Not So (Artifically) Sweet | The Paleo Diet®
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Not So (Artifically) Sweet

By Casey Thaler, B.A., NASM-CPT, FNS
July 8, 2015
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I have had countless clients try to replace their sugar-laden diets with ones rich with artificial sweeteners. While this may work in the short term, it definitely does not work in the long term.1 2 And, the reasons for this are countless.3,

New research shows sugars specifically activate six neurosecretory cells in the brain, which produce Dh44, a homolog of the mammalian corticotropin-releasing hormone.4,5 Artificial sweeteners do not activate these same cells – possibly leaving the brain in a half-finished reward state – potentially leading to more calories being taken in.6,7

Yang, Qing. “Gain Weight by ‘going Diet?’ Artificial Sweeteners and the Neurobiology of Sugar Cravings: Neuroscience 2010.” The Yale Journal of Biology and Medicine 83.2 (2010): 101–108. Print. Yang, Qing. “Gain Weight by ‘going Diet?’ Artificial Sweeteners and the Neurobiology of Sugar Cravings: Neuroscience 2010.” The Yale Journal of Biology and Medicine 83.2 (2010): 101–108. Print.

Another issue with artificial sweeteners is they are typically much, much sweeter than sugar. Just how much sweeter are these manmade creations? Most artificial sweeteners are 200-400 times sweeter than regular table sugar!8 Many researchers argue this leaves the brain expecting a plethora of calories, and also disrupts the brain’s natural reward mechanisms.9

While followers of the Paleo Diet will certainly know that artificial sweeteners have no place in a healthy lifestyle, many who are trying to change their eating habits rely on artificial sweeteners for brief time periods. Not a great idea. As the scientific literature suggests, artificial sweeteners (because they are sweet) encourage sugar craving and sugar dependence.10

Even stevia, which many will argue is a healthier alternative to most artificial sweeteners, is 100-300 times sweeter than table sugar!11 It is certainly not a good idea to be consuming something that sweet on a regular basis – whether it contains sugar or not. Furthermore, artificial sweeteners are typically packaged in foods or drinks that have a laundry list of other negative substances and artificial ingredients.12

Salient scientific studies clearly show how in repeatedly exposing ourselves to sugar, we help to train our flavor preference. In short – the more sweet we eat, the more we crave and expect it. Many studies have shown lowering fat and/or salt intake, over several weeks, leads to less craving of these elements. This is exactly how you should treat sugar and artificial sweeteners.

Sclafani, Anthony. “Sweet Taste Signaling in the Gut.” Proceedings of the National Academy of Sciences of the United States of America 104.38 (2007): 14887–14888. PMC. Web. 7 July 2015. Sclafani, Anthony. “Sweet Taste Signaling in the Gut.” Proceedings of the National Academy of Sciences of the United States of America 104.38 (2007): 14887–14888. PMC. Web. 7 July 2015.

On a granular level, T1R2 and T1R3 sweet taste receptors are found in taste cells in the mouth and enteroendocrine cells in the gut.13 Stimulation of the T1R2 and T1R3 receptors in the mouth by sugars and artificial sweeteners activates intracellular signaling elements, which trigger peripheral taste nerves and brain gustatory pathways. This is one way in which artificial sweeteners actually have a similar effect to sugar – which is not a good thing.

Moreover, research shows substituting sucrose-sweetened drinks for diet drinks does not reduce total energy intake - and may even result in a higher intake during the following day.14 Artificial sweeteners are not the answer.

Even back in 1986, researchers concluded that the data do not support the hypothesis that long-term artificial sweetener use either helps weight loss or prevents weight gain.15

Fernstrom, John D. et al. “Mechanisms for Sweetness.” The Journal of Nutrition 142.6 (2012): 1134S–1141S. PMC. Web. 7 July 2015. Fernstrom, John D. et al. “Mechanisms for Sweetness.” The Journal of Nutrition 142.6 (2012): 1134S–1141S. PMC. Web. 7 July 2015.

So why are artificial sweeteners still used? Well, quite simply: money and industry.

Artificial sweeteners are beneficial to the food industry for a variety of reasons. One – they are cheap, and can help make poor quality foods taste ‘better’. Two – it makes it seem like they care. They sell you the sugar-laden stuff, and then - if you are ‘health conscious’ - you can buy their artificially sweetened product instead. Either way – they win.

I may be preaching to the converted here on The Paleo Diet, but often times even the most disciplined of us slowly let little ‘cheats’ into our diet – without realizing the long term impacts these seemingly innocuous choices may be having on our bodies and brains. If we have any hope of getting out of the current obesity pandemic we currently find ourselves in, it starts with removing all the sweetness (artificial or not) from our collective diet.16,17,18,19,20,21 Your health (and waistline) will thank you for it!

References

[1] Feijó Fde M, Ballard CR, Foletto KC, et al. Saccharin and aspartame, compared with sucrose, induce greater weight gain in adult Wistar rats, at similar total caloric intake levels. Appetite. 2013;60(1):203-7.

[2] Bellisle F, Drewnowski A. Intense sweeteners, energy intake and the control of body weight. Eur J Clin Nutr. 2007;61(6):691-700.

[3] Suez J, Korem T, Zeevi D, et al. Artificial sweeteners induce glucose intolerance by altering the gut microbiota. Nature. 2014;514(7521):181-6.

[4] Available at: //www.endocrinologyadvisor.com/neuroendocrinology/sugar-artificial-sweeteners-satiety/article/423644/. Accessed July 5, 2015.

[5] Dus M, Lai JS, Gunapala KM, et al. Nutrient Sensor in the Brain Directs the Action of the Brain-Gut Axis in Drosophila. Neuron. 2015;87(1):139-51.

[6] Fowler SP, Williams K, Resendez RG, Hunt KJ, Hazuda HP, Stern MP. Fueling the obesity epidemic? Artificially sweetened beverage use and long-term weight gain. Obesity (Silver Spring). 2008;16(8):1894-900.

[7] Blundell JE, Hill AJ. Paradoxical effects of an intense sweetener (aspartame) on appetite. Lancet. 1986;1(8489):1092-3.

[8] Pandurangan M, Park J, Kim E. Aspartame downregulates 3T3-L1 differentiation. In Vitro Cell Dev Biol Anim. 2014;50(9):851-7.

[9] Fernstrom JD, Munger SD, Sclafani A, De araujo IE, Roberts A, Molinary S. Mechanisms for sweetness. J Nutr. 2012;142(6):1134S-41S.

[10] Yang Q. Gain weight by "going diet?" Artificial sweeteners and the neurobiology of sugar cravings: Neuroscience 2010. Yale J Biol Med. 2010;83(2):101-8.

[11] Goyal SK, Samsher, Goyal RK. Stevia (Stevia rebaudiana) a bio-sweetener: a review. Int J Food Sci Nutr. 2010;61(1):1-10.

[12] Kellett GL, Brot-laroche E, Mace OJ, Leturque A. Sugar absorption in the intestine: the role of GLUT2. Annu Rev Nutr. 2008;28:35-54.

[13] Sclafani A. Sweet taste signaling in the gut. Proc Natl Acad Sci USA. 2007;104(38):14887-8.

[14] Lavin JH, French SJ, Read NW. The effect of sucrose- and aspartame-sweetened drinks on energy intake, hunger and food choice of female, moderately restrained eaters. Int J Obes Relat Metab Disord. 1997;21(1):37-42.

[15] Stellman SD, Garfinkel L. Artificial sweetener use and one-year weight change among women. Prev Med. 1986;15(2):195-202.

[16] Swinburn BA, Sacks G, Hall KD, et al. The global obesity pandemic: shaped by global drivers and local environments. Lancet. 2011;378(9793):804-14.

[17] Soeliman FA, Azadbakht L. Weight loss maintenance: A review on dietary related strategies. J Res Med Sci. 2014;19(3):268-75.

[18] Lustig RH. Fructose: metabolic, hedonic, and societal parallels with ethanol. J Am Diet Assoc. 2010;110(9):1307-21.

[19] Isganaitis E, Lustig RH. Fast food, central nervous system insulin resistance, and obesity. Arterioscler Thromb Vasc Biol. 2005;25(12):2451-62.

[20] Lustig RH, Sen S, Soberman JE, Velasquez-mieyer PA. Obesity, leptin resistance, and the effects of insulin reduction. Int J Obes Relat Metab Disord. 2004;28(10):1344-8.

[21] Lustig RH. The neuroendocrinology of obesity. Endocrinol Metab Clin North Am. 2001;30(3):765-85.

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