The major burden of hypertension is in the developing world, where effective drugs may not be affordable or available. Improving the dietary approach would reduce the need for suppressive drug treatments. The epidemiological association between psoriasis, hypertension, diabetes and the metabolic syndrome (Qureshi AA, 2009) suggests a common inflammatory aetiopathogenesis (Spah F, 2008). This case study shows a side benefit of a personalized diet for psoriasis on blood pressure and other metabolic parameters. The propositus had psoriasis for 31 years, when the disease became generalized. Episodes of recurrent pruritic rash ensued. This acute allergy ceased upon discontinuing the spice, Piper guineense, followed by remarkable clearing of the chronic psoriasis. As gradual relapse came on, he eschewed suppressive treatments and investigated dietary effects. Repeated challenge and avoidance testing (over eight years) indicates that certain listed foods (including hydrogenated fats or glutamatergic/ aspartatergic compounds), consistently aggravate psoriasis, and provoke secondary food intolerances. Diary and photographic records show that avoiding these foods/ compounds enables regression of psoriasis. The propositus notes improvement in blood pressure (which rises from 100-110 mm Hg systolic to 120–130 mm Hg during diet-related relapse of psoriasis; serum cholesterol: HDL ratio 2.4; fasting glucose 4.4 mM; PSA 0.4 ug/L; medication nil). This current metabolic profile suggests a role for a personalized, antipsoriatic-type diet in the prevention of chronic disease. Long-term observational case studies may thus indicate dietary modulators of gene expression in chronic disease. As a therapeutic option, personalized nutrition attunes the molecular composition of diet to the individual genome.
Qureshi AA, Choi HK, Setty AR, Curhan GC (2009). Psoriasis and the Risk of Diabetes and Hypertension: A Prospective Study of US Female Nurses. Arch Dermatol 145(4): 379-382.
Späh F (2008). Inflammation in atherosclerosis and psoriasis: common pathogenic mechanisms and the potential for an integrated treatment approach. Br J Dermatol 159 Suppl 2: 10-17.
© 2012 Lippincott Williams & Wilkins, Inc.