ELLAGIC ACID

Potent natural compound associated with strawberries, pomegranate, and especially raw chestnuts. There are no direct anticancer actions shown in clinical trials. But in systemic inflammatory diseases, ellagic acid has been shown to have very good actions in reducing insulin levels, insulin resistance and inflammation levels.

Ellagic acid is one of the main drivers in microbiome health benefits of foods such as pomegranate. There are substantial increases in existing bacteria with anti-inflammatory actions shown from these tests (see References). Other dietary sources include chestnuts and strawberries, especially wild. A supplement may help overcome the low absorption levels.

 

TYPICAL ABSORPTION LEVELS

1-5%

EXAMPLES OF IMPROVED OUTCOMES

NO

PRE-DIAGNOSIS OR PREVENTION

NO

Highlighted Studies

After EA administration, patients reduced their systolic blood pressure (118.1 ± 10.1 to 113.7 ± 7.8 mmHg), diastolic blood pressure (118.1 ± 10.1 to 113.7 ± 7.8 mmHg ), triglycerides (2.8 ± 1.1 to 2.1 ± 0.7 mmol), fasting plasma glucose (6.5 ± 0.5 to 5.7 ± 0.6 mmol/L ), fasting plasma insulin, and insulin secretion, with an increase of insulin sensitivity. In male patients, high-density lipoprotein cholesterol increased [aka “good” cholesterol]. In conclusion, EA improved...

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In the end of the study [polycistic ovary syndrome], EA reduced the FBS, Insulin and IR [insulin reistance], significantly compared the beginning the study—Reduction of CRP and TNF-α [systemic inflammation markers] levels in intervention group after supplementation was significant. EA reduced the TC [cholesterol], TG [tryglycerides] and LDL [cholesterol] significantly compared the beginning the study.

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Analysis of 3 trials involving 142 individuals revealed a significant decrease in CRP levels by 3.00 ng/ml [significant] with ellagic acid supplementation. TAC levels significantly increased [total antioxidant capacity] in individuals taking ellagic acid supplements at doses of 180 and 200 mg/day, with a meaningful enhancement in TAC in studies with an 8-week intervention but not in those lasting 12 weeks. There was no significant correlation between changes in TAC levels and dosage (P, 0.06)...

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At the end of the study, the mean of BS [blood sugar], insulin, IR [insulin resistance], HbA1c, TC, TG, LDL, MDA, CRP [c-reactive protein], TNF-α, and IL-6 were significantly decreased in the intervention group. Also, the mean of TAC and activity of GPx and SOD enzymes significantly increased in the intervention group (p < .05). EA supplementation can be helpful as a diet supplement in patients with type 2 diabetes through improvement in chronic adverse effects

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TABLE OF REFERENCES

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https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9572658/2Human studyEllagic acid consumption after 12 weeks of enhanced insulin sensitivity decreased insulin secretion and improved MetS components. It reduced abdominal obesity, blood pressure, fasting glucose, and triglycerides for males and females with an increasing of HDL-c in only male patients. Additionally, ellagic acid decreased uric acid, VLDL and AST.Additionally, this trial offers information about high-dose EA effects. New assays can be conducted to identify the human minimum effective dose for each component. EA must be studied in a phase 3 clinical trial for inferential information, as single or complementary therapy in some component of MetS or other related disease, offering to patients the benefit of multiple effects through the same regulation pathway.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8325180/2Human studythe results of this study indicated that 8 weeks of supplementation with EA, 200 mg/day, reduced the levels of blood sugar, blood lipids and IR in PCOS patients. Also, with the ameliorating in the status of oxidative stress and inflammatory status, at the end of the study, we saw a significant decrease in the amount of AMH in these patients. These results provide evidence to support the view that polyphenol antioxidant group with reducing the biochemical factors, can play an important role in helping to control the condition of this syndrome.At the end of the study, the mean of FBS, insulin, IR, TC, TG, LDL, MDA, CRP, TNF-α, total testosterone, prolactin and AMH were significantly decreased in the intervention group compared to the placebo group (P < 0.05). Also, there was a significant increase in the mean of TAC after supplementation with EA (P  0.05).
https://www.mdpi.com/2304-8158/13/1/152Human studyhere was no significant change in the gut microbial diversity in both cohorts after 4 weeks of intervention, but there was a significantly increased relative abundance of Coprococcus eutectus, Roseburia faecis, Roseburia inullnivorans, Ruminococcus bicirculans, Ruminococcus calidus, and Faecalibacterium prausnitzii. Pomegranate extract (PE) supplementation led to the augmentation of circulating propionate levels (p = 0.02) and an increasing trend for acetate levels (p = 0.12). The pomegranate extract (PE) supplementation group had an increased level of circulating urolithins compared to the placebo groupn this study, we assessed changes in the gut microbiome and circulating short-chain fatty acids after a four-week oral supplementation of punicalagin-enriched pomegranate extract in healthy subjects. Our results demonstrate a significant increase in the abundance of multiple short-chain producing bacteria in the gut microbiome of the PE group along with an increase in the circulating acetate and propionate levels. Our findings suggest that punicalagin standardized pomegranate extract consumption supports a healthier gut and gut–body communication. Future studies should explore the utility of PE ingestion for clinical conditions such as acne and hidradenitis suppurativa.
https://dmsjournal.biomedcentral.com/articles/10.1186/s13098-021-00633-82Human studyIn conclusion, the results of this study indicated that eight weeks of supplementation with EA, 180 mg/day, reduced the levels of blood sugar, Insulin, IR, and Fetuin-A and increased SIRT1 in patients with type 2 diabetes. These results provide evidence to support the view that polyphenol antioxidant group with reducing the complications of diabetes can play an important role in helping to control the condition of diabetes, including reducing the dose of medications used There were no statistically significant differences at the beginning and end of the study in terms of energy intake, macronutrients, and micronutrients. The effects of Ellagic acid supplementation on FPG, Insulin, IR, STRT1, and, Fetuin-A are shown in Table 3. There were no statistically significant differences between intervention and placebo at the beginning and end of the study. At the end of the study, EA supplementation reduced FPG, Insulin, IR, and Fetuin-A levels and increased SIRT1 level
https://www.sciencedirect.com/science/article/pii/S24058440230905271Lab study EA is beneficial for lowering TC, TG, LDL, and inflammation, and increasing HDL and bile acid secretion. Furthermore, EA demonstrates beneficial effects in the treatment of hypertension, diabetes, and obesity via underlying mechanisms such as decreasing blood glucose and pressure, increasing NO in the blood vessels, improving pancreatic insulin secretion, and decreasing inflammatory cytokines in the body that cause cardiovascular diseasesIn summary, these findings show that EA is a powerful regulator of fasting blood glucose, increasing insulin secretion and RS1 expression, regulating GLUT4 gene expression, and suppressing lipid accumulation and inflammation in adipose tissue (Table 1). According to these studies, the effective dose of EA for treating diabetes in most in vivo studies could be 50–200 mg/kg/day p.o
https://www.mdpi.com/2072-6643/8/11/7441In conclusion, EA displays marked in vitro and in vivo antitumor activity against human bladder cancer, as a result of different effects: inhibition of tumor cell proliferation; migration and invasion of the extracellular matrix in response to VEGF-A; down-modulation of PD-L1; and decreased tumor-associated angiogenesis. Therefore, nutrients rich in EA or dietary supplements based on EA can be a useful support for the prevention and/or treatment of bladder cancer.Although most patients with NMIBC generally have favorable outcomes, local therapy with chemotherapy mainly based on mitomycin C often requires repeated treatments [47]. Interestingly, we found that EA enhanced the antiproliferative effects of mitomycin C. These data suggest that also a less aggressive disease might benefit from local or systemic therapy with this compound, possibly reducing the frequency of administration of the chemotherapeutic agent.Screenshot from 2024-02-20 20-18-17
https://onlinelibrary.wiley.com/doi/full/10.1002/fsn3.36991EA has multiple effects on BC cells including (1) suppresses the growth of BC cells by arresting the cell cycle in the G0/G1 phase, (2) suppresses migration, invasion, and metastatic, (3) stimulates apoptosis in MCF-7 cells via TGF-β/Smad3 signaling axis, (4) inhibits CDK6 that is important in cell cycle regulation, (5) binds to ACTN4 and induces its degradation via the ubiquitin-proteasome pathway, inducing decreased cell motility and invasion in BC cells, (6) inhibits the PI3K/AKT pathway, and (7) inhibits angiogenesis-associated activities including proliferation (reduces VEGFR-2 tyrosine kinase activity). In conclusion, EA exhibits anticancer activity through various molecular mechanisms that influence key cellular processes like apoptosis, cell cycle, angiogenesis, and metastasiMoreover, another study depicted that EA might be a great potential drug adjuvant for cancer treatment and showed that the synergistic effect of EA combined with radiotherapy/chemotherapy resulted in increased DNA damage and apoptosis as well as decreased levels of MGMT expression. Also, due to EA's anti-oxidant and anti-inflammatory properties, the probable side effects of chemo-radiotherapy would be diminished (Xue et al., 2022). Bhosle et al. found that treatment of cancer with EA followed by radiation of 2 Gy would increase oxidative stress and cytotoxicity in tumor cells. They observed decreased levels of SOD, GSH-Px, and catalase in tumor cells

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