Switching off a gene using medication can reduce the risk of heart attacks by 50 percent, researchers have found. The findings can lead to novel medication that can mimic the life-saving gene mutation.

The gene is question is called angiopoietin-like 4 or ANGPTL4. A research team from Germany analyzed the relationship between coronary heart disease and gene mutations.

From 200,000 participants, they analyzed 13,000 distinct genes. The participant pool was made up of box healthy individuals and heart attack patients.

The team found that the participants with a mutated ANGPTL4 gene, their levels of triglyceride in the blood were also significantly lower compared to the participants without the mutated gene.

Triglyceride functions like an energy storage for the body. Unfortunately, high levels of triglycerides can result in increased chances of developing cardiovascular disease.

"Low values [of triglycerides], by contrast, lower the risk," said University of Lübeck's Jeanette Erdmann who was part of the research team.

Technical University of Munich's Heribert Schunkert, the study's lead researcher, added that the triglycerides are the second most crucial type of blood fat. The first is the damaging LDL cholesterol.

Findings showed that triglycerides concentration in the blood were not just affected by predisposition or nutrition. The ANGPTL4 gene was also a key influencer.

"At the core of our data is the lipoprotein lipase (LPL) enzyme. It causes the decomposition of triglycerides in the blood," said Erdmann. The identified gene mutation shut down the ANGPTL4 gene's function and resulted in a significant reduction in the triglycerides levels.

The team found that the body does not even require the ANGPTL4 gene to function well.

"It seems to be superfluous," added Erdmann. The findings were published in the New England Journal of Medicine on March 2.

The study is significant as it could lead new medications to target the ANGPTL4 gene. Novel drugs can shut down the gene and reduce the levels of triglycerides in the blood. This could potentially lead to a groundbreaking reduction in the number of heart attack patients around the world.

However, further research is needed to conclude that the ANGPTL4 gene is absolutely unnecessary.

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