The epidemiological association between psoriasis, hypertension, diabetes and the metabolic syndrome (Mrowietz 2006 Dermatol Res 298:309; Qureshi 2009 Arch Dermatol 145;379) suggests a common inflammatory aetiopathogenesis (Spah 2008 BrJDermatol 159S2:10). Objective: validate a model (induced from observation of dietary effects on psoriasis with side benefit on blood pressure, Chijioke 2012 J Hypertension 30esuppl1:p158) of the aetiopathogenic diet–genome interaction in hypertension.Design and Method:
An open clinical trial involving withdrawal of postulated egregious ingredients. Consenting study participants (SPs) with mild hypertension (BP < 160/100, or on one or two antihypertensives with BP < 140/90) receive personalized categorical food avoidance (PCFA) counseling with emphasis on avoiding certain flavourants, sweeteners and oils, including hydrogenated fats. Personalization addresses secondary intolerance to unfamiliar dietary ingredients.Results:
Fig. 1 shows home BP response (with relapses related to dietary indiscretion) over 4 years in a case with ’GOOD’ dietetic compliance, and who eschews antihypertensive medication. A paired samples t-test shows statistically significant differences between BP values during the first 6 months of 2012 and the last 6 months of 2013 (p < 0.05). Figs 2–6 show the pattern of home BP measurements in 4 recruits who started PCFA counseling on 17Dec2015. PHT5 had a significant reduction in home BP values. Table 1 shows their overall dietetic compliance, with average automated office BP, antihypertensive drug prescription/ adherence and body mass index before and after counselling. 3 out of the 4 later SPs had a fall in AOBP after counselling started. In PHT12 there was a rise in AOBP attributable to POOR dietetic compliance and reduced drug adherence.Conclusions:
The PCFA dietary intervention excludes much of the modern dietary trend: hence it may not be therapeutically useful for patients who lack determination and motivation. However study participants with good PCFA dietetic compliance are showing BP and antihypertensive treatment responses which support the postulated diet-genome interaction in the genesis of hypertension.