17/05/2026
Centella asiatica, aka Gotu Kola.
Thank you for sharing Kerry Bone
In case you haven’t already guessed, one of my favourite herbs is gotu kola (Centella asiatica). This unassuming w**d is a quiet testament to the profound power sometimes concealed within humble origins. Gotu kola bridges traditional wisdom and modern validation, demonstrating clinically proven capacities to restore microcirculatory integrity, enhance collagen architecture and regeneration, and refine connective tissue function. My next two posts reveal how this herb’s therapeutic potential has just been taken to an entirely new level, underpinned by some truly remarkable clinical findings.
Atherosclerotic plaques are fatty build-ups in our artery walls. But more than that, they can be thought of as chronic wounds in the arterial lining, driving the entire cascade of arterial disease, from impaired flow through to heart attacks and strokes. They differ not just in size, but in structure and composition and this strongly influences their risk profile. Using high-resolution ultrasound (including grey-scale imaging), clinicians can assess plaque volume, shape, density and uniformity. On this imaging, denser, more fibrous plaques appear brighter or “white” (echogenic) and tend to be more stable. Softer, lipid-rich plaques appear darker or “black” (echolucent) and are more prone to rupture, thrombosis and embolisation, leading to hard cardiovascular events. This difference is reflected in the underlying biology. Unstable plaque is typically richer in lipids, inflammatory cells, and fragile microvessels, while more stable plaque contains more collagen and organised structure. Rather than viewing plaques as simple obstructions to blood flow, this new understanding treats them as dynamic biological lesions, where vulnerability depends on multiple interacting factors.
A small presurgical study in 40 patients with advanced carotid plaques scheduled for carotid endarterectomy (a surgical procedure to remove atherosclerotic plaque from the carotid artery) compared six months of pine bark extract (150 mg/day) plus gotu kola extract (450 mg/day) against standard care. When the plaques were removed and examined, the differences were striking and consistent across multiple risk features. For example, calcification was present in 32% of treated plaques vs 100% of controls (7/22 vs 18/18), lipid-rich atheroma in 36% vs 89% (8/22 vs 16/18), and inflammatory cell infiltration in 35% vs 100% (7/20 vs 18/18). Markers of vascular instability were also reduced: VCAM-1 (36% vs 72%), ICAM-1 (32% vs 89%), intraplaque thrombosis (23% vs 67%), and haemorrhage (45% vs 78%). Even features linked to plaque fragility, such as neovessel formation and inflammation around thin-walled vessels, were roughly halved in the treatment group. Alongside this, plaque growth over the 6 months was +1.5% vs +4.8% in controls, indicating a meaningful slowing of progression.
Taken together, the gotu kola and pine bark therapy delivered a broad, system-wide shift in plaque phenotype. Specifically, the herbal intervention appears to move plaques away from a “vulnerable” state (lipid-rich, inflamed, angiogenic, thrombosis-prone) toward more stable, organised, and less reactive structures. Moreover, this clinical effect spans multiple biological domains simultaneously: inflammation, endothelial activation, microvascular instability, thrombosis and structural composition. In other words, rather than just shrinking plaques, the herbal combination seems to beneficially change what the plaque is made of and how it behaves.
This discovery has the potential to reframe the discussion around cardiovascular risk. Much of conventional thinking still emphasises plaque burden and lipid levels, but this study highlights that impacting plaque quality—its biology and stability—may be just as important. From a clinical perspective, it raises the possibility that interventions (especially phytotherapy) that act across multiple pathways could meaningfully reduce cardiovascular risk, not by dramatically reducing plaque size and development, but by making plaque less likely to rupture, thrombose and cause events. While the study is small and not outcome-driven, the magnitude and consistency of these morphological changes are intriguing, and they support a more rational true risk-based approach to cardiovascular intervention.
For more information see: https://pubmed.ncbi.nlm.nih.gov/36789998/
