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Sugar & Health

Ten years ago the World Health Organisation (WHO) clearly stated that it recognized higher intakes of sugar threatened the nutrient quality of diets by providing significant energy without specific nutrients, and contributed to weight gain[1].

 

"Significant energy without specific nutrients".

 

Overview

Sugars are characterised by the fact they are soluble in water and have a sweet taste[2].  Natural sugars found in the cell wall of fruits and vegetables are known as intrinsic sugars. Refined sugars such as brown and white sugar, treacle, syrup and sugars from fruit juice are known as extrinsic non-milk sugars.  Artificial sweeteners such as sucralose, aspartame and acesulfame potassium are synthetic chemicals[3] and sugar replacements including xylitol and stevia, are natural products but highly processed[4].

 

Do we need sugar?

A varied diet is likely to contain intrinsic sugars in the form of whole fruit, vegetables, dairy products, and grains.  Individuals have no requirement for any carbohydrate from added sugar[5] and excessive consumption of sugar has been linked to several metabolic abnormalities and adverse health conditions[6].

 

An association does not prove causation but stimulates further research into the true causal agent [7]. 

 

Approximately 75% of sugar produced in the UK is sold directly to manufacturers of food, soft drinks and confectionery[8]. In order to more easily identify specific causal agents certain products have been chosen as the focus of research, such as sugar-sweetened beverages (SSB). In the last few months scientists suggest that the totality of evidence is considered (rather than just short term randomised controlled trials) then we should no longer wait for absolute proof, and action should be taken to limit sugar as a source of harm [9],[10],[11].

 

"Limit sugar as a source of harm".

 

Diets high in sugar are associated with:

 

1) Nutrient Inadequacy
Although trends are not consistent for all age groups, reduced intake of calcium, vitamin A, iron and zinc are observed with increasing intake of added sugar.  Intake of sugars is also inversely associated with fibre intake [6].


2) Obesity

Obesity is a complex metabolic disorder with many factors being involved, the wide array of determinants should always be considered[12].

 

For more than ten years scientists have reported correlations between increased sugar intake and obesity [13], [14], [15], [16], [17], and decrease of sugar intake with weight loss [18] with some contradictions and controversy [19], [20].  A recent (2013) systematic review and meta-analysis published in The British Medical Journal concludes, “Intake of free sugars or sugar sweetened beverages is a determinant of body weight” [21].

 

A closer look at the evidence

*Ebbeling et al., (2002) [13] argue that fundamental changes in the social environment are needed to combat childhood obesity and lists six dietary factors including carbohydrate intake, high glycemic index foods and SSB intake.

 

*Elliot et al., (2002) [14] This review discusses three animal studies showing adiposity increases with a high-fructose diet, along with three human studies reporting the effects of fructose consumption on weight gain.

 

*Ludwig et al., (2001) [15]  Observational data showed BMI increased 0.24kg/m2 for each additional serving of SSB (serving classed as one can soda or one glass). In 548 ethnically diverse school children (mean age 11.7 years) over 2 academic years.

 

*Malik & Hu (2011) [16] Discuss the evidence base that shows clear and consistent associations between SSBs, obesity and related cardio-metabolic diseases.  They also discuss the bias and quality of studies funded by the food industry.

 

*Malik et al., (2012) [17] The authors conclude “SSB intake is a significant contributor to weight gain, can lead to increased risk of Type 2 Diabetes Mellitus and cardiovascular disease”.

 

*Ebbeling et al., (2006) [18]  BMI decreased on average by 0.26 kg/m2 for every serving per day of SSB (360ml or 12fl oz).  This 25-week intervention study included 103 adolescents aged 13-18 years.

 

*Gibson (1996) [19]  A cross sectional survey including 2,097 British adults aged 16-64 years, found that sugar had a weak negative association with BMI.

 

*Forshee et al., (2008) [20] A meta-analysis, which found the association between consumption of SSB and BMI near zero.  Authors were affiliated with Coca Cola, Pepsi Co and The American Beverage Association.

 

3) Type 2 Diabetes (T2D)

High-sugar diets are thought to promote weight gain and insulin resistance predisposing to T2D [22].  The Health Professionals Follow-up Study showed high intakes of sugar-sweetened beverages (SSB) increased the risk for type 2 diabetes [23].  Basu et al., 2013 [24] demonstrated that “soft drink consumption is significantly linked to overweight, obesity, and diabetes worldwide.”  Furthermore a recent European study concluded that the consumption of just one sugar-sweetened drink a day increased the risk of type 2 diabetes by 22% [25].  In addition to this, a recent longitudinal cohort study involving 175 countries showed that, for every additional 150 kilocalorie of sugar consumed daily, there was an 11-fold increase in the risk of developing type 2 diabetes, independent of body mass index and physical activity levels [26].

 

4) Cancer

Cancer prevention recommendations first published in 2007, and updated in 2013 by the World Cancer Research Fund in collaboration with the American Institute of Cancer Research (WCRF/AICR) clearly state sugary drinks should be avoided, and foods high in sugar should be limited [27], [28]. 

 

Evidence shows possible risks of increased sugar consumption and pancreatic cancer [29].  Increased risks have been shown with sugar sweetened beverages and prostate cancer by 38% compared to men that consumed no SSB [30].

 

Overall, studies have produced inconsistent findings on the relationship between dietary sugars and ovarian cancer risk.  The most recent study suggests an increased risk associated with sugary drinks but inconclusive evidence between sugary foods [31].

 

Data from more than 30 years ago showed correlation with breast cancer and consumption of refined sugar [32] and in older women a strong correlation was found between breast cancer mortality and sugar consumption [33].  More recent evidence investigating 1,261 women over a period of 13 years showed that high circulating glucose significantly increased the risk of re-occurrence and death in women with breast cancer and suggested that maintaining healthy blood glucose levels may improve prognosis [34].

 

The National Institute of Health and American Association of Retired Persons (NIH-AARP) Diet and Health Study (2012) included a cohort of 435,686 participants. In gender-combined analyses, added sugars were positively associated with risk of esophageal adenocarcinoma, added fructose was associated with risk of small intestine cancer, and all investigated sugars were associated with increased risk of pleural cancers [35].

 

Furthermore, a 2013 publication that included 378,864 participants, from 9 European countries enrolled in the European Prospective Investigation into Cancer and Nutrition study, concluded, “following WCRF/AICR recommendations (which include avoiding sugary drinks and limiting high sugar foods) could significantly increase longevity” [36].

 

5) Tooth Decay

There is consistent evidence of the importance of sugar as a risk factor for tooth decay [37].  Caries risk is greatest if sugars are consumed at high frequency and it has been shown that many groups of people with habitually high consumption of sugars also have high levels of caries [38].

 

6) Cognitive Function

A 2013 review on the impact of diet and human cognition describes the effects of sugar intake on cognitive functions [39].   Sugar consumption leads to impaired glucose tolerance and insulin resistance, which are associated with cognitive impairment in several cross-sectional studies[39].  The negative influence of a high sugar diet intake and risk for Parkinson’s Disease was provided by a retrospective study in which Parkinson Disease patients reported higher consumption of sweets, cookies, chocolate, desserts, sweetened beverages and candy prior to disease onset [40].

 

There is mixed evidence for the role of sugar in hyperactivity [41] nevertheless, whatever the causal factor underlying the association, undertaking a healthy diet may assist in the management of childhood ADHD [39].

 

7) Gut Flora

Changing to a ‘Western diet’ high in sugar affects gut flora within 24 hours [42] increasing C. innocuum, C. difficile and C. perfringes [43] contributing to dysbiosis and affecting intestinal permeability and barrier function [44]. 

 

8) Liver Function

In human studies, fructose is associated with increasing hepatic fat and inflammation, while fructose and sucrose significantly alter hepatic insulin sensitivity and lipid metabolism. Sufficient evidence exists to support clinical recommendations that fructose intake be limited through decreasing foods and drinks high in added sugars [45], [46].

 

9) Cardiovascular Risk

Yudkin and colleagues in the 1960’s [47] and 1970’s [48] as cited by [49] found that a higher intake of sugar was associated with increased Cardiovascular Disease (CVD).  More recently a cross-sectional study in U.S. adults, showed the consumption of caloric sweeteners was associated with increased dyslipidemia [50]. The Framingham Offspring Study found that individuals who consumed more than one soft drink a day had a 22% higher incidence of hypertension and a 22% higher incidence of hypertriglyceridemia compared with non-consumers [51].  The Nurses Health Study I & II found those who drank more than four soft drinks per day had 44% and 28% higher risk of hypertension, respectively compared to infrequent consumers [52].  Furthermore a recent study with healthy young men aged between 19-25 years who consumed low to moderate amounts of SSB’s (containing 40g fructose or 40g glucose per day), observed potentially harmful cardiovascular effects including an increase in LDL particles, fasting glucose levels and high-sensitivity C-Reactive Protein (hs-CRP) within three weeks [53].

 

Emerging...

Sugar consumption has been hypothesised to cause kidney disease and five studies show the risk is elevated.  Due to conflicting data it has been proposed that alternative research designs are used [54].

 

Conclusions

  • Sugar is becoming more widely available through the increased consumption of processed foods. 

  • Increased sugar consumption is associated with a number of adverse health conditions. 

  • The subject remains contentious due to inconsistent findings and powerful economic interests from the sugar industry and their influence on public health policy.

 

British Medical Journal, Opinions - May 2013

“The dietary advice on added sugar is in desperate need of emergency surgery” [5].

 

 

Take home message:

We're sweet enough as we are, and don't need added sugar in our lives. 

 

 

References:

 

[1] World Health Organisation (2003) Diet, Nutrition and the prevention of Chronic Diseases. Available at: [http://www.iaso.org/site_media/uploads/WHO_TRS_916_Diet_nutrition_and_the_prevention_of_chronic_disease..pdf].  Accessed: 30th June 2013.

 

[2] Webb G (2008) Nutrition: A health promotion approach. 3rd Edn. Hodder Arnold, London.

 

[3] Yang Q (2010) Gain weight by “going diet?” Artificial sweeteners and the neurobiology of sugar cravings. Yale Journal of Biology and Medicine 83:2: 101–108.

 

[4] Gupta C, Prakash D, Gupta S, Goyal S (2012) Role of Low Calorie Sweeteners in Maintaining Dental Health. Middle-East Journal of Scientific Research 11:3:342-346.

 

[5] Malhotra (2013) The dietary advice on added sugar needs emergency surgery. British Medical Journal 2013; 346:f3199.

 

[6] Johnson RK, Appel L, Brands M, Howard B, Lefevre M, Lustig R, Sacks F, Steffen L, Wylie-Rosett J (2009) Dietary sugars intake and cardiovascular health: a scientific statement from the American Heart Association. Circulation 120:1011-20.

 

[7] Bowling A (2009) Research Methods in Health 3rd Edn. McGraw-Hill, New York.

 

[8] Department for Environment, Food and Rural Affairs (DEFRA).  Available at: [https://www.gov.uk].

 

[9] Hu F (2013) Resolved: there is sufficient scientific evidence that decreasing sugar-sweetened beverage consumption will reduce the prevalence of obesity and obesity related disease.  Obesity Reviews [Epub ahead of print].

 

[10] Lustig R, Schmidt L, Brindis C (2012) The Toxic Truth about Sugar.  Nature 482:27-29

 

[11] Willett W & Ludwig D (2013) Science Soring on Sugar.  British Medical Journal 2013; 346:e8077.

 

[12] Srinivasan C (2013) Can adherence to dietary guidelines address excess caloric intake? An empirical assessment for the UK.  Economics and Human Biology.  In press – ahead of print.

 

[13] Ebbeling C, Pawlak D, Ludwig D (2002) Childhood obesity: public-health crisis, common sense cure.  Lancet 360:9331:473-482.

 

[14] Elliott S, Keim N, Stern J, Teff K, Havel P (2002) Fructose, weight gain, and the insulin resistance syndrome American Journal of Clinical Nutrition 76:5:911-922.

 

[15] Ludwig D, Peterson K, Gortmaker S (2001) Relation between consumption of sugar-sweetened drinks and childhood obesity: a prospective, observational analysis.  Lancet 357:9255: 505-508.

 

[16] Malik V & Hu F (2011) Sugar-sweetened beverages and health: where does the evidence stand? American Journal of Clinical Nutrition 94:5:1161-1162.

 

[17] Malik V, Popkin B, Bray G, Despres JP, Hu F (2010)  Sugar-sweetened beverages, obesity, type 2 diabetes mellitus, and cardiovascular disease risk.  Circulation 121:1356-1364.

 

[18] Ebbeling C, Feldman H, Osganian S, Chomitz V, Ellenbogen S, Ludwig D (2006) Effects of Decreasing Sugar-Sweetened Beverage Consumption on Body Weight in Adolescents: A Randomized, Controlled Pilot Study. Pediatrics 117:673- 680.

 

[19] Gibson (1996) Are High-Fat, High-Sugar Foods and Diets Conducive to Obesity? International Journal of Food Sciences and Nutrition 47:5:405-415

 

[20] Forshee R, Anderson P, Storey M (2008) Sugar-sweetened beverages and body mass index in children and adolescents: a meta-analysis. American Journal of Clinical Nutrition 87:6:1662-71.

 

[21] 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.  British Medical Journal 2013;346:e7492

 

[22] Moreira P (2013) High-sugar diets, type 2 diabetes and Alzheimer’s disease.  Current Opinions in Clinical Nutrition 16:4:441-445

 

[23] De Koning L, Malik VS, Rimm EB, Willett WC, Hu FB (2011) Sugar-sweetened and artificially sweetened beverage consumption and risk of type 2 diabetes in men. The American Journal of Clinical Nutrition 93:1321–1327

 

[24] Basu S, Martin McKee, MD, DSc, Gauden Galea, MD, and David Stuckler, PhD, MPH (2013) Relationship of Soft Drink Consumption to Global Overweight, Obesity, and Diabetes: A Cross-National Analysis of 75 Countries.  American Journal of Public health. E-view ahead of print.

 

[25] Consumption of sweet beverages and type 2 diabetes incidence in European adults: results from EPIC-InterAct (2013) The InterAct consortium  Diabetologia.

 

[26] Basu S, Yoffe P, Hills N, Lustig RH (2013) The relationship of sugar to population-level diabetes prevalence: an econometric analysis of repeated cross-sectional data. PLoS One 2013;8:e57873.

 

[27] World Cancer Research Fund and American Institute for Cancer Research (2007) Food Nutrition, Physical Activity and The Prevention of Cancer: A Global Perspective.  Available at: [http://www.dietandcancerreport.org].

 

[28] Perera P, Jewell J, Wiseman M (2013) Nutritional Challenges Facing Low Income Countries: World Cancer Research Fund Global Network and Cancer Prevention.  Cancer Control 44-49.

 

[29] Bosetti C, Bravi F, Turati F, Edefonti V, Polesel J, Decarli A, Negri E Talamini R, Franceschi S, Vecchia C, Zeegers M,  (2013) Nutrient-based dietary patterns and pancreatic cancer risk. Annals of Epidemiology 23:3: 124–128

 

[30] Drake I, Sonestedt E, Gullberg B, Ahlgren G, Bjartell A, Wallström P, Wirfält E (2012) Dietary intakes of carbohydrates in relation to prostate cancer risk: a prospective study in the Malmö Diet and Cancer cohort. American Journal of Clinical Nutrition 96:6:1409-1418

 

[31] King M, Olson S, Paddock L, Chandran U, Demissie K, Lu SE, Parekh N, Rodriguez-Rodriguez L,  Bandera E (2013) Sugary food and beverage consumption and epithelial ovarian cancer risk: a population-based case–control study.  BMC Cancer 13:94.

 

[32] Hems G (1978) The Contributions of Diet and Childbearing to Breast-cancer Rates. British Journal of Cancer 37:6: 974–982.

 

[33] Seely S (1983) Diet and breast cancer: The possible connection with sugar consumption. Medical Hypotheses 11:3:319–327 [Abstract only].

 

[34] Contiero P, Berrino F, Tagliabue G, Mastroianni A, Di Mauro M, Fabiano S, Annulli M, Muti P (2013) Fasting blood glucose and long-term prognosis of non-metastatic breast cancer: a cohort study. Breast Cancer Research and Treatment 138:3:951-959

 

[35] Tasevska N, Jiao L, Cross A, Kipnis V, Subar A, Hollenbeck A, Schatzkin A, Potischman N (2012) Sugars in diet and risk of cancer in the NIH-AARP Diet and Health Study. International Journal of Cancer 130:1:159–169,

 

[36] Vergnaud A, Romaguera D, Peeters P, van Gils CH, Chan D, Romieu I, Freisling H, Ferrari P, Clavel-Chapelon F, Fagherazzi G, Dartois L, Li K, Tikk K, Bergmann MM, Boeing H, Tjønneland A, Olsen A, Overvad K, Dahm CC, Redondo ML, Agudo A, Sánchez MJ, Amiano P, Chirlaque MD, Ardanaz E, Khaw KT, Wareham NJ, Crowe F, Trichopoulou A, Orfanos P, Trichopoulos D, Masala G, Sieri S, Tumino R, Vineis P, Panico S, Bueno-de-Mesquita HB, Ros MM, May A, Wirfält E, Sonestedt E, Johansson I, Hallmans G, Lund E, Weiderpass E, Parr CL, Riboli E, Norat T (2013) Adherence to the World Cancer Research Fund/American Institute for Cancer Research guidelines and risk of death in Europe: results from the European Prospective Investigation into Nutrition and Cancer cohort study. American Journal of Clinical Nutrition 97:5:1107-20.

 

[37] Rugg-Gunn A & Murray J (1983) The role of sugar in the aetiology of dental caries: The epidemiological evidence Journal of Dentistry 11:3:190–199

 

[38] Çolak H, Dülgergil C, Dalli M, Hamidi M (2013) Early childhood caries update: A review of causes, diagnoses, and treatments. Journal of Natural Science Biology and Medicine 4:1: 29–38.

 

[39] Francis H, Stevenson R (2013)  The longer-term impacts of Western diet on human cognition and the brain Appetite 63: 119–128.

 

[40] Hellenbrand W, Seidler A, Boeing H, Robra, BP, Vieregge P, Nischan P, Joerg J, Oertel H, E. Schneider E, Ulm G (1996) Diet and Parkinson's disease I: A possible role for the past intake of specific foods and food groups: Results from a self-administered food-frequency questionnaire in a case-control study. Neurology 47:3:636-643.

 

[41] Johnson R, Gold M, Johnson D, Ishimoto T, Lanaspa M, Zahniser N, Avena N (2011) Attention-Deficit/Hyperactivity Disorder: Is it Time to Reappraise the Role of Sugar Consumption? Postgraduate Medicine 123:5: 39–49.

 

[42] Turnbaugh P, Ridaura V, Faith J, Rey F, Knight R, Gordon J (2009) The Effect of Diet on the Human Gut Microbiome: A Metagenomic Analysis in Humanized Genotobiotic Mice. Science of Translational Medicine 11:1:6.

 

[43] Fukuda S, Toh H, Hase K et al., (2011) Bifidobacteria can protect from enteropathogenic infection through production of acetate. Nature 469: 543–7.

 

[44] Hold (2013) Western lifestyle: a ‘master’ manipulator of the intestinal microbiota?  Gut [Epub ahead of print]

 

[45] Aeberli I, Hochuli M, Gerber P, Sze L, Murer S, Tappy L, Spinas G, Berneis K, (2013) Moderate Amounts of Fructose Consumption Impair Insulin Sensitivity in Healthy Young Men: A randomized controlled trial. Diabetes Care 36:1:150-156

 

[46] Vos M & Lavine J (2013) Dietary fructose in nonalcoholic fatty liver disease.  Hepatology 57:6:2525-2531

 

[47] Yudkin J (1967) Sugar and ischaemic heart disease. Practitioner 198:187:680-3.

 

[48] Yudkin J (1978) Dietary factors in atherosclerosis: sucrose. Lipids 13:370–372.

 

[49] Howard B & Wylie-Rosett J (2002) Sugar and Cardiovascular Disease: A Statement for Healthcare Professionals From the Committee on Nutrition of the Council on Nutrition, Physical Activity, and Metabolism of the American Heart Association.  Circulation 106:4:523-527.

 

[50] Welsh JA, Sharma A, Abramson JL, Vaccarino V, Gillespie C, Vos MB (2010) Caloric sweetener consumption and dyslipidemia among US adults. JAMA 303:1490–1497

 

[51] Dhingra R, Sullivan L, Jacques P, Wang T, Fox C, Meigs J, D'Agostino R, Gaziano J, Vasan R (2007) Soft drink consumption and risk of developing cardiometabolic risk factors and metabolic syndrome in middle aged adults in the community.  Circulation 116:480-488

 

[52] Winkelmayer W, Stampfer M, Willett W, Curhan G (2005) Habitual caffeine intake and the risk of hypertension in women.  The Journal of the American Medical Association 294:2330-2335.

 

[53] Aeberli I, Gerber P, Hochuli M, Kohler S, Haile S, Gouni-Berthold, Berthold H, Spinas G, Berneis K (2011) Low to Moderate sugar sweetened beverage consumption impairs glucose and lipid metabolism and promotes inflammation in healthy young men: a randomised controlled trial. American Journal of Clinical Nutrition 94:479-485.

 

[54] Karalius V & Shoham D (2013) Dietary Sugar and Artificial Sweetener Intake and Chronic Kidney Disease: A Review. Advances in Chronic Kidney Disease 20:2:157–164.

 

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