Gout is frequently linked to excessive alcohol consumption and poor dietary habits, yet recent studies indicate that genetics may play a more significant role in the onset of this painful arthritic condition than was once believed.

An extensive research project conducted by a global team of scientists examined genetic information from 2.6 million individuals across 13 diverse DNA studies, including 120,295 participants diagnosed with gout.

By evaluating and comparing the genetic profiles of those with gout to those without, the research team identified 377 unique DNA regions associated with the condition, with 149 of these regions previously unlinked to gout.

While lifestyle and environmental factors still hold importance, this study underscores the critical genetic influences that determine an individual’s likelihood of developing gout. Moreover, researchers believe that there are still many undiscovered genetic connections to be explored.

“Gout is a chronic condition rooted in genetics, and it is not merely a result of one’s lifestyle choices. We need to dispel the myth that diet and habits are solely responsible for gout,” stated Tony Merriman, an epidemiologist from the University of Otago in New Zealand, at the time of the study’s publication last year.

Gout occurs when uric acid levels in the bloodstream rise, forming sharp crystals in the joints. The immune system reacts to these crystals, resulting in significant pain and discomfort.

Genetics influence all stages of this process, particularly regarding the immune system’s response to the crystals and the transportation of uric acid throughout the body.

Although gout can be episodic, treatments are available. However, the prevailing misconceptions often discourage individuals from seeking appropriate care, which is concerning given the increasing number of cases of the condition being reported.

“This pervasive myth contributes to a sense of shame among gout sufferers, leading many to endure their pain silently and delaying necessary medical consultations for preventive medications that reduce blood urate levels,” asserted Merriman.

This study not only enhances our understanding of gout’s underlying causes but also opens new avenues for treatment, particularly in managing the immune system’s reaction to elevated uric acid levels. In fact, existing medications may be adapted for this purpose.

There are some limitations to consider: much of the data came from individuals of European descent, and some gout cases were self-reported rather than clinically validated. Nevertheless, these findings provide meaningful insight into a condition that has affected many for generations.

“Our hope is that the targets we’ve identified will lead to improved and more accessible treatment options in the future,” said Merriman. “Gout requires more healthcare funding and higher prioritization within our health systems.”

This research article has been published in Nature Genetics.

Note: An earlier version of this article was released in November 2024.