40 steps to completely reverse M.P.B.

[mykal_P]

If you inhibit aromatase you will have an increase in not only testosterone (because estrogen inhibits testosterone production via the feedback loop) but also D.H.T.

Just a question, I thought DHT was made in the scalp by the 5ar enzyme, or is it made other places. Also if more is being made wont propecia just block it since its already in the body. There's got to be a point you would think that a high enough dose of finasteride or dutasteride would blanket every 5ar enzyme not allowing DHT production no matter what the testosterone increase.

 

[Bryan]

If you inhibit aromatase you will have an increase in not only testosterone (because estrogen inhibits testosterone production via the feedback loop) but also D.H.T. because D.H.T. is an estrogen antagonist.

Huh?? How does the fact that DHT is an "estrogen antagonist" explain why DHT would go UP when you reduce estrogen with an aromatase inhibitor?? :shock: :smack:

Seriously, I'm glad to see that you're sloooowly learning some of the basics of endocrinology, after I had to tell you only about, oh, 37 times that both T and DHT go up when you take an aromatase inhibitor. By the way, the actual reason for that is that DHT is made from testosterone, so if you increase testosterone, you tend to increase DHT at the same time. It's as simple as that.

 

[Bryan]

Just a question, I thought DHT was made in the scalp by the 5ar enzyme, or is it made other places.

Both. It's made in the scalp, and numerous other places around the body.

Also if more is being made wont propecia just block it since its already in the body. There's got to be a point you would think that a high enough dose of finasteride or dutasteride would blanket every 5ar enzyme not allowing DHT production no matter what the testosterone increase.

Yes. Oral finasteride doesn't "target" only certain specific body tissues like the scalp or the prostate. It spreads all around the body, inhibiting the 5a-reductase type II enzyme wherever it goes. However, it should be pointed out that there _may_ be more penetration of the drug into certain areas of the body than in others.

 

[dpdr]

misterE

My nutritionist said that avocado oil is rich in beta sitosterol,is true ?

 

[OverMachoGrande]

misterE

My nutritionist said that avocado oil is rich in beta sitosterol,is true ?

Yes

 

[powersam]

1. Decrease testosterone production (low fat/high fiber diet, beta sitosterol, reducing cholesterol levels).


There is little evidence to suggest that this will help male pattern baldness in any way.

If you are going to put such an arrogant title on your thread, you best be ready to back it up with some real evidence.

 

[OverMachoGrande]

1. Decrease testosterone production (low fat/high fiber diet, beta sitosterol, reducing cholesterol levels).


There is little evidence to suggest that this will help male pattern baldness in any way.

You lower testosterone, while increase S.H.B.G. (Sex Hormone Binding Globulin), which regulates the activity of sex hormones.

A high, animal-protein diet decreases S.H.B.G. and promotes "free" testosterone.

A low-fat/high-fiber diet is known to increase S.H.B.G.

 

[powersam]

1. Decrease testosterone production (low fat/high fiber diet, beta sitosterol, reducing cholesterol levels).


There is little evidence to suggest that this will help male pattern baldness in any way.

You lower testosterone, while increase S.H.B.G. (Sex Hormone Binding Globulin), which regulates the activity of sex hormones.

A high, animal-protein diet decreases S.H.B.G. and promotes "free" testosterone.

A low-fat/high-fiber diet is known to increase S.H.B.G.

Show me a study.

 

[OverMachoGrande]

1. Decrease testosterone production (low fat/high fiber diet, beta sitosterol, reducing cholesterol levels).


There is little evidence to suggest that this will help male pattern baldness in any way.

You lower testosterone, while increase S.H.B.G. (Sex Hormone Binding Globulin), which regulates the activity of sex hormones.

A high, animal-protein diet decreases S.H.B.G. and promotes "free" testosterone.

A low-fat/high-fiber diet is known to increase S.H.B.G.

Show me a study.

http://jcem.endojournals.org/cgi/conten ... t/85/1/293
Diet and Sex Hormone-Binding Globulin
C. Longcope, H. A. Feldman, J. B. McKinlay and A. B. Araujo
University of Massachusetts Medical School (C.L.), Worcester, Massachusetts 01655; and New England Research Institutes (H.A.F., J.B.M., A.B.A.), Watertown, Massachusetts 02172

Address all correspondence and requests for reprints to: Dr. C. Longcope, University of Massachusetts Medical School, Worcester, Massachusetts 01655.

The serum concentration of sex hormone-binding globulin (SHBG) is inversely related to weight and in animal studies is inversely related to protein intake. As SHBG can affect the biological activity of testosterone and estradiol, we wished to determine the role of protein intake on SHBG levels in men. Using data from the Massachusetts Male Aging Study we examined cross-sectional relationships between dietary components and SHBG levels in 1552 men (aged 40–70 yr) for whom these factors were known.

Analyzed by multiple regression, controlling for testosterone and estradiol levels, age (P < 0.001) and fiber intake (P = 0.02) were positively correlated to SHBG concentration, whereas body mass index (P < 0.001) and protein intake (P < 0.03) were negatively correlated to SHBG concentration. The intakes of calories, fat (animal or vegetable), and carbohydrate were not related to SHBG concentration. We conclude that age and body mass index are major determinants of SHBG concentrations in older men, and fiber and protein intake are also significant contributors to SHBG levels, but total caloric intake and the intake of carbohydrate or fat are not significant. Thus, diets low in protein in elderly men may lead to elevated SHBG levels and decreased testosterone bioactivity.

http://www.ajcn.org/cgi/content/full/84/6/1456
Long-term low-protein, low-calorie diet and endurance exercise modulate metabolic factors associated with cancer risk1,2,3
Luigi Fontana, Samuel Klein and John O Holloszy
1 From the Division of Geriatrics and Nutritional Science and the Center for Human Nutrition, Washington University School of Medicine, St Louis, MO (LF, SK, and JOH), and the Division of Food Science, Human Nutrition and Health, Istituto Superiore di Sanitá, Rome, Italy (LF)

2 Supported by Clinical Nutrition Research Unit grant DK56351, General Clinical Research Center grant RR00036, and Diabetes Research and Training Center grant DK20579.

3 Reprints not available. Address correspondence to L Fontana, Washington University School of Medicine, 4566 Scott Avenue, Campus Box 8113, St Louis, MO 63110. E-mail: lfontana@im.wustl.edu.

The data from the present study show that consuming a low-protein, low-calorie diet or participating in regular endurance exercise training is associated with a decrease in plasma factors that are linked with some types of cancer. Plasma concentrations of insulin, free sex hormones, and inflammatory markers were lower in subjects consuming a low-protein, low-calorie diet and in subjects who were endurance runners than in nonobese, sedentary subjects who were consuming typical Western diets. Moreover, subjects eating a low-protein, low-calorie diet had much lower plasma IGF-I concentrations and IGF-I:IGFBP-3 than did BMI-matched endurance runners, which suggests that dietary factors may provide additional protective effects, independent of body fat mass. These results help to identify potential mechanisms by which long-term lifestyle modifications in diet or physical activity can selectively reduce circulating factors that are associated with increased cancer risk.

Nutrient intake is a major regulator of circulating IGF-I, which promotes tumor development by stimulating cell proliferation and inhibiting cell death (10–12). Data from epidemiologic studies have shown an association between higher plasma IGF-I concentrations and a greater risk of breast (premenopausal), prostate, and colon cancers (13–16). In rodents, calorie restriction lowers plasma IGF-I concentrations and protects against carcinogenesis, which is reversed by infusing IGF-I (17). Data from several short-term studies conducted in healthy human subjects showed that short-term protein and energy restriction reduces plasma IGF-I concentrations (18, 19).

The results from our study suggest that the effect of protein and energy intakes on IGF-I is not transient and that long-term protein and calorie restriction can cause a chronic decrease in plasma IGF-I concentrations, independent of body fat mass. We found that protein and energy intake were both directly correlated with plasma IGF-I concentrations in sedentary volunteers eating Western diets. Moreover, plasma IGF-I concentrations were lower in our low-protein, low-calorie diet group (9% of calories from protein) than in our lean distance runners and our sedentary control group (16% of calories from protein). The mechanism or mechanisms responsible for the relation between the intake of protein rich in essential amino acids, the intake of calories, and IGF-I that has been shown in other cross-sectional studies (20, 21) is not known, but both decreased IGF-I production and increased clearance may be involved. Decreased dietary protein intake correlates with reduced steady-state concentrations of hepatic IGF-I mRNA (22) and increased clearance of serum IGF-I (23).

Data from epidemiologic studies indicate that obesity is a risk factor for several types of cancer, including colon, breast, endometrial, kidney, and pancreas cancer (1). Increased adipose tissue may be involved in the pathogenesis of specific cancers, because of adipokine production, insulin resistance, hyperinsulinemia, and chronic inflammation (1, 3, 4, 24–27). In addition, higher circulating concentrations of endogenous sex hormones (including estradiol, testosterone, and DHEA) and low plasma SHBG concentrations are associated with an increased risk of breast and endometrial cancers (28–30), possibly because free estrogens and androgens are strong mitogens for mammary cells and stimulate the development and growth of breast tumors (31). We found that our subjects consuming a low-protein, low-calorie diet or performing regular endurance exercise had lower body fat mass and alterations in metabolic factors associated with decreased body fat, including lower plasma concentrations of insulin, leptin, and CRP and greater insulin sensitivity than did nonobese sedentary men and women consuming a Western diet. In addition, our lean subjects had higher plasma SHBG concentrations, which decrease the proportion of free sex hormones (32), than did the sedentary men and women consuming a Western diet. Therefore, the mechanism responsible for the beneficial relation between a low-protein, low-calorie diet or exercise training and these metabolic factors associated with cancer may be related to the effect of reduced calorie intake or increases in energy expenditure on body fat mass.

 

[powersam]

I meant one that shows this affecting hairloss.

 

[OverMachoGrande]

...

 

[OverMachoGrande]

Research into it yourself...Put the pecies together!

I showed you two studies that show diets effect on not only S.H.B.G. but also IGF-1, both of which, are, in my opinion, two huge factors in M.P.B.

 

[powersam]

Research into it yourself...Put the pecies together!

I showed you two studies that show diets effect on not only S.H.B.G. but also IGF-1, both of which, are, in my opinion, two huge factors in M.P.B.

In your opinion.

Show me something that actually prove that they are more than minor factors (at best).

 

[Bryan]

Research into it yourself...Put the pecies together!

I showed you two studies that show diets effect on not only S.H.B.G. but also IGF-1, both of which, are, in my opinion, two huge factors in M.P.B.

In your opinion.

Show me something that actually prove that they are more than minor factors (at best).

We're going to be waiting a long, long, LOOOOONG time for him to show us that they have even a measurable effect on hair!

 

[powersam]

Research into it yourself...Put the pecies together!

I showed you two studies that show diets effect on not only S.H.B.G. but also IGF-1, both of which, are, in my opinion, two huge factors in M.P.B.

In your opinion.

Show me something that actually prove that they are more than minor factors (at best).

We're going to be waiting a long, long, LOOOOONG time for him to show us that they have even a measurable effect on hair!

That's what I thought.

Oddly enough we are still waiting.

 

[abcdefg]

Does high estrogen actually cause gyno or how exactly does that work? What causes a man to get gyno? Its pretty clear science has a LOT to still figure out. It seems for every answer there are 10 more questions you could ask that have no answers.

 

[vauxall]

It seems for every answer there are 10 more questions you could ask that have no answers.

Yes, for example: is that really Sarah Palin in "that bikini"?

 

[powersam]

Does high estrogen actually cause gyno or how exactly does that work? What causes a man to get gyno? Its pretty clear science has a LOT to still figure out. It seems for every answer there are 10 more questions you could ask that have no answers.

Yes science does have a lot to figure out. Cold fusion, gene splicing, how to make out while doing it doggy style, the list goes on.

But yeah, b**ch titties is high on the list.

 

[docj077]

Br J Dermatol. 2009 Jun;160(6):1157-62. Epub 2009 Mar 26. Linksl-Ascorbic acid 2-phosphate promotes elongation of hair shafts via the secretion of insulin-like growth factor-1 from dermal papilla cells through phosphatidylinositol 3-kinase.
Kwack MH, Shin SH, Kim SR, Im SU, Han IS, Kim MK, Kim JC, Sung YK.
Department of Immunology, Kyungpook National University, Daegu, Korea.

BACKGROUND: l-Ascorbic acid 2-phosphate (Asc 2-P), a derivative of l-ascorbic acid, promotes elongation of hair shafts in cultured human hair follicles and induces hair growth in mice. OBJECTIVES: To investigate whether the promotion of hair growth by Asc 2-P is mediated by insulin-like growth factor-1 (IGF-1) and, if so, to investigate the mechanism of the Asc 2-P-induced IGF-1 expression. METHODS: Dermal papilla (DP) cells were cultured and IGF-1 level was measured by reverse transcription-polymerase chain reaction and enzyme-linked immunosorbent assay after Asc 2-P treatment in the absence or presence of LY294002, a phosphatidylinositol 3-kinase (PI3K) inhibitor. Also, hair shaft elongation in cultured human scalp hair follicles and proliferation of cocultured keratinocytes were examined after Asc 2-P treatment in the absence or presence of neutralizing antibody against IGF-1. In addition, keratinocyte proliferation in cultured hair follicles after Asc 2-P treatment in the absence or presence of LY294002 was examined by Ki-67 immunostaining. RESULTS: IGF-1 mRNA in DP cells was upregulated and IGF-1 protein in the conditioned medium of DP cells was significantly increased after treatment with Asc 2-P. Immunohistochemical staining showed that IGF-1 staining is increased in the DP of cultured human hair follicles by Asc 2-P. The neutralizing antibody against IGF-1 significantly suppressed the Asc 2-P-mediated elongation of hair shafts in hair follicle organ culture and significantly attenuated Asc 2-P-induced growth of cocultured keratinocytes. LY294002 significantly attenuated Asc 2-P-inducible IGF-1 expression and proliferation of follicular keratinocytes in cultured hair follicles. CONCLUSIONS: These data show that Asc 2-P-inducible IGF-1 from DP cells promotes proliferation of follicular keratinocytes and stimulates hair follicle growth in vitro via PI3K.

1: Growth Horm IGF Res. 2008 Aug;18(4):335-44. Epub 2008 Mar 5. LinksEffect of topical application of raspberry ketone on dermal production of insulin-like growth factor-I in mice and on hair growth and skin elasticity in humans.
Harada N, Okajima K, Narimatsu N, Kurihara H, Nakagata N.
Department of Translational Medical Science Research, Nagoya City University Graduate School of Medical Sciences, Kawasumi 1, Mizuho-cho, Mizuho-ku, Nagoya 467-8601, Japan.

Sensory neurons release calcitonin gene-related peptide (CGRP) on activation. We recently reported that topical application of capsaicin increases facial skin elasticity and promotes hair growth by increasing dermal insulin-like growth factor-I (IGF-I) production through activation of sensory neurons in mice and humans. Raspberry ketone (RK), a major aromatic compound contained in red raspberries (Rubus idaeus), has a structure similar to that of capsaicin. Thus, it is possible that RK activates sensory neurons, thereby increasing skin elasticity and promoting hair growth by increasing dermal IGF-I production. In the present study, we examined this possibility in mice and humans. RK, at concentrations higher than 1 microM, significantly increased CGRP release from dorsal root ganglion neurons (DRG) isolated from wild-type (WT) mice and this increase was completely reversed by capsazepine, an inhibitor of vanilloid receptor-1 activation. Topical application of 0.01% RK increased dermal IGF-I levels at 30 min after application in WT mice, but not in CGRP-knockout mice. Topical application of 0.01% RK increased immunohistochemical expression of IGF-I at dermal papillae in hair follicles and promoted hair re-growth in WT mice at 4 weeks after the application. When applied topically to the scalp and facial skin, 0.01% RK promoted hair growth in 50.0% of humans with alopecia (n=10) at 5 months after application and increased cheek skin elasticity at 2 weeks after application in 5 females (p<0.04). These observations strongly suggest that RK might increase dermal IGF-I production through sensory neuron activation, thereby promoting hair growth and increasing skin elasticity.

Am J Pathol. 2008 Nov;173(5):1295-310. Epub 2008 Oct 2. LinksOverexpression of mIGF-1 in keratinocytes improves wound healing and accelerates hair follicle formation and cycling in mice.
Semenova E, Koegel H, Hasse S, Klatte JE, Slonimsky E, Bilbao D, Paus R, Werner S, Rosenthal N.
European Molecular Biology Laboratory (EMBL)-Mouse Biology Unit, Campus A. Buzzati-Traverso, Monterotondo-Scalo, Roma, Italy. ekat@embl.it

Insulin-like growth factor 1 (IGF-1) is an important regulator of growth, survival, and differentiation in many tissues. It is produced in several isoforms that differ in their N-terminal signal peptide and C-terminal extension peptide. The locally acting isoform of IGF-1 (mIGF-1) was previously shown to enhance the regeneration of both muscle and heart. In this study, we tested the therapeutic potential of mIGF-1 in the skin by generating a transgenic mouse model in which mIGF-1 expression is driven by the keratin 14 promoter. IGF-1 levels were unchanged in the sera of hemizygous K14/mIGF-1 transgenic animals whose growth was unaffected. A skin analysis of young animals revealed normal architecture and thickness as well as proper expression of differentiation and proliferation markers. No malignant tumors were formed. Normal homeostasis of the putative stem cell compartment was also maintained. Healing of full-thickness excisional wounds was accelerated because of increased proliferation and migration of keratinocytes, whereas inflammation, granulation tissue formation, and scarring were not obviously affected. In addition, mIGF-1 promoted late hair follicle morphogenesis and cycling. To our knowledge, this is the first work to characterize the simultaneous, stimulatory effect of IGF-1 delivery to keratinocytes on two types of regeneration processes within a single mouse model. Our analysis supports the use of mIGF-1 for skin and hair regeneration and describes a potential cell type-restricted action.

 

[DHTHater]

Don't get the point of the french thing in relevance to this discussion,but ok. I'd have to say advantage brian here. He has cited the sources for his findings and disproved the mice thing. He might b**ch but he backs up his evidence.

Unfortunately, Bryan's sources are often mystical ones no one else seems privy to, or are conveniently not online for anyone else to substantiate. While I've found some of the things Bryan says to be universally accepted as true (he seems populist enough with the big 3 etc), and he does seem to show interest in some alternative anti-male pattern baldness compounds that have shown empirical and clinical efficacy (e.g. RU58841, and Topical Green Tea Extract for example),he often tries to refute and debunk things extending further than the evidence supports his argument. It's as if he argues for the sake of argument and in the heat of debate, forgets he doesn't actually have proof to back his claims. When the person he's debating points this out, he too often cites his obscure, outmoded sources that can't be linked.