Everyday our team of researchers in Oxford are inundated with scientific, and medical research articles that have the potential to improve health, wellbeing, and longevity. In this blog we highlight a few of them that caught our attention today.
Young people can eat as much as they want, and exercise infrequently and yet stay lean and healthy. Alas, as we get older we all have to watch what we eat, and exercise regularly to keep in shape and maintain our health. This happens due to our metabolism, the process by which we convert food into energy, deteriorating due to aging.
It would be wonderful if we had a list of things the change during aging in our metabolism. Using this list we maybe able to fix issues using nutrition, lifestyle, and biochemistry, and return to the optimal metabolism of our youth.
Currently, MetaboAge contains 408 metabolites annotated with their biological and chemical information, and more than 1515 aging-related variations, graphically represented on the website grouped by how they were discovered, gender, and age-groups.
Experiments have shown that blood from a young mouse has the ability to rejuvenate the tissues of an older mouse. Likewise, it appears that tissue age can influence the characteristics of red blood cells.
This study analysed red blood cells from 15 and 25-month old mice, and found that age was associated with significant decline of antioxidant capacity and certain metabolic pathways.
Circulation of older red blood cells in younger mice partially restored some of these metabolic pathways, but had minimal to no impact on others.
In a study published in Nature Communication, a team of researchers from the University of Edinburgh used existing data from genome wide association studies (GWAS) to run a multivariate analysis to identify common genomic loci present in each of the three ageing phenotypes: lifespan, healthspan and longevity.
The analysis identified 10 genomic loci which influence all three of the phenotypes, with 5 novel loci that had not been recognised at the genome-wide level before
The team also observed robust evidence for a causative role of haem metabolism in human ageing. Haem is the component of haemoglobin which contains iron.
“Haem synthesis declines with age and its deficiency leads to iron accumulation, oxidative stress, and mitochondrial dysfunction. In turn, iron accumulation helps pathogens to sustain an infection, which is in line with the known increase in infection susceptibility with age. In the brain, abnormal iron homeostasis is commonly seen in neurodegenerative diseases such as Alzheimer’s and Parkinson’s disease and multiple sclerosis”
Protein homeostasis or proteostasis is balanced machinery that controls synthesis, folding, trafficking and degradation of proteins inside and outside of the cell. Ability to maintain proteostasis is essential for cells’ health and loss of it is one of the aspects of aging.
This review article discusses changes to proteostasis caused by aging and methods that allow us to quantify said changes, the majority of them involving sophisticated usage of mass spectrometry.
The article also states that reduced calorie intake, which leads to reduced protein synthesis, may promote longevity. Further studies have shown that specific protein mTOR is inhibited in reduced protein synthesis and its inhibition has a universal effect of longevity promotion across species.