Borrowed Time: The Science of How and Why We Age

by Sue Armstrong

The question of how and why organisms age has teased scientists for centuries. There are myriad competing theories, from the idea that aging is a simple wear and tear process, like the rusting of a car, to the belief that aging and death are genetically programmed and controlled. In fact, there is no clearly defined limit to life, and no single, predictable program playing itself different things are happening within and between tissues, and each system or organ accumulates damage at its own pace, according to the kind of insults imposed on it by daily living. Sometime before 2020, the number of people over sixty-five worldwide will, for the first time, be greater than the number of 0-4 year olds; and by 2050 there are likely to be 2.5 times as many older people in the world as toddlers. Sue Armstrong tells the story of society's quest to understand aging through the eyes of the scientists themselves, as well as through the "ordinary" people who exemplify the mysteries of ageing--from those who suffer from the premature aging condition, Hutchinson-Gilford syndrome, to people still running marathons in their 80s. Borrowed Time will investigate such mind-boggling experiments as transfusing young blood into old rodents, and research into transplanting the first human head, among many others. It will explore where science is taking us and what issues are being raised from a psychological, philosophical and ethical perspective, through interviews with, and profiles of, key scientists in the field and the people who represent interesting and important aspects of aging.

Genres: Science, Nonfiction, Health, Biology, Medical, Genetics, Bodies

272 pages, Hardcover

First published January 24, 2019

Reviews

[Jake · Rating 3 out of 5]

How do we age? Why do we age?

These are good questions. But this book has fallen pray to the horrid pandemic issue of the misleading title - a disease rampant in the pop-sci genre. Neither of these questions are truly answered. Perhaps my expectations are too high, but when a book claims to propose 'the science' i.e. the mechanisms and workings of aging - I correspondingly expect to see some hardcore science. Or perhaps, if not hardcore, then at least a clear and delineated theory. As you can surmise from my circumlocutions meanderings - this is not what the book did. Rather it strung together a bunch of theories and ideas on aging without a clear connection from idea to idea. There was though coherence as a book. Not much, but some.

Do not let my 3 stars dissuade you from reading this. The book was actually quite useful in its survey of some of the literature. Further, do not be persuaded that the jury is out on the topic. Aging is still a mystery. This is something I expect the author no doubt will concede to. I nevertheless am still annoyed by the false advertisement.

Recommended for :
- Health care types (all of you)
- those interested in scientific mysterious
- those enticed by the word senescence
- those interested in biology

[Peter Tillman · Rating 3 out of 5]

Interesting topic, but any positive results seem VERY likely to be too late to benefit me! Hence, since my remaining time is limited [boo hoo!].... -- but younger folk may want to TBR. Here's a good meta-compilation:
https://bookmarks.reviews/reviews/bor...
I read the WSJ review (unpaywalled here, I think?) and it's sensible: basically, author Armstrong says, don't hold your breath. But, who knows, if the zillionaire techies put their $$$$ where their hopes/dreams are.... 😎 ⚡️ 💔? -- or not. Should find some interesting new science along the way!

Came due (new book) and I'm closing it out as DNF, 3.3 arbitrary stars. I might get back to it sometime. Or not. Time will tell....

[Tomislav · Rating 3 out of 5]

I read an advance reader copy of Sue Armstrong’s Borrowed Time: Science Takes a New Look at Old Age in PDF ebook, provided to me by Bloomsbury Publishing through netgalley, in return for promising to write an honest review. The book is scheduled for release on February 26, 2019. Sue Armstrong is a Scottish medical science writer who has published books on medical biology as well as fantasy fiction. Among her prior works is P53: The Gene that Cracked the Cancer Code (which I have not read).

This is not a book to keep for reference, as it is not organized in an order that would be accessible for that purpose, but rather to create fascination, tell the stories of some of the researchers, and give the reader a deeper perspective on science and health news that will break out in the future.

Gerontology is the study of a broad grouping of many specific degenerative diseases. However, it is also a study of some fundamental changes that take place in the cells as we age. Armstrong’s new book takes a fascinating look at the state of the science of cellular aging – telomeres and the Hayflick limit to cell division, prioritization of cellular functions under nutrition shortfalls, senescence as an evolutionarily successful method to shut down potentially cancerous cells, immune system function and degeneration.

The book moves on to cover some of the degenerative diseases which accompany aging, and how they relate to the fundamental cellular changes. Armstrong looks at cancer, HIV, the flu, Parkinson’s Disease, Huntington’s Disease, pneumonia, and others. Being a 63-year-old lifelong cyclist who would qualify for one particular study group, I was personally heartened to hear about the study showing the effect of that on my thymus and immune system!

In the final third of the book, Armstrong focuses on Alzheimer’s Disease, in particular. Accumulation of amyloid beta protein in the cortex of the brain is the trigger. The genetic mutations associated familial Alzheimer’s show the strongest correlation, but familial is only 2-3% of the cases. A number of genetic mutations have been found to associate with sporadic Alzheimer’s, but none of them alone are as strong a correlation. There is also a significant environmental contributor – smoking and air pollution may account for 20% of cases.

No successful drug remedy based on the amyloid beta protein has been found after 20 years of experiments and trials. In response Armstrong suggests that the best therapeutic program may actually lie in wholistic treatment rather than a combination of treatments for degenerative diseases as each appears. She seems to advocate for broad gerontology research, over isolated disease research – but the few examples cited in the last chapter seem more a sign of desperate resignation, rather a direction led from prior work. It is conducting tests of hopeful magic bullets like metformin to alleviate aging as a medical condition itself, rather the continuing the painstaking process of identifying the foundational science of the mechanisms.

So, I felt the strength of the work was in the microbiology of the first section, but then it concentrated overly on Alzheimer’s Disease. I am not in agreement with some of the proposed alternative directions given near the end, although it is hard to argue much with the need for lifestyle and dietary change in modern human lifestyles. And of course, the ultimate criterion of popular science writing is “Did I learn something?” The answer is a definite yes.

[Nicky · Rating 4 out of 5]

I've read one of Sue Armstrong's books before, on the role of the p53 gene in cancer, so despite aging and the science thereof not really being my thing, I thought I'd give it a try. And it was, in fact, riveting. I knew a little about some of the experiments -- I read a paper on sirtuins and resveratrol for my final exam of my BSc, so that gave me some extra context -- but much of the detail was new to me, and Armstrong explains things beautifully and keeps things very clear.

The answer to the question of how and why we age is, of course, "lots of ways and lots of reasons", and the science isn't all the way yet on understanding exact mechanisms and unpicking the many small effects that can add up over a lifetime. Armstrong avoids giving any false certainty, but makes it clear how people in the know expect things to go, and what they're cautious about. Unlike some writers, she doesn't intrude a lot into the narrative (we don't have to hear stories about her neighbour's sister's dog's brother, which some science writers lean on a bit too heavily), or when she does it feels relevant and useful to understand where she stands.

For a field with so many different puzzle-pieces, Armstrong really brings it together well, and I actually found myself reading this all in one day, in great big chunks. Now that's good science writing!

[Tobias Ratschiller · Rating 5 out of 5]

Very good introduction to antiaging research. I particularly liked that it gives a history on the different approaches, which makes it easier to understand how we arrived at where we are.

I would now recommend this as first book for a layman interested in longevity/antiaging . If you are specifically focused on investing, I still recommend Juvenescence: Investing in the Age of Longevity.

[Jeff Wong · Rating 5 out of 5]

This author has compiled a very readable book getting to some of the scientific findings related to the biology of aging. I found her writing to be clear, sufficiently detailed and well constructed. The anecdotes that she shares that support the various theories add to the richness of the prose. It's an enjoyable read.

[Lloyd Downey · Rating 5 out of 5]

Book Extracts: Borrowed time: the science of how and why we age
I’m not expecting to live forever. I just want my superannuation to last until I go. But it’s a very tricky exercise in figuring all this out. Hence my special interest in the subject of aging. But whilst I’ve been researching the subject, I’ve realised that you can live a long and miserable (unhealthy) life or you can, maybe, live a long life in good health until right at the end. (Of course you may get hit by a bus tomorrow). But given the various possibilities, I’d prefer to live the longer healthy life if at all possible. And this book gives, what appears to be, a very thorough coverage of the state of knowledge about the aging process as it stands at the moment. I really learned a lot from the book. I was also impressed that the “free radical” damage as the cause of aging seems to have been de-bunked. And I wonder about this also in all the other contexts where “free radicals” are invoked as the cause of health issues.
Basically, I think Sue Armstrong has done a pretty remarkable job here of teasing out the issues and I’ve extracted some passages below which let her speak for herself. She is a science writer rather than a scientist and I’m a bit ambivalent about having a writer interpret stuff....but, at least, the writer can be a bit more objective than a scientist who has committed to some specific theory. Here are some excerpts from the book.
The fact is that the biggest single risk factor for a host of conditions–from stiffening joints, thinning bones and waning energy to heart failure, cancer, stroke, dementia and the steady loss of hearing and eyesight–is old age.....Anytime now, the number of people aged over 65 years worldwide is set to exceed those under the age of five for the first time in human history, and is projected to be almost twice the number of the very young by 2050.....One cannot ignore the evidence that for too many of us old age is nasty, brutish and long.
A five-year-old girl in the UK today can expect to live to a little over 80 years. But evidence suggests that her last 19 or 20 years will likely be dogged by ill health......‘Over the past 50 years, health care hasn't slowed the ageing process so much as it has slowed the dying process.’ [You just have to love this line].
There is this fundamental property–that longevity is bought, effectively, by investing in better maintenance and repair.’ In 2013 a bunch of scientists working on diverse topics relevant to ageing decided to draw up a list of ‘hallmarks of ageing’–characteristics of the elderly body that ‘represent common denominators of ageing in different organisms,
The nine characteristics that fit this bill are:
1. Instability of the genome.
2. Telomere attrition.
3. Epigenetic alterations.
4. Loss of proteostasis......Proteostasis is the process by which the cell brings order to this potentially unruly mob of individual proteins,
5. Deregulation of nutrient sensing.
6. Mitochondrial dysfunction.
7. Cellular senescence.....Besides shortened telomeres, other forces, such as damage to the DNA or epigenetic alterations, can also cause cells to senesce.
8. Stem-cell exhaustion.......Over the years, these reserves get run down.
9. Altered communication between the cells of the body......result primarily of chronic, low-grade inflammation of the tissues.
When I came into the field 20 years ago, my impression from my colleagues was that the oxidative damage theory was pretty much a done deal,’ said geneticist David Gems......But I suspect it's a folk theory.
Hayflick .....became aware that, at some point, the cells would stop dividing and that this seemed to be a predictable event that occurred after about 50 population doublings.......He was particularly intrigued by the fact that the cells didn't die; they continued to metabolise and could live in that non-dividing state for a year or more. What he had correctly identified as the natural lifespan of cells is known today as the Hayflick limit, and it's become one of the hottest areas of research in gerontology.
Hayflick's game-changing discovery in 1961 raised an obvious question: how do cells know when they have reached their limit?
Over the years scientists have learnt that the length of our telomeres is determined to a certain extent by our genes and that it varies from one tissue and organ to another in our bodies, as the rate of cell division also varies between tissues......The results of telomerase therapy have been inconsistent, unpredictable and not always easy to interpret. This has driven home the message that the picture is a lot more complicated than it seemed early
Cancer and ageing, seem to be two sides of the same coin: ageing is the price we pay for protection against cancer, in that Nature's way of limiting the proliferation of potentially dangerous cells is to put a brake on their ability to divide after a certain length of time.
The system protecting us from cancer does not rely on telomeres alone to limit the life of potentially dangerous cells. Many other things–including UV radiation from sunlight, oxidative stress (those free radicals again), chemicals in the environment, dangerously low levels of oxygen or nutrients, aberrant proteins clogging up the machinery–can damage our DNA and put the brakes on cell division. They do so by setting off a general alarm system controlled by genes known as ‘tumour suppressors’.
The most notable of these tumour suppressors is a gene called simply p53, which is present in all our cells.....It receives signals that the DNA in a dividing cell is damaged; will stop the cell in its tracks and send in the repair team before allowing it to proceed.....If this gene is working properly, it is virtually impossible to get cancer.
As we get older, so too our immune systems age and get less efficient at clearing senescent cells just as we are producing more of the things. ......Senescent cells are not dead but dysfunctional. As they continue to metabolise, they secrete substances into their environment that chew up collagen, the stuff that holds our cells together.
......Senescent cells in the walls of blood vessels tend to forget that they're blood-vessel cells and become bone cells, leaving calcium deposits that cause hardening of the blood vessels and heightened risk of strokes and heart attacks.
But one of the most important ways in which senescent cells are thought to promote ageing is through chronic inflammation
Senescent cells, it seems, are needed to promote tissue repair and for healthy development. ‘But you don't want them sticking around.’..... So, in an old person,’ commented Cox, ‘not only do you have more inflammation because you've got more senescent cells kicking out these inflammatory cytokines, but your immune cells are causing damage as they get to the site of injury.’
There are two schools of thought about how to prevent the damage done by senescent cells. One strategy is to develop agents known as senolytics that will kill the cells, sending them off for recycling. The other is to rejuvenate the cells so that they function normally again.
......So what of the second option described by Cox: simply reversing senescence
Researchers have managed to do this in human cells in lab dishes by switching off p53 and p21, The big danger is that an unrestrained damaged cell might turn cancerous.
If TOR [an enzyme] is working too long or too hard it will drive a cell to senesce. But if you inhibit TOR, you slow down protein production, and you turn on the housekeeping programme that recycles all the worn-out components; senescent cells become younger again,
Rapamycin ....extended the average lifespan of mice by 12 per cent, while also significantly improving their health. ...The drawback with rapamycin, however, is that it can have a range of more or less uncomfortable and serious side effects. [Tests are proceeding with intermittent doses to relieve the side effects.]
Werner's syndrome is........a premature ageing syndrome.....With Werner's syndrome, more than 90 per cent of cells in culture do less than 20 population doublings.......Most of the clinical features seen in people with Werner's syndrome are the result of the accumulation of senescent cells.......The Werner's gene was discoveredin Seattle in 1996.......It was found to be the recipe for an enzyme that unwinds DNA during the process of cell division, when the genome is being copied...... In essence it turns out that tissues where telomerase is turned on are quite protected against the effect of Werner's; tissues that are telomerase-negative aren't protected, and they're badly affected, typically.’’
They have worked out how the chaos in a Werner's cell triggers senescence–how it signals its distress and sets off the cascade of events that bring it to a permanent halt,
At the head of this cascade is a protein that goes by the prosaic name of p38 MAPK. It’s role in inflammatory conditions such as rheumatoid arthritis, psoriasis* and Crohn's disease† has been known for a long time, and a number of big drug companies have been working their socks off to find safe and effective ways of blocking it as a treatment for these diseases........p38 MAPK is not just involved in promoting inflammation, but is a key player in the whole business of responding to stress, and therefore in shutting cells down, causing senescence.......‘One of the problems, is that p38 MAPK is a protein that you can't knock out–it's absolutely critical to a lot of processes.
The conclusion of their research was that p38 MAPK–as a key player in the response to stress–is directly involved in the premature ageing of people with Werner's syndrome....The likelihood is that stress can, under certain circumstances, accelerate ageing in any of us by triggering senescence in our cells even before their time has run out on the telomere clock.
Cellular senescence, [however] could never be the sole mechanism responsible for ageing
The man who really propelled drosophila flies into the mainstream of scientific research was Thomas Hunt Morgan, an embryologist who started using Drosophila in 1908 to study the mechanisms of inheritance...... We now know that around 75 per cent of genes known to be involved in human diseases are also found in Drosophila
With just 100,000 neurons compared with our 100 billion, the fly's brain, too, provides an appealingly simplified system for exploring basic principles of brain function and disease processes......Its brain is remarkably similar to that of mammals, including us....Though it doesn't normally suffer a fly version of dementia, Drosophila does share with us the gene involved in the hereditary form of Alzheimer's disease.....Very recently the fly has been adopted as a model for studying the heart, too–specifically, how the electromechanical signalling system works.
Another stalwart of biological and genetic research is the tiny worm(nematode) Caenorhabditis elegans... The sequencing of its genome in 1998 revealed that the worm has around 19,000 genes arranged on six chromosomes. More than one-third of C. elegans genes have counterparts in humans
Mice are stars in ageing research, too......they're all short-lived.....‘But we could be missing some huge things by only looking at short-lived animals.......A researcher into possums in Venezuela found that they get cataracts and parasites and they'd lose muscle mass–and he could see this in a few months.’ Today he studies what is believed to be the world's longest-lived multicellular animal, Arctica islandica, a species of cold-water clam, [one specimen]. Ming was found to be fully 507 years.....What stands out most clearly as special in the molluscs––is the extraordinary stability of their proteins. So far, the scientists have been unable to pin down the magic ingredient in the clam juice......Why, with so many more dividing cells in their huge bodies, elephants don't have higher rates of cancer than we do. It turns out that elephants have 20 copies of p53, the tumour-suppressor gene......Elephant p53 is a more sensitive version of the gene than ours
In 1993 C. elegans hit the headlines and gave a shot in the arm to ageing research when Cynthia Kenyon, discovered that a mutation in a single gene, known as daf-2, could double the lifespan of the little worm....Tinkering around with daf-2 over the following years, Kenyon's lab managed in 2003 to extend the little worm's lifespan by sixfold, and later another lab was able to extend it tenfold.
The daf-2 gene [can]set off an alarm system [which] activates a caretaker gene called FOXO....The tasks of these genes are, variously, to protect the cells from oxidative stress (free radicals); to repair or recycle damaged components; and to make sure that other proteins in the cell are formed and functioning properly.....Another gene, chico, works high up in the nutrient-sensing network and it triggers the same cascade of events, awakening the caretaker FOXO to go to the nucleus and switch on a battery of protective genes.
Withnin two years a report had come in of mice whose lifespan was extended by 18 per cent by knocking out altogether a single gene that holds the recipe for an insulin receptor specific to fat cells......Whereas invertebrates have only one of the caretaker FOXO gene, humans and other mammals have four. And sure enough, in 2008, a group of scientists
published a paper showing a strong association between a natural variant of the FOXO3 gene and long life......Those who had inherited the gene: had less cancer, cardiovascular disease and cognitive decline than the controls, and were physically stronger and steadier on their feet, despite being on average 11 years older.....The older a person was at death, the later in life they were likely to have suffered their first serious age-related disease–defined as cancer, cardiovascular disease, chronic lung problems, diabetes, dementia or stroke–and the shorter the period of their total lives they had spent as frail old people.
There is abundant evidence that no such master switch exists. Genes such as age-1, daf-2, chico, the FOXOs and their equivalents in other critters form the tip of the iceberg......As of mid-2017, scientists had identified 2,152 genes that affect lifespan (and therefore the rate of ageing) in model organisms, and 307 such genes in humans. From what they have learnt so far, they reckon that some 20–30 per cent of our natural lifespan is accounted for by our genetic heritage, while environmental influences account for the rest.
Not only does calorie restriction extend the lifespan of rodents, but it also delays–often dramatically–the onset of age-related frailty and other pathologies.
Pankaj Kapahi and his colleagues, ....[showed that] when you restrict the diet of a fly, the mechanism by which it's extending lifespan involves TOR. And it's turned out to be true in multiple species now.’......The take-away message there was: maybe you don't have to do this quite so intensively to get the benefits.’...The search is now on to find drugs that might mimic the effects of dietary restriction without the personal pain and disruption.
One of the commonest denominators of all age-related diseases–from cancer, diabetes, furred-up arteries and arthritis to blindness, lung diseases and dementia–is inflammation.
‘As you get older there's a tendency for stem cells to start to become fat cells,’ .....No one yet knows where the healthy balance lies between active and inactive muscles, and her team in Birmingham is running some studies to find out.
Besides causing inflammaging by being permanently switched on at a low level, the immune system itself ages with time.....The evidence is that the immune system gets weaker on all fronts as time goes by, and less efficient at doing its job.... ‘But by the time you're 60 or 70 years old it's really bad......Blundering neutrophils are slow to reach their target, which is one reason why wounds heal so much more slowly as we age...... Tests on healthy older adults found that just two weeks on statins made their neutrophils as good at navigation as a young person's. And they had the same effect on the neutrophils of elderly patients with pneumonia because statins lower the inflammation, improve your neutrophils, and they make [more specialised] T cells function better.
Roughly one in four old people who break a hip will die within a year..... production of DHEAS peaks around the age of 30, declining thereafter, so the balance is not restored in elderly patients with broken hips. With those who didn't become depressed, immune suppression was not such a big deal......‘Bereavement is as powerful a stressor as a hip fracture, and it persists
The cells of the adaptive immune system are the B cells, made by the bone marrow, and the T cells, made by the thymus (hence B and T). The B cells make antibodies–individually tailored weapons–in response to invasion by specific bugs......The T cells, on the other hand, when called upon to fight an invader (typically a virus that gets right inside cells), turn some of their naïve cells–that is, ones that are not yet specialists–into heavily armed killers that can proliferate enormously to produce hundreds of thousands of copies of themselves. These killer cells swarm to the attack, slaying the cells that are infected by the virus.
As they age, .....‘the dendritic cells....are showing reduced uptake of the bug. That makes the T-cell priming very wimpy, because [the dendritic cells] haven't been really activated to a sufficient extent to present enough molecules of the bug to the T cell.......So the sentinels in elderly people are doing a pretty pathetic job of gathering intelligence.......Inadequately stimulated and ageing B cells make poor-quality antibodies, while ageing T cells struggle to produce educated new soldiers, and not only are elderly people especially vulnerable to catching flu, but their response to vaccination–which works by priming the adaptive immune system to produce its specialist weapons–is often poor because of the ageing defence machinery.
People over 75 are almost twice as likely as those below 65 to catch flu when it's around, and one in three of those that do will end up in hospital with a life-threatening illness.
One of the downsides of the dieting strategy, which has proved tantalisingly effective at slowing down the ageing process in so many species, including us, is that it suppresses the immune system.......But with Lord's cyclists this wasn't the case. ‘They had really good thymic output of new T cells,’ she said. ‘The levels we measured were as good as a 20-year-old's.’ What she thinks is happening is that the cyclists’ muscles are much more efficient than those of their le

[FlyingBulgarian Svetli H. · Rating 5 out of 5]

A very interesting read which tries to answer the question of how and why we read - throughout the chapters Sue Armstrong tries to explain different culprits for us getting older. I enjoyed her explanations - it must be quite a feat to take some of the extremely complex research subjects and make them accessible to the average educated reader.

The only thing I would have liked to see which was missing was some practical advice on how to live better and longer. But we can't all have it all.

[Diane Hernandez · Rating 5 out of 5]

If you are interested in the how and why behind aging, Borrowed Time: The Science of How and Why We Age will explain current aging research in an easily understandable manner while opening up a whole new frontier of science to lay readers.

Borrowed Time: The Science of How and Why We Age is definitely a popular science book. The definitions of terms and especially acronyms are written in plain English. The science is clearly explained. However, it is the conclusions drawn that are stunning. Experiments in worms have shown it is possible to extend life tenfold. However, it appears that “ageing is the price we pay for protection against cancer.” Unfortunately, many of the proposed aging solutions caused similar issues. Just a note on the worms: the roundworms carried on the space shuttle Columbia for experimentation were the only survivors of the explosion that killed everything else. Some of their descendants were carried eight years later to the International Space Station on the Endeavor.

I found this book to be really interesting because I didn’t know anything about how the aging process works or any of the multitude of research projects trying to stop it. I would recommend not talking to your 20-something daughter about the importance of the FOXO gene variant, where you basically won the old age lottery. My daughter’s eyes glazed over sometime during the first sentence. I should have started with the fact that fruit flies share 60% of our genes and the worms mentioned above only share 33%. I just have to give this book 4.5 stars rounded up to 5 stars! I couldn’t put it down!

Thanks to Bloomsbury Sigma and NetGalley for a copy in exchange for an honest review.

[Bryan · Rating 5 out of 5]

If you want a heavily science-based review of current ideas on aging and the research on aging that is ongoing, this is highly recommended. It is a readable and objective view of where things currently stand. Even though we have learned a lot about aging, we still have a lot more to learn, and no clear cure for aging is on the horizon, although a number of lines of promising research are under way.

[Kartika Nurfadhilah · Rating 3 out of 5]

Well, I’ve read this book a year ago but I just remember that I haven’t visited my Goodreads account for a while. HUHU, So, yeah, here we go!

Actually, this book was quite boring for me, however, still suits my taste! I bought it at a reasonable and cheap price using a bookstore promotion; the author uses the dictate format (or college look-a-like course book) narration, even though she narrates the story or topic discussion similar to the basic communication dictate book I used during my freshman year. Could you imagine reading this book with course format year? LOL

As the title has talked about the discussion— Borrowed Time: The Science of How and Why We Age was talking about aging and age. She used ‘borrowed time’ means that age is unavoidable therefore we only have a way either to slow the process or to speed the aging, also we have an individual timeline as God already planned the way we live. The book started with the term aging and the process of aging. Then, the author went further about diseases around aging. There were also lots of theories about aging including immortality, but my favorite theory about aging is the aging biology network states that aging is a biological network alteration throughout the times since childhood, and the alteration was done by the automatic program. So, we cannot avoid and change the process, just slow the program.

Because of this book, I managed to read an additional journal about aging HAHAHAH such as this journal (LOL)
1. Induction of pluripotent stem cells from mouse embryonic and adult fibroblast cultures by defined factors -> there’s a chapter about a Japanese researcher trying to reverse the process of aging by using adult tissue back to fetus tissue. Hoping the backward process can cure genetic diseases.
2. Thalidomide: the tragedy of birth defects and the effective treatment of diseases -> we knew the tragedy of thalidomide for affecting the fetus development, but there’s some vision for expanding the utility of drugs instead of developing new kinds of drugs, clinicians, and research want to optimize the current drug for another disease. The tragedy of thalidomide turned out to be effective in curing cancer.
3. Therapeutic potential of metformin in COVID-19 reasoning for its protective role -> just new information, that metformin for diabetics also could be used for chronic COVID-19 patients.

Despite new knowledge, I give 3 stars for this book because of the way the author narrates the book uncomfortably.

[P · Rating 3 out of 5]

The disposable soma theory mentioned in the first chapter was briefly mentioned in The Selfish Gene. In short, the theory says that once we're past our reproductive stage our bodies stop the essential repair and maintenance function that prevents DNA errors from being accumulated. Dawkins suggests that we can extend our lifespans by not having children till the age of, say, 40. The list containing the nine characteristics of ageing was fascinating because it shows us how ageing isn't a simple, linear process affecting a few organs. It's systemic. I had heard of p53 but not of p21. p21 contributes to cellular senescence. But senescent cells are not always bad; they assist in wound healing. There are two major ways to combat ageing - 1. Kill old cells so that new ones (stem cells) can take their place. 2. Resurrect old cells. The latter is a better approach because if we kill too many old cells then it might lead to organ failure. Resurrecting old cells by injecting Yamanaka factors (Oct3/4, Sox2, Klf4, c-Myc) is the best solution we have at the moment, I think. Induced pluripotency is a rapidly developing field. The causative link between leaky gut syndrome and ageing was new. Also interesting was the evolutionary reason for the existence of APOE gene that causes Alzheimer's; the answer is parasites, especially, intestinal worms.

[Shirley · Rating 4 out of 5]

Despite of not understanding 100% of every research’s details, it’s still fascinating to go on this anti-aging researches journey. Anti-aging to me isn’t about living forever; but about how to enjoy life with good health when we are alive!

What hit me the hardest is a research that combines Indian traditional medicine concepts with western scientific methodology to take a more holistic approach to prove initial positive results by changing people’s lifestyles has struggled to seek funding to further their research. I can’t help but wonder is it because of Big Pharma can’t patent ‘healthy lifestyles like exercise and healthy eating’ so they are not keen to invest. See below screenshots of a couple pages that outline those lifestyles tips and the changes they makes!

[Sreena · Rating 4 out of 5]

"Without death, life has no edge, no urgency. Without aging and the inevitable risk of decline and loss, human life loses its poignancy, its urgency, and its depth."

This profound statement resonated deeply with me, serving as a poignant reminder of the intrinsic value and transience of our existence. Armstrong skillfully reminds us that aging is not to be feared but rather embraced as an integral part of the human experience, fostering personal growth and resilience.

The only drawback I could say about this book was that it delves into complex scientific explanations that might overwhelm certain readers without a background in biology or genetics.

Nevertheless, this was a Fascinating Journey into the Mysteries of Aging

[Ira Therebel · Rating 4 out of 5]

A pretty interesting book on how aging happens. Goes through many theories and studies. I didn't even know that fruit flies have a brain similar to ours only smaller and simpler! There is really a lot of research going on and looks like some things may get developed soon enough but at the same time one can also see how many factors are involved so there sure won't be any anti aging pills.

I liked how much was told about Alzheimers. The scariest part of ageing and it is nice to understand it a bit better. Maybe I should start live healthier then.

A very depressing book as one finds out how everything within us stops working but at the same time very interesting to find out/

[Adelyne · Rating 3 out of 5]

I was a bit disappointed with this one, as I have recently read and really enjoyed another book about p53 by this author. I felt like this one was less well-researched, the spectrum of scientists that she interviewed (for a far broader topic) was much more restricted and as a result this book felt a bit repetitive of the opinions of only a small number of researchers in the field. This one also doesn’t have the little quote at the start of every chapter, one of the highlights of the p53 book for me, and I thought the flow from one chapter to the next was also a bit more stuttered. The title is also a bit click-baity, it sort of suggests that the how and why we age is already known (it’s not), and even the theories that are being currently thrown around (and covered in this book) don’t actually answer the question on the subtitle the way it is implied.

That being said, this disappointment does stem from how well I thought the p53 book was written, and this was still a decent effort by Armstrong who does really well in pitching these sorts of scientific concepts. 3.5 stars, 3 on Goodreads. The rounding down is almost 100% due to how much I hate the subtitle!

[Amanda · Rating 3 out of 5]

3.5 stars. This book is heavily science-based, with lots of references to studies, which I appreciate. If you don't, however, this could come across a bit dry. I read a blurb on the back that said someone felt oddly rejuvenated after reading this; I have to say I felt the complete opposite - like I could just feel my body getting older and failing me. Overall a good overview of the different aging mechanisms in the body.

[Valerie · Rating 4 out of 5]

The Clock’s Ticking

Loads of information about the science and biology of the aging process and the effects time has on the body and brain. Dense read if you don’t love learning. Breaks some urban myths about what’s good and not and great explanation of Alzheimer’s. Amazing how the body’s design to defend intrusions can render itself defenseless. It literally fights to the death.

[Roger March · Rating 4 out of 5]

A thoughtful but hard read ...

It has kind of a Popular Science feel to the subject of aging but in the end rescues itself. The magic bullets and miracle cures are dissected into science and you get a good view of how complex aging is to researchers. The Alzheimer's sections are especially disturbing to read. I find it encouraging that there are people are dedicated to persistent even in the face of so much failure.

[Ken · Rating 3 out of 5]

A strong science-based book, easy to read (though I am a biologist... but decades away from cutting edge learning!), and not too detailed, though some of the biochem in the middle third was a bit of a challenge to get through. A little disappointing to read as I'm pushing 60, but overall a good overview of the current theories and research.

[Peter · Rating 5 out of 5]

Great book exploring the science of aging. Author documents multiple lines of ongoing research into the biology of our cells , lots of focus on the brain and Alzheimer’s of course. Research suggests stepping back from focus on age related diseases to keep our biology healthy later into life. Maybe the next 10 years will bear some practical fruit.

[Supinder · Rating 3 out of 5]

The adventures of a journalist that examines the science of longevity. Armstrong skims far too much on the specific detail of the gene sequences involved for this book to be useful. However, she does give an intimate portrait of the main scientists working in the field.

[Elaine Moore · Rating 5 out of 5]

Some old information and some new, Armstrong presents a concise overview of the mechanisms that drive aging. With information on genes, diet, and the immune system, the reader is taken full circle on how older findings were further investigated to show us how we age.

[Kristine Latta · Rating 2 out of 5]

Had to force myself to finish this book despite my interest in the topic. She never pulled back from the granularity of the science to tell a story. The chapters were disjointed and the book was altogether disappointing.

[The Gianelles · Rating 5 out of 5]

Excellent read!!

Very interesting! I didn't know about all of these scientists dedicating so much to finding a "cure" for aging! An excellent read!

[Dixie · Rating 5 out of 5]

Fascinating, and so well and clearly written.

[Robert Maddock · Rating 4 out of 5]

Keeping up with science for me can be challenging. This book has done it for all the influences on aging. Read it if you want to be wowed .

[Steven Ulatt · Rating 4 out of 5]

Great read. A tantalizing glimpse into the future of anti-aging treatments. Gives hope.

[Dagnija · Rating 2 out of 5]

pārāk smalki, lai būtu izklaidējoši

[Meg · Rating 5 out of 5]

So many research rabbit holes from one small book. Invested and entertaining through some very dense subject matter.