DarkDays said:
What if, and this is only a wild swing, the reason why it is harder to get hair back that has been lost longer, and despite treatment, is because of atherosclerosis.
Remember that there are studies showing that those who have pattern baldness(as I think this applies to both genders in more ways than most suspect) are more likely to have various issues with their vascular system, and the head, the infamous horseshoe area, is mostly small capillaries and no larger veins. This in turn gives the follicles less materials to work with(oxygen and nutrients) which then causes DNA damage in the follicle.
Dihydrotestosterone suppresses foam cell formation and attenuates atherosclerosis development.
http://www.ncbi.nlm.nih.gov/pubmed/20427482
Now remember, Minoxidil is a vasodilator so it might actually be taking those veins filled with gunk and making them wider giving the follicle both more blood.
This might explain why wounding works for some as the wound healing initiates angiogenesis that creates new capillaries.
I at least would say that this explains why some people who have been bald for a very long time and then lose all DHT can't grow back their hair completely, as the capillaries are just basically not managing to get enough crap into the follicle, plus the DHT has already damaged the veins.
I know that some will say "but if I cut my hair my scalp bleeds so there is blood there, your theory doesn't hold up!"
Now take into account that it is a question of how much the blood is actually delivering and whether it is managing to get enough to the scalp. There is definitely blood there, but what it is managing to deliver is also of essence and whether it is getting crap out at the same time.
Edit
I also wanted to add that atherosclerosis might explain why finasteride and such lose efficiacy over time as the placque continues to form despite the big 3.
Here is another good study:
Dihydrotestosterone Decreases Tumor Necrosis Factor-
and Lipopolysaccharide-Induced Inflammatory Response
in Human Endothelial Cells
Dihydrotestosterone Decreases Tumor Necrosis Factor-{alpha} and Lipopolysaccharide-Induced Inflammatory Response in Human Endothelial Cells
Giuseppe Danilo Norata, Gianpaolo Tibolla, Paul Maria Seccomandi, Angelo Poletti and Alberico Luigi Catapano
Department of Pharmacological Sciences (G.D.N., G.T., P.M.S., A.L.C.) and Institute of Endocrinology (A.P.), Centre of Excellence on Neurodegenerative Diseases, University of Milan, 20133 Milan, Italy; and Center for the Prevention and Therapy of Global Cardiovascular Risk (G.D.N., A.L.C.), Italian Society for the Study of Atherosclerosis, Bassini Hospital, 20092 Cinisello Balsamo, Italy
Address all correspondence and requests for reprints to: Giuseppe Danilo Norata, Ph.D., Department of Pharmacological Sciences, University of Milan, Italy, Via Balzaretti 9, 20133, Milan, Italy. E-mail:
Danilo.Norata@unimi.it.
Context: An increasing body of evidence suggests that testosterone may exert beneficial effects on the development of atherosclerosis. It was suggested that testosterone may act after conversion into estradiol and activation of the estrogen receptors; however, a direct role of androgens on the vascular wall has been proposed.
Objective: We investigated the effects of dihydrotestosterone on the proinflammatory response observed in human endothelial cells.
Design: Human endothelial cells isolated from umbilical cords were incubated with lipopolysaccharide or TNF{alpha} in the presence or absence of dihydrotestosterone (DHT). mRNA and cellular proteins were processed for gene expression studies, and transient transfection experiments were performed to investigate molecular mechanisms involved in the effects observed.
Setting: These studies took place at the Department of Pharmacological Sciences, University of Milan, Milan, Italy.
Results: Lipopolysaccharide and TNF{alpha} induced VCAM-1 and ICAM-1 mRNA and protein expression, as detected by real-time quantitative PCR, fluorescence-activated cell sorting, and confocal microscopy, but this effect was inhibited when cells were incubated with DHT. In addition, DHT inhibited mRNA expression of IL-6, MCP-1, CD40, TLR4, PAI-1, and Cox-2 and the release of cytokines and chemokines such as GRO, granulocyte-macrophage colony-stimulating factor, and TNF. The DHT effect was counteracted by bicalutamide, an antagonist of the androgen receptor. Furthermore, when cells were cotransfected with a Cox-2 promoter or a 3X-NF-{kappa}B luciferase reporter vector and a plasmid expressing the human androgen receptor, DHT treatment inhibited the increase of the luciferase activity observed with TNF{alpha}.
Conclusion: DHT could positively regulate endothelial function through the control of the inflammatory response mediated by nuclear factor-{kappa}B in endothelial cells.
