The FastDay Forum

Phil, remember that Varady's trials were only for 8 weeks so once we go beyond that we don't know whether fasting every other day might result in metabolic changes designed to reduce weight loss.

We know an obese man can fast for a year and continue to lose weight

[carorees]

Yes, but that is rather extreme! I also read somewhere that fasting was actually used to treat obesity fairly often in the 1950s but it went out of fashion because of excess myocardial infarctions.

it was indeed extreme, but it nails the "starvation mode" myth for what it is.

If fasting is used to treat massive obesity and there are myocardial infarctions how does one differentiate the cause ? http://www.ncbi.nlm.nih.gov/pmc/article ... 2-0024.pdf covers the territory and recommends attention to medical supervision of sodium, potassium etc.

Of course the Protein Sparing Modified Fast procedures are the modern day equivalent of prolonged fasting, with far lower risks.

[carorees]

I don't see that it "nails starvation mode" at all! Just because you are still losing weight does not mean that your body isn't trying to avoid weight loss. I'm sure the patient in question went into starvation mode, but by not eating he had to lose weight. The amazing thing is that the paper claimed he could maintain the weight loss. The problem is always when people stop dieting and start eating normally but their metabolisms do not return to normal, so it becomes impossible to eat normally without gaining weight. Of course it is possible to stay slim by balancing energy intake and expenditure but with the modern availability of food most people cannot manage to keep to a low enough calorie diet to match their new, slower metabolism.

I see one of the main aims of the fast diet as being to allow people to eat normally on feed days and be able to control their weight by having two fast days a week. However, if during the weight loss process they cut calories on feed days too much, or fast for too long on fast days, a slow down in metabolism is likely. This will mean having to have more fast days during maintenance and perhaps never being able to eat normally on feed days.

So, I'm not sure why you doubt the concept of starvation mode...it is well documented. Perhaps it seems irrelevant to the process of weight loss, after all if you cut your calories enough it is inevitable that you will lose weight. Personally speaking, if I have to give up all my treats and fast three times a week or more in order to get to my target weight and to continue that indefinitely to keep the weight off, I know I will fail.

Starvation mode as often used in the sense of "your body will hold onto everything and you will not lose weight" is demonstrable nonsense.

Some reduction in basal metabolic rate per FFM due to calorie restriction is seen in some cases, and not in others, often depending on measurement techniques and similar details. It even seems to be an individual thing where some subjects do show a metabolic reduction and others do not, or show a much smaller one. I'm open minded about a metabolic slow down of up to 200 calories a day, but as it's similar in magnitude to the error in BMR predictions I don't see it as a massive issue.

"The problem is always when people stop dieting and start eating normally but their metabolisms do not return to normal, so it becomes impossible to eat normally without gaining weight." - it is impossible to overeat like they used to, for sure, and at a lower body mass / improved efficiency they need to eat less than they should have been eating too, so yes some adjustments are required.

The studies of overfeeding etc show that metabolic rates are quickly restored after prolonged calorie reduction or fasting, it's part of the process of losing weight to have to learn how to maintain.

Varady used a 20% daily calorie restriction combined with 1 day a week fasting (120 cals only, juice drink) in the food vs liquid study without noting any problems with metabolic rate over 10 weeks.

[carorees]

Hmm, did you read the paper that I reviewed about the various physiological changes occurring with weight loss that act to drive up weight? Even in the absence of a massive metabolic slow down, there are many other factors that act to drive weight up again.

As you say, adjustments have to be made tho maintain the new weight, but midst people are not able to manage it. For those who can...fantastic, but for those like me who can't, anything that makes maintenance harder, such as a change in thyroid function (which is common in post menopausal women) which may be triggered by under eating, increased desirability of food etc etc is a bad thing. This is why I am trying to keep the weight loss going without reassuring to the kind of calorie restriction that involves denying all treats and feeling guilty because in the end the weight will go back on. For this reason I think it is better to use the fast days to create the calorie restriction than reducing feed day calories (except for the necessary adjustment with reducing TDEE), and to try to avoid risking a drop in thyroid function because for those who respond in this way, poor thyroid function carries health problems of its own.

Even if metabolic rates recover on refeeding after a 10% or more drop in body weight (and I need to check that), studies have shown that other changes which drive up weight, including increased hunger, do not. In one study, a year after achieving a reduction in body weight, subjects still felt hungry all the time, despite eating to TDEE for a year.

[carorees]

Some reduction in basal metabolic rate per FFM due to calorie restriction is seen in some cases, and not in others, often depending on measurement techniques and similar details. It even seems to be an individual thing where some subjects do show a metabolic reduction and others do not, or show a much smaller one. I'm open minded about a metabolic slow down of up to 200 calories a day, but as it's similar in magnitude to the error in BMR predictions I don't see it as a massive issue.

Phil, I'd really value your thoughts on the following papers:

http://ajcn.nutrition.org/content/88/4/906.full
http://reference.medscape.com/medline/abstract/22029981
http://www.plosone.org/article/info:doi ... ne.0004377
and
http://clinical.diabetesjournals.org/co ... 3/100.full

I haven't had time to read them fully yet and to work out what, if anything, they imply for 5:2 fasting, weight loss, plateaus and maintenance!

Alternate day fasting (true fasts) effect on metabolic rate is shown at http://ajcn.nutrition.org/content/81/1/ ... nsion.html

After 3 weeks of ADF, during which time the participants lost 1.4kg bodyweight on average, average resting metabolic rate fell from 1597 +/- 68 cals at baseline to 1505 measured on a feed day and 1514 on a fast day (similar variability). Differences not significant.

Fat free mass fell from 53.4 to 52.8 so expressed per kg of FFM the baseline and feed day numbers are 29.9 and 28.5. Per kg body weight 22.8 to 21.9

Phil, I'd really value your thoughts on the following papers:

http://ajcn.nutrition.org/content/88/4/906.full
http://reference.medscape.com/medline/abstract/22029981
http://www.plosone.org/article/info:doi ... ne.0004377
and
http://clinical.diabetesjournals.org/co ... 3/100.full

I haven't had time to read them fully yet and to work out what, if anything, they imply for 5:2 fasting, weight loss, plateaus and maintenance!

I'll have a look.

Slightly old but useful review paper below, points out how exercise (increased energy expenditure) has an effect on metabolic rate etc independent of food restriction (reduced energy intake) - for example it is easier to maintain after a weight loss if exercise is included in the post-diet regime as there is a bigger effect on TDEE than just the exercise itself would suggest.

The Role of Energy Expenditure in Energy Regulation:
Findings from a Decade of Research
Edward Saltzman,M.D. and Susan B. Roberts,Ph.D.

http://clinical.diabetesjournals.org/co ... 3/100.full is a wordy review paper by a 3rd year student.

Conclusions.

Long-term maintenance of weight loss is an important, but often elusive, goal.

Evidence from this review and others cited in the literature find that continued therapy from a health professional is essential for weight loss maintenance success. In support of weight loss maintenance, physician-patient interactions should include a discussion of patient goals, the weight regain phenomenon, decision points in self-care and help-seeking behavior, and conclude with advice about self-monitoring, diet, and exercise.

Paper from 2011 (Australian) highlighted by Carorees http://www.ncbi.nlm.nih.gov/pubmed/?term=22029981

CONCLUSION : One year after initial weight reduction, levels of the circulating mediators of appetite that encourage weight regain after diet-induced weight loss do not revert to the levels recorded before weight loss. Long-term strategies to counteract this change may be needed to prevent obesity relapse.

The paper generated three letters in response (see links at bottom of above abstract). One observed that "In our opinion, the sustained hormonal changes that were observed could be explained completely by persistent weight loss, as compared with baseline." - in other words the post weight loss levels were what they would expect in a less fat person.

A second dug into the data further and observed that " However, data provided in the online Supplementary Appendix (available with the full text of the article at NEJM.org) indicate that there was no significant relationship between weight regain and either the hormone levels at week 10 or changes in the levels from baseline to week 10." - in other words the hormone levels didn't seem to be responsible for weight regain or lack of.

The third contrasted the 31.5% leptin reduction observed in this 8 week VLCD intervention (500-550 calories/day) 13.5 kg weight loss with their own work - "We reported data that showed the preservation of leptin levels despite a relative weight reduction of 3.6% in the Enhance the Metabolic Profile of Women with Insulin Resistance (EMPOWIR) study". The latter was a reduced carb 1200 calorie diet.


In the supplementary appendix it is shown that the only predictor of weight regain after the harsh diet is the tendency to eat, and that isn't statistically significant :-

"Similarly, a least squares regression analysis modeling weight regain percentage on week 10 fasting hormones and VAS scores revealed no significant predictors. A stepwise regression analysis using Akaike information criterion (AIC) chose only VAS scores “urge to eat” and “preoccupation with thoughts of food”, although neither was statistically significant (both p > 0.1)."

In conclusion the paper identifies changes in various hormones and other measures after a 10 week trial with a 1-year follow up. Some of the changes are statistically significant but none are significant predictors of weight gain post diet.

[carorees]

I think you are being a bit disingenuous to dismiss the clinical diabetes paper because the first author is a 3rd year student. The other authors must agree with the findings surely and they are an assistant professor at Johns Hopkins University
School of Medicine, is an associate professor at the Diabetes Research and Training Center at Vanderbilt University Medical Center, is director of the Prevention and Control Core of the Vanderbilt Diabetes Research and Training Center at Vanderbilt University Medical Center and medical director of the Vanderbilt Eskind Diabetes Center and editor-in-chief of Clinical Diabetes.

Be that as it may, the key points that I found in the paper were:

The short- and long-term efficacy of weight loss programs [shows that] with the exception of continuous pharmacological therapy, the pattern of weight regain is evident from 6 months on.

Pre-treatment indicators of future weight regain include older age;69 Mexican-American ethnicity;70 frequent previous diet attempts;71,72 high baseline or maximum weight;73-75 nonmedical triggers for weight loss induction;76 binge eating;77 dietary disinhibition (loss of control while eating);77,78 “all or nothing” thinking;79 perceived barriers to exercise, including “too tired,” “too hard,” “not enough time,” and “no companion”; perceived barriers to diet, including “high cost of healthy foods” and “eating away from home too often”;19,20 and lacking self-efficacy, motivation, realistic weight loss goals, and a strong body image.80

Post-weight loss indicators of weight regain include weight loss > 15-30% of baseline weight;14,81 early regain;82 not responding to early regain;78 perceptions of hunger;83 dissatisfaction with achieved weight loss;80 dietary disinhibition;81 emotional eating;78 binge eating; consuming a diet high in calories, fats, and sugars;14 frequent consumption of fast food (> 2-3 times per week);20 a sedentary lifestyle or decreased frequency and level of physical activity;14 and viewing more than 2-4 hours of television a day.14 Although somewhat counterintuitive, continuation of weight loss efforts is also associated with weight regain.16,73

During the first years of weight loss maintenance, continued effort and attention to weight control is essential. By 2 years, however, maintainers report less reliance on weight loss strategies and reduced attention and effort to weight control, perhaps reflecting new habit assimilation.85 Furthermore, maintenance of weight loss for ≥ 2 years is protective against subsequent regain; by 2 years the likelihood of regaining 2.6 kg in the coming year is only 50%; by 5 years the likelihood drops to 27%.81 Evidence from the NHANES survey similarly supported the contention that among successful weight loss maintainers, years from maximal weight loss is protective against weight regain

For all programs, maximal weight loss occurs in the first 6 months of therapy. For all nonpharmacological programs, weight regain begins shortly thereafter. On average, weight losses at 2 years range between 3 and 6% for nonpharmacological therapies and between 7and 8% for pharmacological therapies. For individuals at risk, these outcomes are within the range known to induce improvements in cardiovascular risk factors and prevent type 2 diabetes

It will be fascinating to see whether the fast diet follows the same pattern described in the above paragraph!

[carorees]

Thanks for looking through the paper on hormone changes.

I just wanted to post the authors' responses to the comments you have highlighted:

We agree with Cordido et al. that the sustained hormonal changes in our study could be explained by the maintenance of a reduced body weight, as compared with baseline, among the subjects. We agree that it would be valuable to compare hormone levels after weight reduction with levels in a weight-stabilized, BMI-matched control group. However, it has previously been shown that after diet-induced weight loss, formerly obese subjects have lower rates of fat oxidation and circulating leptin than do never-obese subjects matched according to age and BMI.1 Furthermore, the fact that some hormone levels increased whereas others decreased in an apparently strategic way to increase hunger also suggests that the hormone changes are not simply caused by the reduced body mass.
Although we did not find significant correlations between individual hormone levels and weight regain, as highlighted by Wing et al. and Cordido et al., we hypothesize that the lack of a significant relationship between individual hormone levels and appetite scores probably reflects the combined influence of several factors on subjective ratings of appetite. We maintain that our findings, as well as those from earlier studies, showing persistent disturbances in appetite-regulating hormones, increased appetite, and reduced energy expenditure2 after diet-induced weight loss indicate a physiological response that encourages weight regain.
We do not dispute that subjects can change their behavior and achieve long-term weight-loss maintenance despite these counterregulatory mechanisms. However, we believe that there is a fundamental difference between a subject who must constantly monitor food intake and energy expenditure to maintain a reduced weight and a never-obese person who can maintain the same weight without conscious monitoring. A disturbing life event that disrupts the necessary routine is likely to encourage weight gain in the weight-reduced subject. We suggest that the development of treatments that are effective and safe for long-term use may be helpful for many obese persons who are unable to maintain significant weight loss with lifestyle interventions alone.
We agree with the suggestion of Mogul et al. that differences between leptin levels in our study and levels in the EMPOWIR trial of a low-glycemic-index diet with metformin are probably due to differences in the study interventions. The difference in weight loss achieved in the two studies (a relative reduction of 14.0% vs. 3.6% of initial weight) probably also contributed to the differences in leptin changes that were observed.

The last paragraph may be important. Many of the studies on weight loss are rather short term and participants often only lose a relatively small % of body weight. Many people doing the fast diet have/are hoping to lose a rather large %. It may be that the 'starvation mode' situation only occurs once a substantial proportion of weight has been lost. The paper I reviewed on the theories of weight 'set points' took the view that the metabolic changes designed to prevent (or delay) starvation come into play at some genetically determined 'set point' and that this varies between people.

If we accept this theory (for the time being) it would imply that starvation mode would not kick in for some time and in fact there are observations that a plateau occurs at around 10% of body weight lost. Possibly most of this is due to not lowering calories in line with reduced TDEE due to reduced body weight, but perhaps also to some people hitting the lower set point.

It is interesting to observe that my OH who is bordering on underweight but who is joining in with fasting for solidarity and in the hope of improving his mental faculties had no problem with fasting for the first few weeks but recently has been finding himself extremely hungry on feed days and very cold all the time. I am wondering if he has hit this lower set point?

Thoughts?

I didn't dismiss it because it was by a third year student, I stated that as a fact (which I didn't notice until after I read it anyway).

I did largely dismiss it as a wordy review paper though

[carorees]

Metabolic and Behavioral Compensations in Response to Caloric Restriction: Implications for the Maintenance of Weight Loss

The introduction to this paper expounds a really interesting theory:

One of the most popular proposed theories by which CR promotes lifespan extension is the rate of living theory [4]. We hypothesized that caloric restriction will reduce energy metabolism in excess of the loss of metabolic mass (metabolic adaption) and therefore will reduce oxidative damage to tissues and organs by lowering the production rates of reactive oxygen species [5]. CR is indeed associated with robust decreases in energy metabolism, including a lowering of resting metabolic rate (or sleeping metabolic rate), reduced thermic effect of meals and a decrease in the energy cost and/or the level of physical activity. However, it is debated whether or not the decrease in total energy expenditure is proportional (or larger; metabolic adaptation) to the loss of metabolic tissues (fat-free and fat mass: FFM and FM). Furthermore, it is not clear if the metabolic adaptation persists once a new stable body weight is reached.

If the longevity comes from the 'starvation mode' itself that would suggest a very different approach to the fast diet!

This study looked at changes in TDEE in three groups of overweight men and women.

The intervention groups achieved a reasonable decrease in body weight after 24 weeks: 10.4% in the calorie restriction (CR) group, 10.0% in the calorie restriction plus exercise (CR+EX) group and 13.9% in the low calorie diet (LCD) group. The CR+EX increased their energy expenditure by 12.5% above baseline through structured aerobic exercise, 5 days per week.

In response to caloric restriction (CR/LCD) we observed a true metabolic adaptation at months 3 and 6 of the intervention. To exclude the contribution of sedentary energy expenditure (the largest component of daily energy expenditure), we adjusted TDEE for sedentary energy expenditure (24h-EE and SMR) and observed that measured TDEE was significantly less than predicted at both month 3 and month 6 of CR. Interestingly no metabolic adaptation was observed in CR+EX. Together, this data indicates that TDEE is reduced with caloric restriction and is likely the result of a metabolic adaptation in the sedentary state accompanied by a reduction in activity-related energy expenditure and reduced levels of physical activity (Figure 3). Therefore, this study supports a ‘metabolic adaptation’ in response to weight loss in humans and demonstrates for the first time a reduction in all components of daily energy expenditure with dietary-induced weight loss, including the level physical activity. Importantly, CR in combination with exercise (CR+EX) did not result in metabolic adaptation while inducing similar changes in body composition as with CR alone.

So their results suggest that 'starvation mode' is a real phenomenon but that it disappears if you make an effort to maintain your exercise levels (phew!).

Whether or not an individual responds to weight loss with a metabolic adaptation has long-term importance for weight maintenance because there is recent data indicating that the metabolic adjustments occurring as a result of CR and weight loss are maintained for up to 6 years following the weight loss [22]. As an alternative hypothesis it would be reasonable to assume two metabolic phases occur in response to CR; an ‘adaptive phase’ when energy expenditure is adjusting to compensate for the reduced availability of energy sources, followed by a ‘maintenance phase’ when energy balance has been re-established and the metabolic and behavioral compensations are therefore complete [37]. The individual group data for CR and LCD in our study may support this viewpoint since we observed a metabolic adaptation early (M3) but a return towards baseline values after an additional 3 months (M6) of weight loss (CR) or weight stability (LCD). We could also conclude that failure to detect a statistically significant adaptation at month 6 however, may be due to limitations in sample size. Considering our sample size of 12 in CR, and the observed mean change in TDEE at 6 months (CR group) adjusted for changes in FFM and FM (−209±114 kcal/d), we would have required 22 volunteers to detect a significant change from baseline with 80% power. This is probably why we did observe a significant metabolic adaptation at both 3 and 6 months of intervention when combining the CR and LCD groups.

It's a shame that they did not speculate in the discussion about whether if we want to improve longevity we should try to keep the metabolic adaptation!