Theory: Cooked Fat =DHT(Dihydrotestosterone) Baldness

[docj077]

This thread is getting out of control.

As I mentioned in the other thread on SHBG, there is no possible way that increased concentrations of SHBG will benefit a man suffering from male pattern baldness long term. Increased SHBG will simply cause the body to produce more testosterone to keep the amount of free testosterone in the body at a constant level. There is a feedback mechanism that governs this process.

In order for this to work, you'd have to put a man on a calorie and carbohydrate restricted diet along with vigorous cardio workouts for a few months to get any hyperinsulinemia under control. That would increase your SHBG...hopefully. Unfortunately, that will also increase our levels of testosterone. This interaction has actually been proven in men taking green tea alone or soy alone, but when you take them together SHBG will go up and 5AR will be inhibited 70%, I believe. Now, the second step of this process would either be 5AR inhibition, androgen receptor antagonism, or steriod synthesis downregulation. Dutasteride or finasteride for the first, flutamide for the second, and something like ketoconazole for the third. A low dose of a drug that inhibits steriod synthesis is probably the way to go if testosterone really increases as much people in this thread says it does.

We could do this, but it would take a far larger committment than simply popping a pill everyday. You'd have to work your *** off for a long time to see results. Also, if you found a doctor that would be willing to help you, you'd be a very lucky man.

 

[DammitLetMeIn]

This thread is getting out of control.

As I mentioned in the other thread on SHBG, there is no possible way that increased concentrations of SHBG will benefit a man suffering from male pattern baldness long term. Increased SHBG will simply cause the body to produce more testosterone to keep the amount of free testosterone in the body at a constant level. There is a feedback mechanism that governs this process.

If this is true, then why:

'Subjects consuming vegetarian diets have demonstrated higher SHBG levels (3, 13), lower T levels (12), and lower levels of available T (3).'

(3) Belanger A, A Locong, C Noel, et al. Influence of diet on plasma steroid and sex plasma binding globulin levels in adult men. Journal of Steroid Biochemistry. 32(6): 829-833, 1989.

(13) Key TJA, L Roe, M Thorogood, et al. British Journal of Nutrition. 64:111-119, 1990.

(12) Howie BJ & TD Shultz. Dietary and hormonal vegetarian Seventh-Day Adventists and nonvegetarian men. American Journal of Clinical Nutrition. 42: 127-134, 1985 July.

And:

Dietary intakes were recorded and plasma androgens and sex-hormone-binding globulin (SHBG) binding capacity were determined. Androstenedione (A), testosterone (T), free T (FT), and SHBG were higher in omnivores than in vegetarians.

http://www.ncbi.nlm.nih.gov/entrez/quer ... t=Abstract

And:

A study published in the Journal of Obstetrics and Gynecology in 2000 provided evidence that choosing low-fat vegetarian meals for as little as two months normalized mentrual irregularities. This study reported that a low-fat vegetarian menu was associated with increased serum sex-hormone binding globulin (SHBG) concentration. SHBG is important for clearing excess estrogens or progesterones and, as such, increasing SHBG levels helps restore hormonal balance.




These studies (the first two) suggest that free testosterone doesn't stay at a constant level and that your body will not always revert to a specific level of Free T regardless of the level of SHBG.

In fact it seems if you want lower free T and higher SHBG, one should adopt a Vegetarian diet.

This is from a cancer doctor Neil D. Barnard M.D.:

By the way, the enzyme (5-alphareductase) that turns testosterone into DHT is also found in the scalp,9 where it works mischief of a different sort. DHT plays a critical role in baldness. Without it, men will not lose their hair, no matter what their genetics may dictate. DHT activity in the scalp may be subject to dietary manipulation.

http://www.cancerproject.org/survival/c ... health.php


But make no mistake that achieving the desired DHT level is paramount because I was reading that DHT is 7 times more analbolic than regular testosterone.

 

[DammitLetMeIn]

You guys might also want to consider thisL:

Your Prostate Would Rather Be a Vegetarian

Changing your eating habits can help prevent prostate problems. The reason is not hard to imagine. The prostate is under hormonal control. In the prostate cells, testosterone is turned into a powerful hormone called DHT (dihydrotestosterone), and DHT is what drives prostate enlargement. This is the conversion that finasteride blocks.
Foods can strongly influence sex hormones, including testosterone. Could it be that cutting out meats and dairy products and adding more vegetables to our plate could turn down the hormonal stimulation of the prostate and prevent prostate problems? That is, in fact, exactly what researchers have found. Daily meat consumption triples the risk of prostate enlargement. Regular milk consumption doubles the risk and failing to consume vegetables regularly nearly quadruples the risk.7 Prostate hyperplasia is reportedly increasing in Asian countries, paralleling the westernization of the diet that has occurred in recent decades.8

The meat-based diet that has become routine in Western countries and is now spreading to other parts of the world encourages many hormone-related conditions, and prostate enlargement is no exception. Even if you grew up as a meat eater, your prostate would rather be a vegetarian.

By the way, the enzyme that turns testosterone into DHT (5-alphareductase) is also found in the scalp,9 where it works mischief of a different sort. DHT plays a critical role in baldness. Without it, men will not lose their hair, no matter what their genetics may dictate. DHT activity in the scalp may be subject to dietary manipulation.

http://www.gan.ca/lifestyle/vegetarian+ ... ms.en.html

 

[DammitLetMeIn]

In order for this to work, you'd have to put a man on a calorie and carbohydrate restricted diet along with vigorous cardio workouts for a few months to get any hyperinsulinemia under control. That would increase your SHBG...hopefully. Unfortunately, that will also increase our levels of testosterone.

The vegetarian studies indicate that testosterone wouldn't necessarily increase.

That is not to say I'm advocating vegetarianism. Just pointing out that a change in diet can increase SHBG as without increasing testosterone.

That all said, it is the levels of DHT which are crucial. However, I don't think levels of DHT in vegetarians are higher, are they?

Also vegetarians could create low SHBG by eating high grain diet so merely eating a vegetarian diet is not fool-proof. IT would seem that it has to be a low GI vegetarian diet.

How would this impact upon male pattern baldness? Well, free T would be lower, SHBG would be higher. DHT - I don't know..but I'm thinking they're lower too because anti-prostate diets are vegetarian.

thoughts?

 

[docj077]

This the latest study that I could find dealing with the relationship between hormones, SHBG, insulin problems, and obesity.

The bolded parts are the most important aspects of the study. The study is small, but it has multiple test groups.

In this study, both the concentration of SHBG and the concentration of testosterone decrease as the population moved more towards having higher BMIs and having what science would consider to be increased insulin resistance.

So, what this thread has been arguing (low SHBG is associated with high testosterone) is actually found to be reversed in larger studies. Insulin resistance may be associated with decreased SHBG, but it is also correlated with decreased testosterone concentrations. The feedback mechanism is in place in "normal individuals" just as it should be. The only way this system could cause male pattern baldness is not if hormones are "out of balance", but if there is a genetic defect in the feedback mechanism.

This study is very new, so the sampling and testing techniques used are highly up to date and the results should be trusted above anything that has been done in this area prior to the 21st century.




Arch Androl. 2006 Sep-Oct;52(5):355-61. Links
Relationship between BMI, total testosterone, sex hormone-binding-globulin, leptin, insulin and insulin resistance in obese men.Osuna JA, Gomez-Perez R, Arata-Bellabarba G, Villaroel V.
Unidad de Endocrinologia, Instituto Autonomo Hospital Universitario de Los Andes, Laboratorio de Andrologia, Centro de Microscopia Electronica, Escuela de Medicina, Universidad de Los Andes, Merida, Venezuela. [email protected]

The objective of this work was to evaluate the relationship between sex steroid hormones, sex hormone-binding-globulin, leptin, insulin and insulin resistance in obese men. Anthropometrical indexes, total testosterone (Tt), free testosterone (fT), estradiol (E), sex hormone-binding-globulin (SHBG), glucemia, insulin and leptin were measured in 77 men, with ages between 20 and 60 years. According to their body mass index (BMI), subjects were grouped into three categories: normal body weight (<24> 30 kg/m2). Insulin resistance index was obtained by the homeostasis assessment model for insulin resistance (HOMA-IR). Total testosterone and SHBG concentrations were lower in the obese group compared with normal and overweight subjects (p < 0.05). The mean insulin concentration was significantly higher in the obese group compared with the other groups (p < 0.05). T was negatively correlated with the BMI (r = -0.447; p < .01), WC (r = -0.464); p < .01, leptin (r = -0.382; p < .01), insulin (r = -0.391; p < 0.01) and also with the HOMA-IR (r = -0.416; p < 0.01). The SHBG negatively and significantly correlated with BMI (r = -0.334; p < 0.01) and WC index (= -0.322; p < 0.01), as well with insulin levels (r = -0.313; p < 0.01) and insulin resistance (= -0.266; p < 0.05). Our results shows that in a sample of men, Tt and SHBG concentrations proportionally diminished with both the increase of BMI and insulin resistance index.

PMID: 16873135 [PubMed - indexed for MEDLINE]


Until the defect is discovered, there is no point arguing this problem. It can not be fixed through diet if there is a defect that prevents adequate feedback inhibition.

 

[DammitLetMeIn]

So, what this thread has been arguing (low SHBG is associated with high testosterone) is actually found to be reversed in larger studies..

Not actually higher testosterone levels, but higher levels of BIOACTIVE (unbound) testosterone. the testosterone level could conceivably remain the same.

That said, when insulin is high, a man gets obese and yes, testosterone should decrease.

Insulin resistance may be associated with decreased SHBG, but it is also correlated with decreased testosterone concentrations

Okkkk....

The feedback mechanism is in place in "normal individuals" just as it should be...

Imo the feedback mechanism when this happens is for the body to produce DHT. Which is why DHT is elevated in older men who tend to have lower overall testosterone levels and high insulin.

The only way this system could cause male pattern baldness is not if hormones are "out of balance", but if there is a genetic defect in the feedback mechanism. ...

I agree the body seeks to return as best it can to normal levels. I don't feel that this is always possible but do feel that the body will always strive to make it so. The production of DHT is one way in which it does this.

DHT is seven times more anabolic than normal testosterone so this would be the easiest way for the body to make sure you're still a man. that is, still able to reproduce.

Until the defect is discovered, there is no point arguing this problem. It can not be fixed through diet if there is a defect that prevents adequate feedback inhibition.

Ok I see what you mean now, however, it is the BIOACTIVITY of the testosterone which is important NOT the overall level of T.

ITs the Free T available which is the crucial factor. And whilst testosterone does decrease, there is STILL LESS Free T available to act on tissues.

This is where the power of DHT comes into play.

In that way, more of that diminished supply of Free T is converted to DHT because this is its most effecient way to exert the androgen effects.

 

[DammitLetMeIn]

Your study shows that the idea of low SHBG means more testosterone acting on tissues is inaccurate.

I accept this.

However, levels of FREE TESTOSTERONE (i.e. what really matters) ARE LOWER in obese individuals despite the high insulin/lower SHBG.

So the best way for the body to use androgens is to make more DHT from less FREE Testosterone because it is 7 times more anabolic than regular T.

So what I'm saying is crucially, a greater percentage of the Free T is converted to DHT in individuals with high insulin.

Thats where the male pattern baldness comes in.

(Indeed, there are some studies which show that abdominal obesity (insulin resistance) increases production of DHT 10 times in the body so any level of insulin resistance is potentially dangerous for DHT levels rising and consequent male pattern baldness).


Some info:

The paradox here is that obese men are hypoandrogenic (low testosterone and DHEA levels) and hyperestrogenic compared to lean men. One possible explanation may lie in their high DHT/T ratio: though their testosterone is low, their "strong testosterone," or dihydrotestosterone (DHT), the stimulator of prostate growth, is relatively high. We see the same situation develop simply with aging: the ratio of DHT to testosterone increases, and so does central obesity ("the bigger the belly, the lower the testosterone").

http://www.antiaging.com/cyberhealth/CyberHealth_3.htm

 

[docj077]

Just so that we're clear on the this here is a study involving 452 men. 73 of the men had metabolic syndrome. Once again, low SHBG is associated with low testosterone in men with metabolic syndrome. The very definition of metabolic syndrome includes insulin resistance.


So, all that you have to prove now is that low testosterone in men with insulin resistance is associated with high DHT and male pattern baldness.


J Am Geriatr Soc. 2006 Dec;54(12):1832-8. Links
Association between hormones and metabolic syndrome in older Italian men.Maggio M, Lauretani F, Ceda GP, Bandinelli S, Basaria S, Ble A, Egan J, Paolisso G, Najjar S, Jeffrey Metter E, Valenti G, Guralnik JM, Ferrucci L.
Clinical Research Branch, National Institute on Aging, Baltimore, Maryland 21225, USA. [email protected]

OBJECTIVES: To determine whether low levels of testosterone, sex hormone binding globulin (SHBG), insulin-like growth factor-1 (IGF-1), and dehydroepiandrosterone sulfate (DHEAS) and high levels of cortisol and leptin would be associated with metabolic syndrome (MS). DESIGN: Cross-sectional. SETTING: Population-based sample of older Italian men. PARTICIPANTS: Four hundred fifty-two men aged 65 and older enrolled in the Invecchiare in Chianti (InCHIANTI) study. MEASUREMENTS: Complete data on testosterone, cortisol, DHEAS, SHBG, fasting insulin, IGF-1 and leptin. MS was defined according to Adult Treatment Panel III criteria. RESULTS: MS was present in 73 men (15.8% of the sample). After adjusting for confounders, total testosterone (P < .05) and log (SHBG) (P < .001) were inversely associated, whereas log (leptin) was positively associated with MS (P < .001). Independent of age, log (SHBG) was positively associated with high-density lipoprotein cholesterol (P < .05) and negatively associated with abdominal obesity (P < .001) and triglycerides (P < .001). Log (leptin) was significantly associated with each component of MS. Cortisol, DHEAS, free and bioavailable testosterone, and IGF-1 were not associated with MS. Having three or more hormones in the lower (for hormones lower in MS) or the upper (for hormones higher in MS) quartile was associated with three times the risk of being affected by MS (odds ratio = 2.8, 95% confidence interval = 1.3-6.9) (P = .005), compared with not having this condition. CONCLUSION: Total testosterone and SHBG are negatively and leptin is positively associated with MS in older men. Whether specific patterns of hormonal dysregulation predict the development of MS should be tested in longitudinal studies.




Also note that this study deals with TOTAL testosterone and not FREE testosterone.


Something else to consider as you're researching this is that older men go through andropause and their levels of testosterone begin to decrease. When this happens their levels of LH and FSH begin to increase similar to a post-menopausal woman. This means that for both men and women the negative feedback mechanism that testosterone normally utilizes to prevent pituitary hormone excretion is no longer in place. Since DHT and testosterone both negatively feedback the pituitary and DHT is the "stronger" hormone there really isn't anyway that the potency of androgens remains the same into old age. It just isn't possible whether there is an increase in DHT or not.

 

[DammitLetMeIn]

So, all that you have to prove now is that low testosterone in men with insulin resistance is associated with high DHT and male pattern baldness.

It would seem that IGF-1 increases/regulates 5ar activity:

http://www.ihop-net.org/UniPub/iHOP/pm/ ... id=8344190

http://endo.endojournals.org/cgi/conten ... 447?ck=nck

IGF-1 higher on balding:

http://www.ncbi.nlm.nih.gov/entrez/quer ... t=Abstract

IGF-1 & balding (2):

http://www.ncbi.nlm.nih.gov/entrez/quer ... t=Abstract

Furthermore:

'Human hair follicles are targets of sex steroids. In particular, androgens induce regression of terminal (large) hair during the development of male-pattern baldness and transform vellus (small) hair to terminal hair in genital skin during puberty.[55] These effects may be associated with high levels of circulating IGF-1 [56] which directly stimulates the activity of the androgen receptor.[57] It is also possible that IGF-1 stimulates the activity of 5-reductase in the skin which increases the local production of dihydrotestosterone converted from testosterone.'[58]

57. Culig Z, Hobisch A, Cronauer MV, radmayr C, Trapman J, Hittmair A, Bartsch G, Klocker H: Androgen receptor activation in prostatic tumor cell lines by insulin-like growth factor-I, keratinocyte growth factor, and epidermal growth factor. Cancer Res 1994;54:5474-8.

58. Horton R, Pasupuletti V, Antonipillai I: Androgen induction of steroid 5 alpha-reductase may be mediated via insulin-like growth factor-I. Endocrinol 1993;133:447-51.


'In summary, regulation of human hair growth by androgen is probably mediated by IGF-1 in the dermal papilla. In male scalp, high levels of IGF-1 may increase the androgen receptor activity and dihydrotestosterone levels and these result in an increased propensity for baldness.'

http://dermatology.cdlib.org/DOJvol5num ... ws/su.html

Baldness & Prostate cancer:

'Our analysis suggests a positive association between prostate cancer and vertex baldness'

'IGF-1 can lead to aberrant activation of the Androgen Receptors'

'The association between T (and IGF-1) and Androgenetic Alopecia was also found in a cross-sectional study'

'analyses of this cohort study have shown positive associations between IGF-1 and prostate cancer'

'Aberrant activation of the Androgen Receptors has been demonstrated in vitro with IGF-1, keratinocyte growth factor, and epidermal growth factor. These agents can directly activate the Androgen Receptors in the absence of androgens and may contribute to the progression of prostate cancer and AA (43 , 44) .

http://cebp.aacrjournals.org/cgi/conten ... /6/549#B13

Also, as levels of Testosterone/Free T decrease with age, DHT increases:

http://www.lef.org/magazine/mag2002/aug ... st_01.html

^
this would correlate with rising insulin as insulin rises as we get older



Moreover, the diet advocated for prostate cancer (associated with higher 5ar activity) based on clinical evidence is thus:

Since there have been no clinical trails on the use of diet alone in the treatment of BPH, the following diet recommendations are based mostly on clinical experience. The diet should be high in protein, low in carbohydrate, low in animal fats, and high in essential fatty acids. Focus on whole, unprocessed foods (legumes, vegetables, fruits, nuts, and seeds).

http://www.drlam.com/A3R_brief_in_doc_f ... lesome.cfm

High Fibre, Low Fat diet lowers serum androgens incl DHT:

http://jcem.endojournals.org/cgi/conten ... 004-1530v1


This diet is said to have a decrease in 5ar activity. Excess dietary fat is proven to increase 5ar activity. Of particular note about this advice is that carbohydrates are low and consequently insulin will not be as high, and neither will IGF-1.


To conclude, whilst I am aware that IGF-1 is necessary to hair growth, overproduction of IGF-1 causes 5ar activity to increase and excess DHT production and thereby baldness.

 

[docj077]

So, all that you have to prove now is that low testosterone in men with insulin resistance is associated with high DHT and male pattern baldness.

It would seem that IGF-1 increases/regulates 5ar activity:

http://www.ihop-net.org/UniPub/iHOP/pm/ ... id=8344190

http://endo.endojournals.org/cgi/conten ... 447?ck=nck

IGF-1 higher on balding:

http://www.ncbi.nlm.nih.gov/entrez/quer ... t=Abstract

IGF-1 & balding (2):

http://www.ncbi.nlm.nih.gov/entrez/quer ... t=Abstract

Furthermore:

'Human hair follicles are targets of sex steroids. In particular, androgens induce regression of terminal (large) hair during the development of male-pattern baldness and transform vellus (small) hair to terminal hair in genital skin during puberty.[55] These effects may be associated with high levels of circulating IGF-1 [56] which directly stimulates the activity of the androgen receptor.[57] It is also possible that IGF-1 stimulates the activity of 5-reductase in the skin which increases the local production of dihydrotestosterone converted from testosterone.'[58]

57. Culig Z, Hobisch A, Cronauer MV, radmayr C, Trapman J, Hittmair A, Bartsch G, Klocker H: Androgen receptor activation in prostatic tumor cell lines by insulin-like growth factor-I, keratinocyte growth factor, and epidermal growth factor. Cancer Res 1994;54:5474-8.

58. Horton R, Pasupuletti V, Antonipillai I: Androgen induction of steroid 5 alpha-reductase may be mediated via insulin-like growth factor-I. Endocrinol 1993;133:447-51.


'In summary, regulation of human hair growth by androgen is probably mediated by IGF-1 in the dermal papilla. In male scalp, high levels of IGF-1 may increase the androgen receptor activity and dihydrotestosterone levels and these result in an increased propensity for baldness.'

http://dermatology.cdlib.org/DOJvol5num ... ws/su.html

Baldness & Prostate cancer:

'Our analysis suggests a positive association between prostate cancer and vertex baldness'

http://cebp.aacrjournals.org/cgi/conten ... /6/549#B13

Also, as levels of Testosterone/Free T decrease with age, DHT increases:

http://www.lef.org/magazine/mag2002/aug ... st_01.html

^
this would correlate with rising insulin as insulin rises as we get older



Moreover, the diet advocated for prostate cancer (associated with higher 5ar activity) based on clinical evidence is thus:

Since there have been no clinical trails on the use of diet alone in the treatment of BPH, the following diet recommendations are based mostly on clinical experience. The diet should be high in protein, low in carbohydrate, low in animal fats, and high in essential fatty acids. Focus on whole, unprocessed foods (legumes, vegetables, fruits, nuts, and seeds).

http://www.drlam.com/A3R_brief_in_doc_f ... lesome.cfm

High Fibre, Low Fat diet lowers serum androgens incl DHT:

http://jcem.endojournals.org/cgi/conten ... 004-1530v1


This diet is said to have a decrease in 5ar activity. Excess dietary fat is proven to increase 5ar activity. Of particular note about this advice is that carbohydrates are low.


To conclude, whilst I am aware that IGF-1 is necessary to hair growth, overproduction of IGF-1 causes 5ar activity to increase and excess DHT production and thereby baldness.

You went through and posted a lot of stuff. Unfortunately, you also proved that the point you're trying make regarding diet and its possible effects on male pattern baldness is invalid.

What the last article you posted regards as significant is really not significant at all with regards to stopping or even reversing male pattern baldness. It's only significant in terms of androgen concentration reduction.

They said:

"We conclude that reduction in dietary fat intake (and increase in fiber) results in 12% consistent lowering of circulating androgens levels without changing the clearance."

Lowering circulating androgens by 12% is nothing compared to the physiological effects of drugs like finasteride or dutasteride. They inhibit the 5AR enzymes so much that circulating levels of DHT can be reduced anywhere from 65-94%.

Not only are the above values important, but those are the values that are required for many men to simply maintain the hair they have. Not every man on propecia regrows their hair. So, somewhere between 65% and 94% inhibition is the magic serum DHT concentration that allows hair follicles to overcome the potent effects of DHT just enough to keep growing in the presence of pro-growth factors like IGF-1.

Like I said, your theory is a bad theory, because you not only think that diet seems to be the key environmental factor in male pattern baldness, but you also think that changing diet can lower circulating hormone levels enough to make a difference. Diet can not and will not influence the potency of DHT or the amount of DHT enough to have an impact on male pattern baldness.

A 12% reduction in androgen levels is not the same as 65% reduction in the most potent androgen in the male body through the use of propecia. They are not equivalent. In fact, the are not even close.

 

[DammitLetMeIn]

You focused on totally the wrong piece of evidence.

Focus not on the androgens but on the fact that high IGF-1 stimulates
5-alpha reductase activity.

THEN, get back to me.


Actually, the last article was the least relevant article of the whole post and was only included to show that diet can have an effect of androgens.

But what is more significant is diets effect on IGF-1.


Focus in particular on this part of the post:

Baldness & Prostate cancer:

'Our analysis suggests a positive association between prostate cancer and vertex baldness'

'IGF-1 can lead to aberrant activation of the Androgen Receptors'

'The association between T (and IGF-1) and Androgenetic Alopecia was also found in a cross-sectional study'

'analyses of this cohort study have shown positive associations between IGF-1 and prostate cancer'

'Aberrant activation of the Androgen Receptors has been demonstrated in vitro with IGF-1, keratinocyte growth factor, and epidermal growth factor. These agents can directly activate the Androgen Receptors in the absence of androgens and may contribute to the progression of prostate cancer and AA (43 , 44) .

http://cebp.aacrjournals.org/cgi/conten ... /6/549#B13


Even Gabe Mirkin M.D. can see it perfectly clearly:

http://www.drmirkin.com/men/M119.htm

 

[DammitLetMeIn]

Like I said, your theory is a bad theory, because you not only think that diet seems to be the key environmental factor in male pattern baldness

It is the key enviromental factor because it raises levels of IGF-1 too high.

but you also think that changing diet can lower circulating hormone levels enough to make a difference.

That wasn't the intention of the post. I probably shouldn't have included that study because you have for some reason chosen to focus on it rather than the rest of the post which is actually relevant.

Diet can not and will not influence the potency of DHT or the amount of DHT enough to have an impact on male pattern baldness.

Is this opinion? Because the science is all there to show that raised IGF-1 levels activate the 5ar enzyme. IGF-1 is raised by diet and insulin levels.

A 12% reduction in androgen levels is not the same as 65% reduction in the most potent androgen in the male body through the use of propecia. They are not equivalent. In fact, the are not even close.

I agree. But returning IGF-1 to its normal level is even better than a 65% reduction in DHT.

Moreover, it won't have anything working against it like Finisteride does with IGF-1.

 

[docj077]

Like I said, your theory is a bad theory, because you not only think that diet seems to be the key environmental factor in male pattern baldness

It is the key enviromental factor because it raises levels of IGF-1 too high.

but you also think that changing diet can lower circulating hormone levels enough to make a difference.

That wasn't the intention of the post. I probably shouldn't have included that study because you have for some reason chosen to focus on it rather than the rest of the post which is actually relevant.

Diet can not and will not influence the potency of DHT or the amount of DHT enough to have an impact on male pattern baldness.

Is this opinion? Because the science is all there to show that raised IGF-1 levels activate the 5ar enzyme. IGF-1 is raised by diet and insulin levels.

A 12% reduction in androgen levels is not the same as 65% reduction in the most potent androgen in the male body through the use of propecia. They are not equivalent. In fact, the are not even close.

I agree. But returning IGF-1 to its normal level is even better than a 65% reduction in DHT.

Moreover, it won't have anything working against it like Finisteride does with IGF-1.

I can only pray that you know that continued use of finasteride is associated with increased concentrations IGF-1 in the hair follicle and people regrow hair with finasteride. IGF-1 is a pro-growth molecule in the hair follicle. IGF-1 controls hair patterning. It doesn't necessarily cause hair loss.

And, no, returning IGF-1 levels to normal is NOT better than a 65% reduction in DHT.

If you think that this is true, then post a study that shows that reducing circulating levels of IGF-1 is equivalent to a 65% reduction in the level of circulating levels of DHT with hair counts and all necessary studies that are needed to prove that such a change increases hair growth, hair density and counts.

As for this:

"Is this opinion? Because the science is all there to show that raised IGF-1 levels activate the 5ar enzyme. IGF-1 is raised by diet and insulin levels."

The science is there to prove that IGF-1 activates the 5AR enzyme in fibroblasts contained within scrotal skin. Try again. I know a little anatomy and I can tell you that your scrotum just happens to not be on your scalp.

Lastly, you need to not post information from non-reputable websites. You're doing it again.

 

[DammitLetMeIn]

I can only pray that you know that continued use of finasteride is associated with increased concentrations IGF-1 in the hair follicle and people regrow hair with finasteride..

I was aware of this. But theres a bigger picture. They are regrowing it from the reduction of DHT which is no longer attaching to follicles.

IGF-1 is a pro-growth molecule in the hair follicle. IGF-1 controls hair patterning. It doesn't necessarily cause hair loss.

Overproduction of it does. The studies are there to prove it.

And, no, returning IGF-1 levels to normal is NOT better than a 65% reduction in DHT.

Considering IGF-1 mediates 5ar activity, I beg to differ.

If you think that this is true, then post a study that shows that reducing circulating levels of IGF-1 is equivalent to a 65% reduction in the level of circulating levels of DHT with hair counts and all necessary studies that are needed to prove that such a change increases hair growth, hair density and counts..

I don't need to. The offending level of DHT would not be reached if IGF-1 levels were not unnecessarily high.

As for this:

"Is this opinion? Because the science is all there to show that raised IGF-1 levels activate the 5ar enzyme. IGF-1 is raised by diet and insulin levels."

The science is there to prove that IGF-1 activates the 5AR enzyme in fibroblasts contained within scrotal skin. Try again. I know a little anatomy and I can tell you that your scrotum just happens to not be on your scalp.

AGAIN you focus on the wrong thing. You just said:

'IGF-1 activates the 5AR enzyme' - thats where you needed to stop, because 5AR enzyme is the same anywhere. Moreover, the studies showing IGF-1 levels aer higher in balding individuals is proof of this.

Lastly, you need to not post information from non-reputable websites. You're doing it again.

Where? Almost all are Medical websties.journals. If you mean Gabe Mirkin M.D <--- I happen to think he's right.

 

[docj077]

I can only pray that you know that continued use of finasteride is associated with increased concentrations IGF-1 in the hair follicle and people regrow hair with finasteride..

I was aware of this. But theres a bigger picture. They are regrowing it from the reduction of DHT which is no longer attaching to follicles.

Prove it.

 

[docj077]

And, no, returning IGF-1 levels to normal is NOT better than a 65% reduction in DHT.

Considering IGF-1 mediates 5ar activity, I beg to differ.

Again, prove it.

 

[DammitLetMeIn]

Prove it.

Are you serious? Everyone knows that DHT attaches to follicles stopping them from growing causing baldness.

A reduction in DHT is undoubtedly going to involve more hair growth.

Any coincidental increase in IGF-1 is because the DHT is no longer there, which allows the follicle to grow hair.

 

[docj077]

Lastly, you need to not post information from non-reputable websites. You're doing it again.

Where? Almost all are Medical websties.journals. If you mean Gabe Mirkin M.D <--- I happen to think he's right.

Only peer reviewed journals are accepted on these forums.

 

[DammitLetMeIn]

Only peer reviewed journals are accepted on these forums.

Thats a pretty lame way to evade the fact that increased IGF-1 is associated with increased 5ar activity and vertex baldness.

Why won't you accept whats there and recognise that high IGF-1 levels means more 5ar activity and more DHT and more baldness?

I actually only included MIrkin's website so you could see from a fellow medic who understood exactly what is going on.

 

[docj077]

Prove it.

Are you serious? Everyone knows that DHT attaches to follicles stopping them from growing causing baldness.

A reduction in DHT is undoubtedly going to involve more hair growth.

Any coincidental increase in IGF-1 is because the DHT is no longer there, which allows the follicle to grow hair.[/quote]

You just proved my point. Thank you. Increased IGF-1 is associated with hair growth and regrowth.