Key findings

  • Approximately 66% of Tsimane had at least one intestinal parasitic infection; over 70% of Orang Asli had a prevalent infection.

  • Inflammaging markers were strongly linked to chronic disease in industrialized populations, but not in Indigenous groups.

  • The study challenges the assumption of universal aging biomarkers, suggesting instead that immune-aging processes are population-specific and heavily influenced by the exposome—the totality of environmental, lifestyle, and infectious exposures.

Inflammation, long considered a hallmark of aging, may not be a universal human experience, according to a new study from Columbia University Mailman School of Public Health. The research suggests that “inflammaging”—chronic, low-grade inflammation associated with aging—appears to be a byproduct of industrialized lifestyles and varies significantly across global populations.

Researchers analyzed data from four populations: two industrialized groups—the Italian InCHIANTI study and the Singapore Longitudinal Aging Study (SLAS)—and two Indigenous, non-industrialized populations—the Tsimane of the Bolivian Amazon and the Orang Asli of Peninsular Malaysia. While the inflammaging signature was similar between the two industrialized populations, it did not hold in the Indigenous groups, where inflammation levels were largely driven by infection rather than age.

Read the full story:

Paywalled Paper:

https://www.nature.com/articles/s43587-025-00888-0

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Many calorie restricted ppl also have minimal inflammation through the lifespan but they still age

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Is this implying that an indigenous population with a parasitic infection has an immune system that is not creating in inflammatory response to the environment unlike the response to the artificial environment in the developed world population?

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Very cool result that intuitively makes sense. Makes you think about how many of those 12 hallmarks are simply long term symptoms of chronic diseases, and how many truly apply to all humans.

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Experts have long pointed to inflammation as a natural part of getting older. But a new paper suggests it might be more a product of our environment.

A new analysis of data gathered from a small Indigenous population in the Bolivian Amazon suggests some of our basic assumptions about the biological process of aging might be wrong.

Inflammation is a natural immune response that protects the body from injury or infection. Scientists have long believed that long-term, low-grade inflammation — also known as “inflammaging” — is a universal hallmark of getting older. But this new data raises the question of whether inflammation is directly linked to aging at all, or if it’s linked to a person’s lifestyle or environment instead.

The study, which was published today, found that people in two nonindustrialized areas experienced a different kind of inflammation throughout their lives than more urban people — likely tied to infections from bacteria, viruses and parasites rather than the precursors of chronic disease. Their inflammation also didn’t appear to increase with age.

if validated in larger studies, the findings could suggest that diet, lifestyle and environment influence inflammation more than aging itself, said Alan Cohen, an author of the paper and an associate professor of environmental health sciences at Columbia University.

The full NY Times article on this research: https://www.nytimes.com/2025/06/30/well/live/aging-inflammation-lifespan-environment.html?unlocked_article_code=1.Tk8.KaSR.X1gnXHdlUTOh&smid=url-share

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Interesting. But so what? I mean, we live (most of us on this site) in a Western environment. There are many things we cannot change (limited control of air quality, for example). We are not going to move into the jungle. The facts are: we Westerners have inflammation that is damaging. Since we are not able to eliminate all sources of said inflammation, then we are obliged to counteract this, including with the use of drugs. In practical terms, since we cannot control all sources of inflammation, we’ll just have to continue with the current means of attenuation regardless.

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Yes - I agree. It’s interesting from a scientific point, but if all people in western, industrial countries have the same inflammation profile then treating it as an aging biomarker isn’t so far off the mark really.

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Yes, I think it’s indicative of what the author concludes about what further research may validate. That diet, lifestyle, and environment influence aging. My take away from this is that western cultures try to avoid inflammation which may not be always so good. Especially, when it comes to things like exercise. Hasn’t it been established that anti inflammatory drugs, NAISD’s, diminish the gains of an exercise program? And exercise has been associated with better aging. Inflammation = good aging.

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It’s important to avoid conflating localized or temporary inflammation and systemic “dry” inflammation. Temporary and localized inflammation is by all means healthy and necessary. When your body is combatting an infection, it involves an inflammatory process. Nobody is proposing to dampend that. Exercise involves temporary inflammation - and we know that trying to tamp down that (through anti-inflammatories or antioxidants), removes a lot of the benefits of exercise, so we don’t do that. Nobody is claiming that the temporary inflammation of exercise is anything but good. That type of inflammation is necessary and beneficial. We don’t try to combat this. That’s not at issue.

What’s at issue is something completely different. It’s a process where the inflammation is constant without an inciting cause - generalized inflammatory state, frequently associated with mTORC1 that doesn’t turn off, but keeps revving the inflammatory process. That’s systemic inflammation - a very different proposition, and here, unlike temporary or localized inflammation we do want to tamp down the process, and no, there are no benefits to this type of inflammation. In Western individuals, this inflammation is commonly associated with aging - called inflammaging. Now, to revisit exercise - why is the inflammation in exercise generated in the first place? In order to rev up the body’s natural mechanism to tamp down on overall inflammation - systemic inflammation - in the process of hormesis. That right there neatly illustrates the distinction - the good temporary inflammation that leads to less systemic inflammation. That’s part of the benefits of exercise - less inflammaging.

So, yes, temporary and localized inflammation that is part of a natural defense mechanism - is GOOD, and should not be tamped down. Systemic “dry” inflammation is NOT GOOD, and yes, it should be tamped down by whatever means we can - lifestyle, diet, exercise, drugs. One of the ways in which rapamycin inhibiting mTORC1 works beneficially is by allowing to tamp down on the destructive continuing revving that apparently happens in old age. Now, maybe there are nuances in how that works in non-Western populations, but I respond to this in the following way: LOOK AT THE ANIMAL DATA.

If we take animal models, anti-inflammatories and mTOR inhibitors WORK. They prolong lifespan and healthspan. And the animals don’t suffer many of the Western lifestyle issues, like sitting around watching TV and eating chips. It works in animals all over the world. Good enough for me. I don’t actually care as much why it works, but that it works. And so, I’ll continue to take rapamycin and anti-inflammatory agents that work against systemic inflammaging, and I let the people in jungles or other cultures find their own ways to slow down aging… and may I add, that longevity records for humans on the whole are reached in the world built on the Western model, including the purported “blue zones” like the Loma Linda in the USA. Somehow they don’t have jungle tribes where people live into their 90’s on average and large numbers are centenarians and some even supercentenarians. Oh, and my cat reminds me, that companion animals living in the rotten West tend to live a great deal longer than their feral brethern who are untouched by the evils of civilization - it’s as if somone needed a reminder of what Thomas Hobbes observed about life in the state of nature without the benefit of civilization: life that is “nasty, brutish and short”. Thanks, but no thanks, I’ll take my pills and go read a book. No inflammaging for me, thank you, but to each their own. YMMV.

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Very interesting the relationship between temporary induced inflammation from exercise curbing the systemic inflammation from aging. And no doubt the data would certainly show the longest lifespans in the world across western cultures. With the occasional indigenous anomalies here or there. Evolution has not been kind to indigenous populations across the globe. So, it’s occasionally nice to see a “win” for a non western population. Plus there are valuable insights to be gained when an outlier population is encountered. Recessive types of genotypes guarantee survival should the environment change. Ours certainly just did with Covid. A virus originating at the fringes of the Western world(civilized world). An interesting point about Western views on aging can be observed by our adoption of Rapamycin. Which looks certainly better than NAISDs at promoting less systemic inflammation and hence better aging, without the inconvenience of caloric restriction or even exercise. Most users of Rapamycin are probably obtaining their Rapamycin from India. A non western country. Circumventing the traditional method of obtaining medicines for the given condition in our society. How long will it take, if ever for western culture to officially adopt Rapamycin as a treatment for systemic inflammation and the associated effect of aging? How will someone profit?

Note, you can get rapamycin in the US with a prescription from doctors who specialize in longevity or simply have a commercial or some other interest.

Profiting financially from rapamycin is unlikely in most circumstances, as it’s now a generic. Profit likely lies in other rapalogs or mTOR inhibitors which can be patented. Tornado, run by Mannick is an example of one such effort. The hope is to develop a drug that is at least as effective, if not more, but has fewer side effects. A drug that can be patented, and has a superior benefit/risk profile than rapamycin. It’s a work in progress.

Ultimately, rapamycin is a stepping stone. We hope for more and much better anti-aging interventions that can give us a vastly greater lifespan and healthspan, in essence preserving and enhancing youth. Sadly - and I don’t want to be pessimistic here - I believe this will occur much further in the future than many life extension enthusiasts assume. I don’t believe it’ll happen within the lifetime of anyone currently alive. Obviously, I hope I’m wrong - I would like nothing more than to have a chance at such a miracle, but realistically it ain’t happening for me who is currently 67 years old. I’ve had a keen interest in this since I was a teenager, and half a century later, no dice. I reckon the next 50 years will be just as long on promise and short on delivery. We aren’t getting out of this alive, I’m afraid, none of us. Future generations, sure. They’ll pity us poor short termers, when they read history, just as we look with horror at the 20-something lifespans of cavemen. We may be some of the last generations to have missed the great lifespan breakthroughs, missing it by a heartbreaking few decades. It’ll be the single greatest tragedy humanity will experience, it’s not like missing out on flight, it’s missing out on the greatest gift the universe has, the miracle of life itself.

And so, we the last generations of the supremely unlucky are taking revenge on the lucky future generations. We’re trashing the environment, we’re leaving these future generations a practically unlivable planet. If we can manage it, perhaps we can even bury the whole thing in a nuclear wasteland, see how they like it. Let them know of the fury of these creatures who have been cheated so badly of life, a fury like that of the Replicants from Blade Runner, knowing that the clock is ticking with relentless cruelty. And so we’re electing leaders all over the world, who will bring on the Armageddon we demand as our final lashing out. You better believe, that as that light is fading and the aged body is giving up, the old men in charge will push that button to go out in a blaze of furious revenge. All you need is one such guy to do it, and the automatic chain reaction of responses will get us there… and there are so many of these old men across the world, one of them is bound to have an itchy finger, just one. Après nous, le déluge.

Oh wait, sorry, I just had a bad dream! In reality Dear Leader and his minions at governmental health agencies are hard at work with our best interests at heart making rapid progress in life prolonging interventions, a glorious future within grasp. Relax, and be happy, the cavalry is coming to rescue you, just obey and get with the program, don’t struggle, don’t cry out, be silent and compliant. Life is but a dream😢.

Meh, but seriously it is what it is, let’s make the best of it. For lunch today, I’m thinking tacos.

Ah… a new study showing inflammation is important… at least in Canada :smile:

Cross-omics risk scores of inflammation markers are associated with all-cause mortality: The Canadian Longitudinal Study on Aging

Inflammation is a critical component of chronic diseases, aging progression, and lifespan. Omics signatures may characterize inflammation status beyond blood biomarkers. We leveraged genetics (polygenic risk score [PRS]), metabolomics (metabolomic risk score [MRS]), and epigenetics (epigenetic risk score [ERS]) to build multi-omics-multi-marker risk scores for inflammation status represented by the level of circulating C-reactive protein (CRP), interleukin 6 (IL-6), and tumor necrosis factor alpha (TNF-α). We found that multi-omics risk scores generally outperformed single-omics risk scores in predicting all-cause mortality in the Canadian Longitudinal Study on Aging. Compared with circulating inflammation biomarkers, some multi-omics risk scores had a higher hazard ratio (HR) for all-cause mortality when including both score and circulating IL-6 in the same model (1-SD IL-6 MRS-ERS: HR = 2.20 [1.55–3.13] vs. 1-SD circulating IL-6 HR = 0.94 [0.67,1.32]. 1-SD IL-6 PRS-MRS: HR = 1.47 [1.35,1.59] vs. 1-SD circulating IL-6 HR = 1.33 [1.18, 1.51]. 1-SD PRS-MRS-ERS: HR = 1.95 [1.40, 2.70] vs. 1-SD circulating IL-6: HR = 0.99 [0.71, 1.39]). In the Nurses’ Health Study (NHS), NHS II, and Health Professional Follow-up Study with available omics, 1 SD of IL-6 PRS and 1-SD IL-6 PRS-MRS had HR = 1.12 [1.00,1.26] and HR = 1.13 [1.01,1.26] among individuals >65 years old without mutual adjustment of the score and circulating IL-6. Our study demonstrates that some multi-omics scores for inflammation markers may characterize important inflammation burden for an individual beyond those represented by blood biomarkers and improve our prediction capability for the aging process and lifespan.

Paywalled paper:

https://www.cell.com/ajhg/abstract/S0002-9297(25)00240-X

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And lemurs are different too…

What can lemurs tell us about inflammation and aging, aka “inflammaging” in humans? That’s the question Elaine Guevara, a biological anthropologist who studies the evolution of life history and aging in primates, set out to understand.

In newly published research on age-related inflammation in ring-tailed and sifaka lemurs, Guevara discovered that perhaps we should rethink the inevitability of inflammaging in humans.

Although similar in many ways, ring-tailed and sifaka lemurs show differences in life pacing and lifespan, making useful comparisons. Because lemurs and humans are primates and share a common ancestor that lived millions of years ago, they offer valuable insights into human evolution.

Her findings, she said, were “surprising.”

“Contrary to our predictions, neither species showed age-related change in either marker of oxidative stress. Neither lemur species exhibited age-related change in inflammation; if anything, contrary to our prediction, ring-tailed lemurs showed marginal declines in inflammation with age,” Guevara said.

This finding, consistent with a few recent studies of other non-human primates, suggests that lemurs avoid the phenomenon of “inflammaging” widely observed in humans.

The study shows inflammaging is not a universal feature of primates, pointing to some differences that might suggest it turns out it’s not even a universal feature of humans, according to Christine Drea, a professor of evolutionary anthropology who was one of the researchers working with Guevara.

full story:

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Also, concerning at least one type of lemur:

https://www.sciencedirect.com/science/article/abs/pii/S0531556518301682

These data show that aging P. coquereli experience only subtle age-related changes, that were not nearly as extensive as reported in humans. This lack of change suggests that unlike humans, lemurs maintain gait competency at high levels, possibly because these animals maintain reproductive capacity close to their age of death and that frailty may be selected against, since gait disability would result in injury and death that would preclude independent living. Although nonhuman primates should experience age-related senescence, their locomotor performance should remain robust throughout their lifetimes, which raises questions about the use of primate models of gait disability, an area that deserves further investigation.