Liver Health

Of 7,810 reports Loop ran with at least one liver enzyme in the latest 12-month window, 21.0% show an elevation in SGPT, SGOT or GGT — the blood markers that rise when liver cells are under strain. On the narrower, more conservative SGPT-only screen, 17.9% are already past the point where the enzyme leaks into the bloodstream faster than a healthy liver allows. India's national picture sits behind this: non-alcoholic fatty liver disease is now estimated to affect around 38% of the adult population, rising well past half in urban cohorts (Duseja et al., Journal of Clinical and Experimental Hepatology, 2023). What the Loop panel adds is the early, sub-clinical layer — strain visible in the enzymes years before a scan would name a disease.

The SGPT distribution:

Most of the dysfunction sits in the mild band — the 41–80 range, where the liver is working harder than it should but has not yet failed. That is the band where the change is reversible and the intervention is behavioural rather than clinical. The population average SGPT of 29.7 U/L sits below the cutoff, but only by a quarter; a healthy working cohort would centre closer to 20.

The 11-point year-on-year fall is mostly a change in the ruler#

The headline any-dysfunction rate fell from 32.2% to 21.0%, but the two numbers are not measuring the same thing. WHI 2025 published on a broader composite screen; the 2026 any-liver definition is a cleaner any-of-three-enzymes cutoff. The comparison that holds across both years is the SGPT-only screen, and that one went the other way — 16.4% to 17.9%, on a sample nearly four times larger. The average SGPT barely moved. Liver strain in this workforce did not improve; the measuring stick changed.

Men carry three times the liver strain women do#

This is the widest gender gap of any biomarker in the 2026 dataset. Nearly one in three men show liver strain against fewer than one in ten women — a 3.3× spread. The average male SGPT (36.2 U/L) is 71% higher than the female average (21.1) and sits a single point below the abnormal threshold, meaning the male centre of distribution is essentially at the cutoff. For women, the marker is rarely the story; for men, it is one of the most reliably abnormal lines on the panel.

The reflex is to attribute this to alcohol, and the survey shows the substance gap is real — men report drinking far more often than women. But the enzyme pattern argues that drink is the smaller part of the story (see the fatty-liver section below). The larger driver is body composition: men accumulate visceral fat — the metabolically active fat wrapped around the abdominal organs — more readily than pre-menopausal women, and visceral fat is the engine of fatty liver.

Liver strain peaks in early career and recedes — the opposite of blood sugar#

Liver dysfunction is highest in the 20s and 30s and falls steadily from there. By the 60s it is nearly half its early-career peak. This inverts the structural pattern of almost every other marker in the report, where dysfunction compounds with age. Blood sugar, lipids, blood pressure — all climb. Liver enzymes do the reverse.

Two mechanisms sit behind the descent. Enzyme levels track the activity of liver injury, not its accumulated history; a young liver under acute metabolic load leaks more enzyme than an older liver that has quietly progressed to fibrosis, where the cells stop leaking because they have stopped functioning. And there is a survivor effect — the heaviest-drinking, highest-load cohort thins out of the working-age sample over time. The reassurance in the falling line is therefore partial. A 28-year-old at SGPT 60 is not safer than a 58-year-old at SGPT 25; the younger liver is louder, the older one quieter.

The early-career peak is itself the finding. The strain is loudest in the 20s and 30s — the decade when most professionals assume their bodies will absorb whatever the schedule demands.

The gender gap is a male phenomenon at every age#

The whole-population gender gap is not spread evenly across the lifespan — it is a young-male story. Men in their 20s and 30s show liver dysfunction at 32–35%, more than four times the rate of women the same age. The male curve then descends through middle age while the female curve drifts gently upward, and by the 60s the two are within four points of each other. Women's liver strain, modest throughout, tends to appear later — consistent with the loss of pre-menopausal metabolic protection. Men's strain is front-loaded into the exact decade the previous section flagged.

Delhi's livers are twice as strained as any other metro's#

Delhi NCR stands alone. Its any-elevation rate of 34.4% is roughly seventy percent above the next metro and nearly double the Bengaluru and Pune readings. On the cleaner SGPT-only measure the gap is starker still — 30.6% against a 15–19% band everywhere else. Most telling, Delhi's average SGPT of 41.2 U/L is the only metro mean that clears the abnormal threshold. This is not a heavy tail dragging up an otherwise healthy city; the entire Delhi distribution is shifted right. The median Delhi report is closer to abnormal than the abnormal reports elsewhere.

The finding replicates. WHI 2025 placed Delhi liver dysfunction at 34.8%; the 2026 reading on a sample nearly six times larger lands at 34.4%. Where the city-level glucose rankings shuffled year to year on sample composition — the Delhi NCR page treats that glucose volatility as a sampling artefact — the Delhi liver signal held its position and its magnitude almost exactly. That stability is what separates a real city effect from a sampling artefact.

Within Delhi the strain is overwhelmingly male. Delhi men show liver dysfunction at 47.5% — close to one in two — against 17.0% for Delhi women. The male rate is the highest single city-by-gender cell in the dataset. Delhi women, at 17.0%, are also the worst-off female metro cohort, running nearly double the female rates in Bengaluru (7.6%), Pune (7.1%) and Hyderabad (6.8%). Whatever Delhi is doing to livers, it does it to both sexes — but it does it hardest to men.

Liver is the one marker where employees look worse than dependents#

On almost every marker in this report the dependent layer — spouses, parents, the people least likely to be screened — is in worse shape than the employee. Liver is the exception. Here the employee runs eight points worse, 23.7% against 15.9%. The reversal is composition, not biology: the employee pool is two-thirds male, the dependent pool nearly two-thirds female, and liver strain is the most male-skewed marker in the dataset. The dependent advantage on liver is a gender advantage in disguise. It does not transfer to the rest of the panel, where dependents remain the higher-risk, lower-screened layer.

The pattern is fatty liver, not drink#

The instinctive read of a male-skewed liver finding is alcohol, and the survey confirms drinking is common — 37.3% of respondents report consuming alcohol at all, 7.8% weekly (the Alcohol page is the survey base for this, and the Substance Mentions page catches only the severe claims tail). But the enzyme chemistry points elsewhere. The shape of the elevation, not its prevalence, tells you the cause.

When the liver is injured by alcohol, AST (SGOT) rises faster than ALT (SGPT) and the ratio climbs above 1.5. When the injury is fatty-metabolic, ALT leads and the ratio falls below 1. In this population the median ratio among elevated cases is 0.65, and 93.6% of elevated cases fall in the sub-1 fatty-liver zone. The alcohol-specific marker, GGT, is co-elevated in fewer than a quarter of cases. The drinking is real, but it is not what most of these enzymes are registering.

The metabolic fingerprint is decisive when liver-elevated reports are set beside liver-normal ones in the same panel:

A report with an elevated liver enzyme is 1.8 times as likely to carry high triglycerides as a report without one, half again as likely to sit below protective HDL, and meaningfully more likely to show glucose dysfunction — the same insulin-resistance signature the Blood Sugar page measures from the glucose end. This is the textbook cluster of metabolic syndrome, and the liver is its most sensitive early instrument. The raised SGPT is rarely the disease itself — it is the visible edge of insulin resistance, central adiposity and dyslipidaemia moving together.

The downstream is metabolic, and it is already in the claims#

The same broad audience whose biomarkers show one in five with liver strain is the audience whose hospital admissions concentrate in metabolically-adjacent categories. Liver disease itself rarely reaches a hospital bed in this cohort — clinically coded liver and hepatic admissions account for roughly 2% of incurred spend, mostly hepatitis and gastrointestinal events rather than end-stage liver disease. The cost of a metabolically strained workforce shows up one organ over.

The fatty liver detected on a blood panel at 32 does not bill the policy. The cardiac event it shares a metabolic root with, twenty years later, does — at over a lakh per admission. The enzyme is the cheapest, earliest signal of a process that the claims file only sees once it has matured into a hospitalisation.