INTRODUCTION
Psoriasis is a chronic immune‑mediated inflammatory skin disease that is strongly associated with metabolic dysregulation and excess adiposity.1 Adipose tissue dysfunction contributes to systemic inflammation, promoting Th17/IL‑17 pathways that drive psoriasis activity.2 Dietary strategies that reduce energy intake either by continuous daily caloric restriction (CCR) or time‑limited/periodic intake such as intermittent fasting (IF) may improve psoriasis severity through weight loss, metabolic improvements, alterations in gut microbiota and immune-metabolic effects (eg, changes in cytokine profiles, autophagy induction, circadian synchronization).3
A recent study demonstrated that a 12-week low-calorie diet in psoriatic patients with non-alcoholic fatty liver disease significantly decreased PASI scores, triglycerides, and liver enzymes, and enhanced quality of life.4 Evidence-based reviews confirm that CCR alleviates symptoms by mitigating metabolic comorbidities, with better pharmacologic response in obese individuals.5
Intermittent fasting (IF), including alternate-day fasting, 5:2 diet, or time-restricted feeding, cycles feeding, and fasting periods, potentially offer superior metabolic benefits over CCR by enhancing insulin sensitivity and reducing inflammation.6 A prospective study on acute time-restricted eating in psoriasis suggests reductions in inflammatory markers.7 Clinical trials indicate IF attenuates psoriasis-like inflammation, with a phase IIb study reporting PASI reductions at week 28.8
The ketogenic diet (Keto), a low-carbohydrate, high-fat regimen promoting ketosis, targets inflammation by limiting glucose availability to immune cells and increasing anti-inflammatory ketones.9 A metabolomic study found very-low-calorie Keto improved psoriasis symptoms through altered metabolic pathways.10 A randomized crossover trial in obese PsA patients showed Keto reduced clinical and biochemical inflammation markers, including IL-1β and IL-2, comparable to Mediterranean diet effects.11
A recent study demonstrated that a 12-week low-calorie diet in psoriatic patients with non-alcoholic fatty liver disease significantly decreased PASI scores, triglycerides, and liver enzymes, and enhanced quality of life.4 Evidence-based reviews confirm that CCR alleviates symptoms by mitigating metabolic comorbidities, with better pharmacologic response in obese individuals.5
Intermittent fasting (IF), including alternate-day fasting, 5:2 diet, or time-restricted feeding, cycles feeding, and fasting periods, potentially offer superior metabolic benefits over CCR by enhancing insulin sensitivity and reducing inflammation.6 A prospective study on acute time-restricted eating in psoriasis suggests reductions in inflammatory markers.7 Clinical trials indicate IF attenuates psoriasis-like inflammation, with a phase IIb study reporting PASI reductions at week 28.8
The ketogenic diet (Keto), a low-carbohydrate, high-fat regimen promoting ketosis, targets inflammation by limiting glucose availability to immune cells and increasing anti-inflammatory ketones.9 A metabolomic study found very-low-calorie Keto improved psoriasis symptoms through altered metabolic pathways.10 A randomized crossover trial in obese PsA patients showed Keto reduced clinical and biochemical inflammation markers, including IL-1β and IL-2, comparable to Mediterranean diet effects.11
