The Frontiers in Neuroscience journal series is the 1st most cited in Neurosciences

General Commentary ARTICLE

Front. Neuroenergetics, 13 January 2012 | https://doi.org/10.3389/fnene.2011.00011

Does sugar addiction really cause obesity?

  • Medical Clinic 1, University of Lübeck, Lübeck, Germany

A commentary on

Carbohydrate-biased control of energy metabolism: the darker side of the selfish brain
by Zilberter, T. (2011). Front. Neuroenergetics 3:8. doi: 10.3389/fnene.2011.00008

Obesity has become the major health problem in many industrialized countries. But why do so many people – who are facing an abundant food offer – stay slim? All organs in the human organism like the heart, liver, kidney lose 40% of their weight during inanition, except the brain, which loses 1% or less (Krieger, 1921). According to the Selfish Brain theory, the brain uses its stress system, i.e., the sympathetic nervous system (SNS) and the hypothalamus–pituitary–adrenal (HPA) system, to actively demand energy from the body (Peters et al., 2011b). In this way, the brain can satisfy its high energy needs, while the rest of the body is only sparsely supplied. The function of the stress system to actively procure the brain with energy is called “brain-pull” function. It has been shown analytically that in the cerebral supply chain a competent brain-pull function protects against body mass gain, even if there is an abundant food offer available (Peters and Langemann, 2009). And why do other people become obese? If the brain-pull function is incompetent, then energy accumulates in the cerebral supply chain: accumulation of energy in the body stores leads to obesity, accumulation of energy (glucose) within the blood vessels culminates in type 2 diabetes (Peters and Langemann, 2009). Thus, the Selfish Brain theory states that people with incompetent brain-pull have to eat more in order to cover the energetic need of their brain, although their body stores are already overfull.

Tanya Zilberter refers to the Selfish Brain theory in her article entitled “carbohydrate-biased control of energy metabolism” (Zilberter, 2011). At the same time, she refers to an apparently related idea proposed by the psychiatrist DuPont (1997), who has used the term “selfish brain” in the context of addiction. Zilberter discusses in her opinion paper the role of carbohydrate addiction as a potential cause of obesity and calls this aspect “darker side of the selfish brain.” She considers addiction as being “highly non-homeostatic” and concludes that “energy intake beyond rigid homeostatic regulation relies on behavior with hedonic rewarding and addictive nuances more characteristic for carbohydrates than for fat.”

Here I would first like to pose the question whether carbohydrate addiction really affects the organism in a non-homeostatic way. Second, I would like to question whether carbohydrate addiction does result in obesity at all. Carbohydrate (sugar) addiction, including tolerance and withdrawal, has been demonstrated in rodents but not in humans (Garber and Lustig, 2011). Bartley G. Hoebel and his team have carried out ground-breaking animal experiments on this theme (Avena et al., 2008). The researchers have induced sugar addiction in rats by exposing them to a 20-days-experimental paradigm, the so-called “daily intermittent sugar and chow” regimen. In fact, the animals fed in this way enhanced their sugar intake. However, these rats regulated their caloric intake by decreasing their chow intake to compensate for the extra calories obtained from sugar, which results in a normal body weight (Colantuoni et al., 2002; Avena and Hoebel, 2003). These experiments clearly demonstrate that homeostatic control is maintained in the animals, which displayed signs of sugar addiction. Thus, there is no experimental evidence that sugar addiction affects metabolism in a non-homeostatic way, nor that sugar addiction is a cause of obesity.

How did “sugar addiction” develop in the experiments, which used the “daily intermittent sugar and chow” paradigm? Animals were food-deprived for 12 h, and food was offered only 4 h after onset of dark, which is the usual time of their first meal (Colantuoni et al., 2002; Avena and Hoebel, 2003). In principle, food deprivation constitutes a stressor, which threatens brain and body energy supply. The stressful effects of caloric restriction become evident to its full extent when the restriction lasts longer; then the brain has to strongly activate the SNS and the HPA-system in order to safeguard brain energy content and mass. In fact, long term caloric restriction in rats leads to a dose-dependent increase in serum corticosterone (Levay et al., 2010), and the animal’s brain mass is conserved, while its body mass decreases (Greenberg and Boozer, 2000). Such brain-mass-preserving effects have also been observed in humans who were on weight reduction diet (Peters et al., 2011a). If now, in the “daily intermittent sugar and chow” paradigm, energy is offered to the rats with a 4-h delay, the prevailing cerebral energy crises can be most quickly resolved by the ingestion of sugar. The unexpected sudden resolution of the difficulties in cerebral energy procurement by intake of sugar prompts a striatal dopamine release as a rewarding signal. The characteristic of the rewarding system is that dopamine release is triggered by unpredicted successes (Schultz, 2007). Dopamine release in the nucleus accumbens helps to acquire and consolidate a behavioral strategy (Kelley, 2004), which safeguards brain energy homeostasis and allows to shut off the stress response; the strategy includes the choice and immediate intake of sugar. In this way, the “daily intermittent sugar and chow” paradigm favors acquisition and consolidation of feeding strategies, which are very effective in maintaining cerebral energy homeostasis in times of food insecurity.

In conclusion, I don’t see any evidence supporting the view that carbohydrate addiction really causes obesity. As mentioned above, the Selfish Brain theory states that the underlying cause of obesity is a brain-pull incompetence. There are many known causes for such an incompetence (i.e., reduced responsiveness) of the brain-pull system, e.g., the habituation to chronic psychosocial stress (Peters and Langemann, 2009; Peters et al., 2011b). The findings on “sugar addiction” in animals should not be linked to human obesity in an overhasty manner, since such ideas might be taken by others to offend those people who have gained weight. In this respect, scientists and clinicians should be particularly cautious, because humans with high body weight do already suffer from severe weight discrimination (Puhl and Heuer, 2009). These humans are known to exert even more rigid cognitive control over their eating behavior than slim subjects do, and these data contradict the notion that a lack of cognitive control causes weight gain (Timko and Perone, 2005; de Lauzon-Guillain et al., 2006; Snoek et al., 2008; Gallant et al., 2010). But even despite such scientific evidence people with high body weight are still accused of being week-willed and hedonistic – only striving at the satisfaction of their lust. The recent progresses in the field of brain energy metabolism, showing that the people who have gained weight just strive at covering their cerebral energy needs (Peters et al., 2011b), can be helpful to relieve them from the burden of weight discrimination.

References

Avena, N. M., and Hoebel, B. G. (2003). A diet promoting sugar dependency causes behavioral cross-sensitization to a low dose of amphetamine. Neuroscience 122, 17–20.

Pubmed Abstract | Pubmed Full Text | CrossRef Full Text

Avena, N. M., Rada, P., and Hoebel, B. G. (2008). Evidence for sugar addiction: behavioral and neurochemical effects of intermittent, excessive sugar intake. Neurosci. Biobehav. Rev. 32, 20–39.

Pubmed Abstract | Pubmed Full Text | CrossRef Full Text

Colantuoni, C., Rada, P., McCarthy, J., Patten, C., Avena, N. M., Chadeayne, A., and Hoebel, B. G. (2002). Evidence that intermittent, excessive sugar intake causes endogenous opioid dependence. Obes. Res. 10, 478–488.

Pubmed Abstract | Pubmed Full Text | CrossRef Full Text

de Lauzon-Guillain, B., Basdevant, A., Romon, M., Karlsson, J., Borys, J. M., and Charles, M. A. (2006). Is restrained eating a risk factor for weight gain in a general population? Am. J. Clin. Nutr. 83, 132–138.

Pubmed Abstract | Pubmed Full Text

DuPont, R. L. (1997). The Selfish Brain: Learning From Addiction. Center City, MN: Hazelden.

Gallant, A. R., Tremblay, A., Perusse, L., Bouchard, C., Despres, J. P., and Drapeau, V. (2010). The Three-Factor Eating Questionnaire and BMI in adolescents: results from the Quebec family study. Br. J. Nutr. 104, 1074–1079.

Pubmed Abstract | Pubmed Full Text | CrossRef Full Text

Garber, A. K., and Lustig, R. H. (2011). Is fast food addictive? Curr. Drug Abuse Rev. 4, 146–162.

Pubmed Abstract | Pubmed Full Text

Greenberg, J. A., and Boozer, C. N. (2000). Metabolic mass, metabolic rate, caloric restriction, and aging in male Fischer 344 rats. Mech. Ageing Dev. 113, 37–48.

Pubmed Abstract | Pubmed Full Text | CrossRef Full Text

Kelley, A. E. (2004). Memory and addiction: shared neural circuitry and molecular mechanisms. Neuron 44, 161–179.

Pubmed Abstract | Pubmed Full Text | CrossRef Full Text

Krieger, M. (1921). Über die Atrophie der menschlichen Organe bei Inanition [On the Atrophy of Human Organs in Inanition]. Z. Angew. Anat. Konstitutionsl. 7, 87–134.

Levay, E. A., Tammer, A. H., Penman, J., Kent, S., and Paolini, A. G. (2010). Calorie restriction at increasing levels leads to augmented concentrations of corticosterone and decreasing concentrations of testosterone in rats. Nutr. Res. 30, 366–373.

Pubmed Abstract | Pubmed Full Text | CrossRef Full Text

Peters, A., Bosy-Westphal, A., Kubera, B., Langemann, D., Goele, K., Later, W., Heller, M., Hubold, C., and Müller, M. J. (2011a). Why doesn’t the brain lose weight, when obese people diet? Obes. Facts 4, 151–157.

CrossRef Full Text

Peters, A., Kubera, B., Hubold, C., and Langemann, D. (2011b). The selfish brain: stress and eating behavior. Front. Neurosci. 5:74. doi: 10.3389/fnins.2011.00074

CrossRef Full Text

Peters, A., and Langemann, D. (2009). Build-ups in the supply chain of the brain: on the neuroenergetic cause of obesity and type 2 diabetes mellitus. Front. Neuroenergetics 1:2. doi: 10.3389/neuro.14.002.2009

Pubmed Abstract | Pubmed Full Text | CrossRef Full Text

Puhl, R. M., and Heuer, C. A. (2009). The stigma of obesity: a review and update. Obesity (Silver Spring) 17, 941–964.

Pubmed Abstract | Pubmed Full Text | CrossRef Full Text

Schultz, W. (2007). Behavioral dopamine signals. Trends Neurosci. 30, 203–210.

Pubmed Abstract | Pubmed Full Text | CrossRef Full Text

Snoek, H. M., Van, S. T., Janssens, J. M., and Engels, R. C. (2008). Restrained eating and BMI: a longitudinal study among adolescents. Health Psychol. 27, 753–759.

Pubmed Abstract | Pubmed Full Text | CrossRef Full Text

Timko, C. A., and Perone, J. (2005). Rigid and flexible control of eating behavior in a college population. Eat. Behav. 6, 119–125.

Pubmed Abstract | Pubmed Full Text | CrossRef Full Text

Zilberter, T. (2011). Carbohydrate-biased control of energy metabolism: the darker side of the selfish brain. Front. Neuroenergetics 3:8. doi: 10.3389/fnene.2011.00008

Pubmed Abstract | Pubmed Full Text | CrossRef Full Text

Citation: Peters A (2012) Does sugar addiction really cause obesity? Front. Neuroenerg. 3:11. doi: 10.3389/fnene.2011.00011

Received: 22 December 2011; Accepted: 31 December 2011;
Published online: 13 January 2012.

Copyright: © 2012 Peters. This is an open-access article distributed under the terms of the Creative Commons Attribution Non Commercial License, which permits non-commercial use, distribution, and reproduction in other forums, provided the original authors and source are credited.

*Correspondence: achim.peters@uksh.de