Gaining Weight Despite Calorie Restriction
This topic comes up time and again on the forums on this website, so here is the explanation with accompanying references on why it doesn't go against any laws of physics to increase in mass when insufficient energy is entering the system.
Yes, weight gain can occur during active calorie restriction.
Every fattist on the planet knows the first law of thermodynamics and they regularly throw it up assuming it debunks the assertion that weight gain could occur in the presence of calorie restriction. I have already addressed the incompleteness of using the first law without the second law when it comes to conservation of energy in the body in the blog post Food Fears One:
“Biologically speaking a calorie is not actually a calorie. [1], [2] Both the first and second laws of thermodynamics are important when identifying how biological systems burn energy. The first law of thermodynamics stipulates that energy is always conserved in a closed system. It means, in the context of eating, that what you take in as energy, you use or store as energy. However, the second law of thermodynamics refers to the quality of the energy that is conserved:
“The quality of matter/energy deteriorates gradually over time…Usable energy is inevitably used for productivity, growth and repair. In the process, usable energy is converted into unusable energy. Thus, usable energy is irretrievably lost in the form of unusable energy.”
“Conservation of energy is maintained when we eat because we export carbon dioxide and water into the greater environment. It is our metabolic pathways, however, that will determine how the energy and matter are distributed among heat, chemical bonds, work and excretion, and dietary composition drives the differentiation of those metabolic pathways.”
The body is an open system, not a closed system. The first and second laws of thermodynamics confirm that a calorie is not a calorie: meaning that metabolic pathways determine the rate at which energy moves from its usable to unusable state. These two laws do not confirm that the body cannot increase in mass in the absence of excess energy coming in from the outside world.
The fact that the body can increase in mass when ostensibly too little energy is being introduced into the body (through dieting) has to do with the balance between catabolism and metabolic suppression.
Catabolism is the destruction of cells throughout your body and this process releases energy into the system when not enough energy is being taken in from the outside environment. You know this as “dieting to lose weight”. But the body uses two processes to survive in the absence of adequate energy: catabolism and metabolic suppression.
There are obvious and observable variations in how calorie restriction impacts individuals both metabolically and in the form of overall reduction of mass. Metabolic changes and efficiencies for maintaining energy balance are not equal from one individual to the next. The efficiency of metabolic suppression appears to be maintained up to six years beyond the point of original calorie restriction. [5] The metabolic suppression also appears to be more aggressive in some than the actual deficit would require. [6] That means restrict a bit and the metabolic response will not only match that deficit, but it will also overcompensate such that excess energy is now available within the system. Some individuals may release that excess into the greater environment (carbon dioxide and water) and others may partition the energy within the system (growth, repair and chemical bonds).
You can therefore gain weight during calorie restriction. This is particularly the case for those with a history of calorie restriction.
“Weight gain during the freshman year averaged 2.1 kg. None of the traditional self-report measures of restraint, disinhibition, or emotional eating were predictive of weight gain. However, both a history of weight loss dieting and weight suppression (discrepancy between highest weight ever and current weight) predicted greater weight gain, and these effects appeared to be largely independent of one another. Individuals who said they were currently dieting to lose weight gained twice as much (5.0 kg) as former dieters (2.5 kg) and three times as much as never dieters (1.6 kg).”
A monozygotic twin study confirms that repetitive intentional weight loss efforts predispose the individual to subsequent further weight gain. [8] A twin study is done to rule in or out genetic predisposition being a contributory factor to the effect being studied. In this case, genetics were ruled out as being a contributory factor. Yet another study on intentional weight loss efforts in preadolescents and adolescents confirmed that frequency of dieting correlated strongly to increased body mass index (BMI) when compared to infrequent or non-dieting controls. [9]
These researchers also noted that binge eating was more common among girls but in both sexes it was associated with dieting— doubling the odds ratio for the girls and not quite doubling it for the boys. [10]
Not surprisingly, fattists will attribute this predilection to gaining weight as a lack of control over binge eating and completely overlook metabolic efficiencies noted in the review from LM Redman et al., that I referenced above.
And as for controlling binge behaviors, Dr. Jane Wardle has made the following assessment of this misguided tactic for maintaining weight:
“…craving for food, preoccupation with eating and loss of control over food intake represent natural psychobiological adaptation to sub-optimal weight and food deprivation. Compulsive eating is therefore best understood in terms of a conflict between a biologically derived drive for food and a culturally derived drive for thinness. Both of these processes have their parallels in the maintenance of dependency disorders. The crucial difference however is that the urge to eat is biologically adaptive, and recovery from compulsive eating depends upon relaxing restraint.”
In the absence of any binges, people experience increases in mass despite a clear deficit in energy intake. Again, I’ll point to the efficiencies of an adaptive metabolism that has been “trained” through repetitive bouts of energy restriction to create energetic surplus.
Furthermore, various environmental pressures additionally impact how efficient the metabolism will be as well as whether the hormone-producing organ that is fat will need to enlarge beyond its inherited set point for health-protective reasons. You will need to read Fat Science in Context as well as Fat Basic Facts One and Two to learn more about how the adipose organ enacts its health-protective functions.
There is no correlation between food intake or activity levels and BMI>30 onset or perseveration. As much as fattists like to believe that binge eating, laziness and lack of control are the reasons for an increase in mass in any individual, the science is not there to support that dogma. To confirm the science behind those assertions, you’ll need to read: Weight Gain Correlates in Literature One and Two.
Beyond the way which your body may have been trained to clamp metabolic function to create surplus energy even when too little food is being consumed, there are three other possible reasons that the fat organ may increase in size and it’s not about the homeodynamic energy system in balance, but rather the role of the fat organ to modulate things in the face of stressors and disease states.
Sleep deficits can be responsible for the increase in size of the adipose organ. Psychosocial stressors have also been linked to adiposity as reflected in this review:
“This systematic, meta-analytic review is the first to confirm that psychosocial stress is positively related to the development of adiposity in prospective studies, although the effects were modest and smaller than assumed in the lay literature. Confidence in the results is increased by the fact that the effect was stronger in studies that were methodologically stronger, controlled for the baseline level of the outcome variable or had longer follow-up”
The correlation between the introduction of artificial light at night and increases in population BMI are well known. Several assessments confirm night-time light’s actual causative role in generating metabolic deviations that result in adipose organ enlargement, as well as disease states, all with no accompanying excess intake of energy. [13],[14],[15],[16],[17]
Finally, there is the possibility that you have a chronic illness, beyond the eating disorder, wherein there may be a need for the fat organ to enlarge in size associated with its immune modulating functions. This is discussed in Weight Gain Correlates in Literature Two.
If you are gaining weight despite conscious efforts to restrict, then stop restricting. If you are gaining weight despite adequate unrestricted refeeding and resting, then allow your metabolism some time to find its way back to a pre-dieting set point.
You live in the modern world with artificial light and inadequate sleep along with whatever cluster of psychosocial stressors surrounds you at present. You might want to cut your fat organ some slack and stop abusing its metabolic-modulating power to manage your modern life.
Manninen, A. H. (2004). Is a calorie really a calorie? Metabolic advantage of low-carbohydrate diets. Journal of the International Society of Sports Nutrition, 1(2), 1-6.
Feinman, R. D., & Fine, E. J. (2004). A calorie is a calorie" violates the second law of thermodynamics. Nutr J, 3(9), 10-1186.
http://www.allaboutscience.org/second-law-of-thermodynamics.htm
Feinman, R. D., & Fine, E. J. (2004). A calorie is a calorie" violates the second law of thermodynamics. Nutr J, 3(9), 10-1186.
Redman, L. M., Heilbronn, L. K., Martin, C. K., De Jonge, L., Williamson, D. A., Delany, J. P., ... & Pennington CALERIE Team. (2009). Metabolic and behavioral compensations in response to caloric restriction: implications for the maintenance of weight loss. PloS one, 4(2), e4377
ibid.
Lowe, M. R., Annunziato, R. A., Markowitz, J. T., Didie, E., Bellace, D. L., Riddell, L., ... & Stice, E. (2006). Multiple types of dieting prospectively predict weight gain during the freshman year of college. Appetite, 47(1), 83-90.
Pietiläinen, K. H., Saarni, S. E., Kaprio, J., & Rissanen, A. (2012). Does dieting make you fat? A twin study. International Journal of Obesity, 36(3), 456-464.
Field, A. E., Austin, S. B., Taylor, C. B., Malspeis, S., Rosner, B., Rockett, H. R., ... & Colditz, G. A. (2003). Relation between dieting and weight change among preadolescents and adolescents. Pediatrics, 112(4), 900-906.
ibid.
Wardle, J. (1987). Compulsive eating and dietary restraint. British Journal of Clinical Psychology, 26(1), 47-55.
Wardle, J., Chida, Y., Gibson, E. L., Whitaker, K. L., & Steptoe, A. (2011). Stress and Adiposity: A Meta‐Analysis of Longitudinal Studies. Obesity, 19(4), 771-778.
Wyse, C. A., Selman, C., Page, M. M., Coogan, A. N., & Hazlerigg, D. G. (2011). Circadian desynchrony and metabolic dysfunction; did light pollution make us fat?. Medical hypotheses, 77(6), 1139-1144.
Stevens, R. G. (2009). Light-at-night, circadian disruption and breast cancer: assessment of existing evidence. International journal of epidemiology, 38(4), 963-970.
Van Drongelen, A., Boot, C. R., Merkus, S. L., Smid, T., & Van Der Beek, A. J. (2011). The effects of shift work on body weight change—a systematic review of longitudinal studies. Scandinavian journal of work, environment & health, 263-275.
Nedeltcheva, A. V., Kilkus, J. M., Imperial, J., Schoeller, D. A., & Penev, P. D. (2010). Insufficient sleep undermines dietary efforts to reduce adiposity. Annals of internal medicine, 153(7), 435-441.
Patel, S. R., & Hu, F. B. (2008). Short sleep duration and weight gain: a systematic review. Obesity, 16(3), 643-653.
