(credit to Dylan and Woo, respectively, for introducing me to those terms)
Empty calories – the potato.
While it has a decent amino acid profile, with only 3 grams of protein it’d take a diabetic amount of potatoes to fulfill your daily protein. By “diabetic,” I mean about a thousand grams of starch. potatoes are just as glycemic as white bread.
Posted in Advanced nutrition, diet, Dietary fat, empty calories, Energy balance, fat, gluten, Grains, insulin, mortality
Tagged Atkins, body composition, calories, carbs, diet, empty calories, energy expenditure, fat, insulin, mortality, obesity, sugar
This isn’t a “magic bullet,” it’s a buckshot aimed at a barn door.
Yes, I think sugar and empty calories
Make no mistake, diabulemia may as well be spelled DIE-abulemia. It’s not a laughing matter. But yeah, well, lemonade, etc. So here it goes
Type I diabetics have low insulin and are lean; type II diabetics have high insulin and are not. Insulin injections in either population promotes hyperplastic fat growth. Sounds scary, right? It is:
This poor soul unfortunately restricted his insulin injections to only two sites. Make all the jokes you want, but the effect is obvious… this is happening everywhere in hyperinsulinemic heavyweights (not just two specific sites).
So what do Type I’s do when they want to lose some fat mass? Stop jabbing themselves with insulin. Unfortunately, it’s really that simple. Type II’s and anyone with excess or hyperplastic fat tissue can do the same with low carb or keto, although this would be a great benefit to their overall health. But for Type I’s… not so much – they need insulin to prevent the horrific manifestations of ketoacidosis, which includes but is not limited to: death.
Type I’s are hyperglycemic because of low insulin; insulin therapy prevents diabetic ketoacidosis, a deadly condition
Type II’s are hyperglycemic because of insulin resistance; a condition that is pathologically neutered via carbohydrate restriction. Type I’s who reduce insulin injections to decrease fat mass are doing just as much damage as Type II’s who DON’T reduce carbohydrate intake.
Diabulemia is akin to an eating disorder. Biologically, the lack of insulin allows fat to be released from adipose tissue with gravitas, and it prevents glucose from being stored in any meaningful capacity. You’re literally pissing calories here, burning ‘em like crazy there; all of which is a helluva lot easier than “eating less moving more” … which is why diabulemics do it (because they have the option [unlike the rest of us]). Diabulemia is good from a fat loss perspective, but will most definitely contribute to severe and possibly deadly complications down the line. Carbohydrate restriction, however, is a win-win-win… (for everyone except The Man, so perhaps it’s a win-win-win… fail)
This isn’t a “magic bullet,” it’s a buckshot aimed at a barn door.
Humans aren’t big rats, but here it is again, anyway:
Leptin deficiency causes insulin resistance induced by uncontrolled diabetes (German et al., 2010)
I’m ignoring the brunt of this paper and only focusing on the positive control groups. [Positive controls… meaning they were included because they would definitely exhibit the expected response.]
Force rats into a state of diabulemia, and their insulin levels plummet, blood glucose soars, and they become ravenously hungry (open squares in the graphs below).
But lo and behold, fat mass atrophy ->
Eat less move more? Well, they certainly didn’t “eat less…” (see above) … and:
nor were they “moving more.” Low insulin seems to have a way to bypass that whole “eat less move more” thing (eg, Metabolic rate per se).
Throwing the baby out with the bathwater works if the baby is fat and the bathwater is insulin. (no, not a fat baby.)
Posted in Advanced nutrition, diet, Dietary fat, empty calories, Energy balance, fat, insulin, Ketosis, TPMC
Tagged Atkins, body composition, calories, carbs, diabetes, diet, empty calories, energy balance, energy expenditure, insulin, mortality, obesity, sugar
Insulin is there to grow fat tissue for the obesity epidemic, not replenish glycogen after yoga.
Teaser: insulin-induce hypoglycemia can get deadly quite fast, and there is no equivalent for the effects of insulin on fat. However, the effects of insulin on fat are 100 times more powerful.
Background: Hormone sensitive lipase (HSL) responds to insulin by inhibiting lipolysis. It halts fat burning. It got its name because it’s THEE most hormone-sensitive lipase in the body. The hormone about which we are speaking is of course insulin. And the enzyme, or at least one of the enzymes as it were, is HSL. To be clear, it takes very little insulin to inhibit HSL. Just a dollop, in fact.
Effect of very small concentrations of insulin on forearm metabolism. Persistence of its action on potassium and free fatty acids without its effect on glucose. (Zierler and Rabinowitz, 1964)
Expt 1. Since we’re all about jabbing people with insulin lately, let’s get at it again. Jab someone with about 100 uU (/min*kg), and muscle and fat vacuum glucose out of the blood. Same goes for potassium; and adipose gets all stingy too… it stops releasing and starts storing fat. This is “healthy,” and its part of why people say insulin, and by extension carbohydrate, causes lean people grow fat tissue.
What do you think would happen in an insulin resistant obese crowd. Less glucose vacuuming, but scrooge adipose will still responds with gravitas, by saving more and spending less? Likely. HSL is like the little piggy’s straw house. The strong young wolf can blow it down. The COPD emphysema wolf can blow it down… because it’s made of straw.
Thus, insulin causes lean people to grow fat tissue, and it causes obese people to grow more fat tissue.
In other words, with regard to common obesity, being resistant to insulin means postprandial hyperglycemia; you can’t handle sugars proper. but it’ll still make you fat(ter).
Expt 2. The interesting part. Try jabbing healthy people with 10x less insulin. Looks like IR obesity! Adipose gets stingy, potassium scrams, but no effect on glucose uptake.
In the figure below: A-DV is muscle; A-SV is adipose. Glucose uptake into fat & muscle is unaffected by a low dose of insulin.
Second figure: with the same dose, adipose goes on a budget SAVE MORE SPEND LESS
Conclusion. In a healthy person, (eg, 
), even very low doses of insulin cause fat growth. This isn’t an issue of high vs. low glycemic issue. The insulin dose used in this study was less than that expected from a respectable low glycemic index meal. This is probably why the glycemic index hasn’t cured the obesity epidemic. On the other hand, dietary fat doesn’t stimulate insulin… just sayin’
Furthermore, perhaps glucose uptake into adipose promotes fat storage under certain conditions, but it’s clearly neither necessary nor essential. Insulin can Miracle Grow fat mass without affecting glucose uptake one iota. I imagine the abundance of 3C precursors simply isn’t “the limiting factor.” And it works just as good with Whole Foods Low GI pa$ta and Wonderbread.
Translation: insulin buttresses fat growth. and it doesn’t matter how much. FYI this probably seems nonsensical at first: carbs stimulate insulin in order to dispose of said carbs, like a logical feedback mechanism. Perhaps. But said insulin cares far more about fat than said carbs. On a scale of 1 to 10 (ie, putting things into “perspective”): insulin is there to grow fat tissue for the obesity epidemic, not replenish glycogen after yoga.
Part II.
Dose-dependent effect of insulin on plasma free fatty acid turnover and oxidation in humans (Bonadonna et al., 1990)
There are a lot of data in this paper, but here are the relevant points:
Infuse insulin at various rates. In the lowest infusion rate, the only aspect of glucose metabolism to respond is hepatic glucose production (second line; HGP declines from 2.0 to 1.34 at the lowest dose):
WRT low dose insulin on glucose metabolism: liver responds, not skeletal muscle. Skeletal muscle doesn’t even look at glucose until insulin infusion reaches 250 – 500 uU, which is probably why back in ’64 they saw absolutely no effect at 10 uU. At 100 uU they saw an effect, but according to these data, it was likely due solely to liver, because skeletal muscle doesn’t seem to care until levels exceed 250 uU (it’s an infusion rate, not an absolute concentration. But that’s neither here nor there). To be clear, 10 uU insulin infusion doesn’t affect glucose metabolism (1964). period. 100 uU modestly affects it (1964), and this is probably so modest because only liver is helping out (1990). At 500 uU, full scale attack on blood glucose.
But fatty acids are obliterated with 5 – 50 x less:
It worked with 10 uU in ’64, and it worked just as well with 100 uU in ’90. (FYI the first paper was published in 1964; this one in 1990).
Furthermore, in the table above glucose metabolism was progressively affected with increasing insulin concentrations. Not so much with FAs:
FA flux is rapidly and completely shut down with a dollop of insulin. Indeed, it is obliterated. Giving more insulin doesn’t do anything, because, well, when you blow down a straw house, it tends to stay down.
But first, a brief primer. In red.
“The glucose muscle-sparing effect of fat-derived fuels”
or, the Randle Cycle 2.0. it’s like a course in life enhancement.
Part I. Intermediary metabolism
The glucose-fatty acid cycle
The Randle Cycle, as originally proposed, states that fatty acid oxidation inhibits glucose oxidation. This is good because during starvation, every tissue than can survive on fatty acids instead of glucose should do so, sparing as much precious glucose as possible for the brain.
The glucose-sparing effect of fat-derived fuels
A critical vital horcrux to this is in the oh-so-humbly-disguised phrase “fat-derived fuels.” The fat-derived fuels are ketones, and they are rescuing the brain from starvation (ie, neuroglycopenia); they do so by supplementing glucose as a fuel source. Ketones are good at this; many tissues are happy to oxidize ketones when they are available.
The glucose muscle-sparing effect of fat-derived fuels
Ketones are derived from fat. During prolonged starvation, glucose comes from skeletal muscle amino acids (eg, alanine). Ketones spare glucose. Thus, ketones spare muscle. QED.
Posted in Advanced nutrition, diet, Dietary fat, Energy balance, insulin, Ketosis, Protein
Tagged Atkins, calories, carbs, energy balance, fat, hypoglycemia, insulin, ketosis, muscle, obesity, protein, sugar
What should you eat before the big feast? (hint: eggs.) And don’t try to compensate in advance by eating less, this will only make you hungrier. Furthermore, foods in your regular diet are probably healthier than holiday fare, so you definitely don’t want to eat fewer healthy foods to make room for empty calories.
Tip 1.
Variation in the effects of three different breakfast meals on subjective satiety and subsequent intake of energy at lunch and evening meal (Fallaize et al., 2012)
Participants were served only one of these for breakfast:
And given unlimited amounts of these for lunch and dinner:
Posted in Advanced nutrition, diet, Dietary fat, empty calories, Energy balance, Exercise, fat, insulin, Protein, Sugar
Tagged Atkins, body composition, calories, carbs, diet, empty calories, energy balance, energy expenditure, exercise, fat, insulin, obesity, protein, sugar
The faux-low carb mouse
Hyperinsulinemia drives diet-induced obesity blah blah blah (Mehran et al., 2012)
The researchers generated a mouse with half as much insulin as normal mice. Physiological insulin levels remain intact, but hyperinsulinemia is genetically inhibited. For the sake of simplicity, we’ll call them “InsKO.”
When fed a high fat diet, normal mice become markedly hyperinsulinemic (pink line) whereas InsKO mice maintain relatively normal insulin levels (red line). Blue lines are chow-fed mice; similar trend but less interesting.
divide and conquer
InsKO mice don’t get fat,
Posted in Advanced nutrition, diet, Dietary fat, empty calories, Energy balance, Exercise, fat, insulin, Sugar
Tagged body composition, calories, carbs, diabetes, diet, empty calories, energy balance, energy expenditure, exercise, fat, insulin, obesity, sugar
What is the biological impact of a history of obesity and weight loss? The metabolic trajectory of two calorically restricted skinny mice depends entirely upon whether or not they used to be fat. The end of this story might be: ‘Tis better to have lost and re-gained than never to have lost at all; or it’s just an interesting new take on the body weight set point theory.
Caloric restriction chronically impairs metabolic programming in mice (Kirchner et al., 2012)
divide and conquer
Part 1.
Study 1. Calorie restricted lean mice: the effect of diet composition.
Posted in Advanced nutrition, diet, Dietary fat, empty calories, Energy balance, fat, pair-feeding, Sugar
Tagged Atkins, body composition, calories, carbs, diet, energy balance, energy expenditure, fat, obesity, sucrose, sugar
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Admittedly, the effect of diet on metabolic rate is small (i.e. statistically non-significant in most cases), but its incredible consistency across space and time suggest it could be true. And given the difficulty of maintaining a reduced body weight after dieting, it might even be important. The following studies are examples of widely differing subject populations in various metabolic conditions; yet the effects of diet on metabolic rate exhibit a phenomenal degree of similarity.
disclaimer: I don’t know what’s more important – metabolic rate per se, the diet behind it, or the resulting hormonal adaptations. All of the diets that are associated with a higher metabolic rate are also predicted to result in lower insulin levels and higher fat oxidation. Thus, we are left with a triumvirate of diet, hormonal milieu, and energy expenditure… all of which are important for body composition and quality of life.
Posted in Advanced nutrition, diet, Dietary fat, Energy balance, Exercise, insulin, Protein
Tagged Atkins, body composition, carbs, energy balance, energy expenditure, exercise, fat, protein, sugar
Weight loss maintenance is not determined by calorie intake… or physical activity… but by The Laws of Energy Balance FTW!!!
Odd, the sensation I felt when reading this news release (gloating?). As reported at a meeting of the Obesity Society, results from the Utah Obesity Study of gastric bypass patients 2 and 6 years after surgery. By the 2 year mark, they lost over 100 pounds, or 36% of their starting weight (went from 296 to 189 pounds). Energy expenditure declined from 2201 to 1736 kcal/day. Food intake went from 2085 to 1638 kcal/day. (Hint: it’s no coincidence that energy expenditure and food intake declined to the exact same degree.) Physical activity and fitness levels increased.
By the 6 year mark, they still weighed 29% less than their starting weight. N.B. that’s an amazing level of success, it’s virtually unheard of in diet intervention studies. +1 for gastric bypass; -1 for nutrition.
Here’s what piqued my interest: during the gradual increase from 189 pounds to 210 pounds, which occurred between years 2 and 6 post-surgery, the most significant factor associated with weight regain was not calorie intake or physical activity… it was metabolic rate. This represents another fail for “eat less move more,” and a win for the Laws of Energy Balance.
So what’s this got to do with The poor, misunderstood calorie?
what we know about metabolic rate:
1) It’s invisible.
2) Fructose vs. The Laws of Energy Balance (circa December, 2011): sugar-sweetened beverages can cause fat gain, not by providing excess calories, but by reducing metabolic rate.
3) Holiday feasts, the freshman 15, and damage control (circa January 2012): overeating a high protein diet causes less fat gain than overeating anything else because it increases metabolic rate.
4) Missing: 300 kilocalories (circa July 2012): after losing weight, subjects assigned to the low carb diet maintained a higher metabolic rate than those on an isocaloric low fat diet.
“Eat less move more” is not the answer. But eating less sugar, more protein, and fewer carbs might be. Nutrition matters.
Posted in Advanced nutrition, diet, empty calories, Energy balance, gastric bypass, Protein, Sugar, TPMC
Tagged calories, carbs, diet, empty calories, energy expenditure, protein, sugar, trans fat
No more pretense or cute backstory; I just like reviewing ingredient profiles of protein bars. It’s a hobby of mine:
Candy in disguise, Op. 73 (circa April 2012)
Decepticon Promicor (soluble corn fiber), Op. 81 (June 2012)
Candy in disguise II, Op. 87 (July 2012)
Protein bar round-up, take II (September 2012)
See?
This is a review of Netrition’s “highest rated” bars. Important notes about this category: these are not necessarily “new” protein bars, or even the bars everyone buy (“best sellers”). They are the bars everyone who votes like the most. They’re not the healthiest either… but some come close.
Continue reading
Posted in Advanced nutrition, diet, Dietary fat, empty calories, fiber, gluten, Protein, Sugar, Uncategorized
Tagged almonds, artificial ingredients, carbohydrates, carbs, diet, empty calories, energy balance, inulin, prebiotics, processed food, protein, sugar
