Did you know that 75 percent of people affected by autoimmune (AI) diseases are women? 

It has long been thought that there is a strong link between female hormones (namely estrogen) and autoimmunity. A new study’s findings support that link.

This study found that T cells, which are involved in AI responses, have estrogen receptor alpha (ERα) on their cell membranes. This receptor binds estradiol, which is the predominant estrogen in women.

Researchers discovered that if they deleted these estrogen receptors in the immune cells of mice who were prone to autoimmune colitis, they were less likely to become sick with the condition.

Related Post: Vitamin D Deficiency’s Role in PCOS and Hashimoto’s Thyroiditis 

estrogen and autoimmune disorders, estrogen levels, postpartum, perimenopause, perimenopausal estrogen, estrogen and autoimmune

Autoimmune Conditions Often Appear When Estrogen Fluctuates

This effect was related to the T cell activations which are involved in AI processes. Hormone receptors on the T cells’ surface seem to be involved in stimulating these cells into “attack mode”. The body ‘s immune system mistakenly attacks healthy tissues in the joints, skin, brain, and various other organs.

The link between extreme estrogen fluctuations and AI diseases may explain why women tend to develop these conditions most often when postpartum, or during perimenopause.

During the postpartum period, these hormone levels go from very high, to very low. Then, over time, estrogen must rise in order for their menstrual cycles to to start again.

Similarly, during perimenopause, many women experience extreme hormone level fluctuations as their bodies adjust to having fewer periods, before they stop menstruating entirely.

Conditions such as Hashimoto’s Thyroiditis, Rheumatoid Arthritis, and Grave’s Disease are often seen at these key points in time.

References:

Imran Mohammad, Inna Starskaia, Tamas Nagy, Jitao Guo, Emrah Yatkin, Kalervo Väänänen, Wendy T. Watford, Zhi Chen. Estrogen receptor α contributes to T cell–mediated autoimmune inflammation by promoting T cell activation and proliferation. Science Signaling, 2018; 11