RESUMO
Intermittent fasting is an increasingly popular dieting technique with many well-studied benefits, such as permitting weight loss in obese patients, lowering low-density lipoprotein cholesterol (LDL-C) levels and triglyceride levels, and optimizing circadian rhythms. A special type of intermittent fasting occurs during Ramadan, when Muslims worldwide fast daily from dawn to sunset for a month. Ramadan fasting has demonstrated several health benefits, including improving the gut microbiome, modifying gut hormone levels, and lowering proinflammatory markers such as cytokines and blood lipids. Although fasting has many health benefits, fasting during Ramadan may aggravate chronic medical conditions. We aim to review the literature devoted to Ramadan fasting and its effects on Muslim patients with gastrointestinal (GI) disorders, such as Inflammatory bowel disease (IBD), peptic ulcer disease (PUD), upper GI bleeding (UGIB), gastroesophageal reflux disease (GERD), and liver conditions. We will discuss recommendations for diet and medication compliance during Ramadan in the recommended pre-Ramadan counseling sessions. In this study, we used PubMed to research journals using the key terms "Ramadan," "intermittent fasting," and "gastrointestinal diseases." The current literature studying the impact of Ramadan on gastrointestinal disorders shows that patients with IBD have a minimal risk of disease exacerbation, although older men with ulcerative colitis (UC) were more prone to exacerbation during fasting. Patients with duodenal ulcers were at a higher risk of hemorrhage after Ramadan fasting. Although with mixed results, studies show patients with liver disease demonstrated improvements in liver enzymes, cholesterol, and bilirubin after Ramadan. Physicians should offer pre-Ramadan counseling to educate patients on the risks of fasting and encourage shared decision-making. To facilitate more definitive discussions between the physician and a Muslim patient, clinicians should seek a deeper understanding of how Ramadan fasting affects certain health conditions and offer accommodations, such as diet and medication adjustments.
RESUMO
Astrocytes and neurons have been shown to swell across a variety of different conditions, including increases in extracellular potassium concentration (^[K+]o). The mechanisms involved in the coupling of K+ influx to water movement into cells leading to cell swelling are not well understood and remain controversial. Here, we set out to determine the effects of ^[K+]o on rapid volume responses of hippocampal CA1 pyramidal neurons and stratum radiatum astrocytes using real-time confocal volume imaging. First, we found that elevating [K+]o within a physiological range (to 6.5 mM and 10.5 mM from a baseline of 2.5 mM), and even up to pathological levels (26 mM), produced dose-dependent increases in astrocyte volume, with absolutely no effect on neuronal volume. In the absence of compensating for addition of KCl by removal of an equal amount of NaCl, neurons actually shrank in ^[K+]o, while astrocytes continued to exhibit rapid volume increases. Astrocyte swelling in ^[K+]o was not dependent on neuronal firing, aquaporin 4, the inwardly rectifying potassium channel Kir 4.1, the sodium bicarbonate cotransporter NBCe1, , or the electroneutral cotransporter, sodium-potassium-chloride cotransporter type 1 (NKCC1), but was significantly attenuated in 1 mM barium chloride (BaCl2) and by the Na+/K+ ATPase inhibitor ouabain. Effects of 1 mM BaCl2 and ouabain applied together were not additive and, together with reports that BaCl2 can inhibit the NKA at high concentrations, suggests a prominent role for the astrocyte NKA in rapid astrocyte volume increases occurring in ^[K+]o. These findings carry important implications for understanding mechanisms of cellular edema, regulation of the brain extracellular space, and brain tissue excitability.
