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When Monty Python sang that ‘every sperm is sacred,’ in their classic hit of the same name from the movie The meaning of life, I hardly imagine that they were thinking about the influence of sperm on biochemistry. However, as Anton von Leeuwenhoek, the father of microscopy, gazed upon his own sperm for the first time in the late 1600s, he was probably thinking that his sperm were great, and had definitely not gone to waste. You see, von Leeuwenhoek discovered the wonderful entities we call sperm, and in his investigations also saw a substance that had crystallised in his samples, which he reported to the Royal Society in 1678. Several other scientists discovered the same crystal independently over the next 200 years, but none saw interest or importance in it until later. That crystalline compound came to be called spermine by dint of its origin, but it wasn’t until the 1920’s that spermine’s chemical structure was revealed, along with that of another related molecule that was named spermidine.
On the other hand, when researchers have supplemented various organisms, from yeast to mice to humans, with polyamines, the levels of polyamines in those organisms increase, cellular activity increases, and mortality decreases. In fact, a study published in 2016 in Nature Medicine made three interesting conclusions: first, spermidine given to mice as a dietary supplement increased their lifespans and seemed to benefit their cardiovascular systems; second, in rats bred for hypertension, spermidine improved their blood pressure; and, third, humans who reported eating diets rich in spermidine-containing foods, like mushrooms, soybeans, and cheddar cheese, were more likely to have lower blood pressure and risk of cardiovascular disease.
How these potentially anti-aging results are achieved is also still in question, but in addition to oxidation defense and upregulation of cell metabolism, it appears that autophagy plays a major role. Autophagy is an essential cellular process by which cells take out the trash, so to speak. If cells aren’t able to remove malformed proteins or damaged organelles, it interferes with their functioning. When the genes for autophagy in cells are disabled, the longevity enhancing effects of spermidine go away, which reinforces its role in this important pathway.
Published on Oct 1, 2016 Dr. Rhonda Patrick speaks with Dr. Valter Longo, a professor of gerontology and biological sciences and director of the longevity institute at the University of Southern California. Dr. Longo has made huge contributions to the field of aging, including the role of fasting and diet in longevity and healthspan in humans as well as metabolic fasting therapies for the treatment of human diseases. In this conversation, Rhonda and Valter discuss... • The effects of prolonged fasting, which refers to 2-3 day fasting intervals in mice and 4-5 days in humans. • Dr. Longo’s work on the fasting-mimicking diet, which is 5 day restricted diet that is meant to simulate some of the biological effects of prolonged fasting while still allowing some food. • How clinical trials have demonstrated efficacy for this diet for type 2 diabetes, multiple sclerosis, and cancer patients. • Fasting as an inducer of differential stress resistance, where it can simultaneously make cancer cells more sensitive to death while also making healthy cells more resistant to these same death stimuli (such as chemotherapy) which might otherwise induce cell death amongst healthy cells as collateral damage. • Fasting as a biological state which humans historically experienced with extreme regularity and we may ultimately need in order to mitigate various disease states. • The effects of prolonged fasting on the immune system, namely, how it clears away damaged white blood cells via autophagy and how this causes hematopoietic stem cells to self renew and make more stem cells and also produce new blood cells to fully replenish the white blood cell population. • How prolonged fasting causes a shift in the immune cell population towards one that is more representative of youth by normalizing the ratio of myeloid cells to lymphoid cells. • The positive effects of prolonged fasting and the fasting-mimicking diet on markers of systemic inflammation, blood glucose levels and other aging biomarkers. • The conclusions of Dr. Longo & Dr. Marcus Bock’s research comparing 1 week of the fasting-mimicking diet followed by 6 months of mediterranean diet to six months of a ketogenic diet in people with multiple sclerosis. • The strange, somewhat paradoxical role of autophagy genes in cancer progression and some of the open questions surrounding the exact role that these genes are playing. • Dr. Longo’s high level thoughts on metformin as an anti-aging drug. • How the growth hormone/IGF-1 axis is one of the most important genetic pathways in aging from yeast to worms to mice to humans.
..humans who reported eating diets rich in spermidine-containing foods, like mushrooms, soybeans, and cheddar cheese, were more likely to have lower blood pressure and risk of cardiovascular disease.
A study jointly led by Drs. Salwa Sebti and Álvaro Fernández, postdoctoral researchers in the Center for Autophagy Research, found that mice with persistently increased levels of autophagy—the process a cell uses to dispose of unwanted or toxic substances that can harm cellular health—live longer and are healthier. The study, published online today, is found in Nature. "Specifically, they have about a 10 percent extension in lifespan and are less likely to develop age-related spontaneous cancers and age-related pathological changes in the heart and the kidney," said Dr. Beth Levine, Director of the Center for Autophagy Research at UT Southwestern.
Autophagy is a phylogenetically conserved mechanism that controls the degradation of subcellular constituents, including misfolded proteins, and damaged organelles. The progression of many neurodegenerative diseases is thought to be driven by the aggregation of misfolded proteins; therefore, autophagic activity is thought to affect disease severity to some extent. In some neurodegenerative diseases, the suppression of autophagic activity accelerates disease progression. Given that the induction of autophagy can potentially mitigate disease severity, various autophagy-inducing compounds have been developed and their efficacy has been evaluated in several rodent models of neurodegenerative diseases.