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Longevity, Healthspan and the Inflammation Epidemic
By Guest Author: Dr. Thomas Maden-Wilkinson, Ph.D
Scientific Director and Associate Professor, Sheffield Hallam University

We talk about wanting to "live longer" as if that were the whole goal. But most people, pressed on it, don't actually want more years in a body that aches, tires early and keeps them out of the activities they care about, we all want more good years. That distinction is the difference between lifespan and healthspan, and it's reshaping how scientists like myself think about ageing. Lifespan is simple: it's the number of years you're alive, full stop. Someone can live to 90 having spent the last thirty managing multiple chronic conditions and declining mobility — a long lifespan, but a short healthspan.
What do we mean by healthspan and longevity?
Healthspan is the portion of life spent free from serious disease, disability and functional decline, where we are strong enough to carry our shopping, sharp enough to hold a conversation, resilient enough to recover from a cold or a knock without it derailing us for weeks. In the UK, life expectancy at birth is now around 79 years for men and 83 for women — but healthy life expectancy, the years lived free of significant illness or disability, is just 60.7 and 60.9 years respectively (The Health Foundation, 2025). That's 18-22 years, on average, spent in declining health at the end of life. And the gap is widening: healthy life expectancy has fallen by roughly two years over the past decade, with the share of life spent in good health dropping from 79% to 77% for men and 77% to 73% for women. People are living about as long as before, just not as well, which is precisely the lifespan/healthspan gap in national data.
Longevity, as researchers now use it, sits above both: the science and practice of extending healthspan so the gap between how long we live and how well we live shrinks. The most meaningful marker of a good longevity strategy isn't a birthday count; it's whether the extra years are ones worth having.
What actually moves healthspan
Healthspan isn't fixed at birth, it responds to a cluster of factors moving together: chronic disease burden, physical activity, diet quality, sleep, and socioeconomic circumstance (in England, the healthy-life-expectancy gap between the most and least deprived areas is now a horrifying 20 years). Running underneath most of these is the level of background inflammation someone is carrying.
A useful way to hold all of this together is the idea of physiological resilience, this our body's buffer against future shocks, not just its current state. Think of it like a bank account. Exercise, good sleep and sound lifestyle choices are deposits: they build capacity before it's needed and allow those reserves to help us when we need it just like a pension or savings account. Chronic inflammation, inactivity and disease are withdrawals: they draw the balance down, often silently, well before symptoms show up. In this concept, healthspan isn't a fixed trait you either have or don', it's a balance you're actively managing, and the direction it's moving in matters more than any single reading.
The twelve hallmarks of ageing — and the thread running through all of them
Ageing biology has organised itself around a shortlist of 12 mechanisms known as the hallmarks of ageing (Baechle et al., 2023). They fall into three tiers —
- Primary hallmarks, where damage first accumulates (primarily through damage to our genes and DNA (genomic instability, telomere attrition, and epigenetic drift) and loss of the ability to rid of waste products from our cells (loss of proteostasis, disabled cellular clean-up).
- Antagonistic hallmarks, the body's compensatory response, turned harmful over time (deregulated nutrient sensing, mitochondrial dysfunction, cellular senescence(keeping of damaged cells).
- Integrative hallmarks, where the ageing phenotype itself shows up (stem cell exhaustion, altered communication between cells and gut dysbiosis).
Chronic inflammation is at the centre of these 12 hallmarks, and the term "inflammaging" has been created (Franceschi et al., 2018). This “inflammaging” once running, feeds back into the other hallmarks creating a self-reinforcing loop. It shows up as a steady drip of inflammatory signalling molecules known as cytokines like IL-6 and TNF-α circulating at levels too low to notice but high enough, over time, to matter (Karpuzoglu et al., 2025).
In a study tracking over 100,000 people, one signal stood out as a stronger predictor of healthspan than almost anything else researchers measured: chronic inflammation. It doesn't just correlate with getting older, it actively predicts who develops heart disease, who becomes frail, who loses cognitive function, and who dies sooner (Furman et al., 2019).
And the effect isn't subtle. One recent study found that people in their 40s with weak "immune resilience" had nearly 10x the mortality rate of those with strong resilience, a gap roughly equivalent to aging 15 years overnight (Manoharan et al., 2025).
The takeaway: your immune system's inflammatory state may matter more for how long and how well you live than most of the things we obsess over.
What's changed isn't human biology, it's the environment it now sits in. Modern life delivers a relentless drip-feed of inflammatory triggers: diets heavy in refined sugar and processed fat, sleep disruption with never ending notifications, sedentary stretches, chronic stress, and environmental exposures our physiology never evolved to handle at this volume. Layer that onto a population living longer, giving inflammaging more decades to compound, and you get what's increasingly described as "an inflammation epidemic". A background hum of inflammatory load most of us carry without realising it and one most routine check-ups aren't set up to catch.
What should we do about it?
Inflammation itself isn't the enemy, it remains an essential repair mechanism, it is a primary driver to helping us repair our muscles after exercise or after injury and helping an infection get cleared. The problem is inflammation that never switches off. The goal isn't to eliminate it; it's to keep it responsive and able to mobilise when needed and resolve when the job is done. The strongest evidence for shifting that balance still sits with lifestyle and diet. Mediterranean-style patterns diets high in vegetables, legumes, olive oil, oily fish, polyphenol-dense plant foods provide consistently and meaningfully lower CRP and IL-6 across trials (Stamerra et al., 2022). Combining this with regular movement, particularly resistance and endurance training, and consistent sleep round out the best-supported levers available.
However, high quality supplementation to help enhance our physiology and dampen that inflammatory hum can directly influence some of those hallmarks of ageing and how our bodies move and feel. Heres just a few examples of how some of the ingredients in Daily Vitals have been shown clinically to support this.
The science behind some of Daily Vitals' anti-inflammatory ingredients
- HydroCurc® (bioavailable curcumin) — Targets inflammation at its source: misfolded proteins that build up with age and trigger inflammatory damage signals. Curcumin interrupts this step directly in cell and animal studies (Read et al., 2020). HydroCurc®'s enhanced-absorption formula solves curcumin's biggest weakness, it'spoor bioavailability and has proven it in humans, to cut IL-6 and TNF-α in placebo-controlled trials (Lorinczova et al., 2022; Fessler et al., 2023).
- Levagen+® (bioavailable PEA) — Silences "zombie cells." Senescent cells stop dividing but refuse to die, instead they sit in your tissue pumping out inflammatory signals (IL-6, IL-1β, TNF-α). Levagen+ has clinical trial data showing it reduces these same markers across multiple conditions (Briskey et al., 2023).
- Resveratrol — A potent free-radical neutralizer with standout cardio- and neuro-protective effects, breaking the cycle where inflammation damages mitochondria and mitochondria fuel more inflammation.
- Astaxanthin — A powerful antioxidant built to get inside the mitochondrial membrane itself, shielding it from oxidative damage at the source (Kim & Kim, 2018). Human data has shown it specifically lowers IL-6 in people who are already metabolically stressed or inflamed (Baolan et al., 2021) and that's exactly the population who stands to benefit most.
None of this happens overnight, and none of it is a single lever pulled once. Resilience, like the balance in any account, is built through repeated deposits: a consistent exercise training habit, a stable sleep routine, a diet and supplement routine that helps dampen inflammation, keeps fibre coming in regularly and keeps us at healthy weight, outweighing the occasional bad week rather than being undone by it.
Every one of us, have issues that crop up as we age, the years ahead are coming regardless. Whether they're spent well is, to a meaningful degree, something we get to influence — and understanding what's quietly driving inflammation in the background, hallmark by hallmark, is one of the more useful places to start.
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