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W dniach 15–17 marca 2022 r. w Instytucie Badawczym Leśnictwa odbyła się XII Sesja Zimowej Szkoły Leśnej, której tematem był „Wpływ zmian klimatu na środowisko leśne”. Spośród licznych propozycji, o wyborze powyższego tematu przesądziło obserwowane od wielu lat systematyczne pogorszanie się stanu zdrowotnego drzewostanów na skutek synergicznego oddziaływania wielu czynników abiotycznych i biotycznych w warunkach zmian klimatu. Współorganizatorem Sesji była Dyrekcja Generalna Lasów Państwowych. Merytoryczne aspekty XII Sesji zostały przygotowane i opracowane przez Radę Programową Zimowej Szkoły Leśnej w składzie: dr hab. Krzysztof Stereńczak, prof. IBL (przewodniczący), prof. dr hab. Bogdan Brzeziecki, mgr inż. Michał Graczyk, prof. dr hab. Andrzej Grzywacz, prof. dr hab. Andrzej Jagodziński, prof. dr hab. Janusz Olejnik, mgr inż. Jan Tabor, mgr inż. Krzysztof Rostek, prof. dr hab. Iwona Skrzecz, dr inż. Klaudia Ziemblińska. Rada Programowa określiła nie tylko zakres problematyki XII Sesji, ale także propozycje tematyczne referatów zamawianych oraz ich autorów. W trakcie trzech dni obrad prelegenci przedstawili 33 referaty. Referaty wygłosili również zaproszeni goście zagraniczni reprezentujący: Uniwersytet w Helsinkach, Czeski Uniwersytet Przyrodniczy w Pradze, Instytut Badań nad Zmianami Globalnymi (Czechy), Uniwersytet Wspólnoty Wirginii, Łotewski Państwowy Instytut Badawczy Leśnictwa oraz Integrated Carbon Observation System. W XII Sesji, która odbyła się w wersji online, wzięło udział niemal 200 osób reprezentujących m.in.: Ministerstwo Klimatu i Środowiska, jednostki organizacyjne Lasów Państwowych, ośrodki uniwersyteckie i instytuty badawcze. Liczne grono stanowili również przedstawiciele ośrodków naukowych oraz polskich uczelni leśnych.

The prevalence of celiac disease increased in recent years. In addition to the genetic and immunological factors, it appears that environmental determinants are also involved in the pathophysiology of celiac disease. Gastrointestinal infections impact the development of celiac disease. Current research does not directly confirm the protective effect of natural childbirth and breastfeeding on celiac disease. However, it seems that in genetically predisposed children, the amount of gluten introduced into the diet may have an impact on celiac disease development. Also western lifestyle, including western dietary patterns high in fat, sugar, and gliadin, potentially may increase the risk of celiac disease due to changes in intestinal microbiota, intestinal permeability, or mucosal inflammation. Further research is needed to expand the knowledge of the relationship between environmental factors and the development of celiac disease to define evidence-based preventive interventions against the development of celiac disease. The manuscript summarizes current knowledge on factors predisposing to the development of celiac disease including factors associated with the western lifestyle.

IntroductionOne of the challenges of personalized medicine is a departure from traditional pharmacology toward individualized, genotype-based therapies. Postmenopausal osteoporosis is a prevalent condition requiring intensive treatment, whose effects are measurable only after a long time, and the goal is bone fracture prevention. This study aimed to determine the influence of VDR gene variation on anti-osteoporotic one-year treatment with denosumab in 63 Polish women with postmenopausal osteoporosis.Materials and methodsThe correlation between bone mineral density (BMD) of the lumbar vertebral column (L1–L4) and femoral neck, and genotype distributions for the ApaI, BsmI, FokI, and TaqI variants of the VDR gene was analyzed. Bone fractures during denosumab therapy were also investigated.ResultsIn the case of the Bsml polymorphism, female patients with BB and Bb genotypes had statistically significantly higher values of BMD and T-score/Z-score indicators, which persisted after a year of denosumab treatment. Our results indicated that the Bsml polymorphism contributes to better bone status, and, consequently, to more efficient biological therapy. The study did not reveal significant differences between changes (delta) in BMD and genotypes for the analyzed VDR gene loci. In the entire study group, one bone fracture was observed in one patient throughout the yearlong period of denosumab therapy.ConclusionsBB and Bb genotypes of the Bsml polymorphism of the VDR gene determine higher DXA parameter values both before and after one-year denosumab therapy in postmenopausal women with osteoporosis.

Inflammatory bowel diseases (IBD) are chronic, progressive and relapsing inflammatory disorders of unknown etiology that may cause disability over time. Data from epidemiologic studies indicate that diet may play a role in the risk of developing and the course of IBD. It is known that the group of beneficial bacteria was reduced in the IBD and that the Mediterranean diet (MD)—which is defined as eating habits characterized by high consumption of plant foods, mainly cereals, vegetables, fruit as well as olive oil, and small portions of dairy products, sweets, sugar and meat products—affects gut microbiota, enriching beneficial bacteria, which support gut barrier function and reduce inflammation. Although several studies support different favorable effects of MD on IBD, adherence to MD by IBD patients is generally low, including patients from the Mediterranean Basin. Patients avoid many products which are elements of MD because there cause gastrointestinal symptoms. Patients should be encouraged to have a healthy and well-balanced diet according to individual tolerance of products. A good option seems to be good modified MD, changing hard-to-digest products to easy digest.

The multifaceted activity of vitamin D in patients with inflammatory bowel disease (IBD) presents a challenge for further research in this area. Vitamin D is involved in the regulation of bone mineral metabolism, it participates in the regulation of the immune system, and it is an underlying factor in the pathogenesis of IBD. Additionally, vitamin D affects Th1 and Th2 lymphocytes, influencing the release of cytokines and inhibiting tumor necrosis factor (TNF) expression and the wnt/β-catenin pathway. As far as IBDs are concerned, they are associated with microbiota dysbiosis, abnormal inflammatory response, and micronutrient deficiency, including vitamin D hypovitaminosis. In turn, the biological activity of active vitamin D is regulated by the vitamin D receptor (VDR) which is associated with several processes related to IBD. Therefore, in terms of research on vitamin D supplementation in IBD patients, it is essential to understand the metabolic pathways and genetic determinants of vitamin D, as well as to identify the environmental factors they are subject to, not only in view of osteoporosis prevention and therapy, but primarily concerning modulating the course and supplementation of IBD pharmacotherapy.

The formation of advanced glycation end-products (AGE) in tissues is a physiological process; however, excessive production and storage are pathological and lead to inflammation. A sedentary lifestyle, hypercaloric and high-fructose diet and increased intake of processed food elements contribute to excessive production of compounds, which are created in the non-enzymatic multi-stage glycation process. The AGE’s sources can be endogenous and exogenous, mainly due to processing food at high temperatures and low moisture, including grilling, roasting, and frying. Accumulation of AGE increases oxidative stress and initiates various disorders, leading to the progression of atherosclerosis, cardiovascular disease, diabetes and their complications. Inborn defensive mechanisms, recovery systems, and exogenous antioxidants (including polyphenols) protect from excessive AGE accumulation. Additionally, numerous products have anti-glycation properties, occurring mainly in fruits, vegetables, herbs, and spices. It confirms the role of diet in the prevention of civilization diseases.

Despite the increasing knowledge with regard to IBD (inflammatory bowel disease), including ulcerative colitis (UC) and Crohn’s disease (CD), the etiology of these conditions is still not fully understood. Apart from immunological, environmental and nutritional factors, which have already been well documented, it is worthwhile to look at the possible impact of genetic factors, as well as the composition of the microbiota in patients suffering from IBD. New technologies in biochemistry allow to obtain information that can add to the current state of knowledge in IBD etiology.

Obesity is a complex and multifactorial problem of global importance. Additionally, obesity causes chronic inflammation, upregulates cell growth, disturbs the immune system, and causes genomic instability, increasing the risk of carcinogenesis. Colorectal cancer is one of the most common cancers, and it has become a global problem. In 2018, there were around 1.8 million new cases and around 881,000 deaths worldwide. Another risk factor of colorectal cancer associated with obesity is poor diet. A Western diet, including a high intake of red and processed meat and a low consumption of whole grains, fruits, vegetables, and fiber, may increase the risk of both colorectal cancer and obesity. Moreover, the Western diet is associated with a proinflammatory profile diet, which may also affect chronic low-grade inflammation. In fact, people with obesity often present gut dysbiosis, increased inflammation, and risk of colorectal cancer. In this article, the association between obesity and colorectal cancer is discussed, including the most important mechanisms, such as low-grade chronic inflammation, gut dysbiosis, and poor diet.

Sarcopenia, which is a decrease in muscle strength and quality of muscle tissue, is a common disorder among patients suffering from inflammatory bowel disease. This particular group of patients often presents with malnutrition and shows low physical activity, which increases the risk of sarcopenia. Another important factor in the development of sarcopenia is an imbalanced ratio of myostatin and follistatin, which may stem from inflammation as well as genetic factors. Currently, research in this area continues, and is aimed at identifying an effective medication for the treatment of this condition. Additionally, we still have no sarcopenia markers that can be used for diagnosis. In this paper, we address the role of myostatin and follistatin as potential markers in the diagnosis of sarcopenia in patients with Crohn’s disease and ulcerative colitis, particularly in view of the genetic and biological aspects. We also present data on new perspectives in the pharmacotherapy of sarcopenia (i.e., myostatin inhibitors and gene therapy). Nevertheless, knowledge is still scarce about the roles of follistatin and myostatin in sarcopenia development among patients suffering from inflammatory bowel disease, which warrants further study.

Several studies have shown increased rates of cardiovascular disease (CVD) in patients suffering from inflammatory bowel disease (IBD), particularly in cases of early atherosclerosis and myocardial infarction. IBD most frequently begins at an early age, patients usually present normal weight and remain under constant care of a physician, as well as of a nutritionist. Therefore, the classical risk factors of CVD are not reflected in the higher prevalence of CVD in the IBD population. Still, both groups are characterised by chronic inflammation and display similar physiopathological mechanisms. In the course of IBD, increased concentrations of pro-inflammatory cytokines, such as C-reactive protein (CRP) and homocysteine, may lead to endothelial dysfunctions and the development of CVD. Furthermore, gut microbiota dysbiosis in patients with IBD also constitutes a risk factor for an increased susceptibility to cardiovascular disease and atherosclerosis. Additionally, diet is an essential factor affecting both positively and negatively the course of the aforementioned diseases, whereas several dietary patterns may also influence the association between IBD and CVD. Thus, it is essential to investigate the factors responsible for the increased cardiovascular (CV) risk in this group of patients. Our paper attempts to review the role of potential inflammatory and nutritional factors, as well as intestinal dysbiosis and pharmacotherapy, in the increased risk of CVD in IBD patients.