January 17, 2008 presentation by Christopher Gardner for the Stanford School of Medicine Medcast lecture series. The case for low-carbohydrate diets is gaining weight. Christopher Gardner, PhD, assistant professor of medicine at the Stanford Prevention Research Center, has completed the largest and longest-ever comparison of four popular diets using real-world conditions, which he discusses – the lowest-carbohydrate Atkins diet came out on top. Stanford University School of Medicine: med.stanford.edu Stanford University Channel on YouTube: www.youtube.com
Video Rating: 4 / 5
So it seems if you are 30-34 bmi, with a gut, you might be insulin resistant, and you should really study Atkins for 8 weeks, and do the diet for a year. Also follow the water advice in case the upcoming study is right about the explanation for differences being the extra water. That’s what it “seems” to be saying.
I wish I had eaten low-carb long ago because, even anecdotally, I do have more energy. I was a good athlete but would have liked the extra energy to use. Nice study. I liked the part showing the effectiveness of Atkins on insulin resistant folks. I also liked how Atkins lowered all numbers for common risk measures for heart disease… even though the control group couldn’t hold to 15% carbs. It appears to be effective even if it isn’t followed exactly… especially if you are insulin resistant.
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I am interested in the formula he gave to see if you have insulin sensitivity. Is is triglycerides divided by HDL with a value of equal or more than 3?
@andrewpmack
None of that matters because it doesn’t work like that. The cause of obesity is not overeating. The cause of weight loss is not undereating. Obesity is a disorder of excess fat accumulation, not a disorder of overeating. So what controls fat accumulation?
The most probable answer: watch?v=M6vpFV6Wkl4
Full title: Authors@Google: Gary Taubes
At 20:00 Gardner says “if all groups had really cut back that many calories they would have all lost 40 lbs.” He attributes the discrepancy in weight loss to false reporting of calories consumed. However, this would require consistent false reporting in some groups but not others.
A better conclusion is that the calories burned in all 4 groups was not the same. The Atkins group had relatively more energy available while the other 3 groups had relatively less energy.
@ABL36
In all examples, the cause is hormones, the effect is activity level.
More T = more active
More insulin = less active
More GH = more active
From there, we can determine in advance who will become a successful athlete. With study and practice, we develop, improve and maintain skill. The more practice, the better the skills. Being leaner/stronger/taller means we get selected for the team, we get more practice time, we become successful athletes.
@ABL36
Growth hormone during child growth determines final adult height. The more GH, the taller we get. There’s a disorder called gigantism where the pituitary produces too much GH. A kid with more GH than another will grow taller, and will be selected for the basketball team. The shorter kid won’t. So, more GH, gets selected, gets more practice, becomes an athlete.
The cause is more GH, the effect is more practice.
@ABL36
If T is the primary factor for strength, what’s the primary factor for obesity? It’s a hormone: Insulin. Just like T and strength, the more insulin the more obesity. Just like T determines if we get selected for the team because of our strength, insulin determines if we get selected for the sprint team because of our leanness and obesity.
@ABL36
The same is true for strength competition. The stronger gets selected for the team, the weaker doesn’t. The cause is greater strength, the effect is more practice.
Strength is primarily a function of muscle mass, which is primarily a function of hormones, namely testosterone. The more T, the greater the muscle mass. We could say that the best athletes are those with the most T.
@ABL36
So what’s the cause and what’s the effect? Is obesity caused by sedentary behavior? In our fat vs lean sprinters, obesity is the cause (does not get selected for the sprint team), sedentary behavior is the effect (gets no practice on the track).
@ABL36
Consider hockey recruiting at a young age. The 10 year old is stronger, faster, smarter than the 9 year old. So when we select who plays, we select the 10 year old. The same is true with fat vs lean. The leaner will be faster, therefore he will be selected for the sprint team. If he’s selected, he will get more practice and eventually become an athlete. The fat kid will not be selected, will not get any practice, will not become an athlete.
@ABL36
“You can be an athlete and not look lean and you can be a non athlete and look lean by genetics.”
That’s correct. But the question wasn’t about athletes, but about lean vs fat. A lean sprinter will tend to be faster than a fat sprinter. Both are athletes, but the leaner of the two tends to win more competitions by virtue of being leaner, not by virtue of being an athlete.
@arrogantcoconut its not the scientists fault dude, its the freaking government. Only certain information is approved by the fucking FDA and a lot of it is old and is bull shit by now.