Microdoses for every day: cadmium as a factor of premature aging

A paper published in Current Developments in Nutrition found that even low-level dietary cadmium intake leads to its deposition in the body and increases signs of aging, including worsening cognitive functions and increasing oxidative stress. This is not a story about acute poisoning: the authors simulated everyday “microdoses” from the diet, and still got an acceleration of “senile” phenotypes.

Background

Cadmium is a cumulative toxicant with a very long tail. It accumulates mainly in the kidneys and liver, and the biological half-life is estimated to be decades; therefore, regulators consider the cumulative (monthly/weekly) dose to be important. WHO/FAO (JECFA) has set a PTMI of 25 µg/kg bw per month, EFSA confirms a TWI of 2.5 µg/kg per week as the threshold associated primarily with the risk of renal toxicity.

• Where does it come from in a "regular" person? For non-smokers, the main contribution is food (crops that absorb cadmium from the soil/fertilizers), for smokers - also tobacco smoke (the tobacco plant actively accumulates cadmium). According to EFSA and WHO, significant sources are: cereals and grain products, vegetables (especially leafy ones), cocoa/chocolate, aquatic mollusks, and regionally - rice; smokers usually have twice as many cadmium biomarkers.
• Who is more vulnerable. With iron deficiency, the intestines increase the transporters of divalent metals (DMT1), and the absorption of cadmium increases; pregnancy and childhood increase sensitivity. Smoking increases the total dose many times over.
• How to measure “cadmium load”. In clinical and population studies, two simple markers are used: blood cadmium reflects recent intake, and urine cadmium reflects the accumulated dose/“store” in the body (especially in the kidneys). It is U-Cd that is more often used in long-term cohort studies and for calculating risk “thresholds” for renal effects.
• Why the topic is related to aging and cognition. Chronic cadmium triggers oxidative stress, mitochondrial dysfunction, maintains low-grade inflammation, and can induce cellular senescence (↑SA-β-gal, p16^INK4a). These mechanisms are the basic “drivers” of tissue aging and cognitive decline. In reviews and modeling studies, cadmium has been repeatedly associated with memory/learning impairment, and in human cohorts (NHANES, etc.), higher Cd levels (in blood/urine) were associated with worse cognitive test results and even with the risk of dementia/Alzheimer's mortality.
• Regional picture and thresholds. According to EFSA estimates, for some Europeans the dietary intake is close to the TWI, and for children the relative load (per kg of body weight) is higher; in China and some regions of Asia, high rice consumers may exceed the monthly JECFA threshold. This explains the interest in even “low” household doses in the diet.
• Why is it that “dietary low doses” are important scientifically? Because of the extremely long half-life, even trace amounts daily can, when “wound up,” produce measurable stress and biological effects—not acute poisoning, but acceleration of aging processes (via ROS stress, mitochondria, inflammation, and senescent cells). Hence the design of the new work: to simulate realistic background intake and look at aging phenotypes and cognitive tests.
• Practical context for health care. Consistent findings:
  • Not smoking is the most powerful measure to reduce cadmium load.
  • Diversification of the diet (cereals/sources of cocoa and leafy greens from controlled chains), diversity of supply geography.
  • Prevention and correction of iron deficiency, which reduces the absorption of cadmium.
  • For monitoring, U-Cd is a priority as a marker of long-term contact.

What exactly did they do?

The researchers modeled long-term, low-level dietary exposure to cadmium and then tested how it would affect the “biology of aging”: behavioral/cognitive tests and biomarkers of oxidative stress. In parallel, they looked at whether cadmium accumulates in tissues at such “low” doses. The conclusion is clear: yes, it does accumulate, and this is enough to shift aging phenotypes to our disadvantage.

Main results

• Cognitive functions were impaired by low-level cadmium compared to controls.
• An increase in oxidative stress (damage from reactive oxygen species) was noted, a classic mechanism associated with aging and neurodegeneration.
• Cadmium was deposited in the body even at “small” dietary doses, confirming that long-term background consumption has a cumulative effect.

Why is this important?

Cadmium is one of the most insidious environmental toxicants: it accumulates over decades (the biological half-life is estimated at 16–30 years) and is associated with damage to the kidneys, bones, blood vessels, and nervous system. The new work adds to the puzzle: even levels close to everyday dietary levels can accelerate brain aging and increase systemic oxidative stress.

Where does "dietary cadmium" come from?

Most often, from products where the soil/water is rich in cadmium or appropriate fertilizers are used: rice, grains, leafy vegetables, cocoa, and shellfish; a separate large share is smoking (tobacco smoke is rich in cadmium). Reviews in recent years emphasize the need to revise the permissible levels and take into account regional differences.

How does this fit into the bigger picture?

Independent studies have linked chronic cadmium exposure to dementia/reduced cognitive performance in the elderly and, in model organisms (flies, rodents), to premature aging and neurodegeneration via mitochondrial dysfunction, inflammation, and ferroptosis-like processes. The new paper reinforces this line of thought even at low dietary exposure levels.

What to do "in practice" today

This is not a reason to panic, but there are common sense steps to reduce the cumulative dose:

• Not smoking (or quitting) is one of the most powerful contributions to reducing your cadmium load.
• Diversify cereals (not just rice), wash/soak leafy greens thoroughly, do not overuse cocoa/chocolate in children.
• Try to choose products from regions with heavy metal monitoring.
• Supporting antioxidant defenses with your diet (vegetables/fruits, sources of selenium and zinc) is not a “detox,” but it helps keep oxidative stress, one of the key pathways for cadmium damage, under control. (These tips are not meant to replace clinical recommendations; discuss diet with your doctor if you have kidney disease, etc.)
  A review of dietary cadmium reminds you that it’s not just the average concentration in a product that matters, but also the frequency of consumption—the risk is compounded “by the penny.”

Limitations and what's next

The authors studied low-level but controlled exposure; the next step is long-term cohort studies with precise dietary intake, biomarkers of accumulation (urine/blood) and neurocognitive outcomes, and an assessment of how much risk is reduced by adjusting key dietary sources of cadmium.

Source: Go YM et al. The Impact of Low Dietary Level Cadmium Exposure on Aging Phenotypes. Current Developments in Nutrition, May 2025.