Theory: Cooked Fat =DHT(Dihydrotestosterone) Baldness

[DammitLetMeIn]

I'm done going back and forth with you.

You don't agree with the contention advanced by myself, and an IGF-1 expert, another person who has been researching hairloss for 9 years, and three M.D.'s.

Thats fair enough and you're entitled to your opinion, but I'm quite simply tired of your attempts to twist facts in order to win an argument where the other side is only interested in the truth.

I don't mind you putting forward science which contends that such a contention may be inaccurate such as the finisteride study you provided but additonal dismissive and somewhat petty comments dismissing the idea out of the water are completely unnecessary.

 

[DammitLetMeIn]

yeah i don't think he reads any of the linked studies anyone else posts that aren't abstracts..

I do read the studies provided. However, I have a decent knowledge of IGF-1 and nothing that I've read in your studies tells me that the theory is inaccurate.

I'm aware that Finisteride is working well for you and I'm truly happy for you but that doesn't mean other theories are automatically dead.

Perhaps you would like to elaborate upon what it is you feel makes the idea inaccurate from your studies?

 

[Bryan]

You have no proof that IGF-1 increases 5AR function in any way as you don't have the peer-reviewed.

I have studies which show that it does in areas DHT sensitive area apart from the scalp

Can you post those studies? I'd be very curious to know how/why IGF-1 would increase 5AR function...

Bryan

 

[DammitLetMeIn]

Can you post those studies? I'd be very curious to know how/why IGF-1 would increase 5AR function...

Bryan

IGF-1 regulating 5-Alpha-Reductase activity:

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

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

-------------------------------------------------------------------------------------
'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

'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.

'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

Gabe Mirkin M.D. points out the connection:

http://www.drmirkin.com/men/M119.htm
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
***IGF-1 can lead to aberrant activation of the Androgen Receptor***

Blok G. J., de Boer H., Gooren L. J., van der Veen E. A. Growth hormone substitution in adult growth hormone-deficient men augments androgen effects on the skin. Clin. Endocrinol., 47: 29-36, 1997

CONCLUSIONS
Overdosage of IGF-I can lead to androgenization, a previously undescribed undesirable effect of IGF-I. Long-term IGF-I treatment necessitates progressive adjustment of the IGF-I dose to avoid overtreatment.

http://www.blackwell-synergy.com/links/ ... 98.00356.x

Here are some excerpts from some other medical Articles cited online:

'Our findings suggest that high levels of IGF-1 may be associated with
increased risk of vertex baldness. Substantial clinical evidence
appears to support this finding.'

'It has also been recently reported that GH treatment of GH-deficient
men increases hair scores in androgen-dependent areas. These effects
can be explained either by IGF-1 directly stimulating the androgen
receptor, or by IGF-1 increasing local 5alpha-reductase activity and
thus stimulating the local conversion of testosterone to
dihydrotestosterone.'

Signorello LB et al. Hormones and hair patterning in men: A role for insulin-like growth factor-1. Journal of the American Academy of Dermatology February, 1999;40:200-203.

 

[SkylineGTR]

yet you still fail to see the studies that point out

1. Hormones effect IGF-1 levels greater then diet.
2. IGF-1 levels decline with age.
3. IGF-1 is regulated by IGFBP-3

The studies you post only say .. can ... may ... possible. Not difinitive.

If IGF-1 were the major cause of baldness they would of already synthesized a supplimental IGFBP-3 seeing that is what regulates IGF-1 MORE then any diet would.

http://www.labcorp.com/datasets/labcorp ... 012300.htm

 

[docj077]

I'm done going back and forth with you.

You don't agree with the contention advanced by myself, and an IGF-1 expert, another person who has been researching hairloss for 9 years, and three M.D.'s.

Thats fair enough and you're entitled to your opinion, but I'm quite simply tired of your attempts to twist facts in order to win an argument where the other side is only interested in the truth.

I don't mind you putting forward science which contends that such a contention may be inaccurate such as the finisteride study you provided but additonal dismissive and somewhat petty comments dismissing the idea out of the water are completely unnecessary.

Good. Maybe you'll post a completed theory lacking in all the holes that your original theory had to begin with. I can't believe that you don't understand that all I'm trying to do is make you work for your opinion. I'm not questioning the results. I'm merely questioning how much you really want to help others when you don't have the problem yourself. Either you're a person with a foolishly large amount of altruistic tendencies, or you really want to help others.

Like I said, the IGF-1 increasing 5AR activity link has been around for years (one article is from 1993). There hasn't been anything done with it since that experiment. At least not in humans. Lowering fat intake and raising the amount of fiber intake appears to lower IGF-1 levels. However, there is no definitive link between that fact and a man with a genetic predisposition to male pattern baldness having his hair loss reversed or stopped. That's the study that needs to be done and both you and I know it. There is also no link between increased IGF-1 levels and frontal baldness.

A perfect study would take a few thousand men (half with baldness and half without with differing Norwood levels); sample their blood for IGF-1 levels, testosterone, SHBG and DHT; sample their scalps (differing regions for each participant); and take those scalp samples and measure the amount of DHT, T, IGF-1,SHBG, and 5AR activity along with amount of TGF-beta activity.

That would pretty much give us the answer to male pattern baldness. What would be even better is if they included a population in the study that was taking finasteride or dutasteride and took the same measurements.



Again, I'm not trying to bring you down or flip your theory against you. I'm just trying to make you work, because you bring up good points, but a lot of your studies don't defend your theory. In fact, many of them are lacking in any support whatsoever.

 

[DammitLetMeIn]

Maybe you'll post a completed theory lacking in all the holes that your original theory had to begin with..

I was actually hoping people would bring forth their own material which may or may not support the theory. There were a multitudinous amount of studies online which I did not have the subscription for and would love to have read.

I can't believe that you don't understand that all I'm trying to do is make you work for your opinion.

Theres a way of doing it, and it doesn't involve cheap digs. Besides you preferred to be consistently negative rather than play devil's advocate regarding the issue.

I'm not questioning the results. I'm merely questioning how much you really want to help others when you don't have the problem yourself..

I told you, I did have a problem. My hair was shedding massively. But it appears to have been some form of telogen effluvium as it is now growing back devoid of any treatments.

Either you're a person with a foolishly large amount of altruistic tendencies, or you really want to help others...

I had a foolishly large amount of free time which has now come to an end. My interest was purely for interest's sake and potential future reference should I ever go down the road of male pattern baldness.

Like I said, the IGF-1 increasing 5AR activity link has been around for years (one article is from 1993). There hasn't been anything done with it since that experiment.

Actually there has. I found a conflicting study earlier today which stated that IGF-1 had no effect on 5ar activity however, growth hormone did. To be honest there needs to be further studies on the issue. But I don't think it is one which should be ignored especially when so many learned individuals have pointed out the link.

Lowering fat intake and raising the amount of fiber intake appears to lower IGF-1 levels. However, there is no definitive link between that fact and a man with a genetic predisposition to male pattern baldness having his hair loss reversed or stopped. That's the study that needs to be done and both you and I know it..

For all I know there IS a study somewhere out there which indicates one way or the other.

The question to be asked is 'would those guys have had vertex balding if their IGF-1 levels were lower'? - who knows.

I actually found another study earlier which stated that insulin (not IGF-1) is able to mimic IGF-1 and impact upon IGF-1 receptors in the hair follicle thus preventing the growth of the hair. This was interesting.

All around it appears that keeping insulin sensitivity is a good idea for hair health and over all health

There is also no link between increased IGF-1 levels and frontal baldness. ..

I personally beleive there is a bigger genetic influence on frontal baldness.

A perfect study would take a few thousand men (half with baldness and half without with differing Norwood levels); sample their blood for IGF-1 levels, testosterone, SHBG and DHT; sample their scalps (differing regions for each participant); and take those scalp samples and measure the amount of DHT, T, IGF-1,SHBG, and 5AR activity along with amount of TGF-beta activity.

That would pretty much give us the answer to male pattern baldness. What would be even better is if they included a population in the study that was taking finasteride or dutasteride and took the same measurements. ..

I agree. But until that time I think its risky to ignore all other studies if one has male pattern baldness. Besides having high insulin isn't good for people anyways.

Again, I'm not trying to bring you down or flip your theory against you. I'm just trying to make you work, because you bring up good points, but a lot of your studies don't defend your theory. In fact, many of them are lacking in any support whatsoever.

Well, I guess you won't have to worry about it anymore. I don't have any time left to research or other stuff. I have to get on with real life again.

 

[wookster]

http://jcem.endojournals.org/cgi/conten ... /83/6/2104

Comparative Rates of Androgen Production and Metabolism in Caucasian and Chinese Subjects1

[...]


Clinically apparent prostate cancer occurs more commonly among Caucasians living in Western countries than in Chinese in the Far East. Prior studies demonstrated diminished facial and body hair and lower levels of plasma 3-androstanediol glucuronide and androsterone glucuronide in Chinese than in Caucasian men. Based upon these findings, investigators postulated that Chinese men could have diminished 5-reductase activity with a resultant decrease in prostate tissue dihydrotestosterone levels and clinically apparent prostate cancer. An alternative hypothesis suggests that decreased 3-androstanediol glucuronide and androsterone glucuronide levels might reflect reduced production of androgenic ketosteroid precursors as a result of genetic or environmental factors. The present study examined 5-reductase activity, androgenic ketosteroid precursors, and the influence of genetic and environmental/dietary factors in groups of Chinese and Caucasian men. We found no significant differences in the ratios of 5ß-:5-reduced urinary steroids (a marker of 5-reductase activity) between Chinese subjects living in Beijing, China, and Caucasians living in Pennsylvania. To enhance the sensitivity of detection, we used an isotopic kinetic method to directly measure 5-reductase activity and found no difference in testosterone to dihydrotestosterone conversion ratios between groups. Then, addressing the alternative hypothesis, we found that the Caucasian subjects excreted significantly higher levels of individual and total androgenic ketosteroids than did their Chinese counterparts. To distinguish genetic from environmental/dietary factors as a cause of these differences, we compared Chinese men living in Pennsylvania and a similar group living in Beijing, China. We detected a reduction in testosterone production rates and total plasma testosterone and sex hormone-binding levels, but not in testosterone MCRs in Beijing Chinese as a opposed to those living in Pennsylvania. Comparing Pennsylvania Chinese with their Caucasian counterparts, we detected no significant differences in total testosterone, free and weakly bound testosterone, sex hormone-binding globulin levels, and testosterone production rates.

Taken together, these studies suggest that environmental/dietary, but not genetic, factors influence androgen production and explain the differences between Caucasian and Chinese men.

 

[wookster]

http://www.hairloss-research.org/february2.html

DIET, INFLAMMATION, AND HAIR LOSS


Several studies have shown a link between diet and hair loss. In short, diets that predispose to inflammation are much more likely to be associated with hair loss than healthier diets, with an abundance of omega-3 fatty acids and phytonutrients. In addition to toxic cytokines, there are other inflammatory pathways that can be mediated via diet modification. A common problem involves over-production of pro-inflammatory hormone-like “messengersâ€￾ (such as prostaglandin) E2) and under-production of anti-inflammatory “messengersâ€￾ (such as prostaglandin E1 and E3). The good news is that omega-3 fatty acids found in fish oils help to suppress the formation of undesirable prostaglandin E2 and promote synthesis of beneficial prostaglandin E3. Gamma linolinic acid (GLA) induces production of the anti-inflammatory prostaglandin E1. What you eat can significantly affect whether you have more of the beneficial prostaglandins (E1 and E3) as opposed to the pro-inflammatory prostaglandin E2. Since prostanglandin E2 is a culprit in inflammation, reducing food that are high in omega-6 fatty acids and increasing omega-3 rich food, such as salmon and other fish can be beneficial. Limiting foods that convert to arachidonic acid can help reduce inflammation. (Arachidonic acid is a precursor to both prostanglandin E2 and the pro-inflammatory cytokine leukotriene B(4)). Another dietary factor that can lead to high levels of arachidonic acid is the over-consumption of high-glycemic index carbohydrates that cause excess production of insulin. Foods that contribute to chronic inflammation and hair loss are foods with the high-glycemic index (things that you digest quickly) like bottled fruit juices or rice cakes, food heavy in polyunsaturated fats or saturated fats, and foods high in arachidonic acid.

Some specific foods to avoid
* Margarine
* Organ meats
* Egg yolks
* Pasta
* Juices (canned or bottled), fresh squeezed OK
* White rice, white bread
* Refined sugar


Good foods
* Salmon
* Oatmeal
* Olives and Olive oil
* Almonds
* Fresh fruits and vegetables
* Avocado and Guacamole
* Flax oil or flax me

 

[OverMachoGrande]

The way I see it... The more animal fat is consumed, the higher the estradiol levels. The more estradiol you have in your body overpowers the testosterone effects... Your body then creates DHT which is 5x stronger than testosterone to balance the effects of the excess estradiol. I believe the reason why some people bald and some don't has to do with the amount of aromatase enzymes and the amount of estrogen in their bodies. DHT is still the enemy, but without all the excess estrogen overwhelming your system, DHT has no purpose.

 

[Guest]

Without reading 48 pages of this thread, can someone summarise what was said? I do believe diet has a part in hair loss, I believe a bad diet can accelerate hair loss.

 

[moxsom]

Re:

As I've said before:

IGF-1 stimulates 5 alpha reductase to cause growth of a beard
IGF-1 stimulates 5 alpha reductase to cause grow of hair in human scrotal skin.
IGF-1 stimulates 5 alpha resuctase to cause acne.
IGF-1 enlarges sebaceous glands.
An IGF-1 expert says it is highly likely that it causes baldness.

You telling me IGF-1 doesn't do the exact same thing in the scalp?

Hey, I have been doing alot of reading on IGF-1. You sir should read this article or even the abstract.

http://www.sciencedirect.com/scienc...erid=10&md5=32d898dfc540190a177aa9ac83cbaebd

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.

Increased IGF-1 showed improvement whilst decreased IGF-1 showed worsening results.

IGF-1 is a mjor player in proliferating and differentiating dermal cells into hair shafts, why would it cause baldness?

 

[moxsom]

And then I read like 15 pages of this thread. Seems like a lot of contradicting studies on IGF-1

 

[Bryan]

The way I see it... The more animal fat is consumed, the higher the estradiol levels. The more estradiol you have in your body overpowers the testosterone effects... Your body then creates DHT which is 5x stronger than testosterone to balance the effects of the excess estradiol.

No it doesn't.

 

[OverMachoGrande]

IGF-1: http://www.ncbi.nlm.nih.gov/pubmed/10827403
IGF-1: http://www.youtube.com/watch?v=mHYFOJBU434
IGF-1/Estrogen: http://www.youtube.com/watch?v=opBJp7jc8wk
IGF-1/Estrogen: http://www.youtube.com/watch?v=2J0F9P9e ... re=channel
Milk: http://www.tbkfitness.com/milk.html
Milk: http://www.rense.com/general26/milk.htm

 

[GreekGod_of_Aesthetics]

Legendary thread. Gonna catch-up with it.
Any TLDR's?