Rush University: Cinnamon to halt the progression of Parkinson's disease

Initial note: This article was previously published and has been updated according to scientific and informative criteria to offer a clear, balanced, and verifiable summary of research on cinnamon and Parkinson's disease. The purpose is informative: it does not replace medical advice. If you have clinical concerns, consult a healthcare professional.

IN BRIEF

• Cinnamon (particularly Cinnamomum verum) can be metabolized into sodium benzoate which, in animal models, shows neuroprotective and neurotrophic effects.
• Studies in mice indicate that sodium benzoate can increase protective proteins (DJ-1, Parkin), neurotrophins (GDNF, BDNF), and improve motor and cognitive behaviors.
• Evidence is predominantly preclinical; there is no robust clinical evidence that cinnamon halts disease progression in humans.
• There are important differences between types of cinnamon: Cassia contains coumarin (liver risk at high doses) while Ceylon contains trace amounts.

Abstract: what does science say?

Research conducted by the Rush University group indicates that components of cinnamon can be metabolized into sodium benzoate (NaB), a molecule studied for its anti-inflammatory and neurotrophic properties. In murine models of neurodegeneration and in cell cultures, sodium benzoate increased the production of neurotrophic factors, protected dopaminergic neurons, and improved certain behavioral parameters. However, this evidence remains experimental: clinical translation requires controlled studies in humans to evaluate efficacy, dosages, product form, and safety. There are safety signals (e.g., coumarin in Cassia) that necessitate caution in long-term or high-dose use.

MAIN SECTION

What cinnamon and its relevant metabolite are

"Cinnamon" refers to the bark and preparations of various species of the genus Cinnamomum. The two most common commercially are Cinnamomum verum (Ceylon, "true") and Cinnamomum cassia (Cassia or "Chinese"). From a chemical perspective, cinnamon contains many active molecules; a relevant metabolic pathway is the conversion, through hepatic metabolism, of some components into sodium benzoate (NaB), a molecule already known as a food preservative and with pharmacological uses in metabolic disorders. The literature also indicates that chemical composition varies between species: Cassia can contain significant amounts of coumarin, a substance associated with liver risks if taken in excess, while Ceylon contains only trace amounts [1].

Proposed biological mechanisms

In experimental models, sodium benzoate appears to act on multiple fronts: reduction of pro-inflammatory activation of microglia and astrocytes, activation of signaling pathways that promote the synthesis of neurotrophins (e.g., BDNF, NT-3, GDNF), and an increase in protective proteins associated with Parkinson's such as DJ-1 and Parkin. These actions have been observed both in cell cultures and in orally treated animals, where NaB was detectable in blood and brain tissue, suggesting that the metabolite crosses the blood-brain barrier [2][3][4][5].

Main experimental evidence

The Rush research group has published a series of preclinical studies showing multiple effects of cinnamon/NaB. In cultures and in mice, NaB reduced inflammatory markers in glial cells [2] and increased DJ-1 in astrocytes and neurons [3]. In murine models of Parkinsonian syndrome, cinnamon supplementation prevented the loss of proteins like Parkin and DJ-1, preserved dopaminergic neurons, and improved motor functions [4]. Other studies by the group have linked NaB to an increase in trophic factors like GDNF through CREB activation, with protection in the substantia nigra in MPTP models [5]. Similar results were observed in experiments on memory and learning, where one month of administration improved hippocampal plasticity in mice with memory deficits [6].

PRACTICAL SECTION

What it means in practice

For the general public: the results are interesting but do not constitute proof that eating cinnamon slows or stops Parkinson's disease in humans. The available research is mostly on animal or cellular models; these models are useful for understanding biological mechanisms and generating hypotheses, but they do not guarantee therapeutic effects in humans. Some practical points:

• Currently, there are no clinical recommendations suggesting the use of cinnamon as a therapy for Parkinson's.
• If moderate dietary use is considered, cinnamon is generally safe; however, Cassia contains coumarin which, if consumed in high doses and for prolonged periods, can increase the risk of liver damage. For this reason, studies suggest caution in choosing the species (Ceylon vs Cassia) and the amount consumed [1].
• Any therapeutic or integrative change should be discussed with a neurologist or trusted doctor, especially in the presence of liver diseases or while on medication affecting the liver.

KEY POINTS TO REMEMBER

• Cinnamon can be converted into sodium benzoate, which in experimental models shows anti-inflammatory and neurotrophic effects [2][1].
• In mice, NaB has been associated with an increase in protective proteins linked to Parkinson's (DJ-1, Parkin) and neurobehavioral improvements [3][4][5].
• The evidence is preclinical: controlled clinical trials demonstrating a clinical effect in human disease are lacking.
• There are safety concerns to consider (coumarin in Cassia): the quality and species of cinnamon matter [1].
• Before using supplements or changing your diet for therapeutic reasons, consult a doctor.

LIMITATIONS OF EVIDENCE

It is crucial to distinguish between types of evidence:

• Observational studies and in vitro/animal studies can indicate biological plausibility but do not prove causality in humans. Many of the favorable results come from murine models or cell cultures; these models do not fully reproduce the complexity of the human brain and the disease.
• Methodological limitations: dosages, route of administration, composition of the cinnamon preparation, plant species, and duration of treatment vary between studies. This makes it difficult to translate experimental protocols into safe and applicable clinical recommendations.
• Context variability: the metabolic state, concomitant pharmacology, age, and liver function of the individual can modify risk/benefit.
• Need for caution: randomized, controlled clinical trials with follow-up are needed to establish efficacy, optimal dosages, and safety profile in humans.

Editorial Conclusion

Research led by the Rush University group has highlighted plausible mechanisms for a possible role of cinnamon's metabolite, sodium benzoate, in modulating glial inflammation, increasing neurotrophic factors, and protecting dopaminergic neurons in experimental models. These results are scientifically relevant because they offer research avenues and potential molecular targets. However, clinical translation is not automatic: currently, the scientific community has robust preclinical evidence but not clinical proof that justifies the use of cinnamon as a therapy for Parkinson's disease. A cautious approach remains appropriate, based on well-designed clinical studies, quality control of cinnamon extracts, and safety monitoring, especially hepatic safety.

Editorial Note

This article has been updated to reflect available peer-reviewed literature and to clarify the limitations and potential of the research. The text is informative and aimed at the general public; it does not replace personalized medical advice.

SCIENTIFIC RESEARCH

Cited sources (Vancouver). Click on the DOI to consult the original article.

1. Creasy R, et al. Cassia cinnamon as a source of coumarin in cinnamon‑flavored food and food supplements in the United States. J Agric Food Chem. 2013;61(27):6785–6791. https://doi.org/10.1021/jf4005862 [1]
2. Jana A, Modi KK, Roy A, Anderson JA, van Breemen RB, Pahan K. Up‑regulation of neurotrophic factors by cinnamon and its metabolite sodium benzoate: therapeutic implications for neurodegenerative disorders. J Neuroimmune Pharmacol. 2013;8(3):739–755. https://doi.10.1007/s11481-013-9447-7 [2]
3. Brahmachari S, Jana A, Pahan K. Sodium benzoate, a metabolite of cinnamon and a food additive, reduces microglial and astroglial inflammatory responses. J Immunol. 2009;183(9):5917–5927. https://doi.org/10.4049/jimmunol.0803336 [3]
4. Khasnavis S, Pahan K. Sodium benzoate, a metabolite of cinnamon and a food additive, upregulates neuroprotective Parkinson disease protein DJ‑1 in astrocytes and neurons. J Neuroimmune Pharmacol. 2011;7(2):424–435. https://doi.org/10.1007/s11481-011-9286-3 [4]
5. Khasnavis S, Pahan K. Cinnamon treatment upregulates neuroprotective proteins Parkin and DJ‑1 and protects dopaminergic neurons in a mouse model of Parkinson's disease. J Neuroimmune Pharmacol. 2014;9(4):569–581. https://doi.org/10.1007/s11481-014-9552-2 [5]
6. Patel D, Jana A, Roy A, Pahan K. Cinnamon and its metabolite protect the nigrostriatum in a mouse model of Parkinson’s disease via astrocytic GDNF. J Neuroimmune Pharmacol. 2019;14(3):503–518. https://doi.org/10.1007/s11481-019-09855-0 [6]
7. Modi KK, Rangasamy SB, Dasarathi S, Roy A, Pahan K. Cinnamon converts poor learning mice to good learners: implications for memory improvement. J Neuroimmune Pharmacol. 2016;11(4):693–707. https://doi.org/10.1007/s11481-016-9693-6 [7]
8. Kundu M, Mondal S, Roy A, Martinson JL, Pahan K. Sodium benzoate, a food additive and a metabolite of cinnamon, enriches regulatory T cells via STAT6‑mediated upregulation of TGF‑β. J Immunol. 2016;197(8):3099–3110. https://doi.org/10.4049/jimmunol.1501628 [8]
9. Rangasamy SB, Dasarathi S, Nutakki A, Mukherjee S, Nellivalasa R, Pahan K. Stimulation of dopamine production by sodium benzoate, a metabolite of cinnamon and a food additive. J Alzheimers Dis Rep. 2021;5(1):295–310. https://doi.org/10.3233/ADR-210001 [9]

Legend: numbers in square brackets in the text correspond to the references in the list above.