Maribel Lucerón-Lucas-Torres

Context: Omega-3 polyunsaturated fatty acids (PUFAs) have demonstrated metabolic benefits in several populations; however, their efficacy in type 1 diabetes mellitus (T1D) is not well established. Objective: The aim of this systematic review and meta-analysis was to assess the efficacy of omega-3 PUFAs supplementation on the lipid and glycemic profile in T1D. Data sources: A systematic search was conducted in Medline, Scopus, Web of Science, and the Cochrane Library, from inception to June 2026. Data extraction: Studies evaluating the effect of omega-3 PUFA supplementation on total cholesterol (TC), low- and high-density lipoprotein cholesterol (LDL-C and HDL-C), triglycerides, fasting plasma glucose (FPG), and glycated hemoglobin (HbA1c) were included. Random-effects meta-analyses of randomized clinical trials (RCTs) and of the pre-post effect of a single intervention arm were performed separately. Heterogeneity was assessed using the I2 statistic. Data analysis: Eighteen studies were included. In the RCTs, omega-3 PUFA supplementation increased HDL-C by 4.47 mg/dL (95% CI, 0.07 to 8.86) with an I2 of 64.87%, and decreased triglycerides by 9.49 mg/dL (95% CI, 16.60 to −2.38) with an I2 of 29.83%. There was no effect on the other outcomes, including TC, LDL-C, FPG, and HbA1c. Finally, the effect on the meta-analyses of pre-post studies was similar to that found in the RCTs. Conclusions: Although omega-3 supplementation has been associated with modest improvements in lipid levels in people with T1D, the results are statistically fragile. No glycemic benefits were observed. Future RCTs focusing on hard cardiovascular outcomes and standardized protocols are necessary to determine the clinical efficacy of omega-3 supplementation beyond surrogate metabolic markers. Systematic Review Registration: PROSPERO registration No. [CRD420261297164].

Background: Chronic kidney disease (CKD) is associated with high cardiovascular morbidity and mortality, which is mediated by arterial stiffness. Pulse wave velocity (PWV), as measured by the aortic (aPWV), brachial‐ankle (baPWV) and carotid‐radial (crPWV) indices or estimated by equations (ePWV), could be a powerful predictor of clinical events and mortality in this population. This study aimed to analyse the association between PWV and all‐cause mortality, cardiovascular mortality, and cardiovascular disease (CVD) risk in populations with CKD. Methods: A systematic search was conducted in PubMed, Scopus, and Web of Science from inception to January 2026. Observational studies estimating the association between PWV, categorically or by an increase of 1 m/s, and the outcomes of interest were included. Random‐effects meta‐analyses were performed, considering the type of PWV studied. The results are presented as hazard ratios (HR) and their 95% confidence intervals (95% CI). Results: Twenty‐eight studies were included in the systematic review, and 22 in the meta‐analyses. Considering a 1 m/s increase in aPWV, HRs of 1.16 (95% CI: 1.06, 1.28), 1.36 (95% CI: 1.15, 1.61), and 1.20 (95% CI: 1.02, 1.41) were found for all‐cause mortality, cardiovascular mortality, and CVD risk, respectively. The remaining associations for aPWV, baPWV, and ePWV were categorical and tended to be higher. Conclusions: Increased PWV was associated with an increased risk of mortality and CVD. However, given the low quality of the current evidence base, these findings should be interpreted with caution and more rigorous studies are needed to confirm their usefulness in clinical practice.

Background/Objectives: Chronic kidney disease (CKD) affects almost 800 million people worldwide. Cardiovascular disease is the main cause of death in this population. Although physical activity is fundamental to systemic health, the evidence regarding its impact on the clinical outcomes of CKD populations is inconclusive. This protocol outlines the methodology for a systematic review and meta-analysis aimed at evaluating the association between physical activity and intensity and all-cause mortality, cardiovascular mortality, and cardiovascular disease. Methods: This protocol adheres to PRISMA-P and Cochrane Handbook guidelines and has been registered with PROSPERO (CRD420261302904). A systematic search will be conducted in MEDLINE, Scopus, Web of Science and the Cochrane Library until June 2026. Studies estimating the association between physical activity and all-cause mortality, cardiovascular mortality and cardiovascular disease in populations with CKD will be included. Two independent reviewers will perform study selection, data extraction and quality assessment using the Study Quality Assessment Tool from the United States National Institute of Health tool. The certainty of the evidence will be evaluated using the Grading of Recommendations, Assessment, Development and Evaluation tool. Narrative synthesis and random-effects meta-analysis will be conducted to calculate pooled effect estimates. Random-effects meta-analyses will be performed according to the level of physical activity, and meta-regressions will be used to control for the association with major covariates. Ethical approval is not required for this study. Results: The results will provide a comprehensive synthesis of the evidence regarding the use of physical activity as a non-pharmacological intervention to modify CKD progression. Conclusions: The findings will be disseminated through peer-reviewed journals and international conferences.

Skin autofluorescence (SAF) is a biomarker of tissue accumulation of advanced glycation end-products, which increase the risk of cardiovascular disease (CVD) and mortality, particularly among individuals with chronic kidney disease (CKD) or diabetes mellitus (DM). The aim was to summarise existing evidence and estimate the association between SAF and all-cause mortality, cardiovascular mortality and CVD. A search of Medline, Scopus, Web of Science and the Cochrane Library was conducted from inception to June 2025. Observational studies estimating the association between SAF and all-cause mortality, cardiovascular mortality and CVD were included. Meta-analyses of these associations were performed by categorising SAF (high vs. low) and by 1 arbitrary unit (AU) increment of SAF, expressed as hazard ratio (HR) or odds ratio (OR) and their 95% confidence intervals. Thirty-two studies were included in the systematic review. Elevated SAF was associated with an increased risk of all-cause mortality, cardiovascular mortality and CVD. Per 1 AU increase, an HR of 1.51 (1.35, 1.69) was obtained for all-cause mortality, an HR of 1.48 (1.16, 1.90) for cardiovascular mortality and an HR of 1.25 (1.13, 1.38) for CVD. However, estimates with OR tended to be higher. Finally, the results were similar in CKD and DM. SAF is a strong predictor of CVD and mortality in general, and in CKD and DM in particular. Integrating SAF measurement into clinical practice could help clinicians implement early and intensive interventions to prevent associated morbidity and mortality, although clinical trials are needed to evaluate its effectiveness.

Noonan syndrome (NS) is a RASopathy, a group of genetic disorders caused by alterations in the RAS/MAPK signalling pathway, and is associated with brain-related disorders, including intellectual developmental disorder (IDD), autism spectrum disorder (ASD), attention deficit hyperactivity disorder (ADHD), epilepsy, and depression and anxiety. However, estimates of prior prevalence vary widely. The aim of this systematic review and meta-analysis was to estimate the prevalence of brain-related disorders (i.e., IDD, ASD, ADHD, epilepsy, and depression and anxiety) in NS. A systematic search of Medline, Scopus, Web of Science and the Cochrane Library was conducted from inception to July 2025. Studies that estimated the prevalence of IDD, ASD, ADHD, epilepsy, and depression and anxiety in the population with NS were included. Genotype was considered when possible. Random-effects meta-analyses of prevalence, expressed as proportions (0–1) and their 95% confidence intervals (95% CI), were performed. Twenty-one studies were included in the systematic review, while 20 were included in the meta-analysis. The IDD prevalence was 0.23 (95% CI: 0.12, 0.35), the ASD prevalence was 0.11 (95% CI: 0.05, 0.17); the ADHD prevalence was 0.31 (95% CI: 0.22, 0.41); the epilepsy prevalence was 0.09 (95% CI: 0.03, 0.15) and the depression and anxiety prevalence was 0.23 (95% CI: 0.08, 0.39). There was hardly any genotype-specific data, particularly for minor mutations. NS is strongly associated with brain-related disorders, which reinforces the need for early and periodic screening in this population. Furthermore, genotype–phenotype correlation studies are required, as there is currently little evidence in this area. What is Known: • Noonan syndrome is a RASopathy characterised by short stature, heart disease and brain-related disorders. • Brain-related disorders include intellectual developmental disorder (IDD), autism spectrum disorder (ASD) and attention deficit hyperactivity disorder (ADHD), among others. What is New: • IDD, ASD and ADHD were estimated to affect 23%, 11% and 31% of individuals, respectively. This is higher than the prevalence in the general population. • The prevalence of seizure disorders and emotional disorders was also high, although the evidence was more limited.

Background/Objectives: Dietary advanced glycation end products (dAGEs) have a pro-inflammatory effect and increase oxidative stress, potentially leading to cancer. The aim of this study was to estimate the association between dAGEs consumption and risk and mortality from overall cancer and according to its site. Methods: A systematic search was conducted in Medline, Scopus, Web of Science, and the Cochrane Library from inception to April 2025. The search strategy was conducted according to the PECO structure adapted to this study, as well as the inclusion criteria, in which the population (P) was the adult population, the exposure (E) was the highest level of dAGEs intake, the comparator (C) was the lowest level of dAGEs intake, and the outcomes (O) were the overall cancer risk, cancer risk by site, and cancer mortality. Results across studies were summarised using random effects and fixed effects. Results: Fourteen studies were included in the systematic review. In the random-effects meta-analysis, high dAGEs intake was associated with Hazard Ratio (HR) = 0.99 [95% Confidence Interval (95% CI): 0.98, 1.00] for overall cancer risk. However, although there was no association with breast cancer (BC), there was an association with invasive BC, with HR = 1.14 (95% CI: 1.05, 1.23). In contrast, in other tumours, there were opposite results depending on the site of the cancer. Conclusions: The reduction in cancer risk is not clinically significant. However, high consumption of dAGEs may increase the risk of BC, particularly the invasive BC, which is a challenge for cancer prevention and subsequent mortality. Due to the limited evidence, further studies are needed to confirm the potential impact of dAGEs, as well as other dietary factors that may play a larger role in cancer development.

Background: It seems that diet is one of the main triggers of migraine; one of the most studied is alcohol, and also, over the years, red wine has been shown to trigger headaches. Therefore, this systematic review and meta-analysis aims to examine the strength of the association between wine consumption and migraine. Methods: In this systematic review and meta-analysis, a search of MEDLINE (via PubMed), Scopus, Cochrane, and Web of Science databases was conducted to assess the association between wine consumption and migraine, covering baseline to December 2023. Pooled Odds Ratio (p-OR) were calculated using the DerSimonian and Laird methods. This study was previously registered in PROSPERO (CRD42024511115). The risk of bias was evaluated using The Quality Assessment Tool for Observational Cohort and Cross-Sectional Studies. Results: Five studies were included in this systematic review, and only four of them were in the meta-analysis. Using the DerSimonian and Laird method, the p-OR for the effect of wine consumption on migraine was 0.63 (95% CI 0.36–1.09). The included studies after the risk of bias assessment showed a moderate risk of bias. Conclusions: The findings of this systematic review and meta-analysis indicate that there is no conclusive evidence to support an increased or decreased risk of migraine associated with wine consumption.

The comment authors pointed out a trend with the omission of meta-analyses for certain types of cancer, and they encourage the authors to clearly specify the types of cancer for which a metaanalysis was carried out and those for which it was not possible. The main reason for this limitation is the limited number of articles available for some cancers in particular. Despite this limitation, a graphical representation has been included for these specific cases, providing the reader with a visual summary of the risk of wine consumption with the available studies, even when a meta-analysis could not be performed. The intention of this graphical representation is to show where the trend in wine consumption and certain types of cancer is pointing so that future studies can support this trend. Substantial heterogeneity and publication bias were investigated and included in the study. In addition, limitations were included regarding the heterogeneity of the included studies in reporting alcohol exposure, as they differed in the methods used to measure wine consumption and did not report the specific volume of wine consumed. This lack of data has influenced the quality of our results because the associations between wine consumption and the development of different types of cancer could not be analyzed by type of wine, amount of wine consumed or sex.Wine, in addition to ethanol, contains nutrients, micronutrients, proteins, and a large amount of phenolic substances that affect human health. 1 The most beneficial components of wine are polyphenols, which are found in the solid parts of the grape, i.e., the skins, seeds, and stems. 2 There are other components that are not polyphenols but also have positive effects on human health, such as melatonin or gallic acid. 3,4 Polyphenols have antioxidant, anti-inflammatory, anticarcinogenic, and antiaging effects, 5 inhibit platelet aggregation, have vasorelaxant effects, modulate lipid metabolism, have neuroprotective effects6, regulate the microbiota, 7,8 and even have chemopreventive effects, among many other benefits. 9 Polyphenols include resveratrol, the polyphenol that has been analyzed the most thus far. 10,11 As a good polyphenol, resveratrol offers multiple benefits to the body by inhibiting LDL oxidation and suppressing platelet aggregation, has antiatherosclerotic properties, promotes vascular relaxation, and has endothelial protective functions. In addition, it regulates various substances, such as nitric oxide synthase, thioredoxin-1, hemeoxygenase-1, vascular endothelial growth factor, manganese superoxide dismutase, and caveolin-1, thus contributing to the prevention of oxidative stress. 12,13 However, the role of resveratrol and flavonoids in health, as the commentary says, is still under study for several reasons, the first of which is from a pharmacological point of view: there is an interaction between resveratrol and certain drugs, such as oral anticoagulants, causing the drug to reach the blood in lower quantities. 14,15 On the other hand, at low doses, resveratrol acts as a cardioprotective agent, but at high doses, it induces apoptosis in cancer cells by exerting a death signal, depressing cardiac function, and increasing the risk of myocardial infarction. 16 With respect to resveratrol in wine, previous evidence shows that the resveratrol dose in wine is at average levels of 7 mg L-1 in red wine and 0.5 mg L-1 in white wine; 17 although resveratrol in the human body is well absorbed, its free fraction in the blood is low and therefore has a low bioavailability compared with that reported in in vitro studies. 18 In addition, evidence over the years has revealed multiple benefits of resveratrol in wine, as it is one of the most interesting polyphenols in wine, as it provides benefits for a wide range of medical problems by reducing oxidative stress and exerting antiinflammatory and antimutagenic effects on diseases such as cancer. 19 On the other hand, although the article focuses on wine consumption, as is reflected in the wording of the article, and some data may indicate that wine consumption may have protective or beneficial effects on health, the comment authors believe it is important to highlight that it is still a type of alcohol and that, as such, it is necessary to draw attention to moderate consumption, but it is true that this work does not show any association, neither negative nor positive, so neither can report that wine consumption increases the risk of cancer. Notably, alcohol consumption is a risk factor for the development of this pathology, which, together with tobacco, may have a concomitant effect. 20 Although the evidence is controversial and seems that the type of alcohol may also influence the development of this pathology, 21 the authors want to stress that although the evidence reports that light-moderate consumption of wine may bring health benefits, caution should be exercised with its consumption, especially in at-risk populations. Therefore, we may highlight that we do not want to recommend wine consumption but rather synthesize the existing evidence on wine consumption, always remembering that safe consumption is zero, that inadequate consumption can be very harmful to health, for many pathologies and that a lifelong abstainer starting to consume can have very detrimental effects on one's health. 22 Finally, in addressing the last point about retracting this scientific article, the authors consider that it is not appropriate because, with our article, we have synthesized data from original studies on wine consumption and different types of cancer; the systematic review and meta-analysis have been carried out in a methodologically correct way, so we believe that it does not justify the article being retracted.

Coenzyme Q10 (CoQ10) has been suggested as an adjunct therapy for endocrine and metabolic disorders. The aim of this study was to synthesise the evidence for the effect of CoQ10 supplementation on lipid and/or glycaemic alterations, including total cholesterol (TC), LDL- and HDL-cholesterol (LDL-C and HDL-C), lipoprotein a, fasting blood glucose (FBG), haemoglobin A1c (HbA1c), fasting insulin and Homeostatic Model Assessment of Insulin Resistance. A systematic search was conducted in Medline, Scopus, Web of Science and the Cochrane Library from their inception to July 2024. Meta-analyses that evaluated the effect of CoQ10 on the lipid or glycaemic profiles were included. Results were expressed as mean difference (MD) or standardised mean difference (SMD). CoQ10 showed an effect on the glycaemic profile, especially on FBG (MD from −11.21 to −5.2 mg/dL, SMD from −2.04 to −0.17) and on HbA1c (MD from −1.83 to −0.12%, SMD of −0.30). CoQ10 may also have an effect on the lipid profile, such as TC, triglycerides, HDL-C and even LDL-C, although the inconsistency of the results was somewhat higher. Supplementation with CoQ10 may be beneficial, especially in populations with diabetes mellitus or other endocrine and metabolic disorders. It could also have some effect on lipid parameters, which, together with the above, may reduce cardiovascular morbidity and mortality, although this is something that needs further research.