Parabens are a family of alkyl esters of 4-hydroxybenzoic acid. The most commonly used include methylparaben, ethylparaben, propylparaben, and butylparaben. These compounds have been reported to disrupt the endocrine system and are believed to affect the central nervous, immune, and reproductive systems, as well as lipid homeostasis, glucose levels, and thyroid function. Given these effects, parabens pose potential health risks, including their possible link to conditions like diabesity - a term describing the dual condition of type 2 diabetes mellitus and obesity. This review explores current literature on how parabens may influence key mechanisms in diabesity, such as gluconeogenesis, glycogenolysis, adipogenesis, insulin resistance, and inflammation. Understanding their role in these metabolic pathways is critical for assessing their contribution to the diabesity epidemic and guiding future research for minimizing their harmful health impacts.

Low back pain (LBP) is a leading global factor in disability among older adults. Movement-evoked pain (MEP) is potentially an important mediator in the disability pathway but is predominantly tested in the laboratory.

We aimed to explore MEP in the natural environment ("daily" MEP) and its correlation with laboratory MEP, along with potential psychological and immunological influences.

Thirty-five older adults with persistent LBP attended a single laboratory session. Pain catastrophizing, pain-related fear of movement, and pain self-efficacy were measured by questionnaire. Resting inflammation and inflammatory reactivity to painful movement were evaluated using serum interleukin-6, tissue necrosis factor alpha, and C-reactive protein (CRP). Laboratory MEP was defined by aggregate pain intensity with a movement provocation test. Daily MEP was measured for the next 7 days using ecological momentary assessment.

Laboratory MEP was strongly correlated with daily MEP (ρ = 0.780, P = <0.001). C-reactive protein (Hedges [g] = 0.266) and interleukin-6 (g = 0.433) demonstrated small to moderate reactivity to painful movement. After controlling for age and multimorbidity, pain catastrophizing and pain self-efficacy explained 24% to 37% variance in laboratory and daily MEP. Resting inflammatory markers were not associated with MEP; however, C-reactive protein reactivity to painful movement explained 19% to 25% variance in laboratory and daily MEP.

Preliminary indication is that laboratory and daily MEP may be proxy measures for one another, and that MEP is influenced by psychological and immunological factors. Future studies will aim to (1) validate findings among older adults with persistent LBP and (2) for clinical phenotyping, clarify complex relationships among psychological and immunological factors with disability pathway components like MEP.

Ectopic fat deposition in skeletal muscle (SKM) due to obesity leads to biochemical and morphological alterations that deteriorate SKM quality and performance. Here, we show that impaired MPST-derived hydrogen sulfide (H2S) signaling contributes to obesity-related SKM dysfunction. Muscle tissues from obese db/db mice exhibit reduced MPST expression, correlating with decreased protein persulfidation and muscle performance in vivo. Mpst-/- mice show similar deficits as db/db mice, confirming the role of MPST. H2S supplementation improves locomotor activity in db/db mice and restores protein persulfidation, including SIRT-1. Myotubes placed in an "obese environment" display a downregulation of MPST, coupled with a reduced SIRT-1 persulfidation leading to an inflammatory state. Exogenous H2S exerts beneficial effects recovering SIRT-1 persulfidation/activity. Finally, muscle biopsies from obese individuals show reduced MPST expression, underscoring the translational relevance to human SKM health. Our study unveils a crucial role for MPST-derived H2S in obesity-associated SKM dysfunction via SIRT-1 persulfidation, highlighting the importance of the MPST/H2S pathway in maintaining healthy SKM function.

The aims of the study were to develop and validate WHOLISTIIC, a data-driven cluster analysis for identifying anthropometric metabolic subtypes.

K-means cluster analysis was performed in 397 424 UK Biobank participants based on five domains, that is, central obesity (waist-to-height ratio), general obesity (body mass index [BMI]), limb strength (handgrip strength), insulin resistance (triglyceride to high-density lipoprotein cholesterol [HDLc] ratio) and inflammatory condition (neutrophil-to-lymphocyte ratio). Replication was done in the NHANES. Cox proportional hazards regression models were used to estimate the associations of clusters with incident adverse health outcomes.

Six replicable clusters were identified. Compared with individuals in cluster 1 (lowest BMI with preserved handgrip strength), individuals in cluster 2 (highest handgrip strength) were not at increased risk of all-cause mortality despite higher BMI, but had small yet significant increased risks of cardiovascular mortality, incident major adverse cardiovascular events (MACE), chronic renal failure and decreased risks of mortality due to respiratory disease, as well as incident dementia; individuals in cluster 3 (lowest handgrip strength and borderline elevated BMI), cluster 4 (highest triglyceride-to-HDLc ratio and moderately elevated BMI), cluster 5 (highest neutrophil-to-lymphocyte ratio and borderline elevated BMI) and cluster 6 (highest BMI) had substantially increased risks of all-cause, cardiovascular, and cancer mortality, incident MACE and chronic renal failure. The associations of anthropometric clusters with the risk of mortality were replicated in the NHANES cohort.

Anthropometric metabolic subtypes identified with easily accessible parameters reflecting multifaceted pathology of overweight and obesity were associated with distinct risks of long-term adverse health outcomes.

Obesity is associated with an increased risk of cardiometabolic morbidity and mortality, which may be attributable to systemic low-grade inflammation. The impact of bariatric surgery-induced weight loss on low-grade inflammation has not yet thoroughly been described. We investigated the effect of Roux-en-Y gastric bypass (RYGB) and sleeve gastrectomy (SG) on the plasma levels of cytokines, chemokines, and cytokine receptors prior to surgery (baseline), and then three and 12 months after surgery.

We recruited 68 individuals (41 females, 27 males) with severe obesity (42.84 ± 6.28) who had been referred for bariatric surgery (RYGB: n = 29, SG: n = 39). Blood samples were collected after an overnight fast at baseline (immediately before surgery), 3 and 12 months after surgery. Eleven patients without obesity or cardiometabolic disease served as controls at baseline. Ninety-two plasma proteins were measured using an Olink Target 96 inflammation panel.

We used a linear mixed model to test differences in inflammatory markers at baseline, across time points and between groups. At baseline, 36 cytokines were found to be differentially expressed between the bariatric surgery patients and controls. Of these cytokines, 13 had significantly decreased three months after bariatric surgery and 27 had significantly decreased 12 months after surgery, compared with baseline. Two cytokines (CCL25 and CCL28) increased markedly after 12 months. Only one cytokine (CCL25) was significantly different between the procedures performed, where it increased in the RYGB group 12 months after surgery.

Individuals with severe obesity have increased expression of plasma inflammatory cytokines compared to controls, but low-grade inflammation improves following bariatric surgery, regardless of whether it is RYGB or SG.

Physical exercise is critical for preventing and managing chronic conditions, such as cardiovascular disease, type 2 diabetes, hypertension, and sarcopenia. Regular physical activity significantly reduces cardiovascular and all-cause mortality. Exercise also enhances metabolic health by promoting muscle growth, mitochondrial biogenesis, and improved nutrient storage while preventing age-related muscle dysfunction. Key metabolic benefits include increased glucose uptake, enhanced fat oxidation, and the release of exercise-induced molecules called myokines, which mediate interorgan communication and improve overall metabolic function. These myokines and other exercise-induced signaling molecules hold promise as therapeutic targets for aging and obesity-related conditions.

Few studies have evaluated the associations between phthalate exposures and maternal inflammation.

To examine cross-sectional associations of urinary phthalate metabolites, individually and as a mixture, with serum inflammatory biomarkers during pregnancy.

A total of 175 pregnant women enrolled in the Environment and Reproductive Health (EARTH) Study between 2005 and 2017 were included. Concentrations of 11 urinary phthalate metabolites and two serum inflammatory biomarkers, including C-reactive protein (CRP) and interleukin-6 (IL-6), were measured. Urinary concentrations of phthalate metabolites were adjusted for specific gravity (SG) before analysis. Linear regression and Bayesian Kernel Machine Regression models were used to examine the associations for individual phthalates and their mixture, respectively. Stratified analyses by pre-pregnancy body mass index (BMI) were also conducted.

No association for urinary phthalate metabolites, individually or as a mixture, was observed with serum CRP overall among pregnant women. Urinary mono-3-carboxypropyl phthalate and monocarboxyisooctyl phthalate were positively associated with serum IL-6 (β [95 % CI] per 1-SD increase in log-transformed, SG-adjusted concentrations: 0.09 [0.01, 0.16] and 0.09 [0.02, 0.17], respectively). Besides, urinary mono-isobutyl phthalate was positively associated with serum IL-6 among women with a pre-pregnancy BMI ≥25 kg/m2 (β [95 % CI] per 1-SD increase: 0.15 [0.00, 0.30]), but not with lower BMI (-0.03 [-0.12, 0.07]). A suggestive positive association between phthalate mixture and serum IL-6 was observed in the high pre-pregnancy BMI group.

Our findings suggest that women with a higher pre-pregnancy BMI may be more vulnerable to the effects of certain phthalates on maternal inflammation reflected by IL-6.

The potential of GLP-1s to change the trajectory of obesity has ignited enthusiasm for these drugs among physicians, patients and policy makers. The "average" reported weight loss of 20-25% of body weight has become reified as the "expected" benefit for patients with previously treatment resistant obesity. In our paper we demonstrate the considerable variation around the average treatment response observed in randomized controlled trials, illustrate that the variation is even more pronounced in real world evidence studies, and examine the role of "biosocial pathogenesis" as a possible explanation for the variation. Biosocial pathogenesis examines the role of both biology and biography on physiological systems that affect both the risk for disease and the response to treatment. Research is needed that enables clinical management to be tailored to the biology and "biography" of patients with obesity and obesity related disorders.

Opuntia ficus-indica (OFI) has attracted much attention as a source of antioxidant and antiinflammatory compounds. We hypothesize that the antioxidant content of OFI cladode extract may improve adipocyte dysfunction resulting from inflammatory stimulation of hypertrophic adipocytes. To this end, the properties of OFI cladode hydroalcoholic extract were evaluated in terms of antioxidant activity, regulation of adipocyte inflammation, and adipocyte/monocyte interaction in human adipocytes rendered dysfunctional by the proinflammatory cytokine tumor necrosis factor-α (TNF-α). The major phenolic compounds identified were isorhamnetin derivatives and phenolic acids, including piscidic and eucomic acids. Our results show that OFI cladode extract exhibits antiradical activities and reduces the adhesion and transmigration activity of monocytes to inflamed adipocytes by inhibiting various cytokines, chemokines, and adhesion molecules such as interleukin (IL)-6 and IL-8 by ∼80%, monocyte chemotactic protein (MCP)-1, C-X-C motif chemokine ligand (CXC-L)10, macrophage colony-stimulating factor (M-CSF) from 40% to 50%, and intercellular adhesion molecule-1 (ICAM-1) by 70% at the higher concentration. In structurally and mechanistically by protein-ligand docking profiling study, piscidic acid proved to be the best potential candidate for a regulatory interaction with the activities of nuclear factor erythroid 2-related factor 2 (NRF-2) and nuclear factor-κB (NF-κB). In summary, these data highlight the potential of OFI as a dietary supplement in nutritional treatments aimed at combating the inflammatory stigmata of obesity.

This study analyzes data from the 2009-2018 National Health and Nutrition Examination Survey (NHANES) to explore the relationship between the Aggregate Index of Systemic Inflammation (AISI), also referred to as the pan-immune-inflammation value (PIV), and Type 2 Diabetes Mellitus (T2DM) among adults in the United States. Furthermore, it evaluates the mediating effect of obesity indicators on this association.

This study included 9,947 individuals from NHANES and applied appropriate weighting techniques. To examine the relationship between AISI and T2DM, we used various statistical models, including weighted multivariable logistic regression, smooth curve fitting, threshold effect analysis, subgroup analysis, trend tests, mediation analysis, and Shapley additive explanations (SHAP) models.

This research included a total of 9,947 participants, with 3,220 diagnosed with T2DM, while 6,727 remained undiagnosed. Weighted multiple logistic regression with all covariates adjusted indicated that with every one-unit increment in AISI/1000, there was an 88.3% likelihood of T2DM occurrence (OR: 1.883, 95% CI: 1.378-2.571). The stratified analysis identified significant differences in this association based on age, biological sex, level of education, poverty-income ratio (PIR), tobacco consumption status, and body mass index (BMI). Interaction tests revealed a positive association between AISI and T2DM, apart from PIR, BMI, age, education attainment, race, gender, tobacco use status, Estimated Glomerular Filtration Rate(eGFR), platelet count, and high blood pressure, with none of the interaction p-values falling below 0.05. Nevertheless, the occurrence of cardiovascular disease (CVD) among participants may affect the strength of this relationship, where an interaction p-value was less than 0.05. Additionally, smoothing curve fitting revealed a nonlinear relationship between AISI and T2DM, marking a significant change at AISI/1000 of 0.21. Mediation analysis indicated that five obesity-related indicators-LAP, VAI, WHtR, WWI and ABSI - partly mediated the association between AISI/1000 and T2DM.

An increase in AISI is associated with an elevated probability of T2DM, with obesity indicators potentially mediating this relationship. Reducing AISI and managing obesity may help prevent T2DM. However, with the cross-sectional design of this study, causal relationships cannot be established. Future research should utilize longitudinal studies to confirm these findings.

To investigate the associations between periodontal inflammation-as determined by the periodontal inflamed surface area (PISA)-and serum inflammatory markers in community-dwelling older adults in Japan.

This cross-sectional study included 470 adults (mean age: 73.1 years). The composite inflammatory marker z-score (CIMZ) was calculated as the sum of the participants' individual z-scores for C-reactive protein (CRP), interleukin-1beta (IL-1β), IL-6 and tumour necrosis factor-α (TNF-α). The associations of PISA (quartiles) with individual biomarkers (continuous, log-transformed) and CIMZ (dichotomized, highest quartile or not) were assessed using linear or Poisson regression models.

Compared with participants in the lowest PISA quartile (Q1), those in Q3 and Q4 had significantly (p < 0.05) higher CRP and IL-6 levels. Statistically significant linear trends (ptrend < 0.05) across the PISA quartiles were observed for CRP and IL-6. The multivariable adjusted prevalence ratios (95% confidence intervals) of high CIMZ (reference: Q1) were 1.20 (0.68-2.14), 1.66 (0.96-2.88) and 1.90 (1.08-3.34) (ptrend = 0.01) in individuals in PISA Q2-Q4.

Older adults with high periodontal inflammation had high serum CRP and IL-6 concentrations and composite summary inflammatory indicator values. Periodontal inflammation is a potential modifiable factor of elevated inflammatory status among older adults in Japan.

Insulin resistance (IR) and obesity represent two major factors closely associated with gout. Triglyceride-glucose body mass index (TyG-BMI), calculated from fasting triglyceride and fasting glucose, has recently been proposed as a surrogate indicator of insulin resistance, potentially offering a simplified method for assessing IR-related risk. The prevalence of gout in the U.S. is higher than in the rest of the world, and the condition is even worse in people with obesity and IR. Therefore, this study aims to explore the correlation of the new index with gout. In this cross-sectional study, 13,307 participants were enrolled from the NHANES database, spanning six survey periods from 2007 to 2008 to 2017-2018. Multivariable logistic regression was used to evaluate the association between TyG-BMI and gout in U.S. adults (> 20 years) and to estimate odds ratios. Restricted cubic spline (RCS) analysis and subgroup analysis were conducted to visualize the results and assess potential differences across specific subgroups. The fully adjusted multivariable logistic regression revealed that a 20-unit increase in TyG-BMI was linked to a 15% higher prevalence of gout (OR = 1.15; 95% CI: 1.11, 1.19). Compared with the lowest TyG-BMI tertile group, the participants in the highest showed a 169% higher prevalence of gout (OR = 2.69, 95% CI: 1.80, 4.00). This association remained consistent and robust across different models and subgroups. No significant interactions were observed between TyG-BMI and stratified variables. TyG-BMI is strongly associated with gout in U.S. adults, indicating the potential application of the new index as a supplementary tool in gout detection. More longitudinal studies are needed to confirm the causal relationship.

Asthma and cardiovascular diseases (CVDs) are the 2 common and complex health problems with a substantial global impact. Epidemiological studies indicate that asthma and CVDs are common, with evidence supporting their cooccurrence. Inflammation, oxidative stress, obesity, metabolic syndrome, smoking, secondhand smoke exposure, physical inactivity, and environmental exposures are all risk factors for asthma and CVDs. In addition, inflammatory and immunological pathways, autonomic dysfunction, endothelial dysfunction, thrombosis, coagulation, and common genetic risk factors contribute to the asthma-CVD relationship. Asthmatic individuals have higher morbidity and mortality rates related to CVDs and high-risk factors. Techniques such as screening for CVDs in asthma patients, pharmaceutical therapy, and lifestyle changes are critical for effectively managing these comorbid illnesses. Understanding the link between asthma and CVD is necessary for integrated and clinical management approaches to enhance patient outcomes and lessen the burden of these related diseases.

Chronic obstructive pulmonary disease (COPD) is a leading cause of global morbidity and mortality. Patients hospitalized with severe acute exacerbations of COPD (AECOPD) represent a high-risk group with poor outcomes and accelerated lung function decline. Body mass index (BMI) shows inconsistent associations with lung function across populations, and its role in AECOPD remains unclear. Understanding this relationship may improve clinical management. Hemoglobin (Hb), essential for oxygen transport, may further influence this association through physiological mechanisms. This study aimed to explore the relationship between BMI and lung function in hospitalized patients with severe AECOPD and to assess whether BMI influences length of hospital stay (LOHS), while evaluating the potential modifying role of Hb.

A retrospective, single-center cross-sectional study was conducted among 579 patients hospitalized for severe AECOPD from 2021 to 2023. Data on BMI, lung function, Hb levels, and LOHS were collected. Nonlinear and threshold effect analyses were used to explore associations between BMI and lung function or LOHS. Subgroup analyses assessed the modifying effect of Hb.

BMI exhibited a nonlinear positive association with FEV1, FVC, FEV1% predicted, and FVC% predicted. Thresholds were identified at 25.39 kg/m² for FEV1, 26.23 kg/m² for FEV1% predicted, 21.67 kg/m² for FVC, and 22.19 kg/m² for FVC% predicted. The association was more pronounced in patients with higher Hb levels. No significant association was found between BMI and LOHS, suggesting that other factors such as infection severity, comorbidities, or treatment strategies may may exert greater influence.

A nonlinear, inverse L-shaped association was observed between BMI and lung function, further modified by Hb levels. These findings highlight the importance of individualized treatment and stratification strategies in severe AECOPD. Future longitudinal studies are needed to validate these observations.

Obesity treatment requires an individualized approach, emphasizing the need to identify metabolic pathways of diagnostic relevance. Toll-like receptors (TLRs), particularly TLR2 and TLR4, play a crucial role in metabolic disorders, as receptor deficiencies improves insulin sensitivity and reduces obesity-related inflammation. Additionally, hydrogen sulfide (H2S) influences lipolysis, adipogenesis, and adipose tissue browning through persulfidation. This study investigates the impact of a high-fat diet (HFD) on low molecular weight sulfur compounds in the visceral adipose tissue (VAT) of C57BL/6 and TLR2-deficient mice. It focuses on key enzymes involved in H2S metabolism: cystathionine beta-synthase (CBS), cystathionine gamma-lyase (CGL), 3-mercaptopyruvate sulfurtransferase (MPST), and thiosulfate sulfurtransferase (TST). In C57BL/6 mice on HFD, MPST activity decreased, while CBS level increased, potentially compensating for H2S production. In contrast, TLR2-deficient mice on HFD exhibited higher MPST activity but reduced level of CBS and CGL activity, suggesting that TLR2 deficiency mitigates HFD-induced changes in sulfur metabolism. TST activity was lower in TLR2-deficient mice, indicating an independent regulatory role of TLR2 in TST activity. Elevated oxidative stress, reflected by increased glutathione levels, was observed in wild-type mice. Interestingly, cysteine and cystine were detectable only in the VAT of the C57BL/6 ND group and were absent in all other groups. The capacity for hydrogen sulfide production in tissues from TLR2-/-B6 HFD group was significantly lower than in the C57BL/6 HFD group. In conclusion, TLR2 modulates sulfur metabolism, oxidative stress, and inflammation in obesity. TLR2 deficiency disrupts H2S production and redox balance, potentially contributing to metabolic dysfunction, highlighting TLR2 as a potential therapeutic target for obesity-related metabolic disorders.

Peripheral arterial disease (PAD) is a common manifestation of atherosclerosis, affecting over 200 million people worldwide. The incidence of PAD is increasing due to the aging population. Common risk factors include smoking, diabetes, and hyperlipidemia, but its exact pathogenesis remains unclear. Nutritional intake is associated with the onset and progression of PAD, although relevant studies remain limited. Some studies suggest that certain nutritional elements may influence the development of PAD. This study aims to explore the relationship between nutrition and PAD using machine learning techniques. Unlike traditional statistical methods, machine learning can effectively capture complex, nonlinear relationships, providing a more comprehensive analysis of PAD risk factor.

Data from National Health and Nutrition Examination Survey (NHANES 1999-2004) were analyzed, including demographic, clinical, and dietary information. Nutrient intake was assessed through 24-h dietary recalls using computer-assisted dietary interview system (CADI) and automated multiple pass method (AMPM) methods. PAD was defined as an ankle-brachial index (ABI) < 0.9. Six ML models-extreme gradient boosting (XGBoost), random Forest (RF), naive bayes classifier (NB), support vector machine (SVM), logistic regression (LR), and decision tree (DT)-were trained on a 70/30 train-test split, with missing data imputed and sample imbalance addressed via synthetic minority oversampling technique (SMOTE). Model performance was evaluated using the area under the receiver operating characteristic curve (AUROC), accuracy, sensitivity, specificity, precision, recall, and F1 score. Shapley additive explanations (SHAP) analysis was used to identify key features. In addition, to further enhance the interpretability of the model, we applied SHAP analysis to identify the features that have a significant impact on PAD prediction. This approach allowed us to determine the contribution of different variables to the model's output, providing deeper insights into how each feature influences the prediction of PAD outcomes.

Of 31,126 participants, 4,520 met the inclusion criteria (mean age 61.2 ± 13.5 years; 48.8% male), and 441 (9.7%) had ABI < 0.9. XGBoost outperformed other models, achieving an AUROC of 0.913 (95% CI, 0.891-0.936) and F1 score of 0.932. With SMOTE, its AUROC improved to 0.926 (95% CI, 0.889-0.936) and F1 score to 0.937. SHAP analysis identified vitamin C, saturated fatty acids, selenium, phosphorus, and protein intake as key predictors of PAD.

This is the first study to apply ML algorithms to examine nutrient intake and PAD in a general population. Vitamin C and phosphorus showed negative correlations with PAD, while saturated fatty acids, protein, and selenium exhibited positive associations.

Klotho is an anti-aging protein, and obesity and inflammation have been identified as having a relationship with Klotho. This study investigated the correlation between weight-adjusted-waist index(WWI), systemic inflammation index(SII) and soluble Klotho (sKlotho) and explored the potential mediating role of SII.

The association between WWI, SII, and sKlotho was investigated using weighted multivariate linear regression, subgroup analysis, and smoothed curve fitting in this cross-sectional study, which was based on NHANES data. The Bootstrap method was used to test for mediation effects. Covariate selection was validated using the variance inflation factor (VIF).

The study involved a total of 9,506 participants. The results showed that WWI (β=-0.03; 95%CI:-0.04,-0.01; p<0.0001) was associated with SII (β=-0.00, 95%CI:-0.00,-0.00:p<0.001) and Ln-sKlotho.There was a negative correlation between both WWI and SII and sKlotho. Subgroup analysis showed that gender, age, education, marital status, family income, HEI, PA, hypertension, diabetes, CKD, alcohol use, smoking, and SII did not affect the negative correlation between WWI and sKlotho (FDR-corrected p>0.1). The mediation analysis showed that SII played a significant mediating effect in the role of WWI on sKlotho, with SII mediating 6.78% of the relationship between WWI and sKlotho.

There is a negative correlation between WWI and sKlotho, and SII may be an important mediator between WWI and sKlotho. Reducing inflammatory conditions in obese populations may increase sKlotho levels, which in turn may delay organismal aging in middle-aged and elderly people.

In this study, we measured the dose-response effect of a 24-week concurrent training (CT) intervention on low-grade systemic inflammation biomarkers in sedentary young healthy adults. A total of 100 untrained participants were randomized to (1) no exercise (control group, n = 35), (2) aerobic + resistance exercise (CT) at moderate intensity (exercise-moderate group; n = 33), or (3) CT at vigorous intensity (exercise-vigorous group, n = 32). Serum concentrations of C-reactive protein (CRP), interleukin-6 (IL-6), IL-7, IL-8, and IL-10, interferon-gamma (IFN-γ), tumor necrosis factor-α, leptin, and adiponectin were determined and compared among the three groups. The exercise-vigorous group members had lower differences in IL-7 levels among them, compared to the exercise-moderate group members (Δ = ‒7.97% vs. 1.90%; p = 0.030; 95% CI [‒0.90, ‒0.04]). The exercise-vigorous group members showed higher differences in CRP values (Δ = 20.1%; F = 3.339; p = 0.046) compared to both the control (Δ = ‒1.91%) and the exercise-moderate (Δ = ‒23.3%) group members, whereas the control group exhibited higher differences in IFN-γ levels compared to the exercise-vigorous group (Δ = 15.3% vs. 2.62%; p = 0.048; 95% CI [‒0.68, ‒0.01]). For individuals in the three groups, body composition and physical fitness correlated overall with leptin. The data show, and we concluded, that the training intervention had no significant effect on low-grade systemic inflammation biomarkers.

The gut is responsible for the digestion and absorption of nutrients, immune regulation, and barrier function. However, factors like poor diet, stress, and infection, can disrupt the balance of the gut microbiota and lead to intestinal inflammation and dysfunction.

This systematic review aims to evaluate the effects of dietary plants-derived essential oil components on gut health and intestinal functions in animal models.

The literature was gathered from the Scopus, Web of Science, PubMed, and Embase databases by using related search terms, such as "dietary plants", "dietary sources", "essential oils", "gut health", "intestine", "anti-inflammatory", "antioxidant", and "gut microbiota".

The results indicate that plant-derived dietary essential oil components, such as butyrolactone-I, carvacrol, cinnamaldehyde, citral, D-limonene, eugenol, farnesol, geraniol, indole, nerolidol, oleic acid, thymol, trans-anethole, vanillin, α-bisabolol, α-linolenic acid, α-pinene, α-terpineol, β-carotene, β-caryophyllene, and β-myrcene have been found to regulate gut health by influencing vital signalling pathways associated with inflammation. Dietary essential oil components modulate the expression of tumor necrosis factor alpha, interleukin 1 beta (IL-1β), interleukin (IL)-6, IL-10, inducible nitric oxide synthase, cyclooxygenase-2, toll-like receptor-4, matrix metalloproteinase, and interferon gamma in mitigating gut inflammation. The primary signalling molecules controlled by these molecules were AMP-activated protein kinase (AMPK), protein kinase B, extracellular signal-regulated kinase, c-Jun N-terminal kinase, mitogen-activated protein kinase, myeloid differentiation primary response 88, nuclear factor erythroid-2-related factor-2, and phosphoinositide 3-kinase (PI3K). Moreover, these phytochemicals have been shown to improve glucose homeostasis by regulating glucose transporter 4, glucagon-like peptide-1, peroxisome proliferator-activated receptor gamma, nuclear factor kappa B, AMPK, PI3K, and uncoupling protein-1. They can also reduce thiobarbituric acid reactive substance, malondialdehyde, and oxidative stress and enhance superoxide dismutase, catalase, and glutathione peroxidase levels.

In conclusion, dietary plants-derived essential oil components have the potential to mitigate inflammation and oxidative stress in the gut. However, additional clinical investigations are necessary to confirm their complete potential in improving human gut health functions.

Adipose-derived stem cells (ADSCs) are mesenchymal stem cells (MSCs) derived from adipose tissue with mesenchymal lineage differentiation potential and remarkable potential in regenerative medicine. ADSCs are easily sourced from adipose tissue, share regenerative characteristics akin to other MSCs. Their convenient adherence to plastic culture flasks, coupled with their capacity for in vitro expansion and multi-lineage differentiation, underscores their promise as a robust tool for tissue repair and enhancement. The accessibility of human adipose tissue and the development of minimally invasive isolation protocols have further propelled the autologous use of ADSCs, fueling excitement in both organ repair and regenerative medicine. Consequently, research in ADSCsis experiencing rapid growth. A detailed overview of the current landscape of ADSCs isolation and differentiation capacity including the latest advancements in ADSCs usage, encompassing ongoing clinical investigations are important considerations to understand their potential to shape the landscape of regenerative medicine.

Alzheimer's disease (AD) is a progressive neurodegenerative disorder characterized by cognitive decline, memory impairment, and synaptic dysfunction. The accumulation of amyloid beta (Aβ) plaques and hyperphosphorylated tau protein leads to neuronal dysfunction, neuroinflammation, and glial cell activation. Emerging evidence suggests that peripheral insulin resistance and chronic inflammation, often associated with type 2 diabetes (T2D) and obesity, promote increased proinflammatory cytokines, oxidative stress, and immune cell infiltration. These conditions further damage the blood-brain barrier (BBB) integrity and promote neurotoxicity and chronic glial cell activation. This induces neuroinflammation and impaired neuronal insulin signaling, reducing glucose metabolism and exacerbating Aβ accumulation and tau hyperphosphorylation. Indeed, epidemiological studies have linked T2D and obesity with an increased risk of developing AD, reinforcing the connection between metabolic disorders and neurodegeneration. This review explores the relationships between peripheral insulin resistance, inflammation, and BBB dysfunction, highlighting their role in glial activation and the exacerbation of AD pathology.

Introduction: Depression is a pervasive global health issue, affecting millions worldwide and causing significant disability. Despite its prevalence, current diagnostic and treatment approaches often yield suboptimal outcomes. The complexity of depression, characterized by diverse causes and symptoms, highlights the urgent need for advanced diagnostic tools and personalized therapies. Biomarkers, particularly genetic and epigenetic depression biomarkers, offer promise in uncovering the biological mechanisms underlying depression, potentially revolutionizing its management. Aim: Primary aim: To identify biomarkers associated with depressive disorders, with a focus on genetic and epigenetic biomarkers. Secondary aim: To optimize the current classification of biomarkers associated with different types of depressive disorders, with a focus on genetic and epigenetic biomarkers. Methods: We integrated findings with strategic keywords extracted from relevant studies, conducting a thorough literature review across the Google Scholar, PubMed, and Web of Science databases. Lastly, final reference inclusion had stringent criteria: recent, diverse peer-reviewed articles in English, all study designs, ensuring up-to-date coverage of genetic and epigenetic depression biomarker research. Results: The review reveals the classification of genetic and epigenetic biomarkers in regard to the type of biomarker, the system of the human body it derives from, and the sampling entity. All of the findings show promise in diagnosing depression, with the potential of predicting treatment outcomes and guiding personalized therapeutic approaches. We defined the significant correlations between genetic and epigenetic biomarker profiles and clinical parameters such as symptom severity and treatment response, thereby enhancing diagnostic accuracy and guiding treatment strategies tailored to individual patient needs across diverse depressive subtypes and treatment responses. Conclusion: Identifying biomarkers associated with depressive disorders, with a focus on genetic and epigenetic biomarkers, represents a critical step toward improving diagnostic precision and treatment efficacy. By elucidating the complex biological underpinnings of depression, this study contributes to the development of targeted therapies that address the diverse needs of individuals affected by this debilitating group of disorders. Future research should focus on validating these genetic and epigenetic biomarkers in larger cohorts and clinical trials to facilitate their clinical implementation and enhance patient outcomes.

Obesity, a worldwide health emergency, is defined by excessive fat accumulation and significantly impacts metabolic health. In addition to its recognized association with cardiovascular disease, diabetes, and other metabolic illnesses, recent studies have revealed the connection between obesity and neurodegeneration. The main reason for this link is inflammation caused by the growth of fat tissue, which activates harmful processes that affect how the brain works. Fat tissue, particularly the fat around the organs, produces various substances that cause inflammation, such as cytokines (TNF-α, IL-6), adipokines (leptin, resistin), and free fatty acids. These chemicals cause low-grade, persistent systemic inflammation, which is becoming more widely acknowledged as a major factor in peripheral metabolic dysfunction and pathology of the central nervous system (CNS). Inflammatory signals in the brain cause neuroinflammatory reactions that harm neuronal structures, change neuroplasticity, and disrupt synaptic function. When obesity-related inflammation is present, the brain's resident immune cells, known as microglia, become hyperactivated, which can lead to the production of neurotoxic chemicals, which can cause neuronal death. This neuroinflammation exacerbates the negative effects of obesity on brain health and is linked to cognitive decline, Alzheimer's disease, and other neurodegenerative disorders. Moreover, the blood-brain barrier (BBB) exhibits increased permeability during inflammatory states, facilitating the infiltration of peripheral immune cells and cytokines into the brain, hence exacerbating neurodegeneration. Adipose tissue is a source of chronic inflammatory mediators, which are examined in this review along with the molecular pathways that connect inflammation brought on by obesity to neurodegeneration. Additionally, it addresses various anti-inflammatory treatment approaches, including lifestyle modifications, anti-inflammatory medications, and gut microbiota modulation, to lessen the metabolic and neurological effects of obesity. Recognizing the link between obesity and inflammation opens up new opportunities for early intervention and the development of targeted treatments to prevent or alleviate neurodegenerative disorders.

Polycystic ovary syndrome (PCOS) is a multifaceted endocrine disorder with reproductive and metabolic dysregulation. PCOS has been associated with inflammation and metabolic syndrome (MetS); however, the moderating effects of inflammation as measured by C-reactive protein (CRP) and menopause on the PCOS-MetS association have not been studied in Hispanic/Latinas with PCOS who have a higher metabolic burden.

We studied the cross-sectional association between PCOS and (1) MetS in 7316 females of the Hispanic Community Health Study/Study of Latinos (HCHS/SOL), (2) subcomponents of MetS including impaired fasting glucose (IFG) and elevated triglycerides (TGL), and (3) effect modification by menopausal status and CRP.

The HCHS/SOL is a multicenter, longitudinal, and observational study of US Hispanic/Latinos. Our study sample included females from visit 2 with self-reported PCOS and MetS (ages 23-82 years).

PCOS (prevalence = 18.8%) was significantly associated with MetS prevalence [odds ratio [odds ratio (OR) = 1.41 (95% confidence interval: 1.13-1.76)], IFG and TGL (OR = 1.42 (1.18-1.72), OR = 1.48 (1.20-1.83), respectively]. We observed effect modification by menopausal status (ORpre = 1.46, Pint= .02; ORpost = 1.34, Pint= .06) and CRP (ORelevated = 1.41, Pint= .04; ORnormal = 1.26, Pint= .16) on the PCOS-MetS association. We also observed a superadditive interaction between CRP and PCOS, adjusting for which resulted in an attenuated effect of PCOS on MetS (OR = 1.29 [0.93-1.78]).

Hispanic/Latino females with PCOS had higher odds of MetS, IFG, and elevated TGL than their peers without PCOS. Interaction analyses revealed that the odds of MetS are higher among PCOS females who have premenopausal status or high inflammation. Interventions in Hispanic/Latinas should target these outcomes for effective management of the disease.

While obesity rates increase worldwide, physical activity levels are reduced. Obesity and physical inactivity may be inversely related to the production of reactive oxygen species (ROS) and cause oxidative stress in the central nervous system. In this study, we aimed to investigate the effects of aerobic physical exercise on the oxidative balance of the prefrontal cortex of rats subjected to overnutrition during lactation. For this, male Wistar rats were subjected to overnutrition during lactation between postnatal day 3 to 21. On postnatal day 23, the two groups of animals were subdivided into trained and untrained animals. Trained rats were subjected to a treadmill training protocol for four weeks, five days/week, 60 min/day, at 50% of maximum running capacity. Our findings demonstrate that overnutrition impairs REDOX balance in the prefrontal cortex through increased prooxidants and reduced antioxidant defenses. On the contrary, exercise tends to restore most of these measures to control levels, possibly due to the increase in mRNA levels of Sirt1 and reduction in Il-6 in the prefrontal cortex. Overnutrition causes oxidative stress in the prefrontal cortex, while exercise re-covers most of its adverse effects through activating anti-inflammatory mechanisms.

The fern "Cyclosorus terminans" (C. terminans) or "Maiden Fern" contains interruptin A and interruptin B. This plant could attenuate obesity, insulin resistance, and fatty liver in rats fed a high-fat/calorie diet. However, the benefits of C. terminans to the gut remain unknown. We investigated the protective effect of C. terminans extract against gut dysfunction in rats exposed to a high-fat/calorie diet.

Male Wistar rats were assigned to receive either (1) a normal diet treated with vehicle, (2) a high-fat/calorie diet treated with vehicle, (3) a high-fat/calorie diet treated with 100 mg per kg per day (mg·kg-1·day-1) of C. terminans extract, or (4) a high-fat/calorie diet treated with 200 mg·kg-1·day-1 of C. terminans extract. The rats were euthanized after 12 weeks of treatment to enable feces and colon tissue collection.

Both 100 and 200 mg·kg-1·day-1 of C. terminans extract reduced body weight (-10.49%; p = 0.030 and -10.54%; p = 0.037, respectively) and ameliorated gut inflammation, gut barrier disruption, changes in short-chain fatty acid levels, and gut dysbiosis caused by high-fat/calorie diet.

C. terminans extract attenuated an increase in body weight and exerted prophylactic effects against gut pathologies induced by high-fat/calorie diet.

The importance of preconception care is now widely recognised. Optimisation of the lifestyle, nutrition, and the health of a couple not only affects the chances of conception and a successful pregnancy but also the health of the resulting offspring. Currently, limited data reinforce the importance of further research examining the role of individual nutrients. The complex interactions that these nutrients have with each other and the resultant effect on fertility should also be a focus for future investigation. Modifiable risk factors such as alcohol, caffeine, and body mass index should be optimised prior to attempting to conceive. New research is examining the role of personalised preconception advice.

This review examines the roles of macronutrients, micronutrients, and lifestyle in fertility and reproductive health. Raising awareness of the importance of the effect of preconception nutrition and lifestyle on hormone balance, gamete development, implantation, and pregnancy should be paramount. This applies to all healthcare professionals who come into contact with people of child-bearing age, as well as the general public.

C-reactive protein (CRP) is a moderately heritable marker of systemic inflammation that is associated with adverse physical and mental health outcomes. Identifying factors associated with genetic liability to elevated CRP in childhood may inform our understanding of variability in CRP that could be targeted to prevent and/or delay the onset of related health outcomes.

We conducted a phenome-wide association study (PheWAS) of genetic risk for elevated CRP (i.e. CRP polygenic risk score [PRS]) among children genetically similar to European ancestry reference populations (median analytic n = 5,509, range = 120-5,556) from the Adolescent Brain and Cognitive DevelopmentSM (ABCD) Study baseline assessment. Associations between CRP PRS and 2,377 psychosocial and neuroimaging phenotypes were estimated using independent mixed effects models nested by recruitment site (or scanner) and family, with ancestral genomic principal components (n = 10), age, and sex, as well as global brain metrics (when relevant) included as fixed effect covariates. Post hoc analyses examined whether: (1) covarying for measured body mass index (BMI) or removing the shared genetic architecture between CRP and BMI altered phenotypic associations, (2) sex moderated CRP PRS associations, and (3) associations were unconfounded by assortative mating or passive gene-environment correlations (using within-family analyses). Multiple testing was adjusted for using Bonferroni and false discovery rate (FDR) correction.

Nine phenotypes were positively associated with CRP PRS after multiple testing correction: five weight- and eating-related phenotypes (e.g. BMI, overeating), three phenotypes related to caregiver somatic problems (e.g. caregiver somatic complaints), as well as weekday video watching (all ps = 1.2 x 10-7 - 2.5 x 10-4, all pFDRs = 0.0002-0.05). No neuroimaging phenotypes were associated with CRP PRS (all ps = 0.0003-0.998; all pFDRs = 0.08-0.998) after correction for multiple testing. Eating and weight-related phenotypes remained associated with CRP PRS in within-family analyses. Covarying for BMI resulted in largely consistent results, and sex did not moderate any CRP PRS associations. Removing the shared genetic variance between CRP and BMI attenuated all relationships; associations with weekday video watching, caregiver somatic problems and caregiver report that the child is overweight remained significant while associations with waist circumference, weight, and caregiver report that child overeats did not.

Genetic liability to elevated CRP is associated with higher weight, eating, and weekday video watching during childhood as well as caregiver somatic problems. These associations were consistent with direct genetic effects (i.e., not solely due to confounding factors like passive gene-environment correlations) and were independent of measured BMI. The majority of associations with weight and eating phenotypes were attributable to shared genetic architecture between BMI and inflammation. The relationship between genetics and heightened inflammation in later life may be partially attributable to modifiable behaviors (e.g. weight and activity levels) that are expressed as early as childhood.

Different dietary choices can influence blood fatty acid profiles, which are crucial for maintaining physiological health and reducing disease risk. In particular, the exclusion of animal foods in vegetarian diets is associated with a higher risk of undersupply of long-chain omega (n)-3 fatty acids, which could, potentially, have a negative effect on inflammation. This study aimed to examine differences in plasma and erythrocyte fatty acid profiles as well as inflammation-related biomarkers between various plant-based diets and a regular omnivores diet.

The Nutritional Evaluation (NuEva) study is a is a parallel-designed trial. Here screening data was used to investigate differences in plasma and erythrocyte fatty acid profiles across omnivores (Western diet; n = 62), flexitarians (n = 69), vegetarians (n = 64) and vegans (n = 57). Furthermore, markers associated with inflammation are investigated and correlated with selected fatty acids.

Flexitarians showed lower erythrocyte saturated fatty acids (SFA) than omnivores, while vegans had the lowest plasma SFA. Vegans had higher erythrocyte monounsaturated fatty acids proportions, like oleic acid, than flexitarians and vegetarians. n-6 fatty acids, particularly linoleic acid, were highest in vegans and vegetarians. Conversely, omnivores had higher arachidonic acid in erythrocytes. Vegans had lower n-3 fatty acids in both plasma and erythrocytes, also reflected in a lower n-3 index (eicosapentaenoic acid (EPA) + docosahexaenoic acid (DHA)) values, indicating a trend with restriction of animal foods: omnivores/flexitarians > vegetarians > vegans. While interleukin (IL)-6, IL-8, IL-10, tumor necrosis factor (TNF)-α and high-sensitive C-reactive protein (hsCRP) did not differ between groups, and vegans had lower leptin levels compared to omnivores.

The NuEva study revealed significant impact of dietary patterns on fatty acid profiles, with vegans and vegetarians displaying lower concentrations of SFA and n-3 fatty acids, including EPA and DHA, compared to omnivores and flexitarians. Despite the clear differences in fatty acid profiles across the diets, the inflammatory markers measured in our healthy collective are comparable.

Registered under ClinicalTrials.gov Identifier no. NCT03582020.

The growing use of glucagon-like peptide 1 (GLP-1) analogs for type 2 diabetes mellitus (DM2) and obesity necessitates studies about their use in patients with inflammatory bowel diseases (IBD).

Data on patients with DM2 were retrieved from an Israeli nationwide cohort of patients with IBD (epi-IIRN), recording GLP-1 analog exposure for at least 6 months. The primary outcome was poor disease outcomes (ie, composite of steroid dependence, initiation of advanced IBD therapy, hospitalization, surgery, or death). Cox proportional hazard models with time-varying covariables were used to assess the impact of GLP-1 use on outcomes during follow-up.

We included 3737 patients (24 338 patient-years) with IBD and DM2 [50.4% ulcerative colitis (UC)], of whom 633 were treated with GLP-1 analogs. Accounting for demographics IBD/DM2 related variables, medication use, and laboratory measurements, GLP-1 analog use was associated with reduced composite outcome in the full cohort (adjusted hazard ratio [aHR] 0.74, 95% confidence interval [CI] 0.62-0.89) and in each subtype [UC (aHR 0.71, 95% CI 0.52-0.96) and Crohn's disease (aHR 0.78, 95% CI 0.62-0.99)]. Similar trends were seen in multivariate analyses of each individual outcome, although only hospitalization was significant (aHR 0.74, 95% CI 0.61-0.91). The protective effect of GLP-1 analogs was seen in patients with obesity (aHR 0.61, 95% CI 0.50-0.77), but not in non-obese (aHR 0.94, 95% CI 0.67-1.31).

GLP-1 analogs are associated with improved outcomes in IBD, specifically in patients with obesity. The mechanisms of these effects require further investigation as well as their role in patients without DM2.

Over the years, there has been a tendency for an increase in global obesity. The World Health Organization's (WHO) 2024 report states that in 2019, more than one billion people were obese, and this condition was responsible for five million deaths, being that obesity is more prevalent among adults compared to adolescents and children. Obesity is a chronic disease characterized by alterations in adipose tissue. When excessive food is consumed and energy expenditure is low, adipose tissue undergoes hypertrophy and hyperplasia. This process activates B cells and induces the transition of anti-inflammatory M2-like macrophages into pro-inflammatory M1-like macrophages. B cells, acting as inflammatory mediators, stimulate pro-inflammatory CD8+ T cells, and promote macrophage infiltration into tissues. This condition triggers inflammation, increases oxidative stress, and ultimately leads to cellular death. During inflammation, an increase of pro-inflammatory cytokines occurs along with a decrease of anti-inflammatory cytokines. By contrast, the increase of oxidative stress is related to an increase of reactive oxygen species (ROS), oxidation of biomolecules, and a decrease in antioxidants. This mechanism for obesity can be mitigated through several healthy lifestyle changes, primarily including regular physical activity and healthy eating. These factors help reduce pro-inflammatory mediators and ROS, lowering inflammation and oxidative stress. Therefore, this review article focuses on studying the bioactive compounds present in the edible leaves of Annona cherimola Mill., Ipomoea batata (L.) Poir., Colocasia esculenta (L.) Schott, Eriobotrya japonica, Cymbopogon citratus, Psidium guajava (L.), and Smallanthus sonchifolius to evaluate their effects on the mechanisms involved in obesity.

This review provides a broad overview of lessons learned in the five years since COVID-19 was identified. It is a bimodal disease, starting with an initially virus-driven phase, followed by resolution or ensuing inappropriate immune activation causing severe inflammation that is no longer strictly virus dependent. Humoral immunity is beneficial for preventing or attenuating the early stage, without benefit once the later stage begins. Neutralizing antibodies elicited by natural infection or vaccination are short-lived and highly vulnerable to viral sequence variation. By contrast, cellular immunity, particularly the CD8+ T cell arm, has a role in preventing or attenuating severe disease, is far less susceptible to viral variation, and is longer-lived than antibodies. Finally, an ill-defined phenomenon of prolonged symptoms after acute infection, termed "long COVID," is poorly understood but may involve various immunologic defects that are hyperactivating or immunosuppressive. Remaining issues include needing to better understand the immune dysregulation of severe disease to allow more tailored therapeutic interventions, developing antibody strategies that cope with the viral spike sequence variability, prolonging vaccine efficacy, and unraveling the mechanisms of long COVID to design therapeutic approaches.

There is active crosstalk between tumor cells and the tumor microenvironment during metastatic progression, a process that is significantly affected by obesity, particularly in breast cancer. Here we analyze the impact of a high fat diet (HFD) on metastasis, focusing on the role of platelets in the formation of premetastatic niches (PMNs). We find that a HFD provokes pre-activation of platelets and endothelial cells, promoting the formation of PMNs in the lung. These niches are characterized by increased vascular leakiness, platelet activation and overexpression of fibronectin in both platelets and endothelial cells. A HFD promotes interactions between platelets, tumor cells and endothelial cells within PMNs, enhancing tumor cell homing and metastasis. Importantly, therapeutic interventions like anti-platelet antibody administration or a dietary switch reduce metastatic cell homing and outgrowth. Moreover, blocking fibronectin reduces the interaction of tumor cells with endothelial cells. Importantly, when coagulation parameters prior to neoadjuvant treatment are considered, triple negative breast cancer (TNBC) female patients with reduced Partial Thromboplastin time (aPTT) had a significantly shorter time to relapse. These findings highlight how diet and platelet activation in pre-metastatic niches affect tumor cell homing and metastasis, suggesting potential therapeutic interventions and prognostic markers for TNBC patients.

Chronic inflammation causes serious medical conditions in many organs and tissues, including female fertility. Here we review the current literature, showing that chronic inflammation has a negative impact on oocyte quality, folliculogenesis, hormone production, immune signaling and other processes that affect fertility in females.

Inflammation has key biological roles in the battle against pathogens and additional key processes in development and tissue homeostasis. However, when inflammation becomes chronic, it can become a serious medical concern. Chronic inflammation has been shown to contribute to the etiology and symptoms of serious medical conditions such as ulcerative colitis, cardiovascular diseases, endometriosis and various cancers. One of the less recognized symptoms associated with chronic inflammation is its effect on reproduction, specifically on female fertility. Here we review the current literature, showing that chronic inflammation has a negative impact on oocyte quality, folliculogenesis, hormone production, immune signaling and other processes that affect fertility in females. We discuss several factors involved in the etiology of chronic inflammation and its effect on female fertility. We also discuss possible mechanisms by which these effects may be mediated and how interventions may mitigate the effect of chronic inflammation. Finally, we discuss the notion that in many cases, the effect of chronic inflammation is tightly correlated with and resembles the effect of aging, drawing interesting parallels between these processes, possibly through the effect of aging-associated inflammaging.

The use of drains in reduction mammoplasty is highly variable among plastic surgeons. However, there is limited evidence to guide surgeons on the optimal timing and conditions for using drains to reduce the risk of seroma formation. The objective of this study was to identify factors that predict the possibility of developing postoperative seroma formation.

Retrospective review of patients who underwent bilateral reduction mammoplasty without intraoperative drain placement at our institution between January 2016 and July 2021 was performed. Demographics, clinical characteristics, and the rate of seroma that required aspiration or drainage were recorded. Univariate time-to-event analyses using Cox regression were performed to identify the predictors of seroma.

A total of 234 patients (468 breasts) were included. The mean age, body mass index, and resection weight were 40.9±17.6 months; 30.7±5.5 kg/m2, and 717.2±388 g, respectively. The superomedial pedicle was used in 268 (57.3%) breast reductions while the inferior pedicle was used in 200 (42.7%) cases. Median follow-up time was 3.2 months (IQR: 2.8 months). Seromas occurred in 17 breasts (3.6%). Patients who were of World Health Organization Obesity Class I (hazards ratio, HR = 15.5, p = 0.01), Class II (HR = 13.9, p = 0.016), and Class III (HR = 27.4, p = 0.004) had increased risk for developing seroma when compared to non-obese patients.

The rate of seroma formation was 3.6% in this cohort. Obesity significantly increased the risk of postoperative seroma formation that required aspiration or surgical drainage; therefore, surgeons who aim to further reduce the risk of seroma should consider using drains for these patients.