Lichen Sclerosis
Q: Hi there - I have been following a Paleo Diet for a few weeks now and there is no doubt that I feel much better for it. I did not need to lose weight and I always regarded myself as pretty fit and healthy. However, a little while back I developed a troublesome skin condition called Lichen Sclerosis. Have you ever been asked about this condition and suggested dietary changes? I think part of the problem is that the etiology is not fully understood but many doctors seem to think it has an autoimmune component though I have read recent research that suggests oxidative damage plays a part and that antioxidant therapy may be useful in treatment. This condition is supposedly incurable (though manageable with potent steroids) but I'm sure it would give a great many people some comfort if simple dietary changes could help. Would be really great to hear your thoughts.
Simon
A: Dear Simon,
The available evidence indicates that an autoimmune component likely occurs with Lichen Sclerosis (LS). With all autoimmune diseases, an autoantigen (self protein) exists and represents the target protein being attacked by the immune system. About 75 % of LS patients maintain an IgG autoantibody to Extra Cellular Matrix Protein 1 (ECM1)1. Acceleration of ECM1 deposition in dermal (skin) blood vessels may underlie the disease symptoms 2, 3. So the question now arises, what causes an accelerated deposition of ECMI in dermal blood vessels in LS patients? The available evidence indicates that increased concentrations of a ubiquitous enzyme in the body called tissue transglutaminase (TG2) is primarily responsible for excessive ECM1 accumulation3. In medical terms, an increase in a concentration of a substance in the bloodstream by another substance is called "upregulation".
So, in LS patients, an upregulation of TG2 causes an upregulation and increased deposition of ECMI in the skin blood vessels in the affected area of the body. The next question to be posed is, what event or events trigger an upregulation of TG2? When we answer this question, then dietary recommendations advocated by the Paleo Diet will make sense. A storage protein called gliadin which is fournd in wheat, rye, barley and oats is known to upregulate TG2 4-7. Hence grain free diets may prove to be therapeutic for LS patients, although no current randomized controlled trials of this intervention strategy have yet been conducted.
Cordially,Loren Cordain, Ph.D., ProfessorReferences:Chan I, Oyama N, Neill SM, Wojnarowska F, Black MM, McGrath JA. Characterization of IgG autoantibodies to extracellular matrix protein 1 in lichen sclerosus. Clin Exp Dermatol. 2004 Sep;29(5):499-504. Kowalewski C, Kozlowska A, Chan I, Górska M, Wozniak K, Jablonska S, McGrath JA.Three-dimensional imaging reveals major changes in skin microvasculature in lipoid proteinosis and lichen sclerosus. J Dermatol Sci. 2005 Jun;38(3):215-24. Epub 2005 Mar 3. Fisher M, Jones RA, Huang L, Haylor JL, El Nahas M, Griffin M, Johnson TS. Modulation of tissue transglutaminase in tubular epithelial cells alters extracellular matrix levels: a potential mechanism of tissue scarring. Matrix Biol. 2009 Jan;28(1):20-31. Epub 2008 Nov 5. Michaelsson, G., Ahs, S., Hammarstrom, I., Lundin, I. P., & Hagforsen, E. Gluten-free diet in psoriasis patients with antibodies to gliadin results in decreased expression of tissue transglutaminase and fewer ki67+ cells in the dermis. Acta Dermato-Venereologica, 2003; 83(6):425-429. Biagi F, Campanella J, Laforenza U, Gastaldi G, Tritto S, Grazioli M, Villanacci V, Corazza GR. Transglutaminase 2 in the enterocytes is celiac specific and gluten dependent. Dig Liver Dis. 2006 Sep;38(9):652-8. Gorgun J, Portyanko A, Marakhouski Y, Cherstvoy E. Tissue transglutaminase expression in celiac mucosa: an immunohistochemical study. Virchows Arch. 2009 Oct;455(4):363-73. Villanacci V, Not T, Sblattero D, Gaiotto T, Chirdo F, Galletti A, Bassotti G. Mucosal tissue transglutaminase expression in celiac disease. J Cell Mol Med. 2009 Feb;13(2):334-40.
Stevia
Q: Is Stevia Paleo? I have attempted to find an answer for this and the information I've found is conflicting at best. Please advise!!Jeff
A: Dear Jeff,
There's some scientific evidence to support the notion that Stevia is safe, even in type 2 diabetes patients1, 2. Furthermore, it has been demonstrated to have antihypertensive properties, as shown by Chan et al.3 and a long-term study4. Having said this, I am not aware of any study examining the potential antinutrient (lectins or saponins) content of the plant, hence we do not know the possible adverse effect of consuming this plant on a daily basis. Hunterh-gatherers used to consume a wide range of plants, thereby minimizing the amount of a single bioactive compound ingested and its toxicity. It is known that rotating the kind of plants is a good strategy in order to decrease food allergy and intolerance.
From an evolutionary standpoint we should look at nutrition as "whole food" rather than nutrients per se. The bottom line is that Stevia seems to be safe, but we need more research to rule out possible side effects.
I hope this is helpful,
Maelán
References
Gregersen S, Jeppesen PB, Holst JJ, Hermansen K. Antihyperglycemic effects of stevioside in type 2 diabetic subjects. Metabolism. 2004 Jan;53(1):73-6. Barriocanal LA, Palacios M, Benitez G, Benitez S, Jimenez JT, Jimenez N, Rojas V. Apparent lack of pharmacological effect of steviol glycosides used as sweeteners in humans. A pilot study of repeated exposures in some normotensive and hypotensive individuals and in Type 1 and Type 2 diabetics. Regul Toxicol Pharmacol. 2008 Jun;51(1):37-41. Epub 2008 Mar 5. Chan P, Tomlinson B, Chen YJ, Liu JC, Hsieh MH, Cheng JT. A double-blind placebo-controlled study of the effectiveness and tolerability of oral stevioside in human hypertension. Br J Clin Pharmacol. 2000 Sep;50(3):215-20. Hsieh MH, Chan P, Sue YM, Liu JC, Liang TH, Huang TY, Tomlinson B, Chow MS, Kao PF, Chen YJ. Clin Ther. 2003 Nov;25(11):2797-808. Efficacy and tolerability of oral stevioside in patients with mild essential hypertension: a two-year, randomized, placebo-controlled study.
