DHEA gets a lot of media coverage for having numerous uses as a nutraceutical (a food with health additives or medical benefits), food supplement, and potent neuro-steroid. You may have questions about DHEA because it’s supposed protective factors are promoted online, in health food stores, and health magazines. It has even been suggested as a neuroprotective treatment for Parkinson’s disease (PD).
What is DHEA?
DHEA (dehydroepiandrosterone) is a naturally made hormone, produced by the adrenal glands. Sometimes called a parent hormone, it is the precursor to the major male and female sex hormones. DHEA levels decrease in the body with age, and it has developed an association with several age-related conditions.1
The DHEA you can buy commercially is a synthetic version of dehydroepiandrosterone. DHEA is not absorbed fully by the body when taken by mouth. It gets modified into sex hormones and your body gets rid of the rest. DHEA is often touted for its healing or restorative value. It has been said to slow or reverse aging, improve thinking skills, and slow the progress of memory loss conditions such as Alzheimer’s or dementia. It has also been promoted for weight loss, anti–aging, immune diseases, weak bones, and muscle conditions. Athletes and trainers have used it to improve physical performance.1 Yet, many of the supplements reported to contain DHEA have quality control issues. Labeling in dietary supplements is often found to be inaccurate when lab tested. Some products were even found to have no active DHEA. So, it is important to discuss taking any supplements with your physician before starting. They can advise on any safety concerns or interactions with your current medications.
There is research to suggest that DHEA may play a role in treating anti-inflammatory conditions. Studies conducted in 2010 and 2011 evaluated synthetic DHEA as a neuroprotective agent in Parkinson’s disease. A few of the tests were on humans, the rest of the test subjects were mice.
Because natural DHEA is not well metabolized by the body, a synthetic version HE3286 was developed that can be metabolized when taken by mouth and has demonstrated safety in clinical trials.2 A key question studied was whether HE3286 could cross the blood-brain barrier. If it could enter the brain tissue to reduce inflammation and protect the neurons in the substantia nigra that are damaged in people with PD, it might hold neuroprotective possibilities as a treatment for Parkinson’s.2 Neuroinflammation is associated with PD, but whether there is a causal relationship between inflammation and neurodegeneration has only recently been studied in PD and other neurodegenerative diseases.3 The preclinical results indicate that HE3286 may have the potential to regulate the inflammatory signals in mice resulting in improved motor function and reduced inflammatory mediator gene expression in the brain.
What’s the bottom line?
There is not a lot of current evidence-based information. More research is needed to determine the possible role synthetic DHEA may have on improving symptoms of PD in humans. Determining why HE3286 is effective and evaluating its potential drawbacks will require further investigation. DHEA can cause serious side effects. Also, using this or any supplement should always be discussed with your physician. DHEA is not considered an approved treatment option for PD at this time.
Mayo Clinic Staff. DHEA Overview. Published December 14, 2017 https://www.mayoclinic.org/drugs-supplements-dhea/art-20364199. Accessed online March 21, 2018.
HE3286 as Treatment for Parkinson's Disease. Therapeutics Development Initiative, 2010. The Michael J. Fox Foundation for Parkinson’s Research. Published 2010. https://www.michaeljfox.org/foundation/grant-detail.php?grant_id=734. Accessed online March 21, 2018.
Nicoletti F, Philippens I, Fagone P, et al. 17α-Ethynyl-androst-5-ene-3β,7β,17β-triol (HE3286) Is Neuroprotective and Reduces Motor Impairment and Neuroinflammation in a Murine MPTP Model of Parkinson's Disease. Parkinsons Dis. 2012;2012:969418. Published August 21, 2012. http://dx.doi.org/10.1155/2012/969418. Accessed online March 18, 2018.