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The Secret Behind Eyelash Growth and Sunscreen's Dark Side

Rebecca James Gadberry November 2006 issue of Skin Inc. magazine

Q. There’s a new growth hormone on the market that supposedly grows eyelashes. What is this ingredient? Does it really work?

A. Renewed lash growth, density and pigmentation have been identified as side effects of several drugs commonly used to treat glaucoma. This effect—known as hypertrichosis—first was described in 1997 in association with the drug latanoprost.1 Since then, more reports have surfaced and similar results have been reported for two other glaucoma drugs, as well—travoprost and bimatoprost. All three are members of the prostaglandin family, which is a group of hormonelike lipid compounds associated with inflammation processes throughout the body.

The effects seen with these drugs may be normal body responses to mild inflammatory agents. During this response, keratinocytes can proliferate, or generate more of the substances that they produce in order to protect the skin or eyes. In the case of the lash-producing keratinocytes lining the eyelids, the rest cycle of the hair follicle—known as telogen—can be shortened, while the hair-growth cycle—known as anagen—is lengthened. This can result in longer, denser lashes that remain rooted in the lash bed for a more significant period than normal. Melanogenesis, the process that creates melanin pigments, also can increase, resulting in greater deposits of melanin in lashes as they are produced by the keratinocytes.

Placebo-controlled studies show that hair growth stimulated by lantanoprost—the most widely studied of the three drugs—occurs very early in the anagen phase.2-4 If lantanoprost use begins at the onset of anagen, results can be seen quickly—sometimes in as little as two to five days5—and can last 14 months or longer.6 The majority of people using lantanoprost will show hair growth after six months of its use, with women exhibiting greater results than men.7 Other studies of these drugs’ effects on lashes indicated that they can produce multiple rows of lashes, as well as a more marked lash curvature. In addition, lantanoprost has been reported to reverse lash alopecia.8-9

Curious researchers also have studied the drugs’ effects on hair growth for the brows and scalp. This research included people with various types of alopecia, or hair loss, with success ranging from no results to those described as remarkable. Even though studies about hair growth on the scalp may show promise, they are still in their infancy. No drugs in this family appear to be ready for the hair-growth market at this time.

Comparisons have been made between lantanoprost and minoxidil, the granddaddy of hair-growth stimulators, which also is thought to act via prostaglandin processes. Although minoxidil does have a thickening effect on women’s lashes and has been used to treat alopecia areata in the lash area, it shows inferior results to the lash growth experienced with latanoprost. In addition, minoxidil must be used continually in order to maintain the results. The effects of latanoprost appear to be more powerful and longer lasting.6

Although these outcomes definitely are desirable, unwanted side effects from the three glaucoma drugs also have been reported, albeit much more rarely. Of the three, lantanoprost appears to produce the least amount of negative effects. These include red, itchy eyes, inflammation or darkening of the irises in blue or green eyes, whitening of the lashes, ingrown lashes, increased pigmentation of the eyelids, and reactivation of herpes keratitis or herpes dermatitis, as well as cystoid macular edema in those susceptible to the condition, which can distort a person’s vision when fluid and protein deposits cause a space on the retinas inside the eyes to thicken and swell. Increased pigmentation in the irises is most common among Asians, although 12–18% of Caucasians are reported to see darkening after one to two years of use. The iris hyperpigmentation experienced with these drugs is thought to be caused by increased melanin formation rather than a rise in melanocytes. Because the latter may be indicative of melanoma, this is comforting news to those who experience this effect.

Related to prostaglandins are growth factors such as vascular endothelial growth factor (VEGF) and epidermal growth factor (EGF). Although neither apparently is used in cosmetics to induce lash growth, last year one company—Jan Marini Skin Research, Inc.—introduced a new product containing an ingredient named Lash Growth Factor. Company owner Jan Marini admits that the ingredient seems to be working on prostaglandins, but is remaining quiet about further details until her patent is filed sometime within the next several months.

Whatever those details are, the effects are remarkably similar to those of the glaucoma drugs. Estheticians, physicians and consumers who use the product containing Lash Growth Factor report noticeable increases in lash growth and density within one to six months of use. Positive effects on brow growth also have been reported. Marini says that alopecia patients sometimes can see results, as well as chemotherapy patients, if they begin using the product after their treatment sessions are completed. However, unlike the glaucoma drugs, Marini adds that her product containing Lash Growth Factor is receiving reports of redness and itching from less than one-tenth of 1% of users. This is significantly less than the occurrence of irritation that frequently is reported with other eye products and glaucoma drugs.


1 M Johnstone, Hypertrichosis and increased pigmentation of eyelashes and adjacent hair in the region of the ipsilateral eyelids of patients treated with unilateral topical latanoprost. Am J Ophthalmol (124), 544–547 (1997)

2 M Sugimoto and Y Uji, Quantitative analysis of eyelash lengthening following topical latanoprost therapy. Can J Ophthalmol (37) 342–345 (2002)

3 R Noecker, S Bulau and J Schwiegerling, Xalatan-induced changes in periocular skin pigmentation and lash dimensions measured using a digital imaging technique. J Invest Ophthalmol (40) S832 (1999)

4 G Stechhi, S Saccucci, S Molinari and F De Gregorio, Eyelash hypertrichosis induced by topical latanoprost: 6-month follow-up study. Acta Ophthalmol Scand (Suppl. 236) 56–57 (2002)

5 R Wolf, H Matz, M Zalish, A Pollack and E Orion, Prostaglandin analogs for hair growth: Great expectations, Dermatology Online Journal 9(3): 7

6 M Johnstone, Brief latanoprost RX induces hypertrichosis [abstract], Invest Ophthalmol Vis Sci (Suppl. 39) S258 (1998)

7 A Reynolds, P Murray, P Colloby, Darkening of eyelashes in a patient treated with latanoprost, Eye (12) 741–743 (1998)

8 S Mansberger and G Coiffi, Eyelash formation secondary to latanoprost treatment in a patient with alopecia, Arch Ophthalmol (118) 718–719 (2000)

9 E Higginbotham, R Feldman, M Stiles and H Dubiner, Latanoprost and timolol combination therapy vs monotherapy. One-year randomized trial. Arch Ophthalmol (120) 915–922 (2002)

Q. Is it true that sunscreens create free radicals in the skin?

A. Yes. This past August, researchers at the University of California gained wide media attention when they announced that three commonly used sunscreen ingredients can produce skin-damaging free radicals if the sunscreen is not reapplied at regular intervals throughout the day when skin is exposed to sunlight.1

The study, which was funded by grants from the National Science Foundation and the National Institutes of Health, is the first of its type to use a unique two-photon laser fluorescence imaging microscope to visibly track what happens when three widely used U.S. Food and Drug Administration (FDA)-approved over-the-counter UV sunscreens—octinoxate (octyl methoxycinnamate), oxybenzone (benzophenone-3) and octocrylene—penetrate the skin’s surface.

Incorporating commonly used levels of each sunscreen into a standard sunscreen base, the researchers were able to view their physiological effects as they made their way from the skin’s surface into deeper epidermal layers. They found that the oxidizing molecules known as reactive oxygen species (ROS)* are lessened significantly when the sunscreens are applied initially. But once the sunscreens leave the skin’s surface and travel into the epidermis, ROS are generated at a higher-than-normal rate within the epidermis—especially when they enter the lower epidermal layers, where cellular DNA is found. If the sunscreen is reapplied, the amount of ROS declines again.

Kerry M. Hanson, a senior research scientist at the University of California, Riverside’s department of chemistry and the study’s lead researcher, concedes that sunscreens can do an excellent job of protecting against sunburn when they are used correctly, which means high SPFs applied uniformly onto the skin every two hours. She adds, “Our data shows, however, that if coverage at the skin’s surface is low, the UV filters in sunscreens that have penetrated into the epidermis can potentially do more harm than good.”

How do the results of this study affect sunscreen use? Following are some suggestions.

  • 1. Look for sunscreen products that keep the ingredients on the skin’s surface for as long as possible. There are various ways to do this, including avoiding skin-penetrants, binding sunscreen ingredients to larger molecules that inhibit penetration or using silicone-based emulsions. Check with your manufacturer to determine how the company is inhibiting sunscreen penetration.


  • 2. Look for UV-stable antioxidants in sunscreen. In a previous study, Hanson determined that an SPF 15 sunscreen featuring octinoxate and avobenzone reduced ROS formation in lower epidermal layers by 90% when compared to bare skin.2 Adding UV-stable vitamin E acetate and sodium ascorbyl phosphate to the same sunscreen reduced ROS formation by an additional 5.5%, for a total of a 95.5% reduction of UV-generated ROS. Other antioxidants believed to be effective against UV-induced ROS include tetrahexyldecyl ascorbate, glycyrrhizates from licorice, coenzyme Q10 (ubiquinone), idebenone, thermus ferment, ethylbisiminomethylguaiacol manganese chloride, green and white teas with a standardized level of epigallocatechin gallate (EGCG), and pomegranate extract with a standardized level of polyphenol ellagic acid. To ensure that your clients receive additional antioxidant protection from their sunscreens, ask your manufacturer for data that shows that the antioxidants contained in the products are effective ROS-inhibitors during UV exposure.


  • 3. Wear high-SPF broad-spectrum sunscreen when in direct sunlight. The American Academy of Dermatology has determined that an SPF of 15 offers high enough protection for most people. Broad-spectrum protection means that the sunscreen protects from both UVB and UVA rays.


  • 4. When in direct sunlight, reapply sunscreen often. The Skin Cancer Foundation recommends high SPFs be reapplied every two hours—more often when swimming or sweating—even with a product touted as resistant or very resistant to these activities. Apply generously wherever skin is exposed to sunlight. Advise clients to use the two-finger rule: Apply a line of sunscreen one-eighth inch wide down the lengths of their index and middle fingers. This amount is enough to cover the entire face, ears, neck, throat and upper chest. The rule applies regardless of whether the sunscreen is in the form of a moisturizer, foundation, blush or dedicated sunscreen product. Be sure to emphasize this even when clients apply sunscreen in foundation or moisturizer. Some people may prefer to apply a separate sunscreen to ensure that they get enough protection.


  • 5. Explain to clients that sunscreens are a last resort when sunlight cannot be avoided. No sunscreen completely blocks UV light, regardless of its SPF. In order to fully protect skin from UV exposure, remind clients to stay out of the sun as much as possible and to cover up when they’re in direct sunlight, sitting by a window or in a car. UVA rays—the sun’s aging rays that may be linked to melanoma—can penetrate glass. For this reason, wearing a high-SPF broad-spectrum UVA/UVB sunscreen daily is a good idea.



1 Sunscreens Can Damage Skin, Researchers Find. University of California, Riverside Newsroom, Office of Strategic Communications (August 29, 2006)

2 K M Hason and R M Clegg, Bioconvertible vitamin antioxidants improve sunscreen photoprotection against UV-induced reactive oxygen species, Journal of Cosmetic Science (54/6), 589–598 (Nov/Dec 2003)

* ROS is the oxygen-based family of free radicals that attacks lipids in cell walls, as well as the skin’s barrier, energy-producing mitochondria in cells and reproductive DNA. These reactions lead not only to inflammation and aging in epidermal and dermal tissues, but some researchers believe that UVA-generated ROS also are the link to the almost threefold rise in melanoma throughout the past 20 years, even though sunscreen use is on the increase worldwide.

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