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Milk Thistle · Silybum marianum
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In one pass Silymarin is not one molecule. Not this — Milk thistle pills protect the liver, lower enzymes, and repair liver damage — It is poorly absorbed and the liver quickly tags it for removal (phase II conjugation), so almost no free compound reaches liver cells. A Cochrane review found no effect on death or complications, and the SyNCH trial, at 3-5x the customary dose, was no better than placebo.
Educational content, not medical advice — consult a clinician.
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Chapter 1
What is actually in the capsule
Silymarin is not one molecule. It is a handful of closely related flavonolignans extracted from the seed, and "silymarin" on the bottle is the collective name for that handful.
The label lists one ingredient, but the capsule holds at least four or five: the most studied are silybin A and B (also called silibinin), plus isosilybin, silychristin, silydianin and a little taxifolin. The part used is the seed, not the leaf or the flower. Milk thistle is one plant, *Silybum marianum*, which has two common names in Chinese.
The one place a hospital genuinely uses it as a drug is mushroom poisoning — and there it is an intravenous injection, not this capsule. If you vomit or have diarrhea after eating wild mushrooms, go to the emergency department now, even if you seem to get better, and tell the doctor it was a wild mushroom.
The label lists one ingredient, but the capsule holds at least four or five: the most studied are silybin A and B (also called silibinin), plus isosilybin, silychristin, silydianin and a little taxifolin. The part used is the seed, not the leaf or the flower. Milk thistle is one plant, *Silybum marianum*, which has two common names in Chinese.
The one place a hospital genuinely uses it as a drug is mushroom poisoning — and there it is an intravenous injection, not this capsule. If you vomit or have diarrhea after eating wild mushrooms, go to the emergency department now, even if you seem to get better, and tell the doctor it was a wild mushroom.
Numbers · How much silybin is in 300 mg
A capsule labeled 300 mg of extract, standardized to 80% silymarin, contains 240 mg of that mixture; the part that is actually silybin is only about half of it, a little over a hundred milligrams. Some studies dose by silymarin and others by silybin, and the two can differ by a factor of two. When two brands' doses do not match, first check which one each is counting.Once the counting is clear, three questions remain: what it does inside a cell, whether a swallowed capsule ever gets there, and why emergency rooms genuinely do use it.
Chapter 2
In a dish, it really does things
Add silybin to liver cells in culture and three things genuinely happen. It crowds into the outer cell membrane and occupies the transporters that carry things inward, so some toxins have a harder time getting in. It mops up some free radicals and, in animal experiments, partly restores depleted glutathione (see Glutathione (GSH)) (see N-acetylcysteine (NAC)). And it weakens the signal that wakes up stellate cells — once awake, stellate cells start mass-producing collagen, which is the scar tissue of the liver.
All three have evidence from the dish. The real question is a physical one: can the concentrations used in those experiments ever reach your liver cells from a capsule you swallow?
All three have evidence from the dish. The real question is a physical one: can the concentrations used in those experiments ever reach your liver cells from a capsule you swallow?
Mechanism · How stellate cells turn liver into scar
The fibrosis step is worth taking apart, because it is the most valuable claim in the whole liver-supplement market.A narrow space runs between liver cells, and stellate cells live in it. In health their job is quiet: store vitamin A and maintain a little of the scaffolding outside the cells (the matrix).
Ongoing injury — alcohol, fat, viruses, drugs — makes the nearby macrophages release a signaling molecule called TGF-β. Stellate cells that receive it transform: they dump their vitamin A stores, grow contractile fibers and start mass-producing collagen. That is scar.
The key question is whether scar is permanent. It used to be thought so; we now know it is not entirely — remove the source of injury and early fibrosis can partly regress. That is exactly why quitting alcohol, losing weight and antiviral treatment are worth far more than any supplement: they act on the source, while a supplement at best negotiates downstream.
In laboratory experiments, silybin weakens the TGF-β signal at this step. Whether it does so in a person is the subject of the chapter What the human trials found.
Chapter 3
Why little of it reaches the liver
Most of the silybin you swallow never gets inside a liver cell.
The first barrier is dissolving: it barely dissolves in water, and the gut can only absorb a molecule that is dispersed in water first. What does not disperse mostly leaves in the stool. The second barrier is tagging: the small amount that is absorbed travels through the portal vein straight to the liver, where the enzymes that handle foreign molecules (phase II enzymes) attach a glucuronide or sulfate group to it. Once tagged, it can no longer cross cell membranes and can only be flushed into bile or urine. So the silybin measured in blood is overwhelmingly the tagged conjugate, not the free form that does the work.
Someone measured this wall: a 5-fold increase in dose raised blood levels of the two silybins 11- to 38-fold, which shows that customary doses are almost entirely intercepted. Curcumin hits the same wall (see Curcumin).
The first barrier is dissolving: it barely dissolves in water, and the gut can only absorb a molecule that is dispersed in water first. What does not disperse mostly leaves in the stool. The second barrier is tagging: the small amount that is absorbed travels through the portal vein straight to the liver, where the enzymes that handle foreign molecules (phase II enzymes) attach a glucuronide or sulfate group to it. Once tagged, it can no longer cross cell membranes and can only be flushed into bile or urine. So the silybin measured in blood is overwhelmingly the tagged conjugate, not the free form that does the work.
Someone measured this wall: a 5-fold increase in dose raised blood levels of the two silybins 11- to 38-fold, which shows that customary doses are almost entirely intercepted. Curcumin hits the same wall (see Curcumin).
Evidence · What enhanced formulations actually fix
Since the wall is there, formulators have of course tried to get around it. On the shelf you will see several approaches:Silybin-phospholipid complex. Complexing silybin with phosphatidylcholine helps it mix into the fatty phase inside the gut. These formulations really do reach blood levels several times higher than plain extract; that part is measurable and real.
Added piperine, nanoparticles, liposomes. Same idea each time: raise absorption, or slow the phase II tagging.
But watch for a substitution here. A higher blood concentration is a pharmacokinetic endpoint; it proves that more of the molecule got in. What you want to know is a clinical endpoint: whether the liver got better. The first cannot answer for the second.
One counterexample is enough: the SyNCH trial used three to five times the customary dose — squarely in the dose range where Hawke 2010 measured blood exposure multiplying — and the result was still negative (Fried 2012). Delivering more of it did not buy a better liver.
So the fair statement about enhanced formulations is: they solved the absorption problem, and there is no evidence that they solved the efficacy problem. The premium buys the former.
Numbers · 5× the dose, 38× the silybin B
Someone measured it properly. A phase I study gave people with chronic hepatitis C but no cirrhosis — four groups of 8 — a dose every 8 hours, escalating through 140, 280, 560 and 700 mg, for 7 days. A 5-fold increase in dose raised steady-state blood exposure to silybin A 11-fold and to silybin B 38-fold — not a straight-line relationship (Hawke 2010). Do not merge the two isomers: 38-fold is silybin B, not a multiplier the two share. Most of the silybin measured in plasma was already in conjugated form.That number runs against intuition, but it means only one thing: at customary doses the clearance pathway is nowhere near full, so almost all of the drug is intercepted; only when the dose is pushed far above customary does the pathway start to saturate and blood levels begin to hold. So the next time you see a claim based on a lab experiment, ask first: can I reach that concentration by swallowing?
Chapter 4
The IV drug for mushroom poisoning
Alpha-amanitin, the toxin in death-cap mushrooms, cannot cross a liver-cell membrane on its own. It has to borrow a door: on the blood-facing side of the liver cell sit two transporters, OATP1B3 and NTCP, whose normal job is retrieving bile acids; the toxin looks like a valid pass, so it gets carried in along with them. What silibinin does here is take the doors: it occupies both transporters so the toxin cannot get in. This is competition between molecules for a transporter, not antioxidant action, and not a boost to glutathione.
The emergency-room injection is not even the same molecular form as the shelf capsule, so the capsule cannot borrow the injection's reputation.
If you vomit or have diarrhea after eating wild mushrooms, get medical care immediately: this poisoning brings a stretch that looks like recovery, and the liver damage happens during that stretch.
The emergency-room injection is not even the same molecular form as the shelf capsule, so the capsule cannot borrow the injection's reputation.
If you vomit or have diarrhea after eating wild mushrooms, get medical care immediately: this poisoning brings a stretch that looks like recovery, and the liver damage happens during that stretch.
Red flag · Why mushroom poisoning fakes a recovery
The most dangerous thing about amatoxin poisoning is not the toxicity itself but its shape in time — and that shape follows directly from the mechanism above.Why nothing happens for the first hours. The toxin locks the pen that copies genes; it does not shatter the cell on contact. Proteins the cell has already built keep working for a while, so for six to twenty-four hours after eating, a person may feel nothing at all. By contrast, most mushrooms that cause vomiting and diarrhea right away are far less lethal. A late onset is itself a danger sign.
Why there is a stretch that looks like recovery. The first wave is severe vomiting and diarrhea, which then eases, and the person looks as though they have pulled through. This is the false recovery period. In reality liver cells are dying in large numbers, just not yet enough to show. Real liver failure surfaces a day or two later.
Why the antidote is a race. Taking the doors only helps while the toxin is still outside the cell. Once it is inside and has locked the polymerase, occupying the doors changes nothing. So every treatment aimed at it works better the earlier it starts.
Red flag: vomiting and diarrhea after eating wild mushrooms — whether or not there was an apparent recovery in between — means going to hospital immediately and telling the clinician that it was a wild mushroom and roughly when it was eaten. Bringing the leftovers or a photo helps. This is not wellness advice; it is an emergency.
Clinical · Four ways the ampoule differs from the capsule
The intravenous product approved in Europe is called Legalon SIL, and its active ingredient is silibinin dihemisuccinate: silibinin rebuilt as a water-soluble salt and injected directly into a vein (Mengs 2012). That step goes around both barriers described in the chapter Why little of it reaches the liver: no gut to cross, and no tagging by the liver before effective concentrations are reached.Set it beside the shelf capsule and there are four differences, not one product in two packages. Form: a dihemisuccinate salt, not the mixture extracted from the seed. Route: intravenous, not oral. Mechanism: occupying transporters and interrupting the gut-liver recirculation, not the antioxidant story in the ads. Indication: death-cap mushroom poisoning, not everyday liver support.
Once the toxin is inside a cell, it locks RNA polymerase II; the cell cannot even build proteins, and liver cells die in sheets. Silibinin also interrupts a second loop: the toxin is excreted into bile and then absorbed again from the gut. Antioxidant action, restoring glutathione, quieting stellate cells — none of them is doing the work here.
The evidence for this injection deserves honesty too. Its support comes mainly from observational registry data, with no — nor should there be, since nobody will assign placebo to a patient with mushroom poisoning. Clear mechanism, widespread clinical use, randomized evidence absent. When an advertisement uses mushroom poisoning to vouch for liver pills, those four differences are where you push back.
Chapter 5
What the human trials found
For those three things from the dish to happen in a person, the molecule first has to get inside the liver cell. The large trials that needed doing have been done, and they asked exactly whether that translates into better outcomes. The answer was negative.
Pooling randomized trials in alcoholic liver disease and hepatitis B and C, milk thistle had no significant effect on mortality or on complications of liver disease. Raising the oral dose to three to five times the customary amount still produced no difference from placebo in liver enzymes or hepatitis C viral load. A steatohepatitis trial that read liver biopsies missed its prespecified primary endpoint.
The "dose was too low" excuse was ruled out as well, by the trial that raised the dose.
Pooling randomized trials in alcoholic liver disease and hepatitis B and C, milk thistle had no significant effect on mortality or on complications of liver disease. Raising the oral dose to three to five times the customary amount still produced no difference from placebo in liver enzymes or hepatitis C viral load. A steatohepatitis trial that read liver biopsies missed its prespecified primary endpoint.
The "dose was too low" excuse was ruled out as well, by the trial that raised the dose.
Evidence · Why early small trials looked positive
Milk thistle collected a batch of positive small trials between the 1970s and the 1990s, and they are the foundation of today's market. There are three reasons they looked positive, none of which requires assuming anyone cheated.Liver enzymes fluctuate on their own. This is the biggest one, and the chapter A lower is not a better liver is devoted to it. In chronic liver disease, transaminase levels naturally rise and fall. If a study enrolls people whose values are high right now, then whatever they are given, the second blood draw tends to be lower than the first — this is called regression to the mean. Without a control group, that fall looks like a drug effect.
Small samples wobble. In a trial of a few dozen people, random variation dominates the result. Producing one attractive number is not hard.
Attractive results are more likely to be published. Small trials with negative results often stay in a drawer and are never submitted, so the literature that survives leans systematically positive.
There is only one antidote to all three: a large sample, randomized, double-blind, with a control group, and the endpoint fixed in advance. That is exactly what the Cochrane pooling and the SyNCH trial did, and their results were negative.
This pattern recurs across supplements. Another textbook case is saw palmetto: the early small trials were uniformly positive, while rigorously designed large trials found no difference from placebo (see Saw Palmetto).
Evidence · The Cochrane review and the SyNCH trial
A Cochrane systematic review pooled the randomized trials in people with alcoholic liver disease and hepatitis B or C: whether all trials were combined or only the methodologically best ones, no significant effect on mortality or on complications of liver disease could be shown (Rambaldi 2007).SyNCH closed off one excuse on purpose: if customary doses barely get in, raise the dose. 154 people with chronic hepatitis C whose interferon treatment had failed were randomized to silymarin 420 mg or 700 mg three times a day, or placebo, for 24 weeks. Result: the fall in liver enzymes did not differ significantly between the three groups, and neither did hepatitis C viral RNA (Fried 2012). Higher-than-customary oral doses did not help the livers of people with hepatitis C, and the "dose was too low" explanation was ruled out.
Evidence · The trial that read liver biopsies
The trial in metabolic dysfunction-associated steatohepatitis — MASH (formerly NASH) — was run rigorously: 99 patients, 700 mg three times a day, for a full 48 weeks, with the endpoint read from liver-biopsy tissue rather than from a blood panel. The primary endpoint was a fall of 30% or more in the disease-activity score without worsening fibrosis — and it was not met. There was a signal on the fibrosis score, but that was a secondary endpoint (Wah Kheong 2017).Why can a secondary endpoint not be the conclusion? A trial measures many things at once, and the more it measures, the more likely one of them looks good by chance alone. The primary endpoint is the one named before the start as the decider, and its value lies in that advance commitment. Picking the pretty number out of the pile afterwards is marketing, not a conclusion. This piece of judgment applies to every supplement claim.
Chapter 6
A lower ALT is not a better liver
(alanine aminotransferase) is an enzyme inside liver cells that works on amino-acid metabolism and normally stays inside the cell. More of it in the blood means something simple: some liver cells have broken open and their enzyme has leaked into the bloodstream. It reads leakage, not liver function.
So if ALT falls after you take something, that does not mean the liver has healed. It tells you only whether liver cells are still breaking right now; it says nothing about how much working capacity the liver has left or how far fibrosis has progressed. In end-stage disease there are few cells left to leak, and ALT can drift back to normal — the worst kind of normal.
It also wobbles up and down by itself. To know whether the liver is still doing its job, look at what it makes, what it clears and how much scar it has. The hepatitis B story covers the other side of this (see Hepatitis B).
So if ALT falls after you take something, that does not mean the liver has healed. It tells you only whether liver cells are still breaking right now; it says nothing about how much working capacity the liver has left or how far fibrosis has progressed. In end-stage disease there are few cells left to leak, and ALT can drift back to normal — the worst kind of normal.
It also wobbles up and down by itself. To know whether the liver is still doing its job, look at what it makes, what it clears and how much scar it has. The hepatitis B story covers the other side of this (see Hepatitis B).
Clinical · What each liver test measures
If you want the numbers on the lab report, they are here. How to interpret your own results must be judged by a clinician who knows your history; this only explains what each marker measures.and : two enzymes that leak
ALT lives mainly in liver cells and is relatively specific to the liver. AST (aspartate aminotransferase) is also found in heart and skeletal muscle, so it rises after hard exercise too. The ratio of the two sometimes offers a clue, but a ratio is not a diagnosis.
ALP and : the bile-duct route
Alkaline phosphatase (ALP) and gamma-glutamyl transferase (GGT) lean toward reflecting a blocked or irritated bile-export pathway. GGT is fairly sensitive to alcohol.
Albumin and clotting: these are the function markers
Albumin is made by the liver, as are most clotting factors. When they fall, the liver's production line is in trouble, which is far more serious than a raised transaminase. Note that albumin's half-life is about three weeks, so it responds slowly and suits the assessment of chronic conditions.
Bilirubin: clearing capacity
Bilirubin is a breakdown product of red blood cells, processed by the liver and excreted into bile. A rise means that processing or excretion is impaired; jaundice is bilirubin becoming visible in the skin and the whites of the eyes.
Elastography and fibrosis scores: how far the scarring has gone
Only this group answers the fibrosis question, and fibrosis is what determines the long-term outcome. Normal transaminases do not mean fibrosis has not progressed.
Red flags · when not to judge for yourself: yellowing of skin or eyes, markedly darker urine, persistent right upper abdominal pain, unusual bruising or gum bleeding, confusion or personality change. With any of these, stop all over-the-counter supplements and seek medical care promptly.
Chapter 7
Safe, but no substitute for treatment
Milk thistle itself rarely harms the liver. The US National Institutes of Health's drug-induced liver injury database, LiverTox, rates its likelihood of causing liver injury as category E: unlikely to cause clinically apparent liver injury, and not recorded as raising liver enzymes (LiverTox 2020). The most common complaints when taken by mouth are bloating, nausea, gas and loose stools. It belongs to the daisy family, so people allergic to ragweed, chrysanthemum, marigold or daisy may react to it too (NCCIH).
The real cost is not side effects but substitution. A bottle of liver pills makes the liver feel handled, while cutting out alcohol, losing weight, getting tested for hepatitis B and stopping liver-damaging drugs have not been done at all.
The real cost is not side effects but substitution. A bottle of liver pills makes the liver feel handled, while cutting out alcohol, losing weight, getting tested for hepatitis B and stopping liver-damaging drugs have not been done at all.
Background · What else goes into a liver pill
Commercial liver products rarely contain milk thistle alone. Here are the usual companions, grouped by what they claim to do. What follows describes the role these molecules play in the body and is not a recommendation to take anything; how prescription drugs are used must be decided by a doctor.Also on the antioxidant route
Reduced glutathione and N-acetylcysteine () often appear together. Their oral predicament resembles silybin's but is not the same: most swallowed glutathione is broken down into amino acids in the gut, whereas NAC supplies the raw material the body uses to make glutathione itself — a different strategy. NAC has a firmly established emergency role in acetaminophen (paracetamol) overdose, which again is an emergency setting, given by mouth or by vein on an emergency protocol, at entirely different doses; do not confuse it with wellness dosing (see N-acetylcysteine (NAC)) (see Glutathione (GSH)).
On the membrane-repair route
Polyenylphosphatidylcholine and similar products aim to supply phospholipid raw material to damaged liver-cell membranes. What cell membranes are made of is real biology; whether supplying it changes clinical outcomes is a separate question, judged the same way as before: by the primary endpoint.
Prescription drugs sitting beside supplements
Some products contain genuine prescription ingredients. Their indication, dose and duration have to be set by a doctor; they are not something to add as you see fit.
Herbal formulas
This group needs the most caution, because natural does not mean safe. The site has a whole story on that sentence, including well-documented cases such as aristolochic acid damaging the kidneys and *Polygonum multiflorum* (he shou wu) damaging the liver (see Herb Safety).
One general rule of thumb: when a single product claims to protect the liver, lower enzymes, cure hangovers, fight fatigue and boost immunity all at once, the breadth of the claim is itself the signal. Interventions that have actually been validated usually have narrow indications.
Safety · Drug interactions, and what really helps
In laboratory experiments it affects some of the liver's drug-processing enzymes, but there is little evidence of clinically meaningful herb-drug interactions in people (LiverTox 2020). Anyone taking prescription drugs — especially anti-rejection drugs, anticoagulants or chemotherapy — should tell their doctor before adding any supplement. *Polygonum multiflorum* (he shou wu) and *Senecio* species are an entirely different matter (see Herb Safety).Faced with any supplement claim, two questions are enough. First, at what concentration was this mechanism seen, and can I reach it by swallowing? Second, does the marker being quoted measure function or leakage, and was it the primary endpoint or picked out afterwards?
What genuinely helps the liver has its own stories on this site. How alcohol is broken down in the liver, and why the first-step product is the damaging one (see Alcohol Metabolism). How fat builds up in liver cells, and why weight loss is the intervention with the strongest evidence (see Fatty Liver). Why the hepatitis B virus cannot be fully cleared, and what to monitor (see Hepatitis B). The liver's whole clearance workshop, and where the idea of "detox" is real and where it is not (see Hepatic System).
This is education about mechanisms, not medical advice. If you have liver disease, take medication or have abnormal lab results, take these questions to your doctor rather than to a shelf.
References · 10
- Federico, A., Dallio, M., & Loguercio, C. (2017). Silymarin/silybin and chronic liver disease: a marriage of many years. Molecules, 22(2), 191. Narrative review of silymarin composition (a flavonolignan mixture in which silybin A/B is the main active fraction) and the proposed antioxidant, membrane-stabilising, and antifibrotic mechanisms, alongside its poor oral bioavailability. 10.3390/molecules22020191
- National Institute of Diabetes and Digestive and Kidney Diseases. (2020). Milk Thistle. In LiverTox: Clinical and Research Information on Drug-Induced Liver Injury. Human trials in chronic liver disease have been 'promising but inconclusive'; milk thistle itself has not been implicated in serum enzyme elevations or clinically apparent liver injury (likelihood score E); intravenous purified silybinin is approved in Europe for Amanita phalloides poisoning. www.ncbi.nlm.nih.gov/books/NBK548817
- National Center for Complementary and Integrative Health. (2025). Milk Thistle: Usefulness and Safety. Trial results for liver disease have been 'conflicting or too limited to allow conclusions'; two NCCIH-funded trials (hepatitis C and nonalcoholic steatohepatitis) showed no benefit. Allergic reactions can occur in people allergic to ragweed, chrysanthemum, marigold, and daisy. www.nccih.nih.gov/health/milk-thistle
- Hawke, R. L., Schrieber, S. J., Soule, T. A., Wen, Z., Smith, P. C., Reddy, K. R., et al. (2010). Silymarin ascending multiple oral dosing phase I study in noncirrhotic patients with chronic hepatitis C. The Journal of Clinical Pharmacology, 50(4), 434-449. Four cohorts of 8 patients dosed 140/280/560/700 mg every 8 h for 7 days: a 5-fold dose increase raised steady-state exposure of silybin A 11-fold and silybin B 38-fold (nonlinear), and plasma silybin circulated predominantly as conjugates — evidence that customary doses achieve very low systemic exposure. 10.1177/0091270009347475
- Letschert, K., Faulstich, H., Keller, D., & Keppler, D. (2006). Molecular characterization and inhibition of amanitin uptake into human hepatocytes. Toxicological Sciences, 91(1), 140-149. Alpha-amanitin cannot cross the hepatocyte membrane unaided — it enters via the sinusoidal uptake transporters OATP1B3 and NTCP, and silibinin inhibits that uptake. 10.1093/toxsci/kfj141
- Mengs, U., Pohl, R.-T., & Mitchell, T. (2012). Legalon SIL: the antidote of choice in patients with acute hepatotoxicity from amatoxin poisoning. Current Pharmaceutical Biotechnology, 13(10), 1964-1970. Reviews the intravenous water-soluble silibinin dihemisuccinate formulation used for Amanita phalloides poisoning; the supporting human data are observational registry series, not randomized trials. 10.2174/138920112802273353
- Rambaldi, A., Jacobs, B. P., & Gluud, C. (2007). Milk thistle for alcoholic and/or hepatitis B or C virus liver diseases. Cochrane Database of Systematic Reviews, (4), CD003620. No significant effect on mortality or complications of liver disease. 10.1002/14651858.CD003620.pub3
- Fried, M. W., Navarro, V. J., Afdhal, N., Belle, S. H., Wahed, A. S., Hawke, R. L., et al. (2012). Effect of silymarin (milk thistle) on liver disease in patients with chronic hepatitis C unsuccessfully treated with interferon therapy: a randomized controlled trial. JAMA, 308(3), 274-282. SyNCH trial, N=154, silymarin 420 or 700 mg three times daily × 24 weeks vs placebo: no significant difference in decline of serum ALT and no difference in HCV RNA — higher-than-customary doses did not help. 10.1001/jama.2012.8265
- Wah Kheong, C., Nik Mustapha, N. R., & Mahadeva, S. (2017). A randomized trial of silymarin for the treatment of nonalcoholic steatohepatitis. Clinical Gastroenterology and Hepatology, 15(12), 1940-1949.e8. N=99, silymarin 700 mg three times daily × 48 weeks: the primary histological endpoint (≥30% reduction in NAFLD activity score without worsening fibrosis) was not met; a reduction in fibrosis score was a secondary finding. 10.1016/j.cgh.2017.04.016
- Chalasani, N., Younossi, Z., Lavine, J. E., Charlton, M., Cusi, K., Rinella, M., et al. (2018). The diagnosis and management of nonalcoholic fatty liver disease: practice guidance from the American Association for the Study of Liver Diseases. Hepatology, 67(1), 328-357. 10.1002/hep.29367