Cognitive breakthrough: Common food preservative shows promise in Alzheimer’s treatment
By willowt // 2025-08-25
Copy
 
  • Sodium benzoate in higher doses (750–1,000 mg/day) improved cognitive function and reduced blood amyloid beta levels in Alzheimer’s patients.
  • The preservative may protect brain cells by blocking enzymes that degrade a key neurotransmitter, D-serine, and reducing oxidative stress.
  • No significant side effects noted; doses tested exceed typical dietary consumption but align with prior schizophrenia studies.
  • Outperforms current therapies in cost, ease of use and safety, addressing critical gaps in treating dementia.
  • Larger trials needed to confirm benefits and clarify if blood amyloid reductions mirror brain changes.
Sodium benzoate, a cheap preservative widely used in sodas and packaged foods, has been linked to improved cognitive function and reduced Alzheimer’s-linked proteins in a recent clinical trial. Researchers found daily doses of the compound at 750 or 1,000 milligrams for 24 weeks boosted memory skills and lowered amyloid beta levels in patients with mild Alzheimer’s, offering a potential low-cost, safe alternative to costly treatments.

Study details: A novel approach to an age-old problem

The randomized trial, led by Dr. Hsien-Yuan Lane at China Medical University, tested 149 patients aged 50-90 with mild Alzheimer’s, assigned to receive placebo or 500, 750 or 1,000 mg of sodium benzoate daily. After six months, participants on the higher doses showed significant improvements in memory recall, word retention and orientation. Critically, their blood levels of amyloid beta 1–40—a protein fragment that clumps into brain plaques—also dropped, a hallmark of the disease. Dr. Thomas Holland, a clinician-researcher at the Rush Institute for Healthy Aging, emphasized the dual impact: “Sodium benzoate may clear amyloid ‘debris’ and protect cellular communication—unlike current drugs that target amyloid alone.” The lower 500 mg dose showed no effect, suggesting a dose-response relationship. Notably, participants with higher baseline amyloid beta 1–42 (a neuroprotective variant) saw greater cognitive gains, hinting that sodium benzoate’s effectiveness may depend on individual disease progression.

How might it work? Clues in cellular machinery

Sodium benzoate’s mechanisms remain under study, but hints emerge from lab research. The compound appears to:
  • Protect key neurotransmitters: By blocking the enzyme D-amino acid oxidase, it preserves D-serine, a molecule crucial for neuron communication. Low D-serine levels correlate with Alzheimer’s and schizophrenia, disorders where the preservative has shown promise in previous studies.
  • Neutralize oxidative stress: Antioxidant effects may shield neurons from damage, boosting beneficial proteins like catalase and glutathione. Earlier trials in Alzheimer’s patients found these levels rose during benzoate treatment.
  • Reduce inflammation: It dampens brain immune cell overactivity linked to neurodegeneration, another pathway behind cognitive decline.
As Holland noted, its multi-pronged approach resembles heart disease care: “We target cholesterol and blood pressure, not one isolated issue.”

Changing the game: Safety, cost and accessibility

Current Alzheimer’s drugs, such as monoclonal antibodies, cost thousands annually, are delivered via infusion, and carry risks like brain swelling. Sodium benzoate’s oral dosing, low expense and tolerance in the trial—no serious side effects reported—could make it a first-line treatment. Lane pointed to prior work in schizophrenia, where up to 2,000 mg/day was safe. However, he stressed cautious optimism: “We need larger trials to understand long-term safety, especially at high doses. Interactions with other preservatives or compounds remain a question.” The FDA allows sodium benzoate in foods at 0.1%, but the recommended therapeutic dose (up to 1,300 mg/day for a 150-lb adult per WHO guidelines) far exceeds dietary intake.

Looking ahead: Overcoming barriers to translation

While promising, gaps exist. Amyloid measured in blood, not the brain, complicates comparisons to standard Alzheimer’s tests like spinal taps or PET scans. Holland likens this to “checking downstream river pollution to infer upstream activity—informative but not definitive.” Future studies must link blood amyloid reductions to clinical outcomes like slowed dementia progression. Large-scale trials are also needed to confirm benefits and monitor long-term safety.

A path forward for affordable dementia care?

Sodium benzoate’s potential is transformative—turning a pantry staple into a potential blockbuster therapy. Its safety, accessibility, and multi-target action align with urgent needs for affordable solutions to Alzheimer’s, a disease affecting 5.3 million Americans alone. Yet challenges remain: While early results are encouraging, robust evidence linking blood biomarkers to brain health and establishing long-term efficacy is essential. For now, this study underscores a thrilling possibility—that dining room to medicine cabinet, the road to dementia prevention may be shorter than we thought. Sources for this article include: TheEpochTimes.com Nature.com PubMed.gov ScienceDirect.com
Copy