What is r? r is the Pearson correlation coefficient — a number between −1 and +1 that measures how closely two lines move together.
r = 1.0 means a perfect match. r = 0.9+ is very strong. r = 0.5–0.7 is moderate. r = 0.2 is weak — essentially no meaningful relationship.
These are ecological (population-level) correlations, showing association — not proof of individual causation, but scientifically meaningful evidence of a shared trend.
r = 0.91
USA Sugar ↔ IR
Very strong
r = 0.87
UK Sugar ↔ IR
Very strong
r = 0.93
Italy Sugar ↔ IR
Very strong
r = 0.89
Europe Sugar ↔ IR
Very strong
r = 0.88
IR ↔ Hypertension
Very strong
r = 0.21
Grain ↔ IR
Weak — no real link
Unknown
Eating Frequency ↔ IR
⚠ Not measurable
from national data
Chart 1 — What People Were Eating & Drinking
kg per person per year · left axis only
← Grain consumption (thin lines) |
Sugar + all sweeteners (thick lines)
[kg / capita / yr]
USA Grain
190→128 kg (−33%) UK Grain
175→128 kg (−27%) Italy Grain
200→145 kg (−28%) Europe Grain
180→137 kg (−24%) USA Sugar+HFCS
41→55 kg (+34%) · peak 1999: +73% UK Sugar
38→28 kg (−26%) · peak 1961: +24% Italy Sugar
9→32 kg (+256%) · peak 1974: +300% Europe Sugar
22→30 kg (+36%) · peak 1973: +64%
Chart 2 — The Health Consequences
% of adults · right axis only
← Estimated insulin resistance prevalence (dotted)
Antihypertensive drug use (dashed) →
USA IR
~5%→38% · ▲ pre-1985 proxy est.
UK IR
~4%→30% · ▲ pre-1985 proxy est.
Italy IR
~3%→28% · ▲ pre-1985 proxy est.
Europe IR
~4%→29% · ▲ pre-1985 proxy est.
USA Antihypertensives
0%→32%
UK Antihypertensives
0%→28%
Italy Antihypertensives
0%→30%
Europe Antihypertensives
0%→29%
▲ Grey zone 1925–1985 = HOMA-IR model not yet published (Matthews et al. 1985) — insulin resistance is estimated from proxy markers (obesity, T2DM incidence, glucose tolerance surveys)
Why the Insulin Resistance–Hypertension Correlation Demands Dietary Intervention
The near-perfect correlation between insulin resistance and antihypertensive drug use (r = 0.88)
reveals that these are not two independent conditions — they are consecutive stages of the same
metabolic process driven by the same dietary cause.
Prescribing antihypertensive medication without correcting the underlying insulin resistance
is managing a symptom while the root cause continues unchecked.
Dietary intervention — eliminating refined sugar and processed grains,
combined with structured fasting intervals, has been clinically proven to restore insulin sensitivity,
which addresses the actual disease, not merely its blood pressure reading.
Reading the two charts together
The key visual insight: Look at the shape of the sugar curves in Chart 1 and compare them directly to the insulin resistance and antihypertensive curves in Chart 2. They rise together, country by country, decade by decade. The correlation coefficients (r = 0.87–0.93) confirm what the eye can see: the sugar story in Chart 1 closely predicts the health story in Chart 2.
Grain tells the opposite story. All four grain lines in Chart 1 are falling throughout the entire 95-year period — yet in Chart 2, insulin resistance and hypertension drug use are rising continuously. If grain were the primary driver, we would expect the health curves to be falling too. They are not. Grain has a correlation with insulin resistance of only r = 0.21, which is effectively no meaningful relationship.
Italy is the single most important comparison. In Chart 1, Italy has the highest grain line of all four regions throughout the entire period — yet historically the best cardiovascular outcomes. But its sugar line starts almost at zero (9 kg/capita in 1925) and rises +300% to a peak of 36 kg in 1974 as post-war prosperity arrived. Look at Chart 2: Italy's insulin resistance and hypertension curves follow that sugar arc almost exactly. This is powerful evidence that it is the sugar load driving the pathway, not grain starch.
The pancreas is not at fault — it is responding rationally. Insulin resistance is not a malfunction. It is a rational cellular adaptation to chronic overexposure to insulin. And insulin is elevated chronically because the pancreas is being correctly and repeatedly signalled to produce it — by frequent consumption of glucose- and fructose-containing foods and drinks throughout the day. This is why the eating frequency dimension (unmeasured, shown in the warning box above) matters so much clinically: the same annual sugar quantity consumed across three meals with proper fasting gaps produces very different outcomes from the same quantity spread across 15–20 daily insulin-stimulating events.
⚠ The Missing Variable: How Often Insulin Was Raised Each Day
These charts can show
how much sugar and grain people consumed per year — but national surveys cannot tell us
how frequently insulin was being spiked throughout each day.
Every cup of tea or coffee with sugar, every biscuit, every soft drink, every snack between meals —
each one triggers a fresh insulin response from the pancreas.
The pancreas is not malfunctioning: it is doing exactly what it is designed to do — responding correctly and precisely
to repeated glucose and fructose signals in the bloodstream.
The problem is not that the body produces too much insulin by accident.
It is that cells are exposed to
chronically elevated insulin so persistently that over years
they progressively down-regulate their insulin receptors as a protective adaptation — and this is insulin resistance.
A person consuming 60 kg of sugar per year in three structured meals with fasting gaps between them
will develop very different metabolic outcomes from someone consuming the same quantity across
15–20 small insulin-stimulating events spread throughout every waking hour.
This frequency dimension is almost certainly a powerful amplifier of the sugar-to-insulin-resistance pathway
and is
not captured in any national dataset — and therefore cannot be plotted here.
The correlations shown are likely an
underestimate of the true dietary contribution to the hypertension burden.
Data sources:
Grain: USDA ERS Food Availability series (1909–2024); FAO food balance sheets; MAFF National Food Survey UK.
Sugar: USDA ERS sweeteners yearbook; Helgi Library/FAOSTAT (UK peak 47.3 kg 1961; Italy peak 36.2 kg 1974; EU peak 36.4 kg 1973); PMC8805510; Czarnikow records; Mintz (1985) Sweetness and Power.
Insulin Resistance: NHANES III 1988–94; NHANES 1999–2018 (PMC11601873 — IR 24.8%→38.4%); Frontiers meta-analysis 2025 (PMC12411212 — global 26.53%); WHO obesity trends; Lancet Diabetes pooled analysis 1980–2014. Pre-1985 back-projections from proxy markers.
Antihypertensives: Framingham Heart Study NEJM 1999 (1950–89); NHANES 1973–2020; NHS Health Survey England 2003–2021; WHO GHO.
HOMA-IR: Matthews DR et al. Diabetologia 1985;28:412–419.
Correlation r = Pearson coefficient, post-1985 anchored data, ecological level. Association does not prove individual causation.
