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There are a variety of reasons why people chew gums; to freshen their breath, to clean their mouth and even to reduce food cravings, theoretically helping them to avoid eating unhealthy foods. However, while some research has shown that chewing gum can indeed decrease the appetite and the motivation to eat,  it has also highlighted the fact that gum chewers' meals can actually end up being less nutritious than those chosen by non-gum-chewers. One study showed, for example, that people who chewed gum were less likely to eat fruit and instead were more motivated to eat junk food. This is likely due to a minty flavor in the gum making fruits and vegetables taste sour or bitter. Regardless of the reason for gum chewing, it can have numerous ill effects on health. This is especially true for people with pre-existing jaw conditions like the painful chronic condition temporomandibular joint disorder (TMJ or TMD). However, even in healthy people, excessive gum chewing can aggravate the cartilage and surrounding joints in the mouth through extra wear and tear. The strain placed on the jaw and surrounding muscles can also increase the incidence of chronic headaches. Chewing gum also causes you to swallow excess air, which can contribute to abdominal pain and bloating seen with irritable bowel syndrome (IBS). Furthermore, chewing gum sends physical signals to the body indicating that food is about to be ingested, resulting in increased production of stomach acid in preparation. Excess stomach acid can have a wide range of negative effects on the digestive system, including ulceration. Sugar free chewing gums often contain artificial sweeteners, such as aspartame or sucralose. Aspartame has been linked to numerous deleterious effects on health, including headaches, insomnia and seizures, as well as changes in metabolism and weight gain. Sucralose consumption can also have numerous ill effects. Animal studies showed that 12 weeks sucralose administration reduced beneficial gut bacteria, increased fecal pH, and altered the expression of enzymes involved in drug metabolism. So next time you chew gum, remember that you may be doing more to your body than just freshening your breath. Gum chewing has been linked to effects on metabolism and appetite, as well as potentially causing harm to the jaw and digestive system. Chewing gum should therefore ideally be kept to a minimum where possible.  Park, E, et al. (2016) Short-term effects of chewing gum on satiety and afternoon snack intake in healthy weight and obese women. Physiol Behav. 159. 64-71.  Hetherington, MM & Boyland, E. (2007) Short-term effects of chewing gum on snack intake and appetite. Appetite. 48(3). 397-401.  Swoboda, C & Temple, JL. (2013) Acute and chronic effects of gum chewing on food reinforcement and energy intake. Eating Behaviours. 14(2). 149-56.  Haggman-Henrikson, B, et al. (2004) Endurance during chewing in whiplash-associated disorders and TMD. J Dent Res. 82(12). 946-50  Blasberg, B & Greenberg, MS. (2003) Temporomandibular disorders In Burket’s Oral Medicine. PMPH, USA  Watemberg, N, et al. (2014) The influence of excessive chewing gum use on headache frequency and severity among adolescents. Pediatr Neurol. 50(1). 69-72.  Silva, AC, et al. (2015) Effect of gum chewing on air swallowing, saliva swallowing and belching. Arg Gastroenterol. 52(3). 190-4.  Friedman, G. (1991) Diet and the irritable bowel syndrome. Gastroenterol Clin North Am. 20(2). 313-24.  Helman, CA. (1988( Chewing gum is as effective as food in stimulating cephalic phase gastric secretion. Am J Gastroenterol. 83(6). 640-2/  Hunt, RH, et al. The stomach in health and disease. Gut. 64(10). 1650-1668.  Humphries, P, et al. (2008) Direct and indirect cellular effects of aspartame on the brain. Eur J Clin Nutr. 62. 451-62.  Feijo Fde, M, et al. (2013) .Saccharin and aspartame, compared with sucrose, induce greater weight gain in adult Wistar rats, at similar total caloric intake levels. Appetite. 60(1). 203-7.  Abou-Donia, MB, et al. (2008) Splenda alters gut microflora and increases intestinal p-glycoprotein and cytochrome p-450 in male rats. J Toxicol Environ Health. 71(21). 1415-29.
Margarita posted a topic in FoodLogic would suggest that consuming fewer calories should result in weight loss, or at the very least, prevent weight gain. However, in the case of artificial sweeteners, which are lower in calories than sugar, there is a paradox in that it has been shown that they can actually cause weight gain. Therefore, diet drinks are potentially far from the ‘healthier’ calorie-free alternative to regular drinks that they claim to be. As the artificial sweeteners present in diet drinks are now thought to contribute to the development of obesity, they could in fact actually be quite unhealthy. Artificial sweeteners such as sucralose and aspartame have zero calories yet are intensely ‘sweet’ tasting, but the brain is not as easily fooled as the tongue. Artificial sweeteners provide less actual ‘sweetness’ satisfaction, and furthermore reduce the satisfaction obtained when ‘real’ sugar is consumed. This can actually lead to increased carbohydrate cravings, boosting the inclination to overindulge.  The first hints at the potential risks of artificial sweeteners arose over two decades ago when studies began revealing that they can stimulate the appetite, with further investigations linking them to increased carbohydrate cravings, the stimulation of fat storage and weight gain. One recent study that followed 474 diet soda drinkers for nearly 10 years, found that they had a staggering 400% greater increase in waist size during the 10 year study period than those who did not drink diet sodas. This increased waist size is not just an aesthetic issue, it is a powerful indicator of the accumulation of visceral fat. This is a dangerous type of fat that gathers around the internal organs, and is strongly linked with type 2 diabetes and heart disease.  In fact waist size is now considered a more powerful predictor of cardiovascular risks than body mass index (BMI). However increased body weight is not the only controversial potential side effect of diet drinks. Early studies showed that some artificial sweeteners caused bladder cancer in laboratory animals,  although further studies failed to provide clear evidence of an association with cancer in humans, leaving the results inconclusive. Reports also suggest an association between the consumption of aspartame, a widely used artificial sweetener, and neurological and behavioural reactions. Aspartame has been shown to have the potential to induce serious adverse reactions, including seizures. So if you’re trying to lose weight, so-called ‘diet’ drinks may not be the healthy alternative that they claim to be. They have the potential for major metabolic, cardiovascular and neurological side effects and can actually contribute to weight gain. That being said, sugary drinks are also potentially damaging to health, so care should also be taken with their consumption. Why not opt for safe and simple water, the benefits of which are well known.  Pepino, MY. (2015) Metabolic effects of non-nutritive sweeteners. Physiol Behav. 152(Pt B). 450-5.  Rudenga, KJ, Small. DM. (2012) Amygdala response to sucrose consumption is inversely related to artificial sweetener use. Appetite. 58(2). 504-7.  Yang, Q. (2010) Gain weight by “going diet?” Artificial sweeteners and the neurobiology of sugar cravings. Yale J Biol Med. 83(2). 101-8.  Rogers, PJ, Blundell, JE. (1989) Separating the actions of sweetness and calories: Effects of saccharin and carbohydrates on hunger and food intake in human subjects. Physiol Behav. 45(6). 1093-9.  Maersk, M, Belza, A, Stødkilde-Jørgensen, H, Ringgaard, S, Chabanova, E, Thomsen, H, Pedersen, SB, Astrup, A, Richelsen, B. (2012) Sucrose-sweetened beverages increase fat storage in the liver, muscle, and visceral fatdepot: a 6-mo randomized intervention study. Am J Clin Nutr. 95(2). 283-9.  Fowler, RP, Williams, K, Hazuda, HP. (2015) Diet soda intake is associated with long-term increases in waist circumference in a biethnic cohort of older adults: the San Antonio Longitudinal Study of Aging. J Am Geriatr Soc. 63(4). 708-15  Abraham, TM, Pedley, A, Massaro, JM, Hoffmann, U, Fox, CS. (2015) Association between visceral and subcutaneous adipose depots and incident cardiovascular disease risk factors. Circulation. 132(17). 1639-47.  Han, TS, Lean, ME. (2016) A clinical perspective of obesity, metabolic syndrome and cardiovascular disease. JRSM Cardiovasc Dis. [epub ahead of print] doi: 10.1177/2048004016633371.  Bastien, M, Poirier, P, Lemieux, I, Després, JP. (2014) Overview of epidemiology and contribution of obesity to cardiovascular disease. Prog Cardiovasc Dis. 56(4). 369-81.  Takayama, S, Sieber, SM, Adamson, RH, Thorgeirsson, UP, Dalgard, DW, Arnold, LL, Cano, M, Eklund, S, Cohen, SM. (1998) Long-term feeding of sodium saccharin to nonhuman primates: implications for urinary tract cancer. J Natl Cancer Inst. 90(1). 19-25.  Kessler, II, Clark, P. (1978) Saccharin, cyclamate and human bladder cancer. No evidence of an association. JAMA. 240(4). 349-55.  Lindseth, GN, Coolahan, SE, Petros,TV, Lindseth, PD. (2014) Neurobehavioural effects of aspartame consumption. Res Nurs Health. 37(3). 185-93.  Maher, TJ, Wurtman, RJ. (1987) Possible neurologic effects of aspartame, a widely used food additive. Environ Health Perspect. 75. 53-7.