Can Ethocyn restore elasticity to your skin?

Ethocyn (chemical name: ethoxyhexyl-bicyclooctanone) is claimed to stimulate the synthesis of elastin in the skin. If true, such capacity would be highly valuable in skin rejuvenation. Elastin is a protein responsible for the skin's ability to bounce back after being stretched. The levels of elastin markedly decline with age, which is one of the major factors in the development of the signs of aging. (See our article about elastin.)

Unfortunately, reliable methods to preserve and/or restore youthful levels of elastin in the skin are scarce at best. That is why the development of Ethocyn in the early 1980s by Dr. Chantal Burnison initially generated so much interest. The problem is that Ethocyn's effectiveness has not been validated by credible published peer-reviewed studies (at least I haven't found any) even though the company refers to some proprietary unpublished research. Perhaps the manufacturer (Chantal Pharmaceutical Corporation) didn't have the budget for the studies comprehensive enough to be published. Or perhaps they were wary of disclosing trade secrets. Or perhaps the supporting data simply wasn't solid enough. Hopefully, time will tell.

Ethocyn molecule is claimed to have a number of physiological effects. Importantly, it blocks the action of the androgenic sex hormone dehydrotestosterone (DHT). It is a well-established fact that DHT levels increase with age. Ethocyn makers claim that age-related decline of elastin synthesis is caused mainly by high level of DHT. Therefore, topical application of Ethocyn presumably blocks DHT in the skin and thereby stimulates elastin synthesis. Such mechanism of action is conceivable but there are serous reservations. In particular, there is little, if any, credible published research proving that high DHT levels suppress the synthesis of elastin. Perhaps the makers of Ethocyn established that fact themselves. Still, an independent peer-reviewed corroboration would help.

Let us assume DHT indeed suppresses elastin synthesis in the skin. Then any agent blocking DHT action or reducing DHT levels would presumably help restore elastin to the skin. Many such agent are known, such as finasteride, dutasteride, spironolactone and so forth. Yet there is no evidence that any anti-DHT agent (except, allegedly, Ethocyn) boosts elsatin synthesis. Perhaps anti-DHT drugs simply have not been studied in that connection. Or perhaps the link between DHT and elastin synthesis, if any, is not causative. Again, more credible research is needed.

Ultimately it is more important to prove that Ethocyn indeed increases elastin synthesis than to establish its exact mechanism of action, whether involving DHT blockade or not. Perhaps the anti-DHT effects of Ethocyn are irrelevant and it boosts elastin via some other pathway. This would still be very good news. However, as long as Ethocyn is backed only by unpublished proprietary research, is it difficult to take its merits at "face value".

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