The Mediterranean diet originates in the food cultures of ancient civilizations which developed around the Mediterranean Basin and is based on the regular consumption of olive oil (as the main source of added fat), plant foods (cereals, fruits, vegetables, legumes, tree nuts, and seeds), the moderate consumption of fish, seafood, and dairy, and low-to-moderate alcohol (mostly red wine) intake, balanced by a comparatively limited use of red meat and other meat products. A few decades ago, the Mediterranean diet drew the attention of medical professionals by proving extended health benefits. The first reports ascertained cardiovascular protection, as multiple large-scale clinical studies, starting with Ancel Keys’ Seven Countries Study, showed a marked reduction of atherosclerotic clinical events in populations with a Mediterranean dietary pattern. Ensuing trials confirmed favorable influences on the risk for metabolic syndrome, obesity, type 2 diabetes mellitus, cancer, and neurodegenerative diseases. While its health benefits are universally recognized today by medical professionals, the present state of the Mediterranean diet is challenged by major difficulties in implementing this protective dietary pattern in other geographical and cultural areas and keeping it alive in traditional Mediterranean territories, also tainted by the unhealthy eating habits brought by worldwide acculturation.

Non-alcoholic fatty liver disease (NAFLD) represents the hepatic expression of the metabolic syndrome and is the most prevalent liver disease. NAFLD is associated with liver-related and extrahepatic morbi-mortality. Among extrahepatic complications, cardiovascular disease (CVD) is the primary cause of mortality in patients with NAFLD. The most frequent clinical expression of CVD is the coronary artery disease (CAD). Epidemiological data support a link between CAD and NAFLD, underlain by pathogenic factors, such as the exacerbation of insulin resistance, genetic phenotype, oxidative stress, atherogenic dyslipidemia, pro-inflammatory mediators, and gut microbiota. A thorough assessment of cardiovascular risk and identification of all forms of CVD, especially CAD, are needed in all patients with NAFLD regardless of their metabolic status. Therefore, this narrative review aims to examine the available data on CAD seen in patients with NAFLD, to outline the main directions undertaken by the CVD risk assessment and the multiple putative underlying mechanisms implicated in the relationship between CAD and NAFLD, and to raise awareness about this underestimated association between two major, frequent and severe diseases.

Eating behavior encompasses the psychological, physiological, and environmental factors influencing food intake. Dysregulation in eating behavior, such as emotional eating, binge eating, or loss of satiety signals, contributes to excessive caloric intake and weight gain. These behaviors are often linked to hormonal imbalances, stress, or genetic predisposition. Obesity is a chronic, multifactorial disease characterized by excessive body fat accumulation, with a body mass index (BMI) ≥ 30 kg/m² often used for diagnosis. It is associated with significant morbidity, including type 2 diabetes, cardiovascular disease, and obstructive sleep apnea. Pathophysiological mechanisms underlying obesity include insulin resistance, leptin dysregulation, and altered gut microbiota, which perpetuate metabolic derangements. Lifestyle interventions remain first-line treatment, but sustained weight loss is challenging for many patients. Bariatric surgery is a therapeutic option for individuals with severe obesity (BMI ≥ 40 kg/m² or ≥35 kg/m² with comorbidities) who have failed conservative management. Procedures such as Roux-en-Y gastric bypass and sleeve gastrectomy alter gastrointestinal anatomy, promoting weight loss through restriction, malabsorption, and hormonal modulation (e.g., increased GLP-1 secretion). Bariatric surgery improves obesity-related comorbidities and enhances quality of life. However, it requires lifelong medical follow-up to address potential nutritional deficiencies and ensure sustainable outcomes.

Type 2 diabetes mellitus (T2DM) undermines health and quality of life (QoL). This cross-sectional study surveyed 138 consenting T2DM patients from North-Eastern Romania with regard to their satisfaction with treatment, diabetes-related impact on QoL, and general health. The Romanian versions of Diabetes Treatment Satisfaction Questionnaire (DTSQ), Audit of Diabetes Dependent Quality of Life (ADDQoL-19), and 36-Item Short Form Health Survey (SF-36) questionnaires were used. Self-reports were analyzed in conjunction with clinical and metabolic profiling. The patients were 57.86 ± 8.82 years old, 49.3% men, treated with oral glucose-lowering drugs, presenting with inadequate glycemic control but without cardiovascular manifestations. The mean DTSQ and ADDQoL scores were 25.46 ± 0.61 and −2.22 ± 1.2, respectively. Freedom to eat, holidays, journeys, leisure, physical health, sex life, freedom to drink, and feelings about the future scored below average. The mean SF-36 physical and mental health scores were 47.78 ± 1.03 and 50.44 ± 1.38, respectively. The mean SF-6D score was 0.59 ± 0.04 (generated retrospectively using SF-36 data). Negative associations were significant between ADDQoL, age (r = −0.16), and body mass index (r = −0.23), p < 0.01. Overall scores did not correlate with diabetes duration (except DTSQ, r = −1.18, p = 0.02) or HbA_1c. The results confirm other researchers’ findings in Europe and nearby countries. Our patients seemed satisfied with treatment despite glycemic imbalance and viewed diabetes as a burden on QoL and especially freedom to eat.

Celiac disease (CD) is a chronic autoimmune disorder triggered by the ingestion of gluten-containing food by genetically predisposed individuals. Hence, treatment of CD consists of permanent avoidance of wheat, rye, barley, and other gluten-containing foods. Lifelong adherence to a gluten-free diet (GFD) improves the symptoms of CD, but recent evidence suggests it is also associated with a higher risk for hepatic steatosis and the coexistence or emergence of other cardiometabolic risk factors. Moreover, a higher risk for liver steatosis is also reported by some authors as a potential extraintestinal complication of the CD itself. Recent nomenclature changes designate the association between hepatic steatosis and at least one of five cardiometabolic risk factors as metabolic dysfunction-associated steatotic liver disease (MASLD). An extended network of potentially causative factors underlying the association between MAFLD and CD, before and after dietary therapy is implemented, was recently described. The individualized treatment of these patients is less supported by evidence, with most of the current recommendations relying on empiric clinical judgment. This review focuses on the causative associations between CD and hepatic injury, either as an extraintestinal manifestation of CD or a side effect of GFD, also referring to potential therapeutic strategies for these individuals.

(1) Background: Type 2 diabetes mellitus (T2DM) contributes to cardiovascular disease and related mortality through the insidious effects of insulin resistance and chronic inflammation. Mitral annular calcification (MAC) is one such degenerative process promoted by T2DM. (2) Methods: This is a post hoc analysis of insulin resistance, inflammation, and hepatic steatosis markers in T2DM patients without atherosclerotic manifestations, but with incidental echocardiographic detection of mild MAC. (3) Results: 138 consenting patients were 49.3% men, 57.86 years old, with a history of T2DM of 6.16 years and HbA_1c 8.06%, of whom sixty had mild MAC (43.47%). The statistically significant differences between patients with/without MAC were higher HOMA C-peptide and C-peptide index for insulin resistance, higher TNF-α for inflammation, and lower estimated glomerular filtration rate. High-sensitive C-reactive protein (hsCRP) was significantly associated with insulin resistance and the strength of the relationship was higher in the MAC group. Predictive of MAC were TNF-α, HOMA C-peptide, and especially hepatic steatosis and hypertension. (4) Conclusions: MAC was more prevalent than reported in the literature. Insulin resistance and inflammation were predictive of MAC, but significant markers differ across studies. Widely available routine tests and echocardiographic assessments are useful in the early identification of mitral annular calcifications in diabetes patients.