Atherosclerosis

Atherosclerosis is an inflammatory condition of the blood vessels, not a disease caused by cholesterol accumulation. 2 Peat argued that the cholesterol found in arterial plaque is a defensive reaction to protect injured tissue, acting as a protective bandage over areas damaged by oxidative stress. 2 The initial insult driving this inflammation is the breakdown of unstable polyunsaturated fats (PUFAs) into free radical products and lipofuscin (age pigment), which can be extracted from every arterial plaque. 2 This process is accelerated by stress hormones like cortisol, estrogen, and growth hormone, which are activated by energy deprivation and further promote the release of damaging free fatty acids. 8

The foundational driver of the metabolic dysfunction underlying atherosclerosis is hypothyroidism. 2 Research from the 1930s demonstrated that thyroid supplementation was sufficient to prevent the condition while simultaneously lowering cholesterol. 1 Broda Barnes’ review of over 70,000 autopsies in a goiter region confirmed that thyroid deficiency causes arterial damage to begin earlier and progress faster, though paradoxically, the incidence of fatal heart attacks dropped when coronary sclerosis increased, suggesting the plaque itself is not the primary killer. 10 Georgi Dinkov has extended this view, noting that mitochondrial dysfunction is a major causal factor in cardiovascular disease, generating the oxidative stress that guarantees a structural pathology will develop. 11

The composition of the plaque confirms the inflammatory, protective model. The majority of the plaque is composed of dead and alive white blood cells, indicating an active immune reaction, with cholesterol rushing in to limit the inflammation. 4 Chemical staining reveals the plaque is full of breakdown products from PUFAs, while the saturated fats remain intact. 5 Dinkov notes that adequate vitamin K status is crucial, as it can reverse calcification of blood vessels, whereas the drug warfarin, a vitamin K antagonist, is known to cause calcification. 4 Peat similarly highlighted that vitamin K, along with substances that increase carbon dioxide like baking soda or niacinamide, helps keep calcium in bones and out of arteries. 9

Therapeutic interventions focus on opposing the inflammatory and calcifying cascade. Vitamin E, in a human-equivalent dose of about 5mg/kg daily, can reduce established atheroma and improve cardiac function, primarily by acting as a PUFA antagonist and inhibiting inflammatory enzymes like COX/LOX. 7 Aspirin in doses of 800mg+ daily has also been shown to reduce plaque. 7 Peat recommended ensuring adequate calcium and vitamin D intake to suppress parathyroid hormone, as elevated PTH is linked to degenerative, inflammatory diseases and bone loss. 9 Iodine injections have a historical precedent for use in atherosclerosis. 6 The condition can manifest extremely early; Danny Roddy referenced a study showing atherosclerotic plaque in the arteries of three-year-old children, illustrating that the metabolic injury accumulates over a lifetime. 2