Non-communicable diseases (NCDs) are rising rapidly in South Africa, prompting the introduction of the Health Promotion Levy (HPL) in 2018 to reduce the consumption of sugar-sweetened beverages. However, the levy remains below the rate recommended by the World Health Organization. One of the central institutions involved in the policy process leading up to and following the introduction of the HPL was the National Economic Development and Labour Council (NEDLAC), a statutory body designed to promote dialogue between government, business, labour, and community constituencies. This study examined NEDLAC's mandate and its actual role in the HPL process, with particular attention to the inclusivity and transparency of its deliberations.

Using an exploratory case study design, the research drew on qualitative content analysis of documents obtained through an access to information request made under South Africa's Promotion of Access to Information Act 2 of 2000. The findings indicate that NEDLAC's engagement with the HPL process fell short of its mandate to advance social equity and inclusive participation in economic decision-making. Community representatives, one of NEDLAC's four official constituencies, were absent from all deliberations on the levy. In contrast, business representatives dominated the discussions, often advancing arguments aligned with the interests of the sugar industry and emphasising potential job losses despite limited supporting evidence. Moreover, the process lacked transparency, particularly regarding the authorship of NEDLAC's HPL Report and the presentation of evidence used to support its conclusions.

NEDLAC's handling of the HPL illustrates how participatory governance structures may, in practice, enable industry influence and weaken public health objectives. To enhance the integrity and effectiveness of policy dialogue on health-related fiscal measures, NEDLAC should adopt clearer procedural guidelines to ensure inclusive representation, strengthen transparency through public access to documentation, and institutionalise the role of civil society in its processes. Such reforms are essential to align participatory mechanisms with public health goals and to safeguard them from corporate capture.

Although there is evidence regarding the effectiveness of probiotics for infantile colic (IC), there are not many studies regarding the efficacy of Bifidobacterium animalis subsp. Lactis BB-12^®, (BB-12^®), for the treatment of IC. This trial aimed to evaluate the efficacy of this subspecies of probiotic administration on IC.

In this double-blind randomized, placebo-controlled clinical trial, infants with IC diagnosis, exclusive breastfeeding, gestational age of more than 37 weeks, and birth weight of more than 2500 grams were included. The selected infants were randomly allocated into the two groups of "BBcare" group, treated with BB-12^® and the control group was treated with a placebo, 5 drops per day, for 6 weeks. The mean of crying time, vomiting episodes, and frequency of defecation at baseline and during follow-ups (40 and 60 days after intervention) were compared between the two studied groups.

In this study, 40 and 38 neonates in "BBcare" and placebo groups completed the study. In the "BBcare" group frequency of defecation, crying time, and vomiting episodes decreased significantly during intervention till 60 days after probiotic administration (P < 0.05). In the placebo group, there was a significant increase in crying and vomiting episodes between baseline and 60 days after intervention (P < 0.05). Between-group analyses indicated that mean of crying time, and vomiting episodes and number of defecations, 60 days after intervention were significantly lower in "BBcare" group (P < 0.05).

The findings of our study offer compelling signals for the effectiveness of BB-12^® in the management of some intestinal problems. Although these findings could be supportive evidence for the important role of gut microbiota as the goal of intervention to improve bowel movement and comfortable defecation in IC, further studies are needed in this field, especially for the evaluation of different types of probiotics in combination with each other's and with different dosages.

Parkinson's disease (PD) is a multifactorial neurodegenerative disorder, and peripheral blood-based biomarkers may help capture disease-related molecular changes. Because protein prenylation is essential for Rab-mediated intracellular trafficking, we investigated whether genes encoding key prenylation enzymes are dysregulated in PD.

Peripheral blood samples were collected from patients with PD and healthy controls. Quantitative real-time PCR was performed for FNTA, FNTB, RABGGTA, RABGGTB, and PGGT1B, using B2M as the endogenous reference gene. Expression was analyzed with efficiency-adjusted ΔCt calculations, and group comparisons, regression analyses, correlation testing, and ROC analyses were performed using standard nonparametric and multivariable approaches.

Four genes, FNTA, FNTB, RABGGTB, and PGGT1B, were significantly downregulated in PD, whereas RABGGTA showed only a weak, non-significant decrease. Individual ROC analyses showed good-to-excellent diagnostic performance for FNTA, FNTB, RABGGTB, and PGGT1B, while RABGGTA performed poorly. A multigene logistic regression model combining FNTA, FNTB, RABGGTB, and PGGT1B yielded excellent discrimination between PD and controls (AUC = 0.9787), with 90.0% overall classification accuracy and satisfactory model calibration. Correlation analyses further suggested coordinated expression patterns among the studied genes, supporting a pathway-level disturbance.

This pilot study identifies coordinated alterations in peripheral expression of prenylation-related genes in Parkinson's disease. The findings support dysregulation of the protein prenylation machinery as a potentially informative molecular feature of Parkinson's disease; however, the contribution of medication exposure and blood-cell composition could not be fully assessed, and independent external validation is required before clinical biomarker utility can be established.

Clinical management of growth hormone (GH) deficiency, acromegaly, and diabetes mellitus is dominated by single-analyte targets: serum insulin-like growth factor-1 (IGF-1) in the GH disorders and glycated hemoglobin in diabetes. This reductive framework obscures a central regulatory fact: GH does not autonomously dictate hepatic IGF-1 output. Whether GH is translated into IGF-1 by the hepatocyte is gated by the concentration of insulin reaching the liver through the portal vein. We propose liver sensitivity to GH (LSG), operationally defined as portal-insulin-determined hepatic GH receptor (GHR) availability, as a unifying variable that places type 1 and type 2 diabetes, obesity, liver failure, and acromegaly on a single continuum rather than treating them as separate phenomena. We develop the molecular basis of insulin-dependent GHR regulation, distinguish the divergent roles of portal versus systemic insulin, and argue that this distinction explains why subcutaneous insulin therapy in type 1 diabetes corrects glycemia while leaving the hepatic GH-resistant state intact. We then re-examine the weight-gain liability of insulinotropic antidiabetic agents, the discordant GH/IGF-1 signatures produced by GLP-1 receptor agonists, the prognostic and potentially therapeutic role of IGF-1 in cirrhosis, and the metabolic limitations of current acromegaly treatment targets when viewed through the LSG framework. The aim is to give the treating physician a mechanistic, rather than purely biochemical, account of how metabolism behaves in these states.

This study aimed to investigate the correlation between six surrogate indexes of insulin resistance (IR) and six inflammatory markers with diabetic peripheral arterial disease (DPAD) in patients with type 2 diabetes mellitus (T2DM).

Clinical and hematological data were retrospectively collected from 300 patients with T2DM admitted to the Endocrinology Department of Wuhu Hospital of Traditional Chinese Medicine (Anhui, China) between January 2024 and May 2025. Patients were divided into two groups: DPAD (n = 207) and T2DM (without DPAD (n = 93)). IR surrogate indexes analyzed included estimated glucose disposal rate (eGDR), Chinese Visceral Adiposity Index (CVAI), triglyceride-glucose (TyG) index, TyG-body mass index (TyG-BMI), metabolic score for insulin resistance (METS-IR), and atherogenic index of plasma (AIP). Inflammatory markers assessed included neutrophil-to-lymphocyte ratio (NLR), platelet-to-lymphocyte ratio (PLR), total cholesterol-to-lymphocyte ratio (TCLR), fibrinogen-to-lymphocyte ratio (FLR), lymphocyte-to-monocyte ratio (LMR), and systemic immune-inflammation index (SII). Factors associated with DPAD were identified and the discriminative ability of IR surrogate indexes and inflammatory markers for DPAD was explored.

Compared with the T2DM group, the DPAD group exhibited significantly higher CVAI, TyG-BMI, METS-IR, AIP, NLR, PLR, TCLR, FLR, and SII (p < 0.05), while eGDR and LMR were significantly lower (p < 0.05). Logistic regression analysis revealed that CVAI, TyG-BMI, METS-IR, AIP, NLR, PLR, FLR, and SII were positively associated with DPAD, whereas eGDR and LMR were inversely associated. eGDR and FLR exhibited significant associations with DPAD in sex and age subgroups. Receiver operating characteristic (ROC) curve analysis revealed that the combined eGDR+CVAI+FLR+LMR model yielded the highest area under the ROC curve (AUC) of 0.742 (95% CI [0.681-0.803]).

IR surrogate indexes and inflammatory markers are closely associated with DPAD risk in T2DM patients. The combined eGDR+CVAI+FLR+LMR model showed the best discriminative ability for DPAD, offering a potential reference for early clinical identification. These findings, however, are hypothesis-generating and require validation in prospective studies.

Diabetes-associated cognitive dysfunction (DACD) arises from interacting metabolic, vascular, inflammatory, and neuronal insults, but evidence for Panax-derived interventions is often overgeneralized across chemically non-equivalent materials. This critical narrative review evaluated whether defined Panax-derived saponins support a coherent mechanism of DACD and identified the evidence needed for translation. A structured multilingual search of eight bibliographic databases, supplemented by a targeted search of Cochrane CENTRAL, followed by deduplication and full-text reassessment, yielded 59 records: 16 A1 in vivo studies relevant to DACD (direct or near-direct), six neural-cell studies, 17 auxiliary Panax/barrier/formulation studies, and 20 contextual records. Purified monomers, the active metabolite compound K, saponin fractions, extracts, formulations, and combination interventions were appraised as non-interchangeable exposures. The most consistent signal was improved learning or memory accompanied by hippocampal or cortical tissue protection. Mechanistic findings converged on three connected but partly parallel processes: impaired brain insulin signaling and neuronal glucose handling; advanced glycation end product/methylglyoxal-associated oxidative and organelle stress; and glial-inflammasome amplification. Causal support was uneven, and brain exposure or central target engagement was rarely demonstrated. Most animal studies used young or adult animals of one sex and preventive or early-treatment designs, while several risk-of-bias domains were insufficiently reported. Panax-derived saponins should therefore be regarded as preclinical modulators of hippocampal metabolic-inflammatory-neuronal injury, not established DACD treatments. Translation requires defined interventions, parent/metabolite profiling, quantitative brain exposure, target-engagement assays, delayed-treatment and reversal designs, and clinically aligned biomarkers.

Short-chain fatty acids (SCFAs) have been proposed as mediators of the relationship between the intestinal microbiome and blood pressure (BP), but their therapeutic relevance in humans remains uncertain. This systematic review evaluated the effects of direct SCFA administration and interventions modifying endogenous fecal or circulating SCFAs on BP in adults. MEDLINE via PubMed, Scopus, and Web of Science Core Collection were searched for randomized controlled trials published from January 1, 2022, through May 31, 2026. The review was reported in accordance with the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) 2020 statement, with study selection, data extraction, and risk-of-bias assessment performed independently by two reviewers. Six randomized controlled trials were included and synthesized narratively because of substantial clinical and methodological heterogeneity. Three trials evaluated direct butyrate administration, while three assessed exercise, plant-derived, dietary, prebiotic, or physical therapy interventions that modified endogenous SCFAs. Direct administration produced inconsistent effects. Conventional oral butyrate increased daytime systolic and diastolic BP relative to placebo in adults with hypertension, whereas acute colon-targeted delivery reduced daytime systolic BP relative to a lower concentration in a small crossover trial. A further oral trial in type 2 diabetes mellitus reported within-group BP reductions without a demonstrated between-group effect. Indirect interventions generally increased plasma or fecal SCFAs alongside improvements in selected BP outcomes, but their multicomponent effects and the absence of formal mediation analyses precluded attributing these responses specifically to SCFAs. Fecal and circulating measurements also showed different relationships with BP, indicating that these compartments are not biologically interchangeable. One study was judged at low risk of bias, two had some concerns, and three were at high risk. Current evidence does not demonstrate a uniform antihypertensive effect of increasing SCFA availability or a reproducible dose-response relationship. Future trials should compare oral and colon-targeted formulations, measure fecal and circulating SCFAs concurrently, use 24-hour ambulatory BP monitoring as the primary outcome, and evaluate whether treatment responses vary by exposure and cardiometabolic phenotype.

Type 2 diabetes mellitus (T2DM) is associated with substantial cardiovascular and renal morbidity, necessitating individualized treatment strategies that target multiple pathophysiological mechanisms. Triple fixed-dose combination (FDC) therapy comprising empagliflozin, sitagliptin, and metformin (ESM) is used in routine clinical practice; however, real-world data describing the clinical characteristics and prescribing patterns of patients receiving this combination in India remain limited.

This multicentric, retrospective, cross-sectional real-world evidence study evaluated demographic characteristics, clinical profiles, comorbidities, glycemic parameters, renal function, and prescribing patterns among adult patients with T2DM receiving empagliflozin-, sitagliptin-, and metformin-based triple FDC therapy in India. Patients receiving empagliflozin 25 mg + sitagliptin 100 mg + metformin 1000 mg (ESM-25) or empagliflozin 10 mg + sitagliptin 100 mg + metformin 1000 mg (ESM-10) were included in the analysis.

A total of 12,843 patients were included, comprising 7,060 receiving ESM-25 therapy and 5,783 receiving ESM-10 therapy. Most patients were aged >50 years (64.2% in both groups), and males constituted 60.4% and 61.2% of the ESM-25 and ESM-10 groups, respectively. Physicians and diabetologists accounted for the majority of prescriptions. Comorbidities were documented in the available medical records for 12.0% of patients, with hypertension and cardiovascular disease (CVD) being the most frequently recorded conditions. Patients receiving ESM-25 therapy demonstrated higher glycemic parameters than those receiving ESM-10 therapy, including HbA1c (8.80% vs 8.68%), fasting plasma glucose (182.38 mg/dL vs 163.96 mg/dL), and postprandial plasma glucose levels (247.99 mg/dL vs 216.54 mg/dL). Differences between dosage groups were observed for urinary albumin-to-creatinine ratio, LDL cholesterol, and triglyceride levels.

Empagliflozin-based triple FDC therapy was prescribed among Indian patients with T2DM, particularly older adults with cardiometabolic comorbidities. Distinct prescribing patterns and clinical characteristics observed between ESM-25 and ESM-10 therapy may reflect individualized treatment selection in routine clinical practice.

Finerenone reduces albuminuria and improves kidney outcomes in patients with diabetic kidney disease (DKD); however, its association with changes in non-albumin proteinuria (NAP), enriched for tubular injury-related proteins, remains unclear. We evaluated whether finerenone treatment was associated with a reduction in NAP and identified clinical phenotypes associated with a greater NAP response.

We retrospectively analyzed 477 patients treated with finerenone who had baseline urine albumin-to-creatinine ratio (uACR) and urine protein-to-creatinine ratio (uPCR) measurements from the same urine specimen. Urine non-albumin protein-to-creatinine ratio (uNAPCR) was calculated as uPCR minus uACR. Patients were stratified by baseline proteinuria severity (uPCR < 500 vs ≥ 500 mg/gCr). The primary outcome was the geometric mean percentage change in uNAPCR after 6 months of finerenone treatment, assessed using linear mixed-effects models. Subgroup interaction analyses were performed to assess differential associations and identify factors associated with greater uNAPCR reduction.

At baseline, median uPCR, uACR, and uNAPCR were 1140 [580, 2290], 716 [328, 1593], and 410 [223, 700] mg/gCr, respectively. At 6 months, uACR and uNAPCR declined by 30.3% and 17.5%, respectively. Subgroup analyses revealed differential associations: patients with higher baseline proteinuria (uPCR ≥ 500 mg/gCr) showed an 18.8% decline in uNAPCR, whereas those with uPCR < 500 mg/gCr showed a non-significant 1.3% change. Changes in uNAPCR were positively correlated with changes in urine N-acetyl-β-D-glucosaminidase-to-creatinine ratio (uNAGCR) (Spearman's ρ = 0.53; p < 0.001).

Finerenone treatment was associated with a reduction in NAP, particularly among patients with higher baseline proteinuria, suggesting a possible effect on tubulointerstitial injury-related processes beyond albuminuria reduction. Prospective multicenter studies are needed to validate uNAPCR as a treatment-response biomarker against clinical endpoints.

As long-term survival rates improve among thyroid cancer patients, the metabolic consequences of thyroidectomy and thyroid hormone therapy have gained increasing importance. While these treatments are crucial for cancer management, their long-term effects on metabolic health remain inadequately understood.

We conducted a retrospective, population-based cohort study utilizing nationwide data from the Korea National Health Insurance Service. We estimated the risk of incident metabolic abnormalities (i) among patients with TC who underwent thyroidectomy compared with matched individuals from the general population without TC, (ii) among TC patients according to thyroidectomy status, and (iii) among TC patients who underwent thyroidectomy, according to thyroid hormone therapy status. The incidence of obesity, diabetes mellitus, hypertension, dyslipidemia, metabolic syndrome, and metabolic dysfunction-associated steatotic liver disease (MASLD) within 5, 8, and 10 years was estimated using multivariable logistic regression models, adjusting for age, sex, household income, alcohol consumption, smoking status, and physical activity.

Thyroidectomy was associated with higher odds of multiple metabolic abnormalities compared with the matched general population without TC and to TC patients without thyroidectomy, with most associations evident from 5 years onward and some from 8 years. Among TC patients who underwent thyroidectomy, thyroid hormone therapy was significantly associated with metabolic abnormalities. In sex-stratified analyses, overall patterns were largely similar; however, MASLD was not significantly associated with thyroidectomy or thyroid hormone therapy in males.

Thyroidectomy and thyroid hormone therapy are associated with incidence of metabolic abnormalities within 5, 8, or 10 years among thyroid cancer survivors. These findings support ongoing metabolic monitoring in thyroid cancer survivors and warrant further studies to determine whether individualized hormone management can reduce long-term metabolic risk.