(B.P.H)-Prostate, Hair Loss, Lycopene and Saw Palmetto

OverMachoGrande

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Here I give quite a few studies regarding BPH, Hair loss, Lycopene and Saw Palmetto, and how they all correlate together.

First I show how Finasteride fights male pattern baldness through the 5-alpha reductase inhabitation, and how it treats BPH;

CNS Drug Rev. 2006 Spring;12(1):53-76.
A new look at the 5alpha-reductase inhibitor finasteride.
Finn DA, Beadles-Bohling AS, Beckley EH, Ford MM, Gililland KR, Gorin-Meyer RE, Wiren KM.
Department of Veterans Affairs Medical Research, Portland Alcohol Research Center, 97239, USA. finnd@ohsu.edu
Finasteride is the first 5alpha-reductase inhibitor that received clinical approval for the treatment of human benign prostatic hyperplasia (BPH) and androgenetic alopecia (male pattern hair loss). These clinical applications are based on the ability of finasteride to inhibit the Type II isoform of the 5alpha-reductase enzyme, which is the predominant form in human prostate and hair follicles, and the concomitant reduction of testosterone to dihydrotestosterone (DHT). In addition to catalyzing the rate-limiting step in the reduction of testosterone, both isoforms of the 5alpha-reductase enzyme are responsible for the reduction of progesterone and deoxycorticosterone to dihydroprogesterone (DHP) and dihydrodeoxycorticosterone (DHDOC), respectively. Recent preclinical data indicate that the subsequent 3alpha-reduction of DHT, DHP and DHDOC produces steroid metabolites with rapid non-genomic effects on brain function and behavior, primarily via an enhancement of gamma-aminobutyric acid (GABA)ergic inhibitory neurotransmission. Consistent with their ability to enhance the action of GABA at GABA(A) receptors, these steroid derivatives (termed neuroactive steroids) possess anticonvulsant, antidepressant and anxiolytic effects in addition to altering aspects of sexual- and alcohol-related behaviors. Thus, finasteride, which inhibits both isoforms of 5alpha-reductase in rodents, has been used as a tool to manipulate neuroactive steroid levels and determine the impact on behavior. Results of some preclinical studies and clinical observations with finasteride are described in this review article. The data suggest that endogenous neuroactive steroid levels may be inversely related to symptoms of premenstrual and postpartum dysphoric disorder, catamenial epilepsy, depression, and alcohol withdrawal.




Endocr Regul. 2010 Jan;44(1):3-8.
Changes of metabolic profile in men treated for androgenetic alopecia with 1 mg finasteride.
Duskova M, Hill M, Starka L.
Objective. Androgenetic alopecia is recognized as a risk factor for cardiovascular diseases, glucose metabolism disorders, and benign prostate hyperplasia and/or carcinoma. Finasteride, used for treatment of androgenetic alopecia at a dose of 1mg/day, is an effective inhibitor of type II 5alpha-reductase, the enzyme responsible for the reduction of testosterone to dihydrotestosterone. Recent studies reported that dihydrotestosterone, among other activities, might play some role in visceral fat metabolism. It thus seemed reasonable to examine whether finasteride treatment of androgenetic alopecia ameliorates some features of metabolic syndrome frequently seen associated with this condition.
Methods. We examined 12 men with premature balding (defined as frontoparietal and vertex hair loss before age 30 with alopecia defined as grade 3 vertex or more on the Norwood-modified Hamilton alopecia classification). Hormonal levels and metabolic parameters were determined and insulin tolerance tests performed for all individuals. Finasteride (1 mg/day) was administrated for 12 months. The hormonal profile and lipid spectrum were monitored after 4, 8 and 12 months of treatment and insulin tolerance tests were repeated after 12 months of the treatment.
Results. After treatment with finasteride the expected changes in the steroid spectrum were seen, namely a decrease in dihydrotestosterone and increase in testosterone, androstenedione and free testosterone index. We observed an initial increase in total cholesterol and HDL- and LDL-cholesterol, which stabilized with prolonged treatment. We founded a significant decrease in glycated hemoglobin HbA1c and insulin resistance measured using rate constant for plasma glucose disappearance (kITT) showed only a borderline decrease.
Conclusions. Finasteride is an efficient 5alpha-reductase inhibitor even at low doses of 1mg/day. In men treated with this dose for 12 months, we observed mild differences in metabolic profile with slight amelioration of glucose metabolism regulation. Keywords: Finasteride - Androgenetic alopecia - Androgens - Lipids - Insulin sensitivity - Metabolic disorders.

Mind you, Initially this drug made DHT go down and Testosterone rise... :whistle:




Eur J Dermatol. 2001 Jul-Aug;11(4):332-4.
Advances in the treatment of male androgenetic alopecia: a brief review of finasteride studies.
Whiting DA.
University of Texas Southwestern Medical Center, Dallas, TX 75246, USA. daddoc@dallasassocderm.com
Finasteride is a type 2 5a-reductase inhibitor and therefore mimics the biochemical profile of inherited type 2 5a-reductase deficiency in men. It was developed to grow hair in androgenetic alopecia and shrink benign prostatic hyperplasia. Various clinical trials of finasteride have confirmed its beneficial effects in androgenetic alopecia in males, but not in females. It can produce visible hair growth in up to 66% of men with mild to moderate alopecia, but importantly can stop hair loss in 91% of patients. In long-term finasteride studies, placebo patients were characterized by significant and progressive hair loss. It can be concluded that finasteride prevents further hair loss by actually continuing to grow enough hair to preserve scalp coverage. This is confirmed by the loss of hair following withdrawal of finasteride in such cases. The proven preservative effect of finasteride, in addition to its restorative effect, is a strong indication for prescribing it in early cases of androgenetic alopecia before much hair has been lost.


Urology. 1998 May;51(5):744-8.
Association of benign prostatic hyperplasia with male pattern baldness.
Oh BR, Kim SJ, Moon JD, Kim HN, Kwon DD, Won YH, Ryu SB, Park YI.
Department of Urology, Chonnam University Medical School, Kwangju, South Korea.
OBJECTIVES: Both benign prostatic hyperplasia (BPH) and male pattern baldness (androgenic alopecia) share the pathogenesis of an androgen-dependent disorder and afflict a large population of elderly men with chronobiologic progress. However, it is unclear whether these diseases are related epidemiologically. We evaluated the association of frequency and severity of male pattern baldness between patients with BPH and a control group. METHODS: A total of 225 patients with BPH (mean age 69.3 +/- 6.5 years) and 1 60 controls (mean age 68.5 +/- 6.4 years), all over 60 years of age, were included in this study. The estimation of baldness severity was based on Norwood's classification (grade I to VII). The International Prostate Symptom Score (IPSS) and genetic tendency for baldness were also evaluated. The difference between IPSS and grade of baldness between the two groups was analyzed by the Mann-Whitney test and the frequency of inherited baldness was compared by the chi-square test. Correlation between severity of baldness and IPSS in each group was estimated by Spearman's rank correlation method. RESULTS: The patients with BPH had an apparently higher grade of male pattern baldness in comparison with that of controls (median value of grade IV versus III, P <0.001). The proportion of men with male pattern baldness of grade IV or higher in the BPH group was significantly larger than that of controls (53.8% versus 36.9%, P <0.01). There was a greater frequency of inherited baldness in the BPH group than in the controls (31.6% versus 12.5%, P <0.001). No significant correlation was noted between baldness severity and IPSS in either group. CONCLUSIONS: This study demonstrates a strong association of BPH with male pattern baldness.





So now we know that Finasteride helps BPH, and enlarged prostate, inhibits the action of 5-alpha reductase from binding with T into DHT.

Now let's see what Lycopene and Saw Palmette can do regarding BPH, Prostate health, Enlarged prostate and male pattern baldness;






Aktuelle Urol. 2009 Jan;40(1):37-43. Epub 2009 Jan 28.
[Tomatoes and lycopene in prevention and therapy--is there an evidence for prostate diseases?]
[Article in German]
Ellinger S, Ellinger J, Müller SC, Stehle P.
Institut für Ernährungs- und Lebensmittelwissenschaften, Fachbereich Ernährungsphysiologie, Universität Bonn, Bonn. ellinger@uni-bonn.de
Tomatoes are discussed to have an important role in the prevention of and therapy for prostate cancer (PCA). Whether or not they are also useful in the primary and secondary prevention of benign prostate hyperplasia (BPH) is not clear. This review summarises the results of original contributions with a focus on interventional studies. Whereas epidemiological studies on BPH prevention provide no evidence for a preventive potential of tomatoes and tomato products, the majority of interventional trials points to an increased DNA resistance against oxidative-induced damage. Even though their effect on a surrogate marker of the IGF pathway cannot be evaluated so far due to insufficient data, the consumption of tomatoes and tomato products may probably protect from PCA--at least when considering low-grade PCA. Thus, regular consumption of these foods can be recommended for the prevention of PCA. Tomato products might also be useful in the therapy for BPH and PCA. The intake of isolated lycopene does not protect from the development of PCA. However, in the doses achieved by consumption of tomato products, lycopene ingestion might also be effective in PCA therapy.





Fitoterapia. 2000 Aug;71 Suppl 1:S21-8.
Botanical derivatives for the prostate.
Cristoni A, Di Pierro F, Bombardelli E.
Scientific Department, Indena S.p.A., Viale Ortles 12, 20139, Milan, Italy. indenami@tin.it
The prostate, after the age of 45 years, may undergo benign hyperplasia (BPH). Its etiology has not yet been completely explained, but different factors play a major role in its occurrence, among them, the sexual hormones (with a fundamental role of 5 alpha reductase). The 5-alpha reductase activity and inflammatory aspects in the prostate tissue can be effectively controlled with the use of highly standardized plant extracts (Pygeum africanum, Serenoa repens, etc.), which yield excellent results in the prophylaxis and treatment of the symptoms linked to prostate hypertrophy. The prostate tissue is not affected only by benign diseases but may also be subject to neoplastic transformation. From an epidemiological point of view, a vegetable derivative, lycopene, was linked with a lower occurrence of prostate carcinoma. A recent clinical study demonstrated that lycopene might not only prevent prostate cancer but also have therapeutic effects.




Evid Based Complement Alternat Med. 2009 Aug 19. [Epub ahead of print]
Inhibition of Inflammatory Gene Expression in Keratinocytes Using a Composition Containing Carnitine, Thioctic Acid and Saw Palmetto Extract.
Chittur S, Parr B, Marcovici G.
Advanced Restoration Technologies, Inc., 9035 North 15th Place, Phoenix, AZ 85020, USA. docgmarcovici@aol.com.
Chronic inflammation of the hair follicle (HF) is considered a contributing factor in the pathogenesis of androgenetic alopecia (Androgenetic Alopecia). Previously, we clinically tested liposterolic extract of Serenoa repens (LSESr) and its glycoside, beta-sitosterol, in subjects with Androgenetic Alopecia and showed a highly positive response to treatment. In this study, we sought to determine whether blockade of inflammation using a composition containing LSESr as well as two anti-inflammatory agents (carnitine and thioctic acid) could alter the expression of molecular markers of inflammation in a well-established in vitro system. Using a well-validated assay representative of HF keratinocytes, specifically, stimulation of cultured human keratinocyte cells in vitro, we measured changes in gene expression of a spectrum of well-known inflammatory markers. Lipopolysaccharide (LPS) provided an inflammatory stimulus. In particular, we found that the composition effectively suppressed LPS-activated gene expression of chemokines, including CCL17, CXCL6 and LTB(4) associated with pathways involved in inflammation and apoptosis. Our data support the hypothesis that the test compound exhibits anti-inflammatory characteristics in a well-established in vitro assay representing HF keratinocyte gene expression. These findings suggest that 5-alpha reductase inhibitors combined with blockade of inflammatory processes could represent a novel two-pronged approach in the treatment of Androgenetic Alopecia with improved efficacy over current modalities.
PMID: 19692448 [PubMed - as supplied by publisher]





a*** Sci. 2009 Apr;25(4):553-7.
Isolation and pharmacological characterization of fatty acids from saw palmetto extract.
Abe M, Ito Y, Suzuki A, Onoue S, Noguchi H, Yamada S.
Department of Pharmacokinetics and Pharmacodynamics, and Global Center of Excellence Program, School of Pharmaceutical Sciences, University of Shizuoka, Suruga, Shizuoka 422-8526, Japan.
Saw palmetto extract (SPE) has been widely used for the treatment of lower urinary-tract symptoms secondary to benign prostatic hyperplasia. The mechanisms of pharmacological effects of SPE include the inhibition of 5alpha-reductase, anti-androgenic effects, anti-proliferative effects, and anti-inflammatory effects. Previously, we showed that SPE bound actively to alpha(1)-adrenergic, muscarinic and 1,4-dihydropyridine calcium channel (1,4-DHP) receptors in the prostate and bladder of rats, whereas its active constituents have not been fully clarified. The present investigation is aimed to identify the main active components contained in hexane and diethyl ether extracts of SPE with the use of column chromatography and preparative HPLC. Based on the binding activity with alpha(1)-adrenergic, muscarinic, and 1,4-DHP receptors, both isolated oleic and lauric acids were deduced to be active components. Authentic samples of oleic and lauric acids also exhibited similar binding activities to these receptors as the fatty acids isolated from SPE, consistent with our findings. In addition, oleic and lauric acids inhibited 5alpha-reductase, possibly leading to therapeutic effects against benign prostatic hyperplasia and related lower urinary-tract symptoms




Biol Pharm Bull. 2009 Apr;32(4):646-50.
Pharmacologically relevant receptor binding characteristics and 5alpha-reductase inhibitory activity of free Fatty acids contained in saw palmetto extract.
Abe M, Ito Y, Oyunzul L, Oki-Fujino T, Yamada S.
Department of Pharmacokinetics and Pharmacodynamics and Global Center of Excellence (COE) Program, School of Pharmaceutical Sciences, University of Shizuoka, Japan.
Saw palmetto extract (SPE), used widely for the treatment of benign prostatic hyperplasia (BPH) has been shown to bind alpha(1)-adrenergic, muscarinic and 1,4-dihydropyridine (1,4-DHP) calcium channel antagonist receptors. Major constituents of SPE are lauric acid, oleic acid, myristic acid, palmitic acid and linoleic acid. The aim of this study was to investigate binding affinities of these fatty acids for pharmacologically relevant (alpha(1)-adrenergic, muscarinic and 1,4-DHP) receptors. The fatty acids inhibited specific [(3)H]prazosin binding in rat brain in a concentration-dependent manner with IC(50) values of 23.8 to 136 microg/ml, and specific (+)-[(3)H]PN 200-110 binding with IC(50) values of 24.5 to 79.5 microg/ml. Also, lauric acid, oleic acid, myristic acid and linoleic acid inhibited specific [(3)H]N-methylscopolamine ([(3)H]NMS) binding in rat brain with IC(50) values of 56.4 to 169 microg/ml. Palmitic acid had no effect on specific [(3)H]NMS binding. The affinity of oleic acid, myristic acid and linoleic acid for each receptor was greater than the affinity of SPE. Scatchard analysis revealed that oleic acid and lauric acid caused a significant decrease in the maximal number of binding sites (B(max)) for [(3)H]prazosin, [(3)H]NMS and (+)-[(3)H]PN 200-110. The results suggest that lauric acid and oleic acid bind noncompetitively to alpha(1)-adrenergic, muscarinic and 1,4-DHP calcium channel antagonist receptors. We developed a novel and convenient method of determining 5alpha-reductase activity using LC/MS. With this method, SPE was shown to inhibit 5alpha-reductase activity in rat liver with an IC(50) of 101 microg/ml. Similarly, all the fatty acids except palmitic acid inhibited 5alpha-reductase activity, with IC(50) values of 42.1 to 67.6 microg/ml. In conclusion, lauric acid, oleic acid, myristic acid, and linoleic acid, major constituents of SPE, exerted binding activities of alpha(1)-adrenergic, muscarinic and 1,4-DHP receptors and inhibited 5alpha-reductase activity.





J Herb Pharmacother. 2005;5(1):17-26.
A preliminary investigation of the enzymatic inhibition of 5alpha-reduction and growth of prostatic carcinoma cell line LNCap-FGC by natural astaxanthin and Saw Palmetto lipid extract in vitro.
Anderson ML.
Research and Development, Triarco Industries, Wayne, NJ 07470, USA. mark.anderson@triarco.com
Inhibition of 5alpha-reductase has been reported to decrease the symptoms of benign prostate hyperplasia (BPH) and possibly inhibit or help treat prostate cancer. Saw Palmetto berry lipid extract (SPLE) is reported to inhibit 5alpha-reductase and decrease the clinical symptoms of BPH. Epidemiologic studies report that carotenoids such as lycopene may inhibit prostate cancer. In this investigation the effect of the carotenoid astaxanthin, and SPLE were examined for their effect on 5alpha-reductase inhibition as well as the growth of prostatic carcinoma cells in vitro. These studies support patent #6,277,417 B1. The results show astaxanthin demonstrated 98% inhibition of 5alpha-reductase at 300 microg/mL in vitro. Alphastat, the combination of astaxanthin and SPLE, showed a 20% greater inhibition of 5alpha-reductase than SPLE alone n vitro. A nine day treatment of prostatic carcinoma cells with astaxanthin in vitro produced a 24% decrease in growth at 0.1 mcg/mL and a 38% decrease at 0.01 mcg/mL. SPLE showed a 34% decrease at 0.1 mcg/mL. CONCLUSIONS: Low levels of carotenoid astaxanthin inhibit 5alpha-reductase and decrease the growth of human prostatic cancer cells in vitro. Astaxanthin added to SPLE shows greater inhibition of 5alpha-reductase than SPLE alone in vitro.




It is important to note here, the effects of Astaxanthin in combination with Saw Palmetto, how how Saw Palmetto becomes more effective.

After viewing these documents, we get better idea on how effective these botanicals are, and how they can be applied to male pattern baldness, with great effectiveness.
 

abcdefg

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What is a quality supplement that mimics exactly what they did here? I dont know if taking separate ones would be the same or not. Not to mention supplement quality and dosing varies a lot . I dont know if its strong enough to do anything even if it does lower DHT a little because you need major androgen level changes to get results not minor ones.
Would this be the right carotenoid then although I dont know what dose would match that - 300 microg/mL in vitro Still seems like finasteride essentially does the same thing.

http://www.amazon.com/NutriGold-Astaxanthin-Liquid-Veggie-Capsules/dp/B006S44THW
 

abcdefg

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Yeah but the question is how powerful are these compared to say finasteride? I mean dose is everything you cant eat 200 tomatos a day for lycopene. I know bald men that eat tomatos full of lycopene like its going out of style didnt help them so its hard for me to believe sometimes that it makes enough of a difference to have some visible effect on male pattern baldness. I also think any supplements/fruits that lower enzymes enough to affect male pattern baldness will have negative sides like anything else just no one knows what those are because its not studied.
Im open to the natural route I just have never seen anyone get major results without medications and there arent any rigorous studies on it I ever saw.
 
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