ALT, AST and GGT liver panel
Reads: Liver
You want it fortified: a protected liver safeguards metabolism, detoxification and whole-body health.
What this marker reads
Liver integrity — the resilience and regenerative capacity of the body's central metabolic and detox organ
What a named body publishes
Each line below is the sentence the issuing body wrote, carried with its own identifier. Nothing here interprets your result — it states what was published, for whom, and by whom.
ALT
“ALT: 'A true healthy normal ALT level ranges from 29 to 33 IU/l for males'; the guideline states 'A normal ALT should be <29-33 IU/l in males' and that clinicians should be educated about outcomes for 'ALT>33 IU/l for men'.” males
ACG Clinical Guideline: Evaluation of Abnormal Liver Chemistries · American Journal of Gastroenterology · 2017 DOI 10.1038/ajg.2016.517 · PMID 27995906
“ALT: 'A true healthy normal ALT level ranges from ... 19 to 25 IU/l for females'; the guideline states 'A normal ALT should be ... 19-25 IU/l in females' and names 'ALT>25 IU/l for women' as the outcome threshold.” females
ACG Clinical Guideline: Evaluation of Abnormal Liver Chemistries · American Journal of Gastroenterology · 2017 DOI 10.1038/ajg.2016.517 · PMID 27995906
“ALT (ALAT): the Nordic Reference Interval Project reference interval for adult men is 0.15-1.1 µkat/L, measured by IFCC-traceable methods at 37 degrees C.” males, adults (not age-stratified)
Nya gemensamma nordiska referensintervall inom klinisk kemi · Läkartidningen 2004;101:901-5 The document
“ALT (ALAT): the NORIP reference interval for adult women is 0.15-0.75 µkat/L.” females, adults (not age-stratified)
Nya gemensamma nordiska referensintervall inom klinisk kemi · Läkartidningen 2004;101:901-5 The document
AST
“AST (ASAT): the NORIP reference interval for adult men is 0.25-0.75 µkat/L.” males, adults (not age-stratified)
Nya gemensamma nordiska referensintervall inom klinisk kemi · Läkartidningen 2004;101:901-5 The document
“AST (ASAT): the NORIP reference interval for adult women is 0.25-0.60 µkat/L.” females, adults (not age-stratified)
Nya gemensamma nordiska referensintervall inom klinisk kemi · Läkartidningen 2004;101:901-5 The document
GGT
“GGT (GT): the NORIP reference interval for men aged 18-40 years is 0.15-1.3 µkat/L.” males, 18-40
Nya gemensamma nordiska referensintervall inom klinisk kemi · Läkartidningen 2004;101:901-5 The document
“GGT (GT): the NORIP reference interval for men over 40 years is 0.20-1.9 µkat/L.” males, >40
Nya gemensamma nordiska referensintervall inom klinisk kemi · Läkartidningen 2004;101:901-5 The document
“GGT (GT): the NORIP reference interval for women aged 18-40 years is 0.15-0.75 µkat/L.” females, 18-40
Nya gemensamma nordiska referensintervall inom klinisk kemi · Läkartidningen 2004;101:901-5 The document
“GGT (GT): the NORIP reference interval for women over 40 years is 0.15-1.2 µkat/L.” females, >40
Nya gemensamma nordiska referensintervall inom klinisk kemi · Läkartidningen 2004;101:901-5 The document
Your laboratory reads your result against its own assay, and this page does not do that for it. What is above is what a named body published and for whom; what is below is the machinery the marker reads and the formulas witnessed on it.
What moves it
Master antioxidant raises it.
APAP-hepatotoxicity review — hepatic glutathione scavenges the reactive metabolite NAPQI; GSH depletion initiates hepatocyte injury and N-acetylcysteine (a GSH precursor) is the clinical antidote. PMC6800176
Tissue renewal raises it.
Michalopoulos 2017 (Hepatostat), Hepatology 65:1384 — after hepatocyte loss, coordinated hepatocyte proliferation restores liver mass (partial-hepatectomy model). PMID 27997988
Reduces scarring lowers it.
TGF-β hepatic fibrosis review 2006 — tgf-β1/Smad3 activates hepatic stellate cells to deposit collagen, driving liver fibrosis. PMID 16420505. Implicated across hepatitis, cirrhosis and hepatocellular carcinoma. Tgf-beta is not one signal — its effect depends on which smad phospho-isoform is engaged, and the paper is titled for it: 'reversible human tgf-beta signal shifting between tumor suppression and fibro-carcinogenesis'. Four forms exist: cytostatic pSmad3C, mitogenic pSmad3L (Ser-213), fibrogenic pSmad2L/C and migratory pSmad2/3L/C. After acute injury tgf-beta raises pSmad3C and terminates proliferation — the tumor-suppressor arm. Under chronic injury the linker-phosphorylated fibrogenic and mitogenic arms dominate. PMID 16420505
Cellular cleanup raises it.
Singh 2009, Nature 458:1131 — hepatic lipophagy clears lipid droplets; its loss drives steatosis and liver injury. doi 10.1038/nature07976
PCOS lowers it.
The source is explicitly bidirectional: while it is recognized that PCOS may contribute to hepatic dysfunction, there is also evidence that the liver may contribute to the features of PCOS. An estimated 50-70 percent of obese women with PCOS have NAFLD, compared to 20-30 percent of obese women without PCOS - roughly a doubling. A rat model shows the mechanism: insulin and hCG treatment induced imbalance between DE novo lipogenesis and mitochondrial beta-oxidation via the PPARa/b-SREBP1/2-ACC1 axis, resulting in varying degrees of hepatic steatosis. Species: that mechanistic arm is rat. PMC11764088
Pathogen tripwire lowers it.
The anatomy is the mechanism: the portal vein gathers blood from the small and large intestine, spleen, and pancreas and directs it into the liver, so as intestinal venous blood drains into the portal vein, the liver becomes the first organ to receive gut microbiota-derived products and metabolites. And the intervention evidence is unusually direct: exogenous conjugated bile acids increase bile acid secretion and reduce bacterial overgrowth, endotoxemia and translocation; FXR agonists RECONSTITUTE microbiota composition, restore epithelial and vascular intestinal barrier function and decrease bacterial translocation and endotoxemia in experimental cirrhosis. Species: experimental cirrhosis is the authors’ phrase - animal models. doi 10.1038/s41522-022-00352-6 · PMC11265038
Innate immune sensor lowers it.
Named across six gut-liver axis reviews. The main alteration is dysbiosis - A decrease in beneficial bacteria, an increase in potentially harmful microbes, and a loss of overall microbial diversity - with intestinal barrier integrity determining the levels of microbial metabolites, ENDOTOXINS and ammonia that reach the liver and systemic circulation. doi 10.1038/s41522-022-00352-6 · PMC11265038
Immune support lowers it.
Two routes, not one: microbial metabolites reach the liver via the portal vein, and separately the immune cells activated by these metabolites can also reach liver through lymphatic circulation. And a targeted mechanism: gut-primed lymphocytes expressing mucosal homing receptors migrate aberrantly to the liver, where they may contribute to biliary epithelial cell injury - the cells are addressed to the gut and arrive at the liver. doi 10.1038/s41522-022-00352-6 · PMC11265038
Calms inflammation lowers it.
Named across six gut-liver axis reviews. The main alteration is dysbiosis - A decrease in beneficial bacteria, an increase in potentially harmful microbes, and a loss of overall microbial diversity - with intestinal barrier integrity determining the levels of microbial metabolites, ENDOTOXINS and ammonia that reach the liver and systemic circulation. doi 10.1038/s41522-022-00352-6 · PMC11265038
Calms body-wide inflammation lowers it.
the main alteration of the gut-liver axis in chronic liver disease is dysbiosis, characterized by a decrease in beneficial bacteria, an increase in potentially harmful microbes, and a loss of overall microbial diversity. doi 10.1038/s41522-022-00352-6 · PMC11265038
What it moves
It lowers PCOS.
An estimated 50-70 percent of obese women with PCOS have NAFLD, compared to 20-30 percent of obese women without PCOS. And the arrow is explicitly bidirectional in the source: while it is recognized that PCOS may contribute to hepatic dysfunction, there is also evidence that the liver may contribute to the features of PCOS. One arrow is drawn, though the relationship runs both ways. doi 10.1038/s41581-026-01066-0 · PMC11725408
It raises Lowers cholesterol.
insulin, fasting insulin, type 2 diabetes and blood lipids share one literature: heart, kidney, liver, and metabolic diseases share interlinked pathological mechanisms, including inflammation, oxidative stress, insulin resistance, and endothelial health issues. These four overlap by nature: fasting insulin is the level, insulin is the signaling, type 2 diabetes is the diagnosis and blood lipids are the substrate. The same driver legitimately reaches all four, and a reader should not mistake four arrows for four independent findings. doi 10.1038/s41581-026-01066-0 · PMC11725408
It raises Micronutrient status.
10.3390/biomedicines11041094 — Micronutrient status is assembled from supplement-trial indices; none of the papers cited studied micronutrient status itself. doi 10.3390/biomedicines11041094
It raises Vitamin D status.
Verbatim: “Vitamin D is then converted by the liver to 25-hydroxyvitamin D, its major circulating form”. PMID 21034990
It raises Iron & oxygen carriage.
The mechanism that makes iron supplementation fail: anemia of inflammation is characterized by the insufficient production of erythropoietin and decreased response of erythroid progenitors to EPO. In addition, it inhibits the release of iron from the body stores and alters the iron status after being stimulated by hepcidin. Inflammation locks iron away - so oral iron given into an inflammatory state does not reach the marrow. Anemia affects 1.62 billion people. And the periodontal link is measured: a meta-analysis of sixteen studies on hemoglobin and iron metabolism in periodontitis - though the authors call the association still controversial and ask for larger cohorts. PMID 835510 · PMC7005133
It raises Gut barrier.
10.3390/biomedicines14051084 — The aging outcome lists the thirteen hallmarks themselves, each mapped to its pathway and labeled with its hallmark number. (from the reviews of this outcome). doi 10.3390/biomedicines14051084
It raises Liver clearance.
10.2147/dddt.s125459 — https://www.merckmanuals.com/professional/clinical-pharmacology/pharmacokinetics/drug-metabolism — The aging outcome lists the thirteen hallmarks themselves, each mapped to its pathway and labeled with its hallmark number. (from the reviews of this outcome). doi 10.2147/dddt.s125459
It raises Gut-liver bile signaling.
Bile acids are synthesized in the liver from cholesterol - the beginning of the gut-liver axis and the route by which cholesterol leaves the body. doi 10.1038/s41522-022-00352-6 · PMC10132248
It raises Thyroid.
10.1093/qjmed/95.9.559 — This link rests on the reviews of this outcome as a whole. No effect size specific to this arm has been reported, so it is shown at reduced weight. (from the reviews of this outcome). doi 10.1093/qjmed/95.9.559
It raises Iron gatekeeper hormone.
Hepcidin is a hepatic hormone. PMC7005133
Formulas that modulate it
Each formula page names this pathway and carries the study behind its claim.
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