
New insights into mitochondria reveal how life expends energy - pmcpinto
http://aging.nautil.us/feature/173/yes-life-in-the-fast-lane-kills-you
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reasonattlm
Bear in mind that the evolution of aging is anything but a settled field. It
is a battleground of many competing views and theories. The evolution of aging
is one of those topics for which the wikipedia page is actually a good place
to start, because right from the top it correctly delivers the understanding
that this field is (a) complicated, (b) not at all unified, and (c) in flux.

[https://en.wikipedia.org/wiki/Evolution_of_ageing](https://en.wikipedia.org/wiki/Evolution_of_ageing)

The fellow here is outlining one particular set of views out of something like
half a dozen with varying degrees of mainstream support, and that any random
selection of evolutionary biologists would take issue with, point by point. He
also simplifies down to a level at which some important points are missed,
such as the existence of mitochondrially targeted antioxidants and what their
ability to slow aging means for various theories of aging and mitochondrial
function.

In fact all of the appearances of mitochondria in this article are in that
bucket of missing important but subtle points. If you want to chase down more
on the viewpoint he discusses in the last section of the article, you should
read up on the membrane pacemaker hypothesis:

[https://www.google.com/#q=Membrane+Pacemaker+Hypothesis](https://www.google.com/#q=Membrane+Pacemaker+Hypothesis)

This is really driven by trying to understand why the outliers on the chart of
resting metabolic rate versus species life span are outliers: naked mole rats,
birds, microbats, etc.

When it comes to what to do about damaged, bad mitochondria in aging, there
are better options than replacement. In fact delivery of good mitochondria as
a therapy is probably not useful at all; the bad mitochondria already
outcompeted the good mitochondria once, and will quickly do so again. It is so
rapid that scientists have never observed this in progress, they only see
cells with all bad mitochondria and cells without any bad mitochondria, never
the transitional state.

(There are two separate things going on in aging vis a vis mitochondria.
Firstly the type of damage to mitochondria that results in bad mitochondria,
under discussion here. Secondly changes in cell signaling and environment that
leads to a sort of general malaise in mitochondrial function and replication
thoughout a tissue without this damage or formation of bad mitochondria, and
that is not really under discussion here or in the article. It is probably a
secondary consequence of other forms of damage and change in aging).

The SENS approach of allotopic expression, moving mitochondrial genes into the
cell nucleus, currently demonstrated for three of the necessary thirteen
genes, is the best and most permanent of solutions to prevent mitochondrial
damage, being a one-time therapy. If something else is used, such as periodic
delivery of replacement mitochondria, it would have to coupled with some kind
of targeted destruction of bad mitochondria. That is a thorny problem, as
anything less than complete destruction is just a short postponement. These
things replicate quickly, and bad mitochondria of the aging-causing sort have
a replication advantage over normal, good mitochondria. I'm not aware of
anyone with a credible approach to that selective destruction yet, however.

~~~
untilHellbanned
Briefly, what's your point?

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cocochanel
"There is a strong relationship between metabolic rate—the rate at which we’re
taking in oxygen and burning up food—and lifespan."

I thought this was disproved. Anyone care to clarify?

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stabbles
Mitochondria is the powerhouse of the cell

