RESUMO
Psoriasis is a common chronic, systemic inflammatory disease, affecting approximately 2% of the population worldwide. Psoriasis is associated with profound psychosocial comorbidity with a burden that extends well beyond the physical signs and symptoms. Psychosocial comorbidities strongly associated with psoriasis include anxiety and depression, suicidal ideation, and substance misuse. There is a substantial unmet need for access to psychological support for people with skin disease in the UK. Recent reports found that while up to 98% of patients felt that their skin disease had affected their emotional or psychological well-being, only 18% sought help. This care gap is largely due to a lack of awareness about the limited available services alongside poor recognition, diagnosis, and triaging. Addressing psychosocial support needs starts with early identification, which can be complex and challenging. Once patients who need further support are identified, outcomes can be improved through prompt and effective treatment of inflammation, cognitive behavioural therapy, meditation and mindfulness-based therapy (including motivational interviewing), and to some extent psychotropic medication. Finally, resources for mental health support are notoriously limited, with dire consequences for patients. It is imperative that a proportion of the new funding promised for mental health services is bookmarked for dermatology patients and adequate provision of multidisciplinary psychodermatology teams to best serve the needs of this population. Ultimately, psoriasis is a complex condition with multifactorial psychological and biological drivers. Psoriasis is associated with high levels of distress, which is often under-recognized. Fully addressing this condition requires a holistic approach to the physical and psychosocial aspects to maximise adherence, efficacy, and optimise patient quality of life.
RESUMO
BACKGROUND: Previous research demonstrated that a high dose of phlorizin-rich apple extract (AE) can markedly inhibit early-phase postprandial glycemia, but efficacy of lower doses of the AE is unclear. OBJECTIVE: To determine whether lower AE doses reduce early-phase postprandial glycemia in healthy adults and investigate mechanisms. DESIGN: In a randomized, controlled, double-blinded, cross-over acute trial, drinks containing 1.8 g (HIGH), 1.35 g (MED), 0.9 g (LOW), or 0 g (CON) of a phlorizin-rich AE were consumed before 75 g starch/sucrose meal. Postprandial blood glucose, insulin, C-peptide, glucose-dependent insulinotropic polypeptide (GIP) and polyphenol metabolites concentrations were measured 0-240 min, acetaminophen concentrations to assess gastric emptying rate, and 24 h urinary glucose excretion. Effects of AE on intestinal glucose transport were investigated in Caco-2/TC7 cells. RESULTS: AE significantly reduced plasma glucose iAUC 0-30 min at all doses: mean differences (95% CI) relative to CON were -15.6 (-23.3, -7.9), -11.3 (-19.6, -3.0) and -8.99 (-17.3, -0.7) mmol/L per minute for HIGH, MEDIUM and LOW respectively, delayed Tmax (HIGH, MEDIUM and LOW 45 min vs. CON 30 min), but did not lower Cmax. Similar dose-dependent treatment effects were observed for insulin, C-peptide, and GIP. Gastric emptying rates and urinary glucose excretion did not differ. Serum phloretin, quercetin and epicatechin metabolites were detected postprandially. A HIGH physiological AE dose equivalent decreased total glucose uptake by 48% in Caco-2/TC7 cells. CONCLUSIONS: Phlorizin-rich AE, even at a low dose, can slightly delay early-phase glycemia without affecting peak and total glycemic response.
