From BMJ Journal “Gut” study (February 17, 2020):
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.
Objective Ageing is accompanied by deterioration of multiple bodily functions and inflammation, which collectively contribute to frailty. We and others have shown that frailty co-varies with alterations in the gut microbiota in a manner accelerated by consumption of a restricted diversity diet. The Mediterranean diet (MedDiet) is associated with health. In the NU-AGE project, we investigated if a 1-year MedDiet intervention could alter the gut microbiota and reduce frailty.
Design We profiled the gut microbiota in 612 non-frail or pre-frail subjects across five European countries (UK, France, Netherlands, Italy and Poland) before and after the administration of a 12-month long MedDiet intervention tailored to elderly subjects (NU-AGE diet).
Results Adherence to the diet was associated with specific microbiome alterations. Taxa enriched by adherence to the diet were positively associated with several markers of lower frailty and improved cognitive function, and negatively associated with inflammatory markers including C-reactive protein and interleukin-17. Analysis of the inferred microbial metabolite profiles indicated that the diet-modulated microbiome change was associated with an increase in short/branch chained fatty acid production and lower production of secondary bile acids, p-cresols, ethanol and carbon dioxide. Microbiome ecosystem network analysis showed that the bacterial taxa that responded positively to the MedDiet intervention occupy keystone interaction positions, whereas frailty-associated taxa are peripheral in the networks.
Conclusion Collectively, our findings support the feasibility of improving the habitual diet to modulate the gut microbiota which in turn has the potential to promote healthier ageing.
Read full study
Microbiome expands the genetic and functional capacity of its human host. Susan Lynch explains that human microbiome develops early in life and that gut microbes shape immune function and relate to disease outcomes in childhood.
She also explores next-generation microbiome therapeutics and research.
From a Science Magazine online article:
They found that these physically active mice had fewer inflammatory cells (leukocytes) than sedentary mice, an effect they traced to diminished activity of hematopoietic stem and progenitor cells (HSPCs). The lower activity of HSPCs was due at least in part to exercise-induced reduction in the levels of leptin, a hormone produced by fat tissue that regulates cells within the hematopoietic bone marrow niche.
Regular physical activity is associated with a lower rate of death from heart disease, but the underlying mechanisms are not fully understood. Frodermann et al. examined the effect of exercise on cardiovascular inflammation, a known risk factor for atherosclerosis, by studying mice that voluntarily ran for long distances on exercise wheels.
To read more: https://science.sciencemag.org/content/366/6469/1091.2
From Sloan Kettering Institute:
Infections with the Enterococcus bacterium are a major threat in healthcare settings. They can lead to inflammation of the colon and serious illnesses such as bacteremia and sepsis, as well as other complications.
Now, an international team led by scientists from Memorial Sloan Kettering has shown for the first time that foods containing lactose, a sugar that’s naturally found in milk and dairy products, help Enterococcus thrive in the gut, at least in mice. They also studied changes in the bodies of people having BMTs. The study was published November 29 in Science.
Their previous research has shown that when harmless strains of microbes are wiped out, often due to treatment with antibiotics, Enterococcus and other harmful types of bacteria can take over due to lack of competition. As part of the new study, which included analysis of microbiota samples from more than 1,300 adults having BMTs, the team confirmed the link between Enterococcus and GVHD.
To read more: https://www.mskcc.org/blog/milking-it-study-mice-suggests-lactose-diet-feeds-dangerous-gut-bacteria?_subsite=research-ski
From a Stanford Medicine online news release:
“What you want is more, small fat cells rather than fewer, large fat cells,” Jackson said. “A large fat cell is not a healthy fat cell. The center is farther away from an oxygen supply, it sends out bad signals and it can burst and release toxic contents.” Large fat cells are associated with insulin resistance, diabetes and inflammation, he added.
Jackson and his colleagues found that when omega-3 fatty acids bind to a receptor called FFAR4 on the cilia of fat stem cells, it prompts the fat stem cells to divide, leading to the creation of more fat cells. This provides the body with more fat cells with which to store energy, something that is healthier than storing too much fat in existing fat cells.
For years, researchers have known that defects in an ancient cellular antenna called the primary cilium are linked with obesity and insulin resistance. Now, researchers at the Stanford University School of Medicine have discovered that the strange little cellular appendage is sensing omega-3 fatty acids in the diet, and that this signal is directly affecting how stem cells in fat tissue divide and turn into fat cells.
To read more: http://med.stanford.edu/news/all-news/2019/11/omega-3-fatty-acids-health-benefit-linked-to-stem-cell-control.html