Background.Traditional Chinese medicine (TCM), when given as a therapy for symptom relief, has gained widespread popularity among diabetic patients. The aim of this study is to analyze the utilization of TCM among type 2 diabetic patients in Taiwan.Methods.The use of TCM for type 2 diabetic patients were evaluated using a randomly sampled cohort of 1,000,000 beneficiaries recruited from the National Health Insurance Research Database.Results.Overall, 77.9%(n=31,289)of type 2 diabetic patients utilized TCM and 13.9%(n=4,351)of them used TCM for the treatment of type 2 diabetes. Among the top ten most frequently prescribed herbal formulae, four remedies,Zhi-Bo-Di-Huang-Wan, Qi-Ju-Di-Huang-Wan, Ji-Sheng-Shen-Qi-WanandBa-Wei-Di-Huang-Wanare derivative formulae ofLiu-Wei-Di-Huang-Wan.In other words,Liu-Wei-Di-Huang-Wanand its derivatives were found to be the most common herbal formulae prescribed by TCM doctors for the treatment of diabetes in Taiwan.Conclusion.Although some evidence does support the use TCM to treat diabetes, the results from the current study may have been confounded by placebo effect, which emphasize the need for well conducted, double-blind, randomized, placebo-controlled studies in order to further evaluate the efficacy ofLiu-Wei-Di-Huang-Wanon patients with type 2 diabetes.

Background. The increased practice of traditional Chinese medicine (TCM) worldwide has raised concerns regarding herb-drug interactions. The purpose of our study is to analyze the concurrent use of Chinese herbal products (CHPs) among Taiwanese insomnia patients taking hypnotic drugs.Methods. The usage, frequency of services, and CHP prescribed among 53,949 insomnia sufferers were evaluated from a random sample of 1 million beneficiaries in the National Health Insurance Research Database. A logistic regression method was used to identify the factors that were associated with the coprescription of a CHP and a hypnotic drug. Cox proportional hazards regressions were performed to calculate the hazard ratios (HRs) of hip fracture between the two groups.Results. More than 1 of every 3 hypnotic users also used a CHP concurrently.Jia-Wei-Xiao-Yao-San(Augmented Rambling Powder) andSuan-Zao-Ren-Tang(Zizyphus Combination) were the 2 most commonly used CHPs that were coadministered with hypnotic drugs. The HR of hip fracture for hypnotic-drug users who used a CHP concurrently was 0.57-fold (95% CI = 0.47–0.69) that of hypnotic-drug users who did not use a CHP.Conclusion. Exploring potential CHP-drug interactions and integrating both healthcare approaches might be beneficial for the overall health and quality of life of insomnia sufferers.

Alzheimer’s disease (AD) has pathological hallmarks including amyloid beta (Aβ) plaque formation. Currently approved single-target drugs cannot effectively ameliorate AD. Medicinal herbs and their derived ingredients (MHDIs) have multitarget and multichannel properties, engendering exceptional AD treatment outcomes. This review delineates how in in vivo models MHDIs suppress Aβ deposition by downregulating β- and γ-secretase activities; inhibit oxidative stress by enhancing the antioxidant activities and reducing lipid peroxidation; prevent tau hyperphosphorylation by upregulating protein phosphatase 2A expression and downregulating glycogen synthase kinase-3β expression; reduce inflammatory mediators partly by upregulating brain-derived neurotrophic factor/extracellular signal-regulated protein kinase 1/2-mediated signaling and downregulating p38 mitogen-activated protein kinase (p38 MAPK)/c-Jun N-terminal kinase (JNK)-mediated signaling; attenuate synaptic dysfunction by increasing presynaptic protein, postsynaptic protein, and acetylcholine levels and preventing acetylcholinesterase activity; and protect against neuronal apoptosis mainly by upregulating Akt/cyclic AMP response element-binding protein/B-cell lymphoma 2 (Bcl-2)-mediated anti-apoptotic signaling and downregulating p38 MAPK/JNK/Bcl-2-associated x protein (Bax)/caspase-3-, Bax/apoptosis-inducing factor-, C/EBP homologous protein/glucose-regulated protein 78-, and autophagy-mediated apoptotic signaling. Therefore, MHDIs listed in this review protect against Aβ-induced cognitive decline by inhibiting Aβ accumulation, oxidative stress, tau hyperphosphorylation, inflammation, synaptic damage, and neuronal apoptosis in the cortex and hippocampus during the early and late AD phases.