[Paleopsych] Economist: Longevity: All you can't eat

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Economist: Longevity: All you can't eat
http://www.economist.com/science/PrinterFriendly.cfm?Story_ID=3809652
5.3.31

[Reply from Steve Harris appended.]

Even a slight decrease in calories may lead to longer lifespans

MOST people would not object to living a few years longer than normal,
as long as it meant they could live those years in good health. Sadly,
the only proven way to extend the lifespan of an animal in this way is
to reduce its calorie intake. Studies going back to the 1930s have shown
that a considerable reduction in consumption (about 50%) can extend the
lifespan of everything from dogs to nematode worms by between 30% and
70%. Although humans are neither dogs nor worms, a few people are
willing to give the calorie-restricted diet a try in the hope that it
might work for them, too. But not many-as the old joke has it, give up
the things you enjoy and you may not live longer, but it will sure seem
as if you did.

Now, though, work done by Marc Hellerstein and his colleagues at the
University of California, Berkeley, suggests that it may be possible to
have, as it were, your cake and eat it too. Or, at least, to eat 95% of
it. Their study, to be published in the American Journal of
Physiology-Endocrinology and Metabolism, suggests that significant gains
in longevity might be made by a mere 5% reduction in calorie intake. The
study was done on mice rather than people. But the ubiquity of previous
calorie-restriction results suggests the same outcome might well occur
in other species, possibly including humans. However, you would have to
fast on alternate days.

Why caloric restriction extends the lifespan of any animal is unclear,
but much of the smart money backs the idea that it slows down cell
division by denying cells the resources they need to grow and
proliferate. One consequence of that slow-down would be to stymie the
development of cancerous tumours.

Cancer is the uncontrolled growth of cells. For a cancer to develop
efficiently, it needs multiple mutations to accumulate in the DNA of the
cell that becomes the tumour's ancestor. To stop this happening, cells
have DNA-repair mechanisms. But if a cell divides before the damage is
repaired, the chance of a successful repair is significantly reduced. A
slower rate of cell division thus results in a slower accumulation of
cancer-causing mutations.

At least, that is the theory. Until now, though, no one has tested
whether reduced calorie intake actually does result in slower cell
division. Dr Hellerstein and his team were able to do so using heavy
water as a chemical "marker" of the process.

Heavy water is heavy because the hydrogen in it weighs twice as much as
ordinary hydrogen (it has a proton and a neutron in its nucleus, instead
of just a proton). Chemically, however, it behaves like its lighter
relative. This means, among other things, that it gets incorporated into
DNA as that molecule doubles in quantity during cell division. So, by
putting heavy water in the diets of their mice, the researchers were
able to measure how much DNA in the tissues of those animals had been
made since the start of the experiment (and by inference how much cell
division had taken place), by the simple expedient of extracting the DNA
and weighing it.

Dr Hellerstein first established how much mice eat if allowed to feed as
much as they want. Then he set up a group of mice that were allowed to
eat only 95% of that amount. In both cases, he used the heavy-water
method to monitor cell division. The upshot was that the rate of
division in the calorie-restricted mice was 37% lower than that in those
mice that could eat as much as they wanted-which could have a
significant effect on the accumulation of cancer-causing mutations.

But calorie-reduction is not all the mice had to endure. They were, in
addition, fed only on alternate days: bingeing one day and starving the
next. There were two reasons for this. First, bingeing and starving is
how many animals tend to feed in the wild. The uncertain food supply
means they regularly go through cycles of too much and too little food
(it also means that they are often restricted to eating less than they
could manage if food were omnipresent). The reasoning here is that
metabolic processes evolved in a particular context and might be
expected to work best in that context. Replicate the evolutionary
context and you might get a better outcome.

The second reason, according to Elaine Hsieh, one of Dr Hellerstein's
colleagues, is that cutting just a few calories overall, but feeding
intermittently, may be a more feasible eating pattern for some people to
maintain than making small reductions each and every day.

Whether modern man and woman, constantly surrounded by food and
advertisements for food, would really be able to forgo eating every
other day is debatable. But even if it does work (and Dr Hellerstein has
yet to prove that reduced cell division translates into longer life) the
temptations of life may prove just too much for wannabe Methuselahs.
_______________________________________________

From: "Steve Harris" <sbharris at ix.netcom.com>
Date: Tue, 5 Apr 2005 16:32:31 -0700
To: "Gerontology Research Group" <grg at lists.ucla.edu>

Argghh.  I saw this and just knew it would be 
misinterpreted.

1) These scientists screwed up, and forgot to have a control 
group which was fed every other day but the 100% caloric 
intake, not 95% of it. So they have *two* independent 
experimental effects, and since they have no control, they 
have no idea which effect is the predominant one on the 
dependent effect they measured, which is (remember) cell 
division (not cancer development or life span).

2) They are measuring a cell division, which is a *proxy* 
for cancer causation and life extension. It probably isn't a 
perfect one, because previous studies have shown that the 
cancer-reducing effects of calorie restriction are NOT 
dependent on interval of feeding, but ONLY on total calories 
consumed. So if these guys see a big effect of interval 
fasting on their proxy cell-division variable, it only 
serves to heighten suspicion that it's not a good 
proxy-variable all the time, not make us think that this 
diet regime will do the same job as a lot of calorie 
restriction. The anticancer effect of any dietary regime 
must be proven *directly*, and there's no getting around it.

3) Finally, due to the difference in specific metabolic 
rates, feeding a mouse every other day is like feeding a 
human every other WEEK. If there are any fasting effects 
that drastically slow down cell division, they're not going 
to work in humans as they do in mice without increasing the 
duration of the human fast by a factor of SEVEN, anyway. So 
it's probably just as well that all this isn't going to turn 
out to be as good a cancer preventive as the researchers 
think it will.

Steve Harris