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Insulin resistance, PCOS, and male pattern baldness

Discussion in 'Men's General Hair Loss Discussions' started by Broons85, Sep 27, 2010.

  1. freakout

    freakout Experienced Member

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    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.

    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.
     
  2. balder

    balder Established Member

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

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

     
  3. S Foote.

    S Foote. Experienced Member

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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.
     
  4. freakout

    freakout Experienced Member

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  5. freakout

    freakout Experienced Member

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    This part is more of a description of the pathology. A root-cause analysis has yet to isolate causative factors.
     
  6. freakout

    freakout Experienced Member

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    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.
     
  7. freakout

    freakout Experienced Member

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    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?
     
  8. freakout

    freakout Experienced Member

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    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?
     
  9. S Foote.

    S Foote. Experienced Member

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    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.
     
  10. squeegee

    squeegee Banned

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  11. guy83

    guy83 Established Member

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    i couldnt understand a word. so drinking a no or a yay
     
  12. Broons85

    Broons85 Member

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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).
     
  13. czvezda

    czvezda New Member

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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.
     
  14. anupamax

    anupamax New Member

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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
     
  15. squeegee

    squeegee Banned

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

    majorsixth Established Member

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    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]
     
  17. squeegee

    squeegee Banned

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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.
     
  18. squeegee

    squeegee Banned

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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
     
  19. Broons85

    Broons85 Member

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    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.
     
  20. powersam

    powersam Senior Member

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    !!!!!

    Been saying this for around 8 years now.
     

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