A retrospective of the fructose alarmism debate.
2010 February 19
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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Errm, Google Alerts doesn’t work if you mis-spell my name.
Oh crap, lemmie fix that
Great recap, Alan.
Loved following this thread. Hope to see you address more controversial issues in the future.
Best,
Mike L.
Great summary Alan!
I missed some of the initial thread and by the time I got back it was too extensive to read in entirety (without losing half of my day).
Great post, and another example of a group scientific, logical thinkers versus a group of nonscientific thinkers. Alan’s team- logical thinkers, and scientists- wins again.
What is a Real Scientist?
Although a person with a science degree might claim to be a scientist, the true test of the scientist is how one thinks. A good scientist:
· Accepts nothing in science absolutely.
· Is willing to change his opinions based on new data.
· Does not rely on Authority.
· Thinks critically.
· Knows that extraordinary claims require extraordinary proof.
· Has an open mind.
· Relies on logic and reason.
· Knows how to form hypotheses and test them.
· Respects the scientific method.
· Examines all the data, not just the data that support his or her view.
· Builds on the work of others, giving them appropriate credit.
· Documents his or her experiments so they can be duplicated by others.
· Knows that if a claim is made, the claimant must provide the proof. (It is not up to others to disprove it.)
· Is intellectually honest
. And drops the ego and admits when their belief system has been refuted by scientific data. It’s not enough to consider the weight of data, but the quality and strength must also be considered.
Of course, all of the points above are not directly applicable to the previous fructose discussion, but some are.
If you lack the skills to evaluate the data it really makes no difference, scientific data is all the same. But if you decide to participate in a scientific debate it’s a good idea to be able to read what you are claiming to be evidence. As I said earlier, anyone interested in scientific data should at least take the time to study research methodology and at least have a basic understanding of the central themes of science and logic.
Alan is seriously like some kind of nutrition hero. It’s like his goal in life is to find things that people worry about and get them to realize that it’s all superstitious nonsense. And the remarkable thing is, 99% of the time – it really is superstitious nonsense.
It really has been life-changing to read some of this stuff — from a completely non-scientific standpoint, I almost feel like there’s a deeper message at play here: intuitively we all know we shouldn’t have to be worrying about fructose, or the GI, or freaking out over meal times, or eating too much fat, and so on. And it’s quite liberating to realize – our intuition was dead on.
What other areas in life are there in which our intuition is dead on? What other things in life are 50x easier than usually believed, but nobody knows this? Making money? Being a rock star? Becoming enlightened?
Anyway, enough lame romantic-era type shit, but you all get the idea.
And BTW Alan, I don’t know how to say this any other way — there may be no limit to the depths I will sink in order to get a vbulletin forum up on this site. forums.alanaragonblog.com FTW – will it ever happen?
I have just learned something: the principle that the most intuitively simple explanation is often the right one is actually the same thing as Occam’s Razor. Sweet!
See that shit right there, brah? Raising my IQ up!
I recently got into a brief dialogue with a coworker about this topic and it all started when she started demonizing HCFS. I usually don’t butt in with my comments but I couldn’t help myself and I used some of the info I learned from here, the AARR, and one of Lyle’s posts. I even linked her to one of the articles. She did seem to kind of acknowledge the facts but was still worried about it.
I told them that these guys, Alan, Lyle, Jamie, etc, really review the research and their ability to analyze data is superb.
Wasn’t impressed at all, would rather listen to the guy actually conducting the research and how the media might distort it.
People get too married to their beliefs of what they see on TV or in the general media (including magazines) and won’t relent no matter what because it maybe helps them justify something they are doing.
I’m proud to say that I USED to be a bro but I have changed my beliefs after seeing the cold hard facts. Isn’t that what learning is all about?
More info on scientific thinking and logic:
Scientific and Nonscientific Approaches to Knowledge
http://www.maxcondition.com/page.php?126
The Fitness Skeptic
http://www.maxcondition.com/page.php?105
Authorities are Fallible
http://www.maxcondition.com/page.php?117
How To Read A Scientific Paper
http://www.biochem.arizona.edu/classes/bioc568/papers.htm
Critical Thinking: What it is and why it counts
http://www.gustrength.com/critcialthinking:facione1
Top 20 logical fallacies
http://www.theskepticsguide.org/resources/logicalfallacies.aspx
Knowledge Summit
http://www.knowledgesummit.net
I think it’s good to be cautious about too much sugar intake. But I think it’s more important to restrict omega-6 intake to reasonable levels.
I read John Yudkin and T. L. Cleave and William Dufty three decades ago and restricted my sugar consumption accordingly thinking I was doing well. However, I got blind sided by omega-6. In 1993 I bumped my shin on a saw horse and was struggling with cellulitis and an ever-deepening sore (ulcer) a week later. Three months of trying various remedies to no avail, I took a few days off work to alternately soak my leg in Epsom salts and elevate. I had a book entitled “Vitamin E: Health Preserver” by Canadian physician and vitamin E researcher Wilfred Shute. Dr. Shute described how he used vitamin E to treat diabetic gangrene, phlebitis, congestive heart failure, and skin ulcers. I obtained some, took it orally, and applied it topically. Worked great. Was able to sleep at night without taking aspirin and the wound filled in with granulated tissue as described in the book.
A little more research and I concluded that I was consuming too much polyunsaturated seed oil, mainly from mayonnaise and salad dressing. I cut those from my diet and my health improved – for a while. More recently I’ve been losing strength and flexibility in my legs to the point where running is impossible and getting up from a chair difficult. I tried stretching and experimented with supplements of various sorts with limited success. Stretching was painful and supplements expensive. Then I heard Dr. Bill Lands utter these words: “…there are some really interesting foods that have more omega-3 than omega-6; but not all. Did you know that peanuts have 4,000 milligrams per 28 gram, one ounce serving of peanuts? 4,000 milligrams of omega-6 and one milligram of omega-3. The United States is the land of peanut butter. Grow our kids. Make our kids healthy. Whoops.”
Whoops indeed! When I learned how much omega-6 was in peanut butter I quit consuming it. That was about three months ago. Recently, I noticed an increase in muscle strength in my legs. In addition, the pain associated with stretching has subsided and I am able to run again and stand up from a chair without thinking about it.
I used to believe that excessive sugar intake was the major cause of clogged arteries. But after listening to Dr. Lands I’m not sure sugar has that much to do with it. Here’s a link to the lecture: http://videocast.nih.gov/summary.asp?live=8108 You can drag the timer button slightly to the right to the 12 minute mark where Dr. Lands begins speaking. If you are unable to play the videocast on you computer you can read a transcript of the lecture at http://www.amazon.com/tag/health/forum/ref=cm_cd_tfp_ef_tft_tp?_encoding=UTF8&cdForum=Fx1EO24KZG65FCB&cdThread=Tx241KS54K89FO7&displayType=tagsDetail
David — While I agree that omega-3 FAs are generally underconsumed (esp. in terms of proportion with omega-6 FAs), I wouldn’t cut out foods I liked on those grounds. I’d just eat less of them, or I’d eat more omega-3 FA. There’s magic in peanut butter, you didn’t know this? I think people can go overboard in their zeal for omega-3 as well, taking a more-is-better approach & swinging the pendulum too far in the other direction. Throwing out peanuts on the sole basis of FA proportion may be a case of throwing the baby out with the bathwater. More reading for you:
http://www.ncbi.nlm.nih.gov/pubmed/18716180
http://www.ncbi.nlm.nih.gov/pubmed/17514537
http://www.ncbi.nlm.nih.gov/pubmed/12672709
http://www.ncbi.nlm.nih.gov/pubmed/18716179
http://www.ncbi.nlm.nih.gov/pubmed/19396658
Insight — I don’t think I’d have enough time to properly nurture a full-fledged forum community. I’ll leave that madness for Lyle
All – Thanks very much for the feedback.
Alan,
What do you think about this video featuring Gary Taubes author of “Good Calories Bad Calories”? http://www.dhslides.org/mgr/mgr060509f/f.htm
It was recently posted on Bodybuilding.com. He claims to be a man of science and states that calories in vs. calories out does not explain obesity. Instead, insulin, glycerol-3 phosphate & carbohydrates are the culprits in making the body store fat regardless of calorie intake or expenditure.
Of course he mentions fructose as being the worst offender.
Perhaps he might be a good candidate for you to continue this debate. He seems like he make a better scientific argument for his case.
@Billy
Alan already thoroughly addressed Taubes and his nonsense in one of his research reviews. Taubes should be forced, as a penance, to rewrite the book (for free) with accurate information and call it “Good Calories, Bad Gary.’
Cheers,
Michael
Billy — I once read an interview with Taubes on T-mag. I was amazed at the misinformation being spewed forth. I have not read GCBC, but from every snippet of it I’ve some across, it sounds to me like he cherry-picks the research that fits his Gripping Story, instead of considering the entirety of the research, then drawing conclusions from there. I am not at all interested in fictional reading at this point in my life. I really wish I had time for it, but then I’d read more of the good stuff in the sci-fi genre. In the meantime, give this a read:
http://www.thebsdetective.com/2009/10/bullshitter-of-day-oct-7th-gary-taubes.html
Alan, you should really read the book (GCBC). At worst, you would be able to rant against it even better.
I really don’t understand how people can discredit a book (or the author) without even reading said book themselves.
Patrick
Patrick — I should really read a lot of things…in the peer-reviewed literature. GCBC is low on the list. And like I said, that T-mag interview was more than enough to cast considerable doubt on Taubes’ objectivity. If you find anything in Krieger’s writeup you find to be false, then feel free to take it up with him & link me to your discussion.
I’m tempted to take Fred up on his “3500 calorie per day meat/egg/fat” diet. I have access to a DEXA scan and can be “overseen” by the head of the exercise physiology department at one of the local universities. When I come back fatter, he’ll still explain it away. Hell, I can present everything at next summer’s “Ancestral Health Symposium.” Interesting n=1 experiment.
Great comments over at Free The Animal, BTW.
Best,
Skyler
If you overfeed on “meat/egg/fat”, you will probably gain weight (a good deal as fat). In the Zero Carb forums that I read, people who overeat on ZC do gain weight. But some are also able to NEAT it away and do not gain. 3500 is not that much. If you want to make sure that you gain, try to intake 10000 kcal. I read posts from people saying they did not gain on 10000 kcal, but that is probably BS.
Patrick
Skyler,
I think the counterargument the Taubes camp would make is that you would then return to your normal bodyweight once you resumed regular eating. This is the layer of details that gets hazy using the GCBC approach. Being on this blog, you’re probably athletically oriented, and I’m guessing may lift weights as well. That’s a helluva of a lot of specific prompting to get from your hormonal profile, in my estimation. I wouldn’t be surprised to learn that you did return to your normal bodyweight, but I would be surprised to learn that this was done completely unconsciously. You’d probably limit calories in some fashion, exercise, etc. The idea that I’m genetically programmed to seek my desk job in order to limit my caloric expenditure and that you in turn would be programmed to increase your conscious exercise to achieve a weight equilibrium just seems several steps too far for me. It’s a shame, because I think there are some good ideas that could have come out from that book, but were buried under mounds of hype. For instance, satiety is discussed a lot, and one person’s recommendation for low carb, meat focused dieting was that people would feel full on it BEFORE they consumed too many calories. Why not just present that? Why not just discuss saturated fat in a diet that matches caloric expenditure? He seemed to be trying to write specifically against the low-fat crowd that he just became a carb critic, and that seems to have lead things like the HFCS crusade.
Aaron
Bray’s Review of Good Calories Bad Calories
http://mindandmuscle.net/articles/jamie-hale/practical-scientist-7
Taubes a man of science? Read my post above -What is a real scientist?
jamie hale
Jamie: “What is a real scientist?”
Very good question !
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2719747/
“I regard consensus science as an extremely pernicious development that ought to be stopped cold in its tracks. Historically, the claim of consensus has been the first refuge of scoundrels; it is a way to avoid debate by claiming that the matter is already settled. Whenever you hear the consensus of scientists agrees on something or other, reach for your wallet, because you’re being had.”
“Let’s be clear: the work of science has nothing whatever to do with consensus. Consensus is the business of politics. Science, on the contrary, requires only one investigator who happens to be right, which means that he or she has results that are verifiable by reference to the real world. In science consensus is irrelevant. What are relevant are reproducible results. The greatest scientists in history are great precisely because they broke with the consensus. There is no such thing as consensus science. If it’s consensus, it isn’t science. If it’s science, it isn’t consensus. Period.”
Patrick
Skyler Tanner said…
“I’m tempted to take Fred up on his “3500 calorie per day meat/egg/fat” diet. I have access to a DEXA scan and can be “overseen” by the head of the exercise physiology department at one of the local universities.” I’ve exchanged a few e-mails with Taubes re: I have a theory. He’s kinda busy right now and wants me to finish reading GCBC before he’ll engage in further debate. I mentioned some individuals that had gained weight on low-carb diets but Taubes said that a proper study was required. Fair enough, but that’s not going to happen any time soon.
If you do do your experiment, will you do a crossover trial i.e. a low-carb bulk followed by a low-carb cut, a rest, then a high-carb bulk followed by a high-carb cut?
Cheers, Nige.
Ahh, a cliff’s version. Perhaps this will encourage some additional bros to educate themselves. Then again, I posted about a 5 sentence response on bb.com and a bro asked me for cliffs
Nigel,
I could do that but I’m really more concerned with the outrageous notion that one wouldn’t gain weight on such a diet. Add in an activity tracker like the Fitbit and a caloric expenditure tracker like the Body Bugg and you’ve got as close to a metabolic chamber as can be managed in free living conditions.
Aaron,
I know I’d return to a lower weight post force feeding because that’s what I do naturally. However, this wasn’t his contention. Like Greg Ellis before me I expect to gain fat, not magically recomp like a test-fueled 18 year old neophyte.
best,
Skyler
Patrick — While I appreciate Michael Crichton’s point of being wary of the concensus, I think Jamie’s punchlist of the scientific mindframe is quite a bit more compplete.
David — That’s way too funny.
All — I see a vision: skylerthescienceproject.com
Yes I agree, Jamie’s links are very good.
Patrick
Over the past decade, it has became increasingly easy for the lay person to access scientific research data. Assuming the layperson has read the data, shouldn’t this mean they are now better equipped to make rational decisions? Not necessarily.
Quote from Randomised Controlled Trials: A user’s Guide (Jadad, 1998):
“Even if RCTs were perfectly designed and readily available to users, they could not influence health care decisions and outcomes if users could not understand them.
During the past 15 years, I have noticed that most people do not understand the concept of randomisation and its strengths, the different sources of bias in RCTs, and the role of RCTs in health care decision making. This could be explained, at least in part, by the fact that most efforts to promote a better understanding of RCTs (and research in general) have focused on researchers in training, particularly graduate students. Little has been done to promote an understanding of research among other users of research. Even though some training programmes for health professionals, policy makers, health planners, and managers include courses on research methodology, they often lack formal activities to promote a better understanding of RCTs. The situation for patients, their family members, and other lay members of the public is even worse. These groups, without whom most RCTs would not exist or would not be needed, have been left unaided to handle research information, let alone RCTs. Journalists who have a profound influence on the dissemination and impact of research information are in a similar situation.
It would be reasonable to assume that those who understand research will be more likely to use it to their advantage than those who do not understand it. People who do not understand research are more likely to ignore it or misuse it. They also have a higher risk of becoming confused, anxious, and frustrated when trying to use research, which could result in worse health outcomes if irrelevant or biased information is used to guide their decisions. The potentially harmful effects of the lack of understanding of users is now compounded by the amount of information available. Until recently, only health care providers had to deal with information overload. Now, with the growth of the Internet, an increasing number of patients, family members, and other lay members of the public are gaining unprecedented access to information and experiencing the effects of information overload.
Against this background, I feel confident in saying that the development and implementation of effective strategies to increase users’ understanding of research, and RCTs in particular, is a top priority. Part of the success of these strategies will depend on the way in which the results from research are presented to users (see above). Part also depends on our ability to recognize, understand, and overcome specific barriers to the adequate use of RCTs by different groups of decision makers. Success will also depend on how well these strategies target all groups of potential and actual users of research.
Timing will be crucial. To date, efforts to promote a better understanding of RCTs and research have focused mainly on adults. Perhaps the effectiveness of such efforts could be enhanced if they were targeted to younger learners. For instance, the basic principles of decision making, research, and critical appraisal in health care could be incorporated in school curricula7,13 and taught using interactive video games and other innovative computer based methods. If children can understand these principles, they will not only be in a better position to participate in health care decisions, but will require little additional education and reinforcement once they become adults fulfilling the roles of health professionals, policy makers, planners, managers, journalists, patients, family members of patients, and other healthy adult members of society.
Efforts to increase our understanding of RCTs should take into account the tendency of human beings to rely excessively on intuition and rules of thumb, to follow inadequately built theories, and to be strongly influenced by vivid experiences and anecdotes. Efforts also need to account for the fact that research information will be modulated, not only by other types of information, but also by the values and preferences of the decision makers and the unique circumstances in which most decisions are made. If trials are to be used efficiently, and if evidence based decision making is to reach its full potential, we will need to couple our efforts to increase the understanding of RCTs with efforts to promote a better understanding of the relationship between RCTs and other study designs, between research information of all kinds and other types of information, and between information available to decision makers, their values and preferences, and the circumstances in which they are making the decisions. We will need a better understanding of the interaction among different groups of decision makers (that is, nurses and physicians, physicians and hospital managers, nurses and patients) in terms of their own information, values, and preferences in different contexts. Gaining this understanding will require different research approaches, input from multiple disciplines, and an enormous commitment at all levels.”
On a final note, the common quasi-experiment- which people often reference as evidence- lacks the strength of a scientifically controlled true or quasi experiment. An example of this type of common experiment would be one in which the trainer advises the trainee to supplement with supplement x. Once the trainee starts the supplement regimen, he/she begins to feel better, get stronger, etc. After 8 weeks the trainee has experienced significant gains, thus the supplement must work. In reality, the trainer and trainee have no idea why or what were the causative factors contributing to the gains. This is not real evidence, and in fact with uncontrolled quasi studies such as this, virtually any type of intervention can be shown to cause positive results.
Truly good stuff Jamie !
Thanks,
Patrick
^^^Yup, what Patrick said.
People who do not understand research are more likely to qualify ANYTHING they read as “research”. I think it happens in other fields besides fitness as well.
Alan bro,
I just finished reading your Jan 08 Issue and got lost here “There are other agents of lipogenesis such as acylation stimulating protein (ASP), which can facilitate fat storage in the absence of insulin”. Does this mean there are other factors to consider besides the energy balance for limiting fat storage (i.e., Is it possible to gain fat while at calorie deficit)?
Can you please give a brief explanation of what you meant?
Thanks
Sameer — My point was there there are various acute (short-term) lipogenic agents aside from insulin, which is actually a multifactorial anticatabolic (& contextually dependent anabolic) agent. Nevertheless, in a net deficit of energy over a period of weeks (or more), these various lipogenic and/or antilipolytic agents ultimately bow to the power of the energy deficit, and fat amd/or weight loss occurs – regardless of the physiological flux of these agents. For more on insulin & fat loss, see the Oct 2008 issue of AARR.
Personally, I think weight loss is easy. It’s preventing obesity that seems more difficult. Is it because it is too easy to eat too many calories nowadays (perhaps because carbs are too easy to binge on) ? Is our metabolism really deregulated ? Is there something in our current diet that effects our satiety ? Perhaps a mix of all this ?
This is what I am really interested in. Weight loss is the easy part, maintaining is more difficult. It looks like _preventing_ obesity would be easier than trying to fix it. But is it just a matter of not eating too much ? Or can we help ourselves, to not eat too much, simply by choosing specific food to this effect ?
In my research so far, I found that there are some food stuff that really helps with satiety. Should we teach our children simply to not overeat or teach them to choose proper food to this effect? Maybe both.
Patrick
Thx Alan
Patrick — We should teach people which foods should predominate the diet & which should comprise minority of the diet. Most people alrteady know what healthy choices and not-so-healthy choices are. The key is gathering up some balls and doing what needs to be done consistently enough, while allowing some flexibility in your plan. This is the nutshell version of how dieters succeed long-term.
Alan-
What can you tell me about trans fat?
It seems that it is Girl Scout Cookie season again and my eyes are immediately drawn to the ingredient list of the Thin Mints and Samoas which contain the words “partially hydrogenated palm kernel and/or cottonseed oil, soybean, and palm oil.”
http://www.girlscoutcookies.org/images/nutrition_info_2009_2010.jpg
What do you think would be a safe amount (in grams) of hydrogenated oils in an average diet?
What about conjugated linoleic acid from grass-fed beef, dairy, etc.?
I’ve always been a little unfamiliar with trans fat. Bros always tell me that if I eat a donut I am guaranteed to die the next day due to the trans fats…but we all know that is not true.
I know you will enlighten me.
“I once read an interview with Taubes on T-mag. I was amazed at the misinformation being spewed forth. I have not read GCBC, but from every snippet of it I’ve some across, it sounds to me like he cherry-picks the research that fits his Gripping Story, instead of considering the entirety of the research, then drawing conclusions from there. I am not at all interested in fictional reading at this point in my life. I really wish I had time for it, but then I’d read more of the good stuff in the sci-fi genre. In the meantime, give this a read”
I feel disappointed when I read reviews like this. GCBC main purpose was to dismantle the lipid hypothesis and show how much more refined carbohydrates contribute to disease of civilization than anything else. That is basically it. Yes, there are flaws with the book. He doesn’t mention every enzyme – he skips over ASP and leptin and he implies that a metabolic advantage exists. He doesn’t mention any of the heat created toxins created when cooking meat. But, these are all minor themes of the book. I am perplexed that people will globally label him as a fraud and a liar because of these details. The work he did was outstanding, even with the flaws. He got way more right than wrong.
@Teddy: I don’t think anyone here’s concerned with the stuff he got right. But then again, that also depends on what you define as “right.” His carbohydrate theory is batshit crazy, but he hit the nail on the head when dismantling the lipid hypothesis. (I have read the book, by the way.)
Teddy — I’ve heard several people say that Taubes does a good job of sticking it to the lipid hypothesis. Great. However, I would ask how much of the book is dedicated to the lipid hypothesis, and how much of it is dedicated to the carb/insulin/obesity nonsense, along with the “exercise doesn’t work” nonsense. Why would I be motivated to read a super-long book (by a journalist, not a scientist) that I might end up giving a C-grade to, at best?
DB — The degree of worry over trans fat intake would depend on how much you plan on going off on those GS cookies. It’s virtually impossible to determine an exact threshold of grams of trans fat beyond which your health is significantly at risk. That said, it’s been postulated that TFA from industrial sources *may* be more risky than TFA from ruminant (meat/dairy) sources. My general advice for you would be to eat those GS cookies & enjoy them — but just don’t make them a major part of your daily diet. 2-3 cookies = no big deal. 2-3 packages of cookies = big deal. As for CLA, the amounts contained in ruminant foods are no biggie as long as you keep your sources relatively lean (for the most part).
Thanks Alan!
“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.”
Again, not to defend Dr. Lustig, but the above statement is a strawman. At no point in his lecture does Dr. Lustig draw a distinction between sucrose and HFCS. Indeed, he goes to great pains to show that they are metabolically identical. When he says, “they’re not the same,” he is unambiguously differentiating between the metabolism of fructose and glucose.
Whether or not you agree with Dr. Lustig’s allegations and conclusions, misrepresenting his positions only damages your own credibility.
Rourke — You miss the point that Lustig takes fructose out of context when discussing effects on hormones that influence appetite. Many of his points would stand if he was talking about isolated fructose in large doses, but alas, speaking of sucrose (or similar) does not support the point of his that I went through great lengths to counter. Misreading my interpretation only damages your credibility…oh wait, I just relayed your own irrelevant point back to you. My bad.
One of the worst things about this is Lustig’s arrogant comment that “real scientists” don’t discuss publicly on blogs. Researchers have to learn to accept that these new forms of media are changing how information is disseminated. This is a great example of how a community of critical thinkers is an improvement over the sheltered status quo that most scientists still live in.
Hopefully Lustig won’t let himself become reinforced in his perspective by an encounter like this.
Nano,
AA,
In the newest promotional video for the “MuscleTech Hardcore Pro Series” line of supplements, Branch Warren and Jonnie Jackson are shown in the lab with MuscleTech’s top chemist, none other than Mr. Issac McNano.
Can you provide any insight as to what they may be discussing? I can only assume (and hope)that they are combining Branch and Jonnie’s real world supplement knowledge with Issac’s book-smarts, so that we can be blessed with some new, ground breaking supplements from MuscleTech!
Thanks,
-BC
Branch — Thanks for stopping in. The problem is, you leave a trail of nano vapor in your wake that lingers like memories of war.
My nano vapors are cryo blasted.
Hmm. Bray joins the fray.
Yep.
Bray GA.
“SUMMARY: The present review concludes on the basis of the data assembled here that in the amounts currently consumed, fructose is hazardous to the cardiometabolic health of many children, adolescents and adults.”
Patrick
“…that in the amounts currently consumed, fructose is hazardous to the cardiometabolic health of many children, adolescents and adults.”
Duh.
So Bray did a bunch of investigation and concluded that America consumes too much sugary beverages? The man’s a revolutionary.
Well, it also tells you that you don’t have to eat abnormal levels (= rats fed with >50E%) of fructose to get a screwed-up metabolism.
Mikael — this depends on dose & context, not sure if I’ve stressed that enough yet…
Should we really be surprised that (a) people are more than willing to believe that a certain macronutrient (rather than how many calories they consume) is responsible for all of our public health ailments, and that (b) there are people of all walks (with credentials, without credentials, etc) willing to feed them the dogmatic swill they are so desperately ready to devour?
Keep in mind, we are a nation of folks who amass infinite credit card debt to buy things we don’t need/can’t afford, then we blame the companies who lent it to us for ‘swindling’ us. We take out ridiculous mortgages that simple math shows we can’t pay, then blame mortgage lenders who had the audacity to lend us the money when we default. Our supposed ‘smartest’ financial gurus lost billions on, essentially, a simple pyramid scam/ponzi scheme (Madoff) that basic logic, ultimately, exposed… We obviously like to live above our means and when the bill comes due, we find someone to blame for our circumstance because it couldn’t possibly be us, right? So why would anyone expect our national approach to food consumption be any different?
Our nation obviously doesn’t like to count, or take personal responsibility. Telling people to budget their finances or count their calories elicits yawns from most of them. They know that taking responsibility would work, most likely, but secretly yearn for (or, worse, believe there is) a back door that would allow them to eschew the ‘rules’. Self-purported gurus or profit-driven companies emerge to pray on these self-delusions, teasing them with the idea that they can somehow ‘beat the system’ and skip the responsibility that monitoring intake/output requires. This gets them ‘excited’… learning that they can find a loophole that absolves them of responsibility. Baseless and obviously flawed mantras emerge: ‘Screw calories, just don’t eat carbs and you won’t get fat’, or ‘ZERO percent interest on balance transfers, because we want to help you get out of debt’.
Why? Because we want to believe we are faultless. We don’t make bad food judgments… some company has merely ‘coerced’ us into making bad choices. We’re not fatter because we eat more… some company has hidden terrible ingredients in our food to make us WANT to eat more. We’re not broke because we have a house /car/wardrobe/lifestyle we can’t afford… some creditor has hidden secret clauses in their lending agreement meant to ‘screw’ us. It’s practically our national philosophy: We are faultless in all things!
Alan is certainly knowledgeable about nutrition, excercise, biochemistry, etc… to be honest, though, any pursuer of logic and reason can deduce from the myriad of scientific evidence available that carbs/fructose, ALONE, haven’t made us fat and sick – neither have fats, carbs, proteins or any other sole factor. But our public problems would indicate that, by and large, we are not a nation of ‘logical’ thinkers – we simply want what we want, when we want it… and, since our own desires and decisions cannot be at fault for our fate, those who give us what we want MUST be.
Our nation’s refusal to acknowledge our own implicitness in our circumstance cartainly hasn’t helped us in addressing our national issues (all issues, not just the ‘nutritional’ ones). And until we assume responsibility for our choices, ‘logic’ will be hard-pressed to enter into our national discourse on any public matter (economy, health, foreign policy, etc). We will be doomed, instead, to replace ‘logic’ with ‘blame’ , and will, thus, continue to be inundated with swill from those who would demonize carbs, fructose, government, business, and (ultimately) all forms of common sense.
Until then, I will continue to find my logic here (and sites like Lyle’s, Martin’s, etc)…
Great site, Alan!
Blake — Thanks for the commentary. Where can I read more of your stuff?
Thank YOU for the blog, Alan. I don’t have one of my own yet… since my expertise is in political studies, about the only writing I usually do is ultra-boring academic-type stuff. I have written a thesis that might manage to put even the most ardent academics to sleep. Perhaps I could create a blog for narcoleptics…
Given my background, I am used to seeing irrational arguments come from folks with advanced degrees – the majority of our politicians are well educated folks, but the nature of their profession is to create consensus among voters so that they can get elected/employed. That means I am used to watching otherwise rational men make irrational arguments to play upon the fears/hopes/beliefs of voters…
As far as my interest in the science of nutrition and fitness, I’m really just a recovering alarmist myself. I was a ‘meal timing’ alarmist who swallowed the supplement company dogma that missing a meal/pill/workout every now and then would lead to fat gain/muscle loss/failure/fitness oblivion/etc. Don’t get me wrong, the strategy ‘worked’ for years – but, for looking so great, I sure was miserable. Then, I started seeking alternative methods to achieve results/fitness happiness, found Lyle McDonald’s writings, which led me to Matrin Berkhan’s site, which led me to yours. And, finally, I realized that all of the crap I had been swallowing was drivel circulated by supplement companies to get me to buy their products. Even a supposedly ‘educated’ guy like me was capable of irrationality in the face of his own ignorance (in this case, my ignorance was a lack of knowledge about the actual science of human performance). My eyes were opened…
So I have followed all of your sites regularly for some time and have never felt compelled to comment on any of them before – even in the face of the compelling debates that often go on. I usually just don’t feel I have NEAR enough knowledge to add much to the debate that isn’t already being contributed. But reading the discussion where you calmly and rationally responded to a supposed ‘scientist’ (as though people with advanced degrees aren’t capable of being poor logicians) while he basically refused to accept your references to ‘updated’ (i.e. more recent than 30 year old) data/studies, and, ultimately, reverted to the always popular argument that most parents use on their children (“because I said so”) reminded me of watching the recent political debates in our country… and made me angry. Watching a familiar scenario from my studied field play out on a site like yours that devotes itself to unbiased research review reminded me that NOTHING is exempt from the ‘political’ anymore… because human psychology applies to all modes of our understanding.
I know how this works (in theory, at least) in the political arena – so I felt I might be able to illustrate an analogous point to remind your readers that this ‘scientist’s’ argument has plenty of precedent… our politicians do it every day, so we shouldn’t be surprised to see it from the ‘good doctor’. Further, we shouldn’t be surprised when it works (i.e. gets a ton of YouTube hits). After all, we are the country that made Brittany Spears a billionaire… so we obviously love to swallow the otherwise unpalatable
Again, thank you for sharing your knowledge, and providing a forum where reason still has merit. It is a welcome respite from that with which I deal everyday!
My aversion to HFCS is more of the practical sort and admittedly extremely unscientific. It tastes horrible, and it prevents proper gelling activity when boiling pectin-based fruits.
Is there any explanation as to why drinks containing HFCS burn my throat while drinks with equivalent amounts of sucrose don’t?
Hi Alan,
I asked:
Alan,
For me the issue is not about obesity or HFCS vs. Sugar and calories. What I found interesting in Dr. Lustig’s presentation was the metabolism of fructose by the liver and the by-products ( Triglycerides and vLDL ). As an adult onset type II diabetic, when my ability to control blood sugar was impared ( through lack of diet and exercise) my triglycerides and LDL numbers were high. Having gotten my A1C number down to about 5.1 my triglyceride and LDL numbers came into line ( dramatically so).
Any thoughts on this portion of Dr. Lustig’s presentation?
You said in response:
Alex — This is yet another fairly grey area that seems to be solved by simple moderation. I’ll quote the section of a paper that touches upon this: Glycated hemoglobin (HbA1c) rises as a result of nonenzymatic modification of hemoglobin by glucose and is a strong risk factor for diabetic complications (especially retinopathy, peripheral vascular disease, and death) (20) and for CHD in nondiabetics (21). Several intervention studies in diabetics and nondiabetics show fructose to markedly lower HbA1c (22–27). Metaregression analysis confirms this as a fructose dose-dependent effect (10) (Fig. 1 A). Neither energy nor macronutrient intakes were confounding factors, but there is still need for studies on the progression of disease over very long durations. A fall in HbA1c caused by moderate to high fructose intake is not entirely expected. A rise in HbA1c would occur should insulin sensitivity be impaired. On the other hand, glycemic control more reflects a relative impairment of pancreatic function; meanwhile, fructose, which is low glycemic, makes little demand on the pancreas.” http://www.ncbi.nlm.nih.gov/pubmed/19386821
We agree on:
“The big picture solution is in managing total caloric balance with a predominance of minimally refined foods and sufficient physical activity.”
But, I don’t think you answered my question. So, permit me to ask again…
Let me start by saying I make ( and neither does Lustig ) *NO* distinction between the health value of table sugar vs. HFCS. I had to watch his presentation 3 times to understand that he was vilifying all sugar ( except that which comes naturally in raw fruits and vegetables ) and not just HFCS. Afterall, there is almost no difference in terms of glucose/fructose ratios between the two…
As I understand it, the reason fructose doesn’t really impact HbA1C is precisely because it is metabolized entirely by the liver. To greatly simplify the situation: When too much fructose enters the liver, the liver can’t process it all fast enough for the body to use as sugar. Instead, it starts making fats from the fructose and sending them off into the bloodstream as triglycerides (& vLDLs).
In my mind, this is potentially bad for at least three reasons:
1) High blood triglycerides are a risk factor for heart disease.
2) Fructose ends up circumventing the normal appetite signaling system, so appetite-regulating hormones aren’t triggered–and you’re left feeling unsatisfied. This is probably at least part of the reason why excess fructose consumption is associated with weight gain.
3) There is some evidence that excess fructose (and I mean from sources like sugar(sucrose) & HFCS) consumption may facilitate insulin resistance, and eventually type 2 diabetes.
Do I have this wrong? Does this clarify why I think we should pay a good deal of attention to what Dr. Lustig is saying?
Consider these charts:
When reduced the amount of sugar in my diet, and increased my exercise levels, I saw dramatic change in my lipid profile ( in 30 days mind you ).
The charts
http://diabeteshacks.com/charts/lipids.png
http://diabeteshacks.com/charts/a1c.png
Alan
Just discovered this site more or less by accident (in Australia) – spent some days at a medical conference last week where several sessions were about obesity.
Yes, everyone always wants the “magic bullet” solution. I am fascinated by the obesity epidemic (Australia is just a little behind the USA). I remember in 1998 watching some archival TV footage on the 30th anniversary of RFK’s death – the “funeral” train’s passage was lined by thousands of people – and they were SO MUCH THINNER than Americans “today” (ie 1998) it was stunning.
Both Dr. Lustig’s lecture and Alan’s review are educational, to be sure. However, I get the feeling that most people are getting caught up in minutia and fail to recognize what to me seems to be the real issue.
The real problem driving excessive consumption seems to be food choice. For example, I assume that the higher consumption of juices goes in hand with lower consumption of fruits and vegetables.
First, juices are more convenient (opening a carton instead of peeling and orange) and easier to consume (drinking instead of chewing and spitting out seeds). This may lead to higher caloric consumption of a fruit juice than the fruit itself.
Second, fruits and veggies have a higher fiber content than their respective juices. Fiber is a satiating nutrient.
Another example may be excessive consumption of highly caloric, sugar filled sauces.
Therefore, I believe that good food choices are probably a natural prevention, so to speak, of excessive involuntary caloric intake. Eat more fibrous foods, drop the soda, etc., and caloric intake will surely drop.
I had a friend that would have a 2 liter coke bottle next to bed in case he woke up thirsty! That plus all the soda he had throughout the day. He recently dropped the soda, and is now ~10-15lbs lighter.
Add poor food choice with a sedentary lifestyle from a young age, and you have a plausible explanation for the increasing obesity and diabetes occurrences in both adults and youths.
So, processed sugars probably do have negative effects on your health and should be kept to a minimum, but it is a volume issue as many have stated. And this volume problem seems to be driven by the greater issue at hand, which is food choices.
To end this post I will admit that I can in no way back my conclusion. Perhaps someone else can. I base my assumptions on observed behaviors of people I know in addition to some common sense.
Last year when taking 3rd year medical students for tutes I asked each group to “solve the obesity crisis” in one week between tutes. I was hoping for a “George Dantzig” moment [http://www.snopes.com/college/homework/unsolvable.asp] but sadly, and I suppose unsurprisingly, they never managed it. I told them if they had I would have ackowledged them in the footnotes of my award-winning papers!
Lustig and others may be on to something, but if it were that easy, it would also be easily solved, and the “solver” would be a multi-millionaire. Again I tell my students that if they had any program that delivered long-term weight loss in over 50% of people who signed up for it, then people would be coming from around the world to see them.
With regard to high-fructose corn syrup, it is barely used here in Australia but we have nearly the same obesity problems as the USA. And yes, I know we eat more sucrose in Australia, but the “uniqueness” of the HFCS argument can’t hold here as the sole explanation of obesity.
Last week I was at the World Congress of Internal Medicine in Melbourne, Australia and there were a few sessions on obesity. Japan is interesting – the BMI’s for men have gone up slowly over the last 30 years or so (but much less than other Western countries), while for women they have remained fairly stationary overall, and have actually FALLEN for women under 40 years of age. And of course people of Japanese descent in Hawaii and South America tend to have the BMI’s of the locals, not of their Japanese forebears.
Rod — Good points made, and I agree with much of them. However, the idea of “dropping” a particular food implies strict abstinence, and in many cases, this is not a realistic nor optimal solution. Decrease? Sure. Drop? Not necessarily. I’d refer you back to this post regarding flexible vs inflexible dieting: http://www.alanaragonblog.com/2010/01/29/the-bitter-truth-about-fructose-alarmism/#comment-1182
Alex,
I’d direct you again to the importance of dose & context. But first off, there is no solid evidence that fructose avoidance will benefit diabetics. What we can solidly conclude is that a reduction in overall carbohydrate intake can benefit certain diabetic circumstances. Further, the detriment or neutrality of fructose (particularly with regards to TG production) would be largely dependent upon chronic energy balance. In a nutshell, if someone is chronically hypercaloric, then liver glycogen would tend to be topped off more often, and thus TG production would occur to a greater extent. In the event of a chronic energy deficit, fructose intake would have a tendency to be directed towards gluconeogenesis. Allow me to direct you to this review indicating that a TG-raising effect in those with type-2 diabetes occurs above a threshold of 60g fructose: http://www.ncbi.nlm.nih.gov/pubmed/19592634
“A dose threshold for the effect of fructose on TG was observed in type 2 diabetes. Only at fructose doses greater than the CDA threshold of >60 g/day (>12% energy for a 2,000-kcal diet) (5) was a TG-raising effect observed in subgroup analyses. This threshold is consistent with the 100 g/day identified across different clinical states (7) and findings from hypercaloric feeding trials with fructose intakes at 25% excess energy in healthy humans, the only trials in which a TG-raising effect has been observed reliably (29,30,32–35). Although our threshold is lower than these estimates, it is higher than the estimated U.S. intake of total fructose of 9.1% energy (45.5 g/day for a 2,000-kcal diet) (8). The inability of low doses to stimulate a quantitatively meaningful DNL response may explain this threshold”
Bottom line: I’d rather support scientific thought than alarmist whistle-blowing.
Mr. Aragon, thoughts on the following?
http://www.ncbi.nlm.nih.gov/pubmed/20219526
It’s just the abstract, but in release (below) they mentioned the “free-floating” nature of the fructose and glucose in HFCS rather than what is found in cane or beet sugar. Would you consider that to be an essential?
http://www.princeton.edu/main/news/archive/S26/91/22K07/index.xml?section=topstories
Enjoy your site.
Some Guy — Rodent response to fructose is vastly different than human response to fructose. I’m currently writing a paper on this very subject. The differences are, well, big.
James Krieger stated 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.”
So, according to Krieger, the enzyme sucrase, which secreted by the tips of the villi of the epithelium in the small intestine, is not actually needed to catalyze the hydrolysis of sucrose to fructose and glucose. So what chemical action in the stomach gets the job done?
David,
Acid can catalyze the hydrolysis of sucrose.
James,
You say stomach acid catalyzes the cleavage of sucrose. This article [http://en.wikipedia.org/wiki/Fructose] says, “Free fructose is absorbed directly by the intestine; however, when fructose is consumed in the form of sucrose, digestion occurs entirely in the upper small intestine.” I’m interested in the truth. Is there research to support your assertion?
David,
Research as far back as 1921 showed that sucrose hydrolysis does occur in the stomach.
http://ajplegacy.physiology.org/cgi/pdf_extract/59/1/413
Now, the extent of sucrose hydrolysis in the stomach is low. It is also dependent upon the amount of time that the sucrose is present in the stomach. The percent hydrolysis will be low when sucrose is consumed on an empty stomach, as the sucrose will not remain present in the stomach long enough for extensive hydrolysis to occur. The majority will be hydrolyzed by sucrase in the small intestine.
With a mixed meal, sucrose will stay present in the stomach much longer, giving much more time for acid hydrolysis in the stomach.
Even if most sucrose is hydrolyzed in the intestine, it makes no difference when compared to HFCS. It’s been shown that the rate of intestinal glucose and fructose absorption, when in free form, is identical to the rate of intestinal glucose and fructose absorption when ingested as sucrose:
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC292710/pdf/jcinvest00261-0118.pdf
Alan,
Love, love, love this post and the thought-provoking comments. I am not an M.D., biochemist, or nutritionist — but as a layperson, I’d like to point out that anyone who wants to observe the effects of a diet very rich in unbound dietary fructose on primates, as opposed to rodents, can just visit their local zoo or turn on the Discovery Channel. The clinical trial period for unbound dietary fructose consumption among primates has been going on for several million years at least. (While the distinction between fresh fruit and refined sweeteners is obvious to most, as are dose and context, it seems not to be in much of the writing I’ve seen lately demonizing poor, defenseless monosaccharides.)
Alan, thanks for the great blog and I can’t wait to read your forthcoming paper comparing rodent and human data.
SED — Thanks for the feedback, glad you liked the melee. As for my article comparing humans & rats, that was done a couple of issues ago in AARR.
This Addictive Commonly Used Food Feeds Cancer Cells, Triggers Weight Gain, and Promotes Premature Aging
Death by sugar may not be an overstatement—evidence is mounting that sugar is THE MAJOR FACTOR causing obesity and chronic disease.
Is sugar a sweet old friend that is secretly plotting your demise?
There is a vast sea of research suggesting that it is. Science has now shown us, beyond any shadow of a doubt, that sugar in your food, in all its myriad of forms, is taking a devastating toll on your health.
The single largest source of calories for Americans comes from sugar—specifically high fructose corn syrup. Just take a look at the sugar consumption trends of the past 300 years:[1]
* In 1700, the average person consumed about 4 pounds of sugar per year.
* In 1800, the average person consumed about 18 pounds of sugar per year.
* In 1900, individual consumption had risen to 90 pounds of sugar per year.
* In 2009, more than 50 percent of all Americans consume one-half pound of sugar PER DAY—translating to a whopping 180 pounds of sugar per year!
Sugar is loaded into your soft drinks, fruit juices, sports drinks, and hidden in almost all processed foods—from bologna to pretzels to Worcestershire sauce to cheese spread. And now most infant formula has the sugar equivalent of one can of Coca-Cola, so babies are being metabolically poisoned from day one if taking formula.
No wonder there is an obesity epidemic in this country.
Today, 32 percent of Americans are obese and an additional one-third are overweight. Compare that to 1890, when a survey of white males in their fifties revealed an obesity rate of just 3.4 percent. In 1975, the obesity rate in America had reached 15 percent, and since then it has doubled.
Carrying excess weight increases your risk for deadly conditions such as heart disease, kidney disease and diabetes.
In 1893, there were fewer than three cases of diabetes per 100,000 people in the United States. Today, diabetes strikes almost 8,000 out of every 100,000 people.[1]
You don’t have to be a physician or a scientist to notice America’s expanding waistline. All you have to do is stroll through a shopping mall or a schoolyard, or perhaps glance in the mirror.
Sugars 101 — Basics of How to Avoid Confusion on this Important Topic
Sucrose
It is easy to become confused by the various sugars and sweeteners. So here is a basic overview:
* Dextrose, fructose and glucose are all monosaccharides, known as simple sugars. The primary difference between them is how your body metabolizes them. Glucose and dextrose are essentially the same sugar. However, food manufacturers usually use the term “dextrose” in their ingredient list.
* The simple sugars can combine to form more complex sugars, like the disaccharide sucrose (table sugar), which is half glucose and half fructose.
* High fructose corn syrup (HFCS) is 55 percent fructose and 45 percent glucose.
* Ethanol (drinking alcohol) is not a sugar, although beer and wine contain residual sugars and starches, in addition to alcohol.
* Sugar alcohols like xylitol, glycerol, sorbitol, maltitol, mannitol, and erythritol are neither sugars nor alcohols but are becoming increasingly popular as sweeteners. They are incompletely absorbed from your small intestine, for the most part, so they provide fewer calories than sugar but often cause problems with bloating, diarrhea and flatulence.
* Sucralose (Splenda) is NOT a sugar, despite its sugar-like name and deceptive marketing slogan, “made from sugar.” It’s a chlorinated artificial sweetener in line with aspartame and saccharin, with detrimental health effects to match.
* Agave syrup, falsely advertised as “natural,” is typically HIGHLY processed and is usually 80 percent fructose. The end product does not even remotely resemble the original agave plant.
* Honey is about 53 percent fructose[2], but is completely natural in its raw form and has many health benefits when used in moderation, including as many antioxidants as spinach.
* Stevia is a highly sweet herb derived from the leaf of the South American stevia plant, which is completely safe (in its natural form). Lo han (or luohanguo) is another natural sweetener, but derived from a fruit.
All Sugars are Not Equal
Glucose is the form of energy you were designed to run on. Every cell in your body, every bacterium—and in fact, every living thing on the Earth—uses glucose for energy.
But as a country, sucrose is no longer the sugar of choice. It’s now fructose.
If your diet was like that of people a century ago, you’d consume about 15 grams per day—a far cry from the 73 grams per day the typical person gets from sweetened drinks. In vegetables and fruits, it’s mixed in with vitamins, minerals, enzymes, and beneficial phytonutrients, all which moderate the negative metabolic effects. Amazingly, 25 percent of people actually consume more than 130 grams of fructose per day.
Making matters worse, all of the fiber has been removed from processed foods, so there is essentially no nutritive value at all. And the very products most people rely on to lose weight—the low-fat diet foods—are often the ones highest in fructose.
It isn’t that fructose itself is bad—it is the MASSIVE DOSES you’re exposed to that make it dangerous.
There are two overall reasons fructose is so damaging:
1. Your body metabolizes fructose in a much different way than glucose. The entire burden of metabolizing fructose falls on your liver.
2. People are consuming fructose in enormous quantities, which has made the negative effects much more profound.
The explosion of soda consumption is the major cause of this.
Today, 55 percent of sweeteners used in food and beverage manufacturing are made from corn, and the number one source of calories in America is soda, in the form of high fructose corn syrup.
Food and beverage manufacturers began switching their sweeteners from sucrose to corn syrup in the 1970s when they discovered that HFCS was not only far cheaper to make, it’s about 20 percent sweeter than conventional table sugar that has sucrose.
HFCS contains the same two sugars as sucrose but is more metabolically risky to you, due to its chemical form.
The fructose and the glucose are not bound together in HFCS, as they are in table sugar, so your body doesn’t have to break it down. Therefore, the fructose is absorbed immediately, going straight to your liver.
Too Much Fructose Creates a Metabolic Disaster in Your Body
Dr. Robert Lustig, Professor of Pediatrics in the Division of Endocrinology at the University of California, San Francisco, has been a pioneer in decoding sugar metabolism. His work has highlighted some major differences in how different sugars are broken down and used by the human body.
I highly recommend watching Lustig’s lecture in its entirety if you want to learn how fructose is ruining your health biochemically.
As I mentioned earlier, after eating fructose, most of the metabolic burden rests on your liver. This is NOT the case with glucose, of which your liver breaks down only 20 percent. Nearly every cell in your body utilizes glucose, so it’s normally “burned up” immediately after consumption.
So where does all of this fructose go, once you consume it?
Onto your thighs. It is turned into FAT (VLDL and triglycerides), which means more fat deposits throughout your body.
Eating Fructose is Far Worse than Eating Fat
However, the physiological problems of fructose metabolism extend well beyond a couple of pant sizes:
* Fructose elevates uric acid, which decreases nitric oxide, raises angiotensin, and causes your smooth muscle cells to contract, thereby raising your blood pressure and potentially damaging your kidneys.[1]
Increased uric acid also leads to chronic, low-level inflammation, which has far-reaching consequences for your health. For example, chronically inflamed blood vessels lead to heart attacks and strokes; also, a good deal of evidence exists that some cancers are caused by chronic inflammation. (See the next section for more about uric acid.)
* Fructose tricks your body into gaining weight by fooling your metabolism—it turns off your body’s appetite-control system. Fructose does not appropriately stimulate insulin, which in turn does not suppress ghrelin (the “hunger hormone”) and doesn’t stimulate leptin (the “satiety hormone”), which together result in your eating more and developing insulin resistance.[3] [4]
* Fructose rapidly leads to weight gain and abdominal obesity (“beer belly”), decreased HDL, increased LDL, elevated triglycerides, elevated blood sugar, and high blood pressure—i.e., classic metabolic syndrome.
* Fructose metabolism is very similar to ethanol metabolism, which has a multitude of toxic effects, including NAFLD (non-alcoholic fatty liver disease). It’s alcohol without the buzz.
These changes are not seen when humans or animals eat starch (or glucose), suggesting that fructose is a “bad carbohydrate” when consumed in excess of 25 grams per day. It is probably the one factor responsible for the partial success of many “low-carb” diets.
One of the more recent findings that surprised researchers is that glucose actually accelerates fructose absorption, making the potential health risks from HFCS even more profound.[1]
You can now see why fructose is the number one contributing factor to the current obesity epidemic.
Is Uric Acid the New Cholesterol?
By now you are probably aware of the childhood obesity epidemic in America—but did you know about childhood hypertension?
Until recently, children were rarely diagnosed with high blood pressure, and when they were, it was usually due to a tumor or a vascular kidney disease.
In 2004, a study showed hypertension among children is four times higher than predicted: 4.5 percent of American children have high blood pressure. Among overweight children, the rate is 10 percent. It is thought that obesity is to blame for about 50 percent of hypertension cases in adolescents today.[1]
Even more startling is that 90 percent of adolescents who have high blood pressure have elevated uric acid levels.
This has led researchers to ask, what does uric acid have to do with obesity and high blood pressure?
In his book, The Sugar Fix: The High-Fructose Fallout That is Making You Fat and Sick, Dr. Robert J. Johnson makes a compelling argument for a previously unrecognized connection between excess sugar consumption and high uric acid levels. However, he promotes artificial sweeteners as an alternative to sugar and makes other recommendations that I don’t agree with.
Dr. Johnson is a conventional physician who has not accepted large parts of natural medicine, however, he is one of the leading researchers defining the extent of fructose toxicity. He has spent many years of his life dedicating himself to uncover this mystery.
There are more than 3,500 articles to date showing a strong relationship between uric acid and obesity, heart disease, hypertension, stroke, kidney disease, and other conditions. In fact, a number of studies have confirmed that people with elevated serum uric acid are at risk for high blood pressure, even if they otherwise appear to be perfectly healthy.
Uric acid levels among Americans have risen significantly since the early half of the 20th Century. In the 1920s, average uric acid levels were about 3.5 ml/dl. By 1980, average uric acid levels had climbed into the range of 6.0 to 6.5 ml/dl and are probably much higher now.
How Does Your Body Produce Uric Acid?
It’s a byproduct of cellular breakdown. As cells die off, DNA and RNA degrade into chemicals called purines. Purines are further broken down into uric acid.
Fructose increases uric acid through a complex process that causes cells to burn up their ATP rapidly, leading to “cell shock” and increased cell death. After eating excessive amounts of fructose, cells become starved of energy and enter a state of shock, just as if they have lost their blood supply. Massive cellular die-off leads to increased uric acid levels.
And cells that are depleted of energy become inflamed and more susceptible to damage from oxidative stress. Fat cells actually become “sickly,” bloating up with excessive amounts of fat.
There is a simple, inexpensive blood test for determining your uric acid level, which I recommend you have done as part of your routine health checkups. Your level should be between 3.0 and 5.5 mg/dl, optimally.
There is little doubt in my mind that your uric acid level is a more potent predictor of cardiovascular and overall health than your total cholesterol level is. Yet virtually no one is screening for this.
Now that you know the truth you don’t have to be left out in the cold, as this is a simple and relatively inexpensive test that you can get at any doctor’s office. Odds are very good your doctor is clueless about the significance of elevated uric acid levels, so it will not likely be productive to engage in a discussion with him unless he is truly an open-minded truth seeker.
Merely get your uric acid level, and if it is over 5 then eliminate as much fructose as you can (also eliminate all beer), and retest your level in a few weeks.
Sugar Sensitization Makes the Problem Even WORSE!
There is yet another problem with sugar—a self-perpetuating one.
According to Dr. Johnson1, sugar activates its own pathways in your body—those metabolic pathways become “upregulated.” In other words, the more sugar you eat, the more effective your body is in absorbing it; and the more you absorb, the more damage you’ll do.
You become “sensitized” to sugar as time goes by, and more sensitive to its toxic effects as well.
The flip side is, when people are given even a brief sugar holiday, sugar sensitization rapidly decreases and those metabolic pathways become “downregulated.” Research tells us that even two weeks without consuming sugar will cause your body to be less reactive to it.
Try it for yourself! Take a two-week sugar sabbatical and see how different you feel.
Are Fruits Good or Bad for You?
Keep in mind that fruits also contain fructose, although an ameliorating factor is that whole fruits also contain vitamins and other antioxidants that reduce the hazardous effects of fructose.
Juices, on the other hand, are nearly as detrimental as soda, because a glass of juice is loaded with fructose, and a lot of the antioxidants are lost.
It is important to remember that fructose alone isn’t evil as fruits are certainly beneficial. But when you consume high levels of fructose it will absolutely devastate your biochemistry and physiology. Remember the AVERAGE fructose dose is 70 grams per day which exceeds the recommend limit by 300 percent.
So please BE CAREFUL with your fruit consumption. You simply MUST understand that because HFCS is so darn cheap, it is added to virtually every processed food. Even if you consumed no soda or fruit, it is very easy to exceed 25 grams of hidden fructose in your diet.
If you are a raw food advocate, have a pristine diet, and exercise very well, then you could be the exception that could exceed this limit and stay healthy.
Dr. Johnson has a handy chart, included below, which you can use to estimate how much fructose you’re getting in your diet. Remember, you are also likely getting additional fructose if you consume any packaged foods at all, since it is hidden in nearly all of them.
Fruit Serving Size Grams of Fructose
Limes 1 medium 0
Lemons 1 medium 0.6
Cranberries 1 cup 0.7
Passion fruit 1 medium 0.9
Prune 1 medium 1.2
Apricot 1 medium 1.3
Guava 2 medium 2.2
Date (Deglet Noor style) 1 medium 2.6
Cantaloupe 1/8 of med. melon 2.8
Raspberries 1 cup 3.0
Clementine 1 medium 3.4
Kiwifruit 1 medium 3.4
Blackberries 1 cup 3.5
Star fruit 1 medium 3.6
Cherries, sweet 10 3.8
Strawberries 1 cup 3.8
Cherries, sour 1 cup 4.0
Pineapple 1 slice
(3.5″ x .75″) 4.0
Grapefruit, pink or red 1/2 medium 4.3
Fruit Serving Size Grams of Fructose
Boysenberries 1 cup 4.6
Tangerine/mandarin orange 1 medium 4.8
Nectarine 1 medium 5.4
Peach 1 medium 5.9
Orange (navel) 1 medium 6.1
Papaya 1/2 medium 6.3
Honeydew 1/8 of med. melon 6.7
Banana 1 medium 7.1
Blueberries 1 cup 7.4
Date (Medjool) 1 medium 7.7
Apple (composite) 1 medium 9.5
Persimmon 1 medium 10.6
Watermelon 1/16 med. melon 11.3
Pear 1 medium 11.8
Raisins 1/4 cup 12.3
Grapes, seedless (green or red) 1 cup 12.4
Mango 1/2 medium 16.2
Apricots, dried 1 cup 16.4
Figs, dried 1 cup 23.0
In addition to limiting your intake of fructose, you should eliminate all sweetened beverages and fruit juices (including all artificial sweeteners) and drink only pure water and raw milk.
You can buy pure glucose (dextrose) as a sweetener for about $1 a pound. It is only 70% as sweet as sucrose, so you’ll end up using a bit more of it for the same amount of sweetness, making it slightly more expensive than sucrose—but still well worth it for your health as it has ZERO grams of fructose.
Remember that glucose can be used directly by every cell in your body and as such is far safer than the metabolic poison fructose.
Beer is also a good beverage to AVOID since it increases uric acid levels, just like fructose does, resulting in many of the same toxic effects.
All alcoholic beverages cause you to produce excess uric acid (and block your kidneys from excreting it), but beer seems to have a more pronounced effect on uric acid levels because it’s a rich source of guanosine, the type of purine that is most readily absorbed by the body.1
76 Additional Ways Sugar Can Ruin Your Health
In addition to throwing off your body’s homeostasis and wreaking havoc on your metabolic processes, excess sugar has a number of other significant consequences.
Nancy Appleton, PhD, author of the book Lick the Sugar Habit[5], contributed an extensive list of the many ways sugar can ruin your health from a vast number of medical journals and other scientific publications.
1. Sugar can suppress your immune system and impair your defenses against infectious disease.[6] [7]
2. Sugar upsets the mineral relationships in your body: causes chromium and copper deficiencies and interferes with absorption of calcium and magnesium.[8] [9] [10] [11]
3. Sugar can cause a rapid rise of adrenaline, hyperactivity, anxiety, difficulty concentrating, and crankiness in children.[12] [13]
4. Sugar can produce a significant rise in total cholesterol, triglycerides and bad cholesterol and a decrease in good cholesterol.[14] [15] [16] [17]
5. Sugar causes a loss of tissue elasticity and function.[18]
6. Sugar feeds cancer cells and has been connected with the development of cancer of the breast, ovaries, prostate, rectum, pancreas, biliary tract, lung, gallbladder and stomach.[19] [20] [21] [22] [23] [24] [25]
7. Sugar can increase fasting levels of glucose and can cause reactive hypoglycemia.[26] [27]
8. Sugar can weaken eyesight.[28] 1
9. Sugar can cause many problems with the gastrointestinal tract including: an acidic digestive tract, indigestion, malabsorption in patients with functional bowel disease, increased risk of Crohn’s disease, and ulcerative colitis.[29] [30] [31] [32] [33]
10. Sugar can cause premature aging.[34] In fact, the single most important factor that accelerates aging is insulin, which is triggered by sugar. 1
11. Sugar can lead to alcoholism.[35]
12. Sugar can cause your saliva to become acidic, tooth decay, and periodontal disease.[36] [37] [38]
13. Sugar contributes to obesity. [39] 1
14. Sugar can cause autoimmune diseases such as: arthritis, asthma, and multiple sclerosis.[40] [41] [42]
15. Sugar greatly assists the uncontrolled growth of Candida Albicans (yeast infections) [43]
16. Sugar can cause gallstones.[44]
17. Sugar can cause appendicitis.[45]
18. Sugar can cause hemorrhoids.[46]
19. Sugar can cause varicose veins.[47]
20. Sugar can elevate glucose and insulin responses in oral contraceptive users.[48]
21. Sugar can contribute to osteoporosis.[49]
22. Sugar can cause a decrease in your insulin sensitivity thereby causing an abnormally high insulin levels and eventually diabetes.[50] [51] [52]
23. Sugar can lower your Vitamin E levels.[53]
24. Sugar can increase your systolic blood pressure.[54]
25. Sugar can cause drowsiness and decreased activity in children.[55]
26. High sugar intake increases advanced glycation end products (AGEs),which are sugar molecules that attach to and damage proteins in your body. AGEs speed up the aging of cells, which may contribute to a variety of chronic and fatal diseases. [56] 1
27. Sugar can interfere with your absorption of protein.[57]
28. Sugar causes food allergies.[58]
29. Sugar can cause toxemia during pregnancy.[59]
30. Sugar can contribute to eczema in children.[60]
31. Sugar can cause atherosclerosis and cardiovascular disease.[61] [62]
32. Sugar can impair the structure of your DNA.[63]
33. Sugar can change the structure of protein and cause a permanent alteration of the way the proteins act in your body.[64] [65]
34. Sugar can make your skin age by changing the structure of collagen.[66]
35. Sugar can cause cataracts and nearsightedness.[67] [68]
36. Sugar can cause emphysema.[69]
37. High sugar intake can impair the physiological homeostasis of many systems in your body.[70]
38. Sugar lowers the ability of enzymes to function.[71]
39. Sugar intake is higher in people with Parkinson’s disease.[72]
40. Sugar can increase the size of your liver by making your liver cells divide, and it can increase the amount of fat in your liver, leading to fatty liver disease.[73] [74]
41. Sugar can increase kidney size and produce pathological changes in the kidney such as the formation of kidney stones.[75] [76] Fructose is helping to drive up rates of kidney disease. 1
42. Sugar can damage your pancreas.[77]
43. Sugar can increase your body’s fluid retention.[78]
44. Sugar is enemy #1 of your bowel movement.[79]
45. Sugar can compromise the lining of your capillaries.[80]
46. Sugar can make your tendons more brittle.[81]
47. Sugar can cause headaches, including migraines.[82]
48. Sugar can reduce the learning capacity, adversely affect your children’s grades and cause learning disorders.[83] [84]
49. Sugar can cause an increase in delta, alpha, and theta brain waves, which can alter your ability to think clearly.[85]
50. Sugar can cause depression.[86]
51. Sugar can increase your risk of gout.[87]
52. Sugar can increase your risk of Alzheimer’s disease.[88] MRI studies show that adults 60 and older who have high uric acid are four to five times more likely to have vascular dementia, the second most common form of dementia after Alzheimer’s.1
53. Sugar can cause hormonal imbalances such as: increasing estrogen in men, exacerbating PMS, and decreasing growth hormone.[89] [90] [91] [92]
54. Sugar can lead to dizziness.[93]
55. Diets high in sugar will increase free radicals and oxidative stress.[94]
56. A high sucrose diet of subjects with peripheral vascular disease significantly increases platelet adhesion.[95]
57. High sugar consumption by pregnant adolescents can lead to a substantial decrease in gestation duration and is associated with a twofold-increased risk for delivering a small-for-gestational-age (SGA) infant.[96] [97]
58. Sugar is an addictive substance.[98]
59. Sugar can be intoxicating, similar to alcohol.[99]
60. Sugar given to premature babies can affect the amount of carbon dioxide they produce.[100]
61. Decrease in sugar intake can increase emotional stability.[101]
62. Your body changes sugar into 2 to 5 times more fat in the bloodstream than it does starch.[102]
63. The rapid absorption of sugar promotes excessive food intake in obese subjects.[103]
64. Sugar can worsen the symptoms of children with attention deficit hyperactivity disorder (ADHD).[104]
65. Sugar adversely affects urinary electrolyte composition.[105]
66. Sugar can impair the function of your adrenal glands.[106]
67. Sugar has the potential of inducing abnormal metabolic processes in normal, healthy individuals, thereby promoting chronic degenerative diseases.[107]
68. Intravenous feedings (IVs) of sugar water can cut off oxygen to your brain.[108]
69. Sugar increases your risk of polio.[109]
70. High sugar intake can cause epileptic seizures.[110]
71. Sugar causes high blood pressure in obese people.[111]
72. In intensive care units, limiting sugar saves lives.[112]
73. Sugar may induce cell death.[113]
74. In juvenile rehabilitation centers, when children were put on low sugar diets, there was a 44 percent drop in antisocial behavior.[114]
75. Sugar dehydrates newborns.[115]
76. Sugar can cause gum disease.[116]
It should now be crystal clear just how damaging sugar is. You simply cannot achieve your highest degree of health and vitality if you are consuming a significant amount of it.
Fortunately, your body has an amazing ability to heal itself when given the basic nutrition it needs, and your liver has an incredible ability to regenerate. If you start making changes today, your health WILL begin to improve, returning you to the state of vitality that nature intended.
References:
* [1] Johnson RJ and Gower T. (2009) The Sugar Fix: The High-Fructose Fallout That is Making You Sick and Fat, Pocket, 416 pp
* [2] “What sweetener should you choose? Sugar? Honey? Agave nectar?” Fitnessspotlight
* [3] Stanhope KL, Schwarz JM, Keim NL, Griffen SC, Bremer AA, Graham JL, Hatcher B, Cox CL, Dyachenko A, Zhang W, McGahan JP, Seibert A, Krauss RM, Chiu S, Schaefer EJ, Ai M, Otokozawa S, Nakajima K, Nakano T, Beysen C, Hellerstein MK, Berglund L and Havel PJ. “Consuming fructose-sweetened, not glucose-sweetened, beverages increases visceral adiposity and lipids and decreases insulin sensitivity in overweight/obese humans,” J Clin Invest. 2009; 119(5):1322-1334
* [4] Park A. “All sugars aren’t the same: Glucose is better, study says,” Time Magazine, April 21, 2009
* [5] Appleton N. Lick the Sugar Habit (1996) Avery, 2nd Ed. 272 pp.
* [6] Sanchez, A., et al. Role of Sugars in Human Neutrophilic Phagocytosis, American Journal of Clinical Nutrition. Nov 1973;261:1180_1184. Bernstein, J., al. Depression of Lymphocyte Transformation Following Oral Glucose Ingestion. American Journal of Clinical Nutrition.1997;30:613
* [7] Ringsdorf, W., Cheraskin, E. and Ramsay R. Sucrose, Neutrophilic Phagocytosis and Resistance to Disease, Dental Survey. 1976;52(12):46_48
* [8] Couzy, F., et al. “Nutritional Implications of the Interaction Minerals,” Progressive Food and Nutrition Science 17;1933:65-87
* [9] Kozlovsky, A., et al. Effects of Diets High in Simple Sugars on Urinary Chromium Losses. Metabolism. June 1986;35:515_518
* [10] Fields, M.., et al. Effect of Copper Deficiency on Metabolism and Mortality in Rats Fed Sucrose or Starch Diets, Journal of Clinical Nutrition. 1983;113:1335_1345
* [11] Lemann, J. Evidence that Glucose Ingestion Inhibits Net Renal Tubular Reabsorption of Calcium and Magnesium. Journal of Clinical Nutrition. 1976 ;70:236_245
* [12] Goldman, J., et al. Behavioral Effects of Sucrose on Preschool Children. Journal of Abnormal Child Psychology.1986;14(4):565_577
* [13] Jones, T. W., et al. Enhanced Adrenomedullary Response and Increased Susceptibility to Neuroglygopenia: Mechanisms Underlying the Adverse Effect of Sugar Ingestion in Children. Journal of Pediatrics. Feb 1995;126:171-7
* [14] Scanto, S. and Yudkin, J. The Effect of Dietary Sucrose on Blood Lipids, Serum Insulin, Platelet Adhesiveness and Body Weight in Human Volunteers, Postgraduate Medicine Journal. 1969;45:602_607
* [15] Albrink, M. and Ullrich I. H. Interaction of Dietary Sucrose and Fiber on Serum Lipids in Healthy Young Men Fed High Carbohydrate Diets. American Journal of Clinical Nutrition. 1986;43:419
* [16] Reiser, S. Effects of Dietary Sugars on Metabolic Risk Factors Associated with Heart Disease. Nutritional Health. 1985;203_216
* [17] Lewis, G. F. and Steiner, G. Acute Effects of Insulin in the Control of Vldl Production in Humans. Implications for The insulin-resistant State. Diabetes Care. 1996 Apr;19(4):390-3 R. Pamplona, M. .J., et al. Mechanisms of Glycation in Atherogenesis. Medical Hypotheses. 1990;40:174-181
* [18] Cerami, A., Vlassara, H., and Brownlee, M. “Glucose and Aging.” Scientific American. May 1987:90. Lee, A. T. and Cerami, A. The Role of Glycation in Aging. Annals of the New York Academy of Science; 663:63-67
* [19] Takahashi, E., Tohoku University School of Medicine, Wholistic Health Digest. October 1982:41:00
* [20] Quillin, Patrick, Cancer’s Sweet Tooth, Nutrition Science News. Ap 2000 Rothkopf, M.. Nutrition. July/Aug 1990;6(4)
* [21] Michaud, D. Dietary Sugar, Glycemic Load, and Pancreatic Cancer Risk in a Prospective Study. J Natl Cancer Inst. Sep 4, 2002 ;94(17):1293-300
* [22] Moerman, C. J., et al. Dietary Sugar Intake in the Etiology of Biliary Tract Cancer. International Journal of Epidemiology. Ap 1993.2(2):207-214.
* [23] The Edell Health Letter. Sept 1991;7:1
* [24] De Stefani, E.”Dietary Sugar and Lung Cancer: a Case control Study in Uruguay.” Nutrition and Cancer. 1998;31(2):132_7
* [25] Cornee, J., et al. A Case-control Study of Gastric Cancer and Nutritional Factors in Marseille, France. European Journal of Epidemiology 11 (1995):55-65
* [26] Kelsay, J., et al. Diets High in Glucose or Sucrose and Young Women. American Journal of Clinical Nutrition. 1974;27:926_936. Thomas, B. J., et al. Relation of Habitual Diet to Fasting Plasma Insulin Concentration and the Insulin Response to Oral Glucose, Human Nutrition Clinical Nutrition. 1983; 36C(1):49_51
* [27] Dufty, William. Sugar Blues. (New York:Warner Books, 1975)
* [28] Acta Ophthalmologica Scandinavica. Mar 2002;48;25. Taub, H. Ed. Sugar Weakens Eyesight, VM NEWSLETTER;May 1986:06:00
* [29] Dufty.
* [30] Yudkin, J. Sweet and Dangerous.(New York:Bantam Books,1974) 129
* [31] Cornee, J., et al. A Case-control Study of Gastric Cancer and Nutritional Factors in Marseille, France, European Journal of Epidemiology. 1995;11
* [32] Persson P. G., Ahlbom, A., and Hellers, G. Epidemiology. 1992;3:47-52
* [33] Jones, T. W., et al. Enhanced Adrenomedullary Response and Increased Susceptibility to Neuroglygopenia: Mechanisms Underlying the Adverse Effect of Sugar Ingestion in Children. Journal of Pediatrics. Feb 1995;126:171-7
* [34] Lee, A. T.and Cerami A. The Role of Glycation in Aging. Annals of the New York Academy of Science.1992;663:63-70
* [35] Abrahamson, E. and Peget, A. Body, Mind and Sugar. (New York: Avon, 1977)
* [36] Glinsmann, W., Irausquin, H., and Youngmee, K. Evaluation of Health Aspects of Sugar Contained in Carbohydrate Sweeteners. F. D. A. Report of Sugars Task Force. 1986:39:00 Makinen K.K.,et al. A Descriptive Report of the Effects of a 16_month Xylitol Chewing_gum Programme Subsequent to a 40_month Sucrose Gum Programme. Caries Research. 1998; 32(2)107_12
* [37] Glinsmann, W., Irausquin, H., and K. Youngmee. Evaluation of Health Aspects of Sugar Contained in Carbohydrate Sweeteners. F. D. A. Report of Sugars Task Force.1986;39:36_38
* [38] Appleton, N. New York: Healthy Bones. Avery Penguin Putnam:1989
* [39] Keen, H., et al. Nutrient Intake, Adiposity, and Diabetes. British Medical Journal. 1989; 1:00 655_658
* [40] Darlington, L., Ramsey, N. W. and Mansfield, J. R. Placebo Controlled, Blind Study of Dietary Manipulation Therapy in Rheumatoid Arthritis, Lancet. Feb 1986;8475(1):236_238
* [41] Powers, L. Sensitivity: You React to What You Eat. Los Angeles Times. (Feb. 12, 1985). Cheng, J., et al. Preliminary Clinical Study on the Correlation Between Allergic Rhinitis and Food Factors. Lin Chuang Er Bi Yan Hou Ke Za Zhi Aug 2002;16(8):393-396
* [42] Erlander, S. The Cause and Cure of Multiple Sclerosis, The Disease to End Disease.” Mar 3, 1979;1(3):59_63
* [43] Crook, W. J. The Yeast Connection. (TN:Professional Books, 1984)
* [44] Heaton, K. The Sweet Road to Gallstones. British Medical Journal. Apr 14, 1984; 288:00:00 1103_1104. Misciagna, G., et al. American Journal of Clinical Nutrition. 1999;69:120-126
* [45] Cleave, T. The Saccharine Disease. (New Canaan, CT: Keats Publishing, 1974)
* [46] Ibid
* [47] Cleave, T. and Campbell, G. (Bristol, England:Diabetes, Coronary Thrombosis and the Saccharine Disease: John Wright and Sons, 1960)
* [48] Behall, K. Influ ence of Estrogen Content of Oral Contraceptives and Consumption of Sucrose on Blood Parameters. Disease Abstracts International. 1982;431437
* [49] Tjäderhane, L. and Larmas, M. A High Sucrose Diet Decreases the Mechanical Strength of Bones in Growing Rats. Journal of Nutrition. 1998:128:1807_1810
* [50] Beck, Nielsen H., Pedersen O., and Schwartz S. Effects of Diet on the Cellular Insulin Binding and the Insulin Sensitivity in Young Healthy Subjects. Diabetes. 1978;15:289_296
* [51] Sucrose Induces Diabetes in Cat. Federal Protocol. 1974;6(97). diabetes
* [52] Reiser, S., et al. Effects of Sugars on Indices on Glucose Tolerance in Humans. American Journal of Clinical Nutrition. 1986;43:151-159
* [53] Journal of Clinical Endocrinology and Metabolism. Aug 2000
* [54] Hodges, R., and Rebello, T. Carbohydrates and Blood Pressure. Annals of Internal Medicine. 1983:98:838_841
* [55] Behar, D., et al. Sugar Challenge Testing with Children Considered Behaviorally Sugar Reactive. Nutritional Behavior. 1984;1:277_288
* [56] Furth, A. and Harding, J. Why Sugar Is Bad For You. New Scientist. Sep 23, 1989;44
* [57] Simmons, J. Is The Sand of Time Sugar? LONGEVITY. June 1990:00:00 49_53
* [58] Appleton, N. New York: LICK THE SUGAR HABIT. Avery Penguin Putnam:1988. allergies
* [59] Cleave, T. The Saccharine Disease: (New Canaan Ct: Keats Publishing, Inc., 1974).131
* [60] Ibid. 132
* [61] Pamplona, R., et al. Mechanisms of Glycation in Atherogenesis. Medical Hypotheses . 1990:00:00 174_181
* [62] Vaccaro O., Ruth, K. J. and Stamler J. Relationship of Postload Plasma Glucose to Mortality with 19 yr Follow up. Diabetes Care. Oct 15,1992;10:328_334. Tominaga, M., et al, Impaired Glucose Tolerance Is a Risk Factor for Cardiovascular Disease, but Not Fasting Glucose. Diabetes Care. 1999:2(6):920-924
* [63] Lee, A. T. and Cerami, A. Modifications of Proteins and Nucleic Acids by Reducing Sugars: Possible Role in Aging. Handbook of the Biology of Aging. (New York: Academic Press, 1990)
* [64] Monnier, V. M. Nonenzymatic Glycosylation, the Maillard Reaction and the Aging Process. Journal of Gerontology 1990:45(4):105_110
* [65] Cerami, A., Vlassara, H., and Brownlee, M. Glucose and Aging. Scientific American. May 1987:00:00 90
* [66] Dyer, D. G., et al. Accumulation of Maillard Reaction Products in Skin Collagen in Diabetes and Aging. Journal of Clinical Investigation. 1993:93(6):421_22
* [67] Veromann, S.et al.”Dietary Sugar and Salt Represent Real Risk Factors for Cataract Development.” Ophthalmologica. 2003 Jul-Aug;217(4):302-307
* [68] Goulart, F. S. Are You Sugar Smart? American Fitness. March_April 1991:00:00 34_38. Milwakuee, WI
* [69] Monnier, V. M. Nonenzymatic Glycosylation, the Maillard Reaction and the Aging Process. Journal of Gerontology. 1990:45(4):105_110
* [70] Ceriello, A. Oxidative Stress and Glycemic Regulation. Metabolism. Feb 2000;49(2 Suppl 1):2729
* [71] Appleton, Nancy. New York; Lick the Sugar Habit. Avery Penguin Putnam, 1988 enzymes
* [72] Hellenbrand, W. Diet and Parkinson’s Disease. A Possible Role for the Past Intake of Specific Nutrients. Results from a Self-administered Food-frequency Questionnaire in a Case-control Study. Neurology. Sep 1996;47(3):644-650
* [73] Goulart, F. S. Are You Sugar Smart? American Fitness. March_April 1991:00:00 34_38
* [74] Ibid.
* [75] Yudkin, J., Kang, S. and Bruckdorfer, K. Effects of High Dietary Sugar. British Journal of Medicine. Nov 22, 1980;1396
* [76] Blacklock, N. J., Sucrose and Idiopathic Renal Stone. Nutrition and Health. 1987;5(1-2):9Curhan, G., et al. Beverage Use and Risk for Kidney Stones in Women. Annals of Internal Medicine. 1998:28:534-340
* [77] Goulart, F. S. Are You Sugar Smart? American Fitness. March_April 1991:00:00 34_38. Milwakuee, WI
* [78] Ibid. fluid retention
* [79] Ibid. bowel movement
* [80] Ibid. compromise the lining of the capillaries
* [81] Nash, J. Health Contenders. Essence. Jan 1992; 23:00 79_81
* [82] Grand, E. Food Allergies and Migraine.Lancet. 1979:1:955_959
* [83] Schauss, A. Diet, Crime and Delinquency. (Berkley Ca; Parker House, 1981)
* [84] Molteni, R, et al. A High-fat, Refined Sugar Diet Reduces Hippocampal Brain-derived Neurotrophic Factor, Neuronal Plasticity, and Learning. NeuroScience. 2002;112(4):803-814
* [85] Christensen, L. The Role of Caffeine and Sugar in Depression. Nutrition Report. Mar 1991;9(3):17-24
* [86] Ibid,44
* [87] Yudkin, J. Sweet and Dangerous.(New York:Bantam Books,1974) 129
* [88] Frey, J. Is There Sugar in the Alzheimer’s Disease? Annales De Biologie Clinique. 2001; 59 (3):253-257
* [89] Yudkin, J. Metabolic Changes Induced by Sugar in Relation to Coronary Heart Disease and Diabetes. Nutrition and Health. 1987;5(1-2):5-8
* [90] Yudkin, J and Eisa, O. Dietary Sucrose and Oestradiol Concentration in Young Men. Annals of Nutrition and Metabolism. 1988:32(2):53-55
* [91] The Edell Health Letter. Sept 1991;7:1
* [92] Gardner, L. and Reiser, S. Effects of Dietary Carbohydrate on Fasting Levels of Human Growth Hormone and Cortisol. Proceedings of the Society for Experimental Biology and Medicine. 1982;169:36_40
* [93] Journal of Advanced Medicine. 1994;7(1):51-58
* [94] Ceriello, A. Oxidative Stress and Glycemic Regulation. Metabolism. Feb 2000;49(2 Suppl 1):2729
* [95] Postgraduate Medicine.Sept 1969:45:602-07
* [96] Lenders, C. M. Gestational Age and Infant Size at Birth Are Associated with Dietary Intake among Pregnant Adolescents. Journal of Nutrition. Jun 1997;1113-1117
* [97] Ibid.
* [98] Sugar, White Flour Withdrawal Produces Chemical Response. The Addiction Letter. Jul 1992:04:00 Colantuoni, C., et al. Evidence That Intermittent, Excessive Sugar Intake Causes Endogenous Opioid Dependence. Obes Res. Jun 2002 ;10(6):478-488. Annual Meeting of the American Psychological Society, Toronto, June 17, 2001 http://www.mercola.com/2001/jun/30/sugar.htm
* [99] Ibid.
* [100] Sunehag, A. L., et al. Gluconeogenesis in Very Low Birth Weight Infants Receiving Total Parenteral Nutrition Diabetes. 1999 ;48 7991_800
* [101] Christensen L., et al. Impact of A Dietary Change on Emotional Distress. Journal of Abnormal Psychology.1985;94(4):565_79
* [102] Nutrition Health Review. Fall 85 changes sugar into fat faster than fat
* [103] Ludwig, D. S., et al. High Glycemic Index Foods, Overeating and Obesity. Pediatrics. March 1999;103(3):26-32
* [104] Pediatrics Research. 1995;38(4):539-542. Berdonces, J. L. Attention Deficit and Infantile Hyperactivity. Rev Enferm. Jan 2001;4(1)11-4
* [105] Blacklock, N. J. Sucrose and Idiopathic Renal Stone. Nutrition Health. 1987;5(1 & 2):9
* [106] Lechin, F., et al. Effects of an Oral Glucose Load on Plasma Neurotransmitters in Humans. Neurophychobiology. 1992;26(1-2):4-11
* [107] Fields, M. Journal of the American College of Nutrition. Aug 1998;17(4):317_321
* [108] Arieff, A. I. Veterans Administration Medical Center in San Francisco. San Jose Mercury; June 12/86. IVs of sugar water can cut off oxygen to the brain
* [109] Sandler, Benjamin P. Diet Prevents Polio. Milwakuee, WI,:The Lee Foundation for for Nutritional Research, 1951
* [110] Murphy, Patricia. The Role of Sugar in Epileptic Seizures. Townsend Letter for Doctors and Patients. May, 2001 Murphy Is Editor of Epilepsy Wellness Newsletter, 1462 West 5th Ave., Eugene, Oregon 97402
* [111] Stern, N. & Tuck, M. Pathogenesis of Hypertension in Diabetes Mellitus. Diabetes Mellitus, a Fundamental and Clinical Test. 2nd Edition, (PhiladelphiA; A:Lippincott Williams & Wilkins, 2000)943-957
* [112] Christansen, D. Critical Care: Sugar Limit Saves Lives. Science News. June 30, 2001; 159:404
* [113] Donnini, D. et al. Glucose May Induce Cell Death through a Free Radical-mediated Mechanism.Biochem Biohhys Res Commun. Feb 15, 1996:219(2):412-417
* [114] Schoenthaler, S. The Los Angeles Probation Department Diet-Behavior Program: Am Empirical Analysis of Six Institutional Settings. Int J Biosocial Res 5(2):88-89
* [115] Gluconeogenesis in Very Low Birth Weight Infants Receiving Total Parenteral Nutrition. Diabetes. 1999 Apr;48(4):791-800
* [116] Glinsmann, W., et al. Evaluation of Health Aspects of Sugar Contained in Carbohydrate Sweeteners.” FDA Report of Sugars Task Force -1986 39 123
Yudkin, J. and Eisa, O. Dietary Sucrose and Oestradiol Concentration in Young Men. Annals of Nutrition and Metabolism. 1988;32(2):53-5
Leonardo — Thanks for that lengthy, yet utterly empty cut/pasted contribution to the discussion.
I’d say that Leonardo can’t spell irony and hasn’t bothered to read any of the actual debate. I would have moderated such an obvious blind dump but thats just me.
OTH thanks for the initial post & this summary.
Thanks for the comment, Jason. I’ll leave Leonardo’s dump up there just for comic relief.