OFFICE OF SCIENCE OUTREACH
DEPARTMENT OF BIOLOGY
Obesity, Type 2 Diabetes, and Fructose
Part 1: The Trends
Since the mid-1970's, Americans have been getting bigger. Not taller, just rounder. This is the "obesity epidemic." Of course, many Americans were overweight before that, but a larger percentage has become obese. The graph below shows a pretty clear change-in-slope at the "1976-1980" timepoint. We would like to know what happened at that time to cause this effect.
After 10-15 years, another alarming trend began. The incidence of Type 2 Diabetes began to increase. Data from the Centers for Disease Control illustrate this very clearly:
http://www.cdc.gov/diabetes/statistics/incidence/images/fig2.gif
Since that time, the incidence of Type 2 Diabetes has increased in parallel with the increase in obesity. In fact. obesity appears to be the single most important factor in developing Type 2 Diabetes.
http://farm2.static.flickr.com/1378/1212880595_7f7ae67524_o.jpg http://medicalmyths.files.wordpress.com/2008/07/diabetes-obesity-risk.gif?w=450&h=338 For over half a century, nutritional advice has been to limit our consumption of fat. The logic, reasonably enough, is that eating fat makes people fat. Furthermore, there is a good correlation between high-fat diets and heart disease. The food industry has done its share in trying to lower fat consumption, by developing low-fat and fat-free substitutes for higher-fat foods. Despite this, however, the USDA reports that from 1970 to 2003, Americans increased fat consumption by 63%, while also increasing grain consumption 43% and sugar consumption 19% -- as part of an overall increase of over 500 calories per day.
That's a lot of calories. In general, the increase in calories has come at a time when Americans are increasingly sedentary. It's no surprise that we gain weight, if we eat more food and exercise less.
But it may not be that simple.
Let's first look at US consumption of fats. The USDA has data:
In accord with dietary recommendations, Americans have cut back on the amount of animal fat we consume (saturated fat). We have increased the amount of poly-unsaturated fats (PUFAs), however. Most of the PUFAs are oils from plant seeds. Food processors seem to use oils from different plants more-or-less interchangeably, judging from the ingredient lists on a variety of products. They all have fairly similar profiles, however, being relatively rich in ω-6 fatty acids, and relatively poor in ω-3 fatty acids. These graphs would seem to absolve animal fat of blame for the obesity epidemic. Do they implicate plant oils?
[Note that the PUFA graph is in grams/day. We can convert it to pounds/year: 35 g/day = 28 pounds/yr. That's roughly twice as much fat as Americans ate in the first half of the 20th century, when the fat was almost all lard, bacon grease, and the like.]
We will need to return to this information. First, however, let's consider our increasing consumption of sugars:
From Johnson RJ et al, AJCN 2007; 86:899-906As it became easier and easier to purify and distribute sugar, we (and the British) clearly ate more of it. The striking increase in obesity comes only in recent decades, with the last 20% increase in sugar consumption. Does this absolve sugar of blame? Some would say yes, because in the early 1970's, the technology was developed to convert corn starch into glucose, and then use a simple enzyme treatment to convert glucose into fructose. With a bit more work, we get HFCS, high-fructose corn syrup. With the invention of HFCS, and the government-subsidy of the corn industry, HFCS became a cost-effective replacement for normal sugar, sucrose.
Apparently, the increase in sugar consumption since about 1975 has been due to HFCS. Could HFCS be the relevant factor in the obesity epidemic and consequent diabetes epidemic?
It is incredibly difficult to disentangle the relative contributions of different factors when there are many involved. It is also difficult when we are dealing with people and population-level data. People, unlike laboratory rats, tend to do what they want, and aren't eager to spend their lives eating a scientist's specified food pellets. Epidemiology produces correlations, but not direct cause-and-effect.
So, we have two correlations: an increase in fat consumption (primarily ω-6 fatty acids), and an increase in sugar consumption (primarily HFCS.) Can we use the methods of modern molecular biology to help us here?
The Trends Molecular Biology → Contact J. Jose Bonner, OSO Director
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