Arterial Stiffness

Arterial Stiffness

Elastin is deposited in the arterial wall early in life and is replaced only marginally thereafter. Over decades of pulsation the elastic lamellae fatigue and fracture, collagen accumulates in their place, and cross-links form between collagen molecules through non-enzymatic glycation. The aorta consequently becomes stiffer with age in every population studied, and between 20 and 30 percent of adults over 60 have a carotid-femoral pulse wave velocity above 10 m/s, the conventional threshold for abnormal stiffening.

The haemodynamic consequence follows from the physics. A compliant aorta absorbs part of each stroke volume during systole and releases it during diastole, smoothing flow and reducing the load on the ventricle. A stiff aorta cannot store that volume, so systolic pressure rises while diastolic pressure falls, widening the pulse pressure. The reflected pressure wave returning from the periphery also travels faster and arrives during systole rather than diastole, adding to peak load. This is the mechanism behind isolated systolic hypertension in older adults, and it explains why the condition is asymptomatic while still increasing cardiac workload measurably.

Ageing is the primary driver. Hypertension accelerates the same process through increased wall stress. Diabetes contributes through advanced glycation end-products, which cross-link collagen directly and are the clearest molecular link between glycaemic exposure and vascular ageing. Chronic kidney disease adds medial calcification, a distinct mechanism of stiffening rather than a variant of the elastin story. Dyslipidaemia, smoking and the oestrogen decline of menopause complete the recognised list.

Two ingredients are graded against this endpoint in the collection, on 7 studies and 1,300 participants between them. Vitamin K2 holds Grade B on 5 studies and 1,200 participants. Its rationale is specific and biologically well defined: matrix Gla protein, an inhibitor of vascular calcification, requires vitamin K-dependent gamma-carboxylation to function, and the uncarboxylated form is measurable in circulation as an index of vascular vitamin K status. This makes K2 unusual among ingredients studied here, since it addresses one identified mechanism of stiffening rather than a general antioxidant or vasodilatory hypothesis. It is also the reason the interaction with vitamin K antagonist anticoagulants is not incidental but pharmacologically direct.

NMN holds Grade C on 2 studies and 100 participants. Its inclusion follows from work on NAD availability and sirtuin signalling in vascular ageing rather than from a body of clinical trial evidence at this endpoint, and two studies with 100 participants cannot support more than a preliminary reading.

No research paper is currently linked to this condition in the collection, so the graded entries above stand on the study counts recorded for them rather than on citable primary sources here. Pulse wave velocity remains the measured quantity, and it responds to blood pressure control, glycaemic control and physical activity on evidence bases considerably larger than either ingredient's.