Skin does show several things that indicate what is right and what is wrong in our body. All disease processes that affect the internal organs also affect the skin and vice versa.
So, we, dermatologists, can identify such problems at a very early stage, and can guide the patient in the right direction, so as to prevent the progression of such diseases.
All diseases are result of interplay of inflammation, oxidative stress and proliferation resulting from imbalance of apoptotic and antiapoptotic factors.
Persistent acne, severe and chronic seborroeic dermatitis (dandruff), multiple benign growths like dermatosis papulosa nigra (DPN) and acrochordon, early onset female pattern hair loss and male pattern hair loss (female and male baldness), acanthosis nigricans (velvety thickening of the skin), chronic candidiasis, recurrent furuncles (boils), etc., can be regarded as cutaneous manifestations of metabolic syndrome (a constellation of hypertension, dyslipidemia, obesity).
Common skin diseases such as prosiasis, lichen planus, vitiligo, atopic dermatitis, alopecia areata etc., are also reported to be aggravated by oxidative stress, in turn linked to our diet and life styles.
Several studies in recent years have found close correlation between dietary factors and development of many skin diseases, especially acne, psoriasis,lichen planus, vitiligo, and metabolic syndrome. Given below are some important updates.
Milk Consumption Worsens Acne and Promotes Chronic Diseases:
Consumption of cow’s milk and cow’s milk protein result in changes of the hormonal axis of insulin, growth hormone and insulin-like growth factor-1(IGF-1) in humans. Raised levels of serum IGF-1 can explain the epidemic incidence of adolescent acne in Western milk-consuming societies. Acne can be regarded as a model for chronic Western diseases with pathologically increased IGF-1-stimulation.
See:
- Melnik B. Milk consumption: aggravating factor of acne and promoter of chronic diseases of Western societies. Journal der Deutschen Dermatologischen Gesellschaft. April 2009;7(4):364–370. DOI: 10.1111/j.1610-0387.2009.07019.x. Free Full text
- Solomons NW. Nature’s Perfect Food Revisited: Recent Insights on Milk Consumption and Chronic Disease Risk. DOI: 10.1301/002966402320243278. Nutrition Reviews. June 2002;60(6):180–182. Abstract
- Danby FW. Acne: Diet and acnegenesis. Indian Dermatol Online J [serial online] 2011 [cited 2011 Aug 21];2:2-5. Available from: http://www.idoj.in/text.asp?2011/2/1/2/79851
Role of diet in acne:
A large body of evidence now exists showing how diet may directly or indirectly influence the development acne.
See:
- Cordain L. Implications for the role of diet in acne. Semin Cutan Med Surg 24:84-91. Available at
http://thepaleodiet.com/download/18/ - Danby FW. Acne: Diet and acnegenesis. Indian Dermatol Online J [serial online] 2011 [cited 2011 Aug 21];2:2-5. Available from: http://www.idoj.in/text.asp?2011/2/1/2/79851
Hyperinsulinemic diseases of civilization: more than just syndrome X [See]
More evidence to link psoriasis with metabolic syndrome:
Several reports in the recent years have suggested associations between psoriasis and metabolic syndrome sidorders. Results of a new study at Reykjavik’s Landspitali, the National University hospital of Iceland suggest that patients — especially women — with psoriasis may be at increased risk for metabolic syndrome. The study involving more than 6,500 people found the prevalence of metabolic syndrome to be higher among patients with psoriasis (40 percent) than among those without (23 percent) [See Love TJ et al. Prevalence of the Metabolic Syndrome in Psoriasis. Arch Dermatol. Published online December 20, 2010. doi:10.1001/archdermatol.2010.370. Abstract | Report
See Other Studies:
- Cohen AD. Psoriasis and the Metabolic Syndrome. Acta Derm Venereol 2007;87:506–509. Full Text
- Gottlieb AB et al. Psoriasis and the Metabolic Syndrome. Journal of Drugs in Dermatology. June, 2008. Full Text
- Sommer DM et al. Increased prevalence of the metabolic syndrome in patients with moderate to severe psoriasis Arch Derm Res. 2006;298(7):321-328. Abstract
- Gisondi P et al. Prevalence of metabolic syndrome in patients with psoriasis: a hospital-based case–control study
British Journal of Dermatology. July 2007;157(1):68–73. Full text - Kimball AB et al. National Psoriasis Foundation clinical consensus on psoriasis co-morbidities and recommendations for screening. J Am Acad Dermatol. 2008 Jun;58(6):1031-42. Epub 2008 Mar 4. Available at http://www.uphs.upenn.edu/dermatol/faculty/pdf/gelfand/NPFcomorbidities.pdf
- Rahat S. Azfar RS, Gelfand JM. Psoriasis and Metabolic Disease: Epidemiology and Pathophysiology. Curr Opin Rheumatol. 2008;20(4):416-422. http://www.uphs.upenn.edu/dermatol/faculty/pdf/gelfand/BOR309.pdf
- More Evidence of Psoriasis Link to Metabolic Diseases Report
- Wolters M. Diet and psoriasis: experimental data and clinical evidence. Br J Dermatol. 2005 Oct;153(4):706-14. Full Text
Diet has been suggested to play a role in the aetiology and pathogenesis of psoriasis. Fasting periods, low-energy diets and vegetarian diets improved psoriasis symptoms in some studies, and diets rich in n-3 polyunsaturated fatty acids from fish oil also showed beneficial effects.
See:
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Wolters M. Diet and psoriasis: experimental data and clinical evidence. Br J Dermatol. 2005 Oct;153(4):706-14. Full Text
Vitiligo and Diet:
Given the pivotal role of oxidative stress in the pathogenesis of vitiligo, food contaminants/additives/preservatives and cosmetic products could aggravate vitiligo because they produce oxidative stress in the skin. Increased consumption of omega-6 or a vegetable source of oils and decreased omega-3 intake may increase, in vivo , the production of free radicals and pro-inflammatory cytokines. Omega-3 fatty acids and eicosapentaenoic acid, in particular, are well-documented inhibitors of pro-inflammatory cytokines such as tumor necrosis factor-α (TNF-α) and appear to exert protection against autoimmunity by enhancing antioxidant enzymes and transforming growth factor-β mRNA levels.
See:
- Namazi MR, Chee Leok G. Vitiligo and diet: A theoretical molecular approach with practical implications. Indian J Dermatol Venereol Leprol [serial online] 2009 [cited 2011 Mar 14];75:116-8. Full text
Male pattern baldness and hyperinsulinemic disorders
See:
- Herreraa CR, Lynch C. Is baldness a risk factor for coronary artery disease? A review of the literature. Journal of Clinical Epidemiology. 1990;43(11):1255-1260. doi:10.1016/0895-4356(90)90026-L. Abstract
- Cordain L et al. Origins and evolution of the Western diet: health implications for the 21st century. Am J Clin Nutr February 2005;81(2):341-354. Full Text athttp://www.ajcn.org/content/81/2/341.full.pdf+html
- Starka L, Duskova M, Cermakova I, Vrbiková J, Hill M. Premature androgenic alopecia and insulin resistance. Male equivalent of polycystic ovary syndrome? Endocr Regul.2005 Dec;39(4):127-31. Abstract at http://www.ncbi.nlm.nih.gov/pubmed/16552990
- Signorello LB et al. Hormones and hair patterning in men: A role for insulin-like growth factor 1? Journal of the American Academy of Dermatology. February 1999;40(2):200-203. Abstract at http://www.eblue.org/article/S0190-9622(99)70188-X/abstract
- Matilainen V, Koskela P, Keinänen-Kiukaanniemi S. Early androgenetic alopecia as a marker of insulin resistance. The Lancet. September 2000;356(9236):1165-1166 doi:10.1016/S0140-6736(00)02763-X. Available at http://download.thelancet.com/pdfs/journals/lancet/PIIS014067360002763X.pdf
Fructose (Fruit Sugar) is a more important cause for metabolic disorders like diabetes, hypertension, fatty liver disease, obesity
See:
- Kimber L. Stanhope et al. Consuming fructose-sweetened, not glucosesweetened, beverages increases visceral adiposity and lipids and decreases insulin sensitivity in overweight/obese humans. The Journal of Clinical Investigation. May 2009;119(5):1332-1334 | Child diabetes blamed on food sweetener: Report
- Sharon S Elliott et al. Fructose, weight gain, and the insulin resistance syndrome. Am J Clin Nutr. 2002;76(5):911-922
- Heather Basciano et al. Fructose, insulin resistance, and metabolic dyslipidemia. Nutrition & Metabolism 2005;2:5
- Xiaosen Ouyang et al. Fructose Consumption as a Risk Factor for Non-alcoholic Fatty Liver Disease. J Hepatol. 2008;48(6):993–999
- Richard J Johnson et al. Potential role of sugar (fructose) in the epidemic of hypertension, obesity and the metabolic syndrome, diabetes, kidney disease, and cardiovascular disease. Am J Clin Nutr. 2007;86(4):899-90
- Michael S. Gersch et al. Fructose, but not dextrose, accelerates the progression of chronic kidney disease. Am J Physiol Renal Physiol 2007;293:F1256-F1261
- Laura Gabriela Sánchez-Lozada et al. How safe is fructose for persons with or without diabetes? Am J Clin Nutr. 2008;88(5):1189-1190.