With the incidence of hair loss and the use of prescription hair loss drugs like Avodart and Propecia skyrocketing — especially for off-label, unapproved use, serious side effects have become a reality for many. Could utilizing this simple combination of supplements be the answer so many are seeking?
As you already know, DHT per se is not the cause of hormonal hair loss. It is the inflammatory process in a patterned area that DHT sets into motion that results in the gradual hair minirturization and decreased growth phases that is known as male or female pattern baldness. Specific inflammatory messengers known as cytokines have been the molecular targets of researchers looking for more direct, effective, and side effect free treatments for MPB. Included among the specific cytokines identified in MPB are Tgf-b, Caspase 1, and NFkB.
Lowering blood levels of DHT is a crude, albeit moderately effective and fairly reliable singular intervention angle of treatment. This can be readily accomplished via Propecia, Proscar, Theaflavin(Black Tea) Extract, Avodart, Green Tea/Soy Isoflavone combination, and Beta Sitosterol/ Astaxanthin combination.
Theaflavin Extract and the combination of Green Tea Extract with Soy Isoflavones give an anti-inflammatory component to their already established ability to reduce blood levels of DHT. In facilitating mechanisms that favorably impact inflammation, and ultimately hair loss it is often the combination of specific compounds, not singular compounds, that give far reaching results. We have already seen this with the unique anti-inflammatory effects of Resveratrol and Curcumin, the interaction of which is far more potent than either one alone. Such is apparently the case with the combo of Green Tea and Soy Isoflavones, which induce a distinctly potent anti-inflammation effect for DHT mediated pathologies, and lower serum DHT to the point of rivaling Dutasteride (Avodart).
Journal of Cerebral Blood Flow & Metabolism (2009) 29, 244–253; doi:10.1038/jcbfm.2008.115; published online 22 October 2008
Dihydrotestosterone stimulates cerebrovascular inflammation through NFκB, modulating contractile function
Rayna J Gonzales, Sue P Duckles and Diana N Krause
1. 1Department of Basic Sciences, University of Arizona College of Medicine-Phoenix, Phoenix, Arizona, USA
2. 2Department of Pharmacology, School of Medicine University of California Irvine, Irvine, California, USA
Correspondence: Dr RJ Gonzales, Department of Basic Medical Sciences, University of Arizona College of Medicine, in partnership with Arizona State University, Phoenix, Arizona 85004, USA. E-mail: email@example.com
Received 9 May 2008; Revised 20 August 2008; Accepted 8 September 2008; Published online 22 October 2008.
Our previous studies show that long-term testosterone treatment augments vascular tone under physiological conditions and exacerbates endotoxin-induced inflammation in the cerebral circulation. However, testosterone can be metabolized by aromatase to estrogen, evoking a balance between androgenic and estrogenic effects. Therefore, we investigated the effect of the nonaromatizable androgen receptor agonist, dihydrotestosterone (DHT), on the inflammatory nuclear factor-κB (NFκB) pathway in cerebral blood vessels. Cerebral arteries were isolated from orchiectomized male rats treated chronically with DHT in vivo. Alternatively, pial arteries were isolated from orchiectomized males and were exposed ex vivo to DHT or vehicle in culture medium. DHT treatment, in vivo or ex vivo, increased nuclear NFκB activation in cerebral arteries and increased levels of the proinflammatory products of NFκB activation, cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS). Effects of DHT on COX-2 and iNOS were attenuated by flutamide. In isolated pressurized middle cerebral arteries from DHT-treated rats, constrictions to the selective COX-2 inhibitor NS398 or the selective iNOS inhibitor L-nil, [L-N6-(Iminoethyl)lysine], were increased, confirming a functional consequence of DHT exposure. In conclusion, activation of the NFκB-mediated COX-2/iNOS pathway by the selective androgen receptor agonist, DHT, results in a state of vascular inflammation. This effect may contribute to sex-related differences in cerebrovascular pathophysiology.
J Nutr Biochem. 2011 May;22(5):502-10. doi: 10.1016/j.jnutbio.2010.04.006.
Dietary soy and tea mitigate chronic inflammation and prostate cancer via NFκB pathway in the Noble rat model.
Hsu A, Bruno RS, Löhr CV, Taylor AW, Dashwood RH, Bray TM, Ho E.
Department of Nutrition and Exercise Sciences, Oregon State University, Corvallis, OR 97331, USA.
Chronic inflammation and nuclear factor-kappa B (NFκB) have been implicated in prostate cancer development; thus, dietary factors that inhibit NFκB may serve as effective chemo-preventative agents. Prostate cancer risk is significantly lower in Asian countries compared to the United States, which has prompted interest in the potential chemopreventative action of Asian dietary components such as soy and green tea. This study examined the effects of dietary soy and tea on NFκB activation and inflammation in vivo using a hormone-induced rat model for prostate cancer. Male Noble rats implanted with estradiol and testosterone were divided into 4 dietary groups: control, soy, tea, or soy+tea. NFκB activation and inflammatory cytokines were measured post implantation. The combination of soy and tea suppressed NFκB p50 binding activity and protein levels via induction of IκBα. Soy and tea also decreased prostate inflammatory infiltration, increased Bax/BcL2 ratio and decreased protein expression of tumor necrosis factor-alpha, interleukin (IL)-6 and IL-1β compared to control. Soy and tea attenuated prostate malignancy by decreasing prostate hyperplasia. These effects were not apparent in groups treated with soy or tea alone. The ongoing in vivo studies thus far suggest that combination of foods, such as soy and tea, may inhibit hormone-induced proinflammatory NFκB signals that contribute to prostate cancer development.
Comment:As mentioned, the combination of Green Tea and Soy Isoflavones dramatically reduce serum DHT, and like their pharmaceutical counterparts Avodart and Propecia, shrink enlarged prostate glands. This combination gives the added dimension of neutralizing specific inflammatory cytokines implicated in Androgenetic hair loss.