The issues with that sort of analysis are explained in the paper I
cite. basically, there are correlations between body size and
longevity and also between metabolic rates and body size, so if you
don’t correct for these effects and you just look at metabolic rate
and longevity you will find correlations. but those correlations
are biased, and if you statistically control for the multiple
correlations between the different traits you find that actually
there is no correlation between metabolic rates and longevity, as we
and others showed.
please see my paper for further details. Speakman has also
published on this, for example:
Speakman JR. Correlations between physiology and lifespan–two
widely ignored problems with comparative studies. Aging Cell.
On 01/02/2015 15:33, Reason wrote:
On 02/01/2015 05:47 AM, J Pedro
I should point out that the idea that metabolic rate
negatively correlates with longevity has now been disproved.
It’s not only that bats and birds are an exception to the idea
that high metabolic rate is associated with short lifespan.
There is no correlation at all between metabolic rate and
longevity in mammals or birds. we have shown this, and so have
others (Speakman, Austad, etc.): http://ift.tt/1D1DIlG
to repeat, Kleiber’s rule is wrong.
What about this study that examines the combination of metabolic
rate and mitochondrial DNA base composition in mammals only?http://ift.tt/1BL2guM
In animal cells, mitochondria are semiautonomous organelles of
virtually “hostile” (bacterial) origin, with their own code and
genome (mtDNA). The semiautonomy and restricted resources could
result in occasional “conflicts of interests” with other cellular
components, in which mitochondria have greater chances to be “the
weakest link,” thus limiting longevity. Two principal questions
are addressed: (1) to what extent the mammalian maximum life span
(MLS) is associated with mtDNA base composition? (2) Does mtDNA
base composition correlate with another important
mitochondria-associated variable—resting metabolic rate (RMR)—and
whether they complement each other in determination of MLS?
Analysis of 140 mammalian species revealed significant
correlations between MLS and the content of the four mtDNA
nucleotides, especially noted for GC pairs (r2 = 0.42; p <
10−17). The most remarkable finding of this study is that
multivariate stepwise analysis selected only the GC content and
RMR, which together explained 77% of variation in MLS (p <
10−25). To the authors' knowledge, it is the highest coefficient
of MLS determination that has ever been reported for a comparable
sample size. Taking into account substantial errors in estimation
of MLS and RMR, it could mean that the GC and RMR explain most of
the MLS biological variation. Other putative players in MLS
determination should have relatively small contribution or their
effects should be realized via the same channels. Although further
research is clearly warranted, the extraordinary high correlation
of mtDNA GC and RMR with MLS suggests a “direct hitting” of the
core longevity targets, inferring mitochondria as a primary object
for longevity-promoting interventions.