Poor diets, including excess added sugar consumption, contribute to the global burden of disease. Subsequently, many nutrition policies have been implemented to reduce added sugar intake and improve population health, including taxes, education, labelling and environmental interventions. A potential consequence of these policy actions is the substitution of added sugars with non-nutritive sweeteners (NNS) in a variety of foods and beverages. NNS are used to reduce the energy and sugar content of foods and beverages while maintaining their palatability. Evidence of the toxicological risks of NNS is inconsistent, though concerns have been raised over the potential substitution effects of ultra-processed foods containing NNS for whole foods. This review aimed to provide an overview of current NNS food supply and consumption patterns, assess added sugar-reduction policies and their impact on NNS, and determine the impact of NNS on food choice, energy intake and diet quality. NNS are widely available in a variety of products, though most commonly in carbonated beverages, dairy products, confectionery, table-top sweeteners and fruit drinks. However, the longitudinal trends of different product categories, and differences between geographies and economy-income levels, require further study. Few studies have examined NNS consumption trends globally, though an increase in NNS consumption in beverages has been observed in some regions. Research examining how the increased availability of low-sugar, NNS-containing products affects global dietary patterns is limited, particularly in terms of their potential substitution effects.

Consumption of sugar and alternative low- or no-energy sweeteners has increased in recent decades. However, it is still uncertain how consumption of sugar and alternative sweeteners during pregnancy affects pregnancy outcomes and long-term offspring health. This review aims to collate the available evidence surrounding the consequences of sugar and alternative sweetener consumption during pregnancy, a so-called secondhand sugar effect. We found evidence that sugar consumption during pregnancy may contribute to increased gestational weight gain and the development of pregnancy complications, including gestational diabetes, preeclampsia and preterm birth. Further, we found a growing body of the animal and human evidence that maternal sugar intake during pregnancy may impact neonatal and childhood metabolism, taste perception and obesity risk. Emerging evidence also suggests that both maternal and paternal preconception sugar intakes are linked to offspring metabolic outcomes, perhaps via epigenetic alterations to the germline. While there have been fewer studies of the impacts of alternative sweetener consumption before and during pregnancy, there is some evidence to suggest effects on infant outcomes including preterm birth risk, increased infant body composition and offspring preference for sweet foods, although mechanisms are unclear. We conclude that preconception and gestational sugar and alternative sweetener consumption may negatively impact pregnancy outcomes and offspring health and that there is a need for further observational, mechanistic and intervention research in this area.

In vitro, both carbohydrate sugars and artificial sweeteners (AS) stimulate the secretion of glucagon-like peptide-1 (GLP-1). It has been suggested that the gut tastes sugars and AS through the same mechanisms as the tongue, with potential effects on gut hormone release. We investigated whether the human gut responds in the same way to AS and carbohydrate sugars, which are perceived by lingual taste as equisweet. We focused on the secretion of gastrointestinal (GI) satiety peptides in relation to appetite perception. We performed a placebo-controlled, double-blind, six-way, cross-over trial including twelve healthy subjects. On separate days, each subject received an intragastric infusion of glucose, fructose or an AS (aspartame, acesulfame K and sucralose) dissolved in 250 ml of water or water only (control). In a second part, four subjects received an intragastric infusion of the non-sweet, non-metabolisable sugar analogue 2-deoxy-d-glucose. Glucose stimulated GLP-1 (P = 0·002) and peptide tyrosine tyrosine (PYY; P = 0·046) secretion and reduced fasting plasma ghrelin (P = 0·046), whereas fructose was less effective. Both carbohydrate sugars increased satiety and fullness (albeit not significantly) compared with water. In contrast, equisweet loads of AS did not affect gastrointestinal peptide secretion with minimal effects on appetite. 2-Deoxy-d-glucose increased hunger ratings, however, with no effects on GLP-1, PYY or ghrelin. Our data demonstrate that the secretion of GLP-1, PYY and ghrelin depends on more than the detection of (1) sweetness or (2) the structural analogy to glucose.

In an intensive livestock production, a shorter suckling period allows more piglets to be born. However, this practice leads to a number of disorders including nutrient malabsorption, resulting in diarrhoea, malnutrition and dehydration. A number of strategies have been proposed to overcome weaning problems. Artificial sweeteners, routinely included in piglets' diet, were thought to enhance feed palatability. However, it is shown in rodent models that when included in the diet, they enhance the expression of Na+/glucose co-transporter (SGLT1) and the capacity of the gut to absorb glucose. Here, we show that supplementation of piglets' feed with a combination of artificial sweeteners saccharin and neohesperidin dihydrochalcone enhances the expression of SGLT1 and intestinal glucose transport function. Artificial sweeteners are known to act on the intestinal sweet taste receptor T1R2/T1R3 and its partner G-protein, gustducin, to activate pathways leading to SGLT1 up-regulation. Here, we demonstrate that T1R2, T1R3 and gustducin are expressed together in the enteroendocrine cells of piglet intestine. Furthermore, gut hormones secreted by the endocrine cells in response to dietary carbohydrates, glucagon-like peptides (GLP)-1, GLP-2 and glucose-dependent insulinotrophic peptide (GIP), are co-expressed with type 1 G-protein-coupled receptors (T1R) and gustducin, indicating that L- and K-enteroendocrine cells express these taste elements. In a fewer endocrine cells, T1R are also co-expressed with serotonin. Lactisole, an inhibitor of human T1R3, had no inhibitory effect on sweetener-induced SGLT1 up-regulation in piglet intestine. A better understanding of the mechanism(s) involved in sweetener up-regulation of SGLT1 will allow the identification of nutritional targets with implications for the prevention of weaning-related malabsorption.

The possible role played by artificial sweeteners in the long-term maintenance of body weight is considered. Although artificial sweeteners can play a role in a short-term energy-controlled diet, the evidence that they are helpful over a longer period is limited. In those in the recommended weight range there is evidence of compensation; that is, the consumption of low-energy foods is followed by an increased energy intake to make up the lost energy. Energy compensation is more likely in those not displaying dietary restraint. The desire to remove sugar from the diet reflects an assumption that its intake is associated with obesity. However, the consumption of energy-dense food, that almost entirely reflects a high fat and low water content, is the best predictor of obesity. Diets offering a high proportion of energy in the form of carbohydrate tend to contain low levels of fat. There are several reports that the use of artificial sweeteners leads to an increased consumption of fat. The weak ability of fat to satisfy hunger makes it easy to overeat fatty foods; in contrast, carbohydrates promote a feeling of ‘fullness’. Various short-term studies have found that carbohydrate consumed as a liquid, rather than a solid, is more likely to result in weight gain.

The long-term physiological effects of refined carbohydrates on appetite and mood remain unclear. Reported effects when subjects are not blind may be due to expectations and have rarely been studied for more than 24 h. The present study compared the effects of supplementary soft drinks added to the diet over 4 weeks on dietary intake, mood and BMI in normal-weight women (n 133). Subjects were categorised as ‘watchers’ or ‘non-watchers’ of what they ate then received sucrose or artificially sweetened drinks (4 × 250 ml per d). Expectancies were varied by labelling drinks ‘sugar’ or ‘diet’ in a counter-balanced design. Sucrose supplements provided 1800 kJ per d and sweetener supplements provided 67 kJ per d. Food intake was measured with a 7 d diary and mood with ten single Likert scales. By 4 weeks, sucrose supplements significantly reduced total carbohydrate intake (F(1,129) = 53·81; P < 0·001), fat (F(2,250) = 33·33; P < 0·001) and protein intake (F(2,250) = 28·04; P < 0·001) compared with sweetener supplements. Mean daily energy intake increased by just under 1000 kJ compared with baseline (t (67 df) = 3·82; P < 0·001) and was associated with a non-significant trend for those receiving sucrose to gain weight. There were no effects on appetite or mood. Neither dietary restraint status as measured by the Dutch Eating Behaviour Questionnaire nor the expectancy procedure had effects. Expectancies influenced mood only during baseline week. It is concluded that sucrose satiates, rather than stimulates, appetite or negative mood in normal-weight subjects.