Andrographis for Liver Protection

Andrographis has been used as a hepatoprotective remedy in Ayurveda, traditional Chinese medicine, and traditional Thai medicine for at least a thousand years. Its Sanskrit name Bhunimba ("earth neem") explicitly identifies it as the terrestrial counterpart of the bitter bile-supporting neem tree. The Chinese name Chuan Xin Lian (literally "through-heart lotus") points to its use for liver-heat, jaundice, and dampness syndromes. The modern molecular story justifies the traditional use: andrographolide is a cholagogue (stimulates bile production and flow), a Nrf2 activator (induces phase-II detoxification enzymes including glutathione-S-transferase, glutathione peroxidase, NAD(P)H quinone oxidoreductase, and heme oxygenase-1), and an inhibitor of CYP-mediated bioactivation of pro-carcinogens. Animal trials document protection against acetaminophen, ethanol, carbon tetrachloride, aflatoxin, and galactosamine hepatotoxicity. This deep-dive walks through the molecular biology, the comparison with the more famous silymarin (milk thistle) model, the clinical applications in fatty liver, hepatitis, and drug-induced liver injury, and the practical dosing for liver-support indications.

Table of Contents

1. Traditional Use as a Hepatoprotective Herb
2. Cholagogue Activity (Bile Flow Stimulation)
3. Nrf2 / Keap1 / ARE Antioxidant Response
4. Phase-II Detoxification Enzyme Induction
5. CYP P450 Inhibition and Carcinogen Bioactivation
6. Acetaminophen (Paracetamol) Hepatotoxicity Protection
7. Alcohol-Induced Liver Injury
8. Non-Alcoholic Fatty Liver Disease (NAFLD)
9. Aflatoxin and Hepatocarcinogenesis
10. Comparison with Silymarin (Milk Thistle)
11. Clinical Applications and Dosing
12. Cautions and Drug Interactions
13. Key Research Papers
14. Connections

Traditional Use as a Hepatoprotective Herb

Andrographis paniculata appears in the Charaka Samhita (~1st-2nd century CE) and the Sushruta Samhita as a remedy for kamala (jaundice), raktapitta (bleeding disorders associated with liver dysfunction), and chronic fevers with liver involvement. The classical Ayurvedic preparation Kalmegh ghana (a concentrated leaf extract) was prescribed for hepatitis, sluggish digestion, and ascites long before modern hepatology distinguished viral hepatitis from autoimmune hepatitis from drug-induced liver injury. Andrographis remains a primary constituent of several traditional polyherbal hepatoprotective formulations including Liv-52 (a Himalaya Drug Company formulation studied in dozens of small trials for fatty liver and hepatitis adjunct).

In traditional Chinese medicine, Chuan Xin Lian is classified as a cold, bitter herb that clears heat, dries dampness, and resolves toxin — the classical syndrome pattern that corresponds to modern conditions including acute viral hepatitis, cholangitis, and cholestatic jaundice. It is also used as a primary herb in TCM formulations for the alarmingly named "damp-heat in the gallbladder" pattern, which translationally corresponds to cholecystitis and cholelithiasis with chronic biliary inflammation.

In traditional Thai medicine, Andrographis (called Fa Thalai Chon) is a Pillar Herb of the National Drug List and is dispensed by the Ministry of Public Health for hepatitis adjunct therapy, along with its better-known URTI applications.

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Cholagogue Activity (Bile Flow Stimulation)

A cholagogue is any agent that increases bile flow from the gallbladder into the duodenum (distinct from a choleretic, which increases bile production by hepatocytes — many cholagogues are also choleretics). Improved bile flow matters clinically for several reasons:

• Bile is the principal route of excretion for fat-soluble metabolic waste, bilirubin (from heme breakdown), cholesterol, and many drugs and their conjugated metabolites. Sluggish bile flow allows these to accumulate in the body
• Bile is required for digestion and absorption of dietary fats and fat-soluble vitamins (A, D, E, K). Cholestatic patients develop fat-soluble vitamin deficiencies and steatorrhea
• Bile-acid recycling through the enterohepatic circulation is a major modulator of cholesterol metabolism, bile-acid-receptor (FXR, TGR5) signaling in the gut and liver, and the gut microbiome
• Bile contains bicarbonate that neutralizes gastric acid in the duodenum and creates the alkaline pH required for pancreatic enzyme function

Andrographis is one of a relatively small number of herbs with documented choleretic and cholagogue activity in controlled animal studies. Andrographolide and the related congeners stimulate hepatocyte bile-acid synthesis and increase the rate of bile-salt secretion into the canaliculus. The effect is modest compared with pharmaceutical cholagogues (ursodeoxycholic acid, dehydrocholic acid) but is meaningful in the context of sluggish digestion, gallbladder hypokinesia, and the lingering biliary effects of post-cholecystectomy syndrome.

Patients reporting symptoms consistent with biliary insufficiency — chronic fat malabsorption, pale stools after fatty meals, post-cholecystectomy diarrhea, gallbladder hypomotility on imaging — may benefit from Andrographis as part of a broader strategy that may also include ox bile supplementation, taurine, and dietary fat moderation.

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Nrf2 / Keap1 / ARE Antioxidant Response

The Nrf2 / Keap1 system is the master regulator of cellular antioxidant and phase-II detoxification gene expression. Under baseline conditions, the transcription factor Nrf2 (nuclear factor erythroid 2-related factor 2) is held in the cytoplasm bound to its repressor Keap1 (Kelch-like ECH-associated protein 1), which targets Nrf2 for proteasomal degradation. When the cell experiences oxidative stress, electrophilic challenge, or exposure to specific Nrf2-activating molecules, key reactive cysteine residues on Keap1 are modified, the Keap1-Nrf2 complex dissociates, and Nrf2 translocates to the nucleus.

In the nucleus, Nrf2 heterodimerizes with small Maf proteins and binds the antioxidant response element (ARE) sequence in the promoter regions of over 200 downstream target genes. The downstream targets include:

• Glutathione synthesis enzymes (glutamate-cysteine ligase catalytic and modifier subunits)
• Glutathione-S-transferases (the major phase-II conjugating enzymes for xenobiotic detoxification)
• NAD(P)H quinone oxidoreductase 1 (NQO1, the principal quinone-detoxifying enzyme)
• Heme oxygenase-1 (HO-1, which catabolizes heme and generates the antioxidants biliverdin/bilirubin and the signaling molecule carbon monoxide)
• Catalase, superoxide dismutase, glutathione peroxidase, thioredoxin reductase (the principal cellular antioxidant enzymes)
• Multi-drug resistance proteins (MRP1-4) that pump conjugated xenobiotic metabolites out of the cell into bile

Andrographolide is a documented Nrf2 activator via covalent modification of Keap1 cysteine residues (analogous to the action of sulforaphane from broccoli sprouts, dimethyl fumarate from the multiple sclerosis drug class, and curcumin). Multiple animal models confirm that andrographolide administration upregulates expression of GST, NQO1, HO-1, and the glutathione synthesis machinery in liver tissue, with measurable increases in hepatic glutathione concentration after a few weeks of dosing.

The protective effect of Nrf2 induction is broad. It buffers against drug-induced and chemical-induced oxidative damage, accelerates clearance of phase-I-activated reactive intermediates, and reduces the rate at which environmental and metabolic toxins damage hepatic DNA. This is the same mechanism behind the cancer-chemoprevention activity of cruciferous vegetables and is part of the broader case for "induce phase-II, inhibit phase-I" detoxification strategies in chronic illness.

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Phase-II Detoxification Enzyme Induction

The conventional hepatic detoxification model divides metabolism into Phase-I (CYP P450-mediated oxidation, reduction, hydrolysis — creates a reactive intermediate from a foreign molecule) and Phase-II (conjugation of the intermediate to glutathione, glucuronide, sulfate, glycine, taurine, methyl — makes it water-soluble for renal or biliary excretion). The reactive Phase-I intermediates are themselves often more toxic than the parent molecule, and the Phase-II enzymes are what neutralize and clear them.

A pattern of relative Phase-I overactivity with Phase-II underactivity is a recurring problem in chronic illness, in genetic detoxification polymorphisms (slow-acetylator NAT2 variants, slow GSTT1/GSTM1 null genotypes), and in the burden of cumulative environmental exposure. The result is accumulation of reactive intermediates that drive chronic oxidative damage and contribute to chemical-induced cancers, autoimmune triggering, and the broad category of multiple chemical sensitivity.

Nrf2 induction is the principal upstream lever for shifting the Phase-I / Phase-II balance toward better conjugation and clearance. Andrographolide is one of the most accessible and well-tolerated Nrf2 activators in the herbal pharmacopeia, alongside sulforaphane (broccoli sprouts), curcumin (turmeric), silymarin (milk thistle), and the carotenoids astaxanthin and beta-carotene.

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CYP P450 Inhibition and Carcinogen Bioactivation

The other half of the detoxification story is Phase-I CYP P450 modulation. The CYP family of approximately 50 hepatic enzymes performs the initial oxidative modification of most foreign molecules — pharmaceuticals, dietary xenobiotics, and many environmental toxins. Three CYP isoforms in particular bioactivate pre-carcinogens into their reactive carcinogenic forms:

• CYP1A1 — converts polycyclic aromatic hydrocarbons (charred meat, cigarette smoke combustion products) into the reactive diol-epoxides that bind DNA and initiate lung and gastric cancer
• CYP1A2 — converts heterocyclic amines (formed in well-done cooked meat) and aromatic amines (bladder carcinogens) into reactive intermediates
• CYP2E1 — bioactivates acetaminophen to the hepatotoxic NAPQI intermediate, activates nitrosamines (cured-meat carcinogens), activates carbon tetrachloride and other halogenated solvents
• CYP3A4 — metabolizes about half of all clinically used pharmaceuticals; also bioactivates aflatoxin B1 to aflatoxin B1-8,9-epoxide, the proximate carcinogenic species for hepatocellular carcinoma

Andrographolide selectively inhibits CYP1A1, CYP1A2, and CYP2B1 (the rat equivalent of CYP2B6) at clinically achievable concentrations. The selectivity is favorable — it preferentially inhibits the bioactivation isoforms while leaving the main drug-metabolizing CYP3A4 less affected, although there is some CYP3A4 interaction at higher doses (a relevant drug-interaction consideration discussed below).

The combination of Phase-I bioactivation inhibition with Phase-II conjugation induction is the textbook example of a "blocker plus suppressor" cancer-chemopreventive agent in the Talalay schema. This is the mechanistic case behind animal-model evidence that long-term andrographolide administration reduces aflatoxin-induced hepatocarcinogenesis, polycyclic-aromatic-hydrocarbon-induced gastric tumors, and chemically induced mammary tumors.

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Acetaminophen (Paracetamol) Hepatotoxicity Protection

Acetaminophen (US) / paracetamol (UK, much of the world) is among the most-used analgesics globally and the leading cause of acute liver failure in the US and several European countries. The hepatotoxic mechanism is well-mapped: acetaminophen is normally glucuronidated and sulfated for excretion, with a small fraction routed through CYP2E1 to the highly reactive intermediate N-acetyl-p-benzoquinone imine (NAPQI). NAPQI is normally rapidly neutralized by hepatic glutathione conjugation. When the acetaminophen dose overwhelms the glucuronidation and sulfation pathways (whether by single overdose or by repeated supratherapeutic dosing in chronic-pain patients), more substrate is shunted through CYP2E1 to NAPQI, and when hepatic glutathione is depleted, NAPQI binds covalently to hepatocyte proteins causing centrilobular necrosis.

The standard rescue therapy is N-acetylcysteine (NAC, a glutathione precursor) given orally or IV within the first hours after overdose. Andrographolide attacks the same problem upstream:

• Inhibits CYP2E1 bioactivation of acetaminophen to NAPQI
• Induces glutathione synthesis via Nrf2 activation, maintaining a larger pool to neutralize whatever NAPQI is generated
• Induces glutathione-S-transferase to accelerate the NAPQI-glutathione conjugation
• Reduces NF-kB-driven inflammatory amplification of the initial centrilobular injury

Multiple animal trials in mice and rats document that prophylactic andrographolide administration substantially reduces the liver-enzyme elevation and histologic necrosis from a hepatotoxic acetaminophen dose. Andrographolide is not a substitute for N-acetylcysteine in acute overdose management, but it is a plausible protective measure for patients who require chronic supratherapeutic acetaminophen for pain control (chronic osteoarthritis, cancer pain, post-surgical pain) and want to reduce cumulative hepatic burden.

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Alcohol-Induced Liver Injury

Alcoholic liver disease (steatosis, alcoholic hepatitis, fibrosis, cirrhosis) is driven by a combination of acetaldehyde toxicity (the proximate ethanol metabolite produced by alcohol dehydrogenase and CYP2E1), oxidative stress from chronic CYP2E1 induction, gut-derived endotoxin (lipopolysaccharide) reaching the liver via the portal vein and activating Kupffer cell TNF-alpha and IL-6 production, and direct toxic effects on hepatocyte mitochondria.

Andrographolide's hepatoprotective effects in alcohol-induced liver injury are well-documented in animal studies and act through several complementary mechanisms:

• Modest CYP2E1 inhibition, reducing the rate of acetaldehyde production
• Glutathione induction, restoring the depleted antioxidant pool that chronic alcohol consumption exhausts
• NF-kB inhibition in Kupffer cells, reducing TNF-alpha amplification of endotoxin-driven inflammation
• Modest gut barrier improvement, reducing the portal endotoxin load that triggers Kupffer activation in the first place

For patients in early recovery from alcohol use disorder with elevated liver enzymes, Andrographis is a reasonable adjunct to alcohol cessation, diet, and conventional management. It does not enable continued drinking and should not be marketed as such. The fundamental treatment is alcohol cessation; Andrographis can support hepatic recovery during the months it takes for established alcoholic steatosis to resolve.

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Non-Alcoholic Fatty Liver Disease (NAFLD)

Non-alcoholic fatty liver disease (now formally renamed metabolic-dysfunction-associated steatotic liver disease, MASLD) affects an estimated 25-30% of adults in developed countries and is now the leading cause of chronic liver disease worldwide. The pathophysiology centers on insulin resistance driving hepatic de novo lipogenesis, mitochondrial dysfunction, oxidative stress, and a chronic low-grade inflammatory state that can progress to non-alcoholic steatohepatitis (NASH) and ultimately to fibrosis, cirrhosis, and hepatocellular carcinoma.

Animal-model and small human pilot trial evidence for Andrographis in NAFLD/MASLD is encouraging:

• Andrographolide activates AMPK, the master regulator of energy metabolism, with downstream effects including reduced hepatic de novo lipogenesis (suppressed SREBP-1c, ACC, FAS expression), increased fatty acid oxidation, and improved insulin sensitivity
• The same Nrf2 induction discussed above buffers against the oxidative-stress component of NASH progression
• NF-kB inhibition reduces the chronic inflammatory state that drives steatosis-to-steatohepatitis progression
• Modest weight reduction and visceral-fat reduction observed in some animal-model studies, although the human evidence is sparse

For NAFLD/MASLD management, Andrographis is again best understood as an adjunct to the foundational interventions (caloric restriction, weight loss of 7-10% of body weight, exercise, low-carbohydrate or Mediterranean dietary pattern, treatment of insulin resistance). It does not replace these. A 3-6 month trial of Andrographis 400-600 mg standardized extract twice daily, combined with the foundational interventions, is reasonable in patients with elevated ALT/AST and biopsy-confirmed or imaging-confirmed steatosis.

See our Fatty Liver Disease page for the broader management context.

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Aflatoxin and Hepatocarcinogenesis

Aflatoxin B1, produced by Aspergillus flavus mold contamination of stored grain, peanuts, tree nuts, and corn, is one of the most potent natural carcinogens known. Chronic dietary aflatoxin exposure is a major contributor to hepatocellular carcinoma (HCC) incidence in much of sub-Saharan Africa and Southeast Asia, often acting synergistically with chronic hepatitis B virus infection. The molecular mechanism is well-mapped: CYP3A4 (and to a lesser extent CYP1A2) oxidizes aflatoxin B1 to the highly reactive aflatoxin-B1-8,9-epoxide, which binds covalently to guanine residues in DNA and produces the characteristic AGG-to-AGT codon-249 mutation in the p53 tumor suppressor gene seen in aflatoxin-driven HCC.

Animal-model studies (predominantly in rat models of aflatoxin-induced HCC) demonstrate that long-term andrographolide administration substantially reduces aflatoxin DNA adduct formation, reduces preneoplastic foci formation in liver, and reduces ultimate HCC incidence. The mechanism is the combination of CYP1A2 inhibition (reducing aflatoxin bioactivation), glutathione-S-transferase induction (accelerating conjugation and excretion of whatever epoxide is formed), and AMPK activation (promoting hepatocyte apoptosis of cells that have sustained DNA damage rather than allowing them to progress to malignant transformation).

For patients in high-aflatoxin-exposure regions (subsistence farmers, populations dependent on home-stored corn and peanuts), Andrographis is a candidate chemopreventive intervention alongside the more important interventions of grain-storage modernization, hepatitis B vaccination, and dietary diversification.

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Comparison with Silymarin (Milk Thistle)

The most-studied hepatoprotective botanical in Western herbal medicine is silymarin from milk thistle (Silybum marianum), a flavonolignan complex with similar Nrf2-activating and membrane-stabilizing properties to andrographolide. The two herbs are mechanistically complementary rather than redundant:

• Silymarin — stronger membrane-stabilizing effect on hepatocyte plasma membrane (particularly important in amanita mushroom poisoning, the classic indication where IV silibinin is approved as primary therapy). Modest Nrf2 activation. Limited CYP inhibition. Modest bile flow stimulation. Extensive evidence base in alcoholic hepatitis, viral hepatitis adjunct, and prevention of chemotherapy-induced liver toxicity.
• Andrographolide — stronger Nrf2 induction and Phase-II enzyme upregulation. Stronger CYP1A1 / CYP1A2 / CYP2E1 inhibition. Stronger NF-kB-mediated anti-inflammatory effect at the Kupffer-cell level. Smaller (but real) evidence base across the same hepatic indications. Additional non-hepatic benefits (URTI, immune modulation, anti-inflammatory) that silymarin does not provide.

The two are often used together in clinical practice. A reasonable combination protocol for hepatic support in chronic liver disease is silymarin 200-400 mg twice daily plus Andrographis 400 mg standardized extract twice daily, taken with food. The combination is well-tolerated, mechanistically synergistic, and not associated with reported interactions between the two herbs.

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Clinical Applications and Dosing

Practical clinical applications and typical dosing:

• Adjunct to chronic viral hepatitis (B, C) — Andrographis 400-600 mg standardized extract twice daily, alongside standard antiviral therapy. May produce modest reduction in ALT/AST and improvement in subjective symptoms. Does not replace antiviral therapy.
• Adjunct to NAFLD/MASLD — Andrographis 400-600 mg twice daily, alongside dietary and weight-management foundation. 3-6 month trial.
• Drug-induced liver injury risk reduction — for patients on chronic potentially hepatotoxic medications (high-dose acetaminophen, methotrexate, isoniazid, amiodarone, statins with mildly elevated ALT), Andrographis 400 mg once or twice daily may provide modest hepatic buffering. Coordinate with prescribing physician.
• Alcohol recovery hepatic support — Andrographis 400-600 mg twice daily for the first 3-6 months of recovery, alongside abstinence, diet, and conventional management.
• Cholagogue for sluggish digestion / post-cholecystectomy syndrome — Andrographis 300-400 mg twice daily, often combined with ox bile, taurine, and digestive enzymes.
• General Phase-II detoxification support — Andrographis 300-600 mg daily, often combined with sulforaphane (broccoli sprout extract), curcumin, and silymarin.

All applications are augmented by the foundational hepatic-health interventions: reduce alcohol intake, optimize macronutrient quality, ensure adequate dietary protein for glutathione synthesis (cysteine is the rate-limiting amino acid), maintain healthy body weight, avoid known environmental hepatotoxins (mold-contaminated foods, industrial solvent exposure, unnecessary medications), and address insulin resistance if present.

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Cautions and Drug Interactions

• Pregnancy — absolute contraindication. Uterine stimulant. Listed as contraindicated by every major regulatory body. Reiterated on every Andrographis page.
• CYP3A4 substrate drugs — Andrographis has modest CYP3A4 inhibitory activity at higher doses. Theoretical risk of increased plasma levels of CYP3A4-substrate drugs including immunosuppressants (tacrolimus, cyclosporine), statins (simvastatin, atorvastatin), calcium channel blockers (amlodipine, felodipine), antiarrhythmics (amiodarone, dronedarone), and many others. Coordinate with prescribing physician and monitor drug levels where applicable.
• CYP1A2 substrate drugs — theoretical risk of altered metabolism of caffeine, theophylline, clozapine, olanzapine, tizanidine. Most interactions are mild and manageable, but worth physician awareness.
• Anticoagulants — modest potentiation of warfarin and other anticoagulants. Monitor INR.
• Acute fulminant liver failure — Andrographis is not indicated in acute liver failure and is not a substitute for emergency hepatology care, N-acetylcysteine in acetaminophen overdose, or liver transplantation evaluation when indicated.
• Active acute hepatitis with high transaminases — defer Andrographis until the acute inflammatory phase has resolved. Use as adjunct in the chronic recovery phase.
• Cholelithiasis (gallstones) with obstruction — Andrographis is a cholagogue and could theoretically increase risk of impacted stone in patients with established symptomatic gallstones. Use cautiously; consult surgeon if obstructive disease is suspected.
• Bitter taste and gastric upset — the standard tolerability issues, manageable with capsule form, food, and divided dosing.

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Key Research Papers

1. Trivedi NP, Rawal UM (2001). Hepatoprotective and antioxidant property of Andrographis paniculata (Nees) in BHC induced liver damage in mice. Indian Journal of Experimental Biology. — PubMed
2. Visen PK, Shukla B, Patnaik GK, Dhawan BN (1993). Andrographolide protects rat hepatocytes against paracetamol-induced damage. Journal of Ethnopharmacology. — PubMed
3. Singh RP, Banerjee S, Rao AR (2001). Modulatory influence of Andrographis paniculata on mouse hepatic and extrahepatic carcinogen metabolizing enzymes and antioxidant status. Phytotherapy Research. — PubMed
4. Trivedi N, Rawal UM, Patel BP (2007). Hepatoprotective effect of andrographolide against hexachlorocyclohexane-induced oxidative injury. Integrative Cancer Therapies. — PubMed
5. Pan CW, Yang SX, Pan ZZ, et al. (2017). Andrographolide ameliorates d-galactosamine/lipopolysaccharide-induced acute liver injury by activating Nrf2 signaling pathway. Oncotarget. — PubMed
6. Roy P, Das S, Bera T, et al. (2010). Andrographolide nanoparticles in leishmaniasis: characterization and in vitro evaluations. International Journal of Nanomedicine. — PubMed
7. Chua LS (2014). Review on liver inflammation and antiinflammatory activity of Andrographis paniculata for hepatoprotection. Phytotherapy Research. — PubMed
8. Bao Z, Guan S, Cheng C, et al. (2009). A novel antiinflammatory role for andrographolide in asthma via inhibition of the nuclear factor-kappaB pathway. American Journal of Respiratory and Critical Care Medicine. — PubMed
9. Handa SS, Sharma A (1990). Hepatoprotective activity of andrographolide from Andrographis paniculata against carbontetrachloride. Indian Journal of Medical Research. — PubMed
10. Pan Y, Abd-Rashid BA, Ismail Z, et al. (2011). In vitro modulatory effects of Andrographis paniculata, Centella asiatica and Orthosiphon stamineus on cytochrome P450 2C19 (CYP2C19). Journal of Ethnopharmacology. — PubMed
11. Bardi DA, Halabi MF, Hassandarvish P, et al. (2014). Andrographis paniculata leaf extract prevents thioacetamide-induced liver cirrhosis in rats. PLOS ONE. — PubMed
12. Nagalekshmi R, Menon A, Chandrasekharan DK, Nair CK (2011). Hepatoprotective activity of Andrographis paniculata and Swertia chirayita. Food and Chemical Toxicology. — PubMed

PubMed Topic Searches

• PubMed: Andrographolide hepatoprotection
• PubMed: Andrographolide Nrf2 detoxification
• PubMed: Andrographis cholagogue
• PubMed: Andrographolide NAFLD
• PubMed: Andrographolide CYP P450

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Connections

• Andrographis Overview
• Andrographis Benefits Hub
• Andrographis for Cold & Flu
• Andrographis Immune Modulation
• Andrographis Anti-Inflammatory
• Milk Thistle (Silymarin)
• Turmeric (Curcumin)
• Dandelion
• N-Acetylcysteine (NAC)
• Taurine (Bile Conjugation)
• Glutathione
• Fatty Liver Disease (NAFLD/MASLD)
• Hepatitis
• Mold and Mycotoxins (Aflatoxin)
• Liver Function Tests (ALT/AST/GGT)
• All Herbs

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