The aim of the study was to evaluate the reproducibility of the Dietary Habits and Nutrition Beliefs Questionnaire (KomPAN) in Polish adolescents and adults, including the assessment of indexes developed based on the questionnaire. In total, the study involved 954 subjects aged 15–65 (53.9% females). Interviews using the interviewer-administered questionnaire (IA-Q) in healthy subjects (n 299) and the self-administered questionnaire (SA-Q) in healthy subjects (n 517) and outpatients (n 138) were conducted and repeated after two weeks. Considering the consumption frequency of 33 food items, the cross-classification (test-retest) agreement of classification into the same category obtained for IA-Q in healthy subjects ranged from 72.2% (fruit juices) to 91.6% (energy drinks); the kappa statistic was >0.60 for all food items. For SA-Q conducted in healthy subjects the cross-classification agreement ranged from 63.8% (vegetable oils, margarines, mixes of butter and margarines) to 84.7% (lard); the kappa statistic was >0.50 for all food items. For SA-Q in outpatients, the cross-classification agreement ranged from 42.0% (both fruit juices and white rice, white pasta, fine-ground groats) to 92.0% (energy drinks); the kappa statistic was ≥0.40 for 20/33 food items. The kappa statistic for lifestyle items ranged 0.42–0.96, and for the nutrition knowledge level it ranged 0.46–0.73. The questionnaire showed moderate to very good reproducibility and can be recommended to assess dietary habits, lifestyle and nutrition knowledge of healthy adolescents and adults and those suffering from chronic diseases, after validation and/or calibration study is carried out. The reproducibility of the interviewer-administered questionnaire was better than its self-administered version. The reproducibility of the self-administered questionnaire was better in healthy subjects than in outpatients.

Type 1 diabetes mellitus is a chronic autoimmune disease associated with degeneration of pancreatic β-cells that results in an inability to produce insulin and the need for exogenous insulin administration. It is a significant global health problem as the incidence of this disorder is increasing worldwide. The causes are still poorly understood, although it certainly has genetic and environmental origins. Vitamin D formed profusely in the skin upon exposure to sunlight, as well as from dietary sources, exhibits an immunomodulatory effect based on gene transcription control. Indeed, vitamin D can downregulate mechanisms connected with adaptive immunity, induce immunological tolerance and decrease auto-aggression-related inflammation. These properties provide the basis for a preventive and therapeutic role of vitamin D. As many studies have demonstrated, appropriate supplementation with vitamin D reduces the risk of autoimmune diseases, including type 1 diabetes mellitus, and alleviates disease symptoms in patients. The aim of this narrative review is to present the molecular mechanisms for the vitamin D immunomodulatory effect as well as review human clinical studies on the use of vitamin D as adjuvant therapy in type 1 diabetes mellitus.

Alzheimer’s disease (AD) is the most common form of neurodegenerative dementia. Metabolic disorders including obesity and type 2 diabetes mellitus (T2DM) may stimulate amyloid β (Aβ) aggregate formation. AD, obesity, and T2DM share similar features such as chronic inflammation, increased oxidative stress, insulin resistance, and impaired energy metabolism. Adiposity is associated with the pro-inflammatory phenotype. Adiposity-related inflammatory factors lead to the formation of inflammasome complexes, which are responsible for the activation, maturation, and release of the pro-inflammatory cytokines including interleukin-1β (IL-1β) and interleukin-18 (IL-18). Activation of the inflammasome complex, particularly NLRP3, has a crucial role in obesity-induced inflammation, insulin resistance, and T2DM. The abnormal activation of the NLRP3 signaling pathway influences neuroinflammatory processes. NLRP3/IL-1β signaling could underlie the association between adiposity and cognitive impairment in humans. The review includes a broadened approach to the role of obesity-related diseases (obesity, low-grade chronic inflammation, type 2 diabetes, insulin resistance, and enhanced NLRP3 activity) in AD. Moreover, we also discuss the mechanisms by which the NLRP3 activation potentially links inflammation, peripheral and central insulin resistance, and metabolic changes with AD.

Alzheimer’s disease and Parkinson’s disease are the most common forms of neurodegenerative illnesses. It has been widely accepted that neuroinflammation is the key pathogenic mechanism in neurodegeneration. Both mitochondrial dysfunction and enhanced NLRP3 (nucleotide-binding oligomerization domain (NOD)-like receptor protein 3) inflammasome complex activity have a crucial role in inducing and sustaining neuroinflammation. In addition, mitochondrial-related inflammatory factors could drive the formation of inflammasome complexes, which are responsible for the activation, maturation, and release of pro-inflammatory cytokines, including interleukin-1β (IL-1β) and interleukin-18 (IL-18). The present review includes a broadened approach to the role of mitochondrial dysfunction resulting in abnormal NLRP3 activation in selected neurodegenerative diseases. Moreover, we also discuss the potential mitochondria-focused treatments that could influence the NLRP3 complex.

Leptin is an adipokine, adipocyte-derived compound, which acts both as a hormone and cytokine. It is mainly synthesized by adipocytes of white adipose tissue. Leptin possesses pleiotropic functions including, among others, stimulation of angiogenesis and production of proinflammatory cytokines. The various types of leptin activity are related to the wide distribution of leptin receptors. This adipokine acts by activating intracellular signaling cascades such as JAKs (Janus kinases), STATs (signal transducers and activators of transcription), and others.In a course of obesity, an increased serum level of leptin coexists with tissue receptor resistance. It has been reported that enhanced leptin levels, leptin receptor impairment, and dysfunction of leptin signaling can influence skin and hair. The previous studies revealed the role of leptin in wound healing, hair cycle, and pathogenesis of skin diseases like psoriasis, lupus erythematosus, and skin cancers. However, the exact mechanism of leptin’s impact on the skin is still under investigation. Herein, we present the current knowledge concerning the role of leptin in psoriasis and selected skin diseases.

The sustainability of education focused on improving the dietary and lifestyle behaviours of teenagers has not been extensively studied. The aim of this study was to determine the sustainability of diet-related and lifestyle-related school-based education on sedentary and active lifestyle, diet quality and body composition of Polish pre-teenagers in a medium-term follow-up study. An education-based intervention study was carried out on 464 students aged 11–12 years (educated/control group: 319/145). Anthropometric measurements were taken and body mass index (BMI) and waist-to-height ratios (WHtR) were calculated, both at the baseline and after nine months. Dietary data from a short-form food frequency questionnaire (SF-FFQ4PolishChildren) were collected. Two measures of lifestyle (screen time, physical activity) and two diet quality scores (pro-healthy, pHDI, and non-healthy, nHDI) were established. After nine months, in the educated group (vs. control) a significantly higher increase was found in nutrition knowledge score (mean difference of the change: 1.8 points) with a significantly higher decrease in physical activity (mean difference of the change: −0.20 points), nHDI (−2.3% points), the z-WHtR (−0.18 SD), and the z-waist circumference (−0.13 SD). Logistic regression modelling with an adjustment for confounders revealed that after nine months in the educated group (referent: control), the chance of adherence to a nutrition knowledge score of at least the median was over 2 times higher, and that of the nHDI category of at least the median was significantly lower (by 35%). In conclusion, diet-related and lifestyle-related school-based education from an almost one-year perspective can reduce central adiposity in pre-teenagers, despite a decrease in physical activity and the tendency to increase screen time. Central adiposity reduction can be attributed to the improvement of nutrition knowledge in pre-teenagers subjected to the provided education and to stopping the increase in unhealthy dietary habits.