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The pathogenesis and prevention of atherosclerosis
A Hässig1, L Wen-Xi, K Stampfli
1Study Group Nutrition and Immunity, Bern, Switzerland.
Insights
A deficiency in glycosaminoglycans, such as heparin, may cause atherosclerosis. Supplementing with glycosaminoglycans could help prevent and treat this condition, offering a new approach to cardiovascular health.
Area of Science:
- Biochemistry
- Cardiovascular Medicine
- Cell Biology
Background:
- Atherosclerosis remains a leading cause of death in industrialized nations.
- Current cholesterol-lowering strategies for atherosclerosis have limited success.
- Arterial degeneration may stem from dysregulation of metabolic processes.
Purpose of the Study:
- To investigate the causal relationship between arterial degeneration and metabolic dysregulation.
- To explore the role of glycosaminoglycan deficiency in atherosclerosis.
- To evaluate the therapeutic potential of glycosaminoglycans in preventing and treating atherosclerosis.
Main Methods:
- Review of existing studies on glycosaminoglycans and atherosclerosis.
- Analysis of the role of heparin and heparinoids in endothelial function.
- Consideration of exogenous glycosaminoglycan supplementation.
Main Results:
- A deficiency in endothelial glycosaminoglycans (heparin, heparinoids) is linked to reduced lipoprotein lipase and antithrombin III activity.
- This deficiency can lead to hyperlipoproteinemia and an increased tendency for thrombosis.
- Exogenous glycosaminoglycan introduction is crucial for adequate synthesis.
Conclusions:
- Glycosaminoglycan deficiency is implicated in the pathogenesis of atherosclerosis.
- Dietary glycosaminoglycan supplementation may offer a viable strategy for preventing and treating atherosclerosis.
- Further research into glycosaminoglycan therapy for cardiovascular health is warranted.
Abstract:
Most measures taken to prevent atherosclerosis still aim at lowering the cholesterol content of the plasma lipoproteins by dietary and pharmacological means. This approach has only proved successful to a limited extent. Diseases secondary to atherosclerosis are still the commonest cause of death in western industrialized countries. As all metabolic processes are regulated by opposing processes of equilibrium, i.e. by processes directed towards performance and recovery, we asked ourselves whether the fatty degeneration and sclerosis of the arteries could be causally related to a continuous dysregulation of these processes. We consider this to be the case, with a continuous deficiency of glycosaminoglycans (heparin, heparinoids) on the endothelial surface of the vessels. Numerous studies indicate that in the case of thinning of the anionic glycosaminoglycan film on the endothelial surface, the lipoprotein-lipase and antithrombin III activity induced by heparin is reduced, as result of which hyperlipoproteinaemia and increased tendency to thrombosis can only by compensated for to an inadequate extent. The formation of glycosaminoglycans is a characteristic of all mesenchymal cells, whereby the exogenous introduction of glycosaminoglycans into the extracellular space is of decisive importance for adequate glycosaminoglycan synthesis. Since Engelberg reported outstanding results obtained with heparin injections in the prevention and treatment of atherosclerotic disorders of the cardiac circulation, we considered it appropriate to use the well-proven dietary supplement of glycosaminoglycans in rheumatology, in the treatment of arthrosis, as well as in the prevention and treatment of atherosclerosis.