Only certain kinds, says reader.
Is cinnamon Good For You?
First, it is important to distinguish “true” (Ceylon) cinnamon from common (“cassia”) cinnamon. There is a glut of products sold and falsely labeled as “Ceylon” cinnamon—which are actually the cheaper cassia from China and Indonesia. Cassia, unlike Ceylon cinnamon, is slightly hepatotoxic and should not be taken as a supplement on a regular basis.
When you eat cinnamon, one of its breakdown products (metabolites) is the antioxidant sodium benzoate (NaB), a widely used food preservative, and a stabilizer in wine-making, added to stop fermentation. NaB’s oral toxicity is roughly equivalent to that of table salt (sodium chloride).
The potential benefits of cinnamon—or its metabolite NaB—in muscle-wasting diseases (e.g., sIBM, ALS) are as follows:
1. It induces muscle growth by upregulating ciliary neurotrophic factor (CNTF), which upregulates follistatin and p21-activated kinase (Pak1), thereby downregulating the muscle atrophy factors myostatin and activin. CNTF also controls muscle wasting in normal aging.
2. NaB is being investigated for treatment of Parkinson’s and Alzheimer’s [300-304], schizophrenia [306-311], and to enhance cognition in healthy persons . In one study, oral administration of either cinnamon or its metabolite NaB suppressed tau phosphorylation, amyloid-beta (Aβ) fibril formation and neuronal degeneration in the hippocampus in a transgenic mouse model of Alzheimer’s disease . Notably, tau phosphorylation and Aβ fibril formation are also hallmarks of sIBM, albeit in sIBM they occur in skeletal muscle as opposed to hippocampal neurons.
3. NaB increases the excretion of ammonia and excess amino acids (e.g., glutamine and glycine), hence is used clinically to treat urea cycle disorders. The benefits of depleting glutamine are discussed under (polyQ). Glycine has been found to be elevated in amyotrophic lateral sclerosis (ALS) . Of possible relevance is that TDP-43 contains a glycine-rich domain that enables TDP-43-mediated protein aggregation [313-315]. Glycine transporters are being investigated as clinical targets for retinal neurodegeneration .
Other effects of cinnamon/NaB not directly relevant to sIBM are that they lower blood sugar, and have variously been used to treat rheumatoid arthritis and hepatic encephalopathy.
300. Journal of Neuroimmune Pharmacology June 2012, Volume 7, Issue 2, pp 424–435 Sodium Benzoate, a Metabolite of Cinnamon and a Food Additive, Upregulates Neuroprotective Parkinson Disease Protein DJ-1 in Astrocytes and Neurons Saurabh Khasnavis and Kalipada Pahan. https://link.springer.com/article/10.1007%2Fs11481-011-9286-3
301. Journal of Neuroimmune Pharmacology June 2013, Volume 8, Issue 3, pp 739–755 Up-Regulation of Neurotrophic Factors by Cinnamon and its Metabolite Sodium Benzoate: Therapeutic Implications for Neurodegenerative Disorders Arundhati Jana, Khushbu K. Modi, Avik Roy, John A. Anderson, Richard B. van Breemen, Kalipada Pahan. https://link.springer.com/article/10.1007%2Fs11481-013-9447-7
302. Saurabh Khasnavis, Kalipada Pahan. Cinnamon Treatment Upregulates Neuroprotective Proteins Parkin and DJ-1 and Protects Dopaminergic Neurons in a Mouse Model of Parkinson’s Disease. Journal of Neuroimmune Pharmacology, 2014; DOI: 10.1007/s11481-014-9552-2 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4167597/
303. Lin, C.H.; Chen, P.K.; Chang, Y.C.; Chuo, L.J.; Chen, Y.S.; Tsai, G.E.; Lane, H.Y. Benzoate, a d-amino acid oxidase inhibitor, for the treatment of early-phase alzheimer disease: A randomized, double-blind, placebo-controlled trial. Biol. Psychiatry 2014, 75, 678–685. https://www.biologicalpsychiatryjournal.com/article/S0006-3223(13)00739-7/fulltext
304. Modi, K.K.; Roy, A.; Brahmachari, S.; Rangasamy, S.B.; Pahan, K. Cinnamon and its metabolite sodium benzoate attenuate the activation of p21rac and protect memory and learning in an animal model of alzheimer’s disease. PLoS ONE 2015, 10, e0130398. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4478015/
305. Piper, J.D.; Piper, P.W. Benzoate and sorbate salts: A systematic review of the potential hazards of these invaluable preservatives and the expanding spectrum of clinical uses for sodium benzoate. Compr. Rev. Food Sci. Food Saf. 2017, 16, 868–880. https://onlinelibrary.wiley.com/doi/full/10.1111/1541-4337.12284
306. Biol Psychiatry. 2018 Sep 15;84(6):422-432. doi: 10.1016/j.biopsych.2017.12.006. Sodium Benzoate, a D-Amino Acid Oxidase Inhibitor, Added to Clozapine for the Treatment of Schizophrenia: A Randomized, Double-Blind, Placebo-Controlled Trial. Lin CH, Lin CH, Chang YC, Huang YJ, Chen PW, Yang HT, Lane HY. https://www.biologicalpsychiatryjournal.com/article/S0006-3223(17)32297-7/fulltext
307. Chue, P.; Lalonde, J.K. Addressing the unmet needs of patients with persistent negative symptoms of schizophrenia: Emerging pharmacological treatment options. Neuropsychiatr. Dis. Treat. 2014, 10, 777–789. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4020880/
308. Hashimoto, K. Targeting of nmda receptors in new treatments for schizophrenia. Expert Opin. Ther. Targets 2014, 18, 1049–1063. https://www.ncbi.nlm.nih.gov/pubmed/24965576
309. 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. 2012, 7, 424–435. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3189510/
310. Lane, H.Y.; Lin, C.H.; Green, M.F.; Hellemann, G.; Huang, C.C.; Chen, P.W.; Tun, R.; Chang, Y.C.; Tsai, G.E. Add-on treatment of benzoate for schizophrenia: A randomized, double-blind, placebo-controlled trial of d-amino acid oxidase inhibitor. JAMA Psychiatry 2013, 70, 1267–1275. https://jamanetwork.com/journals/jamapsychiatry/fullarticle/1746121
311. Lin, C.Y.; Liang, S.Y.; Chang, Y.C.; Ting, S.Y.; Kao, C.L.; Wu, Y.H.; Tsai, G.E.; Lane, H.Y. Adjunctive sarcosine plus benzoate improved cognitive function in chronic schizophrenia patients with constant clinical symptoms: A randomised, double-blind, placebo-controlled trial. World J. Biol. Psychiatry 2015, 18, 1–12. https://www.ncbi.nlm.nih.gov/pubmed/26691576
312. (Praveen, 2014) Front. Synaptic Neurosci., 16 April 2014 The role of D-serine and glycine as co-agonists of NMDA receptors in motor neuron degeneration and amyotrophic lateral sclerosis (ALS)
Praveen Paul and Jackie de Belleroche* |https://doi.org/10.3389/fnsyn.2014.00010
313. Buratti, E., Brindisi, A., Giombi, M., Tisminetzky, S., Ayala, Y. M., and Baralle, F. E. (2005). TDP-43 binds heterogeneous nuclear ribonucleoprotein A/B through its C-terminal tail. J. Biol. Chem. 280, 37572–37584. doi: 10.1074/jbc.M505557200
314. D’ambrogio, A., Buratti, E., Stuani, C., Guarnaccia, C., Romano, M., Ayala, Y. M., et al. (2009). Functional mapping of the interaction between TDP-43 and hnRNP A2 in vivo. Nucleic Acids Res. 37, 4116–4126. doi: 10.1093/nar/gkp342
315. Buratti, E., and Baralle, F. E. (2012). TDP-43: gumming up neurons through protein-protein and protein-RNA interactions. Trends Biochem. Sci. 37, 237–247. doi: 10.1016/j.tibs.2012.03.003
316. Glycine transporter type 1 (GlyT-1) is a potential therapeutic target in retinal neurodegenerative disorders http://semmelweis.hu/pharmacology/kutatas/neurofarmakologiai-kutatocsoport/glycine-transporter-type-1-glyt-1-potential-therapeutic-target-in-retinal-neurodegenerative-disorders/