The role of chronic stress in the development of chronic diseases, especially multimorbidity, through the pathways of increasing allostatic load, and finally, allostatic overload (the state when a compensatory mechanism is likely to fail) is being emphasized. However, allostatic load is a dynamic measure that changes depending on sex, gender, age, level and type of stress, experience of a stressful situation, and coping behaviors. Many other factors such as race, ethnicity, working environment, lifestyle, and circadian rhythm of sleep are also important. The aim of this paper was to synthesize the available information on allostatic load differences, especially those connected to sex/gender and age, and to provide a model for the future study of allostatic load, with a focus on these differences. By carefully studying allostatic load factors, we realized that many studies do not take this allostatic load difference into account in the analysis methods. In this paper, we also support the idea of further research to develop new allostatic load analysis strategies that will include all knowledge about sex/gender differences and that will, in more detail, explain numerous changeable social and educational factors that are currently accepted as biological ones. Furthermore, specific allostatic load biomarkers are expressed differently in different age groups, indicating that the discrepancies cannot be attributed solely to sex/gender disparities. This kind of approach can be valuable, not only for better explaining the differences in the frequency and age of onset of chronic diseases and multimorbidity, but also for the potential planning and development of preventive actions based on the aforementioned sex/gender and age disaparities, in order to prevent the most frequent diseases and to establish specific biomarker cut-off values for each sex/gender and age group.

Functional dyspepsia is a common functional disorder of the gastrointestinal tract that is responsible for many primary care visits. No organic changes have been found to explain its symptoms. We hypothesize that modern lifestyles and environmental factors, especially psychological stress, play a crucial role in the high prevalence of functional dyspepsia and metabolic syndrome. While gastrointestinal tract diseases are rarely linked to metabolic disorders, chronic stress, obesity-related metabolic syndrome, chronic inflammation, intestinal dysbiosis, and functional dyspepsia have significant pathophysiological associations. Functional dyspepsia, often associated with anxiety and chronic psychological stress, can activate the neuroendocrine stress axis and immune system, leading to unhealthy habits that contribute to obesity. Additionally, intestinal dysbiosis, which is commonly present in functional dyspepsia, can exacerbate systemic inflammation and obesity, further promoting metabolic syndrome-related disorders. It is worth noting that the reverse is also true: obesity-related metabolic syndrome can worsen functional dyspepsia and its associated symptoms by triggering systemic inflammation and intestinal dysbiosis, as well as negative emotions (depression) through the brain–gut axis. To understand the pathophysiology and deliver an effective treatment strategy for these two difficult-to-cure disorders, which are challenging for both caregivers and patients, a psychosocial paradigm is essential.

The spectrum, intensity, and overlap of symptoms between functional gastrointestinal disorders (FGIDs) and other gastrointestinal disorders characterize patients with FGIDs, who are incredibly different in their backgrounds. An additional challenge with regard to the diagnosis of FGID and the applicability of a given treatment is the ongoing expansion of the risk factors believed to be connected to these disorders. Many cytokines and inflammatory cells have been found to cause the continuous existence of a low level of inflammation, which is thought to be a basic pathophysiological process. The idea of the gut–brain axis has been created to offer a basic framework for the complex interactions that occur between the nervous system and the intestinal functions, including the involvement of gut bacteria. In this review paper, we intend to promote the hypothesis that FGIDs should be seen through the perspective of the network of the neuroendocrine, immunological, metabolic, and microbiome pathways. This hypothesis arises from an increased understanding of chronic inflammation as a systemic disorder, that is omnipresent in chronic health conditions. A better understanding of inflammation’s role in the pathogenesis of FGIDs can be achieved by clustering markers of inflammation with data indicating symptoms, comorbidities, and psycho-social factors. Finding subclasses among related entities of FGIDs may reduce patient heterogeneity and help clarify the pathophysiology of this disease to allow for better treatment.

Objectives: The main objectives of the research are to examine the incidence of hyperlipoproteinemia in postmenopausal women and to determine the differences in lipid profile considering age, duration of menopause and body mass index in postmenopausal women. Respondents and methods: The research is structured as cross-sectional with historical data. The research used data collected during regular check-ups in primary health care clinics in Osijek Health Center from November 2021 to March 2022. Collected data: demographic data, information on the duration of menopause, body mass, body height, body mass index, values of total, LDL, HDL cholesterol and triglycerides, and data on associated diseases. Results: 98 postmenopausal women were included in the research, of which over 50% had elevated total and LDL cholesterol values, and 39.8% had elevated triglyceride values. Subjects aged 45 to 65 years and subjects with a duration of menopause of 10 or more years had significantly higher values of total and LDL cholesterol while no difference was observed in the lipid profile with regard to the body mass index. Using the SCORE2 table, it was estimated that 65% of the subjects had a very high cardiovascular risk, and only 6% of the subjects achieved the target values of LDL cholesterol in accordance with the cardiovascular risk. Conclusion: There is a very high incidence of hyperlipoproteinemia in postmenopausal women, and the age and duration of menopause have an impact on the poorer achievement of the target values of the lipid profile, while the body mass index showed no impact. Given the high prevalence of subjects with a very high cardiovascular risk (SCORE 2 tables), intensive interventions are needed at all levels of health care, especially at the primary level of health care, which include non-pharmacological and pharmacological methods of treating hyperlipoproteinemia.

Background and Objectives: Chronic kidney disease (CKD) is an increasingly significant global public health issue, with cardiovascular disease being the leading cause of mortality. Endothelial dysfunction plays a critical role, but diagnostic tools have certain limitations. Endocan, a soluble proteoglycan, emerged as a promising endothelial dysfunction marker and potential major adverse cardiovascular event (MACE) predictor in haemodialysis (HD) patients. Materials and Methods: In this single-centre, observational, prospective study, non-diabetic HD patients without prior MACEs were monitored. A total of 75 participants met the inclusion criteria. We measured serum endocan, standard biochemical and anthropometric parameters, and parameters of peripheral and central haemodynamics before and after HD in all participants. Results: Patients with higher endocan were older, had elevated CRP and reduced albumin concentrations, and often had a tunnelled central venous catheter (TCVC) for vascular access. Higher serum endocan levels were independently associated with an increased risk of MACEs (aHR = 4.09, 95%-CI: 1.72–9.74), MACE-related mortality (aHR = 2.64, 95%-CI: 1.23–5.66), and all-cause mortality (aHR = 1.86, 95%-CI: 1.07–3.23), both before and after adjusting for predefined confounders, with the highest endocan tercile exhibiting the shortest event-free survival. Conclusions: Endocan is a valuable marker of inflammation and endothelial dysfunction in non-diabetic HD patients. Its elevated concentration indicates an increased cardiovascular risk and more frequent MACEs. Future multicentre studies with repeated endocan assessments should validate its prognostic and diagnostic utility, particularly in long-term patient follow-up.

Background: Interindividual differences in statin efficacy and tolerability are partly determined by genetic and metabolic factors. The SLCO1B1 c.521T>C polymorphism affects hepatic statin transport, while vitamin D deficiency may influence lipid metabolism and muscular tolerance. This study aimed to assess the impact of SLCO1B1 genotype and vitamin D status on lipid-lowering response and adverse events in postmenopausal women treated with atorvastatin or rosuvastatin. Methods: A total of 145 Croatian postmenopausal women were prospectively followed for 16 weeks. Participants received atorvastatin or rosuvastatin with dose titration to achieve low-density lipoprotein cholesterol (LDL-C) targets. Serum lipids, liver enzymes, and creatine kinase were monitored monthly. Serum levels of 25-hydroxyvitamin D were quantified by LC–MS/MS, while SLCO1B1 c.521T>C genotyping was performed using real-time PCR. Results: Rosuvastatin achieved a higher LDL-C target attainment rate compared with atorvastatin (81.1% vs. 67.6%, p = 0.02). The SLCO1B1 genotype was not associated with lipid response but was significantly associated with adverse effects. In multivariable regression analysis, patients with the T/C genotype had a significantly higher risk of developing adverse effects compared with those with the T/T genotype (OR 7.4, 95% Cl 2.1–26.7, p = 0.002). Vitamin D status showed no significant association with lipid outcomes or adverse events, although participants with severe deficiency exhibited a weaker LDL-C response. Conclusions: Rosuvastatin demonstrated superior lipid-lowering efficacy and tolerability compared with atorvastatin in postmenopausal women. The SLCO1B1 c.521T>C variant primarily affected safety rather than efficacy, while severe vitamin D deficiency might contribute to diminished statin response. Integrating pharmacogenetic and endocrine profiling could enhance individualized statin therapy and cardiovascular prevention in women.