Is Arthritis in Your Genes? Here's What You Should Know

You may know that arthritis occurs in the joints, but did you know that it may also be in your genes? This is to say that arthritis, like many other chronic conditions, seems to have genetic underpinnings that makes it heritable from your parents.

That being said, when it comes to arthritis, there are actually more than 200 distinct types and classifications for the condition. This means that even if you and a best friend or family member have the same diagnosed type, it is highly likely that the two of you would have slightly different specific symptoms.

Various environmental and lifestyle factors play a role in influencing the development and progression of all types of arthritis, but the genetic component in the condition should not be ignored. While a person's specific genes are unlikely to absolutely cause some type of arthritis, having a certain genetic makeup can leave a person predisposed to developing one or more specific types of arthritis.

Fortunately, even if you have such a genetic predisposition, you are not guaranteed to develop arthritis. Furthermore, some forms of arthritis have stronger genetic components than others. This means there is some room for preventative efforts. Learn more about the main types of arthritis and what causes each one:

Forms of Arthritis and their Genetic Causes

1. Osteoarthritis

What many people first think of as arthritis is a kind that primarily affects the elderly, and usually women--osteoarthritis. It is the most common form, and is caused by the degradation of joints, bones, and cartilage of an affected area.

What ends up happening is the cartilage wears thin, and the bones of the joint end up rubbing against each other, leading to inflammation and pain. The pain associated with osteoarthritis can vary widely from person to person, from mild discomfort all the way up to debilitating pain and suffering.

Lifestyle choices (diet, activity levels, obesity, etc), along with increased age, tend to lend the greatest risk for developing osteoarthritis, but there are some genetic components. The genetic bases for developing this type of arthritis vary depending on the particular cause of the joint degradation: collagen, vitamin processing and absorption, immune/inflammatory responses, and cartilage.

Lots of genes, across several different chromosomes form the foundation for the development of osteoarthritis. Chromosomes 1, 2, 4, 6, 7, 9, 11, 12, 13, 16, 19, and X have a number of specific relationships which can result in different forms of osteoarthritis as well as the severity thereof.

Specifically, chromosomes 2, 7, 11, and 16 have a greater weight regarding this process. Genes controlling the production and distribution of collagen (especially collagen type 2) are particularly important: COL2A1 (chromosome 12), COL9A2 and COL11A1 (chromosome 1), COL11A2 (chromosome 6), COMP (chromosome 19), while specific alleles of COL1A1 (chromosome 17) have been shown to reduce the likelihood of hip osteoarthritis in some populations.

Interleukines are a type of cytokine important in the regulation of immune and inflammatory responses, especially with regards to fever, and the operation of macrophages and lymphocytes. Various subtypes of interleukin IL-1 lead to certain presentations of osteoarthritis. Most of the gene locations for the various interleukin subtypes are on chromosome 2, but some are on 9 and 11.

Decreases or changes in estrogen levels have also been linked to an increased incidence of hip and knee osteoarthritis in women. Estrogen receptor alpha (located on chromosome 6) is an important mediator in signal transduction, and is present in several different types of cells throughout the body.

Vitamin D and its corresponding receptor (located on chromosome 12) is responsible for proper bone development and growth, the development of certain cancers, and osteoarthritis (especially in the knees).

The strangely named Frizzled Related Protein gene (located on chromosome 2) is important in the development of cartilage. Mutations in this gene have been found to be the foundation for some types of osteoarthritis in women.

2. Rheumatoid Arthritis

 Rheumatoid arthritis (RA)  is usually caused by an overactive immune system. Immune cells mistakenly attack normal cells and healthy tissues. It can also be caused by other immune products interfering with normal joint movement or organ functioning, usually through inflammation.

Rheumatoid arthritis primarily affects the joints, but it can also affect other connective tissues. Depending on which joints are affected, rheumatoid arthritis can cause secondary conditions such as carpal tunnel syndrome or myelopathy (neurological damage to within the spinal cord).

RA can sometimes affect whole organs including the skin, lungs, kidneys, and nerves. When it affects the skin, a small nodule will form, usually considered to be a necrotizing granuloma. In the lungs, rheumatoid arthritis causes a type of pulmonary fibrosis. In some instances, rheumatoid arthritis can cause kidney damage leading to a form of amyloidosis.

Rheumatoid arthritis offers one specific example of a type that has a strong genetic component. Rheumatoid arthritis is genetically linked to certain classes of the histocompatibility antigen (the specific one, HLA2-DRB1, is located on chromosome 6). Additionally, the tyrosine phosphatase 22 gene (PTPN22, located on chromosome 1), has been implicated in an increased risk for rheumatoid arthritis. Currently, the process for causality between the gene and resulting arthritis is not entirely understood.

When considering twin studies, among identical twins, the dual-occurance rate is roughly 1 in 7. However, among fraternal twins, it falls to roughly 1 in 25. Rheumatoid arthritis affects roughly 1 in 50 people in the population at large, but it is three times more likely to affect women than men. Unlike some other forms of arthritis, rheumatoid arthritis is most likely to first strike during middle age, and rarely starts during childhood, adolescence, and during old age.

3. Gout

Most people do not think of it as a form of arthritis, but gout is a particularly painful and debilitating form of inflammatory arthritis. Gout typically strikes in the feet, usually in the base joint of the big toe of the foot corresponding to the handedness of the individual (right foot in right-handed individuals).

Gout is caused by the accumulation of uric acid in the blood, and once the concentration reaches a certain level, crystals can form in the joints leading to characteristic pain, inflammation, and fever. Roughly 63% of the variability in uric acid production seems to stem from genetic changes.

Prior to recent research, gout was believed to be connected to one of a few serious and rare genetic disorders. Genome wide association studies (GWAS) have shown that gout can have foundations brought about by more mundane genetic changes across a variety of populations.

The most strongly linked genetic change associated with gout is in the Glucose-9 Transporter gene, located on the fourth chromosome (SLC2A). Genetic changes to this gene have been found to be foundational in gout, hyperuricemia, and drastic increases in the risk of developing Alzheimer's Disease.

4. Juvenile Idiopathic Arthritis

Most people think of arthritis as only an “old-person's disease.” However, teenagers and even children can be affected by arthritis. When it strikes this a young person, it is usually called juvenile idiopathic arthritis.

The idiopathic portion of the name is assigned because the ultimate cause of the person's affliction is unknown. Juvenile idiopathic arthritis is thought to arise from a combination of genetic and environmental factors.

Typically, inflammation occurs when the immune system sends molecules and white blood cells to a location of injury or infection to fight the disease and facilitate tissue repair. Normally, the body ends the inflammatory process after it has finished the healing process. This is done to prevent damage to other cells.

However, in those with juvenile idiopathic arthritis, this inflammatory response continues long after the initial cause has been taken care of. Reasons for this extended inflammatory process are unclear, but research is constantly being conducted in order to better understand the underlying processes, and how to prevent further tissue damage.

It is thought that the most likely culprit in direct, genetic causes for JIA comes from changes to the human leukocyte antigen. Genetic changes behind the particular forms of this antigen are brought about by changes to specific locations on the sixth chromosome. There are numerous variations of the HLA gene, allowing for significant variability in the human immune system – though only certain mutations are known to form the genetic basis for JIA.

Recommendations for Managing Arthritis

If you are unlucky enough to develop one of the types of arthritis, the symptoms can be as diverse and intense as there are types of arthritis. Some people experience mild discomfort that can be alleviated just by changing certain behaviors, while others experience crippling pain that robs them of their independence and joy.

While there is no cure for most forms of arthritis, a number of lifestyle choices and treatments do exist that can help sufferers live a fuller life with less pain and debilitation. Diet, exercise, and sleep play key roles in arthritis management. However, participating in appropriate medical care is also crucial. In particular, chiropractic care can offer a drug and surgery free option that can be an effective option for treatment.