Lustig’s delivery is clear, confident, charismatic, and engaging overall. I’m sure many would think that his style is annoyingly smug and preachy, but I find it entertaining. This is a good thing, since the video is about 90 minutes long. Amidst the folly that prompted this post, he offers a few good observations.
First off, he makes a valid point that the public health movement against dietary fat that started in the early 1980’s was a grandiose failure. The climb in obesity to epidemic proportions over the last 30 years is plenty of evidence for this. It was also accurate of him to cite the significant increase in overall caloric consumption over this same time period. Furthermore, he shows an interesting progression of Coca-Cola’s 6.5 oz bottle in 1915 to the 20 oz bottle of the modern day.
Lustig acknowledges the First Law of Thermodynamics as it applies to changes in bodyweight. He attacks the vague expression that “a calorie is a calorie” by pointing out that different nutrients impart different physiological effects and have different roles within the body. His concluding recommendations included kicking out liquid calories except milk, which is generally a good strategy for children. Okay, so far so good. But what does he say that’s so misleading? Let’s take a look.
While Lustig correctly points out that the nation’s overall caloric consumption has increased, he proceeds to blame carbohydrates as being the primary constituent. The thing is, he uses data spanning from 1989-1995 on children aged 2-17. Survey data is far from the gold standard of evidence, but if you’re gonna cite it, you might as well go with something more recent that includes adults.
Here’s the latest from the USDA Economic Research Service (ERS), which tracked the percent of total daily calories of the range of food groups from 1970-2007. The actual spreadsheet of the following figures can be downloaded here, click on the “Percents” tab at the bottom :
- Meats, eggs, and nut kcals decreased 4%.
- Dairy kcals decreased 3%.
- Percentage of fruit kcals stayed the same.
- Percentage of vegetable kcals stayed the same.
- Flour and cereal product kcals increased 3%.
- Added fat kcals are up 7%,
- Added sugars kcals decreased 1%
- Total energy intake in 1970 averaged 2172 kcal. By 2007 this hiked up to 2775 kcal, a 603 kcal increase.
Taking a hard look at the data above, it appears that the rise in obesity is due in large part to an increase in caloric intake across the board, rather than an increase in carbohydrate in particular.
Lustig insufficiently addresses the ‘energy out’ side of the equation. According to the research, it’s possible that over the last couple of decades, we’ve become more sedentary. King and colleagues recently compared the physical activity data in the National Health & Nutrition Examination Survey (NHANES) from 1988-1994 with the NHANES data from 2001-2006, and found a 10% decrease . From a personal observation standpoint, that figure seems conservative (internet surfing for hours after your desk job shift, anyone?). It’s safe to say that all 603 extra daily calories have been landing in the nation’s collective adipose depot.
It’s also safe to say that all this finger-pointing at carbohydrate is just as silly as the finger-pointing toward fat in the ’80’s. Lustig takes the scapegoating of carbohydrate up a notch by singling out fructose. Perhaps the most passionate point he makes throughout the lecture is that fructose is a poison. Well, that’s just what we need in this day and age – obsessive alarmism over a single macronutrient subtype rather than an aerial view of the bigger picture.
Fructose is evil, context be damned
So, is fructose really the poison it’s painted to be? The answer is not an absolute yes or no; the evilness of fructose depends completely on dosage and context. A recurrent error in Lustig’s lecture is his omission of specifying the dosage and context of his claims. A point he hammers throughout his talk is that unlike glucose, fructose does not elicit an insulin (& leptin) response, and thus does not blunt appetite. This is why fructose supposedly leads to overeating and obesity.
Hold on a second…Lustig is forgetting that most fructose in both the commercial and natural domain has an equal amount of glucose attached to it. You’d have to go out of your way to obtain fructose without the accompanying glucose. Sucrose is half fructose and half glucose. High-fructose corn syrup (HFCS) is nearly identical to sucrose in structure and function. Here’s the point I’m getting at: contrary to Lustig’s contentions, both of these compounds have substantial research showing not just their ability to elicit an insulin response, but also their suppressive effect on appetite [3-6].
But wait, there’s more. In studies directly comparing the effect of fructose and glucose preloads on subsequent food intake, one showed no difference , while the majority have shown the fructose preload resulting in lesser food intake than the glucose preload [8-10]. A recent review of the literature on fructose’s effect on satiety found no compelling case for the idea that fructose is less satiating than glucose, or that HFCS is less satiating than sucrose . So much for Lustig’s repeated assertion that fructose and fructose-containing sugars increase subsequent food intake. I suppose it’s easier to sensationalize claims based on rodent data.
In the single human study I’m aware of that linked fructose to a greater next-day appetite in a subset of the subjects, 30% of total daily energy intake was in the form of free fructose . This amounts to 135 grams, which is the equivalent of 6-7 nondiet soft drinks. Is it really that groundbreaking to think that polishing off a half-dozen soft drinks per day is not a good idea? Demonizing fructose without mentioning the dose-dependent nature of its effects is intellectually dishonest. Like anything else, fructose consumed in gross chronic excess can lead to problems, while moderate amounts are neutral, and in some cases beneficial [13-15].
I’m obviously not in favor of replacing anyone’s daily fluid intake with soft drinks, but I can already see a number of straw man arguments headed my way. This is because people have a tendency to think in either-or terms that strictly involve extremes. I’ll quote an elegant review by independent researcher John White that echoes my thoughts :
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.
Atkins, Japan, & alcohol – oh my!
One of Lustig’s opening assertions is that The Atkins diet and the Japanese diet share one thing in common: the absence of fructose. This is flat-out false because it implies that the Japanese don’t eat fruit. On the contrary, bananas, grapefruits, Mandarin oranges, apples, grapes, watermelons, pears, persimmons, peaches, and strawberries are significant staples of the Japanese diet . Lustig’s claim also implies that the Japanese do not consume desserts or sauces that contain added sucrose. This is false as well.
Another oversimplification Lustig makes is that fructose is “ethanol without the buzz,” and that fructose is toxic to the liver. This once again helps me illustrate my point that even in the case of alcoholic beverages, their risk or benefit to health is dose-dependent. Just like his extremist treatment of fructose, Lustig bases his case on the effect of chronic isolated ethanol consumption in large doses. It’s easy to examine ethanol out of its normal context within beverages such as wine, because then you can conveniently ignore the evidence indicating its potential health benefits when consumed in moderation .
Towards the end of Lustig’s lecture, he mentions that fructose within fruit is okay because its effect is neutralized by the fiber content. To a degree, this is a valid claim. However, in building this stance, he uses sugarcane to illustrate just how fiber-dominant natural sources of fructose are, and this is the exception rather than the rule. He claimed that, “Wherever there’s fructose in nature, there’s way more fiber.” That statement is far from universally true. Drawing a few common examples from the major fruits consumed in Japan, a midsize banana contains roughly 27 total grams of carbohydrate, 7 grams of fructose and 3 grams of fiber. A midsize apple contains 25 total grams of carbohydrate, 12 grams of fructose and 4 grams of fiber. Two cups of strawberries contains 24 total grams of carbohydrate, 4 grams of fructose, and 6 grams of fiber.
I would add that fiber is only one of the numerous phytochemicals in fruit that impart health benefits. Thus, it’s not quite as simple as saying that fructose is evil, but once you take it with fiber, you’ve conquered the Dark Side.
I have a great deal of respect for Lustig’s professional accomplishments, and I share his concern for the nation’s penchant for sitting around and overconsuming food and beverages of all sorts. However, I disagree (as does the bulk of the research) with his myopic, militant focus on fructose avoidance. He’s missing the forest while barking up a single tree.
So, what’s the upper safe limit of fructose per day (all sources considered)? Again, this depends on a number of variables, not the least of which are an individual’s physical activity level and lean body mass. Currently in the literature is a liberal camp reporting that fructose intakes up to 90 grams per day have a beneficial effect on HbA(1c), and no significant effects are seen for fasting triacylglycerol or body weight with intakes up to 100 grams per day in adults . The conservative camp suggests that the safe range is much less than this; roughly 25-40 grams per day . Figuring that both sides are biased, the middle figure between the two camps is roughly 50 grams for active adults.
Although the tendency is to get hung up on the trivial minutia of an exact gram amount, it’s not possible to issue a universal number because individual circumstances vary widely (this is a concept that baffles anti-fructose absolutists). The big picture solution is in managing total caloric balance with a predominance of minimally refined foods and sufficient physical activity. Pointing the finger at fructose while dismissing dosage and context is like saying that exercise should be avoided because it makes you fat and injured by spiking your appetite and hurting your joints.
- Economic Research Service, USDA. Loss-Adjusted Food Availability Data. Updated Feb 27, 2009. [ERS/USDA]
- King DE, et al. Adherence to healthy lifestyle habits in US adults, 1988-2006. Am J Med. 2009 Ju; 122(6):528-34. [Medline]
- Melanson KJ, et al. High-fructose corn syrup, energy intake, and appetite regulation. Am J Clin Nutr. 2008 Dec;88(6):1738S-1744S. [Medline]
- Soenen S, Westerterp-Plantenga MS. No differences in satiety or energy intake after high-fructose corn syrup, sucrose, or milk preloads. Am J Clin Nutr. 2007 Dec;86(6):1586-94. [Medline]
- Monsivais P, Perrigue MM, Drewnowski A. Sugars and satiety: does the type of sweetener make a difference? Am J Clin Nutr. 2007 Jul;86(1):116-23. [Medline]
- Akhavan T, Anderson GH. Effects of glucose-to-fructose ratios in solutions on subjective satiety, food intake, and satiety hormones in young men. Am J Clin Nutr. 2007 Nov;86(5):1354-63. [Medline]
- Spitzer L, Rodin J. Effects of fructose and glucose preloads on subsequent food intake. Appetite. 1987 Apr;8(2):135-45. [Medline]
- Rodin J, Reed D, Jamner L. Metabolic effects of fructose and glucose: implications for food intake. Am J Clin Nutr. 1988 Apr;47(4):683–9.
- Rodin J. Comparative effects of fructose, aspartame, glucose and water preloads on calorie and macronutrient intake. Am J Clin Nutr 1990;51:428–35.<!– HIGHWIRE ID=”88:6:1738S:24″ –> [Medline]
- Rodin J. Effects of pure sugar versus mixed starch fructose loads on food intake. Appetite 1991;17:213–9.[Medline]
- <!– HIGHWIRE ID=”88:6:1738S:25″ –>Moran TH. Fructose and satiety. J Nutr. 2009 Jun;139(6):1253S-1256S. Epub 2009 Apr 29. [Medline]
- Teff KL, et al. Dietary fructose reduces circulating insulin and leptin, attenuates postprandial suppression of ghrelin, and increases triglycerides in women. J Clin Endocrinol Metab. 2004 Jun;89(6):2963-72. [Medline]
- Livesy G. Fructose ingestion: dose-dependent responses in health research. J Nutr. 2009 Jun;139(6):1246S-1252S. Epub 2009 Apr 22. [Medline]
- Dolan LC, et al. Evidence-based review on the effect of normal dietary consumption of fructose on development of hyperlipidemia and obesity in healthy, normal weight individuals. Crit Rev Food Sci Nutr. 2010 Jan;50(1):53-84. [Medline]
- Livesey G, Taylor R. Fructose consumption and consequences for glycation, plasma triacylglycerol, and body weight: meta-analyses and meta-regression models of intervention studies. Am J Clin Nutr. 2008 Nov;88(5):1419-37. [Medline]
- White JS. Straight Talk About High-Fructose Corn Syrup: What it is and What it Ain’t. Am J Clin Nutr. 2008 Dec;88(6):1716S-1721S. [Medline]
- Dyck JH, Ito K. Japan’s fruit and vegetable market. Global Trade Patterns in Fruits and Vegetables. [ERS/USDA]
- Saremi A, Arora R. The cardiovascular implications of alcohol and red wine. Am J Ther. 2008 May-Jun;15(3):265-77. [Medline]
- Sánchez-Lozada LG, et al. How safe is fructose for persons with or without diabetes? Am J Clin Nutr. 2008 Nov;88(5):1189-90. [Medline]