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A1CR · Site Admin Joined: 18 Jan 2006 Posts: 559

The following study, located by our good friend CRON4healthyfuture, and analyzed by CRON4healthyfuture and Dean -, shows that early childhood nutrition, and in particular calorie intake, is an important factor determining longevity.

But why? Is it because metabolic events that occur during early childhood are themselves instrumental in controlling lifespan? Or is it because early childhood events impact important things which occur later in life - namely the organism's eventual size and/or appetite, and therefore lifetime calorie intake? This study doesn't tell us definitely, but it is an interesting piece of the puzzle.

From a parent's perspective, to maximize health and longevity this study would suggest:

In early 2004, CRON4healthyfuture noted the following popular accounts of study [1, see below]:

Thanks for posting this interesting study. It appears to show that early
childhood nutrition is an important factor determining longevity, at least
in mice.

Providing the mouse mom with adequate nutrition while the babies are in the
womb appears to be critical. But after birth, if the mom was fed a low-cal,
low-protein diet while the babies were breastfeeding, providing the babies
w/ what could be considered a short-term CR diet, the babies lived longer
than the babies of moms fed ad lib during the breastfeeding period (when
both sets of moms were fed well during pregnancy). In other words, childhood
CR -> increased longevity.

Perhaps most interestingly, mice weaned on a restricted diet for a few weeks
after birth appear (on the surface anyway) not to have been negatively
impacted by a high calorie, highly palatable diet, presumably fed ad lib for
the balance of their life, relative to mice fed a "standard" diet during
adulthood - presumably ad lib as well.

So when the mice who where CR'ed in childhood were subsequently allowed to
gorge to there hearts content on cake and donuts (figuratively speaking -
I'm sure the "cake and donut" diet contained adequate nutrition as well),
they didn't live any shorter lives than mice fed a standard (not as tasty)
rat chow diet.

"The high-calorie diet did not have a noticeable effect on the life span of
well-fed mice weaned on a restricted diet after birth, the researchers
reported."

While on the surface this would *appear* to be strong evidence in favor of
the notion that lifespan is not a linear function of lifetime calorie
intake, there is at least one caveat, as mentioned in the article. Mice
provided adequate nutrition in the womb, and then CR'ed during early
childhood, appear to be small in size, and have a reduced appetite. From the
articles:

"A low-protein diet causes mild growth restrictions"

And

"We think it might be at least in part due to the long-term differences in
appetite," Ozanne says. "If you are born small and then grow very quickly
during lactation, you have a permanently increased appetite, whereas if you
go nice and slowly [i.e. adequately nourished in the womb, and then CR'ed
during early childhood to limit growth], your appetite is permanently
reduced so you're self-regulating and not so prone to obesity. It may well
also alter your propensity to exercise."

The interpretation that the CR'ed baby mice were self-regulating, and didn't
consume as many calories as control mice did over their adult life is
supported by this statement in the abstract:

"Postnatal low-protein animals showed no additional weight gain when given a
highly palatable diet compared with chow-fed litter-mates."

So it appears to me that the "calories, calories, calories" mantra is not
ruled out, or even significantly opposed by this study, at least so far as
can be determined from its abstract and popular press accounts. The
interpretation:

Childhood CR -> stunted growth and reduced appetite -> reduced lifetime
calorie exposure -> extended longevity appears to be very consistent with the results of this study.

But the devil is in the details. In the passage from abstract given above,
what do the authors mean by "compared w/ chow-fed litter-mates"? Mice who
were weaned on an identical low-cal low-protein diet, and then just fed rat
chow (rather than cake and donuts) during adulthood? Or controls feed
standard rodent chow during weaning and adulthood? What were the lifespans
of the different groups? Did they actually measure average calorie intake of
the groups? What were the weights of the various groups, which could be
taken as a (rough) proxy for lifetime calorie intake?

If someone with access to the full paper could post these details [please post them on this forum]

-Dean

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[1] Clin Sci (Lond). 2004 Feb; 106(2): 141-5.

Early programming of weight gain in mice prevents the induction of obesity
by a highly palatable diet.

Ozanne SE, Lewis R, Jennings BJ, Hales CN.

Poor early growth is associated with Type II diabetes, hypertension and
other features of the metabolic syndrome in adulthood. It has been suggested
that this results from the development of a thrifty phenotype by a
malnourished fetus. Such a phenotype would predispose the offspring to the
development of obesity if born into conditions of over-nutrition. The
present study aimed to determine if early nutrition affected subsequent
development of obesity. Mice were established as follows: (a) controls
(offspring of control dams), (b) recuperated (offspring of dams fed a
low-protein diet during pregnancy, but nursed by control dams) and (c)
postnatal low-protein (offspring of control dams nursed by low-protein-fed
dams). Mice were weaned on to standard laboratory chow or a cafeteria diet.
Recuperated offspring, although smaller at birth ( P <0.01), caught up and
exceeded the weight of control offspring by 7 days of age ( P <0.001).
Postnatal low-protein offspring were smaller than controls by 7 days of age
( P <0.001). Recuperated animals gained more weight than controls when given
free access to a highly palatable diet ( P <0.01). Postnatal low-protein
animals showed no additional weight gain when given a highly palatable diet
compared with chow-fed litter-mates. These results suggest that the early
environment has long-term consequences for weight gain. These programmed
responses are powerful enough to block excess weight gain from a highly
palatable diet and, thus, have major implications for the drug-free
regulation of food intake and obesity.

PMID: 14507258