Insulin resistance, PCOS, and male pattern baldness

freakout

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S Foote. said:
OK, as an engineer, i ask questions based on basic common sense.
You're theory tells me you're a mechanical engineer w/ specialty in hydraulics and pipeline networks. Is that right?

I'm into the service, maintainance and troubleshooting of wide-area wireless telecom systems.

S Foote. said:
...so there has to be another factor.

I think this factor is the complex blood supply/drainage that evolved to service the enlarging brain in higher primates.
There's a suggestion that the drainage system is compromised.
There's also a suggestion that the root cause is not within the pilosebaceous units or follicular units.
It's also a suggestion that human physiology are factors in the predisposition to male pattern baldness.

So there's still the question of 'what's difference between balding men and non-balding men within those parameters?

still working on it ... to be continued.
 

balder

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Hypertension and aldosterone levels in women with early-onset androgenetic alopecia.

http://www.ncbi.nlm.nih.gov/pubmed/19906217



Abstract
BACKGROUND:

Few studies have analysed the relationship between androgenetic alopecia (Androgenetic Alopecia) in women and cardiovascular disease. There is reported to be an elevated prevalence of hypertension among men with Androgenetic Alopecia, and it has been proposed that both phenomena may be explained by the presence of hyperaldosteronism. However, no data on blood pressure (BP) and aldosterone levels in women with Androgenetic Alopecia have been published to date.

OBJECTIVES:

The objective of this study was to evaluate aldosterone levels and the presence of systolic and diastolic hypertension in women with early-onset Androgenetic Alopecia and in healthy controls.

PATIENTS AND METHODS:

This case-control study included 40 women with Androgenetic Alopecia and 40 healthy controls from the Department of Dermatology of San Cecilio Hospital, Granada, Spain.

RESULTS:

Patients with Androgenetic Alopecia showed significantly higher systolic BP values (139.43 vs. 107.80 mmHg; P < 0.0001), diastolic BP values (87.65 vs. 67.48 mmHg; P < 0.0001) and aldosterone levels (249.55 vs. 155.14 pg mL(-1); P = 0.002) vs. controls, respectively. A positive correlation between aldosterone levels and systolic and diastolic BP values is described.

CONCLUSIONS:

A higher prevalence of hypertension in women with Androgenetic Alopecia has been found. The elevated aldosterone values in these patients may contribute, alongside other mechanisms, to the development of Androgenetic Alopecia and may also explain the higher prevalence of hypertension. BP screening of women with Androgenetic Alopecia will permit earlier diagnosis of an unsuspected hypertension and initiation of appropriate treatment.

 

S Foote.

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Interesting info folks, thanks.

Freakout i am a mechanical engineer, most of my work over forty years has been related to engines. I started in the engine machining side, then went on to engine developement and trouble shooting. It's more systems engineering, and how one thing effects other things.

I take the same view of physiology.
 

freakout

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freakout

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S Foote. said:
The growing anagen follicle has to grow into the dermal tissue, so what would happen if the dermal tissue doesn't want to move out of the way?

The conclusion i reached is described in the "Hydraulic dermal model" part of the link i posted.

Forget about scalp hair for a moment and consider this. If you transpose the hydraulic principle i suggest onto humans, you notice that the one consistant thing about androgens is they grow hair in certain areas of the body. These areas all have higer concentrations of lymph vessels close to the follicles.

The implication of the theory is that androgens are increasing lymph drainage, so reducing the local fluid pressure and increasing hair growth.

The odd and "opposite" effect is that in some people, this action can reduce scalp growth.
This part is more of a description of the pathology. A root-cause analysis has yet to isolate causative factors.
 

freakout

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S Foote. said:
But there is no direct relationship here as to androgen levels or time period [to the occurrence of male pattern baldness], so there has to be another factor.
Yes. This is very obvious in many cases e.g. Prince William. These cases are already an indication of the existence of causative factors other than androgens which Merck drones deny all the time.
 

freakout

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S Foote. said:
I think this factor is the complex blood supply/drainage that evolved to service the enlarging brain in higher primates.
THe theory points to human envolution and the large blood supply requirement of the human brain as a natural contributor to the predisposition.

It also suggests a compromized drainage system as the 'cause'. This compromized drainage system must be thrown to the other side of the equation - make it the 'effect' of another cause to arrive at the root cause by asking the questions:

What's causing a drainage problem in balding men?
How do non-bald men and hunter-gatherers escape the natural predisposition?

Unlike man-made machine, biological systems are very capable of repairing themselves to a degree beyond the understanding of current medical science. What prevents a compromized drainage system from fixing itself?
 

freakout

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S Foote. said:
The drainage from the scalp can be reduced in this area by androgen increased drainage elsewhere, simple "plumbing" effect because of the complex head feed/ return systems in humans.

This reduced scalp drainage will not build up fluid unless the feed pressure is high. This is why i think there is a proven relationship with high blood pressure and male pattern baldness.
Could you elaborate on this further?

BTW, do you have a copy of hte ligature study? I just found mine:
Treatment for Seborrheic Alopecia:
The Ligature of the Arteries of the Scalp.

Do we have the same study?
 

S Foote.

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idontwanttobebalding said:
S Foote. said:
Interesting info folks, thanks.

Freakout i am a mechanical engineer, most of my work over forty years has been related to engines. I started in the engine machining side, then went on to engine developement and trouble shooting. It's more systems engineering, and how one thing effects other things.

I take the same view of physiology.

What is your opinion on this?


http://www.baldingblog.com/2011/08/04/d ... -be-there/

"The transplanted hair almost always takes on the character of its source. In body hair transplants (chest to scalp) the donor hair often changes a bit, getting longer than when it was growing on the chest. There is no memory that I know of, but I do believe that the character of the skin may influence the character of the hair on a mechanical basis alone".

Here is another article about this.

http://www.newhair.com/resources/mp-200 ... inance.asp

I think the exact procedure itself and size of graft makes a difference, and the healing and fibrosis factor complicates the issue. But it cannot be denied that by some mechanism or mechanisms, the recipient site is effecting the growth characteristics.

We need a lot more transplantation experiments aimed at clearing up these questions.

I personaly think that the transplantation industry does not want these experiments to happen.

I dont know the exact legal position, but transplants are sold on the basis that the follicles are "different". If it was proven that they are not and other factors produced the result, everyone who ever had a bad result may have grounds to sue?

Just my thoughts here.
 

squeegee

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bump! :punk:
 

Broons85

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Drinking small amounts is a yay (or neutral), drinking large amounts is a huge nay. According to that paper, large amounts of alcohol shut off your insulin/sugar metabolism, and that's at the root of hair loss (and most diseases out there).
 

czvezda

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http://www.ncbi.nlm.nih.gov/pubmed/22068870
Aldosterone plays a role in hypertension, and hypertension is prevalent in patients with insulin resistance....This 10-year prospective study demonstrated that plasma aldosterone levels predicted the development of insulin resistance in a general population

http://www.ncbi.nlm.nih.gov/pubmed/19428991
In conclusion, physiological concentrations of sex steroids did not modify aldosterone secretion by human adrenal cells. However, supraphysiological concentrations of DHT-stimulated aldosterone secretion by human adrenal cells by the calmodulin/CaMK and protein kinase C intracellular signaling pathways but independently of the classical androgen receptor. Supraphysiological doses of androgen may promote cardiovascular diseases via stimulation of aldosterone secretion.

Given that androgen receptor antagonist (e.g. RU58841) can stop/reverse male pattern baldness it is not clear how DHT causes male pattern baldness in hypertension/insulin resistance story.
 

anupamax

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Is it possible to scientifically determine if a person was killed by insulin? My stepfather passed recently under very suspicious circumstances. To put it shortly, we have reason to suspect that an insulin injection might have contributed to his death.
____________________________
market samurai ~ marketsamurai ~ marketsamurai.com
 

squeegee

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[youtube:1a1676f7]http://www.youtube.com/watch?v=uFP3_EgJ4N8[/youtube:1a1676f7]
 

majorsixth

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Originally posted by Broons85
if the cells are insulin resistant then they can't grow. Every cell needs insulin to divide. If your hair follicles aren't getting it then they'll stop growing. Then, when you get older, there won't be as many genetic "survival" cues floating around, and insulin is one of those survival cues. So, they'll likely die, leaving you permanently bald.

I completely agree with insulin resistance exacerbating male pattern baldness, if not being the main culprit in some cases, but, in your above statement you make reference to apoptosis of the hair follicle cells following their inability to under take cell division due to no up regulation to glucose.

A lot of guys actually believe this to be true, but it isn't ! The follicle cells just go into permenant telegan state. I know this to be true because i became a norwood 7 at 30 years old, with zero hairs on that shiny bonce, i remained that way for 20 years, then i started using finasteride along with minoxidil 5% and the occasional use of nizoral 2 %. The results where diffused regrowth over a norwood 3 pattern.

So you see if the follicles die like you have stated then this couldn't of possibly occur.

Another interesting point is that medium triglycerides are being used in studies of alzheimer's. This is because there is an hypothesis that insulin resistance plays apart in the condition. Since medium triglycerides require no emulisification these are utilised in the same way carbs are only they carry a different signature so are accepted as an energy source.

For those interested look up Dr Newport [alzheimer's]
 

squeegee

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OBJECTIVE Endothelial progenitor cells (EPCs) are decreased in number and function in type 2 diabetes. Mechanisms by which this dysfunction occurs are largely unknown. We tested the hypothesis that a chronic inflammatory environment leads to insulin signaling defects in EPCs and thereby reduces their survival. Modifying EPCs by a knockdown of nuclear factor-?B (NF-?B) can reverse the insulin signaling defects, improve EPC survival, and decrease neointimal hyperplasia in Zucker fatty rats postangioplasty.


RESEARCH DESIGN AND METHODS EPCs from Zucker fatty insulin-resistant rats were cultured and exposed to tumor necrosis factor-? (TNF-?). Insulin signaling defects and apoptosis were measured in the presence and absence of an NF-?B inhibitor, BAY11. Then, EPCs were modified by a knockdown of NF-?B (RelA) and exposed to TNF-?. For in vivo experiments, Zucker fatty rats were given modified EPCs post–carotid angioplasty. Tracking of EPCs was done at various time points, and neointimal hyperplasia was measured 3 weeks later.


RESULTS Insulin signaling as measured by the phosphorylated–to–total AKT ratio was reduced by 56% in EPCs exposed to TNF-?. Apoptosis was increased by 71%. These defects were reversed by pretreatment with an NF-?B inhibitor, BAY11. Modified EPCs exposed to TNF-? showed a lesser reduction (RelA 20%) in insulin-stimulated AKT phosphorylation versus a 55% reduction in unmodified EPCs. Apoptosis was 41% decreased for RelA knockdown EPCs. Noeintimal hyperplasia postangioplasty was significantly less in rats receiving modified EPCs than in controls (intima-to-media ratio 0.58 vs. 1.62).


CONCLUSIONS In conclusion, we have shown that insulin signaling and EPC survival is impaired in Zucker fatty insulin resistant rats. For the first time, we have shown that this defect can be significantly ameliorated by a knockdown of NF-?B and that these EPCs given to Zucker fatty rats decrease neointimal hyperplasia post–carotid angioplasty.
 

squeegee

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The correlation with Insulin Resistance and male pattern baldness is so there. It is an endothelial dysfunction. Impaired Nitric oxide, chronic inflammation,androgen problems.... male pattern baldness is the male version of PCOS.

http://www.jci.org/articles/view/44478#SEC3
 

Broons85

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majorsixth said:
Originally posted by Broons85
if the cells are insulin resistant then they can't grow. Every cell needs insulin to divide. If your hair follicles aren't getting it then they'll stop growing. Then, when you get older, there won't be as many genetic "survival" cues floating around, and insulin is one of those survival cues. So, they'll likely die, leaving you permanently bald.

I completely agree with insulin resistance exacerbating male pattern baldness, if not being the main culprit in some cases, but, in your above statement you make reference to apoptosis of the hair follicle cells following their inability to under take cell division due to no up regulation to glucose.

A lot of guys actually believe this to be true, but it isn't ! The follicle cells just go into permenant telegan state. I know this to be true because i became a norwood 7 at 30 years old, with zero hairs on that shiny bonce, i remained that way for 20 years, then i started using finasteride along with minoxidil 5% and the occasional use of nizoral 2 %. The results where diffused regrowth over a norwood 3 pattern.

So you see if the follicles die like you have stated then this couldn't of possibly occur.

I never said anything about apoptosis. Apoptosis is one form of cell death. It could be necrosis. You misunderstood me. I'm well aware that the folicles arrest and do not die right away, or maybe ever. I'm not saying the cells will die when you're 30, or 40, or 50. I'm saying that eventually the cells may die. But, the longer they're "resting," because they can't metabolize glucose, the more likely they are to die, either by apoptosis, necrosis, phagocytosis by immune or surrounding cells, etc.
 
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