Category: Uncategorized

THE PARADOX. “But this explanation turns out to be wrong. Since the cost of death to individuals likely exceeds the benefit to the group or species, and because long-lived individuals leave more offspring than short-lived individuals (given equivalent reproductive output), selection would not favor such a death mechanism.” http://www.nature.com/scitable/knowledge/library/the-evolution-of-aging-23651151 View in LinkedIn

GROWTH HORMONE MUTANTS. “Multiple other growth hormone signaling-deficient mouse mutants exhibiting longevity have since been reported.” http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0072255 View in LinkedIn

CLEARING THE WAY. “The famous 19th century German biologist, August Weissmann, for instance, suggested – similar to Lucretius – that selection might favor the evolution of a death mechanism that ensures species survival by making space for more youthful, reproductively prolific individuals.” http://www.nature.com/scitable/knowledge/library/the-evolution-of-aging-23651151 View in LinkedIn

LONGEVITY GENE. “The hypopituitary Ames Dwarf Mouse was the seminal example of single-gene regulation of mammalian longevity. The mice homozygous for a hypomorphic df mutation in the Prophet of Pit1, paired-like homeodomain transcription factor (PROP paired-like homeobox 1) (Prop1) gene have deficient development of the anterior portion of the pituitary gland. Consequently, they are deficient in the production of growth hormone, thyroid stimulating hormone, and prolactin.” http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0072255 View in LinkedIn

2,000 YEAR OLD VIEW. “The Roman poet and philosopher Lucretius, for example, argued in his De Rerum Natura (On the Nature of Things) that aging and death are beneficial because they make room for the next generation, a view that persisted among biologists well into the 20th century.” http://www.nature.com/scitable/knowledge/library/the-evolution-of-aging-23651151 View in LinkedIn

MOUSE MODEL. “Ames dwarf (Prop1df/df) mice are remarkably long-lived and exhibit many characteristics of delayed aging and extended healthspan. Caloric restriction has similar effects on healthspan and lifespan, and causes an extension of longevity in Ames dwarf mice.” http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0072255 View in LinkedIn

THE QUESTION. “Why do we age and die? This poses an evolutionary paradox: natural selection designs organisms for optimal survival and reproductive success (Darwinian fitness), so why does evolution not prevent aging in the first place?” https://lnkd.in/ew9MzD3 View in LinkedIn

CAUSE OF AGING. “It is possible that the etiology of all age-associated diseases is in the molecular state that exists in old cells or cells near the end of their lineage. I’ve been vocal about this for 40 years. And as a consequence of that you don’t make too many friends. But I am more interested in the truth than making friends.” (Hayflick). https://lnkd.in/dQMB4k7 View in LinkedIn

HOW AND WHY WE AGE, Leonard Hayflick, forever the contrarian. "Hearts do not naturally get weaker with age; Regular exercise and a low-fat diet won't slow aging; Curing cancer would only add two years to the average sixty-five-year-old American life. Curing heart disease, however would add fourteen years; Only five percent of people over the age of sixty-five are in nursing homes; No human has lived--or probably can live--past 120 years." https://lnkd.in/eKPhKvH View in LinkedIn

PREDICTION. “It is possible that the etiology of all age-associated diseases is in the molecular state that exists in old cells.” (Hayflick). http://science.howstuffworks.com/life/genetic/hayflick-limit.htm View in LinkedIn