Resource Type: Research

Systematic reviews and meta-analysis of the data show that the link between a high intake of sugars, and overweight and obesity is mediated by energy intake. The body of evidence continues to grow in this area, with a focus on specific sugars like fructose, and the source of kilojoules, for example sugar sweetened beverages. 

Key research

Barclay AW & Brand-Miller J. (2011). The Australian obesity paradox: A substantial decline in sugars intake over the same time frame that overweight and obesity have increased. Nutrients, 3(4):491-504.
The prevalence of obesity has tripled in Australians since 1980. In Australia, the UK and USA, per capita consumption of refined sucrose decreased by 23%, 10% and 20% respectively from 1980 to 2003. In Australia, there was a reduction in sales of nutritively sweetened beverages from 2002 to 2006 and a reduction in percentage of children consuming sugar-sweetened beverages between 1995 and 2007. The findings confirm an “Australian Paradox”—a substantial decline in refined sugars intake over the same timeframe that obesity has increased. The implication is that efforts to reduce sugar intake may reduce consumption but may not reduce the prevalence of obesity.

Brand-Miller J & Barclay AW. (2017). Declining consumption of added sugars and sugar-sweetened beverages in Australia: a challenge for obesity prevention. Am J Clin Nutr, 105(4):854-863.
In Australia, 4 independent data sets confirmed shorter- and longer-term declines in the availability and intake of added sugars, including those contributed by SSBs. The findings challenge the widespread belief that energy from added sugars or sugars in solution are uniquely linked to the prevalence of obesity.

Te Morenga L, Mallard S & Mann J (2013) Dietary sugars and body weight: systematic review and meta-analyses of randomised controlled trials and cohort studies. BMJ, 345:e7492.
In trials of adults with non-restricted diets, a reduced intake of dietary sugars was associated with a decrease in body weight, while an increased sugars intake was associated with a comparable weight increase. The authors concluded the change in body fatness that occurs with modifying intakes seems to be due to changes in energy intakes, since replacing sugars with other carbohydrates (of equal energy) was not associated with weight change.

Other research

Livingstone KM & McNaughton SA. (2017). Dietary patterns by reduced rank regression are associated with obesity and hypertension in Australian adults. Br J Nutr,117(2):248-259.
Obesity prevalence was inversely associated with low dietary energy density (DED), high fibre and high sugar (natural sugars) diets and positively associated with low-fibre and high sugar (added sugars) diets. Hypertension prevalence was higher on low-fibre and high sodium and saturated fat diets. 

Rippe JM & Angelopoulos TJ. (2016). Sugars, obesity, and cardiovascular disease: results from recent randomized control trials. Eur J Nutr, 55:45-53.
This review of randomised trials, systematic reviews and meta-analyses does not support a link between sugar consumption at normal levels and various adverse metabolic and health effects, including those on energy-regulating hormones, obesity, CVD, diabetes, liver fat accumulation and neurologic responses. 

Rippe JM & Angelopoulos TJ. (2016). Added sugars and risk factors for obesity, diabetes and heart disease. Int J Obes, 40:S22-S27.
The normal added sugars in the human diet (for example, sucrose, high-fructose corn syrup and isoglucose) when consumed within the normal range of normal human consumption or substituted isoenergetically for other carbohydrates, do not appear to cause a unique risk of obesity, diabetes or cardiovascular disease.

Khan TA & Sievenpiper JL. (2016). Controversies about sugars: results from systematic reviews and meta-analyses on obesity, cardiometabolic disease and diabetes. Eur J Nutr, 55(Suppl 2):25-43.
The authors conclude sugar content should not be the sole determinant of a healthy diet as there are many other factors in the diet, some providing excess calories while others provide beneficial nutrients. Rather than just focusing on one energy source, we should consider the whole diet for health benefits.

Choo VL, Ha V & Sievenpiper JL. (2015). Sugars and obesity: Is it the sugars or the calories? Nutrition Bulletin, 40(2), 88-96.
Attention needs to remain focused on decreasing overconsumption of all foods associated with overweight and obesity. Sugar‐sweetened beverages and foods are certainly an important place to start but should not draw attention away from the issue of overconsumption in general.

Ahmad R, Mok A, Rangan AM, at al. (2019). Association of free sugar intake with blood pressure and obesity measures in Australian adults. European Journal of Nutrition. Eur J Nutr, 59:651–659.
A higher free sugar intake from beverages was positively associated with BMI, waist circumference and waist-to-height ratio, while free sugar intake from non-beverage sources was inversely associated with these outcomes. Higher free sugar intake from all food source was associated with a reduced risk of high blood pressure.

Wong THT & Louie JCY. (2018). The direct and indirect effect associations of usual free sugar intake on BMI z-scores of Australian children and adolescents. Eur J Clin Nutr, 72:1058–1060.
Free sugar intake was not associated with BMI z-score in this cohort. Instead of focusing on a single energy source in the diet, improving the quality of the whole diet may be a better approach in tackling childhood obesity.

Ambrosini GL, Johns DJ, Northstone K, et al. (2016). Free sugars and total fat are important characteristics of a dietary pattern associated with adiposity across childhood and adolescence. J Nutr, 146(4):778-784.
An energy-dense dietary pattern high in total percentage of energy from total fat and free sugars is associated with greater adiposity in childhood and adolescence.

Prinz P. (2019). The role of dietary sugars in health: molecular composition or just calories? Eur J Clin Nutr, 73:1216–1223.
Current data indicates that dietary sugars are only associated with an increase in obesity when consumed as an excess source of calories, and with that an increase in the risk of diet-related diseases.

Resource Type: Research

Current evidence on a direct link between sugars and cardiovascular disease (CVD) is inconclusive. While there appears to be an association between high sugars intake and CVD risk factors such as weight gain and insulin sensitivity, consumption of sugars at normal levels appears to have no effect.

Key research 

Rippe JM & Angelopoulos TJ. (2016). Sugars, obesity, and cardiovascular disease: results from recent randomized control trials. Eur J Nutr, 55:45-53.
This review of randomised trials, systematic reviews and meta-analyses does not support a link between sugar consumption at normal levels and various adverse metabolic and health effects, including those on energy-regulating hormones, obesity, CVD, diabetes, liver fat accumulation and neurologic responses.

Te Morenga LA, Howatson AJ,  Jones RM, et al. (2014). Dietary sugars and cardiometabolic risk: systematic review and meta-analyses of randomized controlled trials of the effects on blood pressure and lipids. Am J Clin Nutr, 100(1):65-79.
Higher compared with lower sugar intakes significantly raised triglyceride concentrations, total cholesterol, low-density lipoprotein cholesterol and high-density lipoprotein cholesterol. There was a stronger association in studies where energy balance was maintained and when no difference in weight change was reported, indicating the effect of high sugar intake on lipids was independent of effects of sugars on body weight. The effect of sugar intake on blood pressure was greatest in trials ≥8 wk in duration.

Other research

Khan TA, Tayyiba M, Agarwal A, et al. (2019). Relation of total sugars, sucrose, fructose, and added sugars with the risk of cardiovascular disease: a systematic review and dose-response meta-analysis of prospective cohort studies. Mayo Clinic Proceedings, 94(12):2399-2414.
Total sugars, sucrose and fructose were not associated with CVD incidence. Total sugars, fructose, and added sugars were associated with increased CVD mortality, with the threshold for harm above intakes of 133 grams (26% energy) for total sugars, 58 grams (11% energy) for fructose, and 65 grams (13% energy) for added sugars. No harmful association with CVD mortality was seen at lower intakes of these sugars or at any dose for sucrose.

Fattore E, Botta F, Agostoni C & Bosetti C. (2017). Effects of free sugars on blood pressure and lipids: a systematic review and meta-analysis of nutritional isoenergetic intervention trials. Am J Clin Nutr, 105(1):42–56.
In short- or moderate-term isoenergetic intervention trials, the substitution of free sugars for complex carbohydrates had no effect on blood pressure or body weight, and an unclear effect on blood lipid profile. 

Yang Q, Zhang Z, Gregg EW, et al. (2014). Added sugar intake and cardiovascular diseases mortality among US adults. JAMA Intern Med, 174(4):516-524.
Among US adults, the adjusted mean percentage of daily calories from added sugar increased from 15.7% in 1988-1994 to 16.8% in 1999-2004, and decreased to 14.9% in 2005-2010. Most adults consumed 10% or more of calories from added sugar and approximately 10% consumed 25% or more in 2005-2010. The risk of CVD mortality increased exponentially with increasing usual percentage of calories from added sugar, with the relative risk more than double for those who consumed 21% or more of calories from added sugar.

Chiavaroli L, de Souza RJ, Ha V, et al. (2015). Effect of fructose on established lipid targets: A systematic review and meta-analysis of controlled feeding trials. J Am Heart Assoc, 4(9).
Fructose only had an adverse effect on established lipid targets when added to existing diets so as to provide excess calories (+21% to 35% energy). When isocalorically exchanged for other carbohydrates, fructose had no adverse effects on blood lipids.

Sieri S, Agnoli C, Grioni S, et al. (2020). Glycemic index, glycemic load, and risk of coronary heart disease: a pan-European cohort study. Am J Clin Nutr, nqaa157.
High dietary glycemic load (GL) was significantly associated with increased coronary heart disease (CHD) risk in overweight and obese persons, but not in those of normal weight. High dietary glycemic index (GI) was only inconsistently associated with CHD risk. High consumption of available carbohydrate (e.g. white rice and refined wheat) and added sugars (mainly from SSBs), but not starch, was associated with greater CHD risk.

Loader J, Meziat C, Watts R, et al. (2017). Effects of sugar-sweetened beverage consumption on microvascular and macrovascular function in a healthy Population. Arterioscler Thromb Vasc Biol, 37(6):1250-1260.
Compared to water, acute hyperglycemia from SSB consumption impaired microvascular and macrovascular function, while vascular smooth muscle was preserved. To the authors’ knowledge, this is the first study to demonstrate the effects of acute hyperglycemia from SSB alone on vascular function.

Cheungpasitporn W, Thongprayoon C, Edmonds PJ, et al. (2015). Sugar and artificially sweetened soda consumption linked to hypertension: A systematic review and meta-analysis. Clin Exp Hypertens, 37(7):587-93.
This meta-analysis showed a significant association between both sugar-sweetened and artificially-sweetened soda consumption and hypertension, in both males and females. There was an overall 12% and 15% increased risk of hypertension for sugar-sweetened soda and artificially sweetened soda consumption, respectively.

West S, Smail O & Bond B. (2019). The acute influence of sucrose consumption with and without vitamin C co-ingestion on microvascular reactivity in healthy young adults. Microvasc Res, 126:103906.
The consumption of a sugar load representative of commercially available SSBs did not influence microvascular reactivity. The co-ingestion of Vitamin C also failed to influence microvascular reactivity, but did increase the rate of oxygen extraction.

Resource Type: Research

There is no direct or unique causal link between intake of sugars and risk of type 2 diabetes. Research shows that weight gain due to excess energy from any source is a risk factor for type 2 diabetes. New research finds that high dietary glycemic index (GI) and glycemic load (GL) is a factor that likely contributes to type 2 diabetes incidence, while low dietary GI and GL can reduce the risk of type 2 diabetes.

Key research

Lean MEJ & Te Morenga L. (2016). Sugar and Type 2 diabetes. British Medical Bulletin, 120(1):43–53.
Much of the association between sugars and T2DM is eliminated by adjusting data for body mass index (BMI). However, BMI adjustment does not fully account for adiposity. Excess sugar can promote weight gain, thus T2DM, through extra calories, but has no unique diabetogenic effect at physiological levels.

Rippe JM & Angelopoulos TJ. (2016). Sugars, obesity, and cardiovascular disease: results from recent randomized control trials. Eur J Nutr, 55:45-53.
This review of randomised trials, systematic reviews and meta-analyses does not support a link between sugar consumption at normal levels and various adverse metabolic and health effects including those on energy-regulating hormones, obesity, CVD, diabetes, liver fat accumulation and neurologic responses.

Livesey G, Taylor R, Livesey HF, et al. (2019). Dietary glycemic index and load and the risk of type 2 diabetes: assessment of causal relations. Nutrients, 11(6):1436.
All nine of the Bradford-Hill’s criteria for causality were met for GI and GL indicating that the authors can be confident of a role for GI and GL as causal factors contributing to incident T2D. In addition, neither dietary fibre, cereal fibre nor wholegrain were found to be reliable or effective surrogate measures of GI or GL. The cost–benefit analysis suggests food and nutrition advice favours lower GI or GL, and would produce significant potential cost savings in national healthcare budgets.

Jayedi A, Soltani S, Jenkins D, et al. (2020). Dietary glycemic index, glycemic load, and chronic disease: an umbrella review of meta-analyses of prospective cohort studies. Crit Rev Food Sci Nutr, Dec 1: 1-10.
This umbrella review of meta-analyses found a positive association between dietary GI and the risk of type 2 diabetes, coronary heart disease, and colorectal, breast, and bladder cancers, as well as between dietary GL and the risk of coronary heart disease, type 2 diabetes, and stroke. There was no significant association with cancers at other sites. The certainty of evidence ranged from very low to low. 

Other research

Livesey G, Taylor R, Livesey HF, et al. (2019). Dietary glycemic index and load and the risk of type 2 diabetes: a systematic review and updated meta-analyses of prospective cohort studies. Nutrients, 11(6):1280.
Critical analyses of prospective cohort studies provide robust evidence that diets higher in glycemic index (GI) and load (GL), independently of dietary fiber, substantially elevate the risk of type-2 diabetes among healthy populations of men and women.

Biggelaar LJCJ, Eussen S, Sep S, et al. (2017). Associations of dietary glucose, fructose, and sucrose with β-cell function, insulin sensitivity, and type 2 diabetes in the Maastricht study. Nutrients, 9(4):380.
Higher intake of glucose, not fructose and sucrose, was associated with higher insulin sensitivity, independent of dietary fibre. No convincing evidence was found for associations of dietary glucose, fructose, and sucrose with β-cell function in this middle-aged population.

Rippe JM & Angelopoulos TJ. (2016). Added sugars and risk factors for obesity, diabetes and heart disease. Int J Obes, 40:S22-S27.
The normal added sugars in the human diet (for example, sucrose, high-fructose corn syrup and isoglucose) when consumed within the normal range of normal human consumption or substituted isoenergetically for other carbohydrates, do not appear to cause a unique risk of obesity, diabetes or cardiovascular disease.

Imamura F, O'Connor L, Ye Z, et al (2015). Consumption of sugar sweetened beverages, artificially sweetened beverages, and fruit juice and incidence of type 2 diabetes: systematic review, meta-analysis, and estimation of population attributable fraction. BMJ: 351:h3576.
Habitual consumption of sugar sweetened beverages was associated with a greater incidence of type 2 diabetes, independent of adiposity. Although artificially sweetened beverages and fruit juice also showed positive associations with incidence of type 2 diabetes, the findings were likely to involve bias.

Resource Type: Research

Overall the balance of research supports a link between increased frequency of consumption of sugars and incidence of dental decay, but not for total amount of sugars consumed.

Key research 

van Loveren C. (2019). Sugar restriction for caries prevention: amount and frequency. Which is more important? Caries Res, 53(2):168-175.
The results suggest that when fluoride is appropriately used, the relation between sugar consumption and caries is very low or absent. The high correlation between amount and frequency hampers the decision related to which of both is of more importance, but frequency (and stickiness) fits better in our understanding of the caries process. Reducing the amount without reducing the frequency does not seem to be an effective caries preventive approach in contrast to the reciprocity. 

Anderson CA, Curzon MEJ, Van Loveren C, et al. (2009). Sucrose and dental caries: a review of the evidence. Obes Rev, 10 Suppl 1:41-54.
In this review, 6 papers found a positive, significant relationship between sugar quantity and dental caries, 19 of 31 studies reported a significant relationship between sugar intake frequency and dental caries. The balance of studies does not demonstrate a relationship between sugar quantity, but a moderately significant relationship of sugar frequency to dental caries.

Other research

Skafida V & Chambers S. (2018). Positive association between sugar consumption and dental decay prevalence independent of oral hygiene in pre-school children: a longitudinal prospective study. J Public Health (Oxf), 40(3):e275-e283.
Children who snacked all day (rather than eating meals), consumed soft drinks more frequently, or ate sweets or chocolates once a day or more, had a higher chance of dental decay.  There was also an association between decreasing brushing frequency at age 2 and decay at age 5. For children eating sweets or chocolate once a day or more, brushing teeth more often reduced the chance of decay.

Barrington G, Khan S, Kent K, et al. (2019).  Obesity, dietary sugar and dental caries in Australian adults. Int Dental J, 69(5):383-391.
There was a positive association between dental caries experience and being overweight or obese compared with having normal weight or being underweight, as well as between sugar consumption with all four dental caries outcome measures.

Moynihan PJ & Kelly SAM. (2014). Effect on caries of restricting sugars intake; systematic review to inform WHO Guidelines. J Dent Res, 93(1), 8-18.
Of the studies, 42 out of 50 of those in children and 5 out of 5 in adults reported at least one positive association between sugars and caries. There is evidence of moderate quality showing that caries is lower when free-sugars intake is < 10% energy. With the < 5% energy cut-off, a significant relationship was observed, but the evidence was judged to be of very low quality.

Sheiham A & James WPT. (2014). A new understanding of the relationship between sugars, dental caries and fluoride use: implications for limits on sugars consumption. Public Health Nutr, 17(10):2176–2184.
Caries occurred in both resistant and susceptible teeth of children when sugar intakes were only 2–3% of energy intake, provided that the teeth had been exposed to sugars for >3 years. Despite increased enamel resistance after tooth eruption, there was a progressive linear increase in caries throughout life, explaining the higher rates of caries in adults than in children. Fluoride affects progression of caries development but there still is a pandemic prevalence of caries in populations worldwide.

Bernabe E, Vehkalahti MM, Sheiham A, et al. (2016). The shape of the dose-response relationship between sugars and caries in adults. J Dent Res, 95(2): 167-172.
The findings of this longitudinal study among Finnish adults suggest a linear dose-response relationship between sugars and caries, with amount of intake being more important than frequency of ingestion. Also, daily use of fluoride toothpaste reduced but did not eliminate the association between amount of sugars intake and dental caries.

Hong J, Whelton HL, Douglas GVA & Kang J. (2018). Consumption frequency of added sugars and UK children's dental caries. Community Dent Oral Epidemiol, 46:457-464.
Children who consume foods and drinks with added sugar more frequently are more likely to develop dental caries, but higher consumption frequency of drinking water in fluoridated areas might reduce dental caries.

Liska D, Kelley M & Mah E. (2019). 100% fruit juice and dental health: a systematic review of the literature. Front Public Health,7:190.
Prospective cohort studies in children and adolescents found no association between 100% fruit juice intake and tooth erosion or dental caries, but, RCT data in adults suggests that 100% fruit juice could contribute to tooth erosion and dental caries.