Prolonged high glucose levels damage the arterial lining, promoting plaque buildup—a hallmark of CHD. This process narrows the coronary arteries, restricting blood flow to the heart and increasing the risk of angina, heart attacks, and heart failure.
Diabetes also exacerbates existing CHD by accelerating plaque formation and damaging the small cardiac vessels, compounding the risk of heart failure.
Beyond these clinical manifestations, the connection between T2D and CHD is deeply rooted in shared genetic, molecular, and metabolic pathways. Research reveals significant genetic overlap that influences shared risk factors such as insulin resistance, inflammation, and vascular dysfunction.
GENETIC CONNECTION BETWEEN T2D AND CHD
The genetic interplay between T2D and CHD involves multiple genes that contribute to overlapping risk factors. Genome-wide association studies (GWAS) and other genetic research highlight several key pathways and genes involved:
1. COMMON PATHWAY
GENES
• Lipid Metabolism: The genetic connection between T2D and CHD involves certain genes that affect how the body handles lipids (fat). The APOB, APOE, and LPL genes all play crucial roles in how the body processes fats, and mutations in these genes can increase the risk of both T2D and CHD. APOB is involved in transporting fats in the blood, and mutations can lead to higher fat levels, raising the risk of both conditions. APOE affects fat processing, with certain versions, like the 4 variant, linked to elevated fat levels and an increased likelihood of developing T2D and CHD. LPL helps break down triglycerides, and mutations in this gene can lead to higher triglyceride levels, further heightening the risk of both diseases.
This story is from the December 10, 2024 edition of The Daily Guardian.
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This story is from the December 10, 2024 edition of The Daily Guardian.
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