Extreme Hunger Part 2: The Experience and Science

Here you will find answers as to whether you are really hungry during your recovery process or whether it is as you suspect—you are eating because you are bored, experiencing emotional eating, or just plain bingeing for no good reason.

 Lawrence Wang: Flickr.com

Lawrence Wang: Flickr.com

The challenges of hunger, satiation and fullness are quite simply a bit of a mess throughout the recovery process and this causes many a lot of anxiety and grief.

As with the ever-present fear that the metabolism “is broken” many in recovery experience the disconnections between hunger, physical fullness and emotional satiation and worry that the entire energy balance system is “broken” as well.

Neither the metabolism nor the appetite connections are broken due to eating disorders. However, they have developed temporary adaptations that are survival-based.

The Belly Dance

Some portions of this section are also found in the Phases of Recovery Part 4 and were developed in response to the following e-mail I received after having posted Extreme Hunger Part 1:

you describe the pathways of the signals that reach the brain and the GI system, and state that the cells in the body require a high amount of calories to “repair damage” done during restriction. I wonder what specific scientific research has been done to prove this mechanism (that the digestive system plays “catch up”) and on what scientific evidence you base your statements such as " the cells throughout the body are screaming at the brain “More energy now!” ?”

The scientific research on this “catch up” centers on the Minnesota Starvation Experiment. As that experiment can never be duplicated for ethical reasons, most of the research on the topic since that time originates from murine studies.1

Restorative eating is designed to redress deficits

Drs. David M. Garner and Paul E. Garfinkel, researchers in the field of eating disorders responsible for developing numerous psychometric tests for the identification of eating disorder behaviors in individuals, had the following to say on the topic of the kind of reactive eating that was witnessed in the ad libitum (freely, without restraint) re-feeding period that occurred after the initial slow stepped re-feeding period in the Minnesota Starvation Experiment:

During the weekends in particular, some of the men found it difficult to stop eating. Their daily intake commonly ranged between 8,000 and 10,000 calories…
After about 5 months of refeeding, the majority of the men reported some normalization of their eating patterns, but for some the extreme overconsumption persisted: “No. 108 would eat and eat until he could hardly swallow any more and then he felt like eating half an hour later” (p. 847). More than 8 months after renourishment began, most men had returned to normal eating patterns; however, a few were still eating abnormal amounts: “No. 9 ate about 25 percent more than his pre-starvation amount; once he started to reduce but got so hungry he could not stand it” (p. 847)… Serious binge eating developed in a subgroup of men, and this tendency persisted in some cases for months after free access to food was reintroduced; however, the majority of men reported gradually returning to eating normal amounts of food after about 5 months of refeeding. Thus, the fact that binge eating was experimentally produced in some of these normal young men should temper speculations about primary psychological disturbances as the cause of binge eating in patients with eating disorders. These findings are supported by a large body of research indicating that habitual dieters display marked overcompensation in eating behavior that is similar to the binge eating observed in eating disorders (Polivy & Herman, 1985, 1987; Wardle & Beinart, 1981). [emphasis mine]. 2

Abdul Dulloo and his colleagues in 1997 postulated that the fat mass to fat-free mass data collected from the Minnesota Starvation Experiment during the ad libitum re-feeding period suggests “that poststarvation hyperphagia [excess eating] is determined to a large extent by the autoregulatory feedback mechanisms from both fat and lean tissues.” 3 The subjects all returned to pre-starvation fat mass to fat-free mass ratios, although, as mentioned above, it could take beyond a year for that to occur.

Interestingly, a few clinical trials assessing the body fat composition of weight-restoredpatients with an eating disorder suggest that fat mass levels were higher than healthy controls and they remained unevenly distributed at the abdominal and tricep regions after re-feeding. [4], [5] However, I suggest that this data is the result of incomplete recovery processes whereby a specific weight target was applied as a faulty marker of remission. If ad libitum re-feeding and longitudinal assessment are applied beyond the one-year period of weight readjustment, then in fact the clinical findings support my assessment: namely those with eating disorders also return to optimal fat mass to fat-free mass ratios assuming they mimic the re-feeding process seen within the Minnesota Starvation Experiment (i.e., they respond fully to hyperphagia). [6]

Restriction of food intake is very similar to restriction of sleep. The impacts of doing so are cumulative in nature. If you stayed up for 36 hours straight and then went to sleep, would you be concerned if your sleep lasted more than 8 hours? Would you be surprised if you were still tired when you awoke and the subsequent night you found you still required perhaps more sleep than was usual to feel really “caught up” the next morning?

Hyperphagia in recovery

August 2, 2012
Kimberly
Not too long ago, I put some hash browns in the oven and decided to have some toast while I waited. While the toast was in the toaster, I had some cashews and poured myself a bowl of yoghurt—so, essentially, I was having a snack while I waited for the second snack that I was preparing while I waited for the first snack. SNACKCEPTION.

Patients find extreme hunger very upsetting and disturbing in recovery. So pervasive are the misconceptions regarding binge eating and so-called emotional eating as dangerous and unacceptable behaviors that lead to ill health and obesity, it takes herculean focus to maintain respectful responsiveness to the demands for energy that the body is making.

In simplified terms, several hormones including leptin and adiponectin can activate adenosine monophosphate-activated protein kinase (AMPK) and that in turn regulates metabolic choices between anabolism (resulting in the building up of tissue) and catabolism (resulting in the breaking down of tissue). 7 These same hormones also act on the brain and specifically interact with the hypothalamus, which is responsible for identifying whether energy balance is present or absent throughout the entire body. 8 Leptin and adiponectin, as well as resistin and several others, are all generated by cells within the fat organ of your body.

In our current understanding of the cycle of these adipocytokines (as these fat-generated hormones are called as a group), their serum levels are affected by restriction of energy intake (even before catabolism occurs); they “inform” the hypothalamus of an energy deficit; and they activate AMPK to begin the process of catabolism of existing body tissue (made up of cells, obviously) to release energy to support ongoing biological functions.

One of the reasons that those with an active eating disorder often do not appear deficient in many minerals and vitamins may not actually be due to their heavy use of vitamin and mineral supplements, but rather the release of these minerals and vitamins through catabolism of their own body tissue. 9 Catabolism (the destruction of cells and tissue) releases the energy necessary to try to remediate the drop in serum adipocytokine levels while at the same time those levels are signaling the hypothalamus that energy intake is a necessity to reverse the process of catabolism. When you see the word “catabolism,” think cannibalization of your own being.

It is rather obvious to point out that, in the aftermath of restriction, the catabolism (breakdown of tissue) has to be reversed with anabolism (the buildup of tissue).

Nonetheless, this process is complicated further as the gastrointestinal tract has its own nervous system—the enteric nervous system—and specific peptide hormones are released by the gastrointestinal tract in response to the presence of food as well: peptide YY, pancreatic polypeptide, glucagon-like peptide-1, and oxyntomodulin. And these peptides are all presumed to act as postprandial (after a meal) satiety signals. [0

Your gut and your mind

When a person is energy balanced, then hunger, fullness, and satiation are all synchronized. But after just a few weeks (let alone months or years) of catabolizing your own body, these things will be asynchronous when you begin to reverse the damage.

In the earlier phases of recovery, you experience significant sensory dissonance because physical fullness, as identified by your enteric nervous system, and extreme absence of satiation, as experienced by your central nervous system are confirming you are both full and hungry at the same time.

Your enteric nervous system is receiving information that the physical aspects of energy absorption are at peak levels, yet the central nervous system continues to receive information that more anabolism (building up of tissue) is required to return to an energy-balanced state. You are gut-full, body-empty.

And you get complete brain shear as a result and here are just a few first-person explanations of what it feels like (all excised from the Eating Disorder Institute forums):

The concept to me is so confusing, because I can feel not hungry, satiated, or even nauseous with food, but there isn't necessarily fullness in my stomach.”
“Sometimes I would not be full and ask for seconds and it would take ten minutes to reheat. By the time I sat down with that second plate I would think, “actually I’m really full now and I don’t really want this” but I went to the trouble of getting more so I just ate it anyway.”
“I definitely feel some compulsion to “finish everything” now, because I fear being deprived and am still obsessed with food to varying degrees. I am also very, very aware of my hunger. It’s weird that I seriously cannot remember how I ate before I started restricting...”
“I am not quite sure what you mean when you say that you don’t feel the food in your stomach. I think I feel the food in my stomach, and I definitely feel ‘full’, but I still feel the urge to ‘finish everything’, too. Sometimes I feel like I am just forcing the food down. I don’t know whether it’s a lack of fullness or satiation, but I can definitely relate to never feeling full.”
“Even then if there was still food on my plate I would almost force myself to finish it because it ‘tasted so good’. I am really not sure what this is or what it means......if I was not full to bursting I would still feel hungry/not satiated”
“On a day-to-basis, I never feel 100% satisfied after eating either. Maybe 90% if I’m lucky, but there is always room for one more bite. So why not just take the one more bite every single time? Because I worry... :-/ Worry that I’m getting my calories within too short a time period in the day and that I should try to spread them out more; that I’m making up extra calories via “junk” food (I know, I know...)”

For everyone, the brain structures responsible for conscious thought are dealing with a completely novel experience and you can clearly see the profound struggle that it elicits in everyone. Biologically, they are all gut-full, brain-empty.

And look at the contradictions that result in the attempt to describe these sensations! One feels fullness in the stomach, but not satiation and yet the next person will describe the opposite sensations.

Your enteric nervous system is receiving information that the physical aspects of energy absorption are at peak levels, yet the central nervous system continues to receive information that more anabolism (building up of tissue) is required to return to an energy-balanced state.

Try not to get too caught up in what descriptions your conscious mind generates to try to make sense of the nonsensical as you move through these phases of recovery. Your job is to eat. The anxieties about whether it is “normal,” “emotional,” or “the stomach has adapted to more food” are just that: anxieties.

If you feel the need to eat more, then it doesn’t matter how your mind describes that need; the drive to eat is fundamentally sound and all about energy restoration, or anabolism.

And when you reach your energy balanced state yet again, then all your hormones and neurotransmitters will be providing the same message at the same time so hunger, fullness and satiation will not be creating any more strange cross-talk in your mind.


1. Dixon, Deann P., Allison M. Ackert, and Lisa A. Eckel. "Development of, and recovery from, activity-based anorexia in female rats." Physiology & behavior 80, no. 2 (2003): 273-279.

2. Garner, David M., and Paul E. Garfinkel, eds. “Handbook of Treatment for Eating Disorders.” (New York: Guilford Press, 1997), pp.156-157.

3. Dulloo, Abdul G., Jean Jacquet, and Lucien Girardier. "Poststarvation hyperphagia and body fat overshooting in humans: a role for feedback signals from lean and fat tissues." The American journal of Clinical Nutrition 65, no. 3 (1997): 717-723.

4. Mayer, Laurel, B. Timothy Walsh, Richard N. Pierson, Steven B. Heymsfield, Dympna Gallagher, Jack Wang, Michael K. Parides et al. "Body fat redistribution after weight gain in women with anorexia nervosa." The American Journal of Clinical Nutrition 81, no. 6 (2005): 1286-1291.

5. Scalfi, L., A. Polito, L. Bianchi, M. Marra, A. Caldara, E. Nicolai, and F. Contaldo. "Body composition changes in patients with anorexia nervosa after complete weight recovery." European Journal of Clinical Nutrition 56, no. 1 (2002): 15-20.

6. Mayer, Laurel ES, Diane A. Klein, Elizabeth Black, Evelyn Attia, Wei Shen, Xiangling Mao, Dikoma C. Shungu et al. "Adipose tissue distribution after weight restoration and weight maintenance in women with anorexia nervosa." The American Journal of Clinical Nutrition 90, no. 5 (2009): 1132-1137.

7. Hardie, D. Grahame, John W. Scott, David A. Pan, and Emma R. Hudson. "Management of cellular energy by the AMP-activated protein kinase system." FEBS letters 546, no. 1 (2003): 113-120.

8. Flier, Jeffrey S. "Regulating energy balance: the substrate strikes back." Science 312, no. 5775 (2006): 861-864.

9. Casper, Regina C., Barbara Kirschner, Harold H. Sandstead, Robert A. Jacob, and John M. Davis. "An evaluation of trace metals, vitamins, and taste function in anorexia nervosa." The American Journal of Clinical Nutrition 33, no. 8 (1980): 1801-1808.

10. Chaudhri, Owais B., B. C. T. Field, and S. R. Bloom. "Gastrointestinal satiety signals." International Journal of Obesity 32 (2008): S28-S31.