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Re: Calorie Restriction Or Calorie Retention?

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Might this also be seen as another study favoring

maintenance of a low body temperature? CRONies

often experience cold intolerance. Should we just

learn to deal instead of cranking the heat?

-

--- In , Jeff Novick <chefjeff40@...>

wrote:

>

> " ...suggesting that excess calorie retention, rather than

consumption, confers cancer risk. " Cancer Progression in the

Transgenic Adenocarcinoma of Mouse Prostate Mouse Is Related to

Energy Balance, Body Mass, and Body Composition, but not Food Intake

M. Huffman1, S. 1, Watts1, Ada Elgavish2,

Isam A. Eltoum3 and Tim R. Nagy1 Departments of 1 Nutrition

Sciences, 2 Genetics, and 3 Pathology, University of Alabama at

Birmingham, Birmingham, Alabama Requests for reprints: Tim R. Nagy,

Division of Physiology and Metabolism, Department of Nutrition

Sciences, University of Alabama at Birmingham, 419 Webb Building,

1675 University Boulevard, Birmingham, AL 35294-3360. Phone: 205-975-

4088; Fax: 205-934-7050; E-mail: tnagy@... ' + u + '@' + d + ''//--

> . Calorie restriction can inhibit or delay carcinogenesis,

reportedly due to a reduction in calorie intake rather than by

concurrent changes in body mass and/or composition. Our objective was

> to test the hypothesis that body mass and/or composition have an

important effect, independent of energy intake, on the benefits or

hazards associated with calorie restriction or overeating,

respectively. In the first experiment, transgenic mice that

spontaneously develop prostate cancer [transgenic adenocarcinoma of

mouse prostate (TRAMP)] were housed at 27°C or 22°C and pair fed the

same diet for 21 weeks (95% of ad libitum intake at 27°C). In the

second experiment, TRAMP mice were housed at 27°C or 22°C and fed the

same diet ad libitum for 21 weeks. Despite a similar calorie intake,

pair-fed mice at 27°C (PF27) were heavier (28.3 ± 3.3 versus 17.6 ±

1.6 g at 21 weeks; P < 0.001; mean ± SD) and had greater fat (6.4 ±

2.1 versus 1.9 ± 0.3 g; P < 0.001) and lean mass (P < 0.001) than

pair-fed mice at 22°C. Furthermore, PF27 mice had greater levels of

serum leptin (P < 0.001), lower levels of adiponectin (P < 0.05), and

a greater frequency of prostatic adenocarcinoma (P <

> 0.05). In contrast, ad libitum–fed mice housed at 22°C consumed

30% more calories than ad libitum–fed mice at 27°C, but there was no

difference between groups in body composition or cancer progression.

These results imply that the ability of calorie restriction to

inhibit or delay cancer incidence and progression is mediated in part

by changes in energy balance, body mass, and/or body composition

rather than calorie intake per se, suggesting that excess calorie

retention, rather than consumption, confers cancer risk. [Cancer Res

2007;67(1):417–24]

>

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Hi :

I wondered the same thing. But the following sentance seems to rule

out the possibility that ambient temperature affected cancer rates in

this study:

" ..... ad libitum–fed mice housed at 22°C consumed 30% more calories

than ad libitum–fed mice at 27°C, but there was no difference between

groups in body composition or cancer progression. " - the temperatures

were different, but cancer the same, apparently.

And as far as I see from the abstract they didn't measure body

temperature. And don't we know (think we know?) that body

temperature is a function of caloric intake, rather than the

temperature of the local environment? And that lower cancer rates,

at least in rats, is associated with lower caloric intake? So we

probably can draw the conclusion that lower cancer rates are

ASSOCIATED WITH, but not necessarily directly caused by, lower body

temperature.

At least that is my take until some study comes up to show otherwise.

Rodney.

> >

> > " ...suggesting that excess calorie retention, rather than

> consumption, confers cancer risk. " Cancer Progression in the

> Transgenic Adenocarcinoma of Mouse Prostate Mouse Is Related to

> Energy Balance, Body Mass, and Body Composition, but not Food

Intake

> M. Huffman1, S. 1, Watts1, Ada Elgavish2,

> Isam A. Eltoum3 and Tim R. Nagy1 Departments of 1 Nutrition

> Sciences, 2 Genetics, and 3 Pathology, University of Alabama at

> Birmingham, Birmingham, Alabama Requests for reprints: Tim R.

Nagy,

> Division of Physiology and Metabolism, Department of Nutrition

> Sciences, University of Alabama at Birmingham, 419 Webb Building,

> 1675 University Boulevard, Birmingham, AL 35294-3360. Phone: 205-

975-

> 4088; Fax: 205-934-7050; E-mail: tnagy@ ' + u + '@' + d + ''//--

> > . Calorie restriction can inhibit or delay carcinogenesis,

> reportedly due to a reduction in calorie intake rather than by

> concurrent changes in body mass and/or composition. Our objective

was

> > to test the hypothesis that body mass and/or composition have an

> important effect, independent of energy intake, on the benefits or

> hazards associated with calorie restriction or overeating,

> respectively. In the first experiment, transgenic mice that

> spontaneously develop prostate cancer [transgenic adenocarcinoma of

> mouse prostate (TRAMP)] were housed at 27°C or 22°C and pair fed

the

> same diet for 21 weeks (95% of ad libitum intake at 27°C). In the

> second experiment, TRAMP mice were housed at 27°C or 22°C and fed

the

> same diet ad libitum for 21 weeks. Despite a similar calorie

intake,

> pair-fed mice at 27°C (PF27) were heavier (28.3 ± 3.3 versus 17.6 ±

> 1.6 g at 21 weeks; P < 0.001; mean ± SD) and had greater fat (6.4 ±

> 2.1 versus 1.9 ± 0.3 g; P < 0.001) and lean mass (P < 0.001) than

> pair-fed mice at 22°C. Furthermore, PF27 mice had greater levels of

> serum leptin (P < 0.001), lower levels of adiponectin (P < 0.05),

and

> a greater frequency of prostatic adenocarcinoma (P <

> > 0.05). In contrast, ad libitum–fed mice housed at 22°C consumed

> 30% more calories than ad libitum–fed mice at 27°C, but there was

no

> difference between groups in body composition or cancer

progression.

> These results imply that the ability of calorie restriction to

> inhibit or delay cancer incidence and progression is mediated in

part

> by changes in energy balance, body mass, and/or body composition

> rather than calorie intake per se, suggesting that excess calorie

> retention, rather than consumption, confers cancer risk. [Cancer

Res

> 2007;67(1):417–24]

> >

>

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Maybe a raised basal metabolic rate should be seen as an important

clue? Higher BMR would account for decrease in calorie retention.

http://www.nriol.net/basal-metabolic-rate-calculator.asp

External temperature Temperature outside the body also affects basal

metabolic rate. Exposure to cold temperature causes an increase in

the BMR, so as to create the extra heat needed to maintain the

body's internal temperature

> >> >

> >> > " ...suggesting that excess calorie retention,

> >> rather than

> >> consumption, confers cancer risk. "

> >

> >> Huffman DM, MS, Watts A, Elgavish A, Eltoum

> > IA, Nagy TR.

> > Cancer progression in the transgenic adenocarcinoma

> > of mouse prostate mouse is related to energy balance,

> > body mass, and body composition, but not food intake.

> > Cancer Res. 2007 Jan 1;67(1):417-24. Epub 2006 Dec 21.

> >

> > PMID: 17185379 http://tinyurl.com/ypvqto

> >

> >

> >

> >

> >

_____________________________________________________________________

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> > Sucker-punch spam with award-winning protection.

> > Try the free Beta.

> > http://advision.webevents./mailbeta/features_spam.html

> >

>

>

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> Checked by AVG Free Edition.

> Version: 7.5.446 / Virus Database: 268.18.6/709 - Release Date:

3/3/2007

> 8:12 AM

>

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Hi Al

Your comment about Lance Armstrong made me search a little

about his nutrition. He appears to burn 9000 calories per day

when training and consumes tons of Power Bars and sports

drinks, many of which are high in HFCS. A part of me makes

me wonder that despite that his exercise makes him lean,

the amount of fuel passing through his body, and the type

of fuel could contribute to cancer, which he has battled.

http://www.athleteinme.com/tabid/37/id/1c81b4e2-603c-4c18-ab74-cbf05a57304f/Defa\

ult.aspx

Cheers

Arturo

Re: Calorie Restriction Or Calorie " Retention " ?

Posted by: " Al Young " acyoung@... al_young88

Sat Mar 3, 2007 11:31 am (PST)

<snip> So, to my mind, this experiment suggests that excess body mass

itself (calorie retention) contributes to risk. It suggests, for example, that

exercising to leaness is as effective as dieting to leaness (regarding

prostate cancer risk) - that isn't what traditional CR is about;

Lance Armstrong isn't usually considered to be on CR (at, say, 9000 cal/d).

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Hi folks:

Another couple of points about this:

1. It seems to me there is no reason to assume all the benefits of

CR occur through precisely the same mechanism. It may be that

reduced total intake of calories is the key factor causing one set of

benefits (the benefits flowing from reduced oxidative stress,

perhaps?); less hormonal secretion from adipose tissue causing

another benefit; less MET intake another benefit; lower body weight

another; and 'who knows what else that no one has thought of yet' for

some other benefits (better appearance resulting in improved sex life

perhaps? ;; ^ )))).

2. We need to distinguish the factors that rectangularize the

survival curve from those that push the entire curve to the right,

all the way to the bottom. Both are considerable benefits, of

course, but they have different implications.

3. There is no reason to believe all the effects of CR will be

beneficial. One that isn't, for example, is smaller bone size. This

presumably is caused by reduced mechanical stress exerted by lower

body weight on important bones. There may be other negative

effects. But clearly the net benefit is hugely positive.

Rodney.

> >

> > " ...suggesting that excess calorie retention, rather than

> consumption, confers cancer risk. " Cancer Progression in the

> Transgenic Adenocarcinoma of Mouse Prostate Mouse Is Related to

> Energy Balance, Body Mass, and Body Composition, but not Food

Intake

> M. Huffman1, S. 1, Watts1, Ada Elgavish2,

> Isam A. Eltoum3 and Tim R. Nagy1 Departments of 1 Nutrition

> Sciences, 2 Genetics, and 3 Pathology, University of Alabama at

> Birmingham, Birmingham, Alabama Requests for reprints: Tim R.

Nagy,

> Division of Physiology and Metabolism, Department of Nutrition

> Sciences, University of Alabama at Birmingham, 419 Webb Building,

> 1675 University Boulevard, Birmingham, AL 35294-3360. Phone: 205-

975-

> 4088; Fax: 205-934-7050; E-mail: tnagy@ ' + u + '@' + d + ''//--

> > . Calorie restriction can inhibit or delay carcinogenesis,

> reportedly due to a reduction in calorie intake rather than by

> concurrent changes in body mass and/or composition. Our objective

was

> > to test the hypothesis that body mass and/or composition have an

> important effect, independent of energy intake, on the benefits or

> hazards associated with calorie restriction or overeating,

> respectively. In the first experiment, transgenic mice that

> spontaneously develop prostate cancer [transgenic adenocarcinoma of

> mouse prostate (TRAMP)] were housed at 27°C or 22°C and pair fed

the

> same diet for 21 weeks (95% of ad libitum intake at 27°C). In the

> second experiment, TRAMP mice were housed at 27°C or 22°C and fed

the

> same diet ad libitum for 21 weeks. Despite a similar calorie

intake,

> pair-fed mice at 27°C (PF27) were heavier (28.3 ± 3.3 versus 17.6 ±

> 1.6 g at 21 weeks; P < 0.001; mean ± SD) and had greater fat (6.4 ±

> 2.1 versus 1.9 ± 0.3 g; P < 0.001) and lean mass (P < 0.001) than

> pair-fed mice at 22°C. Furthermore, PF27 mice had greater levels of

> serum leptin (P < 0.001), lower levels of adiponectin (P < 0.05),

and

> a greater frequency of prostatic adenocarcinoma (P <

> > 0.05). In contrast, ad libitum–fed mice housed at 22°C consumed

> 30% more calories than ad libitum–fed mice at 27°C, but there was

no

> difference between groups in body composition or cancer

progression.

> These results imply that the ability of calorie restriction to

> inhibit or delay cancer incidence and progression is mediated in

part

> by changes in energy balance, body mass, and/or body composition

> rather than calorie intake per se, suggesting that excess calorie

> retention, rather than consumption, confers cancer risk. [Cancer

Res

> 2007;67(1):417–24]

> >

>

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Consider this:

1) Intermittent Fasting (IF) was shown by Mattson to have the benefits

of CR, and

2) IF does not cause stunting in body size like CR.

The body mass of mice on IF is almost twice that of mice on CR, but

the body composition stays at the lean level. Would you call that

extra weight from IF " calorie retention " ? I don't think so.

What seems to be important is not the *reduction* of calories, but

keeping the right amount of adipose tissue in relation to the body,

i.e., low percentage of body fat. Also, the starvation on the fasting

days for IF, or the continuous deprivation of food in CR affects

glycation of proteins, insulin sensitivity, and other metabolic

functions that probably are important for longevity, delay of cancer

onset, etc.

Given that there at at least two equivalent models for life extension

with different levels of nutrition (IF 100%: CR 60%), it seems

reasonable to consider the hypothesis that body mass and/or

composition have an important effect, independent of energy intake.

But I think that it is also important to consider the TIMING of the

energy intake. IF differs from ad libitium eating only in the TIMING

rather than in the AMOUNT of energy intake.

IMO, whatever happens in our body during periods of starvation is

probably as important for longevity as body composition.

Tony

> > >

> > > " ...suggesting that excess calorie retention, rather than

> > consumption, confers cancer risk. " Cancer Progression in the

> > Transgenic Adenocarcinoma of Mouse Prostate Mouse Is Related to

> > Energy Balance, Body Mass, and Body Composition, but not Food

> Intake

> > M. Huffman1, S. 1, Watts1, Ada Elgavish2,

> > Isam A. Eltoum3 and Tim R. Nagy1 Departments of 1 Nutrition

> > Sciences, 2 Genetics, and 3 Pathology, University of Alabama at

> > Birmingham, Birmingham, Alabama Requests for reprints: Tim R.

> Nagy,

> > Division of Physiology and Metabolism, Department of Nutrition

> > Sciences, University of Alabama at Birmingham, 419 Webb Building,

> > 1675 University Boulevard, Birmingham, AL 35294-3360. Phone: 205-

> 975-

> > 4088; Fax: 205-934-7050; E-mail: tnagy@ ' + u + '@' + d + ''//--

> > > . Calorie restriction can inhibit or delay carcinogenesis,

> > reportedly due to a reduction in calorie intake rather than by

> > concurrent changes in body mass and/or composition. Our objective

> was

> > > to test the hypothesis that body mass and/or composition have an

> > important effect, independent of energy intake, on the benefits or

> > hazards associated with calorie restriction or overeating,

> > respectively. In the first experiment, transgenic mice that

> > spontaneously develop prostate cancer [transgenic adenocarcinoma of

> > mouse prostate (TRAMP)] were housed at 27°C or 22°C and pair fed

> the

> > same diet for 21 weeks (95% of ad libitum intake at 27°C). In the

> > second experiment, TRAMP mice were housed at 27°C or 22°C and fed

> the

> > same diet ad libitum for 21 weeks. Despite a similar calorie

> intake,

> > pair-fed mice at 27°C (PF27) were heavier (28.3 ± 3.3 versus 17.6 ±

> > 1.6 g at 21 weeks; P < 0.001; mean ± SD) and had greater fat (6.4 ±

> > 2.1 versus 1.9 ± 0.3 g; P < 0.001) and lean mass (P < 0.001) than

> > pair-fed mice at 22°C. Furthermore, PF27 mice had greater levels of

> > serum leptin (P < 0.001), lower levels of adiponectin (P < 0.05),

> and

> > a greater frequency of prostatic adenocarcinoma (P <

> > > 0.05). In contrast, ad libitum–fed mice housed at 22°C consumed

> > 30% more calories than ad libitum–fed mice at 27°C, but there was

> no

> > difference between groups in body composition or cancer

> progression.

> > These results imply that the ability of calorie restriction to

> > inhibit or delay cancer incidence and progression is mediated in

> part

> > by changes in energy balance, body mass, and/or body composition

> > rather than calorie intake per se, suggesting that excess calorie

> > retention, rather than consumption, confers cancer risk. [Cancer

> Res

> > 2007;67(1):417–24]

> > >

> >

>

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Guest guest

Lance Armstrong is certainly not alone in terms of elite athletes

consuming and burning such a huge number of calories, so are you

proposing that they are all at elevated risk of cancer? Lance

Armstrong is just one data point, after all. Is there any evidence

that cancer incidence is higher among such athletes in general?

-Dave

>

> Hi Al

> Your comment about Lance Armstrong made me search a little

> about his nutrition. He appears to burn 9000 calories per day

> when training and consumes tons of Power Bars and sports

> drinks, many of which are high in HFCS. A part of me makes

> me wonder that despite that his exercise makes him lean,

> the amount of fuel passing through his body, and the type

> of fuel could contribute to cancer, which he has battled.

>

> http://www.athleteinme.com/tabid/37/id/1c81b4e2-603c-4c18-ab74-

cbf05a57304f/Default.aspx

>

> Cheers

> Arturo

>

> Re: Calorie Restriction Or Calorie " Retention " ?

> Posted by: " Al Young " acyoung@... al_young88

> Sat Mar 3, 2007 11:31 am (PST)

>

> <snip> So, to my mind, this experiment suggests that excess body

mass

> itself (calorie retention) contributes to risk. It suggests, for

example, that

> exercising to leaness is as effective as dieting to leaness

(regarding

> prostate cancer risk) - that isn't what traditional CR is about;

> Lance Armstrong isn't usually considered to be on CR (at, say, 9000

cal/d).

>

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Guest guest

You also have to take a look at the cancer that Armstrong survived

from. His amount of riding has never been dismissed as one of the

possible reasons for his testicular cancer. Millions of GIs have been

in the mode of losing weight on 6000 calories or more per day without

negative effects, but it wasn't taken to the year in and year out

level that

Armstrong took it.

Don White

Seguin, Tx

--- In , " Jewell " <wtjewell@...>

wrote:

>

>

>

>

> I think you would have to consider Lance Armstrong a heavy outlier data

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>Trails wrote:

>>>

c> Consider this: 1) Intermittent Fasting (IF) was

c> shown by Mattson to have the benefits of CR, and

c> The body mass of mice on IF is almost twice that of mice on CR, but

c> the body composition stays at the lean level.

>

> Hi. The problem I'd reflexively anticipate with IF is a change in

> body composition: storing fat on big-eating days, and sacrificing

> protein to be used as fuel on fasting days. (The same would

> presumably hold true for eating one big meal per day.) So you'd

> presumably exchange fat for muscle over time.

>

> If my concern is wrong, then can you suggest what mechanism(s)

> would be responsible? How can IF get the same result as sparse

> grazing? Are you practicing this yourself and found you have

> enhanced or maintained your own leanness? Would a couch potato

> on IF get dramatically different results than an exerciser

> on IF?

>>>

Actually, there is a lot of research and practical experience dealing

with intermittent fasting. Many research papers deal with the effects

of eating in 12-hour intervals such as are practiced by Muslims during

Ramadan, while others are genuine 24-hour intermittent fasting

protocols. None of these reports have found that people get more fat

and less muscle at the end of the experiments. On the contrary, fat

people tend to get leaner. Below are a few papers that represent the

tip of the iceberg on this topic.

With regard to the question: " How can IF get the same result as sparse

grazing? " -- I don't think that anybody knows for sure, but it is hard

to argue with the experimental results that show improvements in many

biomarkers and longevity.

By the way, there is a group of practitioners of Intermittent Fasting

(http://tech./group/fasting/) with about 240 members

who might be able to answer detailed questions about this mode of eating.

Tony

===

Effect of intermittent fasting and refeeding on insulin action in

healthy men

http://jap.physiology.org/cgi/content/full/99/6/2128

Weight, Body Composition, and Indexes of Physical Activity.

The body weight was maintained stable throughout the experiment (86.4

± 2.3 kg, 0.8 ± 0.1% coefficient of variation) and percent body fat

was also unchanged before compared with after the fasting intervention

(Table 1). The level of habitual daily physical activity did not

decrease during fasting days. Thus the average heart rate during

daytime was not different during fasting (79 ± 3 min–1) compared with

nonfasting days (80 ± 3 min–1).

Alternate-day fasting in nonobese subjects: effects on body weight,

body composition, and energy metabolism

http://www.ajcn.org/cgi/content/full/81/1/69

In conclusion, alternate-day fasting is feasible in nonobese subjects

for short time periods, although unlike rodents, the subjects were

unable to maintain their body weight. Furthermore, fat oxidation was

increased and translated into fat mass loss. Hunger on fasting days

did not habituate over the course of the study, which perhaps

indicates the unlikelihood of subjects continuing on this diet for

extended periods of time. Whether alternate-day fasting would promote

weight loss in an obese population is uncertain.

Fast way to better health. Dr. R. Eades

http://www.proteinpower.com/drmike/?p=278

Over the period that we followed the various IF regimens we lost a

little weight because, unlike the rodents, we couldn't eat twice as

much during the eating days as we would have eaten were we not fasting.

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