QUOTE(Listener @ Sep 17 2007, 03:45 PM)
This is all very interesting research and i am pleased that there are ppl like you, still pushing the boundaries on the research of the pathogenesis of acne.
One of the reasons why i believe not washing my face helps my skin is because all the chemicals in surface lipids are used for desquamation etc.. and removing them just further reduces any kind of biochemical status the skin is attempting to achieve.
I read a text called 'the biochemistry of the skin: the brain on the outside' (something like that anyway) and it showed me just how complex the external aspect of the skin is... and it doesn't even start to suggest how complex the internal aspect could be.
I don't know if you recall Ndn but a long long time ago i sent you a PM explaining a theory i had about the acidity of the skin. I now think most of the theory was wrong but in one part i stated i thought the acidity content of the surface lipids was incorrect and any attempt to correct it with BP would have the adverse effect of messing up other chemical factors of the skin.
The question is: If we could increase the amount of linoleic acid for the synthesis of sebum would it also cause the sebum rate to slow down?
From what i read on that page 24 excerpt it would appear that the overproduction of oil causes the dilution of linoleic acid as opposed to the inadequate supply of linoleic acid causes excess oil to be produced.
I hope one day this all can account for results for someone that can piece if all together in a coherent and logical regimen somehow
You are so right, I misread it. It seems that the amount of linoleic acid content stays the same, but the more sebum is produced, the more it gets diluted by oleic acid due to how much free fatty acid (linoleic) is in the blood
I typed out the important aspects of the book on the linoelic acid portion:
A link between comedogensis and a low sebum level of linoleic acid was proposed by Downing and co-authors. They found that patients with acne had a significantly lower level of linoleic acid in their skin surface lipids that normal individuals. Subsequent studies have suggested that this effect relates to the higher sebum secretion rates characteristic of acne, since there is an inverse relationship between the secretion rate and the linoleate content of the surface wax esters, which are purely of sebaceous origin. Conversely, a reduction in the rate of sebum secretion by treatment by treatment with the ant-androgen cyproterone acetate, or with oral isotretinoin, cause a corresponding increase in the linoleic acid content of the sebaceous lipds.
Once sebum synthesis begins, no further lipids are accepted from circulation, so that the more sebum that is synthesized per cell, the more initial linoleate content will be diluted.
It is proposed that when the secretion rate of sebum is high, as in acne, and, as a result, its linoleate concentration is low, the cells of the follicular epithelium might thereby be subjected to lipds that are deficient in essential fatty acids.
I wonder if there is any way to regulate the amount of oleic acid the sebaceous glands can use, perhaps by regulating the production of oleic acid by our bodies (since the body produces the omega 9 fat by itself).
That book on the biochemisty of the skin sounds interesting. It's pretty interesting reading these books regarding just the skin, makes you realize how vast and complex it really is even more so than we know of (our typical information we usually read), there just has to be something we are overlooking.
I also looked up cyproterone acetate as used in the study and found that:
Cyproterone Acetate is used to reduce sex drive in men which have excessive sex drive and for the treatment of pronounced sexual aggression. It is also prescribed to treat severe hirsuitism in woman of childbearing age and also androgenetic alopecia in women. Like cimitedine and other similar type drugs Cyproterone acetate exerts its effects by blocking the binding of DHT dihydrotestosterone to its receptors.