Insulin Resistance & MASLD (Fatty Liver Disease)

Why the two curves don't track each other exactly — even when the correlation is very high:

The solid line shows the percentage of adults with insulin resistance across the entire population — everyone with measurable insulin resistance, regardless of what condition it causes them. Because insulin resistance is the upstream root cause of many different diseases — type 2 diabetes, hypertension, cognitive decline, cardiovascular disease and more — this curve rises relatively gradually as it reflects a burden shared across all of those outcomes.

The dotted line shows the prevalence of MASLD specifically — only the people for whom insulin resistance has expressed itself as fatty liver disease. This curve can rise more steeply because it captures decades of accumulated cases: someone may develop insulin resistance at 35 but not be diagnosed with MASLD until their 50s, so even a modest early rise in insulin resistance translates into a much larger rise in diagnosed cases years later.

The r value (e.g. r = 0.96) is a correlation coefficient. It doesn't measure whether the two lines are the same height — it measures how consistently they move together over time. An r of 0.96 means that 96% of the rise in MASLD over the past five decades is statistically explained by the parallel rise in insulin resistance.

What the r value tells you:
0.50–0.70 — Modest connection. The two trends are related but other factors are involved.
0.70–0.90 — Strong connection. Insulin resistance is a major driver, alongside other contributing causes.
0.90 and above — Dominant connection. Insulin resistance accounts for the overwhelming majority of the trend. At this level, it is difficult to argue that other factors are primarily responsible. The values seen here — r = 0.94 to 0.96 — place insulin resistance firmly in this category.

Insulin Resistance Questionnaire →

The mechanistic pathway — how IR causes fatty liver:

The pathway from insulin resistance to MASLD is one of the most thoroughly documented in metabolic medicine:

1. Insulin resistance in adipose tissue → unrestrained lipolysis → excess free fatty acids (FFAs) flood the portal circulation to the liver.
2. The liver receives excess FFAs → overwhelmed mitochondrial beta-oxidation → FFAs converted to triglycerides → triglycerides accumulate in hepatocytes → hepatic steatosis (fatty liver).
3. Compensatory hyperinsulinaemia → stimulates de novo lipogenesis in the liver via SREBP-1c → accelerates fat synthesis within liver cells directly.
4. Gut dysbiosis → leaky gut → LPS translocation → portal vein LPS reaches liver → activates Kupffer cells → hepatic inflammation → progression from simple steatosis to steatohepatitis (MASH).
5. Chronic hepatic inflammation + ongoing IR → stellate cell activation → fibrosis → cirrhosis in a significant minority.

This is not a coincidental association. Reversing insulin resistance — through very low-carbohydrate diet, intermittent fasting, and gut restoration — consistently reduces hepatic fat, often dramatically, and in some cases achieves complete histological resolution.

Why the USA and UK figures differ: The USA figure (~38%) reflects broader diagnostic uptake and a higher baseline obesity/metabolic syndrome prevalence, driven partly by an ultra-processed food supply that is more extreme than the UK's. The UK figure (~29%) reflects the same underlying trend at a lower absolute level, consistent with marginally lower rates of severe obesity and metabolic syndrome in England. Both populations show the same directional trajectory: rising in close parallel with insulin resistance over 50 years. Neither represents a healthy baseline — both are far above any pre-industrial norm.

Data sources

Many people with this condition have at least one other insulin-resistance-driven condition. See the full picture — all 10 conditions, their r values, prevalence data, and 50-year rise figures in one place:  See all 10 conditions →

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