Sweet And Large

sweetnersA corned beef special with extra Russian dressing, a side of cole slaw, and a hunk of New York cheese cake for dessert, chased with a Diet Coke. This was pretty common lunchtime fare for a raft of patrons at a local eatery. Were they looking to cut calories? Or was diet soda merely the rage? If these folks were trying to fight the Battle of the Bulge, they chose the losing faction. If marketing diet soft drinks, they joined the pack.

Not too long ago scientists re-examined the effects of artificial sweeteners on human physiology, prompted, it seems, by the obesity epidemic that is sweeping the country and a considerable part of the Western World. It is presumed that eliminating the cause will also eliminate the effect. The cause in this case has multiple personalities, starting with saccharin, the oldest fake sugar, discovered at Johns Hopkins in the late 1870’s…from coal tar. Sounds yummy, right? Yep, a little waterproofing/shampoo in your coffee gets the day off to a running start, and it’ll even treat dandruff and kill lice. In its infancy, saccharin was featured on drug store shelves as a sugar replacement for people with diabetes. It was put into soda in the 1940’s for those who wanted to limit sugar intake, which was ironic because sugar was limited during World War II anyway. Saccharin is 300 times sweeter than table sugar and has a bitter aftertaste. Cyclamate came out in the 30’s, and was blended with saccharin to improve the flavor. Both were GRAS—generally recognized as safe—at first, in the late 50’s. In the late 60’s, however, cyclamate was abandoned by the U.S. as a carcinogen, and saccharin was viewed with suspicion. Other countries allow cyclamates to this day. Saccharin had received a warning label, but that was removed in 2000 by the Sweetness Act. How adorable! In 2010, the EPA took saccharin off its hazardous chemical list. Did you know this stuff is made from toluene, which has limited carcinogenic potential but still is paint thinner?

Aspartame was stumbled upon when Big Pharma was looking to make a new ulcer drug in the mid 1960’s. A combination of the amino acids phenylalanine and aspartic acid linked to a methanol backbone, aspartame is supposed to be avoided by those with phenylketonuria, a rare inherited metabolic disorder that fails to process phenylalanine, leading to mental retardation and other serious problems. Popular reports cite aspartame as causative of seizures and mood changes, an allegation that is still hotly debated (Magnuson, 2007) (Pediatrics, 1997). Its sweetness parallels that of saccharin.

Neotame, a product of Monsanto’s NutraSweet, is 7,000 times sweeter than sugar. That was approved in 2002. It’s the sweetest child on the block. Acesulfame potassium (K) hit the streets in dry foods in the 80’s and as a general sweetener in ’03. But the hot one these days is sucralose–Splenda®. It’s the most popular artificial sweetener, used mostly in soft drinks, but also in some baby foods (Why?).

What’s this got to do with obesity? For starters, the brain doesn’t appreciate being fooled. As soon as it gets the message that something sweet is eaten it initiates the secretion of insulin by the pancreas to start metabolizing glucose. When there is no nutritive entity to provide glucose, the brain makes you hungry enough to get some. You then eat.

Dr. Yanina Pepino and her team of researchers at Washington University School of Medicine found that sucralose is not an inert ingredient, but one that has a definite effect on blood sugar peaks. When subjects drank a sucralose beverage prior to drinking a glucose beverage, their sugar levels rose 20 percent higher than when they drank plain water before the glucose drink. The analysts related this to enhanced insulin and glucose responses caused by the artificial sweetener (Pepino, 2013), possibly leading to insulin resistance. True sweet taste cues serve to regulate energy balance, while non-nutritive sweeteners may promote increased food intake and consequent weight gain (Swithers, 2010).

Sucralose has chlorine groups replacing hydroxide groups in a glucose molecule, making it an organochloride that is related to some pesticides and plastics. It has the capability of lowering intestinal pH, making it acidic and hostile to beneficent colonic bacteria. Even after stopping sucralose, the changed pH may persist (Abou-Donia, 2008). Isn’t chlorine used in swimming pool and bathroom cleaners to kill bacteria?

Before sucralose hit the market, similar investigations focused on then-current artificial sweeteners, aspartame paramount among them. Where a 1986 project found ambiguity concerning appetite signals (Blundell, 1986), later study found that aspartame-sweetened carbonated water increased appetite in the short term (Black, 1993), implying a subsequent intake of excess energy. While the cheesecake crowd was enjoying its low-cal sodas, scientists were already looking at weight management in a highly homogeneous group of middle-aged women, learning that heavier gals were more likely to use non-nutritive sweeteners than their normal weight counterparts, but that, in the long term, artificial sweeteners were not able to prevent weight gain or help weight loss (Stellman, 1986). As with much of what we ingest, dose makes the difference. Those imbibing up to three artificially-sweetened drinks a day appear more likely to risk overweight and obesity than those who consume none (Fowler, 2008). For those who exercise, the difference is insignificant.

So, now, what’s the worry, insulin resistance or weight gain? Being a little overweight doesn’t automatically translate to type 2 diabetes, but it is one of the risk factors. Daily consumption of diet soda was associated with a 36% greater relative risk of metabolic syndrome and a 67% greater risk of incident type 2 diabetes, compared to non-consumption, in a 2009 report from the U of TX (Nettleton, 2009). Whatever the concern might be, fake sugars stir the soup and promote insulin release (Malaisse, 1998). One of the mechanisms involves faking out the brain, not only with renegade appetite signals, but also with altered reward processing of the sweet sensation that rightfully belongs outside the sphere of artificial sweeteners (Green, 2012). As with all heath topics, the debate goes on because some people remain completely unaffected. And we thought that only Superman was bulletproof. The bottom line is that artificial sweeteners do not activate the food reward pathways in the same fashion as natural ones (Smeets, 2005).

References

[No authors listed]
“Inactive” ingredients in pharmaceutical products: update (subject review). American Academy of Pediatrics Committee on Drugs.
Pediatrics. 1997 Feb;99(2):268-78.

Abou-Donia MB, El-Masry EM, Abdel-Rahman AA, McLendon RE, Schiffman SS.
Splenda alters gut microflora and increases intestinal p-glycoprotein and cytochrome p-450 in male rats.
J Toxicol Environ Health A. 2008;71(21):1415-29.

Stephen D. Anton, Corby K. Martin, Hongmei Han, Sandra Coulon, William T. Cefalu, Paula Geiselman, Donald A. Williamson
Effects of stevia, aspartame, and sucrose on food intake, satiety, and postprandial glucose and insulin levels
Appetite 55(1); Aug 2010: 37-43

Black RM, Leiter LA, Anderson GH.
Consuming aspartame with and without taste: differential effects on appetite and food intake of young adult males.
Physiol Behav. 1993 Mar;53(3):459-66.

Blundell JE, Hill AJ.
Paradoxical effects of an intense sweetener (aspartame) on appetite.
Lancet. 1986 May 10;1(8489):1092-3.

Brown RJ, de Banate MA, Rother KI.
Artificial sweeteners: a systematic review of metabolic effects in youth.
Int J Pediatr Obes. 2010 Aug;5(4):305-12.

Brusick D, Borzelleca JF, Gallo M, Williams G, Kille J, Wallace Hayes A, Xavier Pi-Sunyer F, Williams C, Burks W.
Expert panel report on a study of Splenda in male rats.
Regul Toxicol Pharmacol. 2009 Oct;55(1):6-12.

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 Aug;16(8):1894-900.

Green E, Murphy C.
Altered processing of sweet taste in the brain of diet soda drinkers.
Physiol Behav. 2012 Nov 5;107(4):560-7.

Magnuson BA, Burdock GA, Doull J, Kroes RM, Marsh GM, Pariza MW, Spencer PS, Waddell WJ, Walker R, Williams GM.
Aspartame: a safety evaluation based on current use levels, regulations, and toxicological and epidemiological studies.
Crit Rev Toxicol. 2007;37(8):629-727.

Malaisse WJ, Vanonderbergen A, Louchami K, Jijakli H, Malaisse-Lagae F.
Effects of artificial sweeteners on insulin release and cationic fluxes in rat pancreatic islets.
Cell Signal. 1998 Nov;10(10):727-33.

Nettleton JA, Lutsey PL, Wang Y, Lima JA, Michos ED, Jacobs DR Jr.
Diet soda intake and risk of incident metabolic syndrome and type 2 diabetes in the Multi-Ethnic Study of Atherosclerosis (MESA).
Diabetes Care. 2009 Apr;32(4):688-94

Pepino MY, Tiemann CD, Patterson BW, Wice BM, Klein S.
Sucralose Affects Glycemic and Hormonal Responses to an Oral Glucose Load.
Diabetes Care. 2013 Apr 30.

Rogers PJ, Carlyle JA, Hill AJ, Blundell JE.
Uncoupling sweet taste and calories: comparison of the effects of glucose and three intense sweeteners on hunger and food intake.
Physiol Behav. 1988;43(5):547-52.

Rudenga KJ, Small DM.
Amygdala response to sucrose consumption is inversely related to artificial sweetener use.
Appetite. 2012 Apr;58(2):504-7.

Smeets PA, de Graaf C, Stafleu A, van Osch MJ, van der Grond J.
Functional magnetic resonance imaging of human hypothalamic responses to sweet taste and calories.
Am J Clin Nutr. 2005 Nov;82(5):1011-6.

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

Swithers SE, Martin AA, Davidson TL.
High-intensity sweeteners and energy balance.
Physiol Behav. 2010 Apr 26;100(1):55-62. Epub 2010 Jan 6.

Qing Yang
Gain weight by “going diet?” Artificial sweeteners and the neurobiology of sugar cravings:Neuroscience 2010
Yale J Biol Med. 2010 June; 83(2): 101–108.

*These statements have not been evaluated by the FDA.
These products are not intended to treat, diagnose, cure, or prevent any disease.

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