Physiology of Binge Eating

In this article, we will dive into a series of reasons as to why binge eating occurs – from neurology to endocrinology.

What is Binge Eating Disorder?

Binge eating disorder is a situation in which a person overconsumes foods over a period of time in a difficult to control manner [1]. This is usually characterized by eating past the feeling of fullness, eating in secret to avoid embarrassment, and distress over the habit of eating large amounts over a specific amount of time [1].

What causes Binge Eating Disorder?

This is a loaded question which spans multiple disciplines, of which I will only explain the physiology in depth in the next section; however, a pattern of psychological, neurophysiological, and genetic factors play their minor and major roles in binge eating.

It seems that those that binge eat may have a slight increase in food reward response and tend to have significantly greater disinhibition (lack of control), although the evidence is mixed (possibly due to different measurement techniques) [4][5][6]. I should also note that there is a noticeable association with depression (again, based on varying measurements) in binge eating individuals [4][5]. This is further evidenced by the aid serotonin reuptake inhibitor drugs (anti-depressants) offer to some [7]. Interestingly, the reporting of hunger is also not always different among binge eating individuals and non, meaning hunger may not always be a driver for these binge eating episodes; although, there are instances in which hunger is elevated in binge eating individuals [4][10]. Compounding these issues, stress may play a triggering role, or at least compound the issue, by showing elevated stress hormone levels in resting conditions in binge eating individuals, but this is dependent on the type of stressor – physical pain increases cortisol levels while psychological stressors seem to have little effect [8][9][23].

So, while I could go on and point out every little factor, the bottom line is there are a number of factors that have been studied, and the outcomes implicate environmental and innate reasons for the occurrence of binge eating.

Understanding the Physiology

As stated previously, this topic spans several disciplines, but there are key physiological factors that may explain binge eating behavior.

First, differences in the brain have been reported [10]. When confronted with food, people with binge eating disorder tend to have higher blood flow to the frontal cortex; this area is characterized as the thought and planning areas of the brain [11]. Not only that, brain activity, be it electrically measured or metabolically measured, shows increases in frontal cortex beta wave production [10]. By comparison, non-binge eating individuals, of similar or lower weights, show lower beta wave production and more alpha wave production [10]. Now, because beta waves are associated with arousal and excitement and alpha waves are associated with relaxation, it would not be farfetched to hypothesize binge eating individuals have an increased excitement to the stimulus of food.

As well as seeing heightened excitation, there is a dampened reward internalized in relation to food cues or other “winning”, “having” outcomes [3][12]. This is evidenced by decreases in corpus striatum activity; this section of the brain is implicated in reward processing [12].

This is an image of the corpus striatum - the emotional processing center of the brain. 

Second, genetics seems to play a role in approximately 50% of binge eating disorder cases [3]. This is an area of great ambiguity as it is clear genetics plays a significant role in the disorders appearance, yet upon study of various genetic coding regions responsible for transcribing a particular dopamine receptor, there is some evidence the receptor is transcribed less in some individuals than others [13]. This may be an explanation for why there is back and forth on if reward sensitivity is increased or decreased – some see an increase, others see a decrease – potentially attributed to the decreased (or normal) expression of this dopamine receptor related gene. Dopamine is released, but the receptor is found in lower quantities in the corpus striatum.

Finally, the last point discussed here (although, there are likely more, these three areas seem to have the greatest impact) is hormonal effect on binge eating. For women, although menstrual hormonal profiles are not different, when estrogen is low and progesterone is low, binge eating is frequent [14][17][18][19][20]. Also, a concurrent increase in progesterone with estrogen leads to an amelioration of estrogen’s anti-binge eating effect, leading to greater risk of binge eating episodes [18]. This means the first week of the menstrual cycle (early to mid follicular phase) and the end of the first week post-ovulation are the highest risks of binge eating [14][15][17][18][19][20].

Increased estrogen seems to reduce hunger and also has an impact on reducing binge eating frequency, unless estrogen is paired with a rise in progesterone [17][18]. Estrogen may be binding estrogen receptors, which stimulate the release of serotonin (5-HT) in the raphe nucleus of the brain, affecting the downstream areas of the brain like the hypothalamus, which is closely related to eating behavior [16][22]. Lower serotonin levels are associated with greater hunger cues, so the increase in estrogen mitigates that issue by stimulating serotonin release [16][21]. Progesterone is thought to inhibit estrogen’s anti-binging effects by acting as a neutral agonist – binding the estrogen receptors on the neural cells, blocking the estrogen from binding and transducing a signal into the cell; this also means that progesterone does not have a direct binge eating promoting effect, independent of estrogen [20].

Shifting focus to the primary stress hormone – cortisol. Although it would seem intuitive to see increases in cortisol with individuals prone to binge eating disorder, the opposite is seen [23]. Those subjected to a psychological stress test saw lower circulating cortisol levels compared to non-binge prone individuals [23]. Interestingly, those same individuals started out with lower cortisol levels, so it may be that chronic cortisol release desensitizes individuals to acute stressors. However, as we mentioned in the previous section, some stress stimuli do increase cortisol levels higher compared non-binge prone individuals – so, the type of stressor matters [8][9][23]. This means that while cortisol likely plays a role, it is likely dependent on the type of stress perceived, which would have a greater impact on different areas of the brain – physical pain affecting the somatosensory cortex and psychological likely impacting the amygdala.

So, how does this operate?

Upon the perception of a stressor, neurons from the original site of perception (for example, the somatosensory cortex) will depolarize neurons to propagate a signal to release epinephrine and other catecholamines from the adrenal gland (in the instance of acute stress), which will inevitably lead to these catecholamines binding to neurons in the hypothalamus [24]. The hypothalamus releases corticotropin releasing factor, which binds the pituitary gland to stimulate it to release adrenocorticotropin hormone [24]. Adrenocorticotropin hormone returns to the adrenal gland (the cortex, as opposed to the medulla), binding it, and stimulating the release of cortisol [24]. Now, the release of cortisol then allows the hormone to bind the hypothalamus, changing its expression of neuropeptides (like neuropeptide Y, POMC, and AgRP – among others) that modulate hunger [24][25].

Now, when it comes to eating and satiety, it would be irresponsible not to investigate the leptin hormone, closely tied to adipose tissue. That said, it seems that leptin may not be as great a factor as one might imagine, because leptin levels are significantly higher in people with binge eating episodes compared to people who do not have binge eating episodes (more leptin generally means an increase in satiety) [26]. However, if we account for increased adiposity in binge eating individuals, we see that effect disappear [27]. So, does leptin have an impact? Unlikely, although certain individuals, not necessarily directly related to binge eating, may have leptin resistance from being obese [28]. However, beyond the normal physiologic role of leptin in energy homeostasis and fatness regulation – leptin seems not to be different between people.

Summary

In summary, there are many factors that play into binge eating disorder, and it is unlikely that one person’s binge eating is immediately related to another’s due to the extreme variability. Factors like the type of stressor, the design of the brain, hunger, depression, hormones, and more, all make binge eating difficult to treat, but if you can understand the patterns within yourself, you will be able to personalize your approach to the problem, regardless of the source of complication (genetic, hormonal, etc.).

Writer: Nicolas Verhoeven

References

[1] Binge Eating Disorder. (2018, February 21). Retrieved from https://www.nationaleatingdisorders.org/learn/by-eating-disorder/bed

[2] Bulik, C. M. (2007). Diagnosis and management of binge eating disorder. World Psychiatry, 6(3), 142-148. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2174583/

[3] Kessler, R. M., Hutson, P. H., Herman, B. K., & Potenza, M. N. (2016). The neurobiological basis of binge-eating disorder. Neuroscience & Biobehavioral Reviews, 63, 223-238. doi:10.1016/j.neubiorev.2016.01.013

[4] Schag, K., Teufel, M., Junne, F., Preissl, H., Hautzinger, M., Zipfel, S., & Giel, K. E. (2013). Impulsivity in Binge Eating Disorder: Food Cues Elicit Increased Reward Responses and Disinhibition. PLoS ONE, 8(10), e76542. doi:10.1371/journal.pone.0076542

[5] Galanti, K., Gluck, M. E., & Geliebter, A. (2007). Test meal intake in obese binge eaters in relation to impulsivity and compulsivity. International Journal of Eating Disorders, 40(8), 727-732. doi:10.1002/eat.20441

[6] Wu, M., Giel, K. E., Skunde, M., Schag, K., Rudofsky, G., De Zwaan, M., … Friederich, H. (2013). Inhibitory control and decision making under risk in bulimia nervosa and binge-eating disorder. International Journal of Eating Disorders, 46(7), 721-728. doi:10.1002/eat.22143

[7] McElroy, S., Guerdjikova, A. I., Mori, N., & O’Melia, A. (2012). Pharmacological management of binge eating disorder: current and emerging treatment options. Therapeutics and Clinical Risk Management, 219. doi:10.2147/tcrm.s25574

[8] GLUCK, M. E., GELIEBTER, A., & LORENCE, M. (2004). Cortisol Stress Response Is Positively Correlated with Central Obesity in Obese Women with Binge Eating Disorder (BED) before and after Cognitive-Behavioral Treatment. Annals of the New York Academy of Sciences, 1032(1), 202-207. doi:10.1196/annals.1314.021

[9] Laessle, R. G., & Schulz, S. (2009). Stress-induced laboratory eating behavior in obese women with binge eating disorder. International Journal of Eating Disorders, 42(6), 505-510. doi:10.1002/eat.20648

[10] Tammela, L. I., Pääkkönen, A., Karhunen, L. J., Karhu, J., Uusitupa, M. I., & Kuikka, J. T. (2010). Brain electrical activity during food presentation in obese binge-eating women. Clinical Physiology and Functional Imaging, 30(2), 135-140. doi:10.1111/j.1475-097x.2009.00916.x

[11] Karhunen, L. J., Vanninen, E. J., Kuikka, J. T., Lappalainen, R. I., Tiihonen, J., & Uusitupa, M. I. (2000). Regional cerebral blood flow during exposure to food in obese binge eating women. Psychiatry Research: Neuroimaging, 99(1), 29-42. doi:10.1016/s0925-4927(00)00053-6

[12] Balodis, I. M., Grilo, C. M., Kober, H., Worhunsky, P. D., White, M. A., Stevens, M. C., … Potenza, M. N. (2013). A pilot study linking reduced fronto-Striatal recruitment during reward processing to persistent bingeing following treatment for binge-eating disorder. International Journal of Eating Disorders, 47(4), 376-384. doi:10.1002/eat.22204

[13] Davis, C., Levitan, R. D., Kaplan, A. S., Carter, J., Reid, C., Curtis, C., … Kennedy, J. L. (2008). Reward sensitivity and the D2 dopamine receptor gene: A case-control study of binge eating disorder. Progress in Neuro-Psychopharmacology and Biological Psychiatry, 32(3), 620-628. doi:10.1016/j.pnpbp.2007.09.024

[14] Klump, K. L., Racine, S. E., Hildebrandt, B., Burt, S. A., Neale, M., Sisk, C. L., … Keel, P. K. (2014). Influences of Ovarian Hormones on Dysregulated Eating. Clinical Psychological Science, 2(5), 545-559. doi:10.1177/2167702614521794

[15] Reed, B. G. (2018). The Normal Menstrual Cycle and the Control of Ovulation. In Endotext. Retrieved from https://www.ncbi.nlm.nih.gov/books/NBK279054/

[16] Xu, P., Cao, X., & Xu, Y. (2015). Targeting brain estrogen receptor for binge eating. Oncotarget, 6(27). doi:10.18632/oncotarget.5239

[17] Kemnitz, J. W., Gibber, J. R., Lindsay, K. A., & Eisele, S. G. (1989). Effects of ovarian hormones on eating behaviors, body weight, and glucoregulation in rhesus monkeys. Hormones and Behavior, 23(2), 235-250. doi:10.1016/0018-506x(89)90064-0

[18] Klump, K. L., Keel, P. K., Racine, S. E., Burt, S. A., Neale, M., Sisk, C. L., … Hu, J. Y. (2013). "The interactive effects of estrogen and progesterone on changes in emotional eating across the menstrual cycle": Correction to Klump et al. (2012). Journal of Abnormal Psychology, 122(1), 137-137. doi:10.1037/a0030842

[19] Edier, C. (2007). Ovarian hormones and binge eating in bulimia nervosa. Psychological Medicine, 37(1), 131-141. Retrieved from https://www.ncbi.nlm.nih.gov/pubmed/17038206

[20] Baker, J. H., Girdler, S. S., & Bulik, C. M. (2012). The role of reproductive hormones in the development and maintenance of eating disorders. Expert Review of Obstetrics & Gynecology, 7(6), 573-583. doi:10.1586/eog.12.54

[21] Neurotransmitters. (2016, December 21). Retrieved from https://www.nationaleatingdisorders.org/toolkit/parent-toolkit/neurotransmitters

[22] Donovan, M. H., & Tecott, L. H. (2013). Serotonin and the regulation of mammalian energy balance. Frontiers in Neuroscience, 7. doi:10.3389/fnins.2013.00036

[23] Rosenberg, N., Bloch, M., Ben Avi, I., Rouach, V., Schreiber, S., Stern, N., & Greenman, Y. (2013). Cortisol response and desire to binge following psychological stress: Comparison between obese subjects with and without binge eating disorder. Psychiatry Research, 208(2), 156-161. doi:10.1016/j.psychres.2012.09.050

[24] Yau, Y. H. (2013). Stress and Eating Behaviors. Minerva Endocrinology, 38(3), 255-267. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4214609/

[25] Arora, S., & Anubhuti. (2006). Role of neuropeptides in appetite regulation and obesity – A review. Neuropeptides, 40(6), 375-401. doi:10.1016/j.npep.2006.07.001

[26] Adami, G., Campostano, A., Cella, F., & Ferrandes, G. (2002). Serum leptin level and restrained eating. Physiology & Behavior, 75(1-2), 189-192. doi:10.1016/s0031-9384(01)00639-4

[27] Adami, G., Campostano, A., Cella, F., & Scopinaro, N. (2002). Serum leptin concentration in obese patients with binge eating disorder. International Journal of Obesity, 26(8), 1125-1128. doi:10.1038/sj.ijo.0802010

[28] Myers, M. G., Leibel, R. L., Seeley, R. J., & Schwartz, M. W. (2010). Obesity and leptin resistance: distinguishing cause from effect. Trends in Endocrinology & Metabolism, 21(11), 643-651. doi:10.1016/j.tem.2010.08.002

"CLICK" for Most Recent