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Research · Lab markers

Gamma-glutamyl transferase (GGT)

GGT is a liver and bile duct enzyme also used to flag drinking. Upper limits run 33 to 40 U/L for women and 45 to 68 for men, lower when set from non-drinkers. Higher values go with more deaths, cardiovascular disease and type 2 diabetes in pooled cohorts. A genetic study found no evidence of a causal role in diabetes.

Checked 2026-11-13
Status
A blood test ordered by a clinician, often alongside other liver tests, and also sold direct to consumers by some US laboratories. FDA classifies gamma-glutamyl transpeptidase test systems as class I devices exempt from premarket notification [1].
Measures
The activity of the enzyme gamma-glutamyl transferase in serum or plasma, used as an indicator of liver and bile duct disease and of alcohol use [1][2].
Also called
GGT, gamma-glutamyl transferase, gamma-glutamyltransferase, gamma-glutamyl transpeptidase, GGTP, gamma-GT, gamma GT, GT, γ-GT, γ-glutamyl transferase
Tested for
liver health, bile duct problems, alcohol use, fatty liver, liver enzymes check, heart disease risk

Strong several reviews agree · Moderate one review or consistent trials · Limited one or a few small studies · Untested no study in people, listed with what it rests on

Reported risks0

No risks sourced yet.

Reference ranges

Each range is the one its source published, in U/L. Also reported in µkat/L. Where sources differ, each is shown.

International Federation of Clinical Chemistry multicenter study, 2010, women

Adult women aged 18 to 85 · [3]

RangeWhat the source calls it
below 6 U/LNo name given
6 to 40 U/L"reference interval"
above 40 U/LNo name given

A laboratory reference interval, the central 95% of results in selected people, not a cut point set for a disease outcome. Measured on systems standardized to the federation's reference measurement systems, in people from Italy, China and Turkey. Upper limits in the Nordic samples were higher than in the other three regions, and those samples were left out of the final interval. The authors conclude that one GGT interval for use worldwide appears unlikely because populations differ [3].

International Federation of Clinical Chemistry multicenter study, 2010, men

Adult men aged 18 to 85 · [3]

RangeWhat the source calls it
below 12 U/LNo name given
12 to 68 U/L"reference interval"
above 68 U/LNo name given

From the same study as the interval for women, with the Nordic samples left out [3].

US national survey laboratory procedure manual, 2017 to 2018, women

Adult women, as the reference range printed for the assay · [2]

RangeWhat the source calls it
below 7 U/LNo name given
7 to 33 U/L"reference range"
above 33 U/LNo name given

The reference range listed in the laboratory manual for the method used in the 2017 to 2018 US National Health and Nutrition Examination Survey (Roche Cobas 6000). It is the range attached to that assay, not one derived from survey participants [2]. A study of an earlier round of the same survey defined abnormal GGT as above 33 U/L in women and above 51 U/L in men [4].

US national survey laboratory procedure manual, 2017 to 2018, men

Adult men, as the reference range printed for the assay · [2]

RangeWhat the source calls it
below 11 U/LNo name given
11 to 51 U/L"reference range"
above 51 U/LNo name given

From the same manual and method as the range for women [2].

American Board of Internal Medicine laboratory reference ranges, 2026, women

Adult women, as the range printed for board examinations · [5]

RangeWhat the source calls it
below 8 U/LNo name given
8 to 40 U/L"reference range"
above 40 U/LNo name given

Published as a reference table for examination candidates. The table does not say how the range was set [5].

American Board of Internal Medicine laboratory reference ranges, 2026, men

Adult men, as the range printed for board examinations · [5]

RangeWhat the source calls it
below 9 U/LNo name given
9 to 50 U/L"reference range"
above 50 U/LNo name given

From the same table as the range for women [5].

Hietala and colleagues, reference population by alcohol use, 2005, men who do not drink

Adult men who abstain from alcohol · [6]

RangeWhat the source calls it
45 or below U/L"normal"
above 45 U/LNo name given

The upper normal limit calculated from the abstainers among 2,485 healthy volunteers (1,156 abstainers in all). The authors set it beside the limit from moderate drinkers to show that GGT responds to low levels of alcohol intake, and that a reference population which includes drinkers yields a higher limit [6].

Hietala and colleagues, reference population by alcohol use, 2005, women who do not drink

Adult women who abstain from alcohol · [6]

RangeWhat the source calls it
35 or below U/L"normal"
above 35 U/LNo name given

From the same abstainer group as the limit for men [6].

Hietala and colleagues, reference population by alcohol use, 2005, men who drink moderately

Adult men drinking a mean of 1 to 40 g of ethanol a day · [6]

RangeWhat the source calls it
66 or below U/L"normal"
above 66 U/LNo name given

The upper normal limit calculated from the moderate drinkers among 2,485 healthy volunteers (1,329 moderate drinkers in all). It is 21 U/L above the limit the same study calculated from men who do not drink [6].

Hietala and colleagues, reference population by alcohol use, 2005, women who drink moderately

Adult women drinking a mean of 1 to 40 g of ethanol a day · [6]

RangeWhat the source calls it
40 or below U/L"normal"
above 40 U/LNo name given

From the same moderate drinker group as the limit for men. It is 5 U/L above the limit calculated from women who do not drink [6].

What has been shown to move it

Shown to lower it3

OrlistatStrong

Liver enzymes in fatty liver disease

Shown to lower liver enzymes in fatty liver disease, ALT by about 9 U/L. Liver fat and scarring were not measured.

The numbers and sources
Effect
In people with metabolic dysfunction-associated steatotic liver disease, orlistat lowered AST by 4.01 U/L (95% CI 1.97 to 6.05), ALT by 8.70 U/L (95% CI 0.90 to 16.51) and GGT by 7.74 U/L (95% CI 0.59 to 14.88) against control. LDL cholesterol fell 5.61 mg/dL, fasting glucose 4.05 mg/dL, HOMA-IR 0.70 and BMI 0.99 kg/m². Blood pressure did not change [6]. A second meta-analysis also found lower ALT, AST, HOMA-IR, BMI, cholesterol, insulin and waist circumference [7].
Population
6 RCTs [6]; 11 studies with 582 participants [7].
Sources
[6], [7]
Caveats
Both reviews measured blood markers, not liver fat on imaging or scarring on biopsy. The trials were small and likely overlap between the reviews. The abstract of [7] does not say whether all 11 studies were randomized.
Fisetin and quercetin (senolytics)Moderate

Liver enzymes and lipids in fatty liver disease (quercetin alone)

Shown to lower liver enzymes, LDL and triglycerides with quercetin alone in people with fatty liver disease, at very low to moderate certainty.

The numbers and sources
Effect
A 2025 meta-analysis of 7 RCTs (540 patients) with metabolic dysfunction-associated steatotic liver disease found that quercetin lowered ALT, AST, GGT, direct bilirubin and C-reactive protein, lowered total cholesterol, LDL and triglycerides, and raised HDL. BMI, body fat, kidney function and TNF-α did not change [10].
Population
540 patients with fatty liver disease in 7 RCTs [10].
Sources
[10]
Caveats
GRADE certainty ranged from very low to moderate. Dose, baseline BMI and age may explain heterogeneity. The abstract gives no pooled effect sizes [10]. None of the trials measured senescent cells.
TurmericModerate

Fatty liver and liver enzymes

Shown to lower the liver enzymes ALT and AST slightly in adults with fatty liver disease, but not in people with diabetes or with piperine added.

In 10 RCTs in prediabetes and diabetes, ALT and AST did not change significantly and GGT fell 2.35 IU/L.

The numbers and sources
Effect
In 15 RCTs (905 patients with nonalcoholic fatty liver disease), curcumin lowered ALT by 4.10 (95% CI -7.16 to -1.04) and AST by 3.27 (95% CI -5.16 to -1.39), with no change in ALP. Curcumin with piperine did not change ALT or AST significantly [36]. In 10 RCTs in prediabetes and diabetes, ALT and AST did not change significantly and GGT fell 2.35 IU/L [37]. Across 18 RCTs of curcuminoids with piperine, AST fell 2.29 IU and the ALT change was not significant (p 0.053) [18].
Population
Adults with nonalcoholic fatty liver disease [36]; adults with prediabetes or diabetes [37]; adults in curcumin with piperine trials [18].
Sources
[36], [37], [18]
Caveats
These are blood enzymes, not measures of liver fat or fibrosis. Results differed by population and formulation [36][37].

Shown to raise it1

Modafinil and armodafinilModerateCommon

Liver enzyme changes

Shown to raise mean GGT and alkaline phosphatase in placebo-controlled trials, mostly within the normal range. ALT and AST did not differ.

The numbers and sources
How common
Common: between 1 in 100 and 1 in 10 people.
Effect
Mean GGT and alkaline phosphatase were higher after modafinil but not placebo, and rose over time, with few values outside the normal range. ALT, AST, albumin and total bilirubin did not differ. "Abnormal liver function" was reported as an adverse reaction in 2% vs 1% on placebo [3].
Population
Adults in placebo-controlled label trials [3].
Sources
[3]
Caveats
The label gives no size for the mean change. The band above is the adverse-reaction rate.

Type in your own result

How it compares with the reference method

Matched the reference method1

LimitedStudied in men

Heavy exercise

One small study found GGT was almost unaltered for 7 days after a weightlifting session that raised AST and ALT.

The numbers and sources
Compared with
The same men's results before exercise, and the laboratory's upper reference limit
Effect
After a single 1-hour weightlifting session in healthy men unused to lifting, GGT, bilirubin and alkaline phosphatase were almost unaltered over 7 days, and no man's GGT went above the upper reference limit. AST, ALT, lactate dehydrogenase, creatine kinase and myoglobin all rose significantly over the same days [16].
Population
15 healthy men, mean age 24.5, 14 analyzed [16].
Sources
[16]
Caveats
One small study of one kind of exercise in men not accustomed to it [16].

Mixed results2

Limited

As a marker of alcohol use

Mixed results: one multicenter study found GGT detected high-risk drinking about as well as carbohydrate deficient transferrin, with results also shifted by weight, sex, age and smoking.

The numbers and sources
Compared with
Alcohol consumption recorded by structured interview
Effect
In 1,863 people recruited in five countries and stratified by alcohol use, age and sex, GGT and carbohydrate deficient transferrin performed comparably on receiver operating characteristic analysis. Both detected high-risk drinking better than intermediate-risk drinking. GGT was influenced by body mass index, sex, age and smoking status [13]. In a second study, GGT in people averaging 1 to 40 g of ethanol a day was higher than in abstainers, and higher again above 40 g a day [6].
Population
1,863 people from Australia, Brazil, Canada, Finland and Japan, mostly community based [13]. 103 heavy drinkers and 92 healthy volunteers, with reference data from 2,485 healthy volunteers [6].
Sources
[13], [6]
Caveats
The first abstract gives no sensitivity or specificity figures. Drinking was self-reported in both studies [13][6].
Moderate

Variation from one test to the next

Shown to vary less between tests than other liver enzymes: 12% of US adults with a raised GGT had a normal result on retest.

The numbers and sources
Compared with
A repeat measurement in the same person
Effect
Among 1,864 US adults measured twice a mean of 17.5 days apart, 12% of those with an initially elevated GGT had a normal result the second time, against 36% for AST and 31% for ALT. The within-person coefficient of variation was 13.8% [14]. In 91 healthy Europeans sampled weekly for 10 weeks, within-person biological variation was 8.9% and variation between people was 41.7%, the widest spread between people of the 9 enzymes studied [15].
Population
1,864 adults in the third US National Health and Nutrition Examination Survey [14]. 91 healthy adults aged 21 to 69 at 6 European laboratories [15].
Sources
[14], [15]
Caveats
The US study had only 2 measurements per person [14]. Neither study states a threshold for agreement, so the result is given as numbers only.

What studies tie it to

Linked in research4

Strong

Death from any cause

Linked to more deaths from any cause, about 7% higher risk for each 5 U/L in a meta-analysis of general population cohorts.

The numbers and sources
Effect
In a meta-analysis of 19 cohort studies, the relative risk of death from any cause was 1.60 (95% CI 1.42 to 1.80) comparing the top and bottom thirds of baseline GGT, and 1.07 (1.04 to 1.10) per 5 U/L higher, consistent with a linear relationship [7]. A second meta-analysis of 35 prospective studies found GGT was associated with increased all-cause and cardiovascular mortality even at levels inside the reference interval [8]. In 14,950 US adults without viral hepatitis followed for 12 years, GGT above 51 U/L in men or 33 U/L in women went with more deaths from any cause (HR 1.5, 95% CI 1.2 to 1.8), from liver disease (HR 13.0, 95% CI 2.4 to 71.5), from neoplasms (HR 1.5, 95% CI 1.01 to 2.2) and from diabetes (HR 3.3, 95% CI 1.4 to 7.6) [4].
Population
Over 9.24 million participants and 242,953 deaths in 19 cohorts, which also covered other liver enzymes [7]. 571,511 participants and 72,196 deaths in 35 studies [8]. 14,950 adults in the third US National Health and Nutrition Examination Survey [4].
Sources
[7], [8], [4]
Caveats
Observational. Many of the pooled studies did not exclude people with liver disease or heavy alcohol use, which the authors of one meta-analysis say may have obscured the results [8]. Liver disease deaths were 0.13% of the US cohort, so the interval around that estimate is wide [4].
Moderate

Heart disease and stroke

Linked to more cardiovascular disease, 23% higher risk per standard deviation of log GGT in a meta-analysis of 29 cohorts.

The numbers and sources
Effect
In a meta-analysis of 29 prospective cohorts, the fully adjusted relative risk of cardiovascular disease was 1.23 (95% CI 1.16 to 1.29) per standard deviation of log baseline GGT, in a log-linear pattern [9]. In US adults, GGT above 51 U/L in men or 33 U/L in women was not significantly associated with cardiovascular death (HR 1.3, 95% CI 0.80 to 2.0) [4].
Population
Over 1.23 million participants and 20,406 cardiovascular outcomes in 29 cohorts, which also covered other liver enzymes [9]. 14,950 US adults [4].
Sources
[9], [4]
Caveats
Observational. The cohorts cannot separate GGT from alcohol intake, body weight and other factors that move with it, beyond the adjustments each study made.
Moderate

Type 2 diabetes

Linked to more type 2 diabetes, 34% higher risk in the top third of GGT across 24 cohorts. A genetic study found no evidence that GGT drives it.

The numbers and sources
Effect
In a meta-analysis of 24 cohort studies, the relative risk of type 2 diabetes comparing the top and bottom thirds of baseline GGT was 1.34 (95% CI 1.27 to 1.42), with a nonlinear dose-response pattern in both men and women and significant heterogeneity between studies [10]. In a Mendelian randomization study, genetically predicted GGT showed no evidence of association with type 2 diabetes (odds ratio 0.92 per standard unit, 95% CI 0.80 to 1.06) [11].
Population
177,307 participants and 11,155 cases of type 2 diabetes in 24 cohorts [10]. Up to 64,094 people with type 2 diabetes and 607,012 controls in the genetic study [11].
Sources
[10], [11]
Caveats
The cohort finding is observational. The genetic result suggests GGT marks a higher risk without causing it [11].
Limited

Cancer

One Swedish cohort of 545,460 people found cancer risk rose across GGT categories, 32% higher at 72 U/L or above than below 18 U/L.

The numbers and sources
Effect
In a Swedish cohort with 37,809 primary cancers, hazard ratios for any cancer against GGT below 18 U/L were 1.07 (95% CI 1.04 to 1.09) at 18 to 36 U/L, 1.18 (1.14 to 1.22) at 36 to 72 U/L and 1.32 (1.26 to 1.38) at 72 U/L or above. Associations with prostate, breast and liver cancer were stronger in people with glucose of 6.11 mmol/L or above [12].
Population
545,460 people older than 20 in the Swedish Apolipoprotein Mortality Risk study [12].
Sources
[12]
Caveats
Observational, one cohort. The abstract does not say whether the analysis adjusted for alcohol intake or smoking [12].

Sources

  1. US Food and Drug Administration. 21 CFR 862.1360, Gamma-glutamyl transpeptidase and isoenzymes test system. Electronic Code of Federal Regulations. https://www.ecfr.gov/current/title-21/section-862.1360
  2. Centers for Disease Control and Prevention, National Center for Health Statistics. National Health and Nutrition Examination Survey 2017-2018 Laboratory Procedure Manual: Gamma-Glutamyltransferase (GGT), serum, Roche Cobas 6000. Performed by the University of Minnesota Advanced Research and Diagnostic Laboratory. https://wwwn.cdc.gov/nchs/data/nhanes/public/2017/labmethods/BIOPRO-J-MET-GGT-508.pdf
  3. Ceriotti F, Henny J, Queraltó J, et al. Common reference intervals for aspartate aminotransferase (AST), alanine aminotransferase (ALT) and γ-glutamyl transferase (GGT) in serum: results from an IFCC multicenter study. Clinical Chemistry and Laboratory Medicine. 2010. https://doi.org/10.1515/cclm.2010.315
  4. Ruhl CE, Everhart JE. Elevated Serum Alanine Aminotransferase and γ-Glutamyltransferase and Mortality in the United States Population. Gastroenterology. 2009. https://doi.org/10.1053/j.gastro.2008.10.052
  5. American Board of Internal Medicine. ABIM Laboratory Test Reference Ranges, January 2026. https://www.abim.org/Media/bfijryql/laboratory-reference-ranges.pdf
  6. Hietala J, Puukka K, Koivisto H, et al. Serum gamma-glutamyl transferase in alcoholics, moderate drinkers and abstainers: effect on GT reference intervals at population level. Alcohol and Alcoholism. 2005. https://doi.org/10.1093/alcalc/agh201
  7. Kunutsor SK, Apekey TA, Seddoh D, Walley J. Liver enzymes and risk of all-cause mortality in general populations: a systematic review and meta-analysis. International Journal of Epidemiology. 2014. https://doi.org/10.1093/ije/dyt192
  8. Long Y, Zeng F, Shi J, et al. Gamma-glutamyltransferase predicts increased risk of mortality: A systematic review and meta-analysis of prospective observational studies. Free Radical Research. 2014. https://doi.org/10.3109/10715762.2014.902055
  9. Kunutsor SK, Apekey TA, Khan H. Liver enzymes and risk of cardiovascular disease in the general population: A meta-analysis of prospective cohort studies. Atherosclerosis. 2014. https://doi.org/10.1016/j.atherosclerosis.2014.06.006
  10. Kunutsor SK, Abbasi A, Adler AI. Gamma-glutamyl transferase and risk of type II diabetes: an updated systematic review and dose-response meta-analysis. Annals of Epidemiology. 2014. https://doi.org/10.1016/j.annepidem.2014.09.001
  11. De Silva NMG, Borges MC, Hingorani AD, et al. Liver Function and Risk of Type 2 Diabetes: Bidirectional Mendelian Randomization Study. Diabetes. 2019. https://doi.org/10.2337/db18-1048
  12. Van Hemelrijck M, Jassem W, Walldius G, et al. Gamma-glutamyltransferase and risk of cancer in a cohort of 545,460 persons: the Swedish AMORIS study. European Journal of Cancer. 2011. https://doi.org/10.1016/j.ejca.2011.03.010
  13. Conigrave KM, Degenhardt LJ, Whitfield JB, et al. CDT, GGT, and AST As Markers of Alcohol Use: The WHO/ISBRA Collaborative Project. Alcoholism: Clinical and Experimental Research. 2002. https://doi.org/10.1111/j.1530-0277.2002.tb02542.x
  14. Lazo M, Selvin E, Clark JM. Brief Communication: Clinical Implications of Short-Term Variability in Liver Function Test Results. Annals of Internal Medicine. 2008. https://doi.org/10.7326/0003-4819-148-5-200803040-00005
  15. Carobene A, Røraas T, Sølvik UØ, et al. Biological Variation Estimates Obtained from 91 Healthy Study Participants for 9 Enzymes in Serum. Clinical Chemistry. 2017. https://doi.org/10.1373/clinchem.2016.269811
  16. Pettersson J, Hindorf U, Persson P, et al. Muscular exercise can cause highly pathological liver function tests in healthy men. British Journal of Clinical Pharmacology. 2008. https://doi.org/10.1111/j.1365-2125.2007.03001.x

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