Michael Pollan says, 'don't listen to scientists'

[jt512]

I see it wasn't obvious that I didn't find your "evidence-based medicine (EBM), as opposed to science-based medicine (SBM)" relevant to my position. Allow me to point that out now.

Well, I think you missed my point, but I'm not going to argue further with you about it.

[Y]our imagination that I was somehow not looking at valid medical research was an incorrect assumption.

I'm afraid that that's your imagination. I never said nor thought that you weren't looking at valid medical research (although I can see from my server logs that you haven't bothered to look at the research I provided a link to in my last post).

There are a dozen or so studies that have found no difference in their outcome measures comparing HFCS and sucrose.

Ok.

There are studies that have looked at fructose vs sucrose.

Studies of fructose vs sucrose aren't relevant to the health effects of HFCS, because HFCS is approximately half fructose and half glucose, nearly the same proportions as sucrose. And HFCS has substituted for sucrose in the American diet, just as sucrose will substitute for HFCS if HFCS use declines. Therefore, the only relevant comparison for the health effects of HFCS are comparisons between HFCS and sucrose.

There are some that have looked at short term calorie intake of HFCS vs sucrose.

And their results are?

What one needs to consider when evaluating these studies are the particulars:

• the time frame
• what specifically was compared
• the sample groups and the sample size

But the most important thing to look at is the

• outcome measure

OK, and how do the studies of HFCS vs sucrose do when evaluated on those parameters—specifically?

Not every study supports the conclusions the researchers claim the results support.

That nice. Now, how do the studies comparing HFCS with sucrose do on that criterion—specifically?

Maybe the problem is in the motivation to market HFCS, maybe the actual substance is not the issue.

If in your opinion there is a problem with that, that in no way implies that there is an adverse health effect with HFCS, and in no way justifies wasting time and money chasing after biologically implausible hypotheses.

The evidence we do have that is undeniable is the rate of HFCS consumption has gone up. The rate of sucrose has gone down as HFCS replaces it. And the rates of obesity have gone up.

You seem to have zero appreciation for how little evidence of causation that implies. First of all, it's mere correlation; but worse, it's an ecologic correlation (ie, a correlation between two summary statistics), and therefore doesn't even imply that the people who are consuming more HFCS are the ones getting fatter. Intake of flour and added fats went up during the same period. Why aren't you demonizing them?

If HFCS was merely added to sucrose consumption, you would easily see more calories consumed and more weight gained. But that is not what we see.

But total caloric intake did go up during that same period.

We see HFCS replacing sucrose and obesity increasing.

Along with total caloric intake.

Until the mechanism underlying the change in obesity increase is clearly understood, I am not willing to rule out HFCS despite the early research that has failed to detect the problem.*

Your posts suggest that your intransigence is influenced by at least five reasons, none of which is valid: (1) you have drastically overrated the evidential value of the parallel trends in HFCS consumption and the prevalence of obesity in the US, a mere ecologic correlation; (2) you underrate the importance of the lack of a plausible biological mechanism; that is, how two substances so close in composition could have significantly different biological effects; (3) you are apparently unaware of evidence that total caloric intake increased during the same period that obesity increased; (4) you have unjustifiably dismissed an entire body of research showing no physiological differences between HFCS and sucrose as "early research"; and (5) you dislike some aspect of the economics or politics underlying the increased use of HFCS in commercial foods.

*ETA: After submitting my response, it occurred to me that by making this statement you have admitted that no amount of evidence showing a lack of adverse effect of HFCS consumption on obesity could persuade you that HFCS is not the cause of the US obesity epidemic. You seem to have just admitted to being a high-fructose corn syrup crank.

ETA2: In another thread, you made this comment about someone's wife who is anti-vaccination:

Start by exploring why your wife distrusts valid scientific evidence and believes in the fear mongering. You need to find out what the barrier is to her accepting evidence before you can provide her with the evidence.

Ironically, I can't help but wonder why you distrust valid scientific evidence about the equivalency of HFCS and sucrose and why you believe in the fear mongering. You should ask yourself what the barrier is to your accepting evidence.

Jay

 

[Skeptic Ginger]

...
I'm afraid that that's your imagination. I never said nor thought that you weren't looking at valid medical research (although I can see from my server logs that you haven't bothered to look at the research I provided a link to in my last post).

That's because I know the difference between scientific evidence and 'evidence' without wasting my time on your false assumptions.

...And their results are?

In the rat study there was a difference at 12 hours and no difference at 24 hours. Since I didn't look for or see obesity studies that compared people sucking on sodas 24 hours a day vs those sucking on them 12 hours a day, I consider the rat study results inconclusive as it applies to the effect of HFCS on human appetite and satiation. Which, BTW, also applies to drawing conclusions about humans from all animal studies.

...OK, and how do the studies of HFCS vs sucrose do when evaluated on those parameters—specifically?

That nice. Now, how do the studies comparing HFCS with sucrose do on that criterion—specifically?

I answered this already. The studies use different outcome measures and it is not certain one can draw conclusions about the overall effect on obesity from the consumption of HFCS vs sucrose.

In order to rule out the effect not being picked up in these studies we need a long term randomized study with a large sample size comparing the effect of HFCS on appetite and satiation. Are you aware of any such study?

...If in your opinion there is a problem with that, that in no way implies that there is an adverse health effect with HFCS, and in no way justifies wasting time and money chasing after biologically implausible hypotheses.

If you have evidence that clearly demonstrates that the increase in obesity in this country which coincidentally correlates with an increase in the substitution of HFCS for sucrose, not the addition of HFCS to an already large consumption of sucrose, has a different clear cause, that would be a reason to quit looking at HFCS.

But we do have the obesity problem, it has gotten worse as HFCS replaced sucrose, and we don't have evidence of a clear cause that is unrelated to the substitution of HFCS for sucrose. So dismissing the hypothesis that HFCS has something to do with the increased obesity would be unwise.

...You seem to have zero appreciation for how little evidence of causation that implies. First of all, it's mere correlation; but worse, it's an ecologic correlation (ie, a correlation between two summary statistics), and therefore doesn't even imply that the people who are consuming more HFCS are the ones getting fatter. Intake of flour and added fats went up during the same period. Why aren't you demonizing them?

You continue to falsely assume I have concluded the HFCS is the cause when all I've said is I don't see enough evidence to rule it out.

...But total caloric intake did go up during that same period.
Along with total caloric intake.

Does the concept of an effect on appetite and satiation just whoosh by you?

...Your posts suggest that your intransigence is influenced by at least five reasons, none of which is valid: (1) you have drastically overrated the evidential value of the parallel trends in HFCS consumption and the prevalence of obesity in the US, a mere ecologic correlation;

Wrong, I have not drawn the conclusions you falsely assume. I recognize all there is is correlation. And yet when I say that over and over, your confirmation bias that I am wrong leads you to read that I am concluding there is evidence of causation.

...(2) you underrate the importance of the lack of a plausible biological mechanism; that is, how two substances so close in composition could have significantly different biological effects;

You are apparently unaware of the complexity of appetite and satiation, and of the other ingredients in HFCS which have been hypothesized to be having an effect on appetite. I posted a link covering this plausible biological mechanism.

...(3) you are apparently unaware of evidence that total caloric intake increased during the same period that obesity increased;

Again, you think I'm saying that HFCS has an effect on fat when I'm suggesting it could be having an effect on appetite. Total calorie intake would of course go up and result in an increase in obesity. To claim I am not aware of the increase in consumption is more confirmation bias on your part. You are building a straw man to argue against.

...(4) you have unjustifiably dismissed an entire body of research showing no physiological differences between HFCS and sucrose as "early research";

Your definition of "entire body of research" is a dozen small studies, with several only done on rats. That is not my definition of an "entire body of research".

... and (5) you dislike some aspect of the economics or politics underlying the increased use of HFCS in commercial foods.

Yes. I have overwhelming evidence that various industries invest millions in propaganda science and it is not hard to find scientists who gladly accept that funding.

You might find "Merchants of Doubt" and interesting book if you have the time. I assure you it is not some left wing anti-corporate piece of junk. It's an extremely well researched and well written history of the last couple decades of science and politics.

The U.S. scientific community has long led the world in research on public health, environmental science, and other issues affecting the quality of life. Our scientists have produced landmark studies on the dangers of DDT, tobacco smoke, acid rain, and global warming. But at the same time, a small yet potent subset of this community leads the world in vehement denial of these dangers.

In their new book, Merchants of Doubt, historians Naomi Oreskes and Erik Conway explain how a loose–knit group of high-level scientists, with extensive political connections, ran effective campaigns to mislead the public and deny well-established scientific knowledge over four decades. In seven compelling chapters addressing tobacco, acid rain, the ozone hole, global warming, and DDT, Oreskes and Conway roll back the rug on this dark corner of the American scientific community, showing how the ideology of free market fundamentalism, aided by a too-compliant media, has skewed public understanding of some of the most pressing issues of our era.

...*ETA: After submitting my response, it occurred to me that by making this statement you have admitted that no amount of evidence showing a lack of adverse effect of HFCS consumption on obesity could persuade you that HFCS is not the cause of the US obesity epidemic. You seem to have just admitted to being a high-fructose corn syrup crank.

Your confirmation bias falsely viewing my position occurs to me.

...ETA2: In another thread, you made this comment about someone's wife who is anti-vaccination:

Ironically, I can't help but wonder why you distrust valid scientific evidence about the equivalency of HFCS and sucrose and why you believe in the fear mongering. You should ask yourself what the barrier is to your accepting evidence.

Jay

It's interesting to me that because I don't see sufficient evidence to rule out the effects of HFCS on appetite and/or satiation people who short sightedly look at an oversimplified view of obesity attack my position. It reminds me of one of the weight threads where some group of forum members judgmentally blame all obesity on will power failure. Genetics and the issues surrounding appetite are dismissed despite overwhelming evidence these things play a big part in the obesity problem. I get the feeling you fall into the "it all about will power" group.

 

[quadraginta]

<snip>

If you have evidence that clearly demonstrates that the increase in obesity in this country which coincidentally correlates with an increase in the substitution of HFCS for sucrose, not the addition of HFCS to an already large consumption of sucrose, has a different clear cause, that would be a reason to quit looking at HFCS.

Take a look at this table (.xls)

"Table 50—U.S. per capita caloric sweeteners estimated deliveries for domestic food and beverage use, by calendar year.", from the USDA.

It does a breakdown of the various sweeteners (refined sugar, HFCS, glucose syrup, honey, etc.) used in U.S. food products from 1966 through 2010. You can see some evidence of the substitution effect you are speaking of in the mid and late seventies, but it is interesting to note that starting in the early eighties the per capita consumption of refined sugar has remained relatively stable.

Meanwhile the overall consumption of caloric sugars per capita increased 34% from 1966 to 1999, and only started to go down in the last ten years or so.

This would seem to support the idea of "additional" consumption of caloric sugars that you are seeking.

In other words there is no real need to search for a mysterious, arcane effect from HFCS. Americans have been eating more sugar. (And likely getting less exercise.)

But we do have the obesity problem, it has gotten worse as HFCS replaced sucrose, and we don't have evidence of a clear cause that is unrelated to the substitution of HFCS for sucrose. So dismissing the hypothesis that HFCS has something to do with the increased obesity would be unwise.

<snip>

The cost of HFCS as compared to refined sugar has been held artificially low in the U.S. since the late seventies, a result of the combined effects of import tariffs and quotas which have made the price of refined sugar in the U.S. twice that of the world market, and government subsidizing of corn production. This has created a marketplace which encouraged the use of HFCS instead of refined sugar in this country, and it has also made the cost of adding caloric sweeteners to a food ridiculously cheap here.

After that market demand took over. Americans like sweet stuff, and they were sold what they wanted.

Tastes are changing, and credit is due to an effort to make the public aware of the dangers of caloric sweeteners. The per capita consumption overall has dropped dramatically since the 1999 high (although still 17% above 1966 levels).

This is a good thing, but letting food alarmists demonize HFCS when the real problem is sugar in general is misguided. When I look at the products on the supermarket shelves that are trying to attract custom by advertising their absence of HFCS they still have sugar in them, and they still have about the same amount of sugar.

Do you think it's a good idea to persuade the public that one kind of sugar is okay and another isn't when there is no clear evidence that it makes any difference at all?

Let's look at another similar scenario. It was the same groups (in many cases the same individuals) of food alarmists who were going on about the dangers of saturated fats back in the eighties, and advocated the substitution of trans-fats. How did that work out?

 

[Almo]

I read The Omnivore's Dilemma, and I found it an excellent book. I didn't find it preachy, or starry-eyed about "natural" foods. Honestly, having read the book and hearing him make these remarks makes me wonder if they are the same person.

I don't think his beef is with the science as much as it is with how marketers and popular media use science to basically trick people into eating crap and thinking it's good for them.

This would make more sense to me, meg. Though that's only on the basis of having read one of his books.

 

[quadraginta]

@Skeptic Ginger.

You had asked for evidence that demonstrated an overall increase in sugar (caloric sweetener) consumption in the U.S. as opposed to a simple substitution of HFCS for refined sugar and relatively stable levels of total consumption.

I am curious if you had any thoughts on the data I linked to in my last post.

 

[Skeptic Ginger]

I got this far with a reply:

DRAFT:

Take a look at this table (.xls)

"Table 50—U.S. per capita caloric sweeteners estimated deliveries for domestic food and beverage use, by calendar year.", from the USDA.

It does a breakdown of the various sweeteners (refined sugar, HFCS, glucose syrup, honey, etc.) used in U.S. food products from 1966 through 2010. You can see some evidence of the substitution effect you are speaking of in the mid and late seventies, but it is interesting to note that starting in the early eighties the per capita consumption of refined sugar has remained relatively stable.

Meanwhile the overall consumption of caloric sugars per capita increased 34% from 1966 to 1999, and only started to go down in the last ten years or so.

This would seem to support the idea of "additional" consumption of caloric sugars that you are seeking.

In other words there is no real need to search for a mysterious, arcane effect from HFCS. Americans have been eating more sugar. (And likely getting less exercise.)

If you look at your table you will see a direct correlation between increasing caloric consumption and increasing HFCS consumption. And in 2003-4 or so as HFCS consumption goes down, so does total caloric consumption.

You have what I call tunnel vision when assessing a patient's symptoms. You've taken the thing that makes the most sense to you based on the evidence, but now you are only looking to confirm that thing rather than taking a systematic approach which continues to consider the differential list.

There are alternative explanations for the obesity correlation. Appetite is a very complex drive. The satiation feedback loop is no simple thing. People typically to have set weights their appetite/satiation tends to maintain. For some people a genetic cause for obesity is clear. Marketing influences what we consume. Habits, behaviors such as eating in front of the TV, social influences, boredom and the like affect our caloric consumption. The fact people gain back more weight than they lose when trying to crash diet is a consistently found occurrence suggesting there is a biologic reason behind it.


The bottom line is you are ruling out the effect of HFCS on appetite and satiation before the data is in. It's fine to have a diagnosis at the top of your differential list. But it is poor practice to stop considering the list until the diagnosis is certain. The data does not yet rule out an affect on appetite regardless there is some preliminary data supporting that conclusion. The results in the rat study cannot be explained. Other ingredients in HFCS have been shown to affect appetite.

The cost of HFCS as compared to refined sugar has been held artificially low in the U.S. since the late seventies, a result of the combined effects of import tariffs and quotas which have made the price of refined sugar in the U.S. twice that of the world market, and government subsidizing of corn production. This has created a marketplace which encouraged the use of HFCS instead of refined sugar in this country, and it has also made the cost of adding caloric sweeteners to a food ridiculously cheap here.

After that market demand took over. Americans like sweet stuff, and they were sold what they wanted.

Tastes are changing, and credit is due to an effort to make the public aware of the dangers of caloric sweeteners. The per capita consumption overall has dropped dramatically since the 1999 high (although still 17% above 1966 levels).

This is a good thing, but letting food alarmists demonize HFCS when the real problem is sugar in general is misguided. When I look at the products on the supermarket shelves that are trying to attract custom by advertising their absence of HFCS they still have sugar in them, and they still have about the same amount of sugar.

Do you think it's a good idea to persuade the public that one kind of sugar is okay and another isn't when there is no clear evidence that it makes any difference at all?

Let's look at another similar scenario. It was the same groups (in many cases the same individuals) of food alarmists who were going on about the dangers of saturated fats back in the eighties, and advocated the substitution of trans-fats. How did that work out?

Contributing to public alarm is a different argument. That's not how I approach risk when it comes to HFCS. I have no need personally to consume HFCS. I prefer to consume less sugar and I'm annoyed the marketers of HFCS have sold food manufacturers on adding it to just about everything. I don't want sugar of any kind in my spaghetti sauce. But I especially don't want enough sugar in it so that it tastes sweet.

I'm sure making products taste sweet is just as much a marketing trick as super-sizing is. Both have a negative impact on the public's health by encouraging obesity. Being a less expensive ingredient is one thing, but adding sweeteners to products that don't need to be sweet is another.

As for the trans fat, saturated fat remains as a contributor to cardiovascular disease. According to the American Heart Association's timeline trans fats were being added to cooking lard beginning in 1911. It's a misconception that trans fat was introduced to replace saturated fat. A more accurate account is that saturated fat was implicated in cardiovascular disease first, (in the late 50s), and trans fat wasn't implicated until the 90s.​

​

Then I got annoyed because I already decided I was not going to waste time on this discussion and here I was investing all this time when I'm comfortable with my current conclusion and don't care about yours.

This time of year I work overtime for 2 months and then it's the Christmas season with a few more things on the time consuming agenda. I have 3-4 other discussions in the politics and religion forums that I also owe replies to backed up before this one. People think I cop out because I don't have an argument, but in reality I don't always feel like the investment in time it takes to properly support a position. Especially when the discussion is like this one with you ignoring everything I have said about appetite stimulation and replying repeatedly with the calorie is a calorie argument. OR, you ignore what I've said about small studies, pilot studies and inconsistent outcome measures and insist that there is enough data to draw a conclusion when I'm convinced there is not.


So that's where I'm at with this. Sorry. This thread is 5th in the queue. It's nothing personal.

 

[jt512]

I got this far with a reply:

DRAFT:

Take a look at this table (.xls)

"Table 50—U.S. per capita caloric sweeteners estimated deliveries for domestic food and beverage use, by calendar year.", from the USDA.

If you look at your table you will see a direct correlation between increasing caloric consumption and increasing HFCS consumption. And in 2003-4 or so as HFCS consumption goes down, so does total caloric consumption.​

Actually, if you look at his table, you'll see no correlation at all between total caloric consumption and HFCS consumption, because the table does not include total caloric consumption. This leads me to believe you didn't actually look at his table, just as you didn't look at the table I presented that showed no difference between HFCS and sucrose consumption on appetite and satiety across six studies.

On the other hand, if you look at this table (.xls), you will see a correlation between HFCS consumption and total caloric intake. If you do the calculation, you'll see that that correlation is 0.91. On the other hand, the correlation between chicken and total caloric intake is 0.98. If you think these correlations are meaningful (they're not), then you should be more concerned about the apparent appetite-stimulating effect of chicken than you are of HFCS.

The bottom line is you are ruling out the effect of HFCS on appetite and satiation before the data is in.

And you continuously fail to evaluate experimental evidence in light of scientific plausibility. The substances in HFCS whose appetite-stimulating effects you're so concerned about amount to just 3–5% of HFCS, and are ordinary di- and oligosaccharides of glucose, which your own body produces during the digestion of starch. After eating a slice of toast, you'll find these same substances in your gut—at least briefly, as they are readily are broken down to glucose.

Jay​

 

[Skeptic Ginger]

Actually, if you look at his table, you'll see no correlation at all between total caloric consumption and HFCS consumption, because the table does not include total caloric consumption. This leads me to believe you didn't actually look at his table, just as you didn't look at the table I presented that showed no difference between HFCS and sucrose consumption on appetite and satiety across six studies.

Oh for pity's sake. I'm talking about the right hand column.

Total caloric sweeteners in pounds

Fine, one eats more concentrated carb calories, not total calories.

If you look at this graph you see the obesity rise leveling off as the HFCS consumption levels off and decreases.

Are there many possible variables? Of course. I'm not failing to evaluate anything. I have said repeatedly, I'm unconvinced we have enough data. If you are satisfied we have enough, that's your prerogative.

And I have said I don't have time to properly post the relevant literature on this topic. Claiming that is the same as not reviewing the literature is one of the problems I see in this forum from time to time. Not everyone has time to post a dissertation on complex subjects. Have either you or Quad taken the time to look at anything in the field of appetite stimulation and suppression? Or are you so convinced you are right you need not bother? At least I've consistently said the data is not in, not that it is in and conclusive. But you both are treating people who don't agree with you as not properly considering the data. I have a particular interest in the insulin appetite feedback loop and have read quite a bit about it over the years. That doesn't mean I have the time to share this with everyone else in a corn sugar discussion. I think it it premature to rule anything out in the obesity problem just as it would be premature to claim we know all there is to know about cancer.

 

[quadraginta]

<snip>

If you have evidence that clearly demonstrates that the increase in obesity in this country which coincidentally correlates with an increase in the substitution of HFCS for sucrose, not the addition of HFCS to an already large consumption of sucrose, has a different clear cause, that would be a reason to quit looking at HFCS.

But we do have the obesity problem, it has gotten worse as HFCS replaced sucrose, and we don't have evidence of a clear cause that is unrelated to the substitution of HFCS for sucrose. So dismissing the hypothesis that HFCS has something to do with the increased obesity would be unwise.
<snip>

I got this far with a reply:

DRAFT:If you look at your table you will see a direct correlation between increasing caloric consumption and increasing HFCS consumption. And in 2003-4 or so as HFCS consumption goes down, so does total caloric consumption.

You have what I call tunnel vision when assessing a patient's symptoms. You've taken the thing that makes the most sense to you based on the evidence, but now you are only looking to confirm that thing rather than taking a systematic approach which continues to consider the differential list.

There are alternative explanations for the obesity correlation. Appetite is a very complex drive. The satiation feedback loop is no simple thing. People typically to have set weights their appetite/satiation tends to maintain. For some people a genetic cause for obesity is clear. Marketing influences what we consume. Habits, behaviors such as eating in front of the TV, social influences, boredom and the like affect our caloric consumption. The fact people gain back more weight than they lose when trying to crash diet is a consistently found occurrence suggesting there is a biologic reason behind it.


The bottom line is you are ruling out the effect of HFCS on appetite and satiation before the data is in. It's fine to have a diagnosis at the top of your differential list. But it is poor practice to stop considering the list until the diagnosis is certain. The data does not yet rule out an affect on appetite regardless there is some preliminary data supporting that conclusion. The results in the rat study cannot be explained. Other ingredients in HFCS have been shown to affect appetite.


Contributing to public alarm is a different argument. That's not how I approach risk when it comes to HFCS. I have no need personally to consume HFCS. I prefer to consume less sugar and I'm annoyed the marketers of HFCS have sold food manufacturers on adding it to just about everything. I don't want sugar of any kind in my spaghetti sauce. But I especially don't want enough sugar in it so that it tastes sweet.

I'm sure making products taste sweet is just as much a marketing trick as super-sizing is. Both have a negative impact on the public's health by encouraging obesity. Being a less expensive ingredient is one thing, but adding sweeteners to products that don't need to be sweet is another.

As for the trans fat, saturated fat remains as a contributor to cardiovascular disease. According to the American Heart Association's timeline trans fats were being added to cooking lard beginning in 1911. It's a misconception that trans fat was introduced to replace saturated fat. A more accurate account is that saturated fat was implicated in cardiovascular disease first, (in the late 50s), and trans fat wasn't implicated until the 90s.​

Then I got annoyed because I already decided I was not going to waste time on this discussion and here I was investing all this time when I'm comfortable with my current conclusion and don't care about yours.

This time of year I work overtime for 2 months and then it's the Christmas season with a few more things on the time consuming agenda. I have 3-4 other discussions in the politics and religion forums that I also owe replies to backed up before this one. People think I cop out because I don't have an argument, but in reality I don't always feel like the investment in time it takes to properly support a position. Especially when the discussion is like this one with you ignoring everything I have said about appetite stimulation and replying repeatedly with the calorie is a calorie argument. OR, you ignore what I've said about small studies, pilot studies and inconsistent outcome measures and insist that there is enough data to draw a conclusion when I'm convinced there is not.


So that's where I'm at with this. Sorry. This thread is 5th in the queue. It's nothing personal.

SG, you seem to be mistaking me for someone who is arguing with you, although the tenor of your response is more that of someone who feels that their authority is being questioned.

I'm not even disagreeing with you all that much. (Yet. )

You indicated that you believed the substitution of HFCS for other caloric sweeteners was a potential cause of obesity, and solicited sources of data which showed an overall increase in the total consumption of caloric sweeteners.

That's what I found for you.

You're welcome.

-------------------------------

As far as food alarmism is concerned, you managed to miss the point entirely.

Of course partially hydrogenated oils with trans-fats have been around for a while. Anyone who has pursued even a passing familiarity with the subject knows about Crisco, at the very least.

People who dig a little deeper know that concerns about coronary health issues exacerbated by trans-fat were being raised as far back as the mid-fifties.

Look at the timeline you linked to, though.

1984

Consumer advocacy groups campaign against using saturated fat for frying in fast-food restaurants.

In response, most fast-food companies begin using partially hydrogenated oils containing trans fat instead of beef tallow and tropical oils high in saturated fats.​

Consumer advocacy groups such as the Center for Science in the Public Interest, a behemoth with a $17 million/yr budget funded mostly by newsletter sales. A lot of newsletter sales.

With articles such as this one, from the CSPI's Mar., 1988, Nutrition Action Healthletter.,

The truth about trans: hydrogenated oils aren't guilty as charged - trans fats

which helped push the fast food industry into using partially hydrogenated vegetable oils exclusively, and even suggested that trans-fats might be good for you.

A decade or so latter the CSPI was hustling even more subscriptions telling everyone trans-fats are killers.

They got it right the second time around. So what? Like a broken clock, they can be right every once in a while, but being right isn't how they make their money. Selling subscriptions is.

This time around they're making a bundle off of HFCS panic, while the manufacturers are predictably marketing "HFCS FREE!!" products in response to public perception ... with a little extra profit margin for their trouble.

Meanwhile, the sweetener shell game still doesn't have anything under any of the cups. Or perhaps more properly there is something under all of them. Calories.

When I look at the labels on the "HFCS FREE!!" products they are not free of caloric sweeteners. Unsurprisingly, they have roughly the same amount.

I wonder how things would have worked out if the industry, instead of naming HFCS "high fructose", which made perfect sense to a food scientist, since it logically distinguished it from the all-glucose corn syrup everyone was already using, had chosen to name the HFCS42 that is used in prepared foods a "high glucose sweetener"?

After all, compared to regular table sugar, it is.

Would we be worrying about the dangers of glucose in our diet, instead?

I bet we would if outfits like the CSPI thought they could up their subscription base with a campaign on the "potential" dangers of "high glucose sweetener".

They have already demonstrated that they aren't particularly wedded to the science behind their campaigns.
​

 

[jt512]

If you look at this graph you see the obesity rise leveling off as the HFCS consumption levels off and decreases.


[qimg]http://i.imgur.com/OvEc8.png[/qimg]

Or so that figure seems to imply. But let's look at what has actually occurred since 1999 ¹ (click on chart to enlarge):

[imgw=600]http://jt512.dyndns.org/images/obesity-hfcs-chicken-lg.png[/imgw]

Indeed, HFCS intake has been in decline since 1999. However, the prevalence of obesity continued to steadily increase for the next seven years. If HFCS were responsible for the obesity epidemic, then by your own argument obesity should have declined during this period. But it did not.

In contrast, look at the remarkable correlation between obesity and intake of chicken! It's almost perfect—literally—its correlation with obesity is 0.99 (compared with only 0.87 for HFCS). Clearly, then, it's not HFCS that's responsible for the obesity epidemic; it's chicken! Who knew?

Of course neither of these conclusions are valid. As I've been trying to convince you, not only does an ecologic correlation not imply causation at the individual level; it doesn't even suggest causation. Obesity correlates directly and casually with total caloric intake. Apparently, chicken is just a good indicator of caloric intake at the population level. And the statistical association between HFCS and obesity is, similarly, meaningless.

As one reviewer recently summed it up:

"A unique linkage between high-fructose corn syrup and obesity postulated by Bray and colleagues in 2004 based on epidemiologic data has now been widely discounted by the scientific community based on prospective data. Major professional groups such as the American Medical Association and the American Dietetic Association have issued statements refuting a unique linkage between high-fructose corn syrup and obesity. An unfortunate aftermath of this saga is that, while the debate on this issue is over in the scientific community, serious misperceptions persist in the public domain and nonrefereed vehicles such as the Internet." ²​

Jay


¹[size=-2] Food intake data taken from http://www.ers.usda.gov/Data/FoodConsumption/spreadsheets/foodloss/Calories.xls (.xls). Source: USDA. Obesity data taken from Table 2 of http://www.cdc.gov/NCHS/data/hestat/obesity_adult_07_08/obesity_adult_07_08.pdf (.pdf) Source: CDC. Obesity was interpolated between observed data by using natural cubic splines. Correlation calculations included both the observed and interpolated points. "Hotlink" is to my own website.[/size]

²[size=-2] Rippe JM. The Health Implications of Sucrose, High-Fructose Corn Syrup, and Fructose: What Do We Really Know? J Diabetes Sci Technol. 2010 July; 4(4): 1008–1011. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2909536/[/size]

 

[Skeptic Ginger]

I said, my reply was a draft I did not finish because I did not have a horse in this race. Now you've both gone off ignoring the fact this thread is not and never was a revisitation of the HFCS debate. That is a debate I don't have the time or desire to invest in today. I posted in the thread because I've read Pollen's "Omnivore's Dilemma" book.

All I ask is that you both knock off the straw man crap. I HAVE MADE NO CLAIMS THAT THE DATA WAS IN AND HFCS IS BAD. I HAVE SAID REPEATEDLY, IMO, THE RESEARCH RESULTS ARE INCONCLUSIVE AS TO THE ROLE IF ANY THE HFCS MIGHT BE PLAYING IN THE OBESITY EPIDEMIC. Also, IMO, I agree with the one blurb I cited that said the author personally chose to avoid the stuff until the data is more clear.


Jay, you have noted chicken consumption correlated with obesity. Two things. I'VE NOT SAID CORRELATION MEANS ANYTHING EXCEPT IT INDICATES HFCS COULD BE A VARIABLE. THAT IS NOT SAYING IT IS A VARIABLE. You are battling a straw man.

And two, regarding the appetite studies:

...showed no difference between HFCS and sucrose consumption on appetite and satiety across six studies.

I addressed this. The outcome measures and methodology in these studies are inconsistent. Again, IMO, I don't think one can say from the studies that they have thoroughly tested the relevant hypothesis of the effect of HFCS on appetite. Sometimes, even with 6 studies, one must look carefully at the actual data and ask oneself, does this really answer the question? In the rat studies the results were mixed, they were not conclusive. In the other studies there was not one that was long term, randomized, well controlled, and had an appropriately sized sample.

The substances in HFCS whose appetite-stimulating effects you're so concerned about amount to just 3–5% of HFCS, and are ordinary di- and oligosaccharides of glucose, which your own body produces during the digestion of starch. After eating a slice of toast, you'll find these same substances in your gut—at least briefly, as they are readily are broken down to glucose.

3-5% is not relevant, nor are anything else about the sugars because we cannot rule out so many variables like ratios, timing, direct effect on gut hormones that might not be the same as metabolite effects, and other unknowns. Unless you do the long term, well controlled, randomized clinical trial with an appropriate sample of people, one can draw tentative conclusions but one cannot be certain one's hypotheses about what is or is not the same about HFCS without a direct test.

There really is a ton of research on what does and does not affect appetite and it is not as simple as most people believe. A PubMed search on appetite regulation returns over 4,000 studies, reviews and commentaries. Do the same search adding HFCS and you get 2 hits. Tell me how that is enough research to call this one concluded?


Quad

SG, you seem to be mistaking me for someone who is arguing with you, although the tenor of your response is more that of someone who feels that their authority is being questioned.

Sorry, I'm mostly annoyed at me for allowing myself to be dragged back into this debate. I've been down this road before. The research is inadequate. It's not like global warming or evolution theory where the science is so overwhelming one can easily argue a position. And it's not my authority that is at issue, it is misrepresenting me as having drawn a conclusion about HFCS when I've said repeatedly I have not drawn a conclusion.

Rather, there is an underlying premise here that seriously oversimplifies the causes of obesity and I don't accept that premise. I have read lots of research on obesity. I have also argued with people in this forum who are ignorantly convinced that obesity is all about will power and overweight people 'choose' to consume more calories than they use.

It's like circumcision, abortion and the politics threads, there's so much collective baggage on the topics it's hard to have an evidence based discussion. Sometimes I'm up for it. Other times it's too time consuming.

 

[jt512]

I'VE NOT SAID CORRELATION MEANS ANYTHING EXCEPT IT INDICATES HFCS COULD BE A VARIABLE. THAT IS NOT SAYING IT IS A VARIABLE. You are battling a straw man.

No, I'm not "battling a straw man"; you're not listening. Correlation does not even indicate that HFCS "could be a variable." It means nothing at all. HFCS intake could, in principle, contribute to obesity whether the correlation between the population-level HFCS intake and the prevalence of obesity were any number between –1 and +1, including 0.

...showed no difference between HFCS and sucrose consumption on appetite and satiety across six studies.

I addressed this. The outcome measures and methodology in these studies are inconsistent.

And you think that's a negative? When studies using a variety of methodologies and outcome measures give consistent results about a hypothesis, that's usually considered to be a strength.

3-5% is not relevant, nor are anything else about the sugars because we cannot rule out so many variables like ratios, timing, direct effect on gut hormones that might not be the same as metabolite effects, and other unknowns. Unless you do the long term, well controlled, randomized clinical trial with an appropriate sample of people, one can draw tentative conclusions but one cannot be certain one's hypotheses about what is or is not the same about HFCS without a direct test.

You've just illustrated the classic criticism of the overly narrow approach to evidence-based medicine: every little hypothesis needs to be decided by a large-scale double-blind randomized controlled trial. There's little regard, if any at all, for the plausibility of the hypothesis or to the basic, underlying science.

There is not now, nor has there ever been, any good reason to suspect that HFCS intake is any more or less obesogenic via any mechanism, including an effect on appetite, than plain old table sugar, regardless of correlations with obesity, rats' preferences for maltose, the presence of impurities in HFCS, and whatever other red herrings that you can imagine "might" be the reason.

Large RCTs should be justified by plausibility of the hypothesis, and by evidence from smaller-scale trials or at least high-quality epidemiology. The HFCS–obesity hypothesis was never plausible in the first place, there is no good epidemiology supporting it, and the small-scale trials that have been conducted have failed to even hint at a connection.

Jay

 

[Skeptic Ginger]

No, I'm not "battling a straw man"; you're not listening.

Classic mistake, 'one is not convinced' does not equal, "not listening".

Correlation does not even indicate that HFCS "could be a variable." It means nothing at all.

You lose the evidence debate if this is your actual premise. I'll give you the benefit of the doubt and consider it hyperbole.

And you think that's a negative? When studies using a variety of methodologies and outcome measures give consistent results about a hypothesis, that's usually considered to be a strength.

You aren't about straw men? Seriously? Do you really think I said, "a variety of methodologies and outcome measures give consistent results about a hypothesis"?

That is not what I said. Try rereading my posts. Let me give you a hint: You have not paraphrased my argument correctly. You have paraphrased it in a way that fits your own narrative. That's what a straw man is.

You've just illustrated the classic criticism of the overly narrow approach to evidence-based medicine: every little hypothesis needs to be decided by a large-scale double-blind randomized controlled trial. There's little regard, if any at all, for the plausibility of the hypothesis or to the basic, underlying science.

Hostility toward evidence based medicine? Or are you still going with changing my argument to one easier for you to address?

There is not now, nor has there ever been, any good reason to suspect that HFCS intake is any more or less obesogenic via any mechanism, including an effect on appetite, than plain old table sugar, regardless of correlations with obesity, rats' preferences for maltose, the presence of impurities in HFCS, and whatever other red herrings that you can imagine "might" be the reason.

Large RCTs should be justified by plausibility of the hypothesis, and by evidence from smaller-scale trials or at least high-quality epidemiology. The HFCS–obesity hypothesis was never plausible in the first place, there is no good epidemiology supporting it, and the small-scale trials that have been conducted have failed to even hint at a connection.

Jay

I'm not asking you to invest in HFCS research. I don't have an interest. I can afford sucrose and don't need cheaper food. What benefit is there for me in consuming foods made with HFCS if I don't have an economic issue with sucrose?

 

[tyr_13]

There is no hypothetically plausible mechanism, no unexplained effect, and testing hasn't yielded a positive answer. That last part means that if there is some effect, it's too small to tell and thus a VERY small problem.

This is what I've got from reading Skeptic Ginger's post yet it's supposed to be some huge issue?

 

[quadraginta]

There is no hypothetically plausible mechanism, no unexplained effect, and testing hasn't yielded a positive answer. That last part means that if there is some effect, it's too small to tell and thus a VERY small problem.

This is what I've got from reading Skeptic Ginger's post yet it's supposed to be some huge issue?

That's sort of my take on it, although I don't feel that it does much good to single out SG.

What I find disturbing is the effect of forcing product ingredient choices on manufacturers and creating an entire industry of fear in the consumer population with such threadbare* evidence.







(* For very low values of "threadbare" that may include "absolutely none at all".)

 

[Skeptic Ginger]

There is no hypothetically plausible mechanism, no unexplained effect, and testing hasn't yielded a positive answer. That last part means that if there is some effect, it's too small to tell and thus a VERY small problem.

This is what I've got from reading Skeptic Ginger's post yet it's supposed to be some huge issue?

I'm not sure what you mean by huge issue.

There is a hypothetically plausible mechanism and that is an affect on appetite regulation.

There are not enough studies with consistent results and with outcome measures that support the conclusion that the effect is small. There are studies that look at outcome measures then draw conclusions which the measures do not support, and there are studies with mixed results. To claim this is the equivalent of conclusive evidence is akin to taking a small in vitro study and drawing a conclusion from it that you then claim applies to an in vivo study which has not been done.

 

[Skeptic Ginger]

....
What I find disturbing is the effect of forcing product ingredient choices on manufacturers and creating an entire industry of fear in the consumer population with such threadbare* evidence....

Just out of curiosity, given the fact the HFCS market is certainly not suffering, who/how is someone profiting from this "entire industry of fear in the consumer population"?

If you read Pollen's account, the corn subsidies paid for with tax dollars distorts the market resulting in the corn growers looking to create new markets for their corn. It's a spiral. Too much corn is grown. But when the price falls the government shores it up keeping corn more profitable than the market would make it. The producers then go creating a market for the crop and when they are successful, that makes farmers plant more corn and so the cycle goes.

One reason the corn sugar is so cheap is because of farm subsidies, not purely because of market forces. Even if you don't think there might be issues with appetite, there are issues with heavily marketing calories and distorting the free market forces. And that was how Pollen addressed the corn market's impact on our diets. I don't recall anything in the book about the evils of HFCS compared to sucrose.

 

[tyr_13]

I'm not sure what you mean by huge issue.

There is a hypothetically plausible mechanism and that is an affect on appetite regulation.

No, there isn't. The proposed mechanism is implausible and has not only not been show to work, has been shown not to work.

Stanhope, K.L., Griffen, S.C., Bair B.R., Swarbrick M.M., Keim N.L., Havel P.J. "Twenty-four-hour endocrine and metabolic profiles following consumption of high-fructose corn syrup-, sucrose-, fructose-, and glucose-sweetened beverages with meals." The American Journal of Clinical Nutrition. 1 May 2008, Volume 87, Issue 5: 1194-1203.

There are not enough studies with consistent results and with outcome measures that support the conclusion that the effect is small. There are studies that look at outcome measures then draw conclusions which the measures do not support, and there are studies with mixed results. To claim this is the equivalent of conclusive evidence is akin to taking a small in vitro study and drawing a conclusion from it that you then claim applies to an in vivo study which has not been done.

If the effect can't be detected through the means already tried, yes, that does mean that it must be either small or masked.

 

[Skeptic Ginger]

No, there isn't. The proposed mechanism is implausible and has not only not been show to work, has been shown not to work.

Stanhope, K.L., Griffen, S.C., Bair B.R., Swarbrick M.M., Keim N.L., Havel P.J. "Twenty-four-hour endocrine and metabolic profiles following consumption of high-fructose corn syrup-, sucrose-, fructose-, and glucose-sweetened beverages with meals." The American Journal of Clinical Nutrition. 1 May 2008, Volume 87, Issue 5: 1194-1203.




If the effect can't be detected through the means already tried, yes, that does mean that it must be either small or masked.

Are you incapable of posting a link?

It's not like it wasn't available.

Thirty-four men and women consumed 3 isocaloric meals with either sucrose- or HFCS-sweetened beverages, and blood samples were collected over 24 h. Eight of the male subjects were also studied when fructose- or glucose-sweetened beverages were consumed.

Results:In 34 subjects, 24-h glucose, insulin, leptin, ghrelin, and TG profiles were similar between days that sucrose or HFCS was consumed. Postprandial TG excursions after HFCS or sucrose were larger in men than in women. In the men in whom the effects of 4 sweeteners were compared, the 24-h glucose and insulin responses induced by HFCS and sucrose were intermediate between the lower responses during consumption of fructose and the higher responses during glucose. Unexpectedly, postprandial TG profiles after HFCS or sucrose were not intermediate but comparably high as after pure fructose.

Conclusions:Sucrose and HFCS do not have substantially different short-term endocrine/metabolic effects. In male subjects, short-term consumption of sucrose and HFCS resulted in postprandial TG responses comparable to those induced by fructose.

(emphasis mine)

So what is it about "not long enough" and "too small a sample size" to draw a broad conclusion do you not understand?

Re the sample:

Thirty-four subjects (18 men and 16 women) with an age range of 20–50 y ( 34.7 ± 1.7 y) participated in the study. Participants were recruited through newspaper advertisements and underwent a telephone interview, a complete blood count, and a serum biochemistry panel to assess eligibility. Respondents with anemia, hepatic or renal disease, diabetes mellitus, fasting serum TG levels > 400 mg/dL, hypertension, eating disorders, or who had surgery for weight loss were excluded from the study. Individuals who smoked; who took thyroid, lipid-lowering, glucose-lowering, antihypertensive, antidepressant, or weight-loss medications; or who were pregnant or lactating were also excluded.

That is not a large scale or even a randomly selected from a large sample test population.

In addition if you would take a bit of time to read some of the >4,000 articles in a PubMed hit on appetite regulation that I linked to above you'd know that we don't know all the regulatory and feedback loops involved. So measuring 24 hour levels of glucose, insulin, leptin, ghrelin, and TG profiles is hardly all there is to appetite regulation.

Here, let me put it in the study author's words:

Studies to determine whether these high postprandial TG levels are sustained during long-term consumption of sucrose and HFCS are needed. Additional studies in women and in subjects with and without components of the metabolic syndrome, as well as dose-response studies, are needed to more fully understand the metabolic effects of fructose-containing sugars.

Your post illustrates the problem good skeptics who are out of their area of expertise often make. That is, taking pilot studies and assuming they are the same as large extensive studies with repeatedly found results when it comes to the predictive value of said results. This is especially true in areas of medical research. Even some of the best studies fail to find consistent outcomes with comparable 'best of' studies. You simply have to interpret these studies extremely cautiously.

 

[tyr_13]

Are you incapable of posting a link?

It's not like it wasn't available.(emphasis mine)

So what is it about "not long enough" and "too small a sample size" to draw a broad conclusion do you not understand?

Re the sample:That is not a large scale or even a randomly selected from a large sample test population.

In addition if you would take a bit of time to read some of the >4,000 articles in a PubMed hit on appetite regulation that I linked to above you'd know that we don't know all the regulatory and feedback loops involved. So measuring 24 hour levels of glucose, insulin, leptin, ghrelin, and TG profiles is hardly all there is to appetite regulation.

Here, let me put it in the study author's words:



Your post illustrates the problem good skeptics who are out of their area of expertise often make. That is, taking pilot studies and assuming they are the same as large extensive studies with repeatedly found results when it comes to the predictive value of said results. This is especially true in areas of medical research. Even some of the best studies fail to find consistent outcomes with comparable 'best of' studies. You simply have to interpret these studies extremely cautiously.

None of that makes the mechanism more plausible. It makes no bio-chemical sense as on absorption they are identical. You say results are mixed, but there are no mixed results.

Why do you believe this justify considering HFCS more dangerous than other caloric sweeteners? There is no evidence that it is, yet you urge caution. Only on the grounds that it hasn't been tested to you liking. You've been doing the skepticism thing a long time, long enough to know that making a claim based on nothing more than 'not enough research to rule it out' is going to be met with, well, skepticism.

Pilot studies are done to see if the effect is even worth pursuing. So far the answer has been, probably not. (Yes I know what the author of that study opined, but their own data doesn't support that conclusion.)