The most promising medical technology on the horizon today

Telomere biology has the potential to extend human life span, to dramatically lower rates of the great remaining killer diseases: heart disease, stroke, and Alzheimer’s.  All three diseases increase exponentially with age, and their toll will be slashed as we we learn how to address the body’s aging clocks.

You would think that the 2009 Nobel Prize might have done more to raise the profile of research in telomere biology, but the field remains a specialized backwater of medical research, and few biologists (fewer doctors) take it seriously as a panacea for the diseases of old age.  If the National Institute of Health has money to put into heart disease and cancer and Alzheimer’s and Parkinson’s diseases, there is no better place to invest than in telomere biology.  Research on these diseases commands multi-billion dollar budgets, because they are considered “medicine”, funded by NIH, while telomere biology is considered “science” and is funded by NSF.  The total NSF budget for all cell biology is only $123 million, and the portion devoted to telomere biology is a few million. The private sector is doing a little better – there are several companies selling herbs that stimulate our own bodies to liberate telomerase.  But this is short-sighted venture capital, and what we need is focused research with a ten-year vision.

There is good reason to think that telomere length is a primary aging clock in the human body.  The body knows perfectly well how to lengthen telomeres, but chooses not to.  All we have to do is to signal the body to activate the telomerase genes that are already present in every cell.   Of course, there is no guarantee that this will work, but compared to the sluggish rate of progress on individual diseases, it’s a pretty good bet, and the target is rather simple.  IMHO, it’s worth a crash research effort.

Three objections raised against telomerase research

1.  “Aging is inevitable because Physics tell us that nothing can last forever.”  This statement refers to the Second Law of Thermodynamics, which says that closed systems, evolving in isolation, must become more disordered over time.  But living systems are open, taking in free energy in the form of food or sunlight, dumping their entropy out into the environment.  There is no reason that such systems cannot maintain themselves indefinitely.  Indeed, growth and maturation would not be possible if this law of physics applied to open thermodynamic systems. Since the 19th Century when the laws of thermodynamics were formulated, it has been understood that aging cannot be explained from physics, and therefore commands an explanation from evolution.

2. “Evolution has been working to maximize animal life spans in order to increase fitness.  It is unlikely that any simple adjustment to physiology that humans can discover will do better than evolution has done over millions of years.”  In fact, evolution has not worked to maximize life span, but only to make it sufficient to assure time for reproduction.  Aging is a form of programmed death, on a flexible but finite schedule.  It is fixed in our genes.  There are mechanisms of aging that have been programmed into living things since the first eukaryotic cells.  Telomere attrition has been used to time the life cycle and form a basis for programmed death for at least a billion years.  Many species of protozoans do not express telomerase during mitosis (but only during conjugation), so their telomeres shorten with each reproduction, leading to a limit of a few hundred reproductions per cell line.  This mechanism is the precursor to telomeric aging that exists to the present day in humans and many other higher animals.

3.  “Expressing telomerase will increase the risk of cancer.” There is a great deal of theoretical concern in this direction, which I think is entirely misguided.  It is true that cancer cells express telomerase.  It is not true that expressing telomerase causes a cell to become cancerous.  This relationship is clearly explained by two seasoned experts (Shay and Wright 2011)

In early studies, the only way of increasing telomerase activity in lab animals was to add extra genes for telomerase.  Technology in the early 2000s did not permit a gene to be added at a targeted location, but only inserted randomly into a chromosome.  Tampering with the structure of DNA in this way is known to increase cancer risk no matter what gene is added or subtracted.  In three of these early studies, cancer rates in mice were increased [1, 2, 3].

There are no lab studies to my knowledge in which activating the native telomerase has increased the risk of cancer.  The modern view is that “while telomerase does not drive the oncogenic process, it is permissive and required for the sustain growth of most advanced cancers.”  Recent perspectives from both Harvard lab of de Pinho and the Spanish lab of Blasco focus on the potential for telomerase to decrease cancer risk, and these were the very people who produced the three studies suggesting caution a decade earlier.

And there are many studies showing that (a) telomerase expression does not increase cancer risk in lab animals, and (b) short telomeres are a very strong cancer risk.  I believe that telomerase activators will greatly reduce the cancer rate, first by eliminating cells that are pro-inflammatory and potentially carcinogenic because their telomeres have become short, and second by rejuvenating the immune system, which is our primary defense against cancer.  I published an article on this subject last year.

Why we might expect big life expectancy gains from extending telomeres

This is the affirmative question, then: what makes me think that telomere extension will have such a powerful effect on diverse aspects of aging biology?

A)    Telomere attrition is an ancient mechanism of aging.

Protists were the first eukaryotic cells, and they appeared on earth a billion years ago (they were a leap up in complexity from bacteria, which had been around 3 billion years before).  In protists, DNA is linear and hence there are telomeres and a need for telomerase.  Since protists reproduce by simple cell division, you would not expect that the cells would “age” or even that the concept of aging could have any meaning for their life cycle.  But a protist cell lineage can age, and indeed some do.  This is the oldest known mechanism of aging, and it is implemented through withholding telomerase.

Paramecia are an example.  When paramecia reproduce, their cells simply fission, the DNA replicates, and no telomerase is expressed.  Hence, telomeres get shorter with each cell division. Paramecia can conjugate, which is a primitive form of sexual gene exchange.  Two paramecium cells merge, mingle their DNA, and then separate.  It is only in the conjugation process that telomerase is expressed.  Therefore, any cell lineage that does not conjugate will die out after a few hundred generations.  This prevents cell colonies from becoming too homogeneous.  Thus aging is a billion years old, and some of the genetic mechanisms of aging have been conserved and passed on through all the transformations of multicellular life (William R Clark has written two accessible books [1, 2] on this topic.)

B)    Telomeres shorten with age in humans.

This has been known for twenty years.

C)    People with shorter telomeres have a much higher risk of mortality.

This was established by Richard Cawthon (2003) in a paper which took the field by surprise.  Researchers before then had assumed on erroneous theoretical grounds that telomere attrition, which was known to occur, could not have anything to do with human aging.  After all, if aging were as simple as telomere attrition, then the body could solve the problem merely by expressing telomerase.  This would enhance individual fitness.  Why would not evolution have found such a simple expedient?  (The answer, of course, is that natural selection favors aging, for the sake of the demographic stability – an evolutionary force not recognized by most evolutionary biologists.)  In Cawthon’s study, the top ¼ of 60-year-olds in terms of telomere length had half the overall mortality risk as the bottom ¼.  Cawthon had access to a unique database of 20-year-old blood samples, and to my knowledge his study has not been replicated or refuted these 11 years.


D)     People with short telomeres have a higher risk of diseases, especially CVD, after adjusting for age.  The association with cardiovascular disease has been consistent, not just in Cawthon’s original study, but also several other studies [Ref Ref Ref].  There are also associations with dementia [Ref, Ref] and with diabetes [Ref, Ref].

E)    Animals with short telomeres also have a higher risk of mortality, after adjusting for age.

This has been established in several bird species [Ref Ref Ref], and in baboons.  In 2003, it was already known that long-lived species tend to lose telomere length more slowly, and short-lived species lose telomeres more rapidly.

F)    In limited studies with mice, telomerase enhancers have led to rejuvenation.  (Mice are expected to be a much less effective target for this strategy than humans, because to all appearances, aging in humans relies on telomere attrition much more so than in mice.)

The first experiment of this type was done in 2008.  In the Spanish lab of Maria Blasco, Tomas-Loba engineered mice that were both cancer-resistant and contained an extra telomerase gene, expressed in some tissues where, even in mice, it would not normally be found.  Cancer-free mice with the extra telomerase lived 18% longer than cancer-free mice with only the normal gene for telomerase.

But soon it was discovered that all the experimental precautions around cancer may not have been necessary.  The same lab Bernardes de Jesus (2011) reported that they could increase health span in mice with the commercial product called TA-65 (widely rumored to be cycloastragenol) with no increase in the incidence of cancer.  Cycloastragenol is a weak telomerase activator compared to man-made chemicals discovered at Sierra Sciences, and even compared to some other herbal extracts.  Nevertheless, the Blasco lab was able to show that the shortest telomeres in the mice were elongated, and that markers of health including insulin sensitivity were improved by short-term treatment with TA-65.

Blasco’s lab then worked with a more potent (though more dangerous) method of telomerase induction: infection with a retrovirus engineered to introduce telomerase into the nuclear DNA of the infected cell.  “Treatment of 1- and 2-year old mice with an adeno associated virus (AAV) of wide tropism expressing mouse TERT had remarkable beneficial effects on health and fitness, including insulin sensitivity, osteoporosis, neuromuscular coordination and several molecular biomarkers of aging.” (Bernardes  de Jesus, Vera et al. 2012)  The mice lived 13% longer when AAV treatment began at age 2 years, and 24% longer when treatment began at 1 year.  There was no increase in cancer incidence.

The most dramatic example of rejuvenation is from the Harvard laboratory of Robert de Pinho.  Normally, mice (unlike people) express telomerase freely through their lifetimes.  These scientists engineered a mouse without the normal (always on) gene for telomerase, but instead had a telomerase gene that could be turned on and off at will by use of a chemical signal that the experimenters could feed to the mice.  As these mice grew older, they developed multiple, severe symptoms of degeneration in the testes, spleen, intestine, nervous system and elsewhere.  All these symptoms were not just halted but reversed when telomerase was turned on late in the animals’ lives. The effect on the nervous system is particularly interesting because nerve cells last a lifetime and do not depend on continual regeneration from stem cells, the way blood and intestinal and skin cells do.  Nevertheless, these mice with telomerase turned off suffered sensory deficiencies and impaired learning that was reversed when the experimenters administered the chemical signal to turn telomerase back on.

A Stanford/Geron research group worked with “skin” grown from human cells in a lab setting.  They found they were able to restore youthful elasticity, softness and texture to the cultured “skin” by infecting the cells with an engineered retrovirus that inserted the gene for telomerase.

G)     In addition to its function in lengthening telomeres, telomerase also acts as a kind of growth hormone.

This fact was suspected as early as the 1990s, and confirmed definitively in a Stanford experiment [Ref, Ref, Ref, Ref].  In this experiment, mice were engineered with “denatured” telomerase that lacked the RNA template for creating telomeres.  Still, the telomerase was shown to induce hair growth.  Telomerase has been shown to activate affect a hormonal signaling pathway called Wnt. Other functions for telomerase are reviewed by Cong and Shay (2008).

H)        In one human case, huge doses of herbal telomerase activators has led to rejuvenation.

I am recently in touch with a physicist from Kansas who has been taking super-high doses of telomerase-activating herbs and supplements for six years and claims to look and feel younger, with improved athletic performance.  He may be an interesting case study.  Jim Green has commented on this blog site.

 The Bottom Line

In my opinion, telomerase activation is a field that offers the most potential for human life extension in the next few years.  This research is languishing for lack of funds, and for lack of attention.

13 thoughts on “The most promising medical technology on the horizon today

  1. I too have been following the science of telomerase (perhaps not as extensively as you) and the scientific evidence of the Hayflick limit and genetic damage due to telomere shortening etc., is quite persuasive. Consequently I have been looking for a telomerase activator that does not cost the earth. I have read that there is a small molecule in a Chinese herbal plant called ‘astragalus membranecus’ which may activate a little of the dormant telomerase gene. There is a product sold in most pharmacies here in New Zealand called ‘Viralex’ which costs only $30 – $40NZ for a month’s supply of capsules that contain 200mg of Astragalus root. It also helps, it says , to boost the immune system. I hate the idea of taking a cocktail of supplements – and I don’t. But I’m willing to give this a try.

    • Dear Zargle –

      Cycloastragenol is the best-documented natural telomerase activator, but not necessarily the most powerful. From in vitro tests, it appears that Silymarin (from Milk Thistle) is about 20 times stronger. And it’s really cheap.

      In other words, Silymarin trumps Cycloastregnol in cell cultures, but we know nothing about what Silymarin does in your body. In contrast, we have at least two papesr about Cycloastragenol in real life, with data from a handful of human subjects: (ref) ,and more than a handful of mice: (ref)

      Product B is a combination of ingredients, headed by Silymarin, and Prod B is in between Cycloastragenol and Silymarin in price. You could reconstruct Product B from constituent ingredients (listed here) at a fraction of the price.

      Inspired by Jim Green, I have just begun experimenting on myself with jumbo doses of Silymarin. In coming months, I promise to let you know the results, if any.

  2. Josh, yes telomeres are an ancient clock, the even occur in paramecial macronuclear DNA – but there -they don’t shorten. So that’s paramecia, they’re weird in any case – but the same is true of mice – their telomeres don’t shorten with aging – and in case the readership doesn’t know, mice last two to three years (I’ve heard of four).
    So what I’m saying is that’s a partial solution – one of the many system involved in aging – elaboration of amyloidogenic proteins like, but not limited to, beta amyloid protein and alpha synuclein (Lewy bodies), the down-grading the efficiency of mitochondria – the deliberate up-regulation of by old cells of pro-inflammatory factors and the production of those factors, by senescent cells, and almost surely result of telomere shortening past the critical length (the telomere is returned to the critical length but no further) – so I would guess that telomere shortening was important for the diseases of aging (as the Baker study seemed to show) but not for aging itself. Telomere length is a good predictor of remaining lifespan – but that doesn’t necessarily mean it causes aging (in fact, as cells that are rejuvenated regrow their telomeres, it means that telomere length is an effect of aging (and/or stress) and not a cause of aging). Anyway the important thing is to get to the cause of aging – attack each arm of the octopus or hydra; amyloid accumulation, DNA damage accumulation, lipofuscin accumulation, ROS production, mitochondrial dysfunction etc. is futile if there is a single head from which the tentacles sprout and by defeating it defeat all the ‘epi-phenomena’ the mechanisms by which aging renders the organism weaker, and more likely to die – in fact with most organisms, inevitably so as the life span unfolds and and stem cells develop all of those symptoms of aging at the cellular level, mitochondrial dysfunction, telomere shortening, ROS production, etc. So – probably rapamycin (if used on the proper schedule for limited periods) will give you a little lifespan boost (and help your health), yet there’s nothing like restoring the hematopoietic stem cells to start producing more lymphoid cells – and is there proof that extending their telomeres will change their ‘potency’ to earlier states – yet there is such proof for other techniques. Again, the phenomenon of cellular rejuvenation proves that aging is not based on such phenomena as telomere shortening, but that telomere shortening is based on aging – reverse aging, change the age phenotypes of the the cells of an organ to an earlier age-phenotype and the telomeres will lengthen, the ROS levels will return to a reducing environment, the mitochondria will increase production of ATP – etc.
    If you’re really interested, Josh will tell you (I give you permission Josh) who I am.

    • I have featured Dr Katcher’s work here and here, and would be happy to go into more depth.

      I agree that aging will most probably need to be attacked from several different angles, even if we work “upstream” at the signaling level. I am not convinced that young hormonal profiles will lead to longer telomeres (unless you go way back to the embryonic stage). I am betting it will work better in reverse, with longer telomeres signaling a younger gene expression profile.

    • Dr. Katcher, I have nowhere near your and Josh’s understanding of the many complicated and inter-related factors which attempt to answer the question: Do short telomeres cause aging, or does aging cause short telomeres?
      However, I have studied telomere biology intensively for the past 11+ years, including working very closely with people like Cal Harley and Bill Andrews whose points-of-view are obviously quite clear and who have influenced my thinking and the direction of my own investigation of the field, so that is disclosure #1. Disclosure #2 is that I am among those Josh mentions who is following the path of offering nutritional supplements which target telomerase activation as well as the other key factors which cause telomere shortening, most importantly oxidative stress and inflammation, as research shows very strongly that:
      –Oxidative stress can reduce telomerase activity by 50-70% and double the rate of telomere shortening [EH Blackburn 2010; Kurz 2004; von Zglinicki 2002]
      –Inflammation also increases the rate of telomere shortening and has a major impact on telomerase activity [Blackburn 2011; Bekaert 2007; Aviv 2009]; Rita Effros [2009 & 2011] has even shown that inhibiting the inflammatory cytokine TNF-alpha can actually increase telomerase activity by 1.25 to 1.78-fold.
      –While I have great respect for those trying to significantly extend human lifespan, I also make no apologies for being among those who are trying, through telomere biology, to extend human Healthspan, in real aging humans, right now.
      You and Josh seem to agree that telomere shortening is important for the diseases of aging; and in fact, there is a wealth of peer-reviewed research that short telomeres and/or lack of telomerase are now considered as causal factors–and should be explored as part of therapy–in at least the following: Type 2 Diabetes [Blackburn, Armanios, L. Rudolph,]; Rheumatoid Arthritis [Weyand & Gorozny, Gabriel,]; aspects of CVD, including Atherosclerosis; Idiopathic Pulmonary Fibrosis [Armanios, Blackburn, Lloyd,]; and HIV’s progression to AIDS [Effros, Yu, Fossel,] This evidence to me is certainly supportive of Josh’s statement that telomere biology is “the most promising medical technology on the horizon today.”

      Finally, you state that “there’s nothing like restoring the hematopoietic stem cells,” and “is there proof that extending their telomeres will change their ‘potency’ to earlier states?” While there may not be absolute proof [yet] in humans, a wealth of research by Blasco, L. Rudolph, DePinho, Sahin, Martens, Aviv, supports very strongly points such as: “Short telomeres are causal of disease, because when they are below a certain length they are damaging for the cells. The stem cells of our tissues do not regenerate and then we have aging of the tissues. [Very exciting is] telomerase activation, because of its potential to reverse aging.” “These findings suggest that telomerase activity and telomere length can directly affect the ability of stem cells to regenerate tissues” (Blasco). “Telomere shortening is one of the mechanisms that can limit the self-renewal of HSCs.” (L. Rudolph). “Limited expression of telomerase is not sufficient to prevent telomere shortening in these cells [HSCs], which is thought ultimately to limit their proliferative capacity” (Martens).
      –And in actual human clinical research of a “weak” to “moderate” natural product-derived telomerase activator, used in combination with a separate dietary supplement pack (of 43 ingredients), there was a statistically significant reduction in the % of critically-short telomeres, and lengthening of critically short telomeres, as measured in leukocytes [Harley/Andrews/Blasco].
      –Now consider a 2010 study by Aviv/Lansdorp/Kimura, concluding that “Robust synchrony [of telomere length] exists among leukocyte subsets throughout the human lifespan. Moreover, telomere length in leukocytes reflects its length in cells up the hematopoietic hierarchy, i.e., HPCs and, by inference, HSCs.”
      –Also, considering that lymphocytes and Adult Stem Cells are among the very few human cell types which naturally express telomerase [Effros; Weyand & Gorozny], it would seem to make sense that the significant reduction in telomerase activity caused by oxidative stress, inflammation (also cortisol and homocysteine) would negatively impact these critical cell types the most, at the risk of sending those with critically-short telomeres into replicative senescence.
      –As Josh concludes, research and research funding in this area is sorely lacking, but it certainly seems to me that if, by intervening with readily-available natural compounds to positively impact telomere length and telomerase activity, we might positively impact the regenerative capacity and potency of HSCs, that is a question worth studying, and measuring.

      By the way, Dr. Katcher, I have a Research Summary readily available about the impact of Telomeres and Telomerase on Adult Stem Cells, which I would be happy to share with you or others if you would like to send your email address to me at: [email protected]. David B. Cross, Founder & President, Telomere Biosciences.

  3. “Josh, yes telomeres are an ancient clock, the even occur in paramecial macronuclear DNA – but there -they don’t shorten. So that’s paramecia, they’re weird in any case – but the same is true of mice – their telomeres don’t shorten with aging – and in case the readership doesn’t know, mice last two to three years (I’ve heard of four).”-Harold Katcher

    Mice have other reasons for being short lived. In fact some say they die mostly from cancer so their long telomeres and telomerase may be a mechanism to cause them to die on time . -link

    “Anyway the important thing is to get to the cause of aging – attack each arm of the octopus or hydra; amyloid accumulation, DNA damage accumulation, lipofuscin accumulation, ROS production, mitochondrial dysfunction etc.”-Harold Katcher

    We would have to look at what exactly is being implemented in negligible senescence organisms to see if all of those need to be addressed.

    We know that even smoking 60 cigarettes a day which should surely increase all forms of damage, doesn’t impede a human from reaching 100 in good health.

    We also know that mechanisms must already exist or be present that allow one of the most metabolically active cells in mammals to live extraordinary long lives far in excess of pretty much any other cells. Neurons live over a century in humans, in other mammals transplant of neurons showed they could live twice as long as original host without genetic modification, it may be the case that human neurons too could live twice as long for all we know. What changes needed implementation to go from 2-3 years to 120+ years in neurons within mammals?

    That would be interesting to know.

    One might say lots of changes or things had to be addressed, but the cells from shorter lived rodents were transplanted unmodified and exceeded twice the lifespan of the original host organism. IF there truly was a serious change needed, at least in these cells, one wouldn’t expect them to live twice as long as the host(and it is believed they could’ve lived even longer).without necessary modification.

      • “Many centenarians manage to avoid chronic diseases even after indulging in a lifetime of serious health risks. For example, many people in the New England Centenarian Study experienced a century free of cancer or heart disease despite smoking as many as 60 cigarettes a day for 50 years. “-wikipedia link

        In the US I believe a pack can be at least 20 cigarettes, 60 is basically 3 packs(even if you take the slightly larger number of 25 used in some it is still close). But in any case the number of people smoking 60+ cigarettes must not be that big. And even if the body has higher than expected resistances, it’s defenses can probably be exceeded by sufficient abuse within a short enough window of time.

  4. While I am excited for research into telomeres, and I hope that future discoveries will lead to medical advances in areas such as cancer, Alzheimers and Parkinsons, the prospect of being able to live indefinitely raises a few concerns.

    I agree that living indefinitely would not be in violation of the laws of thermodynamics, but humans require more than the thermal input from the sun on the earth to stay alive. If dying from age could be prevented then the population would grow at an even faster pace, which is even more unsustainable, (as any population growth is unsustainable). This leaves a few options such as completely halting reproduction of the human species, which would be practically difficult as well widely objected by the general population. The other alternative is to artificially end lives after a set period, which would render the purpose of living indefinitely redundant, as well as introducing an unnecessary burden on those who will eventually have to end a life.

    A use of living indefinitely would be to send humans on trips throughout the universe that might take millions of years to complete. I can advocate indefinite life for such a specific use but not as a general step forward in the evolution of humanity(which would be halted in its tracts by such a prospect). Aside from the philosophical and moral issues, research in telomere biology is essential in our understanding of degenerative diseases such as alzheimers and parkinsons which place great strain on the economy and degrade the quality of life of humanity.

    Thomas Thorburn (14012350)
    Student at University of Pretoria

  5. Hi, Josh:
    I am new to this fascinating blog. Thank you for creating it. People (myself included) too often seek simplistic answers and believe what they want to believe. In my humble opinion cell signaling is everything, and what we are likely to find is that very subtle pathways, and what influence one signal over another, or turn on or off a signal, happens at an electro-chemical level we don’t yet fully understand, yet may have the greatest impact on the science of biology. I note that in one aspect of Dr. DePinho’s work, it was PGC-1B which was significant. PGC dysfunction in ALT positive tumors (see MD Anderson news release on this) had a great impact on survival of test mice, as an example. But what corrupted that cell regulator? What subtle mechanism caused the dysfunction, so that when the PGC was knocked down, the cancerous mice lived longer? And by what mechanism was the cancer so “clever” (for lack of better word, or maybe it is the most appropriate one) that it “knew” to corrupt the PGC in order to accomplish its strategy, even though that strategy is ultimately self-defeating with the death of the host. And of course, can that be said to be a “strategy” at all? Is an intelligence intelligent if it’s success lies in its own destruction. I’m not sure it matters, although it might be helpful to know where a sub-cellular approach is trying to go. Maybe all that matter is that we figure out how it does what it does. But in any event, what triggers the signal, that weird interstitial, electro-chemical space between matter and energy and what influences “things” to move in one direction over another, is to me where the challenge lies. Mechanistic science is immediate, urgent and absolutely relevant to short and intermediate term problem solving (i.e. death!), but until we understand the why it happens as well as the how it happens, we’re somewhat throwing darts.

    But hey, if you throw darts at stock chart, about 50% of the time your picks will be as good as the stock gurus, so I’m all for it.

  6. The purpose of human life is to create a higher form of body. Evolution occurs via in vivo adaption that results from the epi genes reading the enviroment. This can observed both in nature and proved in the lab. The mind, inner desire, etc also influences changes that take place causing a “better” or more evolved “form”.
    To achieve a higher form takes time and application. Currently our lives are far too short for the vast majority of Humans to achieve a state transformational state. However super long live times will apply a pressure to ones being and mind that will facilitate change. I am sure that lower reproductive levels will assist the life extension that will come and of course, all of us staying on Earth is a certain way to extinction eventually by some accident or disaster. Super extended live spans will also see more humans than currently evolve to a higher dimensional state and simply evolve beyond this plane of existence. I am saying that most of the problems that one fears with a super long life span for humans will not actually transpire.

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