Personalized Food Avoidance Dietary Approach for Psoriasis and Hypertension: A Case Study and Pilot Trial

The comorbidity, coheritability and common immune pathways of the inflammatory 'chronic' (non-communicable) diseases, suggest a shared aetiopathogenic mechanism, with phenotypic localization dependent on genetic predisposition, for example, the arteries in hypertension and the skin in psoriasis. Lifelong observation of psoriasis suggests genetically predisposed toxicity of amphiphilic fats, flavor enhancers, and nonsugar sweeteners.

To conduct trials of personalized dietary intervention to abate the phenotypic expression of psoriasis and hypertension.

The interventional case study of psoriasis was conducted by means of repetitive dietary challenge and avoidance testing. We then conducted an open trial of personalized nutrition on nine consenting recruits with uncomplicated essential hypertension. They were counseled on which foods to avoid or to take based on the experience gained in psoriasis. Study participants with 'GOOD' or 'FAIR/POOR' dietary compliance were compared with regard to blood pressure (BP) control, antihypertensive drug treatment requirement (ADTR), and anthropometry.

Data from four FAIR/POOR diet compliers and three GOOD compliers, as at 29 weeks of dietary intervention, showed mean systolic home B P values of 128.1 (±6.74) mmHg and 122.3 (±2.03) mmHg, respectively; the mean systolic automated office B P values were 139.8 (±8.80) mmHg and 108.3 (±5.55) mmHg, respectively; as at 39 weeks of dietary intervention, the mean ADTR scores were 4.2 (±2.12) and 1.03 (±0.57), respectively. Using data at baseline and from all available timepoints after dietary intervention, two-way ANOVA confirmed highly significant improvement of BP control ( P < 0.0001) and reduction of ADTR score ( P = 0.0008) in GOOD compliers. GOOD compliers exhibited significantly more reductions in BMI, abdominal circumference, and triceps skinfold thickness than FAIR/POOR compliers (two-way ANOVA and linear regression: P < 0.05).

These results support the case for adverse dietary exposure avoidance to abate the phenotypic expression of chronic disease.