IngredientsAngelica keiskei Koidzumi, commonly known in Japan as ashitaba (アシタバ or 明日葉), is a popular botanical medicine in Japan containing diverse bioactive components including prenylated chalcones, linear and angular coumarins, and flavanones. The name translates literally to "tomorrow's leaf" in Japanese — harvesting a leaf at the break of day often results in a new sprout growing overnight, being visible the following morning.
It is native to Japan, where it is found on the Pacific Coast, specifically in the area of the Bōsō Peninsula, Miura Peninsula, Izu Peninsula, and the Izu Islands. It has been widely cultivated outside its natural range. It is a perennial, with a typical growth height of 50–120 cm. Like most other members of the carrot family, it produces large umbels of white flowers and has dissected leaves.
This plant is part of the Apiaceae family, along with the carrot, celery, or parsley. It is recognizable by its dissected green leaves, white flowers, and stems containing a yellow sap. In Korea, the plant is known as shinsuncho, meaning "elixir of life." Ashitaba was heavily consumed in Hachijojima (Japan), also known as the "island of longevity."
Leaves and/or stems are the primary extracted parts of the plant. The main use of their stipes, leaves, and taproots is in regional cuisine, where they are used to prepare soba, tempura, shōchū, tea, ice cream, pasta, and other foods. Currently, A. keiskei is also commercialized as a health food and as additives in health drinks. Modern commercial preparations include dried leaf powder in capsule or tablet form, concentrated chalcone extracts standardized to specific active compound percentages, and green juice preparations made from dried leaves and stems. Supercritical CO₂ extraction has been used for certain preparations.
According to ancient documents, the gene-center of Ashitaba is Hachijojima, an island in the Izu archipelago, a moist subtropical region located southerly to Japan. This island is well known as the "Island of Longevity." Historically, inhabitants consumed a diet composed of assorted grains, seaweeds, fish, and the edible, golden-sapped Angelica-like plant known as Ashitaba.
Angelica keiskei (Miq.) Koidz. (Umbelliferae) has traditionally been used to treat dysuria, dyschezia, and dysgalactia as well as to restore vitality. More recently, the aerial parts have been consumed as a health food.
Traditionally, it is seen as a major contributor to the supposedly healthier, extended lives of the local residents, possibly due to the chalconoids that are unique to this species of Angelica. At one point during the Edo period, the haulm's yellow sap was used in the external treatment of smallpox.
In traditional Japanese practice, it was consumed in fresh or dried forms and used as a remedy thought to treat heartburn, stomach ulcers, high blood pressure and cholesterol, hay fever, gout, and constipation.
Longevity- and health-promoting effects have been ascribed to the plant in Asian traditional medicine. In Korea, where the plant is known as shinsuncho, similar health traditions existed. Medicinal uses of Ashitaba have been recorded in early Chinese medicinal texts from the late 1500s, and it was introduced to Japan in the early 1600s.
Various flavonoids, coumarins, phenolics, acetylenes, sesquiterpenes, diterpenes, and triterpenes have been identified as the constituents of A. keiskei. The following classes represent its principal biologically active components:
The chalcone fraction — concentrated especially in the distinctive yellow sap of the stems — is considered the most pharmacologically significant. 4-Hydroxyderricin (4HD) and xanthoangelol (XAG) are major components of the n-hexane/ethyl acetate (5:1) extract of the yellow-colored stem juice of Angelica keiskei. These two prenylated chalcones are considered to be the major active compounds of Ashitaba.
Additional phytochemical constituents documented include isobavachalcone, xanthoangelol (and its variants A–G), cyclohexenones, sesquiterpenes (including ashitabaol), triterpenes, polyacetylenes, and vitamins A, B complex, and K.
DMC has been detected in the stipes and leaves (but not in the roots) of Angelica keiskei koidzumi, to which longevity- and health-promoting effects are attributed in Asian folk medicine. The flavonoid 4,4′-dimethoxychalcone (DMC) is particularly abundant in the plant Angelica keiskei koidzumi, which has been used in Asian traditional medicine, and was documented for its ability to promote autophagy-dependent longevity and health.
From biologically active fractions of A. keiskei roots, two angular furanocoumarins (archangelicin and 8(S),9(R)-9-angeloyloxy-8,9-dihydrooroselol), three linear furanocoumarins (psoralen, bergapten, and xanthotoxin), and several chalcones have been isolated. As is typical with members of the Apiaceae family, Ashitaba contains bioactive furanocoumarins and dihydrofuranocoumarin analogs, some of which have illustrated phototoxic and photogenotoxic effects in studies.
A new antioxidative sesquiterpenoid, ashitabaol A, has been identified from the seeds of Angelica keiskei. The plant also contains chlorophyll, dietary fiber, and several minerals.
Both 4HD and XAG increase glucose uptake and GLUT4 translocation to the plasma membrane. They also stimulate the phosphorylation of 5′ adenosine monophosphate–activated protein kinase (AMPK) and its downstream target acetyl-CoA carboxylase. In addition, phosphorylation of liver kinase B1 (LKB1), which acts upstream of AMPK, is also increased by 4HD and XAG treatment.
4HD and XAG inhibit adipocyte differentiation through AMPK and mitogen-activated protein kinase pathways, resulting in the down-expression of adipocyte-specific transcription factors. Specifically, 4HD and XAG suppress intracellular lipid accumulation and inhibit adipocyte differentiation accompanied by down-expression of adipocyte-specific transcription factors, including CCAAT/enhancer-binding protein-β (C/EBP-β), C/EBP-α, and peroxisome proliferator-activated receptor gamma (PPAR-γ).
LPS-mediated production of nitric oxide (NO) is markedly reduced by 4-hydroxyderricin (10 µM) and xanthoangelol (5 µM) compared with their parent compound, chalcone. They also inhibit LPS-induced secretion of tumor necrosis factor-alpha (TNF-α) and expression of inducible NO synthase (iNOS) and cyclooxygenase-2 (COX-2).
The elevation of plasma plasminogen activator inhibitor 1 (PAI-1), an inhibitor of fibrinolysis, results in a predisposition to thrombosis risk. Ashitaba exudates administered intraperitoneally and orally over long-term suppressed the LPS-induced PAI-1 increase in mouse plasma. Xanthoangelol, xanthoangelols B and D — components of Ashitaba exudates — significantly inhibited TNFα-induced PAI-1 production from human umbilical vein endothelial cells (HUVECs).
The flavonoid 4,4′-dimethoxychalcone (DMC) has been identified as a natural compound with anti-ageing properties. External DMC administration extends the lifespan of yeast, worms, and flies, decelerates senescence of human cell cultures, and protects mice from prolonged myocardial ischaemia. Concomitantly, DMC induces autophagy, which is essential for its cytoprotective effects from yeast to mice. This pro-autophagic response induces a conserved systemic change in metabolism, operates independently of TORC1 signalling, and depends on specific GATA transcription factors.
More recently, DMC treatment was found to selectively eliminate senescent cells, and DMC alone or in combination with quercetin or dasatinib showed high efficiency in the clearance of senescent cells. Mechanistically, DMC inhibits ferrochelatase (FECH) and induces ferritinophagy, which leads to an increase of labile iron pool, triggering ferroptosis of senescent cells.
Ashitaba chalcones 4-hydroxyderricin (4HD) and xanthoangelol (XAG) suppress melanoma development by directly targeting both BRAFV600E and PI3-K, which blocks the activation of downstream signaling. This leads to the induction of G1 phase cell cycle arrest and apoptosis in melanoma cells. 4HD or XAG dramatically attenuated tumor incidence and volume in the BRAF-activated Pten-deficient melanoma mouse model.
Angular type furanocoumarins and chalcones from A. keiskei roots suppressed 12-O-tetradecanoylphorbol-13-acetate (TPA)-stimulated ³²Pi-incorporation into phospholipids of cultured cells; chalcones 4-hydroxyderricin and xanthoangelol were proved to have anti-tumor-promoting activity in mouse skin carcinogenesis induced by DMBA plus TPA.
A critical overview note: Ashitaba is purported to possess cytotoxic, antidiabetic, antioxidative, anti-inflammatory, antihypertensive, and antimicrobial properties. Although many in vitro studies have been conducted on ashitaba's chemical constituents, the in vivo efficacy and clinical relevance of this plant has yet to be confirmed for most of these activities. For several of the areas reviewed below, the evidence base consists primarily of cell culture and animal studies, with limited and often small-scale human clinical evidence.
Human evidence (pilot, uncontrolled): Nine adult subjects defined as patients and candidates with metabolic syndrome ingested Ashitaba green juice (6.2 g/day of granulated powder containing 12.3 mg chalcones) for 8 weeks. For evaluation of efficacy, abdominal fat area, body weight, body fat, and blood parameters were measured. Ingestion of Ashitaba green juice for 8 weeks significantly decreased visceral fat area, body weight, BMI, and body fat. This was an uncontrolled pilot study with no placebo group, severely limiting interpretation.
Human evidence (pilot RCT): A randomized, placebo-controlled, double-blind parallel pilot proof-of-concept study enrolled 15 healthy male subjects (average age 38, average BMI 24.0 ±3.2). The treatment group (N=10) received 200 mg/day ashitaba chalcone powder (total chalcone content: no less than 8%). A two-part pilot study was undertaken to determine Ashitaba's effect on body weight, waist circumference, and visceral fat in overweight adults. There were two 8-week randomized, placebo-controlled, double-blind parallel studies: Part 1 with 15 healthy males and Part 2 with 26 overweight adults. The treatment groups received 200 mg/day ashitaba chalcone powder (8%) and control groups received placebo daily. Weight, visceral fat, subcutaneous fat, total fat, BMI, waist circumference, and body fat were measured at baseline, weeks 4 and 8.
Human evidence (RCT, published 2024): A randomised, placebo-controlled, double-blind, parallel-group study determined whether encapsulated Ashitaba chalcone (16 mg comprising 10.1 mg 4-hydroxyderricin and 5.9 mg xanthoangelol) could reduce obesity in 17 men and 25 women with a BMI of 25 to <30. Participants ingested capsules containing either the chalcone or a placebo daily for 12 weeks. The primary endpoint was changes in visceral fat areas determined by computed tomography (CT) at baseline, and at 8 and 12 weeks later. The primary endpoint, abdominal visceral fat area, was significantly reduced in the chalcone compared with the placebo group 12 weeks after screening (p <0.05). The secondary endpoint, waist circumference, was also significantly decreased in the chalcone compared with the placebo group at weeks 8 and 12 (p <0.05).
A separate 12-week metabolic syndrome study using a standardized sap-derived powder found less consistent results: this pilot study evaluated the effects of ChalCurb® (220 mg capsule) on aspects of metabolic health in 60 adults (30 men, 30 women) with aspects of metabolic syndrome. Subjects were randomly assigned to either the supplement or placebo once a day with dinner for 12 weeks. Quality of life, visceral fat, lipids, HbA1c, body composition, and ghrelin were assessed at baseline and end of study. Change in visceral fat was not different between the groups.
Evidence assessment: The body of human clinical evidence is small in terms of participant numbers and study duration. The 2024 RCT represents the highest-quality data currently available and reported a statistically significant reduction in visceral fat area with a 16 mg chalcone dose; however, the study was relatively small (42 participants). The inconsistency in findings across different preparations and doses warrants further large-scale investigation.
The efficacy of A. keiskei was confirmed in anti-obesity, hepatoprotective, anti-diabetes mellitus, and increasing plasma antioxidants in patients with metabolic syndrome, based on the PMC systematic review published in 2024. Mechanistically, the two prenylated chalcones, 4-hydroxyderricin and xanthoangelol, have exhibited various biological and pharmacological effects, including suppression of adipocyte differentiation in 3T3-L1 cells, suppression of lipid accumulation in HepG2 cells, and prevention of adiposity in high-fat diet–fed mice.
At the receptor level, compounds from Ashitaba have been studied as inhibitors of α-glucosidase and dipeptidyl peptidase IV (DPP-IV), enzymes central to blood glucose regulation. One of the global health issues is diabetes mellitus, characterized by elevated blood glucose levels. The absorption of glucose in the body occurs through the digestion of carbohydrates by the enzyme α-glucosidase, which is responsible for hydrolyzing carbohydrates into sugar.
Evidence assessment: Most antidiabetic evidence in humans is indirect (derived from the broader metabolic syndrome studies). Dedicated human trials specifically targeting glycemic control with standardized A. keiskei preparations remain limited. Mechanistic evidence from cell-culture and animal studies is consistent and robust, but clinical translation is not yet confirmed.
The efficacy of A. keiskei in increasing plasma antioxidants in patients with metabolic syndrome has been demonstrated in human studies. A. keiskei is safe as proven by only mild or no adverse events reported, thus it is prospective to be further developed as an antioxidant nutraceutical. Chalcone-rich preparations have consistently demonstrated free-radical scavenging activity in multiple in vitro assays. A. keiskei koidzumi extracts have been reported to have anti-carcinogenic, anti-diabetic, anti-inflammatory, and anti-hypertensive properties.
Evidence assessment: Antioxidant activity in vitro is well established. Limited human data from metabolic syndrome studies suggest increases in plasma antioxidant capacity, but these findings require replication in dedicated, larger trials.
The in vitro evidence for anti-inflammatory effects of the Ashitaba chalcones is well characterized. Investigations into the effects and underlying molecular mechanisms of 4-hydroxyderricin and xanthoangelol on LPS-induced inflammatory responses in RAW264 mouse macrophages demonstrated that LPS-mediated production of nitric oxide (NO) was markedly reduced by 4-hydroxyderricin (10 µM) and xanthoangelol (5 µM) compared with their parent compound, chalcone. They also inhibited LPS-induced secretion of TNF-α and expression of iNOS and COX-2.
Evidence assessment: Anti-inflammatory effects in cell-culture models are well documented at specific concentrations. No published controlled human clinical trials specifically addressing inflammatory endpoints with A. keiskei preparations were identified in the peer-reviewed literature. Evidence is preclinical only for this indication.
A study clarified that Angelica keiskei exerts actions that lead to the prevention of thrombosis, raising the possibility that ingesting Ashitaba could help prevent thrombotic diseases. These findings suggest that Ashitaba can decrease elevated PAI-1 production, and that daily consumption of Ashitaba products might maintain anticoagulant status by inhibiting elevations in PAI-1.
In a mouse aging model, supplementation with Ashitaba yellow exudate (AYE) decreased levels of the acute-phase and fibrinolytic protein plasma plasminogen, and significantly decreased those of tumor necrosis factor α. These results suggested that continuous intake of AYE throughout life decreases age-induced systemic inflammation and prevents thrombotic tendencies without affecting body weight.
Evidence assessment: Ashitaba is thought to have antithrombotic properties, but this has not yet been scientifically proven in humans. Evidence is derived from in vitro studies on HUVECs and animal models. No human clinical trials specifically evaluating thrombotic or cardiovascular endpoints with Ashitaba have been published.
The crude extracts and pure constituents of A. keiskei have been shown to inhibit tumor growth and ameliorate inflammation, obesity, diabetes, hypertension, and ulcer in preclinical models. Multiple cell-line studies have documented apoptotic activity. For example, 4-hydroxyderricin from Angelica keiskei roots has been shown to induce caspase-dependent apoptotic cell death in HL60 human leukemia cells. The chalcones 4HD and XAG suppress melanoma development by directly targeting both BRAFV600E and PI3-K, blocking downstream signaling, leading to G1 phase cell cycle arrest and apoptosis in melanoma cells, with dramatic attenuation of tumor incidence and volume in a BRAF-activated mouse model.
In hepatocellular carcinoma (HepG2) cells, Angelica keiskei extract produced a dose-dependent reduction in cell viability, with higher dosages causing notable morphological alterations. An antibody apoptotic array indicated significant changes in apoptotic proteins, specifically IGFBP1, BAD, and Bid.
Evidence assessment: All evidence on anticancer activity is preclinical (in vitro and animal studies). No human clinical trials for any oncological indication with Ashitaba or its isolated compounds have been reported. Results are mechanistically interesting but not clinically applicable at this stage.
The flavonoid 4,4′-dimethoxychalcone (DMC) has been identified as a natural compound with anti-ageing properties. External DMC administration extends the lifespan of yeast, worms, and flies, decelerates senescence of human cell cultures, and protects mice from prolonged myocardial ischaemia. Concomitantly, DMC induces autophagy, which is essential for its cytoprotective effects from yeast to mice. This pro-autophagic response induces a conserved systemic change in metabolism, operates independently of TORC1 signalling, and depends on specific GATA transcription factors. DMC has been identified in the plant Angelica keiskei koidzumi, to which longevity- and health-promoting effects are ascribed in Asian traditional medicine.
DMC treatment was found to prevent hair loss, improve motor coordination, and reduce the expression of several senescence-associated secretory phenotype factors (IL-6 and others) in mouse models.
Evidence assessment: The 2019 Nature Communications study by Madeo and colleagues provides compelling multi-organism evidence for pro-autophagic and lifespan-extending effects of DMC. However, all evidence is preclinical (model organisms and human cell cultures). No human clinical trials investigating longevity or aging outcomes with Ashitaba or DMC have been published.
Biochemometric analysis and molecular networking identified the chalcone analogs 4-hydroxyderricin (MIC ≤4.6 µM, IC₅₀ = 2.0 µM) and xanthoangelol (MIC ≤4.0 µM, IC₅₀ = 2.3 µM) as putative active constituents against Staphylococcus aureus. Extracts have also demonstrated anti-viral and anti-bacterial activities in preclinical studies.
Evidence assessment: Antimicrobial activity data are entirely preclinical. Minimum inhibitory concentrations identified in cell-free and cell-culture assays cannot be directly extrapolated to clinical use without pharmacokinetic and human safety/efficacy data.
The administration of Angelica keiskei extracts to ICR mice at 10, 25, and 50 mg/kg per os improves alcohol-induced hepatotoxicity, suggesting that these extracts indirectly protect the liver against free radical attack. Hepatoprotective effects have been confirmed as part of the broader assessment of efficacy in human studies of metabolic syndrome.
Evidence assessment: Primary hepatoprotective evidence is from animal models. Human metabolic syndrome studies have included liver-related biomarkers among their endpoints, but specific hepatoprotective efficacy in humans remains incompletely characterized.
The following dosages are reported directly from identified clinical or formal toxicological studies and should not be interpreted as established therapeutic recommendations:
A. keiskei is safe as demonstrated by only mild or no adverse events reported in clinical studies, and it is prospective to be further developed as an antioxidant nutraceutical. In the Japanese pilot study, 9 subjects ingested Ashitaba green juice for 8 weeks, and all subjects had significantly lower visceral fat, body fat, and body weight at the end of the 8th week, with no adverse clinical changes attributed to Ashitaba.
As is typical with members of the Apiaceae family, Ashitaba contains bioactive furanocoumarins and dihydrofuranocoumarin analogs. Some of these compounds have illustrated phototoxic and photogenotoxic effects in studies. An assessment by the Senate Commission on Food Safety reported that psoralen and its isomer 8-methoxypsoralen are only weakly mutagenic in the absence of UV light, but in the presence of UV radiation, these compounds bind covalently to DNA in bacteria and yeasts, leading to genotoxic and mutagenic effects.
Among natural coumarins, several compounds including psoralen, bergapten, and xanthotoxin — all belonging to the furanocoumarin class — have caused a limited number of skin phototoxic reactions in humans. Typical furanocoumarin intake from food sources is several times below the lowest dose capable of producing phototoxic effects, but the risk of exposure increases in cases of inappropriate storage or processing of foods.
Coumarins are secondary metabolites of numerous higher plant species including Angelica keiskei (Ashitaba). The most important adverse effects of coumarins are hepatotoxicity favored by the ingestion of large doses and possible genetic polymorphism of CYP2A6, and dermatological phototoxic reactions. No specific cases of hepatotoxicity caused by Ashitaba itself have been documented in the clinical literature reviewed.
GLP studies including a bacterial reverse mutation assay, a chromosome aberration assay, and an in vivo micronucleus assay are negative for genotoxicity. A GLP-compliant 90-day repeated oral gavage study of ashitaba yellow sap powder containing 8.45% chalcones in Sprague-Dawley rats resulted in expected known physiological effects on coagulation parameters and plasma lipids at 300 and 1000 mg/kg/day. Ashitaba-related pathology included a dose-related male rat-specific alpha 2-urinary globulin nephropathy at 100, 300, and 1000 mg/kg/day, and jejunal lymphangiectasia in both sexes at 1000 mg/kg/day. The alpha 2-urinary globulin nephropathy finding is considered rat-specific and not directly translatable to human risk.
Various constituents isolated from Ashitaba such as chalcones, flavanones, and coumarins have been precisely characterized with bioactivities. A study clarified that Angelica keiskei exerts actions that lead to the prevention of thrombosis. Given its documented PAI-1 inhibition and antiplatelet chalcone content, there is theoretical potential for additive effects with anticoagulant or antiplatelet drugs, though no human pharmacokinetic interaction studies were identified in the literature reviewed.
Aqueous and ethanol fractions of Angelica keiskei did not induce acute toxicity in the skin of animals, as assessed by anatomical and pathological observations. These aqueous and ethanol fractions of Angelica keiskei have promising potential uses as cosmetic ingredients that do not induce significant levels of skin irritation or phototoxicity.
Review of the physiological effects of Ashitaba on metabolic syndrome risk factors, including blood glucose, obesity, lipid metabolism, and MetS-associated thrombotic tendencies, indicates that although physiological effects appear beneficial, most findings are derived from experimentation using obese and diabetic mouse models, with only a few small clinical reports describing effects on healthy humans. Therefore, larger cohort studies of humans with greater degrees of obesity are needed.
The experimental results demonstrate promise for the medical use of Ashitaba, but considerable work needs to be done to understand the mechanisms of action of its metabolites. The compound DMC in particular, identified and characterized in a landmark 2019 Nature Communications paper, represents one of the most scientifically significant findings associated with the plant, offering mechanistically rigorous evidence for autophagy-mediated anti-aging effects — though entirely in preclinical models to date.
Health conditions that Ashitaba may help support.
Ashitaba's antioxidant activity is among its best-validated properties. A human pilot study demonstrated significant increases in plasma quercetin, lutein, and total antioxidant performance after ingestion. Chalcones have demonstrated potent free-radical scavenging in multiple in vitro systems. A MetS pilot confirmed raised plasma antioxidants in patients.
Ashitaba chalcone XA inhibits platelet aggregation in vivo in mouse tail-bleeding models. Ashitaba exudate reduces PAI-1 (a prothrombotic plasminogen activator inhibitor) in obese, diabetic, and aging mouse models. The Springer Archives of Pharmacal Research review lists anti-thrombotic activity as a confirmed property of ashitaba extracts.
Ashitaba's chalcone 4-HD demonstrated hypotensive action in stroke-prone spontaneously hypertensive rats, reducing blood pressure alongside lipid regulation. The plant is also listed in traditional Japanese use for high blood pressure. Preclinical evidence supports antihypertensive activity, but no human RCTs exist.
Multiple animal studies and a small human pilot study support ashitaba's antidiabetic activity. Its chalcones inhibit α-glucosidase more potently than the drug acarbose in vitro, suppress post-meal glucose spikes in mouse models, and a human metabolic syndrome pilot confirmed anti-diabetic mellitus efficacy. No large-scale RCTs have been conducted.
Ashitaba extract reduced plasma cholesterol in high-fat-diet mice via AMPK-mediated inhibition of hepatic lipogenesis. A rat type 2 diabetes study showed the flavonoid-rich extract reduced total cholesterol comparably to metformin. However, a rat dietary study found no cholesterol reduction at normal dietary doses.
Ashitaba chalcones suppress pro-inflammatory signaling through multiple pathways in cell and animal studies. XA inhibits NF-κB nuclear translocation, and ashitaba exudate reduces TNF-α in obese diabetic mice. In a human bioavailability study, ashitaba consumption raised plasma antioxidant status significantly. No dedicated clinical inflammation trials exist.
The ashitaba compound DMC extends lifespan in yeast, worms, and flies and decelerates senescence in human cell cultures via autophagy induction (Nature Communications, 2019). Ashitaba also contains coumarins that enhance nerve growth factor (NGF) production in vitro. Preclinical neuroprotective effects include protection from demyelination and improved behavioral responses in mice.
Ashitaba chalcones are documented xanthine oxidase (XO) inhibitors in vitro; XO is the enzyme that produces uric acid and is the target of allopurinol. Xanthoangelol was identified as the most potent XO inhibitor among A. keiskei phenolics. Gout is also listed as a traditional use in Japanese folk medicine.
Ashitaba (Angelica keiskei) is a Japanese medicinal plant used as a longevity herb for centuries. It contains 4,4'-dimethoxychalcone (DMC) and chalcones that activate autophagy via AMPK and have been shown to extend lifespan in multiple model organisms. A 2019 Nature Communications study identified DMC as a caloric restriction mimetic extending lifespan by 20% in C. elegans, flies, and mice.
Several animal studies show ashitaba extract suppresses diet-induced obesity via AMPK activation and reduced lipogenesis. Two small human RCTs (8 weeks, 200 mg/day chalcone powder) assessed visceral fat and body composition in overweight adults. Results were pilot-level and require confirmation in larger trials.
Ashitaba chalcone DMC protected mice from myocardial ischemia injury in a Nature Communications study. Ashitaba also reduces PAI-1 (a prothrombotic marker) in animal models of obesity and inflammation, and has antihypertensive and anti-hyperlipidemic properties in preclinical research. No human cardiac outcome trials exist.
Ashitaba chalcones improve insulin sensitivity in animal models via AMPK activation, PTP1B inhibition, and α-glucosidase inhibition. A human metabolic syndrome pilot confirmed antidiabetic activity. XA and 4-HD reduce HOMA-IR (insulin resistance index) in fructose-fed rat models.
A 2024 rat study demonstrated that Angelica keiskei reduced cisplatin-induced nephrotoxicity by lowering serum creatinine, urea nitrogen, and KIM-1 while suppressing NF-κB and COX-2. Earlier rat feeding studies showed no kidney pathology even at excessive doses. No human renal trials exist.
Ashitaba has one randomized double-blind human trial (Noh et al., J Med Food, 2015) showing improvement in some liver function markers in habitual alcohol drinkers. Animal studies further support hepatoprotective effects, and a metabolic syndrome pilot confirmed hepatoprotective activity. Ashitaba has also traditionally been used to support liver function.
Ashitaba has been specifically studied for metabolic syndrome. A pilot study in patients confirmed anti-obesity, hepatoprotective, antidiabetic, and antioxidant efficacy. Two small double-blind RCTs tested chalcone powder (200 mg/day) in overweight/metabolic syndrome adults over 8–12 weeks. Overall, ashitaba holds the most convergent human evidence for MetS.
Ashitaba chalcones activate AMPK — a master regulator of cellular energy metabolism — in adipose tissue and liver. This drives fat oxidation, reduces lipogenesis, and improves insulin signaling in animal models. Human pilot trials targeting metabolic syndrome markers (visceral fat, blood sugar, lipids) used 200–220 mg/day standardized extract.
DMC from ashitaba decelerates senescence in human cell cultures in vitro (Nature Communications, 2019). Traditional Japanese use includes topical ashitaba preparations to promote healthy skin aging. Chalcones also protect cells from oxidative stress, a primary driver of skin aging. No dedicated human clinical dermatology trials exist.
Ashitaba extracts consistently reduced triglyceride levels in multiple rodent studies, including fructose-fed insulin-resistant rats and high-fat-diet mice. The mechanism involves AMPK-mediated suppression of hepatic lipogenesis and enhanced fatty acid oxidation. No dedicated human triglyceride trials have been conducted.
An in vivo rat study demonstrated that topical ashitaba leaf nanoparticle gel (5% nano ethosomal formulation) achieved the best burn wound healing outcomes, attributed to the plant's combined antioxidant, anti-inflammatory, and antibacterial properties. Traditional Japanese use also included topical application of ashitaba sap to cuts and wounds.
Ashitaba has been used in Japanese traditional medicine for centuries to treat persistent heartburn. Preclinical in vitro research identified that its chalcones xanthoangelol and 4-hydroxyderricin inhibit gastric H+/K+-ATPase, the proton pump responsible for acid secretion. No controlled human trials have confirmed efficacy for GERD.
Ashitaba is documented in traditional Japanese medicine as a galactagogue (milk-production enhancer) for breastfeeding mothers, with dysgalactia (insufficient milk secretion) listed as a traditional indication in the Springer Archives of Pharmacal Research review. No human clinical data on lactation efficacy or safety exist.
Ashitaba is documented in traditional Japanese medicine as a laxative and is listed by WebMD as a folk remedy for constipation. A rat feeding study confirmed that high-dose ashitaba significantly increased fecal weight and bile acid excretion, supporting a mild dietary-fiber-mediated laxative effect. No human clinical trials have evaluated this use.
Ashitaba is listed in Japanese traditional medicine as a remedy for stomach ulcers, and is documented as such by WebMD and RxList. Its chalcones inhibit gastric H+/K+-ATPase (proton pump) in vitro, providing a plausible antiulcer mechanism. No controlled human trials for ulcers have been conducted.
Body systems that Ashitaba may help support.
Go back