As a general rule, 10% life extension in mice via metabolic alteration is uninteresting. It depends on the fine details, of course, but most age-slowing interventions so far discovered are in some way upregulating cellular stress response mechanisms, or adjusting growth hormone signaling. Neither of these approaches works anywhere near as well in long-lived mammals, such as our own species, as it does in short-lived mammals, such as mice, and in lower animal species. Short-lived species have life spans that are very plastic in response to environmental cues, such as the lack of nutrients that provoke greater stress response activity. Calorie restriction can extend life in mice by as much as 40%, but certainly doesn’t have that great an effect in humans. Growth hormone receptor
What is the best source of lutein, the primary carotenoid antioxidant in the brain?
Researchers here review the evidence for metabolites produced by the gut microbiome to influence the behavior of innate immune cells in the brain. The gut microbiome changes in composition with age, altering the production of metabolites and inflammatory signaling in ways that degrade tissue function throughout the body. Fixing the many resulting issues at the source by introducing a youthful mix of microbes to the aging gut is a tempting path forward, likely relatively straightforward to achieve via fecal microbiota transplantation from young individuals to old individuals. This short-cut would hopefully evade the onerous requirement to fully understand how exactly harms to the brain result from the aging of the gut microbiome, and thus improve late life health in the near term rather than requiring
The state of the gut microbiome is influential on health, perhaps as much as exercise. The balance of microbial populations shifts with age, reducing beneficial metabolite production, and increasing inflammation. Experiments in animals have shown that resetting those populations towards a more youthful configuration can improve health and extend life. Producing of a greater understanding of how exactly microbial populations produce changes in health is a work in progress, and today’s research is an example of one approach, correlating microbial populations with blood metabolites. Many such metabolites have known associations with aspects of health and aging, which will hopefully guide future research to more effective approaches to intervention. Human gut microbiota produce a variety of molecules, some of which enter the bloodstream and impact health.
The work of George Church combines a broad knowledge of science with an ambitious imagination. Our world needs visionaries, and Church is one of a kind. His Harvard laboratory is at the cutting edge of several key areas of biochemistry. … Continue reading →
There is some debate over whether persistent viral infection, such as by herpesvirus, contributes meaningfully to the onset and development of Alzheimer’s disease. It would be a convenient explanation, given that many people with all of the lifestyle risk factors for neurodegeneration, such as being overweight and sedentary, do not in fact go on to develop Alzheimer’s. The epidemiology is mixed, however, with some studies suggesting yes, some no. Some of the positive data suggests that use of antiviral drugs lowers the risk of Alzheimer’s. More recent work argues that multiple different viral infections are required for a significant effect on Alzheimer’s risk, which might explain why earlier epidemiology has produced conflicting results. Meanwhile, researchers continue to explore the cellular biochemistry that might cause viral
Age-related frailty is a late stage manifestation of degenerative aging, a state of physical weakness and vulnerability that precedes death. Aging is the accumulation of damage and dysfunction, and the burden of such damage and dysfunction needed to produce frailty is one step removed from the amount needed to cause one of the many forms of fatal system failure that cause human mortality. Whether death is eventually due to cardiovascular disease, dementia, or kidney failure, frailty is a proximate indicator. In this long-term population-based prospective cohort comprising 9,912 participants, we evaluated the risk of mortality according to longitudinal repeated measurements of Frailty Index (FI). Both levels of FI and the proportions of frail participants gradually increased with age and there was significant variability in the
In many species, aging of the female reproductive system occurs more rapidly than is the case for other parts of the body. This is one of a few biological systems subject to what appears to be premature aging, relative to other organs. Other examples include the thymus, which atrophies well before late life. Researcher here suggest that mitochondrial quality control, the process of mitophagy, is involved in the aging of oocytes to a great enough degree that upregulation of mitophagy may delay female reproductive aging. Women’s reproductive cessation is the earliest sign of human aging and is caused by decreasing oocyte quality. Similarly, C. elegans’ reproduction declines in mid-adulthood and is caused by oocyte quality decline. Aberrant mitochondrial morphology is a hallmark of age-related dysfunction,
Today’s open access paper underscores the point that prevention and treatment of atherosclerosis should be a high priority in medical research, development, and practice. It is the single largest cause of death in our species, killing a quarter of humanity directly, and arguably another tenth indirectly. Atherosclerosis is the malfunction of macrophage cells responsible for clearing excess and altered cholesterol from blood vessel walls. The result is the accumulation of fatty lesions, and a tipping point in which the contents of the lesion overwhelm the macrophage cells attempting to remove it, thereafter continually adding dead cells to the growing atheroma. Blood vessels are narrowed, weakened, and inflamed. The inevitable rupture produces a stroke or heart attack. Along the way, reduced blood flow contributes to numerous
How might we replicate the protective effects of fasting with food?