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Research Yields Another Clue to How Genetic Diseases Work

Research Yields Another Clue to How Genetic Diseases Work
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For people with chronic diseases such as arthritis and diabetes, “Why me?” is a common question. Now, scientists think they may have an answer. Researchers say they’ve located chemical tags — or genetic modifiers — that can turn certain genes on and off.

What Is It?

In a recent study, researchers at the Johns Hopkins University School of Medicine and the Karolinska Institute in Sweden looked at patients with rheumatoid arthritis (an autoimmune disease), but their work might also apply to people suffering from other chronic conditions such as type II diabetes and heart problems. Researchers compared 354 newly diagnosed rheumatoid arthritis patients and 337 healthy people and examined the white blood cells in both groups. They were looking for differences in the participants’ DNA, specifically chemical tags that could turn genes on and off.

Turns out just having a gene that increases the risk for rheumatoid arthritis doesn’t seal a person’s biological fate. Researchers found that all the patients with rheumatoid arthritis in the study had four specific tags, or DNA methyls, on one cluster of genes that affects the immune response and the risk of developing rheumatoid arthritis. The tags were like a green light for the disease genes: Even though some patients in the healthy group had genes for rheumatoid arthritis, they didn’t develop the disease, presumably because they didn’t have those four specific tags.

Why It Matters

The study is one example of epigenetics, a field of research that studies how genetic modifications can influence the risk for certain diseases. Epigenetic researchers have known about the importance of genetic tags for a while, but they still aren’t sure exactly how these tags end up on our DNA. Scientists suspect some tags aren’t just the cause of diseases, but that they’re actually caused by diseases. Other tags are probably the result of environmental factors (such as diet, stress, and toxins) or certain medications.

Recently, a lot of research in the field has focused on the ways DNA methylation can affect the progression of rheumatoid arthritis [1] [2] [3]. But this study was unique in that researchers were able to figure out which tags contributed to the growth of the disease and which ones only appeared after the arthritis had already developed.

No one’s saying the results of this study are going to lead directly to a cure for rheumatoid arthritis or any other disease. Nor is it likely that researchers will be able to know with 100 percent accuracy who’s going to develop these health problems. But this research is a great step toward being able to predict which people are at risk for certain diseases and, ultimately, trying to prevent them.

Would you want to know if you have the tags that increase your risk for certain diseases? Let us know in the comments below or tweet the author at @ShanaDLebowitz.

Works Cited +

  1. Regulation of DNA Methylation in Rheumatoid Arthritis Synoviocytes. Nakano, K., Boyle, D.L., Firestein, G.S. Division of Rheumatology, Allergy and Immunology, University of California San Diego School of Medicine, La Jolla, CA. Journal of Immunology 2012.
  2. New advances of DNA methylation and histone modifications in rheumatoid arthritis, with special emphasis on MeCP2. Miao, C.G., Yang, Y.Y., He, X., et al. School of Food and Drug, Anhui Science and Technology University, Bengbu, China. Cellular Signaling 2012.
  3. Epigenetics in rheumatoid arthritis. Trenkmann, M., Brock, M., Ospelt, C., et al. Center of Experimental Rheumatology and Zurich Center for Integrative Human Physiology (ZIHP), University of Zurich, Zurich, Switzerland. Clinical Reviews in Allergy and Immunology 2010 Aug;39(1):10-9.

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