Inflammation Hormone Connection

Inflammation is activated by an array of insults such as injury and foreign invasion by viruses and bacteria. What is less expected is the imbalance of hormones which can contribute to increased inflammation. Several hormones play a key role in the increase and decrease of inflammation. When out of balance inflammation increases which contributes to chronic disease.

Hormones that REDUCE inflammation include: TESTOSTERONE, DHEA and CORTISOL. Hormones that INCREASE inflammation include: PROLACTIN, ESTROGEN and INSULIN. (1) These hormone levels vary depending on age, gender, pregnancy and stress levels. Here are just some of the ways these hormones influence inflammation.

TESTOSTERONE: The correlation between testosterone and inflammation has been observed clinically and in research. One article discusses a decrease in inflammation markers IL-6, IL-1beta and TNF-alpha occurring in males on testosterone supplementation  for low functioning testes. (1) The same research indicated the presence of these inflammation markers causing a disruption in formation and release of testosterone in the brain and endocrine organs. (1) Generally,  males who are in adropause (male menopause), experience decline in testosterone and increased inflammation markers.(1) The take home message being testosterone plays a role in protection against systemic inflammation. Additionally, testosterone protects the cardio vascular system. Studies showing higher testosterone in females showed a reduced risk of atherosclerosis demonstrated by reduced size of the most inner layer of the carotid arteries. (2)

DHEA: DHEA has several roles of its own, one of which has become popular for cardiovascular protection . As discussed above, testosterone protects the cardiovascular system at the level of the arterial tissue. DHEA provides antioxidant protection to the Low Density Lipoproteins, or LDL (3). Protecting LDL from oxidation helps to reduce inflammation inside the vessels, thus reducing risk of atherosclerosis. DHEA is also converted to androstenediol and androstenetriol both playing several roles in the immune system including protection against the flu virus. You will notice that Cortisol and DHEA are often seen together in lab work. This is is because CORTISOL is suppressing to the immune system while DHEA counters that suppression by increasing immune activity.

CORTISOL: Unfortunately this hormone has received a bad reputation over the years. While chronically elevated levels can cause harm to the body over time, we would not survive without it.  This hormone functions to help us during times of stress. It works by maintaining our blood sugar, increasing blood pressure and reducing inflammation. All things you would want to function well when running from a tiger, or during times of high stress. When your doctor provides you with a steroid such as cortisone it is mostly to suppress inflammation. Cortisol in our body works the same way. The trick is keeping Cortisol elevated when it should be elevated and low when it should be low. All of which can be reviewed with your Hormone Zone physician.

PROLACTIN: Polactin is released by the anterior pituitary especially during pregnancy and breast feeding. Prolactin is also released outside of the pituitary and binds to prolactin receptors on immune cells. This binding sends chemical signals that increase inflammation. High prolactin levels are seen during flairs in patients with system wide autoimmune disorders such as LUPUS, RHEUMATOID ARTHRITIS and AUTOIMMUNE THYROID disorders such as HASHIMOTOS and GRAVES DISEASE. (4)

ESTROGEN:  It is important to consider the form of estrogen. For example, estradiol is naturally occurring and protective to the breasts and uterus. While estrone and estriol have significant roles but exhibits less protective qualities. Inflammation marker C-Reactive Protein (CRP) was measured in females receiving estrogen therapy from conjugated equine estrogen pill verses estradiol patch. Of the two groups, females receiving the pill of conjugated equine estrogen had a significant increase in CRP levels while patients receiving estradiol patch did not show any change in CRP. (5) This demonstrates that estrogen will impact inflammatory response but the form must be considered.

INSULIN: Insulin resistance and diabetes are associated with damage to small vessels that supply blood to the nerves, kidney and brain. Under normal conditions, insulin acts as a signal to get sugar into the cells. When in states of inflammation insulin is less able to function properly. This is demonstrated by insulin resistance increasing in the presence of inflammatory marker CRP, TNF alpha, MCP-1. The key is, inflammation increases insulin resistance, and insulin resistance increases inflammation. The main goal is to reduce inflammation and prevent insulin resistance to begin with. (6)

At The Hormone Zone we assess each of these hormones as part our annual evaluation. We specialize in hormone balance and health optimization. With over 20 years of combine experience our physicians have devised specific programs to address inflammation. Please contact us to see how proper hormone balance can help you! (480) 338-8070. And remember, healing is always an option.


Maggio, M., Basaria, S., Ceda, G. P., Ble, A., Ling, S. M., Bandinelli, S., . . . Ferrucci, L. (1970, January 01). The relationship between testosterone and molecular markers of inflammation in older men. Retrieved September 27, 2017, from

Hertoghe, T. (2006). The hormone handbook: a quick reference guide therapy for the physician ; the keys to safe hormone replacement therapies ; also adapted for patients who want to understand the details of their treatments. Walton-on-Thames: International Medical Books.


De, A., Bizzarro, A., Pivonello, R., Lombardi, G., & Bellastella, A. (n.d.). Prolactin and autoimmunity. Retrieved October 08, 2017, from

Differential Effects of Oral Versus Transdermal Estrogen Replacement Therapy on C-Reactive Protein in Postmenopausal Women,” by Wanpen Vongpatanasin, MD, et. al., Journal of the American College of Cardiology, Volume 41: 1358-1363, 2003.

Kresser, C., Says, K., Says, K., Says, H., Says, R., Says, B., . . . Says, K. (2017, July 23). How inflammation makes you fat and diabetic (and vice versa). Retrieved October 09, 2017, from


Accessibility Toolbar

Scroll to Top