A practice built on biology.
The Premise
Most people read the quiet shifts of ageing as inevitable decline. The biology suggests something more useful.
At the cellular level, mitochondria gradually lose efficiency. DNA accumulates damage. Chronic low-grade inflammation simmers quietly, sometimes for decades. Muscle fibres thin. Hormonal signalling becomes less precise. Stem cell pools diminish.
None of this is mysterious. It is measurable, mechanistic and, in part, modifiable. That is the entire basis of our work: not a rebellion against ageing, but the recognition that much of what we interpret as unavoidable decline is the cumulative effect of processes that can be influenced.
The Goal
The question is not how long. It is how long in good working order.
Life expectancy has risen steadily for a century. Healthy life expectancy has not risen as fast. The gap between the two is the number of years the average person now spends living with meaningful impairment, and in most countries that gap has been widening.
In 1980 James Fries proposed the alternative: hold function near its peak for as long as possible, so that the period of decline at the end is compressed rather than extended. Not more years at any cost. Fewer bad ones.
Age
Years lived below the independence threshold
Typical trajectory
Capacity erodes from midlife. Length of life is extended; much of the addition is spent in decline.
Compressed morbidity
Function is held near peak for longer. The same endpoint, with the period of dependence made shorter.
After Fries, New England Journal of Medicine, 1980.
Why Age Is The Driver
Heart disease, type 2 diabetes, dementia and most cancers share one risk factor that dwarfs all the others. It is age itself.
Medicine has historically treated these as separate diseases with separate causes. Geroscience makes a different argument: that the biological processes of ageing are the common upstream driver, and that slowing those processes would move every downstream condition at once.
So far that argument is supported much more strongly in animals than in people. Which is why the practical question is a narrower one: not whether ageing can be slowed in general, but which specific process a given product acts on, and how far that has been taken in humans.
The Hallmarks
Twelve processes, one system.
In 2013, López-Otín and colleagues proposed nine hallmarks of ageing: processes that appear during normal ageing, whose acceleration worsens it, and whose attenuation improves it. In 2023 they expanded the set to twelve. It is the framework the field uses, and the one we work from.
Select any hallmark to see what it is, where in the cell it happens, and which other hallmarks it feeds. None of them act alone, which is the single most important thing to understand about them.
Unambiguously harmful processes. Damage accumulates with time, and experimentally accelerating it accelerates ageing.
Responses that are protective at low intensity and damaging when sustained. The dose, and the duration, decide which.
What emerges once damage outpaces repair. These are the hallmarks you can see and feel, the ones that become symptoms.
Mitochondrial dysfunction
Mitochondria are the parts of your cells that turn food and oxygen into usable energy. They become less efficient with age, produce more waste in the process, and are replaced more slowly.
Drives or amplifies
Driven or amplified by
How We Work
How we decide what to carry.
Biology first
We start from the process we are trying to move: mitochondrial decline, chronic low-grade inflammation, epigenetic drift, stem cell exhaustion. Only then do we go looking for a product that moves it.
How we read a study
Human trials carry the most weight, then animal work, then anything done in cells. We check the dose used in the study against the dose in the bottle. Those two questions clear out most of what we see.
A deliberately short list
Most of what reaches us never enters the portfolio. We would rather carry a handful of brands we can answer detailed questions about than forty we cannot.
Healthspan over lifespan
We care about the years you spend in good working order. Strength, clarity and independence, held for as long as your biology allows.
Built for Asian markets
Asian populations differ in genetics, diet and baseline metabolic risk, and every market we work in registers products its own way. Dosing and claims that pass in the US usually have to change before they reach a shelf in Singapore or Jakarta.
Long horizons
Longevity compounds across decades, so we look for products a person could reasonably still be taking in ten years. Most of what trends in a given season fails that test on its own.
Ageing is inevitable.
Passive ageing is not.
Sources
The papers behind this page.
López-Otín C, Blasco MA, Partridge L, Serrano M, Kroemer G. Hallmarks of aging: An expanding universe. Cell, 2023; 186(2):243–278.
The twelve-hallmark framework this page is organised around.
López-Otín C, Blasco MA, Partridge L, Serrano M, Kroemer G. The Hallmarks of Aging. Cell, 2013; 153(6):1194–1217.
The original nine hallmarks.
Fries JF. Aging, natural death, and the compression of morbidity. The New England Journal of Medicine, 1980; 303(3):130–135.
The origin of the compression-of-morbidity argument, and the reason we talk about healthspan rather than lifespan.
Kennedy BK, Berger SL, Brunet A, et al.. Geroscience: linking aging to chronic disease. Cell, 2014; 159(4):709–713.
Sets out why ageing is treated as the shared upstream risk factor for age-related disease.
Franceschi C, Campisi J. Chronic inflammation (inflammaging) and its potential contribution to age-associated diseases. The Journals of Gerontology: Series A, 2014; 69(Suppl 1):S4–S9.
Foundational account of inflammaging.
Horvath S. DNA methylation age of human tissues and cell types. Genome Biology, 2013; 14(10):R115.
The multi-tissue epigenetic clock.
Baker DJ, Wijshake T, Tchkonia T, et al.. Clearance of p16Ink4a-positive senescent cells delays ageing-associated disorders. Nature, 2011; 479(7372):232–236.
Evidence that senescent cells are causal rather than merely correlated, in mice.
de Cabo R, Mattson MP. Effects of Intermittent Fasting on Health, Aging, and Disease. The New England Journal of Medicine, 2019; 381(26):2541–2551.
Review of nutrient-sensing manipulation in humans and animals.
Knowing the mechanism is the easy part.
Deciding which products actually earn a place against it is harder. Tell us what you are trying to improve and we will point you to what fits.
This page is educational. Longevity & Wellness Group does not provide medical advice, diagnosis or treatment, and nothing here is a substitute for consultation with a qualified healthcare professional.