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LEONARD HAYFLICK "and his associates have vehemently condemned "anti-aging medicine" and criticized organizations such as the American Academy of Anti-Aging Medicine. Hayflick has written numerous articles criticizing both the feasibility and desirability of human life extension, which have provoked responses critical of his views.” https://lnkd.in/egWqSRn View in LinkedIn

THE HAYFLICK LIMIT. "Dr. Hayflick noticed that cells grown in cultures reproduce by dividing. They produce facsimiles of themselves (by a process known as mitosis) a finite number of times before the process stops for good and the cell dies. In addition, cells frozen during their lifetimes and later returned to an active state had a kind of cellular memory: The frozen cells picked up right where they left off. In other words, interrupting the cells' life span did nothing to lengthen it.” https://lnkd.in/eXXDjuG View in LinkedIn

PROFESSOR LEONARD HAYFLICK has probably done more for the biology of aging than anybody else. Excerpts from some of his papers will be quoted extensively in the coming sections. He is a contrarian with strong views. http://protein.bio.msu.ru/biokhimiya/contents/v62/full/62111380.html View in LinkedIn

TELOMERE HYPOTHESIS. "A current hypothesis gaining prominence proposes that activation of the enzyme telomerase is necessary for cells to become immortal, or capable of proliferating indefinitely. The theory suggests that almost all cancer cells must attain immortality for progression to malignant states and, hence, require activation of telomerase.” https://lnkd.in/efS2ct4 View in LinkedIn

DISPOSABLE SOMA. "It was considered as “a priori” assumption that bacteria have not separation between soma and germ-line, and therefore under the paradigm of disposable soma theory, that is the soma is the only biological entity that would undergo senescence (aging, the bacteria could not age." https://lnkd.in/d8UFqbd View in LinkedIn

AUTUMN LEAVES seem best to illustrate Weismann’s worn out cell idea; after the wear and tear of a season of respiration, photosynthesis, disease and battering by the elements, leaf defects are multiple and very hard to repair: it is easier to jettison the leaf and start over again than to repair multiple cellular defects. View in LinkedIn

AGING AND SPECIES. “A more parsimonious evolutionary explanation for the existence of aging therefore requires an explanation that is based on individual fitness and selection, not on group selection. This was understood in the 1940's and 1950's by three evolutionary biologists, J.B.S. Haldane, Peter B. Medawar and George C. Williams, who realized that aging does not evolve for the "good of the species". http://www.nature.com/scitable/knowledge/library/the-evolution-of-aging-23651151 View in LinkedIn

FINITE CELL DIVISION."Death takes place because a worn-out tissue cannot forever renew itself, and because a capacity for increase by means of cell division is not everlasting but finite." (Weismann, 1881). http://protein.bio.msu.ru/biokhimiya/contents/v62/full/62111380.html View in LinkedIn

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