Here’s the frustrating part. The science on cinnamon is real: multiple published human RCTs on the active fraction, a responder split from the foundation trial that’s hard to ignore (a manufacturer-reported analysis, not published in the peer-reviewed paper itself, found roughly 83% of the cinnamon group versus 33% of placebo showed a fasting-glucose change), dose-response behavior consistent with a receptor-level mechanism, and several complementary pathways that each move on their own timeline. The research base behind cinnamon’s role in supporting healthy glucose metabolism is reasonably solid.*
What’s sitting on the shelf is a different story. With rare exceptions, the market implementation of that science is a measurement problem: big polyphenol swings between batches of the same product, research citations pinned to doses the product doesn’t actually deliver, species-authentication failures in a meaningful chunk of tested “Ceylon” products, and coumarin “safety” that’s asserted in marketing copy rather than quantified against the EFSA TDI.
You can’t run a meaningful n=1 protocol on a variable you can’t control. And potency that drifts batch to batch is, by definition, an uncontrolled variable.
So here’s what we built for people who track this stuff. SoActive Cinnamon™ is a dual-species cinnamon complex built around a clinically studied, HPLC-standardized water-soluble extract that supports healthy glucose metabolism.* It delivers 500mg of a standardized water-soluble cinnamon extract (Cinnulin PF®), the same 500mg/day dose used in the Ziegenfuss et al. 2006 study, alongside 800mg USDA Organic Ceylon cinnamon (Cinnamomum verum, ~0.004% coumarin, far lower than typical Cassia products). That extract is HPLC-verified to ≥3% Type-A procyanidin polyphenol polymers.
Not aggregate polyphenol content: the specific molecular fraction the literature ties to insulin-receptor function. The dual-species design pairs fast water-soluble extract kinetics (peak plasma concentration for Type-A polymers around 30 to 60 minutes) with fiber-bound Ceylon polyphenols that come on more slowly over several hours. Published Certificates of Analysis are available for independent verification.*
These statements have not been evaluated by the Food and Drug Administration. This product is not intended to diagnose, treat, cure, or prevent any disease. It is intended to support already-healthy metabolic function, not to treat prediabetes, metabolic syndrome, PCOS, or diabetes. Consult your healthcare provider before starting any new supplement regimen. The asterisk () throughout this article refers to this disclaimer.*
How the Dual-Species Design Aims at Verifiable Metabolic Optimization
It’s the first cinnamon formulation we know of engineered specifically for evidence-driven optimizers: a Type-A-standardized extract at the exact 500mg dose from the foundation trial, batch COAs you can actually verify, and a pharmacokinetic design meant to close the single-form coverage gap.
Here’s what’s in it and why. SoActive Cinnamon™ Dual-Cinnamon Complex combines 500mg of a standardized water-soluble cinnamon extract (Cinnulin PF®), a patented 20:1 water-soluble extract of Cinnamomum burmannii that’s HPLC-verified to ≥3% Type-A procyanidin polyphenol polymers and produced through a controlled water-based purification process that strips out most of the coumarin, with 800mg of USDA Organic Cinnamomum verum powder. The two forms do different jobs on different clocks: the extract for immediate-peak kinetics around 30 to 60 minutes, the Ceylon powder for slower, fiber-bound release over several hours.
The design leans on a body of peer-reviewed human research on the Cinnulin PF® ingredient. That includes the Ziegenfuss et al. 2006 study, which reported the fasting-glucose, blood-pressure, and body-composition changes detailed later at 500mg/day (a widely cited 83% responder figure comes from a manufacturer analysis, not the published paper), and the Kort & Lobo 2014 study, which was conducted under an FDA-accepted Investigational New Drug application (IND #110123) with data-safety-monitoring-board oversight. Total daily coumarin exposure comes in around 0.03mg, well below the EFSA TDI, and the COAs are published for independent verification.*
(One thing worth being precise about: an accepted IND permits a clinical trial to proceed. It is not FDA approval or endorsement of any marketed product.) The point of pairing a clinically studied, HPLC-standardized extract with authenticated Ceylon powder is simple: give you the kind of quantifiable, CGM- and biomarker-trackable input that a rigorous n=1 protocol actually needs.*
Put another way, the dual-species approach is built to combine immediate-peak and sustained-release behavior in one dose. The water-soluble extract peaks around 30 to 60 minutes; the fiber-bound Ceylon polyphenols keep coming afterward. Single-form cinnamon products give you one kinetic profile and that’s it.
(Jump to the Multi-Pathway Mechanism section below.)
Your Skepticism About This Category Is Reasonable. Here’s What Actually Changes.
You’ve read the Ziegenfuss abstract. You noticed that some single-ingredient products deliver 250mg, half the studied dose. You went digging through independent testing and found reports of polyphenol variability across products. You’ve pulled COAs from competing products and realized that “standardized to 3% polyphenols” via a Folin-Ciocalteu colorimetric assay is not the same claim as “≥3% Type-A procyanidin polyphenol polymers” verified by HPLC. You asked two brands for a batch COA before buying, and neither one produced one.
Your conclusion, that a lot of this category is analytically weak for personal optimization, is backed by independent testing data.
The failure modes you’ve spotted are real, and they’re specific:
Generic products cite the 500mg Ziegenfuss study while shipping half the dose. You can’t assume the effect at 250mg equals the published research at 500mg. Nobody has characterized the dose-response for Type-A polymer activity as linear, so any personal biomarker data you collect on a half-dose product has no matched published reference frame.
“Clinically studied” language gets slapped on unstandardized whole-powder products. The active molecular fraction, Type-A procyanidin polyphenol polymers, isn’t standardized in whole cinnamon powder. Citing clinical studies on a standardized extract while selling generic Ceylon powder is borrowed clinical credibility from dose-mismatched research.
And Cassia-containing products rarely publish coumarin numbers. “Safe for daily use” is marketing language. The EFSA TDI calculation needs the actual coumarin content per gram of the specific raw material, which generic manufacturers either haven’t tested or won’t publish.
What HPLC standardization, dose-to-research matching, and published safety specs actually change is the list of uncontrolled variables that made your skepticism warranted in the first place. The dual-species design is built to handle the potency variance, the dose mismatch, the species-authentication gap, and the coumarin question together.
Your skepticism was reasonable. What’s different here is the implementation of the science.*
Why Most Cinnamon Formulations Fail the Criteria That Matter
The category tends to fall short for evidence-driven optimizers on four separate dimensions, and any one of them is enough to disqualify a product from a serious n=1 protocol.
Start with whole powder. Organic whole cinnamon runs a cheap $0.15 to $0.40 per serving, but it brings potency variance that’s hard to reconcile with personal data protocols. Independent product testing has reported notable polyphenol variability across cinnamon products, which makes a reproducible dose-response relationship hard to pin down.
If you’re using CGM data or quarterly panels to judge a supplement, variance that big is tough to tell apart from biological noise, and it quietly produces false negatives in your own trials. SoActive Cinnamon™’s HPLC-verified Type-A procyanidin standardization is meant to hold the molecular dose steady batch to batch, so a change you see on CGM is more likely to be the supplement and less likely to be input noise.*
Then there’s the single-ingredient extract problem. These products use a validated ingredient but usually miss on dose-to-research matching. A common online product delivers 250mg per serving, half the 500mg dose from the foundation Ziegenfuss 2006 study. This is the textbook case of borrowed clinical credibility: the ingredient is cited correctly, the dose is arbitrary, the effect size is probably attenuated relative to published data, and your personal biomarker results can’t be cleanly compared to study outcomes. SoActive Cinnamon™ delivers the 500mg standardized-extract dose alongside 800mg organic Ceylon.
Berberine deserves its own note, because it’s the obvious comparison. It has strong meta-analytic biomarker evidence, but it works through a mechanistically narrower pathway than the multi-mechanism cinnamon architecture, and it does so via a route associated with notable GI intolerance at higher doses. If you’re already managing GI sensitivity or stacking several agents, berberine’s tolerance profile creates two problems: adherence risk and confounding in biomarker attribution.
SoActive Cinnamon™’s extract is described in the literature as engaging AMPK through a distinct polyphenol-LKB1 pathway while also supporting insulin-receptor function, PTP1B activity, α-glucosidase activity, and Nrf2/NF-κB signaling. Broader footprint. The two are best understood as stack-compatible rather than substitutable, each covering ground the other doesn’t.*
Finally, the kitchen-sink formulas. Premium multi-ingredient blends sell “comprehensive pathway coverage,” but they wreck the one thing an optimizer needs most: attribution. When 12 to 15 ingredients move a biomarker together, you can’t isolate the driver, which makes the result nearly useless for refining a protocol. Worse, capsule-fill constraints usually mean no single ingredient hits its studied threshold.
A formula stacking 200mg cinnamon with berberine, banaba, gymnema, bitter melon, chromium, and vanadium can’t claim Ziegenfuss 2006’s 500mg outcomes when it’s delivering less than half the dose. SoActive Cinnamon™’s focused design, a 500mg standardized extract plus organic Ceylon, chooses mechanistic depth over taxonomic breadth.*
The Multi-Pathway Mechanism: A Molecular Reference for Protocol Design
Cinnamon’s role in supporting healthy glucose metabolism doesn’t reduce to one mechanism, and that diversity is exactly what tells you which biomarkers might move, on what timeline, and by how much. Use the following as a molecular reference for protocol design. One caveat up front: several of these pathways are characterized mostly in vitro and in preclinical models, and the onset timings are mechanistic estimates, not guaranteed personal outcomes.
Pathway 1, Insulin Receptor Autophosphorylation (estimated onset: 30 to 60 min; potentially CGM-relevant): Type-A procyanidin polyphenol polymers bind the insulin receptor β-subunit and enhance tyrosine-kinase autophosphorylation, which supports receptor activation and, in adipocyte models, enhances insulin-dependent glucose metabolism up to roughly 20-fold (Anderson et al. 2004). This is the acute insulin-support mechanism described in the literature.*
Pathway 2, PTP1B Modulation (estimated onset: 30 to 60 min): That same Type-A polymer fraction modulates protein tyrosine phosphatase 1B (PTP1B), the enzyme that dephosphorylates and switches off the insulin receptor, which effectively supports the receptor’s activation window. The dual action here, activation plus supported signaling, is mechanistically distinct from other metabolic-support approaches.*
Pathway 3, GLUT4 Transporter Mobilization (estimated onset: 30 to 90 min): Downstream of receptor activation, cinnamon polyphenols activate PI3K/Akt phosphorylation in cell models, which promotes GLUT4 vesicle translocation to the plasma membrane. GSK-3β modulation may also support glycogen synthase activity, nudging glucose toward storage as glycogen.*
Pathway 4, AMPK Activation via LKB1 (estimated onset: 30 to 120 min): Water-soluble cinnamon extract activates AMPK via LKB1 kinase in cell models (Shen et al. 2014), a route to supporting glucose uptake that doesn’t depend on insulin. Stack note: this is why cinnamon and berberine read as complementary rather than redundant. They hit AMPK through different upstream nodes, LKB1 versus mitochondrial pathways, with convergent output.*
Pathway 5, α-Glucosidase and α-Amylase Modulation (acute, dose-dependent): Ceylon cinnamaldehyde shows carbohydrate-enzyme inhibition in vitro, with reported IC50 values in the low µg/mL range (for instance, trans-cinnamaldehyde IC50 ~3.8 to 5.4 µg/mL against α-amylase; Anjali, Sadaf & Khare, Indian J Biochem Biophys, 2022). This is an in-vitro assay result only, and it isn’t evidence of a drug-equivalent effect in humans. Mechanistically it slows the rate of intestinal disaccharide hydrolysis, and it’s the one most likely to show up acutely on a postprandial CGM curve. It’s dose-dependent.*
Pathway 6, Nrf2 Transcriptional Activation (estimated onset: 4 to 8 weeks; FRAP/MDA-trackable): Trans-cinnamaldehyde induces substantial Nrf2 transcriptional activation in vitro, upregulating HO-1, NQO1, glutathione-S-transferases, and γ-GCS. That endogenous antioxidant support lines up with the FRAP increase and MDA decrease documented in Roussel et al. 2009 at the same 500mg/day dose. If your quarterly panel includes FRAP and MDA, those are the markers to watch inside a 12-week window.*
Pathway 7, NF-κB Signaling Modulation (estimated onset: 4 to 8 weeks; hs-CRP-trackable): Cinnamon polyphenols support a balanced inflammatory response by modulating IκBα phosphorylation and NF-κB nuclear translocation, with downstream effects on TNF-α, IL-6, and IL-1β signaling in cell models. Eugenol from Ceylon adds COX-2 modulatory activity in vitro. Your candidate biomarker here is hs-CRP on a quarterly panel.*
Pathway 8, Gut Microbiome Prebiotic Support (estimated onset: 4 to 8 weeks; microbiome-panel-trackable): Ceylon’s dietary-fiber content feeds Bifidobacterium and Akkermansia muciniphila. Preclinical and early human data link cinnamon fiber to increases in beneficial taxa and to production of short-chain fatty acids (butyrate, propionate) that signal through GPR41/GPR43 receptors. This one runs on a multi-week adaptation timeline.*
A quick word on pharmacokinetics, because formulation type changes everything about bioavailability and coverage. Water-soluble cinnamon extracts like Cinnulin PF®, produced through a controlled water-based purification process, hit peak plasma concentration around 30 to 60 minutes for Type-A procyanidin polymers.
The high-molecular-weight polymers (roughly 576 to 1,152 Da for dimers through tetramers) show limited direct small-intestine absorption; the larger ones reach the colon, where gut microbiota convert them to bioavailable phenyl-γ-valerolactones and phenylacetic acids that likely contribute to the more sustained effects. Whole cinnamon powder is a different animal. Its polyphenols are locked in plant cell walls with poor aqueous solubility, which means slower, more variable absorption and no pharmacokinetic standardization to speak of.
SoActive Cinnamon™’s dual-species design is meant to get both: the standardized water-soluble extract for that immediate-peak window that’s ideal for postprandial support, and 800mg of organic Ceylon powder whose fiber matrix liberates polyphenols more gradually. One morning dose, meal-time and between-meal coverage.*
Supplements that produce consistent, CGM-observable effects tend to share a profile: they engage insulin-signaling pathways at doses with published human dose-response data. SoActive Cinnamon™ is designed around that profile, engaging multiple complementary pathways: insulin-receptor support via Type-A polyphenols, PTP1B modulation, GLUT4 translocation via PI3K/Akt and AMPK pathways, α-glucosidase modulation supporting healthy postprandial carbohydrate handling, AMPK activation, Nrf2-mediated antioxidant support, NF-κB signaling modulation, and gut-microbiome prebiotic support.
Parameters documented in the underlying research include: postprandial glucose support via carbohydrate-enzyme modulation (acute, dose-dependent), an 8.4% fasting-blood-glucose reduction over 12 weeks in the Ziegenfuss 2006 study population, and an 8.59 mg/dL fasting-blood-sugar reduction in a 150-person Ceylon study. A widely cited 83% responder figure, drawn from a manufacturer-reported analysis rather than the published paper, suggests a reasonable prior for a personal CGM signal. Track fasting glucose and 1-hour postprandial readings before and 8 to 12 weeks after initiation for personal validation.
Biomarker-Framed Outcomes: What to Track, When to Expect Signal, and How to Read It
Frame this as protocol optimization, not transformation. Each item below maps to a specific mechanism, biomarker, timeline, and measurement method. Product-level claims describe support for healthy metabolic function; the specific figures come from published studies and aren’t a promise of personal results.
CGM-Observable Postprandial Glucose Support
Mechanism: α-Glucosidase/α-amylase modulation, plus GLUT4 translocation, plus immediate water-soluble extract peak kinetics at 30 to 60 min.
Biomarker: Postprandial glucose peak magnitude; glucose excursion AUC (1 to 2 hour postprandial window); glucose variability coefficient.
Measurement protocol: Run CGM tracings on matched meals (same composition, same time of day) at baseline and every 2 weeks.
The carbohydrate-enzyme mechanism is acute and dose-dependent, so it’s potentially observable within the first weeks of consistent dosing with an authentic Ceylon component at a meaningful dose. A before/after CGM overlay on the same meal gives you the cleanest personal attribution data.
Identity marker: From “I have good metabolic function” to “I have documented, optimized metabolic function with data to support it.”*
Fasting Glucose Trend and HOMA-IR
Mechanism: Insulin-receptor support (Type-A polymer autophosphorylation), PTP1B modulation, AMPK activation, and Ceylon coverage supporting overnight metabolic function.
Biomarker: Fasting glucose directional trend (weekly CGM morning reading average); HOMA-IR, calculable from fasting glucose plus fasting insulin on quarterly labs.
Measurement protocol: Establish a 2-week fasting-glucose baseline (at least 10 CGM readings pre-intervention).
Calculate HOMA-IR from quarterly labs at baseline and at 12 weeks. Reference figures from the research: mean FBG –8.4% (116.3 → 106.5 mg/dL) at 500mg/day (Ziegenfuss 2006); a ~83% responder figure comes from a manufacturer-reported analysis, not the published study. These describe the study population, not a personal promise.
Identity marker: From “I’m monitoring a stable number” to “I’m tracking a directional trend with a defined mechanism.”
FRAP Antioxidant Capacity and Oxidative Stress Markers
Mechanism: Nrf2 pathway support upregulating HO-1, NQO1, and glutathione-S-transferases, plus direct free-radical scavenging by Ceylon polyphenols.
Biomarker: FRAP (Ferric Reducing Antioxidant Power) plasma assay; MDA (malondialdehyde); plasma thiols.
Measurement protocol: Add FRAP and MDA to a quarterly blood panel at baseline and at 12-week intervals.
Reference figures as reported for Roussel 2009 at the same 500mg/day dose (the significant direction, FRAP and thiols up and MDA down at p<0.05, is confirmed from the study; the exact deltas below are as reported and worth confirming against the full text): FRAP +12% (812→918 µmol/L); MDA –15% (2.7→2.2 µmol/L); plasma thiols +13.7%. These are the markers to compare against published effect sizes.
Identity marker: From “I take antioxidants” to “I track quantified oxidative-stress markers.”
Body Composition and Nutrient Partitioning
Mechanism: AMPK activation supporting fatty-acid oxidation; healthy insulin function favoring glucose storage as muscle glycogen; GSK-3β modulation. Supports healthy body composition when combined with diet and exercise. Biomarker: Lean body mass and body-fat percentage via DEXA; waist circumference; lean:fat ratio over time. Measurement protocol: Run a DEXA scan at baseline and every 12 weeks. Documented in Ziegenfuss 2006 at the 500mg/day dose: LBM +1.1% (DEXA-measured, p<0.002); BF% –0.7% (p<0.02). These are modest absolute changes, measurable with DEXA precision but not reliably with bioimpedance. Identity marker: From “I’m exercising for body composition” to “I’ve added a documented nutrient-partitioning mechanism to my training protocol.”
The Clinical Evidence: Peer-Reviewed Studies, Research-Matched Dosing, and Verifiable PMIDs
SoActive Cinnamon™ is built around the Cinnulin PF® ingredient, which has been studied in multiple peer-reviewed human trials. That includes a study conducted under an FDA-accepted Investigational New Drug application (IND #110123) and the Ziegenfuss et al. 2006 study, with the extract HPLC-verified to ≥3% Type-A procyanidin polyphenol polymers.*
Every citation below carries the PMID or DOI so you can verify it yourself. The studies differ in dose and cinnamon type, and where the dose differs from the 500mg formulation dose, we’ve said so. Each study’s actual population is stated plainly below (prediabetes and metabolic syndrome, impaired fasting glucose, PCOS, and so on).
Those diagnosed or at-risk populations are named so the evidence isn’t overread: the product is intended to support already-healthy metabolic function, not to treat prediabetes, metabolic syndrome, PCOS, or diabetes.
Study 1: Foundation Metabolic Study
Study: Ziegenfuss TN, Hofheins JE, Mendel RW, Landis J, Anderson RA. Journal of the International Society of Sports Nutrition. 2006;3(2):45-53. Design: Randomized, double-blind, placebo-controlled, parallel-group, 12-week trial. n=22 adults with prediabetes and the metabolic syndrome. Intent-to-treat analysis. 21-item chemistry-panel safety monitoring throughout.
Dose: 500mg/day Cinnulin PF® (250mg BID), the same dose as the SoActive extract component.
Key Findings (study population): - FBG: 116.3 → 106.5 mg/dL (–8.4%, p<0.01) - SBP: 133 → 128 mmHg (–3.8%, p<0.001) - LBM: +1.1% (DEXA-measured, p<0.002) - BF%: –0.7% (within-group only, not placebo-controlled; p<0.02)
Responder rate: ~83% of the cinnamon group versus ~33% of placebo showed a fasting-blood-sugar change (manufacturer-reported analysis, not published in the peer-reviewed study)
Safety: No adverse events; chemistry-panel parameters within normal limits throughout
Dose-Research Matching Note: Products delivering 250mg cite this study at half the dose. You can’t assume the effect at 250mg equals half the effect at 500mg, because dose-response for Type-A polymer activity isn’t established as linear.
Study 2: Antioxidant and Oxidative-Stress Biomarkers
Study: Roussel A-M, Hininger I, Benaraba R, Ziegenfuss TN, Anderson RA. Journal of the American College of Nutrition. 2009;28(1):16-21. PMID: 19571155
Design: Double-blind RCT. n=22 overweight or obese adults with impaired fasting glucose. 12 weeks. Dose: 500mg/day Cinnulin PF® (250mg BID), same as the SoActive extract dose.
Key Findings (study population): - FRAP antioxidant capacity: 812→918 µmol/L (+12%, p<0.05) - MDA: 2.7→2.2 µmol/L (–15%, p<0.05) - Plasma thiols: +13.7% (p<0.05) - FBG: 114→102 mg/dL - Positive correlation between plasma glucose and MDA (r=0.74, p=0.014)
Note: the significant direction of the antioxidant changes (FRAP and thiols up, MDA down; all p<0.05) is confirmed; the exact deltas above are as reported and should be confirmed against the full text
Study 3: Athletic Recovery Biomarkers
Study: Bahri S, Adnyana IK, Hasan MF, Apriantono T, Juniarsyah AD. Sport Mont Journal. 2022;20(2):57-61. DOI: 10.26773/smj.220609
Design: Double-blind, one-way crossover. n=16 male weightlifting athletes. 8-week intervention periods. (Cinnulin PF® is named as the extract in the full paper.) Dose: 500mg/day Cinnulin PF®, same as the SoActive extract dose.
Key Findings (study population): - Post-exercise CK (muscle-damage marker): group×time interaction p<0.005 - Post-exercise CRP: p<0.005 - Post-exercise lactate: p=0.012 - Post-exercise glucose: p=0.048 - Maximal lift performance: no significant effect reported, which points to recovery support rather than an acute ergogenic effect
Protocol note: The absence of performance enhancement supports recovery-mechanism specificity rather than a stimulant-adjacent effect.
Study 4: Ceylon Cinnamon Safety and Efficacy (2025)
Study: Muthukuda D, et al. PLOS One. 2025;20(1):e0317904. PMID: 39854533 Design: Randomized, double-blind, placebo-controlled. n=150 adults. 12 weeks. Thorough safety monitoring. Dose: 1000mg/day Ceylon (C. zeylanicum) extract, a Ceylon-specific dose (not the 500mg water-soluble extract).
Key Findings (study population): - FBS: –8.59 mg/dL (baseline-adjusted, p=0.036) across the full adult sample - LDL-C (the trial’s pre-specified primary endpoint): lower than placebo but not statistically significant (p=0.161)
Safety: favorable safety profile; no significant adverse changes in monitored safety parameters A note on how to read this: the trial’s primary endpoint (LDL-C) didn’t reach significance, so the fasting-glucose result is best treated as a secondary finding.
A larger glucose effect seen in a small exploratory subgroup of participants with type 2 diabetes was an underpowered, non-primary analysis, and it isn’t a basis for the product’s general use. Even so, it’s the largest prospective Ceylon-specific RCT to date, and it supports the Ceylon component’s fasting-glucose and safety profile in a general adult sample.
Study 5: Study Conducted Under an FDA-Accepted IND
Study: Kort DH, Lobo RA. American Journal of Obstetrics & Gynecology. 2014;211(5):487.e1-6. PMID: 24813595, conducted under FDA IND #110123
Design: Double-blind, placebo-controlled RCT. n=45 women with polycystic ovary syndrome (PCOS); its primary endpoint was menstrual cyclicity, not a metabolic outcome. 6-month duration, with high attrition: 26 of the 45 completed 3 months and only 17 (38%) completed the full 6 months.
Dose: 1.5 g/day Cinnulin PF® (higher than the 500mg formulation dose).
Relevance: Per the published paper, an IND to use the cinnamon extract was submitted and accepted by the FDA (IND no. 110123), and regular reporting to the FDA and a data-safety-monitoring board was performed. So the extract was studied under a federal clinical-trial oversight framework, a level of prospective safety documentation that’s uncommon for supplement ingredients.
To be clear: an accepted IND permits a clinical trial to proceed. It is not FDA approval or endorsement of any marketed product.
Meta-Analytical Context (Population-Level)
Zarezadeh M, et al. (2023): Umbrella meta-analysis synthesizing multiple independent meta-analyses; pooled fasting-glucose and HOMA-IR reductions across studies. Jafari A, et al. (2025): Large systematic review and meta-analysis (dozens of RCTs, thousands of participants) with GRADE assessment; blood glucose, triglycerides, and blood pressure reduced across the pooled dataset. Together they establish cross-study reproducibility beyond any single trial. (Consistent with, for example, Deyno et al. 2019, a meta-analysis in patients with type 2 diabetes and prediabetes reporting a fasting-glucose reduction of roughly –9.8 mg/dL and HOMA-IR –0.71.)
The Relationship Between Insulin Function and Metabolic Health
Healthy insulin function sits at the center of healthy glucose metabolism. For the optimizer, a standardized clinical-dose cinnamon extract is one of the few natural categories with published human dose-response data and verifiable PMIDs behind a single ingredient. (One of those studies also happened to run under an FDA-accepted IND with DSMB oversight, which is unusual for a supplement ingredient, though an accepted IND is not FDA approval or endorsement of a product.)
SoActive Cinnamon™ ’s peer-reviewed research base, with the Ziegenfuss et al. 2006 study at the 500mg dose (a roughly 83% responder figure comes from a manufacturer analysis, not the published paper), gives you the evidence architecture that n=1 protocols value for producing attributable rather than confounded personal data.*
Technical Differentiation: How SoActive Compares on the Criteria Optimizers Use
Here’s the matrix an evidence-driven optimizer tends to run before committing a supplement to a long-term daily protocol.
FOR OPTIMIZERS USING CONTINUOUS GLUCOSE MONITORS:
✓ Strong fit: SoActive Cinnamon™. The dual-species design supports both acute postprandial glucose handling (α-glucosidase modulation) and a standardized extract at the studied 500mg dose; both are CGM-trackable with reference data from published studies
○ Alternative: A 250mg single-ingredient extract. Same validated ingredient at half the studied dose, so expect a smaller CGM signal relative to research-predicted effect size
✗ Weakest: Generic cinnamon powder. Batch polyphenol variance produces noisy, hard-to-reproduce CGM data
FOR OPTIMIZERS TRACKING QUARTERLY BIOMARKERS (HbA1c, HOMA-IR, FRAP):
✓ Strong fit: SoActive Cinnamon™. Studies document measurable changes at the same extract dose: FBG figures, HOMA-IR directional trends, FRAP +12%; dose-to-research matching keeps your personal data comparable to published effect sizes
○ Alternative: Berberine at typical dose (1,000 to 1,500mg). Strong HOMA-IR evidence, complementary rather than competing; GI tolerance decides feasibility
✗ Weakest: Multi-ingredient blends with undisclosed proprietary blends. You can’t attribute biomarker changes to a specific ingredient
FOR OPTIMIZERS PRIORITIZING INDEPENDENTLY VERIFIABLE DATA:
✓ Strong fit: SoActive Cinnamon™. Every clinical citation includes a PMID; COA available per batch; HPLC-verified Type-A procyanidin standardization is analytically traceable; the FDA IND (#110123) is documented in the published study
○ Alternative: Any product citing the Ziegenfuss 2006 study at the correct 500mg dose with a published COA. Rare, so verify it independently
✗ Weakest: Products citing “clinical studies” without PMIDs, or leaning on dose-mismatched research
FOR OPTIMIZERS RUNNING EXTENDED DAILY PROTOCOLS (12+ MONTHS):
✓ Strong fit: SoActive Cinnamon™. Roughly 0.03mg total daily coumarin (well below the EFSA TDI); the extract was studied under FDA IND oversight with safety-parameter monitoring; self-affirmed GRAS (cinnamon is GRAS as a spice/flavoring under 21 CFR 182.10)
○ Alternative: Organic Ceylon whole powder (authenticated). Safe coumarin profile, but it lacks the HPLC-standardized bioactive content you need for reproducible biomarker results
✗ Weakest: Any Cassia product without published coumarin quantification
FOR OPTIMIZERS BUILDING EVIDENCE-BASED SUPPLEMENT STACKS:
✓ Strong fit: SoActive Cinnamon™. Mechanistically complementary (not redundant) with berberine, myo-inositol, magnesium, and resveratrol through non-overlapping pathway engagement
○ Alternative: Cinnamon + berberine combination products. Just verify the individual doses; most underdose both components
✗ Weakest: “Kitchen-sink” metabolic formulas. They prevent individual biomarker attribution
The HPLC Distinction: Why “3% Polyphenols” ≠ “≥3% Type-A Procyanidin Polymers”
This is one of the most underappreciated quality variables in the whole category, so it’s worth slowing down on.
Colorimetric assays (Folin-Ciocalteu is the common one) measure aggregate reducing capacity. Any compound with phenolic hydroxyl groups adds to the reading: Type-A procyanidin polymers, Type-B procyanidins, cinnamaldehyde, eugenol, catechin, quercetin, and a long list of other plant phenolics. So a product “standardized to 3% polyphenols” via colorimetric assay can carry almost no Type-A polymer and still hit its label claim on the strength of other polyphenolic fractions that don’t share the insulin-receptor mechanism.
HPLC-verified Type-A procyanidin standardization is a different measurement entirely. It uses chromatographic separation to identify and quantify the specific double-linked procyanidin fraction by retention time and UV absorbance. That’s the analytical gold standard, because it tells compounds apart instead of measuring an aggregate color change.
SoActive Cinnamon™ ’s water-soluble extract (Cinnulin PF®) is HPLC-verified to ≥3% Type-A procyanidin polyphenol polymers specifically, the molecular fraction characterized across the peer-reviewed studies. A Certificate of Analysis is available per production batch upon request.*
Technical FAQ: The Questions Evidence-Driven Optimizers Actually Ask
What is the HPLC-verified polyphenol concentration in each serving, and which molecular fraction is standardized?
Each serving delivers 500mg of standardized water-soluble cinnamon extract (Cinnulin PF®) standardized to ≥3% Type-A procyanidin polyphenol polymers via HPLC chromatographic assay, not aggregate colorimetric polyphenol content. The Type-A procyanidin fraction is the double-linked procyanidin class shown to support insulin-receptor β-subunit function in published research (Anderson et al. 2004). That works out to a minimum of about 15mg of Type-A procyanidin polymer content per serving, with chromatographic identity confirmation. A Certificate of Analysis is available per production batch upon request.*
What is the total daily coumarin exposure, and how does it compare to the EFSA TDI?
Coumarin (1,2-benzopyrone) carries a European Food Safety Authority Tolerable Daily Intake of 0.1 mg/kg bodyweight/day, about 7mg/day for a 70kg adult (EFSA, 2004; reaffirmed 2008). Cassia cinnamon at typical supplemental doses can contribute several mg of coumarin.
SoActive Cinnamon™’s two-component design handles it two ways: the controlled water-based purification process removes the large majority of coumarin from the water-soluble extract, and the 800mg of organic Ceylon cinnamon (Cinnamomum verum, ~0.004% coumarin) contributes roughly 0.03mg.
So total daily coumarin exposure lands around 0.03mg, well below the EFSA TDI of ~7mg. The extract was studied under FDA IND #110123 with data-safety-monitoring-board oversight; that six-month study reported no serious adverse events (only minor, self-resolving events such as headache and heartburn).
Broader safety panels, including liver and renal function, were monitored and reported normal in other Ceylon cinnamon trials, such as the 150-person Muthukuda 2025 trial. These statements have not been evaluated by the Food and Drug Administration. This product is not intended to diagnose, treat, cure, or prevent any disease. Consult your healthcare provider.*
Can I take this alongside berberine or other metabolic-support agents?
Cinnamon extract and berberine work through partially overlapping but mechanistically distinct pathways. Berberine engages AMPK largely through a route associated with GI effects that can cap higher doses. The water-soluble cinnamon extract engages AMPK through polyphenol-LKB1 signaling and also supports insulin-receptor function, PTP1B activity, and α-glucosidase activity, areas berberine doesn’t primarily touch.
There are no well-characterized interactions reported. That said, combining multiple metabolic-support agents can have additive effects on blood sugar and warrants monitoring and provider oversight, especially alongside prescription products. Consult your healthcare provider before combining agents.*
When should I expect CGM-observable changes versus quarterly biomarker changes?
Here’s the timeline by mechanism:
- Days 1 to 7: α-Glucosidase modulation is dose-dependent and acute, so postprandial glucose support on CGM may show up within the first week on matched meals. Baseline first: same meal, same time, CGM tracing for 3 consecutive days, then repeat at day 7 to 10.
- Weeks 4 to 8: The fasting glucose directional trend may start to separate from baseline noise as receptor support accumulates. Track the weekly CGM morning average.
- Weeks 8 to 12: Fuller biomarker signal. Calculate HOMA-IR from fasting glucose plus fasting insulin, and compare against the Ziegenfuss 2006 reference figures.
- Months 3 to 6: FRAP, MDA, and hs-CRP via quarterly panels (Roussel 2009 reference data), plus microbiome shifts if you’re running microbiome panel testing.*
Is a Certificate of Analysis available for the current production batch?
Yes. The COA for the current batch is available upon request and includes: HPLC-verified Type-A procyanidin polyphenol polymer concentration (≥3%), coumarin quantification, a heavy-metals panel (USP standards), microbiology (USP standards), and botanical identity confirmation for both Cinnamomum burmannii (extract) and Cinnamomum verum (Ceylon) components. Contact customer support with your order number. Batch numbers are printed on each bottle.*
Protocol Implementation Decision
You’ve evaluated the evidence. The extract dose matches the foundation study. The COA is verifiable. The coumarin architecture is quantified against the EFSA TDI. The dose-to-research matching removes the primary attribution confound. The HPLC standardization targets the specific molecular fraction instead of an aggregate proxy. And the dual-species design is built to deliver both acute postprandial and more sustained coverage from a single morning dose.
SoActive Cinnamon™ is a dual-species cinnamon complex built for evidence-driven metabolic optimizers who want HPLC-standardized Type-A polyphenol content, a clinically studied extract at the studied dose, and biomarker-trackable inputs, without the batch-to-batch potency variance that makes generic cinnamon supplementation so hard to reconcile with rigorous personal data protocols.*
That’s the decision.
→ Learn More About SoActive Cinnamon™
Backed by our 60-day satisfaction guarantee and quality manufacturing standards. Certificate of Analysis available per batch upon request.
These statements have not been evaluated by the Food and Drug Administration. This product is not intended to diagnose, treat, cure, or prevent any disease. Consult your healthcare provider before starting any new supplement regimen.
Complete Molecular and Protocol Reference
Ingredient Profiles: Full Specification
Standardized Water-Soluble Cinnamon Bark Extract (Cinnulin PF®), 500mg per serving
Source & Extraction: A 20:1 water-soluble extract of Cinnamomum burmannii, produced through a controlled water-based purification process. Water-soluble extraction selectively pulls the hydrophilic Type-A procyanidin polyphenol polymers into solution while leaving lipophilic coumarin and volatile cinnamaldehyde behind in the discarded fraction.
Concentration ratio: 500mg extract is roughly equivalent to 10,000mg of whole-cinnamon bioactive content (per the 20:1 ratio). Standardization: ≥3% Type-A procyanidin polyphenol polymers by HPLC chromatographic assay, not colorimetric total polyphenol. The method separates Type-A double-linked procyanidins from Type-B procyanidins, which don’t share the insulin-receptor mechanism.
Pharmacokinetics: The water-soluble format reaches peak plasma concentration around 30 to 60 min post-ingestion. High-MW polymers show limited direct small-intestine absorption; the rest reach the colon, where gut bacteria convert them via ring-fission metabolism to phenyl-γ-valerolactones, phenylacetic acids, and related metabolites that stay detectable in plasma for several hours.
Safety profile: The extract’s GRAS status is self-affirmed, resting on cinnamon’s listing as a GRAS spice/flavoring (21 CFR 182.10) rather than a filed FDA GRAS notice for the branded extract. Coumarin content is greatly reduced post-extraction (typically very low or undetectable with water extraction).
No serious adverse events were reported across its clinical trials; the 6-month FDA-IND-monitored study logged only minor, self-resolving events such as headache and heartburn. Liver and renal function panels were reported normal in other Ceylon cinnamon trials, such as the 150-person Muthukuda 2025 trial.*
Organic Ceylon Cinnamon Powder, 800mg per serving Botanical Authentication:
Cinnamomum verum (syn. C. zeylanicum) from authenticated Sri Lankan sources. Identity is confirmed via HPLC fingerprint and PCR genetic authentication, which addresses the Cassia-substitution problem documented in third-party testing of “Ceylon” products.
Phytochemical Profile: Cinnamaldehyde ~50 to 63% of volatile oils; eugenol ~4 to 10%; linalool; β-caryophyllene; coumarin ~0.004% (versus roughly 0.1 to 1% in Cassia; Woehrlin et al. 2010 and HPLC compositional analyses).
Fiber Content: ~33% dietary fiber (~264mg per 800mg serving), the prebiotic substrate and the basis for the slower, fiber-bound polyphenol liberation.
Trace Mineral Matrix: Chromium, manganese, calcium, potassium, present in whole powder and largely removed by extraction.
Coumarin Safety: 0.004% × 800mg = ~0.032mg per serving, a small fraction of the EFSA TDI.*
Supplement Stack Interaction Notes
Cinnamon + Berberine: Distinct AMPK upstream nodes (LKB1 versus mitochondrial pathways); cinnamon adds insulin-receptor support, PTP1B modulation, and α-glucosidase modulation. Cinnamon’s polyphenol-receptor mechanism doesn’t carry berberine’s GI burden. Stack design: SoActive with breakfast, berberine with the largest carbohydrate meal if GI tolerance permits.
Cinnamon + Myo-Inositol: Distinct, non-overlapping insulin-signaling support (the IPG secondary-messenger pathway). Well tolerated at standard doses (2 to 4g/day).
Cinnamon + Magnesium: Magnesium is a cofactor for insulin-receptor tyrosine kinase, so the extract’s mechanism benefits from adequate Mg status. Additive when Mg is low, neutral when replete.
Cinnamon + Metformin: Different mechanisms. The combined metabolic-support effect warrants glucose monitoring; consult the prescribing provider.*
CGM Protocol Design Reference
Phase 1, Baseline (2 weeks pre-supplementation): Morning fasting glucose (at least 10 readings; record mean and SD). Postprandial protocol: 2 to 3 fixed-composition meals, with CGM recorded at 0/30/60/90/120/180 min on 3 occasions each. Calculate baseline postprandial AUC. Document HOMA-IR from fasting glucose plus insulin.
Phase 2, Intervention (Weeks 1 to 12): 2 capsules with breakfast, consistently. Repeat the postprandial CGM on matched meals at weeks 1, 2, 4, 8, and 12. Track morning fasting glucose weekly. Hold meal composition, exercise timing, and sleep consistent during comparison periods.
Phase 3, Biomarker Assessment (12-week marks): Repeat fasting glucose plus insulin for HOMA-IR. Quarterly panel: FRAP, MDA, hs-CRP, HbA1c, fasting lipids. Compare to the Ziegenfuss 2006 and Roussel 2009 reference figures.
Confound Management: Minimize medication changes, document diet changes that affect postprandial glucose, and keep exercise timing consistent (acute exercise shifts insulin sensitivity for 24 to 48h). If you’re adding berberine, stagger it by at least 4 weeks for attribution clarity.
Extended Technical FAQ
Is the Type-A versus Type-B procyanidin distinction meaningful or academic?
Meaningful. Type-A procyanidins have double interflavanoid linkages; Type-B have single linkages. Anderson et al. 2004 isolated and characterized the Type-A fraction as the active insulin-supporting moiety via Sephadex LH-20 fractionation, and the Type-A-enriched fractions showed dose-dependent glucose-metabolism support while the Type-B-enriched fractions showed minimal activity. A supplement that standardizes to total procyanidin content without specifying Type-A versus Type-B isn’t standardizing to the active class.*
Why does the water-based purification preserve Type-A polymers while removing coumarin?
It comes down to partition-coefficient (log P) differences. Coumarin is moderately lipophilic (log P ≈ 1.5) and partitions into the organic phase; Type-A procyanidin polymers are highly hydrophilic and partition into the aqueous phase. The process exploits that gap to concentrate the active hydrophilic polyphenol fraction while removing most of the coumarin. Cinnamaldehyde (log P ≈ 1.9) is similarly removed, which is one reason the water-soluble extract tends to sit better with the gut than whole Cassia powder.*
What does “dose-to-research matching” actually mean?
It means the formulation delivers the dose used in the study being cited, within a reasonable tolerance. Ziegenfuss 2006 used 500mg/day; SoActive delivers 500mg/day of the same extract, so it’s a match. A 250mg product delivers half. Whether 250mg produces 50%, 25%, or no measurable effect is genuinely unknown, because the sub-500mg dose-response curve for Type-A polymer activity hasn’t been characterized in human trials. That’s the whole difference between personal data you can compare to published literature and personal data you can’t.*
How do I calculate HOMA-IR from my lab results?
HOMA-IR = (fasting glucose in mg/dL × fasting insulin in µIU/mL) / 405. These are general, widely published clinical reference ranges, offered for context rather than as a product claim: <1.5 (good insulin sensitivity); 1.5 to 2.5 (early insulin resistance); >2.5 (significant insulin resistance). The Ziegenfuss 2006 study used DEXA and fasting glucose as primary endpoints rather than HOMA-IR; the Wang 2007 pilot, a 15-person study in women with PCOS, reported improvements in insulin-sensitivity indices, and a secondary review calculates a roughly 44.5% HOMA-IR reduction from that data, consistent with an insulin-support mechanism. Order both fasting glucose and fasting insulin, since glucose alone isn’t enough for HOMA-IR.*
When Practitioners Consider SoActive Cinnamon™ Appropriate
Evidence-driven practitioners and optimization-oriented researchers tend to reach for SoActive Cinnamon™ when:
✓ Optimizers are running CGM protocols and want a supplement with documented postprandial-support mechanisms at a studied dose, so their personal signal is interpretable instead of noisy
✓ Quarterly biomarker tracking (HbA1c, fasting glucose, HOMA-IR, FRAP, hs-CRP) is the primary outcome framework and dose-to-research matching matters
✓ Previous cinnamon supplementation produced inconsistent or null CGM results, plausibly because of potency variance
✓ Extended daily protocols (12+ months) call for a quantified coumarin safety margin with monitored safety data
✓ A stack needs an insulin-receptor-support layer with mechanistically distinct pathway engagement from existing berberine, metformin, or acarbose components
✓ Independent verification of citations (PMIDs), molecular standardization (COA), and regulatory status (self-affirmed GRAS, cGMP) is a due-diligence requirement
And it’s probably not the right addition when:
○ Fasting and postprandial glucose readings are already consistently in a healthy range and there’s little headroom for measurable change
○ A full prescription protocol is already producing satisfactory data and added stack complexity would muddy attribution
○ The primary optimization target sits outside the metabolic pathways where cinnamon’s mechanism contributes
Scientific References & Citations
All clinical citations include PubMed PMIDs or DOIs for independent verification.
Peer-Reviewed Clinical Studies
Bahri, S., Adnyana, I.K., Hasan, M.F., Apriantono, T., & Juniarsyah, A.D. (2022). The effect of cinnamon extract on recovery and performance of weightlifting athletes. Sport Mont Journal, 20(2), 57–61. DOI: 10.26773/smj.220609. 500mg/day Cinnulin PF®. CK, CRP, and lactate reductions; no performance enhancement.
Jafari, A., Mardani, H., Faghfouri, A. H., AhmadianMoghaddam, M., Musazadeh, V., & Alaghi, A. (2025). The effect of cinnamon supplementation on cardiovascular risk factors in adults: a GRADE-assessed systematic review, dose-response and meta-analysis of randomized controlled trials. Journal of Health, Population and Nutrition, 44(1), 233. PMID: 40611215 | DOI: 10.1186/s41043-025-00967-3. Forty-nine RCTs; fasting glucose, triglyceride, and blood-pressure reductions across independent research groups.
Kort, D.H., & Lobo, R.A. (2014). Preliminary evidence that cinnamon improves menstrual cyclicity in women with polycystic ovary syndrome: a randomized controlled trial. American Journal of Obstetrics & Gynecology, 211(5), 487.e1-6. PMID: 24813595. 1.5 g/day Cinnulin PF®; conducted under FDA IND #110123 with FDA/DSMB reporting.
Muthukuda, D., et al. (2025). Effects of Cinnamomum zeylanicum (Ceylon cinnamon) extract on lipid profile, glucose levels and its safety in adults. PLOS One, 20(1), e0317904. PMID: 39854533. Largest Ceylon RCT (n=150); FBS –8.59 mg/dL (p=0.036); favorable safety profile.
Roussel, A-M., Hininger, I., Benaraba, R., Ziegenfuss, T.N., & Anderson, R.A. (2009). Antioxidant effects of a cinnamon extract in people with impaired fasting glucose that are overweight or obese. Journal of the American College of Nutrition, 28(1), 16–21. PMID: 19571155. 500mg/day Cinnulin PF®. FRAP and thiols significantly increased and MDA significantly decreased (all p<0.05); reported deltas ~+12%, +13.7%, and –15% respectively (confirm exact values against full text).
Zarezadeh, M., Musazadeh, V., Foroumandi, E., Keramati, M., Ostadrahimi, A., & Mekary, R. A. (2023). The effect of cinnamon supplementation on glycemic control in patients with type 2 diabetes or with polycystic ovary syndrome: an umbrella meta-analysis on interventional meta-analyses. Diabetology & Metabolic Syndrome, 15(1), 127. PMID: 37316893 | DOI: 10.1186/s13098-023-01057-2. Synthesis of multiple independent meta-analyses in patients with type 2 diabetes or PCOS; pooled fasting-glucose and HOMA-IR reductions.
Ziegenfuss, T.N., Hofheins, J.E., Mendel, R.W., Landis, J., & Anderson, R.A. (2006). Effects of a water-soluble cinnamon extract on body composition and features of the metabolic syndrome in pre-diabetic men and women. Journal of the International Society of Sports Nutrition, 3(2), 45–53. DOI: 10.1186/1550-2783-3-2-45 | PMID: 18500972 | PMC: PMC2129164. 500mg/day Cinnulin PF®. n=22. 12 weeks. FBG –8.4% (p<0.01); SBP –3.8% (p<0.001); LBM +1.1% (p<0.002); BF% –0.7% (p<0.02).
Mechanistic Research
Anderson, R.A., Broadhurst, C.L., Polansky, M.M., et al. (2004). Isolation and characterization of polyphenol type-A polymers from cinnamon with insulin-like biological activity. Journal of Agricultural and Food Chemistry, 52(1):65-70. PMID: 14709014. Primary molecular isolation paper; Type-A versus Type-B activity differences.
Shen, Y., et al. (2014). Cinnamon extract enhances glucose uptake in 3T3-L1 adipocytes and C2C12 myocytes by inducing LKB1-AMPK signaling. PLOS One, 9(2), e87894. PMID: 24551069. Basis for the LKB1-AMPK mechanism.
Deyno, S., Eneyew, K., Seyfe, S., et al. (2019). Efficacy and safety of cinnamon in type 2 diabetes mellitus and pre-diabetes patients: a meta-analysis and meta-regression. Diabetes Research and Clinical Practice, 156, 107815. PMID: 31425768. Fasting-glucose reduction of roughly –9.8 mg/dL and HOMA-IR –0.71 in patients with type 2 diabetes and prediabetes.
Anjali, Sadaf, A., & Khare, S. K. (2022). Evaluation of trans-cinnamaldehyde as an anti-hyperglycemic compound through inhibition of α-amylase. Indian Journal of Biochemistry and Biophysics, 59(2), 183–188. In-vitro α-amylase inhibition data for trans-cinnamaldehyde (source for Pathway 5).
Wang, J.G., et al. (2007). The effect of cinnamon extract on insulin resistance parameters in polycystic ovary syndrome: a pilot study. Fertility & Sterility, 88:240–243. PMID: 17296187. Significant HOMA-IR reduction in a pilot study population.
Regulatory Documentation
U.S. FDA. Investigational New Drug Application IND #110123. Federal oversight framework for the cinnamon-extract clinical trial (Kort & Lobo 2014); DSMB oversight. (An accepted IND permits a trial; it is not approval or endorsement of a marketed product.)
U.S. FDA. Substances Generally Recognized as Safe, 21 CFR 182.10 (cinnamon as a spice and natural seasoning/flavoring; the extract’s source species, Cinnamomum burmannii, is listed there as ‘Cassia, Padang or Batavia’). Basis for the extract’s self-affirmed GRAS status. No branded GRAS Notice (GRN) number for the extract was located in FDA’s GRAS Notice Inventory.
European Food Safety Authority (EFSA). (2004; reaffirmed 2008). Scientific Opinion on coumarin in flavourings and other food ingredients. EFSA Journal, 793:1–47. The coumarin TDI of 0.1 mg/kg bw/day was established in 2004 and reaffirmed in the 2008 opinion.
Bundesinstitut für Risikobewertung (BfR). Health Assessment of Coumarin in Cinnamon Products. Regulatory basis for preferring Ceylon over Cassia at supplemental doses.
Woehrlin, F., Fry, H., Abraham, K., & Preiss-Weigert, A. (2010). Quantification of flavoring constituents in cinnamon: high variation of coumarin in cassia bark from the German retail market and in authentic samples from Indonesia. Journal of Agricultural and Food Chemistry, 58(19), 10568–10575. DOI: 10.1021/jf102112p. Source for the Ceylon-versus-Cassia coumarin comparison.
These statements have not been evaluated by the Food and Drug Administration. This product is not intended to diagnose, treat, cure, or prevent any disease. Consult your healthcare provider before starting any new supplement regimen, especially if you have a medical condition or take medications.
