Is Androgenetic Alopecia a Photoaggravated Dermatosis?

This seems to be going against the anecdotal reports here that sun exposure is beneficial.


Abstract

Progressive thinning of the scalp hair in androgenetic alopecia (AGA) results in a gradual decline in natural protection of the scalp from ultraviolet radiation (UVR). A number of pathologic conditions of the scalp are evidently related to UVR, particularly photosensitive diseases and disorders of the chronically photodamaged bald scalp. The most important chronic effects of UVR are photocarcinogenesis and solar elastosis. Besides these, erosive pustular dermatosis and 'red scalp' are distinct disorders peculiar to the balding scalp. While the consequences of sustained UVR on the unprotected scalp are well appreciated, the effects of UVR on hair loss have widely been ignored. However, clinical observations and theoretical considerations suggest that UVR may have negative effects: acute telogen effluvium from UVR has been described, and the production of porphyrins by Propionibacterium sp. in the pilosebaceous duct, with photoactivation of porphyrins leading to oxidative tissue injury, has been implicated in follicular microinflammation. Alternatively, keratinocytes themselves may respond to physicochemical stress from UVR, besides irritants and pollutants, by producing radical oxygen species and nitric oxide and by releasing proinflammatory cytokines, eventually leading to injury of the putative site of follicular stem cells in the superficial portion of the hair follicle. Since all of these processes involved in hair loss share the common feature that they are induced or exacerbated by exposure to sunlight, it is proposed that AGA is a photoaggravated dermatosis that requires photoprotection.

CausticSymmetry has posted this study before



Dermatology. 2009 Apr 29.
Seasonality of Hair Shedding in Healthy Women Complaining of Hair Loss.
Kunz M, Seifert B, Trüeb RM.

Department of Dermatology, University Hospital of Zürich, Zürich, Switzerland.

Background: A number of otherwise healthy women with or without clinical alopecia complain of recurrent hair loss, presumably reflecting seasonality in the growth and shedding of hair. Objective: To test the hypothesis that periodicity in hair shedding reflects seasonal changes in human hair growth. Methods: Retrospective case study over a period of 6 years of apparently healthy women with the complaint of hair loss. All underwent biochemical investigations, and trichograms were made. Results: After exclusion of patients with a disease or on drugs known to cause hair loss, 823 women remained. Analysis of trichograms demonstrated annual periodicity in the growth and shedding of hair, manifested by a maximal proportion of telogen hairs in summer. A second peak seems to exist, though it is less pronounced, in spring. The telogen rates were lowest in late winter. Conclusions: These results confirm the findings of former authors who have indicated seasonal changes in human hair growth, though this is the first study performed systematically in a representative number of women. Copyright 2009 S. Karger AG, Basel.

JDP,

Intersting thanks. That study doesn't address the cause of the seasonal differences though. For instance it could be change in temperature. It makes sense that those women probably got more sun exposure in the summer and spring, but that is left to speculation. Another thing I can think of would be that people tend to spend more time outdoors exercising when it is warm. UV exposure would be the first thing to come to mind, but not necessarily the cause.

jharsh80 - In the study you listed, the key word is chronic UVR exposure.

Healthy sun exposure will help increase vitamin D and radiate sun energy which provides infrared radiation, which increases nitric oxide.

BTW, I should post this just in case someone gets the wrong idea regarding LLLT

"Studies of hair-bearing human skin

The ESR spectrum of a dark-haired human scalp biopsy is shown in Fig. 2a and comprises a weak background signal due to melanin (17). Ultraviolet irradiation of this sample gave an immediate doublet of the ascorbate radical superimposed upon the melanin signal (Fig. 2b). During irradiation, the combined intensities of the melanin and ascorbate radical signals are approximately three times the intensity of the melanin signal before illumination, and the signals returned to their original intensity when the light was turned off. This is believed to reflect both photoinduced melanin free-radical formation (1 and photosensitized oxidation of ascorbate to the ascorbate radical (either via melanin (19) or via other photosensitizers within the skin itself) and confirms activation of endogenous photosensitizers by UVR and freeradical production in human hair-bearing skin. Application of t-butylhydroperoxide to the epidermis of skin from the same patient gave the ascorbate radical (Fig. 2c); however, after exposure to the ruby laser (five pulses 17 J cm^sup -2^) the spectrum shown in Fig. 2d was obtained (immediately after lasering). A marked increase in the intensity of the melanin signal was observed, but the ascorbate radical could not be detected. Unlike the melanin signal increase induced by UV light, the laser-induced signal increase was found to be irreversible (the signal remaining the same intensity 24 h later) and could reflect either photo- or thermal formation of melanin free radicals. The results show that, although laser light is absorbed by melanin (in the hair and hair follicles) to produce melanin free radicals, this is not accompanied by oxidation of ascorbate (in marked contrast to UV irradiation of similar biopsies). These results show that ruby laser irradiation of hair-bearing skin is not associated with detectable free-radical production."
http://findarticles.com/p/articles/mi_qa3931/is_199909/ai_n8855339/pg_2

jdp,

thanks for that. I wasn't addressing LLT but that is good to know anyway. In fact if I read that conclusion correctly, it is actually supporting the initial abstract I posted, i.e. UV radiation from sunlight is detrimental, but not LLT. Would you say that is correct?

Yes, that's correct. However, I personally believe there is nothing wrong with getting small or modest amounts of UV exposure.

Interestingly, PUVA, which is just a UV light on the scalp has been shown to work well in treating alopecia areata.

jdp710 wrote:Yes, that's correct. However, I personally believe there is nothing wrong with getting small or modest amounts of UV exposure.

Interestingly, PUVA, which is just a UV light on the scalp has been shown to work well in treating alopecia areata.

Me neither- Sun damage and aging from sun is really overplayed IMO. Especially here in CA with everyone constantly wearing sunscreen. No wonder 80% of the U.S. is vitamin D deficient. I still don't intentionally lay out in the sun anymore because I believe it attributed to some unnecessary aging in my case. Then again I was usually drinking beer and smoking at the same time. Have you used niacinamide or NAG topically?

I haven't used niacinamide or NAG/glucosamine topically before so I don't know the best way to mix. I actually have a bunch of bottles of different brands of glucosamine and NAG but all of them I'm sensitive to ... sulfites or free glutamic acid.

Regarding hyperpigmentation, the reason why I don't use anything topically is because my yellow LED lights have worked so well and also works well in preventing fine lines.

hope this helps