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New research suggests that long-term oral nicotine intake helps preserve motor abilities and boosts NAD⁺ levels in older male mice, resulting in behaviors typically observed in younger animals.

Key Findings

  • Continuous oral nicotine consumption throughout much of the lifespan helped older male mice retain exploratory behaviors typical of youth.
  • A behavioral aging clock—based on actions and tissue metabolites—indicated that nicotine-treated aged mice appeared biologically younger.
  • Nicotine intake also altered gut microbiome composition, lowered levels of the harmful ceramide (a metabolite linked to NAD⁺ degradation), and increased NAD⁺ levels in muscles, pancreas, and liver.

Motor Function Protected by Nicotine

Since aging often impairs coordination and stamina, researchers at the Chinese Academy of Sciences assessed nicotine’s impact using various behavior tests. They found that older mice given high-dose nicotine (0.5 g/L in water) for 22 months—roughly equivalent to 65 human years—showed improved coordination, endurance, reduced anxiety, and exhibited exploration behavior similar to that of younger mice.

No Significant Cognitive Impact

Cognitive assessments showed that long-term nicotine neither improved nor harmed memory performance in aging mice. Age-related cognitive changes appeared unaffected by nicotine.

A Dose-Dependent “Younger” Profile

Using their aging clock, researchers noted that aged mice on high-dose nicotine displayed profiles resembling those of much younger mice. In contrast, lower doses produced intermediate results.

Nicotine Alters Gut Bacteria

Nicotine intake, especially at higher doses, increased the ratio of beneficial to harmful gut bacteria—a known marker of aging—and reduced ceramide levels, a byproduct linked to NAD⁺ decline.

Elevated NAD⁺ in Key Tissues

A high nicotine dose led to significant increases in NAD⁺ concentrations in the liver, pancreas, and muscle—but not in white adipose tissue—helping combat the typical age-related drop in NAD⁺.

These NAD⁺ increases corresponded with decreased ceramide and improved exploratory behaviors, mounting evidence that nicotine may rejuvenate metabolic and motor function via gut and metabolic pathways.

“In summary, our findings reveal a previously underappreciated role for oral nicotine in promoting systemic metabolic resilience and preserving motor function during aging,” the researchers concluded.

Implications for Human Aging

If similar effects occur in humans, nicotine—if consumed without the harmful toxins of smoking—might help preserve motor function as we age. However, due to nicotine’s addictive nature and potential to lead to smoking or vaping, the researchers recommend exploring non-addictive compounds with similar molecular effects that could safely elevate NAD⁺ and protect motor abilities.


Model & Dosage Used in the Study:

  • Subjects: C57BL/6J male mice, starting at 7 weeks (equivalent to ~16 human years), studied until 24 months (~69 human years)
  • Dose: Nicotine in drinking water at 0.25 g/L (low dose) and 0.5 g/L (high dose) for 22 months

Summary

  • Preserved motor abilities in aged mice with long-term oral nicotine.
  • No cognitive benefit or harm observed.
  • Younger metabolic profile indicated by behavioral and molecular assessments.
  • Gut microbiome changes and NAD⁺ increases in key tissues noted.
  • Promising, but risky for humans, given nicotine’s addictive properties—future research could explore safer analogs.