% of people. He may be epigenetically predisposed to obesity — not sure if this is prior to his calorie restriction, or if the methylation was induced by his calorie restriction practices
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An alternative model, recently advocated by Berman and colleagues [17], is focused on “solo-WCGWs,” i.e., isolated CpGs occurring in a WCGW sequence context, which are generally methylated in fetal tissue and which would gradually lose methylation as a result of incomplete methylation maintenance during cell division. Approximately 3.7 million solo-WCGWs were identified, with 1.8 million of these mapping to partially methylated domains (PMDs), which largely overlap with late-replicating regions [40]. While hypomethylation at solo-WCGWs is largely seen in cancer and early development (i.e., states of high replicative stress), it is unclear whether DNAm loss in late-replicating regions would play a sufficiently major role in a normal physiological setting or in pre-cancerous states where cells are not under significant replicative stress
Or maybe methylation maintenance during cell division could be extraordinarily good (but there’s probably a reference group of other sites to measure this)
Division rate is lower over time, which is consistent with epigenetic aging rate ALSO slowing over time in older populations
Good. As Dr. Andrei Gudkov wisecracked, “you will die healthy.”
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Alex - what dose of rapamycin have you usually been taking (and for how many years have you been taking it?)
Also - I wonder if rapamycin might be playing a role in this given this research: Rapamycin Prevents Blood Stem Cell Aging, New MIT Study
20mg biweekly (with grapefruit) with some breaks.
I maybe started taking it in 2019/2020? (have to check email archives). Not a lot of time for it to work out its effects
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This is EpiTOC2:
, this may suggest that EpiTOC2 and HypoClock are not capturing proliferation
per se, but something else correlative with turnover within a given tissue or cell type. Further
evidence of this is that the modules in these two clocks did track with passaging in astrocytes.
For EpiTOC2 the navy, light-blue, and cyan modules, but not the pink module, showed strong
increases as a function of passaging, or days in culture. Interestingly, the light-blue and navy
modules exhibited an exponential increase across the lifespan of these cells. This suggests they
are tracking phenomena like genomic instability or activation of senescence pathway
I’m definitely going DEEP into the Levine 2022 paper… Navy is dark blue…
Other
interesting trends include the increase in the green-yellow module, which hits an inflection point
around 43 days in culture (passage 6). This is noteworthy, as this was the point in time when we
began to observe an up-tick in senescence markers and slowing of cell population doublings
(cPD), suggesting cells are beginning to enter a state of growth arrest (Figure S8). The orange
module
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I have worse Hannum than Horvath. Idk what the hell this even means.
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