Re: Metabolic rate and CR- time to say goodbye to the rate of living theory?

[Guest guest]

Pat,The idea that CR lowers the metabolic rate has its basis in the observation that the resting metabolic rate per kilogram of metabolically active tissue decreases in semistarvation studies by 16%.[1]However, both Mattson[2] and Masoro[3] have shown that rodents that have been raised on 40% CR diets eat 18% more food per body weight than the control animals. This leads to the Calorie Restriction Paradox:Mice put on a 40% calorie restricted (CR) diet after 9 weeks of age have an adult body weight that is 51% of the weight of mice fed ad libitum (AL). Considering that CR mice receive 60% of the food eaten by AL mice, CR mice eat 18% more than AL mice on a body weight basis: If the AL mice get F grams of food for a body weight of W, the CR mice get 0.6 F grams of food for a body weight of 0.51 W. Dividing 0.6 F by 0.51 W gives 1.18 food/weight for the CR mice, which is 18% more food. The increased consumption on a weight basis cannot support the idea for reduced metabolism.Tonyhttp://www.scientificpsychic.com/health/crondiet.html[1] Christian Weyer, Roy L Walford, Inge T Harper, Mike Milner, Taber MacCallum, P Tataranni and Ravussin, Energy metabolism after 2 y of energy restriction: the Biosphere 2 experiment, American Journal of Clinical Nutrition, Vol. 72, No. 4, 946-953, October 2000 http://www.ajcn.org/cgi/content/full/72/4/946[2] Mattson, et al. "Intermittent fasting dissociates beneficial effects of dietary restriction on glucose metabolism and neuronal resistance to injury from calorie intake, Proc Natl Acad Sci USA, 2003 May 13; 100(10):6216-6220.http://www.pnas.org/content/100/10/6216.full[3] E J Masoro, et al, "Action of food restriction in delaying the aging process", Proc Natl Acad Sci U S A., 1982 July; 79(13): 4239-4241.>> One of the most persistent notions commonly associated with reduced > uptake of nutritive calories to extend lifespan in several species is > that this effect is achieved through a lowering of metabolic rate. > Can anyone produce evidence to substantiate this? or point to CR > studies that actually focus on metabolic rate/flux or that this idea > is supported by more than unproven hypothesis or mere metaphoric > appeal? Evidence is steadily emerging that the opposite might apply, > that the increase in mitochondrial metabolism «might cause a positive > response to increased formation of ROS and other stressors, leading > to secondary increase in stress defence (mitohormesis), cumulating in > reduced net stress levels and possibly extended life span» (Ristow, > 2007).> > in one review one is told that:> These studies show that DR life extension is not caused by a reduced > metabolic rate, consistent with results in other species.> > http://www.ncbi.nlm.nih.gov/pubmed/17063035?> ordinalpos=16 & itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.P> ubmed_RVDocSum> > in another:> Two possible mechanisms by which DR increases lifespan are reduction > of metabolic rate and reduction of insulin/IGF-1 signalling. > Experimental tests have not supported either possibility.> > http://www.ncbi.nlm.nih.gov/pubmed/15896824?> ordinalpos=1 & itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pu> bmed_DiscoveryPanel.Pubmed_Discovery_RA & linkpos=4 & log$=relatedarticles> & logdbfrom=pubmed> > There is evidence that DR causes increased resistance against > environmental stressors but no decrease of metabolic rate. > > http://www.ncbi.nlm.nih.gov/pubmed/16782293?> ordinalpos=1 & itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pu> bmed_DiscoveryPanel.Pubmed_Discovery_RA & linkpos=2 & log$=relatedarticles> & logdbfrom=pubmed> > The increased life span caused by certain mutations in the nematode > Caenorhabditis elegans has been interpreted in terms of two metabolic > theories of ageing: the oxidative damage theory and the rate of > living theory. New findings support the former, but not the latter > interpretation.> > or:> There is no reduction in metabolic rate or in the rate of generation > of superoxide and hydrogen peroxide from isolated mitochondria in > response to DR. DR acts acutely and rapidly (within 48 h) to reduce > the mortality of flies that are fully fed to the level found in > animals exposed to DR throughout life. > > http://www.ncbi.nlm.nih.gov/pubmed/15935441?> ordinalpos=1 & itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pu> bmed_DiscoveryPanel.Pubmed_Discovery_RA & linkpos=4 & log$=relatedarticles> & logdbfrom=pubmed> > Dietary-restriction had no effect on mass-specific resting metabolic > rate both when measured as oxygen consumption... individual variation > in lifespan in wild-type flies, and life extension by dietary-> restriction and reduced insulin/IGF-1 signalling is not attributable > to differences in metabolic rate.> > http://www.ncbi.nlm.nih.gov/pubmed/15288688?> ordinalpos=1 & itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pu> bmed_DiscoveryPanel.Pubmed_Discovery_RA & linkpos=5 & log$=relatedarticles> & logdbfrom=pubmed > > The above is culled from very recent findings. it seems however that > evidence was offered way back in 1985 but apparently had not caught > much attention...> > The long held belief that reducing food intake lowers the metabolic > rate per unit of metabolic mass may be true in short-term dietary > programs but appears not to be true when a significant portion of the > life span is involved.> > http://www.ncbi.nlm.nih.gov/pubmed/3157325?> ordinalpos=1 & itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pu> bmed_DiscoveryPanel.Pubmed_Discovery_RA & linkpos=4 & log$=relatedarticles> & logdbfrom=pubmed>

[Guest guest]

18% makes sense, Tony, when you consider that energy expenditure may

be 30% to 50% higher than predicted from reduced body mass in CR

animals:

1: Mech Ageing Dev. 2005 Jun-Jul;126(6-7):783-93. Epub 2005 Mar 16.

Links

Energy expenditure of calorically restricted rats is higher than

predicted from their altered body composition.Selman C, T,

Staib JL, Duncan JS, Leeuwenburgh C, Speakman JR.

University of Florida, Department of Aging and Geriatric Research,

College of Medicine, Gainesville, 32608, USA. c.selman@...

Debate exists over the impact of caloric restriction (CR) on the

level of energy expenditure. At the whole animal level, CR decreases

metabolic rates but in parallel body mass also declines. The question

arises whether the reduction in metabolism is greater, smaller or not

different from the expectation based on body mass change alone.

Answers to this question depend on how metabolic rate is normalized

and it has recently been suggested that this issue can only be

resolved through detailed morphological investigation. Added to this

issue is the problem of how appropriate the resting energy

expenditure is to characterize metabolic events relating to aging

phenomena. We measured the daily energy demands of young and old rats

under ad libitum (AD) food intake or 40% CR, using the doubly labeled

water (DLW) method and made detailed morphological examination of

individuals, including 21 different body components. Whole body

energy demands of CR rats were lower than AD rats, but the extent of

this difference was much less than expected from the degree of

caloric restriction, consistent with other studies using the DLW

method on CR animals. Using multiple regression and multivariate data

reduction methods we built two empirical predictive models of the

association between daily energy demands and body composition using

the ad lib animals. We then predicted the expected energy

expenditures of the CR animals based on their altered morphology and

compared these predictions to the observed daily energy demands.

Independent of how we constructed the prediction, young and old rats

under CR expended 30 and 50% more energy, respectively, than the

prediction from their altered body composition. This effect is

consistent with recent intra-specific observations of positive

associations between energy metabolism and lifespan and theoretical

ideas about mechanisms underpinning the relationship between oxygen

consumption and reactive oxygen species production in mitochondria.

PMID: 15888333 [PubMed - indexed for MEDLINE]

> >

> > One of the most persistent notions commonly associated with

reduced

> > uptake of nutritive calories to extend lifespan in several

species is

> > that this effect is achieved through a lowering of metabolic rate.

> > Can anyone produce evidence to substantiate this? or point to CR

> > studies that actually focus on metabolic rate/flux or that this

idea

> > is supported by more than unproven hypothesis or mere metaphoric

> > appeal? Evidence is steadily emerging that the opposite might

apply,

> > that the increase in mitochondrial metabolism «might cause a

> positive

> > response to increased formation of ROS and other stressors,

leading

> > to secondary increase in stress defence (mitohormesis),

cumulating in

> > reduced net stress levels and possibly extended life span»

(Ristow,

> > 2007).

> >

> > in one review one is told that:

> > These studies show that DR life extension is not caused by a

reduced

> > metabolic rate, consistent with results in other species.

> >

> > http://www.ncbi.nlm.nih.gov/pubmed/17063035?

> >

ordinalpos=16 & itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.P

> > ubmed_RVDocSum

> >

> > in another:

> > Two possible mechanisms by which DR increases lifespan are

reduction

> > of metabolic rate and reduction of insulin/IGF-1 signalling.

> > Experimental tests have not supported either possibility.

> >

> > http://www.ncbi.nlm.nih.gov/pubmed/15896824?

> >

ordinalpos=1 & itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pu

> >

bmed_DiscoveryPanel.Pubmed_Discovery_RA & linkpos=4 & log$=relatedarticles

> > & logdbfrom=pubmed

> >

> > There is evidence that DR causes increased resistance against

> > environmental stressors but no decrease of metabolic rate.

> >

> > http://www.ncbi.nlm.nih.gov/pubmed/16782293?

> >

ordinalpos=1 & itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pu

> >

bmed_DiscoveryPanel.Pubmed_Discovery_RA & linkpos=2 & log$=relatedarticles

> > & logdbfrom=pubmed

> >

> > The increased life span caused by certain mutations in the

nematode

> > Caenorhabditis elegans has been interpreted in terms of two

metabolic

> > theories of ageing: the oxidative damage theory and the rate of

> > living theory. New findings support the former, but not the latter

> > interpretation.

> >

> > or:

> > There is no reduction in metabolic rate or in the rate of

generation

> > of superoxide and hydrogen peroxide from isolated mitochondria in

> > response to DR. DR acts acutely and rapidly (within 48 h) to

reduce

> > the mortality of flies that are fully fed to the level found in

> > animals exposed to DR throughout life.

> >

> > http://www.ncbi.nlm.nih.gov/pubmed/15935441?

> >

ordinalpos=1 & itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pu

> >

bmed_DiscoveryPanel.Pubmed_Discovery_RA & linkpos=4 & log$=relatedarticles

> > & logdbfrom=pubmed

> >

> > Dietary-restriction had no effect on mass-specific resting

metabolic

> > rate both when measured as oxygen consumption... individual

variation

> > in lifespan in wild-type flies, and life extension by dietary-

> > restriction and reduced insulin/IGF-1 signalling is not

attributable

> > to differences in metabolic rate.

> >

> > http://www.ncbi.nlm.nih.gov/pubmed/15288688?

> >

ordinalpos=1 & itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pu

> >

bmed_DiscoveryPanel.Pubmed_Discovery_RA & linkpos=5 & log$=relatedarticles

> > & logdbfrom=pubmed

> >

> > The above is culled from very recent findings. it seems however

that

> > evidence was offered way back in 1985 but apparently had not

caught

> > much attention...

> >

> > The long held belief that reducing food intake lowers the

metabolic

> > rate per unit of metabolic mass may be true in short-term dietary

> > programs but appears not to be true when a significant portion of

the

> > life span is involved.

> >

> > http://www.ncbi.nlm.nih.gov/pubmed/3157325?

> >

ordinalpos=1 & itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pu

> >

bmed_DiscoveryPanel.Pubmed_Discovery_RA & linkpos=4 & log$=relatedarticles

> > & logdbfrom=pubmed

> >

>