Research integrity and transparency in CAM journals: an analysis of publication bias and reporting practices (1995-2023) in four leading journals.

Globally, stroke ranks as the second leading cause of death among noncommunicable diseases (NCDs) and the third leading cause of combined mortality and disability (measured in disability-adjusted life years—DALYs) []. From 1990 to 2021, the global burden of stroke increased substantially in low- and lower-middle-income countries, with 69.0% attributable to metabolic risk factors. This disproportionate societal burden significantly shortens productive life expectancy []. Stroke manifests as ischemic and hemorrhagic phenotypes, with ischemic stroke constituting the predominant type [], accounting for 87% of all stroke subtypes in the United States and 63% globally []. Vascular causes of ischemic stroke include large-artery disease, cardioembolic stroke, and small-vessel disease, with the latter also being the most common cause of intracerebral hemorrhage []. Ischemia induces direct neuronal injury, excessive reactive oxygen species (ROS) production, and inflammatory activation, leading to rapid brain tissue pathology, blood–brain barrier disruption, and progressive microvascular damage [,,]. This triggers a cascade of adverse outcomes including cerebral edema, hemorrhagic transformation, neuroinflammation, infarct enlargement, and neurological deficits. Therefore, reducing and preventing stroke-induced neurological damage is crucial for lowering mortality and disability risks in the global population. The INTERSTROKE study indicates that abnormal blood glucose accounts for 3.9% of population-attributable risk in stroke []. Risk factor profiles differ between ischemic stroke subtypes—macroangiopathic atherosclerotic and cerebrovascular disease—but abnormal blood glucose remains a major shared risk factor for both []. Extensive research data support the association between abnormal blood glucose and microcirculatory dysfunction, which triggers key molecular events in atherosclerosis through inducing oxidative stress and inhibiting nitric oxide (NO) bioactivity [,]. Furthermore, emerging evidence indicates that ischemic stroke in diabetic patients exhibits significantly heightened Toll-like receptor 4 (TLR4)-mediated neuroinflammation compared to non-diabetic ischemic stroke [,,]. Thus, optimal glycemic control represents a critical step in enhancing functional recovery in stroke patients. Approximately 16–24% of diabetic patients face stroke risk []. Insulin resistance and hyperinsulinemia predispose to abnormal fatty deposition in intracranial and extracranial arteries, leading to macrovascular complications []. The STOP NIDDM study demonstrated that regular use of acarbose significantly reduces stroke incidence []. A multicenter randomized controlled trial from the UK (UKPDS study) highlighted the importance of intensive glycemic control, showing that a 1% reduction in hemoglobin A1c (HbA1c) lowers stroke risk by 4% []. Studies including the Insulin Resistance Intervention in Stroke (IRIS), Glucose and Insulin in Stroke Trial Pilot (GIST), and Insulin in Acute Ischemic Stroke (INSULINFARCT) all demonstrated the coexistence of abnormal glucose levels and stroke, as well as the therapeutic efficacy of glucose intervention in diabetic stroke patients [,,].