I'd believe Dr. Rassman as much as I believe Merck -- which is a big fat 0%.
He's a propecia-pushing derm prescribing their drugs, and is likely getting some good Merck-funded kickbacks for it -- funny how everytime someone mentions side effects on his blog, he essentially fobs them off or tells them to look elsewhere for the cause of their symptoms instead of the drug. Please...
Anyway, that's just my personal opinion about him. Anecdotally, many guys have experienced dark circles under the eyes while on finasteride, self included. Furthermore, there are studies out there noting the effects 5AR inhibitors (such as finasteride) have on eye function -- or rather, causing dysfunction. Here are some experiences and documents to note:
http://72.14.253.104/search?q=cache:IrB ... cd=1&gl=ca
http://www.merckfrosst.ca/assets/en/pdf ... 2_06-E.pdf
-- As Pondle noted:
"PAGE 7: Although the clinical significance is unclear, a
higher incidence of cataracts (4.2%, finasteride vs. 2.5%, placebo) and diabetes (2.8%, finasteride vs. 1.7%, placebo) was observed in patients receiving finasteride. "
http://www.blackwell-synergy.com/doi/ab ... 04.00770.x
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Effect of Androgen Deficiency on the Human Meibomian Gland and Ocular Surface
ONLINE:
http://jcem.endojournals.org/cgi/conten ... 85/12/4874
PDF:
http://jcem.endojournals.org/cgi/reprint/85/12/4874.pdf
Selected bits:
Our results demonstrate that patients taking antiandrogen treatment, compared with age-related controls, had a:
1) significant increase in the frequency of appearance of tear film debris, an abnormal tear film meniscus, irregular posterior lid margins, conjunctival tarsal injection, and orifice metaplasia of the meibomian glands;
2) significant increase in the degree of ocular surface vital dye staining;
3) significant decrease in the tear film breakup time and quality of meibomian gland secretions; and
4)
significant increase in the frequency of light sensitivity, painful eyes, and blurred vision.
In addition,
the use of antiandrogen pharmaceuticals was associated with significant changes in the relative amounts of lipids in meibomian gland secretions.
Our findings indicate that chronic androgen deficiency is associated with meibomian gland dysfunction and dry eye.
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We also compared the relative frequency of the signs and symptoms of dry eye between patients taking finasteride (n = 4; age, 67.3 ± 2.8 yr; diagnosis, prostatic hypertrophy; average duration of treatment, 3 yr) vs. other antiandrogen medications (i.e. predominantly leuprolide acetate, as well as bicalutamide, goserelin acetate, and flutamide) (n = 11; age, 72.2 ± 2.3 yr; diagnosis, prostatic cancer; average duration of treatment, 3 yr).
The rationale for this comparison was that finasteride, but not the other antiandrogen compounds, might act to inhibit the local conversion of testosterone to DHT (24). If so,
finasteride actions might reflect the importance of local steroidogenesis per se in providing potent androgens to ocular surface tissues.
These comparisons showed that
the left and right eyes of patients taking finasteride had a significantly higher frequency of appearance of conjunctival bulbar injection (finasteride group, 100%; other treatment group, 50%; P < 0.05), lid collarettes (finasteride group, 66.7%; other treatment group, 15%; P < 0.05), metaplasia of meibomian gland orifices (finasteride group, 100%; other treatment group, 54.6%; P < 0.01), and corneal fluorescein staining (finasteride group, 87.5%; other treatment group, 31.8%; P < 0.01).
Finasteride-treated patients also had a significantly greater sensitivity to wind (finasteride group, 75% positive responses; other treatment group, 0% positive responses; P < 0.005).
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Consequently, given that this tissue is an androgen target organ (26), contains both androgen receptor protein and 5-reductase mRNA (9), and responds to androgens with an enhanced lipid synthesis, production and release (11, 12), it would seem that antiandrogen therapy and the resulting androgen deficiency would lead to meibomian gland dysfunction.
... the meibomian gland is a large sebaceous gland, and
androgens are known to control the development, differentiation, and lipid elaboration of sebaceous glands in nonocular sites (27, 28). Antiandrogen treatment and the related androgen insufficiency, in turn, lead to a marked decline in sebaceous gland activity and lipid output.
...
The impact of antiandrogen therapy on the conjunctiva, cornea, lid, and ocular surface symptomatology may have been due, in part, to decreased meibomian gland function. Meibomian gland dysfunction typically leads to an increase in the signs and symptoms of evaporative dry eye. Indeed, this condition has been estimated to be a contributing factor in over 60% of all dry eye patients.
...Another consideration in the response of the conjunctiva and cornea to antiandrogen therapy is that
these tissues express Types 1 and 2 5-reductase mRNA and/or androgen receptor mRNA and protein. Furthermore, androgens have been shown to influence the functional activity of both the conjunctiva and cornea .
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Thus,
finasteride administration, compared with the analogs of LH-releasing hormone or the nonsteroidal antiandrogens,
seemed to be associated with a greater frequency of conjunctival bulbar injection, lid collarettes, metaplasia of meibomian gland orifices, corneal fluorescein staining, and wind sensitivity.
