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The six aging processes at a glance: what research reveals
Aging research understands better than ever what happens in our cells as we age. Six processes get particular attention in the longevity field: oxidative stress, NAD+ decline, inflammaging, sirtuin activity, autophagy and cellular senescence. They are closely connected, and many insights from cell and animal models are now being studied in humans. Clear conclusions for your offer follow from this – from lifestyle to a targeted supply of nutrients.
Aging follows patterns – and research can read them
For a long time, aging was seen as unstoppable wear and tear. Today, research paints a different and far more exciting picture: aging follows patterns that can be described, measured and influenced in experiments. The 2023 update of the hallmarks of aging made exactly this a condition. A process only counts as a hallmark if interventions in it can slow aging in experiments (López-Otín et al., Cell, 2023).
Six of these processes get particular attention in the longevity field. Each one is a fascinating research area of its own – and together they form a picture you can explain clearly to your members, guests or employees. Here you will learn what research describes for each process, which findings are especially promising, and which practical conclusions follow from them.
The six processes at a glance
| Process | The picture | What research describes | Practical conclusion |
|---|---|---|---|
| Oxidative stress | sparks flying in a workshop | Free radicals attack cell components but also act as signals; the body has its own protective systems. | aim for balance; know the nutrients with an authorized claim on cell protection |
| NAD+ decline | a battery that charges more slowly | NAD+ changes with age; precursors boost NAD+ metabolism in humans, too. | keep energy metabolism in view; know vitamin B3 as a building block of NAD+ |
| Inflammaging | a smoldering fire | Chronic inflammation is closely linked to lifestyle factors. | put exercise, diet and stress management at the center |
| Sirtuins | the cell’s caretakers | Sirtuins need NAD+ as fuel; studies in mice show exciting effects. | think of NAD+ and sirtuins as one system |
| Autophagy | the cell’s waste collection | Many interventions that extend lifespan in model organisms stimulate autophagy. | understand diet and energy intake as levers |
| Cellular senescence | retired tenants who won’t move out | Removing senescent cells delayed age-related changes in mice. | follow one of the most dynamic fields; explain animal data as such |
1. Oxidative stress: sparks flying in the workshop
The mitochondria, the cell’s power plants, produce energy – and sparks fly in the process: free radicals. They can attack DNA, proteins and cell membranes. The body has its own protective systems that catch these sparks. Oxidative stress means that more sparks are flying than the protective systems can put out.
What research describes: In 1956, the physician Denham Harman laid a cornerstone of modern aging research with his free radical theory (Harman, Journal of Gerontology, 1956). Since then, oxidative stress has been one of the most intensively studied fields. Today it is clear that free radicals are not just harmful substances but also signals that cells use to respond to stress (López-Otín et al., Cell, 2013). Balance is what matters.
What can be concluded: More is not automatically better. That is also the lesson of a large review of trials with single antioxidant supplements, which found no reduction in mortality (Bjelakovic et al., Cochrane Database of Systematic Reviews, 2012). At the same time, there is a clear, positive basis for your communication: for vitamin C, vitamin E, selenium, zinc and other nutrients, the EU has authorized the claim that they contribute to the protection of cells from oxidative stress (Regulation (EU) No 432/2012). On the genetic side: Oxidative stress and your antioxidant genes.
2. NAD+ decline: a battery that charges more slowly
NAD+ is a helper molecule found in all living cells. It carries electrons during energy production – like a swappable battery that carries energy from station to station. It is also fuel for other enzymes, including the sirtuins.
What research describes: NAD+ levels in cells change with age. In animal models, interventions in how NAD+ is made or used extended both healthspan and lifespan (Verdin, Science, 2015). There are promising data in humans, too: in a randomized, placebo-controlled crossover trial lasting 2 × 6 weeks, the NAD+ precursor nicotinamide riboside was well tolerated and effectively stimulated NAD+ metabolism in healthy middle-aged and older adults. The authors recommend that future trials look more closely at potential benefits for blood pressure and arterial stiffness (Martens et al., Nature Communications, 2018).
What can be concluded: The body builds NAD+ from forms of vitamin B3, among other things. For niacin (vitamin B3), the EU has authorized the claim that it contributes to normal energy-yielding metabolism. For counseling, this means: if you talk about NAD+, you are talking about energy metabolism – and the sirtuins come along with it.
3. Inflammaging: a smoldering fire instead of a blaze
Inflammation is really the body’s fire department: it turns out, puts out the fire and drives back to the station. With age, many people are left with a quiet, smoldering fire – a persistently, slightly raised level of inflammatory activity. The term inflammaging combines “inflammation” and “aging” and was coined in 2000 (Franceschi et al., Annals of the New York Academy of Sciences, 2000).
What research describes: Chronic systemic inflammation is linked to many of the leading causes of disease and disability. It is promoted by factors including infections, physical inactivity, poor diet, environmental toxicants and psychological stress (Furman et al., Nature Medicine, 2019).
What can be concluded: Here lies one of the most encouraging messages of aging research. Several of the most important drivers are lifestyle factors that everyone can influence. Exercise, a balanced diet and good stress management are therefore the logical foundation of every longevity program (more in Lifestyle first). On the genetic side: Chronic inflammation and your immune genes.
4. Sirtuins: the cell’s caretakers
Sirtuins are a family of enzymes that work like caretakers in the cell: they influence which genes are read and keep repair and metabolism running. They need NAD+ as fuel – which is why the two topics often come up together.
What research describes: Sirtuins became famous when studies in yeast, worms and flies linked them to a longer lifespan. In a widely noted study, resveratrol shifted the physiology of middle-aged mice on a high-calorie diet toward that of mice on a standard diet and significantly improved their survival (Baur et al., Nature, 2006) – animal data. Since then, research has been re-testing the early findings with ever stricter controls, showing how important careful study design is; the role of sirtuins remains an active field of research (Burnett et al., Nature, 2011).
What can be concluded: Sirtuins and NAD+ belong together. It follows that energy metabolism, NAD+ and sirtuins should be seen as one connected system – just as research describes them. The mouse data are exciting; in your communication, you label them as animal data.
5. Autophagy: the cell’s waste collection
Autophagy literally means “self-eating.” It refers to the cell’s recycling system: the cell packs up damaged components, breaks them down and reuses the building blocks – a waste collection service with its own recycling center.
What research describes: When autophagy is genetically blocked in mammals, changes appear that resemble aging. Conversely, many interventions that extend lifespan in model organisms stimulate autophagy. With calorie restriction, for example, this effect depends on functioning autophagy (Rubinsztein et al., Cell, 2011). Since the 2023 update, disabled autophagy has been a hallmark of aging in its own right.
What can be concluded: Many of these levers have to do with diet and energy intake. Calorie restriction – eating less energy without nutrient deficiency – is now being studied in humans as well: in a randomized trial, two years of calorie restriction slightly slowed the pace of aging as measured by an epigenetic clock (Waziry et al., Nature Aging, 2023; more in Measuring biological age).
6. Cellular senescence: retired tenants who won’t move out
Senescent cells have stopped dividing but do not die. Picture them as retired tenants who won’t move out and play loud music: they release messengers that can disturb their neighborhood. Yet senescence also has good sides. It curbs the proliferation of damaged cells and helps with wound healing (Baker et al., Nature, 2016).
What research describes: In mice, researchers removed senescent cells using a genetic tool. This delayed age-related changes in several tissues (Baker et al., Nature, 2011). In normal mice, it extended median lifespan and preserved the function of the kidneys, heart and fat tissue (Baker et al., 2016) – a milestone, achieved with animal data.
What can be concluded: Senescence is one of the most dynamic fields in aging research. Research has now taken the step to the first studies in humans, starting with drugs in specific diseases (Justice et al., EBioMedicine, 2019). For your communication, this means: go ahead and tell the fascinating mouse story – but always as what it is.
What you can conclude for your offer
The six processes do not stand side by side; they form a network: NAD+ fuels the sirtuins, senescent cells release pro-inflammatory messengers, and stress can push cells into senescence. Clear conclusions for your offer follow from this:
- Lifestyle as the foundation: exercise, diet and stress management address several drivers at once, above all chronic inflammation.
- Use nutrients in a targeted way: work with the authorized claims – for example on protecting cells from oxidative stress or on normal energy-yielding metabolism.
- Think broadly: a concept that considers several processes fits the network of aging better than a single substance.
- Name the source: explain whether an insight comes from cells, from model organisms or from human studies.
- Communicate cleanly: do not link any of these processes to an efficacy promise – neither for a product nor for a service (more in Advertising longevity).
The planned Novogenia longevity line
A factual note to finish: Novogenia plans to launch a longevity line in 2026. It consists of six building blocks aligned with the six aging processes described here and is designed for different age groups – from the building block for ages 25 and up to the one for ages 50 and up. It is based on our lab’s own literature reviews with a combined 90 referenced PubMed studies. Some popular substances from the US longevity scene, such as NMN, rapamycin and metformin, are deliberately not included; some of them are not permitted as food supplements in the EU.
The line is planned as the Novogenia line and, on request, as a private label. Formulations, quantities and availability may still change before launch. Like all food supplements, the building blocks are not a substitute for a balanced, varied diet and a healthy lifestyle. You will find details on the Novogenia Longevity page.
Frequently asked questions
Which six aging processes are in focus?
Which nutrients may I link to oxidative stress?
What is inflammaging?
What role do animal studies play for sirtuins, autophagy and senescence?
When will the Novogenia longevity line be available?
Related: Longevity and healthspan: what aging research knows · Advertising longevity: what is allowed · The Novogenia longevity line
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Become a partner →The Novogenia longevity lineNote: This guide is general information for businesses and professionals and does not replace medical or legal advice. Novogenia longevity products are food supplements and not a substitute for a balanced, varied diet and a healthy lifestyle; statements in this guide are not promises of cure and not statements on the prevention, treatment or healing of diseases. Recommendations derived from genetic analyses are logical conclusions, not scientifically proven. Regulations can change; errors and changes excepted.
