Psoriasis & Blood Type Diet
How the ER4YT diet can help in psoriasis
Date: 5/18/2006 8:40:44 AM ( 18 y ) ... viewed 8728 times By Dr. Tom Greenfield
http://www.dadamo.com/bloggers/24/archives/00000031.htm
Psoriasis is understood to be an autoimmune disease whereby the concentration of soluble intercellular adhesion molecule-1 (ICAM-1) and other CAMs in serum increase during psoriatic inflammation (1). This is also the case in a variety of other autoimmune diseases. ICAM is a glycoprotein ligand (binding site) expressed on endothelial (surface) cells and also on leucocytes (white blood cells), and is one mechanism for migration of leucocytes towards diseased tissue. In addition to being found in high amounts at psoriatic lesion sites, biopsy of skin that is clinically free of lesions in psoriasis sufferers is characterised by aberrant adhesion molecule expression of (amongst others) ICAM on skin-producing cells (2).
ICAM-1, like the ABO and Lewis blood group antigens, is a cell surface carbohydrate. ICAM-1 is also a signalling molecule that binds leucocytes, which in turn can produce inflammatory agents. Circumstantial evidence would suggest that the principles outlined in the ER4YT book series may favourably affect disease processes related to various cell surface carbohydrate antigens.
Although there is little documented evidence of differences between ABO blood group and psoriasis, research shows that individuals with the A antigen may be more prone to the disease; those with other genetic factors including variations in the subgroups and minor blood groups MNSs, Duffy and Lewis negative, or Le(a-b-) individuals may also have higher incidence of psoriasis (3-6); genetic expression of a type 1 cytokine profile (interleukin-2, interferon-gamma and tumor necrosis factor-alpha) may also play a part in predisposition to psoriatic lesions (3). Candidiasis or altered immune response to Candida albicans may be implicated in the cause of psoriasis (7,8), and effective treatment for this condition differs according to blood group.
Any discussion of which particular elements of the Human Individuality Program approach may be responsible for helping individuals with a condition or disease is speculative until specific research shows otherwise. The concept of eating according to your individual genetic expression is however a holistic one, and appears to take into account many aspects of alterations in health that may relate to psoriasis (such as immune response and inflammation) which may differ between individuals. In practice I have seen some patients with psoriasis respond favourably to changes in their diet over a period of time, but in addition speedy symptom relief can often be achieved with topical application of preparations such as those containing barberry (mahonia) (9).
Specific efforts to reduce ICAM expression may be useful for individuals with psoriasis (10): vitamin A (and natural carotenoids) may help individuals with psoriasis by decreasing local production of ICAM (11), and these may be obtained through diet; the herb Dan shen (Salvia miltiorrhiza) is an example of a natural medicine that may downregulate ICAM expression (12).
Finally, new research suggests that oxidation of fatty acids may also play a part in the of psoriasis (13), and the disease process may be suppressed by blocking the production of an oxidising enzyme. Natural antioxidant substances can be found either through the diet or as supplements, and this may also give more weight to the potential therapeutic action of vitamin A and carotenoids (mentioned above). Eating according to blood group will automatically provide a diet rich in natural carotenes.
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References:
(1)Schopf RE, Naumann S, Rehder M, Morsches B.
Soluble intercellular adhesion molecule-1 levels in patients with psoriasis.
Br J Dermatol. 1993 Jan;128(1):34-7.
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(2) Uyemura K, Yamamura M, Fivenson DF, Modlin RL, Nickoloff BJ.
The cytokine network in lesional and lesion-free psoriatic skin is characterized by a T-helper type 1 cell-mediated response.
Invest Dermatol. 1993 Nov;101(5):701-5.
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(3) Wuepper KD, Coulter SN, Haberman A.
Psoriasis vulgaris: a genetic approach.
J Invest Dermatol. 1990 Nov;95(5):2S-4S. Review.
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(4) Turowska B, Pietrzyk JJ, Turowski G, Kapinska-Mrowska M.
Blood and serum group systems in psoriasis.
Acta Med Pol. 1980;21(2):165-72.
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(5) Walter H, Brachtel R, Eckes L, Hilling M.
Psoriasis vulgaris and genetic markers.
Hum Genet. 1977 Jun 30;37(2):169-81.
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(6) Beckman L, Bergdahl K, Cedergren B, Liden S.
Genetic markers in psoriasis. Correlations to age at onset, continuity of symptoms and the risk of developing the disease.
Acta Derm Venereol. 1977;57(3):247-51.
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(7) Liang YS, Wen HQ, Xiao R. Related Articles, Links
[Serum levels of antibodies for IgG, IgA, and IgM against the fungi antigen in psoriasis vulgaris]
Hunan Yi Ke Da Xue Xue Bao. 2003 Dec;28(6):638-40.
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(8) Waldman A, Gilhar A, Duek L, Berdicevsky I.
Incidence of Candida in psoriasis--a study on the fungal flora of psoriatic patients.
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(9) Augustin M, Andrees U, Grimme H, Schopf E, Simon J.
Effects of Mahonia aquifolium ointment on the expression of adhesion, proliferation, and activation markers in the skin of patients with psoriasis.
Forsch Komplementarmed. 1999 Apr;6 Suppl 2:19-21.
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(10) Yusuf-Makagiansar H, Anderson ME, Yakovleva TV, Murray JS, Siahaan TJ.
Inhibition of LFA-1/ICAM-1 and VLA-4/VCAM-1 as a therapeutic approach to inflammation and autoimmune diseases.
Med Res Rev. 2002 Mar;22(2):146-67.
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(11) Gottlieb S, Hayes E, Gilleaudeau P, Cardinale I, Gottlieb AB, Krueger JG.
Cellular actions of etretinate in psoriasis: enhanced epidermal differentiation and reduced cell-mediated inflammation are unexpected outcomes.
J Cutan Pathol. 1996 Oct;23(5):404-18.
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(12) Ren de C, Du GH, Zhang JT.
Inhibitory effect of the water-soluble extract of Salvia miltiorrhiza on neutrophil-endothelial adhesion.
Jpn J Pharmacol. 2002 Nov;90(3):276-80.
PMID: 12499583
(13) Caspary F, Elliott G, Nave BT, Verzaal P, Rohrbach M, Das PK, Nagelkerken L, Nieland JD.
A new therapeutic approach to treat psoriasis by inhibition of fatty acid oxidation by Etomoxir.
Br J Dermatol. 2005 Nov;153(5):937-44.
PMID: [16225603]
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