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What Happens to Our Body as We Age?
3 sept 20264 min de lectura

What Happens to Our Body as We Age?

There's a moment when your age stops matching how you feel.

The number on your last birthday says one thing, while your body's started saying another.

It's easy to chalk that up to just getting older, and some of it is. But the feeling isn't random. Something specific is shifting inside your cells, and we can name it.

So let's start naming.

The Energy Molecule Runs Low

When you hear the word energy, you probably think about whether you feel tired or wide awake. For your cells, it means something more specific. They turn the food you eat into a usable fuel called ATP, and that conversion depends on a molecule called NAD+.¹ When NAD+ runs low, your cells have less energy to work with.²


As the years pass, the body has a harder time holding onto its NAD+. In one study of human tissue, levels dropped as people aged, in both men and women.³

You'll see this decline described as a fixed law of aging, and the reality is different from what you see out there. Most of the clear measurements come from lab studies, so the full picture in people is still being drawn. That's exactly why it's worth watching. The early results are promising, and they point to a real possibility: that supporting NAD+ as it declines could matter how we age.⁴

The Switches Gets Sluggish

Your cells rely on switches too.


Inside them sits a family of proteins called sirtuins. Flip one on and it sets off the work that keeps a cell healthy: handling stress, making repairs, keeping itself in good shape.⁵

Aging drags on those switches. In that same human tissue study, one of the main sirtuins grew less active as people got older.³

Here's the part worth noticing. Those switches don't run on their own. They need NAD+ to work.⁵ So the molecule that fades as we age is the same one these switches depend on, which means one decline drives another.

Cells Wear Out and Linger

As the years pass, your cells take on damage, and the worn-out ones are meant to be cleared away to make room for fresh ones. Sometimes that doesn't happen. A damaged cell shuts down and waits to be cleared, but the help never comes. Just by staying, it starts making trouble for the healthy cells around it.⁶ There's a whole story in how that unfolds, and we told it in full in [Meet the Zombie Cells Aging Your Body article].


Resveratrol is one to watch in this part of aging. In lab studies on human cells, it's been shown to quiet some of the signals these worn-out cells send out, and researchers are exploring what else it might do here.⁷ That work is still early, which is part of what makes it worth following.

That Lingering Turns Inflammatory

The signals those worn-out cells send are inflammatory, and inflammation isn't a bad thing on its own.⁸ In short bursts it helps, it's how your body handles a cut or a cold. What wears on you is the low, steady kind that builds with age, unevenly, more in some people than others.⁹


This is where turmeric comes in. It's one of the most studied plants for calming inflammation, and it sits in the formula for exactly this reason. How it works, and why it needs black pepper to do its job, is the story we're telling next.

Where that Leaves Us

None of this is your body breaking down. It's a machine that's been running a long time, and like any machine, the parts move a little slower with the miles.


As you can see, NAD+ is tied into a lot of that machinery, flipping the switches and running the energy. That makes it a good system to put our support behind, and it's the reason we formulated our NAD+ Complex the way we did: NAD+ at the center, with supporting ingredients around it to help with how cells age and what comes with it. Not a fix, just a bit of oil in an engine that's earned it.

[Explore Neumina's NAD+ Complex] →

Your cells have been turning over, making energy, and keeping you running for decades, without you ever thinking about it. Time doesn't stop, and the machinery won't run like new. But it can run well, for a long time, and what the research is slowly learning is how to help it keep going.

These statements have not been evaluated by the Food and Drug Administration. This product is not intended to diagnose, treat, cure, or prevent any disease.

References

  1. Amjad S, Nisar S, Bhat AA, et al. Role of NAD+ in regulating cellular and metabolic signaling pathways. Mol Metab. 2021;49:101195. doi:10.1016/j.molmet.2021.101195
  2. Hopp AK, Grüter P, Hottiger MO. Regulation of glucose metabolism by NAD+ and ADP-ribosylation. Cells. 2019;8(8):890. doi:10.3390/cells8080890
  3. Massudi H, Grant R, Braidy N, et al. Age-associated changes in oxidative stress and NAD+ metabolism in human tissue. PLoS One. 2012;7(7):e42357. doi:10.1371/journal.pone.0042357
  4. Peluso A, Damgaard MV, Mori MAS, et al. Age-dependent decline of NAD+ — universal truth or confounded consensus? Nutrients. 2021;14(1):101. doi:10.3390/nu14010101
  5. Borra MT, Smith BC, Denu JM. Mechanism of human SIRT1 activation by resveratrol. J Biol Chem. 2005;280(17):17187-17195. doi:10.1074/jbc.M501250200
  6. Ajoolabady A, Pratico D, Bahijri S, et al. Hallmarks of cellular senescence: biology, mechanisms, regulations. Exp Mol Med. 2025;57:1482-1491. doi:10.1038/s12276-025-01480-7
  7. Pitozzi V, Mocali A, Laurenzana A, et al. Chronic resveratrol treatment ameliorates cell adhesion and mitigates the inflammatory phenotype in senescent human fibroblasts. J Gerontol A Biol Sci Med Sci. 2013;68(4):371-381. doi:10.1093/gerona/gls183
  8. Ohtani N. The roles and mechanisms of senescence-associated secretory phenotype (SASP): can it be controlled by senolysis? Inflamm Regen. 2022;42(1):11. doi:10.1186/s41232-022-00197-8
  9. Franck M, Daunizeau C, Aronoff JE, et al. Inflamm-aging as a diverse and context-dependent process: from species and population differences to individual trajectories. Ageing Res Rev. 2025;113:102880. doi:10.1016/j.arr.2025.102880
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Amy Qin, PhD, RD, CDCES, Nutrition Scientist at Neumina

Amy Qin is a Nutrition Scientist at Neumina with training in both nutrition research and clinical care. She received her PhD in Nutrition and Metabolism from the University of Wisconsin-Madison and completed clinical training at Stanford Hospital and UCSF Benioff Children's Hospital.

Her work focuses on applying nutrition science to metabolism, aging, and chronic disease management in ways that are practical and personalized.