I have been over the concept of “calories in, calories out” numerous times. If caloric intake exceeds caloric expenditure, then you will gain mass, and if caloric intake is less than caloric expenditure, you will lose mass… it’s thermodynamics. So diet soda (with 0 calories) should add nothing to this equation…right?
Well, a 2016 study actually shows otherwise (1). This study aimed to investigate the effect of replacing diet beverages with water or continuing to drink diet beverages in patients with type 2 diabetes during a 24-week weight loss program. The setup was simple: Researchers recruited 81 overweight and obese women with type 2 diabetes who typically consume diet beverages in their diet. Participants were placed on a hypocaloric diet (aimed at weight loss of 7% to 10% of initial body weight, at a rate of 0.5 to 1 kg/wk over 24 weeks) and randomized into two groups. One group would continue to drink diet beverages (they would consume one beverage after lunch 5x a week), while the other group would replace their diet beverage with water.
Now, one would think that if water and diet soda both have 0 calories, then there should be no significant difference in weight loss between groups (we would expect both groups to lose weight at roughly the same rate). However, that is not what the researchers found. Upon completion of the 24 week intervention, both groups lost weight, but the water group (-14.1 +/- 5.3 lbs) lost significantly more weight than the diet beverage group (-11.6 +/-3.5 lbs). In addition, the water group saw significantly better improvements in BMI, fasting plasma glucose, fasting insulin, insulin resistance, and 2 hr postprandial glucose.
So that makes no sense at all…if both water and diet soda are zero calories…did we just break the 1st Law of Thermodynamics? Of course not! This was a free-living study. Participants were given the diet and physical activity recommendations, told to stick to them as best as possible, sent on their way, and would return back for scheduled visits during the 24-weeks.
I agree with the authors in the fact that they claim that the artificial sweeteners found in diet beverages may raise the hedonic desire for sweetened and more energy-dense foods (2–4). Thus, those drinking the diet beverages would theoretically have more sugar cravings, which could only be staved off for so long, thereby leading to more food consumption over time and less weight loss than the water only group. So no, we did not break physics…sorry.
The human body relies on both the homeostatic hunger pathway (KEEP ME ALIVE!) and the hedonistic pathway (MAKE ME HAPPY!). In this case, I will focus on the hedonistic pathway, which is is driven by environmental signals based on reward and desire to consume palatable food for pleasure rather than for metabolic maintenance. Thereby this pathway relies on nutrient availability, palatability, variety, and preferences (5–8).
The visual, gustatory, and olfactory influence of food plays a powerful role in appetite regulation. The sensation of palatable foods utilizes a mesolimbic dopamine pathway. This pathway stretches from the ventral tegmental area to the nucleus accumbens (9,10). Upon sensing palatable food, an influx of dopaminergic transmission to the nucleus accumbens occurs through either direct activation of dopaminergic neurons or indirect inhibition of interneurons containing gamma-aminobutyric acid (GABA) within the ventral tegmental area. The influx of dopamine to the nucleus accumbens modulates behavior to obtain rewards such as enhanced arousal, psychomotor activation, and conditioned learning (11). Whether it is artificial sweeteners, stimulant drugs, or your reaction to going big at the Poker table, they all elicit the same pleasure inducing response which makes you crave more!
So what’s the bottom-line?: I see no problem with drinking diet beverages while trying to adhere to a diet. We have to consider our beverage choices on a continuum:
Everything you consume should have a purpose. Make incremental improvements to your diet. Use this continuum as a guide. Maybe you drink regular soda 7 days a week. Start by subbing out two of those days with diet soda. Progress, and then once you get to all 7 days of diet soda, start adding in sparkling water…rinse and repeat. Water is a powerful tool to improve body composition. Use it wisely.
- Blundell JE, Hill AJ. Paradoxical effects of an intense sweetener (aspartame) on appetite. Lancet. 1986;1:1092–1093
- Nettleton JA, Lutsey PL, Wang Y, Lima JA, Michos ED, Jr Jacobs DR. Diet soda intake and risk of incident metabolic syndrome and type 2 diabetes in the Multi-Ethnic Study of Atherosclerosis (MESA). Diabetes Care. 2009;32(4):688–694
- Rogers PJ, Blundell JE. Separating the actions of sweetness and calories: effects of saccharin and carbohydrates on hunger and food intake in human subjects. Physiol Behav. 1989;45:1093–1099
- Berthoud, H. (2004). Mind versus metabolism in the control of food intake and energy balance. Physiology & Behavior, 81(5), 781–793. doi: 10.1016/j.physbeh.2004.04.034
- Corwin, R., & Hajnal, A. (2005). Too much of a good thing: Neurobiology of non-homeostatic eating and drug abuse. Physiology & Behavior, 86(1–2), 5–8. doi: 10.1016/j.physbeh.2005.06.021\
- Cameron, J., & Doucet, É. (2007). Getting to the bottom of feeding behaviour: who’s on top?. Applied Physiology, Nutrition, And Metabolism, 32(2), 177–189. doi: 10.1139/h06–072
- Leibowitz, S. (2007). Overconsumption of dietary fat and alcohol: Mechanisms involving lipids and hypothalamic peptides. Physiology & Behavior, 91(5), 513–521. doi: 10.1016/j.physbeh.2007.03.018
- Nestler, E. (2001). Molecular basis of long-term plasticity underlying addiction. Nature Reviews Neuroscience, 2(2), 119–128. doi: 10.1038/35053570
- Nestler, E. (2005). Is there a common molecular pathway for addiction?. Nature Neuroscience, 8(11), 1445–1449. doi: 10.1038/nn1578
- de Araujo, I., Oliveira-Maia, A., Sotnikova, T., Gainetdinov, R., Caron, M., Nicolelis, M., & Simon, S. (2008). Food Reward in the Absence of Taste Receptor Signaling. Neuron, 57(6), 930–941. doi: 10.1016/j.neuron.2008.01.032