Irisin has been recently identified as an adipomyokine produced during physical activity and involved in the browning of adipose tissue. Despite the emerging evidence suggesting an inverse relationship between irisin plasma concentrations and adverse metabolic outcomes, the exact impact of diet on irisin levels remains obscure. Thus, we aimed to assess the effects of two dietary patterns, Christian Orthodox fasting (OF) and 16:8 time-restricted eating (TRE), on circulating irisin levels among overweight, metabolically healthy, adults. Plasma irisin, glucose and lipid parameters, calcium homeostasis, and anthropometry were evaluated in 29 Orthodox fasters and 14 age and body mass index (BMI)-matched TRE controls (mean age and BMI, 48.8 years and 28.7 kg/m², respectively) at three, distinct time points—before the implementation of the energy-restricted diets (baseline), at the end of the dietary intervention (7 weeks) and 5 weeks after participants returned to their typical dietary habits (12 weeks from baseline). Repeated measures analysis was applied to assess differences between the two groups and the effect of several indices on irisin levels at all three time points. At 12 weeks, the OF group manifested higher irisin concentrations compared with both its baseline values (64.3 ± 54.4 vs. 43.6 ± 42.2 ng/mL, p = 0.01) and those of the TRE group at the same time point (64.3 ± 54.4 vs. 44.2 ± 26.6 ng/mL, p = 0.04). Glycemic, lipid, and anthropometric parameters were not found to correlate with irisin levels. In contrast, parathyroid hormone (PTH) concentrations at 12 weeks correlated with irisin concentrations (p = 0.04), indicating that lower values of irisin are expected for higher PTH measurements. The findings of this pilot study suggest favorable long-term effects of OF on irisin levels. The interplay between irisin, PTH, and diet warrants further investigation.

Athonian Orthodox fasting (AOF) is characterized by energy- and time-restricted eating (TRE) and is based on the Mediterranean diet. We aimed to investigate the impact of AOF compared to another TRE model on vaspin, omentin, nesfatin, and visfatin levels. We included 25 individuals (mean age 50.3 ± 8.6 years, 24% men) who practiced AOF and abstained from animal products, with the exception of seafood and fish. This group adopted a 12 h eating interval (08.00 to 20.00). In total, 12 participants (mean age 47.7 ± 8.7 years, 33.3% men) who practiced 16:8 TRE (eating from 09:00 to 17:00) and were allowed to consume meat served as the controls. Anthropometric and dietary data and adipokine levels were prospectively collected at three time points: at baseline, after the end of the diets (7 weeks), and 5 weeks after the participants returned to their typical eating habits (12 weeks from baseline). Vaspin levels decreased [795.8 (422.1–1299.4) (baseline) vs. 402.7 (203.8–818.9) (7 weeks) pg/mL, p = 0.002] and omentin levels increased [568.5 (437.7–1196.5) (baseline) vs. 659.0 (555.7–1810.8) (12 weeks) pg/mL, p = 0.001] in the AOF group, while none of the analyzed adipokines changed significantly in the TRE group. The variations observed in vaspin and omentin concentrations in the AOF group were independent of age, sex, changes in anthropometry and fat intake. In conclusion, AOF can significantly reduce vaspin and increase omentin, whose levels are known to increase and decrease, respectively, in obesity and type 2 diabetes. The implications of these findings for cardiometabolic health warrant further investigation.

Anorexia nervosa (AN) is characterized by severe dietary restriction with effects that extend beyond body weight to gastrointestinal function, dietary tolerance and the gut microbiome. Weight restoration remains central to treatment, but studies suggest that microbial composition, microbial metabolites and gastrointestinal symptoms may not recover at the same pace as body mass. This narrative review examines gut microbiome alterations in AN through the clinical context of refeeding and dietetic care. Human and translational studies describe changes in microbial diversity, including shifts in carbohydrate fermenting taxa and their downstream metabolic products such as short-chain fatty acids (including butyrate), mucin-degrading taxa, neuroactive fecal metabolites, immune markers and microbial functional pathways. During refeeding, the substrates available to the gut microbiome are shaped by planned increases in energy intake, the extent to which planned meals are consumed, gastrointestinal tolerance, oral supplement use, constipation, laxative exposure or other medication, dietary variety and the gradual return of fermentable substrates. Current intervention evidence does not support routine use of probiotics, prebiotics or synbiotics for weight restoration, eating-disorder psychopathology or targeted microbiome modulation. Fiber-containing foods, fermented foods and dietary diversity may be relevant to dietary substrate exposure and gastrointestinal tolerance, but their use during AN rehabilitation should be framed as pragmatic dietetic care rather than as established microbiome-specific treatment. Their introduction should remain secondary to adequate energy provision, tolerance, normalization of eating patterns and avoidance of reinforcing restrictive behaviors. Dietitians can translate microbiome-related knowledge into cautious nutritional decision-making while ensuring that patient care remains centered on rehabilitation, safety and dietary adequacy.