I’m trying to make sense of the relationship between insulin growth factor, propecia and resveratrol. I think they’re all linked but I don’t know enough info to know how or why. What I’m thinking is that taking resveratrol will increase IGF-1 in the scalp (while decreasing it in other bodily tissues such as the prostate gland), and thus stop baldness in its tracks.
Here are the studies I’m trying to grasp with:
The expression of insulin-like growth factor 1 in follicular dermal papillae correlates with therapeutic efficacy of finasteride in androgenetic alopecia.
Tang L, Bernardo O, Bolduc C, Lui H, Madani S, Shapiro J.
Division of Dermatology, The University of British Columbia, Vancouver Hospital, Canada.
BACKGROUND: It is generally believed that dihydrotestosterone is one of the pivotal mediators of hair loss in androgenetic alopecia (AGA). Finasteride, which blocks the conversion of testosterone to dihydrotestosterone, has now become an integral part of the current treatment approaches for male AGA. Several lines of evidence support the notion that dermal papilla (DP) cells represent the androgen target within the hair follicle. The specific molecular regulators modulated by androgens within hair follicles in the balding scalp are unknown. OBJECTIVE: The purpose of this study was to identify and quantify changes in expression of specific molecular hair growth regulators in DP of men with AGA treated with finasteride and correlate these findings to clinical efficacy. METHODS: Biopsy specimens were collected from 9 male patients from both the balding area and nonbalding occipital area before and after 4 months of finasteride therapy. DP were microdissected and total RNA was extracted from an equal number of DP from each biopsy specimen. The expression of various cytokines, including insulin-like growth factor (IGF)-1, was determined by reverse transcription polymerase chain reaction. The signals were detected by autoradiography. All 9 patients were given finasteride for 1 year and evaluated for efficacy at month 12. Efficacy was graded on a 7-point scale on the basis of comparison with initial baseline photography. RESULTS: IGF-1 was up-regulated by finasteride treatment in 4 of 9 patients. Among the patients with increased IGF-1 expression, 3 of them showed moderate clinical improvement after 12 months of treatment and another patient remained unchanged. In contrast, 3 patients with decreased IGF-1 expression in the balding scalp showed clinical worsening after 12 months. The other 2 patients without noticeable change in IGF-1 expression showed either slight improvement or no change in their hair condition. CONCLUSION: In a small uncontrolled study of 9 patients with AGA, an increased expression of IGF-1 messenger RNA levels in the DP was associated with patient response to finasteride.
Androgenetic Alopecia and Prostate Cancer: Findings from an Australian Case-Control Study1
Graham G. Giles2, Gianluca Severi, Rod Sinclair, Dallas R. English, Margaret R. E. McCredie, Warren Johnson, Peter Boyle and John L. Hopper
Cancer Epidemiology Centre, Anti-Cancer Council of Victoria, Melbourne, VIC 3053 Australia [G. G. G., D. R. E.]; Division of Epidemiology and Biostatistics, European Institute of Oncology, 1-20141, Milan, Italy [G. S., P. B.]; Department of Dermatology, St. Vincent’s Hospital, Melbourne, VIC 3065 Australia [R. S.]; Department of Preventive and Social Medicine, Dunedin Medical School, University of Otago, New Zealand 9001 [M. R. E. M.]; Cancer Epidemiology Research Unit, New South Wales Cancer Council, Sydney, 2011 New South Wales, Australia [M. R. E. M.]; Department of Public Health, University of Western Australia, Perth, 6009 Australia [D. R. E.]; Royal Melbourne Hospital, Melbourne, 3052 Australia [W. J.]; and Centre for Genetic Epidemiology, University of Melbourne, Melbourne, 3052 Australia [J. L. H.]
The purpose of this study was to examine the relationship between androgenetic alopecia (AA) and prostate cancer with particular emphasis on early age at diagnosis and higher grade tumors. We conducted an age-stratified, population-based case-control study in Australia of men who were diagnosed before 70 years of age during 1994–1997 with histopathology-confirmed adenocarcinoma of the prostate, excluding well-differentiated tumors. Controls were selected from the electoral rolls, and the frequency was matched on age. After excluding subjects with missing values, the analysis was based on 1446 cases and 1390 controls of whom direct observations were made of their pattern of AA during face-to-face interviews. Our data suggest an association between prostate cancer and vertex baldness; compared with men who had no balding, the adjusted odds ratio (OR) was 1.54 (1.19–2.00). No associations were found between prostate cancer and frontal baldness or when frontal baldness was present concurrently with vertex baldness. The ORs were 0.98 (0.79–1.23) and 1.14 (0.90–1.45), respectively. The highest ORs were for high-grade disease in men 60–69 years of age: 1.80 (1.02–3.16) for frontal baldness; 2.91 (1.59–5.32) for vertex baldness; and 1.95 (1.10–3.45) for frontal and vertex baldness. This association between the pattern of AA and prostate cancer points to shared androgen pathways that are worthy of additional investigation.
Carcinogenesis. 2007 Aug 3
Resveratrol Suppresses Prostate Cancer Progression in Transgenic Mice.
Harper CE, Patel BB, Wang J, Arabshahi A, Eltoum IA, Lamartiniere CA.
Department of Pharmacology and Toxicology, University of Alabama at Birmingham, Birmingham, Alabama.
Resveratrol, a natural polyphenolic phytochemical, has been reported to act as an antioxidant and provide anti-cancer activities. We hypothesized that resveratrol would exert a chemopreventive effect against prostate cancer via regulation of sex steroid receptor and growth factor signaling pathways. In the current study, Transgenic Adenocarcinoma Mouse Prostate (TRAMP) males were fed resveratrol (625 mg resveratrol/kg AIN-76A diet) or phytoestrogen-free, control diet (AIN-76A) starting at five weeks of age. Mechanisms of action and histopathology studies were conducted at 12 and 28 weeks of age, respectively. Resveratrol in the diet significantly reduced the incidence of poorly differentiated prostatic adenocarcinoma by 7.7-fold. In the dorsolateral prostate (DLP), resveratrol significantly inhibited cell proliferation, increased androgen receptor (AR), estrogen receptor-beta (ER-beta), and insulin-like growth factor-1 receptor (IGF-1R), and significantly decreased IGF-1, and phospho-extracellular regulating kinase 1 (phospho-ERK 1). In the ventral prostate (VP), resveratrol significantly reduced cell proliferation and phospho-ERKs 1 and 2, but did not significantly alter IGF-1R and IGF-1. Serum total testosterone, free testosterone, estradiol, dihydrotestosterone (DHT), and sex hormone binding globulin (SHBG) concentrations and SV-40 Tag expression in the prostate were not altered in resveratrol-treated mice. Total resveratrol concentration in the blood serum of 12 week old mice treated for three weeks with 625 mg resveratrol/kg diet was 52 +/- 18 nM. The decrease in cell proliferation and the potent growth factor, IGF-1, the down-regulation of downstream effectors, phospho-ERKs 1 and 2, and the increase in the putative tumor suppressor, ER-beta, provide a biochemical basis for resveratrol suppressing prostate cancer development.