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.
Just reducing calories for a short while can help repair your DNA damage, at least if you are a mouse.
Why is this important: Calorie restriction has been shown to improve health, reduce the burden of diseases of aging such as cancer and diabetes, and it have even been shown to increase lifespan in various organisms from worms to rodents.
Key takeaway(s): Calorie restriction without malnutrition slows the biological aging process, and results in lifespan extension in a number of species. Reducing your calorie intake by 40% for a year or two may help you repair your DNA damage.
Could ketogenic diets help treat obesity, and type-2-diabetes?
Why is this important: Metabolic dysfunction caused by obesity, and type-2-diabetes accelerate biological aging. People who are obese, and/or have type-2-diabetes are more likely to suffer from viral and bacterial infections, they are prone to cardiovascular disease, various cancers, and have an elevated risk of dementia and other neurological disorders. By reducing body weight, and making people sensitive to the glucose and insulin in their body we can lower their risk of accelerated biological aging.
Key takeaway(s): Obese patients, and/or patients with type-2-diabetes were more likely to lose weight, and stay on the very-low-calorie-ketogenic-diet (VLCKD) long term, than patients who were on various types of fasting diets, or other low calorie diets. Additionally, not only did the VLCKD patients lose weight, but over a two-year period they were able to reduce their total fat mass, they didn’t suffer from any significant muscle or bone loss, and rarely reported any negative mood or other side-effects.
Could enhancing autophagy increase human lifespan?
Why is this important: Cells degrade aged and damaged interior components in a process called autophagy, which means ‘self-eating’. While this might sound like something undesirable, autophagy is an essential process as it allows cells to remove accumulating toxins and recycle dysfunctional components.There is growing evidence that autophagy plays an important role in longevity. This review highlights what we know.
Key takeaway(s): Autophagy decreases during normal aging while long-lived animals have a high level of autophagy, suggesting that enhanced autophagy is involved in the prolongation of life span. Decreased or defective autophagy accelerates aging, impairing the elimination of mutant and toxic proteins leading to senescence or death of nonrenewable cells. Understanding why autophagy becomes defective with age may lead to new longevity-enhancing strategies.
In adults, adipose tissue consists largely of regular white adipose tissue (WAT), which is adept at storing calories, if possessed in abundance these can be one of the causes of obesity, type 2 diabetes and high blood pressure, otherwise known as metabolic syndrome. Unlike WAT, mitochondria-packed brown adipose tissue (BAT) burns more energy, meaning less calories are hoarded, and the risk of obesity and, therefore, the risk of metabolic syndrome is reduced.
Why is this important: Activating this ‘thermogenic’ fat is thought to be an attractive way to metabolic syndrome, and may result in a metabolic phenotype which favours advanced healthspan.
Key takeaway(s): They found that a distinct pattern of lipid changes in the Ames dwarf mice adipose tissue are associated with increased thermogenesis and improved insulin sensitivity resulting in decreased reactive oxygen species and inflammation. Concluding that “lipid metabolism may underlie the beneficial phenotypes observed in the adipose tissue of Ames dwarf mice”. This research helps progress our knowledge of the intersection between adipose tissue, metabolic syndrome and longevity.
New digital PCR assay for detecting EGFR mutations was developed
Why is this important: In patients with non-small-cell lung cancer the possibility of treatment with tyrosine kinase inhibitors is determined whether specific mutations of EGFR gene are present. However, low throughput and high costs of PCR, that detects said mutations, limits its clinical approach.
What did the researchers do: They developed a new digital PCR assay named dEGFR39, that can detect up to and distinguish between 39 mutations of exons 18-21 of the EGFR gene. This assay is also cost-efficient, requires small sample input and reliable, with the accuracy value of 87.88% in 33 patients.
Key takeaway(s): New enhanced assay will not only allow to screen patients’ blood for EGFR gene mutations for targeted therapy, but also evaluate prognosis after the treatment.