Agave Syrup

Anna brought up agave syrup in a comment on the last post, so I thought I'd put up a little mini-post so everyone can benefit from what she pointed out.

Agave syrup is made from the heart of the agave plant, which is pressed to release a juice rich in inulin. Inulin is a polymer made of fructose molecules. The inulin is then broken down either by heat or by enzymatic processing. The result is a sweet syrup that is rich in fructose.

Agave syrup is marketed as a healthy, alternative sweetener. In fact, it's probably as bad or worse than high-fructose corn syrup (HFCS). They are both a refined and processed plant extract. Both are high in fructose, with agave syrup leading HFCS (estimates of agave syrup range up to 92% fructose by calories). Finally, agave syrup is expensive and inefficient to produce.

The high fructose content gives agave syrup a low glycemic index, because fructose does not raise blood glucose. Unfortunately, as some diabetics learned the hard way, using fructose as a substitute for sucrose (cane sugar) has negative long-term effects on insulin sensitivity.

In my opinion, sweeteners come with risks and there is no free lunch. The only solution is moderation.

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How to Fatten Your Liver

Steatohepatitis is a condition in which the liver becomes inflamed and accumulates fat. It was formerly found almost exclusively in alcoholics. In the 1980s, a new condition was described called nonalcoholic steatohepatitis (NASH), basically steatohepatitis without the alcoholism. Today, NASH is thought to affect more than 2% of the adult American population. The liver has many important functions. It's not an organ you want to break.

This week, I've been reading about how to fatten your liver. First up: industrial vegetable oil. The study that initially sent me on this nerd safari was recently published in the Journal of Nutrition. It's titled "Increased Apoptosis in High-Fat Diet–Induced Nonalcoholic Steatohepatitis in Rats Is Associated with c-Jun NH₂-Terminal Kinase Activation and Elevated Proapoptotic Bax". Quite a mouthful. The important thing for the purpose of this post is that the investigators fed rats a high-fat diet, which induced NASH.

Anytime a study mentions a "high-fat diet", I immediately look to see what they were actually feeding the animals. To my utter amazement, there was no information on the composition of the high-fat diet in the methods section, only a reference to another paper. Apparently fat composition is irrelevant. Despite the fact that a high-fat diet from coconut oil or butter does not produce NASH in rats. Fortunately, I was able to track down the reference. The only difference between the standard diet and the high-fat diet was the addition of a large amount of corn oil and the subtraction of carbohydrate (dextrin maltose).

Corn oil is one of the worst vegetable oils. You've eaten corn so you know it's not an oily seed. To concentrate the oil and make it palatable, manufacturers use organic solvents, high heat, and several rounds of chemical treatment. It's also extremely rich in n-6 linoleic acid. The consumption of corn oil and other n-6 rich oils has risen dramatically in the US in the last 30 years, making them prime suspects in NASH. They have replaced the natural (more saturated) fats we once got from meat and milk.

Next up: fructose. Feeding rats an extreme amount of fructose (60% of calories) gives them nonalcoholic fatty liver disease (NAFLD), NASH's younger sibling, even when the fat in their chow is lard. Given the upward trend of US fructose consumption (mostly from high-fructose corn syrup), and the refined sugar consumed everywhere else (50% fructose), it's also high on my list of suspects.

Here's my prescription for homemade foie gras: take one serving of soybean oil fried french fries, a basket of corn oil fried chicken nuggets, a healthy salad drenched in cottonseed oil ranch dressing, and wash it all down with a tall cup of soda. It's worked for millions of Americans!

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A New Toy

I bought a new toy the other day: a blood glucose meter. I was curious about my post-meal blood glucose after my HbA1c reading came back higher than I was expecting. A blood glucose meter is the only way to know what your blood sugar is doing in your normal setting.

"Glucose intolerance" is the inability to effectively control blood glucose as it enters the bloodstream from the digestive system. It results in elevated blood sugar after eating carbohydrate, which is not a good thing. In someone with normal glucose tolerance, insulin is secreted in sufficient amounts, and the tissues are sufficiently sensitive to it, that blood glucose is kept within a fairly tight range of concentrations.

Glucose tolerance is typically the first thing to deteriorate in the process leading to type II diabetes. By the time fasting glucose is elevated, glucose intolerance is usually well established. Jenny Ruhl talks about this in her wonderful book Blood Sugar 101. Unfortunately, fasting glucose is the most commonly administered glucose test. That's because the more telling one, the oral glucose tolerance test (OGTT), is more involved and more expensive.

An OGTT involves drinking a concentrated solution of glucose and monitoring blood glucose at one and two hours. Values of >140 mg/dL at one hour and >120 mg/dL at two hours are considered "normal". If you have access to a blood glucose meter, you can give yourself a makeshift OGTT. You eat 60-70 grams of quickly-digesting carbohydrate with no fat to slow down absorption and monitor your glucose.

I gave myself an OGTT tonight. I ate a medium-sized boiled potato and a large slice of white bread, totaling about 60g of carbohydrate. Potatoes and bread digest very quickly, resulting in a blood glucose spike similar to drinking concentrated glucose! You can see that in the graph below. I ate at time zero. By 15 minutes, my blood glucose had reached its peak at 106 mg/dL.


My numbers were 97 mg/dL at one hour, and 80 mg/dL at two hours; far below the cutoff for impaired glucose tolerance. I completely cleared the glucose by an hour and 45 minutes. My maximum value was 106 mg/dL, also quite good. That's despite the fact that I used more carbohydrate for the OGTT than I would typically eat in a sitting. I hope you like the graph; I had to prick my fingers 10 times to make it! I thought it would look good with a lot of data points.

I'm going to have fun with this glucose meter. I've already gotten some valuable information. For example, just as I suspected, fast-digesting carbohydrate is not a problem for someone with a well-functioning pancreas and insulin-sensitive tissues. This is consistent with what we see in the Kitavans, who eat a high-carbohydrate, high glycemic load diet, yet are extremely healthy. Of course, for someone with impaired glucose tolerance (very common in industrial societies), fast-digesting carbohydrates could be the kiss of death. The big question is, what causes the pancreas to deteriorate and the tissues to become insulin resistant? Considering certain non-industrial societies were eating plenty of carbohydrate with no problems, it must be something about the modern lifestyle: industrially processed grains (particularly wheat), industrial vegetable oils, refined sugar, lack of fat-soluble vitamins, toxic pollutants and inactivity come to mind. One could make a case for any of those factors contributing to the problem.

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The Rise of Biodiesel Fuel

Aug. 29, 2008

Barack Obama Kicks Off Official Campaign with Bio diesel Plant Tour.
Presidential Candidate Affirms Commitment to Energy Independence and Green Jobs with an Acceptance Speech and Launching his Fall Campaign at Pennsylvania Biodiesel in Monaca, Pennsylvania.

JEFFERSON CITY, Mo.– Last night, millions watched as Sen. Barack Obama accepted the Democratic nomination for President. Today, one of his first stops as the official standard bearer of his party will be a tour of Pennsylvania Biodiesel, a plant located in Monaca, just outside Pittsburgh.

"America heard Sen. Obama's commitment to investment in biofuels and the opportunity for energy independence, a cleaner environment and good paying green jobs that our industry can deliver," said Joe Jobe, CEO of the National Biodiesel Board, from the association's headquarters in Missouri. "We're pleased biodiesel will play a significant role in the presidential campaign discussion. A strategy for helping Americans end our reliance on foreign oil should be a bipartisan goal."

Pat Copple, president of Pennsylvania Biodiesel, said that it is an honor to have Obama visit the plant. "We're eager not only to show Sen. Obama how biodiesel is made, but how it is a sustainable part of our energy solution right now," he said. "We hope he leaves with a strong understanding of how important continued federal support is, including extension of the biodiesel tax incentive."

Pennsylvania Gov. Edward Rendell and Sen. Robert Casey were also scheduled to attend. The state has taken a progressive approach in passing pro-biodiesel legislation. This year, Pennsylvania passed legislation to incentive's production, as well as a 2% mandate that takes effect one year after in-state production exceeds 40 million gallons.

"Sen. Obama made a wise choice to visit a Pennsylvania plant," said Ben Wootton, president of the Pennsylvania Biodiesel Producers Group. "Our state is on the cutting edge of producing the next wave of biofuels and encouraging Americans to make energy independence an achievable goal."

There are 171 biodiesel plants nationwide. Last year, the industry produced 500 million gallons of biodiesel. The NBB is the national trade association of the biodiesel industry and is the coordinating body for biodiesel research and development in the U.S. Its membership is comprised of biodiesel producers, state, national, and international feedstock and feedstock processor organizations, fuel marketers and distributors, and technology providers.

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Inactivity and Weight Gain

Most of the papers I read in the field pay lip-service to some familiar stories: thrifty genes; calories in, calories out; energy density; fat intake; gluttony and sloth.

It may sound counterintuitive, but how do we know that inactivity causes overweight and not the other way around?  In other words, isn't it possible that metabolic deregulation could cause both overweight and a reduced activity level? The answer is clearly yes. There are a number of hormones and other factors that influence activity level in animals and humans. For example, the "Zucker fatty" rat, a genetic model of severe leptin resistance, is obese and hypoactive (I wrote about it here). It's actually a remarkable facsimile of the metabolic syndrome. Since leptin resistance typically comes before insulin resistance and predicts the metabolic syndrome, modern humans may be going through a process similar to the Zucker rat.

Back to the paper. Dr. Nicholas Wareham and his group followed 393 healthy white men for 5.6 years. They took baseline measurements of body composition (weight, BMI and waist circumference) and activity level, and then measured the same things after 5.6 years. In a nutshell, here's what they found:

• Sedentary time associates with overweight at any given timepoint. This is consistent with other studies.


• Overweight at the beginning of the study predicted inactivity after 5.6 years.
  


• Inactivity at the beginning of the study was not associated with overweight at the end.

In other words, overweight predicts inactivity but inactivity does not predict overweight. With the usual caveat that these are just associations, this is not consistent with the idea that inactivity causes overweight. It is consistent with the idea that overweight causes inactivity, or they are both caused by something else.

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The Origins of HEALTH: The Sprouting of a Future

6. Crisis of Identity
Many vegans and vegetarian I know tell me that they got involved with “animal rights” only after they were first involved with human rights. For me, however, it was the opposite. Sometimes I joke that I came through “the backdoor” of the house of social justice. To me, “the environment” was the most important issue. Despite knowing relatively little about local ecosystems and plants as well as the principles of ecology, I thought I felt a deep connection and obligation toward this Other. Again, to me, all humans were equivalent to one another.

In the winter of 2004, the beginning of my second semester, a student would return to Beloit from her semester abroad and set my down a new path in life. Her name was Annie, a member of the OEC who had just returned from a field studies program in Tanzania. She was the second vegan that I knew personally—the first was Rachel, someone who I met during my first week at Beloit. After the first meeting of the semester, I chatted with her about her experiences in Tanzania and somehow the topics of animal rights came up. I told her I had always wanted to see how animals were treated before they were made into food, how they were slaughtered. She lent me a video, which I brought back to my dorm and placed into the VCR. One of my friends, who had just finished watching the Meatrix, decided to join me. In a way, I expected the film to inspire me to commit to vegetarianism—I wanted it too--,but I grievously underestimated the impact it would have on my life.
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The Origins of HEALTH: The Milieu of Modernity

3. The Misanthropic Defense
Somwhat ironically, I had become vegetarian because I cared about the individuality of animals, yet the token environmentalist in me was really just concerned about species—hence the irony in my desire to be a vegetarian hunter. In high school, I tried to rationalize myself out of animal activism. It wasn’t the individual that mattered, but the ecosystem. Thinking about individuals was narrow-minded. The big picture was what was important. These sentiments, however, I do not believe came out of some (ir)rational void; they had emerged from a very particular social milieu. These feelings of detachment from other individuals and the care I felt toward them never existed within the first year or so of going vegetarian.

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