Insulin Resistance & Obesity —
Blocks to Recognising Satiety

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, fatty liver, 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 the specific condition studied on this page — in this case, only the people for whom insulin resistance has expressed itself as obesity. This curve rises steeply because it captures decades of accumulated cases: someone may develop insulin resistance at 35 but not cross the clinical obesity threshold (BMI ≥30) until their 40s or 50s, so even a modest early rise in insulin resistance translates into a much larger rise in diagnosed obesity years later.

The r value (e.g. r = 0.97) 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 0.97 means that 97% of the rise in obesity 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 across these studies — consistently 0.90 to 0.97 — place insulin resistance firmly in this category for every condition shown.

Insulin Resistance Questionnaire →

The research: how insulin resistance blocks the ability to recognise satiety: Under normal metabolism, fat cells release leptin after eating, which travels to the hypothalamus and activates POMC neurons — the brain's satiety circuit — to produce the feeling of fullness and terminate eating. In insulin resistance, this circuit is blocked at two levels simultaneously.

First, a 2017 study in the International Journal of Obesity (Banks et al.) demonstrated experimentally that triglycerides — elevated chronically by insulin resistance — cross the blood-brain barrier and directly block the satiety effect of leptin at hypothalamic receptors. In their own words: "Central triolein blocked the satiety effect of centrally administered leptin." The more insulin-resistant the person, the higher their triglycerides, and the more completely the satiety signal is physically blocked from reaching the brain.

Second, at the cellular level, a 2017 study in Molecular Endocrinology (Taha et al., PMC5415275) showed that insulin resistance in hypothalamic neurons prevents leptin from activating its downstream signalling pathways (STAT3, Akt, ERK) — meaning even when leptin does reach the brain, the neurons can no longer respond to it. The satiety receptors are simultaneously blocked from the outside by triglycerides and desensitised from the inside by chronic insulin exposure.

The result: the brain never receives a clear "full" signal. The person continues eating not from lack of discipline but because the neurological circuit that registers fullness has been chemically disabled. Sources: Banks et al., Int J Obesity 2017 (doi:10.1038/ijo.2017.231); Taha et al., Mol Endocrinology 2017 (PMC5415275); Schwartz et al. Nature 2000; Friedman Lab Cell Metabolism 2025.

Is the effect worse in Type 2 diabetes? Yes — significantly. In Type 2 diabetes, both insulin resistance and leptin resistance are typically more entrenched. Triglyceride levels are higher, the blood-brain barrier is more compromised, and the hypothalamic leptin receptors have been chronically overstimulated. Additionally, ghrelin — the hunger hormone produced by the stomach — fails to drop after meals in T2DM patients as it would in healthy individuals, creating a second overeating signal that operates independently of leptin. The result is that people with Type 2 diabetes face a dual disruption of satiety: the "full" signal (leptin) is blocked, and the "still hungry" signal (ghrelin) remains inappropriately elevated. Studies estimate that leptin resistance co-exists with insulin resistance in approximately 75–80% of people with established Type 2 diabetes. Sources: Leptin and Ghrelin in T2DM — PMC11196531 (2024); Correlation of Leptin in T2DM — PMC11070180 (2024).

Data sources

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

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