I think I bought this book the day it came out and read it immediately, putting aside another book, which I rarely do. But if a Nobel Laureate writes a book about telomeres and aging, it is of course a must-read for every transhumanist. Nonetheless, I am a bit disappointed after reading The Telomere Effect by Elizabeth Blackburn and Elissa Epel. Perhaps my expectations were too high.

I’ve already discussed one point I didn’t like about the book in my previous post. The authors appear to like the shoelace metaphor quite a bit. I found this very confusing because throughout the book, there is no real explanation about how the protective function of telomeres (which is of course important) might correlate with aging.

When I skimmed through the book for this review, I found on page 57 a reference where the authors at least mention the well-known fact that cells stop dividing after the telomeres reach a certain length. Perhaps it would increase the risk of mutations and cancer if chromosomes continued to divide with short telomeres because the genetic material could “easily become unraveled” (p. 49). Unfortunately, the authors don’t go deeper here, which would have been very helpful. Nevertheless, I wanted to add this observation to my previous post.

As I said in the last post, Elizabeth Blackburn is the expert when it comes to telomeres. She won the Nobel Prize in Physiology or Medicine in 2009 (along with two colleagues) for co-discovering telomerase, the enzyme that maintains telomeres. The second author, Elissa Epel, is a health psychologist who studies stress, aging, and obesity.

The topic of the book already becomes clear when you look at the expertise of the two authors. They claim that their research areas are strongly linked and I can tell you that they offer overwhelming evidence. Essentially the book covers three main topics.

First, we learn that aging is indeed linked to telomere shortening. The evidence is nicely presented and easy to understand, although I didn’t discover anything I didn’t already read in other books about the topic. However, this part in the beginning is relatively short and its purpose probably is only to convince you that short telomeres are indeed a problem when it comes to aging and age-related diseases.

The main (and certainly a surprising) thing about the book is that certain behaviors can influence the telomere shortening process. This is how the authors express it (p. 6):

To an extent that has surprised us and the rest of the scientific community, telomeres do not simply carry out the commands issued by your genetic code. Your telomeres, it turns out, are listening to you. They absorb the instructions you give them. The way you live can, in effect, tell your telomeres to speed up the process of cellular aging. But it can also do the opposite. The foods you eat, your response to emotional challenges, the amount of exercise you get, whether you were exposed to childhood stress, and even the level of trust and safety in your neighborhood—all of these factors and more appear to influence your telomeres and can prevent premature aging at the cellular level. In short, one of the keys to a long healthspan is simply doing your part to foster healthy cell renewal.

The third topic describes tips on how you can avoid these behaviors that accelerate telomere shortening.

One of the disappointments from a transhumanist point of view is that the book is not really about radical life extension (p. 12):

Does our research show that by maintaining your telomeres you will live into your hundreds, or run marathons when you’re ninety-four, or stay wrinkle free? No. Everyone’s cells become old and eventually we die.

All right, we are all going to die. That’s sad news, of course—at least if you are a transhumanist. However, even if you are more of an Aubrey de Grey or Michael Fossel follower, it is still worth reading the book.

First of all, if you follow all the advice in the book, you can extend your lifespan at least a little and shorten what the authors call the diseasespan. For most people the diseasespan begins in the early fifties and is “marked by the diseases of aging: cardiovascular disease, arthritis, a weakened immune system, diabetes, cancer, lung disease, and more” (p. 2).

Scared enough? Good! The good news is that you can significantly shorten your diseasespan if you take good care of your telomeres. However, if you expect some secrets in the book on how to accomplish this goal, I have to disappoint you. You can find most of the tips in any common health book. Essentially you have to avoid stress, eat healthy, and exercise. I guess you knew that already. Live healthy and you stay healthy.

Thus, this is not the interesting part of the book. For me the real shockers were the countless studies that link short telomeres to all kinds of external influences. Here is a (short) list that I extracted from different parts of the book (I recommend reading it all, otherwise you won’t get the idea):

Feeling highly threatened (11), processed meats (11), neighborhoods that are low in social cohesion (11), children who are exposed to several adverse life events (11), short telomeres on the parents’ chromosomes (11), stress (63), the times a mother looked after a sick child (75), depression (77), strong threat response (82), angry thoughts (100), mind wandering (100), rumination (100), thought suppression (100), cynical hostility (101), pessimism (102), ironic error (108), anxiety disorder (142), time spent snoring (200), drinking sugared beverages (220), inflammation (225), chronic heavy alcohol use (225), red meat (237), white bread (237), saturated fats (237), omega-6 polyunsaturated fats (238), being stuck in your neighborhood (256), children who live in a neighborhood that is physically disorderly (259), poverty (260), exposure to pesticides (261), alachlor (266), metolachlor (266), triflularin (266), 2,4-D (266), permethrin (266), toxaphene (267), DDT (267), PAHs (267), African Americans who experience more daily discrimination (273), babies whose mothers never completed high school (281), babies whose mothers experienced severe stress and anxiety during pregnancy (289), the more time children spend in an orphanage (296).

Note that the page number in parentheses is just the first location where I found the corresponding cause. I also don’t claim that this list is complete. It is quite likely that I missed a few other things linked to short telomeres. I could have added a second list with things that cause longer telomeres, but I suggest you read the book if you are interested in that.

I find two things amazing here. First, there’s a wide variety of things associated with shorter telomeres. It appears that almost everything known to be “bad” influences telomere length negatively. I suppose soon someone will conduct a study proving that making bad jokes in book reviews is also linked to shorter telomeres.

Unfortunately, the authors rarely give hints on how to explain these links biochemically. Statistical correlation is interesting but it says nothing about causes and effects. Without knowing the biochemical pathways that lead to these correlations, we cannot even say that we have a theory, let alone a confirmed theory. I guess conducting such studies is relatively easy, and if you don’t add a controversial theory, you have a good chance to get published in a peer-reviewed journal (if you know the right people).

However, more interesting to me by far is the sheer number of studies that try to find links between telomere length and external factors. Despite the fact that this is a relatively easy way to get published, it shows that a growing number of scientists believe telomere length is indeed crucial when it comes to explaining aging.

I think this book severely damages the theory that aging is just caused by accumulated damage. Aubrey de Grey’s claim that the telomere theory of aging is pretty much rejected can hardly be true if a Nobel Laureate publishes passages like this (p. XV):

One current, predominant, scientific view of human aging is that the DNA of our cells becomes progressively damaged, causing cells to become irreversibly aged and dysfunctional. But which DNA is damaged? Why did it become damaged? The full answers aren’t known yet, but the clues are now pointing strongly toward telomeres as a major culprit. Diseases can seem distinct because they involve very different organs and parts of the body. But new scientific and clinical findings have crystallized into a new concept. Telomeres throughout the body shorten as we age, and this underlying mechanism contributes to most diseases of aging. Telomeres explain how we run out of the ability to replenish tissue (called replicative senescence). There are other ways cells become dysfunctional or die early, and there are other factors that contribute to human aging. But telomere attrition is a clear and an early contributor to the aging process, and—more exciting—it is possible to slow or even reverse that attrition.

As I mentioned in the introduction of this post, the book disappointed me a bit. When I read the title, I thought Blackburn would present new biochemical details on how telomere shortening causes aging. However, the book does not contain much about this. The fact that so many studies exist about telomere length is interesting, but reading the corresponding lengthy passages without any real scientific (theoretical) meat was not.

If you read health books or occasionally watch health shows on TV, you probably are already familiar with all the book’s health tips. In my view, the authors exaggerate a little by calling this advice “telomere tips” or “telomere maintenance.” That stressful living and sugar consumption shorten your telomeres is interesting. However, I think we all know that stress and this sweet stuff harms you and your body in many other ways.

Anyway, I certainly don’t regret reading the book, and if you are interested in theories of aging and telomeres, you definitely should have a look at The Telomere Effect.