Hypertension

Hypertension is fundamentally an adaptive response to a perceived deficiency of oxygen or glucose delivery, driven by stress signals that become chronic under conditions of metabolic dysfunction. 1 Ray Peat argued that when the body senses inadequate supply, it instructs the heart to pump more blood, a mechanism that becomes pathological when polyunsaturated fatty acids (PUFA) interfere with glucose and oxygen utilization while simultaneously sending false starvation signals to the pituitary and nervous system. 1 A very large proportion of hypertension is simply a symptom of chronic hypothyroidism, where elevated TSH itself acts as a pro-inflammatory factor that increases stress hormones and tightens small blood vessels. 2 This compensatory drive is also seen in the increased cardiac output at the onset of both pregnancy toxemia and essential hypertension, where a smaller blood volume is being pumped more forcefully to maintain tissue perfusion. 2

The physiological regulation of blood pressure is intimately tied to mineral balance and energy metabolism, not simply sodium excess. Peat cited the work of David McCarron extensively, emphasizing that calcium deficiency, rather than high sodium intake, is a primary dietary driver of hypertension. 2 A low calcium status increases the tone of small arteries, while adequate calcium, supported by sodium, helps cells expel calcium and relax. 6 Sodium plays a critical structural role by associating with albumin to exert oncotic pressure, which attracts water into the bloodstream, maintains blood volume, and prevents the leakage of fluid and albumin through capillary walls. 2 When energy metabolism fails—as in diabetes, hypothyroidism, or hyperestrogenism—the physiological loss of sodium occurs, leading to hypo-osmotic fluid retention, cell swelling, and a compensatory adrenergic stress reaction that further raises blood pressure. 9

The hormonal environment dictates the vascular pathology. An increased level of aldosterone is common to both preeclampsia and essential hypertension, where it promotes sodium retention but also increases vascular endothelial growth factor (VEGF), making capillaries leaky and causing edema. 2 Restricting salt paradoxically increases aldosterone production, whereas increasing salt in the diet lowers both aldosterone and VEGF, reducing vascular leakiness. 2 Peat noted that the drug industry's historical approach of treating hypertension and edema with diuretics and low-salt diets mirrored a fundamental misunderstanding of this physiology, analogous to the catastrophic early management of pregnancy toxemia. 9 Newer anti-aldosterone drugs, which are similar in action to progesterone, are effective precisely because they oppose this leakiness and stress cascade. 4

Therapeutically, lowering blood pressure requires improving energy production rather than simply forcing numbers down pharmacologically. Peat recounted the case of a man on a six-month, fat-free diet of milk and sugar whose hypertension, migraines, and fatigue resolved as his cholesterol dropped, attributing the benefit to the high calcium-to-phosphorus ratio of the diet. 5 Supporting thyroid function is central, as thyroid hormone antagonizes the sympathetic stress hormones like adrenaline and serotonin that drive pressure up acutely. 8 Nutrients such as niacinamide, which is anti-lipolytic, and vitamin E, which opposes estrogen and promotes oxidation, can improve circulation by addressing the underlying metabolic interference from free fatty acids. 2 Peat maintained that lowering inflammation and improving glucose oxidation will lower blood pressure while supporting tissue renewal, whereas lowering pressure without restoring energy production merely intensifies existing problems. 4