Some diseases have clear and widely known causes.
Others, however, remain a mystery.
Now, the mystery surrounding the origins of rheumatoid arthritis (RA) may be closer to being solved.
A new report published in the journal
While this has long been suspected, it has never been confirmed in the medical community.
The published study is of considerable length and laden with medical jargon and scientific terminology. However, the findings remain clear: Finding a disease origin or genetic component in conditions like rheumatoid arthritis can eventually further research toward a cure, or at least open up a wider range of treatment options.
Looking at Genetic Traits
The researchers wanted to study whether or not genetic traits across various illnesses were clinically significant.
These genetic variations across a single species are called genetic polymorphisms.
A polymorphism could, for example, mean the difference between a human being born male or female.
Or it could mean the difference between members of the same species developing an autoimmune condition like rheumatoid arthritis, or not.
While genetic variations may be significant, they also might not be.
So the authors of this recent study sought to research these polymorphisms to determine if or how they played a role in certain diseases.
To do so, they studied the human genome through genome-wide association studies. They assigned value to several different biologic mechanisms that were common to certain polymorphisms associated with a myriad of diseases.
One of these conditions was rheumatoid arthritis.
Finding Common Causes
It was found that diabetes, Alzheimer’s, rheumatoid arthritis, and cancer did share certain disease properties and genetic components.
These shared biological properties could be an important development for researchers, medical professionals, and patients living with these conditions.
A statement made to the press and media that was published on the University of Arizona Health Sciences (UAHS) department website summed up the results.
“The discovery of these shared properties offer[s] the opportunity to broaden our understanding of the biological basis of disease and identify new therapeutic targets,” said Dr. Yves A. Lussier, FACMI, who was the lead author of the study and director of the UAHS Center for Biomedical Informatics and Biostatistics.
It is a noteworthy accomplishment in the field of medicine for Lussier and his team to discover the link between these DNA risk variants, gene expression, cellular machinery, and disease biology.
The accomplishment, however, didn’t come easily and wasn’t achieved overnight. Researchers have been analyzing genetic DNA variants for decades — at least 10 years for Lussier and his team.
The UAHS press release states: “When DNA risk variants for a given disease were analyzed in combination, similar biological activities were discovered, suggesting that distinct risk variants can affect the same or shared biological functions and thus cause the same disease. More detailed analyses of variants linked to bladder cancer, Alzheimer’s disease, and rheumatoid arthritis showed that two variants can contribute to disease independently, but also interact genetically. Therefore, the precise combination of DNA variants of a patient may work to increase or decrease the relative risk of disease.”
More Rheumatoid Research
This study wasn’t the only one aimed at finding a genetic component of autoimmune illnesses such as RA.
The Utah Population Database also conducts genome-wide assessment studies looking at the risk of autoimmunity within families, particularly investigating the link between eosinophilic esophagitis (EoE) and other autoimmune diseases.
This population-based study showed increased risk for multiple autoimmune conditions in patients with EoE, and
If doctors and researchers can continue to find links between illnesses, then more patient-tailored drug therapies can evolve.
The customization of treatments is a key component of precision medicine. Establishing these roadmaps to disease is the first step to success.