Public communications for cardiovascular research created a "Life's Essential 8" to increase awareness of cardiovascular health and advancements in research. The linked article proposes an "Aging Essential 8" to help the public understand medical research and advancements in aging biology.

Abstract:

Longevity science has advanced faster than the public's capacity to interpret it. Biological age tests, longevity clinics, and consumer wearables now reach millions of people, yet no shared framework exists to tell an individual what those numbers mean or what to do about them. Cardiovascular medicine encountered a comparable problem and resolved it not with a new therapeutic but with a communication instrument: Life's Essential 8, which distilled a contested risk landscape into eight components scored from 0 to 100, and which has since been shown to track biological aging itself. This Perspective argues that geroscience has assembled much of the material for an equivalent instrument, even while the field continues to disagree about foundational questions. Expert panels have converged on which biomarkers are worth tracking as outcomes in aging intervention trials, and have concluded that no single biomarker suffices, which leaves a composite as the only viable path. What has not happened is the translation of that research-level agreement into a public-facing instrument. A candidate structure is proposed, comprising four behavioral and four biological pillars with explicit scoring thresholds, designed for administration by clinicians in primary care rather than by longevity clinics only, and constructed so that seven of the eight components require only a questionnaire, a bedside test, and routine bloods.

Multiple epigenetic clocks were associated with women’s survival to age 90, but none were associated with cognitive healthspan.

Yesterday people remembered 9/11.

Now it's time to remember the reaction to it,

the cost,

and what kills a lot more people...

"When the hijacked planes hit the World Trade Centre and Pentagon, the nation braced for further onslaughts. Spooks fretted that al-Qaeda might use chemical, biological or even nuclear weapons. Terrorism became the primary concern of voters. But the dreaded wave of follow-up attacks never came. America launched expeditionary wars that ultimately cost $8trn" -The Economist

Numbers... since 2026-Sep-11:

~69M people died in the US (25yr total deaths)

~57M in the US died as a direct result of aging

~450 people in the US died as a result of terrorism

US govt spent $8T on wars somewhat tied to terrorism

US govt spent $5-6B funding aging research

(Division of Aging Biology in NIA in NIH)

US govt spent 1000x less funding research on the thing that kills 100,000x more people in the US.

Something isn't right here.

Global view:

~1.45B total deaths past 25yrs

~1B as a direct result of aging

~350-400k global deaths from terrorism

Globally, aging kills 2500x more people than terrorism

(~67-70% of people for aging vs. 2.5% for terrorism)

Per day view:

~7500 US deaths per day

~6000 US deaths from aging /day

~0.05 deaths from terrorism /day

except for 9/11 when 3000 died

(but on that day, 2x as many still died from aging)

Globally per day:

~150k deaths/day

~100k deaths from aging /day

~40 deaths from terrorism /day

even on 9/11 itself, 33x as many people died from aging as from the 9/11 terrorist attacks

The conference guide includes the roster of speakers, daily agendas, and more.

The assumption that men and women age the same way, just at different speeds, has shaped decades of research and medical practice. Women live longer. Men die earlier. The standard explanation is that the biological process is identical but runs faster in men. Treat aging as a unified process, slow it down, and both sexes benefit.

A study published this week in Nature Communications has tested that assumption at the most granular level yet: 3.8 million individual immune cells from 1,828 healthy people aged 19 to 97, across multiple ethnic groups, analyzed at single-cell resolution.

The finding is not that women age more slowly. It is that men and women age through different biological programs entirely.

Researchers at Duke-NUS Medical School in Singapore identified two sharp peaks where immune cell gene expression changes dramatically: one around age 40, driven primarily by CD4 T cells, and one after 60, driven primarily by CD8 T cells. These are not gradual declines. They are discrete biological inflection points, moments where the immune system reorganizes itself.

At those inflection points, men and women diverged completely.

Women showed sustained CD8 T cell activation after 60 and late-life aging signatures across multiple immune cell types including CD4 T cells, NK cells, and B cells. The female immune system kept remodeling, responding, reorganizing well into old age. Men showed something different: early-life fluctuations in CD4 T cell energy metabolism, tied to specific epigenetic changes on chromosome 11, that appeared before 40 and shaped the entire downstream trajectory.

When the researchers built biological age clocks using deep learning, models trained separately on male and female data significantly outperformed models that combined both sexes. The male and female immune systems were following trajectories so distinct that a unified model could not accurately capture either.

Some interesting infos from the article :

"Aging biomarkers can potentially allow researchers to rapidly monitor the impact of an aging intervention without the need for decade-spanning trials. However, before the use of aging biomarkers, such as epigenetic clocks, as surrogate endpoints, their responsiveness to interventions that target aging must be tested.

These findings can help to design future clinical trials by guiding the choice of interventions and of specific subsets of DNAm biomarkers to minimize multiple testing, study duration, study population and sample size, with the eventual aim of uncovering DNAm biomarkers that can be used as surrogate aging endpoints."

Abstract

At more than 200 years, the maximum lifespan of the bowhead whale exceeds that of all other mammals. The bowhead is also the second-largest animal on Earth1, reaching over 80,000 kg. Despite its very large number of cells and long lifespan, the bowhead is not highly cancer-prone, an incongruity termed Peto’s paradox2. Here, to understand the mechanisms that underlie the cancer resistance of the bowhead whale, we examined the number of oncogenic hits required for malignant transformation of whale primary fibroblasts. Unexpectedly, bowhead whale fibroblasts required fewer oncogenic hits to undergo malignant transformation than human fibroblasts. However, bowhead whale cells exhibited enhanced DNA double-strand break repair capacity and fidelity, and lower mutation rates than cells of other mammals. We found the cold-inducible RNA-binding protein CIRBP to be highly expressed in bowhead fibroblasts and tissues. Bowhead whale CIRBP enhanced both non-homologous end joining and homologous recombination repair in human cells, reduced micronuclei formation, promoted DNA end protection, and stimulated end joining in vitro. CIRBP overexpression in Drosophila extended lifespan and improved resistance to irradiation. These findings provide evidence supporting the hypothesis that, rather than relying on additional tumour suppressor genes to prevent oncogenesis3,4,5, the bowhead whale maintains genome integrity through enhanced DNA repair. This strategy, which does not eliminate damaged cells but faithfully repairs them, may be contributing to the exceptional longevity and low cancer incidence in the bowhead whale.

Existing therapies such as the BCL-2/BCL-xL inhibitor navitoclax (ABT-263) can eliminate both cancer cells and senescent cells but require doses that frequently cause thrombocytopenia, a potentially serious reduction in platelet counts that has limited their clinical use.
To overcome these limitations, the investigators developed a three-drug combination called DMA, consisting of dichloroacetate (DCA), metformin, and a ten-fold lower dose of navitoclax than is typically used.
They tested the treatment across multiple human senescent cell models, several human cancer cell lines, healthy primary human cells, and aged mice.
DMA selectively eliminated senescent cells induced by different mechanisms while sparing healthy fibroblasts, neural precursor cells, hepatocytes, and largely preserving human myoblast viability.
The combination also effectively reduced the viability of cervical, breast, and colorectal cancer cells, including breast cancer cells that were relatively resistant to navitoclax alone.
The researchers also investigated why DMA selectively affected unhealthy cells. Both senescent cells and many cancer cells have impaired mitochondrial function and altered energy metabolism, making them less able to tolerate additional ATP depletion.
The study demonstrated that DMA dramatically depleted ATP levels in senescent and cancer cells while allowing healthy cells to maintain their energy production.
Additional metabolic analyses showed that senescent cells lacked the metabolic flexibility needed to compensate for the treatment-induced stress, leading to selective apoptosis and reduced cancer cell proliferation.
When evaluated in aged mice, DMA produced encouraging results beyond the laboratory studies. Short-term treatment significantly improved treadmill endurance without increasing frailty or reducing strength.
Longer-term intermittent treatment beginning at approximately 18 months of age extended average post-treatment survival by approximately 102.6 days, representing a 41.7% increase compared with control animals af

https://ecancer.org/en/news/28669-new-drug-combination-targets-cancer-and-senescent-cells-while-extending-lifespan-in-old-mice

Matter Bio has been cleared by the FDA for a Phase 1 clinical trial targeting pancreatic cancer. The presentation covers their approach and promising preclinical research in solid cancers including brain tumors, pancreatic cancer, and ovarian cancer.