by Hidaya Aliouche

With the soft drinks levy six months into effect, the prevalence of sugar-averse drinks has flooded the market. Packaged under the litany of pseudonyms ranging from ‘free’, ‘diet’, ‘light’ to the classic ‘zero-sugar’, drinks companies have circumvented this sticky problem by dropping the sweet stuff from their recipes altogether. The rationale behind such a tax is undisputed; sugar consumption is a risk factor for obesity onset in both adults and children.

Obesity is a leading cause of morbidity worldwide. Quantitatively, it is defined in terms of body mass index (BMI), calculated by dividing mass in kilograms by the square of height in metres. A value of >30 indicates obesity; phenotypically, increased fat mass or adiposity is evident. In 2016, the proportion of adults classified as obese was 13%; current projections estimate that by 2030 this will reach 20%. Together with the associated economic strain obesity incurs, it has been hailed as global epidemic, and as such, presents the biggest health-related challenge of the 21st century. The aetiology of obesity is multifactorial; this, coupled with its socially contentious reception means solving the problem is complex.

The acknowledgement that a consistent energy intake that surpasses energy expenditure underpins the cause of fat gain is wholly simplistic. Obesity is the product of a complex interrelation between biological, environmental and behavioural variables. The latter two factors form the social determinants of obesity, and it is these, rather the biological constituent, regarded as the propellants of the global rate of incidence. The time over which the necessary genetic shift that would need to occur to implicate biological factors as causative far exceeds the time elapsed thus far…

The focus on the social determinants has shifted our attention to the food we eat – which is largely influenced by our behaviour; a connection exploited by the food industry. A closer examination of this correlation is predicated on the notion that excessive sugar intake results in an imbalanced energy expenditure. Consequently, the energy balance is tipped in favour of fat mass accumulation. Excess energy intake is not a sugar-specific phenomenon, however. Intuitively speaking, overconsumption of fat, and even protein, is known to elicit the same energy imbalance. What distinguishes sugar from all other food-stuffs is its predominant liquid form.

This makes the task of overconsumption facile, resulting from the poor satiety index of beverages. Solid forms of sugar fare no better – they are notoriously energy-dense and highly palatable – cake, ice cream, chocolate, biscuits, cereals – the list is long and tasty. Unsurprisingly, a strategy for combating expanding waistlines is the reduction in energy intake from sugar. Therein lies the rise of artificial sweeteners, also known as non-nutritive sweeteners (NNSs), the empty counterpart of their energy-laced cousin, sugar.

Figure 1. Types of sweeteners of interest in context. Taken from doi: https://doi.org/10.1136/bmj.k4718 (Published 02 January 2019)

The consumption of NNS from 2008/2009 to 2011/2012 indicates that 44% of soft drinks consumed by adults (aged 19-64) were low calorie, as reported by the National Dietary and Nutrition Survey (NDNS). This is congruent with data reported by the British Soft Drinks Association who reported approximately half of all carbonated drinks sold in 2014 were low or no calorie. Further still, the British Soft Drinks Association reported a decrease in regular calorie drink consumption between 2011-2015 from 62% to 50%.

Figure 2. With the sugar tax in effect, many consumers are turning to the lighter, sweeter version of the traditional white stuff.

The EU have recently issued legislature approving the use of six artificial sweeteners, which includes aspartame, sucralose, saccharin, advantame, neotame and acesulfame potassium-k. On average, their sweetness ranges approximately between 200-500 times greater than sugar. Neotame and advantame are considerably sweeter, ranging from ranging from 7000-13000 and 37,000, respectively!

The health risk associated with their consumption is controversial. Their alleged toxic effects are heterogeneous; migraines, type-2 diabetes, kidney function disorders, premature delivery, hepatotoxicity , cancer, weight gain, metabolic disorders, are samples of a few of the chronic manifestations of toxicity. The controversy surrounding the legitimacy of these concerns is due to the lack of consistent evidence. Furthermore, studies examining phenotypic consequences of NNS consumption utilise mouse models. Human studies have failed, for example, to implicate their role in cancer development.

The contention is augmented by studies that have examined the role of NNS is the prevention of obesity with antagonistic findings prevailing in the literature. Comparative studies between artificial sweeteners and non-artificial sweeteners or sugar provide demonstrable evidence that use of the former aids weight loss. Conversely, some studies have shown that weight gain increases in rats when fed artificial sweeteners.

Observational studies in humans have supported this outcome. These types of studies are unable to determine causality; nonetheless, they stipulate associations, which may be compounded by mechanisms to explain them. A notable long-term study highlighted the dose-dependency of NSS, administered by beverage consumption, and weight gain over a period of 8 years. Those that consumed artificially sweetened beverage showed an increased likelihood of weight-gain compared to non-consumers. The BMI from both groups were adjusted as the relationship between BMI and variables such as sex and age is non-linear. Counterintuitively the NNS consumer groups total daily energy intakes were lower despite their weight gain; a phenomenon that has been echoed in other studies. This posits a plausible explanation to explain the correlation between NNS consumption and weight gain; NNS may work to increase weight without increasing energy intake as one may intuitively assume. This same group also increased their visceral adiposity over a 9 to 10-year period, despite changes in BMI or body weight.

NNS and other health-related issues

Other studies in humans linking the consumption of NNS with dietary choices have also demonstrated mixed outcomes. The inconsistencies in these epidemiological studies, which examine the distribution and determinants of health and disease in populations, arise due to differences in the was these studies are conducted. For example, the way in which NNS consumption is classified and how the subjects are compared. Epidemiological studies that have compared NNS consumption with various other parameters of health have been more conclusive; NNS use and type 2 diabetes, metabolic syndrome , cardiovascular disease, and non-alcoholic fatty liver disease have been positively correlated. Recent systematic reviews have further noted positive associations between NNS use and other negative health outcomes.

So far, the impact of NNS use on ill-health is compelling. There is an undisputed link between the two, however, a strict cause-and-effect relationship remains to be established. Despite this, the role of NNS use in weight management is still confounding – some intervention trials show that NNSs may aid weight management, specifically when participants use these in the context of calorie restriction and intentional weight loss. The inability to determine causal relationships arises from several flaws in the varied methodologies that underpin each study. For example, dietary assessments are often poorly conducted, often due to the questions used to assess the participants dietary habits, or are biased because of a phenomena termed reverse causality. Reverse causality shows a relationship between two variables, but in the reverse cause order. In this context, there is an inherent bias towards NNS use and weight gain, when in fact it is plausible that those who display overweight or obese BMI then consume NNSs to better manage their weight, thus implicating NNS uses as the cause, rather than effect of weight gain. Moreover, the context in which NNS are consumed is unreported; it is unclear whether participants are engaged in weight loss attempts and use NNS as a tool to adhere to calorically controlled diet plans. Finally, differentiated research which looks at specific sweetener effects may provide a clearer overview.

Thus, until future studies mitigate the effects of these limitations by considering the characteristics of participants; particularly their patterns of NNS consumption and reasons for use, determining whether NNSs are helpful for weight loss and maintenance will remain unclear. Further still is the limitation of considering only NNS containing beverages. Investigations that broaden the scope of NNS use to include food and condiments may provide a ‘real-life’ context in which to examine the relationship between NNS use and weight loss.

NNS still remain shrouded in uncertainty. The choice is with the consumer. At this point, the most sensible advice is to exercise moderation, and consider curbing the sweet cravings with nutritive sweeteners such as stevia or xylitol. Do so with caution; although technically sugar-free, these substances are still a type of carbohydrate. Whilst their lower energy content are attractive, they pose an insidious means to accidentally boost your caloric intake!

Further Reading:

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;16:1894‐1900.

Bright OM WD, White MS, Bleich SN, et al. Research priorities for studies linking intake of low calorie sweeteners and potentially related health outcomes. Curr Dev Nutr 2017;1:e000547.

Whitehouse CR, Boullata J, McCauley LA. The potential toxicity of artificial sweeteners. Aaohn J. 2008;56:251–61.

Blackburn, G.L.; Kanders, B.S.; Lavin, P.T.; Keller, S.D.; Whatley, J. The effect of aspartame as part of a multidisciplinary weight-control program on short- and long-term control of body weight. Am. J. Clin. Nutr. 1997, 65, 409–418.

Whitehouse CR, Boullata J, McCauley LA. The potential toxicity of artificial sweeteners. Aaohn J. 2008;56:251–61.

About the Author:

I am a postgraduate student at the University of Manchester. Having completed a degree in Biochemistry I am now working as a clinical and research project assistant. In my spare time, you can find me sweating it out outdoors, crocheting in a corner and baking up a storm (not necessarily in that order…or at the same time).