Sugar, Sweeteners and Public Health: choices, recommendations, taxes Professor Mike Lean Human Nutrition, University of Glasgow 17-19 th November 2016 2nd Nutrition Conference, Dubai
This Lecture is about sweetness
This Lecture is about sweetness
Low Caloric Sweeteners
Glasgow, Scotland
Jamaica Glasgow history: ships, sugar, tobacco
Glasgow history: ships, sugar, tobacco
Sweet Tooth Innate? Or Acquired? Survival value in infancy Human milk is very sweet Sweet Tooth normally persists in childhood Palate normally changes at puberty, to prefer savoury/ umami/ sour/ salt tastes Over-ridden by tolerance to very sweet foods and drinks, through constant exposure into adulthood Possible contributor to obesity? In some studies obese people prefer sweeter tastes and sweet high-fat foods
Sweet tooth reconsidered: Taste responsiveness in human obesity Drewnowski et al, Physiology & Behavior, 35,, 617 622 (1985) BMI <25: preferred foods with 20% lipid and <10% sucrose BMI >30: preferred high-fat (>34% lipid) with <5% sucrose Post-obese: enhanced responses to both sugar and fat Preferred sugar/fat ratio was inversely correlated with BMI We hypothesize that sensory preferences for dietary sugars and fats are determined by body-weight status and may affect the patterns of food consumption. Self-reported preferences may be biased Drenowski works for Nestle..
The group preferring fast food preferred sweet tastes, members of the other group preferred a savory taste The group preferring fast food Consumed an inadequate volume of food, and had an irregular and unbalanced diet. Their intake of green vegetables, vegetables, protein foods, and seaweed was significantly lower than that of the other groups. The food habit score was lower, with irregular meal times and unbalanced diets.
Sweet food and drink taste preference in pregnancy Reduced liking for sweet taste in normal pregnancy Tepper BJ, Seldner AC. Am J Clin Nutr. 1999 Higher hedonic ratings for sweet taste in Gestational Diabetes, related to elevated leptin and insulin concentrations Belzer LM, Smulian JC, Lu SE, Tepper BJ. Chem Senses. 2009
Sweet Tooth is associated with alcohol addiction Preference for a high-concentration sucrose solution in alcoholic men Kampov-Polevoy, et al. Am J Psychiatry 1997
Sugars are sweet Table sugar (sucrose) = glucose + fructose All life on earth depends on sunlight and photosynthesis, making sucrose Sugars includes lactose, in milk and dairy products = glucose + galactose
Assesssing sugar consumption, to relate to diseases, is difficult Many different sugars Present naturally in many foods with health value, and others with health hazards Natural sucrose is exactly the same as added, refined sucrose Added sugar is added to very many foods, and consumers often do not know Distinguishing sugar-sweetened and artificiallysweetened food and drinks can be difficult
Beliefs about possible hazards from sugar and sweeteners often distort the evidence Introduction of sugar in 17 th & 18 th century gave sweetness to common people. Upset the social order and religious control Neophobia is common: accused of causing many diseases, especially type 2 diabetes, and moral corruption Aggressive, intrusive, commercial practices by Big Food companies attracted opposition from articulate media critics Quasi-scientific rationales for hazards, selective use of data, inadequate statistical rigour
Sugar intake and blood glucose Sugar /sucrose MEDIUM-LOW GLYCAEMIC INDEX Sugar /sucrose only elevates blood glucose abnormally if there is ectopic fat in liver and pancreas: Metabolic syndrome Fructose Powell K et al, Am J Clin Nutr 2002; 76:5-56 International Table of Glycemic Index and Glycemic Load Values Chung et al Meta-analysis Am J Clin Nutr 2014
Dietary sugar does not cause diabetes, but SSB do: it is the pattern of eating UK SACN report 2014 c.f. Mann and Te Morenga
Sugar has no direct effect on diabetes, independent of body-weight
Current sucrose consumption c.10% dietary energy Is there a problem with that?
Self-reported data Low CHD-risk population Low SSB consumption Big differences in smoking, alcohol and education with high SSB Adjusted for BMI, not for body fat, or muscle
Existing dietary guidelines to restrict Sugars haven t done much
Further reductions? COMA DRVs 1991: Free sugar<10% total diet energy (population average) US IoM 2005: Added sugars <25% E (individuals) AHA 2014 : Zero-100/150kcal/d (5%E for individuals) (Free sugars half of discretionary calories ) WHO 2015 Free sugars <10%E,<5%E (individuals) SACN 2014 <5% total diet energy (population average) (draft proposal) all individuals <10% E Diabetes UK 2011: ` Focus should be on total energy intake rather than the source of energy in the diet (macronutrient composition) for optimal glycaemic control. (A evidence)
Sugars and Body weight? Possible effect size 0.8kg No evidence for a limit of <10%E or <5%E on body weight change (evidence only dental health)
Dietary sugars and body weight: systematic review and meta-analyses of randomised controlled trials and cohort studies (Te Morenga L 1, Mallard S, Mann J. BMJ 2012) Effect of increasing free sugars on measures of body fatness in adults: <1kg (>8 weeks 2.7kg) Funnel plot of randomised ad libitum trials in adults: evidence of publication bias
Iso-energetic exchanges of free sugars with other carbohydrates or other macronutrient sources Te Morenga L, Mallard S, Mann J. BMJ 2012 No effect on body weight So, Weight gain with SSBs is NOT from the sugar itself. But from patterns of eating and drinking marked by, and probably aggravated by, sweet drinks
Overweight/obesity in children is associated with sugar-sweetened beverages consumption (Te Morenga L, Mallard S, Mann J. BMJ 2012) error: Weight gain with SSBs, not with free sugars SSBs
Zoe and the Yudkin/ Lustig/ McGregor/ Malhotra/ Schofield/ Noakes anti-sugar Band-wagon
Robert Lustig s 3 big fallacies 1. "Sugar causes diseases: unrelated to their calories and unrelated to the attendant weight gain. It's an independent primary-risk factor. 2. Losing the weight doesn't, long-term, solve the metabolic syndrome the addiction to sugar of which obesity is symptomatic. 3. Telling people to simply lose weight is physiologically impossible and it's clinically dangerous. It's a goal that's not achievable.
1. Zoe s favourite paper Greater consumption of sugary drinks is (just) associated with more frequent T2DM (Lustig et al) Data were adjusted for BMI (r 2 reduced) NOT adjusted for greater body fatness/obesity or lower muscle mass Lustig s conclusion is wrong: - Residual confounding from fatness
Sugar Sweetened Beverages and BMI-adjusted risk of diabetes in EPIC-Interact (Europe) Without BMI adjustment With BMI adjustment Romaguera-Bosch et al. Diabetologia 56:1520, 2013
2. Addiction is a normal physiological mechanism, to eating - not to sugar
Low and Non-Caloric Sweeteners have been evaluated by major national and international regulatory authorities They can safely be consumed as part of a balanced diet
Displacement of calories from sugary foods and beverages with low-calorie sweeteners leads to weight loss: Meta-analysis of 15 RCTs N = 1951, men & women Duration = 3 to 78 weeks Mean effect = -0.8 kg Miller and Perez. Am J Clin Nutr 2014;100:765 77
Displacement of calories from SSBs with LCSBs (sucralose & Ace-K): less weight gain in children in the completers but not ITT analysis DRINK trial, n=641, follow-up =18 months
Are artificial Sweeteners also associated with weight gain? a systematic review Brown R. et al, Int J Pediatr Obes. 2010 Eighteen studies were identified. Large, epidemiologic studies show an association between artificially-sweetened beverage consumption and weight gain in children. REVERSE CAUSALITY? Randomized controlled trials do not clearly demonstrate either beneficial or adverse metabolic effects of artificial sweeteners. THE PATTERN OF EATING WITH SNACKING IS CAUSING OBESITY NOT THE SWEETENER ITSELF
Low-Calorie Sweetener and Energy Balance (Fowler, Physiology and Behaviour 2016) Animals: greater weight gain and visceral fat (especially in males) given water with sucralose, aspartame, saccharin, cyclamate Most marked when together with high-sugar high-fat diets Interaction with monosodium glutamate Humans: Saccharin users gain more weight (Stellman & Garfinkel 1986, Colditz 1990) San Antonio Heart study, artificially sweetened drinks associated with weight and waist gain Diet sodas relate to incident CVD: hypertension, diabetes, lipids Reverse causality NOT fully excluded: People with known diseases or risks avoid sodas Most human studies are in women but not all
Low-Energy Sweetened (LES) beverages systematic review (Roger et al IJO 2015) Animal studies: Compulsory feeding ( LES in drinking water) No effect on weight Optional LES (water also available) Sweetened drink alone - no effect Sweetened food too - eat more and gain weight
Low-Energy Sweetened (LES) beverages systematic review (Roger et al IJO 2015) No effect of LES on weight
Low-Energy Sweetened (LES) beverages systematic review (Roger et al IJO 2015) Short-term human studies: LES reduces energy consumption, but with some compensation for reduced energy density of foods Longer term human studies: less weight gain with LES vs sugar no effect vs water
How to resolve the confusing evidence Obesity is being driven by Excessive frequency (grazing, snacking) and portion sizes Of snacks and meals high in both sugar (4kcal/g) and fat (9kcal/g) Unnatural levels of sweetness in drinks and foods, perpetuating a sweet tooth and pushing up demand for sweet snacks Non-caloric sweeteners will reduce energy intakes in short term, and restrict weight gain by c 1kg But long-term, constant normalised exposure to very sweet drinks leads to tolerance, and may increase energy intakes from sweet and fatty foods. So replacing SSBs with diet versions helps but is not sufficient
New York Times 2 October 2015 People have already twigged! Very sweet food and drink is no longer fashionable or cool
Conclusions: To improve public health and reduce obesity Individuals vs weight gain: Put a proper effort behind existing <10% dietary recommendations Teach the importance of balancing all the nutrients which make up healthful diets, and meals Same for people with or without diabetes Use low-calorie sweeteners, but prefer unsweetened water, tea etc Public Health vs obesity epidemic: Limit sweetness globally (not just sugar, not just drinks) Tax (heavily) before banning: all drinks with (progressively) >8% added sugar And those with equivalent sweetness NOT an obsessive, quasi-religious, focus on sugar alone NOT an unworkable*, non-evidence-based, <5%E target
l bottle of 10% sugar Irn Bru (or Cola drink) = 400kcal
Solutions: Replace with 0%, sweetened or Replace with 0%, unsweetened l bottle of 10% sugar Irn Bru (or Cola drink) = 400kcal
Conclusions: To improve public health and reduce obesity Individuals vs weight gain: Put a proper effort behind existing <10% dietary recommendations Teach the importance of balancing all the nutrients which make up healthful diets, and meals Same for people with or without diabetes Use low-calorie sweeteners, but prefer unsweetened water, tea etc Public Health vs obesity epidemic: Limit sweetness globally (not just sugar, not just drinks) Tax (heavily) before banning: all drinks with (progressively) >8% added sugar And those with equivalent sweetness Include juices which are not 100% fruit juice, flavoured dairy drinks, etc To prevent obesity, we need less between-meal snacks and reduced sweetness of snacks and other foods
UK proposed SSB taxation from 2017
Published November 2016 Concise, easy to read
2013-2018 3. People with type 2 diabetes can lose weight, and get rid of their diabetes funded by DiABETES UK to Mike Lean and Roy Taylor Results Dec 2017 Cluster-Randomised Trial: Counterweight-Plus* 810kcal/d LELD and weight maintenance programme vs usual care Both arms follow current clinical guidelines, in primary care 306 patients, BMI >27, diagnosed T2DM <6 years, not on insulin Co-primary endpoints: weight loss >15kg and non-diabetic HbA1c at 12 & 24 months off all drugs (plus life-long clinical monitoring) Mechanistic and Magnetic Resonance studies Qualitative and process evaluation Planned economic analyses * Supported by Cambridge Weight Plan GP data at 12 months: c. 50% have lost >15kg c. 40% have become non-diabetic - off all antidiabetic drugs
2013-2018 funded by DiABETES UK to Mike Lean and Roy Taylor Results Dec 2017 Cluster-Randomised Trial: Counterweight-Plus* 810kcal/d LELD and weight maintenance programme vs usual care Both arms follow current clinical guidelines, in primary care 306 patients, BMI >27, diagnosed T2DM <6 years, not on insulin Co-primary endpoints: weight loss >15kg and non-diabetic HbA1c at 12 & 24 months off all drugs (plus life-long clinical monitoring) Mechanistic and Magnetic Resonance studies Qualitative and process evaluation Planned economic analyses * Supported by Cambridge Weight Plan GP data at 12 months: c. 50% have lost >15kg c. 40% have become non-diabetic - off all antidiabetic drugs
ECO Glasgow April 2019 European Congress on Obesity Published November 2016 Concise, easy to read