In his extremely popular video “Sugar: The Bitter Truth,” watched on YouTube more than 3,300,000 times, Dr. Lustig makes the following key assertions:
- Excess intake of sugar (sucrose or HFCS) is bad for us
- Not all calories are equal; especially with respect to the intake of fat versus carbohydrates (calories from carbs are worse)
- Some sugars are worse than others (e.g., fructose is worse then glucose)
- Sugar-containing beverages should be classified as NON GRAS (Generally Regarded as Safe) by the FDA
While I agree with the first assertion, that excess intake of sugar as a source of calories is bad for us; I also believe that excess calories from any source are bad.
I disagree with the second assertion that Dr. Lustig reinforces with the argument that by reducing intake of fat and replacing it with sugars somehow caused the diabetes epidemic. Are we really to believe that daily three meals at McDonald, even while avoiding sugary beverages and sauces, but eating high fat burgers with bacon and cheese, or daily indulgence with bacon, bread and butter will not lead to obesity and the resultant consequences, so long as no or little sugar is ingested?
The third assertion that somehow fructose is the bad guy and glucose is just fine, or as stated: “Fructose, a poison by itself” has not been substantiated by any clinical study. Most publicly available studies have compared sucrose to HFCS, (that is a 50/50 combination of fructose and glucose vs. a 55 % fructose or a 42 % fructose combination).
While I don’t encourage people to drink sugary beverages, I disagree with the fourth assertion that sugar containing beverages should be classified as non GRAS (Generally Regarded as Safe) by the FDA. Food or food additives are usually classified as non GRAS when normal consumption, in and of itself is harmful, not when excessive intake is harmful. Instead of regulating the supply of the drinks we should be reducing the demand by educating the consumers and providing them with appropriate tools that can educate consumers about all the ingredients in their food and beverages, such as the FoodSmart app, to eat healthily.
It had been suggested in this video and other places that increased intake of sugar, and in particular fructose, are deleterious to health, especially by increasing obesity and diabetes. Such deleterious effects are claimed to exceed those from excess caloric intake from other sources. However, the data to date is equivocal. Data in animals (not cited here) are also very inconclusive despite the quote in the video, which in general tend to select the confirming studies and ignore the contradictory studies. Certainly caloric intake in excess of what is needed will lead to obesity and possibly to diabetes and it is easier to consume calories through soft drinks, but this does not justify the above conclusions and certainly should not lead to legislation to outlaw consumption of sweetened beverages (and fruit juices which are included in this category and have similar effect to sugary beverages). Food or food additives are usually classified as non-GRAS when normal consumption in and of itself is harmful, not when excessive intake is harmful. If we start going down this road than all desserts will be classified as non-GRAS, including ice cream and cakes. And why stop there? Let’s also classify as non-GRAS butter, bleached carbohydrate, eggs, beef…any of those can be harmful when eaten in excess. At some point we must take responsibility for our (and our children’s) actions through education rather than have the food police dictate our life. The FoodSmart app can help you select the healthiest foods to eat healthily, so start your journey today.
The Main Arguments
(Read further to understand my position and it’s scientific backing)
Are some sugars worse than others?
In the United States, consumer foods and products typically use HFCS (high-fructose corn syrup) as a sweetener. It has become very common in processed foods and beverages in the U.S., including breads, cereals, breakfast bars, lunch meats, yogurts, soups, and condiments. Yet from the nutritional point of view only sugary beverages add significant amount to the diet.
HFCS consists of 24% water, and the rest sugars. The most widely used varieties of high-fructose corn syrup are: HFCS 55 (mostly used in soft drinks), which is approximately 55% fructose and 42% glucose; and HFCS 42 (used in beverages, processed foods, cereals and baked goods), which is approximately 42% fructose and 53% glucose. In contrast, corn syrup contains no fructose at all but rather varying amounts of maltose and higher oligosaccharides, depending on the grade. It is converted into HFCS by enzymatic processing. Thus any increase in fructose counts as HFCS.
Reviewing the actual scientific evidence supporting fructose as the villain in the epidemic of obesity yields a vastly different picture than the one presented in the video. Note that, despite the video citing all kinds of data about the harmful effects of fructose, it simultaneously states that, (since sucrose is 50% fructose) “sugar is sugar.”
Indeed, in a study of 59,000 African American women, regular consumption of two or more sugar-sweetened soft drinks and fruit drinks a day was associated with an increased risk of type 2 diabetes mellitus in African American women. The association of diabetes with soft drink consumption was almost entirely mediated by body mass index; whereas the association with fruit drinks consumption was independent of body mass index.1
Another quoted study removed soft drinks from the diet and showed weight loss. However, it is not clear whether that finding was simply due to decreased overall calories, or solely the elimination of the sodas.
Another quote comes from the Nurses’ Study where increased intake of sugary beverages was associated with increased weight. The first problem with this study is that it is an uncontrolled observational study that only collected intake data at the beginning of the study rather than during the many years of the study.
Even allowing for that, the actual study showed that overall, over four years, there was an average gain of 1.45 Kg. Each daily cup of water reduced that weight gain by 0.13 Kg, and each daily sugar sweetened drink increase that weight by 0.36 Kg and fruit juice increased it by 0.22 Kg, OVER THE FOUR YEARS! Hardly an obesity epidemic even if one drinks four sugary drinks a day. 2
Epidemiology of sugar obesity and diabetes:
Let’s look at cross country epidemiology first. The study by Goran compared intake of fructose to incidence of obesity. 3 It concluded that countries with higher availability of HFCS have a higher prevalence of type 2 diabetes, independent of obesity.
However, Marriott evaluated fructose consumption and overall caloric intake from the MHANES database and noted that sweetener availability increased from 1978, peaked in 1999 and decreased through 2005. Total fructose as percent of carbohydrates increased by only 1.2% whereas energy and total carbohydrates increased by 18% and 41%. They note that although comparison of estimates of fructose intakes between data from the 1977-1978 NFCS and the NHANES 1999-2004 showed an increase, this increase was dwarfed by greater increases in total daily energy and carbohydrate intakes. 4
Barclay at al noted the Australian paradox. They note that between 1980 and 2003, when all sources of nutritive sweeteners, including high fructose corn syrups, were considered, per capita consumption decreased in Australia (-16%) and the UK (-5%), but increased in the USA (+23%). In Australia, there was a reduction in sales of nutritively sweetened beverages by 64 million liters from 2002 to 2006 and a reduction in percentage of children consuming sugar-sweetened beverages between 1995 and 2007. Yet the prevalence of obesity in Australia increased three fold during that time! 5.
Gross evaluated per capita nutrient consumption in the United States between 1909 and 1997, obtained from the US Department of Agriculture, and compared this with the prevalence of type 2 diabetes obtained from the Centers for Disease Control and Prevention. Moderate correlation was found between corn syrup consumption and type 2 diabetes.6 Similarly, Montonen examined a cohort of 4304 adults aged 40-60 for 12 years and found increase risk of diabetes with “combined intake of fructose and glucose” but oddly not with not with sucrose intake due to increased intake of sweetened berry juice and soft drinks. 7 Other recent data shows a decrease in intake of sugary beverages since 2005 by about 30%.
Data from 25,506 subjects, aged 12-80 yrs., contained in the NHANES 1999-2006 databases were analyzed for sugar intakes and health parameters. They concluded that dietary fructose was almost always consumed with other sugars. On average, fructose provided 37% of total simple sugar intake and 9% of energy intake. In more than 97% of individuals studied, fructose caloric contribution was lower than that of non-fructose sugars. Fructose and non-fructose sugar intakes had no positive association with blood concentrations of TG, HDL cholesterol, glycohemoglobin, uric acid, blood pressure, waist circumference, and BMI in the adults studied 8
An interesting observation was by Shao, comparing the relationship between food type consumption and rising obesity using the loss-adjusted food availability data from the United States Department of Agriculture (USDA) Economic Research Services (ERS) as well as the obesity prevalence data from the Behavioral Risk Factor Surveillance System (BRFSS) and the National Health and Nutrition Examination Survey (NHANES) at the Centers for Disease Control and Prevention (CDC). Their analysis showed that total calorie intake and consumption of high fructose corn syrup (HFCS) did not correlate with rising obesity trends. Their results surprisingly revealed that consumption of corn products correlated with rising obesity and was independent of gender and race/ethnicity among population dynamics in the U.S. 9
Other reviews and Meta analyses of obesity and DM
White, et al, reviewed the use of HFCS vs. sucrose in the world. Although HFCS use today is nearly equivalent to sucrose use in the United States, we live in a decidedly sucrose-sweetened world: >90% of the nutritive sweetener used worldwide is sucrose. They reviewed the history, composition, availability, and characteristics of HFCS in a factual manner to clarify common misunderstandings that have been a source of confusion to health professionals and the general public alike. In particular, they evaluate the strength of the popular hypothesis that HFCS is uniquely responsible for obesity. Although examples of pure fructose causing metabolic upset at high concentrations abound, especially when fed as the sole carbohydrate source, there is no evidence that the common fructose-glucose sweeteners do the same. Thus, studies using extreme carbohydrate diets may be useful for probing biochemical pathways, but they have no relevance to the human diet or to current consumption. They conclude that the HFCS-obesity hypothesis is neither supported in the United States nor worldwide.10,11
A meta-analysis of controlled feeding studies, including 31 isocaloric diets and 10 hypo caloric diets concluded that most were of poor quality, short (less than 12 weeks) and small (less than 15 patients). Fructose had no overall effect on body weight in isocaloric trials. High doses of fructose in hyper caloric diets lead to increased weight. Thus fructose does not seem to cause weight gain when substituted for other CH. The increased weight with high doses of fructose is likely due to the extra calories.12
In a meta-analysis a literature search was conducted for relevant randomized and controlled intervention studies of crystalline or pure fructose (excluding high-fructose corn syrup). Fructose intake < 90 g/d significantly improved HbA(1c) concentrations dependent on the dose, the duration of study, and the continuous severity of dysglycemia throughout the range of dysglycemia. There was no significant change in body weight at intakes <100 g fructose/d. Fructose intakes of <50 g/d had no postprandially significant effect on triacylglycerol and those of <or=100g/d had no significant effect when subjects were fasting. At >or=100 g fructose/d, the effect on fasting triacylglycerol depended on whether sucrose or starch was being exchanged with fructose. The meta-analysis shows that fructose intakes from 0 to >or=90 g/d have a beneficial effect on HbA(1c). Significant effects on postprandial triacylglycerols are not evident unless >50 g fructose/d is consumed, and no significant effects are seen for fasting triacylglycerol or body weight with intakes of <or=100 g fructose/d in adults.13
An expert panel was convened in 2007 by The Center for Food, Nutrition, and Agriculture Policy to discuss the published scientific literature examining the relationship between consumption of HFCS or “soft drinks” (proxy for HFCS) and weight gain. They concluded that evidence from ecological studies linking HFCS consumption with rising BMI rates is unreliable. Evidence from epidemiologic studies and randomized controlled trials is inconclusive. Studies analyzing the differences between HFCS and sucrose consumption and their contributions to weight gain do not exist.14
Stanhope again reviewed the literature and concluded that there is evidence for effects of fructose intake on lipid profile (primarily TG) but the evidence demonstrating that the commonly consumed sugars increase visceral adipose deposition, DNL, and insulin insensitivity is limited or inconclusive.15
The most recent report by Te Morenga in January 2013 stated that sugar may indeed be deleterious to health. This latest meta-analysis examined the relationship of sugar intake to adiposity in 30 randomized clinical trials and 38 cohort studies. But before you jump into the antisugar camp note that they found that in adults, reduced intake of dietary sugar reduced weight by 0.80 Kg (2 lbs) and increased diatary sugars was associate with weight increase of 0.75 Kg (also 2 lbs) — hardly an obesity epidemic! (I gain and lose 2 lbs every days) Also note that Isoenergetic exchange of dietary sugar with other carbohydrates showed no change in body weight, so it can’t be the fructose. Trials in children showed no overall change in body weight, though increased intake of sodas (but not fruit drinks) increased the chance of being overweight.16
1. Palmer JR, Boggs DA, Krishnan S, Hu FB, Singer M, Rosenberg L. Sugar-sweetened beverages and incidence of type 2 diabetes mellitus in African American women. Archives of internal medicine. Jul 28 2008;168(14):1487-1492.
2. Pan A, Malik VS, Hao T, Willett WC, Mozaffarian D, Hu FB. Changes in water and beverage intake and long-term weight changes: results from three prospective cohort studies. Int J Obes (Lond). Jan 15 2013.
3. Goran MI, Ulijaszek SJ, Ventura EE. High fructose corn syrup and diabetes prevalence: A global perspective. Global public health. Jan 2013;8(1):55-64.
4. Marriott BP, Cole N, Lee E. National estimates of dietary fructose intake increased from 1977 to 2004 in the United States. The Journal of nutrition. Jun 2009;139(6):1228S-1235S.
5. Barclay AW, Brand-Miller J. The Australian paradox: a substantial decline in sugars intake over the same timeframe that overweight and obesity have increased. Nutrients. Apr 2011;3(4):491-504.
6. Gross LS, Li L, Ford ES, Liu S. Increased consumption of refined carbohydrates and the epidemic of type 2 diabetes in the United States: an ecologic assessment. The American journal of clinical nutrition. May 2004;79(5):774-779.
7. Montonen J, Jarvinen R, Knekt P, Heliovaara M, Reunanen A. Consumption of sweetened beverages and intakes of fructose and glucose predict type 2 diabetes occurrence. The Journal of nutrition. Jun 2007;137(6):1447-1454.
8. Sun SZ, Anderson GH, Flickinger BD, Williamson-Hughes PS, Empie MW. Fructose and non-fructose sugar intakes in the US population and their associations with indicators of metabolic syndrome. Food and chemical toxicology: an international journal published for the British Industrial Biological Research Association. Nov 2011;49(11):2875-2882.
9. Shao Q, Chin KV. Survey of American food trends and the growing obesity epidemic. Nutrition research and practice. Jun 2011;5(3):253-259.
10. White JS. Straight talk about high-fructose corn syrup: what it is and what it ain’t. The American journal of clinical nutrition. Dec 2008;88(6):1716S-1721S.
11. White JS. Misconceptions about high-fructose corn syrup: is it uniquely responsible for obesity, reactive dicarbonyl compounds, and advanced glycation endproducts? The Journal of nutrition. Jun 2009;139(6):1219S-1227S.
12. Sievenpiper JL, de Souza RJ, Mirrahimi A, et al. Effect of fructose on body weight in controlled feeding trials: a systematic review and meta-analysis. Annals of internal medicine. Feb 21 2012;156(4):291-304.
13. Livesey G, Taylor R. Fructose consumption and consequences for glycation, plasma triacylglycerol, and body weight: meta-analyses and meta-regression models of intervention studies. The American journal of clinical nutrition. Nov 2008;88(5):1419-1437.
14. Forshee RA, Storey ML, Allison DB, et al. A critical examination of the evidence relating high fructose corn syrup and weight gain. Critical reviews in food science and nutrition. 2007;47(6):561-582.
15. Stanhope KL. Role of fructose-containing sugars in the epidemics of obesity and metabolic syndrome. Annual review of medicine. 2012;63:329-343.
16. Te Morenga L, Mallard S, Mann J. Dietary sugars and body weight: systematic review and meta-analyses of randomised controlled trials and cohort studies. BMJ. 2012;346:e7492.
 BMJ Study.
 Note also in a later study in PlosOne, the Video presenters demonstrate NO correlation between increased sugar and increased weight.
About the Author:
Dr. Yadon Arad is Board certified in Internal Medicine, Endocrinology and Metabolism, and Emergency Medicine. He has extensive experience in various aspects of human and animal Endocrinology, Metabolism, and Preventive Medicine. Dr Arad received a BA in Mathematics, Magna Cum laude, and an MD from the University of Rochester, and trained at Columbia University.
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