Life Ascending
Evolution has no foresight, and does not plan for the future. There is no inventor, no intelligent design. Nonetheless, natural selection subjects all traits to the most exacting tests, and the best designs win out. It is a natural laboratory that belittles the human theatre, scrutinizing trillions of tiny differences simultaneously, each and every generation. (p. 2)
Comments: While evolution has no insight, actions with low fixed costs are often tried out first. There is a pattern here. Tradeoff is often a better description than optimality.
Thermodynamics is one of those words best avoided in a book with any pretence to be popular, but it’s more engaging if seen for what it is: the science of ‘desire’. The existence of atoms and molecules is dominated by ‘attractions’, ‘repulsions’, ‘wants’ and ‘discharges’, to the point that it becomes virtually impossible to write about chemistry without giving it to some sort of randy anthropomorphism. Molecules ‘want’ to lose or gain electrons; attract opposite charges; repulse similar charges; or cohabit with molecules with similar character. A chemical reaction happens spontaneously if all the molecular partners desire to participate; or they can be pressed to react unwillingly through greater force. And of course some molecules really want to react but find it hard to overcome their innate shyness. A little gentle flirtation might prompt a massive release of lust, a discharge of pure energy. … My point is that thermodynamics makes the world go round. If two molecules don’t want to react together, then they won’t be easily persuaded; if they do want to react they will, even if it takes some time to overcome their shyness. Our lives are driven by wants of this kind. (P. 13)
Comments: Try to put the above paragraph to the behavioral paper.
A … disadvantage is that RNA id poor at storing information in comparison with DNA. It is chemically less stable, which is to say it is more reactive than DNA. That, after all, is how RNA catalyses biochemical reactions. But this reactivity means that large RNA genomes are unstable and break down, which imposes a maximum size limit well below that needed for independent existence. A retrovirus is, in fact, already nearly as complex as an RNA-encoded entity can be. (p. 57)
Comment: Put the above to Origin and Evolution of Life.
What photosynthesis achieves --- and what we have so far failed to achieve --- is to come up with a catalyst that can strip the hydrogen from water with a minimal input of energy … So far, all our human ingenuity ends up consuming more energy in splitting water than is gained by the split. (p. 67)
Comment: Put to The Economy of Nature and the Economy of Human Society.
It’s a bit of embarrassment, frankly, that we still don’t know why the maximaland resting metabolic rate tend to be linked in modern mammals, reptiles and birds, or if the link can be in some animals. Certainly, very athletic animals, like the pronghorn antelope, have very high aerobic capacities, around sixty-five times higher than their resting metabolic rates, implying that the two can be disconnected. The same applies to a few reptiles. The American alligator, for example, has an aerobic capacity at least forty times higher than its resting rate. (p. 213)
Comments: The level of output is determined by the level of non-equilibrium. The maintenance of non-equilibrium state takes energy. The further away from equilibrium,, the more energy required. Why the correlation is not absolute? There are other possible tradeoffs. For example, the speed of switching from the resting state to active state may be different. The slower the switching, the less energy is required to maintain the resting state.
There’s the rub. Since the hypothesis was proposed, nearly thirty years ago, there have been many attempts to verify it experimentally, with mixed success. There is indeed a general tendency for resting and maximal metabolic rates to be linked, but little more than that, and there are many exceptions to the rule. It may well be that the two were linked in evolution, even if such a link is not strictly necessary in physiological terms. Without a more specific idea of evolutionary history, it’s hard to say for sure. But as it happens, this time the fissile record might hold the key. It may be that the missing link lies not in physiology, but in the vicissitudes of history. (p. 215)
Comments: I believe it is due to physiology. Read on and see what he says.
True multicellular life can only be achieved by cells ‘prepared’ to subsume themselves entirely to the cause. Their commitment must be policed, and any attempted reversions to independence are punished by death. Nothing else works. Just think about the devastation caused by cancer, even today, after a billion years of multicellular living, to appreciate the impossibility of multicellular life when cells do their own thing. Only death makes multicellular life possible. (p. 267)
Comments: This is very important in discussing institutions. Even individuals have to coordinate the internal complex structures.
Cell death plays an important role in the aging and death of multicellular organisms, and yet there is no law stipulating that all bodily cells should die, or that other equally disposable cells, should not replace them. Some animlas, such as the freshwater anemone Hydra, are essentially immortal --- cell die and are replaced, but the organisms as a whole shows no sign of aging. (p. 268)
Comments: Anemones are sedentary. So the metabolic rates are low. When metabolic rates are low enough, life can become potentially immortal? Think how we may model it. Maybe a smaller sigma. Do some calculation and see what happens.
Comments: This economic way of understanding can be extended systematically into the foundation of understanding biology. Nothing is biology makes sense except in the light of economy.
The point is that it is possible, with finesse, to disentangle sex from longevity, to activate genes responsible for longevity without dismembering sexuality. (p. 276)
Comments: I believe there must be some other trade-offs involved that are not discovered yet.
First and foremost is the fact that lifespan varies with free-radical leak in virtually all species. The faster the leak of the leak of the free radicals, the shorter the lifespan. By and large, the rate that free radicals leak depends on the metabolic rate, which is to say, the rate at which cells consume oxygen. Small animals have fast metabolic rates, their cells guzzling up oxygen as fast as they can, their hearts fluttering at hundreds of beats a minute even when at rest. With such fast respiration, free-radical leak is high, and lifespan is fleeting. Larger animals, in contrast, have a slower metabolic rate, manifesting as a ponderous heart beat and a trickling free-radical leak. They live longer.
The exceptions here really do prove the rule. Many birds, for example, live far longer than they ‘ought to’ on the basis of their metabolic rate. A pigeon, for example, lives for around thirty-five years, a remarkable ten times longer than a rat, despite the fact that pigeons and rats are of similar size, and have a similar metabolic rate. … Gustavo Barja … showed that these differences could be accounted for largely in terms of free-radical leak. In relation to their oxygen consumption, birds leaks nearly ten times fewer free radicals than equivalent mammals. Much the same is true of bats, which also live disproportional long lives. And like birds, bat mitochondria leak far fewer free radicals. Why this should be so is not certain; in earlier books, I have argued that the reason relates to the power of flight. But whatever the reason may be, the unassailable fact is that low free-radical leak equates to long life, whatever the metabolic rate. (p. 280)
Comments: I believe the key is to understand the detailed relation between the rate of free-radical leak and metabolic rate. I suspect the density of mitochondria is higher in flight animals. The flight animals spend more fixed cost to produce mitochondria but are more gentle in using them, which means they work less laboriously and leak less free-radicals while working.
From this perspective, we can see why calorie restriction protects against age-related disease, as well as aging, at least if started early enough in life (before the mitochondria wear out: middle age is fine). By lowering free-radical leak, bolstering mitochondria membranes against damage, and boosting the number of mitochondria, calorie restriction effectively ‘reset’ the clock of life to ‘youth’. In so doing, it switches off hundreds of inflammatory genes, returning genes to their youthful chemical environment, while fortifying cells against programmed death. The combination suppresses both cancer and degenerative disease and slows the rate of aging. It’s likely that, in practice, various other factors are involved (such as the direct immunosuppressive effects of inhibiting TOR), but in principle most benefits of calorie restriction can be explained simply by a reduction in free-radical leak. (p. 282)
Comments: It could be explained by even simpler reasons. Eat less, your digestive system work less. Less wear out.
Page 282 also have long life genes of Japanese. Maybe they are related to low fertility as well. Quote them and comment.