Cannabidiol (CBD) is a naturally occurring, non-psychotropic cannabinoid of the hemp plant L. and has been known to induce several physiological and pharmacological effects. While CBD is approved as a medicinal product subject to prescription, it is also widely sold over the counter (OTC) in the form of food supplements, cosmetics and electronic cigarette liquids. However, regulatory difficulties arise from its origin being a narcotic plant or its status as an unapproved novel food ingredient. Regarding the consumer safety of these OTC products, the question whether or not CBD might be degraded into psychotropic cannabinoids, most prominently tetrahydrocannabinol (THC), under in vivo conditions initiated an ongoing scientific debate. This feature review aims to summarize the current knowledge of CBD degradation processes, specifically the results of in vitro and in vivo studies. Additionally, the literature on psychotropic effects of cannabinoids was carefully studied with a focus on the degradants and metabolites of CBD, but data were found to be sparse. While the literature is contradictory, most studies suggest that CBD is not converted to psychotropic THC under in vivo conditions. Nevertheless, it is certain that CBD degrades to psychotropic products in acidic environments. Hence, the storage stability of commercial formulations requires more attention in the future.
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http://dx.doi.org/10.3390/toxics8020041 | DOI Listing |
Co-existing neuropathological comorbidities have been repeatedly reported to be extremely common in subjects dying with dementia due to Alzheimer disease. As these are likely to be additive to cognitive impairment, and may not be affected by molecularly-specific AD therapeutics, they may cause significant inter-individual response heterogeneity amongst subjects in AD clinical trials. Furthermore, while originally noted for the oldest old, recent reports have now documented high neuropathological comorbidity prevalences in younger old AD subjects, who are more likely to be included in clinical trials.
View Article and Find Full Text PDFCureus
December 2024
Gastroenterology and Hepatology, Monmouth Medical Center, Long Branch, USA.
Lemmel syndrome involves a periampullary duodenal diverticulum (PAD), a pouch-like outpouching near the ampulla of Vater, compressing the common bile duct. We describe a case of severe abdominal pain in a patient who had a large periampullary diverticulum, managed with surgical intervention after an initial failed endoscopic retrograde cholangiopancreatography (ERCP). An elderly female patient in her early 90s arrived at the emergency department with severe cramping pain localized to the right upper quadrant of her abdomen, progressively intensifying over several weeks.
View Article and Find Full Text PDFGastro Hep Adv
September 2024
Gastroenterology Division, Medicine Department, Prince Mohammed Bin Abdulaziz Hospital, Ministry National Guard - Health Affairs, Almadinah, Almunawwarah, KSA.
Situs inversus totalis is a rare congenital disorder defined by the transposition of all viscera to the opposite side of the body. Because of this anatomical alteration, endoscopic retrograde cholangiopancreatography (ERCP) in such a population is significantly challenging. Herein we report a case of a 50-year-old woman presented with epigastric and left upper quadrant pain.
View Article and Find Full Text PDFAME Case Rep
October 2024
Department of Internal Medicine, Unity Hospital, Rochester, NY, USA.
Background: Surgical clip migration is a rare complication that can happen many years following a successful cholecystectomy. It has a similar clinical presentation as choledocholithiasis. The diagnosis is usually made using imaging modalities such as ultrasounds, computed tomography (CT) scans, or magnetic resonance cholangiopancreatography (MRCP).
View Article and Find Full Text PDFMethods Cell Biol
January 2025
Department of Pharmacology, SPP School of Pharmacy & Technology Management, Mumbai, India. Electronic address:
The foremost cause of dementia is Alzheimer's disease (AD). The vital pathological hallmarks of AD are amyloid beta (Aβ) peptide and hyperphosphorylated tau (p-tau) protein. The current animal models used in AD research do not precisely replicate disease pathophysiology, making it difficult for researchers to quickly and effectively gather data or screen potential therapy possibilities.
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