Collagen supplementation (CS) has emerged as a promising therapeutic approach with potential benefits for managing metabolic syndrome (MetS)-related risk factors. This narrative review integrates human evidence with preclinical mechanistic insights into the metabolic actions of collagen. Anti-obesity effects are attributed to increased satiety, gastric distension, GLP-1 secretion, and enhanced fatty acid oxidation mediated by PPAR-α activation and AMPK signalling. In type 2 diabetes, collagen improves glucose homeostasis by enhancing insulin sensitivity, upregulating GLUT-4, and inhibiting DPP-IV, thereby prolonging incretin activity (GLP-1, GIP) and supporting β-cell function. The antihypertensive effect of collagen peptides (CP) is primarily linked to angiotensin-converting enzyme (ACE) inhibition, which reduces angiotensin II levels while promoting bradykinin-mediated vasodilation and nitric oxide release. Additionally, CP has shown potential in improving lipid profiles by modulating PPAR-γ and AMPK, increasing HDL-C and reducing LDL-C and triglycerides. Emerging evidence also supports a role for collagen in restoring gut microbiota balance, increasing short-chain fatty acid production, and reducing pro-inflammatory and oxidative pathways, contributing to systemic metabolic regulation. Overall, these findings suggest CS exerts multi-targeted benefits on MetS components through modulation of endocrine, inflammatory, and metabolic pathways. Nevertheless, larger, long-term clinical trials are warranted to determine optimal dosing regimens, evaluate long-term efficacy, and further elucidate microbiota-mediated effects.

The increasing focus on longevity and cellular health has brought into the spotlight two key compounds, urolithin A (UroA) and spermidine, for their promising roles in autophagy and mitophagy. Urolithin A, a natural metabolite derived from ellagitannins, stimulates mitophagy through pathways such as PTEN induced kinase 1 (PINK1)/ Parkin RBR E3 ubiquitin protein ligase (PRKN), leading to improved mitochondrial health and enhanced muscle function. On the other hand, spermidine, a polyamine found in various food sources, induces autophagy by regulating key signaling pathways such as 5' AMP-activated protein kinase (AMPK) and sirtuin 1, thus mitigating age-related cellular decline and promoting cardiovascular and cognitive health. While both UroA and spermidine target cellular maintenance, they affect overlapping as well as distinct signaling pathways. Thus, they do not have completely identical effects, although they overlap in many ways, and offer varying benefits in terms of metabolic function, oxidative stress reduction, and longevity. This review article aims to describe the mechanisms of action of UroA and spermidine not only on the maintenance of cellular health, which is mediated by the induction and maintenance of autophagy and mitophagy, but also on their potential clinical relevance. The analysis presented here suggests that although both compounds are safe and offer substantial health benefits and are involved in both autophagy and mitophagy, the role of UroA in mitophagy places it as a targeted intervention for mitochondrial health, whereas the broader influence of spermidine on autophagy and metabolic regulation may provide more comprehensive anti-aging effects.

Cognitive decline is a hallmark of brain ageing. Leukocyte telomere length (LTL) has emerged as a candidate biomarker related to brain ageing and neurodegeneration; however, reported associations with cognition and brain structure vary across cohorts. Long‑chain omega‑3 polyunsaturated fatty acids (PUFAs), notably docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA), exert anti‑inflammatory and antioxidant effects that may, in some contexts, relate to slower telomere attrition. Here, we synthesize evidence on n‑3 PUFAs, telomere biology, and cognitive outcomes, integrating clinical, epidemiologic, and experimental data. We emphasize biological plausibility (oxidative stress/inflammation, membrane remodeling, mitochondrial function and expression of telomerase reverse transcriptase (TERT) through PI3K/Akt/mTOR, NRF2 and epigenetic modifications) while acknowledging heterogeneous human findings and methodological considerations (assay variability, life‑course timing, cognitive domains, and biomarker stratification). We outline priorities for future studies to clarify causal pathways and inform dietary strategies that support healthy cognitive ageing.

Growing evidence has linked both the onset and symptoms of various mental disorders to lifestyle factors such as diet, exercise and sleep. The link between diet and mental health in particular in depressive disorders has gained interest in recent years. Previous reviews assessing the link between the Mediterranean diet (MedDiet) and mental health predominantly focused on depression, whilst others failed to integrate a summary of possible underlying mechanisms related to a link between MedDiet and mental health to complement their findings. In the present review, we provide a comprehensive synthesis of evidence on the MedDiet and diverse mental health outcomes complemented by narration of potential mechanisms involved. A literature search was conducted across MEDLINE, PsycINFO, Scopus, Cochrane library, Google scholar, CINAHL and Embase database. A total of 10,249 articles were found through the primary literature search and 104 articles (88 observational and 16 interventional studies) were eligible for inclusion. The Mediterranean diet (MedDiet) has been associated with favourable mental health outcomes in adult populations, including reduced depressive and anxiety symptoms, lower perceived stress, and improved quality of life and overall well-being, both in healthy individuals and those with comorbidities, across diverse geographical settings. Mechanisms involved include anti-oxidant, anti-inflammatory potential of MedDiet and its effect on gut microbiota. Further research is warranted to rigorously establish causal inferences and to guide the optimal incorporation of Mediterranean diet principles into comprehensive prevention and treatment strategies aimed at improving mental health outcomes.