The mechanistic pathway is the most direct of any condition in this series: Insulin resistance → compensatory hyperinsulinaemia → kidneys retain sodium (via ENaC stimulation) → expanded blood volume → raised blood pressure. Simultaneously, elevated insulin activates the sympathetic nervous system, raising heart rate and vascular resistance. High insulin also promotes smooth muscle proliferation in arterial walls → arterial stiffness → sustained hypertension. This is not a coincidental association — it is a well-established causal sequence documented in multiple intervention studies. Reversing insulin resistance through dietary change (low-carbohydrate, intermittent fasting) consistently lowers blood pressure independent of weight loss. Sources: DeFronzo & Ferrannini (1991); Landsberg (2012); Reaven (1988); UKPDS; multiple RCTs.