We may be starting to find out why some people are more susceptible to gout than others. Gout is the highly painful form of arthritis that strikes joints far from the heart: generally, the big toe. Genetics are behind a lot of the diseases we face, and according to the new study, this applies to gout as well.
Scientists found 18 new variations in genes that boost the level of uric acid in the blood. This is the enemy for people who suffer gout, as high levels of uric acid form small crystals in joints and tissues, leading to pain and swelling.
Across the world, about two percent of people have gout. It is the most common form of “inflammatory arthritis.” Scientists believed that understanding how these common genetic variants increase uric acid levels can lead to better treatments and preventative steps against gout.
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Gout isn’t going away, that much we know. Expert researchers say that it is becoming more and more common in the developed world. This is partly due to an aging population and rising levels of obesity. Right now, it affects about one in 70 adults.
The study analyzed genetic data from 140,000 people in previous studies in Europe, the U.S., Japan, and Australia. It is the largest study on this subject. While we know that abnormal levels of uric acid are linked to many common diseases, we don’t know much about “why.”
That is often where science turns to our genes, which dictate so much of what happens to us as we grow older.
For gout, existing therapies to prevent it often cause side effects. What if we could identify new ways to target gout? What if we could have a new crop of therapies, even natural ones, that could improve prevention?
Rest assured this will be an area of much study in the future. We will get to the bottom of gout, and this study is one big step in that direction.
Sources for Today’s Articles:
Why You Might Be Susceptible to Gout
Köttgen, A., et al., “Genome-wide association analyses identify 18 new loci associated with serum urate concentrations,” Nature Genetics, 2012, published online December 23, 2012.