Cracking the Aging Code: The Science Book of the Year

In his new book, Cracking the Aging Code: The New Science of Growing Old and What It Means for Staying Young, Josh Mitteldorf, who has studied aging for decades and writes about it at his website, explores the science of aging and sets forth his own theory as to why we, and virtually all organisms above the level of bacteria, age. (The book has a co-author, Dorion Sagan, but the theory is Mitteldorf’s, and in any case, perhaps because I’ve been an avid reader of his website, the author’s voice seems like Mitteldorf’s alone.)

This is the science book of the year, the best I’ve read in quite awhile.

Mitteldorf is an expert in evolutionary theory (he used to be an astrophysicist), and deftly and skillfully expounds and criticizes the several current theories of aging. He then proposes his own radically different theory. And he’s very convincing. Whatever the fate of his theory, he brings enough evidence to bear both in its favor and against the other theories that, it seems to me, his theory must be reckoned with.

A thorn in the side of evolutionary theory

Aging has been a thorn in the side of evolutionary theory since the beginning. Even Darwin knew and understood this and could not see a way to incorporate aging into the theory of evolution.

Aging poses a conundrum for evolutionary theory because aging manifestly decreases biological fitness, causing lower reproduction and greater mortality. Why wouldn’t evolution have abolished it, or not allowed it to come into existence?

If an organism didn’t age, it would seem to have an advantage: it would never die of aging and it would continue to reproduce throughout its lifetime; hence the longer an organism lived, the more offspring it would leave, and the fitter in evolutionary terms it would be.

Indeed, we do see this in some organisms. Lobsters, for example, apparently do not age, but grow bigger and more fertile with the passage of time. (The record weight for a lobster was 44 lbs.) Mitteldorf describes some species of long-lived shellfish that are almost nothing but feeding and egg-laying machines, cranking out a million eggs daily.

But humans and most animals do age. Animals in the wild have a greater chance of death from predators and infections the older they are. Why hasn’t evolution put a stop to this?

One older idea, that of Peter Medawar, is that the force of natural selection declines with age. If an organism has aged and then dies, any genes that contributed to aging and death have already been passed to its offspring. The idea is that some genes that may cause aging are also necessary for growth and reproduction. Therefore natural selection is unable to eliminate the genes for aging.

Medawar’s idea led to the three main modern theories of aging.

Mutation Accumulation: Genetic mutations are always present in a population; in other contexts, this is known as genetic load. If a mutation is not severe enough to cause death, but causes only, say, a 1% decreased level of fitness, then these genes can stick around in a population for a long time. Essentially, natural selection has not had enough time to get rid of them. An example might be the ApoE4 gene, which raises the risk of dementia and heart disease.

But even a 1% difference in fitness is, as Mitteldorf says, “far from being invisible to natural selection”. Aging animals do not die of senescence usually, but they die at a much greater rate from disease and predators than younger animals. In some arctic species, 60% of deaths in the wild can be attributed to aging. Natural selection should be capable of eliminating the genes that cause this huge death toll, and to be able to do it quickly.

Antagonistic Pleiotropy: Some, maybe most, genes have multiple functions, and this theory says that genes with important functions in youth cannot be weeded out when they cause aging. An example of this might be the hormone IGF-1, which is involved in both growth and aging. Mice without it die shortly after birth — but high levels in older people are associated with cancer and higher mortality.

Mitteldorf describes the work of Michael Rose, who bred fruit flies for longevity in order to see what would happen to fertility. In theory, if he selected long-lived flies and bred them for longevity, their fertility should decrease, given antagonistic pleiotropy. But that’s not what happened; their fertility went up. So there seems no reason that nature can’t separate the function of fertility from aging.

Disposable Soma: Resources, usually in the form of food energy, are always in short supply, so this theory says, so that organisms must allocate these resources to different needs. Damage repair at the cellular level is one of those needs and is an important component of aging, since if the body can repair all of its damage, aging will not occur.  So if resources are lacking, the organism allocates them preferentially to growth and reproduction, and essentially allows itself to age.

The huge counter to this theory is calorie restriction, the most robust life-extending intervention in lab animals. When they are literally starving, animals can live 50% longer than normally fed animals. If resource scarcity were causing aging, we could expect to see the opposite. If you ate more, you would live longer; but such is manifestly not the case. Eat more, die younger — and this holds true for virtually every species of organism which has been put to the test.

Same is true for exercise: if damage and repair are crucial for aging, exercise would make you age faster. Exercise causes damage — yet it makes animals, including humans, live longer.

Hormesis

Both calorie restriction and exercise are examples of hormesis, in which the application of a stress or toxin causes better health and longer life. The organism doesn’t just repair the damage, but becomes stronger and healthier than before.

Hormesis is central to Mitteldorf’s theory of aging. As he says, it looks as if the organism already has potent anti-aging capabilities that, in normal, “easy” times, it does not use. The organism is fully able to slow aging, when the conditions are right.

Aging is not damage that the body can’t control or that natural selection can’t abolish. It isn’t due to lack of resources or pleitropic genes. No.

Aging is programmed.

Programmed Aging and Group Selection

The theory of programmed aging clashes directly with the neo-Darwinian theory of evolution, which is the theory that represents current thinking in biology.

Neo-Darwinian theory states that natural selection takes place at the level of the gene, and only benefits individuals carrying that gene.

Mitteldorf’s theory of programmed aging relies on group selection, a notion that most evolutionary scientists say cannot exist.

Hence my description of Mitteldorf’s theory as radical, since it takes on the entire neo-Darwinian synthesis, and the scientists that back it.

In this light, it’s of more than passing interest that Mitteldorf’s mentor has been another proponent of group selection, David Sloan Wilson, the author of the masterful book Darwin’s Cathedral: Evolution, Religion, and the Nature of Society.

The programmed theory of aging sees aging as a “suicide program”, one that is of no benefit to the individual but which is of great benefit to the group. The organism dials up genes that cause inflammation and other forms of damage, leading to aging and death. Aging is a deliberate effort on the part of the organism, not something it tries to avoid.

Why would organisms do this? The benefit to the group would have to be a very powerful one in order to override the harm to the individual. And indeed it is, according to Mitteldorf.

Organisms age in order to avoid extinction.

In any successful group of organisms, it seems easily possible for the group to overshoot its environment and to succumb to famine or other causes.

All animals are predators in some way or other, depending on other life forms for sustenance, and if the animals are too successful, they risk famine or epidemics and subsequent extinction of the entire group.

Aging is the organisms’ way of buffering the population. In good times, with plentiful food, organisms age and some of them die, thus keeping the group within its environmental limits and in tune with its ecology. The group thrives.

In bad times, with fewer available resources, aging slows. The species does not want every member to die at once, of famine or some other cause. It wants to avoid extinction, an event which means the demise of every gene carried by the species. When the crisis is over, aging resumes.

Criticism

Mitteldorf supplies abundant evidence for his theory, and it makes for fascinating reading. While reading it, I thought of a few objections, which wasn’t easy, as the author is convincing. Note that I am not an evolutionary biologist.

Aging seems too messy a process to be a “suicide program”. If you think of all the ways that aging causes damage, illness, and death, how could multiple sources of these things arise? One gene that caused death would be a lot simpler, and the fact that aging apparently has multiple genetic roots makes one wonder how it could arise by natural selection.

Admittedly, this objection is probably more a matter of taste than of empirical backing.

Another objection is that the mere passage of time seems involved in some aspects of aging, for example, in the accumulation of iron or exposure to antigens.

Iron seems a good example of pleiotropic effects: it’s necessary for growth and reproduction, but causes aging. Furthermore, natural selection might be unable to eliminate its effects on aging. Women with higher iron are more fertile, which might swamp the effect of natural selection on iron causing aging after a person has already had children.

Antigen exposure comes from infectious agents, and is a primary cause of inflammation in aging. The longer we live, the more antigens we’re exposed to, and in fact those exposed to more diseases die younger, i.e. they age faster. But perhaps the organism can’t dial down inflammation, since we need it to fight off pathogens.

Conclusion

Cracking the Aging Code is the best book I’ve read this year, and should be required reading for anyone interested in aging or indeed evolution and biology. Mitteldorf skillfully wends his way through evolutionary theory, its history, and the biology of aging — he even knows his chops when it comes to field biology and ecology.

At the end of the book, he discusses the prospects for anti-aging research as well as what he believes are the best means of slowing aging that we have right now.

His ideas about slowing aging are, I’m happy to say, very much in tune with what I’ve expounded on this site: exercise, intermittent fasting, supplements like berberine and curcumin, aspirin, and more. (He should have mentioned iron.) On the horizon are technical developments like telomerase therapy, which hold great promise in getting to the root mechanisms of aging.

So go read this book.

PS: I cover some of the same ground as to the best way to fight aging in my book, Stop the Clock: The Optimal Anti-Aging Strategy.

PPS: Check out my Supplements Buying Guide for Men.

image_pdfimage_print

Leave a Comment:

35 comments
Josh Mitteldorf says July 10, 2016

Thanks so much, Dennis. My message is new and strange enough that most people take it in slowly, piecemeal. So it is the more gratifying for me to see how clearly you have absorbed the themes of my book.

In answer to your criticism: Why are there multiple, independent and redundant modes of aging? Why do some modes of aging look so much like damage or attrition?

These are deep questions, and my responses are really only a guess.

I think the reason for multiple, redundant aging programs is that the classical evolutionary theorists are right — individual selection for longer life is a powerful and direct evolutionary force. If it were too easy to escape from aging by mutating away a single gene, then it would happen all too often that aging disappears, with disastrous results for the whole community.

I am not surprised to see damaged molecules and physical wear play a role in aging because nature so frequently finds ways to recycle, to repurpose an existing process for a new end. Inflammation is an important defense against microbes, but late in life it is re-purposed for self-destruction. Apoptosis plays an essential role in shaping the body and the brain, but late in life it is re-purposed to make muscles waste away and to destroy brain cells. And in allowing free radical damage to accumulate by withholding the repair mechanisms that are so effective in our youth, nature has once again followed the path of least resistance, adopting the most readily available means to a new end.

Reply
    Hmm says July 17, 2016

    How did you manage to reverse aging and become a child once again?

    Reply
      Josh Mitteldorf says July 17, 2016

      In a clever marketing ploy, the author of Cracking the Aging Code has contrived that this final detail shall be a mystery that you must read the book to resolve.

      Reply
Nick says July 10, 2016

Framing aging as a “suicide program” invites the criticism about multiple, independent modes of aging, because “program” suggests it’s a singular dictate that your body is trying to carry out. Aging, (and death) are advantageous to group survival, in that they allow for more rapid recombinations of DNA and therefore a better chance of adapting to changing environmental conditions. Where the older individuals in the group die off and thereby use less resources, the younger generations adapt to new environmental conditions (and carry forward any previously selected adaptation). So therefore ANY adaptation that leads to aging and death without reducing fitness earlier in life could (and would) become selected over time when death of older individuals increases group survivability. So it makes sense that there would be multiple factors, each independently capable of causing aging and death, rather than just a single cause (or program).

Reply
    Josh Mitteldorf says July 11, 2016

    Nick – What you say makes a lot of sense, but I’ve become wary of making generalizations after surveying the stunning variety of ways to age (and not to age) in nature. There are lifespans of minutes and lifespans of thousands of years. There are insects that live for years with no perceptible sign of aging, then they mate and die in a single day. There are jellyfish and beetles capable of aging backwards, reverting to a larval stage. You can cut off a piece of a starfish and it grows a whole new starfish, which remembers the age of starfish from which the piece was cut. Read more here: http://nautil.us/issue/36/aging/why-aging-isnt-inevitable

    So I;ve become wary of evolutionary theory. There’s nothing we can deduce that doesn’t find an exception somewhere in the biosphere.

    Reply
BC says July 10, 2016

I have thought for some time that aging => death is simply nature’s way of increasing turnover, and thus robustness, within a species. If individual organisms do not die and are not replaced by newer organisms, the micro-evolution (manifestation of diversity within a genome) of the species as a whole is reduced and you do not get, for example, the differentiated beak shapes and lengths of the thrushes that Darwin observed in the Galapagos islands. The thrushes are all still thrushes, but have adapted (manifested pre-existing genetic variations in accordance with) the particulars of the environment. Thus, if the environment changes again, different genetic variations among the newly born will have greater survival fitness and the species will appear to “evolve” little by little. But they are all still thrushes.

So aging => death increases the overall robustness (fitness) of a species at the expense of the individual organism.

Reply
    Josh Mitteldorf says July 11, 2016

    BC – Yes, aging increases population turnover in the community, and so evolution proceeds more efficiently as a result. This sets up a conflict between what’s good for the individual in the short term, and what’s good for the community in the long term. How does natural selection resolve such conflicts? It’s a question with many facets, and the subject of intensive research and stark disagreement in the scientific community.

    Reply
Stuart Mather says July 10, 2016

Hi Dennis,
As always, fascinating. Thanks heaps. The more i intermittent fast the easier to eat just one big meal a day (lunch) over about 1 and a half hours . I’ve always been a slow eater – I just find I enjoy my food more if I don’t gorge. That one meal is certainly bigger than when I used to eat more often though..
I’m finding I also enjoy lifting more when it’s fully fasted too. The more I read about the longevity /health benefits of eating only moderate (about 50g) protein the less i’m finding I obsess about muscle/ strength gain. Getting caught on the ‘need to look ripped’ wheel seems to have more to do with male vanity than strength training itself being the end in itself. Not questioning the power of vanity of course.
My question is about the alpha lipoic acid / acetyl l carnitine combination as a promoter of autophagy while fasted. In other words using it with the other fasting autophagy stuff you recommend like berberine , egcg etc. What’s your take on it?

Reply
    P. D. Mangan says July 11, 2016

    Stuart, I’m not aware that lipoic acid or acetyl carnitine promote autophagy. They have lots of other benefits though.

    Reply
      Stuart Mather says July 18, 2016

      Thanks P. D
      Sorry to hijack this thread btw. But your reply leads me to ask then , if a substance non calorically boosts cellular AMPK levels, it doesn’t necessarilly also promote autophagy?
      Put slightly differently , without raised AMPK , autophagy isn’t possible is it? So in a fasted state (ie after the 12 hrs fasted for autophagy to initialize) boosting AMPK won’t also enhance autophagy?

      Reply
        P. D. Mangan says July 18, 2016

        Stuart, boosting AMPK will increase autophagy, and fasting, just as it increases autophagy, also boosts AMPK. Is that what you had in mind?

        Reply
          Stuart Mather says July 18, 2016

          So things like acetyll – l- carnitine and ALA (the R isomer at any rate) which boost AMPK should also then increase autophagy shouldn’t they? Joseph Cohen at ‘Self Hacked has put together a long list of AMPK boosters (with references)

          Reply
          P. D. Mangan says July 19, 2016

          Yes, whoever that is at that other blog must be reading this one, that I wrote a year and a half ago: http://roguehealthandfitness.com/activating-ampk-lifespan-extension/

          Reply
          Stuart Mather says July 19, 2016

          It seems to be a bit more complicated than just inhibit Mtor, boost autophagy though. NAC is a case in point. It powerfully inhibits Mtor, but also (just as powerfully,apparently) inhibits autophagy.
          Perhaps NAC is just the exception that (dis) proves the rule!
          Also, just a thought, why don’t we all just supplement with rapamycin?

          Reply
          P. D. Mangan says July 20, 2016

          Agree about mTOR and autophagy. AMPK is upstream of mTOR, possibly accounting for the effects of NAC. As for rapamycin, good question. It’s a powerful immune suppressant, not to mention prescription only – and expensive, I understand – so you can’t just take it. That being said, pulse dosing appears to work, such as every other day or even once a week. So, maybe we will be taking it before long. Apparently Mikhail Blagosklonny, the scientist who studies aging, takes it.

          Also of interest regarding weekly dosing, Bergamnini (who’s done great work) took a group of rats and fasted them once a week, and gave them Acipimox, an anti-lipolytic drug similar in effect to niacin, at the time of fasting. He found that this regimen increased autophagy to youthful levels and was as effective as alternate day fasting.

          Reply
          Stuart Mather says July 20, 2016

          Fascinating . Thanks
          For how many hours were the rats fasted once/wk?
          Also, do you think it helps to take all the autophagy boosters (curcumin berberine hydroxycitrate, niacinimide egcg, strenuous exercise etc) every during every fast for maximum autophagic effect ? Or is it counterprodutive to stack them , and better to alternate? Unlike rapamycin, all the others are pretty cheap after all. What approach do you use to maximize the autophagic effect of a fast?

          Reply
          P. D. Mangan says July 20, 2016

          I believe the rats were fasted 24 hours, once weekly. As for the supplements, I think there’s a lot of overlap and taking them together won’t add to autophagy.

          Reply
    Ole says July 27, 2016

    Good question Stuart. There is good reason to believe that antioxidants and in particular alpha-lipoic acid (which is 400 times stronger than vitamin C and vitamin E combined) will inhibit autophagy during intermittent fasting.

    Based on the below, I’ve excluded the use of alpha-lipoic acid during IF.

    http://www.ncbi.nlm.nih.gov/pubmed/20566712

    http://gettingstronger.org/wp-content/plugins/wordpress-toolbar/toolbar.php?wptbto=http%3A%2F%2Fmetamodern.com%2F2010%2F09%2F26%2Fantioxidants-block-cell-repair%2F&wptbhash=aHR0cDovL2dldHRpbmdzdHJvbmdlci5vcmcvMjAxMS8wMy90aGUtY2FzZS1hZ2FpbnN0LWFudGlveGlkYW50cy88d3B0Yj5UaGUgY2FzZSBhZ2FpbnN0IGFudGlveGlkYW50czx3cHRiPmh0dHA6Ly9nZXR0aW5nc3Ryb25nZXIub3JnPHdwdGI%2BR2V0dGluZyBTdHJvbmdlcg%3D%3D

    Reply
      Ole says July 28, 2016

      PS. It would be very interesting to study autophagy during supplementation with targeted antioxidants like MitoQ or SKQ1. It’s known that these supplements inhibit ROS induced apoptosis. But how will they influence autophagy?

      Reply
      Stuart Mather says August 2, 2016

      @ Ole
      Those links are great . Partcularly the one that goes into great detail about how b.i. d NAC supplementation IN THE FASTED STATE (in fact it goes into the detail of saying that the more fasted the body is , the more powerful an inducer of what it calls ‘mitophagy’ (macroautophagy) NAC supplementation is). Lots of references to peer reviewed placebo controlled, crossover double blind VERY well designed studies basically saying that if you were interested in autophagy, NAC (in the fasted state) was the go to supplement.
      Now I’m really confused

      Reply
Transhuman Tees says July 11, 2016

Hey P.D. (And Josh if you’re still here checking comments), I’m wondering if you guys are both familiar with Aubrey De Grey’s work? He’s also written a book on aging called; Ending Aging. He believes there are 7 causes of why we age including Telomeres like you mention in the article, and also believes his team (SENS research foundation) is working towards the cures for those 7 causes.

I think the work he’s doing is where our attention needs to be diverted, but that’s just my opinion, I am relatively new to the whole longevity movement. I just wanted to know if you guys know of the book/Aubrey/SENS?

There is also MFoundation.org which is working in a similar manner I believe.

Another website which you may/may not also be familiar with is FightAging.org, they often have some very interesting articles related to aging research.

Love the blog, need to buy more of your books though! I’m heading in the right direction but could be doing better.

Reply
    P. D. Mangan says July 11, 2016

    Hey TT, yes, I’m aware of de Grey and his work. I’ve read critiques of his SENS plan, but I’m afraid I couldn’t say enough about it myself — though I believe he’s completely right as to the main biological defects seen in aging.

    Reply
      Transhuman Tees says July 11, 2016

      Okay great! Thanks for the reply P.D. much appreciated.

      Reply
    Josh Mitteldorf says July 11, 2016

    Yes – I know Aubrey well, and I’ve worked with him over twelve years. There’s a great deal that Aubrey and I agree on, but Aubrey is not a believer in programmed aging, hence his program emphasizes technical fixes to the things that go wrong in the body, while my program emphasizes biochemical signaling.

    Reply
      Transhuman Tees says July 12, 2016

      Thank you very much for the reply Josh!

      That’s interesting indeed. Like I said above I’m still relatively new to the whole thing, Still trying to learn as much as I can at the moment.

      Your book is on my to read list, and I will be reading more of your blog too. I recently found it through Reddit. There are probably others that I haven’t even come across yet.

      Thanks again to both of you!

      Reply
Frank Budesa says July 11, 2016

It seems that aging even according to this theory could benefit individual genes the same way sexual reproduction does, and group selection isn’t necessary. This pattern of resource availability looks similar to species that have males/females vs ones that don’t (plants at high altitude, etc). Vicar of Bray vs Red Queen

Reply
Justin Irving says July 11, 2016

Looks well worth reading, thanks for sharing this book.

It’s always seemed to me that aging must be somehow encoded into organisms. Take dogs: their aging profile more or less mirrors that of humans, their joints fail, their skin elasticity goes, their hair whitens. They just look *old* in the same way humans do. Yet the age cycle for a dog is about 6 times faster than that of a human, same pattern, different rate. Given that dogs and humans are running more or less the same sort of mammalian hardware, eating more or less similar foods (a dog can live on human food anyway!), it would seem there’s no fundamental reason dogs should age so quickly, yet they do. Must be programmed. If we can find the signals that cause the dog to age faster than the human, maybe we can interrupt that signal and give both of us longer lives.

Reply
    Josh Mitteldorf says July 11, 2016

    Yes! Cynthia Kenyon once said the same thing to me – a one-line proof that aging is programmed.
    (Not everyone sees it that way.)

    Reply
      Stuart Mather says July 18, 2016

      Josh , so the ones who don’t see that aging rates are programmed into different species must have some explanation for the vast variability of aging rates between species.
      I’ve noticed mention of Aubrey de ‘Grey over the years, and watched a fascinating BBC documentary about him a while ago. It basically portrayed him as a bit of a flaky charlatan with pretty well ZERO credibility in the field. You know him. You might want to point out that alcohol is a potent neurotoxin and ask him what on earth anybody serious about maximizing their life span is doing drinking beer regularly.
      My lasting impression from the documentary was that he looked pretty sickly.
      Which isn’t to say that extending maximum human lifespan isn’t a worthy area of research. It’s just that Aubrey de Grey hardly seems like someone who can contribute anything worthwhile to the project.
      Maybe he needs to try intermittent fasting.

      Reply
        P. D. Mangan says July 18, 2016

        De Grey believes, as I recall, that calorie restriction won’t do much for human lifespan, adding maybe a couple years. He could be correct, but I doubt it. This view seems to rely on a trade-off between longevity and reproduction. Since humans put less of their energy into reproduction than, say, a mouse, then CR and by extension fasting wouldn’t do as much. But as we’ve seen, there may be no necessary connection between the two.

        Reply
Allan Folz says July 11, 2016

Great review and great set of comments. I can’t resist quoting Max Planck, “Science advances one funeral at a time.” Apologies if that’s the oldest hackneyed joke among longevity researchers and scientists.

Good old Creative Destruction. Why shouldn’t it be selected for!?

In another context, look what Too Big To Fail makes of an economy — first Japan, and now the US. Or really going back in time, look at the economic lethargy under Hereditary Feudalism.

So again, why shouldn’t aging be selected for? Dogs that age 6-10 times faster than humans… it’s a feature, not a bug.

Reply
ConantheContrarian says July 13, 2016

My explanation for death is religious. Man dies because he is born in fallen flesh prone to sin, and the wages of sin is death. That doesn’t mean that we cannot extend life, and extend it while enjoying good health, but eventually we die. As far as death is concerned, it is programmed into us, it is just that God did the programming and not blind, random, evolution. I am certain that there will be disagreement with me, and I understand that. However, I do appreciate that Mangan is bringing us good information, including Mitteldorf’s research, and I appreciate both of them. Keep opening our eyes, gentlemen.

Reply
    Stuart Mather says July 13, 2016

    The most sensible explanation for why all human belief in tooth fairies, religious or otherwise is necessarily inadequate, I’ve ever heard was that humans are doing the believing. We’re such a limited species after all -limited in this context by the size of our brains. We”re just one bipedal carbon based life form on a humdrum planet (incredibly beautiful and worth not trashing for merely human benefit of course) in ONE of quite a few galaxies in the known universe (light from stars in the forever unknowable universe has not and will not ever reach Earth- at least while our star continues to burn anyway)
    If you really do need to comfort yourself with notions of God, a good start would be realizing that whatever Gods may be would be hoping , even PRAYING that humans grow up intellectually a bit and stop believing in tooth fairies of whatever religious flavour.
    Whenever someone has trouble with the ‘randomness’ of evolution I just think they’re missing the point. It’s the randomness of it that makes it so achingly beautiful isn’t it ? How could any design , intelligent or otherwise, even compare.
    My ”God’ is the physical laws of the Universe. Humans are pretty well at the limits of maximum human abstracting ability even having a good crack at general relativity anyway. So we humans probably won’t even ever be able to even ask the right questions, let alone come up with decent answers. Of course it’s certainly worth asking the ‘why’ questions, but don’t for a moment delude yourself that human notions of ‘God’ are anything but a vain (as in ‘human’) attempt to explain difficult questions that we (if ever) are at least millions of years away from ever being able to answer truthfully.
    Stop being impatient. Do science , particularly the bit about any theory being just a hypothesis.
    And most importantly teach your kids to do science and not try to dress up any particular tooth fairy story as the ;one ring to rule them all’.
    And one of the most telling criticisms of all the so called ‘great’ religions is that they claim to deserve some kind of special respect. Throughout history, humans have always tried to explain the mysteries they become aware of with various creation stories. We’re an impressively creative species after all. Why are any of those accounts more deserving of ‘ hush hush respect the God botherers’ They’re ‘special’. Great outfits and grand notions of course- all of them.
    When I was a lad, I believed in all sorts of stories. And then I grew up. Humans just need to grow up and realize that ‘randomness is the most achingly beautiful refrain of all. Because it isn’t randomness in a vacuum. There are rules – like gravity, and electromagnetic force. Those universal constants CONSTANTLY interact to produce – the universe , past (from our limited temporal perspective at any rate) and future.
    Why is that not enough?

    Reply
    Rick Duker says January 28, 2017

    Death is an enemy because mankind was not originally created to die. Darwinism ascribes God-like intelligence and powers to Evolution and Natural Selection and claiming that this is purely scientific while at the same time denying the existence of God (because that is religious and not scientific). I think Mitteldorf is correct being wary of evolutionary theory. That aging and death are chemically programmed or encoded into living creatures to me is self evident. We all know that what is pro-life for us while we are physically maturing has a pro-death aspect when we are aging. There is nothing wrong with taking prudent steps to increase our healthspan but the root cause of aging is an inherited condition from the firdt human which we are powerless to reverse.

    Reply
Bill says February 20, 2017

Dennis this review of Josh’s book is excellent. I have it and have read it at my leisure. Like you I think it was the science book of the year in 2016 and maybe this year as well..

However Josh does not discuss Jeff Bowle’s proposal that Lutinising Hormone ( LH) and Follicle Stimulating Hormone ( FSH ) which are both dialed up as we age, maybe playing a major role in programmed aging.

Similarly Josh does not spend much time discussing how as we grow older, decreasing levels of Melatonin from the Pineal gland, act as a body trigger, initiating hugely increased destructive, inflamatary levels of LH & FSH.

Jeff presents these ideas in his books ( For example “Alzheimer’s Treatments that actually Worked in Small Studies” ) and he has been taking his own advice for quite a while now. So I wonder whether he has noted any effects in his own life.

Meanwhile for me Melatonin is a part of my own anti aging program. The good thing is it is cheap & bought over the counter and does not need a doctor’s script. It has not toxicity level so it can be taken in high doses replicating the natural melatonin levels of youth. The down side is Melatonin does cause me to wake up feeling ‘groggy’ each morning.

Reply
Add Your Reply