Starting a sensible discussion & compilation of facts as opposed to all the full-caveman-no-water-touching-face-dead-skin-mask threads.
About the acid mantle, lipid barrier, retinoid production and more.
Your skin isn't dead leather & your sebum isn't dead grease. They are ecosystems for enzymes and other substances that play vital roles in skin function. Your sebum contains living cells that produce these substances. Substances that protect and exfoliate. That inhibit DHT production which is a major factor in oily skin, acne and male pattern baldness. Substances that inhibit melanin, reducing hyperpigmentation, Substances that produce retinoids & ceramides. All those things you pay big money for in moisturizers & creams. Those ceramides & other lipids are also stripped away by cleansers. Emulsifying agents are even in lotions & creams you think are helping your skin. Stripping your skin of all these things makes it hard for skin to function and causes the problems we then try to solve with more products. Soaps, cleansers and topicals prevent your skin from functioning.
Acid Mantle - a layer of sebum and sweat that, among other things, makes the surface of your skin slightly acidic which inhibits the overgrowth of harmful microbes. In addition, the various enzymes involved in normal cell desquammation (exfoliation) need an acidic environment to function. Even store bought BHA and AHA topicals need to be the correct PH to function.
Soaps are alkaline and strip it away. It can take hours to recover during which time your skin is vulnerable to microbes and cells don't exfoliate freely without clogging pores. Tap water in most areas is also slightly alkaline, but your skin should recover from the tap water fairly quickly.
Sebum/lipid permeability barrier
- Normal sebum contains enzymes that inhibit the formation of DHT, the form of testosterone that aggravates acne. It also contains enzymes that dissolve the desmosomes that bind your skin cells together so they can exfoliate normally.
Related thread on Sebum and Linoleic Acid: http://www.acne.org/...pical-solution/
Linoleic acid is a major component of normal sebum. A deficiency in linoleic acid has been found to be involved in many skin issues including acne, excema, atopic dermatis, just plain sensitive easily irritated skin, etc. This applies to all mammals. Where linoleic acid is deficient, oleic acid is used. This produces sebum that is greasy looking and sticky which causes skin cells to be clump together and clog pores.
Sphingolipids, ceramides TBC
P. Acnes TBC
Evidence that washing away your sebum stimulates more production of sebum.
Or at least, the abstract of this peer reviewed paper says so. the full text is available here: http://www.nature.co...df/5610517a.pdf I haven't read it yet.
The regulation of epidermal lipid synthesis by permeability barrier requirements.
A major function of the skin is to prevent the loss of fluids. The barrier to fluid loss resides in the intercellular lipids (primarily sterols, fatty acids, and sphingolipids) of the stratum corneum. The epidermis is a very active site of lipid synthesis and when the permeability barrier is disrupted by topical solvents or detergents a marked stimulation of sterol, fatty acid, and sphingolipid synthesis occurs. Essential fatty acid deficient mice, with a chronic disturbance in barrier function, also have an increase in epidermal lipid synthesis. When the defect in barrier function is artificially corrected by occlusion with a water vapor impermeable membrane the increase in epidermal lipid synthesis is prevented, suggesting that water flux may be a regulatory factor. The activity of the key rate limiting enzyme in cholesterol synthesis, HMG CoA reductase is increased following barrier disruption due to both an increased quantity of enzyme and an increase in activation state. Similarly, the activity of serine palmitoyl transferase, the rate limiting enzyme in sphingolipid synthesis is also increased following barrier disruption. Occlusion prevents the increase in HMG CoA reductase and serine palmitoyl transferase activity. When the increase in epidermal lipid synthesis is inhibited by occlusion the characteristic rapid return of stratum corneum lipids and recovery of barrier function is prevented. Moreover, when epidermal cholesterol synthesis is inhibited by lovastatin, an inhibitor of HMG CoA reductase, the rate of recovery of barrier structure and function is delayed. Similarly, B chloroalanine, an inhibitor of serine palmitoyl transferase and sphingolipid synthesis, also impairs barrier recovery. Thus, disruption of the barrier stimulates epidermal lipid synthesis which provides the lipids necessary for the repair of the barrier. The signals that initiate and coordinate this response are yet to be defined, but the understanding of this process may allow for pharmacological interventions that will specifically disrupt the barrier and allow for the transcutaneous delivery of drugs.
Edited by alternativista, 14 July 2014 - 05:45 PM.