Attia separates acute from chronic inflammation, works through which inflammatory markers are actually worth measuring versus which are noise, and what genuinely lowers chronic inflammatory burden. A practical counterpart to the mechanistic literature.
Listen →Dr. Adam Sewell, MD breaks down inflammaging — the persistent, low-grade inflammation that accelerates degeneration across the body's systems — and what actually moves the needle on it.
Listen →In 535 adults with overweight or obesity from the DiOGenes cohort, researchers split insulin resistance into its muscle and liver forms and profiled 1,128 plasma proteins. Muscle insulin resistance tracked 160 proteins dominated by inflammatory pathways, including IL-6 signalling; liver insulin resistance tracked 81 proteins centred on the complement system, with lower IGFBP-1, IGFBP-2, adiponectin and SHBG. Only 12 proteins overlapped. The authors argue this supports tissue-specific rather than one-size-fits-all interventions.
Read source →Three geroscientists (rheumatology, neurology, and critical care) map how chronic low-grade inflammation shows up across specialties — from rheumatologic disease to traumatic brain injury — and where the gap is between wellness-marketing claims and actual evidence on inflammaging tests and treatments.
Listen →Eric Verdin, CEO of the Buck Institute for Research on Aging, on how immune aging — thymic shrinkage, narrowing T-cell diversity, weaker vaccine response — acts as a rate-limiting step in aging, and how chronic inflammation is both a consequence and an accelerant of it. Also covers NAD decline and CD38, the real limits of NMN/NR/IV NAD, rapamycin, and what aging clocks can and can't tell you.
Listen →The inflammaging signature derived from an Italian cohort (InCHIANTI) replicated in another industrialized population (Singapore), but largely vanished in two non-industrialized groups — the Tsimane of the Bolivian Amazon and the Orang Asli of Peninsular Malaysia. In those groups inflammation tracked infection burden rather than age, and showed little association with age-related disease. Suggests inflammaging may be substantially a byproduct of industrialized environments rather than a fixed feature of human aging.
Read source →Pools 13 systematic reviews (11 with meta-analyses) covering resistance, aerobic, combined, HIIT, tai chi, yoga and multimodal training in older adults. Exercise reliably lowered CRP across every review, with resistance training performing best, and reduced TNF-α in most reviews, with HIIT showing particular promise. IL-6 results were inconsistent, with combined aerobic-plus-resistance training doing best, and there was too little data to judge IL-10.
Read source →The design paper for a randomized, double-blind, placebo-controlled trial testing whether clazakizumab, an antibody that blocks interleukin-6, can improve or slow decline in physical, cognitive and vascular function in adults aged 70 and over with low-to-moderate physical function. It is a direct test of the geroscience idea that targeting inflammation itself can extend healthspan. No results yet — this paper describes the rationale and protocol.
Read source →A condensed Huberman Lab episode with Rhonda Patrick on four micronutrients that influence cellular stress responses, inflammation, detoxification and longevity, and why common shortfalls in them may matter more than people assume.
Listen →Maps how age-associated chronic inflammation interacts with the other eleven hallmarks of aging, arguing the crosstalk forms a self-reinforcing cycle that accelerates cellular decline. A good orientation piece for why inflammation sits near the centre of the aging network rather than off to one side.
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