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How Reverse Dieting Can Negatively Impact Bingeing

Disclaimer: This article is not intended as treatment advice for Binge Eating Disorder or Bulimia Nervosa.

 

What is reverse dieting?

 

Reverse dieting is a popular ‘exit strategy’ for competitors and dieters who no longer wish to diet but do not wish to re-gain weight (more specifically, body fat). The idea surfaced as a response to the body’s tendency to promote weight gain and prioritize the replenishing of fat stores once food is reintroduced after a period of caloric restriction. [1] The approach recommends slowly increasing your calories bit by bit from where they are in your deficit in order to match the requirements of the recovering metabolic rate. The idea is that this will allow your body to boost your hormones and metabolic rate bit by bit instead of ‘overshooting’ body fat stores once you return to eating normal amounts of food.

First of all, there is no science to support that claim [2]. However there is a lot of evidence that supports that once a person remains at a deficit their metabolism will continue to be negatively impacted. Reverse dieting is essentially remaining at a deficit but marginally less so as the weeks go by. Less of a deficit is still a deficit and this can be problematic for individuals who are struggling with ‘side effects’ of the hormonal changes that occur when caloric intake is restricted. Some of those side effects being the result of an intense drive to eat like obsessive thoughts about food, extreme hunger, the inability to feel full and even strong uncontrollable urges to binge.

 

What is binging?

 

An accepted definition for binge eating is the following:

 

”Binge eating is when you eat a large amount of food in a short amount of time and feel that you can’t control what or how much you are eating.’’

 

This is a symptom of more serious disorders like Binge Eating Disorder (BED) and Bulimia Nervosa however this is something that can happen to someone with no previous issues with food when they commit to a prolonged diet. The level of hunger required to inspire these urges is more commonly associated with individuals who have dropped a large amount of weight and/or body fat or individuals dieting down from a healthy weight to very low body fat percentages. So basically anyone who has competed in a bodybuilding show…

 

How does dieting affect urges to binge?

 

It only takes a few days of eating at a deficit for hormonal changes to begin to occur within the body as a response to the reduced energy available. Leptin, a hormone primarily secreted by fat cells and plays a role in regulating energy homeostasis, takes a significant hit right off the bat with the potential to drop as much as 50% within your first week of dieting. [3] It’s relatively common knowledge that low leptin levels equal increased hunger but it’s not as well understood that lowered leptin actually affects your feeding behavior. That is – your attitude towards food.

Because leptin acts as an indicator of energy stores in the body, when levels are low it is sensed by the central nervous system which begins to trigger changes in the body that allow it to function more efficiently with the reduced intake and also to promote weight gain. [4] It does so by increasing activity of anabolic circuits in the brain that stimulate eating and reduce energy expenditure while simultaneously inhibiting the activity of neural circuits that act to reduce feeding and boost expenditure. [5-7]

Leptin’s influence on the CNS and peripheral tissues brings on a host of other changes like alterations in thyroid hormone regulation, reduced luteinizing hormone pulsality [7] and reduced fat oxidation but for the purpose of this article I want to address the changes that pertain to low leptin levels and it’s relationship with feeding behavior.

As was mentioned, when the anabolic neural circuits of the brain are activated and catabolic neural circuits inhibited this results in hormonal changes that (amongst other things) encourage increased hunger but also affects your behavior around eating. [7-8] When leptin levels are low, the hunger stimulating hormone ghrelin is higher [9] and satiety hormones like CCK that promote feelings of fullness likely don’t work as well.[10] You may notice that the longer you diet the more you begin to obsess about food, the more food you are able to eat in one sitting, the more random cravings you seem to get, the less full you feel after meals that once would satiate you and the more willpower it requires in order to keep all of these things from derailing you from your deficit. All of this is fueled by those hormonal changes within the body.

After the initial plummet of leptin levels subsequent drops correlate with drops in body fat lost so the leaner you get, the lower your leptin levels fall and the more pronounced these effects can become. Many times these changes in emotional and physical response to available food and the inability to reach satiety results in periods of overeating despite the best efforts of the dieter. In other words, these hormonal changes can trigger urges to binge that can result in binge episodes.

Whether or not they admit it, many bodybuilding competitors have faced the issue of binging on their preps due to the extremity of the deficit and the low levels of body fat required to get on stage. Many times the urges  and intense hunger result in days of guilt ridden binges post-show followed by periods of caloric restriction in order to do damage control. More often than not, this see-saw approach results in these urges resurfacing as they try to force themselves back on a deficit and (as we already learned only takes a few days) once again leptin levels drop and trigger the aggressive ‘anti-starvation’ reactions all over again.

 

So how does this relate to Reverse Dieting?

Since lowered leptin levels are largely responsible for these urges it would seem that correcting lowered leptin levels as soon as possible would be the best way to help yourself with this post-diet. [11-12] While doing my research on how to accomplish this I came across this study.

 

Twenty-four-hour leptin levels respond to cumulative short-term energy imbalance and predict subsequent intake.

This study observes plasma leptin levels in response to maintenance, deficit or surplus calories. Though the participant pool is small, the findings were fascinating. What was of particular interest to me was that they observed leptin levels when returning to maintenance after a period at a deficit. I was under the impression that returning to maintenance would be enough get your body out of the red-zone post-diet and I was eager to see what the results had to show. If you don’t really care about the study details, skip forward to ‘Take Home Point’ section.

 

‘’ We hypothesized that leptin levels acutely respond to caloric excess or insufficiency, thus reflecting the body’s current energy state in nonobese, nonrestrained eaters. By signaling energy balance, leptin plays a role in regulating hunger and satiety, enabling the maintenance of normal weight. To test this hypothesis, 24-h leptin levels were measured as individuals underwent a series of 3-day periods of eucaloric feeding (100% TEE), moderate underfeeding (70% TEE), and overfeeding (130% TEE). In addition, changes in ad libitum intake were compared to changes in leptin levels in nonrestrained eaters.’’

 

They observed six healthy males of ‘non-obese’ weight between 18 and 39 years of age. What I found interesting about the criteria for the participating males was not only were they tested to ensure their blood work indicated good health but they were also screened for healthy eating habits and attitudes towards food. This was so they were less at risk of following disordered eating habits over following their actual hunger cues.

They began by establishing the calorie requirements necessary to maintain the weight of each participant. This is their total energy expenditure (TEE).

The study spanned over 12 days and was divided into four phases, each of them three days in duration.

During the first phase of the experiment, all participants were fed according to their TEE requirements. That is, for the first three days every participant was fed enough calories to maintain their weight.

During the second phase participants were divided into two groups. One group was fed 70% of their TEE requirements (so they were put at a caloric deficit) and the second group was fed 130% of their TEE which put them at a caloric surplus.

During the third phase for both groups intake was returned to 100% of their energy requirements (back to maintenance)

In the fourth phase the participants were divided into the same groups from the second phase and the group that was originally made to consume 70% of their TEE were now switched over to 130% of their TEE and the group originally made to consume 130% of was given 70%.

The study was performed at the Clinical Research Center (CRC) at the University of Chicago Hospital and participants ate all of their meals there under observation.

 

‘’ The first meal after each 3-day treatment period was a breakfast provided in a buffet format. Foods were preweighed and postweighed to calculate energy intake. Subjects were instructed to eat ad libitum, removing their desired portions to their own platter.’’

 

So after every three day phase, the size of the first meal in the following phase was dictated by the test subject and their hunger levels. Whatever they consumed was weighed before and after in order for the calories to be accurately recorded.

At the end of the 12 day period each subject had spent 6 days at their maintenance, 3 days at a deficit and 3 days at a surplus. The design was done in a way that each participant’s energy deficit or energy surplus that was obtained during the second phase was returned to baseline by the end of the 12 day period. That last statement means that their average calorie intake over the 12 day period would still work out to their maintenance calories despite spending a few days at a deficit and a few days at a surplus.

When I saw this study design I assumed that leptin levels would return to baseline in phase three once the 70% of TEE group returned to maintenance calories (moving from diet to maintenance). However this was not the case for either group.

 

‘’ Expressed as a percentage of the 3rd day of the previous eucaloric mesor, fasting leptin levels averaged 92%, 88%, and 80% on the 1st, 2nd, and 3rd days of underfeeding, and 89%, 98%, and 102% on these respective days of overfeeding.’’

‘’ The leptin zenith exhibited an average decrease of 1.2 ± 1.1 ng/mL (−30 ± 21%; P = 0.02) after decreasing intake by 30% of the TEE and an average increase of 0.72 ± 0.45 ng/mL (21 ± 12%; P = 0.01) after increasing intake by 30% of the TEE.’’

 

By day three of the third phase in which everyone was returned to eating 100% of their energy requirements their leptin levels still remained similar to what they were in the previous phase. So that means that those who where put at a deficit still had lowered leptin levels and those who were placed at a surplus still had elevated levels of leptin. At this point the effect of the feeding order was clear in the leptin levels for each participant. Leptin levels were only corrected by the third day of the fourth phase where the deficit group was then put at a surplus and the surplus group was then put at a deficit. So only when the deficit or surplus was corrected.

I think it is worth noting that unlike leptin, insulin levels did return to baseline once the individual returned to maintenance calories in the third phase and this could potentially have a positive effect on one’s appetite. [13-14]

 

‘’When leptin levels increased, ad libitum intake decreased, and when leptin levels decreased, ad libitum intake increased..’’

 

They noticed a correlation between leptin levels and how much food each participant had at their ‘ad libitum’ breakfast. Those who were made to eat 70% of their TEE subsequently ate more at that breakfast whereas those who were put at 130% of TEE ate less. So they noticed a change in feeding behavior/appetite after just 3 days of altered intake.

 

Take Home Point

 

‘’Specifically, we find that that the altered leptin levels resulting from overfeeding and underfeeding were not restored to baseline when the participants were returned to a eucaloric diet, an effect not previously reported. Instead, leptin levels returned to baseline only after the participants crossed over to the complementary dietary treatment and repaid the deficit or surfeit in cumulative energy balance.’’

 

This was the area of the study that I was most interested in as it relates directly to post-diet ‘rehab’. It would appear that simply returning to maintenance calories after a diet was not enough to return leptin levels to baseline. Now, one has to take into consideration that the maintenance period was only for 3 days but other studies where maintenance was sustained for longer periods had similar findings only corrected by exogenous leptin administration [12]. Taking these findings into consideration it would appear that a time at a surplus would better serve an individual aiming to return their leptin levels as close as possible to baseline sooner than later. This is why Reverse Dieting is particularly unhelpful because it keeps the individual at a deficit which means that these hormonal imbalances continue to remain as they are for an extended period as they slowly, calorie by calorie, inch their way back up to a maintenance and THEN towards a surplus. For a person struggling with urges to binge this is, for lack of better phrasing, playing with fire as it greatly prolongs the desired result.

 

How would I advise someone suffering with these urges coming off of a diet keeping in mind that the individual is interested in maintaining their new low weight?

 

My advice would be to prioritize getting rid of the urges as opposed to maintaining your post-diet weight. However, the following advice may be able to accomplish both to some degree. The first step is to immediately return to a surplus for a few days post diet. It’s been shown that high carbohydrate intake has the ability to temporarily boost leptin levels in the short term [15-16] which is the science behind the concept of high-carb refeeds on a diet. Give yourself at least 3 days at a surplus with a hefty amount of carbs and then drop calories to maintenance levels once hunger levels and urges begin to subside. Those surplus days can be untracked (recommended) or tracked depending on your comfort level. But it must be a surplus followed by a maintenance period.

When assisting clients with these urges post-show we give them a few days of ad-libitum eating with no tracking followed by some time at enough calories to maintain their current weight. If their hunger levels continue to remain out of control, we then adjust their numbers slightly to accommodate more food, or depending on the severity of the urges, give them a little more time off of tracking, allow them to eat according to hunger and then put them back at a maintenance when the urges subside. In practice, this intuitive back and forth has allowed things to even out over time with minimal impact on body composition.

One must remember that scale weight will go up regardless due to increased food volume. You’re eating more food so you have more food in your GI tract. This is not the same thing as a change in body composition. You will not maintain your depleted stage weight and trying to force your body to do so is unrealistic. More often than not we observe an initial spike in weight that settles within 2-4 weeks post show once the individual is able to return to their maintenance calories.

When you initially increase your calories you will be working with a lower RMR but only temporarily. Your body will raise your metabolic rate in response to the extra calories along with being given a better change at raising leptin levels which is the goal to take the edge off of your hunger. The sooner you increase your leptin levels the sooner the brain start activating the neural circuits that reduce hunger and raise metabolic rate once more. Remaining at a deficit keeps the levels of circulating leptin and insulin lower which results in the continued activation of the neural circuits that increase hunger and suppress energy expenditure. [4] Returning to maintenance relatively quickly after the surplus hypothetically allows you to quickly put a lid on excessive, unwanted gains. It’s the same desired result of the reverse diet without the continued stress to the system that the deficit would provide but more importantly, you are on the fast track to reduction of your urges to binge. Urges to binge left unchecked or challenged by a persistent deficit could potentially result in multiple binges that promote greater weight gain than a quick, controlled period of overfeeding would produce.

 

Since there are no studies done on the efficacy of Reverse Dieting when it comes to the metabolic response to the slow increase in calories I am not going to rule out the potential for some benefit to this approach, though I am doubtful of it’s efficacy. However, what I can say with certainty is that if you are struggling with binging at the end of your diet Reverse Dieting is definitely not doing you a service.

 

 

[1] Dulloo AG, Jacquet J, Girardier L. Poststarvation hyperphagia and body fat overshooting in humans: a role for feedback signals from lean and fat tissues. Am J Clin Nutr. 1997

[2] Trexler ET, Smith-Ryan AE, Norton LE. Metabolic adaptation to weight loss: implications for the athlete. Journal of the International Society of Sports Nutrition. 2014

[3] Calbet JA, Ponce-González JG, Pérez-Suárez I, de la Calle Herrero J, Holmberg HC. A time-efficient reduction of fat mass in 4 days with exercise and caloric restriction. Scand J Med Sci Sports. 2015

[4] Mantzoros CS, Magkos F, Brinkoetter M, et al. Leptin in human physiology and pathophysiology. American Journal of Physiology – Endocrinology and Metabolism. 2011;301(4):E567-E584. doi:10.1152/ajpendo.00315.2011.

[5] chwartz MW, Woods SC, Porte D Jr, Seeley RJ, Baskin DG. Central nervous system control of food intake. Nature. 2000

[6] Cowley MA, Smart JL, Rubinstein M, Cerdán MG, Diano S, Horvath TL, Cone RD, Low MJ. Leptin activates anorexigenic POMC neurons through a neural network in the arcuate nucleus. Nature. 2001

[7] Park H-K, Ahima RS. Physiology of leptin: energy homeostasis, neuroendocrine function and metabolism. Metabolism: clinical and experimental. 2015

[8]Spiegelman BM, Flier JS. Obesity and the regulation of energy balance. Cell. 2001 Feb 23

[9] Kalra SP, Ueno N, Kalra PS. Stimulation of appetite by ghrelin is regulated by leptin restraint: peripheral and central sites of action. J Nutr. 2005

[10] Wang L, Barachina MD, Martínez V, Wei JY, Taché Y. Synergistic interaction between CCK and leptin to regulate food intake. Regul Pept. 2000

[11] Rosenbaum M, Sy M, Pavlovich K, Leibel RL, Hirsch J. Leptin reverses weight loss-induced changes in regional neural activity responses to visual food stimuli. J Clin Invest. 2008

[12] Kissileff HR, Thornton JC, Torres MI, Pavlovich K, Mayer LS, Kalari V, Leibel RL, Rosenbaum M. Leptin reverses declines in satiation in weight-reduced obese humans. Am J Clin Nutr. 2012

[13]Benoit SC, Blake Smith KA, Clegg DJ, Woods SC. Acute third ventricular administration of insulin decreases food intake in two paradigms. Pharmacol Biochem Behav. 2002

[14] Kalra SP, Dube MG, Pu S, Xu B, Horvath TL, Kalra PS. Interacting appetite-regulating pathways in the hypothalamic regulation of body weight. Endocr Rev. 1999

[15] Romon M, Lebel P, Velly C, Marecaux N, Fruchart JC, Dallongeville J. Leptin response to carbohydrate or fat meal and association with subsequent satiety and energy intake. Am J Physiol. 1999

[16]Dirlewanger M, di Vetta V, Guenat E, Battilana P, Seematter G, Schneiter P, Jéquier E, Tappy L. Effects of short-term carbohydrate or fat overfeeding on energy expenditure and plasma leptin concentrations in healthy female subjects. Int J Obes Relat Metab Disord. 2000

 

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