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.

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

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

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.

Meet Charvie: My New Puppy

I try to focus this blog on weight loss surgery. But you know? I'm human and here is a really cool thing. We have brought home a new puppy and he is a sweetheart bundle of love. The following is from my personal journal September 3:The lights of our dog kennel building have been dark for two years, one month and two days. At twilight, on July 31, 2006 I shut the door to the building, not long

Delicious Wine Reductions for Cool Autumn Nights

So we've had weight loss surgery and are happily losing weight with a restricted diet and the improved ability to exercise. But you know, we didn't have taste bud surgery! We still have taste buds that crave delicious foods - we just want the foods we eat to be satiating and good for us.Let me tell you a culinary secret - it's in the wine! I'm not talking about wine in the glass, I'm talking

A Few Numbers

I went to the doctor's office recently to get some tests done, so I could get a biochemical window into my health. Here's what came back:

• Fasting insulin: 2.3 uIU/mL
• Fasting glucose: 88 mg/dL
• HbA1c: 5.8%
• Total cholesterol: 252 mg/dL
• HDL: 111 mg/dL
• LDL (calculated): 131 mg/dL
• Triglycerides: 48 mg/dL

I was thinking about not posting this for privacy reasons, but I think I'm an interesting enough case study to make it worthwhile.

I'll start from the top. The fasting insulin value is excellent; 2.3 is so low it's outside the "reference range" that's typically encountered. I don't have a trace of hyperinsulinemia, which implies a high degree of insulin sensitivity. I won't be developing metabolic syndrome anytime soon. My fasting blood glucose looks good, not much to say there.

The HbA1c reading is higher than I was hoping/expecting. It's "normal", but on the high end of normal. That could imply mild glucose intolerance. Perhaps a result of years of slamming myself with white flour and sugar. The other possibility is that my blood cells turn over more slowly than usual, which would artificially inflate the HbA1c number. I may buy a glucose meter so I can monitor my post-meal glucose. I wish I had HbA1c data from healthy non-industrial populations with which to compare. 5.8% does associate with a slightly higher risk of heart attack than 5% and below.

The lipid panel looks good. My total cholesterol is on the high side, mostly due to my extremely high HDL. My RN wrote "This is the highest HDL (high density lipoprotein, or 'good cholesterol') I've seen in 22 yrs of clinical practice!!" My triglycerides are very low, which also associates with low CVD risk. My LDL is on the high side, but it's probably the "non-atherogenic large, fluffy" LDL, judging by my HDL, triglyceride and insulin numbers. My triglyceride:HDL ratio and LDL:HDL ratio imply a low risk. Overall, the lipid panel looks very good to my eye.

However, I don't put a lot of faith in the predictive value of blood lipids. The studies that established links between blood lipids and CVD were typically performed in people eating the standard American diet. They don't necessarily imply the same risk in people eating an atypical diet like myself. Case in point, the Kitavans.

Here's a brief overview of my lifestyle:

• Diet, in descending order of calories: added fats like butter, lard, coconut oil and olive oil. Starchy foods like root vegetables, winter squash, legumes and quinoa (latter two always soaked 12-24 hours). Meat, organs and fish, wild or pasture-raised. Pasture-raised eggs. Soaked raw almonds and toasted hazelnuts. Fresh and fermented vegetables. Cheese, yogurt and raw milk. Fruit. Unsweetened chocolate. I estimate my macronutrient intake to be roughly 50% fat, 37% carbohydrate and 13% protein.
  
• Exercise: I cycle commute 30 minutes a day, lift weights briefly 2-3 times a week, sprint once a week, and hike regularly.
• Meditation: several times a week.
• Sleep: 8.5 to 9 hours almost every night.
• Assorted hormesis: weekly 24-hour fast, exercise, cold water swims, sauna.
• Good friends, family, community, relaxation.
  

Here are a few things I'm taking from this:

• I eat a LOT of saturated fat, yet my risk of heart attack is probably very low.
  
• A diet high in saturated fat that includes carbohydrate is compatible with excellent insulin sensitivity, at least in the context of an otherwise good lifestyle.
• I should look into my post-meal blood sugar.