Non-alcoholic fatty liver disease — NAFLD — is now the most common liver disease in the Western world. It affects roughly 25% of the global population. Most people who have it don't know it. And the standard liver test on your annual physical is surprisingly bad at detecting it.
What NAFLD actually is
NAFLD is the accumulation of fat in liver cells in people who drink little or no alcohol. It ranges from simple steatosis (fat accumulation without inflammation) to non-alcoholic steatohepatitis (NASH — fat plus inflammation and cell damage), which can progress to fibrosis, cirrhosis, and liver cancer.
The disease is tightly linked to insulin resistance and metabolic syndrome. In fact, many hepatologists now consider NAFLD to be essentially the liver manifestation of metabolic syndrome. If you have insulin resistance, there's a good chance your liver is storing fat it shouldn't be.
Why standard tests miss it
The standard liver function test — ALT, AST, GGT — can suggest liver damage, but it has a crucial limitation: ALT can be normal even in people with significant fatty liver disease. Studies show that up to 80% of patients with biopsy-proven NAFLD have ALT levels within the normal reference range.
This happens because the "normal" ALT ranges used by most labs were established decades ago, before the NAFLD epidemic. The current recommended upper limits are actually much lower than what most labs report as normal: less than 25 U/L for men and less than 19 U/L for women, according to the EASL/EASD/EASO guidelines.
A practical example
A 48-year-old man has an ALT of 38. His lab report marks this as "normal" (reference range 10–50). But by the evidence-based threshold of <25 for men, this is elevated — and it should trigger a liver ultrasound. At Health Detectors, we use the evidence-based thresholds, not the lab default ranges.
The metabolic cascade
NAFLD doesn't just damage your liver. It's increasingly recognized as an independent cardiovascular risk factor. People with NAFLD have a significantly higher risk of heart attack and stroke — even after controlling for all traditional risk factors. The liver is not just a passive victim of metabolic dysfunction; it actively participates in driving it.
The progression from insulin resistance to fatty liver to cardiovascular disease follows a predictable cascade:
- Insulin resistance → the liver receives more fatty acids than it can process
- Excess fat accumulates in liver cells (steatosis)
- Inflammation begins (NASH)
- The liver produces more triglycerides, more inflammatory markers, more clotting factors
- Cardiovascular risk climbs even as liver enzymes look "normal"
What we do at Health Detectors
Our DETECT panel includes ALT, AST, and GGT — but interpreted against the lower, evidence-based thresholds. If any are elevated (even mildly), or if HOMA-IR suggests insulin resistance, we activate the METABOLIC module, which includes abdominal ultrasound to directly visualize liver fat.
In cases of confirmed steatosis with elevated inflammatory markers or fibrosis risk, we can arrange FibroScan (transient elastography) — a non-invasive test that measures liver stiffness, which correlates with fibrosis stage. This is the test that hepatologists use to decide whether someone needs closer monitoring or intervention.
The good news: early-stage NAFLD is reversible. Weight loss of just 7–10% of body weight has been shown to resolve steatosis in most cases. But you have to know you have it first — and with normal-looking lab results on a standard panel, most people never find out.
References
- EASL-EASD-EASO Clinical Practice Guidelines for the management of NAFLD. J Hepatol. 2016;64(6):1388-1402.
- Prati D, et al. Updated definitions of healthy ranges for serum alanine aminotransferase levels. Ann Intern Med. 2002;137(1):1-10.
- Targher G, et al. Non-alcoholic fatty liver disease and risk of cardiovascular disease. J Hepatol. 2021;75(5):1255-1269.