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.

Lessons From the Pima Indians

At 38% and climbing in 2006, the Pima indians (Akimel O'odham) of Arizona have the highest rate of diabetes of any population in the world. They also have staggering rates of obesity (~70%) and hypertension.

Things were very different for them before 1539, when the Spanish first made contact. They lived on an agricultural diet of beans, corn and squash, with wild fish, game meat and plants. As with most native people, they were thin and healthy while on their traditional diet.

In 1859, the Pima were restricted to a small fraction of their original land along the Gila river, the Pima Reservation. In 1866, settlers began arriving in the region and diverting the Gila river upstream of the reservation for their own agriculture. In 1869, the river went dry for the first time. 1886 was the last year any water flowed to the Pima Reservation in the Gila river.

The Pima had no way to obtain water, and no way to grow crops. Their once productive subsistence economy ground to a halt. Famine ensued for 40 desperate years. The Pima cut down their extensive mesquite forests to sell for food and water. Eventually, after public outcry, uncle Sam stepped in.

The government provided the Pima with subsidized "food": white flour, sugar, partially hydrogenated lard, and canned goods. They promptly became diabetic and overweight, and have remained that way ever since.

The Pima are poster children for mainstream nutrition researchers in the US for several reasons. First of all, their pre-contact diet was probably fairly low in fat, and researchers love to point out that they now eat more fat (comparable to the average American diet). Another reason is that there's another group of Pima in Mexico who still live on a relatively traditional diet and are much healthier. They are genetically very similar, supporting the idea that it's the lifestyle of the American Pima that's causing their problems. The third reason is that the Mexican Pima exercise more than the Arizona Pima and eat a bit less.

I of course agree with the conclusion that their lifestyle is behind their problems; that's pretty obvious. I think most Pima know it too. If they got their water back, maybe things would be different for them.

However, the focus on macronutrients sometimes obscures the fact that the modern Pima diet is pure crap. It's mostly processed food with a low nutrient density. It also contains the two biggest destroyers of indigenous health: white flour and sugar. There are numerous examples of cultures going from a high-fat diet to a lower-fat "reservation food" diet and suffering the same fate: the Inuit of Alaska, the Maasai and Samburu of Kenya, tribes in the Pacific Northwestern US and Canada, certain Aboriginal groups, and more. What do they all have in common? White flour, sugar and other processed food.

The exercise thing is somewhat questionable as well. True, Mexican Pima exercise 2.5 times more than Arizona Pima, but the Arizona Pima still exercise much more than the average American! Women clock in at 3.1 hours a week, while men come in at a whopping 12.1 hours a week! I am a bike commuter and weight lifter, and even I don't exercise that much. So forgive me if I'm a little skeptical of the idea that they aren't exercising enough to keep the weight off. 

The history of the Pima is a heart-wrenching story that has been repeated hundreds, perhaps thousands of times all over the world. Europeans bring in white flour, sugar and other processed food, it destroys a native populations' health, and then researchers either act like they don't understand why it happened, or give unsatisfying explanations for it.

The Pima are canaries in the coal mine, and we can learn a lot from them. Their health problems resemble those of other poor Americans (and wealthier ones also, to a lesser extent). This is because they are both eating similar types of things. The problem is creeping into society at large, however, as we rely more and more on processed wheat, corn, soy and sugar, and less on wholesome food. Obesity in the US has doubled in the past 30 years, and childhood obesity has tripled. Diabetes is following suit. Life expectancy has begun to diminish in some (poor) parts of the country. Meanwhile, our diet is looking increasingly like Pima reservation food. It's time to learn a lesson from their tragedy.

Your Gut Talks to Your Brain

I've been reading through some papers on a gut-brain connection that regulates food intake and blood nutrient balance. I've learned some interesting things.

First of all, when fat hits your small intestine (especially long-chain fatty acids), it sends a message to the brainstem via the vagus nerve. This rapidly inhibits eating behavior.

The hypothalamus can also inhibit glucose production by the liver in response to fat in the bloodstream, by sending it signals via the vagus nerve.

A recent paper that got me interested in all this showed that when you put fatty acids on the upper small intestine, it sends a signal to the brain, which then sends a signal to the liver, increasing insulin sensitivity and decreasing glucose production.

The upper small intestine is not just a passive nutrient sponge. It's a very active player in the body's response to food, coordinating changes in food intake and nutrient disposal.

Diabetes and Your Small Intestine

In the last post, I introduced you to the remarkable antidiabetic effect of gastric bypass surgery. It rapidly reverses diabetes in 83% of patients, and it seems to be due to bypassing the upper small intestine specifically, rather than caloric restriction. This points to a special role of the upper small intestine in regulating food metabolism. I told you I was going to look into the mechanism of why this effect happens, and here's the short answer:

It's complicated and no one understands it completely.

Now for the long answer. Nutrient homeostasis is very important and we have sophisticated ways of coordinating it among different tissues. Part of the small intestine's job is telling the body that nutrients are on their way into the bloodstream. Two ways it conveys this signal are by secreting hormones into the bloodstream, and by sending signals to the brain and liver via parasympathetic nerves.

The small intestine secretes dozens of hormones, one category of which is called the incretins. Incretins by definition increase the secretion of insulin by the pancreas, among other things. They were discovered when researchers realized that oral glucose elicits more of an insulin response than intravenous glucose. The reason is that cells in the upper small intestine secrete incretins when they detect glucose.

There are two known major incretin hormones that are secreted by the small intestine, GIP and GLP-1. There was a recent study by the lab of Blanca Olivan which looked into the levels of incretins in patients who had undergone Roux-en-Y gastric bypass, a common type in which 95% of the stomach and part of the upper small intestine is bypassed.

Their results are very interesting! Compared to controls losing an equivalent amount of weight on a low-calorie diet, the bypass patients saw a HUGE increase in their oral glucose tolerance test (OGTT) GLP-1 secretion (9.8 vs 112.5 pmol/L), a large increase in GIP secretion, and a corresponding increase in insulin secretion (575 vs 769 pmol/L). Two-hour OGTT blood glucose levels went from borderline diabetic to "normal", by American Diabetes Association standards. Fasting glucose and insulin dropped substantially. The bypass group gained considerable glucose control, better than the matched controls on a low-calorie diet.

It looks like part of the mechanism involves whipping the pancreas to produce more insulin in response to glucose. It also affected fasting insulin, although that could simply be due to calorie restriction because it went down in both groups. Interestingly, non-diabetic patients who get a Roux-en-Y bypass often get reactive hypoglycemia, where their pancreas overproduces insulin after a meal and they get dangerously low blood sugar. Dr Mary-Elizabeth Patti calls it "diabetes reversal in people who don't have diabetes". So the effect doesn't seem to be specific to people with diabetes.

There is some suggestion that the effect on incretins is due to bypassing the duodenum, which is part of the upper small intestine. Here's how the (very sophisticated) reasoning goes: when the duodenum doesn't get glucose dumped on it, that somehow increases release of incretins by the small intestine further along the line.

There's actually an antidiabetic drug that mimics GLP-1; it's called Byetta. There's another that inhibits the breakdown of GLP-1 called Januvia. A second effect of GLP-1 is to delay stomach emptying, which both drugs do. They have been effective for some diabetics.

Well this turned into a long post, so I'll follow up on the parasympathetic (nerve) signaling of the small intestine next time.

The Miracle Diabetes Cure You Don't Know About

What would you say if I told you there's a cure for type II diabetes that's effective in 83% of people, extremely rapid, and requires no lifestyle changes? Would you think I was crazy? Well maybe I am, but the cure exists nevertheless.

All it requires is a little intestinal mutilation. It's called gastric bypass surgery. It's an anti-obesity surgery where the digestive tract is re-routed, bypassing 95% of the stomach as well as the duodenum and jejunum, which are parts of the upper small intestine.

The effect was first reported in 1995 by Dr. Walter Pories. Initially, researchers thought the cure was simply from caloric restriction due to a smaller stomach volume, but since then the story has become much more interesting. The key finding was published in 2004 by Dr. Francesco Rubino, who showed that bypassing the duodenum and jejunum but not the stomach of type II diabetic rats was enough to cure their diabetes. The effect wasn't due to caloric restriction, since both groups ate the same amount of food.

What this suggests is that there's some kind of feedback coming from the upper small intestine that affects glucose control and insulin sensitivity. What could be causing it? It just so happens there are some pretty good candidates: hormones called GLP-1 and ghrelin.

I'm going to dive into this and see if I can figure out what's going on.

Sorry for the cheesy post title, I'm practicing for my best-seller. Maybe I should add the word "secret"? How about this: "101 Secret Diabetes Cures THEY Don't Want You to Know About".