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Research · Lab markers

Aspartate aminotransferase (AST)

AST is an enzyme found in liver, muscle, heart and red blood cells. Laboratory sources put its upper limit at 31 to 40 U/L. Values of 20 U/L and above went with more liver disease deaths in one large cohort, while pooled cohorts found no tie to heart disease. One weightlifting session raised it above the limit for days.

Checked 2026-11-13
Status
Part of routine liver and metabolic blood panels, ordered by a clinician and also sold direct to consumers by some US laboratories. FDA classifies AST test systems as class II devices with special controls, exempt from premarket notification within stated limits [1]. Reports print the unit as U/L or IU/L.
Measures
The activity of the enzyme aspartate aminotransferase in serum or plasma. The enzyme is found in liver, heart, skeletal muscle, kidney, brain and other tissues, and in red blood cells [1][2].
Also called
AST, aspartate aminotransferase, aspartate transaminase, aspartate amino transferase, SGOT, serum glutamic oxaloacetic transaminase, ASAT, GOT, AST (SGOT), AST/SGOT
Tested for
liver health, liver damage from alcohol, hepatitis screening, fatty liver, liver enzymes check, muscle damage

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

Adults aged 18 to 85, both sexes · [3]

RangeWhat the source calls it
below 11 U/LNo name given
11 to 34 U/L"reference interval"
above 34 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. From 765 individuals in Italy, China, Turkey and the Nordic countries, measured on systems standardized to the federation's reference measurement systems. The upper limits for women and men differed by 1.7 U/L, which the authors judged small enough to publish one interval for both. The study prints the interval as 0.18 to 0.57 µkat/L [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
0 to 31 U/L"reference range"
above 31 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), standardized against the international federation's formulation. It is the range attached to that assay, not one derived from survey participants. The manual states that hemolysis interferes because red blood cells contain AST, and that hemolyzed specimens are not analyzed for AST [2].

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
0 to 37 U/L"reference range"
above 37 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

Adults, both sexes, as the range printed for board examinations · [4]

RangeWhat the source calls it
below 10 U/LNo name given
10 to 40 U/L"reference range"
above 40 U/LNo name given

One range for both sexes, published as a reference table for examination candidates. The table does not say how the range was set [4].

What has been shown to move it

Shown to lower it6

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.
Milk thistleModerate

Fatty liver disease

Shown to lower liver enzymes in fatty liver disease, ALT by about 7 to 12 U/L, with low certainty and no data on deaths.

The numbers and sources
Effect
In 26 trials (2,375 patients), silymarin lowered ALT (pooled difference -12.39, 95% CI -19.69 to -5.08) and AST (-10.97, 95% CI -15.51 to -6.43), lowered total cholesterol, triglycerides and LDL, and improved steatosis on histology (OR 3.25, 95% CI 1.80 to 5.87) [5]. In a 48-week biopsy trial of 99 adults with NASH, a 30% or greater fall in disease activity score occurred in 32.7% on 700 mg three times a day and 26.0% on placebo (p 0.467). Fibrosis fell by 1 point or more in 22.4% against 6.0% (p 0.023) [6]. A 2025 Cochrane review of 17 RCTs (2,069 adults) found silymarin alone against placebo or no treatment may lower ALT by 7.21 U/L (95% CI -10.62 to -3.80, 6 trials, very low certainty). Silymarin complexes did not lower ALT, and no trial reported deaths or quality of life [7]. In a 2025 meta-analysis of 25 studies (2,283 patients), silymarin alone lowered LDL cholesterol (SMD -0.25), while ALT fell when silymarin was combined with diet or lifestyle change [8].
Population
Adults with fatty liver disease [5][7][8]. 99 adults with biopsy-proven NASH in Malaysia [6].
Sources
[5], [6], [7], [8]
Caveats
The meta-analysis authors state that the effects need confirmation [5]. The biopsy trial missed its primary outcome, and its fibrosis finding was secondary [6]. The Cochrane authors rated the evidence low to very low certainty and called benefits and harms unclear [7].
OrforglipronModerate

Liver tests

Raised liver tests were about as common on orforglipron as on comparators across phase 3 trials, and other causes accounted for every serious case.

The numbers and sources
How common
Uncommon: between 1 in 1,000 and 1 in 100 people.
Effect
Across seven phase 3 trials, mean ALT and AST fell on orforglipron, and raised levels occurred at similar rates on orforglipron and comparators. Six people (0.1%) in each group had ALT or AST at 3 or more times the upper limit with bilirubin at 2 or more times, and other causes accounted for every orforglipron case [13].
Population
11,220 participants, 6,920 on orforglipron, for up to 104 weeks [13].
Sources
[13]
Caveats
A pooled analysis by the manufacturer's investigators. The trials excluded people with markedly raised liver enzymes at screening [13].
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.

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].
Vitamin EModerate

Fatty liver inflammation (NASH)

Shown to improve liver inflammation in adults with NASH without diabetes, 43% against 19% on placebo in one trial. Results on fibrosis disagree.

Across 16 RCTs in fatty liver disease, vitamin E lowered AST (WMD -5.94 IU/L) and ALT (WMD -7.33 IU/L).

The numbers and sources
Effect
After 96 weeks, nonalcoholic steatohepatitis improved in 43% on 800 IU a day and 19% on placebo. Liver enzymes, fat and inflammation fell. Fibrosis scores did not improve [6]. Across 3 placebo-controlled RCTs in steatohepatitis, vitamin E lowered ALT (MD -12.27, 95% CI -16.66 to -7.89) and raised the odds of fibrosis improvement (OR 1.96, 95% CI 1.25 to 3.09). Resolution of steatohepatitis did not differ significantly (OR 1.71, 95% CI 0.69 to 4.27) [7]. Across 16 RCTs in fatty liver disease, vitamin E lowered AST (WMD -5.94 IU/L) and ALT (WMD -7.33 IU/L) [8]. In a Chinese trial, liver histology improved in 29.3% on 300 mg a day and 14.1% on placebo, with gains in steatosis, inflammation and fibrosis stage [9].
Population
247 adults with nonalcoholic steatohepatitis and without diabetes [6]; adults with steatohepatitis in 2 US trials and 1 Chinese trial [7]; adults with metabolic dysfunction-associated steatotic liver disease [8]; 124 adults without diabetes with biopsy-proven steatohepatitis in China [9].
Sources
[6], [7], [8], [9]
Caveats
The 3-trial review is small and its resolution result was heterogeneous [7]. The first large trial found no fibrosis improvement [6], while the pooled analysis and the Chinese trial did [7][9]. The enzyme review could not judge fibrosis or long-term liver outcomes [8].

Shown to raise it7

CBDStrongCommon

Liver enzyme elevation

Shown to raise liver enzymes, about 6 times the odds on placebo, mostly at high doses or with antiepileptic drugs. No cases appeared under 300 mg a day in adults.

In an FDA-run trial of 201 healthy adults, 5 mg/kg a day for 28 days raised ALT or AST above 3 times normal in 5.6% on CBD and 0% on placebo, with increased eosinophilia.

The numbers and sources
How common
Common: between 1 in 100 and 1 in 10 people.
Effect
Across 12 placebo-controlled trials (1,229 participants), CBD raised the odds of liver enzyme elevation (OR 5.85, 95% CI 3.84 to 8.92) and drug-induced liver injury (OR 4.82, 95% CI 2.46 to 9.45). In 28 trials, the pooled rate of enzyme elevation was 7.4% and of liver injury 3.0%. High dose (1,000 mg a day or more, or 20 mg/kg or more) and use with antiepileptic drugs were risk factors. No cases were reported in adults under 300 mg a day, and no severe injury was reported [12]. In an FDA-run trial of 201 healthy adults, 5 mg/kg a day for 28 days raised ALT or AST above 3 times normal in 5.6% on CBD and 0% on placebo, with increased eosinophilia [11]. In the Lennox-Gastaut trial, 9% of CBD patients had raised aminotransferases [2].
Population
Trial participants with epilepsy and healthy adults [2][11][12].
Sources
[2], [11], [12]
Caveats
In the healthy-adult trial, elevations meeting withdrawal criteria were found at day 21 in 2 people and day 28 in 5 [11]. Long-term effects at lower consumer doses were not measured [11].
Atypical antipsychoticsModerateCommon

Raised liver enzymes on quetiapine

Shown to raise the liver enzyme ALT in 5% on quetiapine against 1% on placebo in schizophrenia and mania trials.

The numbers and sources
How common
Common: between 1 in 100 and 1 in 10 people.
Effect
In trials of 3 to 12 weeks, increased ALT was reported in 5% on quetiapine and 1% on placebo, and increased AST in 3% against 1% [3].
Population
719 people on quetiapine and 404 on placebo [3].
Sources
[3]
Caveats
Reported as adverse reactions in short trials, with no data here on how long the rises lasted. The evidence is for quetiapine.
Ezetimibe and fenofibrateModerateCommon

Fenofibrate: liver enzymes and liver injury

Shown to raise ALT above 3 times normal in 5.3% against 1.1% on placebo. The label warns of serious liver injury after approval, including transplant and death.

In label trials, increased AST was 3.4% against 0.5% and abnormal liver tests 7.5% against 1.4%, and raised liver tests caused 1.6% to stop.

The numbers and sources
How common
Common: between 1 in 100 and 1 in 10 people.
Effect
In 10 placebo-controlled trials, ALT rose above 3 times the upper limit in 5.3% on fenofibrate and 1.1% on placebo. In label trials, increased AST was 3.4% against 0.5% and abnormal liver tests 7.5% against 1.4%, and raised liver tests caused 1.6% to stop. In an 8-week study, ALT or AST rises of 3 times or more reached 13% at the higher doses. The label reports serious drug-induced liver injury after approval [7].
Population
439 people on fenofibrate and 365 on placebo, and a pooled 10-trial analysis [7].
Sources
[7]
Caveats
Postmarketing liver injury reports have no denominator.
GnRH drugs for fibroidsModerateStudied in womenCommon

Liver enzyme rises

Shown to raise ALT or AST to 3 times normal or more in about 1% of women on Oriahnn and under 1% on Myfembree, against 0% to 0.4% on placebo.

The numbers and sources
How common
Common: between 1 in 100 and 1 in 10 people.
Effect
ALT rose to 3 times the upper limit or more in 1.1% (4 of 379) on Oriahnn and AST in 1.3% (5 of 379), against none on placebo, peaking at 8 and 6 times the limit, and returning to baseline within 4 months [6]. On Myfembree in fibroid trials, ALT rose in 0.4% (1 of 254) and AST in 0.8% (2 of 254), against 0% and 0.4% on placebo [2]. On leuprolide, 3% of women with fibroids had post-treatment transaminases at least twice baseline and above normal [10].
Population
Premenopausal women with fibroids in the placebo-controlled trials [2][6][10].
Sources
[6], [2], [10]
Caveats
Few events. Both labels contraindicate use in liver disease [2][6].
IsotretinoinModerateVery common

Raised liver enzymes

Shown to raise liver enzymes mildly to moderately in about 15% of people in trials. The label also reports clinical hepatitis.

ALT, AST, GGT and alkaline phosphatase are among the tests the label lists as increased.

The numbers and sources
How common
Very common: more than 1 in 10 people.
Effect
Mild to moderate rises in liver enzymes were seen in about 15% of people in clinical trials, some returning to normal with a lower dose or continued treatment. ALT, AST, GGT and alkaline phosphatase are among the tests the label lists as increased [3]. A meta-analysis found statistically significant changes in hepatic panel means, with ALT averaging 21.77 U/L and AST 22.67 U/L during treatment, and few results outside the normal range [9]. Elevated liver enzymes led to withdrawal from trials in some [1].
Population
Isotretinoin capsule trials [3]; 1,574 patients in 26 studies [9]; 760 people in 11 trials [1].
Sources
[3], [9], [1]
Caveats
The meta-analysis authors concluded that monthly laboratory testing is not supported for standard doses in the standard patient [9].
AllopurinolLimitedCommon

Liver enzymes and liver injury

The label reports rises in AST, ALT and alkaline phosphatase in 1% or more of people, and cases of reversible liver injury.

The numbers and sources
How common
Common: between 1 in 100 and 1 in 10 people.
Effect
The label lists increases in AST, ALT and alkaline phosphatase among reactions occurring in 1% or more, and states that cases of reversible liver injury have occurred, with hepatic necrosis and granulomatous hepatitis reported in under 1% [5]. In a dose-escalation trial, mild rises in liver tests were frequent in both the escalation and control groups [3].
Population
People taking allopurinol, as described in the label [5]; 183 people with gout [3].
Sources
[5], [3]
Caveats
The label gives no placebo rate and no size for the enzyme rises.
OndansetronLimitedCommon

Raised liver enzymes

The label reports ALT or AST above twice the upper limit in 1% to 2% of patients on ondansetron with chemotherapy, transient, with chemotherapy's role unclear.

The numbers and sources
How common
Common: between 1 in 100 and 1 in 10 people.
Effect
AST or ALT exceeded twice the upper limit of normal in about 1% to 2% of 723 patients receiving ondansetron with cyclophosphamide-based chemotherapy. The rises were transient and not related to dose or duration, and symptomatic liver disease did not occur. Liver failure and death have been reported in cancer patients also taking liver-toxic drugs [3].
Population
723 patients in US chemotherapy trials [3].
Sources
[3]
Caveats
No placebo rate is given, and the label states the role of chemotherapy is unclear [3].

Studies disagree1

Tested, and not shown to change it6

Black seed oilModerateHow often is not known

Liver and kidney markers in trials

Liver and kidney markers did not worsen in most trials. Creatinine rose slightly in 3 trials, and doses above 2,000 mg a day were linked to a BUN change.

The numbers and sources
How common
How often is not known: the sources give no rate.
Effect
In 19 trials (1,295 participants), Nigella sativa lowered ALP by 10.8 U/L and BUN by 1.016. Creatinine rose by 0.070 in 3 trials with covariate-adjusted analyses, and doses above 2,000 mg a day were linked to a BUN change in 2 trials [11]. In 70 healthy adults given 200 mg a day of a thymoquinone-rich oil for 90 days, liver and kidney tests did not change and no serious adverse effects were reported [12].
Population
Adults in RCTs [11]. 70 healthy adults [12].
Sources
[11], [12]
Caveats
The safety trial's corresponding author is at Akay Natural Ingredients, the maker of the tested oil [12]. Heterogeneity for ALP and BUN was high [11]. In 16 RCTs in type 2 diabetes, AST, ALT and creatinine did not change significantly [7].
CLAModerate

Liver enzymes

ALT and AST did not change with CLA against control across 22 trials.

The numbers and sources
How common
How often is not known: the sources give no rate.
Effect
In 22 RCTs, ALT and AST did not change with CLA compared with control [9].
Population
Adults in RCTs [9].
Sources
[9]
Caveats
Effect sizes are not given in the abstract.
FenugreekModerate

Liver enzymes

Liver enzymes did not change significantly across 16 controlled trials. Alkaline phosphatase fell at doses above 1 g a day.

The numbers and sources
How common
How often is not known: the sources give no rate.
Effect
A 2026 meta-analysis of 16 controlled trials (1,171 participants) found no significant change in ALT (-1.41 IU/L, 95% CI -3.07 to 0.26), AST (0.03 IU/L, 95% CI -0.12 to 0.18) or alkaline phosphatase (SMD -0.21, 95% CI -0.44 to 0.03). Alkaline phosphatase fell at doses above 1 g a day [10].
Population
Participants in 16 controlled clinical trials [10].
Sources
[10]
Caveats
Liver enzymes are a marker, not a count of liver injury. The authors call for trials in more uniform populations [10].
Garcinia cambogiaModerateHow often is not known

Liver enzymes and side effects in trials

Liver enzymes did not change in short trials. In one trial, gut side effects were twice as common as on placebo.

The numbers and sources
How common
How often is not known: the sources give no rate.
Effect
In pooled trials, garcinia did not change ALT (Hedges' g 0.27, 95% CI -0.20 to 0.73) or AST (Hedges' g -0.08, 95% CI -0.43 to 0.26) [6]. In one trial included in [1], gastrointestinal adverse events were twice as common with hydroxycitric acid as with placebo [1].
Population
444 participants in 9 publications [6]; RCTs [1].
Sources
[1], [6]
Caveats
Trials were short and too small to detect rare liver injury. The registry and case findings [7][8][9][10] and the trial enzyme data describe different things.
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.

ALT, AST, albumin and total bilirubin did not differ. "Abnormal liver function" was reported as an adverse reaction in 2% vs 1% on placebo.

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.
AcetaminophenLimitedHow often is not known

With alcohol

The label warns of severe liver damage with 3 or more alcoholic drinks a day. One short trial in alcoholic patients found no rise in AST.

Mean AST on day 4 was 38.0 against 37.5 U/L, and AST rose above 120 U/L in 4 patients on acetaminophen and 5 on placebo.

The numbers and sources
How common
How often is not known: the sources give no rate.
Effect
The over-the-counter label warns that severe liver damage may occur with 3 or more alcoholic drinks every day while using the product [19]. The prescription combination label states that the risk of acute liver failure is higher in people who drink alcohol while taking acetaminophen [22]. In patients entering an alcohol detoxification center, 1,000 mg four times a day for 2 days did not change liver tests against placebo. Mean AST on day 4 was 38.0 against 37.5 U/L, and AST rose above 120 U/L in 4 patients on acetaminophen and 5 on placebo [29].
Population
201 patients in alcohol detoxification, 102 on acetaminophen and 99 on placebo, with baseline AST and ALT of 120 U/L or below [29].
Sources
[19], [22], [29]
Caveats
The trial gave 2 days of treatment after alcohol had been eliminated, and excluded people with raised enzymes at entry [29].

Type in your own result

How it compares with the reference method

Mixed results2

Moderate

Variation from one test to the next

Shown to vary between tests: 36% of US adults with a raised AST had a normal result when retested about 17 days later.

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, 36% of those with an initially elevated AST had a normal result the second time, and more than 95% of initially normal results stayed normal. The within-person coefficient of variation was 13.9% [12]. In 91 healthy Europeans sampled weekly for 10 weeks under a tightly controlled protocol, within-person biological variation was 9.5% and variation between people was 20.3% [13].
Population
1,864 adults in the third US National Health and Nutrition Examination Survey [12]. 91 healthy adults aged 21 to 69 at 6 European laboratories [13].
Sources
[12], [13]
Caveats
The US study had only 2 measurements per person and lacked a full liver disease history [12]. Neither study states a threshold for agreement, so the result is given as numbers only.
Limited

As a marker of alcohol use

One multicenter study found AST detected high-risk drinking slightly less well than GGT or carbohydrate deficient transferrin.

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, carbohydrate deficient transferrin and GGT performed comparably on receiver operating characteristic analysis, with AST performing slightly less well. All three detected high-risk drinking better than intermediate-risk drinking [14].
Population
1,863 people from Australia, Brazil, Canada, Finland and Japan, mostly community based [14].
Sources
[14]
Caveats
The abstract gives no sensitivity or specificity figures for AST. Drinking was self-reported [14].

Did not match the reference method2

LimitedStudied in men

Heavy exercise

One small study found AST rose above the laboratory's upper limit in every man 3 to 5 days after one weightlifting session.

The numbers and sources
Compared with
The same men's results before exercise, and the laboratory's upper reference limit
Effect
Healthy men used to moderate activity, not including weightlifting, did a single 1-hour weightlifting session. Six had AST above the upper reference limit the next day, and all 14 did on days 3, 4 and 5. The highest value was 16.0 µkat/L against an upper reference limit of 0.7 µkat/L. AST was still significantly higher than before exercise on day 7. Creatine kinase and myoglobin, which come from muscle, rose steeply over the same days, while bilirubin, GGT and alkaline phosphatase were almost unaltered [10].
Population
15 healthy men, mean age 24.5, 14 analyzed [10].
Sources
[10]
Caveats
One small study in men not accustomed to weightlifting. People who train regularly may respond differently, and the study did not test them [10]. The study also reports the ratio of AST to ALT, a separate quantity not placed on this page.
Limited

Muscle injury and disease

Case series: 16 patients with muscle injury and no liver disease had raised AST, falling faster than ALT over the following days.

The numbers and sources
Compared with
Creatine kinase, lactate dehydrogenase and clinical review showing muscle, not liver, as the source
Effect
In a review of 16 patients with muscle necrosis from extreme exercise, polymyositis or seizures and no evidence of liver disease, AST and ALT were both elevated alongside markedly raised creatine kinase and lactate dehydrogenase. In acute cases AST was more than 3 times ALT. The two came closer within a few days because AST declined faster, and they were comparable in chronic muscle injury [11].
Population
16 patients with muscle injury, in three groups: extreme exercise, polymyositis and seizures [11].
Sources
[11]
Caveats
A retrospective review of 16 records. The abstract gives no AST values [11].

What studies tie it to

Linked in research1

Limited

Death from liver disease

One large Korean cohort found deaths from liver disease rose with AST from 20 U/L upward, inside the usual reference range.

The numbers and sources
Effect
In 142,055 Korean adults followed for 8 years, death from liver disease rose with AST even inside the usual reference range. Compared with AST below 20 IU/L, the adjusted relative risk in men was 2.5 (95% CI 2.0 to 3.0) at 20 to 29 IU/L and 8.0 (6.6 to 9.8) at 30 to 39 IU/L. In women it was 3.3 (1.7 to 6.4) and 18.2 (8.1 to 40.4). The cut-off that predicted liver disease in men with the greatest accuracy was 31 IU/L [5].
Population
94,533 men and 47,522 women aged 35 to 59 in the Korea Medical Insurance Corporation study [5].
Sources
[5]
Caveats
Observational, one cohort in one country, with deaths taken from death certificates. The abstract does not say which side of the cut-off a result of exactly 31 falls on, so it is not placed as a range on this page [5].

Mixed results1

Moderate

Type 2 diabetes

Mixed results: 9 pooled cohort studies found no increase in type 2 diabetes with higher AST, while a genetic study found a 25% higher risk.

The numbers and sources
Effect
In a meta-analysis, 9 prospective studies that measured AST gave a relative risk of type 2 diabetes of 1.02 (95% CI 0.99 to 1.04) per standard deviation of log AST, which the authors read as no evidence of increased risk [8]. In a Mendelian randomization study, genetically predicted higher AST was related to more type 2 diabetes (odds ratio 1.25 per standard unit, 95% CI 1.14 to 1.38) [9].
Population
17 studies with 60,359 participants in the meta-analysis, 9 of which measured AST [8]. Up to 64,094 people with type 2 diabetes and 607,012 controls in the genetic study [9].
Sources
[8], [9]
Caveats
The cohort studies are observational. The genetic study's authors read their findings as support for insulin resistance leading to fatty liver, which in turn raises diabetes risk, so AST may mark that process and not drive it [9].

Checked, no link found2

Moderate

Death from any cause

Not linked to death from any cause in a meta-analysis of general population cohorts, where the pooled estimate had a wide interval.

The numbers and sources
Effect
In a meta-analysis of 19 cohort studies of liver enzymes, the authors found no strong evidence of an association of AST with death from any cause. The relative risk comparing the top and bottom thirds of baseline AST was 1.23 (95% CI 0.80 to 1.88) [6].
Population
Over 9.24 million participants and 242,953 deaths across the 19 cohorts, which also covered other liver enzymes. The abstract does not give the number of studies that measured AST [6].
Sources
[6]
Caveats
Observational. The interval runs from 20% lower to 88% higher risk, so a moderate association in either direction is not ruled out [6].
Moderate

Heart disease and stroke

Not linked to cardiovascular disease in a meta-analysis of 29 general population cohorts.

The numbers and sources
Effect
A meta-analysis of 29 prospective cohorts found no evidence of an association of AST with cardiovascular disease, defined as coronary heart disease, stroke or both. Two other enzymes in the same analysis, GGT and alkaline phosphatase, were associated with it [7].
Population
Over 1.23 million participants and 20,406 cardiovascular outcomes across the 29 cohorts, which also covered other liver enzymes [7].
Sources
[7]
Caveats
Observational. The abstract gives no pooled estimate for AST [7].

Sources

  1. US Food and Drug Administration. 21 CFR 862.1100, Aspartate amino transferase (AST/SGOT) test system. Electronic Code of Federal Regulations. https://www.ecfr.gov/current/title-21/section-862.1100
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  13. 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
  14. 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

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