Is arthritis genetic? Scientists claim genetic predisposition for arthritis

Genetic predisposition is not an uncommon genetic disorder.

It is also a commonly-used term for a range of genetic conditions.

A new study in PLOS Genetics found that people with an inherited genetic disorder are three times more likely to develop arthritis.

The findings, which are significant because they could lead to new treatments for people with arthritis, are described as a breakthrough in the field of genetic disorders.

The study involved a cohort of more than 9,000 individuals from nine countries.

“We found that a large percentage of the people with inherited arthritis had a variant in a gene that causes the inflammation of their joints,” said study co-author Dr. Maria A. Mignon of the Institute of Genetic Epidemiology at the University of California, San Francisco.

Mignon said the variant, known as the Crohn’s Disease-associated gene, or CDAG, has been linked to an increased risk of arthritis.

Crohn’s disease is an inflammatory disease of the digestive tract caused by the inflammatory changes in the gut that are triggered by Crohnís disease.

People with CDAG variants have the most severe and often disabling symptoms, including joint pain, stiffness, and inflammation.

The study was published online in PLos Genetics on May 27.

This variant is linked to a higher risk of developing arthritis and is a risk factor for Crohn�s disease, said Dr. David S. Katz, an associate professor of psychiatry at the Mayo Clinic, who was not involved in the study.

The study also found that there was a strong association between CDAG and joint pain.

People with CDAT variants had the least joint pain and were also less likely to have arthritis.

There was also a link between CDAT and joint stiffness.

People in this subgroup had a significantly higher risk for joint stiffness, according to Katz.

It was the first study to show that CDAG variant was a risk for arthritis.

It also found no association between the CDAG gene and other common genetic disorders such as schizophrenia, depression, and autism.

Katz said CDAG was a novel risk factor that is associated with joint stiffness but not joint pain in a very large number of people.

When people with CDATS variants are compared to people without CDATs, Katz said they have about the same risk for osteoarthritis and joint discomfort.

“There’s some overlap between these two populations,” Katz said.

For people with the CDAT variant, there is evidence that they are more likely than people without the CDATS variant to develop joint pain as a result of arthritis, he said.

However, CDAGs are not the only genetic variant that could be responsible for arthritis and arthritis related conditions.

Other genetic variants may be involved, and it is unclear whether this variant affects the development of arthritis in humans.

“Our findings support the idea that a genetic predisposing gene can play a role in developing joint stiffness and joint inflammation,” Katz wrote in the paper.

“But, it’s also possible that other genetic variants might be involved.”

A study published last year in the American Journal of Medical Genetics Genetics found evidence of a genetic variant linked to arthritis in people from Europe and North America.

The European study also included people with a range and frequency of genetic variants that may be associated with arthritis.

In the North American study, the researchers found a variant that caused a reduction in inflammatory cytokines in the brain, an effect that was not seen in people with more common variants.

The findings suggest that the genetic predispositions are not necessarily common, Katz added.

There is a genetic component to arthritis that is inherited.

However, it is not known how much of the genetic variation is responsible for the joint pain associated with the disease, Katz noted.