Key protein not direct cause of heart disease, study reveals
A protein that is widely used as an indicator of a person's heart disease risk does not actually cause heart disease, new research reveals. The findings are important because until now many researchers have viewed C-reactive protein (CRP) as a possible target for heart disease drugs. The research, which was partly funded by the EU, is published in the Journal of the American Medical Association (JAMA). Coronary heart disease is the leading cause of death worldwide. All stages of the disease are characterised by inflammation, and CRP levels in a person's blood are a good indicator of inflammation. Observational studies have also shown that high levels of CRP in the blood are associated with a higher risk of heart disease. However, it was not clear whether CRP was causing heart disease in some way, or whether it was simply a marker of the inflammation involved in heart disease. In this latest study, an international team of researchers studied the genes that control the levels of CRP in the blood and their effect on heart disease. In total they looked at different gene variants in 28,112 people with heart disease and 100,823 people who did not have heart disease. They found that the gene variants linked with different CRP levels are not associated with an increased risk of heart disease, indicating that CRP is unlikely to be directly involved in causing heart disease. In addition, the researchers identified genetic variants in three other genes that affect CRP levels. 'Coronary heart disease is a common cause of death, especially in the UK and other western countries, and scientists have been looking for new ways to treat the disease and reduce mortality,' commented the lead author of the paper, Professor Paul Elliott of the Department of Epidemiology and Public Health at Imperial College London in the UK. 'Some researchers thought C-reactive protein would be a good molecule to target, as raised levels of this protein in the blood are associated with increased risk of coronary heart disease. However our research suggests that the association may not be causal, so attempts to target this protein to reduce the risk of the disease are unlikely to be fruitful. 'We have also discovered new genetic variations that are associated with coronary heart disease. If confirmed in other studies, these might give clues to identify new targets to treat the disease,' he added. EU support for the work came from the CARDIOGENICS ('Identification of genetic roots of coronary artery disease by combining stepwise genome wide association studies with transcriptomic and functional genomic investigation of relevant genetic variants'), EURODIA ('Functional genomics of pancreatic beta cells and of tissues involved in control of the endocrine pancreas for prevention and treatment of type 2 diabetes') and PROCARDIS ('A genome-wide mapping and functional genomics approach to elucidating precocious coronary artery disease') projects, all of which are funded under the 'Life sciences, genomics and biotechnology for health' Thematic area of the Sixth Framework Programme (FP6), as well as the Fifth Framework Programme (FP5) EURO-BLCS ('European birth life-course study') project, which was financed under the 'Quality of life and management of living resources' programme.