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New book on aging

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In his latest podcast, Peter Attia cited Nir Barzilai's new book on aging. Barzilai is the leader of the TAME experiment on metformin and a renowned geroscientist.

Anyone has already read all or part of this book?

 

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I'm going to take a look at some excerpts and reviews.  Most likely it repeats a lot of stuff we already know,  with a few tidbits of new interesting stuff.   In my case, metformin isn't a viable option, even if I were really interested.  Which I'm not. Don't ask why. Anyway,  I'm a bit burnt out on longevity theorizing,  tbh.  Quality on top of quantity, at the moment.

Table of Contents

Introduction

1. One Hundred Years Young
The Mysteries of Aging
What Makes SuperAgers Stay Healthy?
Studying Centenarians
Designing a Study Without a Control Group
Meeting Our First AJ Centenarians and Their Offspring
A Perfect Genome?
Centenarians’ Interactions with Their Environments
Do as I Say, Not as I Do

2. Why We Age
Recent Theories
The Search for Protection from Aging
Eating Less May Lead to More Healthy Years
Unlocking the Secrets in Fat
Caloric Restriction: A Mixed Bag of Effects
Aging Begins Before We’re Born
SuperAgers’ Top Secrets

3. Cholesterol: Is More Better?
Unlocking Cholesterol’s Longevity Secrets
Are there Really Good Gene Mutations?
Solving the Mystery of Helpful Gene Mutations
The Benefits of CETP Personified
A Mutation That Adds Years to Life Span?

4. Growth Hormone: Less Is More
Less Growth May Lead to an Exceptionally Long Life
Growth Hormone Clues from Our Centenarians
Epigenetic Mechanisms Can Increase Longevity
Making the Most of Our Findings
Growth Hormones Don’t “Grow” Life Span

5. Unraveling the Longevity Mystery Deep Inside Our Cells
A Match Made on Earth
Mitochondria’s Hidden Purpose
Resilient to the End
A CohBar Is Born
Searching for Promising Peptides

6. The Quest to Prove Aging Can Be Targeted
Choosing an Existing Drug to Prove Our Point
Getting the FDA on Board
How the TAME Study Works
Who’s Going to Pay for All This?
Metformin Is the Tool, Not the Goal

7. Making Eighty the New Sixty
The Price of Progress
Collaboration Is the Key to Speed
Long, Healthy Life Span Versus Immortality
The Gap Between Making Drugs and Making Drugs Available

8. Stop the Clock
How Old Is Old?
Use It or Lose It
Antioxidants and Hormesis
Thriving in the Shadow of Stress
Preventing the Loss of Muscle Mass as We Age
Exercise Plus Metformin
Feeding Our Longevity
Hydrating Wisely
Prevent Obesity
Nutraceuticals Are in the Works
The Magic Pills We’ve Been Wishing For
When We Eat Matters
Our DNA Has Something to Say
Stay Mentally Sharp
Other Promising Practices
How to Decide What’s Good for You

9. Bright Horizons
The Unparalleled Power of Omics
Personalized Medicine
Advances in Early Detection
Pioneering Explorations
Reversing Cellular Age
Genetic Engineering

Acknowledgments
Index

 

Quote

One of Dr. Barzilai’s most fascinating studies features volunteers that include 750 SuperAgers—individuals who maintain active lives well into their nineties and even beyond—and, more importantly, who reached that ripe old age never having experienced cardiovascular disease, cancer, diabetes, or cognitive decline.

In Age Later, Dr. Barzilai reveals the secrets his team has unlocked about SuperAgers and the scientific discoveries that show we can mimic some of their natural resistance to the aging process..
.  Amazon

Quote

 

Why do some people live past 100 in good health, while others succumb to disease at much younger ages? Barzilai (Inst. for Aging Research, Albert Einstein Coll. of Medicine) explains the latest research into these questions. He studies centenarians to uncover how they differ from the rest of us genetically, biochemically, and physically.

One surprising finding: the dietary and exercise habits of healthy people over age 100 do not differ significantly from those of the general population.

Some theories of aging—decreasing levels of sex hormones, shortened chromosomal telomeres, calorie restriction as protection from aging—have proved to be less predictive than thought.

Barzilai discusses the importance of high levels of "good" HDL cholesterol and the genetic variants that produce them, the research into growth hormone factor, and the difficulty of developing drugs that can replicate these actions.

The author is concerned with extending people's well-being into their later decades and concludes with a series of recommendations based on current research, advising readers to be patient: anti-aging drugs will become available someday.

VERDICT A thoughtful take on aging that should be of interest to all concerned with the overlap between health and aging.—Rachel Owens, Daytona State Coll. Lib., FL  Library Journal

 

 

Edited by Sibiriak

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Thanks sibiriak, the TOC seemed to be interesting so I downloaded the Kindle edition. I'm reading it at a fast pace.

First two interesting things:

  1. Barzilai was part of the panel who examined the documents on the age of J Calment. He says it's highly unlikely that the conspiracy theory (the daughter replaced her) is true. The only paper on it provides no evidence whatsoever and the documents appeared to be genuine.
  2. In his first study on centenarians, the Ashkenazi Jews, the main result was that they exhibited all the unfavorable genetic variants (polymorphisms like APOE4), the same as the control group. In a few words, they had all the unfavorable variants a general, non-centenaries population carries so there was something which prevented these variants to express.

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I heard Nir Barzila talk on Peter Attia's podcast recently and he mentioned something new that I'd not heard before about the CR study in rhesus monkeys. Apparently, early on in Wisconsin study, the study the CR monkeys took a year break from CR because the care takers were being 'compassionate' and feeding the CR monkeys extra food. And it was the cause of the CR group gaining weigh and ending up similar to the ad lib monkeys.

Does he talk about this in his book?

Edited by Matt

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That episode is really funny on the weird side! I'm at the beginning of the book, I'm going to report, as you'll recall Barzilai added that after that, everytime he ran a CR experiment on rats, he made sure to explain the lab guys that giving less food to the rats was meant to lengthen their lives, so it was actually in the best interest of the rats!

If he didn't notice the incoherence in the data, the monkeys study would have turned out to be of no use at all.

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Yeah, that was insane. I didn't find it particularly humorous, I was wondering why those lab guys were not in prison for sabotage. It's outrageous and surely illegal. One can only wonder how many experiments are messed up by sabotage or neglect. Yet another variable in why so much medical science seems to be making such slow progress. Meanwhile here we were agonizing and discussing endlessly about why the results from the NIA study and Wisconsin were so different - who knows what was going on in each lab, since obviously it seems we can't rely on lab reports. One wonders how much of such unreliable reporting goes into other studies. A real mess. It seems like strict controls need to be implemented with cameras and other mechanisms to provide oversight (plus some stiff penalties for criminal behavior); it'll raise costs, but what's the point of saving money when the study results are useless and cannot be relied upon.

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10 hours ago, Matt said:

Apparently, early on in Wisconsin study, the study the CR monkeys took a year break from CR because the care takers were being 'compassionate' and feeding the CR monkeys extra food. And it was the cause of the CR group gaining weigh and ending up similar to the ad lib monkeys.

I didn't watch this interview or read the book in question, so I may be missing something. But you guys do remember that the Wisconsin CR monkeys were the ones that actually did live longer than AL-fed controls, right? Maybe they would have lived even longer had they not had the break from CR as this person seems to be alleging.

Recall from previous discussions, it was the NIA arm of the long-term rhesus monkey study (in which, unlike the Wisconsin arm, they fed both groups a relatively healthy diet) where the results were so disappointing, i.e. the CR monkeys didn't live longer than AL-fed controls.

So while it may be fun to vent, unless I'm missing something all the ranting about fraud and criminal behavior on the part of the researchers seems irrelevant to the question that really matters, i.e. whether serious CR will beat a healthy, obesity-avoiding diet & lifestyle.

--Dean

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Uhm, Dean, you can't be serious. Surely, you understand that there is more than the possibility that you mentioned - in fact I plainly implied the possibility of a completely different scenario, based on these points:

1)The integrity of the Wisconsin has been severely compromised. The fact is that the fraud went on for at least a full year. Who says that it didn't go on - perhaps to a lesser degree - for longer? With full AL feeding there was 0 effect, with partial secret feeding there would've been X, but had there been full integrity, who says the effect might not have been 2X? They got caught in one instance - an egregious one - but that does not imply that therefore there wasn't fraud in other instances in the Wisconsin trail, perhaps better disguised or with lesser effect.

2)If the Wisconsin study was compromised so severely, why do you, Dean, assume that the NIH one was not?? In fact, the researcher who discovered the fraud, Nir Barzilai, immediately drew the conclusion that this might obtain for other CR trails and therefore took immediate measures on other CR trails under his control (involving rats). So if this problem is potentially so widespread that it compelled Barzilai to act in other trails, I think there is a non-zero possibility that the NIH was fatally flawed along the same lines, except there was no Nir Barzilai to challenge the protocol.

So based on these two points I think it's entirely possible that there was fraud perpetrated at both trials, except it was belatedly descovered in the case of the Wisconsin study. Do I know that for a fact? No, but how is this not plausible? In fact, if you heard about two groups of bankers where money didn't perform as expected, and you discovered in one group that there was fraud, and when the fraud was stopped the performance was now improved as expected, why would you NOT assume that the exact same thing must be happening at the other group where the money is again not behaving as expected. In fact, it's very damning. It's not proof, but at the very least is highly suspicious and a compelling indicator demanding a thorough investigation.

In other words, Dean, you need to sharpen your possibility models, because you appear to be missing some pretty big potential outcomes :)

 

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10 hours ago, TomBAvoider said:

In fact, if you heard about two groups of bankers where money didn't perform as expected, and you discovered in one group that there was fraud, and when the fraud was stopped the performance was now improved as expected, why would you NOT assume that the exact same thing must be happening at the other group where the money is again not behaving as expected.

Your bank fraud anology completely misses my point. The Wisconsin monkey results did perform as expected - i.e. the CR monkeys in the Wisconsin trial did live longer despite the alleged hiatus during which they may have been fed ad lib for one year out of the ~25 year experiment. In short, feed monkeys a lesser amount of a crappy diet for most of their adult life and they will live longer. No duh. 

It is a free country, so you are free to engage in speculations about rampant fraud elsewhere in CR research, including the (disappointing) NIA monkey study. But in the good old days of this forum it was enjoyable to engage in arguments grounded in evidence not mere speculation, cynicism and conspiracy theories. 

--Dean 

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Dr Barzilai on the book hints at the same things hinted at in the podcast. The experiment was probably continued and the results have been succinctly described. This is the relevant excerpt:

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By the way, I'm only posting small excerpts here and, insofar as I could read, at 26% of the content, I advise the purchase of the book, it deserves to be read. If the excerpts are judged to be possibly illegal, I'll be ready to edit them or I suggest the moderators themselves to delete them.

we discussed very extensively on lipids, but I don't remember about MDPs

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He goes on with a specific chapter on cholesterol, chapter 3

Edited by mccoy

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Barzilai expresses his ideas that CR in humans probably increases longevity in obese and overweight people, whereas its benefits on people with ideal or lower than average BMI are dubious. He adds that probably teh benefits of CR are a function of individual genetics, as it has observed in different strains of lab rats.

We discussed the above. That would imply that CR must be very finely tuned, depending on individual genetics and % of CR, besides all the other rules of optimum nutrition we all know very well.

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Dean,

I completely agree with you -- I'm surprised at Tom's unjustified speculation.

HOWEVER, I remember that at one of the last few CR Society Meetings -- I think the last one -- a question was addressed to the panel of invited guests (the last presentation of each CR Society Conference) -- about the disappointing result of the NIA monkey study -- in nt finding life extension in the CR'd group.

One of the invited presenters in the panel answered:  He said that he was aware of the design of the NIA study -- and that there was problems in obtaining enough similar monkeys for both groups -- and that additional monkeys were added, that were very different for the two groups, both in sex and race.  the presenter regarded this as being more than sufficient to cause one to ignore the fact that there was no obvious boost in lifespan for the CR'ed group.

Tapes were made of all of the CR Society meetings -- this information, in detail, is on the relevant CD.  I recall that at least one member of these Forums has them.

  --  Saul

 

 

Edited by Saul
add more info

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Chapter 4 is an extensive report on the studies on IGF-1 and centenaries, the broad conclusion is that high/exogenous GH does not increase longevity and health span, outside the period of puberty. As a whole, lower IGF-1 prevails in centenaries and is correlated to longevity, especially so in women. Barzilai, unlike Longo and Attia, gives no optimum values nor goes down the rabbit hole of various IGF types, stopping at the IGF-1R receptors.

The apparent drawbacks of low IGF-1 on cognition and the musculoskeletal system are discussed, they are lesser in women.

We've discussed some of these aspects. For example, I have low IGF-1 but not impaired muscle growth. In my case evidently the INS/IGF-1↦ PIK3↦AKT pathway which stimulates mTOR becomes MFG↦ PIK3↦AKT, that is Insulin and IGF-1 are substituted by the mechanogrowth factor which is released by the mechanic stress ensuing from resistance exercise. For muscle growth, exercise prevails over physiological concentrations of IGF-1 and insulin

Edited by mccoy

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I'll buy the book soon, thanks mccoy for sharing it!

I don't remember him thinking the NIA study was compromised in the same way when he was talking on the podcast.

I'm not much of a conspiracy theorist myself, but there is some interesting data that doesn't agree with what we see in humans based on the CALERIE study or Fontana's work on CRSociety members. Or what we see happen in rodents who do live longer.

In the NIA study, the body weight of old onset CR vs the control was not really any different in the study. Does this agree with the effect we see of carefully imposed CR in humans? It does not.

Quote

"Bodyweight of the old-onset NIA control and CR males were not significantly different at either mid-age or advanced ages, and old-onset NIA male controls weighed significantly less than UW controls."

But their diet was healthier and they did weigh 15% less than the UW controls. And with that, lived quite a few years longer. So clearly quality of diet plays a role, too. 

But both studies were a mixed bag of results when it came to the response or lack thereof to CR. Michael already did a really good analysis on this so I won't go into any detail. But the inconsistent response to CR regarding hormones, glucose, cholesterol, triglyceride trajectories; especially for female CR monkeys: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3832985/figure/F9/ (and body weight in some cases).

Quote

"Importantly, the median survival estimates for old-onset males were very high, similar to what has been reported previously as the 90th percentile for this species (∼35 years of age). Six of the original 20 monkeys have lived beyond 40 years of age, the previous maximal lifespan recorded, and one old-onset CR male monkey is currently 43 years old, which is a longevity record for this species. Median survival estimates for old-onset females, ∼27 and ∼28 for controls and CR respectively, were also greater than national median lifespan estimates, with one remaining female currently 38 years of age. The clear benefit in survival estimates for monkeys within the old-onset cohort compared to UW controls suggests that food intake can and does influence survival." 

https://www.nia.nih.gov/news/calorie-restriction-improves-health-survival-rhesus-monkeys

Mccoy said:

Quote

 

Barzilai expresses his ideas that CR in humans probably increases longevity in obese and overweight people, whereas its benefits on people with ideal or lower than average BMI are dubious. He adds that probably teh benefits of CR are a function of individual genetics, as it has observed in different strains of lab rats.

We discussed the above. That would imply that CR must be very finely tuned, depending on individual genetics and % of CR, besides all the other rules of optimum nutrition we all know very well.

 

It's probably true that each of us can tolerate CR to a lesser or greater degree, but understanding when we've pushed it too far is still difficult. There were follow up studies looking at predictors of whether or not CR works, and maintenance of body fat under extreme CR was an important one. Nothing new... as this was observed by researchers who studied CR mice or rats years ago.

I've looked at cohorts and the numbers for offspring of nonagenarians centenarians and despite them at the time being close to our older CR Society members, their numbers with regards to cholesterol, glucose, blood pressure (systolic 142  +/- 19 for LLS cohort) are really not all impressive (see here). And as you know, they are predisposed to also living much longer and healthier.

I think a person on life-long CR with a very healthy plant-based diet would be in much greater shape at 100 than your average centenarian.

Luigi Fontana still appears to be fairly optimistic about the strong effect of CR on health and potentially lifespan. I've heard him several times saying that he expects people on moderate calorie restriction (and implementing several other strategies) to reach 100, 110, or even longer in some cases.

I thought the study looking at the transcriptional profile of people on CR quite interesting but never got much attention. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3714316/

It just shows that many of the important and common genes or pathways that regulate longevity in animals and humans are affected by humans on CR (from CR Society.) I don't know if CALERIE did anything similar? 

I'm still obviously very optimistic about the effect of CR in humans. I still think for most people, there is a lot of improvement than can be made to their healthspan and lifespan.

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Hi Matt!

Please review my last posting -- I edited it with some important added material about the NIA study.

  --  Saul

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6 hours ago, Dean Pomerleau said:

...you are free to engage in speculations about rampant fraud elsewhere in CR research, including the (disappointing) NIA monkey study. But in the good old days of this forum it was enjoyable to engage in arguments grounded in evidence not mere speculation, cynicism and conspiracy theories. 

Wouldn't it also be pretty easy for anyone with access to the data to verify "feed fraud" anyway?  I mean if at any point the CR primates were gaining weight that would be a pretty good indication, maybe they would be expected to gain a little weight as they got older, but should still maintain some reasonable fraction of weight vs. controls (ad lib).

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3 hours ago, Saul said:

HOWEVER, I remember that at one of the last few CR Society Meetings -- I think the last one -- a question was addressed to the panel of invited guests (the last presentation of each CR Society Conference) -- about the disappointing result of the NIA monkey study -- in nt finding life extension in the CR'd group.

One of the invited presenters in the panel answered:  He said that he was aware of the design of the NIA study -- and that there was problems in obtaining enough similar monkeys for both groups -- and that additional monkeys were added, that were very different for the two groups, both in sex and race.  the presenter regarded this as being more than sufficient to cause one to ignore the fact that there was no obvious boost in lifespan for the CR'ed group.

Tapes were made of all of the CR Society meetings -- this information, in detail, is on the relevant CD.  I recall that at least one member of these Forums has them.

  --  Saul

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But in the good old days of this forum it was enjoyable to engage in arguments grounded in evidence not mere speculation, cynicism and conspiracy theories. 

Well, it's not "groundless" speculation, when you have two trials that both involve CR'd monkeys and both show disappointing results, until one of them gets a comptroller - Nir Barzilai - and surprise surprise he discovers fraud which upon being corrected suddenly has the results in his trial diverge from the disappointing path. Had the Wisconsin trial not had a Nir Barzilai we'd all be speculating about why it is that both trials in CR monkeys failed. But the Wisconsin trial had Barzilai, and so it suddenly showed results. The NIH trial didn't have Barzilai and continued to show disappointing results. In our banker group analogy both groups show the same "surprising" results until one of them gets a comptroller (Barzilai), and then suddenly the result is as expected, meanwhile the one without the comptroller continues on showing "surprising" results - wouldn't it be natural to wonder if both weren't afflicted by the same problem with one group being lucky to have been checked by the comptroller? How is that "groundless" speculation?

And yes, in the old days we engaged in arguments without such speculation, because we didn't know that fraud was even a factor to consider. This is new information. With this new information, a whole new field of possibilities opens up that previously was out of bounds. It seems to me a dereliction of duty not to consider this possibility given this new context and new information. In fact, far from condemning me as a conspiracy fan, I would excoriate myself as being needlessly trusting. Because I certainly didn't suggest - and to my discredit it didn't even occur to me - that misconduct could be a factor in the results of these studies. And yet this was a factor in the Wisconsin studies - we don't know what the ultimate results would've been in the Wisconsin studies without the year long fraud impact on health of the monkeys. But once this possibility has been shown I would be a fool not to consider in the other case that also has a strikingly odd outcome. As the saying goes, "fool me once". But it seems the right approach is to say "sure there's fraud in this very monkey trial", but hey, it's not kosher to now consider the very same possibility in the other "surprising" result of the NIH trial. Meanwhile, the fact that there was minimal difference between the weights of the controls and the CR'd monkeys at Wisconsin were the tipoff that something was wrong, and yet, only Barzilai picked up on that - why didn't the OTHER scientists involved immediately raise alarms? That's extremely damning. The fact that there were also miminmal differences in weight between the controls and CR'd monkeys at NIH is not something that fills me with confidence. I expect CR'd monkeys to show LESS weight than ad lib monkeys - this seems to me fundamental to the very premise of CR. But oh, nothing to see here, right? and it's mere conspiracy thinking to wonder about the integrity of the other trial. Now that fraud is demonstrably on the table, it changes the parameters of the discussion very fundamentally, and it is impossible to ignore. My only fault here was in being insufficiently skeptical to begin with, and not that I'm now chastenend into considering this possibility after such a horrendous loss of credibility in the reported results. I'd be a fool not to consider this possibility given the precedent. 

Edited by TomBAvoider

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Chapter 5 of the book deals with MDPs, Mitochodria-derived peptides, something I don't remember has ever been discussed here (I probably  totally overlooked it).

MDPs like humanin and IGF-1 BP3, very new stuff to me.

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Even the seemingly highest quality studies can have a multitude of problems, known, and unknown.  For this reason it seems fair to look at the preponderance of evidence, weighing more heavily the highest quality evidence - a sort of fuzzy mental meta-analysis if you will.

Unfortunately with the cost, length, and other barriers, prospective life-long monkey trials like these two in CR are unlikely to occur ( except much more modestly in shorter lived more distant primates like lemurs, has produced some publications, with note underway).  Lest of all in people.

So what are we left with?  Longo’s so called pillars of evidence including biomarkers, other animal models, natural history studies, etc.... and making the best of the data we do have.

Matt’s citation of the summary from the NIH corresponds to an extensive 2017 effort and collaboration between the two centers “to more fully assess possible explanations for the discrepant findings between the two studies” [through] “comprehensive assessment of longitudinal data from both sites highlighting differences that may have contributed to the dissimilar outcomes.”

Though the authors were in my estimation appropriately cautious and qualified in their analysis concluded

Data from both study locations suggest that the CR paradigm is effective in delaying the effects of ageing in nonhuman primates but that the age of onset is an important factor in determining the extent to which beneficial effects of CR might be induced

and that

Taken together, data from both UW and NIA studies support the concept that lower food intake in adult or advanced age is associated with improved survival in nonhuman primates

Even presuming agreement here (dissent and healthy skepticism and counter-interpretation of the evidence are proud and valuable scientific traditions) , to what extent restricted calories yielded benefit through prevention of obesity, metabolic syndrome and related factors versus by true “CR” restricting calories beyond that point remains an open question.  So this still does not answer Dean’s question ( or proposal).  There is lots of room for interpretation.

The skeptic will argue that the controls are sedentary and overfed ( and a quick glance at their diet compared to NIA is certainly reminiscent of the standard American diet - pretty terrible) while the optimist may concede this point but still argue that the controls were a bit too restricted in their feeding protocol and point toward the superior glucoregulatory control and some biomarkers and reduced cancer incidence in CR group at both centers.  

It is easy to go back and forth in debate indefinitely from there.  For example that the lower cancer and better glucose disposal if helpful must statistically speaking be hindered by other poor outcomes at the NIA site given a failure to show appreciable net life-extension.... and then a number of potential counter-counter arguments from there, such as that these deaths are perhaps avoidable or artifacts of the study protocol.....

Potential objections are in practice subjectively weighed in mind and discourse, depending on how one perceived those other pillars of evidence.  
 

Such as Matt’s citation above investigating transcrional profiles among CR persons documenting “The PI3K and AKT transcripts were significantly down-regulated 1.7 and 2 folds” , upregulation of AMPK, downstream transcripts of FOXO3A, the sirtuins, PGC-1α, etc. as we see in other model organisms under CR.  In your Bayesian mental model of “truth” how much ( if any ) does that push your overall appraisal in one direction or another? 

The point is, the pillars of evidence are at a minimum subjective - certainly in the absence of a strong enough stacking of data one way or another relative to the null hypothesis on CR. 
 

People are different than model animals.  Surrogates are still just surrogates.  There is biological plausibility, and a portfolio of data, and with no prospect for a true CR RCT in man.  

Given the inexact science, where does that leave us?

1) Look at all the pillars

2) Read the studies yourself, and understand them.  It doesn’t matter how many times the 2017 study has been cited if you don’t scrutinize it yourself - and the evidence and publications consistent and inconsistent with it.  

3) Respect science and the limitations of the boundaries of knowledge.  The larger the departure from a strong evidence base and common practice, the more caution that is warranted.  This does not mean being a “sheep” and following the herd off the cliff of the standard American lifestyle.  Every choice not taken is a choice as well, and both have consequences, for worse or better.  It does mean educating yourself, performing due diligence, and consulting colleagues and professionals as appropriate for your situation.  Proactive pursuit of a healthy lifestyle is not easy, but it is well worth the effort.

Best,

Mechanism

PS-, if you have not read it yet, this reference is a real beauty.  I hope this helps a little.  Stay safe and be well!!

(1)

Mattison JA, Colman RJ, Beasley TM, et al. Caloric restriction improves health and survival of rhesus monkeys. Nat Commun. 2017;8:14063. Published 2017 Jan 17. doi:10.1038/ncomms14063

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5247583/

 

 

 

 

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I'm through reading the book. Probably the most interesting thing is the pharmaceutical aspect of longevity drugs, the concepts, what's under way, what are the expectations. Nir Barzilai is very optimistic, about this.We all would like to share his optimism

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I ordered the book from amazon and should have it here next week. However, I'm of two minds about books on longevity. It seems they rarely stand the test of time - perhaps inevitably - what is exciting and new today becomes the disappointment and wrong roads of tomorrow. So many drugs, so many hopes, and all end up ultimate failures. Hard to get excited over a book that one already knows is probably badly out of date by the time of publication. In this way, such speculative books are hard to enjoy in re-reading. Unlike timeless works of fiction, these time limited (can be argued *also* works of "fiction") books are not frequently re-read decades or even years down the road. But I like Barzilai's enthusiasm, so I'm happy to support his efforts through the buying of his merch :)

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9 hours ago, TomBAvoider said:

But I like Barzilai's enthusiasm, so I'm happy to support his efforts through the buying of his merch

👍

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