What is the coumarin content difference between cassia and Ceylon cinnamon and how does it affect liver risk?

Checked on January 25, 2026
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Executive summary

Cassia cinnamon contains orders of magnitude more coumarin than Ceylon (true) cinnamon—typical cassia powders show coumarin in the low thousands of mg/kg while Ceylon samples are near or below detection limits—creating a real potential for chronic coumarin exposure from routine cassia use [1] [2] [3]. Regulatory bodies set a tolerable daily intake (TDI) for coumarin because high intake has been associated with elevated liver enzymes and, in severe cases, liver inflammation in susceptible subjects, yet human case-series and cohort data remain mixed and mechanisms are not fully resolved [3] [4].

1. Cassia versus Ceylon — how big is the chemical gap?

Analyses of retail cinnamon repeatedly show that cassia varieties contain much higher coumarin concentrations: multiple surveys report cassia ranging from roughly 1,740–7,670 mg per kg and even up to 12,200 mg/kg in some reports, while tested Ceylon samples were typically below detection or only a few hundred mg/kg at most—orders of magnitude lower and often effectively trace amounts [2] [1] [3]. Published summaries state cassia can contain up to about 1% coumarin whereas true Ceylon cinnamon contains only trace amounts (~0.004% in some cited figures), a difference frequently expressed as hundreds-fold to two-hundred-fifty-fold lower in Ceylon [1] [5].

2. What those concentrations mean for everyday intake

Because typical household measures concentrate the spice, a single teaspoon (about 2.6 g) of cassia cinnamon can deliver several milligrams of coumarin—estimates put that between roughly 6.9 and 18 mg per teaspoon depending on the cassia sample—enough that daily use of a teaspoon could exceed conservative regulatory daily intake guidance for many adults [6] [3]. Regulators such as EFSA and national institutes use a TDI of 0.1 mg/kg body weight/day (and some reassessments suggest similar or slightly different benchmarks), so routine cassia use—especially in children or small adults—can push exposure above those limits [3] [2].

3. Liver risk: animal data, human signals, and the uncertainty

Animal studies show coumarin can cause liver and other organ toxicity and has tumorigenic effects in rodents, which underpins regulatory caution; human data are less definitive—observational reports and a Japanese study of Kampo medicines found liver-test abnormalities but did not demonstrate a clear dose–response above or below the TDI in that cohort, leaving causality and individual susceptibility unresolved [5] [4]. Regulatory agencies note that in especially sensitive persons even comparatively small coumarin doses can cause reversible liver damage, and surveys of food products highlight that chronic elevated intake "can lead to elevation of liver enzymes, and in severe cases to inflammation of the liver"—a conservative stance intended to protect susceptible subgroups [3] [7].

4. Who is most at risk and why consumption patterns matter

Risk concentrates in people who consume cinnamon daily in measurable amounts—habitual users of supplements, daily smoothie or porridge fans, children with lower body weight, and people with pre-existing liver disease or on hepatotoxic drugs—because cumulative coumarin exposure, not single small culinary uses, drives concern [6] [7]. Authorities such as Germany’s BfR explicitly recommend Ceylon for regular consumers because its low coumarin levels substantially reduce the probability of exceeding intake limits [3] [7].

5. Practical implications and limits of available evidence

From a pragmatic standpoint, switching to verified Ceylon cinnamon markedly reduces coumarin exposure—practical guides and tests for quill appearance or sourcing are promoted because many supermarket products are cassia and powder labels often omit species, which complicates consumer choices [8] [7]. At the same time, human data that would definitively quantify liver risk thresholds, identify genetic susceptibility factors (e.g., CYP2A6 polymorphisms) and define safe long-term therapeutic use are incomplete; one clinical series found no significant difference in liver-test abnormalities around the TDI, underscoring persistent uncertainty [4].

6. Clear takeaway

Scientifically, the difference is simple and consequential: cassia contains substantially more coumarin than Ceylon (often by hundreds-fold), and that higher content can push routine consumers above regulatory tolerable intake levels with potential for liver enzyme elevations or, in rare susceptible cases, liver inflammation—so those using cinnamon daily, giving it to children, or with liver concerns should prefer verified Ceylon or limit cassia intake [1] [2] [3] [6]. Existing research supports precaution, yet gaps in human mechanistic and susceptibility data mean absolute risk estimates remain imprecise [4].

Want to dive deeper?
How much cassia cinnamon (in grams or teaspoons) would exceed EFSA's TDI for various body weights?
What are the known genetic or medical risk factors that increase human susceptibility to coumarin hepatotoxicity?
How often is 'Ceylon' cinnamon mislabeled in retail markets and what tests verify true Ceylon cinnamon?