Johns HopkinsResearchers from Johns Hopkins University School of Medicine claim to have identified why some people’s blood platelets are more inclined to cluster faster as compared to others. This is said to be the largest review of the human genetic code until now. The experts observed a septet of overactive genes that were capable of controlling that bodily function.

Platelets help to fight infection and seal wounds and on the other hand they speed up cardiovascular diseases that cause fatal heart attacks or strokes. Researchers examined platelets stickiness in the blood sample collected from 5000 American men and women. They further compared this to some 2.5 million single possible changes in the human genetic code. This was done in order to observe which genes stood out across the entire group increased or slowed down platelets clustering. The participants enlisted for the research included both men and women with no previous chronic health problems.

“Our results give us a clear set of new molecular targets, the proteins produced from these genes, to develop tests that could help us identify people more at risk for blood clots and for whom certain blood-thinning drugs may work best or not. We can even look toward testing new treatments that may speed up how the body fights infection or recovers from wounds,” says co-senior research investigator and cardiologist Lewis Becker, M.D., a professor at the Johns Hopkins University School of Medicine.

Researchers observed that seven genes considerably affected the speed and duration of the platelets to cling together. They also revealed how many of them would bunch together. Becker revealed that among these, three genes were previously linked with platelets collection. Researcher’s grouped major pieces of the genetic puzzle that may help understand as to why some people’s blood is prone to clot as compared to others. This helped them comprehend as to how healing was promoted and succession of a disease was blocked.

Becker shares that this research was possible by merging information from two very old studies that included why healthy people suffer from heart disease. This data was collected from 2,800 white men and women who joined in the Massachusetts-based Framingham Heart research. They started collecting samples since 2003 from 2000 similar participants that included 800 blacks who joined in the Genetic research of Aspirin Responsiveness (GeneSTAR) at Johns Hopkins since 2002. This was led by Becker’s wife and research co-investigator Diane Becker, M.P.H., Sc.D., a professor at the both Hopkins’ School of Medicine and the University’s Bloomberg School of Public Health.

Researchers examined platelet samples for their stickiness in reaction to adding various concentrations of three chemicals that are usually found in the blood. These included adenosine diphosphate, or ADP which is an energy molecule unconfined by platelets into the blood to allure and bundle with other platelets, epinephrine that is known to be a stress hormone attached to inflammation and vascular disease and collagen is known to be the most widespread protein in the human body.

Researchers correlated clumping results with outcomes from gene chip surveys of the human genome. This enabled them to arrange millions of different genetic alterations to identify which specific genes are more active than others. Researchers considered genetic analysis to be a massive undertaking and it took nearly two years to complete.

“Our combined study results really do set the path for personalizing a lot of treatments for cardiovascular disease to people based on their genetic make up and who is likely to benefit most or not at all from these treatments” quotes co-senior research investigator and cardiologist Lewis Becker, M.D.

The team’s next steps are to examine various platelet antagonists or blood thinning agents namely aspirin that is the most frequently used drug in heart and vascular diseases. This will be done to highlight which hereditary factors may separate people who are aspirin-resistant or not, and as to why the drug works for most but not all.

This article was reported in the issue of Nature Genetics online on June 7.