Caloric Sweeteners and Health: What is the Truth?
- G. Harvey Anderson
Professor Departments of Nutritional Sciences and Physiology Faculty of Medicine, University of Toronto. November 2 , 2016
Caloric Sweeteners and Health: What is the Truth? G. Harvey - - PowerPoint PPT Presentation
Caloric Sweeteners and Health: What is the Truth? G. Harvey Anderson Professor Departments of Nutritional Sciences and Physiology Faculty of Medicine, University of Toronto. November 2 , 2016 Conflicts o of Interest Consultant to many
Professor Departments of Nutritional Sciences and Physiology Faculty of Medicine, University of Toronto. November 2 , 2016
associations.
Travenol, EliLily, PepsiCo, Kraft, Alliance for Potato Research and Education, American Beverage Association,Winston Strawn LLP
McDonalds, Hillshire Brands, Unilever, Heinz, ADM, Healthy Grains Institute, Canadian Sugar Institute.
Regulatory Affairs (15 Food Industry Members)
based on preventing the displacement of foods that are major sources of essential micronutrients
that added sugars negatively impacts the health risks for obesity, type II diabetes, cardiovascular disease and dental carries
energy (strong recommendation) Based on moderate quality evidence from
Based on very low quality evidence from ecological studies
Results from a failure to achieve energy balance Unclear whether obesity develops in susceptible individuals because physiological mechanisms of food intake control are compromised first
the environment and become compromised
(Ebbeling et al, JAMA 2004)
The WHO's nutrition director, Dr Francesco Branca, said "nutritionally, people don't need any sugar in their diet". October 2016
declined in 20 years
caloric sweetener consumption and see public support in taking action.
John L Sievenpiper, MD, PhD, FRCPC1,2,3,4
1Associate Professor, Department of Nutritional Sciences, University of Toronto 2Consultant Physician, Division of Endocrinology & Metabolism, St. Michael’s Hospital 3Scientist, Li Ka Shing Knowledge Institute, St. Michael’s Hospital 4Knowledge Synthesis Lead, Toronto 3D Knowledge Synthesis Unit, St. Michael’s Hospital
October 21, 2016
http://www.sign.ac.uk/guidelines/fulltext/50/annexb.html http://www.cnpp.usda.gov/Publications/NutritionInsights/Insight38.pdf http://www.nice.org.uk/niceMedia/pdf/GDM_Chapter7_0305.pdf
Systematic Reviews & meta-analyses RCTs Non-randomized controlled trials (NRCT) Cohorts studies Case-control studies Cross-sectional studies Case series/time series Expert opinion
Decreasing bias
13 cohort comparisons, n=108,170 (14,752 cases)
Relative Risk: 0.88 [0.74, 1.06] p = 0.17
Tsilas et al., CMAJ, under review
Benefit harm
Risk ratio IV random, 95% CI
6 cohort comparisons, n=107,972 (3,833 cases)
Relative Risk: 1.04 (0.84, 1.29) p = 0.72
Tsilas et al., CMAJ, under review
Benefit harm
Risk ratio IV random, 95% CI
8 cohort comparisons, n=192,332 (4,535 cases)
High BMI = Body Mass Index ≥ 29 kg/m2 Low BMI = Body Mass Index < 29 kg/m2
Relative Risk: 0.89 (0.80, 0.98) p = 0.02
Tsilas et al., CMAJ, under review
Benefit harm
Risk ratio IV random, 95% CI
Meta-analysis of 17 cohorts, N=464,937 (38,253 cases), FU=12y (3-21y)
Unadjusted for adiposity Adjusted for adiposity Adjusted for adiposity & within person variation Imamura et al. BMJ. 2015 Jul 21;351:h3576. RR= 1.28 (1.12-1.46) RR=1.27 (1.10-1.46)* RR= 1.18 (1.09-1.28) RR= 1.13 (1.06-1.21) *Calibrated for publication bias
Mozaffarian et al. NEJM 2011;364:2392-2404
+3.35lb +1.69lb +0.57lb +1.00lb +0.95 lb +0.28 to 0.36lb +0.65lb
Increased servings of different foods contribute to weight change over 4 year intervals:
NHS I (1986-2006), NHS II (1991-2003) and HPFS (1986-2006), N=120 877
+0.93 lb
**Multivariate adjustment for age, BMI, sleep, physical activity, alcohol, television watching, smoking, and all dietary factors**
Mozaffarian et al. NEJM 2011;364:2392-2404
Increased servings of different foods contribute to weight change over 4 year intervals:
NHS I (1986-2006), NHS II (1991-2003) and HPFS (1986-2006), N=120 877
**Multivariate adjustment for age, BMI, sleep, physical activity, alcohol, television watching, smoking, and all dietary factors**
Summary of 5 systematic reviews and meta-analyses or individual prospective cohort studies
Sievenpiper et al. Can J Diabetes. 2016 Aug;40(4):287-95
Benefit Harm Food source of sugars Cohort comparisons Participants Cases Median Follow-up Risk ratios (95% CIs) I2 Fried foods [104] Processed meat [105] SSBs [14] French fries [106] High GI diet [107] Red meat [105] Potatoes [106] High GL diet [107] 2 9 17 1 20 10 1 30 111,631 371,492 464,937 84,555 394,039 442,101 84,555 710,314 10,323 26,256 38,253 4,496 35,715 28,228 4,496 46,115 25y 14y 12y 20y 11y 14y 20y 11y 1.55 (1.32 to 1.83) 1.51 (1.25 to 1.83) 1.28 (1.12 to 1.46) 1.21 (1.09 to 1.33) 1.19 (1.14 to 1.24) 1.19 (1.04 to 1.37) 1.16 (1.05 to 1.29) 1.13 (1.08 to 1.17)
73%*
93%*
0.5 1 1.5 2
“Substitution trials”= Energy from sugars substituted for
“Addition trials”= Energy from sugars “added” to the diet “Subtraction trials” = Energy from sugars “subtracted” from the diet Ad libitum trials = Energy from sugars is freely replaced with other macronutrients
Sugars mediate weight change through excess calories
Te Morenga et al. BMJ. 2012;345:e7492 Kaiser et al. Obes Rev. 2013 Aug;14(8):620-33. Malik et al. AJCN. 2013 Oct;98(4):1084-102.
1. It is difficult to separate the contribution of fructose-containing sugars from that
2. Any threshold for the effect of sugars on body weight and cardiometabolic risk is highly dependent on energy balance, nutrient adequacy (food sources). 3. There are many pathways to overconsumption leading to weight gain and
influence on weight gain and cardiometabolic risk and represent the best
4. Targeting sugars as a source of excess calories remains a prudent strategy, as sugary foods and beverages can be a proximate pathway to overconsumption. 5. One cannot choose a healthy diet by sugars alone! A little sugar helps the wholegrains, fibre, fruits, and dairy/non-dairy alternatives to go down.
Is the evidence enough for setting policy and regulations?
Garcia-Bailo et al., OMICS, 13:69-80, 2009
Visit 1
Thr/Thr Thr/Ile + Ile/Ile 50 75 100 125
86 g 112 g
Genotype Sugars (g/d)
P= 0.01
Visit 2
Thr/Thr Thr/Ile + Ile/Ile 50 75 100 125
82 g 111 g
Genotype Sugars (g/d)
P= 0.003
Eny et al., Physiol. Genomics, 33:355-60, 2008
Thr/Thr Thr/Ile + Ile/Ile 100 125 150
115 g 131 g
Genotype Sugars (g/d)
P= 0.007
Eny et al., Physiol. Genomics, 33:355-60, 2008
Food intake: No Effect of Beverage on Meal Intake.
Values are means ± SEM; n=29.
600 650 700 750 800 850 900 950 1000 1050 Water 1% Milk Orange Juice Regular Cola Diet Cola Food Intake (kcal)
Panahi et al. (2013) Appetite 65: 75-82.
Values are means ± SEM; n=29. Means with a different superscript letters are significantly different, P<0.05 (treatment effect using proc mixed, Tukey’s post hoc).
Adults: All caloric beverages with meals add calories, but milk results in the lowest post-prandial glucose
50 100 150 200 250 300 Water 1% Milk Fruit Drink Regular Cola Diet Cola
Blood Glucose AUC (mmol/L * min)
c a ab bc ab
200 400 600 800 1000 1200 1400 Water 1% Milk Orange Juice Regular Cola Diet Cola
Total Caloric Intake (Kcal)
b a b b a Panahi et al. (2013) Appetite 65: 75-82.
Values are means ± SEM; n=32. Means with different supers script letters are significantly different. One-way ANOVA (Drink; P < 0.001) S Vein (MSc Thesis) n Presss APNM 2016
All caloric beverages consumed ad libitum during a meal add to total meal-time energy intake, but 1% milk favours a lower post- meal blood glucose and subjective appetite score and adds to nutrient intake.
Panahi et al. (2013) Appetite 65: 75-82.
based on preventing the displacement of foods that are major sources of essential micronutrients
that added sugars negatively impacts the health risks for obesity, type II diabetes, cardiovascular disease and dental carries
energy (strong recommendation) Based on moderate quality evidence from
Based on very low quality evidence from ecological studies
NUTRITION LABEL CHANGES IN THE U.S.
Added Sugars Mandatory
52
Mary R. L’Abbé, PhD
Earle W. McHenry Professor and Chair, Department of Nutritional Sciences
Professor Departments of Nutritional Sciences and Physiology Faculty of Medicine, University of Toronto. November 2 , 2016