A Closer Look At: Insulin & IGF-1.

[purecontrol]

However a baked food is completely different from being raw. As a substance such a food is heated is begins to break down, a microwaved potato is even high glycimic than a baked one.

What does it break down into?

Worst things you can do for you insulin sensativity

#2 Fat with high glycimic foods.

Do you deny that fat lowers the glycemic index of carbohydrates?

#1 I don't think I need to give a lesson, and you know every well why it causes a higher glucose load and insulin

#2 Once again, I don't need to give a lesson. And you know that a fat combined with a simple carb will prolong the insulin levels which is the whole problem in the first place, not to mention all the other negative effects it has.

What you should have done was paid attention to the fact that the most important part is the insulin levels, as that is what is causing the problem ie insulin sensativity.

For instance a lot of people don't know that Fats such as Fish oil cause a large release of insulin. Just because as good is shown to be "low" glycimic does not mean that there is a lower amount of insulin released.

 

[Bryan]

#1 I don't think I need to give a lesson, and you know every well why it causes a higher glucose load and insulin

I didn't even mention the words "higher glucose load" or "insulin" at all. Rather than make a pointless comment about something I didn't even ask you, please answer the question that I _did_ ask you. I may have a follow-up question for you, if you can see your way to doing that.

 

[purecontrol]

#1 I don't think I need to give a lesson, and you know every well why it causes a higher glucose load and insulin

I didn't even mention the words "higher glucose load" or "insulin" at all. Rather than make a pointless comment about something I didn't even ask you, please answer the question that I _did_ ask you. I may have a follow-up question for you, if you can see your way to doing that.

Brian stick to the post and quit taking it off subject your ego has no place here.

Thanks

 

[OverMachoGrande]

#1 I don't think I need to give a lesson, and you know every well why it causes a higher glucose load and insulin

I didn't even mention the words "higher glucose load" or "insulin" at all. Rather than make a pointless comment about something I didn't even ask you, please answer the question that I _did_ ask you. I may have a follow-up question for you, if you can see your way to doing that.

Brian stick to the post and quit taking it off subject your ego has no place here.

Thanks

Yeah Bryan, take your hidden-agenda elsewhere!

 

[Bryan]

Brian stick to the post and quit taking it off subject your ego has no place here.

Does this mean you're not going to answer the question that I asked you?

 

[somone uk]

hmm interesting i have just read research on minoxidil and the mechanism of minoxidil seems to have a lot to do with insulin
i don't know if' it's specially insulin or IGF 1 but research seems to show that in vitro only slows down hair regression in an insulin free environment (where the hair regresses faster) and in an environment rich in insulin the hair regression is the same rate with or without minoxidil

so it seems in other words
with minoxidil -----> amount of insulin doesn't matter
with insulin ------> amount of minoxidil doesn't matter

since i seem to get results from minoxidil it seems my hair must have a poor supply of insulin :dunno:
saying that no study has been done inside a living body

 

[OverMachoGrande]

Brian stick to the post and quit taking it off subject your ego has no place here.

Does this mean you're not going to answer the question that I asked you?

What about the question I asked you?

I asked for your take on IGF-1. Why would you come to an IGF-1 post and start asking questions about potatoes? All you said was IGF-1 was beneficial to hair.Why do you think that?

 

[Bryan]

What about the question I asked you?

What about it? I answered it.

I asked for your take on IGF-1.

I gave it to you.

Why would you come to an IGF-1 post and start asking questions about potatoes?

Because the poster "purecontrol" said something about them.

All you said was IGF-1 was beneficial to hair.Why do you think that?

I've already cited some of the medical evidence for that, as has at least one other poster.

 

[OverMachoGrande]

I've already cited some of the medical evidence for that, as has at least one other poster.

I have shown strong evidence that IGF-1 contributes to the balding process. Just read the first two posts!

 

[OverMachoGrande]

...

 

[OverMachoGrande]

...

 

[somone uk]

afro haircut anyone?
i particularly like the square one on the left :innocent:

 

[JLL]

isn't that tito jackson next to the turkish emperor?

 

[moxsom]

According to the book: Hair & It's Disorders: Biology, Pathology & Management by Francisco M. Camacho, Valerie A. Randall, Vera H. Price....

IGF-1 Inhibits catagen and telogen phases of the hair growth cycle, and promotes the phase switch back to anagen again. According to Francisco M. Camacho, Valerie A. Randall, Vera H. Price: "telogen is best viewed as the pre-regeneration state of the hair follicle, that is, whenever a hair follicle seeks to regenerate itself following severe damage, it enters catagen in order to deconstruct itself and become and telogen follicle again. In fact, rapid catagen introduction is the most effective way to return to the telogen state and to reconstruct a new fiber factory. In addition, the return to telogen by partial organ suicide at the extended period of hair growth may also be associated with the inherent risk of hair shaft production going awry.Thus re-entering the telogen state during cycling may be crucial for the prevention of malignant degeneration. The proposed telogen default sate, therefore, is more than a 'mere' resting state, and is clinically important, since it may be pharmaceutically targeted, for example by hair drugs that prolong anagen for the treatment of alopecia".

http://books.google.com/books?id=iCqCdO ... en&f=false

I think your outlook of catagen induction is a little flawed. Yes you must go through catagen to start the anagen phase again but this is not something you want happening over and over (as you propose would happen with low levels of IGF-1). Remember that a full hair cycle lasts from 2 - 6 years. Each time your hair cycles and is under the influenece of androgen damage the hair becomes weaker and weaker and the telogen and catagen phases become longer.

Inhibiting catagen and telogen is a GOOD thing and anagen phase elongation would provide you with thicker and healther hairs. From my reading IGF-1 is good for hair growth.

J Am Acad Dermatol. 2003 Aug;49(2):229-33.
The expression of insulin-like growth factor 1 in follicular dermal papillae correlates with therapeutic efficacy of finasteride in androgenetic alopecia.
Tang L, Bernardo O, Bolduc C, Lui H, Madani S, Shapiro J.

Try reading this paper. It states that those patients on finasteride who showed the greatest improvement had an upregulation of IGF-1, while those who showed clinical worsening had down-regulated IGF-1. How does your theory hold in light of this?

 

[Bryan]

J Am Acad Dermatol. 2003 Aug;49(2):229-33.
The expression of insulin-like growth factor 1 in follicular dermal papillae correlates with therapeutic efficacy of finasteride in androgenetic alopecia.
Tang L, Bernardo O, Bolduc C, Lui H, Madani S, Shapiro J.

Try reading this paper. It states that those patients on finasteride who showed the greatest improvement had an upregulation of IGF-1, while those who showed clinical worsening had down-regulated IGF-1. How does your theory hold in light of this?

THANK YOU so much for citing that study for misterE!

I've cited at least one other study for him myself, showing that IGF-1 seems to be an important growth factor for human hair (not that it matters much, because he doesn't listen to what anybody tells him). Hopefully he'll eventually get off his anti-IGF-1 kick.

 

[OverMachoGrande]

According to the book: Hair & It's Disorders: Biology, Pathology & Management by Francisco M. Camacho, Valerie A. Randall, Vera H. Price....

IGF-1 Inhibits catagen and telogen phases of the hair growth cycle, and promotes the phase switch back to anagen again. According to Francisco M. Camacho, Valerie A. Randall, Vera H. Price: "telogen is best viewed as the pre-regeneration state of the hair follicle, that is, whenever a hair follicle seeks to regenerate itself following severe damage, it enters catagen in order to deconstruct itself and become and telogen follicle again. In fact, rapid catagen introduction is the most effective way to return to the telogen state and to reconstruct a new fiber factory. In addition, the return to telogen by partial organ suicide at the extended period of hair growth may also be associated with the inherent risk of hair shaft production going awry.Thus re-entering the telogen state during cycling may be crucial for the prevention of malignant degeneration. The proposed telogen default sate, therefore, is more than a 'mere' resting state, and is clinically important, since it may be pharmaceutically targeted, for example by hair drugs that prolong anagen for the treatment of alopecia".

http://books.google.com/books?id=iCqCdO ... en&f=false

I think your outlook of catagen induction is a little flawed. Yes you must go through catagen to start the anagen phase again but this is not something you want happening over and over (as you propose would happen with low levels of IGF-1). Remember that a full hair cycle lasts from 2 - 6 years. Each time your hair cycles and is under the influenece of androgen damage the hair becomes weaker and weaker and the telogen and catagen phases become longer.

Inhibiting catagen and telogen is a GOOD thing and anagen phase elongation would provide you with thicker and healther hairs. From my reading IGF-1 is good for hair growth.

J Am Acad Dermatol. 2003 Aug;49(2):229-33.
The expression of insulin-like growth factor 1 in follicular dermal papillae correlates with therapeutic efficacy of finasteride in androgenetic alopecia.
Tang L, Bernardo O, Bolduc C, Lui H, Madani S, Shapiro J.

Try reading this paper. It states that those patients on finasteride who showed the greatest improvement had an upregulation of IGF-1, while those who showed clinical worsening had down-regulated IGF-1. How does your theory hold in light of this?

How do you explain the fact that IGF-1 inhibits the production of S.H.B.G.? How do you explain the studies on calorie restriction (which reduces both insulin and IGF-1) that is shown to increases life span and slow aging? How do explain IGF-1's role in prostate enlargement, breast cancer and acne? And how do explain that high IGF-1 and low IGFBP-3 is shown to cause vertex balding?

How can I get off my anti-IGF-1 kick knowing all this?

 

[moxsom]

Okay I will only adress the last part because in reality it is the only thing you brought up that has to do with balding.

You clearly never learned the difference between correlation and causation. Because an increase in IGF-1 and a decrease in IGFB3 is correlated with vertex balding it does NOT mean it is the cause of vertex balding.

For example, say that I find that students who go to school in colder temperatures have much higher marks then those that go to school in warmer temperatures. I cannot say that cold temperatures cause the higher marks for these students, there could be MANY other factors, such as different teaching systems, parenting, etc.. Likewise with the vertex balding study, perhaps all these men had much more sensitive androgen receptors, or much higher levels of DHT, which would attribute to vertex balding more so then IGF-1.

Also you clearly haven't even read the entire study and you should stop looking so much into abstracts as they only tell very little of the research being discussed.

I have read that In androgen-responsive tissue, IGF-1 may act locally to positively mediate the induction of 5a-reductase by dihydrotestosterone. But there is also plenty of evidence that IGF-1 also promotes hair growth.

It's more than a 2 sided die though, and growth factors can effect a multitude of pathways, and in this instance it is unclear wether the damage done by androgens (possibly metiated in part by IGF-1) is greater then that of proper hair growth induction by IGF-1. In my readings I have concluded that I would rather upregulate IGF-1, especially since I inhibit the 5a-reductase enzyme via proscar.

 

[OverMachoGrande]

Butyrate is a short-chain fatty acid produced by microbial fermentation of dietary fiber and starch. According to this study: Butyrate increases IGFBP-3. Low IGFBP-3 levels have been shown to play a role in prostate enlargement (which involves the same hormones and growth factors associated with M.P.B.).
I personally think that dietary fiber plays a huge role in M.P.B. due to the fact in lowers estrogen and increases S.H.B.G. and now, right below it says that it reduces IGF-1!

Anyway here is the study:

Differential Activation of the IGF Binding Protein-3 Promoter by Butyrate in Prostate Cancer Cells
Junko Tsubaki, Vivian Hwa, Stephen M. Twigg and Ron G. Rosenfeld
Department of Pediatrics (J.T., V.H., R.G.R.), Oregon Health Sciences University, Portland, Oregon 97201; and Kolling Institute of Medical Research (S.M.T.), University of Sydney, Royal North Shore Hospital, Sydney, New South Wales 2065, Australia

Address all correspondence and requests for reprints to: Vivian Hwa, Department of Pediatrics, School of Medicine NRC5, Oregon Health Sciences University, 3181 Southwest Sam Jackson Park Road, Portland, Oregon 97201-3402.

http://endo.endojournals.org/cgi/conten ... 143/5/1778


Abstract.
Sodium butyrate (NaB), a dietary micronutrient, is a potent growth inhibitor that initiates cell differentiation in many cell types, including prostate cancer cells. The molecular mechanisms by which these effects occur remain largely unknown. In this study, we investigated the effects of NaB on the expression of IGF binding protein (IGFBP)-3, a known growth regulator, in two human prostate cancer cell lines (PC-3 and LNCaP).

Treatment with NaB (0–10 mM) caused a dose-dependent stimulation of IGFBP-3 mRNA expression and parallel increases in protein levels. A specific histone deacetylase inhibitor, trichostatin A (TSA) similarly induced IGFBP-3 expression, indicating that histone hyperacetylation may be critical in the regulation of IGFBP-3 expression.

To investigate the molecular mechanism of NaB-regulated IGFBP-3 expression, 1.87 kb of the human IGFBP-3 gene promoter was cloned into the pGL2-basic luciferase reporter vector. In both PC-3 and LNCaP cells, NaB (10 mM) significantly increased luciferase activity 20- to 30-fold, compared with the untreated control. However, using 5' sequential deletion constructs of the IGFBP-3 promoter, the NaB response sequences in the IGFBP-3 promoter were different in PC-3 and LNCaP cells. Our studies identified a region, -75 to +69 from the start of transcription (+1), that is fully inducible by NaB treatment in LNCaP cells, but not in PC-3 cells. Unlike other well characterized NaB-regulated genes, Sp1 DNA sequences are not involved in NaB up-regulation of IGFBP-3 gene in LNCaP cells. Further deletion studies identified two independent regions critical for NaB-induced transactivation in LNCaP cells. These regions contain consensus binding sites for p53 and GATA, respectively, but mutational analyses and gel shift assays suggested that, while the p53 response element is required for NaB responsiveness, neither p53 nor GATA are involved.

In summary, we have demonstrated that 1) NaB significantly up-regulates IGFBP-3 mRNA and protein levels in PC-3 and LNCaP prostate cancer cells; and 2) novel butyrate- responsive elements lacking consensus Sp1 sites are used in LNCaP cells.

 

[moxsom]

Butyrate is a short-chain fatty acid produced by microbial fermentation of dietary fiber and starch. According to this study: Butyrate increases IGFBP-3. Low IGFBP-3 levels have been shown to play a role in prostate enlargement (which involves the same hormones and growth factors associated with M.P.B.).
I personally think that dietary fiber plays a huge role in M.P.B. due to the fact in lowers estrogen and increases S.H.B.G. and now, right below it says that it reduces IGF-1!

Your making vast assumptions right here. Yes, prostate enlargement and androgenic alopecia share some pathways there is MANY differences in the mechanisms of each.

For example, prostate enlargement is due to proliferation of many cells (epithelial I think), not adrogen mediated damage like in the dermal papilla of hair follicles on the scalp. Although both cell lines have androgen receptors sensitive to DHT.

I encourage you to start reading some of the basics before you start making such large assumptions. Read on the mechanisms of prostate cancer or enalrgement first before trying to solve both prostate cancer and male pattern baldness.

 

[abcdv12]

Taking a tablespoon of psyllium (fiber) , has dramatically reduced my hair fall.
and also it made my scalp and existing hair look very healthy.
But it is too late for me as i am allready a NW6.