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An important update on E5.
Here we look at an attempt to replicate the amazing results with E5 from Dr Katcher’s 2020 paper by an institute that has been set up in Brazil.
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Next in our New Year countdown, a study found that traumatic experiences during childhood may impair muscle function later in life.
Read more.
A University of Michigan study has shown that traumatic experiences during childhood may get “under the skin” later in life, impairing the muscle function of people as they age.
Continue reading “Childhood Trauma Leaves Lasting Imprint on Muscle Function” »
Benonisdottir et al. review the genetics of reproductive traits and examine how these associate with links to health, behavior, aging and longevity as well as outcomes for offspring.
Using an AI tool, researchers at Karolinska Institutet have analyzed brain images from 70-year-olds and estimated their brains’ biological age. They found that factors detrimental to vascular health, such as inflammation and high glucose levels, are associated with an older-looking brain, while healthy lifestyles were linked to brains with a younger appearance.
The results are presented in a paper titled “Biological brain age and resilience in cognitively unimpaired 70-year-old individuals” in Alzheimer’s & Dementia.
Every year, over 20,000 people in Sweden develop some form of dementia, with Alzheimer’s disease accounting for approximately two-thirds of cases. However, the speed at which the brain ages is affected by various risk and health factors.
Furthermore, GDF-15 levels have been positively associated with the aging process. In fact, Tanaka et al. (Tanaka et al. 2018) showed that this cytokine had the strongest positive correlation with age in humans, and several reports describe higher levels of GDF-15 in older individuals (Semba et al. 2020; Doerstling et al. 2018; Liu et al. 2020). Aging is characterized by a decline in physiological function and changes in body composition, being a major risk factor for a variety of chronic diseases. As such, GDF-15 is also associated with several age-related diseases, including cardiovascular disease (Echouffo-Tcheugui et al. 2021), cancer (Wischhusen et al. 2020), metabolic syndrome (Ho et al. 2023; Carballo-Casla et al. 2022), or diabetes (Ouyang et al. 2020; Merchant et al. 2023), among others (Candia et al. 2021; Iglesias et al. 2023). In addition, it has been proposed as a biomarker for the risk of death in patients with cardiovascular conditions and an accurate all-cause mortality marker (Candia et al. 2021; Iglesias et al. 2023; Nopp et al. 2021). GDF-15 has also been positively associated with deteriorated muscle function and sarcopenia (Semba et al. 2020; Kim et al. 2022, 2020; Nakajima et al. 2019; Lee et al. 2022), a highly prevalent condition among the elderly that increases the risk of frailty (Picca et al. 2020).
It is widely accepted that human aging may be influenced by epigenetic alterations (López-Otín et al. 2023). In this sense, age biomarkers based on DNA methylation have proven useful in predicting the risk of age-related diseases and mortality (Fransquet et al. 2019). Among several developed epigenetic clocks, DNAm GrimAge has shown a higher prediction capacity of mortality and morbidity risk (Lu et al. 2022). Notably, GDF-15 is one of the markers included for the calculation of this clock (Lu et al. 2019). Thus, understanding the interplay between GDF-15 and aging can be crucial for improving the assessment of and management of age-associated conditions.
For all this, the aim of this study was to characterize the changes in circulating GDF-15 levels with age in a population of healthy individuals from the Balearic Islands and investigate its potential associations with different epigenetic and biological clocks, physical performance and other age-related biomarkers.
Mayo Clinic researchers have identified interleukin-23 receptor (IL-23R) as a significant biomarker of cellular senescence and aging in both mice and humans. Experiments show that IL-23R levels in the bloodstream increase with age and can decrease, reflecting senescent cell clearing, with senolytic therapies.
Cellular senescence occurs when cells stop dividing but do not trigger apoptosis mechanisms that would allow them to die naturally. Instead, they are stuck in a zombie-like state, where they still have the urge to feed and carry out metabolic activities, but with increasingly incoherent cell signaling and increased pro-inflammatory cytokine secretions.
Senescent cell activity has been linked to several age-related diseases, including those of the immune, cardiovascular, metabolic, pulmonary, musculoskeletal and neurological systems.
Chimeric antigen receptor (CAR) T cells targeting uPAR, a cell-surface protein that is upregulated on senescent cells, eliminate senescent cells in vitro and in vivo and reduce liver fibrosis in mice.
Andrew Cassy had spent his working life in a telecommunications research department until a diagnosis of Parkinson’s disease in 2010 pushed him into early retirement. Curious about his illness, which he came to think of as an engineering problem, he decided to volunteer for clinical trials.
“I had time, something of value that I could give to the process of understanding the disease and finding good treatments,” he says.
In 2024, he was accepted into a radical trial. That October, surgeons in Lund, Sweden, placed neurons that were derived from human embryonic stem (ES) cells into his brain. The hope is that they will eventually replace some of his damaged tissue.
Ignore pseudo-science supplements promising to solve inflammation & prevent illness, and learn the truth about recalibrating your body’s defences for long-term health.
