Methylation Clocks and True Biological Age

The good news is that the DataBETA project has found a home.  After several months of seeking a university partner, I am thrilled to be working with Moshe Szyf’s lab at McGill School of Medicine.  DataBETA is a broad survey of things people do to try to extend life expectancy, combined with evaluation of these strategies (and their interactions!) using the latest epigenetic clocks.  Szyf was a true pioneer of epigenetic science, back in an era when epigenetics was not yet on any of our radar screens. No one has more experience extracting information from methylation data.


DataBETA is just the kind of study that is newly possible, now that methylation clocks have come of age. Studies of anti-aging interventions had been impractical in the past, because as long as the study depends on people dying of old age, it is going to take decades and cost $ tens of millions. Using methylation clocks to evaluate biological age shortcuts that process, potentially slashing the time by a factor of 10 and the cost by a factor of 100.  But it depends critically on the assumption that the methylation clocks remain true predictors of disease and death when unnatural interventions are imposed. Is methylation an indicator, a passive marker of age? Or do changing methylation patterns cause aging?

Two types of methylation changes with age

Everyone agrees that methylation changes with age are the most accurate measure we have, by far, of a person’s chronological age—and beyond this, the GrimAge clock and PhenoAge clock are actually better indications of a person’s life expectancy and future morbidity than his chronological age.

Everyone agrees that methylation is a program under the body’s control. Epigenetic signals control gene expression, and gene expression is central to every aspect of the body’s metabolism, every stage of life history. Sure, there is a loss of focus in methylation patterns with age, sometimes called “epigenetic drift”.  But there is also clearly directed change, and it is on the directed changes that methylation clocks are based.

But there are two interpretations of what this means. (1) There is the theory that aging is fundamentally an epigenetic program. Senescence and death proceed on an evolutionarily-determined time schedule, just as growth and development unfold via epigenetic programming at an earlier stage in life. Several prominent articles were written even before the first Horvath clock proposing this ideas [ref, ref], and I have been a proponent of this view from early on [ref]. If you think this way, then methylation changes are a root cause of aging, and restoring the body to a younger epigenetic state is likely to make the body younger.

(2) The other view, based on an evolutionary paradigm of purely individual selection, denies that programmed self-destruciton is a biological possibility. Since there is a program in late-life epigenetic changes, it must be a response and not a cause of aging. Aging is damage to the body at the molecular and cellular level. In response to this threat, the body is ramping up its repair and defense mechanisms, and this accounts for consistency of the methylation clock. In this view, setting back the methylation pattern to a younger state would be counter-productive. To do so is to shut off the body’s repair mechanisms and to shorten life expectancy.

So, if you believe (1) then setting back the bodys methylation clock leads to longer life, but if you believe (2) then setting back the bodys methylation clock leads to shorter life.

I think there is good reason to support the first interpretation (1). Epigenetics is fundamentally about gene expression. If you drill down to specific changes in gene expression with age, you find that glutathione, CoQ10=ubiquinone, SOD and other antioxidant defenses are actually dialed down in late life when we need them more. You find that inflammatory cytokines like NFκB are ramped up, worsening the chronic inflammation that is our prominent enemy with age.  You find that protective hormones like pregnenolone are shut off, while damaging hormones like LH and FSH are sky high in women when, past menopause, they have no use for them. There is a method in this madness, and the method appears to be self-destruction.

Until this year, I have been very comfortable with this argument, and comfortable promoting the DataBETA study, which is founded in the premise that setting back the methylation clock is our best indicator of enhanced life expectancy. The thing that made me start to question was the story of Lu and Horvath’s GrimAge clock, which I blogged about back in March. 

The GrimAge clock is the best predictor of mortality and morbidity currently available, and it was built not directly on a purely statistical analysis of direct associations with m&m, but based on indirect associations with such things as inflammatory markers and smoking history. (This is a really interesting story, and I suggest you go back and read the March entry if you have not already. The story has been told in this way nowhere else.)

(Please be patient, I’m getting to the point.) Years of smoking leave an imprint on the body’s methylation patterns, and this imprint (but not the smoking history itself) is part of the GrimAge clock. I asked myself, How does smoking shorten life expectancy? I have always assumed that smoking damages the lungs, damages the arteries, damages the body’s chemistry. Smoking shortens lifespan not through instructions imprinted in the epigenetic program, but quite directly through damaging the body’s tissues. Therefore, the epigenetic shadow of smoker-years that contributes to the GrimAge clock is not likely to be programmed aging of type (1), but rather programmed protection, type (2).

For me, this realization marked a crisis. I have begun to worry that setting back the methylation clock does not always contribute positively to life expectancy. The canonical example is that if we erased the body’s protective response to the damage incurred by smoking, we would not expect the smoker to live longer.

The bottom line

I now believe there are two types of methylation changes with age. I remain convinced that type (1) predominates, and that setting these markers to a younger state is a healthy thing to do, and that it offers genuine rejuvenation. But there are also some type (2) changes with age—how common they are, I do not know—and we want to be careful not to set these back to a younger, less protected state. 

The methylation clocks promise a new era in medical research on aging, an era in which we can know what works without waiting decades to detect mortality differences between test and control groups. But it is only type (1) methylation changes that can be used in this way. So it is an urgent research priority to distinguish between these two types of directed changes.

This is a difficult problem, because the obvious research method would be to follow many people with many different methylation patterns for many decades—exactly the slow and costly process that the methylation clocks were going to help us avoid. My first hunch is that we might find a shortcut experimenting with cell cultures. Using CRISPR, we can induce methylation changes one-at-a-time in cell lines and then assess changes in the transcriptome, and with known metabolic chemistry, make an educated guess whether these changes are likely to be beneficial or the opposite. As stated, this probably will not work because methylation on CpGs tends to work not via individual sites but on islands that are typically ~1,000 base pairs in length. Perhaps changes in the transcriptome can be detected when we intervene to methylate or demethylate an entire CpG island.

Perhaps there is a better way. I invite suggestions from people who know more biology than I know for experimental ways to distinguish type (1) from type (2) methylation changes with age.

58 thoughts on “Methylation Clocks and True Biological Age

  1. Apologies for the unrelated question but it’s extremely difficult to find an answer for this: Why should niacinamide be avoided while NR, NMN, and NAD+ seem to offer rejuvenating benefits? Someone mentioned this in here a few months ago and I recently heard David Sinclair mention this as well. Thanks in advance.

  2. Great questions Josh!
    I find the topic of the methylation clock astonishing – there is still so much more to discover. In relation to the question if setting back the methylation clock would be beneficial or damaging in a smoker/former smoker: In a perfect scenario where setting back the methylation clock equals real rejuvenation, would that not mean that the damages from smoking would be just repaired like in a young person? I mean most young people who smoke do not suffer immediate consequences, but will accumulate damage that gets much more noticeable once our body diminishes its capacity for repair und begins to slowly selfdestruct. On the other hand I can see the point from scenario two in which the setting back will only create more room for the damage to expand. But why exactly would that happen? Would only some part of the signaling for inflammation/ malicious growth change whereas the actual cells are unaffected so that the damage they once suffered would not be reversed but even increased?
    By the way sorry for my English if there are too many errors, I am not a native speaker.

  3. Additionally (and I know that is a little late but it has some link to your previous post) I am currently working on my thesis project: It will be about P.gingivalis in relation to Alzheimer´s disease and/or pancreatic cancer (I am still discussing this with my tutor). I am going to do case control study to analyze the concentration of P.gingivalis in patients with AD or Pancreatic cancer vs a group of matched controls to see if there is a statistical significant difference in the bacterial load from the crevicular fluid samples of the two groups. If you are interested I will be happy to share the results with you. You just will have to be a bit more patient as I am just starting the project 🙂

    Best regards from Ecuador,
    Cynthia

    • Not quite “nothing”, we understand telomere shortening because of cell culture. But not nearly everything, either… look what happens when you transplant organs from shortlived pigs into longlived humans, e.g.

  4. I highly encourage McGill to invite participation by the University of British Columbia authors of “High-Resolution Single-Cell DNA Methylation Measurements Reveal Epigenetically Distinct Hematopoietic Stem Cell Subpopulations” https://www.cell.com/stem-cell-reports/article/S2213-6711(18)30308-4/fulltext
    Using their single-cell protocol with longitudinal samples could tease out answers to whether or not methylation clocks show causes or effects.

    • This is the area where I am awaiting the next breaktrough in aging research.

      “An atlas of the aging lung mapped by single cell transcriptomics and deep tissue proteomics”
      Open Access article.

      “Ageing affects DNA methylation drift and transcriptional cell-to-cell variability in mouse muscle stem cells”
      Nature communications

      Key takeaway for me:
      Aging effects are more pronounced in ECM and ECM related gene expression (maybe feedback control is not so tight as in the cytosol)

      Stem cells age much more slowly according to the epigenetic clock then terminally differentiated cells

      • Here’s what the BC researchers could contribute:
        “Current analytical strategies for single-cell DNA methylation measurements average DNA methylation in fixed genomic bins or over defined genomic regions.

        However, inference across cells (as well as sequence context) assumes homogeneity across cells, which is at cross-purposes with the generation of single-cell molecular measurements through the potential to mask rare subpopulations.”

  5. How it was established that smoking (substances that lungs and the body are treated during smoking) do not change these methylations directly? Thus it’s not a direct cause of smoking but indirect organism reaction?

    • Those are my thoughts too. It is possible that smoking happens to piggy-back on one of the processes that increase methylation age. So that the damage we perceive in the tissues is not the direct result of the chemicals ‘destroying’ structures, but of those chemicals promoting a harmful gene expression.

      I think what Josh was getting at, partly, is that since the GrimAge clock sites are not the same as the DNAm chronological age sites, then these are unlikely to be a result of an evolutionary conserved ageing program.

      But it’s also true that most other eAge clocks so far show little overlap. So it could be too early to characterize any of them as independent processes. We could be looking at parts of the same puzzle.

      I think that the story so far, is that processes that seem to increase cell turn-over and cell proliferation appear correlated with an increase in epigenetic age (or epigenetic measure of morbidity in this case). Think of radiation, alcohol abuse (liver cell turn-over), or obesity (higher cell proliferation?). And on the opposite side, caloric restriction or rapamycin use. Hard to say where exercise fits, a reduced caloric availability perhaps?. At least, that’s my current guess.

      Smoking probably increases cell turn over in the lungs. Although I am not so sure in other tissues in the body. If this is the upstream cause of the epigenetic changes, then it would be difficult to separate from other commonly attributed causes of ageing, such as senes. cell accumulation, telomere shortening or stem cell depletion. Or we are looking at different stages of the same underlying process.

      • Smoking might be the most convoluted lifestyle factor and therefore can easily mislead us. It causes damage in many unrelated ways.

        Some of the damage that is currently entirely attributed to smoking requires additional factors. Japanese smoke more but get less cancer, until they move, so it’s not simply different genetics (my guess is difference of ingredients in food).

        One of the ways commercial cigarettes cause damage is radiation. The tobacco plant’s roots go deep into the ground, reaching high levels of radioactive minerals, but just the low cost fertilizer alone raises levels dramatically. Radiation damage of course can not just affect DNA and cause mutations but other parts of the cells as well.

        Comparison: The Most Radioactive Places on Earth
        https://youtu.be/TRL7o2kPqw0?t=529

        Lower levels of oxygen –due to blood cells being busy transporting waste instead– probably leave very different traces than radiation damage and carcinogens that don’t exist until the moment a cigarette is fired up and the number of different molecules goes way up due to the activation energy from the lighter.

  6. Maybe this has been already asked. I live in Switzerland. Could I participate to the DataBETA study? Is it available in EU? I noticed some of the entries in the questionnaire are asked using non-SI units of measure which is not a problem though.

    • I hope to have a European partner to make it esy for EU subjects to participate. I’m also exporing contacts in China. Both these extensions will be valuable for broadening the array of anti-aging measure the program can sample.

      • Thank you Josh for the reply. Even greater news. I could leverage my participation also to gain insight and match with my data incl. supplementation, biomarkers (quite extensive), drugs and lifestyle changes over about 20 years and match with my genotype information.
        I have tried with no success to motivate the local Zymo reps and never received a reply from Zymo about accessibility here of their test (they are alternative too I know about).
        Good luck with you project and thank you for the hard work!

  7. Thanks for your hard work Josh. Can I ask how DataBeta is different from the Age Reversal Network’s project announced at RAADfest 2019?

    “The mission of Vitality in Aging (VIA) Research Group is to break new ground by trying to capture all the factors that influence healthy aging. The factors examined will run the full gamut from the basics of nature to the complexities of nurture. We will examine genetic and epigenetic influences on biological age, as well as the numerous factors that come into play after we are born with the hand dealt us: simple lifestyle factors and choices such as diet and exercise, pathogens to which we have been exposed, and of course therapies we have undergone in the hopes of slowing the decline in health so many of us experience as we age.
    Most of the above work will be conducted via our Longitudinal Study. But we will also conduct numerous intervention trials examining promising but neglected treatments that have shown efficacy in animal models, but never made it to human trials”.
    https://vitalityinaging.org/

    • The VIA program aims to validate the methylation clocks, to prove that they are a good measure of biological age under all circumstances. Logically, the VIA program is a prerequisite to DataBETA. But I’m leapfrogging the validation stage — which could take 15 years — and plunging forward on the assumption that methylation tests will valid. DataBETA is a 3-year project.

      If VIA finds that some methylation tests work better than others for this kind of study, then we’ll be able to revisit our data retroactively, since we’re measuring 850,000 methylation sites, not just the few hundred that are used in the Horvath clocks. Fifteen years from now, we’ll be able to go back and reinterpret our findings based on what VIA reports.

  8. Hi Josh.

    You’ve talked before about how a non aging (selfish) individual would be bad for the group.

    I think I see a parallel in the cells that survive in the aged body. Whenever I look into an aspect of aging, I always see the same thing. The cells that survive are the ones that are the worst at doing their job for the body. Everyone seems to assume that a mysterious process called aging is causing these cells to fail with age. But what if it is a selection process that leaves the most selfish cells alive?

    I can give concrete examples. Briefly, epidermal stem cells respond to stress signals through asymmetric division producing a replacement stem cell plus epidermal skin cell. But naturally some stem cells are more resistant to stress and instead with the appropriate growth signal they divide symmetrically, with two(more stress resistant) stem cells spreading out and eventually coming to dominant the epidermis. In this way skin replenishment requires ever greater stress signals and fails. Another example. Fibroblasts produce collagen from glycine at a limited rate that necessities recycling of most of the collagen produced. But eventually more collagen has to be made and this requires diversion of glycine from glutathione production and a rise in ROS (the glutathione level decline with age is secondary to declines in the blood levels of glycine and cysteine).This means the cells that produce most collagen are the most likely to die. Again, you’re always left with the most selfish cells.

    I can give other examples and references. Just food for thought.

    Best regards and good luck with your project.

    • I’m the wrong person to ask about this, since I’m prejudiced against the idea. I come to the table thinking that there are powerful incentives for cooperation of cells within a single individual because they all have the same DNA, and the only way that that DNA can survive long-term is if the individual does well.

      It’s certainly true that sometimes cells within the body fight selfishly among themselves and try to reproduce more than the next cell line. That’s called “cancer”.

      • I wouldn’t describe this process as programmed or a cell vs organism decision. It’s just based on the fact that cells will have a natural range of responses to a given stimuli, and that the cells that respond less will often survive longer, eventually desensitising the organism to that stimuli. The repair system of the body (adult stem cells) work in exactly this way. A given level of tissue damage (but not less) is sufficient to trigger ASC release from the bone marrow. But over time repeated stimulation leaves the remaining population in the bone marrow less sensitive to the signal and so repair can only be triggered with a stronger signal.

        This is an entirely different view from internal, cell autonomous aging. A young person is born with a range of cells from the most to the least responsive, but he dies with only least responsive cells left. This is actually highly supportive of cellular reprogramming as a solution to aging rather than a downstream consequence of some ‘damage’. By this view of aging methylation clocks might not necessary be measuring a cell intrinsic process but a change in the makeup of a cell population perhaps.

        • From a clinical standpoint , it is amazing how trauma to a hip vs. trauma to an ankle, differ markedly in their repair mechanisms. The cartilage in an ankle is able to completely repair and rejuvenate in a very similar manner as a salamander is able to regrow a tail. In contrast, hip cartilage barely repairs at all and is usually a chronic problem.

          • Hi Paul.

            Interestingly, I had a long standing knee problem that only healed once I started taking a hydrolysed collagen supplement. It may be that some joints turn over collagen less than others and require a really strong signal to do so. I’m not sure why this would be the case.

    • This is also true for iPSC colonies. iPSC expansion favors those cells which are more efficient in bypassing mitotic checkpoints.

      Journal of Clinical Medicine
      Review
      iPS-Cell Technology and the Problem of Genetic Instability—Can It Ever Be Safe for Clinical Use?

  9. Maximum Life Span
    All these techniques would more or less enhanced life expectancy. But maximal life span remained the same in the last 25 years. Due to lack of documentation we can not extend that further back in time.
    If the maximal life span does not increase this imply that there is no rejuvenation. Only the aging process is slowed down asymptotically to a maximum age which is specific for each species
    https://www.ncbi.nlm.nih.gov/pubmed/28511176

    • I’ve seen this theme many times before, and I haven’t been able to make sense of it. How can we know if maximal lifespan has increased when we haven’t waited for treated people to die? Why do you define “rejuvenation” only with respect to maximal lifespan, and not average lifespan? If I increase my life expectancy by 10 years, simultaneously feeling more energetic and rolling back my arthritis and blood lipids, would you say that’s not “rejuvenation” because I won’t live more than 122 years?

      • Ok, if you see it like this you can can consider it a relative rejuvenation. For example a 50 years old man who took those treatments when he will be 70 will be like one who is 60.
        I think that there is an optimal path for attaining the maximal life span. This optimal path includes optimal genetics and optimal environmental factors. Those who passed 110 years old, had by chance attained this optimal path
        There will never be the case when a 50 years old man with any treatment will attain in the future the status of a 40 years old (for example) That’s the real rejuvenation. At most the aging process will very much slowed down asymptotically to an certain age

    • Thanks for this, Bill. I think the evidence has been pointing this way for a whole now. The previous work from Blasco showed mean and Max lifespan were correlated with rate of telomere shorteningover many species. Presumably the rate of shortening is the same in this new strain of mice, but with longer telomeres they avoid accumulating any ‘shorts’ for longer.

      • I think that telomerase activity is only harmful once a malignant mutation has already ocurred. But if you start with already long telomeres and then just maintain them with telomerase, it would help avoid the DNA from fraying and thus prevent malignant changes in your genome.

        Now I wonder what would happen if we would CRISP-engineer some mice not only with hyperlong telomeres but also with overexpressed telomerase activity!?

        • I agree Cynthia. I think that most malignancies arise because a large enough number of cells get short enough telomeres and up the mutation rate such that there is sufficient chance for 1 cell to switch telomerase back on. This and the senescence of the immune system explains the exponential rise of cancer with age.

          There might however be some rarer, non age related cancers that can take advantage of long telomeres (even with long telomeres the chance of an oncogenic mutation is not zero). They might also be virus related. This would put an upper limit on the benefits of telomere length as these cancers could strike the young, and we know evolution will not like that.

          But Blasco now has all the tools to tease these answers out. She needs a much bigger group of hyper long telomere mice for starters.

          Incidentally, I’d urge everyone to watch Josh’s interview over on Ira Pastor’s IdeaXme YouTube channel. It’s really great.

          • Yes, just seen the Ira Pastor’s IdeaXme YouTube interview and liked very much the touch of wisdom Josh is bringing to this community. Thank you for sharing. I was not aware of the other aspects of Josh’s thought. A wisdom everyone can bring to her/his own life.

  10. Josh, love your blog!

    I’m sure you may be aware that the statement “the other view, based on an evolutionary paradigm of purely individual selection, denies that programmed self-destruciton is a biological possibility.” is based on a narrow interpretation of evolutionary theory – that an individual’s capacity for survival and reproduction are all that contribute to genetic impact on evolution. For social creatures, the impact of the individual may go beyond their own survival, particularly when factoring in their impact on their own progeny within family groups – hence the evolutionary justification for humans having the capacity to greatly exceed their reproductive years (grandparents increase the survival chances for their children and grandchildren). This may generate much more complex tenets for your essay: now instead of two hypotheses paired to two interpretations of the implications of evolutionary theory, the alternative possibility that programmed changes during the non-reproductive phase of the human lifespan may impart evolutionary advantages is raised. Indeed, these changes may simultaneously permit the benefits of a long lifespan to provide additional nurturing and support for parents burdened with offspring that require a significant investment, while limiting the competition between parents and their own children that might have occurred if humans were reproductively capable up to the end of such long lives. Or it could be as simple as, non-reproductive parents would have the time to help with grandchildren, whereas they would not if they were raising additional batches of their own kids.

    Again, love your site. Cheers, JWIV

    • Thanks for engaging on this, John. This is the subject of my book, and I’ve thought about it from various angles. I’ve concluded that the inclusive fitness model which still predominates in evolutionary theory today is too narrow to encompass all the forms of altruism we see in nature. It’s not just humans–you may be familiar with the fruiting body of the amoeba, as a very low-level example. Many examples of coevolution at levels high and low are also difficult to explain with the narrow model.

      In my book, I propose that the key to understanding the vastly greater scope of altruism we see in nature is that animal communities are tied together by a common food source, and it is a compelling imperative to preserve and cultivate that food source, not to overexploit it. I refer you to Cracking the Aging Code (MacMillan, 2016) or the academic book on the same theme, from CRC Press.

      • Hi Josh, on the subject of food availability. I was wondering if you have seen the Max Planck Inst. study from this past summer titled ‘Relaxed Selection Limits Lifespan by Increasing Mutation Load’ on the genome of different species of killifish, which vary in lifespan from months to a few years.

        Their conclusion was that mutational load on genes likely to affect lifespan accumulate in the short lived variants. So they are coming out strong in favour of the Medawar hypotheses of ageing.

        I was thinking this could also be interpreted an adaptation to avoid completely starving the cell line, so that a small number of larvae survive if both adults and young are competing for the same food source.

        But they seem confident the former is the underlying evolutionary reason, through genetic drift bottlenecks on the short lived species.

  11. Josh, perhaps story #1 (programmed aging) and story #2 (aging as damage response) can be reconciled more simply: you have often wondered what is the primary “clock” that would drive programmed aging.  What if the driver is simply accumulated damage?

    In other words, the more damage that accrues to the organism, the more repair mechanism are *intentionally* turned off, allowing damage to accumulate to the point that the organism dies.

    Then it would be unsurprising that something like smoking advances methylation age.

    This theory might appear to have some problems with hormesis effects (eg exercise), but not if we assume that the aging clock is driven by specific types of damage, eg mutagens.

    Are there experimental results or observations that speak against this explanation?

    If not, how could it be tested?

  12. Hi Josh,
    I just finished David Sinclair’s new book and watched your interview on “Ideaxme” on youTube. You both seem to have similar philosophies which I applaud heartily.

    I am a washed-up aviator and a failed geologist who threw away his degree to answer the siren call of flying. Following this blog has been difficult but rewarding due to a lack of training in biology and organic chemistry.

    I recommend Sinclair’s new book “Lifespan: Why We Age_and Why We Don’t Have To” to others with my handicap because it makes this blog more understandable for me by tying all the modalities together.

    Thanks to you, Josh, and all your contributors for lighting the way.

    James Flint

  13. Just watched Josh’s interview with Ira and it leads to some questions in my mind about our little endeavors here on this site.

    Namely, if Josh’s central thesis is correct and aging, and by extension death, is vital to our survival as a species, so much so that it’s integrated into a genetic death program, then why are we trying to slow- and even reverse- the aging process?

    Will these interventions be only for a select few? If for the masses, then are we doing something that will just lead us all to mass extinction via starvation and epidemics when we all die at once?

    Have we thought this through to its logical conclusion?

    • I am convinced that the extension of life, if it will be attained will not be for all. It will be a very few rich which will benefit from this extension.
      See what happened with the introduction of the automation. If the needs of the humanity would have been maintained only to proper food and housing then with the means that we have today we’ll all have to spend the majority of time in leisure which is not the case for the majority.
      But the rich ones have used the progress to create new needs and we have to work today more than in the past (albeit the work has other nature).
      Something similar will happen if there will discovered techniques to prolong significantly the life. No one could say which the future “needs” will arise based on this as no one could foresaw 200 years ago the needs of contemporary people.

    • Well all species go extinct, even with various programs built in to enhance the group survival. Humans could be different. We can go beyond our genetics and become something completely different. The defeat of the diseases of aging is but the first part of this story. It doesn’t necessarily mean this will be bad for the planet, although other pressures will certainly arise.

    • Paul –    Yes, of course. Your questions have been increasingly on my mind. They are the subject of the last chapter of my book. At minimum, I think we life extensionists need to be equally advocates for preserving biodiversity and for population control. Further afield, I believe the paradigm of Western scientific reductionism is wrong, and is leading us away from our hearts and away from our communities and away from the biosophere to which we belong.    Death is not the end of all. I don’t know this in a conventional sense, but I have seen abundant evidence (unpusblishable by most scientific journals) and I sense it intuitively.    Of course, these sentiments will not be popular among the communities that are my most loyal blog readers. 
      – Josh

  14. I see no mention of acetylation or histone acetylation. Is there any connection that you can see in regard to aging? Or is it part of the methylation process you reference here?

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