
The structural biologist, who has devoted his life to studying the processes behind aging, discusses the surprising things he has learned and the public misunderstandings about longevity.

The structural biologist, who has devoted his life to studying the processes behind aging, discusses the surprising things he has learned and the public misunderstandings about longevity.
In a recent interview with Wired, Nobel laureate Venkatraman Ramakrishnan discusses his book Why We Die, in which he argues that death is not genetically programmed but rather a consequence of evolution favoring reproduction over longevity. Here are some of the most thought-provoking excerpts:
WIRED: Professor Ramakrishnan, the crucial question in your book is why we die. But exactly what is death?
Venki Ramakrishnan: By death, we mean the irreversible loss of the ability to function as a coherent individual. It is the result of the failure of a critical system or apparatus, for example, heart, brain, lung, or kidney failure. In this sense there is an apparent paradox: When our organism, as a whole, is alive, millions of cells within us are constantly dying, and we do not even realize it. On the other hand, at the time of death, most of the cells in our bodies are still alive, and entire organs are still functioning and can be donated to people in need of transplantati
The longevity industry is no longer science fiction.
Inside Retro's Bid to Make Humans Live Ten Years Longer
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As you age you naturally lose neurons and muscle mass and experience a decline in fertility and wound healing ability. Previous research in animals has offered several potential techniques for turning back the biological clock in specific tissues, including exercise and calorie restriction. However,...
New COO Michael Ringel says company is confident as it prepares for clinical studies in glaucoma and NAION later this year.
Individual and additive effects of vitamin D, omega-3 and exercise on DNA methylation clocks of biological aging in older adults from the DO-HEALTH trial | Nature Aging
Abstract
While observational studies and small pilot trials suggest that vitamin D, omega-3 and exercise may slow biological aging, larger clinical trials testing these treatments individually or in combination are lacking. Here, we report the results of a post hoc analysis among 777 participants of the DO-HEALTH trial on the effect of vitamin D (2,000 IU per day) and/or omega-3 (1 g per day) and/or a home exercise program on four next-generation DNA methylation (DNAm) measures of biological aging (PhenoAge, GrimAge, GrimAge2 and DunedinPACE) over 3 years. Omega-3 alone slowed the DNAm clocks PhenoAge, GrimAge2 and DunedinPACE, and all three treatments had additive benefits on PhenoAge. Overall, from baseline to year 3, standardized effects ranged from 0.16 to 0.32 units (2.9–3.8 months). In summary, our trial indicates a small protective effect of omega-3 treatment on slowing biological aging over 3 years across several clocks, with an additive protective effect of omega-3, vi
The thymus is a small but vital internal organ. Thymocytes generated in the bone marrow migrate to the thymus where they mature into T cells of the adaptive immune system. One of the important contributions to the aging of the immune system is that the thymus steadily atrophies with advancing age, l...
The study seeks to determine whether rapamycin increases the lifespan of dogs, with the hope that it may also help extend human lives.
New epigenetic clock based on easy-to-collect cheek cells accurately predicts mortality.
Over the past decade, several epigenetic clocks have been developed to track physiological aging. Until recently, all had been based on the DNA methylome of blood cells – onerous and stressful to collect. But now, scientists from the US have shown for the first time that their new epigenetic c...
David Sinclair Supplements: A Deep Dive To His Supplement Regimen
Get the latest insights on David Sinclair's 2024 Supplement Protocol and discover why he's chosen NMN, Resveratrol, and more for optimal longevity.
Exploring the Latest Supplements, Vitamins, and Medications in Sinclair's Longevity Regimen
Do We Have to Die?
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Maybe, maybe not. More research is needed.
A metabolic atlas of blood cells in young and aged mice identifies uridine as a metabolite to rejuvenate aged hematopoietic stem cells - Nature Aging
Through metabolic screening, we identified uridine as a potential regulator to rejuvenate aged HSPCs.
Inhibition of IL-11 signalling extends mammalian healthspan and lifespan - Nature
Here we examined whether IL-11, a pro-inflammatory cytokine of the IL-6 family, has a negative effect on age-associated disease and lifespan.
Researchers publishing in Aging have found a molecule linking exercise to the inhibition of cellular senescence, one of the hallmarks of aging. Exercise against senescence […]
Researchers publishing in Aging have found a molecule linking exercise to the inhibition of cellular senescence, one of the hallmarks of aging.
Researchers have published a method of rescuing cells from damaged mitochondria and cellular senescence, potentially alleviating major aspects of aging. Bad mitochondria must be consumed A core part of autophagy involves selective autophagy receptors (SARs), which build […]
The researchers investigated whether NAD precusors, including nicotinamide and NR, along with the well-known compound rapamycin could rescue mitophagy, and they found positive results for all of these compounds.
TERT activation targets DNA methylation and multiple aging hallmarks
TAC promoted tissue rejuvenation, including new neuron formation, and alleviated multiple aging hallmarks in aged mice, revealing the regenerative potential of adult tissues through physiological TERT activation.
An analysis of oral microbes in older adults has indicated an association between microbial diversity and executive function performance [1]. […]
The authors elaborate on the potential mechanisms underlying the connection between oral microbial dysbiosis and cognitive function impairment.
Recent epigenome-wide studies have identified a large number of genomic regions that consistently exhibit changes in their methylation status with aging across diverse populations, but the functional consequences of these changes are largely unknown. On the other hand, transcriptomic changes are mor...