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Why Do We Feel Hungry? Explaining the Human Drive to Eat

By Dr. Marc Bubbs ND, MSc, CISSN, CSCS
June 4, 2021
Dan Gold/ Unsplash.com
Dan Gold/ Unsplash.com

In the 1970s, the prevalence of obesity in America was a mere five percent of the population, and families ate most of their meals at home. [1]

Today, almost 30 percent of the United States is obese, and half of our meals are from restaurants, convenience stores, or fast food. [1] Ultra-processed foods have become a large part of the standard American diet (SAD), and their high caloric value is a major contributor to overconsumption and weight gain. [2,3]

In the past 50 years—the blink of an eye in evolutionary terms—the waistline and health of the nation have worsened at an unprecedented and alarming rate. Why?

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How energy expenditure works

The term “energy balance” describes an interplay between how much food you consume (i.e. energy intake) and how much energy you expend (i.e. energy expenditure)—combining both the energy your body naturally uses at rest and energy used from movement and activity you perform in a day.

Tracking energy balance is not simply a matter of measuring the calories in your food and the energy expenditure displayed on a FitBit or other tracking device. What often gets missed is how tightly these two factors are connected; changing one inevitably influences the other.

In the 1950s, this effect was first illustrated in a study of mill workers in Calcutta, India. [6] Heavy physical demands were commonplace for some workers, while others had more sedentary day-to-day roles. Researchers found that the amount of food eaten in the canteen was proportional to the level of energy in their daily work.

In other words, the workers had an innate sense of how much they needed to eat to maintain energy balance.

Fast forward to the 1990s, the first studies involving simultaneous measurements of energy expenditure and human eating behavior were conducted as researchers looked to assess the impact of exercise on appetite control. [7]

What did they find? Interestingly, it wasn’t fat mass driving energy intake. Instead, it was the fat-free mass (FFM), like skeletal muscle and organ tissue, that was a principal driver. [8,9]

Incredibly, fat mass was either unrelated or negatively associated with food (energy) intake.

The finding that FFM drives energy intake has been replicated in nine different countries and four continents; the relationship is very strong and appears to be independent of culture. [10-20]

How appetite plays a role

Our bodies were designed to balance our appetite with our activity levels. However, there is a disconnect of this system in obese individuals, making it harder for them to regulate weight. [6,7] So, if energy expenditure no longer drives energy intake in this scenario, how does appetite fit into the equation? Let’s explore.

Traditional scientific thinking about appetite control is centered around the idea that the purpose of appetite is to regulate bodyweight and adipose (fat) tissue. And according to this theory of appetite, the fat cell is at the heart of the regulatory process. [24]

Regulation implies that there is an optimal weight or level of adipose tissue that is tightly controlled. If we drop below that optimal balance, appetite increases. Once we exceed our needs to stay in balance, appetite is suppressed. In essence, obesity is the result of this regulation going haywire.

However, what if it’s not a tightly regulated system? That is, what if our bodies neither monitor nor “care” how much fat mass we put on?

An emerging group of scientists are turning the question upside down: If bodyweight is under physiological regulation, they ask, why do we have an obesity epidemic? [25] Can an evolutionary perspective yield further insight?

In nature, biological systems exhibit a wide range of strategies to favor survival under various conditions. A few other biological principles, other than regulation, come into play including adaptation, feedback, and dynamic stability. All of these may help guide energy balance beyond just simple regulation.

In fact, an important evolutionary principle states, “a system will have adaptive properties which contribute to biological organization, but which does not need to incorporate a process of regulation.” [4]

In other words, there is an emerging hypothesis that energy expenditure (EE) drives energy intake (EI) in a way that does not require regulation. The “drive to eat” in humans is most definitely purposeful (to support bodily processes) and occurs from biological signals, but this emerging hypothesis proposes it’s independent of negative feedback.

This is a clear distinction from the traditional regulatory model of appetite. In fact, scientists question whether the “existence of lipostatic (fat) regulation of body fatness is an illusion.” Their belief that there may be no regulatory processes goes against the current conventional wisdom on weight gain. [26]

Our diet of ultra-processed food has hijacked these evolutionary drivers of eating. This affects the various signals our brain uses to control appetite, such as blood glucose, nutrient density, and satiety hormones, and can fool our bodies into always being hungry.

Hunger signals in the brain

If the drive to eat is not regulated, what factors impact it?

According to the “drive to eat” theory, the brain is also a contributor in the drive to eat. The brain receives signals from a variety of sources that can all trigger the drive to eat. Here is a brief list:

  • an empty stomach
  • low blood glucose
  • lack of immediate nutrients
  • low gastro-intestinal activity
  • influence of the hormones leptin and ghrelin
  • other events indicating a lack of recent ingestion [28-33]

This new “drive to eat” model acknowledges that weight gain and the accumulation of fat mass do exert an inhibitory influence on the factors listed above (via leptin signaling,) but they are not the biggest factors. Energy expenditure and resting metabolic rate exert the greatest influence on why we eat as humans. [4]

Note that the “drive to eat” theory in humans doesn’t attempt to explain food choice, satiety, food reward, consumer behavior, or thought processes around eating that are believed to be major contributors to our current obesity epidemic.

How to combat obesity

What does all this mean with respect to solving our current obesity epidemic?

A new line of research proposes that fat-free mass (FFM) and resting metabolic rate (RMR) are the major long-term factors impacting our drive to eat, regardless of culture. Our diet of ultra-processed food has hijacked these evolutionary drivers of eating. This affects the various signals our brain uses to control appetite, such as blood glucose, nutrient density, and satiety hormones, and can fool our bodies into always being hungry.

To combat this issue, be sure to incorporate resistance training into your routine. The amount of muscle you carry is a pivotal factor in supporting a healthy RMR, as well as increasing your energy expenditure. Avoid ultra-processed foods, exercise daily, and eat enough protein (at least 1.2g/kg/day) each day to lay the foundation for health and longevity.

The Evidence Against Eating Ultra-Processed Foods Continues to Mount
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  1. NHS Digital, Statistics On Obesity, Physical Activity and Diet, England, 2019 2019 https://digital.nhs.uk/data-and-information/publications/statistical/statistics-on-obesity-physical-activity-and-diet/statistics-on-obesity-physical-activity-and-diet- england-2019 2019.
  2. M. Hopkins, G. Finlayson, C. Duarte, S. Whybrow, P. Ritz, G.W. Horgan, et al., Modelling the associations between fat-free mass, resting metabolic rate and energy intake in the context of total energy balance, Int. J. Obes. (Lond.) 40 (2) (2016) 312–318, https://doi.org/10.1038/ijo.20...;
  3. M. Hopkins, G. Finlayson, C. Duarte, C. Gibbons, A.M. Johnstone, S. Whybrow,
    et al., Biological and psychological mediators of the relationships between fat mass, fat-free mass and energy intake, Int. J. Obes. 43 (2) (2018) 233–242, https://doi. org/10.1038/s41366-018-0059-4.
  4. J. Blundell, C. Gibbons, K Beaulieu et al.The drive to eat in homo sapiens: Energy expenditure drives energy intake. Physiology &Behavior 219 (2020) 112846. https://doi.org/10.1016/j.physbeh.2020.112846
  5. D.P. Speechly, R Buffenstein, Appetite dysfunction in obese males: evidence for role of hyperinsulinaemia in passive overconsumption with a high fat diet, Eur. J. Clin. Nutr. 54 (3) (2000) 225–233.
  6. J. Mayer, P. Roy, K.P Mitra, Relation between caloric intake, body weight, and physical work: studies in an industrial male population in West Bengal, Am. J. Clin. Nutr. 4(2) (1956) 169–175.
  7. N.A. King, V.J. Burley, J.E Blundell, Exercise-induced suppression of appetite: effects on food intake and implications for energy balance, Eur. J. Clin. Nutr. 48 (10) (1994) 715–724.
  8. J.E. Blundell, P. Caudwell, C. Gibbons, M. Hopkins, E. Naslund, N.A. King, et al., Body composition and appetite: fat-free mass (but not fat mass or BMI) is positively associated with self-determined meal size and daily energy intake in humans, Br. J. Nutr. 107 (3) (2012) 445–449, https://doi.org/10.1017/S00071...;
  9. J.E. Blundell, P. Caudwell, C. Gibbons, M. Hopkins, E. Naslund, N.A. King, et al., Role of resting metabolic rate and energy expenditure in hunger and appetite control: a new formulation, Dis. Model. Mech. 5 (5)(2012) 608–613, https://doi. org/10.1242/dmm.00983710.1242/dmm.009837.
  10. J. McNeil, G. Lamothe, J.D. Cameron, M.E. Riou, S. Cadieux, J. Lafreniere, et al., Investigating predictors of eating: is resting metabolic rate really the strongest proxy of energy intake? Am. J. Clin. Nutr. 106 (5) (2017) 1206–1212, https://doi. org/10.3945/ajcn.117.153718.
  11. [22]  P. Caudwell, G. Finlayson, C. Gibbons, M. Hopkins, N. King, E. Naslund, et al., Resting metabolic rate is associated with hunger, self-determined meal size, and daily energy intake and may represent a marker for appetite, Am. J. Clin. Nutr. 97 (1) (2013) 7–14, https://doi.org/10.3945/ajcn.111.029975.
  12. M. Hopkins, C. Duarte, K. Beaulieu, G. Finlayson, C. Gibbons, A.M. Johnstone, et al., Activity energy expenditure is an independent predictor of energy intake in hu- mans, Int. J. Obes. (Lond.) (2019), https://doi.org/10.1038/s41366-018-0308-6.
  13. P. Piaggi, M.S. Thearle, J. Krakoff, S.B Votruba, Higher daily energy expenditure and respiratory quotient, rather than fat-free mass, independently determine greater ad libitum overeating, J. Clin. Endocrinol. Metab. 100 (8) (2015) 3011–3020, xtagstartza href="
  14. J.D. Cameron, R.J. Sigal, G.P. Kenny, A.S. Alberga, D. Prud'homme, P. Phillips,et al., Body composition and energy intake – skeletal muscle mass is the strongest predictor of food intake in obese adolescents: the hearty trial, Appl. Physiol. Nutr.Metab. 41 (6) (2016) 611–617, https://doi.org/10.1139/apnm-2015-0479.
  15. A. Grannell, W. Al-Najim, A. Mangan, N. Kapoor, W.P. Martin, J.C. Murphy, et al., Fat free mass is positively associated with hunger and energy intake at extremes of obesity, Appetite 143 (2019) 104444, , https://doi.org/10.1016/j.appet.2019. 104444.
  16. X. Bi, C.G. Forde, A.T. Goh, C.J Henry, Basal metabolic rate and body composition predict habitual food and macronutrient intakes: gender differences, Nutrients 11 (11) (2019), https://doi.org/10.3390/nu11112653.
  17. U. Vainik, K. Konstabel, E. Latt, J. Maestu, P. Purge, J Jurimae, Diet misreporting can be corrected: confirmation of the association between energy intake and fat-free mass in adolescents, Br. J. Nutr. 116 (8) (2016) 1425–1436, https://doi.org/10. 1017/s0007114516003317.
  18. G. Sanchez-Delgado, F. Acosta, B. Martinez-Tellez, G. Finlayson, C. Gibbons,
    I. Labayen, et al., Brown adipose tissue volume and 18F-FDG uptake are not asso- ciated with energy intake in young human adults, Am. J. Clin. Nutr. (2019), https:// doi.org/10.1093/ajcn/nqz300.
  19. L.J. Moran, M. Noakes, P.M. Clifton, G.A. Wittert, C.W. Le Roux, M.A. Ghatei, et al., Postprandial ghrelin, cholecystokinin, peptide YY, and appetite before and after weight loss in overweight women with and without polycystic ovary syndrome, Am. J. Clin. Nutr. 86 (6) (2007) 1603–1610, https://doi.org/10.1093/ajcn/86.5.1603.
  20. M. Hopkins, G. Finlayson, C. Duarte, C. Gibbons, A.M. Johnstone, S. Whybrow,
    et al., Biological and psychological mediators of the relationships between fat mass, fat-free mass and energy intake, Int. J. Obes. 43 (2) (2018) 233–242, https://doi. org/10.1038/s41366-018-0059-4.
  21. A.M. Johnstone, S.D. Murison, J.S. Duncan, K.A. Rance, J.R Speakman, Factors influencing variation in basal metabolic rate include fat-free mass, fat mass, age, and circulating thyroxine but not sex, circulating leptin, or triiodothyronine, Am. J. Clin. Nutr. 82 (5) (2005) 941–948, https://doi.org/10.1093/ajcn/82.5.941.
  22. P. Caudwell, G. Finlayson, C. Gibbons, M. Hopkins, N. King, E. Naslund, et al., Resting metabolic rate is associated with hunger, self-determined meal size, and daily energy intake and may represent a marker for appetite, Am. J. Clin. Nutr.97 (1) (2013) 7–14, https://doi.org/10.3945/ajcn.111.029975.
  23. Y.Y. Lam, E. Ravussin, Variations in energy intake: it is more complicated than we think, Am. J. Clin. Nutr. 106 (5) (2017) 1169–1170, https://doi.org/10.3945/ajcn.117.167742.
  24. G.C Kennedy, The role of depot fat in the hypothalamic control of food intake in the rat, Proc. R. Soc. Lond. Ser. B Biol. Sci. 140 (901) (1953) 578–592.
  25. J.R. Speakman, If body fatness is under physiological regulation, then how come we have an obesity epidemic? Physiology 29 (2) (2014) 88–98, https://doi.org/10.1152/physiol.00053.2013.
  26. J.R. Speakman, R.J. Stubbs, J.G Mercer, Does body mass play a role in the reg- ulation of food intake? Proc. Nutr. Soc. 61 (4) (2002) 473–487, https://doi.org/10.1079/pns2002194.
  27. F.J. Smith, D.W. Driscoll, L.A Campfield, Short term effects of fructose on blood glucose dynamics and meal initiation, Physiol. Behav. 44 (4–5) (1988) 625–631, https://doi.org/10.1016/0031-9384(88)90328-9.
  28. F.J. Smith, L.A Campfield, Meal initiation occurs after experimental induction of transient declines in blood glucose, Am. J. Physiol. 265 (6 Pt 2) (1993) R1423–R14R9, https://doi.org/10.1152/ajpregu.1993.265.6.R1423.
  29. L.A. Campfield, F.J Smith, Functional coupling between transient declines in blood glucose and feeding behavior: temporal relationships, Brain Res. Bull. 17 (3) (1986) 427–433.
  30. M. Kojima, K Kangawa, Ghrelin: structure and function, Physiol. Rev. 85 (2) (2005) 495–522, https://doi.org/10.1152/physre...;
  31. G. Pradhan, S.L. Samson, Y Sun, Ghrelin: much more than a hunger hormone, Curr. Opin. Clin. Nutr. Metab. Care 16 (6) (2013) 619–624, xtagstartza href="
  32. T.D. Müller, R. Nogueiras, M.L. Andermann, Z.B. Andrews, S.D. Anker, J. Argente, et al., Ghrelin, Mol Metab 4 (6) (2015) 437–460, https://doi.org/10.1016/j. molmet.2015.03.005.
  33. D.E. Cummings, J.Q. Purnell, R.S. Frayo, K. Schmidova, B.E. Wisse, D.S Weigle, A preprandial rise in plasma ghrelin levels suggests a role in meal initiation in hu- mans. Diabetes 50 (8) (2001) 1714–1719.
  34. M.W. Schwartz, S.C. Woods, D. Porte Jr., R.J. Seeley, D.G Baskin, Central nervous system control of food intake, Nature 404 (6778) (2000) 661–671, https://doi.org/ 10.1038/35007534.
  35. [79]  G.J. Morton, D.E. Cummings, D.G. Baskin, G.S. Barsh, M.W Schwartz, Central nervous system control of food intake and body weight, Nature 443 (7109) (2006) 289 295.
  36. A. Oswal, G.S.H Yeo, The leptin melanocortin pathway and the control of body weight: lessons from human and murine genetics, Obes. Rev. Offic. J. Int. Assoc. Study Obes.8 (4) (2007) 293–306, https://doi.org/10.1111/j.1467-789X.2007. 00378.x.
  37.  M. Franco, P. Orduñez, B. Caballero, J.A. Tapia Granados, M. Lazo, J.L. Bernal, et al., Impact of energy intake, physical activity, and population-wide weight loss on cardiovascular disease and diabetes mortality in Cuba, 1980–2005, Am. J. Epidemiol. 166 (12) (2007) 1374–1380, https://doi.org/10.1093/aje/kwm226.

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