Estimating Steatotic Liver Disease Prevalence Among US Veterans

Steatotic liver disease (SLD) is the most common cause of chronic liver disease in the United States.¹ Updated SLD nomenclature acknowledge the dual pathology of SLD—metabolic and alcohol—and categorizes SLD spectrum ranging from predominantly metabolic dysfunction–associated steatotic liver disease (MASLD) to dual effects of both metabolic and alcohol (metabolic-associated alcohol-related liver disease (MetALD)) to predominantly alcohol-driven (alcohol-associated liver disease (ALD)) subsets.² Existing US studies report that among adults with SLD, 86%–92% were of MASLD subtypes, 6%–7% MetALD, and 2%–3% ALD.^3,4 There are also other potential etiologies of SLD that are less common and contribute to a smaller proportion of the overall SLD population (eg drug induced liver injury, viral hepatitis, cryptogenic liver disease).² However, ALD or MetALD may be more prevalent than these previous estimates due to limited data on and under-reporting of alcohol use in existing datasets. Alcohol use screening in outpatient clinics has been mandated in the Veterans Affairs (VA) health system since 2004 with performance metrics consistently showing >90% of Veterans screened.⁵ Hence, VA populations provide a unique opportunity to evaluate alcohol use and alcohol-related disorders. To better understand the contribution of alcohol use to SLD prevalence, we conducted a cross-sectional study of all US Veterans (age ≥18 years) receiving care at VA health-care facilities from January 1, 2010, to December 31, 2024, to characterize the prevalence of MASLD, MetALD, and ALD, which will provide important data to improve health-care resource planning and health policy decisions.

Identification of MASLD, MetALD, or ALD was based on recently updated international SLD nomenclature and aligns with recent SLD studies in VA populations.^2,6 Specifically, MASLD was defined as presence of hepatic steatosis (HS) (HS index > 36) and ≥1 concurrent cardiometabolic risk factors (CMRFs) in patients with no alcohol use. CMRF included elevated body mass index (>25 kg/m² in non-Asians or >23 kg/m² in Asians), diabetes mellitus or insulin resistance, hypertension or on antihypertension therapy, elevated triglycerides (>150 mg/dL) or on hypertriglyceridemia treatment, and low high-density lipoprotein cholesterol (<40 mg/dL in men or <50 mg/dL in women) or on lipid-lowering therapy. Alcohol use was assessed using documented Alcohol Use Disorders Identification Test-Concise (AUDIT-C) scores and categorized as no alcohol use (AUDIT-C = 0), low-risk alcohol use (AUDIT-C = 1–2 for women and 1–3 for men), and high-risk alcohol use (AUDIT-C ≥ 3 for women and ≥ 4 for men). MetALD = HS + ≥1 CMRF in patients in low-risk alcohol use. ALD = HS + high-risk alcohol use (±CMRF). We utilized the AUDIT-C score that was nearest to the time of HS diagnosis. Patients with other causes of chronic liver disease were excluded and we did not evaluate other etiologies of SLD that are less common (eg drug induced liver injury, viral hepatitis, cryptogenic liver disease).

Prevalence of MASLD, MetALD, or ALD was based on a patient’s first diagnosis meeting aforementioned criteria during the study period and divided by total number of Veterans actively engaged with the health-care system (ie ≥1 annual health-care encounter). Prevalence (per 100,000 persons) was stratified by sex, age groups, and race/ethnicity. Comparisons of prevalence between groups utilized the z-statistic using standard equations. Statistical analyses were performed using SQL and SAS version 9.4 (SAS Institute, Cary, NC). Statistical significance was defined as 2-tailed P < .05. This study was approved by Stanford University Institutional Review Board and VA Palo Alto Healthcare System Scientific Research Committee.

Among 6,192,643 Veterans, we identified 534,494 (8.6%) with MASLD, 356,619 (5.8%) with MetALD, and 119,422 (1.9%) with ALD (Figure 1). Among all three SLD subtypes, the majority were men and of non-Hispanic White race/ethnicity (Table A1). Mean age of patients with MASLD (67.1 ± 12.0) was older than patients with MetALD (63.1 ± 13.0) or ALD (61.3 ± 13.5). The proportion of patients with body mass index > 30 kg/m² or concurrent diabetes mellitus was highest in patients with MASLD. Overall prevalence of MASLD was higher than MetALD (8631 vs 5759 per 100,000 persons) or ALD (8631 vs 1928 per 100,000 persons) (Table). Prevalence of MASLD was significantly higher in males vs females (8683 vs 8116 per 100,000 persons, P < .001). Compared to non-Hispanic Whites, all other non-White race/ethnic groups had significantly higher prevalence of MASLD. Increasing age was associated with increasing prevalence of MASLD. Similar trends were seen for MetALD, with higher prevalence in males vs females, and higher prevalence in non-White ethnic minorities (Table). When compared to non-Hispanic whites, significantly higher prevalence of ALD was observed in Black/African Americans (2526 vs 2067 per 100,000 persons, P < .001) and Hispanics (2664 vs 2067 per 100,000 persons, P < .01). Similar to MASLD and MetALD, increasing age was associated with increasing prevalence of ALD.

Figure 1.

Number of Veterans with MASLD, MetALD, and ALD, 2010–2024.

Table.

Prevalence of MASLD, MetALD, and ALD.

Variables	MASLD			MetALD			ALD
	Prevalence per 100,000	95% CI	P value	Prevalence per 100,000	95% CI	P value	Prevalence per 100,000	95% CI	P value
Total	8631	(8551–8711)		5759	(5679–5838)		1928	(1851–2007)
Sex
Female	8116	(7851–8382)	Reference	5336	(5074–5599)	Reference	1745	(1487–2003)	Reference
Male	8683	(8598–8767)	< .001	5801	(5718–5884)	< .01	1947	(1865–2029)	.144
Race/Ethnicity
Non-Hispanic white	8937	(8835–9040)	Reference	5930	(5829–6032)	Reference	2067	(1967–2167)	Reference
American Indian or Alaska Native	11,183	(10,155–12,219)	< .001	5908	(4902–6923)	.966	2796	(1804–3797)	.156
Asian or Pacific Islander	11,313	(10,653–11,976)	< .001	7977	(7326–8632)	< .001	1820	(1186–2457)	.453
Black or African American	12,043	(11,830–12,256)	< .001	8329	(8120–8540)	< .001	2526	(2322–2731)	< .001
Hispanic	12,858	(12,526–13,191)	< .001	8340	(8013–8667)	< .001	2664	(2346–2984)	< .001
Age
18–29 y	232	(13–461)	Reference	328	(99–558)	Reference	145	(1–375)	Reference
30–39 y	2465	(2219–2712)	< .001	3194	(2947–3442)	< .001	1494	(1249–1740)	< .001
40–49 y	3396	(3203–3590)	< .001	3841	(3647–4036)	< .001	1450	(1258–1642)	< .001
50–59 y	5970	(5799–6142)	< .001	5415	(5245–5586)	< .001	1924	(1756–2092)	< .001
60–69 y	11,210	(11,032–11,388)	< .001	7011	(6836–7187)	< .001	2357	(2186–2529)	< .001
70 y and over	21,155	(20,967–21,343)	< .001	10,858	(10,676–11,040)	< .001	3135	(2959–3311)	< .001

CI, confidence interval.

While existing data among US populations have reported MASLD accounting for 86%–92% of SLD,^3,4 our analyses of national VA data provide strikingly different observations, with MASLD accounting for ∼53% of patients with SLD, followed by 35% with MetALD, and 12% with ALD (Figure A1). Unlike limitations of existing datasets with missing or limited alcohol use data, the VA cohort incorporating consistent alcohol use assessments may provide more accurate estimates of SLD subtype distributions. These data emphasize that alcohol use may play a greater impact on the prevalence of SLD than previously estimated. Our data also demonstrate higher prevalence of MetALD and ALD than 2 recent systematic reviews and meta-analyses evaluating global prevalence of SLD subtypes, among which MetALD represented 10%–11% of the SLD cohort.^7,8 The higher prevalences of MetALD and ALD in our current study align with existing epidemiological studies reporting on rising trends of advanced ALD (eg alcohol-associated hepatitis and alcohol-related cirrhosis).9, 10, 11 These increasing trends in advanced ALD are the downstream complications of alcohol-related SLD, which has historically been under-reported given aforementioned limitations in accurately assessing alcohol use in large datasets. We also observed higher prevalence of MASLD and MetALD in males vs females and in non-White ethnic minorities vs non-Hispanic whites, and increasing prevalence of all SLD subtypes with increasing age.

A strength of national VA data is incorporation of alcohol use data available for >90% of Veterans. However, the predominantly male and majority non-Hispanic white demographic may limit generalizability of these findings to other populations. High-risk alcohol use in Veterans is more prevalent than in the general US adult populations,¹² which may have contributed to higher prevalences of MetALD and ALD. In the current study, we defined MASLD and MetALD based on recently updated nomenclature which requires presence of HS and at least 1 CMRF. Hence a patient with HS and no alcohol or low-level alcohol but without any CMRFs was not included in either MASLD or MetALD groups, which may have led to some misclassification bias. In addition, our current study utilized AUDIT-C scores for estimating alcohol use to categorize SLD subtypes, which is practical, easy to assess, and aligns with current evidence that even low levels of alcohol should be avoided in SLD. However, AUDIT-C may be subject to recall bias as well as under-reporting bias, and while AUDIT-C data are more comprehensively available due to routine assessment in the VA health system, more objective measures (eg phosphatidylethanol testing) may be more accurate in assessing alcohol use. Sick quitter effect bias should also be considered, such that individuals who quit drinking due to being too sick (eg cirrhosis) may be inappropriately classified into individuals who are lifelong alcohol abstainers. Furthermore, incorporating alcohol biomarkers (eg phosphatidylethanol) in routine assessment of alcohol use may improve MetALD identification. It is also important to note that while MASLD, MetALD, and ALD together comprise the vast majority of SLD subtypes, there are other potential etiologies that could contribute to SLD that represent a much smaller proportion of the SLD population.

Conclusion

Among a national cohort of Veterans, we observed prevalences of MetALD and ALD that are higher than previous estimates among US adults. These data continue to highlight the alarming detrimental impact of alcohol use in contributing to chronic liver disease and emphasize that alcohol use may have a greater impact on earlier subtypes of SLD subtypes than previously understood.