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Apigenin

Sleep & Recovery

Last reviewed: May 26, 2026

Also Known As: 4',5,7-trihydroxyflavone, chamomile flavonoid, Matricaria chamomilla active flavonoid

Supplement Class: Plant flavonoid / GABA-A receptor partial agonist (benzodiazepine binding site) / CD38 inhibitor (NAD+ preservation)

Evidence Tier: Moderate (chamomile extract) — Mao et al. 2016's 38-week GAD RCT (n=179), Amsterdam et al. 2012, and Adib-Hajbaghery & Mousavi 2017's elderly sleep trial, all using chamomile extract standardized to apigenin content. Limited (standalone pure apigenin) — animal and cell evidence documented via Avallone et al. 2000 (GABA-A binding) and Escande et al. 2013 (CD38 inhibition); direct human RCTs of standalone 50 mg apigenin are sparse and the popular dose is extrapolated rather than directly validated.

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What is apigenin?

Apigenin is a plant flavonoid found in highest concentration in dried chamomile flowers (the source of chamomile tea), as well as in parsley, celery, and citrus peels. It is the principal active flavonoid behind chamomile's traditional calming and sleep-supporting effects, and has gained substantial recent popularity — largely via Andrew Huberman's recommendations — as a standalone supplement at 50 mg pre-bed. The primary mechanism reported is partial agonism at the benzodiazepine binding site of GABA-A receptors (Avallone et al. 2000) — the same site targeted by benzodiazepines and alcohol, but with a ceiling on activation discussed as theoretically preventing the deep receptor adaptation responsible for benzodiazepine dependence. A secondary mechanism, documented separately, is CD38 inhibition (Escande et al. 2013), which preserves NAD+ levels by reducing the activity of a major NAD+-consuming enzyme — a longevity-relevant arm that complements rather than duplicates NAD+ precursor supplements (NMN, NR). The strongest human evidence is from chamomile extract RCTs (Mao et al. 2016's GAD trial, Amsterdam et al. 2012, Adib-Hajbaghery & Mousavi 2017's elderly sleep trial), where apigenin is the principal active flavonoid. Standalone pure-apigenin trials at the 50 mg supplemental dose are sparse — the popular protocol is extrapolated from animal data and chamomile dosing rather than directly RCT-validated. Apigenin is discussed alongside sleep peptides like DSIP, Selank, and Epitalon via complementary mechanism layers spanning both sleep and NAD+/longevity peptide clusters.

Reported benefits:

  • Anxiolytic effect in GAD via chamomile extract (Mao et al. 2016, Amsterdam et al. 2012)
  • Improved sleep quality in elderly populations (Adib-Hajbaghery & Mousavi 2017)
  • GABA-A receptor partial agonism at the benzodiazepine binding site, with theoretically minimal dependence risk
  • CD38 inhibition preserving NAD+ levels, documented in cell culture and obese-mouse models (Escande et al. 2013)
  • Anti-inflammatory effects via NF-κB modulation
  • Mast cell stabilization, reported in some research

Common dose: 50 mg pure apigenin taken 30–60 minutes before bed, commonly paired with a small amount of dietary fat given apigenin's poor water solubility. The Huberman-protocol dose, extrapolated from animal data and chamomile evidence rather than direct human RCT validation. Lower doses (25 mg) are used by sensitive users; higher doses (75–100 mg) are occasionally used without additional evidence behind them.

Reported safety considerations: CYP2C9 and CYP3A4 inhibition, affecting metabolism of warfarin, statins, and some antidepressants — clinician coordination is standard guidance. Asteraceae allergies (ragweed, daisies, chrysanthemums) carry possible cross-reactivity with chamomile-derived apigenin. Pregnancy is a commonly discussed contraindication for concentrated supplements.

On this page
  1. 1.How does apigenin work?
  2. 2.What does the evidence say apigenin does?
  3. 3.How is apigenin dosed?
  4. 4.How apigenin is taken
  5. 5.What does apigenin stack with?
  6. 6.Side effects and interactions
  7. 7.What isn't established about apigenin
  8. 8.Product-quality considerations
  9. 9.Apigenin FAQ
  10. 10.References
  11. 11.Published Studies

How does apigenin work?

Apigenin is reported to work primarily through partial agonism at the benzodiazepine binding site of GABA-A receptors — the same receptor family targeted by benzodiazepines and alcohol, but with a ceiling on activation that is discussed as preventing the deep receptor adaptation responsible for benzodiazepine dependence. A secondary, separately documented mechanism is CD38 inhibition (Escande et al. 2013), which preserves NAD+ levels and provides a longevity-relevant arm distinct from the sleep mechanism.

  1. GABA-A partial agonism at the benzodiazepine site. Avallone et al. 2000 reports apigenin displaces a specific radioligand from the central benzodiazepine binding site on GABA-A receptors and reduces GABA-evoked currents in cultured cerebellar granule cells in a manner consistent with partial-agonist pharmacology. Apigenin produces submaximal receptor activation even at high concentrations, structurally distinct from full agonists like benzodiazepines and discussed as protective against the deep receptor downregulation that drives benzodiazepine dependence.
  2. Inhibitory neurotransmission modulation. By enhancing GABA-A receptor activity, apigenin is reported to amplify inhibitory neurotransmitter tone in the CNS, reducing neuronal firing and producing the calming, sleep-supporting effects observed in animal models.
  3. CD38 inhibition and NAD+ preservation. CD38 is an enzyme that consumes NAD+, particularly in immune cells and tissues with elevated inflammation, with CD38 activity reported to increase with age. Escande et al. 2013 identifies apigenin as a pharmacological CD38 inhibitor, reporting that apigenin treatment raises NAD+ levels and reduces protein acetylation in cell culture, and that apigenin administration to obese mice raises NAD+ levels and improves glucose and lipid homeostasis — a mechanism distinct from NAD+ precursor supplementation (NMN, NR), which works on the input side.
  4. Anti-inflammatory effects. Apigenin is reported to modulate NF-κB signaling and reduce inflammatory cytokine production, per the Salehi et al. 2019 review — a mechanism discussed as supporting the broader longevity-relevant case and the chamomile-apigenin evidence in GI and skin inflammation contexts.
  5. Mast cell stabilization. Apigenin has been documented as a mast cell stabilizer in some research, reducing histamine release and inflammatory mediator production — discussed as underlying chamomile's traditional use in allergy and skin contexts.
  6. Bioavailability constraint. Apigenin is poorly water-soluble, and oral bioavailability is reported as modest. Coadministration with dietary fat is discussed as a means of modestly improving absorption — a central practical constraint for translating in-vitro and animal effects to clinical outcomes.

What does the evidence say apigenin does?

Apigenin's evidence base is heterogeneous. The strongest evidence comes from chamomile extract studies — where apigenin is the principal active flavonoid — for anxiety and sleep in clinical populations. Standalone pure-apigenin trials are sparse and mostly animal-based. The CD38/NAD+ longevity mechanism is well-documented in cell and mouse studies but human-untested.

  1. Chamomile extract for anxiety (Strong via chamomile, indirect for standalone apigenin). Mao et al. 2016 (38-week RCT, n=179) and Amsterdam et al. 2012 document anxiolytic and mood effects of chamomile extract standardized to apigenin content in patients with generalized anxiety disorder. Apigenin is discussed as the principal active flavonoid driving the effect, though these trials studied the whole extract rather than isolated apigenin.
  2. Standalone pure apigenin for anxiety/sleep (Limited human, animal-supported). Animal models consistently report sedative and anxiolytic effects of pure apigenin via the GABA-A benzodiazepine-site mechanism, with sedative effects reported to be blocked by flumazenil (the benzodiazepine antagonist), supporting the proposed mechanism. Direct standalone-apigenin human RCTs at the 50 mg evening dose are sparse — the popular protocol is extrapolated from animal data and chamomile evidence.
  3. Sleep in older adults (Moderate via chamomile). Adib-Hajbaghery & Mousavi 2017 reports sleep quality improvement with chamomile extract in elderly adults. The trial's open-label design is a methodological limitation, but the finding supports the use case in age-related GABAergic decline contexts.
  4. CD38 inhibition and NAD+ preservation (Documented in cells and mice, human-untested). Escande et al. 2013 reports apigenin inhibits CD38, raises NAD+ levels, and improves glucose/lipid parameters in obese mice. Human clinical NAD+ elevation from oral apigenin at typical supplemental doses has not been directly demonstrated in the sources reviewed for this page.
  5. Anti-inflammatory effects (Mechanistic). NF-κB inhibition and cytokine reduction are documented across multiple in vitro and animal studies per the Salehi et al. 2019 review. Translation to human clinical outcomes for specific inflammatory conditions is not robustly RCT-tested.
  6. Cancer adjunct research (Preclinical). Extensive preclinical work discussed in the Salehi et al. 2019 review suggests apigenin has anti-cancer effects via apoptosis induction and angiogenesis inhibition. Human trial data is essentially absent.
  7. Skin and allergy applications (Modest via chamomile). Chamomile has traditional use for skin inflammation and allergic contexts, with the mast cell stabilization mechanism discussed as supporting this use case; human evidence specific to apigenin is modest.

How is apigenin dosed?

Apigenin dosing is relatively simple in practice — 50 mg pre-bed is the dominant supplemental protocol, popularized by Andrew Huberman's recommendations. The 50 mg dose is extrapolated from animal data and chamomile extract scaling rather than direct human RCT validation. Reported doses range from 25–100 mg, with limited evidence supporting the higher end.

Prof. Peptide reports what trials established and what research communities practice, labelled separately. Neither is a recommendation.

  1. Standard pre-bed dose. 50 mg pure apigenin taken 30–60 minutes before bed, commonly paired with a small amount of dietary fat for absorption — the popular Huberman-protocol dose.
  2. Lower starting dose. 25 mg is used by some sensitive users, or as an initial tolerance check; reported by some as sufficient for sleep effects.
  3. Chamomile extract alternative. 400–1,500 mg/day chamomile extract standardized to apigenin content (about 1.2% apigenin in the Mao et al. 2016 trial product). Provides apigenin alongside other chamomile flavonoids and has a stronger RCT record than standalone apigenin.
  4. Higher dose. 75–100 mg is occasionally used but has limited additional evidence behind it.
  5. Chamomile tea (culinary). 1–2 cups per evening provides roughly 1–10 mg apigenin — discussed as a pleasant wind-down ritual, far below the supplemental dose studied for a discrete effect.

Reported timeline: acute sleep effects within 30–60 minutes. Anxiolytic chronic effects, per the chamomile-extract trials, are reported to emerge over 4–8 weeks. CD38/NAD+ effects, if clinically relevant in humans, would be expected to require chronic dosing, though this has not been directly tested.

Label math. A label reading "apigenin 50 mg" is understood to mean 50 mg pure apigenin, typically from chamomile extract concentrated to 98%+ apigenin. "Chamomile extract 500 mg standardized to 5% apigenin" provides 25 mg apigenin per serving — the distinction matters for comparing products.

How apigenin is taken

Apigenin is taken orally as capsules of standardized extract, occasionally as powder. The practical considerations reported are bioavailability (poorly water-soluble — commonly paired with dietary fat), timing (30–60 minutes pre-bed for sleep), and source quality (chamomile-derived 98%+ pure apigenin is the studied form).

AspectReported
FrequencyOnce nightly for the sleep protocol; chronic anxiolytic use is discussed as once daily, evening preferred to leverage the sleep-supportive effect.
Best time of day30–60 minutes before bed; morning dosing is generally avoided given the calming effect during waking hours.
FoodWith a small amount of dietary fat — apigenin is poorly water-soluble. A few nuts, a teaspoon of olive oil, or a small piece of dark chocolate is a common accommodation to modestly improve absorption.
FormPure apigenin extract (typically 98%+ from chamomile source) is the most-studied form. Synthetic apigenin exists but is rare in commercial products. Chamomile extract standardized to apigenin content is an evidence-supported alternative.
Standardization markerLabels reading "98% apigenin" or "pure apigenin" with the chamomile source disclosed are considered the clearer standard. Independent testing has occasionally found products with significantly less apigenin than labeled — third-party testing is the relevant screen.
CyclingNo cycling is reported as pharmacologically required — the partial-agonist pharmacology is discussed as theoretically preventing tolerance development, and no tolerance has been documented at clinical doses in the sources reviewed.

What does apigenin stack with?

Apigenin's GABA-A partial agonism plus CD38 inhibition spans both the sleep and longevity supplement clusters. It is discussed as pairing cleanly with sleep peptides, NAD+ precursors, and other GABAergic supplements.

With peptides

Apigenin is discussed alongside the Russian-origin sleep and longevity peptide cluster, spanning both the sleep and NAD+/longevity peptide clusters via its dual mechanism. DSIP (delta sleep-inducing peptide) is reported to act directly on slow-wave sleep architecture. Selank (a tuftsin analog) is reported to provide anxiolytic effects via GABA-A receptor sensitivity modulation — the same broad target as apigenin but at a different mechanism layer. Epitalon adds a pineal-axis longevity arm — telomere maintenance and circadian regulation, discussed as complementary to apigenin's CD38/NAD+ longevity arm. NAD+ peptide provides direct NAD+ delivery alongside apigenin's consumption-side preservation. No known negative interaction is documented in the sources reviewed for this page.

With supplements

  1. NMN or NAD+ precursors — apigenin's CD38 inhibition is discussed as preserving the NAD+ that NMN/NR provide, addressing both sides of the NAD+ balance equation.
  2. Magnesium glycinate — a GABA-A positive allosteric modulator, discussed as pairing with apigenin's benzodiazepine-site partial agonism at the same receptor.
  3. Glycine — reported body-temperature regulation for sleep onset plus inhibitory neurotransmission via a different mechanism.
  4. L-theanine — alpha-wave induction plus GABAergic enhancement via a different mechanism.
  5. Melatonin — circadian signaling via the MT1/MT2 receptor, a different mechanism from apigenin's GABA-A target.
  6. Tart cherry — a natural melatonin, tryptophan, and anthocyanin botanical matrix, discussed as a compatible botanical sleep-stack pairing.
  7. Quercetin — another flavonoid documented as a CD38 inhibitor alongside apigenin in the Escande et al. 2013 paper, with anti-inflammatory effects, and a common co-occupant in longevity stacks.

With lifestyle factors

  1. Pre-bed timing with dietary fat. 30–60 minutes before target bedtime, paired with a small amount of fat for absorption.
  2. Alcohol or sedative combination. The same GABA-A receptor system as benzodiazepines and alcohol is involved, raising additive CNS depression risk; separate dosing is standard guidance.
  3. Chamomile tea as adjunct. A wind-down ritual that adds a small amount of apigenin alongside other chamomile flavonoids, complementing supplemental dosing.
  4. Pregnancy. Concentrated supplemental doses are commonly avoided given uterine activity concerns at high doses; culinary chamomile tea is generally considered safer in pregnancy, but clinician coordination is standard guidance.

Side effects and interactions

Apigenin shows a favorable safety profile at supplemental doses across the sources reviewed. The main considerations reported are CYP enzyme inhibition (affecting metabolism of certain medications), Asteraceae allergy contraindications, and additive sedation with other CNS depressants.

Common (mostly transient)

  1. Mild drowsiness — intentional for sleep applications, undesirable if dosed during waking hours.
  2. Mild GI discomfort — reported occasionally, generally at higher doses or on an empty stomach.
  3. Vivid dreams — occasionally reported, discussed as likely tied to GABAergic effects on sleep architecture.
  4. No documented serious adverse events at standard supplemental doses across the human research base reviewed.

Less common (watch-list)

  1. Asteraceae (daisy family) allergy reactions. Users with allergies to ragweed, chrysanthemums, daisies, or marigolds may react to chamomile-derived apigenin — a synthetic source is a possible alternative for these users.
  2. Pregnancy uterine activity concerns. Concentrated apigenin is theoretically discussed as capable of triggering uterine activity at high doses; supplemental apigenin is commonly avoided during pregnancy.
  3. Hypotension at very high doses — apigenin has modest blood-pressure-lowering effects reported in some animal studies.

Drug and supplement interactions

  1. CYP2C9 and CYP3A4 substrates. Apigenin is reported to inhibit these cytochrome P450 enzymes, potentially affecting metabolism of warfarin, statins, certain antidepressants, and some calcium channel blockers. Clinically meaningful for narrow-therapeutic-index drugs; clinician coordination is standard guidance.
  2. Anticoagulants (warfarin, apixaban, rivaroxaban). A mild antiplatelet effect plus CYP2C9 inhibition affecting warfarin metabolism is reported; INR monitoring for warfarin users and clinician coordination is standard guidance.
  3. Alcohol and benzodiazepines. The same GABA-A receptor system is involved, raising additive CNS depression risk; combining without medical guidance is discouraged.
  4. Z-drugs (zolpidem, eszopiclone). The same GABA-A target is involved, raising additive sedation risk.
  5. Other GABAergic supplements — generally compatible (see Stacks section above), with attention to total inhibitory tone if stacking aggressively.

What isn't established about apigenin

Apigenin has rapidly gained popularity, largely via Andrew Huberman's recommendations, but the evidence base for standalone pure apigenin remains thinner than the popularity suggests. Several open questions affect how confidently it can be recommended.

Standalone apigenin vs chamomile extract evidence gap. The strongest human RCT evidence is for chamomile extract (Mao et al. 2016, Amsterdam et al. 2012) standardized to apigenin content — not standalone purified apigenin. The 50 mg supplemental dose is extrapolated from animal data and chamomile dosing rather than direct human RCT validation of standalone apigenin. Whether pure apigenin at 50 mg produces the same effects as chamomile extract's broader flavonoid matrix is mechanistically reasonable but not directly demonstrated.

CD38/NAD+ human translation. Escande et al. 2013's mechanism is documented in cell culture and obese mice. Whether oral apigenin at supplemental doses meaningfully elevates human NAD+ levels, and whether this translates to longevity outcomes, is essentially untested in the sources reviewed. The mechanism is documented; the clinical translation is mechanistically reasonable but not RCT-validated.

Bioavailability constraint. Apigenin is poorly water-soluble. Oral bioavailability is reported as modest, even with dietary fat coadministration. This absorption gate may account for some apigenin trials showing smaller effects than preclinical work would predict.

Long-term safety beyond a few weeks. Most clinical trials reviewed extend to weeks or a few months. Multi-year continuous supplemental apigenin use is not directly RCT-characterized, though the partial-agonist pharmacology is discussed as theoretically protective against tolerance and dependence.

CYP inhibition clinical significance. CYP2C9 and CYP3A4 inhibition is a documented mechanism. The clinical-significance threshold for users on chronic CYP-substrate medications is not precisely characterized in the sources reviewed.

Product quality variance. Independent testing has occasionally found apigenin products with significantly less apigenin than labeled, and some products may contain other chamomile flavonoids or undisclosed compounds.

Healthy young-adult evidence. Most chamomile-apigenin trials reviewed are in older adults or anxiety populations. Whether apigenin produces meaningful effects in healthy young adults beyond mild relaxation is mechanistically reasonable but not directly demonstrated.

Product-quality considerations

Apigenin is available primarily as standalone extract supplements (typically 50 mg capsules) and as chamomile extract products with varying apigenin standardization. Quality is reported to vary — independent testing has found products with significantly less apigenin than labeled.

Quality markers reported in the category

  • 98%+ pure apigenin standardized extract — the studied form. Lower-purity products dilute the per-mg apigenin content.
  • Source disclosed — chamomile extract is the conventional and trial-validated source; some products use parsley or synthetic apigenin instead.
  • 50 mg per capsule — matching the common evening protocol. Lower-dose (25 mg) and higher-dose (75–100 mg) products also exist.
  • Third-party testing — USP, NSF, or ConsumerLab certification. HPLC verification of apigenin content is the relevant additional check given documented label variance.
  • cGMP-certified manufacturing facility.
  • Certificate of Analysis (COA) available on request — signals manufacturer transparency about testing.
  • No proprietary sleep blends that obscure the actual apigenin dose alongside other ingredients.
  • Price relative to extraction cost. High-purity apigenin extraction is moderately expensive; implausibly low-priced products often underdeliver on actual content.
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Apigenin FAQ

How much apigenin is typically taken?

50 mg taken 30–60 minutes before bed is the most common protocol, popularized in part by Andrew Huberman's recommendations. This dose is extrapolated from animal data and chamomile extract studies rather than direct human RCTs of pure apigenin — the evidence base is thinner than the popularity suggests. Higher doses (100 mg) are sometimes used but lack additional evidence; lower doses (25 mg) are reported by some users as sufficient. Dietary fat alongside dosing is commonly recommended for absorption, since apigenin is poorly water-soluble.

How does apigenin compare to chamomile tea?

A large dose difference. A typical cup of chamomile tea provides roughly 1–5 mg apigenin; a 50 mg supplement provides 10–50× that amount in concentrated form. Chamomile extract products (standardized to specific apigenin content) sit between the two. Tea is discussed as a pleasant wind-down ritual providing apigenin alongside other chamomile flavonoids and aromatic compounds, relevant to the overall sensory and habit-formation arm of sleep hygiene. The supplement delivers the concentrated dose-dependent effect studied in animal models and extrapolated to human use.

Does apigenin cause dependence or tolerance like benzodiazepines?

Current evidence suggests no. Apigenin is a partial agonist at the benzodiazepine binding site on GABA-A receptors, meaning it has a ceiling on receptor activation that is discussed as preventing the deep receptor downregulation and chronic adaptation responsible for benzodiazepine dependence. Long-term human dependency studies on standalone apigenin are limited, but no concerning signals have been reported so far. The partial-agonist pharmacology is structurally distinct from full agonists like benzodiazepines.

Is the CD38/NAD+ longevity mechanism well established?

The mechanism — CD38 inhibition preserving NAD+ — is documented in cell and animal studies (Escande et al. 2013). Apigenin inhibits CD38, the enzyme that consumes NAD+, meaning it acts on a different layer than NAD+ precursor supplements (NMN, NR, oral NAD+). Combining a precursor (input side) with apigenin (consumption side) is described as mechanistically coherent. Whether oral apigenin at typical human supplemental doses produces meaningful NAD+ elevation, and whether this translates to longevity outcomes, remains unproven in humans — the mechanism is documented in mice, not directly tested in human trials.

Does apigenin stack with DSIP or other sleep peptides?

The combination is discussed as mechanistically complementary. DSIP (delta sleep-inducing peptide) is reported to act directly on slow-wave sleep architecture — a peptide-level intervention on sleep depth. Selank (a tuftsin analog) is reported to provide anxiolytic effects via GABA-A receptor sensitivity modulation — the same broad GABA-A target as apigenin but at a different mechanism layer (Selank modulates receptor sensitivity; apigenin is a partial agonist at the benzodiazepine binding site). Epitalon adds a pineal-axis longevity arm — telomere maintenance and circadian regulation. The four-component combination (DSIP, Selank, Epitalon, apigenin) is discussed as covering sleep architecture, anxiolytic GABA-A modulation, pineal-axis longevity, and benzodiazepine-site partial agonism plus CD38/NAD+ preservation from four distinct mechanism layers, with no known negative interaction documented.

Does apigenin combined with NMN or NAD+ make mechanistic sense?

The mechanism layering is described as biochemically coherent. NMN and NAD+ precursors operate on the input side, feeding the salvage pathway to raise NAD+ levels. Apigenin operates on the consumption side, inhibiting CD38, the major NAD+-consuming enzyme reported to increase in activity with aging and inflammation. Combining the two addresses both ends of the NAD+ balance equation: more substrate in (NMN/NR), less destruction (apigenin via CD38 inhibition). This combination is not rigorously RCT-validated as a combination, but the pharmacological rationale is discussed as mature.

What about apigenin during pregnancy?

Concentrated apigenin supplements are commonly discussed as a pregnancy contraindication. Chamomile — and by extension apigenin — has historically been associated with uterine activity concerns at high doses, with a theoretical risk of triggering contractions. Culinary chamomile tea (1–2 cups daily) is generally considered acceptable during pregnancy in most clinical practice, but concentrated 50 mg supplements deliver far higher apigenin per dose than tea provides. The evidence base for supplemental apigenin in pregnancy is essentially absent; clinician coordination is the standard guidance.

Does apigenin help with anxiety, or only sleep?

Both, with related mechanisms — but the anxiety evidence comes mostly from chamomile extract studies rather than standalone apigenin. Chamomile extract has shown anxiolytic effects in RCTs in adults with generalized anxiety disorder; apigenin is the principal active flavonoid in chamomile, so the effect is reported to likely operate through apigenin's GABA-A partial agonism. Effect sizes are described as modest — not benzodiazepine-class — but real. Direct standalone-apigenin anxiety trials are limited.

References

  1. Salehi B, Venditti A, Sharifi-Rad M, et al. The therapeutic potential of apigenin. Int J Mol Sci. 2019;20(6):1305. https://pubmed.ncbi.nlm.nih.gov/30875872/
  2. Mao JJ, Xie SX, Keefe JR, Soeller I, Li QS, Amsterdam JD. Long-term chamomile (Matricaria chamomilla L.) treatment for generalized anxiety disorder: a randomized clinical trial. Phytomedicine. 2016;23(14):1735-1742. https://pubmed.ncbi.nlm.nih.gov/27912875/
  3. Amsterdam JD, Shults J, Soeller I, Mao JJ, Rockwell K, Newberg AB. Chamomile (Matricaria recutita) may provide antidepressant activity in anxious, depressed humans: an exploratory study. Altern Ther Health Med. 2012;18(5):44-49. https://pubmed.ncbi.nlm.nih.gov/22894890/
  4. Escande C, Nin V, Price NL, et al. Flavonoid apigenin is an inhibitor of the NAD+ase CD38: implications for cellular NAD+ metabolism, protein acetylation, and treatment of metabolic syndrome. Diabetes. 2013;62(4):1084-1093. https://pubmed.ncbi.nlm.nih.gov/23172919/
  5. Adib-Hajbaghery M, Mousavi SN. The effects of chamomile extract on sleep quality among elderly people: a clinical trial. Complement Ther Med. 2017;35:109-114. https://pubmed.ncbi.nlm.nih.gov/29154054/
  6. Avallone R, Zanoli P, Puia G, Kleinschnitz M, Schreier P, Baraldi M. Pharmacological profile of apigenin, a flavonoid isolated from Matricaria chamomilla. Biochem Pharmacol. 2000;59(11):1387-1394. https://pubmed.ncbi.nlm.nih.gov/10751547/

Published Studies

Plain-English summaries of the peer-reviewed studies behind the claims above. Click any title to read the source paper.

International Journal of Molecular Sciences · 2019Open Access
The Therapeutic Potential of Apigenin →

Salehi B, Venditti A, Sharifi-Rad M, et al.

A comprehensive review of apigenin's bioactive properties covering GABAergic mechanism (benzodiazepine-site partial agonism on GABA-A receptors), anti-inflammatory effects, anxiolytic and sedative effects in animal models, and emerging human evidence primarily via chamomile extract trials. A frequently cited single-source reference for the apigenin evidence landscape and mechanism case.

Phytomedicine · 2016Open Access
Long-Term Chamomile (Matricaria chamomilla L.) Treatment for Generalized Anxiety Disorder: A Randomized Clinical Trial →

Mao JJ, Xie SX, Keefe JR, Soeller I, Li QS, Amsterdam JD

A 38-week randomized clinical trial of chamomile extract (1,500 mg/day, standardized to 1.2% apigenin) in 179 patients with generalized anxiety disorder. Chamomile produced significant reductions in GAD severity versus expected relapse rates, with the effect maintained over long-term follow-up. The cleanest human RCT evidence for chamomile-apigenin in anxiety, though it studies chamomile extract rather than pure standalone apigenin.

Alternative Therapies in Health and Medicine · 2012Paywalled
Chamomile (Matricaria recutita) May Provide Antidepressant Activity in Anxious, Depressed Humans: An Exploratory Study →

Amsterdam JD, Shults J, Soeller I, Mao JJ, Rockwell K, Newberg AB

A secondary analysis of a chamomile clinical trial exploring whether chamomile extract provides antidepressant activity alongside its established anxiolytic effect. Reports a signal toward reduced depressive symptoms in patients with comorbid anxiety and depression. Cited as supporting evidence for the chamomile-apigenin mood effect.

Diabetes · 2013Open Access
Flavonoid Apigenin Is an Inhibitor of the NAD+ase CD38: Implications for Cellular NAD+ Metabolism, Protein Acetylation, and Treatment of Metabolic Syndrome →

Escande C, Nin V, Price NL, et al.

Identifies apigenin (alongside quercetin) as a pharmacological CD38 inhibitor. Reports that apigenin treatment raises intracellular NAD+ levels and reduces global protein acetylation in cell culture, and that apigenin administration to obese mice increases NAD+ levels and improves glucose and lipid homeostasis. The foundational mechanism reference specifically identifying apigenin (not a synthetic analog) as the CD38-inhibiting compound behind the NAD+ preservation claim.

Complementary Therapies in Medicine · 2017Open Access
The Effects of Chamomile Extract on Sleep Quality Among Elderly People: A Clinical Trial →

Adib-Hajbaghery M, Mousavi SN

A clinical trial of chamomile extract (400 mg twice daily) in 60 elderly adults with poor sleep quality. Reports chamomile significantly improved sleep quality scores over the trial period. Methodology is weaker than a placebo-controlled design but supports the sleep-effect use case in older populations where endogenous GABAergic tone declines with age.

ChamomileGABA-A Partial AgonistCD38 InhibitorNAD+ PreservationAnxiolyticSleep

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