The Long and the Short of It: The Science of Life Span and Aging
by Jonathan Slivertown. It takes a while to develop good instinct to select new science books. I have wasted enough time reading my quota of pop science books over the years but Slivertown book is a well written and packed with latest research. I learned a lot in the past few days on why I am wired to kick the bucket and I hope, we reduce the sufferings in future but never conquer death.
By comparison, an organism carrying a gene for later maturity and longer life will plod slowly toward posterity and fast become history. It is just arithmetic. Imagine two banks that pay you compound interest on your savings. Which will earn you more, one that pays 5 percent a month or one that pays 5 percent a year? Monthly compound interest at 5 percent will turn $ 100 into nearly $ 180 in a year, a return forty times better than the $ 5 you will get from the tardy bank. That’s exactly the kind of advantage that short life and early reproduction confers on organisms. And by the way, if you find a bank paying even 2 percent a month, be sure to let me know. The puzzle of longevity, then, is not why we die so soon, but rather why we live so long.
On Senescence:
by Jonathan Slivertown. It takes a while to develop good instinct to select new science books. I have wasted enough time reading my quota of pop science books over the years but Slivertown book is a well written and packed with latest research. I learned a lot in the past few days on why I am wired to kick the bucket and I hope, we reduce the sufferings in future but never conquer death.By comparison, an organism carrying a gene for later maturity and longer life will plod slowly toward posterity and fast become history. It is just arithmetic. Imagine two banks that pay you compound interest on your savings. Which will earn you more, one that pays 5 percent a month or one that pays 5 percent a year? Monthly compound interest at 5 percent will turn $ 100 into nearly $ 180 in a year, a return forty times better than the $ 5 you will get from the tardy bank. That’s exactly the kind of advantage that short life and early reproduction confers on organisms. And by the way, if you find a bank paying even 2 percent a month, be sure to let me know. The puzzle of longevity, then, is not why we die so soon, but rather why we live so long.
On Senescence:
Although in the richest countries life expectancy has approximately doubled over the last 200 years, the mortality rate doubling time has not declined. The explanation for this paradox is that senescence has not been reduced; it has just been postponed to later life. 32 We have no idea what further gains in life expectancy may be made in the future, but we can say that such gains are unlikely to be made at the expense of senescence. Senescence does come to a stop in extreme old age, but by then the annual mortality rate is so high that this buys very little extra time. The grinding to a halt of senescence in the very old is probably caused by death winnowing out the frailest, leaving behind those who have enjoyed more robust health than average throughout their lives.
In summary, Medawar’s idea is that the ability of natural selection to alter the genetic future diminishes with the age of individuals and that this, by default, permits mutations that cause senescence to accumulate over evolutionary time. One might say that natural selection retires in old age. Peter Medawar went a step further with his argument, pointing out that some mutations that have beneficial effects on health and reproduction during youth might also have deleterious effects in old age. Such double-acting mutations would accelerate the evolution of senescence because they would actually be favored by natural selection and not just passively accumulate. Double-acting genes that have reproductive benefits in youth but health penalties in old age can be compared to a children’s seesaw, with life span represented by a plank that connects youth and old age. Raising one end of the seesaw results in lowering the other. Natural selection elevates youth, but it is indifferent to the plunge in old age that results at the other end of the plank.
Plants & Cancer:
One reason plants are spared fatal cancers must be that plant cells are immobilized by a boxlike cell wall that prevents them spreading around the plant body in the way that animal cells are able to do. The phenomenon of metastasis that kills so many cancer patients cannot occur in plants. It has also been suggested that the division of a cell is more tightly controlled by the influence of neighboring cells in plants than in animals, which makes it much harder for a single mutant plant cell to multiply out of control.
Long-lived trees also defend themselves with chemicals. The fragrant resin produced by conifers, for example, is an important part of their armory, flooding wounds with antiseptic when the trees are damaged. The dried heartwood of a ponderosa pine can contain as much as 86 percent resin by weight. 26 Oil extracted from eastern red cedar wood is an effective termite and moth deterrent. Chests lined with the wood were traditionally used in New England to store and protect winter clothes from attack by moths during the summer months.
Telomeres:
The DNA molecules in a human cell are extremely thin and long. Stretched out in a line, the DNA in a single cell would be between six and nine feet long. 21 Packing such molecules into a tiny cell is a feat of natural nanoengineering to be marveled at. The packages of hyper-coiled DNA in cells are called chromosomes, and each human cell has 23 pairs of these. The process that copies the DNA in a chromosome has a problem when it gets to the end of the molecule, where it tends to stop short, leaving loose ends like the unraveling sleeves of an old sweater. This problem was fixed very early in the evolution of the eukaryotes by the placement of a cap, called a telomere, at either end of each chromosome. Elizabeth Blackburn and her collaborators, working at Yale and later at the University of California, Berkeley, discovered the structure of telomeres, which turned out to be made of a repeating DNA sequence of six bases. The telomeres do not keep a chromosome from getting shorter at the ends each time it is replicated, but they prevent the genes in the chromosome from being clipped by taking the hit for them. Each time a cell divides, the telomeres on the chromosomes of its daughter cells get shorter. Of course the telomeres eventually get clipped to a nub, and at that point the cells lose the ability to divide and enter a state called replicative senescence.
The association of telomere length with survival may be direct, indirect, or both. For example, short telomeres could have a direct effect on susceptibility to infection if they handicap the rate at which new white blood cells, whose job it is to fight infection, are generated by cell division. Telomere length might equally well be an indirect marker of other aging processes such as oxidative stress. Telomere replication is known to be more sensitive to oxidative stress than replication of other parts of the chromosome, and this sensitivity may cause telomeres to shorten.
In summary, Medawar’s idea is that the ability of natural selection to alter the genetic future diminishes with the age of individuals and that this, by default, permits mutations that cause senescence to accumulate over evolutionary time. One might say that natural selection retires in old age. Peter Medawar went a step further with his argument, pointing out that some mutations that have beneficial effects on health and reproduction during youth might also have deleterious effects in old age. Such double-acting mutations would accelerate the evolution of senescence because they would actually be favored by natural selection and not just passively accumulate. Double-acting genes that have reproductive benefits in youth but health penalties in old age can be compared to a children’s seesaw, with life span represented by a plank that connects youth and old age. Raising one end of the seesaw results in lowering the other. Natural selection elevates youth, but it is indifferent to the plunge in old age that results at the other end of the plank.
Plants & Cancer:
One reason plants are spared fatal cancers must be that plant cells are immobilized by a boxlike cell wall that prevents them spreading around the plant body in the way that animal cells are able to do. The phenomenon of metastasis that kills so many cancer patients cannot occur in plants. It has also been suggested that the division of a cell is more tightly controlled by the influence of neighboring cells in plants than in animals, which makes it much harder for a single mutant plant cell to multiply out of control.
Long-lived trees also defend themselves with chemicals. The fragrant resin produced by conifers, for example, is an important part of their armory, flooding wounds with antiseptic when the trees are damaged. The dried heartwood of a ponderosa pine can contain as much as 86 percent resin by weight. 26 Oil extracted from eastern red cedar wood is an effective termite and moth deterrent. Chests lined with the wood were traditionally used in New England to store and protect winter clothes from attack by moths during the summer months.
Telomeres:
The DNA molecules in a human cell are extremely thin and long. Stretched out in a line, the DNA in a single cell would be between six and nine feet long. 21 Packing such molecules into a tiny cell is a feat of natural nanoengineering to be marveled at. The packages of hyper-coiled DNA in cells are called chromosomes, and each human cell has 23 pairs of these. The process that copies the DNA in a chromosome has a problem when it gets to the end of the molecule, where it tends to stop short, leaving loose ends like the unraveling sleeves of an old sweater. This problem was fixed very early in the evolution of the eukaryotes by the placement of a cap, called a telomere, at either end of each chromosome. Elizabeth Blackburn and her collaborators, working at Yale and later at the University of California, Berkeley, discovered the structure of telomeres, which turned out to be made of a repeating DNA sequence of six bases. The telomeres do not keep a chromosome from getting shorter at the ends each time it is replicated, but they prevent the genes in the chromosome from being clipped by taking the hit for them. Each time a cell divides, the telomeres on the chromosomes of its daughter cells get shorter. Of course the telomeres eventually get clipped to a nub, and at that point the cells lose the ability to divide and enter a state called replicative senescence.
The association of telomere length with survival may be direct, indirect, or both. For example, short telomeres could have a direct effect on susceptibility to infection if they handicap the rate at which new white blood cells, whose job it is to fight infection, are generated by cell division. Telomere length might equally well be an indirect marker of other aging processes such as oxidative stress. Telomere replication is known to be more sensitive to oxidative stress than replication of other parts of the chromosome, and this sensitivity may cause telomeres to shorten.
No comments:
Post a Comment