When is a calorie not a calorie?

[Elite121]

[MOD EDIT: Topic split from Protein detox]

Protein shakes are just another food at the end of the day.

I don"t think anything replaces wholesome food

If this drops your 'energy in' below your 'energy use' you'll lose weight, not good if you're trying to gain, but good if you're wanting to drop weight.

Which law of thermodynamics are you referring to?

[fit2fight]

If this drops your 'energy in' below your 'energy use' you'll lose weight, not good if you're trying to gain, but good if you're wanting to drop weight.

Which law of thermodynamics are you referring to?

The Second Law of Thermodynamics states that "in all energy exchanges, if no energy enters or leaves the system, the potential energy of the state will always be less than that of the initial state." This is also commonly referred to as entropy. Once the potential energy locked in carbohydrates is converted into kinetic energy (energy in use or motion), the organism will get no more until energy is input again. In the process of energy transfer, some energy will dissipate as heat. Entropy is a measure of disorder: cells are NOT disordered and so have low entropy. The flow of energy maintains order and life. Entropy wins when organisms cease to take in energy and die.

So lose weight (until death) would be right no?

[Elite121]

If this drops your 'energy in' below your 'energy use' you'll lose weight, not good if you're trying to gain, but good if you're wanting to drop weight.

Which law of thermodynamics are you referring to?

The Second Law of Thermodynamics states that "in all energy exchanges, if no energy enters or leaves the system, the potential energy of the state will always be less than that of the initial state." This is also commonly referred to as entropy. Once the potential energy locked in carbohydrates is converted into kinetic energy (energy in use or motion), the organism will get no more until energy is input again. In the process of energy transfer, some energy will dissipate as heat. Entropy is a measure of disorder: cells are NOT disordered and so have low entropy. The flow of energy maintains order and life. Entropy wins when organisms cease to take in energy and die.

So lose weight (until death) would be right no?

If a calorie is a calorie it violates the 2nd law of thermodynamics.

[teamfatboy]

Actually, putting aside the debate about "matter can neither be created nor destroyed, only transformed", isn't Nate's fundamental point still valid... if a body ingests less calories than it expends, regardless of the actual numbers, then some form of tissue must be used to make up the difference?

And so, if OP wants to steer clear of shakes, the difference would have to be made up somehow...?

If the issue's the cost, shop around for cheaper protein - including some of the advertisers...

[thatwaslight]

Which law of thermodynamics are you referring to?

The Second Law of Thermodynamics states that "in all energy exchanges, if no energy enters or leaves the system, the potential energy of the state will always be less than that of the initial state." This is also commonly referred to as entropy. Once the potential energy locked in carbohydrates is converted into kinetic energy (energy in use or motion), the organism will get no more until energy is input again. In the process of energy transfer, some energy will dissipate as heat. Entropy is a measure of disorder: cells are NOT disordered and so have low entropy. The flow of energy maintains order and life. Entropy wins when organisms cease to take in energy and die.

So lose weight (until death) would be right no?

If a calorie is a calorie it violates the 2nd law of thermodynamics.

How so?

[Im Hungry]

I'd have to agree with Nate

If a calorie is a calorie it violates the 2nd law of thermodynamics.

a calorie is a unit measure of energy in a lab environment only. the body is not that lab environment. To prove: a 1000 cals from protein (say chicken eggs and protein shakes) will promote fat loss whereas 1000 cals from carbs (= 10 cups cooked rice) will promote weight gain.

Whats that say about calories in relation to the human body?

(to qualify: In a non starving individual excess protein is broken down and excreted)

[ani_m0L]

Damn, is this the nerd-a-thon forum?

[nate225]

Damn, is this the nerd-a-thon forum?

LMAO ani-moL!

I'm enjoying sitting back and watching this one!

I'm all for scientific debate but lets not get complex for the sake of it - its all pretty simple in this case - the labcoats can come off gentlemen!

Eat more than you need = gain weight, Eat less = lose weight. Period. :nod:

[thatwaslight]

Damn, is this the nerd-a-thon forum?

LMAO ani-moL!

I'm enjoying sitting back and watching this one!

I'm all for scientific debate but lets not get complex for the sake of it - its all pretty simple in this case - the labcoats can come off gentlemen!

Eat more than you need = gain weight, Eat less = lose weight. Period. :nod:

Questions Nate, is this a proven theory? is there anecdotal evidence to support this? as fore mentioned this violates the 2nd law of thermodynamics and plus i read it on the innuhnet so how can you be right?

[Dubble_D]

hormonal differences between calorie from protein and other calories such as from fat. just mentioned it on the worlds heaviest man program on prime. Did not go into details.

[nate225]

Questions Nate, is this a proven theory? is there anecdotal evidence to support this? as fore mentioned this violates the 2nd law of thermodynamics and plus i read it on the innuhnet so how can you be right?

There was this study with a significant sample size, from memory it was every fucking person who ever ate food - all that ate more than they expended got heavier, all that ate less than they expended got lighter! LOL. No post grad quals needed to comprehend that one.

Great pisstake btw thatwaslight, I hope?!

For anyone taking this seriously you may wish to find another sport that doesn't require you to constantly modify your bodyweight! :grin:

hormonal differences between calorie from protein and other calories such as from fat. just mentioned it on the worlds heaviest man program on prime. Did not go into details.

Sounds way to much like "my medical condition makes me put on weight".

Unless you've got tumours growing its the food going down your throat making you gain weight.

[Dubble_D]

It is obvious, you are what you eat.

How ever I am still interested in how a calorie from protein differs from a calorie from fat or carb?

I find it interesting.

[nate225]

How ever I am still interested in how a calorie from protein differs from a calorie from fat or carb?

It doesn't.

A calorie is a calorie. Period.

It is simply a unit of measure. Like a kilometre equals a kilometre.

The pathways utilised in the body to access that calorie differ for different substrates (carb, protein, lipids, alcohol etc). A first year biochem paper might be worth doing if metabolism floats your boat Dubble_D?

We've hijacked this thread enough! Back to protein shakes! :grin:

[Dubble_D]

Thanks Nate,

A calorie is a calorie, thats why I am a marine and costal ecology major and thankfully I have managed to stay clear of Biochem!

I guess a protein detox is when you have to much muscle and want to lose some, personally I can't afford to do that.

[Elite121]

The Second Law of Thermodynamics states that "in all energy exchanges, if no energy enters or leaves the system, the potential energy of the state will always be less than that of the initial state." This is also commonly referred to as entropy. Once the potential energy locked in carbohydrates is converted into kinetic energy (energy in use or motion), the organism will get no more until energy is input again. In the process of energy transfer, some energy will dissipate as heat. Entropy is a measure of disorder: cells are NOT disordered and so have low entropy. The flow of energy maintains order and life. Entropy wins when organisms cease to take in energy and die.

So lose weight (until death) would be right no?

If a calorie is a calorie it violates the 2nd law of thermodynamics.

How so?

http://www.nutritionj.com/content/3/1/9

[Mr_Krabs]

I hate to be an ass here but a calorie is a calorie in the calorimeter in which they measured the energy output by burning it.

Not all calories are created equal in biological metabolic systems, we are ignorring the fact that the body is better equipped to use or store energy from some macros over others.

[Phedder]

I hate to be an ass here but a calorie is a calorie in the calorimeter in which they measured the energy output by burning it.

But the body is not a calorimeter and should not be considered as one.

Not all calories are created equal in biological metabolic systems, we are ignorring the fact that the body is better equipped to use or store energy from some macros over others.

Why are we ignoring that fact? That's a fundamental point that cannot be ignored, Calorie intake from differing ratios of macro-nutrients may be the same, but the body cannot utilize the macros with the same efficiency so the net calories gained by the body can be altered dependent on the ratio of macros consumed. The two different ratios will net the same result in a calorimeter, but not in the human body which is what matters when it comes to diet.

Thanks for posting that article elite, was a fascinating read.

[Elite121]

No one eats calories; calories are just a measurement (as is an centimeter) and have no substance. A calorie is a unit of heat equal to the amount of heat required to raise the temperature of one kilogram of water by one degree at one atmosphere pressure.Does this sound like a human body?

I don't agree with the common held knowledge of "A calorie is a calorie" To imply that its saying that the body is a heat engine! The human body is not a heat engine!The human body is more like a complex chemical factory than it is a heat engine.

Food is converted in to complex substances and structures and not as a machine designed for heat production, which the measurement of a calorie is.

A scientist named Adolph Fick proved in 1893 that living cells cannot be heat engines. Biological systems like humans are isothermal (equal temperature) systems. Cells cannot act as heat engines, for they have no means of permitting heat to flow from a warmer to a cooler body.

Nobel Prize-winner, Hans Krebs, mentioned in his book about another Nobel Prize-winner, Otto Warburg, M.D., Ph.D. “Fick made it clear in 1893 that living cells cannot be heat engines…”

Herman Taller, M.D, author of Calories Don’t Count stated, “One could assert with absolute certainty that the calorie theory has no scientific basis whatsoever”

In 2003, Harvard University study found people on a low carbohydrate diet could eat 25,000 more calories than those on a high carbohydrate diet over a 12-week period and they gained no additional weight. If the calorie theory was correct then the low carbohydrate group should have gained a little over 3kg's of fat.

http://harvardscience.harvard.edu/medic ... ve-low-fat

In another study conducted at Harvard University, some participants ate only carbohydrates, while other participants ate twice as many calories of only protein. Although the protein eaters ate twice as many calories as the carbohydrates eaters, they didn't gain any weight, whereas the carbohydrates eaters gained weight despite eating fewer calories.

http://www.ncbi.nlm.nih.gov/pubmed/19246357

So again is a calorie a calorie?

A number of recent studies that have shown that subjects following low-carb diets actually lose more weight than their counterparts on low-fat, high carb diets despite the fact that the low-carbers consumed considerably more calories.Take a look at this earlier study to see more:

http://www.ajcn.org/cgi/reprint/23/7/948

I also don't agree with the the calories in calories out theory..heres why.

ttp://video.google.com/videoplay?docid= ... 661765149#

And on another note if it was that simple calorie in calories out then why then are there 300 million people worldwide that are obese, and over a billion overweight, according to the World Health Organization (WHO). Clearly the calories in calories out theory is not working!

And a big thing when people talk about calories in calorie out is that they almost never mention a very important aspect Hormones...its beyond me that people ignore this.Hormones have a huge part to play. Think INSULIN it governs how much fat we accumulate in our fat tissue. Insulin is lipogenic.

http://atvb.ahajournals.org/cgi/content ... ct/9/4/479

http://cat.inist.fr/?aModele=afficheN&cpsidt=2770384

An important thing to remember is, it's not the amount of calories eaten, it’s the content of the calories. If we eat foods that will be used for energy and body structure, like proteins and natural fats, we do NOT have to worry about getting fat. On the other hand, if we load up on carbs, which are not used for building the body structure, the body must release insulin to treat the excess sugar from the carbs and then will ultimately store this sugar as fat.

Eat for nutrition not for calories

[Mr_Krabs]

I hate to be an ass here but a calorie is a calorie in the calorimeter in which they measured the energy output by burning it.

But the body is not a calorimeter and should not be considered as one.

Not all calories are created equal in biological metabolic systems, we are ignorring the fact that the body is better equipped to use or store energy from some macros over others.

Why are we ignoring that fact? That's a fundamental point that cannot be ignored, Calorie intake from differing ratios of macro-nutrients may be the same, but the body cannot utilize the macros with the same efficiency so the net calories gained by the body can be altered dependent on the ratio of macros consumed. The two different ratios will net the same result in a calorimeter, but not in the human body which is what matters when it comes to diet.

Thanks for posting that article elite, was a fascinating read.

LOL wrong end of stick much? :pfft:

We're on the same page bro :grin:

[nate225]

Elite - I appreciate all the research, (I haven't had a chance to look at yet but will), but you are starting to sound a little like a low carb zealot seeking to convert the masses!!! It's not Elite Atkins by any chance? :grin:

Your statement re: Insulin is lipogenic, whilst being true you forget to state that insulin is also anabolic in relation to skeletal muscle...... :nod: Point being it's not all bad, you just manipulate it to suit your particular needs at the time.

You state An important thing to remember is, it's not the amount of calories eaten, it’s the content of the calories. If we eat foods that will be used for energy and body structure, like proteins and natural fats, we do NOT have to worry about getting fat. On the other hand, if we load up on carbs, which are not used for building the body structure, the body must release insulin to treat the excess sugar from the carbs and then will ultimately store this sugar as fat.

Again this may have some basis, however when eating to meet your needs (as opposed to 'loading up on carbs'), you will simply replace the glycogen in muscle, liver and maintain blood glucose levels; NOT as you state "ultimately store this sugar as fat". This will however occur if you are eating more carbs than you need to meet your total energy requirements, as it would with any other macro (lets ignore the negligible thermic effect of protein to keep it simple?).

Your comment And on another note if it was that simple calorie in calories out then why then are there 300 million people worldwide that are obese, and over a billion overweight, according to the World Health Organization (WHO). Clearly the calories in calories out theory is not working!

Yep something aint working! But the theory holds strong. Obesogenic environment is a term you may or may not heard. Less physical activity in our lives than our predecessors and more calorie-dense foods available - READ: Less energy used, more energy consumed. In short more fat asses!

I'm not having a crack at you Elite, I appreciate a good debate (and the research you have done to support your argument) but I don't think we'll see eye to eye on this one!

I do however like your last statement though "Eat for nutrition not for calories" - I've never counted calories personally. By adjusting the volumes & type of food however I adjust my calorie intake by default, and gain/lose weight accordingly.

Nate

[Elite121]

Elite - I appreciate all the research, (I haven't had a chance to look at yet but will), but you are starting to sound a little like a low carb zealot seeking to convert the masses!!! It's not Elite Atkins by any chance? :grin:

Your statement re: Insulin is lipogenic, whilst being true you forget to state that insulin is also anabolic in relation to skeletal muscle...... :nod: Point being it's not all bad, you just manipulate it to suit your particular needs at the time.

Its a common held belief that raising insulin post workout leads to an anabolic effect on skeletal muscle....but then again it may have a catabolic effect, bad news for some supplement companies and the industry funded research...

You state An important thing to remember is, it's not the amount of calories eaten, it’s the content of the calories. If we eat foods that will be used for energy and body structure, like proteins and natural fats, we do NOT have to worry about getting fat. On the other hand, if we load up on carbs, which are not used for building the body structure, the body must release insulin to treat the excess sugar from the carbs and then will ultimately store this sugar as fat.

Again this may have some basis, however when eating to meet your needs (as opposed to 'loading up on carbs'), you will simply replace the glycogen in muscle, liver and maintain blood glucose levels; NOT as you state "ultimately store this sugar as fat". This will however occur if you are eating more carbs than you need to meet your total energy requirements, as it would with any other macro (lets ignore the negligible thermic effect of protein to keep it simple?).

Your comment And on another note if it was that simple calorie in calories out then why then are there 300 million people worldwide that are obese, and over a billion overweight, according to the World Health Organization (WHO). Clearly the calories in calories out theory is not working!

Yep something aint working! But the theory holds strong. Obesogenic environment is a term you may or may not heard. Less physical activity in our lives than our predecessors and more calorie-dense foods available - READ: Less energy used, more energy consumed. In short more fat asses!

The Caloric Balance Hypothesis is flawed:

When a female enters puberty she gains weight this has absolutely nothing to do with caloric balance controlling fat tissue, but more to do with hormones.

We have a worldwide epidemic of obesity in 6 month olds,and we also have obesity and malnutrition strongly linked. The energy balance hypothesis completely ignores this evidence.

Another example is Lipodystrophy that shows people who are morbidly obese in the lower body and rail thin in the upper body and vice versa.What does the calorie balance hypothesis have to do with any of that?

http://video.google.com/videoplay?docid ... 661765149#

Does overeating calories really make us fat over the long term?

Role of Nonexercise Activity Thermogenesis in Resistance to Fat Gain in Humans

James A. Levine, Norman L. Eberhardt, Michael D. Jensen *

Humans show considerable interindividual variation in susceptibility to weight gain in response to overeating. The physiological basis of this variation was investigated by measuring changes in energy storage and expenditure in 16 nonobese volunteers who were fed 1000 kilocalories per day in excess of weight-maintenance requirements for 8 weeks. Two-thirds of the increases in total daily energy expenditure was due to increased nonexercise activity thermogenesis (NEAT), which is associated with fidgeting, maintenance of posture, and other physical activities of daily life. Changes in NEAT accounted for the 10-fold differences in fat storage that occurred and directly predicted resistance to fat gain with overfeeding (correlation coefficient = 0.77, probability < 0.001). These results suggest that as humans overeat, activation of NEAT dissipates excess energy to preserve leanness and that failure to activate NEAT may result in ready fat gain.

Autonomic nervous system activity in weight gain and weight loss

L. J. Arone, R. Mackintosh, M. Rosenbaum, R. L. Leibel and J. Hirsch

Laboratory of Human Behavior and Metabolism, Rockefeller University, New York, New York 10021-6399, USA.

Studies in both animals and humans indicate that the autonomic nervous system (ANS) responds to changes in systemic energy balance. In the present study, ANS response to weight change was examined by sequential blockade of cardiac autonomic innervation with parasympathetic (atropine) and sympathetic (esmolol) blockers. Change in heart period (interbeat interval) from baseline after atropine defined the amount of parasympathetic control (PC), and the subsequent change after esmolol defined the amount of sympathetic control (SC). In nonobese subjects, weight gain to 10% above initial body weight resulted in a decrease in PC and an increase in SC, and conversely, weight loss to 10% below initial weight resulted in an increase in PC and a decrease in SC. In obese subjects, weight loss resulted in the same pattern of changes in PC and SC. The major changes were in the parasympathetic arm of the ANS. These findings support the hypothesis that the ANS acts to oppose weight change.

Does a sedentary lifestyle really make us fat? Or is it inactivity that appears to be a consequence, not a cause, of being overweight?

Contribution of a sedentary lifestyle and inactivity to the etiology of overweight and obesity: current evidence and research issues.

Jebb SA, Moore MS.

MRC Human Nutrition Research, Cambridge, United Kingdom.

Abstract

PURPOSE: The etiology of overweight and obesity is clearly multifactorial, but ultimately it is determined by the long-term balance between energy intake and expenditure. This review will consider the effects on body weight and the risk of obesity of sedentary lifestyles, within the context of dietary habits. METHODS: The data from ecological, cross-sectional, and prospective studies that have assessed physical activity and dietary intake and their relationship to body weight were reviewed. RESULTS: Ecological analyses imply that the increase in the prevalence of obesity is more strongly related to lower levels of physical activity than higher energy intakes. However, there is a paucity of pertinent data from cross-sectional or prospective studies. There is some evidence that both a high proportion of dietary fat and low levels of physical activity may increase the likelihood of weight gain. However, even the most comprehensive studies are unable to account for more than a small proportion of the interindividual variance in weight gain, so it is difficult to usefully assess their relative importance. Furthermore, there are insufficient data that pertain to "sedentary lifestyles" to segregate any putative effect from a protective effect of exercise. All the data in this review is NHLBI Evidence category C. CONCLUSIONS: This review provides clear evidence that low levels of physical activity are associated with an increased risk of weight gain and obesity. On balance, the evidence is suggestive of a causal link, but the experimental designs are too weak is provide conclusive evidence. The potential effect of interactions between diet and activity have largely been ignored. To make progress in this area, a number of key issues need to be resolved with regard to the methodology, study design, and statistical analysis of prospective epidemiological studies. In the meantime, data need to be drawn from other sources, particularly those studies designed to elucidate the mechanism of action of diet and physical activity in the etiology of obesity, to establish rational interventions to guide public health policies.

ORIGINAL RESEARCH COMMUNICATION

Time spent being sedentary and weight gain in healthy adults: reverse or bidirectional causality?1,2,3

Ulf Ekelund1, Søren Brage1, Herve Besson1, Stephen Sharp1 and Nicholas J Wareham1

1 From the Medical Research Council Epidemiology Unit, Institute of Metabolic Science, Cambridge, United Kingdom

Background:Whether obesity is a cause or a consequence of a sedentary lifestyle has not yet been fully elucidated, which leaves uncertainty about the direction of causality.

Objective:We aimed to assess the longitudinal associations between objectively measured time spent being sedentary (sedentary time) and obesity indicators.

Design:The study was a prospective, population-based cohort study in 393 middle-aged healthy whites (n = 176 M, 217 F). Sedentary time (% of daytime hours) was measured by individually calibrated monitoring of the heart rate. Body weight (BW), body mass index (BMI), and waist circumference (WC) were assessed by standard clinical procedures. Fat mass (FM) was assessed with bioimpedance. All measurements were collected at baseline and at 5.6-y follow-up.

Results:At baseline, sedentary time was significantly correlated with FM (partial r = 0.10, P = 0.043) and WC (partial r = 0.11, P = 0.027) after adjustment for sex and age. At follow-up, sedentary time was significantly correlated with BW (partial r = 0.19, P < 0.0001), BMI (partial r = 0.20, P < 0.0001), WC (partial r = 0.15, P = 0.003), and FM (partial r = 0.19, P < 0.0001). Sedentary time did not predict any of the obesity indicators at follow-up. In contrast, BW (β = 0.33; 95% CI: 0.15, 0.50), BMI (1.10; 0.58, 1.63), FM (0.59; 0.11, 0.40), and WC (0.44; 0.23, 0.66) predicted sedentary time at follow-up after adjustment for sex, baseline age, baseline sedentary time, baseline physical activity energy expenditure, and follow-up time.

Conclusion:BMI, FM, and WC may predict sedentary time, but our results do not suggest that sedentary time predicts future obesity.

[Phedder]

I hate to be an ass here but a calorie is a calorie in the calorimeter in which they measured the energy output by burning it.

But the body is not a calorimeter and should not be considered as one.

Not all calories are created equal in biological metabolic systems, we are ignorring the fact that the body is better equipped to use or store energy from some macros over others.

Why are we ignoring that fact? That's a fundamental point that cannot be ignored, Calorie intake from differing ratios of macro-nutrients may be the same, but the body cannot utilize the macros with the same efficiency so the net calories gained by the body can be altered dependent on the ratio of macros consumed. The two different ratios will net the same result in a calorimeter, but not in the human body which is what matters when it comes to diet.

Thanks for posting that article elite, was a fascinating read.

LOL wrong end of stick much? :pfft:

We're on the same page bro :grin:

Yeah I realise that, I was agreeing with you but trying to explain somewhat simply to others reading this thread why we shouldn't ignore it. I hope it didn't come off as an attack, wasn't even directly replying to you, just in general on what you said.

[nate225]

The Caloric Balance Hypothesis is flawed:

When a female enters puberty she gains weight this has absolutely nothing to do with caloric balance controlling fat tissue, but more to do with hormones.

We have a worldwide epidemic of obesity in 6 month olds,and we also have obesity and malnutrition strongly linked. The energy balance hypothesis completely ignores this evidence.

Both the above are general statements that don't really lend any support to your argument Elite. However the earlier statement intriques me though, and it may be worth investigating to see if hormones really play such a big role or is it that confounding variables impact on the weight gain here? (e.g. hormones, particularly estrogen etc which increase masively at this point leading to changes in eating habits, satiety etc, bone growth such as broadening of hips at puberty, water retention from hormone level changes etc).

The latter statement re: babies has adds to the obesogenic environment argument - traditionally high rates of breast feeding vs feed on demand formulas, introduction of high calorie wemi-solids pre 6 months etc.

Another example is Lipodystrophy that shows people who are morbidly obese in the lower body and rail thin in the upper body and vice versa.What does the calorie balance hypothesis have to do with any of that?

Not sure what you're getting at Elite? Has this changed over the years? Lack of physical activity leads to lack of muscle development, if that is what 'rail thin' refers to? If you are talking purely about fat distribution with 'rail thin' then hormones do have a role to play. No debate there.

Does overeating calories really make us fat over the long term?

Role of Nonexercise Activity Thermogenesis in Resistance to Fat Gain in Humans

James A. Levine, Norman L. Eberhardt, Michael D. Jensen *

Humans show considerable interindividual variation in susceptibility to weight gain in response to overeating. The physiological basis of this variation was investigated by measuring changes in energy storage and expenditure in 16 nonobese volunteers who were fed 1000 kilocalories per day in excess of weight-maintenance requirements for 8 weeks. Two-thirds of the increases in total daily energy expenditure was due to increased nonexercise activity thermogenesis (NEAT), which is associated with fidgeting, maintenance of posture, and other physical activities of daily life. Changes in NEAT accounted for the 10-fold differences in fat storage that occurred and directly predicted resistance to fat gain with overfeeding (correlation coefficient = 0.77, probability < 0.001). These results suggest that as humans overeat, activation of NEAT dissipates excess energy to preserve leanness and that failure to activate NEAT may result in ready fat gain.

Autonomic nervous system activity in weight gain and weight loss

L. J. Arone, R. Mackintosh, M. Rosenbaum, R. L. Leibel and J. Hirsch

Laboratory of Human Behavior and Metabolism, Rockefeller University, New York, New York 10021-6399, USA.

Studies in both animals and humans indicate that the autonomic nervous system (ANS) responds to changes in systemic energy balance. In the present study, ANS response to weight change was examined by sequential blockade of cardiac autonomic innervation with parasympathetic (atropine) and sympathetic (esmolol) blockers. Change in heart period (interbeat interval) from baseline after atropine defined the amount of parasympathetic control (PC), and the subsequent change after esmolol defined the amount of sympathetic control (SC). In nonobese subjects, weight gain to 10% above initial body weight resulted in a decrease in PC and an increase in SC, and conversely, weight loss to 10% below initial weight resulted in an increase in PC and a decrease in SC. In obese subjects, weight loss resulted in the same pattern of changes in PC and SC. The major changes were in the parasympathetic arm of the ANS. These findings support the hypothesis that the ANS acts to oppose weight change.

Not sure where you are going with this Elite? It's well established individuals have differing basal metabolic rates. The 'jittering' thing has been known for years - if only I had it to keep the BF down! :grin: It changes the amount of calories an individual needs to eat to 'break even' but doesn't negate the 'calorie is a calorie' theory unless I missed something?

Does a sedentary lifestyle really make us fat? Or is it inactivity that appears to be a consequence, not a cause, of being overweight?

Contribution of a sedentary lifestyle and inactivity to the etiology of overweight and obesity: current evidence and research issues.

Jebb SA, Moore MS.

MRC Human Nutrition Research, Cambridge, United Kingdom.

Abstract

PURPOSE: The etiology of overweight and obesity is clearly multifactorial, but ultimately it is determined by the long-term balance between energy intake and expenditure. This review will consider the effects on body weight and the risk of obesity of sedentary lifestyles, within the context of dietary habits. METHODS: The data from ecological, cross-sectional, and prospective studies that have assessed physical activity and dietary intake and their relationship to body weight were reviewed. RESULTS: Ecological analyses imply that the increase in the prevalence of obesity is more strongly related to lower levels of physical activity than higher energy intakes. However, there is a paucity of pertinent data from cross-sectional or prospective studies. There is some evidence that both a high proportion of dietary fat and low levels of physical activity may increase the likelihood of weight gain. However, even the most comprehensive studies are unable to account for more than a small proportion of the interindividual variance in weight gain, so it is difficult to usefully assess their relative importance. Furthermore, there are insufficient data that pertain to "sedentary lifestyles" to segregate any putative effect from a protective effect of exercise. All the data in this review is NHLBI Evidence category C. CONCLUSIONS: This review provides clear evidence that low levels of physical activity are associated with an increased risk of weight gain and obesity. On balance, the evidence is suggestive of a causal link, but the experimental designs are too weak is provide conclusive evidence. The potential effect of interactions between diet and activity have largely been ignored. To make progress in this area, a number of key issues need to be resolved with regard to the methodology, study design, and statistical analysis of prospective epidemiological studies. In the meantime, data need to be drawn from other sources, particularly those studies designed to elucidate the mechanism of action of diet and physical activity in the etiology of obesity, to establish rational interventions to guide public health policies.

ORIGINAL RESEARCH COMMUNICATION

Time spent being sedentary and weight gain in healthy adults: reverse or bidirectional causality?1,2,3

Ulf Ekelund1, Søren Brage1, Herve Besson1, Stephen Sharp1 and Nicholas J Wareham1

1 From the Medical Research Council Epidemiology Unit, Institute of Metabolic Science, Cambridge, United Kingdom

Background:Whether obesity is a cause or a consequence of a sedentary lifestyle has not yet been fully elucidated, which leaves uncertainty about the direction of causality.

Objective:We aimed to assess the longitudinal associations between objectively measured time spent being sedentary (sedentary time) and obesity indicators.

Design:The study was a prospective, population-based cohort study in 393 middle-aged healthy whites (n = 176 M, 217 F). Sedentary time (% of daytime hours) was measured by individually calibrated monitoring of the heart rate. Body weight (BW), body mass index (BMI), and waist circumference (WC) were assessed by standard clinical procedures. Fat mass (FM) was assessed with bioimpedance. All measurements were collected at baseline and at 5.6-y follow-up.

Results:At baseline, sedentary time was significantly correlated with FM (partial r = 0.10, P = 0.043) and WC (partial r = 0.11, P = 0.027) after adjustment for sex and age. At follow-up, sedentary time was significantly correlated with BW (partial r = 0.19, P < 0.0001), BMI (partial r = 0.20, P < 0.0001), WC (partial r = 0.15, P = 0.003), and FM (partial r = 0.19, P < 0.0001). Sedentary time did not predict any of the obesity indicators at follow-up. In contrast, BW (β = 0.33; 95% CI: 0.15, 0.50), BMI (1.10; 0.58, 1.63), FM (0.59; 0.11, 0.40), and WC (0.44; 0.23, 0.66) predicted sedentary time at follow-up after adjustment for sex, baseline age, baseline sedentary time, baseline physical activity energy expenditure, and follow-up time.

Conclusion:BMI, FM, and WC may predict sedentary time, but our results do not suggest that sedentary time predicts future obesity.

This is gold Elite! :nod:

Regardless of the position you or I take, it seems allowing oneself to become obese, (whether you choose to believe it was through hormones & food type choices or through sheer calorific overload), starts a self perpetuating cycle in terms of sedentary lifestyle.

I probably haven't given your research the time it deserves - I will if/when I get a chance - unfortunately I'm trying to hold down a job at the moment! :grin:

[thatwaslight]

Questions Nate, is this a proven theory? is there anecdotal evidence to support this? as fore mentioned this violates the 2nd law of thermodynamics and plus i read it on the innuhnet so how can you be right?

There was this study with a significant sample size, from memory it was every fucking person who ever ate food - all that ate more than they expended got heavier, all that ate less than they expended got lighter! LOL. No post grad quals needed to comprehend that one.

Great pisstake btw thatwaslight, I hope?!

:grin: fabulous debate, maybe 300 million people are over weight because they dont understand that the calorie being a calorie violates the second law of thermodynamics nate! :shock: :pfft:

[Elite121]

The Caloric Balance Hypothesis is flawed:

When a female enters puberty she gains weight this has absolutely nothing to do with caloric balance controlling fat tissue, but more to do with hormones.

We have a worldwide epidemic of obesity in 6 month olds,and we also have obesity and malnutrition strongly linked. The energy balance hypothesis completely ignores this evidence.

Both the above are general statements that don't really lend any support to your argument Elite. However the earlier statement intriques me though, and it may be worth investigating to see if hormones really play such a big role or is it that confounding variables impact on the weight gain here? (e.g. hormones, particularly estrogen etc which increase masively at this point leading to changes in eating habits, satiety etc, bone growth such as broadening of hips at puberty, water retention from hormone level changes etc).

The latter statement re: babies has adds to the obesogenic environment argument - traditionally high rates of breast feeding vs feed on demand formulas, introduction of high calorie wemi-solids pre 6 months etc.

The examples may be general but are real world examples and do back my argument against the caloric balance hypothesis that says very much that inactivity and overeating leads to fat gain PERIOD...I assume you believe this hypothesis by your previous post:

Yep something aint working! But the theory holds strong. Obesogenic environment is a term you may or may not heard. Less physical activity in our lives than our predecessors and more calorie-dense foods available - READ: Less energy used, more energy consumed. In short more fat asses!

In regards to the babies comment, HFCS is a culprit in obesity that plays a huge role affecting genetics to produce this disorder. I think there are more factors affecting childhood obesity that go beyond calories.Take for example children in 3rd world countries where they are undernourished and they still end up obese.. something else is affecting their fat accumulation.

Another example is Lipodystrophy that shows people who are morbidly obese in the lower body and rail thin in the upper body and vice versa.What does the calorie balance hypothesis have to do with any of that?

Not sure what you're getting at Elite? Has this changed over the years? Lack of physical activity leads to lack of muscle development, if that is what 'rail thin' refers to? If you are talking purely about fat distribution with 'rail thin' then hormones do have a role to play. No debate there.

Again the caloric balance theory states you get fat by overeating and lack of activity....this is not true my example of Lipodystrophy hopefully shows you how faulty the hypothesis is.Lipodystrophy is hormonally caused characterized by degenerative and abnormal functioning of the adipose tissue present in an individual's body and not by exercise and diet.(Calorie balance hypothesis)

Does overeating calories really make us fat over the long term?

Role of Nonexercise Activity Thermogenesis in Resistance to Fat Gain in Humans

James A. Levine, Norman L. Eberhardt, Michael D. Jensen *

Humans show considerable interindividual variation in susceptibility to weight gain in response to overeating. The physiological basis of this variation was investigated by measuring changes in energy storage and expenditure in 16 nonobese volunteers who were fed 1000 kilocalories per day in excess of weight-maintenance requirements for 8 weeks. Two-thirds of the increases in total daily energy expenditure was due to increased nonexercise activity thermogenesis (NEAT), which is associated with fidgeting, maintenance of posture, and other physical activities of daily life. Changes in NEAT accounted for the 10-fold differences in fat storage that occurred and directly predicted resistance to fat gain with overfeeding (correlation coefficient = 0.77, probability < 0.001). These results suggest that as humans overeat, activation of NEAT dissipates excess energy to preserve leanness and that failure to activate NEAT may result in ready fat gain.

Autonomic nervous system activity in weight gain and weight loss

L. J. Arone, R. Mackintosh, M. Rosenbaum, R. L. Leibel and J. Hirsch

Laboratory of Human Behavior and Metabolism, Rockefeller University, New York, New York 10021-6399, USA.

Studies in both animals and humans indicate that the autonomic nervous system (ANS) responds to changes in systemic energy balance. In the present study, ANS response to weight change was examined by sequential blockade of cardiac autonomic innervation with parasympathetic (atropine) and sympathetic (esmolol) blockers. Change in heart period (interbeat interval) from baseline after atropine defined the amount of parasympathetic control (PC), and the subsequent change after esmolol defined the amount of sympathetic control (SC). In nonobese subjects, weight gain to 10% above initial body weight resulted in a decrease in PC and an increase in SC, and conversely, weight loss to 10% below initial weight resulted in an increase in PC and a decrease in SC. In obese subjects, weight loss resulted in the same pattern of changes in PC and SC. The major changes were in the parasympathetic arm of the ANS. These findings support the hypothesis that the ANS acts to oppose weight change.

Not sure where you are going with this Elite? It's well established individuals have differing basal metabolic rates. The 'jittering' thing has been known for years - if only I had it to keep the BF down! :grin: It changes the amount of calories an individual needs to eat to 'break even' but doesn't negate the 'calorie is a calorie' theory unless I missed something?

My point is that inactivity does not lead to long term weight gain.Inactivity is a consequence, not a cause, of being overweight.

Does a sedentary lifestyle really make us fat? Or is it inactivity that appears to be a consequence, not a cause, of being overweight?

Contribution of a sedentary lifestyle and inactivity to the etiology of overweight and obesity: current evidence and research issues.

Jebb SA, Moore MS.

MRC Human Nutrition Research, Cambridge, United Kingdom.

Abstract

PURPOSE: The etiology of overweight and obesity is clearly multifactorial, but ultimately it is determined by the long-term balance between energy intake and expenditure. This review will consider the effects on body weight and the risk of obesity of sedentary lifestyles, within the context of dietary habits. METHODS: The data from ecological, cross-sectional, and prospective studies that have assessed physical activity and dietary intake and their relationship to body weight were reviewed. RESULTS: Ecological analyses imply that the increase in the prevalence of obesity is more strongly related to lower levels of physical activity than higher energy intakes. However, there is a paucity of pertinent data from cross-sectional or prospective studies. There is some evidence that both a high proportion of dietary fat and low levels of physical activity may increase the likelihood of weight gain. However, even the most comprehensive studies are unable to account for more than a small proportion of the interindividual variance in weight gain, so it is difficult to usefully assess their relative importance. Furthermore, there are insufficient data that pertain to "sedentary lifestyles" to segregate any putative effect from a protective effect of exercise. All the data in this review is NHLBI Evidence category C. CONCLUSIONS: This review provides clear evidence that low levels of physical activity are associated with an increased risk of weight gain and obesity. On balance, the evidence is suggestive of a causal link, but the experimental designs are too weak is provide conclusive evidence. The potential effect of interactions between diet and activity have largely been ignored. To make progress in this area, a number of key issues need to be resolved with regard to the methodology, study design, and statistical analysis of prospective epidemiological studies. In the meantime, data need to be drawn from other sources, particularly those studies designed to elucidate the mechanism of action of diet and physical activity in the etiology of obesity, to establish rational interventions to guide public health policies.

ORIGINAL RESEARCH COMMUNICATION

Time spent being sedentary and weight gain in healthy adults: reverse or bidirectional causality?1,2,3

Ulf Ekelund1, Søren Brage1, Herve Besson1, Stephen Sharp1 and Nicholas J Wareham1

1 From the Medical Research Council Epidemiology Unit, Institute of Metabolic Science, Cambridge, United Kingdom

Background:Whether obesity is a cause or a consequence of a sedentary lifestyle has not yet been fully elucidated, which leaves uncertainty about the direction of causality.

Objective:We aimed to assess the longitudinal associations between objectively measured time spent being sedentary (sedentary time) and obesity indicators.

Design:The study was a prospective, population-based cohort study in 393 middle-aged healthy whites (n = 176 M, 217 F). Sedentary time (% of daytime hours) was measured by individually calibrated monitoring of the heart rate. Body weight (BW), body mass index (BMI), and waist circumference (WC) were assessed by standard clinical procedures. Fat mass (FM) was assessed with bioimpedance. All measurements were collected at baseline and at 5.6-y follow-up.

Results:At baseline, sedentary time was significantly correlated with FM (partial r = 0.10, P = 0.043) and WC (partial r = 0.11, P = 0.027) after adjustment for sex and age. At follow-up, sedentary time was significantly correlated with BW (partial r = 0.19, P < 0.0001), BMI (partial r = 0.20, P < 0.0001), WC (partial r = 0.15, P = 0.003), and FM (partial r = 0.19, P < 0.0001). Sedentary time did not predict any of the obesity indicators at follow-up. In contrast, BW (β = 0.33; 95% CI: 0.15, 0.50), BMI (1.10; 0.58, 1.63), FM (0.59; 0.11, 0.40), and WC (0.44; 0.23, 0.66) predicted sedentary time at follow-up after adjustment for sex, baseline age, baseline sedentary time, baseline physical activity energy expenditure, and follow-up time.

Conclusion:BMI, FM, and WC may predict sedentary time, but our results do not suggest that sedentary time predicts future obesity.

This is gold Elite! :nod:

Regardless of the position you or I take, it seems allowing oneself to become obese, (whether you choose to believe it was through hormones & food type choices or through sheer calorific overload), starts a self perpetuating cycle in terms of sedentary lifestyle.

I probably haven't given your research the time it deserves - I will if/when I get a chance - unfortunately I'm trying to hold down a job at the moment! :grin: