Saturday, May 17, 2008

US Fructose Consumption Trends

As you may have noticed, I suspect fructose is involved in overweight and other health problems. It seems to have adverse effects on fat deposition in the liver and insulin sensitivity that could be related to its association with weight gain. I looked through USDA estimated per capita consumption of different sweeteners to get an idea of how fructose consumption has changed in the US in the time since adult obesity rates have doubled.

In 1970, we ate an estimated 72.5 lb/year of cane and beet sugar (sucrose) per person, which is 50% fructose and 50% glucose. We also ate 0.4 lb/year of corn syrup, which is most commonly 55% fructose, 45% glucose. Consumption of other unspecified sweeteners was 12.0 lb/year, for a total intake of 84.9 lb/year of added sweeteners.

In 2007, we ate an estimated 44.2 lb/year of sucrose, 40.1 lb/year of corn syrup, and 12.9 lb/year of other unspecified sweeteners, for a
total added sweetener intake of 97.2 lb/year. Doing the math, and generously assuming that the "other" sweeteners are 100% honey (~50% fructose), here are the results:
  • 1970: 42.5 lb/year of added fructose.
  • 2007: 50.6 lb/year of added fructose.
At 19%, it's not a staggering increase, but it's definitely significant. I also think it's an underestimate, because it doesn't include fruit juice or total fruit consumption, both of which have increased. Other notable findings: grain intake has increased 41% between 1970 and 2005, due chiefly to rising consumption of processed wheat products. Added fats and oils have increased 63% in the same time period, with the increase coming exclusively from vegetable fats. The use of hydrogenated shortening has more than doubled.

What has caused the dramatic expansion of American waistlines in the last 30 years? No one knows for sure, but I think it's probably related to diet since the percentage of people who exercise has actually
increased in the same time period. My money is on the wheat and sugar, with possible contributions from hydrogenated oil, polyunsaturated vegetable oils and chemical pollutants. The reason is that wheat and sugar seem to have devastating metabolic effects on populations throughout the world, such as the Pima.


.^ said...

I've pondered this a bit myself. The HFCS thing seems a bit hard to pin down in that it's only marginally more fructose than ordinary sugar.

In New Zealand, where I live, morbid obesity is rare. Sure, "middle-aged spread" is common, including at my place, but the "epidemic" that I keep hearing about from the US is yet to reach our shores in its most virulent form.

Yet we eat plenty of sugar, and I have all my life. HFCS is not a major feature though since we don't produce or import much corn and cane sugar is readily available from, for instance, Fiji.

So that leads us back to HFCS as prime suspect for the US problem, but at only 5% more fructose ...?

Anyway, it doesn't seem to add up.

Stephan Guyenet said...

Hi Chainey,

I agree that the difference in fructose between sucrose and HFCS isn't very large. I just looked at the sweetener consumption stats for New Zealand and they're similar to the US. The Kuna also eat a fair amount of sugar and are healthy. So basically, I agree that the relationship is murky.

My guess is that fructose is probably not sufficient by itself to cause major problems, but acts synergistically with other elements of the diet to cause metabolic problems.

Do New Zealanders eat much processed food, or is it mostly homemade? Do they eat mostly animal or vegetable fats? Full-fat or low-fat milk? Do they eat a lot of wheat, and if so, in what form? If it's bread, does it tend to be sourdough?

We're going to get to the bottom of this!

.^ said...

I'm not sure I can assess NZers' diets objectively--My own diet since leaving home has bounced around between several extremes.

My guess would be that middle-class NZ families eat much like middle-class families in most other "Western" countries (US, Canada, Aus, NZ, Britain, etc.) with perhaps a bit less processed food.

For instance, I had never heard of "egg beaters" before a few weeks ago and was kind of amazed that such a product exists (people can't crack an egg?)

Stephan Guyenet said...

Well then I suppose the HFCS stands out. Do New Zealanders eat a lot of trans fat?

Oh yeah, egg beaters. That stuff is a crime against humanity. It's basically egg whites in a carton. It's more for getting rid of the cholesterol in the yolks than for convenience. I guess nobody told them egg yolks don't raise serum cholesterol...

Debs said...

"Crack an egg? Um, what's an egg?" - Average American

It sounds like the detrimental changes to our diet you're describing have arrived en masse -- increased fructose, sucrose, vegetable oil, wheat, chemical pollutants, processed foods and additives, etc.

Perhaps our bodies could have handled an increase in one such ingredient, but the combined effect overwhelms and shuts down the systems we have in place to compensate and regulate. Maybe HFCS/fructose is such a problem partly because of everything else we're eating, and partly because it's substantially detrimental enough to push us far past the tipping point.

Stephan Guyenet said...

That's about what I'm thinking as well.

Ronald Pottol said...

The author of Good Calories Bad Calories was thinking HFCS was a major cause of obesity when he started research, but he no longer believes that. It seems that it was more trying to cut down on dietary fat, and eating quite a lot more carbs as a result.

Stephan Guyenet said...

Hi Ronald,

You're right, Taubes doesn't really point the finger at HFCS. Don't get me wrong, I don't think fructose is THE culprit. Actually, I'm less convinced than ever after seeing that it's only increased by 20%. Although I will say that it's a hell of a correlation that HFCS consumption has increased by 700% in the same time period as the obesity epidemic explosion.

But I still think it has the potential to be a major contributor to health problems. The epidemic of nonalcoholic steatohepatitis (fatty liver) that's affecting the overweight in Amercia may have something to do with fructose. Overfeeding rats with fructose causes steatohepatitis. Once your liver is foie gras, you can forget about having good insulin sensitivity. I think it's all tied together.

Average fructose statistics also hide the fact that some people consume massive amounts of it in the form of soda, while others consume virtually none.

I think too much sugar is unhealthy, but it's probably not sufficient to cause massive metabolic problems without the aid of other problematic foods. The Kuna eat their fair share of sugar.

TedHutchinson said...

Excellent new free full text online research dealing the detrimental effects of HFCS and fructose.
Consuming fructose-sweetened, not glucose-sweetened, beverages increases visceral adiposity and lipids and decreases insulin sensitivity in overweight/obese humans

(a) The increase in VAT in subjects consuming fructose and the increase in the expression of lipogenic genes in SAT in subjects consuming glucose suggest that fructose and glucose have differential effects on regional adipose distribution. We believe that these results are novel and warrant further investigation.

(b) In addition to increases of postprandial TG and fasting and postprandial apoB, we show for what we believe is the first time that fructose consumption increases plasma concentrations of fasting sdLDL, oxidized LDL, and postprandial RLP-C and RLP-TG in older, overweight/obese men and women, whereas glucose consumption does not. These changes may be associated with increased risk of cardiovascular disease.

(c) Fructose consumption increased hepatic fractional DNL, and postprandial LPL activity was lower in subjects consuming fructose compared with those consuming glucose. These results suggest that both increased DNL and decreased LPL-mediated clearance contribute to fructose-induced postprandial hypertriglyceridemia.

(d) Consumption of fructose at 25% of energy requirements with an ad libitum diet decreased glucose tolerance and insulin sensitivity in older overweight/obese adults compared with glucose consumption.

(e) VAT accumulation and increases of 24-hour TG exposure, peak postprandial TG concentrations, and postprandial RLP-C concentrations in response to fructose consumption were more pronounced in men than in women. Consumption of sugar-sweetened beverages resulted in greater decreases in insulin sensitivity in women than in men.