What is the metabolic difference between cola light and normal cola?

Diana Artene

This article refers not only to cola light or to a specific brand in particular, but to the difference in metabolic impact between the consumption of cola light and soda drinks containing “sugars”.

To start, let’s define exactly what is used to sweeten light or “sugar-free” soda drinks and what is used to sweeten normal or cola “with sugars”.

“Normal” soda drinks do not contain actual sugar – which is biochemically a disaccharide called sucrose, consisting of glucose + fructose, biochemically bound to each other – but High Fructose Corn Syrup (abbreviated to HFCS) – which is basically a mixture of the same two monosaccharides but unbound to each other and the fructose to glucose proportion in the made-up mixture is quite different from the one in natural sugar.

Light soda contains a lot of chemicals that are mostly inedible, among which aspartame, acesulfame potassium (Ace K) and sucralose (Splenda). However, despite the fact that aspartame is so controversial that it was removed from the market temporarily in some “civilized” countries, it is actually the most commonly used artificial sweetener in the world.

So, when we compare the metabolic impact of normal soda drinks with light soda drinks, we mainly actually compare the metabolic impact of HFCS to aspartame.

Aspartame is an artificial sweetener – also named in European Union countries E951 – used for sweetening “light”, “zero”, “diet” or other “sugar-free” soda drinks.

Although it is sweet, aspartame is not a carbohydrate but a protein.

After consumption, aspartame is broken down in the small intestine – under the action of peptidases produced by the small intestine cells – into methanol, phenylalanine and aspartic acid. Thus, the health risks potentially associated with aspartame frequent intake may be due to:

  • methanol and its metabolites toxicity – with carcinogenic potential
  • increased plasma levels of phenylalanine and aspartic acid – which are potentially harmful for the brain normal function
  • increased norepinephrine and dopamine catecholamine concentrations – with addictive potential

However, aspartame is declared “safe for human consumption” in over 130 countries at doses below 40 mg/ day per kg of body weight.

But since these seemingly informative numbers means nothing to the average human, let’s see an illustrative example:

  • a can of 330 ml of light soda drink contains about 200 mg of aspartame
  • a 70 kg adult can theoretically consume a maximum of 2.800 mg of aspartame per day,
  • that is: about 14 cans of 330 ml light soda drinks – and of course, most people keep their soda drinking way below this level.

However, aspartame is also found in many other drinks, foods, drugs and chewing gums – the total daily aspartame intake being almost impossible to estimate as “safe” or “unsafe”.

We can say that no one drinks 14 cans of soda per day, so it’s safe.

And we can say that we actually don’t know all the aspartame intake from other food and drinks, thus it isn’t safe.

But we just don’t really know.

Despite the legal reinsurance that EFSA (European Food Safety Authority) has given us on December 10, 2013, there are many studies conducted by other scientists demonstrating the following consequences of aspartame intake:

  • weight gain (3)
  • increased risk of diabetes (4)
  • increased risk of multiple myeloma, non-Hodgkin’s lymphoma and leukemia (5,6)
  • increased risk of cardiovascular disease (7)
  • disordered appetite (8)
  • migraines, depression and irritability (9)

On the other hand, HCFS is a kind of artificial fructose, called in the European Union countries and HFCS-55, used mainly for the sweetening of normal soda drinks – which actually can also be called “sugar-free” because they also contain no actual sugar.

Sugar is a disaccharide composed of a molecule of glucose biochemically linked to a molecule of fructose. The disaccharidases secreted by the small intestinal mucosa are required for sugar to be digested into glucose and fructose and further absorbed into the blood.

HFCS is a mixture of individual monosaccharides – the same glucose and fructose, but as they come biochemically separated the body doesn’t have to contribute to their digestion and intestinal absorption in any way. Thus HCFS is extremely absorbable even when the intestinal mucosa is inflamed, unlike sugar that requires the integrity of the mucosa intestinal for digestion and absorption.

After the fast absorption, the glucose from the HFCS mixture generates an insulin secretion spike followed by reactive hypoglycemia, and the contained fructose is converted inside the liver directly into VLDL fat that will be deposited locally.

Thus, as studies after studies continue to show, consumption of HFCS sweetened soda drinks leads to:

  • weight gain (10)
  • hepatic steatosis (11)
  • increased risk of kidney disease (12)
  • increased risk of cardiovascular disease (13)
  • decreased perception of satiety (14)
  • decreased perception of pleasure (15)
  • increased hunger and appetite (16)

In addition, if we take into account that all the enzymes and hormones involved in digestion are secreted long before these beverages actually reach the digestive system, it is clear that both of these aspartame sweetened or HFCS sweetened soda drink variants have an impact on the secretion of digestive enzymes, incretins and insulin, both types leaving the body “high and dry”.

Neither cola light type drinks nor normal cola type drinks provide the body with the real sugar usable as a source of energy, but with synthetic chemicals whose consumption generates de novo lipogenesis.

De novo lipogenesis translates to gradual weight gain, dyslipidemia, liver and kidney steatosis, and a disordered appetite built up on a gradually increasing craving that will make you want to consume them daily.

When one decides whether to consume normal soda drinks or light soda drinks, what one decides is actually just where he or she wants to deposit the fat formed de novo – inside the body – the mechanisms leading to increased fat deposits happening after the consumption both types (17).

Of course, you can continue to “don’t worry, no sugar” and drink them “just for the taste of it”, but keep in mind that you are doing it on your increasing fat.

Quoted studies

(1) “Scientific Opinion on the re-evaluation of aspartame (E 951) as a food additive”. EFSA Journal 11 (12): 263. 10 December 2013. doi:10.2903/j.efsa.2013.3496.

(2) http://www.efsa.europa.eu/en/press/news/131210.htm

(3) Fowler, Sharon P. et al. “Fueling the Obesity Epidemic? Artificially Sweetened Beverage Use and Long‐term Weight Gain.” Obesity 16.8 (2008): 1894-1900.

(4) Sakurai, Masaru et al. “Sugar-sweetened beverage and diet soda consumption and the 7-year risk for type 2 diabetes mellitus in middle-aged Japanese men.” European journal of nutrition 53.1 (2014): 251-258.

(5) Belpoggi, Fiorella et al. “Results of Long‐Term Carcinogenicity Bioassay on Sprague‐Dawley Rats Exposed to Aspartame Administered in Feed.” Annals of the New York Academy of Sciences 1076.1 (2006): 559-577.

(6) Aune, Dagfinn. “Soft drinks, aspartame, and the risk of cancer and cardiovascular disease.” The American journal of clinical nutrition 96.6 (2012): 1249-1251.

(7) Dhingra, Ravi et al. “Soft drink consumption and risk of developing cardiometabolic risk factors and the metabolic syndrome in middle-aged adults in the community.” Circulation 116.5 (2007): 480-488.

(8) Qing Yang. Gain weight by “going diet?” Artificial sweeteners and the neurobiology of sugar cravings: Neuroscience 2010. The Yale Journal of Biology and Medicine. June 2010.

(9) Lindseth, Glenda N. et al. “Neurobehavioral Effects of Aspartame Consumption.” Research in nursing & health 37.3 (2014): 185-193.

(10) Basciano, Heather, Lisa Federico, and Khosrow Adeli. “Fructose, insulin resistance, and metabolic dyslipidemia.” Nutrition & metabolism 2.1 (2005): 5.

(11) Collison, Kate S. et al. “Diabetes of the Liver: The Link Between Nonalcoholic Fatty Liver Disease and HFCS‐55.” Obesity 17.11 (2009): 2003-2013.

(12) Johnson, Richard J., L. Gabriela Sanchez-Lozada, and Takahiko Nakagawa. “The effect of fructose on renal biology and disease.” Journal of the American Society of Nephrology 21.12 (2010): 2036-2039.

(13) Tappy, Luc et al. “Fructose and metabolic diseases: new findings, new questions.” Nutrition 26.11 (2010): 1044-1049.

(14) Dekker, Mark J. et al. “Fructose: a highly lipogenic nutrient implicated in insulin resistance, hepatic steatosis, and the metabolic syndrome.” American Journal of Physiology-Endocrinology and Metabolism 299.5 (2010): E685-E694.

(15) Cameron, Jameason D., and Éric Doucet. “Reinforcement and food hedonics: a look at how energy deprivation impacts food reward.” Handbook of Behavior, Food and Nutrition. Springer New York, 2011. 2285-2305.

(16) Bellisle, F., and A. Drewnowski. “Intense sweeteners, energy intake and the control of body weight.” European Journal of Clinical Nutrition 61.6 (2007): 691-700.

(17) Feijó Fde M, Ballard CR, Foletto KC, Batista BA, Neves AM, Ribeiro MF, Bertoluci MC. Saccharin and aspartame, compared with sucrose, induce greater weight gain in adult Wistar rats, at similar total caloric intake levels. Appetite. January 2013. doi: 10.1016/j.appet.2012.10.009.