Lithium is a naturally occurring trace mineral found in rocks, soil, and water. Humans have been exposed to small amounts of lithium throughout history through natural water sources and food grown in mineral-rich soil.

While lithium is best known as a prescription medication used at high doses for bipolar disorder, it also exists at much lower levels in nature. These nutritional-level amounts are sometimes referred to as “microdosed lithium.”

In NOVOS Core, lithium is included at 1 mg per serving, a microdose that is hundreds of times lower than typical prescription levels. It is included for its potential role in supporting biological pathways associated with healthy aging and brain resilience, which are explored in more detail below.

This Article Covers:

• What’s microdosed lithium
• How it’s linked to longer lifespan
• Its role in epigenetics, telomeres, and brain health
• Effects on mitochondria, autophagy, and inflammation
• The difference between microdosed and pharmaceutical lithium
• Why it’s included in NOVOS Core

Key Takeaways

✔ Lithium is a naturally occurring trace mineral found in rocks and water.
✔ Some population studies associate higher trace lithium in drinking water with lower mortality-related outcomes, but they don’t prove causation.
✔ Preclinical research links lithium to longevity and stress resilience in model organisms.
✔ Mechanistically, lithium can influence targets like GSK-3 and pathways connected to cellular maintenance (including autophagy).
✔ NOVOS Core contains 1 mg lithium per serving, far below typical prescription doses

Is Lithium Linked to a Longer Life?

Evidence in Model Organisms:

One reason lithium has attracted attention in longevity research is that lifespan effects have been observed in multiple model organisms, where researchers can test interventions across the full lifespan under controlled conditions.

In C. elegans (nematode worms), lithium exposure has repeatedly been linked to longer survival. In one of the foundational studies, lithium increased survival during normal aging, with reported effects reaching up to ~46% median lifespan extension depending on conditions (R,R).
A later study also reported that lithium can increase both lifespan and healthspan, alongside improvements in age-related mitochondrial energetic function.

In Drosophila (fruit flies), dietary lithium has also been shown to extend lifespan, within a specific dose range. In the Cell Reports study, lithium extended lifespan in female flies at concentrations between 1–25 mM, increasing median lifespan by ~16% and maximum lifespan by ~18% (with higher doses shortening lifespan) (R).

Evidence in Humans:

At the microdose used in NOVOS Core, lithium’s human evidence base comes mainly from long-term observational research, especially studies that compare naturally varying trace lithium levels in drinking water across regions, rather than short randomized clinical trials.

Across years of follow-up, higher background lithium exposure has been associated with several population-level outcomes, including:

• Lower all-cause mortality in some regional analyses (R;R)
• Lower Alzheimer’s disease–related mortality or dementia-related outcomes in ecological and review-level evidence (still not causal) (R,R).
• Lower suicide rates in many (but not all) ecological studies, supported by multiple systematic reviews/meta-analyses, again, association only (R;R)

Some studies also report that higher trace lithium exposure correlates with measurable lithium biomarkers (e.g., in urine or blood) in the population, suggesting real uptake, though the health implications at these levels remain an active research question  (R;R).

Because these studies are observational and often ecological (regional averages), they cannot prove that lithium causes longer life. But together, they help explain why microdosed lithium has become a topic of interest in healthy aging research, and why controlled clinical studies are still needed.

How Does Microdosed Lithium Support Healthy Aging?

How Does Microdosed Lithium Improve Epigenetic Health and Support Telomere Length?

As we age, epigenetic regulation, the molecular “software” that helps control which genes are active or silenced, can become less stable. This shift is linked to reduced cellular resilience and altered stress-response signaling (R).

Lithium has been shown to influence several pathways that intersect with epigenetic regulation, especially through its well-characterized inhibition of GSK-3 and downstream effects on gene transcription and cellular stress signaling. (R, R)

Because most mechanistic data comes from cell/animal studies and from clinical psychiatric use (higher doses than nutritional microdoses), the best-supported way to describe microdosed lithium is that it is biologically plausible, not that it “proves” these effects in healthy people at 1 mg (R).

1) Epigenetic signaling and gene-expression programs

Reviews of lithium’s biology describe epigenetic involvement across DNA methylation, histone modifications, and noncoding RNAs, largely in the context of lithium’s clinical effects and cellular models, supporting the idea that lithium can modulate gene-expression programs related to cellular maintenance and stress response (R).

2) BDNF and neuro-resilience signaling

Lithium has been reported to increase BDNF in human clinical contexts (e.g., Alzheimer’s disease cohorts treated with lithium), consistent with a broader body of preclinical work linking lithium to neurotrophic signaling. (R)
Note: These results come from clinical dosing contexts, so they inform plausibility, not a guaranteed effect at microdose.

3) Telomerase activity and telomere-related markers

In bipolar-disorder cohorts, long-term lithium treatment has been associated with longer telomeres and with changes in telomerase-related biology (e.g., increased TERT expression/telomerase activity in some studies). (R, R, R)
However, telomere outcomes are not uniform across all studies and remain an active research area—especially when extrapolating to low nutritional doses. (R, R)

How Does Lithium Activate Autophagy?

One hallmark of aging is the accumulation of damaged proteins and dysfunctional cellular components, contributing to impaired proteostasis and cellular stress (R).

Lithium has been shown in experimental systems to promote autophagy, the cell’s internal recycling and quality-control system. Unlike some other autophagy activators, lithium can stimulate autophagy through inositol depletion pathways, independently of mTOR signaling (R, R).

In preclinical models, lithium-induced autophagy has been associated with:

• Enhanced clearance of misfolded or aggregation-prone proteins
• Improved cellular stress resistance
• Better maintenance of proteostasis

These mechanisms are widely studied in aging biology, although most direct evidence comes from cellular and animal research rather than nutritional-dose human trials (R, R).

How Does Microdosed Lithium Support Mitochondria?

Mitochondrial function declines with age, contributing to reduced energy production, increased oxidative stress, and impaired cellular resilience (R).

In model organisms and experimental systems, lithium has been linked to improvements in mitochondrial function and stress resistance. In C. elegans, lithium treatment was shown to mitigate age-related decline in mitochondrial turnover and energetics. (R)

Mechanistically, lithium’s modulation of stress-response pathways and redox signaling may help:

• Improve mitochondrial efficiency under stress
• Reduce oxidative damage
• Support cellular energy balance

Most of these findings come from preclinical research; direct human data at nutritional microdoses remain limited. (R, R)

How Does Lithium Reduce Inflammaging?

Chronic low-grade inflammation, often referred to as inflammaging, is a key contributor to age-related cognitive and physical decline. (R)

Lithium has demonstrated anti-inflammatory effects in experimental and clinical contexts, particularly within the brain. In cellular and animal studies, lithium reduces pro-inflammatory signaling and modulates microglial activation. (R)

In clinical psychiatric populations, lithium treatment has been associated with neuroprotective effects and improved markers related to neuronal resilience. (R)

Additionally, experimental data suggest lithium may influence neural progenitor cell biology and neurogenesis, although these findings largely come from preclinical or therapeutic-dose research. (R)

Together, these findings support the hypothesis that lithium interacts with pathways involved in inflammation and brain aging, though long-term randomized trials at microdose levels are still needed.

What Is the Difference Between Microdosed Lithium and Pharmaceutical Lithium?

Microdosed Lithium	Pharmaceutical Lithium
~0.3–3 mg elemental lithium per day	~300–1200 mg lithium salts per day
Nutritional-level intake aimed at supporting healthy aging biology	Prescribed to treat bipolar disorder and other psychiatric conditions
Does not require blood-level monitoring at nutritional doses	Requires medical supervision and regular blood monitoring
Included in NOVOS Core (1 mg elemental lithium)	Available by prescription only

NOVOS CORE & Lithium

At just 1 mg per serving, the microdosed lithium in NOVOS Core supports your biology without side effects, offering a gentle but powerful tool to promote healthy aging.