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Anyone who alleges that Environ products thin out the skin is either completely
ignorant of the action of vitamin A, or are merely spreading malicious rumors.
The facts about the action of vitamin A and the anti-oxidants on the skin are
backed by extensive and profound medical research over the past 50 years.
There are no remaining doubts about the role and action of vitamin A.
The facts are as follows:
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Vitamin A is the central driving factor in the development of normal,
healthy human tissue including all parts of the skin. This is from
conception to death. If vitamin A was to disappear tomorrow for some
mysterious reason, no more humans would be born in the normal,
recognizable form. We are human because of vitamin A.
Skin becomes thin because of a general lack of vitamin A, sun damage,
loss of sex hormones, general ageing and excess cortisone.
The only proven method that exists to thicken skin is the use of vitamin
A. It is an over-simplification to say that it is only vitamin A, but fact of
the matter is that without it the other treatments do not work. This is a
simple physiological fact.
Vitamin A improves skin quality and thickness to such an extent that one
has to go to extraordinary measures in order to get enough vitamin A
into the skin like using ionto and sonophoresis or the Cosmetic Roll-CIT.
If the opposite were true, such treatments would destroy skin and not
help even more than just simple application.
Environ products are especially good at improving skin health because
of its carefully balanced combination of vitamin A and anti-oxidants in
carefully selected carrier and stabilizing ingredients.
Any product range which does not include molecules proven to stimulate
tissue development (differentiation) is essentially making a false claim.
The different molecules involved in this process are well identified.
Their receptors in the cell nucleus have been identified. The mechanisms
by which new skin cells are produced are described in enough detail to
know that vitamin A is the only molecule without which the tissue
differentiation system would collapse.
The only time when vitamin A can make the skin thin is when the socalled retinoid reaction occurs. This is an irritant contact dermatitis. It is
transient and does not leave any damage to the skin. Environ products
goes out of its way in training to ensure that the pattern of application
and the principles of skin treatment are adhered to which avoids this
problem. The thinner skin here is a result of the inflammatory reaction,
but reverses as soon as the reaction subsides and the vitamin A receptors
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are more active again. Medium to long term usage of the Environ
products leads to histologically proven thicker and more vital skin.
It would be a lie to say that Environ products contain absolutely every
molecule required to rejuvenate skin, because the information describing
the complete system does not exist. Any cream has limited space to
include different essential molecules. The truth is that no single molecule
can be claimed to drive the entire process, but vitamin A is undoubtedly
the key to the whole process. There must always be a fine balance of
elements with sufficient concentrations of vitamin A to manage this
process properly.
I think that it is very important to speak to any therapist to try and gather
as much accurate information as you can on the origins of such rumours.
Perhaps one can educate people to the truth of the matter in the process.
Please ask them for references in the published medical literature to
support their allegations, or other articles they may have read, which
could have instilled this erroneous idea into their thinking. Should we be
challenged on this subject in a similar manner, you may supply them
with the list of references I have attached at the bottom.
References
[1].Introduction, Braham Shroot, Retinoids A Clinician's Guide, Second Edition, page 1,
Edited by Nicholas J Lowe and Ronald Marks , Publisher Martin Dunitz 1998.
[2.] Vitamin A and Caretenoids: Flexible Actions of Inflexible Molecules, James Allen
Olson, Retinoids: From Basic Science to Clinical Applications, Edited by M A Livrea
and G Vidali, Page 11 - 19 Published by Birkhauser 1994.
[3] F Chytil New Horizons in Retinoid Research,
Retinoids: From Basic Science to Clinical Applications, Edited by M A Livrea and G
Vidali, Published by Birkhauser 1994.
[4] Tazarotene and other novel receptor- and function-selective retinoids S Nagpal and R
A S Chandraratna Retinoids & Lipid-soluble vitamins in clinical practice. Vol. 14
Number 1, Page 2 – 6.
[5] Induction of cytochrome P450 3A by retinoids in rat hepatocyte culture,
Jurima-Romet M, Neigh S and Casley W L, Human and Experimental Toxicology, 1997,
16, page 198-203.
[6] Retinoid transport in rodents, William S Blaner et al, Retinoids: From Basic Science
to Clinical Applications, Edited by M A Livrea and G Vidali, page 53- 78 Published by
Birkhauser 1994.
[7] Modulation of retinoid metabolism by binding proteins.
David E Ong et al. Retinoids: From Basic Science to Clinical Applications, Edited by M
A Livrea and G Vidali , page 79-89 Published by Birkhauser 1994.
[8] Retinoic Acid Synthesis from Holocellular Retinol Binding Protein
S Ottonello et al. Retinoids: From Basic Science to Clinical Applications, Edited by M A
Livrea and G Vidali, page 91-102 Published by Birkhauser 1994.
[9] Transport Mechanisms and Specific Receptors, Braham Shroot, Retinoids A
Clinician's Guide, Second Edition, page 9, Edited by Nicholas J Lowe and Ronald Marks,
Publisher Martin Dunitz 1998.
[10] Retinoid nuclear receptors. Roshantha AS Chandraratna, Elliott S Klein
Retinoids A Clinician's Guide, Second Edition, page 22-32, Edited by Nicholas J Lowe
and Ronald Marks, Publisher Martin Dunitz 1998.
[11] Retinoid Response Pathways Magnus Pfahl,
Retinoids: From Basic Science to Clinical Applications, Edited by M A Livrea and G
Vidali, page 115-126 Published by Birkhauser 1994.
[12] Vitamin D - a modulator of cell proliferation. R Gniadecki
Retinoids & Lipid-soluble vitamins in clinical practice. Vol. 13 Number 2, page 55-59
May 1997.
[13] Transcriptional activation of the human p21waf1/cip1 gene by retinoic acid receptor.
Liu M, Iavorone A and Freedman LP, The Journal of Biological Chemistry, 1996, 271,
31723-31728.
[14] Ultra-violet Irradiation of human skin causes functional vitamin A deficiency,
preventable by all-trans retinoic acid pre-treatment. Wang et al., Nature Medicine 1999,
5, 418 - 422.
[15] Retinoids in the management of renal cell carcinoma, B Escudier and P Y Dietrich ,
Retinoids 1998 , Volume 14 Number 2 , p51-53.
[16] Blomhoff R. Vitamin A in Health and Disease, Marcel Dekker, New York 1994.
[17] Receptors, Models for Binding, Trafficking and Signalling, Douglas Lauffenburger,
Jennifer Linderman, Oxford University Press 1993.
[18] Rusting of the Epidermal Engine, R Marks, Retinoids 1999, Vol. 15 No3,
Page 86-88.
[19] Introduction to Mathematics for Life Scientists, E Batschelet, Springer Verlag
Berlin , 1973.
[20] Ligand Induced Transcription By Nuclear Receptors, D M Heery, M G Parker,
Retinoids 1997, Vol. 13 No 1, Page 26 – 30.
[21] New Retinoids For Use In Breast Cancer, L Isnardi, P Raffo and S Toma, Retinoids
1998, Vol. 14 No 1, Page 78-80.
[22] Editorial, E J Woods, Retinoids 1998, Vol. 14 No 1, Page 77.
[23] John S Strauss, Dermatology in General Practice, T. B. Fitzpatric et al, Third Edition
McGraw Hill 1987, Page 666-679.
[24] Retinoylation Of Proteins In Vivo: Potential Physiological an Pharmacological
Implications A M Myhre et al, Retinoids, Vol. 15 No 3 August 1999, 112 – 117.
[25] How Good Are Sunscreens?, R Marks, Retinoids 1997, Vol. 13 No 1, Page 133-136.
[26] Robert A Schwatrz et al, Epithelial Pre-cancerous Lesions, Dermatology in General
Practice, T. B. Fitzpatric et al, Third Edition McGraw Hill 1987, Page 736-740.
[27] Retinoid Receptors, H Törmä, Retinoids 1997, Vol. 15 No 3, Page 101.