Written by Jon Hutchinson - http://www.sportandexercisereview.com

An article in ‘Dietetics Today’, a magazine produced by the British Dietetic Association, (the Association of British Dieticians) was titled ‘Low Calorie Sweeteners – friend or foe?’ The writer used several references to conclude that there is a considerable weight of evidence in favour of consumption of Low Calorie Sweeteners (LCS) and that it was unfortunate that selected misinformation claiming the contrary were in effect raising unfounded concerns over safety. All well and good, until you read that the article by Professor Peter Rogers of the University of Bristol was sponsored by ‘Thirst for Knowledge’ – an educational initiative funded by Coca Cola. Undoubtedly there are misunderstandings surrounding LCS, but is an industry which promotes their use best placed to study them? Whilst assurances that studies are kept apart from the sponsor, the underlying expectation of a ‘bang for their buck’ may not offer the best vision of independent research.

The term ‘Dietician’ is often confusing amid the range of nutritionists out there. A Dietician is regulated by law and only those registered with the statutory regulator, the Health & Care Professions Council (HCPC) can use the title of Dietitian/Registered Dietitian. This needs to be clarified in the light in which the article was published.

 

There may be many who would question the validity of publishing work which could be influential on the work of those who read the magazine, given its elevated status, if it might be no more than the paid opinion of someone with a clear conflict of interest, even though the sponsorship was set out on the page.

The difficulty in assessing the efficacy of LCS lies in the inherent nature of research, most of which is confined to parameters that are the scientific equivalent of trying to dance in a coffin. It’s of little value proving that they contribute to weight loss if they also cause long term health issues. Of course each aspect of the conundrum is worthy of its own little piece of investigation, but no conclusion should be offered about their overall effect unless all are taken into account.

The history of LCS is worth visiting, if only to understand how we got here, the discovery of most would make Lab technicians the World over wince, given that the artificial sweetness was only discovered when the scientist, after mixing a concoction simply stuck their finger in and tasted it. The improbably named Constantine Fahlberg found Saccharin whilst testing Coal Tar derivatives, whilst the most controversial, Aspartame, was the result of combining two natural amino acids – Phenylalanine and Aspartate. James Schlatter was in fact trying to produce new ulcer drugs, but stuck his finger in the resulting mix, tasted it and found that it was incredibly sweet. In many cases, the objection to LCS is that they are an invention of ‘Big Pharma’, those Companies who prowl the Earth with the express desire to kill us all whilst filling their bank accounts, but the truth is most sweeteners where born of simple accident.

There are realistically two considerations for LCS, the first is their intended use as a method of weight loss, the second is their effects on health.

Most of the studies so far have used mice and rats, hardly a true reflection of how sweeteners will affect the human population, although that hasn’t stopped many from taking those results and applying them to you and me there is a World of difference even though we may only be a few genes apart. An example is Saccharin, which is 300 times sweeter than Sucrose. Saccharin has a bitter aftertaste and is mixed with Cyclamate in order to make it more palatable. It was recognised as safe by the United States Federal Food, Drug and Cosmetics Act. In 1969, the Food and Drug Administration (FDA) banned Cyclamate due to its carcinogenic potential and Saccharin too fell foul of the FDA and a ban on that was planned in 1977 although this was commuted to a warning label on all products containing the substance. The connection between Cyclamate and cancer was later refuted and the suggested link between bladder cancer and Saccharin was found to be unique to the physiology of rats (1).

Most people choose LCS as an intuitive method of weight control, reducing sugar intake and therefore restricting calories. The issues surrounding sugar intake have been highlighted recently by Jamie Oliver and the Medical Profession in general, so the use of LCS makes sense, but does the science agree? The answer is no, but sometimes yes.. in human trials, several studies through the 80’s suggested that there was a correlation between LCS use and weight gain, including the San Antonio Heart Study (2), The American Cancer Society study (3) and the Nurses Health Study (4), altogether accounting for around 115,000 subjects, but a 2002 study for the American Journal of Clinical Nutrition showed that obese adults in a ten week period of consuming sucrose drinks or LCS drinks lost more weight on the LCS (5) . The idea of switching from sugar or high fructose soft drinks to low calorie alternatives should reduce overall energy intake and therefore weight. There are a number of suggestions why this appears not to happen, most of them are not really backed by any study. The explanation would appear to lie in a combination of psychology and physiology. One theory is that of overcompensation, that the sweetness but lack of energy in LCS leads to a lack of feeling full and could in turn lead to increased overall energy intake, or that people are aware that they have consumed fewer calories and therefore may feel free to eat a little more. Interestingly, sweetness is an appetite enhancer and that is the case whether it is sugar or LCS. One study compared the reported feeling of appetite in male subjects after Aspartame given either as a drink, or in a capsule (the reason for the capsule was that the subject would be consuming the sweetener, but wouldn’t be able to taste it). The results showed that those who had consumed the drink were hungrier afterwards (6). The important finding with regard to appetite is that several studies showed that appetite increased after LCS to a greater extent than sugar or glucose, which again suggests that LCS may lead to a greater urge to eat more than they would have otherwise, negating the effect of the energy reduction of LCS consumption (7, 8, 9).

The use of LCS can also have a different effect on the brain pathways than sugar. There is increasing evidence that LCS do not activate the food reward pathways in the same way as sugar, the lack of calories in LCS is not missed by the brain which leads to a sustained hunger afterwards (10, 11).

This brings up quite naturally the question of inducing an Insulin response, which seems to be a common assertion within the fitness and nutrition industry – that drinking a diet drink leads to the release of the hormone with negative effects on the body. The studies seem quite clear on this one, Artificial Sweeteners do not cause an insulin response. (12, 13, 13a, 13b, 13c, 13d ). Although some studies have suggested an altered insulin response when LCS is combined with other sugars. A key phrase from a 2010 paper in the British Medical Journal was quite clear –

“There is no consistent evidence that low-energy sweeteners cause insulin release or affect blood pressure in normal subjects”. (13e)

The reason why a sweet substance doesn’t always lead to an insulin response could possibly be compared to the use of a carbohydrate mouth rinse, of which Professor Asker Jeukendrup is probably the most prominent researcher at present. If you take a carbohydrate solution, swill it in your mouth and spit it out, the immediate effect on your body is as if you had ingested it. The exact mechanism of why this happens isn’t fully understood but it seems the receptors in the mouth tell the brain that carbs are on the way and the brain says wonderful! Let’s go! – if you try the same thing with a sweetener, the effect doesn’t happen, which would suggest that the receptors in the mouth can tell the difference between the two and sends signals to the brain accordingly, which may also explain the lack of insulin production. However, the continued use of LCS is subject to a number of studies for their long term effects on the body’s response to sweetness. The same brain pathways described earlier that govern the process of sensing sugars and dealing with them appropriately might become degraded by consuming LCS over time by desensitising the receptors (14). Although the studies are confined to rats, some brain imaging of humans has leant support to the theory (15).

When discussing artificial sweeteners, a special mention has to go to Aspartame, possibly the most controversial of them all. If any substance has caused such a fuss it may yet to be found. One of the most serious accusations levelled against it is that it can cause cancer. In 1984, animal studies showed no evidence (16, 17) but some 15 years later a study (18) suggested otherwise. There was speculation that the rise in brain tumours through the 80’s could be ascribed to Aspartame and subsequent studies using rats seemed to confirm an issue, the rats being fed Aspartame over a two year period resulting in 12 out of 320 of the rodents developing brain tumours (19), but later trials didn’t confirm those results. A further study tested the link between mothers to be consuming Aspartame products and the incidence of brain tumours in their children, but no link was found (20). There are many internet sites which link Aspartame to a myriad of diseases and ailments from Fibromyalgia to Migraines and Arthritis to liver damage and premature births. The truth is that these are anecdotal at best as little if any research has been carried out to try and investigate these side effects, it’s not to say they are not true, just that there is no evidence to support them.

aspartame

One relatively new area of research is the effect that LCS may have on gut bacteria. In 2014 the journal Nature (21) tested for changes in gut bacteria in mice and found that continued use of LCS did indeed lead to a change in those bacteria which in turn led to increasing glucose intolerance. They found similar results in human subjects and concluded that ‘massive’ use of LCS should be reassessed. Another study from last year (22) reviewed the new evidence and quoted from one of those studies –

“that dietary sugar alternatives meant to stave off the risk of obesity and diabetes may actually increase disease risk due to microbial alterations”

Although another recent investigation (23) found less convincing evidence for the change in gut bacteria but nevertheless expressed the need for further research given the serious nature of the issue given the high consumption of LCS

The conclusion is that LCS are not a fail safe way to lose weight as people may eat more to satisfy the feeling of fullness. More research is needed to gauge the long term effects of these sweeteners on the body’s response to sweetness, whether continued exposure to it changes the way we process sugar in general and how, for athletes, the inclusion of them might affect performance if the body reacts differently to them. Whilst many of the fears surrounding LCS are unfounded, the recent research suggesting changes in gut bacteria could be a game changer, if further work confirms the initial findings, the use of LCS will come under intense pressure and will almost certainly lead to calls for a reduction or even an end to their continued use.

1 Nettleton, J A (2009) ‘Diet soda intake and risk of incident metabolic syndrome and type

2 diabetes in the multi ethnic study of atherosclerosis’ Diabetes Care 32 (4) 688-694

2 Fowler S P, et al (2008) Fueling the obesity epidemic? Artificially sweetened beverage use and long-term weight gain. Obesity 16 1894–1900

3 Stellman S D, Garfinkel L. (1986) Artificial sweetener use and one-year weight change among women. Preventative Medicine. 15 195–202

4 Colditz GA, et al (1990). Patterns of weight change and their relation to diet in a cohort of healthy women. American Journal of Clinical Nutrition 51 1100–1105.

5 Raben A, et al (2002) Sucrose compared with artificial sweeteners: different effects on ad libitum food intake and body weight after 10 wk of supplementation in overweight subjects. American Journal of Clinical Nutrition 76 (4) 721-729.

6 Black R M, et al. (1993) Consuming aspartame with and without taste: differential effects on appetite and food intake of young adult males. Physiology Behaviour. 53 459–466

7 Blundell, J E, Hill , A J. (1986) Paradoxical effects of an intense sweetener (aspartame) on appetite. Lancet. 1092–1093

8 Rogers, P J (1988). Uncoupling sweet taste and calories: comparison of the effects of glucose and three intense sweeteners on hunger and food intake. Physiology Behaviour. 547–552

9 Lavin, J H, et al (1997). The effect of sucrose- and aspartame-sweetened drinks on energy intake, hunger and food choice of female, moderately restrained eaters. International Journal of Obesity Related Metabolic Disorder. 37–42

10 Haase, L, et al. (2009) Cortical activation in response to pure taste stimuli during the physiological states of hunger and satiety. NeuroImage. 1008–1021

11 Liem, D G, de Graaf, C. (2004) Sweet and sour preferences in young children and adults: role of repeated exposure. Physiological Behaviour. 421–429

12 Brown, R J, et al. (2009) Ingestion of diet soda before a glucose load augments glucagon-like peptide-1 secretion. Diabetes Care. 32 (2) 184–186

13 Brown RJ, et al. (2012) Effects of diet soda on gut hormones in youths with diabetes. Diabetes Care. 959–964

13a Moller, S A (1991) Effect of aspartame and protein, administered in phenylalanine-equivalent doses, on plasma neutral amino acids, aspartate, insulin and glucose in man. Pharamcological Toxicology 68 (5) 408-412

13b Wolf-Novak, L C et al (1990) Aspartame ingestion with and without carbohydrate in phenylketonuric and normal subjects: effect on plasma concentrations of amino acids, glucose, and insulin. Metabolism 39 (4) 391-396

13c Horowitz, D L (1988) Response to single dose of aspartame or saccharin by NIDDM patients. Diabetes Care 11 (3) 230-234

13d Ma, J (2009) Effect of the artificial sweetener, sucralose, on gastric emptying and incretin hormone release in healthy subjects. American Journal of Physiology Gastrointest Liver Physiology. 296 (4) 735-739

13e Renwick, A G (2010) Sweet-taste receptors, low-energy sweeteners, glucose absorption and insulin release. British medical Journal 104 (10) 1415-1420

14 Swithers, S E, et al. (2012) Experience with the high-intensity sweetener saccharin impairs glucose homeostasis and GLP-1 release in rats. Behav Brain Res. 1–14

15 Green E, Murphy C. (2012) Altered processing of sweet taste in the brain of diet soda drinkers. Physiology Behaviour 560–567.

16 Hagiwara, A, (1984) Effects of three sweeteners on rat urinary bladder carcinogenesis initiated by N-butyl-N-(4hydroxybutylnitrosoamine. Gann 763-768

17 Ishii H, (1981) Incidence of brain tumors in rats fed aspartame. Toxicology Letters 433-437.

18 Olney, J W, et al. (1996) Increasing brain tumour rates: is there a link to aspartame? Journal Neuropathology and Experimental Neurology 1115- 1123.

19 Study E33-34 in Master file 134 on aspartame. On file at the FDA Hearing Clerk’s Office 2001.

20 Gurney, J G, et al. (1997) Aspartame consumption in relation to childhood brain tumor risk: results from a case-control study. National Cancer Institute 1072-1074

21 Suez, J et al (2014) Artificial sweeteners induce glucose intolerance by altering the gut microbiota. Nature 514 181-186

22 Bokulich, N A (2014) A Bitter Aftertaste: Unintended Effects of Artificial Sweeteners on the Gut Microbiome Cell Metabolism 20 (5) 701-703

23 Frankenfeld, C L (2015) High-intensity sweetener consumption and gut microbiome content and predicted gene function in a cross-sectional study of adults in the United States. Annals of Epidemiology 25 (10) 736-742

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