I wrote a long post, but I gave up. Too many ad hominems. So I'll start again but try to stick to the topic as best I can.
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Because of this well-known role of insulin, one of the more puzzling explanations offered by some – including a few respected scientists and medical professionals — for weight gain is that elevated insulin is to blame because of its involvement in “fat storage”. In addition, they argue that the reason why a diet lower in carbohydrates works for weight loss is because of reduced levels of the peptide hormone.
It’s an easy conclusion to make. The logic goes that carbohydrates through their stimulation of insulin are fattening beyond their contribution of energy as kilocalories. It doesn’t matter how much you eat, so long as you avoid carbs to lose weight.
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It can't be puzzling if it's an easy conclusion to make.
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Another growing belief floating mainly around fitness circles is that it’s best to forego foods containing carbs when heading to the gym. It’s for fear that the carbs’ action on insulin will squash fat burning stimulated by exercise. Then again, some low-carb proponents have also argued, physical activity as a means to expend energy for weight management is pointless altogether. Again, carbs are really all that matter because of their action on insulin.
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There's various reasons for this belief. The main reason is the effect of carbs on insulin sensitivity. As glycogen is depleted, cells becomes insulin sensitive. As cells are insulin sensitive, blood insulin level drops. As insulin level drops, its effect on fat tissue is thus less. Eating carbs would replete glycogen, causing cells to shut down insulin receptors, in turn causing blood insulin level to rise again, on top of the insulin spike we get just from eating carbs, with the ultimate greater effect on fat tissue. Makes sense to me.
Exercise makes us hungry, so we eat more. No exercise, less food intake, more weight lost. Also, since the goal is to lose weight, this means we're fat, and exercise is just harder to do when you're fat. Better to wait until we get leaner through low-carb, then do exercise at this point since it's now much easier. I see no problem with any of this.
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Where does all the extra energy from excess protein and fat go when overconsumed? And what about protein’s own effects in stimulating insulin or insulin’s role in promoting satiety? These questions are often overlooked or not easily answered by those that promote the “insulin is a fat storage hormone” proposition.
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No, they are just overlooked by you, so you can make a point that we're not that smart. What extra energy are you talking about? As far as I know, low-carb blunts hunger, so we eat less. If anything, we undereat. So your argument of "when they are overconsumed" is a red herring just to make a point. But to please the audience, we have a few experiments of overeating on low-carb, the latest I found is this:
http://www.dietdoctor.com/what-happ...on-an-lchf-diet
As he noted, his waist shrunk. So whatever excess he ate, most certainly did not go to belly fat. That should answer your red herring, Mr Science Writer.
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Out to help repair insulin’s reputation is obesity researcher Stephan Guyenet
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I'll pretend I didn't read that bit.
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Exercise researcher John Ivy, Ph.D., of the University of Texas, is in agreement that insulin is an often-misunderstood hormone and also makes the point that insulin’s specific action following meals does not relate to long-term fat storage. “The most important thing is calories burned in a day,” he comments.
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That's just not true. The nature of insulin does not change just because we're eating or we're fasting. To borrow a phrase from our CICO proponents, insulin is insulin is insulin. When insulin is high, the effect on fat tissue is the same regardless.
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As previously shared on this blog, Ivy emphasizes that understanding how to make the best use of insulin and carbohydrate can be critical for long-term weight management. The main reason is because of their support to muscle maintenance and growth. Ivy reminds that insulin’s role extends well beyond its action on promoting fatty acid synthesis. The hormone also both prevents protein breakdown and boosts protein synthesis in muscle. Although protein by itself promotes insulin’s release (again, often overlooked by low-carb proponents), carbohydrates can boost both these effects.
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That's so true. The functions of insulin go well beyond promoting fatty acid synthesis. Let's see, from
http://en.wikipedia.org/wiki/Insuli...ogical_effects:
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Physiological effects
The actions of insulin on the global human metabolism level include:
-Control of cellular intake of certain substances, most prominently glucose in muscle and adipose tissue (about two-thirds of body cells)
-Increase of DNA replication and protein synthesis via control of amino acid uptake
-Modification of the activity of numerous enzymes.
The actions of insulin (indirect and direct) on cells include:
-Increased glycogen synthesis – insulin forces storage of glucose in liver (and muscle) cells in the form of glycogen; lowered levels of insulin cause liver cells to convert glycogen to glucose and excrete it into the blood. This is the clinical action of insulin, which is directly useful in reducing high blood glucose levels as in diabetes.
-Increased lipid synthesis – insulin forces fat cells to take in blood lipids, which are converted to triglycerides; lack of insulin causes the reverse.[clarification needed (see talk)]
-Increased esterification of fatty acids – forces adipose tissue to make fats (i.e., triglycerides) from fatty acid esters; lack of insulin causes the reverse.
-Decreased proteolysis – decreasing the breakdown of protein
-Decreased lipolysis – forces reduction in conversion of fat cell lipid stores into blood fatty acids; lack of insulin causes the reverse.
-Decreased gluconeogenesis – decreases production of glucose from nonsugar substrates, primarily in the liver (the vast majority of endogenous insulin arriving at the liver never leaves the liver); lack of insulin causes glucose production from assorted substrates in the liver and elsewhere.
-Decreased autophagy - decreased level of degradation of damaged organelles. Postprandial levels inhibit autophagy completely.[30]
-Increased amino acid uptake – forces cells to absorb circulating amino acids; lack of insulin inhibits absorption.
-Increased potassium uptake – forces cells to absorb serum potassium; lack of insulin inhibits absorption. Insulin's increase in cellular potassium uptake lowers potassium levels in blood. This possibly occurs via insulin-induced translocation of the Na+/K+-ATPase to the surface of skeletal muscle cells.[31][32]
-Arterial muscle tone – forces arterial wall muscle to relax, increasing blood flow, especially in microarteries; lack of insulin reduces flow by allowing these muscles to contract.
-Increase in the secretion of hydrochloric acid by parietal cells in the stomach
-Decreased renal sodium excretion.
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Bolded the pertinent parts. Let's analyze this stuff. Basically, fuel and protein. What happens to all fuels? They all get stored. Glycogenesis, lipogenesis. Their release is inhibited. Glycogenolysis, lipolysis. Sure, protein synthesis and proteolysis are affected, which suggests we'll end up with bigger muscles. But here's the problem. All cellular functions require fuel, and all the fuels are being stored and their release is being inhibited. Nothing left for normal functions, like protein synthesis. What we really end up with is emaciation of lean tissue, and hypertrophy of fat tissue, all due to fuel partitioning from the global actions of insulin. And I'm not even a science writer.
There's one bit in there that struck me. It's "decreased autophagy". I've read that word before. Chaperone-mediated autophagy. That's the recycling of glycated protein inside cells, due to the action of ketones. And this means there's a bit missing in the Wikipedia list of things insulin does: Inhibition of ketogenesis at the liver and other cells capable of it. Ya, insulin inhibits the recycling of glycated protein inside cells (through its inhibition of ketogenesis at the liver), protein which could otherwise be used elsewhere, but ultimately end up gunking up the works inside cells.
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Diabetes researcher Joseph Henson, Ph.D., of University of Leicester, affirms that physical activity’s powerful effects on promoting insulin sensitivity makes it the “first line” of defense for prevention and treatment of insulin resistance. But while perhaps timing nutrients for after exercise may be best, he says that just getting any activity is what counts most. “A single bout of exercise can increase insulin sensitivity for at least 16 hours post exercise in healthy people as well as people with type 2 diabetes,” Henson comments.
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Ya, if you eat high-carb. But if you eat low-carb, low-carb is the first line of offense. As we restrict dietary carbohydrates, glycogen is depleted all the time, relatively speaking. This means all cells are insulin sensitive all the time. Exercise is just overkill at this point.
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On the other hand, the lack of activity, or general muscle contraction, Henson argues, can exacerbate insulin resistance and decrease insulin sensitivity, which are prerequisites for type 2 diabetes. Henson’s recent research suggests that probably more important than exercising regularly is simply avoiding staying sedentary for too long for cardiovascular health.
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Ya, that's true. But the primary prerequisite of diabetes type 2 is hyperglycemia. And the primary effect of dietary carbohydrates is hyperglycemia. Did somebody say "puzzling" earlier?
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In a review paper last year, Westerterp-Plantega (along with colleagues Sofie Lemmens and Klaas Westerterp) wrote that controlled trials have shown that the answer is that it is the relatively higher protein of the diets including Atkins, South Beach Diet, Paleo, etc., and not the relatively lower carbohydrate content that has led to the success of these approaches for weight loss. The reason is that dietary protein acts on three “metabolic targets”: it increases satiety, stimulates energy expenditure, and spares fat-free muscle (helping to maintain resting energy expenditure).
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How much more protein, exactly? The A-TO-Z study shows protein intake was the same in all diets tested. The bolded part, the same is true of dietary fat. It increases satiety due to its action on speed of digestion, stimulates energy expenditure due to its action on ketogenesis, and spares fat-free muscle due to its action on chaperone-mediated autophagy. Low-carb is inherently high-fat.
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Westerterp-Plantenga’s hypotheses are now supported further by a new study of which she was the lead author published earlier this year. The study compared two energy-restricted diets, one normal in protein (0.8g/kg/d) and one higher in protein (1.2g/kg/d) on 72 overweight and obese men and women. While both groups lost weight, as expected, the group that consumed more protein retained more muscle and had a higher resting metabolism (this was independent of physical activity).
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Low-carb is typically ad libitum. In spite of unrestricted caloric intake, low-carb produces better weight loss. How can we explain this by testing energy-restricted diets? In another study we discussed here (I forget which one exactly), Eout was higher with low-carb than with high-carb, with protein intake presumably remaining constant. Even with the A-TO-Z study, which didn't measure Eout, we must conclude that Eout was higher on Atkins, because it produced the greatest weight loss.