A completely random picture of a lab mouse
According to those idiots over at the Guardian, “Harvard scientists reverse the ageing process in mice – now for humans”. As if that were not miraculous enough, the Guardian also claims that “Now they believe they might be able to regenerate human organs”. Here at the Hub we would love nothing more than for this story to be true, but alas it is one of the hugest piles of sensationalist bullshit I have seen on the net in quite a while. The scientific research cited by the Guardian does not support these sensationalist claims and the Guardian knows this. But they don’t give a damn because sensationalism sells – big time! The Guardian knows that sloppy, idiotic bloggers and news organizations across the web will regurgitate anything they see without hardly the slightest attempt at fact checking. And hence this bogus story has been an enormous hit. The story already has more than 15,000 Facebook likes and this number is sure to grow. It has been picked up and rehashed as a legitimate scientific story by major news outlets, including the Wall Street Journal, Digg, Endgadget, Wired, and many more. Congratulations to the Guardian and the author of the story, Ian Sample – you have created a story that sells well, but your reputation is utter crap.
First let us take a brief look at the scientific research that Guardian correspondent Ian Sample claims will reverse aging and allow us to regenerate human organs. Scientists at Harvard genetically altered mice so that they lacked an enzyme, telomerase, that is responsible for maintaining proper telomeres. Telomeres are repeated sequences of DNA at the ends of our DNA that protect the DNA from damage. Without the ability to produce the telomerase enzyme, the mice had essentially nonfunctioning telomeres, leaving their DNA unprotected and prone to extensive damage and malfunction over time. To no one’s surprise, as these mice grew and lived out their lives within the laboratory their bodies quickly broke down. Their organs began to fail – they lost their sense of smell, they became infertile, they were weak. With the mice now in this degraded state (that we are lead to believe approximates aging), the Harvard researchers then proceeded to give the mice regular injections to reactivate the telomerase enzyme to see what would happen to them.
So what happened to the mice once their broken, dying bodies were finally given injections to activate the vital telomerase enzyme that they had thus far been denied? In what will be a surprise to nobody (except apparently the Harvard researchers and Ian Sample at the Guardian) the bodies of the mice stopped their decay. As if this were not miraculous enough, the bodies of the mice also seemed to regain some of their lost vitality and function now that their DNA was allowed to function properly. Isn’t that amazing?
Any reasonable person would quickly summarize this research as something like “take away a vital enzyme from an organism and it starts to decay, give the enzyme back to the organism and decay stops, allowing the natural process of repair and growth in the organism to proceed”. The research sheds some light on how crucial telomerase and telomeres are to the proper function of an organism, but unless you are an expert in that field this is a non-story. This research is a long, long way from leading to a reversal in aging. Unless, that is, you are Ian Sample working for the Guardian, in which case apparently you have just stumbled upon a fantastic piece of research that you can use to create a misleading and sensationalist story that will sell to mindless readers and bloggers.
I can’t figure out what is more ridiculous here. Is the Guardian story itself the most ridiculous thing, or is the fact that the story was blindly syndicated by thousands of news outlets and believed by millions of readers across the world even more ridiculous? Ian Sample and the Guardian must be laughing all the way to the bank with the traffic this story is generating for them. Readers will correctly point out that I am only aiding their little game by giving the story even more prominence and calling it out in this post. To that all I can say is that I can’t stop people from reading the Guardian’s BS, but at least I can do my part to show the world what complete crap it is. The Guardian has gained itself a hugely popular story, but at what cost to it’s reputation? Sadly, most people probably won’t even care. But I can hope.
Image source [rama]
Comments
Please research your data well.
The Harvard Research is valid. Normal cells or somatic cells are Telomerase Negative. Ie similar to the knock off mice created by the Harvard Scientists. In humans only Germ or sexual cells like sperm are telomerase positive.
It is not that you took away something from the mice and gave it back to them.They were simulating a normal condition, which is cellular senescence or the Hay flick limit in normal cells.
The research proves that Telomeres are a component of aging and that activating Telomerase in a telomerase deprived cell leads to extended cell division. This has been proven more than once with extension up to 200 replications from the base figure of 80.
Sorry but The Guardian was right and so were the groups syndicating the article.
Dr. Bob Shalaby FRCSE.
HI Keith since you are so cranked about the Depinho study I thought would share another one with you, kinda the grandaddy of them all if you will. You might recognize a Noble prize winner in there somewhere and jeez look there is that pesky DePinho again!
Cell. 1999 Mar 5;96(5):701-12.
Longevity, stress response, and cancer in aging telomerase-deficient mice.
Rudolph KL, Chang S, Lee HW, Blasco M, Gottlieb GJ, Greider C, DePinho RA.
Department of Adult Oncology, Dana Farber Cancer Institute, Boston, Massachusetts 02115, USA.
Abstract
Telomere maintenance is thought to play a role in signaling cellular senescence; however, a link with organismal aging processes has not been established. The telomerase null mouse provides an opportunity to understand the effects associated with critical telomere shortening at the organismal level. We studied a variety of physiological processes in an aging cohort of mTR-/- mice. Loss of telomere function did not elicit a full spectrum of classical pathophysiological symptoms of aging. However, age-dependent telomere shortening and accompanying genetic instability were associated with shortened life span as well as a reduced capacity to respond to stresses such as wound healing and hematopoietic ablation. In addition, we found an increased incidence of spontaneous malignancies. These findings demonstrate a critical role for telomere length in the overall fitness, reserve, and well being of the aging organism.
The same group went on to do a different version of the DePinho study reversing many of the clinical signs of aging in generally accepted mouse model of aging using . Then Bill Andrews and Walter funk xenografted old human skin onto mice and made it young again with telomerase. The skin was not genetically modified. ( Funk Exp Cell Resv 2000). yep I can’t for the life of me understand why so many bright people are excited about all this “old” news .
And how about those TA-65 people doing a study ( it was too small to mean anything right) in a no name journal ( it didn’t have drug company support so it can’t be worthwhile) with some prestigious scientists ( at least that Depinho guy wasn’t there again!) showing improved biomarkers of aging and lengthening of the critically short telomeres after 1 year of use.
And then Passos and other went on to show how telomere length/function controls cellular gatekeeper, mitochondria function and biogenesis while others showed the same for FOXO and mTor previously thought to be the sole domains of sirtuins and CR. You are right what is all this fuss about!!! All this hype makes me want to OD on a bottle of resveratrol after I calorie restrict myself into misery
I read this article, went away, thought about it, then came back and realized all I took away from it was an image of some guy screaming “bullsh*t” a lot. I’m new to Singularity Hub and its unfortunate that this had to be one of the first articles I read. This site really needs to weed out some of the bullsh*t its contributors produce if it wants to become a respectable source for tech news. This article reads like a poorly thought out Facebook rant.
You need to read the paper a little more carefully – it’s not the absence of the telomerase that caused the damage, it’s the absence of the TELOMERES. The knockout mice were fine until their telomeres got so short that the cells stopped functioning.
This is precisely what happens in normal ageing – it’s just that it takes a lot longer if the natural telomerase is still around.
The obvious next step is to do the same thing with mice that have naturally occuring telomerase.
I think you miss the point of what the Harvard scientists were trying to figure out. They caused speedy damage to mice to shorten the experiment time, so they could see if telomerase would actually REVERSE the damage, not stop or slow it down. You say it isn’t a surprise to anyone but the Guardian or Harvard, but it IS surprising that damage was REVERSED, not hindered. I personally would have expected damage to be significantly hindered if not even at all. This goes to show that aging is something that could be reversed, even if we don’t have a step-by-step guide on how to do it yet.
I think you miss the point of what the Harvard scientists were trying to figure out. They caused speedy damage to mice to shorten the experiment time, so they could see if telomerase would actually REVERSE the damage, not stop or slow it down. You say it isn’t a surprise to anyone but the Guardian or Harvard, but it IS surprising that damage was REVERSED, not hindered. I personally would have expected damage to be significantly hindered if not even at all. This goes to show that aging is something that could be reversed, even if we don’t have a step-by-step guide on how to do it yet.
I thought this up in high school. I imagined that the aging process was a result of a net degeneration of genetic information which codes for everything to the pigments in your hair to the hormones that maintain bone density. Cells, as they divide, erode telomeres at the ends of chromosomal DNA. When a fetus develops cellular division is at a max and would consume telomeres very quickly but an enzyme, telomerase, repairs the telomeres by adding to them, thus counteracting telomere erosion. As we age the expression levels of the gene that makes telomerase declines and genetic damage accumulates. All you have to do is make a genetic modification that reactivates the telomerase gene in an older individual and that person should stop aging in this way. It has only been recently that technology to make changes with such specificity in complex eukaryotic organism’s genetics has been possible. I’m glad to see a confirmation of my speculations. Of course your going to see great propaganda stating this is impossible or that it will induce cancer. I’m sure the idea of an ageless civilization scares somebody out there.
well maybe not now but I bet we are on the edge of finding something that works but then we will have over population problems and then who knows what …
I’m always skeptical that replacing any natural chemical which our bodies are responsible for making on their own (hormones, enzymes etc.) with a medication is going to be as effective, so I read that story with skepticism too. But, how do we know that it’s not going to work, at least to an extent? The shortening of telomeres seems to be because death and birth are necessary for natural selection, so the evolutionary process benefited from this feature which we as individuals consider a bug. So we should be able to correct this shortcoming somehow; it’s an obvious mechanism that we can attack and see how that turns out. Hopefully they take the next step and try to prevent the normal aging of the mice rather than causing the problem first and then fixing it. But sometimes you have to take a machine apart to figure out how it works.
Mice engineered to overexpress telomerase from the outset live significantly longer lives. (Unpublished data, but nobel prize worthy!)
That is impressive!
Isn’t the real lesson that the aging-reversal did indeed happen, which isn’t somehow a priori guaranteed. I mean if you artificially age an organism in an oxygen chamber, they don’t de-age once you take them out. This de-aging didn’t have to be possible, but they observed it, and it turned out to be quite complete. So this research certainly is interesting, and this article is stupid for panning it. Now, for the Guardian article – yes, they left out crucial information and mislead their readers. But this is still very interesting research.
lump1, I agree with much of your statement. I believe this statement from the story supports this:
“The research sheds some light on how crucial telomerase and telomeres are to the proper function of an organism, but unless you are an expert in that field this is a non-story. This research is a long, long way from leading to a reversal in aging.”
I can’t believe how many of you are defending this research and the Guardian. For those of you that think the research is so effective against aging, perhaps you would be interested in signing up for the same trial the mice had. We will take telomerase away from your bodies for several months, and then after your body is sick and dying we will give telomerase back to your body and watch you regain a small portion of your former health. We will all then rejoice that we have helped you to reverse aging! I am pretty sure NONE of you would sign up for such a trial…but go ahead, keep on defending the Guardian
Wow – you’re amazingly arrogant and wildly annoying. Your own personal “journalism” is painful to read. You’re essentially yelling “you’re science is wrong and I’ll prove it by throwing English at you!” Back up your statements with some facts instead of assumptions. As stated above there’s been plenty of prior work done on this enzyme that correlates with this research.
Instead of foaming at the mouth like some internet troll – try a shot at some good journalism yourself.
So I guess you would like to sign up for this treatment? Please explain to me how in the world this treatment will allow you to live longer?
I am signing up for the Patton protocol using TA-65 and recommending it to all my well to so patients. If they cant afford it I am recommending Astragalus extract.
I don’t have to be a mouse and delete my telomeres in order to believe in something.
Kieth, what you fail to realize is that all human beings, every single last one of us, are already signed up for the very trial you describe. NO HUMAN BEING HAS ACTIVE TELOMERASE. That is why we age the way we do. If we can find a way to activate our telomerase, then it is entirely possible that we will experience aging reversal. Of course that is easier said than done, and the technology that Dr. dePinho used on the mice is not appropriate for humans, but that doesn’t mean it’s impossible. This man (http://www.popsci.com/science/article/2011-07/man-who-would-stop-time ) has dedicated his life to doing just that. He is very close to having a drug that humans could take that would activate telomerase. Will it stop or reverse aging? No one knows, but Dr. dePino’s research makes it very likely!
I think the title is BS. An article I read elsewhere of the same topic had a different title that had something like, “Scientists may be able to hinder aging with new finding” or something like that.
The BS is not in the Guardian’s story but in Keith’s post. I don’t think it is done maliciously, it’s just that he doesn’t know enough about telomere biology to be able to properly critique the science behind the story.
The mice were never injected with the telomerase enzyme or anything else. They had a pellet containing a molecule that activates telomerase placed under their skin. The telomerase activating molecule gets into the blood stream and is carried to the cells where it penetrates the nucleus of the cell and turns on the hitherto shut off gene that controls the enzyme. That in turn causes the telomeres to grow longer which rejuvenates the cells. These mice that were made to be old before their time were made young again and that is big news. I think I also was getting older “before my time” and am only too glad to be taking the telomerase activator TA-65 from T.A. Sciences with the idea of making my cells younger as happened in the mice.
Noel Thomas Patton
“Is the Guardian story itself the most ridiculous thing, or is the fact that the story was blindly syndicated by thousands of news outlets and believed by millions of readers across the world even more ridiculous?”
Well the latter certainly wont be considered very ridiculous since that happens for all types of stories all the time. “The New York Times” writes up something political thats utter rubbish, it gets picked up by outlets all over the US and the world, and only a minority of people ever gives it a second thought.
Keith you’d better go study biology again. The results are not at all expected. At very most one would expect the aging process (yes aging) to be arrested and more likely just retarded. The fact that it seemed to be reversed is pretty spectacular.
And have you even read the original article? I seriously doubt you could even begin to comprehend. Maybe you shouldn’t comment about things you have little understanding of.
http://www.nature.com/nature/journal/vaop/ncurrent/full/nature09603.html
I think there is more to it than your cynical observations suggest. I doubt this would even make it out of a classroom if the tests were not monitored over a long enough period of time where ageing would take place regardless of any modifications to the mice’ DNA!
The BBC’s recent Moral Maze debate on Radio 4, “Should we welcome treatments to reverse the ageing process?” was premised upon the same uncritical interpretation of the Harvard research.
Hypocritical much?
12/2/2010 – Harvard Scientists Reverse the Aging Process in Mice – Total Bullsh*t
An article describing how the work with telomerase is a non-story to all but the medical expertise. It cites multiple websites, including the Wall Street Journal for blowing this story out of proportion. When inspecting the WSJ they clearly well define what the research was about.
10/8/2009 – http://singularityhub.com/2009/10/08/nobel-prize-in-medicine-awarded-for-work-in-aging/
Article from Singularity Hub about telomerase studies, and the fact that it won three scientists the nobel prize in medicine that year.
Singularity Hub, I am disappoint.
Sorry folks my question is not directly about this article but it is about sensational claims that is being discussed in these comments. I am wondering whether the following product is genuine and can do what it claims about DNA testing or it is all …?
https://www.23andme.com/
Our generation may be out of luck, but those who will be born to our generation have a very good chance. I would even go farther; the only thing that could prevent their chance would be a failure mode of this now ancient paradigm.
I suspect that if you want a chance yourself, you may need to save your pre-degenerated cells, which could then be propagated and used in therapies future therapies.
My own idea, and I am not a biologist, is that some hope may exist with a combination of telomerase therapy and aggressive cancer treatment and prevention. I have a hunch that the reason telomerase is not fully expressed may be that it is costly in terms or energy and/or cancer.
Telomere shortening could also serve to protect DNA… in the sense that other errors develop in DNA even with full telomeres, so there could be a benefit to letting those errors expire with time. Does that make sense?
We need a higher order (an extropic) process for pruning errors or instilling ourselves with newly propagated cells (e.g., a 26 years old (ahhh!) Blair stem line). The first order of pruning takes place already when our immune system battles cancer. We just need to augment that process.
Reverse aging = Slowed aging
Telomerase is also used by cancer cells to become immortal. No drug works as well as the natural equilibrium regulaed by the body.
Telomerase is not a “drug”. Telomerase is an enzyme already present within our cell’s nucleus. Telomerase is active in cancer cells, but inactive in our regular cells. Our cells age and become senescent whereas cancer cells do not. If our regular cells had active telomerase, they would also not age, that is, they would retain youthful functioning. Considering that it is our immune system’s cells that FIGHT cancer, it is entirely possible that having active telomerase in our normal cells would give us much better cancer defenses!
I do not understand the author’s anger. I found the tone of this article nonprofessional. I do not understand why the emphasize should be place on the Guardian story rather than on the mere research and its implications. Basically, I do not understand the whole point – almost 90% of all scientific articles (especially those in Nature & Science) drastically exaggerate their findings. This could be called scientific marketing. To pick up so seriously on this particular research article as the biggest culprit and turn it almost into a scapegoat is neither fair nor particularly interesting. It’s been for a long time obvious that claiming to have obtained the whole puzzle by connecting only 2-3 pieces together is meaningless in the context of achieving big unambiguous conclusions. Unfortunately, this is what science nowadays has turned into – untested small hypotheses based on max 1-2 component experiments are being published as to suggest their conclusions are universal. Scientists should start understanding that using diverse combinations of methods is the only way to reach valid conclusions about something that is dependent upon an enormous number of degrees of freedom, such as aging for example. Unfortunately #2, the required fast-pace research leads to more and more bad articles, which more and more are superficially being used by not only journalists, but also other scientists to come up with practical products, which then turn out to be useless and in many cases harmful. That’s why wise people say “Move faster slowly”. I could only hope this to become applicable to scientific research in near future.
I was delighted to finally see someone out there recognizing the media coverage of this minor scientific report for what it is: an interesting study of the rapidity of late-life telomerase replenishment, of zero significance for translation as a therapy for normally-aging humans. It’s surprising and a bit disheartening to see so many commenters either insisting that it really, really does have to mean something for extending healthy human life, and/or defending the Guardian for being no more sloppy and headline-hungry than the existing, pathetically low standard of the media landscape. Thank you, Keith, for pointing out the nature of this fertilizer.
I wrote about the same study on my blog yesterday:
http://inhumanexperiment.blogspot.com/2010/11/jumping-head-first-into-fountain-of.html
But it’s not just the Guardian that exaggerated the whole thing; I quote the Daily Mail article in the post, and it’s the same bullshit.
If you look at the statements from the professor involved in the study, I think it’s clear that he’s partly to blame for all the hype. No wonder the media got so excited.
I see this news steer up some heat, but if we throw away bad journalism there still is a fact that some damage from aging can be cured. I don’t know if there is a difference between a normal aging and an artificial, but still I welcome the research.
I think that you Keith, should have focused more on research results and should have given your opinion about what it could mean for science in the future, instead writing about someone’s bad journalism. This is the kind of Singularity Hub I used to know.
However, I welcome your skepticism for it drives the humanity forward
Wow, that was a shocking level of anger over a little sensationalism.
I think we would all agree that there is too little funding for researching into fighting aging. And we might even agree with the point that Aubrey de Grey has made that part of the problem lies with the “pro-death trance” (or whatever precisely he calls it). Surely an article that goes around the world ten times over and generates a lot of enthusiasm for aging research – raising the possibility of reversing aging – isn’t a bad thing.
Yes, yes, it’s a bit over the top and lots more research has to be done to prove that it works in mice with normal telemerase levels and then with other mammals, etc. (of course, the same could be said for any research in mice models – but I still get excited when I read about a vaccine test clearing amyloid in mice engineered to produce amyloid) But so what… The excitement is the main thing here and I think that you need to dial back the science nerd pedantry a little bit. Relax, have a drink, and enjoy the fact that there may be a few million more people today who now accept a major premise of transhumanism/singularitarianism.
I have to agree with Keith. The headline is BS. The research itself might have some merit, but tabloid style journalism isn’t the way to present it. How many science based publications aimed at the general public could have told this story? The Guardian isn’t the place I’d be looking for science stories.
Yes, the headline is BS.
“So what happened to the mice once their broken, dying bodies were finally given injections to activate the vital telomerase enzyme that they had thus far been denied? In what will be a surprise to nobody (except apparently the Harvard researchers and Ian Sample at the Guardian) the bodies of the mice stopped their decay. As if this were not miraculous enough, the bodies of the mice also seemed to regain some of their lost vitality and function now that their DNA was allowed to function properly. Isn’t that amazing?”
But then he suggests that there’s nothing interesting about the degree of regeneration noted by the researchers. I doubt they agree.
Hypocritical much?
The point he is making is that these mice were specifically bred to be telomerase deficient; these were not regular mice, but mice that had a vital part of their genome knocked-out. Instead of aging regularly, theirs accelerated, as would be expected, and adding telomerase into their bodies merely covered for their defficiency.
This is no different then other tests that use “knock-out” mice. This is like if the mice had been bred for diabetes and injected with insulin. As with insulin-deficient mice, these telomerase-deficient mice have some of their symptoms lessened with injections of the lacking enzyme. This is merely a conformation of known knowledge and merely offers hope for new studies on regular mice, nothing more.
If this had been done in geriatric, regular mice, this study would hold some weight, but, at the moment, this study is no different for any knock-out test and is nothing worth sensationalizing.
Yes, but the point that many of you seem to be missing is that we humans are already “knocked out” Unlike normal mice, normal humans don’t have active telomerase. This means that just possibly if we were able to find a way to activate our telomerase, we might see the same dramatic results as was seen with Dr. dePinho’s mice.
Wired, might have picked up the story and the catchy title, but their reporting was sound their article was extremely skeptical as it should be, and pointed out the facts.
The reversal of tissue degeneration that was at least similar to what one would expect from aging is significant.
“In what will be a surprise to nobody (except apparently the Harvard researchers…)…”
Your overreaction is nearly as bad as the sensationalist claims made in the guardian article.
Harvard Scientists Reverse the Aging Process in Mice – Total Bullsh*t written by Keith Kleiner is Total Bullsh*t. See I can do it too. Keith the only thing that the guardian journalist is guilt of it what all journalists are guilty of, sensationalizing and diluting the details. Sensationalism draws in readers who would have otherwise not picked up a science journal. Diluting of the publication is for the common man or specialist in another field who cares less to get a degree in the specialty to understand the thesis.
But to call the article total bullshit. Total Keith? You mean 100% bullshit on Harvard scientists? Could you not have done the same with a title like “Guardian sensationalized Harvard Telomerase Research”.
I don’t approve of sensationalism but i did read the article with the necessary skepticism as i did yours. Thank you for at least citing the research so i could read it myself and reserve judgement.
Harvard Scientists Reverse the Aging Process in Mice – Total Bullsh*t written by Keith Kleiner is Total Bullsh*t. See I can do it too. Keith the only thing that the guardian journalist is guilt of it what all journalists are guilty of, sensationalizing and diluting the details. Sensationalism draws in readers who would have otherwise not picked up a science journal. Diluting of the publication is for the common man or specialist in another field who cares less to get a degree in the specialty to understand the thesis.
But to call the article total bullshit. Total Keith? You mean 100% bullshit on Harvard scientists? Could you not have done the same with a title like “Guardian sensationalized Harvard Telomerase Research”.
I don’t approve of sensationalism but i did read the article with the necessary skepticism as i did yours. Thank you for at least citing the research so i could read it myself and reserve judgement.
Here’s yet another perspective -
http://video.foxnews.com/v/4441847/signs-of-aging-can-be-stopped
Sometimes transhumanist blogs and forums behave like a clique with echo. We have no faith in Google AI research or in the algorithms of Numenta because it doesn’t want to create an artificial scientist as Ben Goertzel want (and also because Hawkins does not seem to believe in the singularity). We have to speak ill of the rejuvenation of mices at Harvard (published by The Guardian and FoxNews) because Aubrey de Grey thinks that what they did has no value to rejuvenate naturally aged mice… Come on, folks, this study has merit, starting with the largest one, shake the very strong belief that it is impossible to do anything against aging!
So basically you’re upset with:
a) A title that implied they could/should/would look into this with humans.
b) A random comment about the possibility that this could regenerate human organs, or as sensible people would interpret this as a way to reduce the decline in health of said organs.
c) Other random things about this article getting press-
Oh, wait. I see what you did there. Good job at getting people to come to your article by calling bullshit to another. Whether it’s true or not, you completely go off on a little tangent rather than directly dispute all the supposed “facts.” I only believe the original to an extent but can also see there are always possibilities out there.
The good news is that the public is being tuned into the idea of anti-aging, and the article presents the prospect of extreme longevity in a good light. While the article did vastly exaggerate the implications of this research, it may have a net good on the world.
That Guardian “Article” also mentions 2 other things that made it look to me like bad journalism: The theory of free radicals is mentioned whichs also became questionable recently.
And they claim that telomerase can cause cancer in adults which most scientist I heard do not belive. (Because cancer cells already grow anyways so with telomerase just the healthy other cell live longer too)
Maybe you should check your facts before you start spewing venom. Research on telomeres has sound science behind it. “The expression of telomerase is suppressed in normal human somatic cells but activates in tumorgensis.” See Counter et al. 1998 Oncegene 16(9):1217-22.
The 2009 Nobel prize was awarded to Elizabeth H. Blackburn, Carol W. Greider and Jack W. Szostak for their work for the discovery of “how chromosomes are protected by telomeres and the enzyme telomerase” Currently the only known species to increase telomere length with age is Leach’s Storm Petrels (see http://rspb.royalsocietypublishing.org/content/270/1522/1387.full.pdf).
The only real crime here is that they act like this is something new when in fact this research has been going on for many many years now.
Hello. I’m not a specialist at all, but this study seems to show that it’s possible to reverse the consequences of a degradation with an enzyme, yes. But this degradation could be an important part of the aging process. If you boost a vital enzyme (metabolism, in the cells, etc..), you will have an effect, but which one ? Local, general, useful, not useful…? In this case, the authors have boosted this enzym and it seems to reverse this part of aging process, a general and useful effect (but is it going to last ? Will the mice live longer, or less ? etc.) Difficult for me to say just “bull sh*t”..
What is bullsh*t is to make claims like “Harvard scientists reverse the ageing process in mice – now for humans” and “Now they believe they might be able to regenerate human organs”. Those are very large claims relative to this research, and yet those are almost certainly the claims that allowed the story to become such a sensation.
ok, it’s a critic on the form (sorry for my english…). In fact i didn’t read the Guardian article, but this one http://www.nature.com/news/2010/101128/full/news.2010.635.html and the abstract, and it made an echo with the 2009 Nobel prize. Anyway the today society lacks of dreams (differents from the money dream, the consommation dream…), so if some searchers can show their work (done to go further…) via a dream…
It’s pretty reasonable to think that if we can cause this in one animal (particularly a mammal), then we can cause it in humans too. Maybe not using the exact same method, but still doing an essentially similar thing
Not to be mean here…but why do you think that is reasonable? Have you done studies with mice and translated them to humans? It really isn’t all that reasonable – you can’t engineer a knock-in human (at least under the FDA’s guidance) so how would you suggest moving these results to a clinical application?
Might just be the bitter biomedical engineering in me that thinks organogenesis and cell biology studies such as this one (take a vital protein away, see what happens, then add it back) are just silly…but I’d be interested in hearing from someone who thinks its “reasonable” for clinical applications.
So explain how you would know what would happen unless you took it away and then put it back?
>> I’d be interested in hearing from someone who thinks its “reasonable” for clinical applications.
You’re hearing from him! “you can’t engineer a knock-in human” You’re right, but that doesn’t mean that you can’t find a drug to activate telomerase in humans. Sierra Sciences has over three hundred compounds that activate telomerase in human cells. With standard techniques of medical chemistry they will soon have a candidate drug. Any other questions?
Why didn’t they just introduce the enzyme into the healthy, non-engineered genetically old mice, and show it reverses the ageing process? Because it won’t work, what they did works only in genetically damaged mice, but will have no effect on ACTUAL ageing process!
Or because ageing is complex, not only a telomere’s question. In this study, they have isolated the telomerase effect and reverse the consequences of the absence of this enzyme. It’s a confirmation (mice only for the moment) of its influence on ageing and a confirmation of the possibility of retro-acting this influence… A little step, but a real step, no…?
There are a lot of real steps done around every day, but not everyone can afford such advertisement because not everyone is from Harvard.
Sure, so many studies, very promising, are not known… But if a lot of people, via the buzz around this study, discover this research field, maybe the journalists will be more attentive to the next abstracts and publications about this theme…
So when you call this a non-story, do you mean the results are not what was reported? Or are the results as reported but the implications not nearly so wide-reaching? Or is this just a, “sure, we knew this is what would happen”? There is a lot of room for criticism of what passes for scientific journalism today, but this article is just as bad.
What is meant is that “the results are as reported but the implications not nearly so wide-reaching?”
The beginning of the story, and especially the title, are completely disproportionate and sensationalist when compared to the bottom of the story (ie, to the actual description of the experiment).
2 Chilean newspapers (maybe even more) also published this same story.. I guess the article made a snowball effect of mediocre journalism.
Thank you for saying this is unwarranted enthusiasm! This so-called “breakthrough” is really just another small step on a long climb.
Guess you’ll have to wait until reality intrudes itself forcefully on your angry belief system. In the meantime, you might try reading “Cells, Aging, and Human Disease” (Oxford University Press, 2004) for some deeper understanding of how aging actually works.