Thursday, September 18, 2008

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 pump glucose into the tissues 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.


The bottom line is that my glucose control seems good, so I don't know why my HbA1c is on the high side. Maybe I have a slow rate of erythrocyte turnover?

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.

Clean Eating: It Works for Us

Every now and then a new product comes along and I think, "Wow! What a great idea." Well, just this week I held in hand my first copy of the Oxygen publication "Clean Eating" magazine. The subtitle: Improving your life one meal at a time.Finally! A mainstream magazine we can use to support, benefit and enhance our post surgical weight loss surgery way of life.Have you seen it yet?I have in hand

Wednesday, September 17, 2008

Men and Weight Loss Surgery: Social Stigma?

We are having an interesting discussion on the Men & Weight Loss Surgery Message Board in the Neighborhood. Our new member ScottL, who is considering surgical weight loss. He presented statistics from the American Obesity Association that indicate men are not necessarily less obese than women, yet a significantly smaller population of men than women have obesity surgery. Scott asks the question

Monday, September 15, 2008

Evolution in Your Face

The debate between proponents of evolution and intelligent design (ID) rages on in certain parts of the US. It mostly centers around which one to emphasize, and whether to teach ID at all.

Here's how science is supposed to work: you get the best possible data, and then you create the most logical interpretation of it. I think all interpretations should be presented, including ID and antique scientific theories, but if we want to call it 'science class' then we shouldn't put on kid gloves for anything. The process of teaching science requires cultivating skepticism and independent thinking, and students should be allowed to come to their own conclusions with the facts in front of them.


What many people don't realize is that the facts point overwhelmingly toward evolution. Many American teachers have been tying their hands with the same wimpy anecdotes for decades. Evolution is not just about the fossil record and a few moths somewhere; it's a dynamic process that's happening around us at all times.

I'm constantly dealing with it in the lab. For example, sometimes by chance I'll create a mutant strain of yeast that grows slowly. I'll streak it out on a petri dish. Five days later, one out of twenty of the colonies growing on that plate will have mutated into faster-growing strains. These mutations are called 'suppressors' because they suppress slow growth. If I then take all the yeast on that plate and put them in liquid medium, by the next day, 99% of the cells will be of the faster-growing variety. The slow ones get left in the dust. That's natural selection.

Another example is antibiotic resistant bacteria. All you need is a selective pressure, in this case an antibiotic, and over time if an organism survives it will rise to the occasion. Bacteria are frighteningly rapid at adapting because there is a huge population of them and they have an extremely short generation time. But the same process applies to all organisms, usually on a longer timescale.


Science teachers should use the full repertoire of evidence supporting evolution, including allowing students to participate in natural selection experiments in yeast and bacteria. I think if students could
see evolution, if it became tangible for them, they would realize the debate is a charade. Believe ID if you wish, but don't call it science.

Sunday, September 14, 2008

After WLS: Not What I Was Expecting

I read and write a lot about weight loss surgery, and more importantly, LIVING after weight loss surgery. Recently I received an email from a disappointed post-surgical weight loss patient. This patient had only lost 10 (ten) pounds. She was discouraged and anxious. And she was 7 (seven) days post surgery ready to give the 5 Day Pouch Test a try since "the surgery did not work for her." How sad

Saturday, September 13, 2008

9 Years Post Weight Loss Surgery

Hello Neighbors!Today marks nine years since I was gut-whacked; uh, I mean had laporoscopic gastric bypass surgery in San Diego, California. Nine years. You know, some times I do not remember what it was like to be morbidly obese. Then again, most of the time I never forget what being overweight was like.A couple of days ago I bought a new pair of denium jeans: size 8. I was pretty disgusted with

Friday, September 12, 2008

Inactivity and Weight Gain

Every now and then I read a paper that restores a little bit of my faith in obesity research. Most of the papers I read in the field pay lip-service to the same tired old stories: thrifty genes; calories in, calories out; energy density; fat intake; gluttony and sloth. None of which make sense upon close examination. The "overweight is due to sloth" theory, in its many forms, is one of the most often repeated. The main evidence for it is that overweight people tend to move less than thin people, which seems to be true. Exercise also burns calories, which can come from fat.

It may sound counterintuitive, but how do we know that inactivity causes overweight and not the other way around? Gary Taubes asked this question in Good Calories, Bad Calories. 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.

I've pointed out before that the "we're fat because we exercise less" theory is probably incorrect. It's based on assumptions that fall apart on close examination. Exercise is healthy, but it's not the most effective way to achieve or maintain an optimal weight. The body compensates for the calories burned during exercise by a phenomenon known as "hunger". Certain obesity researchers have stubbornly tried to deny this, because it puts a kink in the "calories in, calories out" hypothesis, but anyone who has ever gotten out of their recliner knows it's true. I believe overweight is largely caused by diet composition. If that's the case, then changing diet composition is obviously going to be a more effective treatment than exercise, which doesn't address the root cause of the problem. This idea is supported by numerous diet intervention trials.