"Starvation Mode" / isocaloric diets

[Gr3g_Lycan]

1. I have seen various posts about people cutting calories but not losing fat. Some responses refer to this as "starvation mode", and all I can find are anecdotal references to "starvation mode". However we don know Very Low Calorie Diets work.

Is "starvation mode" broscience? Where is the research?


2. There is some research underway on what "causes different people to gain or lose weight when they appear to eat and exercise the same amount"
http://www.physorg.com/news9144.html

We do know that there are genes associated with diabetes, and these have effects on insulin sensitivity, which affects metabolism.

So what solid research is there on isocaloric diets (ie people eating the same calories) and the ability to lose/gain weight?

[Emma-Leigh]

Originally Posted by GregT

1. I have seen various posts about people cutting calories but not losing fat. Some responses refer to this as "starvation mode", and all I can find are anecdotal references to "starvation mode". However we don know Very Low Calorie Diets work.

Is "starvation mode" broscience? Where is the research?


2. There is some research underway on what "causes different people to gain or lose weight when they appear to eat and exercise the same amount"
http://www.physorg.com/news9144.html

We do know that there are genes associated with diabetes, and these have effects on insulin sensitivity, which affects metabolism.

So what solid research is there on isocaloric diets (ie people eating the same calories) and the ability to lose/gain weight?

Questions that will impact on the answer:
1. Are we talking about 'VLCD used to treat morbid obesity' or 'diets in everyday people when trying to lose weight' or 'very lean people when trying to get cut'?
[that is - when considering the answer the pre-existing physiological and hormonal state of the individual is very important]

2. How much of a calorie deficit are you thinking the people will be at? 25%? 50%? How long are people on the diet for? 1 month? 6 months?
[the degree and length of deficit is going to impact on the degree of metabolic impact]

3. Are we to assume that the diet is configured such that 'macro and micronutrients' are adequate for the person in question?
[that is - protein/ EFA's and vitamins/minerals]

4. Male or female?
[yes, it is very important]

5. Lots of exercise? No exercise?
[also very important]

6. You mention 'isocaloric' (which to most people the diet is 33/33/33)... What are you asking in this....? Did you mean 'weight loss while eating maintenance calories'?

[Phosphate bond]

Originally Posted by GregT

So what solid research is there on isocaloric diets (ie people eating the same calories) and the ability to lose/gain weight?

If there was a difference in "Calories Out" or weight lifting intensity between diet A and diet B there might be weight change differences. (especially if there was a total body water shift from any difference in resistance training performance)

Unfortunately most long term diet studies don't seem to include weight lifting.

[gekkoboy14]

Originally Posted by Emma-Leigh

Questions that will impact on the answer:
1. Are we talking about 'VLCD used to treat morbid obesity' or 'diets in everyday people when trying to lose weight' or 'very lean people when trying to get cut'?
[that is - when considering the answer the pre-existing physiological and hormonal state of the individual is very important]

2. How much of a calorie deficit are you thinking the people will be at? 25%? 50%? How long are people on the diet for? 1 month? 6 months?
[the degree and length of deficit is going to impact on the degree of metabolic impact]

3. Are we to assume that the diet is configured such that 'macro and micronutrients' are adequate for the person in question?
[that is - protein/ EFA's and vitamins/minerals]

4. Male or female?
[yes, it is very important]

5. Lots of exercise? No exercise?
[also very important]

6. You mention 'isocaloric' (which to most people the diet is 33/33/33)... What are you asking in this....? Did you mean 'weight loss while eating maintenance calories'?

why is sex important?

[Emma-Leigh]

Originally Posted by gekkoboy14

why is sex important?

.... long story short: Females are 'pre-set' to 'fat'.

In the eyes of mother nature we be but ‘baby incubators’. And anything that threatens our reproductive viability is seen as a bad thing... As a consequence, we have more 'safety' mechanisms in place in regards to 'calorie deficiency' which ensure we maintain 'baby food' around our butts/ thighs at all costs. So if you take a female and drop calories too much + add too much activity => the body doesn't like it and you get a metabolic down regulation as a consequence. And this is disproportionately so/ much more so than for a male given the same changes/ situation...

Good for the species. Bad for the individual.

[RC2008]

Originally Posted by Emma-Leigh

.... long story short: Females are 'pre-set' to 'fat'.

In the eyes of mother nature we be but ?baby incubators?. And anything that threatens our reproductive viability is seen as a bad thing... As a consequence, we have more 'safety' mechanisms in place in regards to 'calorie deficiency' which ensure we maintain 'baby food' around our butts/ thighs at all costs. So if you take a female and drop calories too much + add too much activity => the body doesn't like it and you get a metabolic down regulation as a consequence. And this is disproportionately so/ much more so than for a male given the same changes/ situation...

Good for the species. Bad for the individual.

Lmao aweosme post

[Emma-Leigh]

*sigh* It's only funny 'cause it's true....

[daYDreAmErX]

Originally Posted by Emma-Leigh

*sigh* It's only funny 'cause it's true....

So true

I can lose weight and it usually last 10-15 days After that, my body shuts down and wants me to eat. It's not about craving, it's like a natural sign hahaha

[Gr3g_Lycan]

Maybe I phrased my questions vaguely. The questions are independent.

Q1- its there any scientific basis in "starvation mode". That is, if you cant lose fat consuming X calories, then somehow you can lose fat increasing to X+Y calories.


Q2- assume we have people all consuming X calories per day and doing the same exercise. Will people converge to the same fat percentage and and muscle mass? What is the scientific basis of any differences? This is a deceptively simple question that lies at the heart of body composition.

Anecdotally, taking boarding school or college dorms as an example, where people eat the same food & do the same exercise, the fat people remain fat and the thin people remain thin. Is this really the case and why from a scientific perspective?

[Emma-Leigh]

Originally Posted by GregT

Maybe I phrased my questions vaguely. The questions are independent.

Q1- its there any scientific basis in "starvation mode". That is, if you cant lose fat consuming X calories, then somehow you can lose fat increasing to X+Y calories.


Q2- assume we have people all consuming X calories per day and doing the same exercise. Will people converge to the same fat percentage and and muscle mass? What is the scientific basis of any differences? This is a deceptively simple question that lies at the heart of body composition.

Anecdotally, taking boarding school or college dorms as an example, where people eat the same food & do the same exercise, the fat people remain fat and the thin people remain thin. Is this really the case and why from a scientific perspective?

In response to question 1:-
'Starvation mode'.... I really, really don't like that term. But yes - there IS certainly evidence for metabolic response to dieting. This can either be a 'slight' decrease in energy output (as seen in moderate calorie restriction) - which is not really all that significant and is easily overcome and reversed.... Or a more severe and longer term response (as seen in those who have dieted severely or for a long period of time - resulting in large changes in body weight and hormonal regulation) eg: Key's et. al. studies.

This is why I put in all of the above qualifiers.... As mentioned above - it is often worse in females.... Worse when you severely restrict calories.... worse if you are doing lots of cardio..... Worse if you lost a substantial amount of lean mass during the diet.... worse if you have not a lot of fat mass to begin with.... worse if basic nutrient requirements are not meet..... etc etc...

Basically:
a. 'starvation mode' is not what most people think it is
b. but yes - there is a metabolic response to dieting and it is observed frequently in studies
(on a tangent - this is actually the main concept at the base of 'calorie restriction = longer life"... You slow the metabolism down and you get a decreased rate of oxidative damage/ tissue decay and an increase in lifespan).


In response to question 2:-
a. No people will not reach the same fat % and muscle mass.

b. The scientific basis of the difference is in peoples phenotype (genetics + environment in which they were raised) [eg: thrifty v's non thrifty genetics.... your set point..... if your mother was 'large' while you were in utero.... if you were 'large' when a child or duing your teenage years.... ]... And this is the million dollar question that thousands around the world are trying to answer ($$$$ for an obesity 'cure').

If you are interseted in the area do some reading on the 'Thrifty gene' and the 'metabolic responses to calorie restriction'....

[chosenone28]

I am interested in the metabolic response to dieting. Could you reccomend any good books/sites/articles in reference to this Emma?

Thanks.

[GoutDeMiel]

god some of you people are sofaking smart

[Emma-Leigh]

Originally Posted by chosenone28

I am interested in the metabolic response to dieting. Could you reccomend any good books/sites/articles in reference to this Emma?

Thanks.

^^
http://forum.bodybuilding.com/showth...hp?t=110624041

Pubmed. is the best place to go for easily 'sourced' research on the matter.
^
Do the tutorials to learn how to search effectively.
Then some terms you might want to look up -
- 'thrifty gene'
- 'drifty gene'
- 'phenotype' & 'obesity'
- 'evolution' & 'obesity'
- 'calorie restriction'
^^
etc etc...

Also - look into the Minnesota 'Starvation Study' (Keys et al.) - although it is from mid last century it really is a 'landmark' study in relation to the physiological and psychological concequences of calorie restriction/ starvation.

[imccarthy]

Originally Posted by Emma-Leigh

.... long story short: Females are 'pre-set' to 'fat'.

In the eyes of mother nature we be but ?baby incubators?. And anything that threatens our reproductive viability is seen as a bad thing... As a consequence, we have more 'safety' mechanisms in place in regards to 'calorie deficiency' which ensure we maintain 'baby food' around our butts/ thighs at all costs. So if you take a female and drop calories too much + add too much activity => the body doesn't like it and you get a metabolic down regulation as a consequence. And this is disproportionately so/ much more so than for a male given the same changes/ situation...

Good for the species. Bad for the individual.

Is this why female bodybuilders and fitness competitor almost always diet on less than 1000 calories a day? It sure sounds like starvation but that's the only way most women can get down to single digits.

[Emma-Leigh]

Originally Posted by imccarthy

Is this why female bodybuilders and fitness competitor almost always diet on less than 1000 calories a day? It sure sounds like starvation but that's the only way most women can get down to single digits.

No. They do that because they are working with bro-science-blinkered trainers who only know 'one way' of training and are therefore not being managed appropriately.

[KLMARB]

Originally Posted by chosenone28

I am interested in the metabolic response to dieting. Could you reccomend any good books/sites/articles in reference to this Emma?

Thanks.

A basic understanding is Berardi's "Hungry, Hungry, Hormones" found in the archives...

[Passion4Pump]

Originally Posted by Emma-Leigh

In response to question 1:-
'Starvation mode'.... I really, really don't like that term. But yes - there IS certainly evidence for metabolic response to dieting. This can either be a 'slight' decrease in energy output (as seen in moderate calorie restriction) - which is not really all that significant and is easily overcome and reversed.... Or a more severe and longer term response (as seen in those who have dieted severely or for a long period of time - resulting in large changes in body weight and hormonal regulation) eg: Key's et. al. studies.

This is why I put in all of the above qualifiers.... As mentioned above - it is often worse in females.... Worse when you severely restrict calories.... worse if you are doing lots of cardio..... Worse if you lost a substantial amount of lean mass during the diet.... worse if you have not a lot of fat mass to begin with.... worse if basic nutrient requirements are not meet..... etc etc...

Basically:
a. 'starvation mode' is not what most people think it is
b. but yes - there is a metabolic response to dieting and it is observed frequently in studies
(on a tangent - this is actually the main concept at the base of 'calorie restriction = longer life"... You slow the metabolism down and you get a decreased rate of oxidative damage/ tissue decay and an increase in lifespan).

I'm really glad I came across this thread before I made a new one! Emma-Leigh, I'd like to say that as someone with a hunger for nutritional knowledge, it's a joy to read your posts. I hope you wouldn't mind responding to a couple of questions that I have that are related to this topic.

Generally, at what percent of restriction and for how long will the metabolic impact of a diet become significant. I'm not really sure how to qualify significant, but let's set the threshold pretty low (at what point would you start worrying about it?). We'll say that the subject is male, is performing lots of exercise, is very lean and trying to get cut, and assume that the diet is configured such that 'macro and micronutrients' are adequate for the person in question. I realize that at this point I'm still leaving at least two free "parameters". But if it makes it easier, assume that the person is in about a 33% deficit. How long would it take for such a restriction to cause a noticable impact on metabolism? Would it occur significantly quicker if restriction were 50%? 70%? Even more specifically, to what extent would abbreviating such periods with caloric excess help. How long would these periods have to be to "reverse" the effects?

Of course, I'm not asking you to answer each of these questions individually. But hopefully through this barrage of questions you understand the type of knowledge I seek. I tried to leave out specific numbers because I feel like a more general answer would be more satisfying to give, would help others more, and would certainly make me smarter and more able to apply it to a variety of situations. Whatever your answer is, I appreciate any attention you pay to this.

[Emma-Leigh]

Originally Posted by Passion4Pump

Emma-Leigh, I'd like to say that as someone with a hunger for nutritional knowledge, it's a joy to read your posts. I hope you wouldn't mind responding to a couple of questions that I have that are related to this topic.

Thank you... and not at all - although my answer is probably going to be more frustrating to you than anything!

At what percent of restriction and for how long will the metabolic impact of a diet become significant. I'm not really sure how to qualify significant, but let's set the threshold pretty low (at what point would you start worrying about it?). We'll say that the subject is male, is performing lots of exercise, is very lean and trying to get cut, and assume that the diet is configured such that 'macro and micronutrients' are adequate for the person in question. I realize that at this point I'm still leaving at least two free "parameters". Assume that the person is in about a 33% deficit. How long would it take for such a restriction to cause a noticable impact on metabolism? Would it occur significantly quicker if restriction were 50%? 70%?

My answer to this is 'it still depends' - > Genetics is one of the key components as to the metabolic response of an individual to a diet (see above information re thrifty/ drifty metabolism). So:
1. if the person is of poor genetic stock...
2. if the person is already very lean....
3. if the person does +++ cardio and drops cals by 33%...
then they are not only pretty stupid ( ) but they will also likely adapt metabolically pretty quickly... Dropping their NEAT + decreasing BMR to some degree too.

The decrease in metabolism would happen almost immediately for some things (eg: decreased food intake = decreased TEF = less energy expended.... lack of incoming energy = decreased NEAT = decreased energy expended)... but would take longer for some of the other things.... But I would be kidding someone if I could pinpoint a specific time frame for these things.

If they were of better genetic standing + if they made an obvious effort to continue to maintain as much NEAT as possible - the decrease would be less marked. It would still occur - but to a lesser extent and a slower rate.

Even more specifically, to what extent would abbreviating such periods with caloric excess help. How long would these periods have to be to "reverse" the effects?

The effects of re-feeds are very well known (the re-feed may only need to be 5 hrs in duration... or it may need to be up to 6 weeks in length for reversal) -> and if you want more info into this look up LEPTIN and but if you are looking at a specific % increase associated with a refeed I, once again, couldn't say.

[Emma-Leigh]

A few articles related to the area:

Int J Obes Relat Metab Disord. 2001 Dec;25 Suppl 5:S22-9. Links
An adipose-specific control of thermogenesis in body weight regulation.Dulloo AG, Jacquet J.
Institute of Physiology, Department of Medicine, University of Fribourg, Fribourg, Switzerland. abdul.dulloo@unifr.ch

Much of our understanding about 'adaptive thermogenesis' as a control system in mammalian weight regulation derives from studies of experimental starvation and overfeeding, and these have served to characterize its functional role as an 'attenuator' of energy imbalance. By applying a system-analysis approach in evaluating data on the energetics of starvation and refeeding, evidence is presented here in support of the hypothesis that there are in fact two distinct control systems underlying adaptive thermogenesis. In one of them, the efferent limb is primarily under the control of the sympathetic nervous system (SNS), whose functional state is dictated by overlapping or interacting signals arising from a variety of environmental stresses, including food deprivation, deficiency of essential nutrients, excess energy intake and exposure to cold or to infections; it is hence referred to as the non-specific control of thermogenesis, and is likely to occur primarily in organs/tissues with a high specific metabolic rate (eg liver, kidneys, brown fat). The other is independent of the functional state of the SNS and is dictated solely by signals arising from the state of depletion of the adipose tissue fat stores; it is hence referred to as the adipose-specific control of thermogenesis, and is postulated to occur primarily in the skeletal muscle. While suppression of this adipose-specific thermogenesis during both starvation and refeeding leads to energy conservation, the energy spared during refeeding is directed specifically at the replenishment of the fat stores, so that it functions as an 'accelerator' of fat recovery. These two distinct control systems for adaptive thermogenesis have been incorporated in a compartmental model of body weight and body composition regulation. This is used to provide a mechanistic explanation as to how, during weight recovery, they can operate simultaneously but in opposite directions--with activation of thermogenesis under non-specific control being energy-dissipating, while suppression of thermogenesis under adipose-specific control being energy-conserving--and could hence explain the paradox of a high efficiency of fat recovery co-existing with an overall state of enhanced thermogenesis and hypermetabolism. Elucidating the components of the adipose-specific control of thermogenesis (ie its sensors, signals and effector mechanisms) will have important implications for our understanding of body composition regulation, and hence for the development of more effective strategies in the management of cachexia and obesity.

Am J Clin Nutr. 1998 Sep;68(3):599-606.Links
Adaptive reduction in basal metabolic rate in response to food deprivation in humans: a role for feedback signals from fat stores.Dulloo AG, Jacquet J.
Department of Physiology, Faculty of Medicine, University of Geneva, Switzerland.

We assessed the importance of lean and fat tissue depletion as determinants of the adaptive reduction in basal metabolic rate (BMR) in response to food deprivation by reanalyzing the data on BMR and body composition for the 32 men participating in the classic Minnesota experiment of semi-starvation and refeeding. We used individual data on BMR, body fat, and fat-free mass (FFM) assessed during the control (prestarvation) period, at weeks 12 and 24 of semistarvation (S12 and S24), and week 12 of restricted refeeding (R 12) to calculate an index of the reduction in thermogenesis at S12, S24, and R12, defined as the change in BMR adjusted for changes in FFM and fat mass, and an index of the state of depletion of the fat mass and FFM compartments at these times, defined as the deviation in fat mass or FFM relative to control values. The results indicated a positive relation between the reduction in thermogenesis and the degree of fat mass depletion (but not FFM depletion) during weight loss as well as during weight recovery (r = 0.5, P < 0.01). Furthermore, the residual variance was predicted by the initial (prestarvation) percentage fat and the cormic index (sitting height/height). Taken together, these results in normal-weight men responding to severe food deprivation reveal anthropometric predictors for human interindividual variability in the capacity for energy conservation and suggest that the adaptive reduction in BMR is partly determined by an autoregulatory feedback control system linking the state of depletion of fat stores to compensatory mechanisms that suppress thermogenesis.

Br J Nutr. 1999 Nov;82(5):339-56.Links
The control of partitioning between protein and fat during human starvation: its internal determinants and biological significance.Dulloo AG, Jacquet J.
Institute of Physiology, University of Fribourg, Switzerland. abdul.dulloo@unifr.ch

Human subjects vary in the extent to which their body's protein and fat compartments are mobilized for fuel during starvation. Although an inverse association between the initial adiposity and the contribution of protein as fuel during starvation has been known for nearly a century, interest in the quantitative importance and functional significance of the initial percentage fat as a determinant of biological variation in energy-partitioning between protein and fat (and hence in determining the partitioning characteristic of the individual) is relatively recent. The present paper addresses these issues by revisiting the classic Minnesota experiment of semi-starvation and refeeding from a standpoint of system physiology. In a quantitative analysis of the relationship between the initial body composition (ration FAT0: fat-free mass (FFM)0) and the composition of weight loss (ratio delta FAT: delta FFM) in the thirty-two men in the Minnesota study, the arguments are put forward that the fraction of FFM lost when the fat stores reach total depletion is independent of the initial percentage fat, and that this fraction represents the 'dispensable' component of the protein compartment that is compatible with life (i.e. the protein energy-reserve, rp). The concepts are developed that (1) the initial percentage body fat (which reflects the initial ratio FAT0:FFM0) provides a 'memory of partitioning' which dictates the control of partitioning between protein and fat in such a way that both the protein energy-reserve (rp) and the fat energy-reserve (rf) each complete depletion simultaneously, a strategy that would ensure maximum length of survival during long-term food scarcity, and that (2) variability in the relative sizes of these two energy reserves (i.e. in rf:rp) could, in addition to the initial percentage fat, also contribute to human variability in energy-partitioning. The basic assumptions underlying this re-analysis of the Minnesota data, and the concepts that are derived from it, have been integrated in the simple mathematical model for predicting the partitioning characteristic of the individual. This model is used to explain how variability in the fraction of the protein compartment that could function as an energy reserve (rp) can be as important as the initial percentage fat in determining inter-individual variability in protein-sparing during the early phase of starvation, in fuel partitioning during prolonged starvation, or in the maximum percentage weight loss during starvation. The elucidation of factors underlying variability in the size of the protein energy-reserve may have important implications for our understanding of the pathophysiology of starvation and age-associated susceptibility to muscle wasting, and in the clinical management of cachexia and obesity.

Sports Med. 2006;36(3):239-62.Links
The role of diet and exercise for the maintenance of fat-free mass and resting metabolic rate during weight loss.Stiegler P, Cunliffe A.
Department of Human and Health Sciences, University of Westminster, London, UK. Stieglp@wmin.ac.uk

The incidence of obesity is increasing rapidly. Research efforts for effective treatment strategies still focus on diet and exercise programmes, the individual components of which have been investigated in intervention trials in order to determine the most effective recommendations for sustained changes in bodyweight. The foremost objective of a weight-loss trial has to be the reduction in body fat leading to a decrease in risk factors for metabolic syndrome. However, a concomitant decline in lean tissue can frequently be observed. Given that fat-free mass (FFM) represents a key determinant of the magnitude of resting metabolic rate (RMR), it follows that a decrease in lean tissue could hinder the progress of weight loss. Therefore, with respect to long-term effectiveness of weight-loss programmes, the loss of fat mass while maintaining FFM and RMR seems desirable. Diet intervention studies suggest spontaneous losses in bodyweight following low-fat diets, and current data on a reduction of the carbohydrate-to-protein ratio of the diet show promising outcomes. Exercise training is associated with an increase in energy expenditure, thus promoting changes in body composition and bodyweight while keeping dietary intake constant. The advantages of strength training may have greater implications than initially proposed with respect to decreasing percentage body fat and sustaining FFM. Research to date suggests that the addition of exercise programmes to dietary restriction can promote more favourable changes in body composition than diet or physical activity on its own. Moreover, recent research indicates that the macronutrient content of the energy-restricted diet may influence body compositional alterations following exercise regimens. Protein emerges as an important factor for the maintenance of or increase in FFM induced by exercise training. Changes in RMR can only partly be accounted for by alterations in respiring tissues, and other yet-undefined mechanisms have to be explored. These outcomes provide the scientific rationale to justify further randomised intervention trials on the synergies between diet and exercise approaches to yield favourable modifications in body composition.

[Emma-Leigh]

And some more:

1: Int J Obes Relat Metab Disord. 1996 May;20(5):393-405.Links
Autoregulation of body composition during weight recovery in human: the Minnesota Experiment revisited.Dulloo AG, Jacquet J, Girardier L.
Department of Physiology, Faculty of Medicine, University of Geneva, Switzerland.

OBJECTIVES: To gain insights into the control systems underlying human variability in the regulation of body composition during weight recovery, as well as the disproportionate recovery of fat relative to lean tissue, the classical Minnesota Experiment conducted on 32 men subjected to long-term semi-starvation and refeeding was revisited with the following objectives: (1) to determine whether the control of energy-partitioning between lean and fat tissues during weight loss and weight recovery is an individual characteristic, and if a predictor can be statistically identified, (2) to determine whether the reduction in thermogenesis during weight loss persists during weight recovery, and underlies the disproportionate recovery of fat tissue and (3) to integrate the control of energy-partitioning and that of thermogenesis in order to explain the pattern of lean and fat tissue mobilisation and deposition during weight loss and weight recovery. METHODS: Individual data on body weight, body fat, fat-free-mass (FFM), and basal metabolic rate (BMR), assessed during the control baseline period (i.e. prior to weight loss), at the end of 24 weeks of semi-starvation, and at the end of a 12 week period of restricted refeeding, were used to calculate the following parameters: (i) a quantitative index of energy-partitioning, the P-ratio, defined as the proportion of body energy mobilised as protein during weight loss, or as the proportion of body energy deposited as protein during weight recovery, (ii) a quantitative index of changes in thermogenesis, defined as the change in BMR adjusted for FFM (or for both FFM and fat mass) and (iii) the degree of replenishment of fat and FFM compartments, defined as the recovery of body fat and FFM (during refeeding) as a percentage of that lost during semi-starvation. RESULTS: This re-analysis indicates the following: (i) a large inter-individual variability in P-ratio during both weight loss and weight recovery, but for a given individual, the P-ratio during refeeding is strongly correlated with the P-ratio during semi-starvation, (ii) body composition during the control period is the most important predictor of variability in P-ratio, such that the higher the initial % body fat, the lower the proportion of energy mobilised as protein, and hence the greater the propensity to mobilise fat during semi-starvation and to subsequently deposit fat during refeeding and (iii) at week 12 of refeeding, the change in adjusted BMR is found to be reduced by a magnitude which is inversely proportional to the degree of fat recovery, but is unrelated to the degree of FFM recovery. A quantitative relationship is derived between the P-ratio during refeeding, the % fat recovery, and the P-ratio during semi-starvation. CONCLUSIONS: Evidence is presented here suggesting that (i) human variability in the pattern of lean and fat tissue deposition during weight recovery is to a large extent determined by individual variations in the control of energy-partitioning, for which the initial % body fat is the most important predictor and (ii) the disproportionate gain in fat relative to lean tissue during weight recovery is contributed by a reduction in thermogenesis (i.e. increased efficiency of food utilization) for accelerating specifically the replenishment of the fat stores. These control systems, operating via energy-partitioning and thermogenesis, have been integrated into a compartmental model for the regulation of body composition during underfeeding/refeeding, and can be used to explain the individual pattern of lean and fat tissue deposition during weight recovery in situations ranging from the rehabilitation after malnutrition to the relapse of obesity.

Ann N Y Acad Sci. 2000 May;904:359-65. Links
Body fat content influences the body composition response to nutrition and exercise.Forbes GB.
University of Rochester School of Medicine and Dentistry, New York 14642, USA.

In most situations involving a significant change in body weight, both fat-free body mass (FFM) and body fat participate, but the relative contribution of FFM and fat to the total weight change is influenced by the initial body fat content. Overfeeding: In experiments of at least 3-weeks' duration, the weight gain of thin people comprises 60-70% lean tissues, whereas in the obese it is 30-40%. Underfeeding: In humans, there is an inverse curvilinear relationship between initial body fat content and the proportion of weight loss consisting of lean tissue. The same trend holds for animals and birds, including loss during hibernation. Another factor is the magnitude of the energy deficit: as energy intake is reduced, lean tissue makes up an increasing fraction of the total weight loss. Exercise: If individuals lose much weight with exercise, the result is usually some loss of lean tissue as well as fat, and once again the proportion of lean loss to total weight loss is greater in thin people than in those who have larger body fat burdens. Members of twin pairs often differ in weight. In thin individuals, lean accounts for about half of the intrapair weight difference, whereas in the obese it accounts for only one quarter. Body fat content must be taken into account in evaluating body composition changes induced by nutrition and exercise.

[Ted Nugent]

Originally Posted by KLMARB

A basic understanding is Berardi's "Hungry, Hungry, Hormones" found in the archives...

reps for a link to that

[Passion4Pump]

Originally Posted by Emma-Leigh

Thank you... and not at all - although my answer is probably going to be more frustrating to you than anything!


My answer to this is 'it still depends' - > Genetics is one of the key components as to the metabolic response of an individual to a diet (see above information re thrifty/ drifty metabolism). So:
1. if the person is of poor genetic stock...
2. if the person is already very lean....
3. if the person does +++ cardio and drops cals by 33%...
then they are not only pretty stupid ( ) but they will also likely adapt metabolically pretty quickly... Dropping their NEAT + decreasing BMR to some degree too.

The decrease in metabolism would happen almost immediately for some things (eg: decreased food intake = decreased TEF = less energy expended.... lack of incoming energy = decreased NEAT = decreased energy expended)... but would take longer for some of the other things.... But I would be kidding someone if I could pinpoint a specific time frame for these things.

If they were of better genetic standing + if they made an obvious effort to continue to maintain as much NEAT as possible - the decrease would be less marked. It would still occur - but to a lesser extent and a slower rate.



The effects of re-feeds are very well known (the re-feed may only need to be 5 hrs in duration... or it may need to be up to 6 weeks in length for reversal) -> and if you want more info into this look up LEPTIN and but if you are looking at a specific % increase associated with a refeed I, once again, couldn't say.

I, too, often must respond to questions on this topic with "well... it depends". There's just never a simple answer to anything, which is what makes it so intriguing to me. I guess the next logical questions would be

1) What would be your checklist for minimizing any decrease in metabolism that would result from cutting?

and, if that depends on too many things, then

2) Is there any way to tell if, and to what extent, my metabolism has slowed down?

In the mean time, i will diligently struggle through those articles you posted.

[MrLovrLovr]

Besides your body functioning from innate food processing pumped - regular exercise will keep your metabolism functioning .

tricking your body once in awhile with refeeds works for most people .

Metabolism slowing ? feeling ugh for starters