Search Results (3,286)

This paper presents a new, quick method for testing the content of magnetic forms of iron in organic soils. These forms are an important marker of changes occurring in the environment. This method is based on impedance spectroscopy of a measuring coil inside which the tested material is placed—the material serves as the core of the coil. Unlike EIS (electrochemical impedance spectroscopy), the new method does not use electrodes, is sensitive to magnetic forms of iron, and is non-contact (the measuring current does not flow through the tested material). The results of research on three materials, including brown peat and silt with plant detritus, are presented in this paper. The results showed that changes in the standardized components of the measuring coil impedance in the frequency range of 100–135 kHz enable the determination of the content of ferromagnetic iron oxide (Fe₃O₄). The proposed method is very sensitive to soil oxide content in the range of 0% to 8%. Additionally, elemental composition analysis was performed using ICP-AES (inductively coupled plasma–atomic emission spectroscopy), which allowed for comparison of iron and other metal content with impedance measurement results. The final results confirm the usefulness of impedance spectroscopy as a non-destructive method for studying sedimentary environments and assessing their mineral properties. Full article

Background: Population aging increases susceptibility to cognitive decline, anxiety, and metabolic dysregulation, yet safe and effective interventions remain limited. Saffron (Crocus sativus L.) has been traditionally used to enhance mood and cognition, and its main metabolites, crocins and safranal, exert neuroprotective, anxiolytic, and metabolic effects. However, variability in extract composition and frequent adulteration hinder reproducibility. Objectives: To clarify the efficacy of genuine saffron preparations in aging, we investigated a saffron extract standardized for safranal and crocin content (SSE). Methods: Safranal bioavailability was first characterized in rats, followed by an evaluation of behavioral, neuroendocrine, and metabolic outcomes after 35 days of oral SSE administration (25 or 200 mg/kg/day) in 25-month-old male C57BL/6 mice. Behavioral performance was assessed using open field and novel object recognition tests, while molecular analyses targeted neuropeptides in the hypothalamus and amygdala, hippocampal plasticity markers, cortical inflammatory proteins, and hepatic lipid metabolism genes. Results: SSE administration induced a rapid but transient increase in the plasma’s safranal, confirming its bioavailability. In aged mice, the low dose prevented age-related weight loss and modulated hepatic lipid metabolism, whereas the high dose reduced anxiety-like behavior and improved recognition memory. The anxiolytic effects are consistent with elevated hypothalamic Npy, an anxiolytic peptide, reduced amygdalar Crh, a key mediator of stress and anxiety, and decreased hypothalamic Hcrt, an arousal modulator. The improvement in memory is associated with modulation of the cortical and hippocampal inflammatory and endocannabinoid proteins involved in neural plasticity. Conclusions: These findings highlight content-standardized saffron extracts as a promising multi-target nutraceuticals for healthy aging. Full article

Background/Objectives: Kidney cancer (RC) is a significant global health burden. Renal cell carcinoma (RCC) is the most common form of kidney cancer. Its predominant histological subtype is clear cell renal cell carcinoma (ccRCC), which is frequently diagnosed at an advanced local stage or with metastases. Detecting cancer at an early stage significantly increases the likelihood of a cure; therefore, research on new markers and a thorough understanding of tumor biology are essential. This study investigated the significance of aromatase (ARO), cathepsin S (CTSS), and matrix metalloproteinase 1 (MMP-1) as potential biomarkers in ccRCC. Methods: ARO, CTSS, and MMP-1 concentrations in plasma were determined using SPRi biosensors. Appropriate antibodies were used as biorecognition molecules in the biosensors. The samples analyzed came from 60 patients with histopathologically confirmed clear cell renal cell carcinoma (ccRCC) and from 26 patients diagnosed with chronic cystitis or benign prostatic hyperplasia (BPH). Results: A statistically significant increase (p < 0.00001) in the concentration of all proteins compared with the control samples was observed at the T3–T4 stage. The ARO concentration was already statistically significantly higher at the T1–T2 stage (p < 0.00001). The ROC curve for aromatase demonstrated high sensitivity and specificity for detecting ccRCC, with a cut-off point of 7.53 ng mL⁻¹. A moderate positive correlation was also found between the concentrations of the three tested substances in renal cancer, which may indicate potential interactions in the tumor’s pathogenesis. Conclusions: SPRI testing has been shown to be an alternative to standard methods for detecting potential ccRCC markers. The biosensors used in the study can simultaneously determine ARO, CTSS, and MMP-1. The results obtained suggest the potential importance of these proteins in the development of ccRCC, and our work proposes a new diagnostic technique that may aid in the diagnosis of ccRCC. Full article

Previous studies have shown that plasma amyloid-beta oligomers (AβOs), the toxic form of amyloid-beta (Aβ), are a critical issue in the development or worsening of Alzheimer’s disease (AD) and can be regarded as a blood marker for screening in dementia. We examined plasma AβOs with their related biomarkers in a case–control study to clarify these issues. A total of 16 patients diagnosed with Alzheimer’s dementia (AD) and 16 cognitively normal controls (NCs) were recruited to compare their plasma biomarkers, AβO, Aβ_1-40, and Aβ_1-42, also referring to other parameters like APOE ε4 status, Clinical Dementia Rating^®-Sum of Boxes (CDR^®-SB), and Mini Mental Status Examination (MMSE) scores. In plasma concentrations of Aβ_1-40, Aβ_1-42, and AβO, the mean concentrations were significantly different between the two groups. There is a significant increase in the concentrations of Aβ_1-40 and AβO, while Aβ_1-42 is decreased in individuals with AD compared to NC. AβO was statistically associated with the Aβ_1-40 and Aβ_1-42/Aβ_1-40 ratio. Higher plasma concentrations of AβO were significantly associated with AD compared to non-dementia controls. This suggests that AβOs can be potential plasma biomarkers to screen in AD. However, a study recruiting more individuals is necessary to examine the association, if any. Full article

Background/Objectives: Post-COVID-19 pulmonary fibrosis (PCPF) and idiopathic pulmonary fibrosis (IPF) exhibit significant clinical and pathophysiological overlap, suggesting convergent molecular pathways driving fibrosis. This prospective longitudinal study investigates the sustained dysregulation of matrix metalloproteinases (MMP)-2 and MMP-9 and its relationship with evolving systemic inflammation and endothelial dysfunction in convalescent COVID-19 patients, with comparative analysis to IPF. Methods: We conducted a prospective observational study of 86 patients at 6 and 12 months post-SARS-CoV-2 infection, stratified by high-resolution CT evidence of PCPF (FB+ group, n = 32) or absence of fibrosis (FB− group, n = 54). Gene expression of MMP-2 and MMP-9 in peripheral blood leukocytes and circulating levels of MMP-2, MMP-9, pro-inflammatory cytokines (TNF-α, IL-6), and endothelial dysfunction markers (Endothelin-1 [ET-1], adhesion molecules) were quantified via qRT-PCR and ELISA. A pre-pandemic healthy control group (HD, n = 20) and an IPF patient group (n = 10) served as comparators. Results: A significant, sustained elevation of MMP-2 and MMP-9 was observed in all post-COVID-19 patients versus HDs, most pronounced in the FB+ group and qualitatively similar to IPF. A critical divergence emerged: FB− patients showed resolution of systemic inflammation (reduced TNF-α, IL-6), whereas FB+ patients exhibited persistent cytokine elevation. Critically, a delayed, severe endothelial dysfunction, characterized by a profound surge in ET-1 and elevated adhesion molecules, manifested exclusively in the FB+ cohort at 12 months. Positive correlations linked plasma MMP-2/9 levels with ET-1 (r_s = 0.65, p = 0.004; r_s = 0.49, p = 0.009) and ET-1 with sICAM-1 (r_s = 0.68, p = 0.01). Conclusions: The development of PCPF is associated with a distinct pathogenic triad: sustained MMP dysregulation, failure to resolve inflammation, and severe late-phase endothelial dysfunction. The correlative links between these components suggest a self-reinforcing loop. This systemic signature mirrors patterns in IPF, underscoring shared final pathways in fibrotic lung disease and identifying the MMP–inflammation–endothelial axis as a promising target for biomarker development and therapeutic intervention. Full article

Background: Visceral adiposity has emerged as a clinically relevant determinant of early cardiometabolic dysfunction in pediatric type 1 diabetes mellitus (T1DM), yet its assessment remains underutilized in routine practice. This study evaluated ultrasonographically measured epicardial adipose tissue thickness (EATT) and perirenal adipose tissue thickness (PrATT) as markers of metabolic risk, insulin sensitivity, and subclinical atherosclerosis in children and adolescents with T1DM. Methods: This cross-sectional study included 150 participants with T1DM and 152 age- and sex-matched healthy controls. Anthropometric data, biochemical parameters, hepatic steatosis grade, and insulin sensitivity indices (eGDR) were collected. EATT and PrATT were measured via standardized echocardiographic and abdominal ultrasonographic protocols. Carotid intima–media thickness (cIMT) was assessed as an indicator of subclinical atherosclerosis. Correlation and multivariable logistic regression analyses were performed to identify independent predictors of T1DM status and cardiometabolic risk. Results: Children with T1DM exhibited significantly higher PrATT and EATT values compared with controls (both p < 0.05). All eGDR indices were markedly lower in the T1DM group, reflecting reduced insulin sensitivity. PrATT and EATT showed strong or moderate correlations with hsCRP, hepatic steatosis, atherogenic index of plasma, and multiple anthropometric markers. Both visceral fat depots were positively associated with cIMT. Logistic regression identified PrATT, EATT, hsCRP, cIMT, and eGDR-BMI as independent predictors of case status. Subgroup analyses demonstrated more pronounced visceral adiposity and metabolic impairment among participants with BMI ≥85th percentile. Conclusions: Ultrasonographically measured PrATT and EATT provide valuable insight into early cardiometabolic risk in youth with T1DM, independent of BMI. Their associations with insulin resistance, inflammation, and subclinical atherosclerosis highlight their potential utility as accessible markers for early risk stratification in pediatric diabetes. Routine incorporation of visceral fat assessment may support earlier identification of high-risk individuals and more targeted preventive strategies. Full article

Background/Objectives: Cardiac sarcoidosis (CS) is a challenging diagnosis due to its subclinical progression and the limitations of existing screening tools. Cardiac magnetic resonance (CMR) and PET/CT imaging have improved diagnosis and detection. Aldosterone, a hormone with known profibrotic effects, may offer additional diagnostic value. We therefore aimed to determine whether plasma aldosterone level is associated with myocardial fibrosis, independent of active inflammation, in CS. Methods: This observational study included 541 patients with biopsy-proven sarcoidosis and preserved left ventricular ejection fraction (LVEF ≥ 50%). All underwent CMR with extracellular volume (ECV) mapping and 18F-FDG PET/CT to assess myocardial fibrosis and inflammation, respectively. Plasma aldosterone levels were also measured. Results: Plasma aldosterone levels were significantly higher in patients with cardiac sarcoidosis (172 [IQR 106–235] pg/mL) compared to those without cardiac involvement (143 [100–205] pg/mL, p = 0.02). Aldosterone was independently associated with the presence of late gadolinium enhancement (LGE) on CMR (OR 1.002 per 1 pg/mL increase; 95% CI 1.001–1.004, p = 0.04) and with higher ECV values (β = 0.008 per 1 pg/mL, p = 0.001). Regression analysis showed that aldosterone is associated with ECV (b-0.009, CI: 0.002–0.016, p = 0.009) and there was no interaction according to LGE status indicating a relationship with diffuse myocardial fibrosis even in the absence of visible scarring. No association was observed with T1-, T2-, or PET/CT-defined inflammation. Conclusions: Plasma aldosterone is a robust marker of myocardial fibrosis in sarcoidosis, particularly in early or subclinical stages. Its correlation with ECV—but not with inflammatory imaging markers—suggests its link with myocardial diffuse fibrotic remodeling before, and independently of, overt scarring or inflammation. Full article

Preeclampsia (PE) is the onset of hypertension in pregnancy with systemic involvement; PE poses significant risks of cerebral complications, including eclampsia and long-term cognitive impairment. This review explores the potential of neurological biomarkers—neurofilament light chain (NfL), neuron-specific enolase (NSE), S100 Calcium Binding Protein B (S100B), and tau—as indicators of cerebral injury in PE. A literature search identified studies comparing biomarker levels in preeclamptic and healthy pregnancies. Findings reveal elevated plasma levels of NfL, NSE, S100B, and Tau in PE, with NfL showing the strongest association with blood–brain barrier dysfunction, cognitive symptoms, and disease severity. Variations between plasma and cerebrospinal fluid levels suggest impaired BBB integrity rather than increased central nervous system production. Despite promising correlations, limitations include small sample sizes, lack of standardized thresholds, and limited CSF data. While NfL emerges as a particularly promising marker for risk stratification, further research is needed to validate the clinical utility of these biomarkers in routine PE management. Full article

Circulating irisin, a myokine implicated in energy expenditure and adipose tissue regulation, has been increasingly studied as a potential biomarker of metabolic dysfunction. This study evaluated the relationship between serum irisin and metabolic indices, including the atherogenic index of plasma (AIP), the lipid accumulation product (LAP), and hypertriglyceridemic-waist (HTGW) phenotype in individuals with prediabetes (PreDM) and newly diagnosed type 2 diabetes mellitus (T2DM). A total of 138 participants (48 PreDM, 90 T2DM) were assessed for anthropometric, glycemic, and lipid parameters. Serum irisin levels were measured by enzyme-linked immunosorbent assay (ELISA) and correlated with insulin resistance indices (Homeostatic Model Assessment of Insulin Resistance (HOMA-IR), Quantitative Insulin Sensitivity Check Index (QUICKI)), glycemic control (glycosylated hemoglobin A1c (HbA1c)), and composite lipid markers (total triglycerides-to-high-density lipoprotein cholesterol (TG/HDL-C)). Group differences were evaluated using non-parametric tests; two-way ANOVA assessed interactions between phenotypes and markers; multiple linear regression (MLR) and logistic regression models explored independent associations with metabolic indices and HTGW; receiver operating characteristic (ROC) analyses compared global and stratified model performance. Serum irisin was significantly lower in T2DM than in PreDM (median 140.4 vs. 230.7 ng/mL, p < 0.0001). Irisin levels remained comparable between males and females in both groups. Post hoc analysis shows that lipid indices and irisin primarily distinguish HTGW phenotypes, especially in T2DM. In both groups, irisin correlated inversely with HOMA-IR, AIP, and TG/HDL-C, and positively with QUICKI, indicating a possible compensatory role in early insulin resistance. MLR analyses revealed no independent relationship between irisin and either AIP or LAP in PreDM, while in T2DM, waist circumference remained the strongest negative predictor of irisin. Logistic regression identified age, male sex, and HbA1c as independent predictors of the HTGW phenotype, while irisin contributed modestly to overall model discrimination. ROC curves demonstrated good discriminative performance (AUC = 0.806 for global; 0.794 for PreDM; 0.813 for T2DM), suggesting comparable predictive accuracy across glycemic stages. In conclusion, irisin levels decline from prediabetes to overt diabetes and are inversely linked to lipid accumulation and insulin resistance but do not independently predict the HTGW phenotype. These findings support irisin’s role as an integrative indicator of metabolic stress rather than a stand-alone biomarker. Incorporating irisin into multi-parameter metabolic panels may enhance early detection of cardiometabolic risk in dysglycemic populations. Full article

Background/Objectives: Intermittent fasting and ketogenic dietary approaches are increasingly investigated for their potential metabolic benefits in obesity. However, their long-term neuroendocrine effects—particularly those involving Orexin-A, a peptide implicated in energy regulation—remain poorly understood. The objective of this study was to compare the long-term metabolic, inflammatory, and orexinergic responses to different dietary strategies in adults with obesity. Methods: In this 12-month randomized, three-arm trial, 30 adults with obesity (BMI ≥ 30 kg/m²) were randomly assigned (1:1:1) to a hypocaloric ketogenic diet (KD), a 16:8 time-restricted eating regimen (TRF16:8), or a 5:2 intermittent fasting protocol (ADF5:2). Anthropometric parameters, body composition, fasting glucose, lipid profile, inflammatory cytokines (CRP, IL-6, TNF-α, IL-10), and plasma Orexin-A levels were assessed at baseline and every 3 months. Dietary adherence was monitored through structured logs and monthly assessments. Statistical analyses included repeated-measures models with sensitivity analyses adjusted for age and sex. Results: All participants completed the intervention. The ketogenic diet produced the largest sustained reductions in BMI, fat mass, fasting glucose, and total cholesterol over 12 months. TRF16:8 elicited more rapid early metabolic improvements and showed the most consistent longitudinal increase in Orexin-A levels. The ADF5:2 protocol resulted in moderate improvements across outcomes. In all groups, increases in Orexin-A were associated with markers of improved metabolic flexibility and reduced inflammation; however, mediation analyses were exploratory and non-causal. Between-group differences remained significant for fat mass, glucose, and Orexin-A trajectories after correction for multiple comparisons. Conclusions: The ketogenic diet was associated with the most pronounced long-term metabolic improvements, whereas 16:8 time-restricted eating yielded faster early responses and the most stable enhancement in Orexin-A levels. These findings indicate distinct metabolic and neuroendocrine adaptation profiles across dietary strategies. Given the small sample size, results should be interpreted cautiously, and larger trials are warranted to clarify the role of Orexin-A as a potential biomarker of dietary response in obesity. Full article

Background: Atherosclerosis and its associated chronic inflammation of the arterial wall disrupt fatty acid metabolism, leading to changes in plasma fatty acid composition. These alterations can be used to improve disease diagnosis and risk stratification by the development and application of specific lipidomic indices. Objectives: The objectives of this study are to evaluate the performance of conventional fatty acid indices and enhance diagnostic efficiency in atherosclerosis by introducing novel index based on plasma PUFA n-6 and n-3 content (Omega-6/3 Balance Index, O6/3-BI), as well as the perspective SFA/MUFA ratio (stearic/oleic acid ratio, C18:0/C18:1n-9) and a logit function combining PUFA and SFA/MUFA biomarkers. Methods: Plasma fatty acids were quantified by LC-MS/MS in healthy controls (n = 50) and patients with carotid atherosclerosis (n = 52), stratified by atorvastatin, rosuvastatin, or no statin therapy. The conventional indices (the Omega-3 Status (EPA + DHA), AA/EPA, and the omega-6/omega-3 ratio), and pathway ratios (C18:0/C18:1n-9; and C20:4n-6/C22:4n-6), as well as the newly introduced PUFA index and combined PUFA-SFA/MUFA logit function, were calculated. Their diagnostic performance for distinguishing atherosclerosis was assessed by a receiver operating characteristic (ROC) analysis with the cross-validation and calculation of Cliff’s Δ effect size. Results: The conventional parameters demonstrated a poor to low discrimination ability of the atherosclerosis patients’ groups from healthy controls (area under the ROC curve, AUC 0.548–0.711). In statin-treated patients, these conventional markers lost significance. The newly introduced PUFA index and SFA/MUFA ratio demonstrated improved patients’ discrimination with AUC 0.734–0.780 for the former and strong predictive power with AUC 0.831–0.858 for the latter marker and maintained their diagnostic value under statin therapy. The most significant positive effect size was observed for the SFA/MUFA ratio with Cliff’s Δ = 0.67–0.71. The combined PUFA-SFA/MUFA logit function also demonstrated a strong predictive power with AUC = 0.880 (Cliff’s Δ = −0.76), outperforming any single index. Conclusions: The newly introduced lipidomic index based on the PUFA content, SFA/MUFA ratio, and a logit function combining PUFA-SFA/MUFA biomarkers demonstrated a substantially better discrimination of atherosclerosis-related fatty acid metabolic disturbances than conventional fatty acid biomarkers. Full article

This study intends to assess oxidative stress markers and endogenous enzymes in plasma and peritumoral adipose tissues (PATs) obtained from normal subjects and patients with stages I-IV colorectal cancer (CRC). 63 participants were recruited, including 23 patients with colorectal cancer and 40 healthy subjects. CRC patients had increased circulating malondialdehyde (MDA) and protein carbonyl concentrations, as well as reduced superoxide dismutase (SOD) and catalase activities, compared to normal volunteers. (p < 0.05). The findings aligned with the oxidative parameters assessed in peritumoral adipose tissue. Superoxide production in PAT was dramatically higher in the CRC group compared to the control group (p < 0.05). Moreover, oxidative stress markers were progressively altered in relation to CRC stages. Nuclear factor erythroid 2-related factor 2 (Nrf2)/heme oxygenase-1 (HO-1) protein expression was reduced in PAT isolated from CRC compared to normal subjects and associated with CRC stages. CRC patients showed a systemic and peritumoral oxidative imbalance, along with elevated superoxide production in the PAT. The oxidative modifications worsened with the progression of CRC stage and were associated with the downregulation of the Nrf2/HO-1 antioxidant cascade in peritumoral adipose tissue. Full article

Background/Objectives: Aurora kinases (AURKs) are key regulators of mitosis, and their dysregulation contributes to plasma cell disorders, including multiple myeloma (MM) and plasma cell leukemia (PCL). Methods: The expression and prognostic relevance of AURK family members were examined, and the therapeutic potential of AURKA inhibition was evaluated. Results: Gene expression analysis demonstrated significant upregulation of AURKA in PCL. Treatment of MM cells with the selective AURKA inhibitor LY3295668 induced dose-dependent cytotoxicity, caspase-3/7 activation, and cellular senescence. Similarly, selinexor, a selective exportin-1 inhibitor, elicited dose-dependent cytotoxicity and apoptosis. Combined treatment with LY3295668 and selinexor significantly improved apoptosis compared with either agent alone, and AURKA knockdown further sensitized MM cells to selinexor, thereby increasing apoptosis. In bortezomib-resistant MM cells and primary PCL samples, the combination therapy induced cytotoxicity and caspase-3/7 activation. Conclusions: These findings underscore AURKA expression as a prognostic marker in plasma cell disorders and support the therapeutic potential of combining AURKA inhibition with selinexor for bortezomib-resistant MM and PCL. To explore biomarker-driven strategies for optimizing therapeutic outcomes, future studies are warranted. Full article

Background: Irisin, an exercise-induced myokine, has emerged as a potent neuroprotective factor, though a systematic synthesis of its role across neurological disorders is lacking. This review systematically evaluates clinical and preclinical evidence on irisin’s association with neurological diseases and its underlying mechanisms. Methods: Following PRISMA 2020 guidelines, a systematic search of PubMed/MEDLINE, Scopus, Web of Science, Embase, and Cochrane Library was conducted. The review protocol was prospectively registered in PROSPERO. Twenty-one studies were included, comprising predominantly preclinical evidence (n = 14), alongside clinical observational studies (n = 6), and a single randomized controlled trial (RCT) investigating irisin in cerebrovascular diseases, Parkinson’s disease (PD), Alzheimer’s disease (AD), and other neurological conditions. Eligible studies were original English-language research on irisin or FNDC5 and their neuroprotective effects, excluding reviews and studies without direct neuronal outcomes. Risk of bias was independently assessed using SYRCLE, the Newcastle–Ottawa Scale, and RoB 2, where disagreements between reviewers were resolved through discussion and consensus. Results were synthesized narratively, integrating mechanistic, pre-clinical, and clinical evidence to highlight consistent neuroprotective patterns of irisin across disease categories. Results: Clinical studies consistently demonstrated that reduced circulating irisin levels predict poorer outcomes. Lower serum irisin was associated with worse functional recovery and post-stroke depression after ischemic stroke, while decreased plasma irisin in PD correlated with greater motor severity, higher α-synuclein, and reduced dopamine uptake. In AD, cerebrospinal fluid irisin levels were significantly correlated with global cognitive efficiency and specific domain performance, and correlation analyses within studies suggested a closer association with amyloid-β pathology than with markers of general neurodegeneration. However, diagnostic accuracy metrics (e.g., AUC, sensitivity, specificity) for irisin as a standalone biomarker are not yet established. Preclinical findings revealed that irisin exerts neuroprotection through multiple mechanisms: modulating microglial polarization from pro-inflammatory M1 to anti-inflammatory M2 phenotype, suppressing NLRP3 inflammasome activation, enhancing autophagy, activating integrin αVβ5/AMPK/SIRT1 signaling, improving mitochondrial function, and reducing neuronal apoptosis. Irisin administration improved outcomes across models of stroke, PD, AD, postoperative cognitive dysfunction, and epilepsy. Conclusions: Irisin represents a critical mediator linking exercise to brain health, with consistent neuroprotective effects across diverse neurological conditions. Its dual ability to combat neuroinflammation and directly protect neurons, demonstrated in preclinical models, positions it as a promising therapeutic candidate for future investigation. Future research must prioritize the resolution of fundamental methodological challenges in irisin measurement, alongside investigating pharmacokinetics and sex-specific effects, to advance irisin toward rigorous clinical evaluation. Full article

Biomarker-based prevention is rapidly expanding, driven by advances in molecular diagnostics, genetic profiling, and commercial direct-to-consumer (DTC) testing. General practitioners (GPs) increasingly encounter biomarker results of uncertain relevance, often introduced outside the guideline frameworks. This creates new challenges in interpretation, communication, and equitable resource use in primary care. This narrative review synthesizes evidence from population-based studies, guideline frameworks, consensus statements, and communication research to evaluate the predictive value, limitations, and real-world implications of biomarkers in asymptomatic adults. Attention is given to polygenic risk scores, DTC genetic tests, neurodegenerative and cardiovascular biomarkers, and emerging multi-omics and aging markers. Several biomarkers, including high-sensitivity cardiac troponins, N-terminal pro–B-type natriuretic peptide, lipoprotein(a), coronary artery calcium scoring, and plasma p-tau species, showed robust predictive validity. However, many widely marketed biomarkers lack evidence of clinical utility, offer limited actionable benefits, or perform poorly in primary care populations. Unintended consequences, such as overdiagnosis, false positives, psychological distress, diagnostic cascades, and widening inequities, are well documented. Patients often misinterpret unvalidated biomarker results, whereas DTC testing amplifies demand without providing adequate counseling or follow-up. Only a minority of biomarkers currently meet the thresholds of analytical validity, clinical validity, and clinical utility required for preventive use in general practices. GPs play a critical role in contextualizing biomarker results, guiding shared decision-making, and mitigating potential harm. The responsible integration of biomarkers into preventive medicine requires clear communication, strong ethical safeguards, robust evidence, and system-level support for equitable, patient-centered care. Full article