In finance, a foreign exchange option (commonly shortened to just FX option or currency option) is a derivative financial instrument that gives the right but not the obligation to exchange money denominated in one currency into another currency at a pre-agreed exchange rate on a specified date.[1] See Foreign exchange derivative. The foreign exchange options market is the deepest, largest and most liquid market for options of any kind. Most trading is over the counter (OTC) and is lightly regulated, but a fraction is traded on exchanges like the International Securities Exchange, Philadelphia Stock Exchange, or the Chicago Mercantile Exchange for options on futures contracts. The global market for exchange-traded currency options was notionally valued by the Bank for International Settlements at $158.3 trillion in 2005 For example, a GBPUSD contract could give the owner the right to sell? Eagles Long Road Out Of Eden Rar File. 1,000,000 and buy $2,000,000 on December 31. In this case the pre-agreed exchange rate, or strike price, is 2.0000 USD per GBP (or GBP/USD 2.00 as it is typically quoted) and the notional amounts (notionals) are?1,000,000 and $2,000,000.

This type of contract is both a call on dollars and a put on sterling, and is typically called a GBPUSD put, as it is a put on the exchange rate; although it could equally be called a USDGBP call. If the rate is lower than 2.0000 on December 31 (say 1.9000), meaning that the dollar is stronger and the pound is weaker, then the option is exercised, allowing the owner to sell GBP at 2.0000 and immediately buy it back in the spot market at 1.9000, making a profit of (2.0000 GBPUSD? 1.9000 GBPUSD)? 1,000,000 GBP = 100,000 USD in the process. If instead they take the profit in GBP (by selling the USD on the spot market) this amounts to 100,000 / 1.9000 = 52,632 GBP.

In finance, a foreign exchange option (commonly shortened to just FX option or currency option) is a derivative financial instrument that gives the right but not the.

Although FX options are more widely used today than ever before, few multinationals act as if they truly understand when and why these instruments can add to shareholder value. To the contrary, much of the time corporates seem to use FX options to paper over accounting problems, or to disguise the true cost of speculative positioning, or sometimes to solve internal control problems. The standard clich? About currency options affirms without elaboration their power to provide a company with upside potential while limiting the downside risk. Options are typically portrayed as a form of financial insurance, no less useful than property and casualty insurance. This glossy rationale masks the reality: if it is insurance then a currency option is akin to buying theft insurance to protect against flood risk. The truth is that the range of truly non-speculative uses for currency options, arising from the normal operations of a company, is quite small.

In reality currency options do provide excellent vehicles for corporates' speculative positioning in the guise of hedging. Corporates would go better if they didn't believe the disguise was real. Let's start with six of the most common myths about the benefits of FX options to the international corporation -- myths that damage shareholder values. Historically, the currency derivative pricing literature and the macroeconomics literature on FX determination have progressed separately. In this Chapter I argue the joint study of these two strands of literature and give an overview of FX option pricing concepts and terminology crucial for this interdisciplinary study. I also explain the three sources of information about market expectations and perception of risk that can be extracted from FX option prices and review empirical methods for extracting option-implied densities of future exchange rates. As an illustration, I conclude the Chapter by investigating time series dynamics of option-implied measures of FX risk vis-a-vis market events and US government policy actions during the period January 2007 to December 2008.

Chapter 2: This Chapter proposes using foreign exchange (FX) options with different strike prices and maturities to capture both FX expectations and risks. We show that exchange rate movements, which are notoriously difficult to model empirically, are well-explained by the term structures of forward premia and options-based measures of FX expectations and risk. Although this finding is to be expected, expectations and risk have been largely ignored in empirical exchange rate modeling. Using daily options data for six major currency pairs, we first show that the cross section options-implied standard deviation, skewness and kurtosis consistently explain not only the conditional mean but also the entire conditional distribution of subsequent currency excess returns for horizons ranging from one week to twelve months. At June 30 and September 30, the value of the portfolio was?1,050,000. Note, however, that the notional amount of Ridgeway's hedging instrument was only?1,000,000.

Therefore, subsequent to the increase in the value of the pound (which is assumed to have occurred on June 30), a portion of Ridgeway's foreign currency exchange risk was not hedged. For the three-month period ending September 30, exchange rates caused the value of the portfolio to decline by $52,500.

Of that amount, only $50,000 was offset by changes in the value of the currency put option. The difference between those amounts ($2,500) represents the exchange rate loss on the unhedged portion of the portfolio (i.e., the 'additional'?50,000 of fair value that arose through increased share prices after entering into the currency hedge). At June 30, the additional?50,000 of stock value had a U.S. Dollar fair value of $45,000. At September 30, using the spot rate of 0.85:1, the fair value of this additional portion of the portfolio declined to $42,500. Ridge way will exclude from its assessment of hedge effectiveness the portion of the fair value of the put option attributable to time value. That is, Ridgeway will recognize changes in that portion of the put option's fair value in earnings but will not consider those changes to represent ineffectiveness.

Aitan Goelman, the CFTC’s Director of Enforcement, stated: “The setting of a benchmark rate is not simply another opportunity for banks to earn a profit. Countless individuals and companies around the world rely on these rates to settle financial contracts, and this reliance is premised on faith in the fundamental integrity of these benchmarks. The market only works if people have confidence that the process of setting these benchmarks is fair, not corrupted by manipulation by some of the biggest banks in the world.” The Commission finalized rules to implement the Dodd-Frank Wall Street Reform and Consumer Protection Act regarding Regulation of Off-Exchange Retail Foreign Exchange Transactions and Intermediaries. The Commission also finalized Conforming Changes to existing Retail Foreign Exchange Regulations in response to the Dodd-Frank Act. Additional information regarding these final rules is provided below, including rules, factsheets, and details of meetings held between CFTC Staff and outside parties.

January 29, 2010 Excellent stuff, as usual, Alan. I do have a quick question with relation to high fructose corn syrup, and perhaps you could share your quick thoughts(admittedly I don’t have a massive knowledge in this area, so the question stems strictly from a claim I often hear bandied about, which may or may not be true.or perhaps somewhere in between). A common indictment of HFCS is that it is derived from GMO corn. While there’s absolutely no debate in terms of sucrose versus HFCS given their ratios of fructose and glucose, is there any merit at all (based upon what is currently known) about whether or not this is a problem to one degree or another?

Based upon the types of folks who tend to make that claim, it is tempting to say it is more alarmism, but I figured it would be best to just ask someone knowledgeable like you than simply accepting what those folks are saying. January 30, 2010 Hi, Alan, here is SturmBG from Lyle’s forum (the falesly accused paleotard). When I was watching the video (some time ago) I was thinking about pretty much the same points you did. But there is something else – this guy is obviously trying to sound cogently and he is doing it good while actually advocating some correct points.

How about the possibility that he knows that he is exxagerating for the sake of being more interesting? If I had to speak in front of an audience that is not exceptionaly knowledgeble about the topic, I would speak something like him. What do you think about that? January 30, 2010 Good post Alan, and, personally, I’m a little tired of all the alarmist talk when it comes to carbs/sugar. We are a nation of gluttons, who, as you pointed out, have increased our caloric intakes and moved much less over the past 25 years. And most dietary tribes (low-fat, low-carb, vegetarianism, etc.) will focus so much on one macronutrient that they miss the overall pictures that calories are king!

I guess I’m just trying to figure out how much of all this is simply for profit or are many of these researchers that myopic? January 30, 2010 Fine, Sturm, you’re not a paleotard. You’re justa fucking retard apologist for groups like the paleo fucks and Lustwig. How about the possibility that he’s just an alarmist dipshit who should be ignored completely because he can’t even get basic concepts right?

Or do you have to constantly make excuses for EVERYONE making bullshit claims like him, the paleo cult fucks, Dean Peat, etc. Because that’s what you seem to constantly do.

“Oh, they make some good points.” Yeah, a broken clock is right twice a day too. Because someone makes one good point doesn’t change the fact that EVERYTHING ELSE THEY ARE SAYING IS COMPLETELY FUCKING RETARDEDLY WRONG.

January 30, 2010 Lustig goes on and on about it being a “quantity issue.” I don’t know what more he could have said to mention the fact that the dangers of frucotse are dose-dependent, right in line with what Yudkin proposed. Besides, if we are eating too many calories as you allude to, why are we doing that? And perhaps the appetite perversion of fructose is not experienced meal to meal, but creates a steadily upward-creeping disparity between metabolism and appetite. Plus, gaining 40 pounds of fat in 40 years is only 1/20th of a serving of peanut butter per day.

We’re talking about something very subtle. A tiny disparity for the vast majority of people.

January 30, 2010 Hi, I preach the treachery of HFCS so my mission/bias is clear. “HFCS is nearly identical to sucrose in structure and function.” In my humble opinion it is the “nearly identical” that is killing us.

Have you considered the ratios of fructose:glucose in sucrose and HFCS? HFCS is 55%fructose:45%glucose. This appears to be close to the 50:50 ratio found in sucrose, until you do the math. 55%:45% = 55/45 =1.22. This means that in every can of Coke (bottled in the USA) there is, compared to glucose, 22% extra fructose. In everyday terms this means that drinking 5 HFCS-55 sweetened beverages is equivalent to drinking 4 1/4 cans of sucrose sweetened be beverage plus 3/4 can of pure fructose sweetened beverage.

Considering that the average teen chugs one of two cans a day, that’s a lot of extra fructose. I’ve always wondered why the CRA, Corn Refiners Assoc., chose that ratio. Were they just trying to find a ratio that simulated sucrose-like sweetness, or were they looking for something extremely sweet so end manufacturers could use less, or perhaps they wanted something a little more addictive? At any rate, they chose the ratio, not mother nature.

Back to the facts: Sucrose is a disaccharide.The fructose and glucose are chemically linked. Our gut has the enzyme sucrase. It’s responsibility is to cleave the disaccharide so the simple sugars, fructose and glucose, can enter the bloodstream.

Enzymes function as biological catalysts and also serve as gatekeepers; they regulate entry of sugars into the bloodstream. In contrast, HFCS is only a gemisch, a mixture of fructose and glucose, not requiring sucrase control. The fructose is shunted directly to the liver for metabolism. When you drink something with HFCS-55 you might as well have an I.V. To your portal vein. Btw: Food manufacturers are always trying to stay one step ahead of the consumer.

I was reading the ingredients on a bottle of low cal fruit water. No HFCS, good; no fructose, good; but wait there’s levuloselevulose is fructose. You’ve made some good points, but you’re skirting the issue as to the basic reasons of our obesity, type II diabetes crisis. Two thirds of our intake of HFCS comes through sweetened beverages.

It is estimated that per capita intake of HFCS is about 70 lbs per year. That’s a lot of extra fructose assaulting our livers. If you look at CDC’s obesity vs. HFCS and sucrose chart, you will notice that obesity really started to climb in 1984-1985.

That was the year that the big boys, Coke and Pepsi, switched to HFCS-55. Ditch HFCS, especially HFCS-55. To your health. January 30, 2010 Cynth, “You’ve made some good points, but you’re skirting the issue as to the basic reasons of our obesity, type II diabetes crisis. Two thirds of our intake of HFCS comes through sweetened beverages.” Step back for two seconds, and think logically. What’s to blame, HFCS or people overconsuming food and drink?

Would they be taking in that much fructose if they even just had 1 can of sweetened drink per day? How about no cans, and only fruit?

Still a problem? It’s tough I know. It’s easy to blame one thing for all of the problems but seriously it comes down to something so simple as people over consuming and being lazy. January 31, 2010 Alan – Feel free to delete this if you feel it’s irrelevant or redundant.

Just something I came across several years ago that I thought was interesting: “Some facts about High Fructose Corn Syrup (HFCS): • HFCS contains approximately equal ratios of fructose and glucose, similar to sugar (sucrose, cane sugar), honey, or invert sugar. • Many parts of the world, including Australia, Mexico and Europe, have rising rates of obesity and diabetes despite having little or no HFCS in their foods and beverages. Department of Agriculture data show that per capita consumption of HFCS has been declining in recent years, yet the incidence of obesity and diabetes in the United States remains on the rise.

• HFCS has not increased the amount of fructose in the U.S. Diet since being introduced. While HFCS use has increased, the use of sucrose has significantly decreased. Since HFCS and sucrose share basically the same composition, the amount of fructose in use has remained nearly the same for the last 30 years.” Unfortunately, the author of this article provided no sources. Can you confirm any of this information? February 1, 2010 Mr.

Aragon, I suggest it is you who should take a better look at the data. Despite documented increases in daily caloric intake in the last 30 years, total dietary fat intake has remained relatively stable (5.3 gm decrease in men, 5 gm increase in women), while the percentage of calories from saturated fat has decreased. Although high-fat feeding can induce overnutrition and metabolic syndrome in experimental animal and human models, it does so only in the presence of concomitant carbohydrate.

However, carbohydrate intake has skyrocketed during this same period. Centers for Disease Control.

Trends in intake of energy and macronutrients–United States, 1971-2000. 53, 80-82 (2004). Chanmugam, P. Did fat intake in the United States really decline between 1989-1991 and 1994-1996? 103, 867-872 (2003). The Japanese diet does have fructose; but it is only in fruit.

There are no added sugars in their diet. That is what we are talking about here; added dietary sugars; not endogenous ones.

Indeed, I am not alone; the American Heart Association has revised their recommended consumption of added sugars down from 22 tsp/day to 6 or 9 tsp/day. Johnson, R.K. Dietary sugars intake and cardiovascular health. A scientific statement from the American Heart Association. Circulation 120, 1011-1020 (2009).

It is about dose, and it is about context. I say so in the video, please do not misquote me. Hard spirits do not cause metabolic syndrome, but beer and shochu do; because the ethanol is delivered along with glucose. Same with fructose in soda or juice; as the only way to get fructose is with glucose combined (HFCS or sucrose); so they are congruent. Fructose always comes with glucose; and the two together overwhelm the liver’s capacity to process either one, generating metabolic syndrome through the pathways described in the video. Athyros VG, Liberopoulos EN, Mikhailidis DP, Papageorgiou AA, Ganotakis ES, Tziomalos K, Kakafika AI, Karagiannis A, Lambropoulos S, Elisaf M. Association of drinking pattern and alcohol beverage type with the prevalence of metabolic syndrome, diabetes, coronary heart disease, stroke, and peripheral arterial disease in a Mediterranean cohort.

After viewing your critique, I will maintain my position, and I suggest you rethink yours. Sincerely, Robert Lustig, M.D. February 1, 2010 @Pikku: Most of the studies showing that sweet food/drink is more desirable than cocaine have been done on rats.

“Discussion First, our findings seem to run counter to seminal research in monkeys showing that the large majority of individuals prefer high doses of intravenous cocaine over dry food, regardless of the amount of food available and even despite severe weight loss. However, in most previous studies, except one, the food option contained no or only modest concentrations of sweet tastants, which probably explains why it was neglected in favor of high doses of cocaine. In addition, in those studies that employed lightly sweetened food pellets, the amount of effort required to obtain the food option was ten times higher than to obtain cocaine, thereby favoring drug choices. However, in one choice study, all monkeys clearly preferred, ceteris paribus, the highest dose of cocaine over a 1-g sucrose pellet. The discrepancy between this latter study and the present study may suggest either that sweetened beverages are more rewarding than sweetened dryfoods (which may induce thirst in addition to reward) and/or that one 1-g sucrose pellet is not enough to surmount the rewarding effects of the highest doses of cocaine*. Finally, one cannot rule out the possibility that this discrepancy could also reflect an interspecific gap between rodents and primates, the latter being hypothetically more susceptible to cocaine reward than the former.

Future research is needed to tease apart these different hypotheses.” *1g of sucrose doesn’t do much for me. 1g of coke, on the other hand;-D @Alan: What about my comment about certain varieties of apple having a very high sugar content?

February 2, 2010 I don’t have an exact moment for you. Probably late in the video. I also don’t see why you are hung up on dosage, as the biochemistry speaks for itself. Fructose would not be the first chemical that humans can tolerate in low amounts but is damaging in high doses.

Florine in water? Omega-6 fats? Lustig did not enumerate a specific amount, and rightly so, as it is specific to individuals, as Alan pointed out. Along with his discussion of fiber, he generalized that fructose occurring in nature come in safe amounts with benefits that override the fructose dangers. February 2, 2010 Considering that just about everything is dose-dependent in the world of nutrition/pharmacology/toxicology, unless he explicitly says fructose isn’t, why jump to that conclusion?

If fructose is indeed “poison”, as he claims, it clearly can only be so in the chronic, dose-dependent sense, or else we would all be quite sick or even dead already. This is really a mountain being made out of a molehill. Scrutinize his actual publications if you really think you have a legitimate gripe against Lustig’s theses. February 2, 2010 You’ve missed a critical part of the picture Alan. In 1999, the USDA asked more firms (food companies) that weren’t being taken into account prior to this point to report their total sales of vegetable oil. They then threw the numbers into the mix in 2000 and did not adjust for years prior.

This makes it appear like a huge increase in added fats when in fact this is not the case. This also makes it look like total fat intake or calories is the cause of obesity epidemic but not so.

But you’re in good company – Michael Pollan gets this wrong too. From the USDA information I have, the only macronutrient that significantly increased was carbohydrate between 1982 and 2000. Grain and flour consumption went way up. Fruit consumption went up.

Added sugars went way up as did vegetable consumption. Total fat isn’t really changing because meat consumption goes down from 2002 to 2007. So in fact, it is certainly not added fats that have caused an obesity epidemic as is touted in the industry. Indeed if anything it is the total carbohydrate that has caused the obesity epidemic and not total calories. But this is always the key issue.

Yes, total calories went up, but the calories were sugar. So, which is responsible for people getting fatter? Well, we don’t know. That’s why you have to do randomized controlled trials and they have to be designed in such away that they test this question in particular. This is why we need to convince someone in a position of authority to do metabolic ward studies and feed half a dozen men 3500 calories of a balanced diet and feed another half a dozen 3500 calories of a ketogenic diet. If the former stay fat and the latter lose weight, then it’s not the calories they consumed that made the difference, but the difference in the type of calories. Biochemistry suggests that this may very well be true.

From my experience with clients I know this to be true. February 2, 2010 Nicholas said: “I don’t have an exact moment for you. Probably late in the video.” or earlier, or maybe it was somewhere in the middle on second thought – maybe he didn’t say it at all.

Nicholas: “I also don’t see why you are hung up on dosage, as the biochemistry speaks for itself.” Because the dose makes the poison, Nicholas – the very point Alan hammered home and the very point that you insist Dr. Lustig agreed with. Nicholas: “Fructose would not be the first chemical that humans can tolerate in low amounts but is damaging in high doses. Florine in water? Omega-6 fats?” A fanciful red herring. ANYTHING in a high enough dose can be deleterious to health – even foods that are considered healthy and nutrient dense.

If we are going to make comparison’s can we at least make them somewhat relevant? Lustig were being honest, he would state that fructose consumption within the context of an otherwise healthy and hypocaloric diet would not likely do jack squat to anyone’s health. If he feels otherwise, he ought to show evidence of this.

February 2, 2010 Hello again Fred! It is refreshing to hear you say “we don’t know if it’s calories or carbs/sugar”. The thing is, though that metabolic ward studies HAVE been done and the majority show that it IS in fact calories that make the biggest difference in weight.

Which leaves your only supportive evidence as “I know it’s the carbs because I’ve seen it”. I agree that it would be ideal to have more RTC’s including metabolic ward studies, but let’s seek some middle ground here for a minute.

Nobody is suggesting you just eat x number of calories – without any regard for macro composition. But when protein is matched and adequate, the fat and carb chips can fall where they may and people will lose weight – provided they are in a deficit. February 2, 2010 “It is refreshing to hear you say “we don’t know if it’s calories or carbs/sugar”. The thing is, though that metabolic ward studies HAVE been done and the majority show that it IS in fact calories that make the biggest difference in weight. Which leaves your only supportive evidence as “I know it’s the carbs because I’ve seen it”. ****That’s not exactly what I am saying Mike.

And would you be so kind as to list the references for these studies you say have been done? As far as I am aware they have not. The only ward studies I know of were not ketogenic vs standard USDA fare and not maintenance level calorically. And I gave several references as to other studies that do show a metabolic advantage to truly low carb diets on that godforsaken message board. When you see a 7 foot tall 13 year old at a table eating a huge portion of food do you think even for a second that his height is caused by his eating enormous amounts of calories? Of course not. You know the child has a hormonal abnormality.

Why then if you see a fat person eating an enormous amount of food do you blame his obesity on his caloric consumption? Obesity is a disorder of excess fat accumulation. Let that sink in deep.

“I agree that it would be ideal to have more RTC’s including metabolic ward studies, but let’s seek some middle ground here for a minute. Nobody is suggesting you just eat x number of calories – without any regard for macro composition. But when protein is matched and adequate, the fat and carb chips can fall where they may and people will lose weight – provided they are in a deficit.” ****Provided they are in a deficit. And when they are in a deficit, they are always eating less carbohydrate usually significantly less on their new found diets. The conventional wisdom is to say “See it’s the calories.” But all lower calories diets decrease total carbohydrate intake. And no one can keep up eating a low calorie diet for long.

We’re talking ad libitum diet composition. If you were to match protein intake and assuring adequate protein intake for both groups, do you really think that if the subjects were fed maintenance level calories (if there is such a thing) one group getting pure fat and the other pure sugar there would be no difference in body composition after say a 6 month period? February 2, 2010 Fred you stated – “When you see a 7 foot tall 13 year old at a table eating a huge portion of food do you think even for a second that his height is caused by his eating enormous amounts of calories?

Of course not. You know the child has a hormonal abnormality. Why then if you see a fat person eating an enormous amount of food do you blame his obesity on his caloric consumption?” This is a constant argument point you use. In fact, I have seen you use this stance at least 3 times.

It seems you and guys like Taubes have a common theme. Your theme is to pull out circus sideshow cases and make them relevant for the general population. It couldn’t possibly be the average client I track and monitor is usually 25% under what their recommend caloric intake due to their lifestyle and work habits. It couldn’t possibly be the 2000 calorie meals, of both fat and carbohydrates, people are eating in one sitting. Yes, there is room for discussion on why people overeat and how to better optimize diets. The majority of us fall in a close line to what a proper macro distribution should be.

No one ever says to mainline fructose. What we do say, or I should say for myself, is there is a fundamental base of energy distribution and it is king. It is possible and frequent due to genetics and lifestyle habits, that energy and apdatation has a large margin to move around in, but energy demand is the base to build everything on. Your 7ft 13 year old boy isn’t the middle line, he is the top of the scale.

The rest of the people fall closer to the middle of that line. While he may not be normal, he isn’t void of following those same principles. His body functions on energy demand the exact same way mine does, it is just at a higher level of energy demand. You are adjusting the wrong line.

Instead of placing the movement into freak hormonal response you need to place it in energy needs and demands. Then and only then will you start to make a genuine change in client response because you base is starting off with common sense and something measurable.

February 2, 2010 Mike: the lecture clearly stated that fructose is a chronic use, non-acute poison, as opposed to alcohol. In any case, keep in mind this is a lecture, not a dissertation nor academic paper. It may be forgiven for missing or not clarifying some points. I think overall the message is correct. Mountains over molehills. Weelittleme: have you been to Japan? Their Coke tastes like club soda.

There is more fresh food with little corn syrup (ie real food). There may not be absolute zero fructose, but you are being nit picky. Bottom line is that Japanese eat less sugar. February 2, 2010 Mike — I’ll interject my feedback to your quotes: • HFCS contains approximately equal ratios of fructose and glucose, similar to sugar (sucrose, cane sugar), honey, or invert sugar. ^^^Yes, this is true for the most common types of HFCS on the market.

• Many parts of the world, including Australia, Mexico and Europe, have rising rates of obesity and diabetes despite having little or no HFCS in their foods and beverages. ^^^It’s true that HFCS is not used extensively outside of the US, and yet obesity has been on the rise worldwide. Department of Agriculture data show that per capita consumption of HFCS has been declining in recent years, yet the incidence of obesity and diabetes in the United States remains on the rise. ^^^This is not true. While added sugars as a whole are decreased as a percentage of total calories, HFCS consumption has increased significantly.

• HFCS has not increased the amount of fructose in the U.S. Diet since being introduced.

While HFCS use has increased, the use of sucrose has significantly decreased. Since HFCS and sucrose share basically the same composition, the amount of fructose in use has remained nearly the same for the last 30 years.” ^^^This doesn’t sound too far off, according to the latest ERS/USDA data. February 2, 2010 Chris — You said: “This is really a mountain being made out of a molehill.” Funny enough, this is exactly my point about Lustig’s spotlighting of fructose while downplaying other important factors, not to mention its dose-dependent effect.

Nicholas — In your fervor to defend Lustig, you’re misrepresenting his statement, which was explicitly that, “The Japanese diet does have fructose; but it is only in fruit. There are no added sugars in their diet.”. February 3, 2010 Oh and I forgot to say something about the HFCS vs. Sugar debate.

Here in Bulgaria we don’t use almost any HFCS at all. We didn’t have a problem going obese.

And when somebody sais “HFCS (or sugar) is to be blamed for obesity” may be they have to take a look at the pacific countries (in some countries obesity is 90%+) and ask themselfs if it isn’t more of a cultural than diet reason. My point is that people are obese because they want to do what makes them obese (consume calories). February 3, 2010 I’m dog tired so this will be a short post. Lustig has made it clear here that there is context and dose-response but he continues to obfuscate – not commenting on the context of calories or dose ranges.

If you watch the video, the message seems pretty clear – fructose is TOXIC. Context is an afterthought. This is what is disingenuous and perhaps what Alan (and others) are objecting to. To quote Lustig himself in this video; (At about the 20:15 mark) “Sugar and HFCS are both the same – they are both equally bad. They’re both dangerous they’re both poison I said it – poison.

My charge before the end of tonight is to convince you that fructose is poison”. Hmmm sounds like his thesis may have something to do with oh, I don’t know convincing us that fructose is poison?

In terms of caloric context, Lustig proclaims (at about the 21 min. Mark) “It has nothing to do with calories, it’s poison by itself”.

These are caustic statements – statements that demand immediate qualification. By not contextualizing these bold proclamations it makes Lustig sound agenda-driven. This is contrary to scientific thought and in my mind, reduces his message to some good points mixed in with a lot of noise.

That’s all for tonight folks. February 3, 2010 Dr. Lustig — Please see my interjections to your numbered quotes below. ____________________________________________________________ 1. Despite documented increases in daily caloric intake in the last 30 years, total dietary fat intake has remained relatively stable (5.3 gm decrease in men, 5 gm increase in women), while the percentage of calories from saturated fat has decreased. Although high-fat feeding can induce overnutrition and metabolic syndrome in experimental animal and human models, it does so only in the presence of concomitant carbohydrate. However, carbohydrate intake has skyrocketed during this same period.

Centers for Disease Control. Trends in intake of energy and macronutrients–United States, 1971-2000. 53, 80-82 (2004).

Chanmugam, P. Did fat intake in the United States really decline between 1989-1991 and 1994-1996? 103, 867-872 (2003). ____________________________________________________________ ^^^As I mentioned to Fred, I’ve laid out data that has been updated as recently as Feb 2009. If there are discrepancies between that & what you have, then that’s not surprising, since self-reported surveys are generally problematic (subject to recall bias & inconsistent interview methods) in the first place. But let’s assume for a second that the USDA/ERS data showing a decrease in percent of added sugars is incorrect. It doesn’t change the fact that singling out fructose, HFCS, or sugar consumption as THE most culpable agent of the rise in obesity is merely speculative, and insufficiently supported by the bulk of the controlled data.

I’ll quote a rather exhaustive review by Forshee et al [Crit Rev Food Sci Nutr. 2007;47(6):561-82.]: “The evidence that HFCS consumption uniquely increases the risk of weight gain is very weak. Few studies directly explore the relationship between HFCS, body weight, and BMI. The only evidence directly linking HFCS consumption and weight gain is ecological data.

Ecological data are widely recognized as insufficient for establishing cause-effect relationships. HFCS consumption and weight gain have major gaps. The hypothesis that the increasing levels of HFCS in the food supply has increased the F:G ratio is not supported by the USDA ERS food availability data. The impact of HFCS consumption on BMI must be put in context with other broad economic and societal changes during the past several decades. Many other plausible explanations for rising overweight and obesity rates exist, including a decrease in smoking; 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, 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. The expert panel concluded that the currently available evidence is insufficient to implicate HFCS per se as a causal factor in the overweight and obesity problem in the United States.” ____________________________________________________________ 2.

The Japanese diet does have fructose; but it is only in fruit. There are no added sugars in their diet. That is what we are talking about here; added dietary sugars; not endogenous ones. Indeed, I am not alone; the American Heart Association has revised their recommended consumption of added sugars down from 22 tsp/day to 6 or 9 tsp/day. Johnson, R.K. Dietary sugars intake and cardiovascular health.

A scientific statement from the American Heart Association. Circulation 120, 1011-1020 (2009). ____________________________________________________________ ^^^We’re not in total disagreement here since we’ve both mentioned that the Japanese DO indeed eat fruit as a regular part of their diet. However, you’re still skirting the fact that you mentioned explictly in the beginning of your video that the Japanese diet “eliminates fructose”. Furthermore, aside from it being a contradictory claim, you said explicitly that the only source of fructose in the Japanese diet is “only in fruit. There are no added sugars in their diet.” This is simply false.

Sushi rice is made with about 1 tbsp sucrose per cup of uncooked rice. There are numerous Japanese desserts & sweets that all have added sugar as an ingredient. Even some non-dessert items have added sugar within dips and sauces such as teriyaki. ____________________________________________________________ 3. It is about dose, and it is about context. I say so in the video, please do not misquote me.

Hard spirits do not cause metabolic syndrome, but beer and shochu do; because the ethanol is delivered along with glucose. Same with fructose in soda or juice; as the only way to get fructose is with glucose combined (HFCS or sucrose); so they are congruent. Fructose always comes with glucose; and the two together overwhelm the liver’s capacity to process either one, generating metabolic syndrome through the pathways described in the video. Athyros VG, Liberopoulos EN, Mikhailidis DP, Papageorgiou AA, Ganotakis ES, Tziomalos K, Kakafika AI, Karagiannis A, Lambropoulos S, Elisaf M. Association of drinking pattern and alcohol beverage type with the prevalence of metabolic syndrome, diabetes, coronary heart disease, stroke, and peripheral arterial disease in a Mediterranean cohort.

____________________________________________________________ ^^^If it’s really your position that it’s about dosage and context, then we are not in fundamental disagreement. However, based on my observations of the reactions of those on fitness message boards, that certainly has not been the predominant take-home message absorbed by the viewers.

If indeed you were delivering an objective message about dosage & context, it was lost amongst the alarmist claims. The majority are unversed and unfamiliar with the research, and come away with the sentiments that JLB & RayC mentioned – fructose is the devil, and overall calories pale in comparison. I’ll also add that many people have gotten the incorrect impression that HFCS & sucrose have an appetite-stimulatory effect due to the fructose content. That’s false according to the available research. Let me also add the fact that unless I missed it, you neglected to provide anything concrete in terms of a safe fructose dosage range, nor any contextual guidelines in which to frame such a range.

After viewing your response, I will maintain my position, and I suggest you rethink the content and delivery of your next lecture. Let me suggest that you place a little more emphasis on dose-dependence rather than painting a black-white picture of fructose that crucially downplays the importance of context. I also suggest that you re-check your claims concerning the Japanese diet if you’re going to use it as a salient introductory point of the lecture.

Thanks for engaging in discussion, I’ll await your response. February 3, 2010 “This is a constant argument point you use. In fact, I have seen you use this stance at least 3 times. It seems you and guys like Taubes have a common theme.

Your theme is to pull out circus sideshow cases and make them relevant for the general population.” Circus sideshow cases? Obese people were used as circus sideshow cases years ago when obesity was very rare. You couldn’t put a fat lady in a circus act today as she’d look normal. The point is excessive height as well as excessive fat accumulation is a hormonal disorder. It is a disorder of excess fat accumulation. Obese people eat more (some don’t eat that much) because much of what they eat gets stored as fat rather than being made available for energy.

When this happens, they remain hungry since too many of the caories went to storage rather than to building/maintaining. The rest of your post reflects the common thinking on the matter and if you try to keep people lean by feeding them less total calories you’ll find very poor long term results. And every single time a fitness professional decreases someones calories they also decrease their total carb intake and alter the type of carbs from highly refined to fibrous. You will never get an obese person lean by lowering their calories and yet keeping the refined sugars high. February 3, 2010 “Fred — If you can present a more recent update than the USDA data that I linked, you’ll be in a better position to argue. I’ve laid out data that has been updated as recently as Feb 2009.

If there are discrepancies between that & what you have, then that’s not surprising, since self-reported surveys are generally problematic (subject to recall bias & inconsistent interview methods) in the first place. I agree with you that well-controlled prolonged hypercaloric comparisons of varying macronutrient intakes are lacking.” I don’t understand. My point was that in 2000 the RDA asked many more companies to report on vegetable oil. The spike from 1999 to 2000 was due to previous underreporting. They did not however go BACK and adjust. Therefore the percentage of nutrients are all askew.

My USDA table is from 2006. Carbohydrate is still far and away the greatest macronutrient increase. February 3, 2010 “In studies directly comparing the effect of fructose and glucose preloads on subsequent food intake, one showed no difference [7], while another showed it was actually the fructose preload that resulted in lesser food intake than the glucose preload [8]. A recent review of the literature on fructose’s effect on satiety found no compelling case for the idea that fructose is less satiating than glucose, or that HFCS is less satiating than sucrose [9]. So much for Lustig’s repeated assertion that fructose and fructose-containing sugars increase subsequent food intake.

I suppose it’s easier to sensationalize claims based on rodent data.” Alan, you smashed that claim. In addition, other factors influence hunger, appetite, and subsequent food intake; these factors include neurochemical factors (e.g. Serotonin, endorphins, dopamine etc.), gastric signals (e.g. Peptides, stomach distention), hedonistic qualities of food (e.g. Taste, texture, smell), genetic, environmental (e.g. Food availability, cost, etc.), and emotional factors (stress, depression, etc.) (Freedman et al., 2001). When considering food consumption in everyday life it is important to consider the above-mentioned factors.

It is impractical to consider one nutrient’s impact, while ignoring other factors that influence satiety. “Demonizing fructose without mentioning the dose-dependent nature of its effects is intellectually dishonest.” Agreed.

When discussing the benefits or dangers of a substance it’s important to consider dosage. “A chemical can’t simply be classified as “dangerous” or “safe”: it always depends on the amount, or dose, received. The effects of a chemical will change with different amounts, so that below a certain dose it may be harmless or beneficial and at a higher dose it may be toxic. We all know that a little aspirin is good for us, whereas 50 tablets could cause acute renal failure, coma, and heart failure from salicylate poisoning” (Sense About Science, Making Sense of Chemical Stories). “One of Lustig’s opening assertions is that The Atkins diet and the Japanese diet share one thing in common: the absence of fructose.” Really? I wonder why he would make a claim that is so easily refuted?

On another note, let’s say this assertion (fantasy) was correct. Does he assume the absence of fructose in a hypercaloric diet results in weight loss?

Does he assume fructose consumption in a hypocaloric diet results in weight gain? Does he assume that everyone following the Atkins and Japanese Diet are lean? Does he understand correlation doesn’t mean causation? Keith Stanovich, cognitive scientist, says “There is no excuse for making causal inferences on the basis of correlational evidence when it is possible to manipulate variables in a way that would legitimately justify a causal inference.” There are two major classes of ambiguity present in a simple correlation between two variables (Stanovich, 2007): the directionality problem, and the third-variable problem. Directionality problem: before deciding that a correlation between A and variable B is due to changes in A causing changes in B, we must consider the direction of causation may be the opposite, from B to A.

Third- variable problem: the two variables may not indicate a causal path in either direction, but occurs because both variables are related to a third variable. “However, I disagree (as does the bulk of the research) with his myopic, militant focus on fructose avoidance.” So do basic logic and a plethora of scientific evidence. “Pointing the finger at fructose while dismissing dosage and context” is utter nonsense. Cynthia- Please re-read my comments on correlation and causation. Please refer to any basic manual on logic. Other good references include Stanovich- How to Think Straight About Psychology, Patten- Understanding Research Methods, Aragon- Girth Control. There is an ample amount of data explaining the difference between correlation and causation.

Lusting- “The Japanese diet does have fructose; but it is only in fruit. There are no added sugars in their diet. That is what we are talking about here; added dietary sugars; not endogenous ones.” Apparently, you are under the assumption that natural sugars are always safer than laboratory made sugars (never mind their molecular structures are identical, cannot be distinguished). This false assumption is generally derived from the idea that processes performed by living things are fundamentally different than ones created through chemical laboratory processes. Ok, never mind that every living process is fundamentally a chemical process.

Would you be surprised if I told you some of the world’s most dangerous toxins are all natural? They include ricin, abrin, botulinum, and strychnine—highly evolved chemical weapons used by organisms for self-defense and territorial expansion. Indeed, every plant and microbe carries a variety of mostly uncharacterized, more or less toxic attack chemicals, and synthetic chemicals are no more likely to be toxic than natural ones (Silver, 2006). Other examples of dangerous natural substance include water hemlock, arsenic and mercury. The chemical reality- whether a substance is manufactured by people, copied from nature or extracted directly from nature, tells us little at all about its properties. To reiterate, in terms of chemical safety, “industrial”, “synthetic”, “artificial” and “man-made” are not necessarily more damaging and “natural” does not necessarily mean better. Lee Silver, Professor of Biology at Princeton Univ & Author of Challenging Nature, discussing natural food myths- Peter- “but still in most cases people need to see something exxagarated to actually find it interesting.” So, that makes it all right to perpetuate fallacious information?

Where do we draw the line and how can we ever expect to gain any real knowledge if interesting info takes precedence over evidence-based claims? Nicholas- You said “I watched the video once (but very carefully and with some rewind), and I thought Dr. Lustig communicated dose and context of fructose adequately during the 90 minutes. It was not headlined for you, but it was covered.” When asked to specify where it occurred you said “I don’t have an exact moment for you.

Probably late in the video. I also don’t see why you are hung up on dosage, as the biochemistry speaks for itself.” How about you watch the video again and locate the moment Lustig communicated dose. Your comment is like saying a study says xx but I can’t tell you exactly where or when I saw it, it was in Obesity Research or the Journal of Nutrition or one of those things. Not sure, but I know I saw it. Why get hung up on dosage? Once again, “[a] chemical can’t simply be classified as “dangerous” or “safe”: it always depends on the amount, or dose, received.

The effects of a chemical will change with different amounts, so that below a certain dose it may be harmless or beneficial and at a higher dose it may be toxic. We all know that a little aspirin is good for us, whereas 50 tablets could cause acute renal failure, coma, and heart failure from salicylate poisoning” (Sense About Science, Making Sense of Chemical Stories). JLB- “This is where you’re copping out. You’re implying that Dr. Lustig was clear about context and dosage, yet, you dance around the fact that he did not specify any threshold below which adverse effects are not seen to any degree of concrete significance. The message to most who view this video is clear, and it is alarmist against fructose. Deny all you want, but at least support your argument with more than a mess of excuses.” I agree.

Nicholas puts forth a pitiful argument. Nicholas again- “There may not be absolute zero fructose, but you are being nit picky. Bottom line is that Japanese eat less sugar.” Why not just say they eat less sugar? Is that nit picky? Saying the Japanese diet is absent- not present, not existing- of fructose means no fructose.

Actually, this lack of nit pickiness is one of the most common problems with communication. Japanese eat less sugar, so what? Please refer to the info I posted above discussing correlation and causation. Mike Howard- “Sugar and HFCS are both the same – they are both equally bad. They’re both dangerous they’re both poison I said it – poison. My charge before the end of tonight is to convince you that fructose is poison”. Thanks Mike for pointing that out.

Seems like when he comments on the blog he is trying to wiggle his way out of some of the assertions made on the video. I would recommend he look at the scientific data- maybe all of the available data, distinguish the strengths of different types of evidence, invest some time into studying logic (science of reason), admit he is fallible, pay credit where credit is due- to Alan Aragon, and if he has a team of research data associates get rid of them and get some new ones. Alan- “After viewing your response, I will maintain my position, and I suggest you rethink the content and delivery of your next lecture. Let me suggest that you place a little more emphasis on dose-dependence rather than painting a black-white picture of fructose that crucially downplays the importance of context. I also suggest that you re-check your claims concerning the Japanese diet if you’re going to use them as a salient introductory point of the lecture.” As I said previously, I would recommend he look at the scientific data- maybe all of the available data, distinguish the strengths of different types of evidence, invest some time into studying logic (science of reason), admit he is fallible, pay credit where credit is due- to Alan Aragon, and if he has a team of research data associates get rid of them and get some new ones. Mike Howard again- “Another little bit that makes me question Lustig’s nutritional knowledge he claims that the sodium content of coke – at 55mg is like “drinking a pizza” and claims it makes us more thirsty.” It sounds like this guy definitely needs to spend some time researching nutrition.

Final comments: Numerous studies have shown that sugar-containing liquids, when consumed in place of usual meals, may lead to significant and sustained weight loss (Drewnowski, A & Bellisle, F 2007) “The hypothesis that fructose, HFCS, and caloric beverages play a unique role in obesity and type 2 diabetes beyond their inherent energy contributions has generated tremendous attention from scientists and the media, but no credible scientific support” says John S. And President of White Technical Research (White, 2008) “The American Medical Association helped put to rest a common misunderstanding about high fructose corn syrup and obesity, stating that ‘high fructose syrup does not appear to contribute to obesity more than other caloric sweeteners.’ Even former critics of high fructose corn syrup dispelled myths and distanced themselves from earlier speculation about the sweetener’s link to obesity in a comprehensive scientific review published in the December 2008 American Journal of Clinical Nutrition” (Science Blog, 2009).

The addition of HFCS to a negative energy diet does not cause weight gain. You don’t have to get rid of all the sodas in your pantry just make sure to drink in moderation. February 3, 2010 Fred you stated – “Circus sideshow cases? Obese people were used as circus sideshow cases years ago when obesity was very rare. You couldn’t put a fat lady in a circus act today as she’d look normal.” Fred, the circus ladies back in the day at their lowest weight were in the 500lb range and sometimes very short in height.

If you look at the tale of one lady, Baby Ruth, she was 300 pounds by the age of ten. You consider that normal? You should also check out how easy it was for her to lose weight and the effort they had to go through to get her to gain more weight for what she was doing. In United States it is estimated less than 0.20 of the entire population are above 500 pounds. While this number has increased and while we become desensitized with programs on television and outliers of extreme morbid obsesity, it isn’t normal. The average person see the effects of their body increase overtime due to a lack of movement in correlation with a increase in calorie consumption.

This study shows that the average fitness level of the morbidly obese (body mass indexes between 40.0 and 49.9) walked an average of 2,500 steps a day. This leaves the burning very close to a BMR level of expenditure. Vanhecke, Barry A.

Franklin, Wendy M. Miller, Adam T. DeJong, Catherine J. Coleman, Peter A.

Cardiorespiratory Fitness and Sedentary Lifestyle in the Morbidly Obese. Clinical Cardiology, 2009; 32 (3): 121 DOI: 10.1002/clc.20458 Fat, carbs or protein, it is highly easy to out eat that type of activity especially when there is such a disruption in the endocrine system. Its funny how you seem to think we miss those disruptions, we don’t but it doesn’t toss aside energy balance. Fred you stated – “The point is excessive height as well as excessive fat accumulation is a hormonal disorder.” Fred, you got get over the height thing.

Not to mention you are comparing apples and oranges. Excessive growth hormone is the likely factor of excessive height. Growth hormone is usually blunted in those with obesity. This comparison doesn’t make sense at all. In terms you might understand, it is much like relating your stance to the event that took place when the Ninja Turtles walked in the green goo. That was one hell of a endocrine disruption but you don’t see me using that as a go between for the morbidly obese do you? Fred you stated – “It is a disorder of excess fat accumulation.

Obese people eat more (some don’t eat that much) because much of what they eat gets stored as fat rather than being made available for energy. When this happens, they remain hungry since too many of the caories went to storage rather than to building/maintaining.” This statement doesn’t even make sense. Fred you stated – “The rest of your post reflects the common thinking on the matter and if you try to keep people lean by feeding them less total calories you’ll find very poor long term results.” Trying to “keep people lean” is not what I am suggesting. In the process of achieving a leaner state, people need to consume less calories. Once they have achieved a leaner state, calorie consumption can be whatever the hell you want it to be depending on your movement and training lifestyle. Fred you stated – “And every single time a fitness professional decreases someones calories they also decrease their total carb intake and alter the type of carbs from highly refined to fibrous. You will never get an obese person lean by lowering their calories and yet keeping the refined sugars high.” Actually you can Fred but this is a flawed argument stance.

You also are assuming more metabolic advantage towards decreased carbohydrates which isn’t always the case either. Some people crash on low carb and decrease their daily activity (as well as see severe depletion in mental function). This leads to faster stalls or binge incidences on the rebound. For others it is smooth sailing, it just depends.

You will only find a success with a small population of people who fit into a certain criteria but hey, that is fine. I have no problem using critical thought and assessment of situation to aid different people and pick up your slack. See, that is the ironic part of your argument Fred. You claim hormonal abnormalities bridge a large scale and are responsible for differences. I agree; we are all different.

Isn’t it funny how you are the one who wants to solve that by “one size fits all.”. February 3, 2010 Leigh – I don’t want to hijack Alan’s blog with our discussion any further but I’d be happy to continue the debate on my forum You’ll have to explain why some people who eat more calories then maintenance do not gain fat and why some do. Hormones regulate fat storage.

No insulin, no fat storage regardless of the calories ingested. Your thinking on the matter is 2 dimensional.

We can discuss this at length on my site if you wish. And there is no slack for you to pick up. ALL my clients who follow my recommended low carb ad libitum plan lose fat quite well. Have you ever tried it? February 3, 2010 Fred H. – Continually citing anecdotal reports does not help further your cause. There may be limited research, but a recent study suggests that the ketogenic diet does not offer a metabolic advantage over a standard, reduced-calorie diet (see: “Ketogenic low-carbohydrate diets have no metabolic advantage over nonketogenic low-carbohydrate diets.”).

Regardless of your personal experience, the results of controlled scientific studies seem to indicate that specific macronutrient composition is largely irrelevant when comparing calorie- *and* protein-matched diets. February 3, 2010 Fred, There’s no way you can present someone’s testimonial and imply that it’s conclusive evidence of the superiority of low carb, high fat. You can grab the same type of testimonials claiming the same results from the promoters of low fat diets like the Pritikin diet, Body for Life, or any diet for that matter. Whatever it takes to get the person to stick with a calorie deficit is the right diet for that person.

Also, testimonials should be taken with a grain of salt because there’s plenty of uncontrolled variables. I agree with Leigh Peele that you have a one-size-fits-all approach that ignores individual differences. Here’s a quote from Alan about low-carb zealots on Jamie Hale’s site that reminded me of you: “A key point that must be made is that the research is not sufficient grounds to be dogmatic about low-carbing in the first place. On the whole, studies do not match protein intakes between diets. Adequate protein intakes have multiple advantages (ie, LBM support, satiety, thermic effect), and they simply end up being compared to inadequate protein intakes.

Thus, it’s not lower carb intake per se that imparts any advantage, it’s the higher protein intake. Once you match protein intake between diets, the one with more carbs is actually the one with the potential for a slight metabolic advantage.

Furthermore, the majority of the research compares dietary extremes (high-carb/low-fat/low-protein versus low-carb/high-fat/moderate protein). The funny part is, the majority of long-term trials (12 months or more) STILL fail to show a significant weight loss difference. Note that these trials use the sedentary obese, so in the fit population, any weight loss differences would be even more miniscule. Once again, keep in mind that the lack of significant difference in weight loss is seen despite unequal protein intakes between treatments. There’s a large middle ground here that tends to get ignored by the ‘metabolic advantage’ folks, who are incorrect to begin with. It’s always either-or for them, when in fact, individual carbohydrate demands vary widely. For some folks, low-carb is warranted.

For others, it isn’t. It always amazes me how hard that concept is to grasp for low-carb absolutists. What I find to be a common thread among people who deny that individual carbohydrate requirements vary widely is a lack of client experience, particularly with different types of athletes. The minute someone says that EVERYONE should severely restrict carbohydrate, it’s obvious that you’re dealing with a cherry-picking low-carb zealot who is unfamiliar with the totality of research evidence, and has limited field experience.”.

February 3, 2010 I’m just getting caught up on this discussion but wanted to make a comment on the Japanese diet, which seems to have been misrepresented and is in need of desperate clarification. I am a specialist in East Asian international affairs and have spent a great deal of time in Japan for research purposes. Anyone who claims that the Japanese don’t consume added sugars is operating from a position of pure ignorance. As someone with first-hand experience of Japan’s dietary culture, I would argue the Japanese are even more fond of desserts and sugary snacks than Americans. Bakeries serving all variety of desserts both Western and Asian are ubiquitous, easily as ubiquitous as Starbucks is here in Seattle.

I would argue that fructose consumption through HFCS-loaded sweetened drinks and dessert products is even more common than it is in America. There’s an entire konbini (short for convenience store) culture (コンビニ) alive and thriving in the land of the rising sun, unparalleled by anything we know here in the States. Japan is the home of what’s known as tabehoudai (食べ放題), which translates to “all-you-possibly-can eat,” and differs from a buffet in that the entire purpose of said endeavor is to consume as much food as possible in a given time limit (typically 60 – 120 minutes). Customers pay a nominal fee (equivalent to about $10-20 American) and are allowed to eat as much as they can within that time frame. This tends to become quite the competitive endeavor amongst inebriated company men. Speaking of which There’s also the ever-popular drinking variant, nomihoudai (飲み放題) where one’s goal is to drink as much as possible for a given time period, and operates in the same manner of tabehoudai, opening up the bar for 60 – 120 minutes.

Many restaurants encourage you to purchase both for a discount so you can drink and eat yourself sick at the same time. And let’s not forget the popular kuiadore (食いあどれ), where in similarity to the American pub crawl, the Japanese head out to literally “eat til they drop” or “eat til they’re dead,” the literal translation of the phrase. Workers in Osaka will typically get off work and begin their binge at 5:00pm, not stopping until midnight, when the last train home departs the station. The major difference between Japan and America? The Japanese walk, and walk, and walk, and walk, and walk, and walk some more and can manage the calories in versus calories out issue far better than we Americans.

Anyone who believes that the Japanese, in daily practice, eat more healthfully than the average American needs to go abroad. As a parting thought, anyone familiar with Japanese cooking knows that nearly every single sauce used has a foundation consisting of soy sauce and sugar (as syrup, honey, or straight-up cane sugar).

February 3, 2010 I hope that Dr. Lustig does the responsible thing and comments further, perhaps with a modified stance based on the evidence discussed here. I have a bad feeling that he may have taken his ball and ran home.

I hope not, though. This type of discussion just goes to show that anyone can have holes in his case, be it a doctor, professor, or both. What we don’t see enough of is people of high academic credentials admitting any degree of wrong.

Thanks to everyone contributing, this really has been an enlightening read. February 4, 2010 Interesting comments. Mr Aragon thanks for writing this article.

Especially enjoyed the points you raised on context-dropping. Jamie Hale wrote the following: “The chemical reality- whether a substance is manufactured by people, copied from nature or extracted directly from nature, tells us little at all about its properties. To reiterate, in terms of chemical safety, “industrial”, “synthetic”, “artificial” and “man-made” are not necessarily more damaging and “natural” does not necessarily mean better.” This is a very important point and what she is referring to is intrinsicism.

This occurs when people treat value (or non-value) as a non-relational property of an object. In this case, the good is not determined objectively by the metaphysical (in this case biological) *relationship* between the food and the person eating it with their life being the standard. Instead the value is seen as contained somewhere (where?) in non man-made substances and to the extent to which man applies his mind to modify these substances or create new ones, he destroys this “good”. February 4, 2010 Ryan. You took the words right out of my mouth.

I’ve been living in Japan for 6 years. I spent 3 years in Hokkaido in the north and I’ve now completed 3 in Tokyo. I took Japanese cooking lessons once a week for about four months when I lived in Hokkaido and I was astounded by the amount of “traditional” dishes are prepared with sucrose.

In addition to the forms you mentioned as being staple ingredients in traditional Japanese dishes, sucrose is also paired with sake (rice wine) in a liquid called mirin. Another staple ingredient is called ryori-shu or cooking alcohol.

Together with soy sauce, and in differing proportions, these three ingredients constitute the “typical” Japanese taste of traditional foods. Just to give an example, a typical homestyle meal called “teishoku” may consist of the following: 1. A piece of fish. Seasoning may be salt or teriyaki sauce (combo soy sauce, sugar, mirin, and ryori-shu) or A breaded and deep-fried paddy of ground meat or potato.

Seasoning is a sweet, brown sauce similar to BBQ sauce. A vegetable dish: Usually a seaweed like “hijiki”.

Seasoning (combo of soy sauce, sugar, mirin, and ryori-shu) or Shredded cabbage that is companion to the breaded and deep-fried paddy. Seasoning is mayonaise, and it’s not sugar-free, or low-fat. A pickle dish: pickled vegetable in small quantity but more often than not it has been sweetened with sugar. Rolled egg dish: Called “tamago-yaki”. Eggs beaten with sugar, soy sauce and soup stock and then fried and rolled into a cube shape. Miso soup or “O-suimono”. The latter, is a soup made of a combo of soy sauce, sugar, mirin, and ryori-shu.

Just on a separate note, nothing in Japan besides milk and yogurt is produced “low-fat” or “fat-free” and nothing else is offered as “low carb” or “sugar-free”. The more fat on a cut of meat, the more expensive it is.

I live near a restaurant that sells a steak dinner for 80-120 USD of which the steak is more white than red. When I say “astounded” I don’t mean to imply I think it’s terrible and should be eliminated. I simply didn’t expect it.

I certainly wouldn’t avoid any particular “traditional” or home-cooked meal based on the sucrose content. February 4, 2010 RG and Ryan, Good posts, but far too measured. I tuned out from this thread long ago when posters who clearly have never been to Japan started discussing the merits of the “Japanese diet.” Sorry folks, the days of a conservative bowl of rice, raw fish, and a bowl of miso are long gone. Pastries, Starbucks, every fast food imaginable, and a insane amount of “snacks” purchased from vending machines designed for the starship Enterprise are the norm for the 21st century. Let’s not forget the alcohol. It is EVERYWHERE, even on the train platforms- and no, not just a conservative shot of sake. Best of luck finding a train at 9pm that didn’t have a couple of hopelessly inebriated salary men passed out in the corner or butchering “Sweet Caroline.” Is my rambling a sweeping generalization?

But so are the inferences that every one of Japan’s 175 million residents follows a Spartan, zero-sugar, non-processed diet. Please don’t make the egregious error of justifying or advocating a particular dietary protocol based on what is ostensibly a cultural stereotype. February 4, 2010 I really have literally zero credibility and expert knowledge on nutrition or human body but to hear someone who supposedly has that kind of knowledge say “why then do some people gain fat when eating above maintenance and some don’t” is just plain sad.

It’s obviously that if someone isn’t gaining weight when supposedly eating above maintenance that he/she ISN’T eating above maintenance. Either the amount of ingested calories isn’t above maintenance or the maintenance level has increased due to fidgeting and other non-voluntary movements or thermic effect of ingested food (“fast” metabolism, as a lay-man would put it). Unless someone has a kind of metabolic dysfunction, how can anyone GAIN fat/weight while not eating ABOVE maintenance and some one NOT GAIN fat/weight while eating above maintenance. It seems that at any given time there’s one particular macro-nutrient (dietary fat, sugar, starch) that somehow magically poses the power to give out more energy than it actually holds. And that’s against some quite fundamental physical laws, isn’t it? “You’ll have to explain why some people who eat more calories then maintenance do not gain fat and why some do.

” ^^ Please Fred Hahn, can you explain why you think that? It’s not possible to gain weight when your body is using more energy than you give to it.

February 4, 2010 Blimey! This thread’s grown like Topsy.it must be the HFCS;-p I think that slim/active/healthy people can eat what they damn well like whereas fat/inactive/metabolically-impaired people can’t. Anyway, back to apples “The fruit’s sugar content has risen by up to 50 per cent over the last decade” (from ~10% to ~15%). You asked for some decent evidence. Here’s all I could find on PubMed under Apple “Sugar Content”:-.

“RESULTS: The total sugar content of most cultivars from integrated cultivation ranged between 115 and 160 g/kg.”. February 4, 2010 Nigel — That study doesn’t tell us anything about an increase in sugar content of the apples. It merely tells us that they contain a range of 12-16 grams of carbohydrate per 100g serving.

A midsize apple has a total mass of appx 182g, so according to that study, it will contain 12-16% carbs, which equals 21.8-29.1g. This is an average of ~25g, which is exactly as it’s been for ages.

Quoting my article above: “A midsize apple contains 25 total grams of carbohydrate, 12 grams of fructose and 4 grams of fiber.”. February 4, 2010 Here is what has changed and continues to change since Crisco was introduced in 1913 – the consumption of processed foods.

Fructose is part of that over-all picture that began 100 years ago. We eat more, we move less.

But I believe if we were eating food that way we did in just the 1950’s on our farm, we would have less of a problem. I look through my HS yearbook and can only find 2-3 pictures of teenage men or women over weight, none obese. It was rare for parents to be more than a few pounds overweight until they were over 60. Here is a study that suggests many of those extra calories are in beverages.

Though fructose is not an evil food, consuming it in large quantities easily while watching TV or playing video games contributes to the problem but the obestiy problem though not caused by fructose alone, is certainly aided by economic and social policy just as tobacco use was years ago. The decline in cancer rates is attributed to falls in the number of tobacco users. If we want to do something meaningful to prevent a generation of youth growing up with NAFLD, then we need to do something about our policy regarding fructose production. It isn’t fructose, but the societalpolicy of profit before people that creates these problems. February 4, 2010 Alan, ya got me.

I can’t find any studies showing the increase in the sugar content of apples. That still leaves the problem of the metabolically-impaired. If a baby is chronically over-fed and becomes a fat kid/teen/adult with Metabolic Syndrome/Syndrome-X, that person is at a high risk of having NAFLD, high TGs, sdLDL-C etc. Metabolically-impaired people who eat lots of fruit can deteriorate into full-blown diabetics..

From, an Agatston score of 1157 puts this person at a 20% risk of MI/death within the next 12 months. February 4, 2010 The other part of the picture that people are missing is that Americans have become MUCH lazier and rely much more heavily on a sedentary lifestyle. Furthermore, as stated above, Japanese foods and the trend of liking desserts is just as high there as in the USA. However, among many favoring factors, they do walk more day-to-day compared to those living in the USAmost notably either in a car, behind a desk, in front of a TV or Playstation, in bed, no more Physical Education in schools, etc. I think it is clear that nobody is promoting suagry liquid consumption (either from socrose or HFCS) on any party in this debate, and it is definitely part of the puzzle to obesity. However, this is mainly because of the overconsumption from all foods as stated by Alan.

Furthermore, Jamie pointed out that there is a HUGE difference when it is consumed on a hypocaloric diet than compared to a hypercaloric diet. Factor in physical activity, and it makes even more of a difference. February 4, 2010 Nigel — I’ll quote that blog post you linked: “However, Mitch somehow failed to follow our restriction on fruit, which we limit to no more than two 4 oz servings per day, preferably berries. He thought we said “Eat all the fruit you want.” And so he did. Mitch had a banana, orange, and blueberries for breakfast.

For lunch, along with some tuna or soup, he’d typically have half a melon, a pear, and red grapes. For snacks, he’d have an apple or nectarine. After dinner, it wasn’t unusual for Mitch to have another piece of fruit for dessert.” ^^^Based on the above, it appears the subject in this case study not only has a metabolic impairment, but also a mental one. For him to turn a recommendation of 2 servings of fruit a day into 20 servings, who knows what else he did to screw up dietary compliance.

Again, anything in chronic excess = not a good idea. February 5, 2010 If you all agree that fructose at a certain level is damaging, then I challenge you to come up with a number. Try it, and you might see why Dr. Lustig does not, because it would be highly specific to the individual. Some of you focus on calories, when the issue with fructose is really metabolic disorder which would cause you to regulate your body weight poorly. If your hormonal signals of insulin, leptin, etc. Worked properly, then you will tend to stay the same weight.

Yes, exercise and other can help you maintain this balance, which allows you to consume more fructose (mentioned in the lecture during the biochemistry). In addition, some populations (including Japanese) handle carbs better. Come up with a one-size-fits-all number for fructose now when you have to deal with diet, genetics, exercise, etc.? That’d be like using the ridiculous RDA allowances. As for Japan, it should not be denied that less sugar is consumed overall, despite the existence of dessert shops and drinking houses. Some of the population obviously will go for that.

Japan does have over a 100 million people after all. “No” sugar obviously was not to be taken literally. Given that Dr. Lustig is not a lawyer, I can forgive him for that. February 5, 2010 “Drop Good Calorie Bad Calorie, and start reading biochemistry/endocrinology books and peer-reviewed studies. You’ll probably have much more clever thing to say. I doubt you understand how complexe metabolism regulation is.

If it was just as simple as excess insulin, obesity would not be hard to treat.” Excess circulating insulin/insulin insensitivity is the major aspect of fat storage. And when you read the text books that fact slaps you in the face. JLB – You speak as if you have great client experience using different diets.

ATZ you said: “I think you’re doing a great job in showing everybody here you have not a clue (other than what you read in GCBC) on the subject. Your inane ramblings, strawmen and anecdotal counter arguments do more to discredit yourself than anyone here could.” Yes ATZ you’re right – GCBC is the only book I’ve ever read on the subject. I know nothing more than that.

I was asked last year by Dr. Mary Vernon of the American Society of Bariatric Physicians to speak at an upcoming conference. I’ve written 2 book on the subject and have over 70 hours of continuing ed on the subject. I run a gym that for the past 12 years has shed hundreds of pounds off of people and been on the T0day show twice, and oh I forget 2 dozen other major TV and radio shows including Oprah and friends with Dr. But yes your’re right, I’ve no clue. I should just shut up. Carry on – you’re giving me a good laugh too.

February 5, 2010 Fred, I’m not going to pretend that I’m a guru or some sort of authority on fitness. I’m just a student taking notes. However, I’m keen enough to know who’s who in the fitness industry. I’m educated enough to know who respects the real science, and who puts out the pseudoscience.

It’s obvious that you have a ways to go before you get to the level of Alan or Lyle. And that’s not a personal dig at you, it’s just that very few people in the entire industry, in my opinion, are at their level. Canopus Xplode Professional 4.0 Free Download on this page. Can’t even fit them on one hand. I can see that you work hard to whet your craft, so let me suggest that you pay more attention and learn from the real gurus, not the ones who are so attached to their dogma that their quality of info has stopped improving 15 years ago.

February 5, 2010 @Fred Hahn You stated “Hormones regulate fat storage. No insulin, no fat storage regardless of the calories ingested. ” So, you really believe that no insulin = no fat storage? If so, yes, start reading something else than GCBC such Alan’s research review, as a starter. BTW, it is impossible to have no insulin around.

Why is still possible to lose weight then? Also, why is it that in studies where they used drugs to inhibit insulin secretion they showed no difference in weight loss?

If you could drop off weight from some ppl at your gym, it’s simply because somehow you affected the energy equation by having them eat less and move more. Why is it so hard to accept as true? Sorry but going on Oprah is not giving you any good credit.

This subject has been beaten to death by Lyle McDonald, Alan Aragon and Anthony Colpo. All that you are doing is wishful thinking and showing once again how people are stubborn when it comes to changing their mind. You’re doing a diservice to your client by ignoring this.

Anyway, the low-carb infatuation is fadding now, so you better take the train while you can. I know it ain’t easy after telling so many ppl that low-carb is magic but hey they will trust you much more if they see that you can change your mind when the evidences tell you to do so! February 5, 2010 “This subject has been beaten to death by Lyle McDonald, Alan Aragon and Anthony Colpo.” All of whom don’t get it – not fully at least. But there in good company.

“Also, why is it that in studies where they used drugs to inhibit insulin secretion they showed no difference in weight loss?” I’d need to read the studies to see if they are in fact done well. There are many reasons why this could be. Like the Barry Sears study that was mentioned here on this thread. Quite flawed and biased. “You’re doing a diservice to your client by ignoring this. ” I don’t think my clients who are losing body fat extremely effortlessly and improving their internal health markers dramatically are feeling ‘disserviced.’ “Anyway, the low-carb infatuation is fadding now, so you better take the train while you can.

I know it ain’t easy after telling so many ppl that low-carb is magic but hey they will trust you much more if they see that you can change your mind when the evidences tell you to do so!” I never said LC was ‘magic.’ Quite the contrary. I’ve said what the physiology textbooks say – that the hormone insulin regulates body fat storage and keeping insulin under control is key to getting leaner an staying lean and certainly key for not becoming obese. And if you think the low carb issue is fading you have not a clue of what is going on in the world of bariatric medicine.

You are as wrong as wrong can be. Watch the show Face OFF this coming Feb. 22 at 11:35 PM.

Excess carbohydrate intake is the primary source for adipose tissue stores. Try to get fat on an all fat-meat diet.

Do the experiment. I dare any of you to try this. Eat 3500 calories of pure fatty meat/fish and eggs for one month.

I guarantee you will will get leaner of you are somewhat over fat and more muscular if already lean and training. I bet you NONE of you will try. “It’s not possible to gain weight when your body is using more energy than you give to it.” Assuming it is using it rather than storing it. Hormones regulate fat storage. When hormones are screwed with you can indeed store more fat than ‘usual.’ And they are screwed with when you eat too much sugar. Why most of you can’t understand this is truly mind boggling.

Why so many of you want to hold onto the age old calorie nonsense is frightening. What do you say to your clients – eat enough protein and the rest is up to you so long as you eat less calories than you are now? Eat two chicken large breasts a day and the rest in bagels, poptarts and cookies?

Listen, no hard feelings. We all choose to help our clients as best as we can. I have yet to fail a client by a combo of strength training and low sugar/don’t count caloire dieting. February 5, 2010 “Eat 3500 calories of pure fatty meat/fish and eggs for one month.” I doubt if most people could keep that up. My guess is that most people would eventually lower their calorie intake as they get tired of eating just meat and eggs. Although I admit that that would probably lead to weight loss!

🙂 But the problem isn’t really weight loss, it’s weight maintenance. Most people who lose weight gain the weight back. I lost 65 pounds, plateaued, and then gained most of it back. This was on a diet where my main carb source was fruit and whipped cream too much fructose, I guess! We need sustainable diets that people can adhere to. An all meat diet is not sustainable for most people, so I don’t think it’s relevant to real people living in the real world. February 5, 2010 “Excess carbohydrate intake is the primary source for adipose tissue stores.

Try to get fat on an all fat-meat diet. Do the experiment. I dare any of you to try this.

Eat 3500 calories of pure fatty meat/fish and eggs for one month. I guarantee you will will get leaner of you are somewhat over fat and more muscular if already lean and training. I bet you NONE of you will try.” Do you have any studies to support this?

This is quite an outrageous claim to make without having any form of evidence to back it up. This type of extreme diet would work for people that are in excess of 500 lbs, but that’s about itplus there is no balance to this ridiculous all fatty meat diet, so it is not a realistic option for anybody. I’m more interested about the effects of an all fatty meat diet with zero fiberdoesn’t seem like it would be too pleasant. February 5, 2010 What is your academic background Fred? I looked on your website but could not find anything. In this world of pseudo-science, someone should at least have some academic credibility if he wants to talk about science and research. I don’t see how someone without at least an MSc can understand biostatistics and research enough to be able to critically analyse a research paper.

Do you have this? Not an ad hominem here, just being realistic. Without basic science background, it’s not quite easy to understand biochemistry and endocrinology. So, what credibility do you have regarding this?

You say you read textbook, but do you have the academic background to understand what’s written in there? If you really believe that’s it’s impossible to gain weight as long as you eat only fat and protein, we’ve hit an impass and there is nothing more I can say. You’re a wishful thinker, and really, the only thing I can do is to never read anything from you and make sure that anyone I know will not refer to your stuff. BTW, I know people who bulked (more muscle AND more body fat) on a keto diet, so, if anecdote worth anything, and you seem to consider so, you are wrong 😉.

February 5, 2010 Original comment by Fred Hahn: “Excess carbohydrate intake is the primary source for adipose tissue stores. Try to get fat on an all fat-meat diet.

Do the experiment. I dare any of you to try this.

Eat 3500 calories of pure fatty meat/fish and eggs for one month. I guarantee you will will get leaner of you are somewhat over fat and more muscular if already lean and training. I bet you NONE of you will try.” Uh yeah, a keto-bulk? Tried it and the only weight i GAINED was FAT. Explain that? February 5, 2010 @ Fred – I find it ultimately ironic that you accuse others of “not getting it” or being narrow-minded when it would appear that it is you who has the absolutist views on nutrition and strength training.

So far all you’ve delivered is conjecture, anectdote and horn-tooting about your radio and TV appearances. Jim Karras, David Kirsh, Jorge Cruize, Tony Little – heck even Richard Simmons have all been on those shows too. That doesn’t make them authorities on matters of nutrition or fitness. This speaks to your business acumen – not your knowledge. There is absolutely NO WAY that someone with such a hard-lined stances on nutrition could be looking at the scientific data objectively. February 5, 2010 @ Nicholas, I don’t even know where to begin, but I’ll just say that there is obviously some affiliation/infatuation with Dr.

Lustig on your part. I’m sorry, but he does not get a get-out-of-bullsh*tting-free card because a)he isn’t a lawyer b) is speaking to lay people or c) made some good points. Lustig even confirmed what he meant on this thread and he still got called out for his BS. It’s not up to us to speculate what he may have meant by what he said. If he feels strongly, he’ll come back and defend his position. February 5, 2010 FRED, Please define “excess carbohydrate intake”? And, at what point does this occur?

Also, please show research showing the following in a hypocaloric state causes fat gain: You stated: “Assuming it is using it rather than storing it. Hormones regulate fat storage. When hormones are screwed with you can indeed store more fat than ‘usual.’ And they are screwed with when you eat too much sugar.” Even diabetics who are Insulin-Dependant lose weight when calories are below maintenance. February 6, 2010 ****************** that the hormone insulin regulates body fat storage and keeping insulin under control is key to getting leaner an staying lean and certainly key for not becoming obese. ********************** Fred, this is a key statement that you continue to make, but it’s a statement that is overly simplistic and ignores the highly complicated realm of adipose tissue regulation. I’ve pointed this out to you before, but you always ignore it because it doesn’t conveniently fit with the Taubes hypothesis. There are numerous hormones that are involved in the regulation of fat metabolism.catecholamines, IL-6, growth hormone, leptin, etc.

You also seem very stuck on hormones, but you ignore the fact that there are many non-hormonal factors that are involved in the regulation of adipose tissue stores. There are also extremely complicated interactions between all of these factors, which ultimately lead to the regulation of body fat stores. The fact is, fat cells can and do take up glucose and fatty acids in the complete absence of insulin. Fat cells can and do create triglycerides in the complete absence of insulin. The body is full of redundant biochemical pathways which are involved in the increase of adipose tissue stores.

************** Try to get fat on an all fat-meat diet. ************** And there are people here who posted that they have. I know you’re a fan of anecdotes. Do their anecdotes not count? *************** You’ll fail.

****************** Yeah, they’ll fail because they’ll get sick of eating meat & eggs all the time and they won’t be able to eat enough in the first place. I remember trying Di Pasquale’s “Anabolic Diet” years ago, which involved 5 days of ketogenic eating and a 2-day weekend carb load. I could barely get in 2000 – 2500 calories per day during the ketogenic cycle, partly because I didn’t have the appetite and partly because I got mentally sick of constantly eating meat. ************ Why most of you can’t understand this is truly mind boggling ************* No, what is mind-boggling is how you continue to adhere to a simplistic, grade-school level of understanding of adipose tissue regulation.

February 6, 2010 In reference to a direct comparison of fructose consumption by the Japanese in Japan vs. Japanese in Hawaii: Diabetes Care. 1979 Mar-Apr;2(2):161-70. Diabetes mellitus and its vascular complications in Japanese migrants on the Island of Hawaii.

Kawate R, Yamakido M, Nishimoto Y, Bennett PH, Hamman RF, Knowler WC. Japanese migrants and their offspring on the island of Hawaii and Japanese living in Hiroshima were examined for diabetes mellitus and its vascular complications. The same methods and investigators were used in both locations. Death certificates of Japanese and Caucasians dying on the island during the past 26 yr were analyzed. Diabetes, defined as a venous serum glucose concentration of at least 200 mg/dl 2 h after a 50-g oral glucose load, was significantly more common in the Hawaiian Japanese than in the Hiroshima Japanese subjects. This suggests that diabetes is more prevalent in Japanese in Hawaii than in Japan, although lack of knowledge about the total population of Japanese migrants in Hawaii makes this generalization uncertain. The proportion of deaths attributed to diabetes was much higher in Japanese migrants and their offspring in Hawaii than in Japan.

During the 1950s, the proportional death rate from diabetes was about half as large in Japanese Hawaiians as in Caucasian Hawaiians, but it increased to become 1.6 times the Caucasian rate during the 1970s. A nutritional study revealed that the total caloric intake was similar in Japanese in Hawaii and Hiroshima, although the estimated level of physical activity was less in the Hawaiian subjects. Consumption of animal fat and simple carbohydrates (sucrose and fructose) were at least twice as high in Hawaiian as in Hiroshima Japanese. Conversely, Hiroshima Japanese consumed about twice the amount of complex carbohydrate as the Hawaiian Japanese. These observations support the hypothesis that a high fat, high simple carbohydrate, low complex carbohydrate diet and/or reduced levels of physical activity increase risk of diabetes. The proportion of deaths attributed to ischemic heart disease was higher in both diabetic and nondiabetic Japanese Hawaiians than in diabetic subjects in Japan. The rates were similar for Japanese and Caucasians in Hawaii.

There was no evidence of an environmental influence on the development of microangiopathy (retinopathy) in diabetes, as the prevalence of diabetic retinopathy (stratified for diabetes duration) was similar in Japanese subjects in Hawaii and in Japan, and it was similar to previous reports from England. On the other hand, diabetes alone did not appear to account for the greater prevalence of macroangiopathy in Hawaiian Japanese than in Hiroshima. Thus environmental factors, possibly including diet, appear to be involved in the development of macrovascular complications of diabetes. February 6, 2010 Dr. Lustig, You gotta love the soup of confounding variables that limits epidemiological research. I don’t need to tell you that correlational research is useful for generating hypotheses, but not cause-and-effect relationships (a task achievable only through randomized controlled trials). This is a point I already made in my previous post, which I’ll re-quote since it didn’t sink in the first time [Crit Rev Food Sci Nutr.

2007;47(6):561-82]: “The evidence that HFCS consumption uniquely increases the risk of weight gain is very weak. Few studies directly explore the relationship between HFCS, body weight, and BMI. The only evidence directly linking HFCS consumption and weight gain is ecological data. Ecological data are widely recognized as insufficient for establishing cause-effect relationships. HFCS consumption and weight gain have major gaps. The hypothesis that the increasing levels of HFCS in the food supply has increased the F:G ratio is not supported by the USDA ERS food availability data. The impact of HFCS consumption on BMI must be put in context with other broad economic and societal changes during the past several decades.

Many other plausible explanations for rising overweight and obesity rates exist, including a decrease in smoking; 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, 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.” ^^^In light of the above, I’ll quote the study you posted to illustrate my point [Diabetes Care. 1979 Mar-Apr;2(2):161-70]: “These observations support the hypothesis that a high fat, high simple carbohydrate, low complex carbohydrate diet and/or reduced levels of physical activity increase risk of diabetes.”. February 6, 2010 Mr. Aragon, since you seem to be unswayed by anything but randomized controlled trials in humans, and only those at fructose doses that are reasonable, and since you seem to like to journal quote, then here is just a sampling that demonstrates that fructose, and not just extra calories, is behind dyslipidemia, insulin resistance, visceral adiposity, and hepatic steatosis.

J Clin Invest. 2009 May;119(5):1322-34. Consuming fructose-sweetened, not glucose-sweetened, beverages increases visceral adiposity and lipids and decreases insulin sensitivity in overweight/obese humans. 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, Havel PJ.

Department of Molecular Biosciences, UCD, Davis, California 95616, USA. Studies in animals have documented that, compared with glucose, dietary fructose induces dyslipidemia and insulin resistance. To assess the relative effects of these dietary sugars during sustained consumption in humans, overweight and obese subjects consumed glucose- or fructose-sweetened beverages providing 25% of energy requirements for 10 weeks. Although both groups exhibited similar weight gain during the intervention, visceral adipose volume was significantly increased only in subjects consuming fructose. Fasting plasma triglyceride concentrations increased by approximately 10% during 10 weeks of glucose consumption but not after fructose consumption.

In contrast, hepatic de novo lipogenesis (DNL) and the 23-hour postprandial triglyceride AUC were increased specifically during fructose consumption. Similarly, markers of altered lipid metabolism and lipoprotein remodeling, including fasting apoB, LDL, small dense LDL, oxidized LDL, and postprandial concentrations of remnant-like particle-triglyceride and -cholesterol significantly increased during fructose but not glucose consumption. In addition, fasting plasma glucose and insulin levels increased and insulin sensitivity decreased in subjects consuming fructose but not in those consuming glucose. These data demonstrate that dietary fructose specifically increases DNL, promotes dyslipidemia, decreases insulin sensitivity, and increases visceral adiposity in overweight/obese adults.

Schwarz JM, Noworolski SM, Lee GA, Wen M, Dyachenko A, Prior J, Weinberg M, Herraiz L, Rao M, Mulligan K. Effects of short-term feeding with high- vs low- fructose isoenergetic diets on hepatic de novo lipogenesis, liver fat content and glucose regulation.

Diabetes 1476P (2009). We studied the effects of fructose on intrahepatic lipid accumulation. Seven subjects were scanned at baseline and after each of two successive 7-day isocaloric diets, one high in fructose, one high in complex carbohydrates in a randomized crossover fashion. All subjects had higher intrahepatic lipid after the high fructose diet versus the complex carbohydrate diet, regardless of diet order (median increase = 133%, median lipids/water = 0.021 vs. 0.018, respectively; p=0.031). Visceral and subcutaneous fat were measured in 5 of these subjects, resulting in an average VAT/SAT ratio of 114% ± 16% for the high fructose diet versus the complex carbohydrate diet. These results suggest that fructose is unique in increasing intrahepatic lipid accumulation.

In addition, you have completely ignored the thread that by inducing insulin and leptin resistance, fructose increased and persistent food intake both at the hypothalamic and the nucleus accumbens level. So while controlled and pair-feeding fructose consumption does not result in increased total aggregate weight gain vs. Glucose (as shown in the Stanhope article), the signals of starvation and reward cause individuals to overeat, generating obesity in free-range situations. There are also new studies demonstrating changes in the nucleus accumbens by PET scan, which equate fructose with other substances of abuse. Avena NM, Rada P, Hoebel BG. Evidence for sugar addiction: behavioral and neurochemical effects of intermittent, excessive sugar intake.

Neurosci Biobehav Rev. I could go on, but our manuscript in Nature Reviews, entitled “The role of fructose in non-alcoholic fatty liver disease and metabolic syndrome” will speak for itself in due course. The defense rests. I shall not respond any further, as I have satisfied your criteria for objectivity and experimental and mechanistic rigor, and I have better things to do than engage in this continued puerile one-upsmanship.

I’ll let the public decide who they wish to believe. And thus far, based on the 230,000 YouTube hits and numerous blogs extolling this line of reasoning, I’ll take my chances.

Sincerely (for the final time), Robert Lustig, M.D. February 7, 2010 Dr Lustig: Did you even look at the methodology of the paper you cited? “The amount of sugar consumed by the subjects in this study, 25% of energy requirements, is considerably higher than 15.8%, the current estimate for the mean intake of added sugars by Americans (58).

However, recent reports (59–63) suggest that the sugar intake from beverages alone approaches or exceeds 15% of energy in adolescents and adults up to 40 years of age. The large SDs in several of these reports suggest that at least 16% of the studied populations was consuming over 25% of daily energy requirements from sugar-sweetened beverages (59, 62, 63). ” Or did you just fail to read Alan’s article?

“In the single human study I’m aware of that linked fructose to a greater next-day appetite in a subset of the subjects, 30% of total daily energy intake was in the form of free fructose [10]. This amounts to 135 grams, which is the equivalent of 6-7 nondiet soft drinks. Is it really that groundbreaking to think that polishing off a half-dozen soft drinks per day is not a good idea? Demonizing fructose without mentioning the dose-dependent nature of its effects is intellectually dishonest.

Like anything else, fructose consumed in gross chronic excess can lead to problems, while moderate amounts are neutral, and in some cases beneficial [11-13].” Context, Herr Doctor, Context. And this: “And thus far, based on the 230,000 YouTube hits and numerous blogs extolling this line of reasoning, I’ll take my chances.” is just as laughable as Fred using his Oprah appearances to back up his position. Science is not decided in the court of public opinion. February 7, 2010 “The defense rests. I shall not respond any further, as I have satisfied your criteria for objectivity and experimental and mechanistic rigor, and I have better things to do than engage in this continued puerile one-upsmanship.” Translation: I can’t really say much more but “if you overeat on fructose you’re marginally worse off than overeating on anything else”, so I’ll take my ball and go home. “I’ll let the public decide who they wish to believe.

And thus far, based on the 230,000 YouTube hits and numerous blogs extolling this line of reasoning, I’ll take my chances.” lmao. That’s how science works, right?

Pick a conclusion, cherry-pick til it looks right, and sell it to people without the scientific background to evaluate your claims. Oh and push that “MD” title, too.

When you don’t have a leg to stand on, appeal to authority. It’d be unbelievable if I weren’t seeing it with my own eyes. February 7, 2010 Dr. Lustig — This is not one-upmanship, it’s called you being on the hot seat for dishing out misleading information. You have deftly evaded the acknowledgement of errors you made regarding the Japanese diet and the effect of fructose-containing sugars on satiety. Last but not least, you continually evade the acknowledgement of the importance of dosage & context, as evidenced by your latest post, which I’ll review. Please see my comments after your sections: ____________________________________________________________ J Clin Invest.

2009 May;119(5):1322-34. Consuming fructose-sweetened, not glucose-sweetened, beverages increases visceral adiposity and lipids and decreases insulin sensitivity in overweight/obese humans. ____________________________________________________________ ^^^The most significant design limitation was the far-fetched dosing of fructose and glucose, and the use of specially designed beverages that scarcely exist among major commercial brands. Specifically, soft drinks are rarely sweetened exclusively with fructose, and rarely is there an all-glucose soft drink available through major commercial pipelines. Most nondiet soft drinks are sweetened with sucrose or similar (ie, HFCS), which is roughly an even split of glucose and fructose. To illustrate the questionability of the dose, 25% of total daily calories coming from these drinks would be roughly 600 calories, which equates to 150 grams of either fructose or glucose.

Achieving that total would require a daily intake of 7 cans of nondiet soda. You mean to tell me that drinking 7 cans of nondiet softdrinks per day is a bad idea? Wow, thanks for the enlightenment. According to the text, the average intake of added sugars among Americans is 15.8%. This means that fructose intake is half of that, at 7.9% – about 3 times less than the 25% imposed in this study. Dosage & context, remember? ____________________________________________________________ Schwarz JM, Noworolski SM, Lee GA, Wen M, Dyachenko A, Prior J, Weinberg M, Herraiz L, Rao M, Mulligan K.

Effects of short-term feeding with high- vs low- fructose isoenergetic diets on hepatic de novo lipogenesis, liver fat content and glucose regulation. Diabetes 1476P (2009). ____________________________________________________________ ^^^I can’t find this study. If anyone reading this even finds the abstract, please link me.

Can you tell me what fructose dose was used here? I’m going to guess it’s an artificially high amount that only serves to create a strawman argument on your part. Again, the same principles of my argument would apply in this case. ____________________________________________________________ In addition, you have completely ignored the thread that by inducing insulin and leptin resistance, fructose increased and persistent food intake both at the hypothalamic and the nucleus accumbens level. So while controlled and pair-feeding fructose consumption does not result in increased total aggregate weight gain vs.

Glucose (as shown in the Stanhope article), the signals of starvation and reward cause individuals to overeat, generating obesity in free-range situations. There are also new studies demonstrating changes in the nucleus accumbens by PET scan, which equate fructose with other substances of abuse.

Avena NM, Rada P, Hoebel BG. Evidence for sugar addiction: behavioral and neurochemical effects of intermittent, excessive sugar intake. Neurosci Biobehav Rev.

____________________________________________________________ ^^^You already acknowledged that I “seem to be unswayed by anything but randomized controlled trials in humans, and only those at fructose doses that are reasonable”, so why even present this research on intermittently fed rats? Scroll up to my article and you’ll see linked references for RCTs that compared the satiating effects of various sugars on humans. ____________________________________________________________ I could go on, but our manuscript in Nature Reviews, entitled “The role of fructose in non-alcoholic fatty liver disease and metabolic syndrome” will speak for itself in due course. ____________________________________________________________ ^^^I’m sure that this is a wonderful paper, as long as it takes dosage & context into account when drawing its conclusions.

Based on everything you’ve presented thus far, I’m not gonna hold my breath. ____________________________________________________________ The defense rests. I shall not respond any further, as I have satisfied your criteria for objectivity and experimental and mechanistic rigor, and I have better things to do than engage in this continued puerile one-upsmanship.

I’ll let the public decide who they wish to believe. And thus far, based on the 230,000 YouTube hits and numerous blogs extolling this line of reasoning, I’ll take my chances. ____________________________________________________________ ^^^I’m sure that the majority of the public who has seen your lecture, but not this blog’s discussion, is impressed and beguiled with your delivery. However, if you were to put your objective lenses on and take a close look at what transpired here, you DECISIVELY failed to capture the belief of most people reading this. PS – Thanks for participating in the discussion, even if your last post was your white flag.

It’s been fun, and I can guarantee that you learned something, whether you’re ready to come to terms with it or not. February 7, 2010 This thread has become a vindication for those of us who carry the good fight against the predatory media alarmism made ubiquitous by the egos who fail to temper their practice with ethics. I’m elated at seeing how some very conscientious, well-read, and wickedly intelligent fitness nerds can take to task marketing mavens, fitness gurus, and yes, even M.D.’s who base their careers on murky hypotheticals. For me, this thread has become a glowing illustration of positive community.

It makes me smile knowing that a groundswell of critical thought is emerging against the dominant pseudo-scientific mainstream. Lustig’s case, it’s easy to see how readily politicized researchers become when their baby, the research or theory that serves as the bedrock of their career, doesn’t hold water in the real-world. It suddenly isn’t about the science anymore, is it? It’s about the YouTube video hits. A man who has committed his life to solving the ailments of our civilization has cited his number of YouTube hits in response to a direct, contextual criticism of his work.

This saddens me, but gives me hope knowing that people like Alan, and Jamie, and Leigh, and Lyle, and Mike, and James, and Roger, and JC, and everyone else who has built this rebellion are slowly making a name, making a dent into the rampant B.S. That cripples so many well-meaning folk who just want to get in shape.

Whether you’re sitting on the side of the lay-public like Hahn, or occupying a seat in the ivory tower like Dr. Lustig, when you play with theoretical fire you’re bound to get empirically burned. Bravo, Alan, bravo. February 7, 2010 “I’ll let the public decide who they wish to believe. And thus far, based on the 230,000 YouTube hits and numerous blogs extolling this line of reasoning, I’ll take my chances.” So I guess because you have so many YouTube hits, everything in your video must be trueLOL If YouTube hits are so important, the “Chocolate Rain” guy must be a geniushe has 47 million plus hits, and he’s not even an MD.

And by the way, I’m guessing that the majority of those 230,000 hits were people that didn’t even watch the whole videothey clicked on the link thinking the topic was intriguing, then realized that it was 1 hour and 29 minutes longthat was when they figured out that watching the entire video would be a waste of time, so instead, they all went out and exercised, so then they could eat their fructose with no fear. Good work Alan. Although his ignorance still shines bright, hopefully he will remember the day when Alan Aragon laid the smack down on his high fructose candy ass. February 7, 2010 It is 2010, a man walked on the Moon, a remote controlled car is cruising around on Mars, yet some people STILL believe the Earth is flat, some people still vigorously claim evolution isn’t happening. Only a few people on this board are experts regarding food, I suppose mr. Aragon is one of them, having watched the video of dr.

Lustig’s lecture and having read mr. Aragon’s critique here, I fail to understand why there is such an interesting note of negativity from some posters toward dr. Because, as they say he speaks more on the sensationalist side? Some professors tend to lecture this way and it’s a good thing, because there will be very little sleepers in the classroom. Being passionate about a truthiness does not make him wrong. Lustig proven the theory about fructose, so that all doubt is removed?

Well apparently not. So, I’m not sure what the majority opinion here is, that fructose is neutral, or that it is good? Are there any arguments to consume more fructose?

To go, as Alan put it, out of your way to get pure fructose and use it generously on everything you eat, and why not? Maybe you, who doubt dr. Lustig should do that, I’ll see to it that you get your Darwin award in a few years. Seriously, what our good doctor proposes is NOT unhealthy, it seems so even to a non professional nutritionist such as myself. Furthermore, doesn’t it make perfect sense to eliminate simple sugars from your diet? Drink plain water, don’t sweeten your anything and also, lower saturated fats as much as you can, increase non-saturated fats intake, increase fiber intake. In my gym, evey guy I talked to knows that.

February 7, 2010 @Fred Hahn: “The point is excessive height as well as excessive fat accumulation is a hormonal disorder. ” Except that fat accumulation is in the individuals control based on calorie consumption and activity levels. I’ve never heard of a diet and exercise routine that can make you taller or shorter. One of the above situations is almost completely out of the control of the individual, and aside from malnutrition affecting final genetic potential, there is not much one can do to infuence and manipulate height.

That is completely the opposite of what is true for fat accumulation. Stop giving people excuses and acting like obesity is more of a disease than an eating disorder. February 7, 2010 Michael K., “So, I’m not sure what the majority opinion here is, that fructose is neutral, or that it is good? Are there any arguments to consume more fructose?” The majority opinion is that fructose is not “poison” and that dosage needs to be taken into consideration before demonizing a simple monosaccharide. Lustig failed to provide any studies suggesting that moderate fructose consumption is hazardous to your health. “Seriously, what our good doctor proposes is NOT unhealthy, it seems so even to a non professional nutritionist such as myself. Furthermore, doesn’t it make perfect sense to eliminate simple sugars from your diet?

Drink plain water, don’t sweeten your anything and also, lower saturated fats as much as you can, increase non-saturated fats intake, increase fiber intake. In my gym, evey guy I talked to knows that.” I’m not a “professional nutritionist” either, but I can tell you – Artificial sweeteners are generally considered to be safe and can help promote hydration.

– There is no reason to “lower saturated fats as much as you can.” – Increasing non-saturated fat and fiber intake can lead to problems as well (increased caloric intake and/or immunosuppressant effects and hormonal issues, respectively). Hope that helps clear things up. February 7, 2010 Dr. Lustig, That was a very weak display of ‘scientific’ debating. In fact, it was a nearly perfect display of poor reasoning skills and denial of the research evidence. Alan was clear, logical, and evidence-based.

You appeared confused, frustrated, and quite ignorant. I have to echo others’ thoughts about using Youtube as a base of support for your credibility. At least you got me to chuckle. Apparently, you’re no better than Fred Hahn when it comes to forming strong logical arguments. I would suggest that you have your esteemed colleagues have a look at this discussion. Perhaps they can come across to you about how you fell short, as well as how you might improve your mindset and practice as a scientist and teacher.

February 7, 2010 On a whim, I emailed Dr. Lustig thanking him for contributing, and I even praised him for his tenacity despite our disagreement. His initial response was cordial, but contentious. The last thing I want to do is spend my time in a private email debate with him.

I let him know that the point of our discussion in the first place is to educate the public, so I invited him to re-engage with me over here, for the learning benefit of the readers. His second response was less cordial, more contentious, and more bristling toward the idea of coming back here. He even had some choice descriptors of the contributors to this discussion, which I’m sure is why he disallowed me to post our email exchange publicly. Here’s the key point I want to level at Dr.

Lustig, who I asked to respond again, but probably will not: If you are such an illustrious academician and scientist compared to the “naysayers” of this discussion who are merely “pseudo-scientists”, then your arguments should have stood strongly on the merit of their scientific defensibility. But, they were EASILY crumbled. Furthermore, valid arguments against your claims were repeatedly ignored. The large gaps in the accuracy of your material were also repeatedly ignored.

You made an extremely weak showing here, and trust me that plenty of, as you say, “real scientists” had their eyes on this discussion, watching in disappointment as your case floundered and essentially got crushed. With all that said, you’re welcome to come back and attempt to rectify your failure to communicate relevant facts. February 8, 2010 I watched the entire 1.5 hour video and I definitely came away with the message that the ill effects of HFCS is dose dependant. I checked my hamburger buns and several other products in my kitchen and most contained HFCS (it was often in the first five ingredients listed).

Other than those buns and a few other products (I use sparingly) I don’t drink soda, juice, or eat a lot of sweet and/or processed foods, but I am still apparently exposed to a fair amount of HFCS. I can easily envision how many other American’s who eat much more processed food, soda, and juice products than I are ingesting a great deal more daily. So it would seem to me the dose comes in the form of the cumulative exposure we, by virtue of HFCS being added to a great many products, consume on a regular basis. So I did not come away from watching the video with a fear of HFCS consumed in moderation, however, I did come away with a good appreciation for how difficult it is for the typical American to do so given how ubiquitous it is in food products. From what I understood of the biochemistry involved (and forgive me if I misspeak, I am a layperson trying to grasp this), sugar (sucrose) is not as harmful by far as HFCS due to the difference in the way it is metabolized in the liver.

Therefore, that Japanese consume a lot of sweet products does not necessarily do away with the underlying argument made in the video if these products are sweetened with sugar and not HFCS (as is the case in a great many products in the US). Ryan, can you speak to the the type of sweetener most commonly used in Japan? Anyone, was Dr. Lustig’s explanation of how HFCS is metabolized in the liver as opposed to sucrose incorrect? Are they not metabolized differently? Finally, I am disappointed with the responses from Dr.

Lustig and didn’t find them compelling. Although I don’t necessarily find the arguments against his theory compelling either (although generally better presented) as many have put too much emphasis on Dr. Lustig’s lack of stressing dose dependence which I personally did feel he conveyed in the video. February 8, 2010 @Frank: I suppose I expressed myself unclearly the first time, I’ll say things as they are: replacing SFAs with PUFAs is healthier than not doing it.

This is consistent with what I believe. @Mike L: it seems to me Lustig defined fructose as poison because it has the traits of the poison, it can only be broken down in the liver, and will under certain conditions (not coming in naturally balanced – with fibers) lead to chronic disease. I understand exactly why you guys have a problem with this sensationalistic definition, and I do give you that it does go over the edge, but he’s still right. This poison won’t kill you, but alcohol won’t kill you either if you consume it in moderate amounts. Why would you need artificial sweeteners?

I never had a sweet tooth for anything sweet, and time I put sugar in my coffee, tea, or anything else is long gone. Please provide a reference to “- Increasing non-saturated fat and fiber intake can lead to problems as well (increased caloric intake and/or immunosuppressant effects and hormonal issues, respectively).”. @Roy Baty: if you tell me Zeus will drag me to Hades with an acceleration of 9.8 meters per second per second, I’ll tell you your reasoning is false, but I’ll admit the numbers are still correct. The proving and disproving part – get serious, we all know how this one goes.

Also, I would like to see more discussion with dr.Lustig, I hope he will come back regardless of what he said in his last post and e-mail. Scientifically, any theory should and must go through a process of evaluation, it must stand to be criticised, looked at and debated from any imaginable angle NO MATTER how obviously correct it seems to the scientist behind it. February 8, 2010 I have a few isssues with your comments. First, your studies, who is financing them? It has been my experience that the studies that say fructose and high fructose corn syrup are “ok in moderation” are funded by someone with something to gain. Also so it is not fair to compare the fructose in a starwberry or any other natural food that God created to the fructose in a fruit snack, juice, or any otehr food tha man creates!!

And how do you define ‘moderation’ when most of the products that are on our shelves contain HFCS, its in ketchup, in juices, in cereal, in granola bars, it is in too many foods that Americans consume! If you want to look at some good unbiased nutrition facts, look up Dr. James Chestnut, but please don’t help people buy into the lie about our processed foods. Our country has an obesity problem because the additives in our foods are killing our metabolisms. Oh and one last thing, don’t go to a diet pop to avoid the sugar and HFCS, you get aspertame, and that is a poison, it was approved with the knowldge it caused cancer!

February 8, 2010 @Amy Southwick Aspartame is perfectly safe, at least in the dosage we are getting. Aspartame: a safety evaluation based on current use levels, regulations, and toxicological and epidemiological studies. PMID: 17828671 “The studies provide no evidence to support an association between aspartame and cancer in any tissue.

The weight of existing evidence is that aspartame is safe at current levels of consumption as a nonnutritive sweetener.” There was no conflict of interest reported in this review. The problem might more lie in the fact that product containing aspartame are highly processed. February 8, 2010 James, which HFCS formulation are you comparing sucrose to? 🙂 Also, I think one of the major points here is that we have so much more weight problems and accompanying diseases not because HFCS, but because sucrose or HFCS are ADDED to damn near everything that is processed, especially in America – this has got to be partly responsible for weight gains. Sauces have grown immensely popular and all of them contain sugar, some to an almost obscene amount.

Fact is, people love sugar and food industry loves to make money, connect the two and you get sugar everywhere. Again, why does everything you put in your mouth have to be sweet? Are you kicking the ‘fructose alarmism’ horse because you’re basically okay with consuming ~100 pounds of sugar annually?

The truth is probably (as I can, with my modest knowledge, only sense it) that there is not just one factor to be blamed for worldwide weight gains, there must be several. Sugar is only one of them, (over)processed foods may be another, perhaps denaturalization of foods (pesticides, growth hormones in animals etc.) we grow are yet another. So maybe noone here is completely right, and noone is really wrong. February 8, 2010 Ganine — You mention that you “did not come away from watching the video with a fear of HFCS consumed in moderation,” except the rest of your comment shows otherwise. Notice how you implied a significant difference in sugar-sweetened foods versus HFCS-sweetened foods. That’s incorrect. Chronic overconsumption of either one is a bad idea.

As for HFCS in various refined products, the amount will vary considerably. Those buns you’re scared of likely do not have much more than about 1 gram of HFCS per slice. How many buns will you be munching on today? You’re better off keeping an eye on total carbs for the day while predominating your diet with minimally refined foods rather than fretting over every gram of HFCS in the minor amount of refined foods you eat. Michael K — Your extremist stance on dietary intake is unproven and unproductive.

It might even be detrimental. This is where experience comes in, and I can tell you that most people eventually react rebelliously to orders of strict food avoidance. Eliminate SFA. No sugar allowed.

All bullshit. Even the Okinawans have added sugar in their diets. Moderation is a good thing when it comes to dietary habits. Rigid food avoidance, false designation of food taboos, and a dichotomous all-or-nothing approach has a stronger association with adverse outcomes than a more flexible approach. By the way, this is not just my field observation, it’s in the literature as well (yes, this is correlational research, but it’s better than a baseless defense of food avoidance practices): Rigid vs.

Flexible dieting: association with eating disorder symptoms in nonobese women. Rigid dieting strategies: relationship with adverse behavioral outcomes.

Amy — It looks like you’ve been drinking the alarmist coolaid quite a bit, immersing yourself in scare-mongering. Please refer to James & Frank’s responses to you.

As for research funding source, it should be factored into perspective, but not viewed as a reason to dismiss research completely. Would it make sense to dismiss the large body of low-carb research funded by the beef industry? All the egg research funded by the egg industry?

The creatine & beta-alanine research funded by EAS? The fish oil research funded by the fishing industry? All pharmaceutical research that’s industry-sponsored? Of course not. Take funding source into consideration, sure.

But don’t dismiss data completely based on funding source. If you read my article carefully, I shoot right in the middle of the liberal & the conservative recommendations in the literature because both sides are biased. February 8, 2010 Alan: Thank you for the reply. “You mention that you ‘did not come away from watching the video with a fear of HFCS consumed in moderation,’ except the rest of your comment shows otherwise. Notice how you implied a significant difference in sugar-sweetened foods versus HFCS-sweetened foods.

That’s incorrect.” In reference to your above comment, I didn’t imply anything. I asked a straight forward questionare they, or are they not, metabolized differently? I admitted I didn’t know much about the subject and was simply seeking clarification on this point.

If they are metabolized differently, that would “seem” to be potentially significant. Again, I don’t know much about biochemistry, but the very little I do know is that a very small change in chemical composition can radically alter a substance and hence the bodies reaction to that substance. The answer I got from James (thank you, James), lead me to believe they are metabolized differently since he said there is a “little” difference in how they are metabolized; he did not say there is “no” difference. If there is any difference, no matter how slight, then the implication is they “may” not be metabolized the same.

Whether that little bit of difference leads to the problems being hypothesized by Dr. Lustig or not is a completely different matter. Again, I was only trying get some clarity re: if they are metabolized differently or not. “Chronic overconsumption of either one is a bad idea.” Agreed. But the question would seem to be does one have more of a detrimental hit than the other.

And if so, than that detrimental effect combined with cumulative exposure (obtained by virtue of it’s ubiquity) extrapolated out over several years “might” be a problem. Not saying it is or isn’t, but I’m keeping an open mind to the issue. Once more, I was just trying to get a handle on if there is ANY difference, and what that difference is, re: metabolism. ” As for HFCS in various refined products, the amount will vary considerably.” I’d imagine that is true, but HFCS would seem to be in quite a lot of products. “Those buns you’re scared of likely do not have much more than about 1 gram of HFCS per slice.

How many buns will you be munching on today? You’re better off keeping an eye on total carbs for the day while predominating your diet with minimally refined foods rather than fretting over every gram of HFCS in the minor amount of refined foods you eat.” You are completely mischaracterizing my statement. I am not “scared” of the buns at all LOL. I actually ate 2 right after I wrote my post. I eat a small amount of carbs during the day and I usually eat the majority of my carbs post workout ( I had just deadlifted before having my burgers).

I do keep an eye on total carbs for the day, and other than my buns, tend to not eat processed foods. I am not “fretting” in the least over my buns (well, not the ones I eat anyway). I understand your blog post is on “alarmism,” but please don’t automatically assume your posters to be alarmist, lest you be an alarmist alarmist.

February 8, 2010 Ganine, 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. February 8, 2010 The funniest thing about this whole notion is that it leads to the idea that fruits are bad for you. When the fuck did fruits become a bad thing to have in your diet?

All because guys like Lustig and other alarmist idiots can’t understand simple dose-response relationships. And yes, it is alarmism. People are so scared of everything now.

Shut up and eat. Despite what God-girl said about Jesus making more pure fructose or whatever her superstitious ramblings were saying, there’s just nothing to support the idea that moderate amounts of fructose are harmful. Why this is challenged with the “SO YOU SUPPORT EATING 10,000 POUNDS OF SUGAR!!!!” strawman is beyond me. If you over-eat anything, you get fat. Now we just need Fred Hahn to come back and say you can’t put on fat by over-eating steak and eggs. Is the education system really this broken?

Fructose doesn’t get a pass to violate first principles of thermodynamics. Neither does insulin. If you people are postulating magic, you better damn well have research showing the magic wand. February 8, 2010 Alan, calling my stance extreme is a bit unfounded. Beseides, I fail to see how my statements brought up the rigid vs flexible dieting, unless you would call “no drugs, tobacco and alcohol” rigid dieting too. Perhaps I lacked precision in my posts – of course I never proposed we replace ALL SFAs with PUFAs, since that would be impossible – just avoid SFAs, which is mainly animal fat. I do propose the elimination of all centrifugal sugars (that does not include foods that naturally contain sugars, even honey) but of course it’s not really necessary to eliminate them in absolute terms, just don’t add sugar – you’ll get it in anyway somehow.

However much fibers you eat, it’s probably not enough, so I propose you eat some more. Add olive oil and fish oil to your diet.

Do you really think that’s extreme or are you just trying to bully me? February 8, 2010 holy fuck. Ryan Zielonka February 8, 2010 “You are correct that the obesity epidemic is multifactorial, which is why it is erroneous for anyone to blame one factor for obesity.” bullshit i can easily blame all the time spent reading this god damned comment thread while munching on deep-fried HFCS (stroopwafels, mmmm) rather than training or doing something otherwise useful. My simple translation of reality is that the psychological effects of teh sugars, while independent of and thus not changing the phsyiological, can dominate. Thus, the result is (get this) people fucking eat more. February 8, 2010 @ Michael I don’t want to be picky, but here, to quote you, you said, a few post ago: “lower saturated fats as much as you can” is somewhat in the idea of “of course I never proposed we replace ALL SFAs with PUFAs” Of course it’s not possible, but your first sentence implies that if this could be done, you would recommend it, when this is clearly not a necessity. Quoting you again: “just avoid SFAs” Why would someone need to do this?

Althought the epidemiology is quite clear that PUFA are beneficial when they replace SFAs (but adding more SFAs to one’s diet is not deleterious to health – a very important distinction), i’m still convince there are important confounding factors since many mechanistic studies found that n-6 promote inflammation & oxidation after a certain threshold. Again, dosage is important here (as always).

But by telling people to avoid SFA you, first, pertain a myth that must die now, and second, perpetuate extremist behavior of food avoidance, as Allan pointed out. February 9, 2010 Really Frank? Since my opinion on SFAs is in accord with most of what google finds when looking for saturated fats I must conclude what I think is not extreme, but mainstream (unless you call mainstream opinion extreme-?) – that doesn’t in any way mean it is correct, but I would very much like you to prove your point by providing a few credible links/studies. I found this one ( )claiming that we should increase SFA intake, sadly, it cites no sources, here’s an article at the Harvard’s page in my favor:. Don’t get me wrong, I’m not defending my camp to death, I’m merely looking for the truth. February 9, 2010 Excellent resource, thanx for that.

February 9, 2010 @ Michael Read these, Michael. Meta-analysis of prospective cohort studies evaluating the association of saturated fat with cardiovascular disease. PMID: 20071648 A systematic review of the evidence supporting a causal link between dietary factors and coronary heart disease. PMID: 19364995 Dietary Fat and Coronary Heart Disease: Summary of Evidence from Prospective Cohort and Randomised Controlled Trials. PMID: 19752542 The last one can be downloaded for free. These are all systematic review of the literature, which are consider very high quality evidence, done by independant researchers. I don’t wait for the mainstream to change it’s view to go with what the science say 🙂 If you look for the truth, then the truth is that SFAs are not related to CHD, but by replacing them with PUFAs you can further decrease your risk.

These papers are all very clear. There’s also 3 others review out there published in the last two years, but it’s no as high quality evidence, so these 3 should make it. February 9, 2010 One of the least convincing arguments from the above is that HFCS is the same as table sugar. I understand this — but the argument does not stop there. These assertions come loaded with the implication that table sugar is safe over the long term in the ever-increasing dosage which human beings are consuming. If the metabolic pathways for fructose lead to a higher amount of undesirable end-products within the human body then it is irrelevant as to whether its source is HFCS or by pouring refined, white sugar down your gob. So what of it?

Is table sugar a long term health risk? Should we be consuming more, or less? What is the ideal daily dosage? How can we relate this to the rise of HFCS as an additive in almost all processed foods? February 9, 2010 Mike K, It looks to me like instead of trying to find the truth, you’re groping for evidence that fits your beliefs, and ignoring the rest.

Refer to Frank’s response for the big picture about saturated fat. Also, that other study you cited is correlational.

Not that this means it’s useless, but it can’t show cause-and-effect, and it can’t necesarily distinguish the role of decreasing activity levels and a lot of other variables from soft drink intake. Also, I think you’re misrepresenting Alan’s stance. He advocates “a predominance of minimally processed foods” in the diet. That study you linked suggests the dangers of excess soft drink consumption combined with other typically bad lifestyle habits of the population at large. Are you even reading Alan’s responses? You are in fact proving yourself to be an extremist by missing the point continually.

February 9, 2010 I’ll take a stab at this >>Is table sugar a long term health risk? Depends on context and dose >>Should we be consuming more, or less?

If “we” is already obese people consuming excess calories and if “we” want to gain more weight, yes you “should”, but why concentrate on sugar? In this case fat (butter, lard, cream) would be a better, more concentrated way to get more calories. If “we” is anorexic women about to die, IMHO hell yes you “should” (although you might disagree) if “we” is everybody in the US – the answer is “depends”.

My answer is “I don’t know” if “we” is people with insulin resistance who’ve carefully experimented on their own diets and found they do well on high fat diets and badly on high carbohydrate, probably you shouldn’t. >>What is the ideal daily dosage?

You have been reading along in the last 150 or so posts, right? >>How can we relate this to the rise of HFCS as an additive in almost all processed foods? What do you mean by “this” in “relate this” – the preceding 4 questions, the stuff in the 1st paragraph? February 9, 2010 Bill, You had stated the following: “These assertions come loaded with the implication that table sugar is safe over the long term in the ever-increasing dosage which human beings are consuming.” My point was that these assertions do not come loaded with such an implication.

In regards to your other questions, Sam actually addressed them quite well. There are no straightforward answers because they completely depend upon the context, which is something Alan has been pointing out both in his blog post and in the comments. For example, too much sugar for a sedentary person is completely different from too much sugar for a marathon runner.

People always want nice, simple answers to their dietary questions, but when it comes to the complexity of the human body, nice simple answers rarely exist. Do I feel that the U.S.

Population consumes too much sugar on average? But do I know what the “optimal” level might be?

No, because that is a question related to individual needs, which, again, require context. ************* If the metabolic pathways for fructose lead to a higher amount of undesirable end-products within the human body then it is irrelevant as to whether its source is HFCS or by pouring refined, white sugar down your gob. ************* I’m going to use your above statement as an example. The metabolic pathways for fructose only lead to higher amounts of “undesirable end-products” under certain conditions. Under other conditions, fructose is harmless and can even be beneficial. This is why context needs to be taken into consideration.

February 9, 2010 Basically, the energy status of the body. This can be partly reflected by liver glycogen content. I won’t go into the detailed biochemistry, but fructose will take different metabolic pathways in the liver depending upon liver glycogen status. In fact, liver glycogen status is a powerful mediator of fructose metabolism in that it regulates the enzymes which are involved in fructose metabolism.

If you are in an energy deficit, liver glycogen is not full. In this case, fructose is directed towards gluconeogenesis (production of new glucose to be released into the blood) and replenishment of liver glycogen. If you are in an energy surplus, liver glycogen is full. In that case, fructose is directed towards triglyceride and VLDL formation (the “undesirable end products” you refer to). If you are in energy balance, there will be a balance between triglyceride formation from fructose, and triglyceride and fructose oxidation, and there won’t be any accumulation of visceral fat.

Thus, fructose will only exert harmful effects if you’re overeating in the first place. February 10, 2010 Alan, Under the heading “Boooo, Doc” you say: “ he proceeds to blame carbohydrates as being the primary constituent [for increases in caloric consumption]” You then go on to cite USDA figures in an unusual way (by simply subtracting the 2007 percentage of total diet from the 1970 percentage). For example, Meat etc was 17 percent of the US diet in 2007 and 21 percent in 1970, so you say meat consumption ‘decreased by 4%’. However the underlying reality is that between 1970 and 2007 US Meat, eggs and nuts consumption increased by 10% (see the Meat tab in the link you provide). Using the same method, fructose consumption (see sugars tab and adjust for percentage fructose) increased by 20.6% in the same period or by 43.8% (if you use trough [1975] to peak [1999]). You then draw the conclusion “it appears that the rise in obesity is due in large part to an increase in caloric intake across the board, rather than an increase in carbohydrate in particular.” And whilst it is undoubtedly true that you won’t get fat without increasing the number of calories you consume, your statement says nothing about the underlying cause of the increase in consumption.

It seems to me that what Lustig is actually saying is that fructose exerts a metabolic effect which results in the up-regulating of our appetite control system. If that is correct then the result of that up-regulation would be a gradual increase in the amount of (all) food that we eat. The USDA data is not probative of anything other than caloric increase, but it behaves as Lustig’s hypothesis would predict. The expected outcome would be a sustained increase in total caloric consumption and the USDA data bears that out, doesn’t it? Cheers David. February 10, 2010 Alan, Under the heading “Fructose is evil, context be damned” you say: “[Lustig says] that unlike glucose, fructose does not elicit an insulin (& leptin) response, and thus does not blunt appetite Lustig is forgetting that most fructose has an equal amount of glucose attached to it Here’s the point I’m getting at: contrary to Lustig’s contentions, both of these compounds have substantial research showing not just their ability to elicit an insulin response, but also their suppressive effect on appetite.” You cite four studies as authority for that statement.

Each of those studies comes to an identical conclusion: HFCS (55% fructose) is not materially worse for you than sucrose (50% fructose) (or vice versa). The studies were funded by [3] PepsiCo North America, [4] Suikerstichting Nederland [Dutch Sugar Industry], [5] the American Beverage Association and the Corn Refiners Association and [6] International Life Sciences Institute North America – ILSI has significant links to producers and purveyors of sugar and HFCS products. And while I doubt funding source changed what was an entirely predictable outcome, I think it would have been good to mention it when citing the articles.

What I don’t understand is how citing four studies which say that sugar and HFCS have identical effects (including on [next meal] satiety) addresses the point Lustig makes about fructose versus glucose and long term appetite control. And I certainly don’t understand how you get from there to the conclusion that because fructose (on its own) is not a normal part of our diet, we don’t have to worry about substances that include it (such as HFCS and Sugar). Cheers David. February 10, 2010 >>What I don’t understand is how citing >>four studies which say that sugar and >>HFCS have identical effects >>(including on [next meal] satiety) >>addresses the point Lustig makes >>about fructose versus glucose and >>long term appetite control. My understanding of Alan’s stance: using biochemistry, to single out one single mechanism of satiety has not panned out when tested in the real world, where there are other biochemical pathways involved. If fructose’s satiating effect is negative, why does it not make you much hungrier than glucose in the preload studies? And if the biochemistry has not given you the result you predicted in the short term, why will it give you the result you predict in the long term?

And besides, the biochemistry goes both ways – fructose preferentially refills liver glycogen, an important contributor to satiety (an alternative path to leptin). Glucose refills liver glycogen less effectively than fructose. Why concentrate on one of fructose’s effects and ignore one that rebuts the argument? February 10, 2010 >>because fructose (on its own) is not >>a normal part of our diet, we don’t >>have to worry about substances that >>include it (such as HFCS and Sugar) Where did you see that? I see stuff like AA: >>Is it really that groundbreaking to >>think that polishing off a half-dozen >>soft drinks per day is not a good >>idea? And this: AA: >>I’m obviously not in favor of >>replacing anyone’s daily fluid >>intake with soft drinks, but I can >>already see a number of straw man >>arguments headed my way.

February 10, 2010 Great one Alan. I just got through reading all the comments. I have only two points to make.

I’m urging everyone with websites to post only the debate between Alan and Lustig. I doubt many people will read through all these comments and the world deserves to see the misinformation that Lustig is spreading and how he ran away from a logical argument after being defeated.

I feel sorry for Fred Hahn’s clients. I’ve never heard such poorly made arguments and an utter refusal to listen to reason.

February 10, 2010 Alan, You go on (under the same heading) to cite two studies by Rodin as authority for the proposition that Lustig’s “assertion that fructose and fructose-containing sugars increase subsequent food intake” is wrong. Rodin’s studies were designed to determine the effect of a fructose or glucose solution on the amount of food consumed at a subsequent meal. To make the solutions taste the same (fructose is much sweeter than glucose), Rodin’s team added aspartame to the glucose solution. What she found was that subjects who drank the fructose solution ate less at a subsequent meal. Whether that was because fructose is satiating or because aspartame or glucose (or both) are not could not be determined from the studies. She also noted that elapsed time between the load and the meal affected the outcome. Studies on the appetite stimulating effects of aspartame are all over the shop, but a recent meta review and longitudinal study came down on the side that it could be.

(see: ) Interesting though this undoubtedly is, I can’t see how it relates to Lustig’s hypothesis which I understand to be that fructose produces long term hormonal disruption by creating insulin (and leptin) resistance. Under that hypothesis surely any effect observable after one meal would be meaninglessly small (and surely undetectable) amongst the tidal shifts of insulin (and glucagon) occurring after ingestion of any food (not just fructose, glucose and aspartame)?

You round out this section of your article by quoting White who you say is ‘an independent researcher’. Let’s put aside for a moment the fact that White works closely with the Corn Refiners Association and ILSI. Let’s also try to ignore the fact that the paper from which you quote was supported by the American Society for Nutrition (whose membership list is a roll call of the processed food industry) and focus on what he says.

After admitting that studies which feed human subjects pure fructose will produce ‘metabolic anomalies’, he reverts to the argument that since HFCS is only 55% fructose those studies don’t count (when considering HFCS). He then spends the remainder of the scientific part of the paper comparing HFCS to sugar and concluding that they are (surprisingly) pretty much the same. He then compares HFCS consumption to worldwide obesity rates and concludes there is no association. That shouldn’t come as too much of a shock since the US is the primary consumer of HFCS (pretty much everywhere else dominantly uses sugar). But by then it seems that White has forgotten his earlier point that HFCS and sugar are metabolically identical and so doesn’t include sugar consumption in his analysis. In the passage you quote approvingly (from the abstract), White refers to ‘studies using extreme carbohydrate diets’, but the only two human studies he references on this point (in the paper) tested subjects at 0%, 7.5% and 15% exposure and found metabolic problems at all levels (except 0%). Does that sound like an extreme diet to you?

Cheers David. February 11, 2010 Louis: You are right that people in Asia exercise more and stay thin despite a high carb intake. Lustig did not miss this point in the lecture – he stated that exercise increased the rate of, I believe, the citric acid cycle which keeps the liver from converting the glucose into fat and distributing it into the bloodstream. In addition, only 20% of glucose is subject to this process, while ALL of fructose is. So there is in fact a huge difference between an active Asian eating rice versus a sedentary American consuming fructose. Ganine: The lecture never said HFCS is bad, sucrose is okay.

In fact, it stated that the two are almost equivalent. These are just two examples of the lecture being interpreted unfairly or erroneously.

I have no affiliation with Dr. Lustig whatsoever. I merely agree with his findings as most convincing, and most conforming to my own observations. In addition the research he cites and arguments he delivers seem to be in line with the latest science. In the end, the alarmism of fructose really is about the disruption of hormone regulation. If you believe it fructose is fine, I’d like to hear alternative theories on why Americans have such high rates of diabetes, high blood pressure, and other degenerative diseases.

Some biochemistry will be convincing. February 11, 2010 @ David Gillespie: Could you possibly be selling a book you wrote about how to be an alarmist sugarphobe? I don’t know why but I have a strong hunch that you do: How can you go bashing the AMERICAN SOCIETY FOR NUTRITION from a position of an IT guy who lost a bunch of weight and is now blaming teh sugars for getting you fat?

Do you even realize you are EXACTLY the type of guy Alan is trying to prevent the cloning of, due to lectures by Robert “I’m credible because of Youtube hits” Lustig? February 11, 2010 Scientist’s rule #7: if you, in an open debate, mention the popularity of your work on the internet as a reference to it being true, you lose all credibility, your points become invalid, your work is annihilated and your ph.d. Revoked, you become an Ogre and are thereafter forever banished from the land you live in. I find it interesting how David Gillespie’s major points (and entire posts actually) are widely ignored and nobody seems to realize there just MIGHT be a conflict of interest here, and we are not talking about a few dollars more or less, we’re talking about profits of a industry so huge, from which only Coca Cola spends more than 2.5 billion US on advertising alone. Don’t you think they would maybe spill a few bucks of that money into funding a study or two that says their product is perfectly okay?????????????????? If I were the board of directors, anyone who didn’t agree with that would get fired.

Out of a cannon. Tobacco industry had to back down, because the arguments against tobacco were just way too overwhelming and the correlation too undoubtful, but they still fought decades, regardless – and here there is an industry that feeds us what tastes great on our tongues Something that takes years of careful observation has never been easy to prove, and even so, it can easily be ‘disproved’ by another ‘study’ and people are relieved, because they like it the way it is. I have reached a conclusion, and I will stick with it, unless someone comes up with a persuasive argument, backed up by clean, independent studies. February 11, 2010 >>In the end, the alarmism of fructose really is about the disruption >>of hormone regulation. If you believe it fructose is fine, I’d like >>to hear alternative theories on why Americans have such high rates >>of diabetes, high blood pressure, and other degenerative >>diseases. Some biochemistry will be convincing.

Could simply be aging. Older people weigh more, get more diabetes & cancer & heart disease, and the average age in the US is rising. Sandy Schwarc has a lot of pieces on the “Obesity Epidemic”.

February 11, 2010 Nicolas said: “In the end, the alarmism of fructose really is about the disruption of hormone regulation. If you believe it fructose is fine, I’d like to hear alternative theories on why Americans have such high rates of diabetes, high blood pressure, and other degenerative diseases. Some biochemistry will be convincing.” Sorry, this is not how science works. We could generate hundreds or possibly even thousands of hypotheses as to why this is the case. It is doubtful that any one variable is responsible. The fructose alarmists are the ones making a specific claim. The onus of proof is on them and they’ve done a piss poor job at it so far!

February 11, 2010 >>Coca Cola spends more than 2.5 billion US on advertising >>alone. Don’t you think they would maybe spill a few bucks of that >>money into funding a study or two that says their product is >>perfectly okay?????????????????? If I were the board of directors, >>anyone who didn’t agree with that would get fired.

Out of a IMHO you put the emphasis on the wrong side of the issue. The bigger risk is from researchers and the researcher/politico with an ax to grind, who makes results conform to his own prejudgments.

Saturated fat phobia being a case in point. For corporations the risk from a backlash to this kind of activity is huge. The only safe way to proceed is to commission the study and if the findings are not to your liking, don’t allow publication. You couldn’t realistically commission a study with that objective. At the very least, you don’t put anything like that, or that could be interpreted that way on paper or in an email.

My understanding of current US “justice system” is that if you’re sued and the plaintiff asks for documents, you have to turn them over. And if a jury gets wind that your company likes to pay for “appropriate science” the result will be disastrous for the company. Put yourself in the position of an executive about to order a study and specify the results you want to see. How are you going to communicate that?

How sure are you that no one you meet with is recording? Sure you have no disgruntled employees? Any place like Coke or Pepsi, with lawyers up the wazoo, will not ignore a judge’s discovery order. The lawyers have too much to lose. The companies do to, although they may not realize it. Emails, meeting minutes, voice mails, notes regarding phone calls.

It’s all discoverable. If there were orders or threats to find a specific result these orders would be found, by, among others, CSPI.

This obviously does not preclude wink and smirk activity, but threats, and even hints, of firing are out. Returning to that question: you’re that executive – want to risk your $300,000 per year job just to get a wee little article published?

February 11, 2010 Fred Hahn, have you not come across Lex Rooker and other bloggers who are doing very carefully controlled self experiments, who gained weight on zero carb? Eades says: >>The metabolic advantage brought about by low-carb dieting is >>probably somewhere in the neighborhood of a 100-300 calories, which >>isn’t all that much. This isn’t very far from what Lyle says, is it? (minus the cussing: ) doesn’t QUITE sound like “you can eat a plate of pork chops piled to the ceiling and not get fat” And yes, I could eat a plate of pork thops, piled to the ceiling, plus some bacon and eggs, plus some duck pate (love that stuff) no juice, no bread, no cereal (no carbs) every day.

I can overeat meat like anybody’s business. I used to have 32 ounces of steak and a small salad for dinner all the time).

5,000 calories a day of steak, no carbs??( BRING IT ON. February 11, 2010 David, Since you agree that sucrose or HFCS has appetite-suppressive effects in the short-term, I find it amusing that you’re quick to assume this would automatically flip-flop the opposite way in the long term, particularly within the context that their consumption isn’t artificially high as in studies commonly used for scaremongering purposes. As for your critique of John White’s article, you point out that 2 of the studies cited therein indicate the metabolic risks of a moderate amount of fructose despite White’s mentioning of an extreme amount of fructose being the problem. Okay, that’s fine.

However, this doesn’t make his statement false, as I’ve shown in my rebuttal to Lustig’s final post. Also, you have to look at the totality of the evidence.

Have a look at the following review, which objectively examines the gamut of research and shows that your alarmist stance on fructose is unfounded: Evidence-based review on the effect of normal dietary consumption of fructose on development of hyperlipidemia and obesity in healthy, normal weight individuals. In agreement with RayC, your dismissal of the American Society for Nutrition’s credibility on the basis of their membership is ludicrous. The ASN publishes some of the highest quality nutrition-related research, in terms of both the investigators and the content. They hold high standards of rigor in the conflict-of-interest department, requiring transparency from all involved. In sum, the ASN is one of the most well-respected scientific information resources – for deserved reason. The study I cited above is published by the CRC press, which publishes a range of scientific material, including engineering, physics, and medicine.

All nonfictional material. If we were to apply your logic behind the dismissal of the ASN, we could just as easily dismiss the credibility of your book “Sweet Poison: Why Sugar Makes Us Fat”, since its publisher (Penguin Books Australia) has a bestseller list predominated by FICTION: But would that be a fair or logical dismissal? Not on those grounds. A better basis for skepticism towards your stance would be the fact that you fit the one-sided alarmist archetype to a stunning degree. The message behind your agenda is oversimplified, and in denial of the importance of dosage & context. Did you skip over the research I linked regarding the association between rigid dieting and adverse behavioral outcomes? Here, I’ll link it again: Rigid vs.

Flexible dieting: association with eating disorder symptoms in nonobese women. Rigid dieting strategies: relationship with adverse behavioral outcomes. The black & white, good/bad picture you paint is not only incorrect, but it’s counterproductive to properly educating the public. You are very quick to discredit scientists and scientific organizations that don’t fit your pre-existent beliefs, but what makes you more credible? I’m very satisfied with my track record with freeing people from various irrational food phobias. You on the other hand, are en route to doing just the opposite. To illustrate, I’ve captured the main point driven home at the end of each one of your videos.

February 11, 2010 David, I also want to add that in your promotional campaign, you use your own testimony as the major selling point for your book. You let yourself get 88 lbs overweight.

And sugar was to blame for this? Well, that sounds like a good enough reason to write a book. Get really fat, adopt a quasi-religious faith about the good and evil of various foods, then write a book about it.

You should have stuck to being a corporate lawyer, because this new gig of yours as the Superhero Against Sugar is a joke. Alan put forth a noble message against extremism, alarmism, and the labeling of foods as good or evil. Frankly, I’m enjoying watching him own the hell out of you and your ilk. February 11, 2010 David: Could it be that your job right now as a software guy is biasing your views?

All the software guys I know drink lots of soft drinks, both diet and non. But they also eat a lot of whatever gets in front of their faces. Alan has plenty of experience with clients who used to have a crazy good-bad perspective of food. I would even say that I had a mortal fear of some foods. Why was I so neurotic about food?

Mainly because of books like yours, that give too much false power to a food, and take all the power away from the dieter. I’ve been much better off ever since I accepted that as long as the majority of what I eat is healthy, the minority of what I eat can be whatever I want. Even sugary stuff.

If I were you, I would think twice about pushing your own personal neurosis and limited personal experience onto everyone. Thanks Alan for the great service you provide, Lisa. February 11, 2010 “David Gillespie is a recovering corporate lawyer, co-founder of a successful software company and consultant to the IT industry. He is also the father of six young children (including one set of twins). With such a lot of extra time on his hands, and 40 extra kilos on his waistline, he set out to investigate why he, like so many in his generation, was fat. He deciphered the latest medical findings on diet and weight gain and what he found was chilling. Being fat was the least of his problems.

He needed to stop poisoning himself. Web site: ” Hey David I got fat from eating too much fried chicken, pizza, steak, and fries. I never go for the sugar, and I have no sweet tooth to speak of. Am I not poisoning myself because I avoid sugar? Please do tell.

February 11, 2010 You know, I get a kick out of knowing I can maintain sub-10% bodyfat (despite being a former fat boy with shitty genetics and thyroid issues) on frozen pizza, Starbucks’ mochas, cookies, rice, Gatorade, and Chinese buffets only by obeying the laws of thermodynamics. I was actually FATTER when I did the Paleo-tard/low-carb thing, which I followed strictly for close to two years. I avoided HFCS like the plague and used practically zero condiments. Why was I fatter? Because inevitably I’d blow my diet when I wanted some starch or was put into a situation where I had no other option. And instead of a sane serving I’d demolish boxes of cereal and anything resembling sugar because 97% of the time I deprived myself of it.

I feel bad for you Paleo/low-carb folks. Really, I do. It’s a whole lot of pain and suffering you endure for no good reason. Moreover, I feel terrible for your children, especially if you impose your diet zealotry upon them.

I’ll take my moderated starch, sugar, and HFCS intake with a side of abs any day over the stress associated with any asinine mainstream eating guidelines. February 11, 2010 One last caveat.

I work with a highly respected physician in Seattle who does sports performance work for elite athletes. She specializes in treating legitimate over-training, also known in the medical community as general adaptation disorder. 99% of the people who believe they’re over-trained have only over-reached. I was diagnosed with over-training disorder in April 2008 and am still recovering from it. Guess what the number one common denominator is amongst athletes, recreational or professional, who are diagnosed with over-training? Chronically insufficient carbohydrate intake.

There’s a dark side to this zealotry that never gets discussed on boards because these folks get sick. Really sick from the kind of deprivation advocated by these fad diets. And they never come back because they’re getting medical treatment for borderline, sub-clinical or full-blown eating disorders fueled by this stuff. February 11, 2010 Alan, Thank you for taking the time to respond. You are clearly missing my point, so I’ll be more explicit. The papers you cite in favour of your argument are funded by people who stand to benefit from sugar, HFCS or fructose being painted in a positive (or at least not detrimental) light. You do yourself (and your arguments) no favours by linking again (as your response) to a paper ([12] in your original list) paid for by Tate & Lyle (the world’s largest sugar producer) which you describe as objective.

That piece regurgitates the work of Livesey ([13] in your list) which was in turn paid for by Danisco (the world’s largest fructose producer). Even putting that aside, when we look closely at the papers you cite, the analysis (such as there is) is suspect. I’ve given examples above and you even concede that is the case with White.

The science (not paid for by sugar producers – over 3,000 at last count) says fructose is dangerous because it has metabolic effects to which we are not adapted (and no other foodstuff seems to fall into that category). The obvious question then (given your ‘track record’) is: Why have you not cited any of the recent human studies which contradict the view perpetuated by the sugar producers (aside from Teff which you dismiss on the grounds of quantity)? Cheers David.

February 11, 2010 David, What good is it for Alan to respond to you if you ignore the research review he just linked refuting your “Fructose = BAD” stance? And he’s the one supposedly remiss here? And I suppose it’s convenient to ignore the research review Michael Miller posted too. Why don’t you post the research you have refuting Alan’s position instead of crowing on and on about funding source.

I’m sure that we all would be happy to see the evidence you can present to support your stance. We’re all here to learn, no sense in witholding your secrets. February 12, 2010 Sam, There’s a definite lag time with the Paleo thing. “Better” is relative.

I’ve seen too many folks dig themselves into a spiraling black hole with low-carb/paleo dieting. If you go back three plus years ago, you can find me fingers in ears proselytizing party-line low-carb zealotry on fitness websites. It may take years (it did for me), but there will be an inevitable physiological or psychological backlash. It’s human nature -we crave what we can’t have. Moreover, many paleo folks go from pure dietary hedonism to strict asceticism, never experiencing a middle ground. Because the diet “worked” doesn’t mean that it’s the only, let alone ideal path to progress. February 12, 2010 Oh, please do email Dr.

Lustig and ask him to join this debate. Do you want to know what side he would come down on? Hint: In his video he admits that some people can eat sugar all day long and suffer no ill effects.

Hint: when he posted here he specifically said he also considers dose and context of the greatest importance hint: he wouldn’t take any side that says “the only safe amount is zero” I’m assuming you can take a hint. Might be a very bad assumption, from what I’ve been reading.

February 12, 2010 Alan, you’re definitely in the same class as Anthony Colpo. Collect x number of scientific studies and you can support any positon. Same goes for any other person.

What most people fail to realize is the complex nature of metabolism and that anyone that claims to have “the answer” is arrogant and unteachable. There is always the urge to develop a unified theory of any area when that goal is only possible by ignoring facts that interfere with that theory. Like Einstein once said, “everything should be made as simple as possiblebut not simpler.”. February 12, 2010 >>There’s a definite lag time with the Paleo thing. Doesn’t seem to have kicked in for me. I went mostly paleo in Sept 2003, went from 190# to 160# in 5 months (at 6’1″, that was pretty skinny), started going to the gym, and muscled up to 180.

A few years into that transformation, I cut out the last little bit of grain and most of the dairy. I find it completely effortless to eat this way. Starchy foods make me sleepy and lethargic, which prompts me to binge on sweets to get my blood sugar back up; it’s why I got fat on a predominantly vegetarian diet that was largely based on whole grains and beans. I now get the carbs I need from vegetables and fruit.

My blood sugar stays nice and even, I have energy, I sleep well. It’s ludicrous to suggest that I’m somehow destined to crash and burn because I no longer eat foods that wreak havoc on my endocrine system. February 12, 2010 David Gillespie, It is nothing more than intellectual laziness to discount a paper or papers based on funding source alone. What people need to understand about study funding is that just because a company funds a study, it does not mean the company had any hands in the actual research or outcomes of the paper. I published a study on glutamine supplementtion which was funded by EAS, which sells glutamine as a supplement. However, EAS had absolutely no say on the methodology of the study, the outcomes, or whether or not we published the results.

We did publish the results, which were a mix of positive and negative results. Should funding source be cause for increased skepticism? But it is not a valid reason to dismiss a paper. If a paper is to be dismissed, it should be dismissed on the grounds of its methodology. You have a vested financial interest in espousing low-carbohydrate diets given that you sell a book related to this. Does this mean that we should automatically dismiss anything you say based on this reason alone?

************* The science (not paid for by sugar producers – over 3,000 at last count) says fructose is dangerous because it has metabolic effects to which we are not adapted (and no other foodstuff seems to fall into that category). ************** Apparently you have not been reading what Alan has been writing, which is that the dose and context needs to be taken into consideration when discussing fructose. Methanol (wood alcohol) is toxic to the human body. However, it is present in all the fruits we eat.

Does this mean we should stop eating fruit? Of course not, because the amount of methanol is not high enough to have harmful effects.

It’s all about dose and context. February 12, 2010 Dear Ed, You said: “Alan, you’re definitely in the same class as Anthony Colpo. Collect x number of scientific studies and you can support any positon.

Same goes for any other person. What most people fail to realize is the complex nature of metabolism and that anyone that claims to have “the answer” is arrogant and unteachable. There is always the urge to develop a unified theory of any area when that goal is only possible by ignoring facts that interfere with that theory. Like Einstein once said, ‘everything should be made as simple as possiblebut not simpler.' ” Anthony Colpo really has nothing to do with this, but nice ad hominem. Anyways, you’re correct that its possible to cherry-pick the literature to support your position, and people do it all the time. If you take a look at Alan’s reference list, he included a few reviews and meta-analyses of the literature.

You understand what they are, right? And why I would bring them up, right? I also included one a few posts above this one in this comments section. You should read the reviews. The one I posted is the most recent. It is very illuminating.

While some people enjoy calling him “Alan Arogant [sic]” and others “don’t like the cut of his jib,” everybody knows that he, and James Krieger, realize “the complex nature of metabolism.” Because they understand “the complex nature of metabolism” they don’t claim to “have ‘the answer’.” Instead, like any intellectually honest and open-minded person would do, they look to the body of evidence for “the answer.” They examine the evidence and see in which direction its pointing. They aren’t afraid to say, “I don’t know.” Intellectually honest and intelligent people know that the most credible evidence is contained in the scientific literature (RCTs, reviews, and meta-analyses), more specifically in peer-reviewed journal articles. Intellectually dishonest people, however, begin their mission with a conclusion in hand, and then proceed to engage in rationalization, omission, and verbal gymnastics in an attempt to force reality to fit their conclusion. Those whom you claim to be “arrogant and unteachable” used to believe all kinds of nonsense. One day they learned how to analyze the literature, examine how one study fits into the bigger picture, and generally think for themselves. Once again Ed, I invite you to read the reviews and meta-analyses. Cheers, Michael Miller.

February 12, 2010 Ted — like, totally, bro. Ed — If you actually read the material more carefully, you’ll see that you & I are in agreement on the complexity of the matter, and that oversimplistic black/white statements can’t be made. JLB — Yes, David is blatantly ignoring the evidence. David — Review James’ response to you regarding funding. Also, you keep mentioning the multitude of non-vested studies refuting my position that the harm of fructose is context & dose-dependent, yet you’ve posted none of it.

Mike Miller posted a review in agreement with my position, I’ll re-link it for you to potentially ignore again, but you can’t dismiss it on the basis of sponsorship: I’ll also re-link another lit review that supports my stance, you can ignore this too if you want: Sam — I’m a paleovegan warrior. All — Thanks for the feedback.

February 12, 2010 As someone who has struggled with insulin resistance, pre-diabetes, obesity, hypertension, fatty liver diseasethere is no doubt in my mind that I was exposed to harmful levels of refined sugars and carbs, and that my tolerance for those substances is now extremely low. All of the above conditions are being successfully treated by low carb dieting: specifically removing sucrose, HFCS, honey, molasses, maple syrup, crystallized fructose, agave nectar, evaporated cane juice or any other refined sweetener from my diet. Some of you anti-alarmists in this thread would just label my problems as being a slothful gluttonthe typical fat, lazy American.

And you’d be wrong. A person who works with athletes and fitness freaks may not be alarmed by the effects of refined sugars. But a person who has actually suffered from those effects and who has lost family members to diabetes-related causesmight be considerably more alarmed. Likewise, a doctor/researcher who works with obese toddlers may also be quite alarmed. There’s your context. Fructose is becoming even more prevalent as “healthy” sweetener with products like Vitaminwater being sweetened by crystalline fructose and organic processed foods being sweetened by agave nectar (which can be much higher in%fructose than sucrose or HFCS).

I find that VERY alarming, and I’m thankful that Dr. Lustig is speaking out. February 12, 2010 DAVID GILLESPIE: I pointed out before you are setting up a straw may by claiming Alan says “eat unlimited sugar”.

He wrote no such thing but you continue spouting this nonsense. Alan: Watch your calories, watch your sugars, don’t eat too much of either, just be moderate, don’t be hysterical in eating or in avoidance. David: “AHA says dont drink 4 cans of pop a day (regardless if you ‘re a young athlete or an old bed-ridden man), Alan doesn’t give a hard and fast number, so Alan is a sugar industry sponsored satan/sugar worshipper” HEY DAVID – would it be possible for you to stick your fingers in your ears any harder than they are, or shout llalalalallalalallalal IM NOT LISTENING l;lalalallalallala would that be possible? February 12, 2010 ************ Some of you anti-alarmists in this thread would just label my problems as being a slothful gluttonthe typical fat, lazy American. And you’d be wrong. *************** Terry, you are constructing a strawman.

No one here would label your problems as from being a slothful glutton. The only point being made here is that, if someone is going to claim that fructose is extremely harmful, they need to consider the dose and the context. There’s nothing wrong with reducing sugars in your diet. No one here is saying you shouldn’t do that. But that doesn’t mean that people should be going around claiming that sugar is going to kill you and that it’s extremely harmful. Again it’s about dosage and context. ************** A person who works with athletes and fitness freaks may not be alarmed by the effects of refined sugars.

But a person who has actually suffered from those effects and who has lost family members to diabetes-related causesmight be considerably more alarmed. Likewise, a doctor/researcher who works with obese toddlers may also be quite alarmed. There’s your context. ****************** And your “context” has been taken out of context and is built around your strawman.

You talk as if the effects of refined sugars are the same, regardless of the dose. That’s exactly what Alan here is refuting. And is there individual variation in people’s response to sugars?

But that doesn’t mean that sugar is this evil thing that should be avoided at all times. February 12, 2010 Terry: I agree with you. I bet a lot of us here do. From one of my posts, re: should you eat more sugar >>if “we” is people with insulin resistance who’ve carefully experimented >>on their own diets and found they do well on high fat diets and badly >>on high carbohydrate, probably you shouldn’t. Everyone should be afraid OF THE THINGS THAT PERTAIN TO THEM. Scattershot hysteria or mass fear can mis-direct and waste badly needed resources. I wondered above about Dr.

Lustig’s contention about a pediatric obesity epidemic. I don’t believe it because of similar stuff that happened in the past.

February 12, 2010 @James Krieger – Strawman? Let’s look at the one you just built. You are incorrectly stating that my (and Dr. Lustig’s) position is “sugar is an evil thing that must be avoided at all times.” My argmuent is that obesity and diabetes is running rampant, and for the 10’s of millions of Americans who are suffering from impaired glucose metabolismsugar (and more specifically, fructose) is actually dangerous and should be heavily restricted in their diet. Just because fructose is safe for most people at low doses, doesn’t mean that it is safe for all people at the doses that many Americans are consuming it.

February 12, 2010 David, Thanks for your reply 🙂 Below is a chart from the AHA paper you linked to. Perhaps you needed to look a little closer at the recommendations and at least report them in their entirety – without omitting context. Notice how the added sugar allowance for active males is 18 tsp.

At 4g per tsp, that’s 72 grams. Since sugar is half fructose, this amounts to 36 grams of fructose.

Add a couple of fruit servings to this, and you end up with 50 grams, which is exactly what I listed in my article as an approximate upper safe limit for active adults. Let me be clear that I was referring to total dietary fructose per day, not just fructose from added sugar. And like I said in the article, the applicability of this limit is going to vary according to the individual. But if we were to pick a generalized upper safe limit of daily fructose intake based on the research evidence as a whole, it lands right around the neighborhood of 50 grams.

I also qualified this claim by stating that it’s not productive to get hung up on a particular number, because individual requirements vary. With that said, the 50g figure is well within the 50-100g limit listed in this meta-analysis:, and also well within the 60g limit listed in this other meta-analysis James linked.

February 12, 2010 @Matt and @J.C. James was trying to fight my strawman with a strawman of his own.

Sorry, if I didn’t point that out clearly enough. Yes, I think we can all agree that dosing and context is important. In fact, that’s the whole point. The doses of fructose in the American diet have gotten very high, and many people can’t handle it. I’m alarmed so I guess I’m an alarmist. I get alarmed when I see obese teenagers drinking sugary beverages. I get alarmed when I hear diabetic co-workers say they are using agave nectar, because it has a low glycemic index.

I get alarmed when my friend is drinking Vitaminwater, because he thinks it’s healthy due to containing natural “fruit sugar” instead of table sugar. I guess I just can’t understand why more people aren’t alarmed Oh well, I should know better than to argue nutrition with peopleit’s almost as pointless as arguing politics and religion.

February 12, 2010 @ Alan: “Good job, Dave man” = lmfao, priceless. @ Terry: What you’re doing is having a hissie fit over the type of sugars people are taking in. Guess what, if they had a goddamn clue about the big picture, they’d be just fine. Once people figure out that TOTAL CARBS matter most, the rest falls into place from there. And yes, I was formerly obese, but not anymore. What happened is I got educated, and I learned that reaching your goals in the long term has nothing to do with “this food = good, that food = bad”.

I know this stuff is difficult to grasp, but take your time, the lights will flip on eventually. February 12, 2010 Alan, You really do indulge me with your time and attention. I appreciate it. The AHA make it abundantly clear in the conclusion that they recommend a maximum of 144 calories of added sugar for men and 80 calories for women. Of course there are exceptions for individuals with particularly high calorie burns, but they say their recommendations are for “most American men [and women].” If by ‘context’ you mean your article is intended only to apply to individuals consuming 3,000 calories per day (and living an ‘active’ lifestyle as defined by the AHA [walking more than 3 miles per day on top of independent living]) then perhaps you should have said that. If that was indeed your intention, then I sincerely apologise for interfering. That aside, would you mind answering the question I posed at the end of my last comment: “Why is it that neither the AHA analysis, nor any of these studies made the cut when you were performing your objective review of the evidence on fructose ‘alarmism’, but almost every review ever performed on behalf of the sugar industry made the list?” Cheers David.

PS The article which James linked to (and you endorsed) was funded by the Coca-Cola Company (among others) and only serves to illustrate my point. February 12, 2010 @RayCinLA – “I know this stuff is difficult to grasp, but take your time, the lights will flip on eventually.” Wow, really Ray? Condescending much?

I’m glad you have everything figured out! Heck, if everyone were as smart as you there wouldn’t be a problem with obesity in America. Unfortunately, just last year I had my primary care physician and the nutritionist he sent me to both telling me to go on a low fat/high carb diet to control my cholesterol and triglycerides. Both of them knowing full well that my fasting blood glucose was high. There are so many people in the medical/diet/nutrition field that have NOT figured it out.

Maybe you could go flip their lights on for them? February 12, 2010 David, You need to read closer. That study was NOT funded by the Coca-Cola company. The research was supported by a scholarship, two fellowships, and a grant from the Canadian government. A TRAVEL grant was funded by the Coca-Cola company, which had nothing to do with the funding of the study itself. This travel funding was provided after the study had already been completed. It is repeatedly evident from your posts here that you do not thoroughly investigate things.

You also ignored my post about study funding, and how it’s not an adequate reason for dismissing a study. On top of that, if a potential financial conflict of interest is such a problem for you, then that would mean that everything you say is meaningless as you have a vested financial interest in low-carb diets since you sell a book on them. February 12, 2010 hey David Gillespie: THANK YOU SO MUCH for not answering many of the questions directed at you – shows a lot about you You again pretend that Alan recommends everyone consume a lot of fructose, as if the numbers for active people are be applied to everybody. This has been your pattern from the start – right after your first post I asked DG: because fructose (on its own) is not a normal part of our diet, we DG: don’t have to worry about substances that include it (such as DG: HFCS and Sugar) Where did you see that? I see stuff like AA: >>Is it really that groundbreaking to >>think that polishing off a half-dozen >>soft drinks per day is not a good >>idea? You continue the pattern throughout, up to and including this last post, DG: If by ‘context’ you mean your article is intended only to apply DG: to individuals consuming 3,000 calories per day (and living an DG: ‘active’ lifestyle your reading comprehension leaves much to be desired A small sedentary female’s context differs from an active young large male.

Do you know the meaning of the word context? If you do then apparently you forget what it means when it comes time to type On to the AHA paper: What’s your point? If anyone had written above “small sedentary women can eat a ton of fructose” then that paper might have some relevance but no one wrote that. Everyone wrote different people should consume different amounts I don’t know who you think you’re convincing, but anyone who can read can check up on your distortions all the way through Here’s my guess as to your next post: “you are an agent of the sugar industry.

I bet you’re funded by Coca Cola. You say we should all eat 600 grams of fructose per day. February 13, 2010 David, Please re-read James’ response to you. Not only are you incorrect about the study’s funding source, but your hasty dismissal based on funding source is negligent in the first place. You are working backwards. Instead of investigating the evidence and then drawing conclusions, you’re set on your beliefs, and are on a mission to select evidence that you think supports your personal dogma.

Regarding the set of papers you cited, I’ll address the RCTs. But before I even go there, do you realize that about half of the studies you cited are published by the ASN, which you discredited for having vested financial interests? Good grief, Dave. On with the RCTs. — Stanhope, et al: I’ll just re-quote my response to Lustig, “To illustrate the questionability of the dose, 25% of total daily calories coming from these drinks would be roughly 600 calories, which equates to 150 grams of either fructose or glucose. Achieving that total would require a daily intake of 7 cans of nondiet soda.

You mean to tell me that drinking 7 cans of nondiet softdrinks per day is a bad idea? Wow, thanks for the enlightenment. According to the text, the average intake of added sugars among Americans is 15.8%. This means that fructose intake is half of that, at 7.9% – about 3 times less than the 25% imposed in this study. Dosage & context, remember?” — James, et al: You mean to tell me that when children cut back their caloric intake (in this case from soft drinks), they lose weight? — Ebbeling, et al: See my comment above.

— Hallfrisch, et al. Let’s look at the design of this trial. Would you really put sedentary hyperinsulinemic subjects on a diet consisting of 15% protein, 43% carb, and 42% fat (60% of which was saturated FA), and 5 grams of fiber? I hope you’re beginning to see the lack of relevance here. Also, this study is 27 years old, so I find it funny that you’re having me look at it while you chose to ignore the recent systematic reviews & meta-analyses of RCTs presented in our discussion. For the 3rd time, this data has to first be put into context, and then factored into the entire body of evidence, which indeed has been wrung out in the following recent metas & reviews, which all happen to support my stance: I’ll leave you with a quote from the following recent review originally linked by Michael Miller: “There is at present not the single hint that HFCS may have more deleterious effect on body weight than other sources of sugar. Regarding the relationship between fructose or sucrose intake and cardiovascular risk factors or type 2 diabetes, the evidence is even sparser.

Given the number of confounding variables, there is clearly a need for intervention studies in which the fructose intake of high fructose consumers is reduced to better delineate the possible pathogenic role of fructose. At present, short-term intervention studies however suggest that a high-fructose intake consisting of soft drinks, sweetened juices, or bakery products can increase the risk of metabolic and cardiovascular diseases. There is, however, no objective ground to support that moderate intake of fructose, or of fructose consumed with fruits or honey, is unsafe. February 13, 2010 So, I had decided that I wasn’t going to post another comment because everything that needed to be said was said already. But then, and I had to show everyone here. REMOVE FRUCTOSE entirely from your diet, it is a sort of poison on terms of irritating the endocrine system. It triggers fat storage hormone ESTROGEN.

Detoxifying from fructose is compulsory for normal health. This means STRICTLY removing soft drinks HFCS (fructose) laced, STRICTLY all fruits, STRICTLY fruit juices and alcohol (fructose) from diet. The very usual reaction to removing fructose from the body is to lose several kg (15kg?) of weight without exercise. Your food cravings will vanish entirely too.

Try also to remove milk products from your diet (casein triggers estrogen). Remove gluten (it triggers estrogen). Omega 6 fats can cause allergic reaction (triggering estrogen) – can offset it with omega 3 intake. Some veggies have chemicals sprayed on them during growing. Washing them is not enough to avoid allergic reaction. Try to cook it instead of eating raw. The out of normal reactions are usually caused by allergens in food.

And many health problems including obesity, stubborn fat, depression are fully traced to Estrogen elevated presence in the body. Passion flower, chamomile, damiana, garlic can lower estrogen. Drink lots of water, soda water is OK it doesn?t cause allergy. Drink green tea for it burns calories and can help you lose weight. Green tea will work for you very well after estrogen is vastly lowered. After removing products irritating hormonal system there will be a much fewer products to chose from as the food to eat.

Try to see it positive – this was price to pay for getting healed. There is nothing bad in following some narrow path if that is the only way of staying healthy. February 14, 2010 Alan, I see that you have grasped my point.

Just like Lustig, the AHA has indeed reviewed all the evidence (not just the evidence paid for by the sugar industry). The conclusion they reached was also similar to that reached by Lustig: fructose is dangerous and Americans need to drastically reduce their intake.

The conclusion is not alarmist. It is prudent. You on the other hand appear to have reviewed only the evidence produced by the sugar industry. In that ‘context’ you have arrived at a recommendation which is approximately three times higher than the AHA recommendation for most American men and five times higher than for women. I see little point discussing the matter further, so this will be my last comment on this thread. I do however wish to extend my sincere thanks for the courtesy you have shown in constantly responding to my comments. It was very much appreciated.

Cheers David. February 14, 2010 I guess this is mostly in response to Ryan Zielonka – but also anyone else re: the Japanese Diet Living in Japan 7 years out of the last 10 – in Kyushu/Fukuoka – I’m going to have to disagree a bit with some earlier assertions.

While yes, I do agree it’s incorrect to state that the Japanese diet has no added fructose – that’s clearly incorrect – it seems to me, and lots of folks I’ve lived with and around – that the Japanese diet consumes far less processed carbs and sugar than the Western diet. Shoot, one of the first things I, my wife and others things often commented when we first got here with the ubiquitous pastry shops is how much lighter and less sweet their wares are compared to the west. Folks I’ve shared “American” chocolate with, for example, often complain to me that it is too sweet for the “Japanese” taste. The staples of the Japanese diet are still, in my experiences, seafood, miso, sea vegetables, fermented vegetables and massive, massive amounts of rice. But they do eat fruit.

Man, when it’s mikan season, it seems like that’s all they eat. [I kid.] But they tend to eat seasonally. Not constantly.

People are far less likely to spend the day sucking down HFCS colas – in fact the first few times I popped open soda cans at my desk people thought I’d brought beer to work, so uncommon is the regular drinking of cokes and whatnot but they do drink down bottle after bottle and thermos after thermos of green tea [and cup after cup of black coffee.] By that alone, I can’t see how there’s any way Japan consumes more HFCS [percentage wise] than the US, giving the sheer amount of liquid sugar via soda the US puts away. Tabehodai’s and nomihodai’s are, for most folks, not regular affairs. As opposed to the weekly or bi-weekly Golden Corral all-you-can-eat [plus all the sweet tea you can drink] buffets of my American youth. February 14, 2010 David, I felt it was important to respond to each of your contentions because you’re exactly the type that can effectively spread misinformation. You’re articulate & well-mannered.

However, you’re also unobjective. And that’s the problem. For example, you’ve been shown various studies pooling together the body of controlled reasearch and arriving at a safe dose of fructose that’s in line with what I mentioned in my article. In response, you called foul due to funding source. I & others explained the folly of that, and you ignored us. You’re probably still in denial that you’re wrong about the funding source of the study James linked indicating a 60g threshold, and I bet you’re also going to ignore the review posted by Michael Miller, as well as the rest of the evidence. Also, you have to realize that the AHA’s paper is just one of several scientific reviews on this topic.

Therefore, it in and of itself is not the Gospel. Like any other review, it’s needs to be factored into the body of research as a whole. But even looking at the AHA’s recommendations in isolation, they STILL don’t support your stance. Pay attention and take notes The AHA’s added sugar recommendations are based on the assumption that added sugars will comprise half of your ‘discretionary kcals’, which are miscellaneous, flexible kcals that can technically can come from ANY proportion of added sugar, solid fat, or alcohol [ Note: the idea of discretionary kcals boggles the mind of absolutists who have no grasp of dietary flexibility]. 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. Here’s the kicker: if we were to look at the entirety of the research, that 50g limit is actually towards the lower end. Feel free to re-read the above, as well as everyone’s responses to your comments. Despite your articulate delivery, you have tenaciously ignored the facts.