I’m fairly certain that most of you reading this are familiar with the veteran strength coach/author Mark Rippetoe, best known for Starting Strength and his collab with Lon Kilgore, Practical Programming for Strength Training. To say that these books are influential cult classics that get consistently glowing reviews would be an understatement. Given this, I had my expectations set pretty high regarding Mark’s general approach to the acquisition and dissemination of knowledge. But, it turns out I was wrong in my assumptions – at least about the nutritional aspect of his message board.

Pubmed, Schmubmed

Having recently registered at the Starting Strength Forums, I randomly engaged in discussion with a member who was worried about combining carbs and fat in the same meal. One of the members stepped in and attempted to justify the carb-fat separation tactic. In Socratic fashion, I helped him discover that there wasn’t anything about his claim that he could substantiate from a scientific standpoint. But that’s not the kicker. After some browsing, I ran into a rather unique forum rule. Here are some key sections from a stickied thread in the subforum of the resident nutrition coach John Sheaffer (who posts as “Johnny Pain” on Mark’s forums):

“…there are many other places (where many of you may already be members) for you guys to post studies and talk about medline, and Pubmed, and argue the validity of someone’s research…”

“I am largely not interested in that sort of thing. It takes too much time away from the important stuff, and the people who are doing the real science in the gym and at the table. I am not into arguing with people on the internet.”

“I will continue to answer questions that are relevant to the board. I have been legitimately enjoying this so far, and have met some great people. Do not however, bother posting threads or individual posts that include discussion of or links to studies. They will be deleted.”

Now, don’t get me wrong. I can appreciate simplistic/no-brainer/default-based approaches to helping out forum members. But in this particular realm, isn’t it kind of odd to literally forbid scientific research-related discussion? If John is not interested in getting into scientific debates, then that’s fine. But to prohibit this from occurring in his subforum even if he’s not involved is, well, an interesting way to run a community.

Prohibiting discussion that includes citing scientific research shifts the bias too far in the direction of anecdote/personal testimony. Heck, there are dozens of methods out there with a ton of testimony behind them and very little actual merit. Published research is not, cannot, and will never be the end-all judge. However, it’s an indispensable tool that helps separate the empty claims from the ones backed by objective evidence (however limited that evidence might be).

Nutritional mythology 101

And of course, you always have to laugh when scientific research is cited when it’s convenient, and dismissed when it doesn’t match up with someone’s personally held beliefs/anecdotes. Funny how that works. Now, let me give you a perfect example of why research should be discussed on training/nutrition forums. Have a look at this quote from John:

“Separate your carbs and fats. In each meal, you will have a portion of protein in addition to either carbs or fats, but not both. In the earlier half of the day, your meals should be Protein + Carb (P/C) in order to fill your muscle glycogen stores for your athletic activities. Later in the day (afternoon to evening, depending on your individual metabolism), when you are more sedentary, your meals should be Protein + Fat (P/F). Since carbs produce an insulin response, removing the carbs at this time will decrease the likelihood that you will store your excess calories as fat. Your final meal of the day should be *only* protein. Also, your PWO meal, regardless of what time of the day it is, must be a P/C meal.”

The above quote is so packed with broscience, it’s enough to provide a strong case for more research-based discussion on John’s subforum. Regarding the “don’t mix carbs with fat” myth, I wrote an article debunking it here. As for warning against carbs at night, there’s nothing inherently fattening about night-time carbs unless they contribute to a chronic surplus of calories that isn’t used for building lean tissue. The ONLY reason cutting carbs out of the evening works for controlling fat gain in some folks is because it restricts total caloric intake for the day.

“No carbs at night” is nothing more than a calorie-cutting-for-dummies tactic. Can it work? Yes, it can. In the case of people who tend to overeat carbo-liscious foods at night, this can serve as a default solution, but it’s not a guideline that should be universally recommended. What works just as well is cutting back on an equivalent amount of calories earlier in the day. There are no night-time insulin fairies ready & waiting to store carbs in the fat tissue — at least not at any greater rate than they would do so during the day.

Is there research to back up the claim that shifting the majority of your carbs to the later part of the day won’t magically chub you up or make it tougher to lose fat? Yes there is – and this occurred despite exercise being in the earlier part of the day for both groups compared [1]. For those who put a lot of stock in case studies, the lack of fattening effect of pre-bed carbs has plenty of examples - particularly in Martin Berkhan’s clientele [2].

Come at me, bro

If I had a chance to discuss these issues with John or Mark on the Starting Strength Forums, I would have gladly done so. However, it’s clear that Mark is not interested in discussing it with me, as seen in this thread. John hasn’t said a word about it yet, and I sincerely encourage him to do so. I’m easy to reach, and willing to field any challenges to any of the claims I’ve made. I won’t hold my breath, though. To relay John’s own words stuck at the top of his subforum:

“I am not into arguing with people on the internet. I think it’s gay to do so. I think it makes you a pussy. If people have a problem with the way I handle my board, please go to another forum and talk trash on me. It’s ok. People do it all the time. Better yet, catch up with me at an event that I am attending and voice your concern to me in person. That’s how it should be anyway, right?”

To the above quote, I would counter that there’s no way it can’t be productive to calmly & intelligently discuss any topic by presenting scientific evidence to support your case, while being open to research that perhaps you were not aware of. But hey, learning and staying informed about the scientific side of things takes considerable effort. And apparently, some people have no interest in delving into anything beyond their pre-existent beliefs. I personally think that there’s ALWAYS room for learning from scientific research, especially if you include science to justify your methods of practice. Disagree? Then come at me, bro.

_________________________________________________________________________

References

1. Keim NL, et al. Weight loss is greater with consumption of large morning meals and fat-free mass is preserved with large evening meals in women on a controlled weight reduction regimen. J Nutr. 1997 Jan;127(1):75-82. [Medline]
2. Berkhan M. Client Updates. (note that in many cases there’s even some fat with the carbs in those large evening meals – shocking, I know) [Leangains]

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Three hundred…

After 300 comments and counting, it’s safe to agree with Nigel Kinbrum that my recent fructose article “has caused a bit of a stir in the nutritional blogosphere.”  The intense debate (& discussion) that ensued inspired me to re-cap some things I feel were most interesting. There was plenty of learning to be had on both sides of the fence. Here are the highlights as I see them:

• Dr. Robert Lustig showed up, to the excitement and anticipation of all, including me. He went 3 rounds with me, which was actually more than I expected.
• In round one, he defended his position using  survey data that was contrary to the ERS/USDA data, which is well and good. I don’t disagree that survey data in general is pretty messy and equivocal, not to mention, incapable of establishing causal relationships. He then repeated his claim that the Japanese diet contains no fructose outside of fruit. Perhaps due to hasty error, he says, “That is what we are talking about here; added dietary sugars; not endogenous ones.”  I’m going to assume he meant to say intrinsic sugars, not endogenous sugars.  In any case, this idea that the Japanese do not add sugar to their diets is completely false – regardless of which regional or traditional aspect of Japan you’re talking about (this actually was never specified). He also mentioned the revised recommendations of the American Heart Association (AHA), which David Gillespie follows up on towards the end of the discussion, where the full picture is omitted until I post it up (I’ll get to that). 
• In my rebuttal to Lustig’s initial comment, I first point out the limitations of epidemiological data, as well as Lustig’s neglect of the numerous factors that have contributed to a reduction in energy expenditure, such as, “an increase in sedentary occupations; an increase in two-income households and single-parent households; transportation and infrastructure changes that discourage physical activity; a decrease in PE classes and extracurricular sports programs in schools; an increase in sedentary forms of entertainment (i.e. TV/movie viewing, video games, internet, etc.); demographic changes (i.e. aging population, immigration, etc.); a decrease in food costs with increase in food availability and changes in food consumption patterns” (study here).  I  finish off by pointing out the error of the claim regarding the Japanese diet, and mention Lustig’s omission of giving concrete numbers in his lecture regarding the dose-dependent safety of fructose in the diet.
• Lustig’s 2nd round defense was merely a cut/paste of the abstract of a 31 year-old epidemiological study showing that, “a high fat, high simple carbohydrate, low complex carbohydrate diet and/or reduced levels of physical activity increase risk of diabetes.”  My rebuttal to this was simple. I pointed out how Lustig was not only using uncontrolled data to support his stance, but he was being selective about what the observational data showed. I used the study he posted plus two more recent studies to show the common thread among each of them: an increase in fat, an increase in sugar, and a decrease in physical activity was associated with adverse health effects. Clearly, it’s incorrect to selectively scapegoat the single factor of your personal choice. 
• In Lustig’s final defense, he first cites as study wherein roughly 150 grams of fructose (the equivalent of 6-7 cans of non-diet soda), increased visceral adiposity and reduced insulin sensitivity in overweight & obese subjects. Does this surprise anyone? The study he cited used a fructose dose that’s 3 times the average American intake. He then goes on to cite rodent research despite his acknowledgement of my demand for human interventions using non-stratospheric doses of fructose. All this, after my multiple citations of human research showing the contrary.  To top everything off, Lustig cited his Youtube popularity as a basis of accuracy and credibility. That was not a good move. My rebuttal to Lustig’s final comment is right here.
• I emailed Lustig, thanking him for the discussion, and he responded by preaching to me more of his gospel. I politely asked that he take his argument back to the blog since the purpose of the whole discussion in the first place is to educate the public. He would have none of that, quipping that “real scientists” don’t go tit-for-tat on blogs, they go to journal clubs to discuss research with other “real scientists.”  If his case was as strong as he thinks it was, he wouldn’t have gotten embarrassed by the opposition.
• As I mentioned in response to a straight-shooting article by Martin Berkhan, Lustig probably has more education and native intelligence than he knows what to do with. However, as he demonstrated, you can be the most brilliant guy in the world & still find yourself fumbling over groundless claims.
• Comments by Ryan Zielonka (here), RG (here), DSD  (here), and Rob (here) illustrate the regional heterogeneity of the Japanese diet, and how it can’t be simply pegged as fructose-free aside from the fruit intake.
• Fred Hahn brought his classic carbophobic flair (here), which was well-rebutted by Mike Howard (here) and Leigh Peele (here). 
• Ganine asked the question of whether or not HFCS has different metabolic effects than regular sugar (sucrose). James Krieger came in with a follow-up response stating that, “The only practical difference between sucrose and HFCS is in the bonding. The glucose & fructose in HFCS is mainly free and unbonded, while it is bonded in sucrose. However, this makes no *meaningful* difference in regards to metabolism in the body. The bonds in sucrose are quickly broken when sucrose hits the acid environment of the stomach. This means that once sucrose hits the stomach, it’s no different from HFCS. Once you get to the small intestine, metabolism is *exactly* the same. This *little bit of difference* does not lead to the problems Dr. Lustig talks about. The fact is, HFCS and sucrose are identical as far as your body is concerned. The difference in bonding wouldn’t make a shred of difference in regards to your health.”
• Speaking of James Krieger, I’d like to direct anyone interested in fructose metabolism to this fine tutorial here.
• In response to Mike K’s advocacy of food avoidance, I posted research indicating an association between inflexible, all-or-nothing eating habits and adverse conditions. To quote Stewart et al, “The study found that individuals who engage in rigid dieting strategies reported symptoms of an eating disorder, mood disturbances, and excessive concern with body size/shape. In contrast, flexible dieting strategies were not highly associated with BMI, eating disorder symptoms, mood disturbances, or concerns with body size.” 
• Here’s a quote from a similar study by Smith et al: “Subjects were administered questionnaires measuring dietary restraint, overeating, depression and anxiety. Measurements of height and weight were also obtained in order to calculate BMI. Canonical correlation was performed to evaluate the relationship of dietary restraint variables with overeating variables, body mass, depression and anxiety. The strongest canonical correlation (r=0.65) was the relationship between flexible dieting and the absence of overeating, lower body mass and lower levels of depression and anxiety.”
• Indeed, correlation doesn’t automatically equal causation, but the two studies I cited above build a far better case than the baseless assumptions of folks who assert their dietary perfectionism onto the world around them.
• Ardent sugarphobe David Gillespie presented some very engaging arguments. However, he ignored all other posters, as well as the evidence I presented. He correctly pointed out that John White’s HFCS article contained a citation of research that did not support the point he was making (good catch, David!). However, he went on to dismiss reams of data on the grounds of funding source. He also incorrectly accused a study of being funded by the Coca Cola company, when in fact, Coke funded the travel expenses after the study was already complete. As James pointed out, the study was funded by a scholarship, two fellowships, and a grant from the Canadian government. Beyond that, studies should not be judged solely on funding source; the weight of their scrutiny should rest on their quality of design.
• David responded by citing the AHA’s recommendations, which I’ll quote him as saying, “Of particular note is their final recommendation that an adult male should consume no more than 144 calories (38 g) per day in added sugars (which would be 19g of fructose).”  The problem with this is that it omits the range of doses the AHA listed for various populations, which went as high as 19 teaspoons of sugar per day for active males, which is double the figure that David emphasized. Of course, it’s convenient to leave out the higher end when you’re building a case that’s biased toward sugar avoidance. Go here to see my response to this, which includes a screen shot of the chart in the AHA paper.
• In my final rebuttal to David, I explain what discretionary calories are, and how their intended use further supports the point I made in my original article. To quote my response, “The discretionary allotment for an active male is 512 kcal, and a sedentary one is 290 kcal. The average of this is 401 kcal. Technically, it wouldn’t violate the AHA’s recommendations if someone’s entire discretionary kcals came from sugar, which in the case of 401 kcals is about 100g, which equates to 50g fructose, which brings us right back to the exact number I listed as the upper safe limit in my original article.”
• An honorable mention is deserved for the most epic comment, by Jamie Hale.

I want to give sincere thanks everyone who contributed to this discussion. Speaking of meaningful contributors, go visit the brand-new blog of a highly astute bro of mine, Mike Miller. To end off, I encourage anyone interested to check out the following scientitic reviews for further information on the topic of fructose:

http://www.ncbi.nlm.nih.gov/pubmed/19592634 

http://www.ncbi.nlm.nih.gov/pubmed/18996880

http://www.ncbi.nlm.nih.gov/pubmed/20047139 

http://www.ncbi.nlm.nih.gov/pubmed/20086073

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Dr. Robert Lustig, professor of pediatrics at the University of California at San Francisco, is the star of the video above. While he presents some material that’s scientifically sound, he also makes enough errors to warrant a healthy dose of criticism. There’s a ton of material he goes over, so instead of writing a multi-chapter opus, I’ll discuss the aspects that I feel are the most relevant and interesting.

Bravo, Doc

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.

Boooo, Doc

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 [1]:

• 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 [2]. 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 [7], 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 [11]. 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 [12]. 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 [16]:

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 [17]. 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 [18].

Partial redemption

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.

Summing up

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 [15]. The conservative camp suggests that the safe range is much less than this; roughly 25-40 grams per day [19].  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.

.

Note: for those with little tolerance for reading through over 400 comments, there’s a summary of the discussion here.  .

References

1. Economic Research Service, USDA. Loss-Adjusted Food Availability Data. Updated Feb 27, 2009. [ERS/USDA]
2. King DE, et al. Adherence to healthy lifestyle habits in US adults, 1988-2006. Am J Med. 2009 Ju; 122(6):528-34. [Medline]
3. Melanson KJ, et al. High-fructose corn syrup, energy intake, and appetite regulation. Am J Clin Nutr. 2008 Dec;88(6):1738S-1744S. [Medline]
4. 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]
5. 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]
6. 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]
7. Spitzer L, Rodin J. Effects of fructose and glucose preloads on subsequent food intake. Appetite. 1987 Apr;8(2):135-45. [Medline]
8. 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.
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. [Medline]
10. Rodin J. Effects of pure sugar versus mixed starch fructose loads on food intake. Appetite 1991;17:213–9.[Medline]
11. Moran TH. Fructose and satiety. J Nutr. 2009 Jun;139(6):1253S-1256S. Epub 2009 Apr 29. [Medline]
12. 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]
13. Livesy G. Fructose ingestion: dose-dependent responses in health research. J Nutr. 2009 Jun;139(6):1246S-1252S. Epub 2009 Apr 22. [Medline]
14. 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]
15. 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]
16. 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]
17. Dyck JH, Ito K. Japan’s fruit and vegetable market. Global Trade Patterns in Fruits and Vegetables. [ERS/USDA]
18. Saremi A, Arora R. The cardiovascular implications of alcohol and red wine. Am J Ther. 2008 May-Jun;15(3):265-77. [Medline]
19. 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]

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