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Estrogen: you’ll miss it when it’s gone

When we were living in caves and fighting wild lions, we didn’t make it to menopause. Now, we do.

Estrogen does a lot for our bodies, including our skin and scalp. Estrogen deficiency, like the one that comes with menopause, leads to aging and delayed skin repair. In addition to “normal” menopause (around 50), many women go through early menopause, have to contend with the effects of removal of the ovaries or deal with estrogen suppressants (to control the growth of a tumor that responds to estrogen).

How does menopause affect skin and hair?

The answer is complicated, so I hope you will bear with me. But first, why is the “how” important? Because if we know how estrogen supports the skin, and its mechanism of action, then maybe we can help alleviate the damage we can see in the mirror when estrogen goes down. For example, we know that estrogen accelerates the healing process, but how does it do it?
How estrogen affects our body
  • Estrogen inhibits the macrophage migration inhibitory factor (MIF, a pro-inflammatory factor)
  • Estrogen protects cells against oxidative damage caused by ROS*.
  • Estrogen seems to be the most important factor in delayed healing in the elderly.
  • Estrogen deficiency leads to telomerase inhibition, telomere shortening, and reduced cell proliferation.
Obviously, it is not surprising that menopause (and the other ways we can into estrogen deficiency) plays havoc with our body.
I see two ways to deal with estrogen deficiency
1) Hormone supplementation (hormone replacement, HRT). However, if/when cells that possess estrogen receptors become cancerous (and some will if we live long enough), then you are done with hormone replacement. Also, hormone supplementation has been linked to some nasty types of cancer (in particular, invasive lobular breast cancer) and HRT will accelerate cancer progress.
NOTE:  Phytoestrogens are not a remedy when dealing with cancer cells positive for estrogen receptors: if a phytoestrogen binds to the receptors, it will turn on the cancerous cells as well. What matters is not whether a chemical is made by plants but what is its mechanism of action.
2) Bypass estrogen receptors. How? Look at the mechanisms by which estrogen helps your skin and hair and use actives that can do that job without binding to estrogen receptors. This is especially important when dealing with cancer possessing receptors for estrogen. Apigenin will inhibit MIF.
The first strategy is easy: use phytoestrogens to mimic the action of the diminishing estrogen. Examples: soy isoflavones, our phytoestrogen booster, Elixir 10. These botanical extracts and pure chemicals add some great qualities to their phytoestrogenic activity.
The second strategy involves finding actives that can do what estrogen does without binding with estrogen receptors. For example, make up for the antioxidation power lost when estrogen declines, like ROS terminator, or promote telomerase activity without “touching” estrogen receptors, like apocynin.
Look at our products that deal with multiple aspects of skin aging. Our Vitamin A cream with ROS BioNet and apocynin will help renew the skin, disarm ROS*, and help with telomeres without touching estrogen receptors.  We have a similar product that will help with scalp health, preventing hair loss.
The good news? Skin Actives has products that can help with the changes caused by menopause, and we continue to assemble the best actives that can benefit your skin while keeping you safe.  I will keep you posted.
References (I include these for the benefit of those who want to get into the amazingly complicated world of estrogen)
Affinito, P., Palomba, S., Sorrentino, C., Di Carlo, C., Bifulco, G., Arienzo, M.P. and Nappi, C. (2013) Effects of postmenopausal hypoestrogenism on skin collagen, Maturitas. 33 (1999) 239-247.
Ashcroft, G.S., Greenwell-Wild, T., Horan, M.A., Wahl, S.M. and Ferguson, M.W. (1999) Topical estrogen accelerates cutaneous wound healing in aged humans associated with an altered inflammatory response, Am. J. Pathol. 155: 1137-1146.
Ashcroft, G.S., Mills, S.J., Lei, K., Gibbons, L., Jeong, M.J., Taniguchi, M., Burow, M., Horan, M.A., Wahl, S.M. and Nakayama, T. (2003) Estrogen modulates cutaneous wound healing by downregulating macrophage migration inhibitory factor, J. Clin. Invest. 111: 1309-1318
Bayne, S., Jones, M.E., Li, H., Pinto, A.R., Simpson, E.R. and Liu, J.P. (2008) Estrogen deficiency leads to telomerase inhibition, telomere shortening and reduced cell proliferation in the adrenal gland of mice, Cell. Res. 18 (2008) 1141-1150.
Bottai, G., Mancina, R., Muratori, M., Di Gennaro, P. and Lotti, T. (2013) 17β‐estradiol protects human skin fibroblasts and keratinocytes against oxidative damage, Eur. Acad. Dermatol. Venereol. 27:1236-1243
Emmerson, E. and M.J. Hardman (2012) The role of estrogen deficiency in skin ageing and wound healing, Biogerontology. 13: 3-20.
Hardman, M.J. and G.S. Ashcroft (2008) Estrogen, not intrinsic aging, is the major regulator of delayed human wound healing in the elderly, Genome Biol. 9: R80, 1-17.
Hardman MJ, Waite A, Zeef L, Burow M, Nakayama T, Ashcroft GS. Macrophage migration inhibitory factor: a central regulator of wound healing. Am J Pathol. 2005 Dec;167(6):1561-74. doi: 10.1016/S0002-9440(10)61241-2.
Inoue, T., Miki, Y., Abe, K., Hatori, M., Hosaka, M., Kariya, Y., Kakuo, S., Fujimura, T., Hachiya, A., Aiba, S. and Sasano, H. (2011) The role of estrogen-metabolizing enzymes and estrogen receptors in human epidermis, Mol. Cell. Endocrinol. 344: 35-40
Thornton, M.J.(2013) Estrogens and aging skin, Dermatoendocrinol. 5: 264-270
Tresguerres, J.A., Kireev, R., Tresguerres, A.F., Borras, C., Vara, E. and Ariznavarreta, C. (2008) Molecular mechanisms involved in the hormonal prevention of aging in the rat, J. Steroid. Biochem. Mol. Biol. 108 (2008) 318-326
Wilkinson, H. N., & Hardman, M. J. (2017). The role of estrogen in cutaneous ageing and repair. Maturitas, 103, 60–64. doi:10.1016/j.maturitas.2017.06.026
Yoshihisa, Y., Andoh, T., Rehman, M. U., & Shimizu, T. (2019). The regulation of protein kinase casein kinase II by apigenin is involved in the inhibition of ultraviolet B‐induced macrophage migration inhibitory factor‐mediated hyperpigmentation. Phytotherapy Research. doi:10.1002/ptr.6597
Zouboulis CC1, Chen WC, Thornton MJ, Qin K, Rosenfield R. (2007) Sexual hormones in human skin. Horm. Metab. Res. 39: 85-95
DISCLAIMER: These claims have not been evaluated by the FDA and are not intended to diagnose, cure, treat or prevent any disease.