New research could help explain why thousands of Covid-19 survivors are facing debilitating neurological symptoms months after initially getting sick. WSJ breaks down the science behind how the coronavirus affects the brain, and what this could mean for long-haul patients. Illustration: Nick Collingwood/WSJ
From iScience / Cell.com (June 26, 2020):
…the beneficial effects of TRE are dose dependent, with greater reductions in body weight, fat mass, and improvement in glucose tolerance when a 9-h protocol was implemented versus 12 and 15 h. The optimal TRE time frame to recommend for people has not been tested. Clear improvements have been noted after 6-, 8-, 9-, and 10-h protocols. It is likely that the greater time restriction would result in greater weight losses, which may maximize the metabolic benefits.
Eating out of phase with daily circadian rhythms induces metabolic desynchrony in peripheral metabolic organs and may increase chronic disease risk. Time-restricted eating (TRE) is a dietary approach that consolidates all calorie intake to 6- to 10-h periods during the active phase of the day, without necessarily altering diet quality and quantity.
TRE reduces body weight, improves glucose tolerance, protects from hepatosteatosis, increases metabolic flexibility, reduces atherogenic lipids and blood pressure, and improves gut function and cardiometabolic health in preclinical studies. This review discusses the importance of meal timing on the circadian system, the metabolic health benefits of TRE in preclinical models and humans, the possible mechanisms of action, the challenges we face in implementing TRE in humans, and the possible consequences of delaying initiation of TRE.
We observed that increased adherence to the MedDiet modulates specific components of the gut microbiota that were associated with a reduction in risk of frailty, improved cognitive function and reduced inflammatory status.
Dr Philip Smith, Digital and Education Editor of Gut and Consultant Gastroenterologist at the Royal Liverpool Hospital interviews Professor Paul O’Toole; who is Professor of Microbial Genomics, Head of School of Microbiology and Principal Investigator in APC Microbiome Ireland, an SFI funded centre at University College Cork, Ireland, on “Mediterranean diet intervention alters the gut microbiome in older people reducing frailty and improving health status: the NU-AGE 1-year dietary intervention across 5 European countries” published in paper copy in Gut in July 2020.
First up this week, Staff Writer Jennifer Couzin-Frankel talks with host Sarah Crespi about a rare inflammatory response in children that has appeared in a number of COVID-19 hot spots.
Next, Julian Dowdeswell, director of the Scott Polar Research Institute and professor of physical geography at the University of Cambridge, talks with producer Meagan Cantwell about tracing the retreat of Antarctica’s glaciers by examining the ocean floor. Finally, Kiki Sanford interviews author Danny Dorling about his new book, Slowdown: The End of the Great Acceleration―and Why It’s Good for the Planet, the Economy, and Our Lives.
Read Digital “Yale Medicine Magazine”May 2020 Issue
From a BMJ Open Journal study release (February 20, 2020):
Aspirin is an inhibitor of prostaglandin production and may influence the cellular basis of bone remodelling responsible for maintaining the material and structural strength of bone.
The consistent findings of reduced risk of fracture across studies included in this review is encouraging. It is important to keep in mind that studies were quite diverse in design, populations included, data collection methods and follow-up periods and we did observe high heterogeneity especially for fracture risk. While we need to interpret this finding with some caution, there appeared to be a consistent indication that aspirin use is associated with positive bone outcomes.
The anti-inflammatory effects of aspirin via prostaglandin inhibition have recently gained attention. Chronic low-grade inflammation contributes to age-related cardiovascular, neurological, respiratory and musculoskeletal conditions. Low-grade inflammation is associated with increased bone loss and fracture risk. Prostaglandin, an important inflammatory mediator, is likely to have a key role in bone remodelling attributable to inflammation. Prostaglandin E2 stimulates bone resorption and formation and is produced largely from cyclooxygenase-2 induction. Prostaglandins acutely inhibit osteoclast function. However, their chronic effect is to stimulate bone resorption by increasing replication of osteoclast precursors, and differentiation to mature osteoclasts.