WHY WE BORN ON EARTH?
a) I don't know
b) Its was god's choice
c) none of the above
Answers
Answer:
b) it was God's choice
Explanation:
it was our fortune
c. none of the above
Myth 1: We die to make room for younger generations.
Genes are selfish, and each individual body is a vehicle for a collection of genes. These genes are selected to favor the survival of copies of themselves. Since parents and offspring use the same resources, the death of a parent creates room ecologically for just one offspring. Each gene in the parent has a 50% chance of appearing in this offspring. But it has a 100% chance of appearing in the parent, because it’s already there. It’s never, then, in the evolutionary interests of a parent to die so an offspring can replace it.
Myth 2: We die because our cells/DNA get damaged with age.
This is like saying bad drivers die because of blood loss. It’s a proximate mechanism of death, not the evolutionary cause of mortality. Our somatic cells (the cells that are part of our body) do indeed suffer occasional mutations as they divide. These mutations can kill or damage cells, which is annoying but not generally a big problem as we can make more. However, the worst mutations do something much more dangerous: they help cells to survive and proliferate. That’s how you get cancer. Because this risk accumulates over time, cells are normally allowed only a limited number of divisions before they undergo cellular senescence, that is, they die. But the genes that cause cellular senescence can also stop working. So that’s one of the ways in which we get old: our somatic cell lineages get older, damaged and mutated, and some become cancerous.
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However, the cell/DNA damage idea assumes that this isn’t something evolution can counteract and that’s clearly false. Lifespan and cancer rates differ between species, and not in the ways you would expect if they were determined by cell/DNA damage. For instance, once you take into account body size and phylogeny, DNA repair doesn’t correlate with lifespan. Lifespan does, however, correlate with ecology: mammal species who typically lead risky lives die younger (even if you protect them from those risks). At one extreme, in the harsh Australian bush we find the male agile antechinus, who dies of stress at the end of a single breeding season. At the other extreme, the naked mole rat can live for three decades in its peaceful underground colonies.
This gets even more puzzling when you start to look at genomics. We have a whole suite of genes devoted to keeping our genome pristine. My favorite is a clever gene called P53 that acts as a “gatekeeper” for cell division. If the cell has too many mutations, P53 will halt division and activate repair mechanisms. If that doesn’t fix things, it will make the cell commit suicide. Mutations that break P53 are involved in about half of all human cancers. Now, here’s the rub: there’s a whole family of genes related to P53 in other mammals, and some work better than others. Naked mole rats, as it happens, have two particularly awesome versions that completely protect them against cancer.
We also know that it’s perfectly feasible for genetic modification to immortalize cell lineages, and that going through a haploid stage is not essential for maintaining cell viability. How do we know this? From the strange case of the 11,000 year old dog. The dog as an individual is long dead, but her cells survive today as an infectious cancer on other dogs’ genitalia. There’s also a quaking aspen in Utah whose roots are at least 80,000 years old.
The same applies to permanent organ damage. Some organs heal and regenerate, some don’t. Some species can regenerate organs that others can’t. A salamander can grow a whole new leg. There’s even a jellyfish that can reverse its development when it’s damaged. All in all, natural selection is clearly capable of creating creatures who can fix cellular and DNA damage and repair damaged organs.
So: evolution can fix these problems for us, and it doesn’t. What the heck, evolution, aren’t we friends?
Well, no, actually, evolution is not our friend. If anything, it’s our genes’ friend and there’s a very good reason our genes don’t actually care about us.
Mutations are a problem evolution can fix. But death isn’t. Accidents happen. Diseases happen. Sabre-toothed cats happen (well, not any more, but you get the point). No matter how hard our genes try to help us survive, sometimes they’re going to fail. These failures are often, as far as your genes are concerned, random. That means our genes can’t afford to get too invested in the survival of any individual. In the long term, the only way a gene can survive is to spread — to copy itself through a population.
So from a gene’s-eye view, every investment in your survival is a potential trade-off with the creation and survival of your potential descendants. And, rather obviously, the more likely you are to die randomly, the less it makes sense for your genes to invest in the survival side of the equation.