– and Why We Don’t Have To — A conversation with David Sinclair.
David Andrew Sinclair AO is an Australian biologist who is a professor of genetics and co-Director of the Paul F. Glenn Center for the Biology of Aging at Harvard Medical School.
The Italian version is “Longevità”, here: https://www.verduci.it/prodotto/longevita/
https://media.blubrry.com/drjohnday/p/drjohnday.com/podcasts/Podcast217.mp3 Podcast: Play in new window | DownloadSubscribe: Apple Podcasts | Android | RSS6 Foods to Reverse Aging with Lithium Could a microscopic dose of the psychoactive drug lithium, which occurs naturally in mineral water and certain foods, actually be the secret to less heart disease, better moods, and a longer life? In this article, I share how eating six foods may reverse aging with lithium.
“In our current study we were able to uncover important limitations for the use of metformin as longevity medicine,” says Dr. Ermolaeva. In contrast to the positive longevity effects in young organisms that received metformin, lifespan is shortened through metformin intake at an older age. “Previous studies that provided evidence of an extended longevity by metformin usually examined animals treated with metformin from young adult or middle age until the end of life. In contrast, we have looked at treatment windows covering the entire life span, or restricted to early life or to late life”. The study also utilized a human cell culture model of replicative aging to assess human responses to metformin at a cellular level and compare them to organismal responses of the worms.
**Metformin longevity benefits are reversed with age**
The research team led by Dr. Ermolaeva found that the very same metformin treatment that prolonged life when C. elegans worms were treated at young age, was highly toxic when animals of old age were treated. Up to 80% of the population treated at old age were killed by metformin within the first 24 hours of treatment. Consistently, human primary cells demonstrated a progressive decrease in metformin tolerance as they approached replicative senescence. The researchers were able to link this detrimental phenotype to the reduced ability of old cells and old nematodes to adapt to metabolic stressors like metformin. Under these circumstances, the exact same dose of the drug that increased longevity of young-treated organisms by triggering adaptive stress responses was harmful in animals treated at old age, which were unable to activate such protective signals.
Metformin is a common type 2 diabetes drug. Recently, it was found to extend life span of young non-diabetic animals but the responses of older organisms to metformin remain unexplored. Researchers at the Leibniz Institute on Aging—Fritz Lipmann Institute (FLI) in Jena, Germany, and the Friedrich Schiller University Jena found that mitochondrial dysfunction abrogates metformin benefits in aged C. elegans and late passage human cells. Moreover, the same metformin regime that prolongs the lifespan of young nematodes was toxic in old animals by inducing deleterious metabolic changes. These findings suggest that aging sets a limit for the health span benefits of metformin outside of diabetes.
While people today are getting older and older, diseases that are associated with age (e.g. cardiovascular diseases, cancer, dementia and diabetes) are also increasing. Reaching late life while staying healthy is of high priority. Recently, the drug metformin, which has been used for decades to treat patients suffering from type 2 diabetes, was linked to the reduced risk of cancer development and showed potential to alleviate cardiovascular diseases in humans. Furthermore, a life-prolonging effect of metformin has recently been shown in mice, flies and worms. So, does this make metformin the new miracle drug to prolong life and even delay aging-associated diseases?
The first clinical testing of a potential life-prolonging effect of metformin in aged humans without diabetes has been initiated by the American Federation for Aging Research (AFAR). However, the long-term effects of metformin in a non-diabetic cohort at different age have not been investigated yet. Researchers at the Leibniz Institute on Aging—Fritz Lipmann Institute (FLI) in Jena, and their colleagues from the Friedrich Schiller University Jena (FSU), Germany, have now addressed these questions. They used the nematode C. elegans and human primary cells to investigate the metabolic response of young and old non-diabetic organisms to metformin treatment in detail. The current study has now been published in the journal Nature Metabolism.
Aging link
~~~ “The telomere biology of humans is closer to the telomere biology of birds than those of traditional laboratory models. In both humans and birds, telomere length is measured in a minimally-invasive way from small blood samples,” says Collegium Researcher Antoine Stier from the University of Turku (Finland), the main author of the research article.
While authors of the study had reasons to expect shorter telomeres in chicks born from eggs injected with thyroid hormones, they were quite surprised to find that those chicks actually exhibited longer telomeres right after birth.” “Based on the natural decline of telomere length observed with age in the same collared flycatcher population, we estimated that chicks hatching from thyroid hormones injected eggs were approximately four years younger at birth than chicks hatched from control eggs,” adds Collegium Researcher Suvi Ruuskanen.
Although the molecular mechanisms underlying such effects remain to be discovered, the new findings suggest that prenatal thyroid hormones might have a role in setting the ‘biological age’ at birth.
The environment provided by the mother during embryo development has major consequences on later-life health and lifespan. This can arise through effects on cellular aging which is often estimated with the length of telomeres. Telomeres are the protective end caps of chromosomes and their length is a marker of biological age.
While telomeres normally shorten with age, short telomeres at a given age predict higher disease and mortality risks. Prenatal exposure to maternal stress hormones as well as instability during embryo development have previously been found to result in short telomeres, i.e. accelerated cellular aging.
Here’s my latest video, “Longevity Genes: APOE”!
A reduced mortality risk and an increased lifespan has been reported for people who have APOE2 alleles, when compared with APOE3 or APOE4, but beyond associations, data for lifespan in APOE-expressing mice was recently reported, evidence that supports a causative role for APOE on longevity.
Summary: YTHDF2 is a key protein that assists in creating healthy blood cells by regulating the body’s inflammatory response.
Source: University of Edinburgh
The study is the first to reveal a protein that has a crucial role in protecting the blood’s stem cells, which continually produce all blood and immune cells needed in the body, from premature aging.
A genetic disposition that plays a role in the development of the heart in the embryo also appears to play a key role in the human immune system. This is shown by a recent study led by the University of Bonn (Germany). When the gene is not active enough, the immune defense system undergoes characteristic changes, causing it to lose its effectiveness. Doctors speak of an aging immune system, as a similar effect can often be observed in older people. In the medium term, the results may contribute to reduce these age-related losses. The study is published in the journal Nature Immunology.
The gene with the cryptic abbreviation CRELD1 has so far been a mystery to science. It was known to play an important role in the development of the heart in the embryo. However, CRELD1 remains active after birth: Studies show that it is regularly produced in practically all cells of the body. For what purpose, however, was previously completely unknown.
The Bonn researchers used a novel approach to answer this question. Nowadays, scientific studies with human participants often include so-called transcriptome analyses. By these means, one can determine which genes are active to what extent in the respective test subjects. Researchers are also increasingly making the data they obtain available to colleagues, who can then use it to work on completely different matters. “And this is exactly what we did in our study,” says Dr. Anna Aschenbrenner from the LIMES Institute at the University of Bonn and member of the ImmunoSensation² Cluster of Excellence.
Host Mark Sackler and panelists discuss the challenges of getting governments and the public on board with one of the basic principles of longevity research: that the cause of all chronic diseases of aging is aging itself.
Peter and Dan continue their conversation about the Abundance Platinum Longevity trip, where Peter and a select group of entrepreneurs, executives and investors spent five days learning from the top longevity and immunology experts in two of California’s top biotech hubs.
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At high concentrations, reactive oxygen species—known as oxidants—are harmful to cells in all organisms and have been linked to aging. But a study from Chalmers University of Technology, Sweden, has now shown that low levels of the oxidant hydrogen peroxide can stimulate an enzyme that helps slow down the aging of yeast cells.
One benefit of antioxidants, such as vitamins C and E, is that they neutralize reactive oxygen species —known as oxidants—which may otherwise react with important molecules in the body and destroy their biological functions. Larger amounts of oxidants can cause serious damage to DNA, cell membranes and proteins for example. Our cells have therefore developed powerful defense mechanisms to get rid of these oxidants, which are formed in our normal metabolism.
It was previously believed that oxidants were only harmful, but recently, scientists have begun to understand that they also have positive functions. Now, the new research from Chalmers University of Technology shows that the well-known oxidant hydrogen peroxide can actually slow down the aging of yeast cells. Hydrogen peroxide is a chemical used for hair and tooth whitening, among other things. It is also one of the metabolically produced oxidants that is harmful at higher concentrations.