No evidence for that. In fact, it was estimated that even if a police state prevented reproduction by every carrier of, say, the cystic fibrosis gene, the incidence of the disease would fall only by half in 10,000 years, due to repeated spontaneous mutations. And we need to know a lot more about “harmful” genes that have survived thousands of years in the population: those genes are likely to have been helpful at some time and in some conditions (like sickle cell anemia, a gene that actually protects the carrier from malaria.)
Yes, though the incidence is low (1 in 10,000 births.) The diseases are all ones that most people, and even doctors, have not heard of.
Many things are possible, including determining individual persons’ genomes, to compute risk for many common and rare diseases. This will be debated: does it increase or decrease the cost of health care? We are also well into looking, say, at the genomes of 1000 people with Disease X, and comparing them with those of 1000 people without it; and identifying the genes that are associated with having the disease. That leads to identifying what actually is going wrong, a thing we actually don’t know, most of the time.
A big topic, and one that should be discussed by the public, not just the doctors and the politicians. A lot of what we consider desirable (good looks, brains) seem to be very multigenic, that is, you’d have to have the right version of dozens of genes; it would be really hard to design a kid like that.
That can and does happen, though it seems that the best pathogens learn instead to fool the immune system by understanding how it works and then turning parts of it off. HIV is good at preventing the development of the most effective anti-HIV lymphocytes, for example.
Fat. It gets broken down to 2-carbon units which are then whirled through the Krebs cycle in the mitochondria. A fat has 3 fatty acid chains, each in the 12 to 18-carbon range, so that’s a lot of carbon to oxidize (burn) compared to the 6 carbons in glucose.
Probably not much. There are a few papers indicating that leptin made by inflammatory cells cab extend the lifespan of autoimmune T cells, but the significance of this in human disease has not been studied.
They depend on mutations, just like sexually-reproducing creatures. But all recessive mutations (to only one of two chromosomes, where you need both chromosomes mutated to see a change) are not, therefore, expressed; while with sex, there is a chance to each parent to donate a recessive mutation, for good or for bad. So asexual change is slow. As was seen when the potato crop in Ireland got the Blight and was completely killed, resulting in starvation. Or as we’re seeing with bananas; only one strain (Cavendish) is grown almost everywhere, and it’s sick, as you can see in the grocery store.