Bexfield waged an epic battle against the insurance company that lasted several years and consisted of countless emails, YouTube videos, and even help from David Segal, aka “The Haggler” from the New York Times. In the end, Presbyterian reimbursed his $198,000 original payment for the procedure and paid $204,000 in interest.

Wow, the good guy wins. Was not expecting that ending!

http://www.halt-ms.org/forpatients.html

In autoimmunity the problem is that the immune system is misconfigured in some way - so culling existing immune cells and replacing with fresh ones stands a good chance of getting rid of the cell-based misconfiguration. That is true whether or not the misconfiguration is understood; it is a good shortcut past lack of knowledge.

This has worked for other autoimmune diseases, but is sufficiently drastic that the research community has abandoned it in favor of even marginally effective treatments for conditions where those exist. For example there were promising results in the burn-and-rebuild approach for rheumatoid arthritis a way back, but then biologics arrived offering control and less pain for some patients, and that line of research died out.

It will probably return with the advent of more targeted therapies that are not as harsh as chemotherapy, ways to selectively destroy only immune cells with specified surface chemistry. This sort of thing is underway in the cancer research community, and the technologies produced will have very broad application: safe and painless removal of immune cells, fat cells, senescent cells - anything we don't want and can be distinguished. This is a big deal but still in the works; the issue isn't destroying the cells, but rather coming up with sufficiently discriminating targeting systems.

There is an assumption in the research community that, yes, stochastic DNA damage and epigenetic drift in tissues has to be important in aging in ways other than cancer, but there isn't any good experiment to demonstrate that this is in fact the case. If anything the available evidence points in the opposite direction, such as mice loaded with a large multiple of the normal level of point mutations that don't appear to suffer any consequences as a result.

When you look at what kills the most people, cardiovascular disease, it all appears to be fairly directly linked to a combination of degredation of elasticity in blood vessel walls (cross-links in the extracellular matrix, a metabolic waste product issue), damaged lipids in blood vessel walls spawning self-reinforcing damage generators (mitochondrial DNA damage, inflammation), and things of that ilk, which lead to hypertension and runaway bad feedback loops in blood pressure and the body's response to same, and then catastrophic failures or blockages in blood vessels. Stem cells and their declining activity are something of a secondary issue in the background, and don't really figure in the important path through this pathology. If your skin and blood vessel walls are loaded up with cross-links that the body cannot break down and increasingly inelastic as a result then it doesn't matter how youthful your stem cells are, you are still on the path to death.

There are strong indications that aging, and dying, is an entirely programmed-in part of our genetic structure. We age and die, not because of DNA copy errors, but because DNA sabotages itself and the cell it's in over time. There are, of course, ageless cells. The most obvious example being procreation-related cells, but there's many different kinds (for instance, muscle cells have very different aging clocks).

Multiple "death clocks" have been identified, telomeres being the most famous, that measure number of cell divisions, others measure the amount of energy expended by the cell, genetic quality, and presumably a few other things. Exceed the limits on any one of them, and the cell commits suicide. But if you're close to the limit, the cells will "senescence", which means they'll be less active and less worried about making mistakes. But this is an active, controlled process, not an accidental result of gene degradation. All of your cells contain logic somewhat like this :

  do_something() {
    if (rand() > age/150) {
      don't do it
    }
    if (rand() > age/300) {
      kill the cell off
    }
    actually do it
  }

Also there are plenty of animals and plants, smaller ones, that don't age. Which has the surprising consequences that death (caused by old age at least) has an origin. There must be a point in history where evolution decided we'd grow old and die.

There's a very interesting book about this subject :

http://www.amazon.com/Sex-Origins-Death-William-Clark/dp/019...

As to why aging exists in multicellular organisms, the evolutionary explanations tend to work whether or not aging is a matter of failure to evolve longevity-assurance mechanisms because selection pressure is low in post-reproductive life, failure to restrict selection of enhancements in youth that go on to cause harm in old age because selection pressure is low in post-reproductive life (such as an adaptive immune system that kills pathogens very efficiently in youth, but which goes haywire sometimes to attack the owners tissues, and suffers structural failure after exposure to too many pathogens), or a matter of the selected evolution of death programs. A compelling explanation is that species that age most likely outcompete those that do not during periods of environmental change.

http://dx.doi.org/10.1371/journal.pone.0024328

Thanks for this (and the link). It seems very obvious but I hadn't thought of it or read about it at all.

There is no logic, because life do not do long term planning.

You don't have to go back many generations before being in your 40s was impressive. It was highly likely that the combined stresses of living would take you out in some way or other.

Once we reach the age of procreation, evolution is pretty much done with us.

It seems to me that the same argument could be used against the whole group of social animals. It doesn't work. Older people organize the group, they protect the young, ... One needs to look at evolution like it's at play for groups of people as much as it is at play for individuals themselves.

Besides there are many things that are tough to explain in evolution. Riddle me this. Humans are 7 billion, and have a generational length of 20 years, more or less. Bacteria are 9999999999 trillion (at least) and have a generational length that is somewhere between minutes and hours.

How do humans stay alive with that sort of competition ? Evolution becomes more efficient with shorter generational lengths and larger numbers of individuals. Sorry to break it to you, but bacteria have got us beat, by a LOT (and the gain should compound over time). Why haven't all larger plants and animals died out from infection long before humans or even mammals existed ?

I wonder if the chemotherapy doesn't act to kill or suppress some of the cancer risk until the immune system reboots.